diabetes care 2013

Introduction

The American Diabetes Association(ADA) has been actively involved inthe development and dissemination

of diabetes care standards, guidelines, andrelated documents for many years. Thesestatements are published in one or moreof the Association’s professional journals.This supplement contains the latest updateof the ADA’s major position statement,“Standards of Medical Care in Diabetes,”which contains all of the Association’s keyrecommendations. In addition, containedherein are selected position statements oncertain topics not adequately covered inthe “Standards.” ADA hopes that this is aconvenient and important resource for allhealth care professionals who care forpeople with diabetes.

ADA Clinical Practice Recommenda-tions consist of position statements thatrepresent official ADA opinion as denotedby formal review and approval by theProfessional Practice Committee and theExecutive Committee of the Board ofDirectors. Consensus reports and system-atic reviews are not official ADA recom-mendations; however, they are producedunder the auspices of the Association byinvited experts. These publications maybe used by the Professional Practice Com-mittee as source documents to update the“Standards.”

ADA has adopted the following def-initions for its clinically related reports.

ADA position statement. An officialpoint of view or belief of the ADA.Position statements are issued on scien-tific or medical issues related to diabetes.They may be authored or unauthored andare published in ADA journals and otherscientific/medical publications as appro-priate. Position statements must be re-viewed and approved by the ProfessionalPractice Committee and, subsequently,by the Executive Committee of the Boardof Directors. ADA position statementsare typically based on a systematic re-view or other review of published litera-ture. They are reviewed on an annual basisand updated as needed. A list of recent

position statements is included on p. e3 ofthis supplement.

ADA scientific statement. A scholarlysynopsis of a topic related to diabetes,which may or may not contain clinical orresearch recommendations. Any recom-mendations included represent the officialpoint of view or belief of the ADA. WorkGroup Reports fall into this category. Sci-entific statements are published in the ADAjournals and other scientific/medical pub-lications as appropriate. Scientific state-ments must be reviewed and approved bythe Professional Practice Committee and,subsequently, by the Executive Committeeof the Board of Directors. A list of recentscientific statements is included on p. e4 ofthis supplement.

Systematic review. A balanced reviewand analysis of the literature on a scien-tific or medical topic related to diabetes.Effective January 2010, technical reviewswere replaced by systematic reviews, forwhich a priori search and inclusion/exclusion criteria are developed and pub-lished. The systematic review provides ascientific rationale for a position state-ment and undergoes critical peer reviewbefore submission to the ProfessionalPractice Committee for approval. A listof past systematic reviews is included onp. e1 of this supplement.

Consensus report. A comprehensive ex-amination by a panel of experts (i.e., con-sensus panel) of a scientific or medicalissue related to diabetes. Effective January2010, consensus statements were re-named consensus reports. The categorymay also include task force and expertcommittee reports. Consensus reports donot have the Association’s name includedin the title or subtitle and include a dis-claimer in the introduction stating that anyrecommendations are not ADA position. Aconsensus report is typically developedimmediately following a consensus confer-ence at which presentations are made onthe issue under review. The statement

represents the panel’s collective analysis,evaluation, and opinion at that point intime based in part on the conferenceproceedings. The need for a consensusreport arises when clinicians or scientistsdesire guidance on a subject for which theevidence is contradictory or incomplete.Once written by the panel, a consensusreport is not subject to subsequent reviewor approval and does not represent officialAssociation opinion. A list of recent con-sensus reports is included on p. e2 of thissupplement.

Professional Practice Committee. TheAssociation ’s Professional PracticeCommittee is responsible for reviewingADA systematic reviews, scientific state-ments, and position statements, as wellas for overseeing revisions of the latter asneeded. Appointment to the Profes-sional Practice Committee is based onexcellence in clinical practice and/orresearch. The committee comprisesphysicians, diabetes educators, regis-tered dietitians, and others who haveexpertise in a range of areas, includingadult and pediatric endocrinology, epi-demiology, and public health, lipidresearch, hypertension, and preconcep-tion and pregnancy care. All members ofthe Professional Practice Committee arerequired to disclose potential conflictsof interest (listed on p. S109).

Grading of scientific evidence. Therehas been considerable evolution in theevaluation of scientific evidence and inthe development of evidence-based guide-lines since the ADA first began publishingpractice guidelines. Accordingly, we de-veloped a classification system to grade thequality of scientific evidence supportingADA recommendations for all new andrevised ADA position statements.

Recommendations are assigned rat-ings of A, B, or C, depending on thequality of evidence (Table 1). Expertopinion (E) is a separate category forrecommendations in which there is asyet no evidence from clinical trials, inwhich clinical trials may be impractical,or in which there is conflicting evidence.Recommendations with an “A” rating arebased on large well-designed clini-cal trials or well-done meta-analyses.

c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c c

DOI: 10.2337/dc13-S001© 2013 by the American Diabetes Association. Readers may use this article as long as the work is properly

cited, the use is educational and not for profit, and thework is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

care.diabetesjournals.org DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 S1

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Generally, these recommendations havethe best chance of improving outcomeswhen applied to the population to whichthey are appropriate. Recommendations

with lower levels of evidence may beequally important but are not as well sup-ported. The level of evidence supportinga given recommendation is noted either

as a heading for a group of recommenda-tions or in parentheses after a given rec-ommendation.

Of course, evidence is only one compo-nent of clinical decision making. Clinicianscare for patients, not populations;guidelines must always be interpretedwith the needs of the individual patientin mind. Individual circumstances,such as comorbid and coexisting dis-eases, age, education, disability, and,above all, patients’ values and prefer-ences, must also be considered and maylead to different treatment targets andstrategies. Also, conventional evidencehierarchies, such as the one adapted bythe ADA, may miss some nuances thatare important in diabetes care. Forexample, while there is excellent evi-dence from clinical trials supportingthe importance of achieving multiplerisk factor control, the optimal way toachieve this result is less clear. It isdifficult to assess each component ofsuch a complex intervention.

ADA will continue to improve andupdate the Clinical Practice Recommen-dations to ensure that clinicians, healthplans, and policymakers can continueto rely on them as the most authorita-tive and current guidelines for diabetescare. Our Clinical Practice Recom-mendations are also available on theAssociation’s website at www.diabetes.org/diabetescare.

Table 1dADA evidence-grading system for clinical practice recommendations

Level ofevidence Description

A Clear evidence from well-conducted, generalizable, randomized controlled trialsĆ that are adequately powered, including:

c Evidence from a well-conducted multicenter trialc Evidence from a meta-analysis that incorporated quality ratings in theĆ analysis

Compelling nonexperimental evidence, i.e., the “all or none” rule developed byĆ the Centre for Evidence-Based Medicine at OxfordSupportive evidence from well-conducted randomized controlled trials that areĆ adequately powered, including:

c Evidence from a well-conducted trial at one or more institutionsc Evidence from a meta-analysis that incorporated quality ratings in theĆ analysis

B Supportive evidence from well-conducted cohort studies, including:c Evidence from a well-conducted prospective cohort study or registryc Evidence from a well-conducted meta-analysis of cohort studies

Supportive evidence from a well-conducted case-control studyC Supportive evidence from poorly controlled or uncontrolled studies, including:

c Evidence from randomized clinical trials with one ormoremajor or Ćthree ormoreĆ minor methodological flaws that could invalidate the resultsc Evidence from observational studies with high potential for bias (such as caseĆ series with comparison to historical controls)c Evidence from case series or case reports

Conflicting evidence with the weight of evidence supporting the recommendationE Expert consensus or clinical experience

S2 DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 care.diabetesjournals.org

Introduction

http://www.diabetes.org/diabetescare

http://www.diabetes.org/diabetescare

Summary of Revisions for the 2013Clinical Practice Recommendations

Revisions to the Standardsof Medical Care inDiabetesd2013In addition to many small changes relatedto new evidence since the prior year, andto clarify recommendations, the follow-ing sections have undergone more sub-stantive changes:

c Section II.C. Screening for Type 1Diabetes has been revised to includemore specific recommendations.

c Section IV. Prevention/Delay of Type 2Diabetes has been revised to reflectthe importance of screening for andtreating other cardiovascular risk fac-tors.

c Section V.C.a. Glucose Monitoring hasbeen revised to highlight the need forpatients on intensive insulin regimensto do frequent self-monitoring of bloodglucose.

c Section V.D. Pharmacological andOverall Approaches to Treatment hasbeen revised to add a section with morespecific recommendations for insulintherapy in type 1 diabetes.

c Section V.F. Diabetes Self-ManagementEducation and Support has been revisedto be consistent with the newly revised

National Standards for Diabetes Self-Management Education and Support.

c Section V.K. Hypoglycemia has beenrevised to emphasize the need to assesshypoglycemia and cognitive functionwhen indicated.

c Section V.M. Immunization has beenupdated to include the new Centers forDisease Control and Prevention (CDC)recommendations for hepatitis B vac-cination for people with diabetes.

c Section VI.A.1. Hypertension/BloodPressure Control has been revised tosuggest that the systolic blood pressuregoal for many people with diabetes andhypertension should be ,140 mmHg,but that lower systolic targets (such as,130 mmHg) may be appropriate forcertain individuals, such as youngerpatients, if it can be achieved withoutundue treatment burden.

c Section VI.A.2. Dyslipidemia/LipidManagement and Table 10 have beenrevised to emphasize the importance ofstatin therapy over particular LDLcholesterol goals in high-risk patients.

c Section VI.B. Nephropathy Screeningand Treatment and Table 11 have beenrevised to highlight increased urinaryalbumin excretion over the terms

micro- andmacroalbuminuria, other thanwhen discussion of past studies requiresthe distinction.

c SectionVI.C. Retinopathy Screening andTreatment has been revised to includeanti–vascular endothelial growth factortherapy for diabetic macular edema.

c Section IX.A. Diabetes Care in theHospital has been revised to include arecommendation to consider obtainingan A1C in patients with risk factors forundiagnosed diabetes who exhibit hy-perglycemia in the hospital.

Revised Position Statementc The position statement “Diagnosis andClassification of Diabetes Mellitus” hasbeen revised slightly to add newer in-formation about monogenic forms ofdiabetes.

Revisions to the NationalStandards for DiabetesSelf-Management Educationand Supportc The task force report “National Standardsfor Diabetes Self-Management Educationand Support” represents a major revisioncompleted in 2012.





S U M M A R Y O F R E V I S I O N S



Executive Summary: Standards ofMedical Care in Diabetesd2013

Current criteria for thediagnosis of diabetesc A1C $6.5%. The test should be per-formed in a laboratory using a methodthat is NGSP certified and standardizedto the Diabetes Control and Compli-cations Trial (DCCT) assay; or

c fasting plasma glucose (FPG) $126mg/dL (7.0 mmol/L). Fasting is de-fined as no caloric intake for at least8 h; or

c 2-h plasma glucose $200 mg/dL (11.1mmol/L) during an oral glucose toler-ance test (OGTT). The test should beperformed as described by the WorldHealth Organization, using a glucoseload containing the equivalent of 75 ganhydrous glucose dissolved inwater; or

c in a patient with classic symptoms ofhyperglycemia or hyperglycemic crisis,a random plasma glucose $200 mg/dL(11.1 mmol/L);

c in the absence of unequivocal hyper-glycemia, result should be confirmedby repeat testing.

Testing for diabetes inasymptomatic patientsc Testing to detect type 2 diabetes andprediabetes in asymptomatic peopleshould be considered in adults ofany age who are overweight or obese(BMI $25 kg/m2) and who haveone or more additional risk fac-tors for diabetes (see Table 4 ofthe “Standards of Medical Care inDiabetesd2013”). In those withoutthese risk factors, testing should be-gin at age 45 years. (B)

c If tests are normal, repeat testing at leastat 3-year intervals is reasonable. (E)

c To test for diabetes or prediabetes, theA1C, FPG, or 75-g 2-h OGTT are ap-propriate. (B)

c In those identified with prediabetes,identify and, if appropriate, treat othercardiovascular disease (CVD) risk fac-tors. (B)

Screening for type 2diabetes in childrenc Testing to detect type 2 diabetes andprediabetes should be considered inchildren and adolescents who are over-weight and who have two or more ad-ditional risk factors for diabetes (seeTable 5 of the “Standards of MedicalCare in Diabetesd2013”). (E)

Screening for type 1diabetesc Consider referring relatives of thosewith type 1 diabetes for antibody test-ing for risk assessment in the settingof a clinical research study. (E)

Detection and diagnosisof gestational diabetesmellitusc Screen for undiagnosed type 2 diabetesat the first prenatal visit in those withrisk factors, using standard diagnosticcriteria. (B)

c In pregnant women not previouslyknown to have diabetes, screen forgestational diabetes mellitus (GDM)at 24–28 weeks of gestation, using a75-g 2-h OGTT and the diagnostic cutpoints in Table 6 of the “Standards ofMedical Care in Diabetesd2013.” (B)

c Screenwomenwith GDM for persistentdiabetes at 6–12 weeks postpartum,using the OGTT and nonpregnancydiagnostic criteria. (E)

c Women with a history of GDM shouldhave lifelong screening for the de-velopment of diabetes or prediabetes atleast every 3 years. (B)

c Women with a history of GDM foundto have prediabetes should receivelifestyle interventions or metformin toprevent diabetes. (A)

Prevention/delay of type 2diabetesc Patients with impaired glucose toler-ance (IGT) (A), impaired fasting glucose

(IFG) (E), or an A1C 5.7–6.4% (E)should be referred to an effective on-going support program targeting weightloss of 7% of body weight and in-creasing physical activity to at least 150min/week of moderate activity suchas walking.

c Follow-up counseling appears to beimportant for success. (B)

c Based on the cost-effectiveness of diabetesprevention, such programs should becovered by third-party payers. (B)

c Metformin therapy for prevention oftype 2 diabetes may be considered inthose with IGT (A), IFG (E), or an A1C5.7–6.4% (E), especially for those withBMI .35 kg/m2, aged ,60 years, andwomen with prior GDM. (A)

c At least annual monitoring for the de-velopment of diabetes in those withprediabetes is suggested. (E)

c Screening for and treatment of modifi-able risk factors for CVD is suggested. (B)

Glucose monitoringc Patients on multiple-dose insulin(MDI) or insulin pump therapy shoulddo self-monitoring of blood glucose(SMBG) at least prior to meals andsnacks, occasionally postprandially, atbedtime, prior to exercise, when theysuspect low blood glucose, after treat-ing low blood glucose until they arenormoglycemic, and prior to criticaltasks such as driving. (B)

c When prescribed as part of a broadereducational context, SMBG results maybe helpful to guide treatment decisionsand/or patient self-management forpatients using less frequent insulin in-jections or noninsulin therapies. (E)

c When prescribing SMBG, ensure thatpatients receive ongoing instructionand regular evaluation of SMBG tech-nique and SMBG results, as well astheir ability to use SMBG data to adjusttherapy. (E)

c Continuous glucosemonitoring (CGM)in conjunction with intensive insulinregimens can be a useful tool to lowerA1C in selected adults (aged$25 years)with type 1 diabetes. (A)

c Although the evidence for A1C loweringis less strong in children, teens, and





E X E C U T I V E S U M M A R Y



younger adults, CGMmay be helpful inthese groups. Success correlates with ad-herence to ongoing use of the device. (C)

c CGM may be a supplemental tool toSMBG in those with hypoglycemia un-awareness and/or frequent hypoglyce-mic episodes. (E)

A1Cc Perform the A1C test at least twotimes a year in patients who are meet-ing treatment goals (and who havestable glycemic control). (E)

c Perform the A1C test quarterly in pa-tients whose therapy has changed orwho are not meeting glycemic goals. (E)

c Use of point-of-care testing for A1Cprovides the opportunity for moretimely treatment changes. (E)

Glycemic goals in adultsc Lowering A1C to below or around 7%has been shown to reduce microvas-cular complications of diabetes, andif implemented soon after the di-agnosis of diabetes is associated withlong-term reduction in macrovasculardisease. Therefore, a reasonable A1Cgoal for many nonpregnant adults is,7%. (B)

c Providers might reasonably suggestmore stringent A1C goals (such as,6.5%) for selected individual pa-tients, if this can be achieved withoutsignificant hypoglycemia or other ad-verse effects of treatment. Appropriatepatients might include those with shortduration of diabetes, long life expec-tancy, and no significant CVD. (C)

c Less stringent A1C goals (such as,8%) may be appropriate for patientswith a history of severe hypoglycemia,limited life expectancy, advanced mi-crovascular or macrovascular compli-cations, extensive comorbid conditions,and those with long-standing diabetesin whom the general goal is difficult toattain despite diabetes self-managementeducation (DSME), appropriate glucosemonitoring, and effective doses ofmultiple glucose-lowering agents in-cluding insulin. (B)

Pharmacological and overallapproaches to treatmentInsulin therapy for type 1 diabetesc Most people with type 1 diabetes shouldbe treated with MDI injections (three tofour injections per day of basal andprandial insulin) or continuous sub-cutaneous insulin infusion (CSII). (A)

c Most people with type 1 diabetesshould be educated in how to matchprandial insulin dose to carbohydrateintake, premeal blood glucose, andanticipated activity. (E)

c Most people with type 1 diabetesshould use insulin analogs to reducehypoglycemia risk. (A)

c Consider screening those with type 1diabetes for other autoimmune dis-eases (thyroid, vitamin B12 deficiency,celiac) as appropriate. (B)

Pharmacological therapy forhyperglycemia in type 2 diabetesc Metformin, if not contraindicated andif tolerated, is the preferred initialpharmacological agent for type 2 di-abetes. (A)

c In newly diagnosed type 2 diabeticpatients with markedly symptomaticand/or elevated blood glucose levels orA1C, consider insulin therapy, with orwithout additional agents, from theoutset. (E)

c If noninsulin monotherapy at maximaltolerated dose does not achieve or main-tain the A1C target over 3–6 months,add a second oral agent, a glucagon-likepeptide-1 (GLP-1) receptor agonist, orinsulin. (A)

c A patient-centered approach should beused to guide choice of pharmacologi-cal agents. Considerations includeefficacy, cost, potential side effects,effects on weight, comorbidities, hy-poglycemia risk, and patient prefer-ences. (E)

c Due to the progressive nature of type 2diabetes, insulin therapy is eventuallyindicated for many patients with type 2diabetes. (B)

Medical nutrition therapyGeneral recommendationsc Individuals who have prediabetes ordiabetes should receive individualizedmedical nutrition therapy (MNT) asneeded to achieve treatment goals,preferably provided by a registered di-etitian familiar with the components ofdiabetes MNT. (A)

c Because MNT can result in cost-savingsand improved outcomes (B), MNTshould be adequately covered by in-surance and other payers. (E)

Energy balance, overweight, andobesityc Weight loss is recommended for alloverweight or obese individuals whohave or are at risk for diabetes. (A)

c For weight loss, either low-carbohydrate,low-fat calorie-restricted, or Mediterra-nean diets may be effective in the shortterm (up to 2 years). (A)

c For patients on low-carbohydrate di-ets, monitor lipid profiles, renal func-tion, and protein intake (in those withnephropathy) and adjust hypoglyce-mic therapy as needed. (E)

c Physical activity and behavior modifi-cation are important components ofweight loss programs and are mosthelpful inmaintenance ofweight loss. (B)

Recommendations for primaryprevention of type 2 diabetesc Among individuals at high risk fordeveloping type 2 diabetes, structuredprograms that emphasize lifestyle changesthat include moderate weight loss (7%bodyweight) and regular physical activity(150 min/week), with dietary strategiesincluding reduced calories and reducedintake of dietary fat, can reduce the riskfor developing diabetes and are thereforerecommended. (A)

c Individuals at risk for type 2 diabetesshould be encouraged to achieve theU.S. Department of Agriculture (USDA)recommendation for dietary fiber (14 gfiber/1,000 kcal) and foods contain-ing whole grains (one-half of grainintake). (B)

c Individuals at risk for type 2 diabetesshould be encouraged to limit theirintake of sugar-sweetened beverages(SSBs). (B)

Recommendations for managementof diabetesMacronutrients in diabetes managementc The mix of carbohydrate, protein, andfat may be adjusted to meet the meta-bolic goals and individual preferencesof the person with diabetes. (C)

c Monitoring carbohydrate, whether bycarbohydrate counting, choices, orexperience-based estimation, remainsa key strategy in achieving glycemiccontrol. (B)

c Saturated fat intake should be ,7% oftotal calories. (B)

c Reducing intake of trans fat lowers LDLcholesterol and increases HDL choles-terol (A); therefore, intake of trans fatshould be minimized. (E)

Other nutrition recommendationsc If adults with diabetes choose to usealcohol, they should limit intake to amoderate amount (one drink per dayor less for adult women and two drinksper day or less for adult men) and


Executive Summary

should take extra precautions to pre-vent hypoglycemia. (E)

c Routine supplementation with anti-oxidants, such as vitamins E and C andcarotene, is not advised because of lackof evidence of efficacy and concern re-lated to long-term safety. (A)

c It is recommended that individualizedmeal planning include optimization offood choices to meet recommended di-etary allowance (RDA)/dietary referenceintake (DRI) for all micronutrients. (E)

Diabetes self-managementeducation and supportc People with diabetes should receiveDSME and diabetes self-managementsupport (DSMS) according to NationalStandards for Diabetes Self-Manage-ment Education and Support whentheir diabetes is diagnosed and asneeded thereafter. (B)

c Effective self-management and qualityof life are the key outcomes of DSMEand DSMS and should be measuredand monitored as part of care. (C)

c DSME and DSMS should addresspsychosocial issues, since emotionalwell-being is associated with positivediabetes outcomes. (C)

c DSME and DSMS programs are ap-propriate venues for people with pre-diabetes to receive education andsupport to develop and maintain be-haviors that can prevent or delay theonset of diabetes. (C)

c Because DSME and DSMS can resultin cost-savings and improved out-comes (B), DSME and DSMS should beadequately reimbursed by third-partypayers. (E)

Physical activityc Adults with diabetes should be advisedto perform at least 150 min/week ofmoderate-intensity aerobic physicalactivity (50–70% of maximum heartrate), spread over at least 3 days/weekwith no more than 2 consecutive dayswithout exercise. (A)

c In the absence of contraindications,adults with type 2 diabetes should beencouraged to perform resistancetraining at least twice per week. (A)

Psychosocial assessmentand carec It is reasonable to include assessment ofthe patient’s psychological and socialsituation as an ongoing part of themedical management of diabetes. (E)

c Psychosocial screening and follow-upmay include, but are not limited to,attitudes about the illness, expectationsfor medical management and out-comes, affect/mood, general and di-abetes-related quality of life, resources(financial, social, and emotional), andpsychiatric history. (E)

c Screen for psychosocial problems suchas depression and diabetes-relateddistress, anxiety, eating disorders,and cognitive impairment when self-management is poor. (B)

Hypoglycemiac Individuals at risk for hypoglycemiashould be asked about symptomaticand asymptomatic hypoglycemia ateach encounter. (C)

c Glucose (15–20 g) is the preferredtreatment for the conscious individualwith hypoglycemia, although any formof carbohydrate that contains glucosemay be used. If SMBG 15 min aftertreatment shows continued hypogly-cemia, the treatment should be re-peated. Once SMBG glucose returns tonormal, the individual should con-sume a meal or snack to prevent re-currence of hypoglycemia. (E)

c Glucagon should be prescribed for allindividuals at significant risk of severehypoglycemia, and caregivers or familymembers of these individuals shouldbe instructed on its administration.Glucagon administration is not limitedto health care professionals. (E)

c Hypoglycemia unawareness or one ormore episodes of severe hypoglycemiashould trigger re-evaluation of thetreatment regimen. (E)

c Insulin-treated patients with hypogly-cemia unawareness or an episode ofsevere hypoglycemia should be advisedto raise their glycemic targets to strictlyavoid further hypoglycemia for at leastseveral weeks, to partially reverse hy-poglycemia unawareness, and to re-duce risk of future episodes. (A)

c Ongoing assessment of cognitive func-tion is suggestedwith increased vigilancefor hypoglycemia by the clinician,patient, and caregivers if low cognitionand/or declining cognition is found. (B)

Bariatric surgeryc Bariatric surgery may be considered foradults with BMI$35 kg/m2 and type 2diabetes, especially if the diabetes orassociated comorbidities are difficult tocontrol with lifestyle and pharmaco-logical therapy. (B)

c Patients with type 2 diabetes who haveundergone bariatric surgery need lifelonglifestyle support and medical monitor-ing. (B)

c Although small trials have shown gly-cemic benefit of bariatric surgery inpatients with type 2 diabetes and BMI30–35 kg/m2, there is currently in-sufficient evidence to generally recom-mend surgery in patients with BMI,35kg/m2 outside of a research protocol. (E)

c The long-term benefits, cost-effectiveness,and risks of bariatric surgery in in-dividuals with type 2 diabetes should bestudied in well-designed controlledtrials with optimal medical and lifestyletherapy as the comparator. (E)

Immunizationc Annually provide an influenza vaccineto all diabetic patients $6 months ofage. (C)

c Administer pneumococcal polysaccha-ride vaccine to all diabetic patients $2years of age. A one-time revaccinationis recommended for individuals .64years of age previously immunizedwhen they were,65 years of age if thevaccine was administered .5 yearsago. Other indications for repeat vac-cination include nephrotic syndrome,chronic renal disease, and other im-munocompromised states, such as af-ter transplantation. (C)

c Administer hepatitis B vaccination tounvaccinated adults with diabetes whoare aged 19 through 59 years. (C)

c Consider administering hepatitis B vac-cination to unvaccinated adults withdiabetes who are aged $60 years. (C)

Hypertension/bloodpressure control

Screening and diagnosisc Blood pressure should be measured atevery routine visit. Patients found tohave elevated blood pressure shouldhave blood pressure confirmed on aseparate day. (B)

Goalsc People with diabetes and hypertensionshould be treated to a systolic bloodpressure goal of ,140 mmHg. (B)

c Lower systolic targets, such as ,130mmHg, may be appropriate for certainindividuals, such as younger patients, ifit can be achieved without unduetreatment burden. (C)

c Patients with diabetes should be trea-ted to a diastolic blood pressure ,80mmHg. (B)


Executive Summary

Treatmentc Patients with a blood pressure.120/80mmHg should be advised on lifestylechanges to reduce blood pressure. (B)

c Patients with confirmed blood pressure$140/80 mmHg should, in addition tolifestyle therapy, have prompt initia-tion and timely subsequent titration ofpharmacological therapy to achieveblood pressure goals. (B)

c Lifestyle therapy for elevated blood pres-sure consists of weight loss, if overweight;Dietary Approaches to Stop Hyperten-sion (DASH)-style dietary pattern in-cluding reducing sodium and increasingpotassium intake; moderation of alcoholintake; and increasedphysical activity. (B)

c Pharmacological therapy for patientswith diabetes and hypertension shouldbe with a regimen that includes eitheran ACE inhibitor or an angiotensinreceptor blocker (ARB). If one class isnot tolerated, the other should besubstituted. (C)

c Multiple-drug therapy (two or moreagents at maximal doses) is generallyrequired to achieve blood pressuretargets. (B)

c Administer one or more antihyperten-sive medications at bedtime. (A)

c If ACE inhibitors, ARBs, or diureticsare used, serum creatinine/estimatedglomerular filtration rate (eGFR) andserum potassium levels should bemonitored. (E)

c In pregnant patients with diabetes andchronic hypertension, blood pressuretarget goals of 110–129/65–79 mmHgare suggested in the interest of long-term maternal health and minimizingimpaired fetal growth. ACE inhibitorsand ARBs are contraindicated duringpregnancy. (E)

Dyslipidemia/lipidmanagementScreeningc In most adult patients with diabetes,measure fasting lipid profile at leastannually. (B)

c In adults with low-risk lipid values(LDL cholesterol ,100 mg/dL, HDLcholesterol .50 mg/dL, and trigly-cerides,150mg/dL), lipid assessmentsmay be repeated every 2 years. (E)

Treatment recommendations andgoalsc Lifestyle modification focusing on thereduction of saturated fat, trans fat, andcholesterol intake; increase of n-3 fatty

acids, viscous fiber and plant stanols/sterols; weight loss (if indicated); andincreased physical activity should berecommended to improve the lipidprofile in patients with diabetes. (A)

c Statin therapy should be added to life-style therapy, regardless of baselinelipid levels, for diabetic patients:

c with overt CVD (A)c without CVDwho are over the age of40 years and have one or more otherCVD risk factors (family history ofCVD, hypertension, smoking, dysli-pidemia, or albuminuria). (A)

c For lower-risk patients than the above(e.g., without overt CVD and under theage of 40 years), statin therapy shouldbe considered in addition to lifestyletherapy if LDL cholesterol remainsabove 100 mg/dL or in those withmultiple CVD risk factors. (C)

c In individuals without overt CVD, thegoal is LDL cholesterol ,100 mg/dL(2.6 mmol/L). (B)

c In individuals with overt CVD, a lowerLDL cholesterol goal of ,70 mg/dL(1.8 mmol/L), using a high dose of astatin, is an option. (B)

c If drug-treated patients do not reachthe above targets on maximal toleratedstatin therapy, a reduction in LDLcholesterol of;30–40% from baselineis an alternative therapeutic goal. (B)

c Triglyceride levels ,150 mg/dL (1.7mmol/L) and HDL cholesterol .40mg/dL (1.0 mmol/L) in men and .50mg/dL (1.3 mmol/L) in women aredesirable (C). However, LDL choles-terol–targeted statin therapy remainsthe preferred strategy. (A)

c Combination therapy has been shownnot to provide additional cardiovascu-lar benefit above statin therapy aloneand is not generally recommended. (A)

c Statin therapy is contraindicated inpregnancy. (B)

Antiplatelet agentsc Consider aspirin therapy (75–162 mg/day) as a primary prevention strategy inthose with type 1 or type 2 diabetes atincreased cardiovascular risk (10-yearrisk .10%). This includes most menaged .50 years or women aged .60years who have at least one additionalmajor risk factor (family history ofCVD, hypertension, smoking, dyslipi-demia, or albuminuria). (C)

c Aspirin should not be recommendedfor CVD prevention for adults with

diabetes at low CVD risk (10-year CVDrisk,5%, such as inmen aged,50yearsand women aged ,60 years with nomajor additional CVD risk factors), sincethe potential adverse effects from bleed-ing likely offset the potential benefits. (C)

c In patients in these age-groups withmultiple other risk factors (e.g., 10-year risk 5–10%), clinical judgment isrequired. (E)

c Use aspirin therapy (75–162mg/day) as asecondary prevention strategy in thosewith diabetes with a history of CVD. (A)

c For patients with CVD and docu-mented aspirin allergy, clopidogrel (75mg/day) should be used. (B)

c Combination therapy with aspirin(75–162 mg/day) and clopidogrel (75mg/day) is reasonable for up to a yearafter an acute coronary syndrome. (B)

Smoking cessationc Advise all patients not to smoke or usetobacco products. (A)

c Include smoking cessation counselingand other forms of treatment as a routinecomponent of diabetes care. (B)

Coronary heart diseasescreening and treatmentScreeningc In asymptomatic patients, routinescreening for coronary artery disease(CAD) is not recommended, as it doesnot improve outcomes as long as CVDrisk factors are treated. (A)

Treatmentc In patients with known CVD, considerACE inhibitor therapy (C) and use as-pirin and statin therapy (A) (if notcontraindicated) to reduce the risk ofcardiovascular events. In patients with aprior myocardial infarction, b-blockersshould be continued for at least 2 yearsafter the event. (B)

c Avoid thiazolidinedione treatment in pa-tients with symptomatic heart failure. (C)

c Metformin may be used in patients withstable congestive heart failure (CHF) ifrenal function is normal. It should beavoided in unstable or hospitalizedpatients with CHF. (C)

Nephropathy screening andtreatmentGeneral recommendationsc To reduce the risk or slow the pro-gression of nephropathy, optimize glu-cose control. (A)


Executive Summary

c To reduce the risk or slow the pro-gressionof nephropathy, optimize bloodpressure control. (A)

Screeningc Perform an annual test to assess urinealbumin excretion in type 1 diabeticpatients with diabetes duration of $5years and in all type 2 diabetic patientsstarting at diagnosis. (B)

c Measure serum creatinine at least an-nually in all adults with diabetes re-gardless of the degree of urine albuminexcretion. The serum creatinine shouldbe used to estimate glomerular filtra-tion rate (GFR) and stage the levelof chronic kidney disease (CKD), ifpresent. (E)

Treatmentc In the treatment of the nonpregnantpatient with modestly elevated (30–299 mg/day) (C) or higher levels($300 mg/day) of urinary albuminexcretion (A), either ACE inhibitors orARBs are recommended.

c Reduction of protein intake to 0.8–1.0g/kg body wt per day in individualswith diabetes and the earlier stages ofCKD and to 0.8 g/kg body wt per dayin the later stages of CKD may improvemeasures of renal function (urine al-bumin excretion rate, GFR) and isrecommended. (C)

c When ACE inhibitors, ARBs, or diu-retics are used, monitor serum creati-nine and potassium levels for thedevelopment of increased creatinine orchanges in potassium. (E)

c Continued monitoring of urine albu-min excretion to assess both responseto therapy and progression of disease isreasonable. (E)

c When eGFR is ,60 mL/min/1.73 m2,evaluate and manage potential com-plications of CKD. (E)

c Consider referral to a physicianexperienced in the care of kidneydisease for uncertainty about the eti-ology of kidney disease, difficultmanagement issues, or advancedkidney disease. (B)

Retinopathy screening andtreatment

General recommendationsc To reduce the risk or slow the pro-gression of retinopathy, optimize gly-cemic control. (A)

c To reduce the risk or slow the pro-gression of retinopathy, optimize bloodpressure control. (A)

Screeningc Adults and children aged $10 yearswith type 1 diabetes should have aninitial dilated and comprehensive eyeexamination by an ophthalmologist oroptometrist within 5 years after theonset of diabetes. (B)

c Patients with type 2 diabetes shouldhave an initial dilated and compre-hensive eye examination by an oph-thalmologist or optometrist shortlyafter the diagnosis of diabetes. (B)

c Subsequent examinations for type 1and type 2 diabetic patients should berepeated annually by an ophthalmolo-gist or optometrist. Less frequent exams(every 2–3 years) may be consideredfollowing one or more normal eye ex-ams. Examinations will be requiredmore frequently if retinopathy is pro-gressing. (B)

c High-quality fundus photographs candetect most clinically significant di-abetic retinopathy. Interpretation ofthe images should be performed by atrained eye care provider. While retinalphotography may serve as a screeningtool for retinopathy, it is not a sub-stitute for a comprehensive eye exam,which should be performed at leastinitially and at intervals thereafter asrecommended by an eye care pro-fessional. (E)

c Womenwith pre-existing diabetes whoare planning pregnancy or who havebecome pregnant should have a com-prehensive eye examination and becounseled on the risk of developmentand/or progression of diabetic reti-nopathy. Eye examination should oc-cur in the first trimester with closefollow-up throughout pregnancy andfor 1 year postpartum. (B)

Treatmentc Promptly refer patients with any levelofmacular edema, severe nonproliferativediabetic retinopathy (NPDR), or anyproliferative diabetic retinopathy (PDR)to an ophthalmologist who is knowl-edgeable and experienced in the man-agement and treatment of diabeticretinopathy. (A)

c Laser photocoagulation therapy is in-dicated to reduce the risk of vision lossin patients with high-risk PDR, clini-cally significant macular edema, and insome cases of severe NPDR. (A)

c Anti–vascular endothelial growth fac-tor (VEGF) therapy is indicated for di-abetic macular edema. (A)

c The presence of retinopathy is not acontraindication to aspirin therapy forcardioprotection, as this therapy doesnot increase the risk of retinal hemor-rhage. (A)

Neuropathy screening andtreatmentc All patients should be screened fordistal symmetric polyneuropathy (DPN)starting at diagnosis of type 2 diabetesand 5 years after the diagnosis of type 1diabetes and at least annually thereafter,using simple clinical tests. (B)

c Electrophysiological testing is rarelyneeded, except in situations where theclinical features are atypical. (E)

c Screening for signs and symptoms ofcardiovascular autonomic neuropathy(CAN) should be instituted at diagnosisof type 2 diabetes and 5 years after thediagnosis of type 1 diabetes. Specialtesting is rarely needed and may notaffect management or outcomes. (E)

c Medications for the relief of specificsymptoms related to painful DPN andautonomic neuropathy are recom-mended, as they improve the quality oflife of the patient. (E)

Foot carec For all patients with diabetes, performan annual comprehensive foot exami-nation to identify risk factors predic-tive of ulcers and amputations. Thefoot examination should include in-spection, assessment of foot pulses,and testing for loss of protective sen-sation (LOPS) (10-g monofilamentplus testing any one of the following:vibration using 128-Hz tuning fork,pinprick sensation, ankle reflexes, orvibration perception threshold). (B)

c Provide general foot self-care educationto all patients with diabetes. (B)

c A multidisciplinary approach is rec-ommended for individuals with footulcers and high-risk feet, especiallythose with a history of prior ulcer oramputation. (B)

c Refer patients who smoke, have LOPSand structural abnormalities, or have ahistory of prior lower-extremity com-plications to foot care specialists forongoing preventive care and lifelongsurveillance. (C)

c Initial screening for peripheral arterialdisease (PAD) should include a historyfor claudication and an assessment ofthe pedal pulses. Consider obtainingan ankle-brachial index (ABI), as manypatientswith PAD are asymptomatic. (C)


Executive Summary

c Refer patients with significant claudica-tion or a positive ABI for further vascularassessment and consider exercise, med-ications, and surgical options. (C)

Assessment of commoncomorbid conditionsc For patients with risk factors, signs,or symptoms, consider assessmentand treatment for common diabetes-associated conditions (see Table 14 ofthe “Standards of Medical Care inDiabetesd2013”). (B)

Children and adolescentsc As is the case for all children, childrenwith diabetes or prediabetes should beencouraged to engage in at least 60 minof physical activity each day. (B)

Type 1 diabetesGlycemic controlc Consider age when setting glycemicgoals in children and adolescents withtype 1 diabetes. (E)

Screening and managementof chronic complications inchildren and adolescentswith type 1 diabetesNephropathyc Annual screening for microalbuminuria,with a random spot urine sample foralbumin-to-creatinine ratio (ACR), shouldbe considered once the child is 10years of age and has had diabetes for5 years. (B)

c Treatment with an ACE inhibitor, ti-trated to normalization of albumin ex-cretion, should be considered whenelevated ACR is subsequently con-firmed on two additional specimensfrom different days. (E)

Hypertensionc Blood pressure should be measured ateach routine visit. Children found tohave high-normal blood pressure orhypertension should have blood pres-sure confirmed on a separate day. (B)

c Initial treatment of high-normal bloodpressure (systolic or diastolic bloodpressure consistently above the 90thpercentile for age, sex, and height) in-cludes dietary intervention and exer-cise, aimed at weight control andincreased physical activity, if appro-priate. If target blood pressure is notreached with 3–6 months of lifestyleintervention, pharmacological treat-ment should be considered. (E)

c Pharmacological treatment of hyperten-sion (systolic or diastolic blood pressureconsistently above the 95th percentilefor age, sex, and height or consistently.130/80 mmHg, if 95% exceeds thatvalue) should be considered as soon asthe diagnosis is confirmed. (E)

c ACE inhibitors should be consideredfor the initial treatment of hypertension,following appropriate reproductivecounseling due to its potential tera-togenic effects. (E)

c The goal of treatment is a blood pres-sure consistently ,130/80 or belowthe 90th percentile for age, sex, andheight, whichever is lower. (E)

DyslipidemiaScreeningc If there is a family history of hyper-cholesterolemia or a cardiovascularevent before age 55 years, or if familyhistory is unknown, then considerobtaining a fasting lipid profile onchildren .2 years of age soon afterdiagnosis (after glucose control hasbeen established). If family history isnot of concern, then consider the firstlipid screening at puberty ($10 yearsof age). For children diagnosed withdiabetes at or after puberty, considerobtaining a fasting lipid profile soonafter the diagnosis (after glucose con-trol has been established). (E)

c For both age-groups, if lipids are ab-normal, annual monitoring is reason-able. If LDL cholesterol values are withinthe accepted risk levels (,100 mg/dL[2.6 mmol/L]), a lipid profile repeatedevery 5 years is reasonable. (E)

Treatmentc Initial therapy may consist of optimiza-tion of glucose control and MNT using aStep 2 American Heart Association(AHA) diet aimed at a decrease in theamount of saturated fat in the diet. (E)

c After the age of 10 years, the additionof a statin in patients who, after MNTand lifestyle changes, have LDL cho-lesterol .160 mg/dL (4.1 mmol/L) orLDL cholesterol .130 mg/dL (3.4mmol/L) and one or more CVD riskfactors is reasonable. (E)

c The goal of therapy is an LDL cholesterolvalue,100 mg/dL (2.6 mmol/L). (E)

Retinopathyc The first ophthalmologic examinationshould be obtained once the child is$10 years of age and has had diabetesfor 3–5 years. (B)

c After the initial examination, annual rou-tine follow-up is generally recommended.

Less frequent examinations may be ac-ceptable on the advice of an eye careprofessional. (E)

Celiac diseasec Consider screening children with type 1diabetes for celiac disease by measuringtissue transglutaminase or antiendo-mysial antibodies, with documentationof normal total serum IgA levels, soonafter the diagnosis of diabetes. (E)

c Testing should be considered in chil-dren with growth failure, failure to gainweight, weight loss, diarrhea, flatu-lence, abdominal pain, or signs ofmalabsorption or in children with fre-quent unexplained hypoglycemia ordeterioration in glycemic control. (E)

c Consider referral to a gastroenterolo-gist for evaluation with possible en-doscopy and biopsy for confirmation ofceliac disease in asymptomatic childrenwith positive antibodies. (E)

c Children with biopsy-confirmed celiacdisease should be placed on a gluten-freediet andhave consultationwith a dietitianexperienced in managing both diabetesand celiac disease. (B)

Hypothyroidismc Consider screening children with type1 diabetes for thyroid peroxidase andthyroglobulin antibodies soon afterdiagnosis. (E)

c Measuring thyroid-stimulating hormone(TSH) concentrations soon after diagnosisof type 1 diabetes, after metabolic controlhas been established, is reasonable. Ifnormal, consider rechecking every 1–2years, especially if the patient developssymptoms of thyroid dysfunction, thyro-megaly, or an abnormal growth rate. (E)

Transition from pediatric toadult carec As teens transition into emergingadulthood, health care providers andfamilies must recognize their manyvulnerabilities (B) and prepare the de-veloping teen, beginning in early tomid adolescence and at least 1 yearprior to the transition. (E)

c Both pediatricians and adult healthcare providers should assist in pro-viding support and links to resourcesfor the teen and emerging adult. (B)

Preconception carec A1C levels should be as close to normal aspossible (,7%) in an individual patientbefore conception is attempted. (B)


Executive Summary

c Starting at puberty, preconceptioncounseling should be incorporated inthe routine diabetes clinic visit for allwomen of childbearing potential. (C)

c Women with diabetes who are con-templating pregnancy should be eval-uated and, if indicated, treated fordiabetic retinopathy, nephropathy,neuropathy, and CVD. (B)

c Medications used by suchwomen shouldbe evaluated prior to conception, sincedrugs commonly used to treat diabet-es and its complications may be con-traindicated or not recommended inpregnancy, including statins, ACE in-hibitors, ARBs, and most noninsulintherapies. (E)

c Since many pregnancies are un-planned, consider the potential risksand benefits of medications that arecontraindicated in pregnancy in allwomen of childbearing potential andcounsel women using such medi-cations accordingly. (E)

Older adultsc Older adults who are functional, cog-nitively intact, and have significant lifeexpectancy should receive diabetescare with goals similar to those de-veloped for younger adults. (E)

c Glycemic goals for some older adultsmight reasonably be relaxed, using in-dividual criteria, but hyperglycemialeading to symptoms or risk of acutehyperglycemic complications shouldbe avoided in all patients. (E)

c Other cardiovascular risk factorsshould be treated in older adults withconsideration of the time frame ofbenefit and the individual patient.Treatment of hypertension is indicatedin virtually all older adults, and lipidand aspirin therapy may benefit thosewith life expectancy at least equal to thetime frame of primary or secondaryprevention trials. (E)

c Screening for diabetes complicationsshould be individualized in olderadults, but particular attention shouldbe paid to complications that wouldlead to functional impairment. (E)

Cystic fibrosis–relateddiabetesc Annual screening for cystic fibrosis–related diabetes (CFRD) with OGTTshould begin by age 10 years in allpatients with cystic fibrosis who do nothave CFRD (B). Use of A1C as a

screening test for CFRD is not recom-mended. (B)

c During a period of stable health, thediagnosis of CFRD can be made incystic fibrosis patients according tousual glucose criteria. (E)

c Patients with CFRD should be treatedwith insulin to attain individualizedglycemic goals. (A)

c Annual monitoring for complicationsof diabetes is recommended, beginning5 years after the diagnosis of CFRD. (E)

Diabetes care in the hospitalc All patients with diabetes admitted tothe hospital should have their diabetesclearly identified in the medical record.(E)

c All patients with diabetes should havean order for blood glucose monitoring,with results available to all members ofthe health care team. (E)

c Goals for blood glucose levels:c Critically ill patients: Insulintherapy should be initiated fortreatment of persistent hyperglyce-mia starting at a threshold of nogreater than 180mg/dL (10mmol/L).Once insulin therapy is started, aglucose range of 140–180 mg/dL(7.8–10 mmol/L) is recommendedfor the majority of critically illpatients. (A)

c More stringent goals, such as 110–140 mg/dL (6.1–7.8 mmol/L)may be appropriate for selectedpatients, as long as this can be ach-ieved without significant hypoglyce-mia. (C)

c Critically ill patients require an in-travenous insulin protocol that hasdemonstrated efficacy and safety inachieving the desired glucose rangewithout increasing risk for severehypoglycemia. (E)

c Non–critically ill patients: Thereis no clear evidence for specificblood glucose goals. If treated withinsulin, the premeal blood glucosetargets generally ,140 mg/dL (7.8mmol/L) with random blood glu-cose ,180 mg/dL (10.0 mmol/L)are reasonable, provided these tar-gets can be safely achieved. Morestringent targets may be appropri-ate in stable patients with previoustight glycemic control. Less strin-gent targets may be appropriatein those with severe comorbidi-ties. (E)

c Scheduled subcutaneous insulin withbasal, nutritional, and correction com-ponents is the preferred method forachieving and maintaining glucose con-trol in non–critically ill patients. (C)

c Glucose monitoring should be initiatedin any patient not known to be diabeticwho receives therapy associated withhigh risk for hyperglycemia, includinghigh-dose glucocorticoid therapy, ini-tiation of enteral or parenteral nutri-tion, or other medications such asoctreotide or immunosuppressive med-ications (B). If hyperglycemia is docu-mented and persistent, consider treatingsuch patients to the same glycemic goalsas patients with known diabetes. (E)

c A hypoglycemia management protocolshould be adopted and implementedby each hospital or hospital system. Aplan for preventing and treating hy-poglycemia should be established foreach patient. Episodes of hypoglycemiain the hospital should be documentedin the medical record and tracked. (E)

c Consider obtaining an A1C on patientswith diabetes admitted to the hospital ifthe result of testing in the previous 2–3months is not available. (E)

c Consider obtaining an A1C in patientswith risk factors for undiagnosed di-abetes who exhibit hyperglycemia inthe hospital. (E)

c Patients with hyperglycemia in thehospital who do not have a prior di-agnosis of diabetes should have ap-propriate plans for follow-up testingand care documented at discharge. (E)

Strategies for improvingdiabetes carec Care should be alignedwith componentsof the Chronic Care Model (CCM) toensure productive interactions betweena prepared proactive practice team andan informed activated patient. (A)

c When feasible, care systems shouldsupport team-based care, communityinvolvement, patient registries, andembedded decision support tools tomeet patient needs. (B)

c Treatment decisions should be timelyand based on evidence-based guide-lines that are tailored to individualpatient preferences, prognoses, andcomorbidities. (B)

c A patient-centered communicationstyle should be employed that in-corporates patient preferences, assessesliteracy and numeracy, and addressescultural barriers to care. (B)


Executive Summary

Standards ofMedical Care inDiabetesd2013AMERICAN DIABETES ASSOCIATION

D iabetes mellitus is a chronic illnessthat requires continuing medical careand ongoing patient self-management

education and support to prevent acutecomplications and to reduce the risk oflong-term complications. Diabetes care iscomplex and requires multifactorial riskreduction strategies beyond glycemic con-trol. A large body of evidence exists thatsupports a range of interventions to improvediabetes outcomes.

These standards of care are intendedto provide clinicians, patients, researchers,payers, and other interested individualswith the components of diabetes care,general treatment goals, and tools to eval-uate the quality of care. Although individ-ual preferences, comorbidities, and otherpatient factors may require modification ofgoals, targets that are desirable for mostpatients with diabetes are provided. Spe-cifically titled sections of the standardsaddress children with diabetes, pregnantwomen, and people with prediabetes.These standards are not intended to pre-clude clinical judgment or more extensiveevaluation and management of the patientby other specialists as needed. For moredetailed information about management ofdiabetes, refer to references (1–3).

The recommendations included arescreening, diagnostic, and therapeuticactions that are known or believed tofavorably affect health outcomes of patientswith diabetes. A large number of theseinterventions have been shown to be cost-effective (4). A grading system (Table 1),developed by the American Diabetes Asso-ciation (ADA) and modeled after existingmethods, was utilized to clarify and codifythe evidence that forms the basis for therecommendations. The level of evidencethat supports each recommendation islisted after each recommendation usingthe letters A, B, C, or E.

These standards of care are revisedannually by the ADA’s multidisciplinaryProfessional Practice Committee, incor-porating new evidence. For the currentrevision, committee members systemati-cally searched Medline for human stud-ies related to each subsection andpublished since 1 January 2011. Recom-mendations (bulleted at the beginningof each subsection and also listed inthe “Executive Summary: Standards ofMedical Care in Diabetesd2013”) wererevised based on new evidence or, insome cases, to clarify the prior recom-mendation or match the strength of thewording to the strength of the evidence.A table linking the changes in recom-mendations to new evidence can be re-viewed at http://professional.diabetes.org/CPR. As is the case for all positionstatements, these standards of care werereviewed and approved by the ExecutiveCommittee of ADA’s Board of Directors,which includes health care professionals,scientists, and lay people.

Feedback from the larger clinicalcommunity was valuable for the 2013revision of the standards. Readers whowish to comment on the “Standards ofMedical Care in Diabetesd2013” areinvited to do so at http://professional.diabetes.org/CPR.

Members of the Professional PracticeCommittee disclose all potential finan-cial conflicts of interest with industry.These disclosures were discussed at theonset of the standards revision meeting.Members of the committee, their em-ployer, and their disclosed conflicts ofinterest are listed in the “ProfessionalPractice Committee for the 2013 ClinicalPractice Recommendations” table (seep. S109). The ADA funds developmentof the standards and all its position state-ments out of its general revenues and

does not use industry support for thesepurposes.

I. CLASSIFICATION ANDDIAGNOSIS

A. ClassificationThe classification of diabetes includesfour clinical classes:

c Type 1 diabetes (results from b-celldestruction, usually leading to absoluteinsulin deficiency)

c Type 2 diabetes (results from a pro-gressive insulin secretory defect on thebackground of insulin resistance)

c Other specific types of diabetes due toother causes, e.g., genetic defects inb-cell function, genetic defects in in-sulin action, diseases of the exocrinepancreas (such as cystic fibrosis), anddrug- or chemical-induced (such as inthe treatment of HIV/AIDS or after or-gan transplantation)

c Gestational diabetes mellitus (GDM)(diabetes diagnosed during pregnancythat is not clearly overt diabetes)

Some patients cannot be clearly clas-sified as type 1 or type 2 diabetic. Clinicalpresentation and disease progression varyconsiderably in both types of diabetes.Occasionally, patients who otherwisehave type 2 diabetes may present withketoacidosis. Similarly, patients with type1 diabetes may have a late onset and slow(but relentless) progression of diseasedespite having features of autoimmunedisease. Such difficulties in diagnosis mayoccur in children, adolescents, andadults. The true diagnosis may becomemore obvious over time.

B. Diagnosis of diabetesFor decades, the diagnosis of diabetes wasbased on plasma glucose criteria, eitherthe fasting plasma glucose (FPG) or the2-h value in the 75-g oral glucose toler-ance test (OGTT) (5).

In 2009, an International ExpertCommittee that included representativesof the ADA, the International Diabetes


Originally approved 1988. Most recent review/revision October 2012.DOI: 10.2337/dc13-S011© 2013 by the American Diabetes Association. Readers may use this article as long as the work is properly



P O S I T I O N S T A T E M E N T

Federation (IDF), and the EuropeanAssociation for the Study of Diabetes(EASD) recommended the use of the A1Ctest to diagnose diabetes, with a thresholdof $6.5% (6), and the ADA adopted thiscriterion in 2010 (5). The diagnostic testshould be performed using a method thatis certified by the NGSP and standardizedor traceable to the Diabetes Control andComplications Trial (DCCT) reference as-say. Although point-of-care (POC) A1C as-says may be NGSP certified, proficiencytesting is not mandated for performingthe test, so use of these assays for diagnosticpurposes could be problematic.

Epidemiological datasets show a sim-ilar relationship for A1C to the risk ofretinopathy as has been shown for thecorresponding FPG and 2-h PG thresh-olds. The A1C has several advantages tothe FPG and OGTT, including greaterconvenience (since fasting is not required),evidence to suggest greater preanalyticalstability, and less day-to-day perturbationsduring periods of stress and illness. Theseadvantages must be balanced by greatercost, the limited availability of A1C testingin certain regions of the developing world,and the incomplete correlation betweenA1C and average glucose in certain indi-viduals. In addition, HbA1c levels may varywith patients’ race/ethnicity (7,8). Some

have posited that glycation rates differ byrace (with, for example, African Americanshaving higher rates of glycation), but this iscontroversial. A recent epidemiologicalstudy found that, when matched for FPG,African Americans (with and without dia-betes) indeed had higher A1C than whites,but also had higher levels of fructosamineand glycated albumin and lower levels of1,5 anhydroglucitol, suggesting that theirglycemic burden (particularly postpran-dially) may be higher (9). Epidemiologicalstudies forming the framework for recom-mending use of the A1C to diagnose diabe-tes have all been in adult populations.Whether the cut point would be the sameto diagnose children or adolescents withtype 2 diabetes is an area of uncertainty(3,10). A1C inaccurately reflects glycemiawith certain anemias and hemoglobinopa-thies. For patients with an abnormal hemo-globin but normal red cell turnover, such assickle cell trait, an A1C assay without inter-ference fromabnormal hemoglobins shouldbe used (an updated list is available at www.ngsp.org/interf.asp). For conditions withabnormal red cell turnover, such as preg-nancy, recent blood loss or transfusion, orsome anemias, the diagnosis of diabetesmust employ glucose criteria exclusively.

The established glucose criteria forthe diagnosis of diabetes (FPG and 2-h

PG) remain valid as well (Table 2). Just asthere is less than 100% concordance be-tween the FPG and 2-h PG tests, there isno perfect concordance between A1C andeither glucose-based test. Analyses of theNational Health and Nutrition Examina-tion Survey (NHANES) data indicate that,assuming universal screening of the un-diagnosed, the A1C cut point of $6.5%identifies one-third fewer cases of undiag-nosed diabetes than a fasting glucose cutpoint of$126 mg/dL (7.0 mmol/L) (11),and numerous studies have confirmedthat at these cut points the 2-h OGTTvalue diagnoses more screened peoplewith diabetes (12). However, in practice, alarge portion of the diabetic population re-mains unaware of its condition. Thus, thelower sensitivity of A1C at the designatedcut point may well be offset by the test’sgreater practicality, and wider applicationof a more convenient test (A1C) may actu-ally increase the number of diagnosesmade.

As with most diagnostic tests, a testresult diagnostic of diabetes should berepeated to rule out laboratory error,unless the diagnosis is clear on clinicalgrounds, such as a patient with a hyper-glycemic crisis or classic symptoms ofhyperglycemia and a random plasmaglucose $200 mg/dL. It is preferablethat the same test be repeated for confir-mation, since there will be a greater likeli-hood of concurrence in this case. Forexample, if the A1C is 7.0% and a repeatresult is 6.8%, the diagnosis of diabetes isconfirmed. However, if two different tests(such as A1C and FPG) are both above thediagnostic thresholds, the diagnosis of di-abetes is also confirmed.

On the other hand, if two differenttests are available in an individual and theresults are discordant, the test whose resultis above the diagnostic cut point should berepeated, and the diagnosis is made basedon the confirmed test. That is, if a patientmeets the diabetes criterion of the A1C (tworesults$6.5%) but not the FPG (,126mg/dL or 7.0 mmol/L), or vice versa, that per-son should be considered to have diabetes.

Since there is preanalytical and ana-lytical variability of all the tests, it is alsopossible that when a test whose result wasabove the diagnostic threshold is re-peated, the second value will be belowthe diagnostic cut point. This is leastlikely for A1C, somewhat more likely forFPG, and most likely for the 2-h PG.Barring a laboratory error, such patientsare likely to have test results near themargins of the threshold for a diagnosis.The health care professional might opt to

Table 1dADA evidence grading system for clinical practice recommendations

Level ofevidence Description

A Clear evidence from well-conducted, generalizable RCTs that are adequatelypowered, including:c Evidence from a well-conducted multicenter trialc Evidence from a meta-analysis that incorporated quality ratings in theanalysis

Compelling nonexperimental evidence, i.e., “all or none” rule developed by theCentre for Evidence-Based Medicine at the University of Oxford

Supportive evidence from well-conducted RCTs that are adequately powered,including:c Evidence from a well-conducted trial at one or more institutionsc Evidence from ameta-analysis that incorporated quality ratings in the analysis

B Supportive evidence from well-conducted cohort studiesc Evidence from a well-conducted prospective cohort study or registryc Evidence from a well-conducted meta-analysis of cohort studies

Supportive evidence from a well-conducted case-control studyC Supportive evidence from poorly controlled or uncontrolled studies

c Evidence from randomized clinical trials with one or more major or three ormore minor methodological flaws that could invalidate the results

c Evidence from observational studies with high potential for bias (such as caseseries with comparison with historical controls)

c Evidence from case series or case reportsConflicting evidence with the weight of evidence supporting the recommendation

E Expert consensus or clinical experience


Position Statement

follow the patient closely and repeat thetesting in 3–6 months.

The current diagnostic criteria fordiabetes are summarized in Table 2.

C. Categories of increased riskfor diabetes (prediabetes)In 1997 and 2003, the Expert Committeeon Diagnosis and Classification of Diabe-tes Mellitus (13,14) recognized an inter-mediate group of individuals whoseglucose levels, although not meeting cri-teria for diabetes, are nevertheless toohigh to be considered normal. These per-sons were defined as having impaired fast-ing glucose (IFG) (FPG levels 100 mg/dL[5.6 mmol/L] to 125 mg/dL [6.9 mmol/L])or impaired glucose tolerance (IGT) (2-hvalues in the OGTT of 140 mg/dL [7.8mmol/L] to 199 mg/dL [11.0 mmol/L]). Itshould be noted that the World HealthOrganization (WHO) and a number ofother diabetes organizations define the cut-off for IFG at 110 mg/dL (6.1 mmol/L).

Individuals with IFG and/or IGT havebeen referred to as having prediabetes,indicating the relatively high risk for thefuture development of diabetes. IFG andIGT should not be viewed as clinicalentities in their own right but rather riskfactors for diabetes aswell as cardiovasculardisease (CVD). IFG and IGT are associatedwith obesity (especially abdominal or vis-ceral obesity), dyslipidemia with high tri-glycerides and/or lowHDL cholesterol, andhypertension.

As is the case with the glucose mea-sures, several prospective studies that

used A1C to predict the progression todiabetes demonstrated a strong, continu-ous association between A1C and sub-sequent diabetes. In a systematic review of44,203 individuals from 16 cohort stud-ies with a follow-up interval averaging 5.6years (range 2.8–12 years), those with anA1C between 5.5 and 6.0% had a substan-tially increased risk of diabetes with 5-yearincidences ranging from 9 to 25%. An A1Crange of 6.0–6.5% had a 5-year risk of de-veloping diabetes between 25 to 50% andrelative risk (RR) 20 times higher comparedwith anA1Cof 5.0% (15). In a community-based study of black and white adultswithout diabetes, baseline A1C was astronger predictor of subsequent diabetesand cardiovascular events than was fast-ing glucose (16). Other analyses suggestthat an A1C of 5.7% is associated withdiabetes risk similar to that in the high-risk participants in the Diabetes PreventionProgram (DPP) (17).

Hence, it is reasonable to consider anA1C range of 5.7–6.4% as identifying in-dividuals with prediabetes. As is the casefor individuals found to have IFG andIGT, individuals with an A1C of 5.7–6.4%should be informed of their increased riskfor diabetes as well as CVD and counseledabout effective strategies to lower their risks(see Section IV). As with glucose measure-ments, the continuum of risk is curvilinear,so that as A1C rises, the risk of diabetes risesdisproportionately (15). Accordingly, inter-ventions should be most intensive andfollow-up particularly vigilant for thosewith A1Cs above 6.0%,who should be con-sidered to be at very high risk.

Table 3 summarizes the categories ofprediabetes.

II. TESTING FOR DIABETES INASYMPTOMATIC PATIENTS

Recommendationsc Testing to detect type 2 diabetes andprediabetes in asymptomatic peopleshould be considered in adults of anyage who are overweight or obese (BMI$25 kg/m2) and who have one or moreadditional risk factors for diabetes (Table4). In those without these risk factors,testing should begin at age 45. (B)

c If tests are normal, repeat testing at leastat 3-year intervals is reasonable. (E)

c To test for diabetes or prediabetes, theA1C, FPG, or 75-g 2-h OGTT are appro-priate. (B)

c In those identified with prediabetes,identify and, if appropriate, treat otherCVD risk factors. (B)

Formany illnesses, there is a major dis-tinction between screening and diagnostictesting. However, for diabetes, the sametests would be used for “screening” as fordiagnosis. Diabetes may be identified any-where along a spectrum of clinical scenar-ios ranging from a seemingly low-riskindividual who happens to have glucosetesting, to a higher-risk individual whomthe provider tests because of high suspicionof diabetes, to the symptomatic patient.The discussion herein is primarily framedas testing for diabetes in those withoutsymptoms. The same assays used for test-ing for diabetes will also detect individualswith prediabetes.

A. Testing for type 2 diabetes andrisk of future diabetes in adultsPrediabetes and diabetes meet establishedcriteria for conditions in which early de-tection is appropriate. Both conditions arecommon, increasing in prevalence, andimpose significant public health burdens.There is a long presymptomatic phasebefore the diagnosis of type 2 diabetes isusually made. Relatively simple tests areavailable to detect preclinical disease. Ad-ditionally, the duration of glycemic burdenis a strong predictor of adverse outcomes,and effective interventions exist to preventprogression of prediabetes to diabetes (seeSection IV) and to reduce risk of compli-cations of diabetes (see Section VI).

Type 2 diabetes is frequently not di-agnosed until complications appear, andapproximately one-fourth of all peoplewith diabetes in the U.S. may be undiag-nosed. The effectiveness of early identifica-tion of prediabetes and diabetes throughmass testing of asymptomatic individualshas not been proven definitively, andrigorous trials to provide such proof areunlikely to occur. In a large randomizedcontrolled trial (RCT) in Europe, generalpractice patients between the ages of 40–69 years were screened for diabetes and

Table 2dCriteria for the diagnosis ofdiabetes

A1C$6.5%. The test should be performed ina laboratory using a method that is NGSPcertified and standardized to the DCCTassay.*

ORFPG $126 mg/dL (7.0 mmol/L). Fasting isdefined as no caloric intake for at least 8 h.*

OR2-h plasma glucose$200mg/dL (11.1mmol/L)during an OGTT. The test should beperformed as described by the WHO, usinga glucose load containing the equivalent of75 g anhydrous glucose dissolved in water.*

ORIn a patient with classic symptoms ofhyperglycemia or hyperglycemic crisis,a random plasma glucose $200 mg/dL(11.1 mmol/L).

*In the absence of unequivocal hyperglycemia, re-sult should be confirmed by repeat testing.

Table 3dCategories of increased risk fordiabetes (prediabetes)*

FPG 100 mg/dL (5.6 mmol/L) to 125 mg/dL(6.9 mmol/L) (IFG)

OR2-h plasmaglucose in the 75-gOGTT140mg/dL(7.8 mmol/L) to 199 mg/dL (11.0 mmol/L)(IGT)

ORA1C 5.7–6.4%

*For all three tests, risk is continuous, extending be-low the lower limit of the range and becoming dis-proportionately greater at higher ends of the range.


Position Statement

then randomly assigned by practice toroutine care of diabetes or intensive treat-ment of multiple risk factors. After 5.3years of follow-up, CVD risk factors weremodestly but significantly more improvedwith intensive treatment. Incidence of firstCVD event and mortality rates were notsignificantly different between groups(18). This study would seem to add sup-port for early treatment of screen-detecteddiabetes, as risk factor control was excel-lent even in the routine treatment armand both groups had lower event ratesthan predicted. The absence of a controlunscreened arm limits the ability to defi-nitely prove that screening impacts out-comes. Mathematical modeling studiessuggest that screening independent ofrisk factors beginning at age 30 yearsor age 45 years is highly cost-effective(,$11,000 per quality-adjusted life-year gained) (19).

Recommendations for testing for di-abetes in asymptomatic, undiagnosedadults are listed in Table 4. Testing shouldbe considered in adults of any age withBMI $25 kg/m2 and one or more of theknown risk factors for diabetes. In addi-tion to the listed risk factors, certain med-ications, such as glucocorticoids andantipsychotics (20), are known to in-crease the risk of type 2 diabetes. Thereis compelling evidence that lower BMI cutpoints suggest diabetes risk in some racialand ethnic groups. In a large multiethniccohort study, for an equivalent incidencerate of diabetes conferred by a BMI of 30kg/m2 in whites, the BMI cutoff value was

24 kg/m2 in South Asians, 25 kg/m2 inChinese, and 26 kg/m2 in African Ameri-cans (21). Disparities in screening rates,not explainable by insurance status, arehighlighted by evidence that despitemuch higher prevalence of type 2 diabe-tes, non-Caucasians in an insured popu-lation are no more likely than Caucasiansto be screened for diabetes (22). Becauseage is a major risk factor for diabetes, test-ing of those without other risk factorsshould begin no later than age 45 years.

The A1C, FPG, or the 2-h OGTT areappropriate for testing. It should be notedthat the tests do not necessarily detectdiabetes in the same individuals. Theefficacy of interventions for primary pre-vention of type 2 diabetes (23–29) hasprimarily been demonstrated among in-dividuals with IGT, not for individualswith isolated IFG or for individuals withspecific A1C levels.

The appropriate interval betweentests is not known (30). The rationalefor the 3-year interval is that false nega-tives will be repeated before substantialtime elapses, and there is little likelihoodthat an individual will develop significantcomplications of diabetes within 3 yearsof a negative test result. In the modelingstudy, repeat screening every 3 or 5 yearswas cost-effective (19).

Because of the need for follow-up anddiscussion of abnormal results, testingshould be carried out within the healthcare setting. Community screening outsidea health care setting is not recommendedbecause people with positive tests may not

seek, orhave access to, appropriate follow-uptesting and care. Conversely, there may befailure to ensure appropriate repeat testingfor individuals who test negative. Commu-nity screening may also be poorly targeted; i.e., it may fail to reach the groupsmost at riskand inappropriately test those at low risk (theworried well) or even those already diag-nosed.

B. Screening for type 2 diabetesin childrenRecommendationsc Testing to detect type 2 diabetes andprediabetes should be considered in chil-dren and adolescents who are overweightand who have two or more additionalrisk factors for diabetes (Table 5). (E)

The incidence of type 2 diabetes inadolescents has increased dramatically inthe last decade, especially in minoritypopulations (31), although the diseaseremains rare in the general pediatric pop-ulation (32). Consistent with recom-mendations for adults, children andyouth at increased risk for the presenceor the development of type 2 diabetesshould be tested within the health caresetting (33). The recommendations ofthe ADA consensus statement “Type 2Diabetes in Children and Adolescents,”with some modifications, are summa-rized in Table 5.

C. Screening for type 1 diabetesRecommendationsc Consider referring relatives of thosewith type 1 diabetes for antibody test-ing for risk assessment in the settingof a clinical research study. (E)

Generally, people with type 1 diabetespresent with acute symptoms of diabetesand markedly elevated blood glucoselevels, and some cases are diagnosed withlife-threatening ketoacidosis. Evidencefrom several studies suggests that mea-surement of islet autoantibodies in rela-tives of those with type 1 diabetesidentifies individuals who are at risk fordeveloping type 1 diabetes. Such testing,coupled with education about symptomsof diabetes and follow-up in an observa-tional clinical study, may allow earlieridentification of onset of type 1 diabetesand lessen presentation with ketoacidosisat time of diagnosis. This testing may beappropriate in those who have relativeswith type 1 diabetes, in the context of

Table 4dCriteria for testing for diabetes in asymptomatic adult individuals

1. Testing should be considered in all adults who are overweight (BMI $25 kg/m2*)and have additional risk factors:

c physical inactivityc first-degree relative with diabetesc high-risk race/ethnicity (e.g., African American, Latino, Native American, Asian

American, Pacific Islander)c women who delivered a baby weighing .9 lb or were diagnosed with GDMc hypertension ($140/90 mmHg or on therapy for hypertension)c HDL cholesterol level ,35 mg/dL (0.90 mmol/L) and/or a triglyceride

level .250 mg/dL (2.82 mmol/L)c women with polycystic ovary syndromec A1C $5.7%, IGT, or IFG on previous testingc other clinical conditions associated with insulin resistance (e.g., severe obesity,

acanthosis nigricans)c history of CVD

2. In the absence of the above criteria, testing for diabetes should begin at age 45 years.3. If results are normal, testing should be repeated at least at 3-year intervals, with

consideration of more frequent testing depending on initial results (e.g., those withprediabetes should be tested yearly) and risk status.

*At-risk BMI may be lower in some ethnic groups.


Position Statement

clinical research studies (see, for example,http://www.diabetestrialnet.org). However,widespread clinical testing of asymptomaticlow-risk individuals cannot currently berecommended, as it would identify veryfew individuals in the general populationwho are at risk. Individuals who screenpositive should be counseled about theirrisk of developing diabetes and symptomsof diabetes, followed closely to prevent de-velopment of diabetic ketoacidosis, andinformed about clinical trials. Clinicalstudies are being conducted to test variousmethods of preventing type 1 diabetes inthose with evidence of autoimmunity.Some interventions have demonstratedmodest efficacy in slowing b-cell loss earlyin type 1 diabetes (34,35), and further re-search is needed to determine whetherthey may be effective in preventing type1 diabetes.

III. DETECTION ANDDIAGNOSIS OF GDM

Recommendationsc Screen for undiagnosed type 2 diabetesat the first prenatal visit in those withrisk factors, using standard diagnosticcriteria. (B)

c In pregnant women not previouslyknown to have diabetes, screen for

GDM at 24–28 weeks of gestation,using a 75-g 2-h OGTT and the di-agnostic cut points in Table 6. (B)

c Screen womenwith GDM for persistentdiabetes at 6–12 weeks postpartum,using the OGTT and nonpregnancydiagnostic criteria. (E)

c Women with a history of GDM shouldhave lifelong screening for the de-velopment of diabetes or prediabetes atleast every 3 years. (B)

c Women with a history of GDM foundto have prediabetes should receivelifestyle interventions or metformin toprevent diabetes. (A)

For many years, GDM was defined asany degree of glucose intolerance withonset or first recognition during preg-nancy (13), whether or not the conditionpersisted after pregnancy, and not ex-cluding the possibility that unrecognizedglucose intolerance may have antedatedor begun concomitantly with the preg-nancy. This definition facilitated a uniformstrategy for detection and classification ofGDM, but its limitations were recognizedfor many years. As the ongoing epidemicof obesity and diabetes has led to moretype 2 diabetes in women of childbearingage, the number of pregnant women withundiagnosed type 2 diabetes has increased(36). Because of this, it is reasonable to

screen women with risk factors for type2 diabetes (Table 4) for diabetes at theirinitial prenatal visit, using standard diag-nostic criteria (Table 2). Women with di-abetes found at this visit should receivea diagnosis of overt, not gestational,diabetes.

GDM carries risks for the mother andneonate. The Hyperglycemia and Ad-verse Pregnancy Outcome (HAPO) study(37), a large-scale (;25,000 pregnantwomen) multinational epidemiologicalstudy, demonstrated that risk of adversematernal, fetal, and neonatal outcomescontinuously increased as a function ofmaternal glycemia at 24–28 weeks, evenwithin ranges previously considered nor-mal for pregnancy. For most complica-tions, there was no threshold for risk.These results have led to careful recon-sideration of the diagnostic criteria forGDM. After deliberations in 2008–2009, the International Association ofDiabetes and Pregnancy Study Groups(IADPSG), an international consensusgroup with representatives frommultipleobstetrical and diabetes organizations,including ADA, developed revised rec-ommendations for diagnosing GDM.The group recommended that all womennot known to have prior diabetesundergo a 75-g OGTT at 24–28 weeksof gestation. Additionally, the group de-veloped diagnostic cut points for the fast-ing, 1-h, and 2-h plasma glucosemeasurements that conveyed an oddsratio for adverse outcomes of at least1.75 compared with women with themean glucose levels in the HAPO study.Current screening and diagnostic strate-gies, based on the IADPSG statement(38), are outlined in Table 6.

These new criteria will significantlyincrease the prevalence of GDM, primar-ily because only one abnormal value, nottwo, is sufficient to make the diagnosis.The ADA recognizes the anticipated sig-nificant increase in the incidence of GDMdiagnosed by these criteria and is sensitiveto concerns about the “medicalization” ofpregnancies previously categorized as nor-mal. These diagnostic criteria changes arebeing made in the context of worrisomeworldwide increases in obesity and diabe-tes rates, with the intent of optimizing ges-tational outcomes for women and theirbabies.

Admittedly, there are few data fromrandomized clinical trials regarding ther-apeutic interventions in women who willnow be diagnosed with GDM based ononly one blood glucose value above the

Table 5dTesting for type 2 diabetes in asymptomatic children*

Criteriac Overweight (BMI .85th percentile for age and sex, weight for height .85th percentile, orweight .120% of ideal for height)

Plus any two of the following risk factors:c Family history of type 2 diabetes in first- or second-degree relativec Race/ethnicity (Native American, African American, Latino, Asian American, PacificIslander)

c Signs of insulin resistance or conditions associated with insulin resistance (acanthosisnigricans, hypertension, dyslipidemia, polycystic ovary syndrome, or small-for-gestational-age birth weight)

c Maternal history of diabetes or GDM during the child’s gestationAge of initiation: age 10 years or at onset of puberty, if puberty occurs at a younger ageFrequency: every 3 years

*Persons aged 18 years and younger.

Table 6dScreening for and diagnosis of GDM

Perform a 75-g OGTT, with plasma glucose measurement fasting and at 1 and 2 h, at 24–28weeks of gestation in women not previously diagnosed with overt diabetes.

The OGTT should be performed in the morning after an overnight fast of at least 8 h.The diagnosis of GDM is made when any of the following plasma glucose values are exceeded:

c Fasting: $92 mg/dL (5.1 mmol/L)c 1 h: $180 mg/dL (10.0 mmol/L)c 2 h: $153 mg/dL (8.5 mmol/L)


Position Statement

specified cut points (in contrast to the oldercriteria that stipulated at least two abnor-mal values). However, there is emergingobservational and retrospective evidencethat women diagnosed with the newcriteria (even if they would not havebeen diagnosed with older criteria) haveincreased rates of poor pregnancy out-comes similar to those of women withGDM by prior criteria (39,40). Expectedbenefits to these pregnancies and offspringare inferred from intervention trials thatfocused on women with more mild hyper-glycemia than identified using older GDMdiagnostic criteria and that found modestbenefits (41,42). The frequency of follow-up and blood glucose monitoring for thesewomen is not yet clear, but likely to be lessintensive than for women diagnosed by theolder criteria. It is important to note that80–90% of women in both of the mildGDM studies (whose glucose values over-lapped with the thresholds recommendedherein) could be managed with lifestyletherapy alone.

The American College of Obstetri-cians and Gynecologists announced in2011 that they continue to recommenduse of prior diagnostic criteria for GDM(43). Several other countries haveadopted the new criteria, and a reportfrom the WHO on this topic is pendingat the time of publication of these stand-ards. The National Institutes of Health isplanning to hold a consensus develop-ment conference on this topic in 2013.

Because some cases of GDM mayrepresent pre-existing undiagnosed type2 diabetes, women with a history ofGDM should be screened for diabetes6–12 weeks postpartum, using nonpreg-nant OGTT criteria. Because of their pre-partum treatment for hyperglycemia, useof the A1C for diagnosis of persistent di-abetes at the postpartum visit is not rec-ommended (44). Women with a historyof GDM have a greatly increased subse-quent risk for diabetes (45) and shouldbe followed up with subsequent screen-ing for the development of diabetes orprediabetes, as outlined in Section II.Lifestyle interventions or metforminshould be offered to women with a his-tory of GDM who develop prediabetes,as discussed in Section IV. In the pro-spective Nurses’ Health Study II, risk ofsubsequent diabetes after a history ofGDM was significantly lower in womenwho followed healthy eating patterns.Adjusting for BMI moderately, but notcompletely, attenuated this association(46).

IV. PREVENTION/DELAYOF TYPE 2 DIABETES

Recommendationsc Patientswith IGT (A), IFG (E), or anA1Cof 5.7–6.4% (E) should be referred to aneffective ongoing support program tar-geting weight loss of 7% of body weightand increasing physical activity to at least150 min/week of moderate activity suchas walking.

c Follow-up counseling appears to beimportant for success. (B)

c Based on the cost-effectiveness of diabetesprevention, such programs should becovered by third-party payers. (B)

c Metformin therapy for prevention oftype 2 diabetes may be considered inthosewith IGT (A), IFG (E), or anA1Cof5.7–6.4% (E), especially for those withBMI .35 kg/m2, aged ,60 years, andwomen with prior GDM. (A)

c At least annual monitoring for the de-velopment of diabetes in those withprediabetes is suggested. (E)

c Screening for and treatment of modifi-able risk factors for CVD is suggested. (B)

RCTs have shown that individuals athigh risk for developing type 2 diabetes(those with IFG, IGT, or both) can signif-icantly decrease the rate of onset of diabeteswith particular interventions (23–29).These include intensive lifestyle modifica-tion programs that have been shown to bevery effective (;58% reduction after 3years) and use of the pharmacologicalagents metformin, a-glucosidase inhibi-tors, orlistat, and thiazolidinediones, eachof which has been shown to decrease inci-dent diabetes to various degrees. Follow-upof all three large studies of lifestyle interven-tion has shown sustained reduction in therate of conversion to type 2 diabetes, with43% reduction at 20 years in the Da Qingstudy (47), 43% reduction at 7 years in theFinnish Diabetes Prevention Study (DPS)(48), and 34% reduction at 10 years inthe U.S. Diabetes Prevention ProgramOutcomes Study (DPPOS) (49). A cost-effectiveness model suggested that lifestyleinterventions as delivered in the DPP arecost-effective (50), and actual cost datafrom theDPP andDPPOS confirm that life-style interventions are highly cost-effective(51). Group delivery of the DPP interven-tion in community settings has the poten-tial to be significantly less expensive whilestill achieving similar weight loss (52).

Based on the results of clinical trialsand the known risks of progression ofprediabetes to diabetes, persons with an

A1C of 5.7–6.4%, IGT, or IFG should becounseled on lifestyle changes with goalssimilar to those of the DPP (7% weightloss and moderate physical activity of atleast 150 min/week). Regarding drugtherapy for diabetes prevention, metfor-min has a strong evidence base and dem-onstrated long-term safety (53). For otherdrugs, issues of cost, side effects, and lackof persistence of effect in some studies(54) require consideration. Metforminwas less effective than lifestyle modifica-tion in the DPP and DPPOS, but may becost-saving over a 10-year period (51). Itwas as effective as lifestyle modificationin participants with a BMI of at least 35kg/m2, but not significantly better thanplacebo than those over age 60 years(23). In women in the DPP with a historyof GDM,metformin and intensive lifestylemodification led to an equivalent 50% re-duction in the risk of diabetes (55). Met-formin therefore might reasonably berecommended for very high-risk individ-uals (those with a history of GDM, thevery obese, and/or those with more severeor progressive hyperglycemia).

People with prediabetes often haveother cardiovascular risk factors, such asobesity, hypertension, and dyslipidemia.Assessing and treating these risk factors isan important aspect of reducing cardio-metabolic risk. In the DPP and DPPOS,cardiovascular event rates have been verylow, perhaps due to appropriate manage-ment of cardiovascular risk factors in allarms of the study (56).

V. DIABETES CARE

A. Initial evaluationA complete medical evaluation should beperformed to classify the diabetes, detectthe presence of diabetes complications,review previous treatment and risk factorcontrol in patients with established diabe-tes, assist in formulating a managementplan, and provide a basis for continuingcare. Laboratory tests appropriate to theevaluation of each patient’s medical condi-tion should be performed. A focus on thecomponents of comprehensive care (Table7) will assist the health care team to ensureoptimal management of the patient withdiabetes.

B. ManagementPeople with diabetes should receive med-ical care from a team that may includephysicians, nurse practitioners, physician’sassistants, nurses, dietitians, pharmacists,and mental health professionals with


Position Statement

expertise and a special interest in diabetes.It is essential in this collaborative and in-tegrated team approach that individualswith diabetes assume an active role in theircare.

The management plan should beformulated as a collaborative therapeuticalliance among the patient and family,the physician, and other members of thehealth care team. A variety of strategiesand techniques should be used to provideadequate education and development

of problem-solving skills in the variousaspects of diabetes management. Imple-mentation of the management plan re-quires that the goals and treatment planare individualized and take patient pref-erences into account. The managementplan should recognize diabetes self-management education (DSME) and on-going diabetes support as an integralcomponent of care. In developing theplan, consideration should be given tothe patient’s age, school or work schedule

and conditions, physical activity, eatingpatterns, social situation and cultural fac-tors, and presence of complications of di-abetes or other medical conditions.

C. Glycemic control

1. Assessment of glycemic controlTwo primary techniques are available forhealth providers and patients to assess theeffectiveness of the management plan onglycemic control: patient self-monitoringof blood glucose (SMBG) or interstitialglucose, and A1C.

a. Glucose monitoringRecommendationsc Patients on multiple-dose insulin (MDI)or insulin pump therapy should doSMBG at least prior to meals and snacks,occasionally postprandially, at bedtime,prior to exercise, when they suspect lowblood glucose, after treating low bloodglucose until they are normoglycemic,and prior to critical tasks such as driv-ing. (B)

c When prescribed as part of a broadereducational context, SMBG results maybe helpful to guide treatment decisionsand/or patient self-management forpatients using less frequent insulin in-jections or noninsulin therapies. (E)

c When prescribing SMBG, ensure thatpatients receive ongoing instructionand regular evaluation of SMBG tech-nique and SMBG results, as well as theirability to use SMBG data to adjust ther-apy. (E)

c Continuous glucose monitoring (CGM)in conjunction with intensive insulinregimens can be a useful tool to lowerA1C in selected adults (aged$25 years)with type 1 diabetes. (A)

c Although the evidence for A1C lower-ing is less strong in children, teens, andyounger adults, CGM may be helpfulin these groups. Success correlates withadherence to ongoing use of the device.(C)

c CGM may be a supplemental tool toSMBG in those with hypoglycemiaunawareness and/or frequent hypogly-cemic episodes. (E)

Major clinical trials of insulin-treatedpatients that demonstrated the benefits ofintensive glycemic control on diabetescomplications have included SMBG aspart of multifactorial interventions, sug-gesting that SMBG is a component ofeffective therapy. SMBG allows patientsto evaluate their individual response to

Table 7dComponents of the comprehensive diabetes evaluation

Medical historyc Age and characteristics of onset of diabetes (e.g., DKA, asymptomatic laboratory finding)c Eating patterns, physical activity habits, nutritional status, and weight history; growth anddevelopment in children and adolescents

c Diabetes education historyc Review of previous treatment regimens and response to therapy (A1C records)c Current treatment of diabetes, including medications, medication adherence and barriersthereto, meal plan, physical activity patterns, and readiness for behavior change

c Results of glucose monitoring and patient’s use of datac DKA frequency, severity, and causec Hypoglycemic episodes

c Hypoglycemia awarenessc Any severe hypoglycemia: frequency and cause

c History of diabetes-related complicationsc Microvascular: retinopathy, nephropathy, neuropathy (sensory, including history of footlesions; autonomic, including sexual dysfunction and gastroparesis)

c Macrovascular: CHD, cerebrovascular disease, and PADc Other: psychosocial problems*, dental disease*

Physical examinationc Height, weight, BMIc Blood pressure determination, including orthostatic measurements when indicatedc Fundoscopic examination*c Thyroid palpationc Skin examination (for acanthosis nigricans and insulin injection sites)c Comprehensive foot examination

c Inspectionc Palpation of dorsalis pedis and posterior tibial pulsesc Presence/absence of patellar and Achilles reflexesc Determination of proprioception, vibration, and monofilament sensation

Laboratory evaluationc A1C, if results not available within past 2–3 months

If not performed/available within past yearc Fasting lipid profile, including total, LDL and HDL cholesterol and triglyceridesc Liver function testsc Test for urine albumin excretion with spot urine albumin-to-creatinine ratioc Serum creatinine and calculated GFRc TSH in type 1 diabetes, dyslipidemia or women over age 50 years

Referralsc Eye care professional for annual dilated eye examc Family planning for women of reproductive agec Registered dietitian for MNTc DSMEc Dentist for comprehensive periodontal examinationc Mental health professional, if needed

*See appropriate referrals for these categories.


Position Statement

therapy and assess whether glycemic tar-gets are being achieved. Results of SMBGcan be useful in preventing hypoglycemiaand adjusting medications (particularlyprandial insulin doses), medical nutritiontherapy (MNT), and physical activity.

The frequency and timing of SMBGshould be dictated by the particular needsand goals of the patient. SMBG is espe-cially important for patients treated withinsulin tomonitor for and prevent asymp-tomatic hypoglycemia and hyperglyce-mia. Most patients with type 1 diabetesand others on intensive insulin regimens(MDI or insulin pump therapy) should doSMBG at least prior to meals and snacks,occasionally postprandially, at bedtime,prior to exercise, when they suspect lowblood glucose, after treating low bloodglucose until they are normoglycemic,and prior to critical tasks such as driving.For many patients, this will require test-ing 6–8 times daily, although individualneeds may be greater. Although there arefew rigorous studies, a database study ofalmost 27,000 children and adolescentswith type 1 diabetes showed that, afteradjustment for multiple confounders, in-creased daily frequency of SMBG was sig-nificantly associated with lower A1C(20.2% per additional test per day, level-ing off at five tests per day) and with feweracute complications (57). The optimalfrequency of SMBG for patients on non-intensive regimens, such as those withtype 2 diabetes on basal insulin, is notknown, although a number of studieshave used fasting SMBG for patient or pro-vider titration of the basal insulin dose.

The evidence base for SMBG forpatientswith type 2 diabetes on noninsulin therapyis somewhat mixed. Several randomizedtrials have called into question the clinicalutility and cost-effectiveness of routineSMBG in non–insulin-treated patients(58–60). A recent meta-analysis suggestedthat SMBG reduced A1C by 0.25% at 6months (61), while a Cochrane review con-cluded that the overall effect of SMBG insuch patients is small up to 6 months afterinitiation and subsides after 12months (62).

Because the accuracy of SMBG isinstrument and user dependent (63), itis important to evaluate each patient’smonitoring technique, both initially andat regular intervals thereafter. Optimaluse of SMBG requires proper review andinterpretation of the data, both by the pa-tient and provider. Among patients whochecked their blood glucose at least oncedaily, many reported taking no actionwhen results were high or low (64). In

one study of insulin-naïve patients withsuboptimal initial glycemic control, useof structured SMBG (a paper tool to col-lect and interpret 7-point SMBG profilesover 3 days at least quarterly) reducedA1C by 0.3% more than in an active con-trol group (65). Patients should be taughthow to use SMBG data to adjust food in-take, exercise, or pharmacological therapyto achieve specific goals, and the ongoingneed for and frequency of SMBG should bere-evaluated at each routine visit.

Real-time CGM through the measure-ment of interstitial glucose (which corre-lates well with plasma glucose) is available.These sensors require calibration withSMBG, and the latter are still recommendedfor making acute treatment decisions.CGM devices have alarms for hypo- andhyperglycemic excursions. A 26-week ran-domized trial of 322 type 1 diabetic pa-tients showed that adults aged $25 yearsusing intensive insulin therapy and CGMexperienced a 0.5% reduction in A1C(from;7.6 to 7.1%) compared with usualintensive insulin therapy with SMBG (66).Sensor use in children, teens, and adults toage 24 years did not result in significantA1C lowering, and there was no significantdifference in hypoglycemia in any group.Importantly, the greatest predictor of A1Clowering in this study for all age-groupswas frequency of sensor use, which waslower in younger age-groups. In a smallerRCT of 129 adults and children with base-line A1C ,7.0%, outcomes combiningA1C and hypoglycemia favored the grouputilizing CGM, suggesting that CGM is alsobeneficial for individuals with type 1 dia-betes who have already achieved excellentcontrol (67).

A trial comparing CGM plus insulinpump to SMBG plus multiple injectionsof insulin in adults and children with type1 diabetes showed significantly greaterimprovements in A1C with “sensor-augmented pump” therapy (68,69), butthis trial did not isolate the effect of CGMitself. Overall, meta-analyses suggest thatcompared with SMBG, CGM lowers A1Cby ;0.26% (70). Altogether, these datasuggest that, in appropriately selected pa-tients who are motivated to wear it most ofthe time, CGM reduces A1C. The technol-ogymay be particularly useful in thosewithhypoglycemia unawareness and/or fre-quent episodes of hypoglycemia, althoughstudies as yet have not shown significantreductions in severe hypoglycemia (70).CGM forms the underpinning for the de-velopment of pumps that suspend insulindelivery when hypoglycemia is developing

and for the burgeoning work on “artificialpancreas” systems.

b. A1CRecommendationsc Perform the A1C test at least twotimes a year in patients who are meet-ing treatment goals (and who havestable glycemic control). (E)

c Perform the A1C test quarterly in pa-tients whose therapy has changed orwho are not meeting glycemic goals. (E)

c Use of POC testing for A1C providesthe opportunity for more timely treat-ment changes. (E)

Because A1C is thought to reflect aver-age glycemia over several months (63) andhas strong predictive value for diabetescomplications (71,72), A1C testingshould be performed routinely in all pa-tients with diabetes, at initial assessmentand then as part of continuing care. Mea-surement approximately every 3 monthsdetermines whether patient’s glycemic tar-gets have been reached and maintained.For any individual patient, the frequencyof A1C testing should be dependent onthe clinical situation, the treatment regimenused, and the judgment of the clinician.Some patients with stable glycemia wellwithin target may do well with testingonly twice per year, while unstable orhighly intensively managed patients (e.g.,pregnant type 1 diabetic women) may betested more frequently than every 3months. The availability of the A1C resultat the time that the patient is seen (POCtesting) has been reported in small studiesto result in increased intensification of ther-apy and improvement in glycemic control(73,74). However, two recent systematicreviews andmeta-analyses found no signif-icant difference in A1C between POC andlaboratory A1C usage (75,76).

The A1C test is subject to certainlimitations. Conditions that affect eryth-rocyte turnover (hemolysis, blood loss)and hemoglobin variants must be consid-ered, particularly when the A1C resultdoes not correlate with the patient’s clin-ical situation (63). In addition, A1C doesnot provide a measure of glycemic vari-ability or hypoglycemia. For patientsprone to glycemic variability (especiallytype 1 diabetic patients or type 2 diabeticpatients with severe insulin deficiency),glycemic control is best judged by thecombination of results of self-monitoringand the A1C. The A1Cmay also serve as acheck on the accuracy of the patient’s me-ter (or the patient’s reported SMBG


Position Statement

results) and the adequacy of the SMBGtesting schedule.

Table 8 contains the correlation be-tween A1C levels and mean plasma glu-cose levels based on data from theinternational A1C-Derived Average Glu-cose (ADAG) trial utilizing frequentSMBG and CGM in 507 adults (83% Cau-casian) with type 1, type 2, and no diabe-tes (77). The ADA and the AmericanAssociation for Clinical Chemistry havedetermined that the correlation (r 50.92) is strong enough to justify reportingboth an A1C result and an estimated av-erage glucose (eAG) result when a clini-cian orders the A1C test. The table in pre-2009 versions of the “Standards of Medi-cal Care in Diabetes” describing the cor-relation between A1C and mean glucosewas derived from relatively sparse data(one 7-point profile over 1 day per A1Creading) in the primarily Caucasian type 1diabetic participants in the DCCT (78).Clinicians should note that the numbersin the table are now different, as they arebased on;2,800 readings per A1C in theADAG trial.

In the ADAG trial, there were no sig-nificant differences among racial and eth-nic groups in the regression lines betweenA1C and mean glucose, although therewas a trend toward a difference betweenAfrican/African American participantsand Caucasian ones. A small study com-paring A1C to CGM data in type 1 di-abetic children found a highly statisticallysignificant correlation between A1C andmean blood glucose, although the corre-lation (r 5 0.7) was significantly lowerthan in the ADAG trial (79). Whether

there are significant differences in howA1C relates to average glucose in childrenor in African American patients is an areafor further study. For the time being, thequestion has not led to different recom-mendations about testing A1C or to dif-ferent interpretations of the clinicalmeaning of given levels of A1C in thosepopulations.

For patients in whom A1C/eAG andmeasured blood glucose appear discrep-ant, clinicians should consider the possi-bilities of hemoglobinopathy or alteredred cell turnover, and the options of morefrequent and/or different timing of SMBGor use of CGM.Othermeasures of chronicglycemia such as fructosamine are avail-able, but their linkage to average glucoseand their prognostic significance are notas clear as is the case for A1C.

2. Glycemic goals in adultsRecommendationsc Lowering A1C to below or around 7%has been shown to reduce microvas-cular complications of diabetes and ifimplemented soon after the diagnosisof diabetes is associated with long-termreduction in macrovascular disease.Therefore, a reasonable A1C goal formany nonpregnant adults is ,7%. (B)

c Providers might reasonably suggestmore stringent A1C goals (such as,6.5%) for selected individual pa-tients, if this can be achieved withoutsignificant hypoglycemia or other ad-verse effects of treatment. Appropriatepatients might include those with shortduration of diabetes, long life expec-tancy, and no significant CVD. (C)

c Less stringent A1C goals (such as,8%) may be appropriate for patientswith a history of severe hypoglycemia,limited life expectancy, advanced mi-crovascular or macrovascular complica-tions, extensive comorbid conditions,and those with long-standing diabetes inwhom the general goal is difficult to at-tain despite DSME, appropriate glucosemonitoring, and effective doses of mul-tiple glucose-lowering agents includinginsulin. (B)

Hyperglycemia defines diabetes, andglycemic control is fundamental to themanagement of diabetes. The DCCT(71), a prospective RCT of intensive ver-sus standard glycemic control in patientswith relatively recently diagnosed type 1diabetes, showed definitively thatimproved glycemic control is associ-ated with significantly decreased rates of

microvascular (retinopathy and nephro-pathy) and neuropathic complications.Follow-up of the DCCT cohorts in the Ep-idemiology of Diabetes Interventions andComplications (EDIC) study (80,81) dem-onstrated persistence of these microvascu-lar benefits in previously intensively treatedsubjects, even though their glycemic con-trol approximated that of previous stan-dard arm subjects during follow-up.

The Kumamoto Study (82) and UKProspective Diabetes Study (UKPDS)(83,84) confirmed that intensive glycemiccontrol was associated with significantlydecreased rates of microvascular and neu-ropathic complications in patients withtype 2 diabetes. Long-term follow-up ofthe UKPDS cohorts showed persistence ofthe effect of early glycemic control onmost microvascular complications (85).

Subsequent trials in patients withmore long-standing type 2 diabetes, de-signed primarily to look at the role ofintensive glycemic control on cardiovas-cular outcomes, also confirmed a benefit,although more modest, on onset or pro-gression of microvascular complications.The Veterans Affairs Diabetes Trial(VADT) showed significant reductionsin albuminuria with intensive (achievedmedian A1C 6.9%) compared with stan-dard glycemic control, but no differencein retinopathy and neuropathy (86,87).The Action in Diabetes and Vascular Dis-ease: Preterax and Diamicron MR Con-trolled Evaluation (ADVANCE) study ofintensive versus standard glycemic con-trol in type 2 diabetes found a statisticallysignificant reduction in albuminuria, butnot in neuropathy or retinopathy, with anA1C target of ,6.5% (achieved medianA1C 6.3%) compared with standard ther-apy achieving amedian A1C of 7.0% (88).Analyses from the Action to Control Car-diovascular Risk in Diabetes (ACCORD)trial have shown lower rates of onset orprogression of early-stage microvascularcomplications in the intensive glycemiccontrol arm compared with the standardarm (89,90).

Epidemiological analyses of the DCCTand UKPDS (71,72) demonstrate a curvi-linear relationship between A1C and mi-crovascular complications. Such analysessuggest that, on a population level, thegreatest number of complications will beaverted by taking patients from very poorcontrol to fair or good control. These anal-yses also suggest that further lowering ofA1C from7 to 6% is associatedwith furtherreduction in the risk of microvascularcomplications, albeit the absolute risk

Table 8dCorrelation of A1C with averageglucose

A1C (%)

Mean plasma glucose

mg/dL mmol/L

6 126 7.07 154 8.68 183 10.29 212 11.810 240 13.411 269 14.912 298 16.5

These estimates are based on ADAG data of;2,700glucose measurements over 3 months per A1Cmeasurement in 507 adults with type 1, type 2, andno diabetes. The correlation between A1C and av-erage glucose was 0.92 (ref. 77). A calculator forconverting A1C results into eAG, in either mg/dL ormmol/L, is available at http://professional.diabetes.org/eAG.


Position Statement

reductions become much smaller. Giventhe substantially increased risk of hypogly-cemia (particularly in those with type 1 di-abetes, but also in the recent type 2 diabetestrials), the concerning mortality findings inthe ACCORD trial (91), and the relativelymuch greater effort required to achievenear-normoglycemia, the risks of lower gly-cemic targets may outweigh the potentialbenefits on microvascular complicationson a population level. However, selectedindividual patients, especially those withlittle comorbidity and long life expectancy(who may reap the benefits of further low-ering of glycemia below 7%), may, basedon provider judgment and patient prefer-ences, adopt more intensive glycemic tar-gets (e.g., an A1C target,6.5%) as long assignificant hypoglycemia does not becomea barrier.

CVD, a more common cause of deathin populations with diabetes than micro-vascular complications, is less clearlyimpacted by levels of hyperglycemia orthe intensity of glycemic control. In theDCCT, there was a trend toward lowerrisk of CVD events with intensive control,and in 9-year post-DCCT follow-up of theEDIC cohort participants previously ran-domized to the intensive arm had a sig-nificant 57% reduction in the risk ofnonfatalmyocardial infarction (MI), stroke,or CVD death compared with those pre-viously in the standard arm (92). The ben-efit of intensive glycemic control in thistype 1 diabetic cohort has recently beenshown to persist for several decades (93).

In type 2 diabetes, there is evidencethat more intensive treatment of glycemiain newly diagnosed patients may reducelong-term CVD rates. During the UKPDStrial, there was a 16% reduction in car-diovascular events (combined fatal ornonfatal MI and sudden death) in theintensive glycemic control arm that didnot reach statistical significance (P 50.052), and there was no suggestion ofbenefit on other CVD outcomes such asstroke. However, after 10 years of follow-up, those originally randomized to inten-sive glycemic control had significantlong-term reductions in MI (15% withsulfonylurea or insulin as initial pharma-cotherapy, 33% with metformin as initialpharmacotherapy) and in all-cause mor-tality (13% and 27%, respectively) (85).

Three more recent large trials(ACCORD, ADVANCE, and VADT) sug-gested no significant reduction in CVDoutcomes with intensive glycemic controlin participants who had more advancedtype 2 diabetes than UKPDS participants.

All three of these trials were conducted inparticipants with more long-standing di-abetes (mean duration 8–11 years) andeither known CVD or multiple cardiovas-cular risk factors. Details of these threestudies are reviewed extensively in anADA position statement (94).

The ACCORD study enrolled partici-pants with either known CVD or two ormore major cardiovascular risk factorsand randomized them to intensive glyce-mic control (goal A1C,6%) or standardglycemic control (goal A1C 7–8%). Theglycemic control comparison was haltedearly due to the finding of an increasedrate of mortality in the intensive arm com-pared with the standard arm (1.41% vs.1.14% per year; HR 1.22; 95% CI 1.01–1.46), with a similar increase in cardiovas-cular deaths. This increase in mortality inthe intensive glycemic control arm wasseen in all prespecified patient subgroups.The primary outcome of ACCORD (non-fatal MI, nonfatal stroke, or cardiovascu-lar death) was nonsignificantly lower inthe intensive glycemic control groupdue to a reduction in nonfatal MI, bothwhen the glycemic control comparisonwas halted and all participants transi-tioned to the standard glycemic controlintervention (91), and at completion ofthe planned follow-up (95).

Exploratory analyses of the mortalityfindings of ACCORD (evaluating vari-ables including weight gain, use of anyspecific drug or drug combination, andhypoglycemia) were reportedly unable toidentify a clear explanation for the excessmortality in the intensive arm (91). TheACCORD investigators subsequentlypublished additional epidemiologicalanalyses showing no increase in mortalityin the intensive arm participants whoachieved A1C levels below 7% nor inthose who lowered their A1C quickly af-ter trial enrollment. In fact, although therewas no A1C level at which intensive armparticipants had significantly lower mor-tality than standard arm participants, thehighest risk for mortality was observed inintensive arm participants with the high-est A1C levels (96).

The role of hypoglycemia in the ex-cess mortality findings was also complex.Severe hypoglycemia was significantlymore likely in participants randomizedto the intensive glycemic control arm.However, excess mortality in the inten-sive versus standard arms was only sig-nificant for participants with no severehypoglycemia, and not for those with oneor more episodes. Severe hypoglycemia

was associated with excess mortality ineither arm, but the association was stron-ger in those randomized to the standardglycemic control arm (97). Unlike thecase with the DCCT trial, where lowerachieved A1C levels were related to sig-nificantly increased rates of severe hypo-glycemia, in ACCORD every 1% declinein A1C from baseline to 4 months into thetrial was associated with a significant de-crease in the rate of severe hypoglycemiain both arms (96).

The primary outcome of ADVANCEwas a combination of microvascularevents (nephropathy and retinopathy)and major adverse cardiovascular events(MI, stroke, and cardiovascular death).Intensive glycemic control (to a goal A1C,6.5% vs. treatment to local standards)significantly reduced the primary endpoint. However, this was due to a significantreduction in themicrovascular outcome, pri-marily development of macroalbuminuria,with no significant reduction in the macro-vascular outcome. There was no differencein overall or cardiovascular mortality be-tween the intensive compared with thestandard glycemic control arms (88).

The VADT randomized participantswith type 2 diabetes uncontrolled oninsulin or maximal-dose oral agents (me-dian entry A1C 9.4%) to a strategy ofintensive glycemic control (goal A1C,6.0%) or standard glycemic control,with a planned A1C separation of at least1.5%. The primary outcome of the VADTwas a composite of CVD events. The cu-mulative primary outcome was nonsig-nificantly lower in the intensive arm(86). An ancillary study of the VADTdemonstrated that intensive glycemiccontrol significantly reduced the primaryCVD outcome in individuals with lessatherosclerosis at baseline (assessed bycoronary calcium) but not in personswith more extensive baseline atheroscle-rosis (98). A post hoc analysis showed acomplex relationship between durationof diabetes before glycemic intensifica-tion and mortality: mortality in the inten-sive vs. standard glycemic control armwas inversely related to duration of dia-betes at the time of study enrollment.Those with diabetes duration less than15 years had a mortality benefit in the in-tensive arm, while those with duration of20 years or more had higher mortality inthe intensive arm (99).

The evidence for a cardiovascular ben-efit of intensive glycemic control primarilyrests on long-term follow-up of studycohorts treated early in the course of type


Position Statement

1 and type 2 diabetes and subset analyses ofACCORD, ADVANCE, and VADT. Agroup-level meta-analysis of the latter threetrials suggests that glucose lowering has amodest (9%) but statistically significantreduction in major CVD outcomes, pri-marily nonfatal MI, with no significanteffect onmortality.However, heterogeneityof the mortality effects across studies wasnoted, precluding firm summary measuresof the mortality effects. A prespecified sub-group analysis suggested that major CVDoutcome reduction occurred in patientswithout known CVD at baseline (HR 0.84,95% CI 0.74–0.94) (100). Conversely, themortality findings in ACCORD and sub-group analyses of the VADT suggest thatthe potential risks of intensive glycemiccontrol may outweigh its benefits in somepatients, such as those with very long du-ration of diabetes, known history of severehypoglycemia, advanced atherosclerosis,and advanced age/frailty. Certainly, provid-ers should be vigilant in preventing severehypoglycemia in patients with advanceddisease and should not aggressively at-tempt to achieve near-normal A1C levelsin patients in whom such a target cannotbe safely and reasonably easily achieved.Severe or frequent hypoglycemia is an ab-solute indication for the modification oftreatment regimens, including settinghigher glycemic goals. Many factors, in-cluding patient preferences, should betaken into account when developing a pa-tient’s individualized goals (101).

Recommended glycemic goals formany nonpregnant adults are shown inTable 9. The recommendations are basedon those for A1C values, with listed bloodglucose levels that appear to correlatewith achievement of an A1C of ,7%.

The issue of pre- versus postprandialSMBG targets is complex (102). Elevatedpostchallenge (2-h OGTT) glucose valueshave been associated with increased car-diovascular risk independent of FPG insome epidemiological studies. In diabeticsubjects, some surrogate measures ofvascular pathology, such as endothelialdysfunction, are negatively affected bypostprandial hyperglycemia (103). It isclear that postprandial hyperglycemia,like preprandial hyperglycemia, contrib-utes to elevated A1C levels, with its rela-tive contribution being higher at A1Clevels that are closer to 7%. However,outcome studies have clearly shownA1C to be the primary predictor of com-plications, and landmark glycemic con-trol trials such as the DCCT and UKPDSrelied overwhelmingly on preprandialSMBG. Additionally, an RCT in patientswith known CVD found no CVD benefitof insulin regimens targeting postpran-dial glucose compared with thosetargeting preprandial glucose (104). Areasonable recommendation for post-prandial testing and targets is that for in-dividuals who have premeal glucosevalues within target but have A1C valuesabove target, monitoring postprandialplasma glucose (PPG) 1–2 h after the startof themeal and treatment aimed at reduc-ing PPG values to,180 mg/dL may helplower A1C.

Glycemic goals for children are pro-vided in Section VIII.A.1.a. As regards goalsfor glycemic control for women withGDM, recommendations from the FifthInternational Workshop-Conference onGestational Diabetes Mellitus (105) wereto target maternal capillary glucose con-centrations of:

c preprandial:#95mg/dL (5.3 mmol/L),and either:

c 1-h postmeal:#140mg/dL (7.8mmol/L)or

c 2-h postmeal:#120mg/dL (6.7mmol/L)

For women with pre-existing type 1or type 2 diabetes who become pregnant, arecent consensus statement (106) recom-mended the following as optimal glycemicgoals, if they can be achieved without ex-cessive hypoglycemia:

c premeal, bedtime, and overnight glu-cose 60–99 mg/dL (3.3–5.4 mmol/L)

c peak postprandial glucose 100–129mg/dL (5.4–7.1 mmol/L)

c A1C ,6.0%

D. Pharmacological and overallapproaches to treatment

1. Insulin therapy for type 1 diabetesRecommendationsc Most people with type 1 diabetes shouldbe treated with MDI injections (threeto four injections per day of basal andprandial insulin) or continuous sub-cutaneous insulin infusion (CSII). (A)

c Most people with type 1 diabetesshould be educated in how to matchprandial insulin dose to carbohydrateintake, premeal blood glucose, andanticipated activity. (E)

c Most people with type 1 diabetesshould use insulin analogs to reducehypoglycemia risk. (A)

c Consider screening those with type 1diabetes for other autoimmune dis-eases (thyroid, vitamin B12 deficiency,celiac) as appropriate. (B)

The DCCT clearly showed that inten-sive insulin therapy (three or more in-jections per day of insulin, CSII, or insulinpump therapy) was a key part of im-proved glycemia and better outcomes(71,92). At the time of the study, therapywas carried out with short- and intermedi-ate-acting human insulins. Despite bettermicrovascular outcomes, intensive insulintherapy was associated with a high rate insevere hypoglycemia (62 episodes per 100patient-years of therapy). Since the time ofthe DCCT, a number of rapid-acting andlong-acting insulin analogs have been de-veloped. These analogs are associated withless hypoglycemia with equal A1C lower-ing in type 1 diabetes (107,108).

Recommended therapy for type 1 di-abetes consists of the following components:

Table 9dSummary of glycemic recommendations for many nonpregnant adults with diabetes

A1C ,7.0%*Preprandial capillary plasma glucose 70–130mg/dL* (3.9–7.2 mmol/L)Peak postprandial capillary plasma glucose† ,180 mg/dL* (,10.0 mmol/L)

c*Goals should be individualized based on:c duration of diabetesc age/life expectancyc comorbid conditionsc known CVD or advanced microvascular complicationsc hypoglycemia unawarenessc individual patient considerations

c More or less stringent glycemic goals may be appropriatefor individual patients

c Postprandial glucose may be targeted if A1C goals arenot met despite reaching preprandial glucose goals

†Postprandial glucose measurements should be made 1–2 h after the beginning of the meal, generally peaklevels in patients with diabetes.


Position Statement

1) use of MDI injections (three to four in-jections per day of basal and prandial in-sulin) or CSII therapy; 2) matching ofprandial insulin to carbohydrate intake,premeal blood glucose, and anticipatedactivity; and 3) for most patients (espe-cially if hypoglycemia is a problem), useof insulin analogs. There are excellent re-views available that guide the initiationand management of insulin therapyto achieve desired glycemic goals(107,109,110). Although most studies ofMDI versus pump therapy have been smalland of short duration, a systematic reviewand meta-analysis concluded that therewere no systematic differences in A1C orrates of severe hypoglycemia in childrenand adults between the two forms of inten-sive insulin therapy (70).

Because of the increased frequencyof other autoimmune diseases in type 1diabetes, screening for thyroid dysfunc-tion, vitamin B12 deficiency, or celiacdisease should be considered based onsigns and symptoms. Periodic screeningin absence of symptoms has been recom-mended, but the effectiveness and opti-mal frequency are unclear.

2. Pharmacological therapy for hyper-glycemia in type 2 diabetesRecommendationsc Metformin, if not contraindicated and iftolerated, is the preferred initial pharma-cological agent for type 2 diabetes. (A)

c In newly diagnosed type 2 diabeticpatients with markedly symptomaticand/or elevated blood glucose levels orA1C, consider insulin therapy, with orwithout additional agents, from theoutset. (E)

c If noninsulin monotherapy at maximaltolerated dose does not achieve or main-tain the A1C target over 3–6 months,add a second oral agent, a glucagon-likepeptide-1 (GLP-1) receptor agonist, orinsulin. (A)

c A patient-centered approach should beused to guide choice of pharmacologicalagents. Considerations include efficacy,cost, potential side effects, effects onweight, comorbidities, hypoglycemiarisk, and patient preferences. (E)

c Due to the progressive nature of type 2diabetes, insulin therapy is eventuallyindicated for many patients with type 2diabetes. (B)

The ADA and EASD have recentlypartnered on guidance for individualiza-tion of use of medication classes andcombinations in patients with type 2

diabetes (111). This 2012 position state-ment is less prescriptive than prior algo-rithms and discusses advantages anddisadvantages of the available medicationclasses and considerations for their use. Apatient-centered approach is stressed,taking into account patient preferences,cost and potential side effects of eachclass, effects on body weight, and hypo-glycemia risk. The position statement re-affirms metformin as the preferred initialagent, barring contraindication or intoler-ance, either in addition to lifestyle coun-seling and support for weight loss andexercise, or when lifestyle efforts alonehave not achieved ormaintained glycemicgoals. Metformin has a long-standingevidence base for efficacy and safety, isinexpensive, and may reduce risk of car-diovascular events (85). When metforminfails to achieve or maintain glycemic goals,another agent should be added. Althoughthere are a number of trials comparingdual therapy to metformin alone, few di-rectly compare drugs as add-on therapy.Comparative effectiveness meta-analyses(112) suggest that overall each new classof noninsulin agents added to initial ther-apy lowers A1C around 0.9–1.1%.

Many patients with type 2 diabeteseventually benefit from insulin therapy.The progressive nature of type 2 diabetesand its therapies should regularly beexplained in a matter-of-fact manner topatients, avoiding using insulin as a threator describing it as a failure or punishment.Providing patients with an algorithm forself-titration of insulin doses based onSMBG results improves glycemic controlin type 2 diabetic patients initiatinginsulin (113). For more details on phar-macotherapy for hyperglycemia in type2 diabetes, including a table of informa-tion about currently approved classesof medications for treating hyperglyce-mia in type 2 diabetes, readers are referredto the ADA-EASD position statement(111).

E. MNTGeneral recommendationsc Individuals who have prediabetes ordiabetes should receive individualizedMNT as needed to achieve treatmentgoals, preferably provided by a regis-tered dietitian familiar with the com-ponents of diabetes MNT. (A)

c Because MNT can result in cost-savingsand improved outcomes (B), MNTshould be adequately covered by in-surance and other payers. (E)

Energy balance, overweight, and obesityc Weight loss is recommended for alloverweight or obese individuals whohave or are at risk for diabetes. (A)

c For weight loss, either low-carbohydrate,low-fat calorie-restricted, or Mediterra-nean diets may be effective in the short-term (up to 2 years). (A)

c For patients on low-carbohydrate diets,monitor lipid profiles, renal function,and protein intake (in those with ne-phropathy) and adjust hypoglycemictherapy as needed. (E)

c Physical activity and behavior modifi-cation are important components ofweight loss programs and are mosthelpful in maintenance of weightloss. (B)

Recommendations for primaryprevention of type 2 diabetesc Among individuals at high risk for de-veloping type 2 diabetes, structuredprograms that emphasize lifestylechanges that include moderate weightloss (7% body weight) and regularphysical activity (150 min/week), withdietary strategies including reducedcalories and reduced intake of dietaryfat, can reduce the risk for developingdiabetes and are therefore recom-mended. (A)

c Individuals at risk for type 2 diabetesshould be encouraged to achieve theU.S. Department of Agriculture (USDA)recommendation for dietary fiber (14 gfiber/1,000 kcal) and foods containingwhole grains (one-half of grain intake).(B)

c Individuals at risk for type 2 diabetesshould be encouraged to limit theirintake of sugar-sweetened beverages(SSBs). (B)

Recommendations for managementof diabetesMacronutrients in diabetes managementc The mix of carbohydrate, protein, andfat may be adjusted to meet the meta-bolic goals and individual preferencesof the person with diabetes. (C)

c Monitoring carbohydrate, whether bycarbohydrate counting, choices, or ex-perience-based estimation, remains a keystrategy in achieving glycemic control. (B)

c Saturated fat intake should be ,7% oftotal calories. (B)

c Reducing intake of trans fat lowers LDLcholesterol and increases HDL choles-terol (A); therefore, intake of trans fatshould be minimized. (E)


Position Statement

Other nutrition recommendationsc If adults with diabetes choose to usealcohol, they should limit intake to amoderate amount (one drink per day orless for adult women and two drinksper day or less for adultmen) and shouldtake extra precautions to prevent hypo-glycemia. (E)

c Routine supplementation with anti-oxidants, such as vitamins E and C andcarotene, is not advised because of lackof evidence of efficacy and concern re-lated to long-term safety. (A)

c It is recommended that individualizedmeal planning include optimization offood choices to meet recommended di-etary allowance (RDA)/dietary referenceintake (DRI) for all micronutrients. (E)

MNT is an integral component of di-abetes prevention, management, and self-management education. In addition to itsrole in preventing and controlling diabetes,the ADA recognizes the importance ofnutrition as an essential component of anoverall healthy lifestyle. A full review of theevidence regarding nutrition in preventingand controlling diabetes and its complica-tions and additional nutrition-related rec-ommendations can be found in the ADAposition statement “Nutrition Recommen-dations and Interventions for Diabetes”(114), which is being updated as of 2013.Achieving nutrition-related goals requires acoordinated team effort that includes the ac-tive involvement of the person with predia-betes or diabetes. Because of the complexityof nutrition issues, it is recommended that aregistered dietitian who is knowledgeableand skilled in implementing nutritiontherapy into diabetes management andeducation be the team member who pro-vides MNT.

Clinical trials/outcome studies ofMNT have reported decreases in A1C at3–6 months ranging from 0.25 to 2.9%with higher reductions seen in type 2diabetes of shorter duration. Multiplestudies have demonstrated sustained im-provements in A1C at 12months and lon-ger when a registered dietitian providedfollow-up visits ranging from monthly to3 sessions per year (115–122). Studies innondiabetic individuals suggest thatMNT reduces LDL cholesterol by 15–25mg/dL up to 16% (123) and support arole for lifestyle modification in treatinghypertension (123,124).

Although the importance of weight lossfor overweight and obese individuals is welldocumented, an optimal macronutrientdistribution and dietary pattern of weight

loss diets has not been established. Asystematic review of 80 weight loss studiesof $1-year duration demonstrated thatmoderate weight loss achieved throughdiet alone, diet and exercise, and meal re-placements can be achieved and main-tained (4.8–8% weight loss at 12 months)(125). Both low-fat low-carbohydrate andMediterranean style eating patterns havebeen shown to promote weight loss withsimilar results after 1 to 2 years of follow-up (126–129). A meta-analysis showedthat at 6 months, low-carbohydrate dietswere associated with greater improvementsin triglyceride andHDLcholesterol concen-trations than low-fat diets; however, LDLcholesterol was significantly higher on thelow-carbohydrate diets (130).

Because of the effects of obesity oninsulin resistance, weight loss is an im-portant therapeutic objective for over-weight or obese individuals who are atrisk for diabetes (131). The multifactorialintensive lifestyle intervention used in theDPP, which included reduced intake of fatand calories, led to weight loss averaging7% at 6 months and maintenance of 5%weight loss at 3 years, associated with a58% reduction in incidence of type 2 di-abetes (23). An RCT looking at high-riskindividuals in Spain showed that theMediterranean dietary pattern reducedthe incidence of diabetes in the absenceof weight loss by 52% compared with thelow-fat control group (132).

Although our society abounds withexamples of high-calorie nutrient-poorfoods, large increases in the consumptionof SSBs have coincided with the epidemicsof obesity and type 2 diabetes. In a meta-analysis of eight prospective cohort stud-ies (n5 310,819), a diet high in consump-tion of SSBs was associated with thedevelopment of type 2 diabetes (n 515,043). Individuals in the highest versuslowest quantile of SSB intake had a 26%greater risk of developing diabetes (133).

For individuals with type 2 diabetes,studies have demonstrated that moderateweight loss (5% of body weight) is associ-ated with decreased insulin resistance, im-proved measures of glycemia and lipemia,and reduced blood pressure (134); longer-term studies ($52 weeks) showed mixedeffects onA1C in adultswith type 2diabetes(135–137), and in some studies resultswere confounded by pharmacologicalweight loss therapy. Look AHEAD (Actionfor Health in Diabetes) is a large clinical trialdesigned to determine whether long-termweight loss will improve glycemia and pre-vent cardiovascular events in subjects with

type 2 diabetes. One-year results of the in-tensive lifestyle intervention in this trialshow an average 8.6% weight loss, signifi-cant reduction of A1C, and reduction inseveral CVD risk factors (138), with benefitssustained at 4 years (139). At the time thisarticle was going to press, the LookAHEADtrial was halted early, after 11 years of fol-low-up, because there was no significantdifference in the primary cardiovascularoutcome between the weight loss and stan-dard care group (http://www.nih.gov/news/health/oct2012/niddk-19.htm). Multiplecardiovascular risk factors were improvedwith weight loss, and those participantson average were on fewer medications toachieve these improvements.

Although numerous studies have at-tempted to identify the optimal mix ofmacronutrients for meal plans of peoplewith diabetes, a recent systematic review(140) confirms that there is nomost effec-tive mix that applies broadly, and thatmacronutrient proportions should be indi-vidualized. It must be clearly recognizedthat regardless of the macronutrient mix,total caloric intake must be appropriate toweight management goal. Further, individ-ualization of the macronutrient composi-tion will depend on the metabolic statusof the patient (e.g., lipid profile, renal func-tion) and/or food preferences. A variety ofdietary meal patterns are likely effective inmanaging diabetes including Mediterra-nean-style, plant-based (vegan or vegetar-ian), low-fat and lower-carbohydrate eatingpatterns (127,141–143).

It should be noted that the RDA fordigestible carbohydrate is 130 g/day and isbased on providing adequate glucose as therequired fuel for the central nervous systemwithout reliance on glucose productionfrom ingested protein or fat. Althoughbrain fuel needs can be met on lowercarbohydrate diets, long-term metaboliceffects of very low-carbohydrate diets areunclear and such diets eliminate manyfoods that are important sources of energy,fiber, vitamins, and minerals and are im-portant in dietary palatability (144).

Saturated and trans fatty acids are theprincipal dietary determinants of plasmaLDL cholesterol. There is a lack of evi-dence on the effects of specific fatty acidson people with diabetes, so the recom-mended goals are consistent with thosefor individuals with CVD (123,145).

Reimbursement for MNTMNT, when delivered by a registereddietitian according to nutrition practiceguidelines, is reimbursed as part of the


Position Statement

Medicare program as overseen by theCenters for Medicare and Medicaid Serv-ices (CMS), as well as many health in-surance plans.

F. Diabetes self-managementeducation and supportRecommendationsc People with diabetes should receiveDSME and diabetes self-managementsupport (DSMS) according to NationalStandards for Diabetes Self-Manage-ment Education and Support whentheir diabetes is diagnosed and asneeded thereafter. (B)

c Effective self-management and qualityof life are the key outcomes of DSMEand DSMS and should be measuredand monitored as part of care. (C)

c DSME and DSMS should addresspsychosocial issues, since emotionalwell-being is associated with positivediabetes outcomes. (C)

c DSME and DSMS programs are appro-priate venues for people with prediabetesto receive education and support to de-velop and maintain behaviors that canprevent or delay the onset of diabetes. (C)

c Because DSME and DSMS can result incost-savings and improved outcomes (B),DSME and DSMS should be adequatelyreimbursed by third-party payers. (E)

DSME and DSMS are essential ele-ments of diabetes care (146–151), and re-cently updated National Standards forDiabetes Self-Management Education andSupport (152) are based on evidence for itsbenefits. Education helps people with dia-betes initiate effective self-management andcope with diabetes when they are first di-agnosed. Ongoing DSME and DSMS alsohelp people with diabetes maintain effec-tive self-management throughout a lifetimeof diabetes as they face new challenges andtreatment advances become available.DSME helps patients optimize metaboliccontrol, prevent and manage complica-tions, and maximize quality of life in acost-effective manner (153).

DSME and DSMS are the ongoingprocesses of facilitating the knowledge,skill, and ability necessary for diabetesself-care. This process incorporates theneeds, goals, and life experiences of theperson with diabetes. The overall objec-tives of DSME and DSMS are to supportinformed decisionmaking, self-care behav-iors, problem-solving, and active collabo-ration with the health care team to improveclinical outcomes, health status, and qual-ity of life in a cost-effective manner (152).

Current best practice of DSME is askill-based approach that focuses onhelping those with diabetes make in-formed self-management choices. DSMEhas changed from a didactic approachfocusing on providing information tomore theoretically based empowermentmodels that focus on helping those withdiabetes make informed self-managementdecisions. Care of diabetes has shifted toan approach that is more patient centeredand places the person with diabetesand his or her family at the center of thecare model working in collaborationwith health care professionals. Patient-centered care is respectful of and respon-sive to individual patient preferences,needs, and values and ensures that patientvalues guide all decision making (154).

Evidence for the benefits of DSME andDSMSMultiple studies have found that DSME isassociated with improved diabetes knowl-edge and improved self-care behavior(146), improved clinical outcomes suchas lower A1C (147,148,150,151,155–158), lower self-reported weight (146), im-proved quality of life (149,156,159),healthy coping (160), and lower costs(161). Better outcomes were reported forDSME interventions that were longer andincluded follow-up support (DSMS)(146,162–165), that were culturally(166,167) and age appropriate (168,169)and were tailored to individual needs andpreferences, and that addressed psychoso-cial issues and incorporated behavioralstrategies (146,150,170,171). Both indi-vidual and group approaches have beenfound effective (172,173). There is growingevidence for the role of community healthworkers and peer (174–180) and lay lead-ers (181) in delivering DSME and DSMS inconjunction with the core team (182).

Diabetes education is associated withincreased use of primary and preventiveservices (161,183) and lower use of acute,inpatient hospital services (161). Patientswho participate in diabetes education aremore likely to follow best practice treat-ment recommendations, particularlyamong the Medicare population, andhave lower Medicare and commercialclaim costs (184,185).

The National Standards for DiabetesSelf-Management Education andSupportThe National Standards for Diabetes Self-Management Education and Support aredesigned to define quality DSME and

DSMS and to assist diabetes educatorsin a variety of settings to provide evidence-based education and self-managementsupport (152). The standards, recently up-dated, are reviewed and updated every 5years by a task force representing key or-ganizations involved in the field of diabeteseducation and care.

DSME and DSMS providers and peo-ple with prediabetesThe new standards for DSME and DSMSalso apply to the education and support ofpeople with prediabetes. Currently, thereare significant barriers to the provision ofeducation and support to those with pre-diabetes. However, the strategies for sup-porting successful behavior change andthe healthy behaviors recommended forpeople with prediabetes are largely iden-tical to those for people with diabetes. Asbarriers to care are overcome, providers ofDSME and DSMS, given their training andexperience, are particularly well equippedto assist people with prediabetes in de-veloping and maintaining behaviors thatcan prevent or delay the onset of diabetes(152,186).

Reimbursement for DSME and DSMSDSME, when provided by a program thatmeets national standards for DSME and isrecognized by the ADA or other approvalbodies, is reimbursed as part of theMedicareprogram as overseen by the CMS. DSMEis also covered by most health insuranceplans. Although DSMS has been shown tobe instrumental for improving outcomes, asdescribed in the “Evidence for the benefits ofDSME and DSMS,” and can be provided informats such as phone calls and via tele-health, it currently has limited reimburse-ment as face-to-face visits included asfollow-up to DSME.

G. Physical activityRecommendationsc Adults with diabetes should be advisedto perform at least 150 min/week ofmoderate-intensity aerobic physicalactivity (50–70% of maximum heartrate), spread over at least 3 days/weekwith no more than two consecutivedays without exercise. (A)

c In the absence of contraindications,adults with type 2 diabetes should beencouraged to perform resistance train-ing at least twice per week. (A)

Exercise is an important part of thediabetes management plan. Regular exer-cise has been shown to improve blood


Position Statement

glucose control, reduce cardiovascular riskfactors, contribute to weight loss, andimprove well-being. Furthermore, regularexercise may prevent type 2 diabetes inhigh-risk individuals (23–25). Structuredexercise interventions of at least 8 weeks’duration have been shown to lower A1C byan average of 0.66% in people with type2 diabetes, even with no significant changein BMI (187). Higher levels of exercise in-tensity are associated with greater improve-ments in A1C and in fitness (188). A jointposition statement of the ADA and theAmerican College of Sports Medicine(ACSM) summarizes the evidence for thebenefits of exercise in people with type 2diabetes (189).

Frequency and type of exerciseThe U.S. Department of Health and HumanServices’ Physical Activity Guidelines forAmericans (190) suggest that adults overage 18 years do 150 min/week of moder-ate-intensity, or 75 min/week of vigorousaerobic physical activity, or an equivalentcombination of the two. In addition, theguidelines suggest that adults also domuscle-strengthening activities that in-volve all major muscle groups $2 days/week. The guidelines suggest that adultsover age 65 years, or those with disabili-ties, follow the adult guidelines if possibleor (if this is not possible) be as physicallyactive as they are able. Studies included inthe meta-analysis of effects of exercise in-terventions on glycemic control (187)had a mean number of sessions perweek of 3.4, with a mean of 49 min persession. The DPP lifestyle intervention,which included 150 min/week of moder-ate-intensity exercise, had a beneficialeffect on glycemia in those with predia-betes. Therefore, it seems reasonable torecommend that people with diabetestry to follow the physical activity guide-lines for the general population.

Progressive resistance exercise im-proves insulin sensitivity in older menwith type 2 diabetes to the same or even agreater extent as aerobic exercise (191).Clinical trials have provided strong evidencefor the A1C lowering value of resistancetraining in older adults with type 2 dia-betes (192,193) and for an additive ben-efit of combined aerobic and resistanceexercise in adults with type 2 diabetes(194,195). In the absence of contraindi-cations, patients with type 2 diabetesshould be encouraged to do at least twoweekly sessions of resistance exercise (ex-ercise with free weights or weight ma-chines), with each session consisting of

at least one set of five or more differentresistance exercises involving the largemuscle groups (189).

Evaluation of the diabetic patient beforerecommending an exercise programPrior guidelines suggested that beforerecommending a program of physical activ-ity, the provider should assess patients withmultiple cardiovascular risk factors for cor-onary artery disease (CAD). As discussedmore fully in Section VI.A.5, the area ofscreening asymptomatic diabetic patientsfor CAD remains unclear, and a recent ADAconsensus statement on this issue con-cluded that routine screening is not recom-mended (196). Providers should use clinicaljudgment in this area. Certainly, high-riskpatients should be encouraged to start withshort periods of low-intensity exercise andincrease the intensity and duration slowly.

Providers should assess patients forconditions that might contraindicate cer-tain types of exercise or predispose toinjury, such as uncontrolled hyperten-sion, severe autonomic neuropathy, se-vere peripheral neuropathy or history offoot lesions, and unstable proliferativeretinopathy. The patient’s age and pre-vious physical activity level should beconsidered.

Exercise in the presence of nonoptimalglycemic controlHyperglycemia. When people with type1 diabetes are deprived of insulin for 12–48 h and are ketotic, exercise can worsenhyperglycemia and ketosis (197); there-fore, vigorous activity should be avoidedin the presence of ketosis. However, it isnot necessary to postpone exercise basedsimply on hyperglycemia, provided thepatient feels well and urine and/or bloodketones are negative.Hypoglycemia. In individuals taking in-sulin and/or insulin secretagogues, phys-ical activity can cause hypoglycemia ifmedication dose or carbohydrate con-sumption is not altered. For individualson these therapies, added carbohydrateshould be ingested if pre-exercise glucoselevels are,100 mg/dL (5.6 mmol/L). Hy-poglycemia is rare in diabetic individualswho are not treated with insulin or insulinsecretagogues, and no preventive mea-sures for hypoglycemia are usually ad-vised in these cases.

Exercise in the presence of specificlong-term complications of diabetesRetinopathy. In the presence of prolifer-ative diabetic retinopathy (PDR) or severe

non-PDR (NPDR), vigorous aerobic orresistance exercise may be contraindi-cated because of the risk of triggeringvitreous hemorrhage or retinal detach-ment (198).Peripheral neuropathy. Decreased painsensation in the extremities results inincreased risk of skin breakdown andinfection and of Charcot joint destruc-tion. Prior recommendations have ad-vised non–weight-bearing exercise forpatients with severe peripheral neuropa-thy. However, studies have shown thatmoderate-intensity walking may notlead to increased risk of foot ulcers orreulceration in those with peripheralneuropathy (199). All individuals withperipheral neuropathy should wearproper footwear and examine their feetdaily to detect lesions early. Anyonewith a foot injury or open sore shouldbe restricted to non–weight-bearing ac-tivities.Autonomic neuropathy. Autonomic neu-ropathy can increase the risk of exercise-induced injury or adverse event throughdecreased cardiac responsiveness to exer-cise, postural hypotension, impaired ther-moregulation, impaired night vision due toimpaired papillary reaction, and unpredict-able carbohydrate delivery from gastropa-resis predisposing to hypoglycemia (200).Autonomic neuropathy is also strongly as-sociated with CVD in people with diabetes(201,202). People with diabetic autonomicneuropathy should undergo cardiac inves-tigation before beginning physical activitymore intense than that to which they areaccustomed.Albuminuria and nephropathy. Physicalactivity can acutely increase urinary pro-tein excretion. However, there is no evi-dence that vigorous exercise increases therate of progression of diabetic kidneydisease, and there is likely no need forany specific exercise restrictions for peo-ple with diabetic kidney disease (203).

H. Psychosocial assessment and careRecommendationsc It is reasonable to include assessment ofthe patient’s psychological and socialsituation as an ongoing part of themedical management of diabetes. (E)

c Psychosocial screening and follow-upmay include, but is not limited to, at-titudes about the illness, expectationsfor medical management and out-comes, affect/mood, general and di-abetes-related quality of life, resources(financial, social, and emotional), andpsychiatric history. (E)


Position Statement

c Screen for psychosocial problems suchas depression and diabetes-relateddistress, anxiety, eating disorders,and cognitive impairment when self-management is poor. (B)

It is important to establish that emotionalwell-being is part of diabetes care and self-management. Psychological and socialproblems can impair the individual’s(204–207) or family’s ability to carry outdiabetes care tasks and therefore compro-mise health status. There are opportuni-ties for the clinician to assess psychosocialstatus in a timely and efficient manner sothat referral for appropriate services canbe accomplished. A systematic review andmeta-analysis showed that psychosocialinterventions modestly but significantlyimproved A1C (standardizedmean differ-ence 20.29%) and mental health out-comes. However, there was a limitedassociation between the effects on A1Cand mental health, and no interventioncharacteristics predicted benefit on bothoutcomes (208).

Key opportunities for screening ofpsychosocial status occur at diagnosis,during regularly scheduled managementvisits, during hospitalizations, at discov-ery of complications, or when problemswith glucose control, quality of life, oradherence are identified. Patients arelikely to exhibit psychological vulnerabil-ity at diagnosis and when their medicalstatus changes (e.g., the end of the hon-eymoon period), when the need for in-tensified treatment is evident, and whencomplications are discovered (206).

Depression affects about 20–25% ofpeople with diabetes (207) and increasesthe risk forMI and post-MI (209,210) andall-cause (211) mortality. Other issuesknown to impact self-management andhealth outcomes include but are not limitedto attitudes about the illness, expectationsfor medical management and outcomes,affect/mood, general and diabetes-relatedquality of life, diabetes-related distress(212,213), resources (financial, social,and emotional) (214), and psychiatric his-tory (215–217). Screening tools are avail-able for a number of these areas (170).Indications for referral to a mental healthspecialist familiar with diabetes manage-ment may include gross disregard for themedical regimen (by self or others) (217),depression, possibility of self-harm, debil-itating anxiety (alone or with depression),indications of an eating disorder (218), orcognitive functioning that significantlyimpairs judgment. It is preferable to

incorporate psychological assessmentand treatment into routine care ratherthan waiting for identification of a specificproblem or deterioration in psychologicalstatus (170). Although the clinician maynot feel qualified to treat psychologicalproblems (219), utilizing the patient-provider relationship as a foundationcan increase the likelihood that the pa-tient will accept referral for other services.Collaborative care interventions andusing a team approach have demon-strated efficacy in diabetes and depres-sion (220,221).

I. When treatment goals are not metFor a variety of reasons, some people withdiabetes and their health care providersdo not achieve the desired goals of treat-ment (Table 9). Rethinking the treatmentregimen may require assessment of barri-ers including income, health literacy,diabetes distress, depression, and com-peting demands, including those relatedto family responsibilities and dynamics.Other strategies may include culturallyappropriate and enhanced DSME andDSMS, co-management with a diabetesteam, referral to a medical social workerfor assistance with insurance coverage, orchange in pharmacological therapy. Initi-ation of or increase in SMBG, utilizationof CGM, frequent contact with the pa-tient, or referral to a mental health pro-fessional or physician with specialexpertise in diabetes may be useful.

J. Intercurrent illnessThe stress of illness, trauma, and/or sur-gery frequently aggravates glycemic con-trol and may precipitate diabeticketoacidosis (DKA) or nonketotic hyper-osmolar statedlife-threatening conditionsthat require immediate medical care to pre-vent complications and death. Any condi-tion leading to deterioration in glycemiccontrol necessitatesmore frequentmonitor-ing of blood glucose and (in ketosis-pronepatients) urine or blood ketones. Markedhyperglycemia requires temporary adjust-ment of the treatment program and, if ac-companied by ketosis, vomiting, oralteration in level of consciousness, imme-diate interaction with the diabetes careteam. The patient treated with noninsulintherapies or MNT alone may temporarilyrequire insulin. Adequate fluid and caloricintake must be assured. Infection or dehy-dration is more likely to necessitate hospi-talization of the person with diabetes thanthe person without diabetes.

The hospitalized patient should betreated by a physician with expertise inthe management of diabetes. For furtherinformation on management of patientswith hyperglycemia in the hospital, seeSection IX.A. For further informationon management of DKA or hyperglycemicnonketotic hyperosmolar state, refer to theADA statement on hyperglycemic crises(222).

K. HypoglycemiaRecommendationsc Individuals at risk for hypoglycemiashould be asked about symptomaticand asymptomatic hypoglycemia ateach encounter. (C)

c Glucose (15–20 g) is the preferredtreatment for the conscious individualwith hypoglycemia, although any formof carbohydrate that contains glucosemay be used. If SMBG 15 min aftertreatment shows continued hypogly-cemia, the treatment should be re-peated. Once SMBG glucose returns tonormal, the individual should consume ameal or snack to prevent recurrence ofhypoglycemia. (E)

c Glucagon should be prescribed for allindividuals at significant risk of severehypoglycemia, and caregivers or familymembers of these individuals shouldbe instructed on its administration.Glucagon administration is not limitedto health care professionals. (E)

c Hypoglycemia unawareness or one ormore episodes of severe hypoglycemiashould trigger re-evaluation of thetreatment regimen. (E)

c Insulin-treated patients with hypogly-cemia unawareness or an episode ofsevere hypoglycemia should be advisedto raise their glycemic targets to strictlyavoid further hypoglycemia for at leastseveral weeks, to partially reverse hy-poglycemia unawareness, and to re-duce risk of future episodes. (A)

c Ongoing assessment of cognitive func-tion is suggestedwith increased vigilancefor hypoglycemia by the clinician, pa-tient, and caregivers if low cognitionand/or declining cognition is found. (B)

Hypoglycemia is the leading limitingfactor in the glycemic management of type1 and insulin-treated type 2 diabetes (223).Mild hypoglycemia may be inconvenientor frightening to patients with diabetes,and more severe hypoglycemia can causeacute harm to the person with diabetes orothers, if it causes falls, motor vehicle


Position Statement

accidents, or other injury. A large cohortstudy suggested that among older adultswith type 2 diabetes, a history of severehypoglycemia was associated with greaterrisk of dementia (224). Conversely, in asubstudy of the ACCORD trial, cognitiveimpairment at baseline or decline in cog-nitive function during the trial was signif-icantly associated with subsequentepisodes of severe hypoglycemia (225).Evidence from the DCCT/EDIC trial,which involved younger adults and ado-lescents with type 1 diabetes, suggested noassociation of frequency of severe hypo-glycemia with cognitive decline (226). Asdiscussed in the Section VIII.A.1.a, a fewstudies have suggested that severe hypo-glycemia in very young children is associ-ated with mild impairments in cognitivefunction.

As described in the Section V.b.2,severe hypoglycemia was associated withmortality in participants in both the stan-dard and intensive glycemia arms of theACCORD trial, but the relationships withachieved A1C and treatment intensitywere not straightforward. An associationof severe hypoglycemia with mortalitywas also found in the ADVANCE trial(227), but its association with other out-comes such as pulmonary and skin disor-ders raises the question of whether severehypoglycemia is a marker for a sicker pa-tient, rather than a cause of mortality. Anassociation of self-reported severe hypo-glycemia with 5-year mortality has alsobeen reported in clinical practice (228).At the time this statement went to press,the ADA and The Endocrine Society werefinalizing a Hypoglycemia Work Groupreport, where the causes of and associa-tions with hypoglycemia are discussed indepth.

Treatment of hypoglycemia (plasmaglucose,70 mg/dL) requires ingestion ofglucose- or carbohydrate-containingfoods. The acute glycemic response cor-relates better with the glucose contentthan with the carbohydrate content ofthe food. Although pure glucose is thepreferred treatment, any form of carbohy-drate that contains glucose will raiseblood glucose. Added fat may retard andthen prolong the acute glycemic response.Ongoing activity of insulin or insulin sec-retagoguesmay lead to recurrence of hypo-glycemia unless further food is ingestedafter recovery.

Severe hypoglycemia (where the in-dividual requires the assistance of an-other person and cannot be treated withoral carbohydrate due to confusion or

unconsciousness) should be treated usingemergency glucagon kits, which require aprescription. Those in close contact with,or having custodial care of, people withhypoglycemia-prone diabetes (familymembers, roommates, school personnel,child care providers, correctional institu-tion staff, or coworkers) should be in-structed in use of such kits. An individualdoes not need to be a health care pro-fessional to safely administer glucagon.Care should be taken to ensure that un-expired glucagon kits are available.

Prevention of hypoglycemia is a crit-ical component of diabetes management.Particularly for insulin-treated patients,SMBG and, for some patients, CGM todetect incipient hypoglycemia and assessadequacy of treatment are a key compo-nent of safe therapy. Patients should un-derstand situations that increase their riskof hypoglycemia, such as when fasting fortests or procedures, during or after in-tense exercise, and during sleep and thatincrease the risk of harm to self or othersfrom hypoglycemia, such as with driving.Teaching people with diabetes to balanceinsulin use, carbohydrate intake, andexercise is a necessary but not alwayssufficient strategy for prevention. In type1 diabetes and severely insulin-deficienttype 2 diabetes, the syndrome of hypo-glycemia unawareness, or hypoglycemia-associated autonomic failure, can severelycompromise stringent diabetes controland quality of life. The deficient counter-regulatory hormone release and autonomicresponses in this syndrome are both riskfactors for, and caused by, hypoglycemia. Acorollary to this “vicious cycle” is that sev-eral weeks of avoidance of hypoglycemiahas been demonstrated to improvecounter-regulation and awareness to someextent in many patients (229). Hence,patients with one or more episodes ofsevere hypoglycemia may benefit fromat least short-term relaxation of glycemictargets.

L. Bariatric surgeryRecommendationsc Bariatric surgery may be considered foradults with BMI$35 kg/m2 and type 2diabetes, especially if the diabetes orassociated comorbidities are difficult tocontrol with lifestyle and pharmaco-logical therapy. (B)

c Patients with type 2 diabetes who haveundergone bariatric surgery need life-long lifestyle support and medicalmonitoring. (B)

c Although small trials have shown gly-cemic benefit of bariatric surgery inpatients with type 2 diabetes and BMI30–35 kg/m2, there is currently in-sufficient evidence to generally rec-ommend surgery in patients with BMI,35 kg/m2 outside of a research pro-tocol. (E)

c The long-termbenefits, cost-effectiveness,and risks of bariatric surgery in indivi-duals with type 2 diabetes should bestudied in well-designed controlled trialswith optimalmedical and lifestyle therapyas the comparator. (E)

Gastric reduction surgery, either gas-tric banding or procedures that involvebypassing, transposing, or resecting sec-tions of the small intestine, when part of acomprehensive team approach, can be aneffective weight loss treatment for severeobesity, and national guidelines supportits consideration for people with type2 diabetes who have BMI of 35 kg/m2

or greater. Bariatric surgery has beenshown to lead to near- or complete nor-malization of glycemia in ;40–95% ofpatients with type 2 diabetes, dependingon the study and the surgical procedure(230–232). A meta-analysis of studies ofbariatric surgery involving 3,188 patientswith diabetes reported that 78% had re-mission of diabetes (normalization ofblood glucose levels in the absence ofmedications) and that the remission rateswere sustained in studies that had follow-up exceeding 2 years (233). Remissionrates tend to be lower with proceduresthat only constrict the stomach andhigher with those that bypass portionsof the small intestine. Additionally, thereis a suggestion that intestinal bypass pro-ceduresmay have glycemic effects that areindependent of their effects on weight,perhaps involving the incretin axis.

There is also evidence for diabetesremission in subjects who are less obese.One randomized trial compared adjust-able gastric banding to “best available”medical and lifestyle therapy in subjectswith type 2 diabetes and BMI 30–40 kg/m2

(234). Overall, 73% of surgically treatedpatients achieved “remission” of their di-abetes compared with 13% of those trea-ted medically. The latter group lost only1.7% of body weight, suggesting thattheir therapy was not optimal. Overallthe trial had 60 subjects, and only 13had a BMI under 35 kg/m2, making it dif-ficult to generalize these results widely todiabetic patients who are less severelyobese or with longer duration of diabetes.


Position Statement

In a recent nonrandomized study of 66people with BMI of 30–35 kg/m2, 88%of participants had remission of theirtype 2 diabetes up to 6 years after surgery(235).

Bariatric surgery is costly in the short-term and has some risks. Rates of mor-bidity andmortality directly related to thesurgery have been reduced considerablyin recent years, with 30-day mortalityrates now 0.28%, similar to those oflaparoscopic cholecystectomy (236).Longer-term concerns include vitaminand mineral deficiencies, osteoporosis,and rare but often severe hypoglycemiafrom insulin hypersecretion. Cohortstudies attempting to match subjectssuggest that the procedure may reducelonger-term mortality rates (237). Recentretrospective analyses and modelingstudies suggest that these proceduresmay be cost-effective, when one considersreduction in subsequent health care costs(238–240).

Some caution about the benefits ofbariatric surgery might come from recentstudies. Propensity score–adjusted anal-yses of older severely obese patients withhigh baseline mortality in Veterans Af-fairs Medical Centers found that the useof bariatric surgery was not associatedwith decreased mortality compared withusual care during a mean 6.7 years offollow-up (241). A study that followedpatients who had undergone laparo-scopic adjustable gastric banding(LAGB) for 12 years found that 60%were satisfied with the procedure. Nearlyone out of three patients experiencedband erosion, and almost half requiredremoval of their bands. The authors’ con-clusion was that “LAGB appears to resultin relatively poor long-term outcomes”(242). Studies of the mechanisms of gly-cemic improvement and long-term bene-fits and risks of bariatric surgery inindividuals with type 2 diabetes, espe-cially those who are not severely obese,will require well-designed clinical trials,with optimal medical and lifestyle ther-apy of diabetes and cardiovascular riskfactors as the comparator.

M. ImmunizationRecommendationsc Annually provide an influenza vaccineto all diabetic patients $6 months ofage. (C)

c Administer pneumococcal polysaccharidevaccine to all diabetic patients $2 yearsof age. A one-time revaccination is rec-ommended for individuals.64 years of

age previously immunized when theywere ,65 years of age if the vaccinewas administered.5 years ago. Otherindications for repeat vaccination in-clude nephrotic syndrome, chronicrenal disease, and other immunocom-promised states, such as after trans-plantation. (C)

c Administer hepatitis B vaccination tounvaccinated adults with diabetes whoare aged 19 through 59 years. (C)

c Consider administering hepatitis B vac-cination to unvaccinated adults withdiabetes who are aged$60 years. (C)

Influenza and pneumonia are common,preventable infectious diseases associatedwith high mortality and morbidity in theelderly and in people with chronic dis-eases. Though there are limited studiesreporting the morbidity and mortality ofinfluenza and pneumococcal pneumoniaspecifically in people with diabetes, ob-servational studies of patients with a va-riety of chronic illnesses, includingdiabetes, show that these conditions areassociated with an increase in hospital-izations for influenza and its complica-tions. People with diabetes may be atincreased risk of the bacteremic form ofpneumococcal infection and have beenreported to have a high risk of nosocomialbacteremia, which has a mortality rate ashigh as 50% (243).

Safe and effective vaccines are avail-able that can greatly reduce the risk ofserious complications from these diseases(244,245). In a case-control series, influ-enza vaccine was shown to reduce dia-betes-related hospital admission by asmuch as 79% during flu epidemics(244). There is sufficient evidence to sup-port that people with diabetes haveappropriate serological and clinical re-sponses to these vaccinations. The Cen-ters for Disease Control and Prevention(CDC) Advisory Committee on Immuni-zation Practices recommends influenzaand pneumococcal vaccines for all indi-viduals with diabetes (http://www.cdc.gov/vaccines/recs/).

Late in 2012, the Advisory Commit-tee on Immunization Practices of the CDCrecommended that all previously unvac-cinated adults with diabetes aged 19through 59 years be vaccinated againsthepatitis B virus (HBV) as soon as possibleafter a diagnosis of diabetes is made andthat vaccination be considered for thoseaged $60 years, after assessing risk andlikelihood of an adequate immune re-sponse (246). At least 29 outbreaks of

HBV in long-term care facilities and hos-pitals have been reported to the CDC,with the majority involving adults withdiabetes receiving “assisted blood glucosemonitoring,” in which such monitoring isdone by a health care professional withresponsibility for more than one patient.HBV is highly transmissible and stable forlong periods of time on surfaces such aslancing devices and blood glucose meters,even when no blood is visible. Blood suf-ficient to transmit the virus has also beenfound in the reservoirs of insulin pens,resulting in warnings against sharingsuch devices between patients.

The CDC analyses suggest that, ex-cluding persons with HBV-related riskbehaviors, acute HBV infection is abouttwice as high among adults with diabetesaged $23 years compared with adultswithout diabetes. Seroprevalence of anti-body toHBV core antigen, suggesting pastor current infection, is 60% higher amongadults with diabetes than those without,and there is some evidence that diabetesimparts a higher HBV case fatality rate.The age differentiation in the recommen-dations stems from CDC economic mod-els suggesting that vaccination of adultswith diabetes who were aged 20–59 yearswould cost an estimated $75,000 perquality-adjusted life-year saved, whilecost per quality-adjusted life-year savedincreased significantly at higher ages. Inaddition to competing causes of mortalityin older adults, the immune response tothe vaccine declines with age (246).

These new recommendations regard-ing HBV vaccinations serve as a reminderto clinicians that children and adults withdiabetes need a number of vaccinations,both those specifically indicated becauseof diabetes as well as those recommendedfor the general population (http://www.cdc.gov/vaccines/recs/).

VI. PREVENTION ANDMANAGEMENT OF DIABETESCOMPLICATIONS

A. CVDCVD is the major cause of morbidity andmortality for individuals with diabetesand the largest contributor to the directand indirect costs of diabetes. The commonconditions coexisting with type 2 diabetes(e.g., hypertension and dyslipidemia) areclear risk factors for CVD, and diabetesitself confers independent risk. Numerousstudies have shown the efficacy of con-trolling individual cardiovascular riskfactors in preventing or slowing CVD in


Position Statement

people with diabetes. Large benefits areseen when multiple risk factors are ad-dressed globally (247,248). There is evi-dence that measures of 10-year coronaryheart disease (CHD) risk among U.S.adults with diabetes have improved signif-icantly over the past decade (249).

1. Hypertension/blood pressurecontrolRecommendationsScreening and diagnosisc Blood pressure should be measured atevery routine visit. Patients found tohave elevated blood pressure shouldhave blood pressure confirmed on aseparate day. (B)

Goalsc People with diabetes and hypertensionshould be treated to a systolic bloodpressure goal of ,140 mmHg. (B)

c Lower systolic targets, such as ,130mmHg, may be appropriate for certainindividuals, such as younger patients,if it can be achieved without unduetreatment burden. (C)

c Patients with diabetes should be treatedto a diastolic blood pressure,80mmHg.(B)

Treatmentc Patients with a blood pressure .120/80 mmHg should be advised on life-style changes to reduce blood pressure.(B)

c Patients with confirmed blood pressure$140/80 mmHg should, in addition tolifestyle therapy, have prompt initia-tion and timely subsequent titration ofpharmacological therapy to achieveblood pressure goals. (B)

c Lifestyle therapy for elevated bloodpressure consists of weight loss, ifoverweight; Dietary Approaches toStop Hypertension (DASH)-style di-etary pattern including reducing so-dium and increasing potassium intake;moderation of alcohol intake; and in-creased physical activity. (B)

c Pharmacological therapy for patientswith diabetes and hypertension shouldbe with a regimen that includes eitheran ACE inhibitor or an angiotensinreceptor blocker (ARB). If one class isnot tolerated, the other should be sub-stituted. (C)

c Multiple-drug therapy (two or moreagents at maximal doses) is generallyrequired to achieve blood pressuretargets. (B)

c Administer one or more antihyperten-sive medications at bedtime. (A)

c If ACE inhibitors, ARBs, or diuretics areused, serum creatinine/estimated glo-merular filtration rate (eGFR) and serumpotassium levels should be monitored.(E)

c In pregnant patients with diabetes andchronic hypertension, blood pressuretarget goals of 110–129/65–79 mmHgare suggested in the interest of long-term maternal health and minimizingimpaired fetal growth. ACE inhibitorsand ARBs are contraindicated duringpregnancy. (E)

Hypertension is a common comor-bidity of diabetes, affecting themajority ofpatients, with prevalence depending ontype of diabetes, age, obesity, and ethnic-ity. Hypertension is a major risk factor forboth CVD and microvascular complica-tions. In type 1 diabetes, hypertension isoften the result of underlying nephropa-thy, while in type 2 diabetes it usuallycoexists with other cardiometabolic riskfactors.

Screening and diagnosisMeasurement of blood pressure in theoffice should be done by a trained in-dividual and follow the guidelines es-tablished for nondiabetic individuals:measurement in the seated position,with feet on the floor and arm supportedat heart level, after 5 min of rest. Cuff sizeshould be appropriate for the upper armcircumference. Elevated values should beconfirmed on a separate day.

Home blood pressure self-monitoringand 24-h ambulatory blood pressuremonitoring may provide additional evi-dence of “white coat” and masked hyper-tension and other discrepancies betweenoffice and “true” blood pressure. Studiesin nondiabetic populations found thathome measurements may better correlatewith CVD risk than office measurements(250,251). However, the preponderanceof the evidence of benefits of treatment ofhypertension in people with diabetes isbased on office measurements.

Treatment goalsEpidemiological analyses show that bloodpressure .115/75 mmHg is associatedwith increased cardiovascular event ratesand mortality in individuals with diabetes(252–254) and that systolic blood pres-sure above 120mmHg predicts long-termend-stage renal disease (ESRD). Random-ized clinical trials have demonstrated thebenefit (reduction of CHD events, stroke,and nephropathy) of lowering blood

pressure to ,140 mmHg systolic and,80 mmHg diastolic in individuals withdiabetes (252,255–257). The evidence forbenefits from lower systolic blood pres-sure targets is, however, limited.

The ACCORD trial examinedwhether blood pressure lowering to sys-tolic blood pressure ,120 mmHg pro-vides greater cardiovascular protectionthan a systolic blood pressure level of130–140 mmHg in patients with type 2diabetes at high risk for CVD (258). Theblood pressure achieved in the intensivegroup was 119/64 mmHg and in the stan-dard group 133/70mmHg; the goals wereattained with an average of 3.4 medica-tions per participant in the intensivegroup and 2.1 in the standard therapygroup. The hazard ratio for the primaryend point (nonfatal MI, nonfatal stroke,and CVD death) in the intensive groupwas 0.88 (95% CI 0.73–1.06, P 5 0.20).Of the prespecified secondary end points,only stroke and nonfatal stroke were sta-tistically significantly reduced by inten-sive blood pressure treatment, with ahazard ratio of 0.59 (95% CI 0.39–0.89,P 5 0.01) and 0.63 (95% CI 0.41–0.96,P 5 0.03), respectively. Absolute strokeevent rates were low; the number neededto treat to prevent one stroke over thecourse of 5 years with intensive bloodpressure management is 89. Serious ad-verse event rates (including syncope andhyperkalemia) were higher with intensivetargets (3.3% vs. 1.3%, P5 0.001). Ratesof albuminuria were reduced with moreintensive blood pressure goals, but therewere no differences in renal function inthis 5-year trial (and in fact more adverseevents related to reduced eGFRwithmoreintensive goals) nor in other microvascu-lar complications.

Other recent randomized trial datainclude those of the ADVANCE trial inwhich treatment with an ACE inhibitorand a thiazide-type diuretic reduced therate of death but not the compositemacrovascular outcome. However, theADVANCE trial had no specified targetsfor the randomized comparison, and themean systolic blood pressure in the in-tensive group (135mmHg)was not as lowas the mean systolic blood pressure evenin the ACCORD standard-therapy group(259). Post hoc analysis of achieved bloodpressure in several hypertension treat-ment trials has suggested no benefit oflower achieved systolic blood pressure.As an example, among 6,400 patientswith diabetes and CAD enrolled in onetrial, “tight control” (achieved systolic


Position Statement

blood pressure,130 mmHg) was not as-sociated with improved cardiovascularoutcomes compared with “usual care”(achieved systolic blood pressure 130–140 mmHg) (260). Similar findingemerged from an analysis of another trial,but additionally those with achieved sys-tolic blood pressure (,115 mmHg) hadincreased rates of CVD events (thoughlower rates of stroke) (261).

Observational data, including thosederived from clinical trials, may be in-appropriate to use for defining bloodpressure targets since sicker patientsmay have low blood pressure or, con-versely, healthier or more adherent pa-tients may achieve goals more readily. Arecent meta-analysis of randomized trialsof adults with type 2 diabetes comparingprespecified blood pressure targets foundno significant reduction in mortality ornonfatal MI. There was a statisticallysignificant 35% relative reduction instroke, but the absolute risk reductionwas only 1% (262). Other outcomes, suchas indicators of microvascular complica-tions, were not examined. Anothermeta-analysis that included both trialscomparing blood pressure goals and trialscomparing treatment strategies con-cluded that a systolic treatment goal of130–135 mmHg was acceptable. Withgoals,130 mmHg, there were greater re-ductions in stroke, a 10% reduction inmortality, but no reduction of otherCVD events and increased rates of seriousadverse events. Systolic blood pressure,130 mmHg was associated with re-duced onset and progression of albumin-uria. However, there was heterogeneity inthemeasure, rates of more advanced renaldisease outcomes were not affected, andthere were no significant changes in reti-nopathy or neuropathy (263).

This change in the “default” systolicblood pressure target is not meant todownplay the importance of treating hy-pertension in patients with diabetes or toimply that lower targets than ,140mmHg are generally inappropriate. Theclear body of evidence that systolic bloodpressure over 140 mmHg is harmful sug-gests that clinicians should promptly ini-tiate and titrate therapy in an ongoingfashion to achieve and maintain systolicblood pressure below 140 mmHg in vir-tually all patients. Additionally, patientswith long life expectancy (in whom theremay be renal benefits from long-termstricter blood pressure control) or thosein whom stroke risk is a concern might,as part of shared decision making,

appropriately have lower systolic targetssuch as ,130 mmHg. This would espe-cially be the case if this can be achievedwith few drugs and without side effects oftherapy.

Treatment strategiesAlthough there are no well-controlledstudies of diet and exercise in the treat-ment of elevated blood pressure or hy-pertension in individuals with diabetes,the DASH study in nondiabetic individu-als has shown antihypertensive effectssimilar to pharmacological monotherapy.Lifestyle therapy consists of reducingsodium intake (to below 1,500 mg/day)and excess body weight; increasing con-sumption of fruits, vegetables (8–10 serv-ings per day), and low-fat dairy products(2–3 servings per day); avoiding excessivealcohol consumption (no more than twoservings per day for men and no morethan one serving per day for women)(264); and increasing activity levels(252). These nonpharmacological strate-gies may also positively affect glycemiaand lipid control and as a result shouldbe encouraged in those with even mildlyelevated blood pressure. Their effects oncardiovascular events have not been es-tablished. Nonpharmacological therapyis reasonable in diabetic individuals withmildly elevated blood pressure (systolicblood pressure .120 mmHg or diastolicblood pressure.80 mmHg). If the bloodpressure is confirmed to be$140 mmHgsystolic and/or $80 mmHg diastolic,pharmacological therapy should be initi-ated along with nonpharmacologicaltherapy (252).

Lowering of blood pressure with regi-mens based on a variety of antihypertensivedrugs, including ACE inhibitors, ARBs,b-blockers, diuretics, and calcium channelblockers, has been shown to be effective inreducing cardiovascular events. Severalstudies suggested that ACE inhibitors maybe superior to dihydropyridine calciumchannel blockers in reducing cardiovascu-lar events (265–267). However, a variety ofother studies have shown no specific ad-vantage to ACE inhibitors as initial treat-ment of hypertension in the generalhypertensive population, but rather an ad-vantage on cardiovascular outcomes of ini-tial therapy with low-dose thiazide diuretics(252,268,269).

In people with diabetes, inhibitors ofthe renin-angiotensin system (RAS) mayhave unique advantages for initial or earlytherapy of hypertension. In a nonhyper-tension trial of high-risk individuals,

including a large subset with diabetes,an ACE inhibitor reduced CVD outcomes(270). In patients with congestive heartfailure (CHF), including diabetic sub-groups, ARBs have been shown to reducemajor CVD outcomes (271–274), and intype 2 diabetic patients with significantnephropathy, ARBs were superior to cal-cium channel blockers for reducing heartfailure (275). Though evidence for dis-tinct advantages of RAS inhibitors onCVD outcomes in diabetes remains con-flicting (255,269), the high CVD risks as-sociated with diabetes, and the highprevalence of undiagnosed CVD,may stillfavor recommendations for their use asfirst-line hypertension therapy in peoplewith diabetes (252).

Recently, the blood pressure arm ofthe ADVANCE trial demonstrated thatroutine administration of a fixed combi-nation of the ACE inhibitor perindopriland the diuretic indapamide significantlyreduced combined microvascular andmacrovascular outcomes, as well as CVDand total mortality. The improved out-comes could also have been due tolower achieved blood pressure in theperindopril-indapamide arm (259). An-other trial showed a decrease inmorbidityand mortality in those receiving benaze-pril and amlodipine compared with bena-zepril and hydrochlorothiazide (HCTZ).The compelling benefits of RAS inhibitorsin diabetic patients with albuminuria orrenal insufficiency provide additional ra-tionale for use of these agents (see SectionVI.B). If needed to achieve blood pressuretargets, amlodipine, HCTZ, or chlorthali-done can be added. If eGFR is ,30 mL/min/m2, a loop diuretic rather than HCTZor chlorthalidone should be prescribed.Titration of and/or addition of furtherblood pressure medications should bemade in timely fashion to overcome clin-ical inertia in achieving blood pressuretargets.

Evidence is emerging that health in-formation technology can be used safelyand effectively as a tool to enable attain-ment of blood pressure goals. Usinga telemonitoring intervention to directtitrations of antihypertensive medicationsbetween medical office visits has beendemonstrated to have a profound impacton systolic blood pressure control (276).

An important caveat is that mostpatients with hypertension requiremultiple-drug therapy to reach treatmentgoals (252). Identifying and addressingbarriers to medication adherence (suchas cost and side effects) should routinely


Position Statement

be done. If blood pressure is refractorydespite confirmed adherence to optimaldoses of at least three antihypertensiveagents of different classifications, one ofwhich should be a diuretic, cliniciansshould consider an evaluation for sec-ondary forms of hypertension. Growingevidence suggests that there is an associ-ation between increase in sleep-timeblood pressure and incidence of CVDevents. A recent RCT of 448 participantswith type 2 diabetes and hypertensiondemonstrated reduced cardiovascularevents and mortality with medianfollow-up of 5.4 years if at least one an-tihypertensive medication was given atbedtime (277).

During pregnancy in diabetic womenwith chronic hypertension, target bloodpressure goals of systolic blood pressure110–129mmHg and diastolic blood pres-sure 65–79 mmHg are reasonable, as theycontribute to long-term maternal health.Lower blood pressure levels may be asso-ciated with impaired fetal growth. Duringpregnancy, treatment with ACE inhibi-tors and ARBs is contraindicated becausethey can cause fetal damage. Antihyper-tensive drugs known to be effective andsafe in pregnancy include methyldopa,labetalol, diltiazem, clonidine, and pra-zosin. Chronic diuretic use during preg-nancy has been associated with restrictedmaternal plasma volume, which mightreduce uteroplacental perfusion (278).

2. Dyslipidemia/lipid managementRecommendationsScreeningc In most adult patients with diabetes,measure fasting lipid profile at leastannually. (B)

c In adults with low-risk lipid values(LDL cholesterol ,100 mg/dL, HDLcholesterol .50 mg/dL, and trigly-cerides,150 mg/dL), lipid assessmentsmay be repeated every 2 years. (E)

Treatment recommendations and goalsc Lifestyle modification focusing on thereduction of saturated fat, trans fat, andcholesterol intake; increase of n-3 fattyacids, viscous fiber, and plant stanols/sterols; weight loss (if indicated); andincreased physical activity should berecommended to improve the lipidprofile in patients with diabetes. (A)

c Statin therapy should be added to life-style therapy, regardless of baselinelipid levels, for diabetic patients:c with overt CVD (A)c without CVD who are over the age of40 years and have one or more other

CVD risk factors (family history ofCVD, hypertension, smoking, dysli-pidemia, or albuminuria) (A)

c For lower-risk patients than the above(e.g., without overt CVD and under theage of 40 years), statin therapy shouldbe considered in addition to lifestyletherapy if LDL cholesterol remainsabove 100 mg/dL or in those withmultiple CVD risk factors. (C)

c In individuals without overt CVD, thegoal is LDL cholesterol ,100 mg/dL(2.6 mmol/L). (B)

c In individuals with overt CVD, a lowerLDL cholesterol goal of ,70 mg/dL(1.8 mmol/L), using a high dose of astatin, is an option. (B)

c If drug-treated patients do not reachthe above targets on maximal toleratedstatin therapy, a reduction in LDLcholesterol of;30–40% from baselineis an alternative therapeutic goal. (B)

c Triglycerides levels ,150 mg/dL (1.7mmol/L) and HDL cholesterol .40mg/dL (1.0 mmol/L) in men and .50mg/dL (1.3 mmol/L) in women aredesirable (C). However, LDL cholesterol–targeted statin therapy remains thepreferred strategy. (A)

c Combination therapy has been shownnot to provide additional cardiovascu-lar benefit above statin therapy aloneand is not generally recommended. (A)

c Statin therapy is contraindicated inpregnancy. (B)

Evidence for benefits of lipid-loweringtherapyPatients with type 2 diabetes have anincreased prevalence of lipid abnormali-ties, contributing to their high risk ofCVD. Multiple clinical trials demon-strated significant effects of pharmacolog-ical (primarily statin) therapy on CVDoutcomes in subjects with CHD and forprimary CVD prevention (279,280). Sub-analyses of diabetic subgroups of largertrials (281–285) and trials specifically insubjects with diabetes (286,287) showedsignificant primary and secondary pre-vention of CVD events 1/2 CHD deathsin diabetic populations. Meta-analyses in-cluding data from over 18,000 patientswith diabetes from 14 randomized trialsof statin therapy, followed for a mean of4.3 years, demonstrate a 9% proportionalreduction in all-cause mortality and 13%reduction in vascular mortality, for eachmmol/L reduction in LDL cholesterol(288). As is the case in nondiabetic indi-viduals, absolute reductions in “hard”CVD outcomes (CHD death and nonfatal

MI) are greatest in people with high base-line CVD risk (known CVD and/or veryhigh LDL cholesterol levels), but overallthe benefits of statin therapy in peoplewith diabetes at moderate or high riskfor CVD are convincing.

There is an increased risk of incidentdiabetes with statin use (289,290), whichmay be limited to those with risk factorsfor diabetes. These patients may benefitadditionally from diabetes screeningwhen on statin therapy. In an analysis ofone of the initial studies suggesting thatstatins are linked to risk of diabetes, thecardiovascular event rate reduction withstatins outweighed the risk of incident di-abetes even for patients at highest risk fordiabetes. The absolute risk increase wassmall (over 5 years of follow-up, 1.2% ofparticipants on placebo developed diabe-tes and 1.5% on rosuvastatin) (291). Therelative risk-benefit ratio favoring statinsis further supported by meta-analysis ofindividual data of over 170,000 personsfrom 27 randomized trials. This demon-strated that individuals at low risk of vas-cular disease, including those undergoingprimary prevention, received benefitsfrom statins that included reductions inmajor vascular events and vascular deathwithout increase in incidence of cancer ordeaths from other causes (280).

Low levels of HDL cholesterol, oftenassociated with elevated triglyceride lev-els, are the most prevalent pattern ofdyslipidemia in persons with type 2 di-abetes. However, the evidence base fordrugs that target these lipid fractions issignificantly less robust than that forstatin therapy (292). Nicotinic acid hasbeen shown to reduce CVD outcomes(293), although the study was done in anondiabetic cohort. Gemfibrozil has beenshown to decrease rates of CVD events insubjects without diabetes (294,295) andin the diabetic subgroup of one of thelarger trials (294). However, in a large trialspecific to diabetic patients, fenofibratefailed to reduce overall cardiovascularoutcomes (296).

Combination therapy, with a statinand a fibrate or statin and niacin, may beefficacious for treatment for all three lipidfractions, but this combination is associ-ated with an increased risk for abnormaltransaminase levels, myositis, or rhabdo-myolysis. The risk of rhabdomyolysis ishigher with higher doses of statins andwith renal insufficiency and seems to belower when statins are combined withfenofibrate than gemfibrozil (297). In theACCORD study, the combination of


Position Statement

fenofibrate and simvastatin did not re-duce the rate of fatal cardiovascularevents, nonfatal MI, or nonfatal stroke,as compared with simvastatin alone, inpatients with type 2 diabetes who wereat high risk for CVD. Prespecified sub-group analyses suggested heterogeneityin treatment effects according to sex,with a benefit of combination therapyfor men and possible harm for women,and a possible benefit for patients withboth triglyceride level $204 mg/dL andHDL cholesterol level #34 mg/dL (298).The AIM-HIGH trial randomized over3,000 patients (about one-third with di-abetes) with established CVD, low levelsof HDL cholesterol, and triglyceride levelsof 150–400 mg/dL to statin therapy plusextended release niacin or matching pla-cebo. The trial was halted early due to lackof efficacy on the primary CVD outcomeand a possible increase in ischemic strokein those on combination therapy (299).Hence, combination lipid-lowering ther-apy cannot be broadly recommended.

Dyslipidemia treatment and targetlipid levelsFor most patients with diabetes, the firstpriority of dyslipidemia therapy (unlesssevere hypertriglyceridemia with risk ofpancreatitis is the immediate issue) is tolower LDL cholesterol to a target goal of,100 mg/dL (2.60 mmol/L) (300). Life-style intervention, including MNT, in-creased physical activity, weight loss,and smoking cessation, may allow somepatients to reach lipid goals. Nutrition in-tervention should be tailored according toeach patient’s age, type of diabetes, phar-macological treatment, lipid levels, andother medical conditions and should fo-cus on the reduction of saturated fat, cho-lesterol, and trans unsaturated fat intakeand increases in n-3 fatty acids, viscousfiber (such as in oats, legumes, citrus),and plant stanols/sterols. Glycemic con-trol can also beneficially modify plasmalipid levels, particularly in patients withvery high triglycerides and poor glycemiccontrol.

In those with clinical CVD or over age40 years with other CVD risk factors,pharmacological treatment should beadded to lifestyle therapy regardless ofbaseline lipid levels. Statins are the drugsof choice for LDL cholesterol loweringand cardioprotection. In patients otherthan those described above, statin treat-ment should be considered if there is aninadequate LDL cholesterol response tolifestyle modifications and improved

glucose control, or if the patient hasincreased cardiovascular risk (e.g., multi-ple cardiovascular risk factors or longduration of diabetes). Very little clinicaltrial evidence exists for type 2 diabeticpatients under the age 40 years, or fortype 1 diabetic patients of any age. In theHeart Protection Study (lower age limit40 years), the subgroup of;600 patientswith type 1 diabetes had a reduction inrisk proportionately similar to that of pa-tients with type 2 diabetes, although notstatistically significant (282). Althoughthe data are not definitive, considerationshould be given to similar lipid-loweringgoals in type 1 diabetic patients as in type2 diabetic patients, particularly if theyhave other cardiovascular risk factors.

Alternative lipoprotein goalsVirtually all trials of statins and CVDoutcome tested specific doses of statinsagainst placebo, other doses of statin, orother statins, rather than aiming for spe-cific LDL cholesterol goals (301). Placebo-controlled trials generally achieved LDLcholesterol reductions of 30–40% frombaseline. Hence, LDL cholesterol lower-ing of this magnitude is an acceptable out-come for patients who cannot reach LDLcholesterol goals due to severe baselineelevations in LDL cholesterol and/or in-tolerance of maximal, or any, statin doses.Additionally for those with baseline LDLcholesterol minimally above 100 mg/dL,prescribing statin therapy to lower LDLcholesterol about 30–40% from baselineis probably more effective than prescrib-ing just enough to get LDL cholesterolslightly below 100 mg/dL.

Clinical trials in high-risk patients,such as those with acute coronary syn-dromes or previous cardiovascular events(302–304), have demonstrated that moreaggressive therapy with high doses of sta-tins to achieve an LDL cholesterol of,70mg/dL led to a significant reduction infurther events. Therefore, a reduction inLDL cholesterol to a goal of,70 mg/dL isan option in very high-risk diabetic pa-tients with overt CVD (305). Some ex-perts recommend a greater focus onnon–HDL cholesterol, apolipoprotein B(apoB), or lipoprotein particle measure-ments to assess residual CVD risk instatin-treated patients who are likely tohave small LDL particles, such as peoplewith diabetes (306), but it is unclearwhether clinical management wouldchange with these measurements.

In individual patients, LDL choles-terol lowering with statins is highly

variable, and this variable response ispoorly understood (307). Reduction ofCVD events with statins correlates veryclosely with LDL cholesterol lowering(279). If initial attempts to prescribe astatin leads to side effects, cliniciansshould attempt to find a dose or alterna-tive statin that the patient can tolerate.There is evidence for significant LDLcholesterol lowering from even ex-tremely low, less than daily, statin doses(308). When maximally tolerated dosesof statins fail to significantly lower LDLcholesterol (,30% reduction from thepatient’s baseline), there is no strong ev-idence that combination therapy shouldbe used to achieve additional LDL cho-lesterol lowering. Niacin, fenofibrate,ezetimibe, and bile acid sequestrants alloffer additional LDL cholesterol loweringto statins alone, but without evidencethat such combination therapy for LDLcholesterol lowering provides a signifi-cant increment in CVD risk reductionover statin therapy alone.

Treatment of other lipoprotein frac-tions or targetsHypertriglyceridemia should be ad-dressed with dietary and lifestyle changes.Severe hypertriglyceridemia (.1,000mg/dL) may warrant immediate pharma-cological therapy (fibric acid derivative,niacin, or fish oil) to reduce the risk ofacute pancreatitis. In the absence of se-vere hypertriglyceridemia, therapy target-ing HDL cholesterol or triglycerides lacksthe strong evidence base of statin therapy.If the HDL cholesterol is,40 mg/dL andthe LDL cholesterol is between 100 and129 mg/dL, a fibrate or niacin might beused, especially if a patient is intolerant tostatins. Niacin is the most effective drugfor raising HDL cholesterol. It can signif-icantly increase blood glucose at high doses,but at modest doses (750–2,000 mg/day)significant improvements in LDL choles-terol, HDL cholesterol, and triglyceridelevels are accompanied by only modestchanges in glucose that are generally ame-nable to adjustment of diabetes therapy(299,309,310).

Table 10 summarizes common treat-ment goals for A1C, blood pressure, andLDL cholesterol.

3. Antiplatelet agentsRecommendationsc Consider aspirin therapy (75–162mg/day) as a primary prevention strategyin those with type 1 or type 2 diabetes


Position Statement

at increased cardiovascular risk (10-yearrisk .10%). This includes most menaged .50 years or women aged .60years who have at least one additionalmajor risk factor (family history of CVD,hypertension, smoking, dyslipidemia, oralbuminuria). (C)

c Aspirin should not be recommendedfor CVD prevention for adults withdiabetes at low CVD risk (10-year CVDrisk ,5%, such as in men aged ,50years and women aged,60 years withno major additional CVD risk factors),since the potential adverse effects frombleeding likely offset the potentialbenefits. (C)

c In patients in these age-groups withmultiple other risk factors (e.g., 10-year risk 5–10%), clinical judgment isrequired. (E)

c Use aspirin therapy (75–162 mg/day)as a secondary prevention strategy inthose with diabetes with a history ofCVD. (A)

c For patients with CVD and docu-mented aspirin allergy, clopidogrel (75mg/day) should be used. (B)

c Combination therapy with aspirin (75–162mg/day) and clopidogrel (75mg/day)is reasonable for up to a year after anacute coronary syndrome. (B)

Aspirin has been shown to be effectivein reducing cardiovascular morbidity andmortality in high-risk patients with pre-vious MI or stroke (secondary prevention).Its net benefit in primary preventionamong patients with no previous cardio-vascular events is more controversial, bothfor patients with and without a history ofdiabetes (311). Two recent RCTs of aspirinspecifically in patients with diabetes failedto show a significant reduction in CVD endpoints, raising further questions about theefficacy of aspirin for primary prevention inpeople with diabetes (312,313).

The Antithrombotic Trialists’ (ATT)collaborators recently published an indi-vidual patient-level meta-analysis of thesix large trials of aspirin for primary pre-vention in the general population. Thesetrials collectively enrolled over 95,000participants, including almost 4,000with diabetes. Overall, they found that as-pirin reduced the risk of vascular eventsby 12% (RR 0.88, 95% CI 0.82–0.94).The largest reduction was for nonfatalMI with little effect on CHD death (RR0.95, 95% CI 0.78–1.15) or total stroke.There was some evidence of a differencein aspirin effect by sex. Aspirin signifi-cantly reduced CHD events in men butnot in women. Conversely, aspirin hadno effect on stroke in men but signifi-cantly reduced stroke in women. Notably,sex differences in aspirin’s effects have notbeen observed in studies of secondaryprevention (311). In the six trials exam-ined by the ATT collaborators, the effectsof aspirin on major vascular events weresimilar for patients with or without diabe-tes: RR 0.88 (95%CI 0.67–1.15) and 0.87(95% CI 0.79–0.96), respectively. Theconfidence interval was wider for thosewith diabetes because of their smallernumber.

Based on the currently available evi-dence, aspirin appears to have a modesteffect on ischemic vascular events withthe absolute decrease in events depend-ing on the underlying CVD risk. Themain adverse effects appear to be anincreased risk of gastrointestinal bleed-ing. The excess risk may be as high as 1–5per 1,000 per year in real-world settings.In adults with CVD risk greater than 1%per year, the number of CVD events pre-vented will be similar to or greater thanthe number of episodes of bleeding in-duced, although these complications donot have equal effects on long-termhealth (314).

In 2010, a position statement of theADA, the American Heart Association(AHA), and the American College ofCardiology Foundation (ACCF) updatedprior joint recommendations for primaryprevention (315). Low-dose (75–162mg/day) aspirin use for primary preven-tion is reasonable for adults with diabetesand no previous history of vascular dis-ease who are at increased CVD risk (10-year risk of CVD events over 10%) andwho are not at increased risk for bleeding.This generally includes most men overage 50 years andwomen over age 60 yearswho also have one or more of the follow-ing major risk factors: 1) smoking, 2) hy-pertension, 3) dyslipidemia, 4) familyhistory of premature CVD, and 5) albu-minuria.

However, aspirin is no longer recom-mended for those at low CVD risk(women under age 60 years and menunder age 50 years with no major CVDrisk factors; 10-year CVD risk under 5%)as the low benefit is likely to be out-weighed by the risks of significant bleed-ing. Clinical judgment should be used forthose at intermediate risk (younger pa-tients with one or more risk factors, orolder patients with no risk factors; thosewith 10-year CVD risk of 5–10%) untilfurther research is available. Use of aspirinin patients under the age of 21 years iscontraindicated due to the associatedrisk of Reye syndrome.

Average daily dosages used in mostclinical trials involving patients with di-abetes ranged from 50 to 650 mg butwere mostly in the range of 100 to 325mg/day. There is little evidence to sup-port any specific dose, but using thelowest possible dosage may help reduceside effects (316). In the U.S., the mostcommon low dose tablet is 81 mg. Al-though platelets from patients with dia-betes have altered function, it is unclearwhat, if any, impact that finding has onthe required dose of aspirin for cardio-protective effects in the patient with di-abetes. Many alternate pathways forplatelet activation exist that are indepen-dent of thromboxane A2 and thus notsensitive to the effects of aspirin (317).Therefore, while “aspirin resistance” ap-pears higher in the diabetic patients whenmeasured by a variety of ex vivo and invitro methods (platelet aggregometry,measurement of thromboxane B2), theseobservations alone are insufficient to em-pirically recommend higher doses of as-pirin be used in the diabetic patient at thistime.

Table 10dSummary of recommendations for glycemic, blood pressure, and lipid control formost adults with diabetes

A1C ,7.0%*Blood pressure ,140/80 mmHg**LipidsLDL cholesterol ,100 mg/dL (,2.6 mmol/L)†

Statin therapy for those with history of MI or age over 401other risk factors

*More or less stringent glycemic goals may be appropriate for individual patients. Goals should be in-dividualized based on duration of diabetes, age/life expectancy, comorbid conditions, known CVD or ad-vanced microvascular complications, hypoglycemia unawareness, and individual patient considerations.**Based on patient characteristics and response to therapy, lower systolic blood pressure targets may beappropriate. †In individuals with overt CVD, a lower LDL cholesterol goal of,70mg/dL (1.8mmol/L), usinga high dose of a statin, is an option.


Position Statement

Clopidogrel has been demonstratedto reduce CVD events in diabetic individ-uals (318). It is recommended as adjunc-tive therapy in the first year after an acutecoronary syndrome or as alternative ther-apy in aspirin-intolerant patients.

4. Smoking cessationRecommendationsc Advise all patients not to smoke or usetobacco products. (A)

c Include smoking cessation counselingand other forms of treatment as a rou-tine component of diabetes care. (B)

A large body of evidence from epide-miological, case-control, and cohort stud-ies provides convincing documentationof the causal link between cigarette smok-ing and health risks. Much of the workdocumenting the impact of smoking onhealth did not separately discuss resultson subsets of individuals with diabetes,but suggests that the identified risks are atleast equivalent to those found in thegeneral population. Other studies of in-dividuals with diabetes consistently dem-onstrate that smokers have a heightenedrisk of CVD, premature death, and in-creased rate of microvascular complica-tions of diabetes. Smoking may have arole in the development of type 2 diabetes.One study in smokers with newly diag-nosed type 2 diabetes found that smokingcessation was associated with ameliorationofmetabolic parameters and reducedbloodpressure and albuminuria at 1 year (319).

The routine and thorough assessmentof tobacco use is important as a means ofpreventing smoking or encouraging ces-sation. A number of large randomizedclinical trials have demonstrated the effi-cacy and cost-effectiveness of brief coun-seling in smoking cessation, including theuse of quitlines, in the reduction oftobacco use. For the patient motivatedto quit, the addition of pharmacologicaltherapy to counseling is more effectivethan either treatment alone. Special con-siderations should include assessment oflevel of nicotine dependence, which isassociated with difficulty in quitting andrelapse (320).

5. CHD screening and treatmentRecommendationsScreeningc In asymptomatic patients, routinescreening for CAD is not recommended,as it does not improve outcomes as longas CVD risk factors are treated. (A)

Treatmentc In patients with known CVD, considerACE inhibitor therapy (C) and use as-pirin and statin therapy (A) (if notcontraindicated) to reduce the risk ofcardiovascular events. In patients with aprior MI, b-blockers should be contin-ued for at least 2 years after the event. (B)

c Avoid thiazolidinedione treatment inpatients with symptomatic heart fail-ure. (C)

c Metformin may be used in patientswith stable CHF if renal function isnormal. It should be avoided in unstableor hospitalized patients with CHF. (C)

Screening for CAD is reviewed in arecently updated consensus statement(196). To identify the presence of CADin diabetic patients without clear or sug-gestive symptoms, a risk factor–based ap-proach to the initial diagnostic evaluationand subsequent follow-up has intuitiveappeal. However, recent studies con-cluded that using this approach fails toidentify which patients with type 2 diabe-tes will have silent ischemia on screeningtests (201,321).

Candidates for cardiac testing includethose with 1) typical or atypical cardiacsymptoms and 2) an abnormal restingECG. The screening of asymptomatic pa-tients remains controversial. Intensivemedical therapy that would be indicatedanyway for diabetic patients at high riskfor CVD seems to provide equal outcomesto invasive revascularization (322,323).There is also some evidence that silentmyocardial ischemia may reverse overtime, adding to the controversy concern-ing aggressive screening strategies (324).Finally, a recent randomized observa-tional trial demonstrated no clinical ben-efit to routine screening of asymptomaticpatients with type 2 diabetes and normalECGs (325). Despite abnormal myocar-dial perfusion imaging in more than onein five patients, cardiac outcomes wereessentially equal (and very low) inscreened compared with unscreened pa-tients. Accordingly, the overall effective-ness, especially the cost-effectiveness, ofsuch an indiscriminate screening strategyis now questioned.

Newer noninvasive CAD screeningmethods, such as computed tomography(CT) and CT angiography have gained inpopularity. These tests infer the presenceof coronary atherosclerosis by measuringthe amount of calcium in coronary arter-ies and, in some circumstances, bydirect visualization of luminal stenoses.

Although asymptomatic diabetic patientsfound to have a higher coronary diseaseburden have more future cardiac events(326–328), the role of these tests beyondrisk stratification is not clear. Their rou-tine use leads to radiation exposure andmay result in unnecessary invasive testingsuch as coronary angiography and revas-cularization procedures. The ultimatebalance of benefit, cost, and risks ofsuch an approach in asymptomatic pa-tients remains controversial, particularlyin the modern setting of aggressive CVDrisk factor control.

In all patients with diabetes, cardio-vascular risk factors should be assessedat least annually. These risk factorsinclude dyslipidemia, hypertension,smoking, a positive family history ofpremature coronary disease, and thepresence of micro- or macroalbu-minuria. Abnormal risk factors shouldbe treated as described elsewhere inthese guidelines. Patients at increasedCHD risk should receive aspirin and astatin, and ACE inhibitor or ARB therapyif hypertensive, unless there are contra-indications to a particular drug class.Although clear benefit exists for ACEinhibitor and ARB therapy in patientswith nephropathy or hypertension, thebenefits in patients with CVD in theabsence of these conditions are less clear,especially when LDL cholesterol is con-comitantly controlled (329,330).

B. Nephropathy screening andtreatmentRecommendationsGeneral recommendationsc To reduce the risk or slow the progres-sion of nephropathy, optimize glucosecontrol. (A)

c To reduce the risk or slow the pro-gression of nephropathy, optimizeblood pressure control. (A)

Screeningc Perform an annual test to assess urinealbumin excretion in type 1 diabeticpatients with diabetes duration of $5years and in all type 2 diabetic patientsstarting at diagnosis. (B)

c Measure serumcreatinine at least annuallyin all adults with diabetes regardless of thedegree of urine albumin excretion. Theserum creatinine should be used to esti-mate GFR and stage the level of chronickidney disease (CKD), if present. (E)

Treatmentc In the treatment of the nonpregnantpatient with modestly elevated (30–299


Position Statement

mg/day) (C) or higher levels ($300mg/day) of urinary albumin excretion(A), either ACE inhibitors or ARBs arerecommended.

c Reduction of protein intake to 0.8–1.0g/kg body wt per day in individualswith diabetes and the earlier stages ofCKD and to 0.8 g/kg body wt per day inthe later stages of CKD may improvemeasures of renal function (urine al-bumin excretion rate, GFR) and isrecommended. (C)

c When ACE inhibitors, ARBs, or diu-retics are used, monitor serum creati-nine and potassium levels for thedevelopment of increased creatinine orchanges in potassium. (E)

c Continued monitoring of urine albu-min excretion to assess both responseto therapy and progression of disease isreasonable. (E)

c When eGFR ,60 mL/min/1.73 m2,evaluate and manage potential com-plications of CKD. (E)

c Consider referral to a physician expe-rienced in the care of kidney disease foruncertainty about the etiology of kid-ney disease, difficult management is-sues, or advanced kidney disease. (B)

Diabetic nephropathy occurs in 20–40%of patients with diabetes and is the singleleading cause of ESRD. Persistent albu-minuria in the range of 30–299 mg/24 h(historically called microalbuminuria)has been shown to be the earliest stageof diabetic nephropathy in type 1 diabetesand a marker for development of nephrop-athy in type 2 diabetes. It is also a well-established marker of increased CVD risk(331,332). Patients with microalbuminuriawho progress to more significant levels($300 mg/24 h, historically called mac-roalbuminuria) are likely to progress toESRD (333,334). However, a number ofinterventions have been demonstrated toreduce the risk and slow the progressionof renal disease.

Intensive diabetes management withthe goal of achieving near-normoglycemiahas been shown in large prospective ran-domized studies to delay the onset andprogression of increased urinary albuminexcretion in patients with type 1(335,336) and type 2 (83,84,88,89) dia-betes. The UKPDS provided strong evi-dence that control of blood pressure canreduce the development of nephropathy(255). In addition, large prospective ran-domized studies in patients with type 1diabetes have demonstrated that achieve-ment of lower levels of systolic blood

pressure (,140 mmHg) resulting fromtreatment using ACE inhibitors provides aselective benefit over other antihyperten-sive drug classes in delaying the progres-sion of increased urinary albumin excretionand can slow the decline in GFR in patientswith higher levels of albuminuria (337–339). In type 2 diabetes with hypertensionand normoalbuminuria, RAS inhibitionhas been demonstrated to delay onset ofmicroalbuminuria (340,341). In the latterstudy, there was an unexpected higher rateof fatal cardiovascular events with olmesar-tan among patients with preexisting CHD.

ACE inhibitors have been shown toreduce major CVD outcomes (i.e., MI,stroke, death) in patients with diabetes(270), thus further supporting the use ofthese agents in patients with albuminuria, aCVD risk factor. ARBs do not prevent onsetof albuminuria in normotensive patientswith type 1 or type 2 diabetes (342,343);however, ARBs have been shown to reducethe rate of progression from micro- to mac-roalbuminuria as well as ESRD in patientswith type 2 diabetes (344–346). Some ev-idence suggests that ARBs have a smallermagnitude of rise in potassium comparedwith ACE inhibitors in people with ne-phropathy (347,348). Combinations ofdrugs that block the renin-angiotensin-aldosterone system (e.g., an ACE inhibitorplus an ARB, a mineralocorticoid antago-nist, or a direct renin inhibitor) provideadditional lowering of albuminuria (349–352). However, such combinations havebeen found to provide no additional car-diovascular benefit and have higher ad-verse event rates (353), and their effectson major renal outcomes have not yetbeen proven.

Other drugs, such as diuretics, cal-cium channel blockers, and b-blockers,should be used as additional therapy tofurther lower blood pressure in patientsalready treated with ACE inhibitors orARBs (275), or as alternate therapy inthe rare individual unable to tolerateACE inhibitors or ARBs.

Studies in patients with varying stagesof nephropathy have shown that proteinrestriction of dietary protein helps slowthe progression of albuminuria, GFR de-cline, and occurrence of ESRD (354–357), although more recent studies haveprovided conflicting results (140). Die-tary protein restriction might be consid-ered particularly in patients whosenephropathy seems to be progressing de-spite optimal glucose and blood pressurecontrol and use of ACE inhibitor and/orARBs (357).

Assessment of albuminuria status andrenal functionScreening for increased urinary albuminexcretion can be performed by measure-ment of the albumin-to-creatinine ratioin a random spot collection; 24-h ortimed collections are more burdensomeand add little to prediction or accuracy(358,359). Measurement of a spot urinefor albumin only, whether by immunoas-say or by using a dipstick test specific formicroalbumin, without simultaneouslymeasuring urine creatinine, is somewhatless expensive but susceptible to false-negative and false-positive determina-tions as a result of variation in urineconcentration due to hydration and otherfactors.

Abnormalities of albumin excretionand the linkage between albumin-to-creatinine ratio and 24-h albumin excre-tion are defined in Table 11. Because ofvariability in urinary albumin excretion,two of three specimens collected within a3- to 6-month period should be abnormalbefore considering a patient to have de-veloped increased urinary albumin excre-tion or had a progression in albuminuria.Exercise within 24 h, infection, fever,CHF, marked hyperglycemia, andmarked hypertension may elevate urinaryalbumin excretion over baseline values.

Information on presence of abnormalurine albumin excretion in addition tolevel of GFR may be used to stage CKD.The National Kidney Foundation classifi-cation (Table 12) is primarily based onGFR levels and therefore differs fromother systems, in which staging is basedprimarily on urinary albumin excretion(360). Studies have found decreasedGFR in the absence of increased urine al-bumin excretion in a substantial percent-age of adults with diabetes (361). Serumcreatinine should therefore be measuredat least annually in all adults with

Table 11dDefinitions of abnormalities inalbumin excretion

CategorySpot collection

(mg/mg creatinine)

Normal ,30Increased urinaryalbumin excretion* $30

*Historically, ratios between 30 and 299 have beencalled microalbuminuria and those 300 or greaterhave been called macroalbuminuria (or clinical al-buminuria).


Position Statement

diabetes, regardless of the degree of urinealbumin excretion.

Serum creatinine should be used toestimate GFR and to stage the level ofCKD, if present. eGFR is commonlycoreported by laboratories or can beestimated using formulae such as theModification of Diet in Renal Disease(MDRD) study equation (362). Recent re-ports have indicated that the MDRD ismore accurate for the diagnosis and strat-ification of CKD in patients with diabetesthan the Cockcroft-Gault formula (363).GFR calculators are available at http://www.nkdep.nih.gov.

The role of continued annual quanti-tative assessment of albumin excretionafter diagnosis of albuminuria and insti-tution of ACE inhibitor or ARB therapyand blood pressure control is unclear.Continued surveillance can assess bothresponse to therapy and progression ofdisease. Some suggest that reducing al-buminuria to the normal (,30 mg/g) ornear-normal range may improve renaland cardiovascular prognosis, but this ap-proach has not been formally evaluated inprospective trials.

Complications of kidney disease cor-relate with level of kidney function.Whenthe eGFR is,60 mL/min/1.73 m2, screen-ing for complications of CKD is indicated(Table 13). Early vaccination against hepa-titis B is indicated in patients likely to prog-ress to end-stage kidney disease.

Consider referral to a physician expe-rienced in the care of kidney disease whenthere is uncertainty about the etiology ofkidney disease (heavy proteinuria, activeurine sediment, absence of retinopathy,rapid decline in GFR, resistant hyperten-sion). Other triggers for referral may in-clude difficult management issues (anemia,secondary hyperparathyroidism,metabolicbone disease, or electrolyte disturbance) oradvanced kidney disease. The threshold forreferral may vary depending on the fre-quency with which a provider encountersdiabetic patients with significant kidney

disease. Consultation with a nephrologistwhen stage 4CKDdevelops has been foundto reduce cost, improve quality of care, andkeep people off dialysis longer (364). How-ever, nonrenal specialists should not delayeducating their patients about the progres-sive nature of diabetic kidney disease; therenal preservation benefits of aggressivetreatment of blood pressure, blood glucose,and hyperlipidemia; and the potential needfor renal replacement therapy.

C. Retinopathy screening andtreatmentRecommendationsGeneral recommendationsc To reduce the risk or slow the pro-gression of retinopathy, optimize gly-cemic control. (A)

c To reduce the risk or slow the pro-gression of retinopathy, optimize bloodpressure control. (A)

Screeningc Adults and children aged $10 yearswith type 1 diabetes should have aninitial dilated and comprehensive eyeexamination by an ophthalmologist oroptometrist within 5 years after theonset of diabetes. (B)

c Patients with type 2 diabetes shouldhave an initial dilated and compre-hensive eye examination by an oph-thalmologist or optometrist shortlyafter the diagnosis of diabetes. (B)

c Subsequent examinations for type 1and type 2 diabetic patients should berepeated annually by an ophthalmologistor optometrist. Less frequent exams(every 2–3 years) may be consideredfollowing one ormore normal eye exams.Examinations will be required more fre-quently if retinopathy is progressing. (B)

c High-quality fundus photographs candetect most clinically significant di-abetic retinopathy. Interpretation ofthe images should be performed by atrained eye care provider. While retinalphotography may serve as a screeningtool for retinopathy, it is not a substitute

for a comprehensive eye exam, whichshould be performed at least initiallyand at intervals thereafter as recom-mended by an eye care professional. (E)

c Womenwith pre-existing diabetes whoare planning pregnancy or who havebecome pregnant should have a com-prehensive eye examination and becounseled on the risk of developmentand/or progression of diabetic reti-nopathy. Eye examination should oc-cur in the first trimester with closefollow-up throughout pregnancy andfor 1 year postpartum. (B)

Treatmentc Promptly refer patients with any levelof macular edema, severe NPDR, or anyPDR to an ophthalmologist who isknowledgeable and experienced in themanagement and treatment of diabeticretinopathy. (A)

c Laser photocoagulation therapy is in-dicated to reduce the risk of vision lossin patients with high-risk PDR, clini-cally significant macular edema, and insome cases of severe NPDR. (A)

c Anti–vascular endothelial growth fac-tor (VEGF) therapy is indicated for di-abetic macular edema. (A)

c The presence of retinopathy is not acontraindication to aspirin therapy forcardioprotection, as this therapy doesnot increase the risk of retinal hemor-rhage. (A)

Diabetic retinopathy is a highly specificvascular complication of both type 1 andtype 2 diabetes, with prevalence stronglyrelated to the duration of diabetes. Di-abetic retinopathy is the most frequentcause of new cases of blindness amongadults aged 20–74 years. Glaucoma, cata-racts, and other disorders of the eye occurearlier and more frequently in people withdiabetes.

In addition to duration of diabetes,other factors that increase the risk of, orare associated with, retinopathy includechronic hyperglycemia (365), nephrop-athy (366), and hypertension (367). In-tensive diabetes management with thegoal of achieving near-normoglycemiahas been shown in large prospective ran-domized studies to prevent and/or delaythe onset and progression of diabetic ret-inopathy (71,83,84,90). Lowering bloodpressure has been shown to decrease theprogression of retinopathy (255), al-though tight targets (systolic ,120mmHg) do not impart additional benefit(90). Several case series and a controlledprospective study suggest that pregnancy

Table 12dStages of CKD

Stage DescriptionGFR (mL/min/1.73 m2

body surface area)

1 Kidney damage* with normal or increased GFR $902 Kidney damage* with mildly decreased GFR 60–893 Moderately decreased GFR 30–594 Severely decreased GFR 15–295 Kidney failure ,15 or dialysis

*Kidney damage defined as abnormalities on pathological, urine, blood, or imaging tests. Adapted from ref.359.


Position Statement

in type 1 diabetic patients may aggravateretinopathy (368,369); laser photocoa-gulation surgery can minimize this risk(369).

One of the main motivations forscreening for diabetic retinopathy is thelong-established efficacy of laser photo-coagulation surgery in preventing visualloss. Two large trials, the Diabetic Reti-nopathy Study (DRS) in patients withPDR and the Early Treatment DiabeticRetinopathy Study (ETDRS) in patientswith macular edema, provide the stron-gest support for the therapeutic benefitsof photocoagulation surgery. The DRS(370) showed that panretinal photocoag-ulation surgery reduced the risk of severevision loss from PDR from 15.9% in un-treated eyes to 6.4% in treated eyes, withgreatest risk-benefit ratio in those withbaseline disease (disc neovascularizationor vitreous hemorrhage).

The ETDRS (371) established thebenefit of focal laser photocoagulationsurgery in eyes with macular edema, par-ticularly those with clinically significantmacular edema, with reduction of dou-bling of the visual angle (e.g., 20/50 to20/100) from 20% in untreated eyes to8% in treated eyes. The ETDRS also veri-fied the benefits of panretinal photocoag-ulation for high-risk PDR and in older-onset patients with severe NPDR or less-than-high-risk PDR.

Laser photocoagulation surgery inboth trials was beneficial in reducing therisk of further visual loss, but generally notbeneficial in reversing already diminished

acuity. Recombinant monoclonal neutral-izing antibody to VEGF is a newly ap-proved therapy that improves vision andreduces the need for laser photocoa-gulation in patients with macular edema(372). Other emerging therapies for reti-nopathy include sustained intravitreal de-livery of fluocinolone (373) and thepossibility of prevention with fenofibrate(374,375).

The preventive effects of therapy andthe fact that patients with PDR or macularedema may be asymptomatic providestrong support for a screening programto detect diabetic retinopathy. As retinop-athy is estimated to take at least 5 years todevelop after the onset of hyperglycemia,patients with type 1 diabetes should havean initial dilated and comprehensive eyeexamination within 5 years after the onsetof diabetes. Patients with type 2 diabetes,who generally have had years of undiag-nosed diabetes and who have a significantrisk of prevalent diabetic retinopathy attime of diabetes diagnosis, should have aninitial dilated and comprehensive eye exam-ination soon after diagnosis. Examinationsshould be performed by an ophthalmologistor optometrist who is knowledgeable andexperienced in diagnosing the presence ofdiabetic retinopathy and is aware of itsmanagement. Subsequent examinationsfor type 1 and type 2 diabetic patients aregenerally repeated annually. Less frequentexams (every 2–3 years) may be cost effec-tive after one or more normal eye exams,and in a population with well-controlledtype 2 diabetes there was essentially no

risk of development of significant retinop-athy with a 3-year interval after a normalexamination (376). Examinations will berequired more frequently if retinopathy isprogressing (377).

The use of retinal photography withremote reading by experts has great po-tential in areas where qualified eye careprofessionals are not available and mayalso enhance efficiency and reduce costswhen the expertise of ophthalmologistscan be utilized for more complex exami-nations and for therapy (378). In-personexams are still necessary when the photosare unacceptable and for follow-up of ab-normalities detected. Photos are not asubstitute for a comprehensive eyeexam, which should be performed at leastinitially and at intervals thereafter as rec-ommended by an eye care professional.Results of eye examinations should bedocumented and transmitted to the refer-ring health care professional.

D. Neuropathy screening andtreatmentRecommendationsc All patients should be screened for distalsymmetric polyneuropathy (DPN) start-ing at diagnosis of type 2 diabetes and 5years after the diagnosis of type 1 diabetesand at least annually thereafter, usingsimple clinical tests. (B)

c Electrophysiological testing is rarelyneeded, except in situations where theclinical features are atypical. (E)

c Screening for signs and symptoms ofcardiovascular autonomic neuropathy(CAN) should be instituted at diagnosisof type 2 diabetes and 5 years after thediagnosis of type 1 diabetes. Specialtesting is rarely needed and may notaffect management or outcomes. (E)

c Medications for the relief of specificsymptoms related to painful DPN andautonomic neuropathy are recom-mended, as they improve the quality oflife of the patient. (E)

The diabetic neuropathies are hetero-geneous with diverse clinical manifesta-tions. They may be focal or diffuse. Mostcommon among the neuropathies arechronic sensorimotor DPN and autonomicneuropathy. Although DPN is a diagnosisof exclusion, complex investigations toexclude other conditions are rarely needed.

The early recognition and appropri-ate management of neuropathy in thepatient with diabetes is important for anumber of reasons: 1) nondiabetic

Table 13dManagement of CKD in diabetes

GFR Recommended

All patients Yearly measurement of creatinine, urinary albumin excretion, potassium45–60 Referral to nephrology if possibility for nondiabetic kidney disease exists

(duration of type 1 diabetes ,10 years, heavy proteinuria, abnormalfindings on renal ultrasound, resistant hypertension, rapid fall in GFR,or active urinary sediment on ultrasound)

Consider need for dose adjustment of medicationsMonitor eGFR every 6 monthsMonitor electrolytes, bicarbonate, hemoglobin, calcium, phosphorus,parathyroid hormone at least yearly

Assure vitamin D sufficiencyConsider bone density testingReferral for dietary counseling

30–44 Monitor eGFR every 3 monthsMonitor electrolytes, bicarbonate, calcium, phosphorus, parathyroidhormone, hemoglobin, albumin, weight every 3–6 months

Consider need for dose adjustment of medications,30 Referral to nephrologist

Adapted from http://www.kidney.org/professionals/KDOQI/guideline_diabetes/.


Position Statement

neuropathies may be present in patientswith diabetes and may be treatable; 2) anumber of treatment options exist forsymptomatic diabetic neuropathy; 3) upto 50% of DPNmay be asymptomatic andpatients are at risk for insensate injury totheir feet; and 4) autonomic neuropathy,and particularly CAN, is associated withsubstantial morbidity and even mortality.Specific treatment for the underlyingnerve damage is currently not available,other than improved glycemic control,which may modestly slow progression(89) but not reverse neuronal loss. Effec-tive symptomatic treatments are availablefor somemanifestations of DPN (379) andautonomic neuropathy.

Diagnosis of neuropathyDPN. Patients with diabetes should bescreened annually for DPN using testssuch as pinprick sensation, vibration per-ception (using a 128-Hz tuning fork), 10-gmonofilament pressure sensation at thedistal plantar aspect of both great toes andmetatarsal joints, and assessment of anklereflexes. Combinations of more than onetest have .87% sensitivity in detectingDPN. Loss of 10-g monofilament percep-tion and reduced vibration perceptionpredict foot ulcers (380). Importantly, inpatients with neuropathy, particularlywhen severe, causes other than diabetesshould always be considered, such as neu-rotoxic medications, heavy metal poison-ing, alcohol abuse, vitamin B12 deficiency(especially in those taking metformin forprolonged periods (381), renal disease,chronic inflammatory demyelinating neu-ropathy, inherited neuropathies, and vas-culitis (382).Diabetic autonomic neuropathy. Thesymptoms and signs of autonomic dys-function should be elicited carefully dur-ing the history and physical examination.Major clinical manifestations of diabeticautonomic neuropathy include restingtachycardia, exercise intolerance, ortho-static hypotension, constipation, gastro-paresis, erectile dysfunction, sudomotordysfunction, impaired neurovascular func-tion, and, potentially, autonomic failure inresponse to hypoglycemia (383).

CAN, a CVD risk factor (93), is themost studied and clinically importantform of diabetic autonomic neuropathy.CAN may be indicated by resting tachy-cardia (.100 bpm), orthostasis (a fall insystolic blood pressure.20 mmHg uponstanding without an appropriate heartrate response); it is also associated withincreased cardiac event rates. Although

some societies have developed guidelinesfor screening for CAN, the benefits of so-phisticated testing beyond risk stratifica-tion are not clear (384).

Gastrointestinal neuropathies (e.g.,esophageal enteropathy, gastroparesis,constipation, diarrhea, fecal inconti-nence) are common, and any section ofthe gastrointestinal tract may be affected.Gastroparesis should be suspected in in-dividuals with erratic glucose control orwith upper gastrointestinal symptomswithout other identified cause. Evalua-tion of solid-phase gastric emptying usingdouble-isotope scintigraphy may be doneif symptoms are suggestive, but test re-sults often correlate poorly with symp-toms. Constipation is the most commonlower-gastrointestinal symptom but canalternate with episodes of diarrhea.

Diabetic autonomic neuropathy isalso associated with genitourinary tractdisturbances. In men, diabetic autonomicneuropathy may cause erectile dysfunc-tion and/or retrograde ejaculation. Eval-uation of bladder dysfunction should beperformed for individuals with diabeteswho have recurrent urinary tract infec-tions, pyelonephritis, incontinence, or apalpable bladder.

Symptomatic treatmentsDPN. The first step in management ofpatients with DPN should be to aim forstable and optimal glycemic control. Al-though controlled trial evidence is lack-ing, several observational studies suggestthat neuropathic symptoms improve notonly with optimization of control, butalso with the avoidance of extreme bloodglucose fluctuations. Patients with painfulDPN may benefit from pharmacologicaltreatment of their symptoms: manyagents have confirmed or probable effi-cacy confirmed in systematic reviews ofRCTs (379), with several U.S. Food andDrug Administration (FDA)-approved forthe management of painful DPN.Treatment of autonomic neuropathy.Gastroparesis symptoms may improvewith dietary changes and prokineticagents such as metoclopramide or eryth-romycin. Treatments for erectile dysfunc-tion may include phosphodiesterase type5 inhibitors, intracorporeal or intraure-thral prostaglandins, vacuum devices, orpenile prostheses. Interventions for othermanifestations of autonomic neuropathyare described in the ADA statement onneuropathy (380). As with DPN treat-ments, these interventions do not changethe underlying pathology and natural

history of the disease process, but mayhave a positive impact on the quality oflife of the patient.

E. Foot careRecommendationsc For all patients with diabetes, performan annual comprehensive foot exami-nation to identify risk factors predictiveof ulcers and amputations. The footexamination should include inspection,assessment of foot pulses, and testing forloss of protective sensation (LOPS) (10-gmonofilament plus testing any one ofthe following: vibration using 128-Hztuning fork, pinprick sensation, anklereflexes, or vibration perception thresh-old). (B)

c Provide general foot self-care educationto all patients with diabetes. (B)

c A multidisciplinary approach is rec-ommended for individuals with footulcers and high-risk feet, especiallythose with a history of prior ulcer oramputation. (B)

c Refer patients who smoke, have LOPSand structural abnormalities, or havehistory of prior lower-extremity com-plications to foot care specialists forongoing preventive care and lifelongsurveillance. (C)

c Initial screening for peripheral arterialdisease (PAD) should include a historyfor claudication and an assessment ofthe pedal pulses. Consider obtainingan ankle-brachial index (ABI), as manypatients with PAD are asymptom-atic. (C)

c Refer patients with significant claudi-cation or a positive ABI for furthervascular assessment and consider ex-ercise, medications, and surgical op-tions. (C)

Amputation and foot ulceration, con-sequences of diabetic neuropathy and/orPAD, are common and major causes ofmorbidity and disability in people withdiabetes. Early recognition and manage-ment of risk factors can prevent or delayadverse outcomes.

The risk of ulcers or amputations isincreased in people who have the follow-ing risk factors:

c Previous amputationc Past foot ulcer historyc Peripheral neuropathyc Foot deformityc Peripheral vascular diseasec Visual impairment


Position Statement

c Diabetic nephropathy (especially pa-tients on dialysis)

c Poor glycemic controlc Cigarette smoking

Many studies have been publishedproposing a range of tests that mightusefully identify patients at risk for footulceration, creating confusion amongpractitioners as to which screening testsshould be adopted in clinical practice. AnADA task force was therefore assembledin 2008 to concisely summarize recentliterature in this area and then recommendwhat should be included in the compre-hensive foot exam for adult patients withdiabetes. Their recommendations are sum-marized below, but clinicians should referto the task force report (385) for furtherdetails and practical descriptions of howto perform components of the comprehen-sive foot examination.

At least annually, all adults with di-abetes should undergo a comprehensivefoot examination to identify high-riskconditions. Clinicians should ask abouthistory of previous foot ulceration oramputation, neuropathic or peripheralvascular symptoms, impaired vision, to-bacco use, and foot care practices. Ageneral inspection of skin integrity andmusculoskeletal deformities should bedone in a well-lit room. Vascular assess-ment would include inspection and as-sessment of pedal pulses.

The neurologic exam recommendedis designed to identify LOPS rather thanearly neuropathy. The clinical examina-tion to identify LOPS is simple andrequires no expensive equipment. Fivesimple clinical tests (use of a 10-g mono-filament, vibration testing using a 128-Hztuning fork, tests of pinprick sensation,ankle reflex assessment, and testing vi-bration perception threshold with a bio-thesiometer), each with evidence fromwell-conducted prospective clinical co-hort studies, are considered useful in thediagnosis of LOPS in the diabetic foot.The task force agrees that any of the fivetests listed could be used by clinicians toidentify LOPS, although ideally two ofthese should be regularly performed dur-ing the screening examdnormally the10-g monofilament and one other test.One or more abnormal tests would sug-gest LOPS, while at least two normal tests(and no abnormal test) would rule outLOPS. The last test listed, vibration as-sessment using a biothesiometer or simi-lar instrument, is widely used in the U.S.;

however, identification of the patient withLOPS can easily be carried out withoutthis or other expensive equipment.

Initial screening for PAD shouldinclude a history for claudication and anassessment of the pedal pulses. A diag-nostic ABI should be performed in anypatient with symptoms of PAD. Due tothe high estimated prevalence of PAD inpatients with diabetes and the fact thatmany patients with PAD are asymptom-atic, an ADA consensus statement on PAD(386) suggested that a screening ABI beperformed in patients over 50 years of ageand be considered in patients under 50years of age who have other PAD risk fac-tors (e.g., smoking, hypertension, hyper-lipidemia, or duration of diabetes .10years). Refer patients with significantsymptoms or a positive ABI for furthervascular assessment and consider exer-cise, medications, and surgical options(386).

Patients with diabetes and high-riskfoot conditions should be educated re-garding their risk factors and appropriatemanagement. Patients at risk should un-derstand the implications of the loss ofprotective sensation, the importance offoot monitoring on a daily basis, theproper care of the foot, including nailand skin care, and the selection of appro-priate footwear. Patients with LOPSshould be educated on ways to substituteother sensory modalities (hand palpation,visual inspection) for surveillance of earlyfoot problems. The patients’ understand-ing of these issues and their physical abil-ity to conduct proper foot surveillanceand care should be assessed. Patientswith visual difficulties, physical con-straints preventing movement, or cogni-tive problems that impair their ability toassess the condition of the foot and to in-stitute appropriate responses will needother people, such as family members,to assist in their care.

People with neuropathy or evidenceof increased plantar pressure (e.g., ery-thema, warmth, callus, or measuredpressure) may be adequately managedwith well-fitted walking shoes or athleticshoes that cushion the feet and redistrib-ute pressure. Callus can be debridedwith a scalpel by a foot care specialistor other health professional with experi-ence and training in foot care. Peoplewith bony deformities (e.g., hammer-toes, prominent metatarsal heads, bun-ions) may need extra-wide or -depthshoes. People with extreme bonydeformities (e.g., Charcot foot) who

cannot be accommodated with commercialtherapeutic footwear may need custom-molded shoes.

Foot ulcers and wound care mayrequire care by a podiatrist, orthopedicor vascular surgeon, or rehabilitationspecialist experienced in the managementof individuals with diabetes. Guidelinesfor treatment of diabetic foot ulcers haverecently been updated (387).

VII. ASSESSMENT OFCOMMON COMORBIDCONDITIONS

Recommendationsc For patients with risk factors, signs orsymptoms, consider assessment andtreatment for common diabetes-asso-ciated conditions (see Table 14). (B)

In addition to the commonly appre-ciated comorbidities of obesity, hyperten-sion, and dyslipidemia, diabetes is alsoassociated with other diseases or condi-tions at rates higher than those of age-matched people without diabetes. A fewof the more common comorbidities aredescribed herein and listed in Table 14.

Hearing impairmentHearing impairment, both high frequencyand low/mid frequency, is more commonin people with diabetes, perhaps due toneuropathy and/or vascular disease. In anNHANES analysis, hearing impairmentwas about twice as great in people withdiabetes compared with those without,after adjusting for age and other riskfactors for hearing impairment (388).Controlling for age, race, and other demo-graphic factors, high frequency loss inthose with diabetes was significantly asso-ciated with history of CHD and with pe-ripheral neuropathy, while low/midfrequency loss was associated with lowHDL cholesterol and with poor reportedhealth status (389).

Table 14dCommon comorbidities for whichincreased risk is associated with diabetes

Hearing impairmentObstructive sleep apneaFatty liver diseaseLow testosterone in menPeriodontal diseaseCertain cancersFracturesCognitive impairmentDepression


Position Statement

Obstructive sleep apneaAge-adjusted rates of obstructive sleepapnea, a risk factor for CVD, are signifi-cantly higher (4- to 10-fold) with obesity,especially with central obesity, in menand women (390). The prevalence in gen-eral populations with type 2 diabetes maybe up to 23% (391), and in obese partic-ipants enrolled in the Look AHEAD trialexceeded 80% (392). Treatment of sleepapnea significantly improves quality oflife and blood pressure control. The evi-dence for a treatment effect on glycemiccontrol is mixed (393).

Fatty liver diseaseUnexplained elevation of hepatic trans-aminase concentrations is significantlyassociated with higher BMI, waist circum-ference, triglycerides, and fasting insulin,and with lower HDL cholesterol. Type 2diabetes and hypertension are indepen-dently associated with transaminase ele-vations in women (394). In a prospectiveanalysis, diabetes was significantly associ-ated with incident nonalcoholic chronicliver disease and with hepatocellular car-cinoma (395). Interventions that improvemetabolic abnormalities in patients withdiabetes (weight loss, glycemic control,treatment with specific drugs for hyper-glycemia or dyslipidemia) are also benefi-cial for fatty liver disease (396).

Low testosterone in menMean levels of testosterone are lower inmen with diabetes compared with age-matched men without diabetes, butobesity is a major confounder (397). Theissue of treatment in asymptomatic men iscontroversial. The evidence for effects of tes-tosterone replacement on outcomes ismixed, and recent guidelines suggest thatscreening and treatment of men withoutsymptoms are not recommended (398).

Periodontal diseasePeriodontal disease is more severe, butnot necessarily more prevalent, in pa-tients with diabetes than those without(399). Numerous studies have suggestedassociations with poor glycemic control,nephropathy, and CVD, but most studiesare highly confounded. A comprehensiveassessment, and treatment of identifieddisease, is indicated in patients with dia-betes, but the evidence that periodontaldisease treatment improves glycemic con-trol is mixed. A meta-analysis reported asignificant 0.47% improvement in A1C,but notedmultiple problemswith the qual-ity of the published studies included in the

analysis (400). Several high-quality RCTshave not shown a significant effect (401).

CancerDiabetes (possibly only type 2 diabetes) isassociated with increased risk of cancersof the liver, pancreas, endometrium, co-lon/rectum, breast, and bladder (402).The association may result from sharedrisk factors between type 2 diabetes andcancer (obesity, age, and physical inactiv-ity) but may also be due to hyperinsuline-mia or hyperglycemia (401,403). Patientswith diabetes should be encouragedto undergo recommended age- and sex-appropriate cancer screenings and to re-duce their modifiable cancer risk factors(obesity, smoking, and physical inactivity).

FracturesAge-matched hip fracture risk is signifi-cantly increased in both type 1 (summaryRR 6.3) and type 2 diabetes (summary RR1.7) in both sexes (404). Type 1 diabetesis associated with osteoporosis, but intype 2 diabetes an increased risk of hipfracture is seen despite higher bone min-eral density (BMD) (405). One studyshowed that prevalent vertebral fractureswere significantly more common in menand women with type 2 diabetes, butwere not associated with BMD (406). Inthree large observational studies of olderadults, femoral neck BMD T-score andthe WHO fracture risk algorithm(FRAX) score were associated with hipand nonspine fracture, although fracturerisk was higher in diabetic participantscompared with participants without dia-betes for a given T-score and age or for agiven FRAX score risk (407). It is appro-priate to assess fracture history and riskfactors in older patients with diabetes andrecommend BMD testing if appropriatefor the patient’s age and sex. For at-riskpatients, it is reasonable to consider stan-dard primary or secondary preventionstrategies (reduce risk factors for falls, en-sure adequate calcium and vitamin D in-take, avoid use of medications that lowerBMD, such as glucocorticoids), and to con-sider pharmacotherapy for high-risk pa-tients. For patients with type 2 diabeteswith fracture risk factors, avoiding use ofthiazolidinediones is warranted.

Cognitive impairmentDiabetes is associated with significantlyincreased risk of cognitive decline, agreater rate of cognitive decline, andincreased risk of dementia (408,409).In a 15-year prospective study of a

community-dwelling people over theage of 60 years, the presence of diabetesat baseline significantly increased the age-and sex-adjusted incidence of all-causedementia, Alzheimer disease, and vascu-lar dementia compared with rates in thosewith normal glucose tolerance (410). In asubstudy of the ACCORD study, therewere no differences in cognitive outcomesbetween intensive and standard glycemiccontrol, although there was significantlyless of a decrement in total brain volumeby magnetic resonance imaging in partic-ipants in the intensive arm (411). The ef-fects of hyperglycemia and insulin on thebrain are areas of intense research interest.

DepressionAs discussed in Section V.H, depression ishighly prevalent in people with diabetesand is associated with worse outcomes.

VIII. DIABETES CARE INSPECIFIC POPULATIONS

A. Children and adolescentsRecommendationsc As is the case for all children, childrenwith diabetes or prediabetes should beencouraged to engage in at least 60 minof physical activity each day. (B)

1. Type 1 diabetesThree-quarters of all cases of type 1 di-abetes are diagnosed in individuals ,18years of age. It is appropriate to considerthe unique aspects of care and manage-ment of children and adolescents withtype 1 diabetes. Children with diabetesdiffer from adults in many respects, in-cluding changes in insulin sensitivity re-lated to sexual maturity and physicalgrowth, ability to provide self-care, super-vision in child care and school, andunique neurologic vulnerability to hypo-glycemia and DKA. Attention to such is-sues as family dynamics, developmentalstages, and physiological differences re-lated to sexual maturity are all essentialin developing and implementing an opti-mal diabetes regimen. Although recom-mendations for children and adolescentsare less likely to be based on clinical trialevidence, expert opinion and a review ofavailable and relevant experimental dataare summarized in the ADA statement oncare of children and adolescents with type1 diabetes (412).

Ideally, the care of a child or adoles-cent with type 1 diabetes should be pro-vided by a multidisciplinary team ofspecialists trained in the care of children


Position Statement

with pediatric diabetes. At the very least,education of the child and family shouldbe provided by health care providerstrained and experienced in childhooddiabetes and sensitive to the challengesposed by diabetes in this age-group. It isessential that DSME, MNT, and psycho-social support be provided at the time ofdiagnosis and regularly thereafter by in-dividuals experiencedwith the educational,nutritional, behavioral, and emotional needsof the growing child and family. It isexpected that the balance between adultsupervision and self-care should be definedand that it will evolve with physical, psy-chological, and emotional maturity.

a. Glycemic controlRecommendationsc Consider age when setting glycemicgoals in children and adolescents withtype 1 diabetes. (E)

While current standards for diabetesmanagement reflect the need to lowerglucose as safely possible, special consid-eration should be given to the uniquerisks of hypoglycemia in young children.Glycemic goals may need to be modifiedto take into account the fact that mostchildren,6 or 7 years of age have a formof “hypoglycemic unawareness,” includ-ing immaturity and a relative inability torecognize and respond to hypoglycemicsymptoms, placing them at greater riskfor severe hypoglycemia and its sequelae.In addition, and unlike the case in type 1diabetic adults, young children below theage of 5 years may be at risk for perma-nent cognitive impairment after episodesof severe hypoglycemia (413–415). Fur-thermore, the DCCT demonstrated thatnear-normalization of blood glucose lev-els was more difficult to achieve in ado-lescents than adults. Nevertheless, theincreased frequency of use of basal-bolusregimens and insulin pumps in youthfrom infancy through adolescence hasbeen associated with more childrenreaching ADA blood glucose targets(416,417) in those families in whichboth parents and the child with diabetesparticipate jointly to perform the re-quired diabetes-related tasks. Further-more, recent studies documentingneurocognitive sequelae of hyperglyce-mia in children provide another compel-ling motivation for achieving glycemictargets (418,419).

In selecting glycemic goals, the bene-fits on long-term health outcomes ofachieving a lower A1C should be balanced

against the risks of hypoglycemia and thedevelopmental burdens of intensive regi-mens in children and youth. Age-specificglycemic and A1C goals are presented inTable 15.

b. Screening and managementof chronic complications inchildren and adolescentswith type 1 diabetes

i. NephropathyRecommendationsc Annual screening for microalbuminuria,with a random spot urine sample foralbumin-to-creatinine ratio, should beconsidered once the child is 10 years ofage and has had diabetes for 5 years. (B)

c Treatment with an ACE inhibitor, ti-trated to normalization of albumin ex-cretion, should be considered whenelevated albumin-to-creatinine ratio issubsequently confirmed on two addi-tional specimens from different days. (E)

ii. HypertensionRecommendationsc Blood pressure should be measured ateach routine visit. Children found tohave high-normal blood pressure orhypertension should have blood pres-sure confirmed on a separate day. (B)

c Initial treatment of high-normal bloodpressure (systolic or diastolic blood pres-sure consistently above the 90th percen-tile for age, sex, and height) includesdietary intervention and exercise, aimedat weight control and increased physicalactivity, if appropriate. If target bloodpressure is not reached with 3–6 monthsof lifestyle intervention, pharmacologicaltreatment should be considered. (E)

c Pharmacological treatment of hyperten-sion (systolic or diastolic blood pressureconsistently above the 95th percentile forage, sex, and height or consistently.130/80 mmHg, if 95% exceeds thatvalue) should be considered as soon asthe diagnosis is confirmed. (E)

c ACE inhibitors should be consideredfor the initial treatment of hypertension,following appropriate reproductivecounseling due to its potential terato-genic effects. (E)

c The goal of treatment is a blood pres-sure consistently ,130/80 or belowthe 90th percentile for age, sex, andheight, whichever is lower. (E)

It is important that blood pressuremeasurements are determined correctly,using the appropriate size cuff, and withthe child seated and relaxed. Hypertension

should be confirmed on at least threeseparate days. Normal blood pressurelevels for age, sex, and height and appro-priate methods for determinations areavailable online at www.nhlbi.nih.gov/health/prof/heart/hbp/hbp_ped.pdf.

iii. DyslipidemiaRecommendationsScreeningc If there is a family history of hypercho-lesterolemia or a cardiovascular eventbefore age 55 years, or if family history isunknown, then consider obtaining afasting lipid profile on children.2 yearsof age soon after diagnosis (after glucosecontrol has been established). If familyhistory is not of concern, then considerthe first lipid screening at puberty ($10years of age). For children diagnosedwith diabetes at or after puberty, con-sider obtaining a fasting lipid profilesoon after the diagnosis (after glucosecontrol has been established). (E)

c For both age-groups, if lipids are ab-normal, annual monitoring is reason-able. If LDL cholesterol values are withinthe accepted risk levels (,100 mg/dL[2.6 mmol/L]), a lipid profile repeatedevery 5 years is reasonable. (E)

Treatmentc Initial therapy may consist of optimi-zation of glucose control and MNTusing a Step 2 AHA diet aimed at adecrease in the amount of saturated fatin the diet. (E)

c After the age of 10 years, the additionof a statin in patients who, after MNTand lifestyle changes, have LDL choles-terol.160mg/dL (4.1mmol/L), or LDLcholesterol .130 mg/dL (3.4 mmol/L)and one or more CVD risk factors, isreasonable. (E)

c The goal of therapy is an LDL choles-terol value,100mg/dL (2.6mmol/L). (E)

People diagnosed with type 1 diabetesin childhood have a high risk of earlysubclinical (420–422) and clinical (423)CVD. Although intervention data arelacking, the AHA categorizes childrenwith type 1 diabetes in the highest tierfor cardiovascular risk and recommendsboth lifestyle and pharmacological treat-ment for those with elevated LDL choles-terol levels (424,425). Initial therapyshould be with a Step 2 AHA diet, whichrestricts saturated fat to 7% of total calo-ries and restricts dietary cholesterol to200 mg/day. Data from randomized clin-ical trials in children as young as 7monthsof age indicate that this diet is safe and


Position Statement

does not interfere with normal growthand development (426,427).

Neither long-term safety nor cardio-vascular outcome efficacy of statin therapyhas been established for children. How-ever, recent studies have shown short-termsafety equivalent to that seen in adults andefficacy in lowering LDL cholesterol levels,improving endothelial function and caus-ing regression of carotid intimal thickening(428–430). No statin is approved for useunder the age of 10 years, and statin treat-ment should generally not be used in chil-dren with type 1 diabetes prior to this age.For postpubertal girls, issues of pregnancyprevention are paramount, since statins arecategory X in pregnancy. See Section VIII.Bfor more information.

iv. RetinopathyRecommendationsc The first ophthalmologic examinationshould be obtained once the child is$10 years of age and has had diabetesfor 3–5 years. (B)

c After the initial examination, annualroutine follow-up is generally recom-mended. Less frequent examinationsmay be acceptable on the advice of aneye care professional. (E)

Although retinopathy (like albuminuria)most commonly occurs after the onset ofpuberty and after 5–10 years of diabetesduration (431), it has been reported inprepubertal children and with diabetesduration of only 1–2 years. Referrals

should be made to eye care professionalswith expertise in diabetic retinopathy, anunderstanding of the risk for retinopathyin the pediatric population, and experi-ence in counseling the pediatric patientand family on the importance of early pre-vention/intervention.

v. Celiac diseaseRecommendationsc Consider screening children with type1 diabetes for celiac disease by measuringtissue transglutaminase or antiendomysialantibodies, with documentation of nor-mal total serum IgA levels, soon after thediagnosis of diabetes. (E)

c Testing should be considered in chil-dren with growth failure, failure to gainweight, weight loss, diarrhea, flatulence,abdominal pain, or signs of malabsorp-tion or in children with frequent un-explained hypoglycemia or deteriorationin glycemic control. (E)

c Consider referral to a gastroenterolo-gist for evaluation with possible en-doscopy and biopsy for confirmation ofceliac disease in asymptomatic childrenwith positive antibodies. (E)

c Children with biopsy-confirmed celiacdisease should be placed on a gluten-free diet and have consultation with adietitian experienced in managing bothdiabetes and celiac disease. (B)

Celiac disease is an immune-mediated dis-order that occurs with increased frequencyin patients with type 1 diabetes (1–16% of

individuals compared with 0.3–1% in thegeneral population) (432,433). Symptomsof celiac disease include diarrhea, weightloss or poor weight gain, growth failure,abdominal pain, chronic fatigue, malnutri-tion due to malabsorption, and othergastrointestinal problems, and unexplainedhypoglycemia or erratic blood glucose con-centrations.

Screening for celiac disease includesmeasuring serum levels of tissue trans-glutaminase or antiendomysial antibodies,then small bowel biopsy in antibody-positive children. Recent European guide-lines on screening for celiac disease inchildren (not specific to children with type1 diabetes) suggested that biopsy mightnot be necessary in symptomatic childrenwith positive antibodies, as long as furthertesting such as genetic or HLA testing wassupportive, but that asymptomatic but at-risk children should have biopsies (434).One small study that included childrenwith and without type 1 diabetes sugges-ted that antibody-positive but biopsy-neg-ative children were similar clinically tothose who were biopsy positive and thatbiopsy-negative children had benefitsfrom a gluten-free diet but worsening on ausual diet (435). Because this study wassmall and because children with type 1 di-abetes already need to follow a careful diet,it is difficult to advocate for not confirmingthe diagnosis bybiopsy before recommend-ing a lifelong gluten-free diet, especially inasymptomatic children. In symptomaticchildren with type 1 diabetes and celiac

Table 15dPlasma blood glucose and A1C goals for type 1 diabetes by age-group

Values by age (years)

Plasma blood glucose goalrange (mg/dL)

A1C RationaleBeforemeals

Bedtime/overnight

Toddlers and preschoolers (0–6) 100–180 110–200 ,8.5% c Vulnerability to hypoglycemiac Insulin sensitivityc Unpredictability in dietary intake and physical activityc A lower goal (,8.0%) is reasonable if it can beachieved without excessive hypoglycemia

School age (6–12) 90–180 100–180 ,8% c Vulnerability of hypoglycemiac A lower goal (,7.5%) is reasonable if it can beachieved without excessive hypoglycemia

Adolescents and young adults (13–19) 90–130 90–150 ,7.5% c A lower goal (,7.0%) is reasonable if it can beachieved without excessive hypoglycemia

Key concepts in setting glycemic goals:c Goals should be individualized and lower goals may be reasonable based on benefit-risk assessment.c Blood glucose goals should be modified in children with frequent hypoglycemia or hypoglycemia unawareness.c Postprandial blood glucose values should be measured when there is a discrepancy between preprandial blood glucose values and A1Clevels and to help assess glycemia in those on basal/bolus regimens.


Position Statement

disease, gluten-free diets reduce symptomsand rates of hypoglycemia (436).

vi. HypothyroidismRecommendationsc Consider screening children with type1 diabetes for thyroid peroxidase andthyroglobulin antibodies soon afterdiagnosis. (E)

c Measuring thyroid-stimulating hor-mone (TSH) concentrations soon afterdiagnosis of type 1 diabetes, after me-tabolic control has been established,is reasonable. If normal, consider re-checking every 1–2 years, especially ifthe patient develops symptoms of thy-roid dysfunction, thyromegaly, or anabnormal growth rate. (E)

Autoimmune thyroiddisease is themostcommon autoimmune disorder associ-ated with diabetes, occurring in 17–30%of patients with type 1 diabetes (437).About one-quarter of type 1 diabetic chil-dren have thyroid autoantibodies at thetime of diagnosis of their diabetes (438),and the presence of thyroid autoantibod-ies is predictive of thyroid dysfunction,generally hypothyroidism but less com-monly hyperthyroidism (439). Subclini-cal hypothyroidism may be associatedwith increased risk of symptomatic hypo-glycemia (440) and with reduced lineargrowth (441). Hyperthyroidism altersglucose metabolism, potentially resultingin deterioration of metabolic control.

c. Self-managementNo matter how sound the medical regi-men, it can only be as good as the abilityof the family and/or individual to imple-ment it. Family involvement in diabetesremains an important component of opti-mal diabetes management throughoutchildhood and adolescence. Health careproviders who care for children and adoles-cents, therefore, must be capable ofevaluating the educational, behavioral, emo-tional, and psychosocial factors that impactimplementation of a treatment plan andmust workwith the individual and family toovercome barriers or redefine goals as ap-propriate.

d. School and day careSince a sizable portion of a child’s day isspent in school, close communicationwith and cooperation of school or daycare personnel is essential for optimal di-abetes management, safety, and maximalacademic opportunities. See the ADA po-sition statement on diabetes care in the

school and day care setting (442) for fur-ther discussion.

e. Transition from pediatric to adultcareRecommendationsc As teens transition into emergingadulthood, health care providers andfamilies must recognize their manyvulnerabilities (B) and prepare the de-veloping teen, beginning in early tomid adolescence and at least 1 yearprior to the transition. (E)

c Both pediatricians and adult healthcare providers should assist in pro-viding support and links to resourcesfor the teen and emerging adult. (B)

Care and close supervision of diabetesmanagement is increasingly shifted fromparents and other older adults through-out childhood and adolescence. How-ever, the shift from pediatrics to adulthealth care providers often occurs veryabruptly as the older teen enters the nextdevelopmental stage referred to as emerg-ing adulthood (443), a critical period foryoung people who have diabetes; duringthis period of major life transitions, youthbegin to move out of their parents’ homeand must become more fully responsiblefor their diabetes care including the manyaspects of self management, making med-ical appointments, and financing healthcare once they are no longer covered un-der their parents’ health insurance(444,445). In addition to lapses in healthcare, this is also a period of deteriorationin glycemic control, increased occurrenceof acute complications, psycho-social-emotional-behavioral issues, and emergenceof chronic complications (444–447).

Though scientific evidence continuesto be limited, it is clear that early andongoing attention be given to compre-hensive and coordinated planning forseamless transition of all youth frompediatric to adult health care (444,445).A comprehensive discussion regardingthe challenges faced during this period,including specific recommendations, isfound in the ADA position statement “Di-abetes Care for Emerging Adults: Recom-mendations for Transition From Pediatricto Adult Diabetes Care Systems” (445).

The National Diabetes Education Pro-gram (NDEP) has materials available tofacilitate the transition process (http://ndep.nih.gov/transitions/), and The EndocrineSociety (in collaboration with the ADAand other organizations has developedtransition tools for clinicians and youth/

families (http://www.endo-society.org/clinicalpractice/transition_of_care.cfm).

2. Type 2 diabetesThe incidence of type 2 diabetes in ado-lescents is increasing, especially in ethnicminority populations (31). Distinctionbetween type 1 and type 2 diabetes inchildren can be difficult, since the preva-lence of overweight in children continuesto rise and since autoantigens and ketosismay be present in a substantial number ofpatients with features of type 2 diabetes(including obesity and acanthosis nigri-cans). Such a distinction at the time ofdiagnosis is critical because treatment reg-imens, educational approaches, and die-tary counsel will differ markedly betweenthe two diagnoses.

Type 2 diabetes has a significant in-cidence of comorbidities already presentat the time of diagnosis (448). It is recom-mended that blood pressure measurement,a fasting lipid profile, microalbuminuria as-sessment, and dilated eye examination beperformed at the time of diagnosis. There-after, screening guidelines and treatmentrecommendations for hypertension, dysli-pidemia, microalbuminuria, and retinopa-thy in youthwith type 2 diabetes are similarto those for youth with type 1 diabetes. Ad-ditional problems that may need to be ad-dressed include polycystic ovarian diseaseand the various comorbidities associatedwith pediatric obesity such as sleep apnea,hepatic steatosis, orthopedic complica-tions, and psychosocial concerns. TheADA consensus statement on this subject(33) provides guidance on the prevention,screening, and treatment of type 2 diabetesand its comorbidities in young people.

3. Monogenic diabetes syndromesMonogenic forms of diabetes (neonataldiabetes or maturity-onset diabetes of theyoung) represent a small fraction of chil-dren with diabetes (,5%), but the readyavailability of commercial genetic testingis now enabling a true genetic diagnosiswith increasing frequency. It is importantto correctly diagnose one of the mono-genic forms of diabetes, as these childrenmay be incorrectly diagnosed with type 1or type 2 diabetes, leading to nonoptimaltreatment regimens and delays in diag-nosing other family members.

The diagnosis of monogenic diabetesshould be considered in the followingsettings: diabetes diagnosed within thefirst 6 months of life; in children withstrong family history of diabetes but with-out typical features of type 2 diabetes


Position Statement

(nonobese, low-risk ethnic group); in chil-drenwithmild fasting hyperglycemia (100–150 mg/dL [5.5–8.5 mmol]), especially ifyoung and nonobese; and in children withdiabetes but with negative autoantibodieswithout signs of obesity or insulin resis-tance. A recent international consensusdocument discusses in further detail the di-agnosis and management of children withmonogenic forms of diabetes (449).

B. Preconception careRecommendationsc A1C levels should be as close to normalas possible (,7%) in an individual pa-tient before conception is attempted. (B)

c Starting at puberty, preconceptioncounseling should be incorporated inthe routine diabetes clinic visit for allwomen of childbearing potential. (C)

c Women with diabetes who are con-templating pregnancy should be eval-uated and, if indicated, treated fordiabetic retinopathy, nephropathy,neuropathy, and CVD. (B)

c Medications used by such womenshould be evaluated prior to conception,since drugs commonly used to treat di-abetes and its complications may becontraindicated or not recommended inpregnancy, including statins, ACE in-hibitors, ARBs, and most noninsulintherapies. (E)

c Since many pregnancies are unplanned,consider the potential risks and benefitsof medications that are contraindicatedin pregnancy in all women of child-bearing potential and counsel womenusing such medications accordingly. (E)

Major congenital malformations re-main the leading cause of mortality andserious morbidity in infants of motherswith type 1 and type 2 diabetes. Obser-vational studies indicate that the risk ofmalformations increases continuouslywith increasing maternal glycemia duringthe first 6–8weeks of gestation, as definedby first-trimester A1C concentrations.There is no threshold for A1C values be-low which risk disappears entirely. How-ever, malformation rates above the 1–2%background rate of nondiabetic pregnan-cies appear to be limited to pregnancies inwhich first-trimester A1C concentrationsare .1% above the normal range for anondiabetic pregnant woman.

Preconception care of diabetes ap-pears to reduce the risk of congenitalmalformations. Five nonrandomizedstudies compared rates of major malfor-mations in infants between women who

participated in preconception diabetescare programs and women who initiatedintensive diabetes management after theywere already pregnant. The preconcep-tion care programsweremultidisciplinaryand designed to train patients in diabetesself-management with diet, intensifiedinsulin therapy, and SMBG. Goals wereset to achieve normal blood glucose con-centrations, and .80% of subjects ach-ieved normal A1C concentrations beforethey became pregnant. In all five studies,the incidence of major congenital malfor-mations in women who participated inpreconception care (range 1.0–1.7% ofinfants) was much lower than the inci-dence in women who did not participate(range 1.4–10.9% of infants) (106). Onelimitation of these studies is that partici-pation in preconception care was self-selected rather than randomized. Thus,it is impossible to be certain that the lowermalformation rates resulted fully fromimproved diabetes care. Nonetheless,the evidence supports the concept thatmalformations can be reduced or preven-ted by careful management of diabetes be-fore pregnancy.

Planned pregnancies greatly facilitatepreconception diabetes care. Unfortu-nately, nearly two-thirds of pregnanciesin women with diabetes are unplanned,leading to a persistent excess of malfor-mations in infants of diabetic mothers. Tominimize the occurrence of these devas-tating malformations, standard care for allwomen with diabetes who have child-bearing potential, beginning at the onsetof puberty or at diagnosis, should include1) education about the risk of malforma-tions associated with unplanned pregnan-cies and poor metabolic control and 2)use of effective contraception at all times,unless the patient has good metaboliccontrol and is actively trying to conceive.

Women contemplating pregnancyneed to be seen frequently by a multidis-ciplinary team experienced in the man-agement of diabetes before and duringpregnancy. The goals of preconceptioncare are to 1) involve and empower thepatient in the management of her diabe-tes, 2) achieve the lowest A1C test resultspossible without excessive hypoglycemia,3) assure effective contraception until sta-ble and acceptable glycemia is achieved,and 4) identify, evaluate, and treat long-term diabetes complications such asretinopathy, nephropathy, neuropathy,hypertension, and CHD (106).

Among the drugs commonly used inthe treatment of patients with diabetes, a

number may be relatively or absolutelycontraindicated during pregnancy. Sta-tins are category X (contraindicated foruse in pregnancy) and should be discon-tinued before conception, as should ACEinhibitors (450). ARBs are category C(risk cannot be ruled out) in the first tri-mester but category D (positive evidenceof risk) in later pregnancy and shouldgenerally be discontinued before preg-nancy. Since many pregnancies are un-planned, health care professionals caringfor any woman of childbearing potentialshould consider the potential risks andbenefits of medications that are contrain-dicated in pregnancy.Women usingmed-ications such as statins or ACE inhibitorsneed ongoing family planning counsel-ing. Among the oral antidiabetic agents,metformin and acarbose are classified ascategory B (no evidence of risk in hu-mans) and all others as category C. Poten-tial risks and benefits of oral antidiabeticagents in the preconception period mustbe carefully weighed, recognizing thatdata are insufficient to establish the safetyof these agents in pregnancy.

For further discussion of preconcep-tion care, see the ADA’s consensus state-ment on pre-existing diabetes andpregnancy (106) and the position state-ment (451) on this subject.

C. Older adultsRecommendationsc Older adults who are functional, cog-nitively intact, and have significant lifeexpectancy should receive diabetescare with goals similar to those de-veloped for younger adults. (E)

c Glycemic goals for some older adultsmight reasonably be relaxed, using in-dividual criteria, but hyperglycemialeading to symptoms or risk of acutehyperglycemic complications shouldbe avoided in all patients. (E)

c Other cardiovascular risk factorsshould be treated in older adults withconsideration of the time frame ofbenefit and the individual patient.Treatment of hypertension is indicatedin virtually all older adults, and lipidand aspirin therapy may benefit thosewith life expectancy at least equal to thetime frame of primary or secondaryprevention trials. (E)

c Screening for diabetes complicationsshould be individualized in olderadults, but particular attention shouldbe paid to complications that wouldlead to functional impairment. (E)


Position Statement

Diabetes is an important health condi-tion for the aging population; at least 20%of patients over the age of 65 years havediabetes, and this number can be expectedto grow rapidly in the coming decades.Older individuals with diabetes havehigher rates of premature death, functionaldisability, and coexisting illnesses such ashypertension, CHD, and stroke than thosewithout diabetes. Older adults with diabe-tes are also at greater risk than other olderadults for several common geriatric syn-dromes, such as polypharmacy, depres-sion, cognitive impairment, urinaryincontinence, injurious falls, and persistentpain.

A consensus report on diabetes andolder adults (452) influenced the follow-ing discussion and recommendations.The care of older adults with diabetes iscomplicated by their clinical and func-tional heterogeneity. Some older individ-uals developed diabetes years earlier andmay have significant complications; oth-ers who are newly diagnosed may havehad years of undiagnosed diabetes withresultant complications or may have trulyrecent-onset disease and few or no com-plications. Some older adults with diabe-tes are frail and have other underlyingchronic conditions, substantial diabetes-related comorbidity, or limited physicalor cognitive functioning. Other older in-dividuals with diabetes have little comor-bidity and are active. Life expectancies arehighly variable for this population, butoften longer than clinicians realize. Pro-viders caring for older adults with diabe-tes must take this heterogeneity intoconsideration when setting and prioritiz-ing treatment goals.

There are few long-term studies inolder adults demonstrating the benefits ofintensive glycemic, blood pressure, andlipid control. Patients who can beexpected to live long enough to reap thebenefits of long-term intensive diabetesmanagement, who have good cognitiveand functional function, and who chooseto do so via shared decision making maybe treated using therapeutic interventionsand goals similar to those for youngeradults with diabetes. As with all patients,DSME and ongoing DSMS are vital com-ponents of diabetes care for older adultsand their caregivers.

For patients with advanced diabetescomplications, life-limiting comorbid ill-ness, or substantial cognitive or func-tional impairment, it is reasonable to setless intensive glycemic target goals. Thesepatients are less likely to benefit from

reducing the risk of microvascular com-plications and more likely to suffer seri-ous adverse effects from hypoglycemia.However, patients with poorly controlleddiabetes may be subject to acute compli-cations of diabetes, including dehydration,poor wound healing, and hyperglycemichyperosmolar coma. Glycemic goalsat a minimum should avoid these conse-quences.

Although control of hyperglycemiamay be important in older individualswith diabetes, greater reductions in mor-bidity and mortality may result fromcontrol of other cardiovascular risk fac-tors rather than from tight glycemic con-trol alone. There is strong evidence fromclinical trials of the value of treatinghypertension in the elderly (453,454).There is less evidence for lipid-loweringand aspirin therapy, although the benefitsof these interventions for primary andsecondary prevention are likely to applyto older adults whose life expectanciesequal or exceed the time frames seen inclinical trials.

Special care is required in prescribingand monitoring pharmacological therapyin older adults. Costs may be a significantfactor, especially since older adults tendto be on many medications. Metforminmay be contraindicated because of renalinsufficiency or significant heart failure.Thiazolidinediones, if used at all, shouldbe used very cautiously in those with, orat risk for, CHF and have also beenassociated with fractures. Sulfonylureas,other insulin secretagogues, and insulincan cause hypoglycemia. Insulin use re-quires that patients or caregivers have goodvisual and motor skills and cognitive abil-ity. Dipeptidyl peptidase 4 (DPP-4) inhib-itors have few side effects, but their costsmay be a barrier to some older patients; thelatter is also the case for GLP-1 agonists.

Screening for diabetes complicationsin older adults also should be individual-ized. Particular attention should be paidto complications that can develop overshort periods of time and/or that wouldsignificantly impair functional status,such as visual and lower-extremity com-plications.

D. Cystic fibrosis–related diabetesRecommendationsc Annual screening for cystic fibrosis–related diabetes (CFRD) with OGTTshould begin by age 10 years in all pa-tients with cystic fibrosis who do nothave CFRD (B). Use of A1C as a

screening test for CFRD is not recom-mended. (B)

c During a period of stable health, thediagnosis of CFRD can be made incystic fibrosis patients according tousual glucose criteria. (E)

c Patients with CFRD should be treatedwith insulin to attain individualizedglycemic goals. (A)

c Annual monitoring for complicationsof diabetes is recommended, beginning5 years after the diagnosis of CFRD. (E)

CFRD is the most common comorbidityin persons with cystic fibrosis, occurringin about 20% of adolescents and 40–50%of adults. The additional diagnosis of di-abetes in this population is associatedwith worse nutritional status, more severeinflammatory lung disease, and greatermortality from respiratory failure. Insulininsufficiency related to partial fibrotic de-struction of the islet mass is the primarydefect in CFRD. Genetically determinedfunction of the remaining b-cells and in-sulin resistance associated with infectionand inflammation may also play a role.Encouraging new data suggest that earlydetection and aggressive insulin therapyhave narrowed the gap in mortality be-tween cystic fibrosis patients with andwithout diabetes and have eliminatedthe sex difference in mortality (455).

Recommendations for the clinicalmanagement of CFRD can be found inthe recent ADA position statement on thistopic (456).

IX. DIABETES CARE INSPECIFIC SETTINGS

A. Diabetes care in the hospitalRecommendationsc All patients with diabetes admitted to thehospital shouldhave their diabetes clearlyidentified in the medical record. (E)

c All patients with diabetes should havean order for blood glucose monitoring,with results available to all members ofthe health care team. (E)

c Goals for blood glucose levels:c Critically ill patients: Insulin ther-apy should be initiated for treatmentof persistent hyperglycemia startingat a threshold of no greater than 180mg/dL (10 mmol/L). Once insulintherapy is started, a glucose range of140–180 mg/dL (7.8–10 mmol/L) isrecommended for the majority ofcritically ill patients. (A)

c More stringent goals, such as 110–140 mg/dL (6.1–7.8 mmol/L) may be


Position Statement

appropriate for selected patients, aslong as this can be achieved withoutsignificant hypoglycemia. (C)

c Critically ill patients require an intrave-nous insulin protocol that has demon-strated efficacy and safety in achievingthe desired glucose range without in-creasing risk for severe hypoglycemia. (E)

c Non–critically ill patients: There is noclear evidence for specific blood glucosegoals. If treated with insulin, the pre-meal blood glucose targets generally,140 mg/dL (7.8 mmol/L) with ran-domblood glucose,180mg/dL (10.0mmol/L) are reasonable, providedthese targets can be safely achieved.More stringent targets may be appro-priate in stable patients with previoustight glycemic control. Less stringenttargets may be appropriate in thosewith severe comorbidities. (E)

c Scheduled subcutaneous insulin withbasal, nutritional, and correction com-ponents is the preferred method forachieving and maintaining glucose con-trol in non–critically ill patients. (C)

c Glucose monitoring should be initiatedin any patient not known to be diabeticwho receives therapy associated withhigh risk for hyperglycemia, includinghigh-dose glucocorticoid therapy, initi-ation of enteral or parenteral nutrition,or other medications such as octreotideor immunosuppressive medications. (B)If hyperglycemia is documented andpersistent, consider treating such pa-tients to the same glycemic goals as pa-tients with known diabetes. (E)

c A hypoglycemia management protocolshould be adopted and implementedby each hospital or hospital system. Aplan for preventing and treating hypo-glycemia should be established for eachpatient. Episodes of hypoglycemia inthe hospital should be documented inthe medial record and tracked. (E)

c Consider obtaining an A1C on patientswith diabetes admitted to the hospital ifthe result of testing in the previous 2–3months is not available. (E)

c Consider obtaining an A1C in patientswith risk factors for undiagnosed di-abetes who exhibit hyperglycemia inthe hospital. (E)

c Patients with hyperglycemia in thehospital who do not have a prior di-agnosis of diabetes should have ap-propriate plans for follow-up testingand care documented at discharge. (E)

Hyperglycemia in the hospital can re-present previously known diabetes,

previously undiagnosed diabetes, or hos-pital-related hyperglycemia (fastingblood glucose $126 mg/dL or randomblood glucose $200 mg/dL occurringduring the hospitalization that reverts tonormal after hospital discharge). The dif-ficulty distinguishing between the secondand third categories during the hospitali-zation may be overcome by measuring anA1C in undiagnosed patients with hyper-glycemia, as long as conditions interferingwith A1C utility (hemolysis, blood trans-fusion) have not occurred. The manage-ment of hyperglycemia in the hospital hasoften been considered secondary in im-portance to the condition that promptedadmission (457). However, a body of lit-erature now supports targeted glucosecontrol in the hospital setting for poten-tial improved clinical outcomes. Hyper-glycemia in the hospital may result fromstress, decompensation of type 1 or type 2or other forms of diabetes, and/or may beiatrogenic due to withholding of antihy-perglycemic medications or administra-tion of hyperglycemia-provoking agentssuch as glucocorticoids or vasopressors.

There is substantial observational ev-idence linking hyperglycemia in hospital-ized patients (with or without diabetes) topoor outcomes. Cohort studies as wellas a few early RCTs suggested that in-tensive treatment of hyperglycemia im-proved hospital outcomes (457–459). Ingeneral, these studies were heterogeneousin terms of patient population, blood glu-cose targets and insulin protocols used,provision of nutritional support, and theproportion of patients receiving insulin,which limits the ability to make meaning-ful comparisons among them. Recent tri-als in critically ill patients have failed toshow a significant improvement in mor-tality with intensive glycemic control(460,461) or have even shown increasedmortality risk (462). Moreover, these re-cent RCTs have highlighted the risk ofsevere hypoglycemia resulting from suchefforts (460–465).

The largest study to date, NICE-SUGAR (Normoglycaemia in IntensiveCare Evaluation and Survival Using Glu-cose Algorithm Regulation), a multicen-ter, multinational RCT, compared theeffect of intensive glycemic control (target81–108 mg/dL, mean blood glucose at-tained 115 mg/dL) to standard glycemiccontrol (target 144–180 mg/dL, meanblood glucose attained 144 mg/dL) onoutcomes among 6,104 critically ill par-ticipants, almost all of whom required me-chanical ventilation (462). Ninety-day

mortality was significantly higher inthe intensive versus the conventionalgroup in both surgical and medical pa-tients, as was mortality from cardiovascu-lar causes. Severe hypoglycemia was alsomore common in the intensively treatedgroup (6.8% vs. 0.5%, P , 0.001). Theprecise reason for the increased mortalityin the tightly controlled group is un-known. The results of this study lie instark contrast to a famous 2001 single-center study that reported a 42% relativereduction in intensive care unit (ICU)mortality in critically ill surgical patientstreated to a target blood glucose of 80–110mg/dL (458). Importantly, the controlgroup in NICE-SUGAR had reasonablygood blood glucose management, main-tained at a mean glucose of 144 mg/dL,only 29 mg/dL above the intensively man-aged patients. Accordingly, this study’sfindings do not disprove the notion thatglycemic control in the ICU is important.However, they do strongly suggest that itmay not be necessary to target blood glu-cose values,140 mg/dL and that a highlystringent target of,110 mg/dL may actu-ally be dangerous.

In a recent meta-analysis of 26 trials(N5 13,567), which included the NICE-SUGAR data, the pooled RR of death withintensive insulin therapy was 0.93 ascompared with conventional therapy(95% CI 0.83–1.04) (465). Approxi-mately half of these trials reported hypo-glycemia, with a pooled RR of intensivetherapy of 6.0 (95% CI 4.5–8.0). Thespecific ICU setting influenced the find-ings, with patients in surgical ICUs ap-pearing to benefit from intensive insulintherapy (RR 0.63, 95% CI 0.44–0.91),whereas those in other medical andmixed critical care settings did not. Itwas concluded that, overall, intensive in-sulin therapy increased the risk of hypo-glycemia but provided no overall benefiton mortality in the critically ill,although a possible mortality benefit topatients admitted to the surgical ICU wassuggested.

1. Glycemic targets in hospitalizedpatients

Definition of glucose abnormalities inthe hospital settingHyperglycemia in the hospital has beendefined as any blood glucose.140 mg/dL(7.8 mmol/L). Levels that are significantlyand persistently above this may requiretreatment in hospitalized patients. A1Cvalues .6.5% suggest, in undiagnosed


Position Statement

patients, that diabetes preceded hospitali-zation (466). Hypoglycemia has been de-fined as any blood glucose ,70 mg/dL(3.9 mmol/L). This is the standard defini-tion in outpatients and correlates with theinitial threshold for the release of counter-regulatory hormones. Severe hypoglyce-mia in hospitalized patients has been de-fined bymany as,40mg/dL (2.2mmol/L),although this is lower than the;50mg/dL(2.8 mmol/L) level at which cognitive im-pairment begins in normal individuals(467). As with hyperglycemia, hypoglyce-mia among inpatients is also associatedwith adverse short- and long-term out-comes. Early recognition and treatmentof mild to moderate hypoglycemia (40–69 mg/dL [2.2–3.8 mmol/L]) can preventdeterioration to a more severe episodewith potential adverse sequelae (468).

Critically ill patientsBased on the weight of the availableevidence, for the majority of critically illpatients in the ICU setting, insulin infusionshould be used to control hyperglycemia,with a starting threshold of no higher than180 mg/dL (10.0 mmol/L). Once intrave-nous insulin is started, the glucose levelshould be maintained between 140 and180mg/dL (7.8 and 10.0mmol/L). Greaterbenefit maybe realized at the lower end ofthis range. Although strong evidence islacking, somewhat lower glucose targetsmay be appropriate in selected patients.One small study suggested that medicalintensive care unit (MICU) patients treatedto targets of 120–140 mg/dL had less neg-ative nitrogen balance than those treated tohigher targets (469). However, targets,110 mg/dL (6.1 mmol/L) are not recom-mended. Use of insulin infusion protocolswith demonstrated safety and efficacy, re-sulting in low rates of hypoglycemia, arehighly recommended (468).

Non–critically ill patientsWith no prospective RCT data to informspecific glycemic targets in non–criticallyill patients, recommendations are basedon clinical experience and judgment(470). For the majority of non–criticallyill patients treated with insulin, premealglucose targets should generally be,140mg/dL (7.8 mmol/L) with random bloodglucose ,180 mg/dL (10.0 mmol/L), aslong as these targets can be safely achieved.To avoid hypoglycemia, considerationshould be given to reassessing the insulinregimen if blood glucose levels fall below100 mg/dL (5.6 mmol/L). Modification ofthe regimen is required when blood

glucose values are ,70 mg/dL (3.9mmol/L), unless the event is easily ex-plained by other factors (such as a missedmeal). There is some evidence that system-atic attention to hyperglycemia in theemergency room leads to better glycemiccontrol in the hospital for those subse-quently admitted (471).

Occasional patients with a prior his-tory of successful tight glycemic control inthe outpatient setting who are clinicallystable may be maintained with a glucoserange below the above cut points. Con-versely, higher glucose ranges may beacceptable in terminally ill patients or inpatients with severe comorbidities, as wellas in those in patient care settings wherefrequent glucose monitoring or closenursing supervision is not feasible.

Clinical judgment, combined withongoing assessment of the patient’s clini-cal status, including changes in the trajec-tory of glucose measures, the severity ofillness, nutritional status, or concurrentuse of medications that might affect glu-cose levels (e.g., steroids, octreotide),must be incorporated into the day-to-day decisions regarding insulin dosing(468).

2. Antihyperglycemic agents inhospitalized patientsIn the hospital setting, insulin therapy isthe preferred method of glycemic controlin majority of clinical situations (468). Inthe ICU, intravenous infusion is the pre-ferred route of insulin administration.When the patient is transitioned off intra-venous insulin to subcutaneous therapy,precautions should be taken to preventhyperglycemia escape (472,473). Outsideof critical care units, scheduled subcuta-neous insulin that delivers basal, nutri-tional, and correction (supplemental)components is preferred. Typical dosingschemes are based on body weight, withsome evidence that patients with renal in-sufficiency should be treated with lowerdoses (474). Prolonged therapy withsliding-scale insulin (SSI) as the soleregimen is ineffective in the majority ofpatients, increases risk of both hypogly-cemia and hyperglycemia, and has re-cently been shown in a randomized trialto be associated with adverse outcomes ingeneral surgery patients with type 2 diabe-tes (475). SSI is potentially dangerous intype 1 diabetes (468). The reader is referredto several recent publications and reviewsthat describe currently available insulinpreparations and protocols and provideguidance in use of insulin therapy in

specific clinical settings including paren-teral nutrition (476), enteral tube feedingsand with high dose glucocorticoid therapy(468).

There are no data on the safety andefficacy of oral agents and injectable non-insulin therapies such as GLP-1 analogsand pramlintide in the hospital. They aregenerally considered to have a limited rolein the management of hyperglycemia inconjunction with acute illness. Continu-ation of these agents may be appropriatein selected stable patients who areexpected to consume meals at regularintervals, and they may be initiated orresumed in anticipation of discharge oncethe patient is clinically stable. Specificcaution is required with metformin, dueto the possibility that a contraindicationmay develop during the hospitalization,such as renal insufficiency, unstable he-modynamic status, or need for an imagingstudy that requires a radio-contrast dye.

3. Preventing hypoglycemiaIn the hospital, multiple risk factors forhypoglycemia are present. Patients withor without diabetes may experience hy-poglycemia in the hospital in associationwith altered nutritional state, heart fail-ure, renal or liver disease, malignancy,infection, or sepsis. Additional triggeringevents leading to iatrogenic hypoglycemiainclude sudden reduction of corticoste-roid dose, altered ability of the patient toreport symptoms, reduction of oral in-take, emesis, new NPO status, inappro-priate timing of short- or rapid-actinginsulin in relation to meals, reduction ofrate of administration of intravenous dex-trose, and unexpected interruption ofenteral feedings or parenteral nutrition.

Despite the preventable nature ofmanyinpatient episodes of hypoglycemia, insti-tutions are more likely to have nursingprotocols for the treatment of hypoglyce-mia than for its prevention. Tracking suchepisodes and analyzing their causes areimportant quality-improvement activities(468).

4. Diabetes care providers in thehospitalInpatient diabetes management may beeffectively championed and/or providedby primary care physicians, endocrinolo-gists, intensivists, or hospitalists. Involve-ment of appropriately trained specialistsor specialty teams may reduce length ofstay, improve glycemic control, and im-prove outcomes (468). In the care of di-abetes, implementation of standardized


Position Statement

order sets for scheduled and correction-dose insulin may reduce reliance onsliding-scale management. As hospitalsmove to comply with “meaningful use”regulations for electronic health records,as mandated by the Health InformationTechnology Act, efforts should be madeto assure that all components of struc-tured insulin order sets are incorporatedinto electronic insulin order sets (477,478).

A team approach is needed to estab-lish hospital pathways. To achieve glyce-mic targets associated with improvedhospital outcomes, hospitals will needmultidisciplinary support to develop in-sulin management protocols that effec-tively and safely enable achievement ofglycemic targets (479).

5. Self-management in the hospitalSelf-management of diabetes in the hos-pital may be appropriate for competentadult patients who have a stable level ofconsciousness, have reasonably stabledaily insulin requirements, successfullyconduct self-management of diabetes athome, have physical skills needed tosuccessfully self-administer insulin andperform SMBG, have adequate oral in-take, and are proficient in carbohydratecounting, use of multiple daily insulininjections or insulin pump therapy, andsick-day management. The patient andphysician, in consultation with nursingstaff, must agree that patient self-management is appropriate under theconditions of hospitalization.

Patients who use CSII pump therapyin the outpatient setting can be candidatesfor diabetes self-management in the hos-pital, provided that they have the mentaland physical capacity to do so (468). Ahospital policy and procedures delineat-ing inpatient guidelines for CSII therapyare advisable, and availability of hospitalpersonnel with expertise in CSII therapyis essential. It is important that nursingpersonnel document basal rates and bolusdoses taken on a regular basis (at leastdaily).

6. MNT in the hospitalThe goals of MNT are to optimize glyce-mic control, to provide adequate caloriesto meet metabolic demands, and tocreate a discharge plan for follow-upcare (457,480). The ADA does not en-dorse any single meal plan or specifiedpercentages of macronutrients, and theterm “ADA diet” should no longer beused. Current nutrition recommenda-tions advise individualization based on

treatment goals, physiological parame-ters, and medication usage. Consistentcarbohydrate meal plans are preferredby many hospitals because they facilitatematching the prandial insulin dose to theamount of carbohydrate consumed (481).Because of the complexity of nutrition is-sues in the hospital, a registered dietitian,knowledgeable and skilled in MNT,should serve as an inpatient team mem-ber. The dietitian is responsible for inte-grating information about the patient’sclinical condition, eating, and lifestylehabits and for establishing treatmentgoals in order to determine a realisticplan for nutrition therapy (482,483).

7. Bedside blood glucose monitoringPOC blood glucose monitoring per-formed at the bedside is used to guideinsulin dosing. In the patient who isreceiving nutrition, the timing of glucosemonitoring should match carbohydrateexposure. In the patient who is not re-ceiving nutrition, glucose monitoring isperformed every 4 to 6 h (484,485). Morefrequent blood glucose testing rangingfrom every 30 min to every 2 h is requiredfor patients on intravenous insulin infusions.

Safety standards should be estab-lished for blood glucose monitoring pro-hibiting sharing of finger-stick lancingdevices, lancets, needles, and meters toreduce the risk of transmission of bloodborne diseases. Shared lancing devices carryessentially the same risk as is conferred fromsharing of syringes and needles (486).

Accuracy of blood glucose measure-ments using POC meters has limitationsthat must be considered. Although theFDA allows a 1/2 20% error for bloodglucose meters, questions about the ap-propriateness of these criteria have beenraised (388). Glucose measures differ sig-nificantly between plasma and wholeblood, terms that are often used inter-changeably and can lead to misinterpre-tation. Most commercially availablecapillary blood glucose meters introduce acorrection factor of ;1.12 to report a“plasma-adjusted” value (487).

Significant discrepancies betweencapillary, venous, and arterial plasmasamples have been observed in patientswith low or high hemoglobin concentra-tions, hypoperfusion, and the presence ofinterfering substances particularlymaltose, as contained in immunoglobu-lins (488). Analytical variability has beendescribed with several POCmeters (489).Increasingly newer generation POC bloodglucose meters correct for variation in

hematocrit and for interfering substances.Any glucose result that does not correlatewith the patient’s status should be con-firmed through conventional laboratorysampling of plasma glucose. The FDAhas become increasingly concerned aboutthe use of POC blood glucose meters inthe hospital and is presently reviewingmatters related to their use.

8. Discharge planning and DSMETransition from the acute care setting is ahigh-risk time for all patients, not just thosewith diabetes or new hyperglycemia. Al-though there is an extensive literatureconcerning safe transition within andfrom the hospital, little of it is specific todiabetes (490). It is important to rememberthat diabetes discharge planning is not aseparate entity, but is part of an overall dis-charge plan. As such, discharge planningbegins at admission to the hospital and isupdated as projected patient needs change.

Inpatients may be discharged to var-ied settings, including home (with orwithout visiting nurse services), assistedliving, rehabilitation, or skilled nursingfacilities. The latter two sites are generallystaffed by health professionals, so diabe-tes discharge planning will be limited tocommunication of medication and dietorders. For the patient who is dischargedto assisted living or to home, the optimalprogram will need to consider the typeand severity of diabetes, the effects of thepatient’s illness on blood glucose levels,and the capacities and desires of the pa-tient. Smooth transition to outpatient careshould be ensured. The Agency for Health-care Research and Quality (AHRQ) recom-mends that at a minimum, discharge plansinclude the following:

c Medication reconciliation: The pa-tient’s medications must be cross-checked to ensure that no chronicmedications were stopped and to en-sure the safety of new prescriptions.

c Whenever possible, prescriptions fornew or changed medication should befilled and reviewedwith the patient andfamily at or before discharge.

c Structured discharge communication:Information on medication changes,pending tests and studies, and follow-upneeds must be accurately and promptlycommunicated to outpatient physicians.

c Discharge summaries should be trans-mitted to the primary physician as soonas possible after discharge.

c Appointment keeping behavior isenhanced when the inpatient team


Position Statement

schedules outpatient medical follow-up prior to discharge. Ideally the in-patient care providers or case managers/discharge planners will schedule fol-low-up visit(s) with the appropriateprofessionals, including the primarycare provider, endocrinologist, and di-abetes educator (491).

Teaching diabetes self-management topatients in hospitals is a challenging task.Patients are ill, under increased stress relatedto their hospitalization and diagnosis, andin an environment not conducive to learn-ing. Ideally, people with diabetes should betaught at a time and place conducive tolearning: as an outpatient in a recognizedprogram of diabetes education. For thehospitalized patient, diabetes “survivalskills” education is generally a feasible ap-proach to provide sufficient informationand training to enable safe care at home.Patients hospitalized because of a crisis re-lated to diabetes management or poor careat home need education to prevent subse-quent episodes of hospitalization. An as-sessment of the need for a home healthreferral or referral to an outpatient diabeteseducation program should be part of dis-charge planning for all patients.

DSME cannot wait until discharge,especially in those new to insulin ther-apy or in whom the diabetes regimen hasbeen substantially altered during thehospitalization.

It is recommended that the followingareas of knowledge be reviewed andaddressed prior to hospital discharge:

c Identification of health care providerwho will provide diabetes care afterdischarge

c Level of understanding related to thediagnosis of diabetes, SMBG, and ex-planation of home blood glucose goals

c Definition, recognition, treatment, andprevention of hyperglycemia and hy-poglycemia

c Information on consistent eatingpatterns

c When and how to take blood glucose–loweringmedications including insulinadministration (if going home on in-sulin)

c Sick-day managementc Proper use and disposal of needles andsyringes

It is important that patients be pro-vided with appropriate durable medicalequipment, medication, supplies, andprescriptions at the time of discharge in

order to avoid a potentially dangeroushiatus in care. These supplies/prescrip-tions should include the following:

c Insulin (vials or pens) if neededc Syringes or pen needles (if needed)c Oral medications (if needed)c Blood glucose meter and stripsc Lancets and lancing devicec Urine ketone strips (type 1)c Glucagon emergency kit (insulin-treated)c Medical alert application/charm

More expanded diabetes education canbe arranged in the community. An out-patient follow-up visit with the primarycare provider, endocrinologist, or diabeteseducator within 1 month of discharge isadvised for all patients having hyperglyce-mia in the hospital. Clear communicationwith outpatient providers either directly orvia hospital discharge summaries facilitatessafe transitions to outpatient care. Provid-ing information regarding the cause or theplan for determining the cause of hyper-glycemia, related complications and co-morbidities, and recommended treatmentscan assist outpatient providers as theyassume ongoing care.

B. Diabetes and employmentAny person with diabetes, whether in-sulin treated or noninsulin treated,should be eligible for any employmentfor which he/she is otherwise qualified.Employment decisions should never bebased on generalizations or stereotypesregarding the effects of diabetes. Whenquestions arise about the medical fitnessof a person with diabetes for a particularjob, a health care professional with ex-pertise in treating diabetes should per-form an individualized assessment. Seethe ADA position statement on diabetesand employment (492).

C. Diabetes and drivingA large percentage of people with diabetesin the U.S. and elsewhere seek a license todrive, either for personal or employmentpurposes. There has been considerable de-bate whether, and the extent to which,diabetes may be a relevant factor in de-termining the driver ability and eligibilityfor a license.

People with diabetes are subject to agreat variety of licensing requirements ap-plied by both state and federal jurisdic-tions, which may lead to loss ofemployment or significant restrictionson a person’s license. Presence of a medicalcondition that can lead to significantly

impaired consciousness or cognition maylead to drivers being evaluated for fitness todrive. For diabetes, this typically ariseswhen the person has had a hypoglycemicepisode behind the wheel, even if this didnot lead to a motor vehicle accident.

Epidemiological and simulator datasuggest that people with insulin-treateddiabetes have a small increase in risk ofmotor vehicle accidents, primarily due tohypoglycemia and decreased awarenessof hypoglycemia. This increase (RR 1.12–1.19) is much smaller than the risks asso-ciated with teenage male drivers (RR 42),driving at night (RR 142), driving on ruralroads compared with urban roads (RR9.2), and obstructive sleep apnea (RR2.4), all of which are accepted for unre-stricted licensure.

The ADA position statement on di-abetes and driving (493) recommendsagainst blanket restrictions based on thediagnosis of diabetes and urges individualassessment by a health care professionalknowledgeable in diabetes if restrictionson licensure are being considered. Pa-tients should be evaluated for decreasedawareness of hypoglycemia, hypoglyce-mia episodes while driving, or severe hy-poglycemia. Patients with retinopathy orperipheral neuropathy require assess-ment to determine if those complicationsinterfere with operation of a motor vehi-cle. Health care professionals should becognizant of the potential risk of drivingwith diabetes and counsel their patientsabout detecting and avoiding hypoglyce-mia while driving.

D. Diabetes management incorrectional institutionsPeople with diabetes in correctional facil-ities should receive care that meets na-tional standards. Because it is estimatedthat nearly 80,000 inmates have diabetes,correctional institutions should havewritten policies and procedures for themanagement of diabetes and for trainingof medical and correctional staff in di-abetes care practices. See the ADA posi-tion statement on diabetes managementin correctional institutions (494) for fur-ther discussion.

X. STRATEGIES FORIMPROVING DIABETES CARE

Recommendationsc Care should be aligned with compo-nents of the Chronic Care Model(CCM) to ensure productive inter-actions between a prepared proactive


Position Statement

practice team and an informed acti-vated patient. (A)

c When feasible, care systems shouldsupport team-based care, communityinvolvement, patient registries, andembedded decision support tools tomeet patient needs. (B)

c Treatment decisions should be timelyand based on evidence-based guide-lines that are tailored to individualpatient preferences, prognoses, andcomorbidities. (B)

c A patient-centered communicationstyle should be employed that in-corporates patient preferences, assessesliteracy and numeracy, and addressescultural barriers to care. (B)

There has been steady improvement in theproportion of diabetic patients achievingrecommended levels of A1C, blood pres-sure, and LDL cholesterol in the last 10years, both in primary care settings and inendocrinology practices. Mean A1C na-tionally has declined from 7.82% in 1999–2000 to 7.18% in 2004 based onNHANESdata (495). This has been accompanied byimprovements in lipids and blood pressurecontrol and led to substantial reductions inend-stage microvascular complications inthose with diabetes. Nevertheless in somestudies only 57.1% of adults with diag-nosed diabetes achieved an A1C of ,7%,only 45.5% had a blood pressure,130/80mmHg, and just 46.5% had a total choles-terol ,200 mg/dL, with only 12.2% ofpeople with diabetes achieving all threetreatment goals (496). Evidence also sug-gests that progress in risk factor controlmay be slowing (497). Certain patientgroups, such as patients with complex co-morbidities, financial or other social hard-ships, and/or limited English proficiency,may present particular challenges to goal-based care (498,499). Persistent variationin quality of diabetes care across providersand across practice settings even after ad-justing for patient factors indicates thatthere remains potential for substantial fur-ther improvements in diabetes care.

Although numerous interventions toimprove adherence to the recommendedstandards have been implemented, a ma-jor barrier to optimal care is a deliverysystem that too often is fragmented, lacksclinical information capabilities, oftenduplicates services, and is poorly de-signed for the coordinated delivery ofchronic care. The CCM has been shownin numerous studies to be an effectiveframework for improving the quality ofdiabetes care (500). The CCM includes

six core elements for the provision of op-timal care of patients with chronic dis-ease: 1) delivery system design (movingfrom a reactive to a proactive care deliverysystem where planned visits are coordi-nated through a team based approach),2) self-management support, 3) decisionsupport (basing care on evidence-based,effective care guidelines), 4) clinical infor-mation systems (using registries that canprovide patient-specific and population-based support to the care team), 5)community resources and policies (iden-tifying or developing resources to supporthealthy lifestyles), and 6) health systems(to create a quality-oriented culture). Re-definition of the roles of the clinic staffand promoting self-management on thepart of the patient are fundamental tothe successful implementation of theCCM (501). Collaborative, multidisci-plinary teams are best suited to providesuch care for people with chronicconditions such as diabetes and to facili-tate patients’ performance of appropriateself-management (163,165,220,502).

NDEP maintains an online resource(www.betterdiabetescare.nih.gov) to helphealth care professionals design and im-plement more effective health care deliv-ery systems for those with diabetes. Threespecific objectives, with references to lit-erature that outlines practical strategies toachieve each, are outlined below.

Objective 1: Optimize provider andteam behaviorThe care team should prioritize timely andappropriate intensification of lifestyle and/or pharmaceutical therapy of patients whohave not achieved beneficial levels of bloodpressure, lipid, or glucose control (503).Strategies such as explicit goal settingwith patients (504); identifying and ad-dressing language, numeracy, or culturalbarriers to care (505–508); integrating evi-dence-based guidelines and clinical infor-mation tools into the process of care(509–511); and incorporating caremanage-ment teams including nurses, pharmacists,and other providers (512–515) have eachbeen shown to optimize provider and teambehavior and thereby catalyze reduction inA1C, blood pressure, and LDL cholesterol.

Objective 2: Support patient behaviorchangeSuccessful diabetes care requires a sys-tematic approach to supporting patients’behavior change efforts, including a)healthy lifestyle changes (physical activ-ity, healthy eating, nonuse of tobacco,

weight management, effective coping),b) disease self-management (medicationtaking and management; self-monitoringof glucose and blood pressure when clin-ically appropriate), and c) prevention ofdiabetes complications (self-monitoringof foot health; active participation inscreening for eye, foot, and renal compli-cations; immunizations). High-qualityDSME has been shown to improve patientself-management, satisfaction, and glu-cose control (184,516), as has deliveryof ongoing DSMS so that gains achievedduringDSME are sustained (134,135,152).National DSME standards call for anintegrated approach that includes clinicalcontent and skills, behavioral strategies(goal-setting, problem solving), and ad-dressing emotional concerns in eachneeded curriculum content area.

Objective 3: Change the systemof careThe most successful practices have an in-stitutional priority for providing high qual-ity of care (517). Changes that have beenshown to increase quality of diabetes careinclude basing care on evidence-basedguidelines (518), expanding the role ofteams and staff (501,519), redesigning theprocesses of care (520), implementing elec-tronic health record tools (521,522), acti-vating and educating patients (523,524),and identifying and/or developing and en-gaging community resources and publicpolicy that support healthy lifestyles(525). Recent initiatives such as thePatient-Centered Medical Home showpromise to improve outcomes through co-ordinated primary care and offer new op-portunities for team-based chronic diseasecare (526). Alterations in reimbursementthat reward the provision of appropriateand high-quality care rather than visit-based billing (527) and that can accommo-date the need to personalize care goals mayprovide additional incentives to improvediabetes care (528).

It is clear that optimal diabetes man-agement requires an organized, system-atic approach and involvement of acoordinated team of dedicated healthcare professionals working in an environ-ment where patient-centered high-qualitycare is a priority.

References1. American Diabetes Association. Medical

Management of Type 1 Diabetes. Alexandria,VA, American Diabetes Association, 2012

2. American Diabetes Association. MedicalManagement of Type 2 Diabetes.


Position Statement

Alexandria, VA, American Diabetes As-sociation, 2012

3. American Diabetes Association. Therapyfor Diabetes Mellitus and Related Dis-orders. Alexandria, VA, American Di-abetes Association, 2009

4. Li R, Zhang P, Barker LE, ChowdhuryFM, Zhang X. Cost-effectiveness of in-terventions to prevent and control di-abetes mellitus: a systematic review.Diabetes Care 2010;33:1872–1894

5. American Diabetes Association. Diagnosisand classification of diabetes mellitus.Diabetes Care 2010;33(Suppl. 1):S62–S69

6. International Expert Committee. In-ternational Expert Committee report onthe role of the A1C assay in the diagnosisof diabetes. Diabetes Care 2009;32:1327–1334

7. Ziemer DC, Kolm P, Weintraub WS,et al. Glucose-independent, black-whitedifferences in hemoglobin A1c levels:a cross-sectional analysis of 2 studies.Ann Intern Med 2010;152:770–777

8. Kumar PR, Bhansali A, RavikiranM, et al.Utility of glycated hemoglobin in di-agnosing type 2 diabetes mellitus:a community-based study. J Clin Endo-crinol Metab 2010;95:2832–2835

9. Selvin E, Steffes MW, Ballantyne CM,Hoogeveen RC, Coresh J, Brancati FL.Racial differences in glycemic markers:a cross-sectional analysis of community-based data. Ann Intern Med 2011;154:303–309

10. Nowicka P, Santoro N, Liu H, et al.Utility of hemoglobin A(1c) for di-agnosing prediabetes and diabetes inobese children and adolescents. DiabetesCare 2011;34:1306–1311

11. Cowie CC, Rust KF, Byrd-Holt DD, et al.Prevalence of diabetes and high risk fordiabetes using A1C criteria in the U.S.population in 1988-2006. Diabetes Care2010;33:562–568

12. Picón MJ, Murri M, Muñoz A,Fern�andez-Garc�ıa JC, Gomez-Huelgas R,Tinahones FJ. Hemoglobin A1c versusoral glucose tolerance test in postpartumdiabetes screening. Diabetes Care 2012;35:1648–1653

13. Expert Committee on the Diagnosis andClassification of Diabetes Mellitus. Re-port of the Expert Committee on theDiagnosis and Classification of DiabetesMellitus. Diabetes Care 1997;20:1183–1197

14. Genuth S, Alberti KG, Bennett P, et al.;Expert Committee on the Diagnosisand Classification of Diabetes Mellitus.Follow-up report on the diagnosis ofdiabetes mellitus. Diabetes Care 2003;26:3160–3167

15. Zhang X, Gregg EW, Williamson DF,et al. A1C level and future risk of di-abetes: a systematic review. DiabetesCare 2010;33:1665–1673

16. Selvin E, Steffes MW, Zhu H, et al. Gly-cated hemoglobin, diabetes, and car-diovascular risk in nondiabetic adults.N Engl J Med 2010;362:800–811

17. Ackermann RT, Cheng YJ, WilliamsonDF, Gregg EW. Identifying adults at highrisk for diabetes and cardiovascular dis-ease using hemoglobin A1c NationalHealth and Nutrition Examination Sur-vey 2005-2006. Am J PrevMed 2011;40:11–17

18. Griffin SJ, Borch-Johnsen K, Davies MJ,et al. Effect of early intensive multifac-torial therapy on 5-year cardiovascularoutcomes in individuals with type 2 di-abetes detected by screening (ADDI-TION-Europe): a cluster-randomisedtrial. Lancet 2011;378:156–167

19. Kahn R, Alperin P, Eddy D, et al. Ageat initiation and frequency of screen-ing to detect type 2 diabetes: a cost-effectiveness analysis. Lancet 2010;375:1365–1374

20. Erickson SC, Le L, Zakharyan A, et al.New-onset treatment-dependent di-abetes mellitus and hyperlipidemia as-sociated with atypical antipsychotic usein older adults without schizophrenia orbipolar disorder. J Am Geriatr Soc 2012;60:474–479

21. Chiu M, Austin PC, Manuel DG, ShahBR, Tu JV. Deriving ethnic-specific BMIcutoff points for assessing diabetes risk.Diabetes Care 2011;34:1741–1748

22. Sheehy A, Pandhi N, Coursin DB, et al.Minority status and diabetes screening inan ambulatory population. DiabetesCare 2011;34:1289–1294

23. Knowler WC, Barrett-Connor E, FowlerSE, et al.; Diabetes Prevention ProgramResearch Group. Reduction in the in-cidence of type 2 diabetes with lifestyleintervention or metformin. N Engl J Med2002;346:393–403

24. Tuomilehto J, Lindström J, Eriksson JG,et al.; Finnish Diabetes Prevention StudyGroup. Prevention of type 2 diabetesmellitus by changes in lifestyle amongsubjects with impaired glucose tolerance.N Engl J Med 2001;344:1343–1350

25. Pan XR, Li GW, Hu YH, et al. Effects ofdiet and exercise in preventing NIDDMin people with impaired glucose toler-ance. The Da Qing IGT and DiabetesStudy. Diabetes Care 1997;20:537–544

26. Buchanan TA, Xiang AH, Peters RK, et al.Preservation of pancreatic beta-cellfunction and prevention of type 2 di-abetes by pharmacological treatment ofinsulin resistance in high-risk Hispanicwomen. Diabetes 2002;51:2796–2803

27. Chiasson JL, Josse RG, Gomis R,HanefeldM, Karasik A, LaaksoM; STOP-NIDDM Trial Research Group. Acarbosefor prevention of type 2 diabetes melli-tus: the STOP-NIDDM randomised trial.Lancet 2002;359:2072–2077

28. Gerstein HC, Yusuf S, Bosch J, et al.;DREAM (Diabetes REduction Assess-ment with ramipril and rosiglitazoneMedication) Trial Investigators. Effect ofrosiglitazone on the frequency of di-abetes in patients with impaired glucosetolerance or impaired fasting glucose:a randomised controlled trial. Lancet2006;368:1096–1105

29. Ramachandran A, Snehalatha C, Mary S,Mukesh B, Bhaskar AD, Vijay V; IndianDiabetes Prevention Programme (IDPP).The Indian Diabetes Prevention Pro-gramme shows that lifestyle modifica-tion and metformin prevent type 2diabetes in Asian Indian subjects withimpaired glucose tolerance (IDPP-1).Diabetologia 2006;49:289–297

30. Johnson SL, Tabaei BP, Herman WH.The efficacy and cost of alternativestrategies for systematic screening fortype 2 diabetes in the U.S. population45-74 years of age. Diabetes Care 2005;28:307–311

31. Dabelea D, D’Agostino RB Jr, Mayer-Davis EJ, et al.; SEARCH for Diabetes inYouth Study Group. Testing the accel-erator hypothesis: body size, beta-cellfunction, and age at onset of type 1(autoimmune) diabetes. Diabetes Care2006;29:290–294

32. Liese AD, D’Agostino RB Jr, HammanRF, et al.; SEARCH for Diabetes in YouthStudy Group. The burden of diabetesmellitus among US youth: prevalenceestimates from the SEARCH for Diabetesin Youth Study. Pediatrics 2006;118:1510–1518

33. American Diabetes Association. Type 2diabetes in children and adolescents.Diabetes Care 2000;23:381–389

34. Pescovitz MD, Greenbaum CJ, Krause-Steinrauf H, et al.; Type 1 DiabetesTrialNet Anti-CD20 Study Group. Rit-uximab, B-lymphocyte depletion, andpreservation of beta-cell function. NEngl J Med 2009;361:2143–2152

35. Orban T, Bundy B, Becker DJ, et al.;Type 1 Diabetes TrialNet AbataceptStudy Group. Co-stimulation modulationwith abatacept in patients with recent-onset type 1 diabetes: a randomised,double-blind, placebo-controlled trial.Lancet 2011;378:412–419

36. Lawrence JM, Contreras R, Chen W,Sacks DA. Trends in the prevalence ofpreexisting diabetes and gestationaldiabetes mellitus among a racially/ethnically diverse population of preg-nant women, 1999-2005. Diabetes Care2008;31:899–904

37. Metzger BE, Lowe LP, Dyer AR, et al.;HAPO Study Cooperative ResearchGroup. Hyperglycemia and adversepregnancy outcomes. N Engl J Med2008;358:1991–2002

38. Metzger BE, Gabbe SG, Persson B, et al.;International Association of Diabetes


Position Statement

and Pregnancy Study Groups ConsensusPanel. International association of di-abetes and pregnancy study groups rec-ommendations on the diagnosis andclassification of hyperglycemia in preg-nancy. Diabetes Care 2010;33:676–682

39. O’Sullivan EP, Avalos G, O’Reilly M,Dennedy MC, Gaffney G, Dunne F; At-lantic DIP collaborators. Atlantic Diabetesin Pregnancy (DIP): the prevalence andoutcomes of gestational diabetes mellitususing newdiagnostic criteria. Diabetologia2011;54:1670–1675

40. Lapolla A, Dalfrà MG, Ragazzi E, De CataAP, Fedele D. New International Asso-ciation of the Diabetes and PregnancyStudy Groups (IADPSG) recommen-dations for diagnosing gestational di-abetes compared with former criteria:a retrospective study on pregnancy out-come. Diabet Med 2011;28:1074–1077

41. Landon MB, Spong CY, Thom E, et al.;Eunice Kennedy Shriver National In-stitute of Child Health and Human De-velopment Maternal-Fetal MedicineUnits Network. A multicenter, random-ized trial of treatment for mild gesta-tional diabetes. N Engl J Med 2009;361:1339–1348

42. Crowther CA, Hiller JE, Moss JR,McPhee AJ, Jeffries WS, Robinson JS;Australian Carbohydrate IntoleranceStudy in Pregnant Women (ACHOIS)Trial Group. Effect of treatment of ges-tational diabetes mellitus on pregnancyoutcomes. N Engl J Med 2005;352:2477–2486

43. Committee on Obstetric Practice. Com-mittee opinion no. 504: screening anddiagnosis of gestational diabetes melli-tus. Obstet Gynecol 2011;118:751–753

44. Kim C, Herman WH, Cheung NW,Gunderson EP, Richardson C. Compar-ison of hemoglobin A1c with fastingplasma glucose and 2-h postchallengeglucose for risk stratification amongwomen with recent gestational diabetesmellitus. Diabetes Care 2011;34:1949–1951

45. Kim C, Newton KM, Knopp RH. Gesta-tional diabetes and the incidence of type2 diabetes: a systematic review. DiabetesCare 2002;25:1862–1868

46. Tobias DK, Hu FB, Chavarro J, Rosner B,Mozaffarian D, Zhang C. Healthful di-etary patterns and type 2 diabetes mel-litus risk among women with a history ofgestational diabetesmellitus. Arch InternMed 2012;172:1566–1572

47. Li G, Zhang P,Wang J, et al. The long-termeffect of lifestyle interventions to preventdiabetes in the China Da Qing DiabetesPrevention Study: a 20-year follow-upstudy. Lancet 2008;371:1783–1789

48. Lindström J, Ilanne-Parikka P, PeltonenM, et al.; Finnish Diabetes PreventionStudy Group. Sustained reduction in theincidence of type 2 diabetes by lifestyle

intervention: follow-up of the FinnishDiabetes Prevention Study. Lancet 2006;368:1673–1679

49. Knowler WC, Fowler SE, Hamman RF,et al.; Diabetes Prevention Program Re-search Group. 10-year follow-up of di-abetes incidence and weight loss in theDiabetes Prevention Program OutcomesStudy. Lancet 2009;374:1677–1686

50. Herman WH, Hoerger TJ, Brandle M,et al.; Diabetes Prevention Program Re-search Group. The cost-effectiveness oflifestyle modification or metformin inpreventing type 2 diabetes in adults withimpaired glucose tolerance. Ann InternMed 2005;142:323–332

51. Diabetes Prevention Program ResearchGroup. The 10-year cost-effectiveness oflifestyle intervention or metformin fordiabetes prevention: an intent-to-treatanalysis of the DPP/DPPOS. DiabetesCare 2012;35:723–730

52. Ackermann RT, Finch EA, Brizendine E,Zhou H, Marrero DG. Translating theDiabetes Prevention Program into thecommunity. The DEPLOY Pilot Study.Am J Prev Med 2008;35:357–363

53. Diabetes Prevention Program ResearchGroup. Long-term safety, tolerability,and weight loss associated with metfor-min in the Diabetes Prevention ProgramOutcomes Study. Diabetes Care 2012;35:731–737

54. DREAM Trial Investigators. Incidence ofdiabetes following ramipril or rosiglita-zone withdrawal. Diabetes Care 2011;34:1265–1269

55. Ratner RE, Christophi CA, Metzger BE,et al.; Diabetes Prevention Program Re-search Group. Prevention of diabetes inwomen with a history of gestational di-abetes: effects of metformin and lifestyleinterventions. J Clin Endocrinol Metab2008;93:4774–4779

56. Orchard TJ, Temprosa M, Barrett-Connor E, et al.; The Diabetes Pre-vention Program Outcomes StudyResearch Group; prepared on behalf ofthe DPPOS Research Group. Long-termeffects of the Diabetes Prevention Pro-gram interventions on cardiovascularrisk factors: a report from the DPP Out-comes Study. Diabet Med. 19 July 2012[Epub ahead of print]

57. Ziegler R, Heidtmann B, Hilgard D,Hofer S, Rosenbauer J, Holl R; DPV-Wiss-Initiative. Frequency of SMBGcorrelates with HbA1c and acute com-plications in children and adolescentswith type 1 diabetes. Pediatr Diabetes2011;12:11–17

58. Farmer A, Wade A, Goyder E, et al. Im-pact of self monitoring of blood glucosein the management of patients with non-insulin treated diabetes: open parallelgroup randomised trial. BMJ 2007;335:132

59. O’Kane MJ, Bunting B, Copeland M,Coates VE; ESMON Study Group. Effi-cacy of self monitoring of blood glucosein patients with newly diagnosed type 2diabetes (ESMON study): randomisedcontrolled trial. BMJ 2008;336:1174–1177

60. Simon J, Gray A, Clarke P, Wade A, NeilA, Farmer A; Diabetes Glycaemic Edu-cation and Monitoring Trial Group. Costeffectiveness of self monitoring of bloodglucose in patients with non-insulintreated type 2 diabetes: economic eval-uation of data from the DiGEM trial. BMJ2008;336:1177–1180

61. Farmer AJ, Perera R, Ward A, et al. Meta-analysis of individual patient data inrandomised trials of self monitoring ofblood glucose in people with non-insulin treated type 2 diabetes. BMJ2012;344:e486

62. Malanda UL, Welschen LMC, RiphagenII, Dekker JM, Nijpels G, Bot SD. Self-monitoring of blood glucose in patientswith type 2 diabetes mellitus who are notusing insulin. Cochrane Database SystRev 2012;2012(Issue 1):CD005060

63. Sacks DB, Arnold M, Bakris GL, et al.;National Academy of Clinical Bio-chemistry. Position statement executivesummary: guidelines and recommenda-tions for laboratory analysis in the di-agnosis and management of diabetesmellitus. Diabetes Care 2011;34:1419–1423

64. Wang J, Zgibor J, Matthews JT, Charron-Prochownik D, Sereika SM, Siminerio L.Self-monitoring of blood glucose is as-sociated with problem-solving skills inhyperglycemia and hypoglycemia. Di-abetes Educ 2012;38:207–218

65. Polonsky WH, Fisher L, Schikman CH,et al. Structured self-monitoring of bloodglucose significantly reduces A1C levelsin poorly controlled, noninsulin-treatedtype 2 diabetes: results from the Struc-tured Testing Program study. DiabetesCare 2011;34:262–267

66. Tamborlane WV, Beck RW, Bode BW,et al.; Juvenile Diabetes Research Foun-dation Continuous Glucose Monitor-ing Study Group. Continuous glucosemonitoring and intensive treatment oftype 1 diabetes. N Engl J Med 2008;359:1464–1476

67. Beck RW, Hirsch IB, Laffel L, et al.; Ju-venile Diabetes Research FoundationContinuous Glucose Monitoring StudyGroup. The effect of continuous glucosemonitoring in well-controlled type 1diabetes. Diabetes Care 2009;32:1378–1383

68. Bergenstal RM, Tamborlane WV,Ahmann A, et al.; STAR 3 Study Group.Effectiveness of sensor-augmented in-sulin-pump therapy in type 1 diabetes. NEngl J Med 2010;363:311–320


Position Statement

69. Slover RH, Welsh JB, Criego A, et al.Effectiveness of sensor-augmented pumptherapy in children and adolescents withtype 1 diabetes in the STAR 3 study. Pe-diatr Diabetes 2012;13:6–11

70. Yeh HC, Brown TT, Maruthur N, et al.Comparative effectiveness and safety ofmethods of insulin delivery and glucosemonitoring for diabetes mellitus: a sys-tematic review and meta-analysis. AnnIntern Med 2012;157:336–347

71. The Diabetes Control and ComplicationsTrial Research Group. The effect of in-tensive treatment of diabetes on the de-velopment and progression of long-termcomplications in insulin-dependent di-abetes mellitus. N Engl J Med 1993;329:977–986

72. Stratton IM, Adler AI, Neil HA, et al.Association of glycaemia with macro-vascular and microvascular complica-tions of type 2 diabetes (UKPDS 35):prospective observational study. BMJ2000;321:405–412

73. Cagliero E, Levina EV, Nathan DM. Im-mediate feedback of HbA1c levels im-proves glycemic control in type 1 andinsulin-treated type 2 diabetic patients.Diabetes Care 1999;22:1785–1789

74. Miller CD, Barnes CS, Phillips LS, et al.Rapid A1c availability improves clinicaldecision-making in an urban primarycare clinic. Diabetes Care 2003;26:1158–1163

75. Al-Ansary L, Farmer A, Hirst J, et al.Point-of-care testing for Hb A1c in themanagement of diabetes: a systematicreview and metaanalysis. Clin Chem2011;57:568–576

76. Gialamas A, St John A, Laurence CO,Bubner TK; PoCT Management Com-mittee. Point-of-care testing for patientswith diabetes, hyperlipidaemia or co-agulation disorders in the general prac-tice setting: a systematic review. FamPract 2010;27:17–24

77. Nathan DM, Kuenen J, Borg R, Zheng H,Schoenfeld D, Heine RJ; A1C-DerivedAverage Glucose Study Group. Trans-lating the A1C assay into estimated av-erage glucose values. Diabetes Care2008;31:1473–1478

78. Rohlfing CL, Wiedmeyer HM, Little RR,England JD, Tennill A, Goldstein DE.Defining the relationship betweenplasma glucose and HbA(1c): analysis ofglucose profiles and HbA(1c) in the Di-abetes Control and Complications Trial.Diabetes Care 2002;25:275–278

79. Wilson DM, Kollman; Diabetes Researchin Children Network (DirecNet) StudyGroup. Relationship of A1C to glucoseconcentrations in children with type 1diabetes: assessments by high-frequencyglucose determinations by sensors. Di-abetes Care 2008;31:381–385

80. The Diabetes Control and Complica-tions Trial/Epidemiology of Diabetes

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81. Martin CL, Albers J, Herman WH, et al.;DCCT/EDIC Research Group. Neurop-athy among the diabetes control andcomplications trial cohort 8 years aftertrial completion. Diabetes Care 2006;29:340–344

82. Ohkubo Y, Kishikawa H, Araki E, et al.Intensive insulin therapy prevents theprogression of diabetic microvascularcomplications in Japanese patients withnon-insulin-dependent diabetes melli-tus: a randomized prospective 6-yearstudy. Diabetes Res Clin Pract 1995;28:103–117

83. UK Prospective Diabetes Study (UKPDS)Group. Effect of intensive blood-glucosecontrol with metformin on complica-tions in overweight patients with type 2diabetes (UKPDS 34). Lancet 1998;352:854–865

84. UK Prospective Diabetes Study (UKPDS)Group. Intensive blood-glucose controlwith sulphonylureas or insulin com-pared with conventional treatment andrisk of complications in patients withtype 2 diabetes (UKPDS 33). Lancet1998;352:837–853

85. Holman RR, Paul SK, Bethel MA,Matthews DR, Neil HA. 10-year follow-up of intensive glucose control in type 2diabetes. N Engl J Med 2008;359:1577–1589

86. Duckworth W, Abraira C, Moritz T,et al.; VADT Investigators. Glucosecontrol and vascular complications inveterans with type 2 diabetes. N Engl JMed 2009;360:129–139

87. Moritz T, Duckworth W, Abraira C. Vet-erans Affairs Diabetes Trialdcorrections.N Engl J Med 2009;361:1024–1025

88. Patel A, MacMahon S, Chalmers J, et al.;ADVANCE Collaborative Group. In-tensive blood glucose control and vas-cular outcomes in patients with type 2diabetes. N Engl J Med 2008;358:2560–2572

89. Ismail-Beigi F, Craven T, Banerji MA,et al.; ACCORD Trial Group. Effect ofintensive treatment of hyperglycaemiaon microvascular outcomes in type 2diabetes: an analysis of the ACCORDrandomised trial. Lancet 2010;376:419–430

90. Chew EY, Ambrosius WT, Davis MD,et al.; ACCORD Study Group; ACCORDEye Study Group. Effects of medicaltherapies on retinopathy progression intype 2 diabetes. N Engl J Med 2010;363:233–244

91. Gerstein HC, Miller ME, Byington RP,et al.; Action to Control CardiovascularRisk in Diabetes Study Group. Effects of

intensive glucose lowering in type 2 di-abetes. N Engl J Med 2008;358:2545–2559

92. Nathan DM, Cleary PA, Backlund JY,et al.; Diabetes Control and Compli-cations Trial/Epidemiology of DiabetesInterventions and Complications (DCCT/EDIC) Study Research Group. Intensivediabetes treatment and cardiovasculardisease in patients with type 1 diabetes.N Engl J Med 2005;353:2643–2653

93. Nathan DM, Zinman B, Cleary PA, et al.;Diabetes Control and ComplicationsTrial/Epidemiology of Diabetes Inter-ventions and Complications (DCCT/EDIC) Research Group. Modern-dayclinical course of type 1 diabetes mellitusafter 30 years’ duration: the Diabetes Con-trol and Complications Trial/Epidemiologyof Diabetes Interventions and Complica-tions and Pittsburgh Epidemiology ofDiabetes Complications experience (1983-2005). Arch Intern Med 2009;169:1307–1316

94. Skyler JS, Bergenstal R, Bonow RO, et al.;American Diabetes Association; Ameri-can College of Cardiology Foundation;American Heart Association. Intensiveglycemic control and the prevention ofcardiovascular events: implications ofthe ACCORD, ADVANCE, and VA Di-abetes Trials: a position statement of theAmerican Diabetes Association and ascientific statement of the AmericanCollege of Cardiology Foundation andthe American Heart Association. Di-abetes Care 2009;32:187–192

95. Gerstein HC, Miller ME, Genuth S, et al.;ACCORD Study Group. Long-term ef-fects of intensive glucose lowering oncardiovascular outcomes. N Engl J Med2011;364:818–828

96. Riddle MC, Ambrosius WT, Brillon DJ,et al.; Action to Control CardiovascularRisk in Diabetes Investigators. Epidemi-ologic relationships between A1C andall-cause mortality during a median 3.4-year follow-up of glycemic treatment inthe ACCORD trial. Diabetes Care 2010;33:983–990

97. Bonds DE, Miller ME, Bergenstal RM,et al. The association between symp-tomatic, severe hypoglycaemia andmortality in type 2 diabetes: retrospec-tive epidemiological analysis of the AC-CORD study. BMJ 2010;340:b4909

98. Reaven PD, Moritz TE, Schwenke DC,et al. Intensive glucose-lowering therapyreduces cardiovascular disease events inVeterans Affairs Diabetes Trial participantswith lower calcified coronary atheroscle-rosis. Diabetes 2009;58:2642–2648

99. Duckworth WC, Abraira C, Moritz TE,et al.; Investigators of the VADT. Theduration of diabetes affects the responseto intensive glucose control in type2 subjects: the VA Diabetes Trial.


Position Statement

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100. Turnbull FM, Abraira C, Anderson RJ,et al.; Control Group. Intensive glucosecontrol and macrovascular outcomes intype 2 diabetes. Diabetologia 2009;52:2288–2298

101. Ismail-Beigi F, Moghissi E, Tiktin M,Hirsch IB, Inzucchi SE, Genuth S. In-dividualizing glycemic targets in type 2diabetes mellitus: implications of recentclinical trials. Ann InternMed 2011;154:554–559

102. American Diabetes Association. Post-prandial blood glucose. Diabetes Care2001;24:775–778

103. Ceriello A, Taboga C, Tonutti L, et al.Evidence for an independent and cu-mulative effect of postprandial hyper-triglyceridemia and hyperglycemia onendothelial dysfunction and oxidativestress generation: effects of short- andlong-term simvastatin treatment. Circu-lation 2002;106:1211–1218

104. Raz I,Wilson PW, Strojek K, et al. Effectsof prandial versus fasting glycemia oncardiovascular outcomes in type 2 di-abetes: the HEART2D trial. DiabetesCare 2009;32:381–386

105. Metzger BE, Buchanan TA, Coustan DR,et al. Summary and recommendationsof the Fifth International Workshop-Conference on Gestational DiabetesMellitus. Diabetes Care 2007;30(Suppl.2):S251–S260

106. Kitzmiller JL, Block JM, Brown FM, et al.Managing preexisting diabetes for pr-egnancy: summary of evidence andconsensus recommendations for care.Diabetes Care 2008;31:1060–1079

107. DeWitt DE, Hirsch IB. Outpatient in-sulin therapy in type 1 and type 2 di-abetes mellitus: scientific review. JAMA2003;289:2254–2264

108. Rosenstock J, Dailey G, Massi-BenedettiM, Fritsche A, Lin Z, Salzman A. Re-duced hypoglycemia risk with insulinglargine: a meta-analysis comparing in-sulin glargine with human NPH insulinin type 2 diabetes. Diabetes Care 2005;28:950–955

109. American Diabetes Association. IntensiveDiabetes Management. Alexandria, VA,American Diabetes Association, 2009

110. Mooradian AD, BernbaumM, Albert SG.Narrative review: a rational approach tostarting insulin therapy. Ann Intern Med2006;145:125–134

111. Inzucchi SE, Bergenstal RM, Buse JB,et al.; American Diabetes Association(ADA); European Association for theStudy of Diabetes (EASD). Managementof hyperglycemia in type 2 diabetes:a patient-centered approach. PositionStatement of the American Diabetes As-sociation (ADA) and the European As-sociation for the Study of Diabetes

(EASD). Diabetes Care 2012;35:1364–1379

112. Bennett WL, Maruthur NM, Singh S,et al. Comparative effectiveness andsafety of medications for type 2 diabetes:an update including new drugs and 2-drug combinations. Ann Intern Med2011;154:602–613

113. Blonde L,MerilainenM, Karwe V, RaskinP; TITRATE Study Group. Patient-di-rected titration for achieving glycaemicgoals using a once-daily basal insulinanalogue: an assessment of two differentfasting plasma glucose targets–theTITRATE study. Diabetes Obes Metab2009;11:623–631

114. Bantle JP, Wylie-Rosett J, Albright AL,et al.; American Diabetes Association.Nutrition recommendations and inter-ventions for diabetes: a position statementof the American Diabetes Association.Diabetes Care 2008;31(Suppl. 1):S61–S78

115. DAFNE Study Group. Training in flexi-ble, intensive insulin management toenable dietary freedom in people withtype 1 diabetes: dose adjustment fornormal eating (DAFNE) randomisedcontrolled trial. BMJ 2002;325:746

116. Franz MJ, Monk A, Barry B, et al. Effec-tiveness of medical nutrition therapyprovided by dietitians in the manage-ment of non-insulin-dependent diabetesmellitus: a randomized, controlled clinicaltrial. J Am Diet Assoc 1995;95:1009–1017

117. Goldhaber-Fiebert JD, Goldhaber-FiebertSN, Trist�anML,NathanDM. Randomizedcontrolled community-based nutritionand exercise intervention improves gly-cemia and cardiovascular risk factors intype 2 diabetic patients in ruralCosta Rica.Diabetes Care 2003;26:24–29

118. Lemon CC, Lacey K, Lohse B, HubacherDO, Klawitter B, Palta M. Outcomesmonitoring of health, behavior, andquality of life after nutrition interventionin adults with type 2 diabetes. J Am DietAssoc 2004;104:1805–1815

119. Miller CK, Edwards L, Kissling G,Sanville L. Nutrition education improvesmetabolic outcomes among older adultswith diabetes mellitus: results from arandomized controlled trial. Prev Med2002;34:252–259

120. Wilson C, Brown T, Acton K, Gilliland S.Effects of clinical nutrition educationand educator discipline on glycemiccontrol outcomes in the Indian HealthService. Diabetes Care 2003;26:2500–2504

121. Graber AL, Elasy TA, Quinn D, Wolff K,Brown A. Improving glycemic control inadults with diabetes mellitus: shared re-sponsibility in primary care practices.South Med J 2002;95:684–690

122. Gaetke LM, Stuart MA, Truszczynska H.A single nutrition counseling session

with a registered dietitian improvesshort-term clinical outcomes for ruralKentucky patients with chronic diseases.J Am Diet Assoc 2006;106:109–112

123. Van Horn L, McCoin M, Kris-EthertonPM, et al. The evidence for dietary pre-vention and treatment of cardiovasculardisease. J Am Diet Assoc 2008;108:287–331

124. Appel LJ, Moore TJ, Obarzanek E, et al.;DASH Collaborative Research Group. Aclinical trial of the effects of dietary pat-terns on blood pressure. N Engl J Med1997;336:1117–1124

125. FranzMJ, VanWormer JJ, Crain AL, et al.Weight-loss outcomes: a systematic reviewand meta-analysis of weight-loss clinicaltrials with a minimum 1-year follow-up. JAm Diet Assoc 2007;107:1755–1767

126. Foster GD, Wyatt HR, Hill JO, et al. Arandomized trial of a low-carbohydratediet for obesity. N Engl J Med 2003;348:2082–2090

127. Stern L, Iqbal N, Seshadri P, et al. Theeffects of low-carbohydrate versus con-ventional weight loss diets in severelyobese adults: one-year follow-up of arandomized trial. Ann Intern Med 2004;140:778–785

128. Foster GD, Wyatt HR, Hill JO, et al.Weight and metabolic outcomes after 2years on a low-carbohydrate versus low-fat diet: a randomized trial. Ann InternMed 2010;153:147–157

129. Shai I, Schwarzfuchs D, Henkin Y, et al.;Dietary Intervention Randomized Con-trolled Trial (DIRECT) Group. Weightloss with a low-carbohydrate, Mediter-ranean, or low-fat diet. N Engl J Med2008;359:229–241

130. Nordmann AJ, Nordmann A, Briel M,et al. Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovas-cular risk factors: a meta-analysis ofrandomized controlled trials. Arch In-tern Med 2006;166:285–293

131. Norris SL, Zhang X, Avenell A, et al.Long-term effectiveness of weight-lossinterventions in adults with pre-diabetes: a review. Am J Prev Med 2005;28:126–139

132. Salas-Salvado J, Bullo M, Babio N, et al.Reduction in the incidence of type 2 di-abetes with the Mediterranean diet: re-sults of the PREDIMED-Reus nutritionintervention randomized trial. DiabetesCare 2011;34:14–19

133. Malik VS, Popkin BM, Bray GA, DesprésJP, Willett WC, Hu FB. Sugar-sweetenedbeverages and risk of metabolic syn-drome and type 2 diabetes: a meta-analysis. Diabetes Care 2010;33:2477–2483

134. Klein S, Sheard NF, Pi-Sunyer X, et al.;American Diabetes Association; NorthAmerican Association for the Study ofObesity; American Society for ClinicalNutrition. Weight management through


Position Statement

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135. Norris SL, Zhang X, Avenell A, et al. Ef-ficacy of pharmacotherapy for weightloss in adults with type 2 diabetes mel-litus: a meta-analysis. Arch Intern Med2004;164:1395–1404

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219. Beverly EA, Hultgren BA, Brooks KM,Ritholz MD, Abrahamson MJ, WeingerK. Understanding physicians’ challengeswhen treating type 2 diabetic patients’social and emotional difficulties: a quali-tative study. Diabetes Care 2011;34:1086–1088

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309. Elam MB, Hunninghake DB, Davis KB,et al. Effect of niacin on lipid and lipo-protein levels and glycemic control inpatients with diabetes and peripheralarterial disease. The ADMIT Study:a randomized trial. JAMA 2000;284:1263–1270

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329. Braunwald E, Domanski MJ, Fowler SE,et al.; PEACE Trial Investigators. An-giotensin-converting-enzyme inhibition

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Position Statement

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377. Fong DS, Aiello L, Gardner TW, et al.;American Diabetes Association. Reti-nopathy in diabetes. Diabetes Care 2004;27(Suppl. 1):S84–S87

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Position Statement

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414. Rovet J, Alvarez M. Attentional func-tioning in children and adolescents withIDDM. Diabetes Care 1997;20:803–810

415. Bjørgaas M, Gimse R, Vik T, Sand T.Cognitive function in type 1 diabeticchildren with and without episodes ofsevere hypoglycaemia. Acta Paediatr1997;86:148–153

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Position Statement

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480. Schafer RG, Bohannon B, Franz MJ,et al.; American Diabetes Association.Diabetes nutrition recommendations for


Position Statement

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Position Statement

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Position Statement

Diagnosis and Classification of DiabetesMellitusAMERICAN DIABETES ASSOCIATION

DEFINITION ANDDESCRIPTION OF DIABETESMELLITUSdDiabetes is a group ofmetabolic diseases characterized by hy-perglycemia resulting from defects in in-sulin secretion, insulin action, or both.The chronic hyperglycemia of diabetes isassociated with long-term damage, dys-function, and failure of different organs,especially the eyes, kidneys, nerves, heart,and blood vessels.

Several pathogenic processes are in-volved in the development of diabetes.These range from autoimmune destruc-tion of the b-cells of the pancreas withconsequent insulin deficiency to abnor-malities that result in resistance to insulinaction. The basis of the abnormalities incarbohydrate, fat, and protein metabo-lism in diabetes is deficient action of in-sulin on target tissues. Deficient insulinaction results from inadequate insulin se-cretion and/or diminished tissue respon-ses to insulin at one or more points in thecomplex pathways of hormone action.Impairment of insulin secretion and de-fects in insulin action frequently coexist inthe same patient, and it is often unclearwhich abnormality, if either alone, is theprimary cause of the hyperglycemia.

Symptoms ofmarked hyperglycemia in-cludepolyuria,polydipsia,weight loss,some-times with polyphagia, and blurred vision.Impairment of growth and susceptibility tocertain infections may also accompanychronic hyperglycemia. Acute, life-threaten-ing consequences of uncontrolled diabetesare hyperglycemia with ketoacidosis or thenonketotic hyperosmolar syndrome.

Long-term complications of diabetesinclude retinopathy with potential lossof vision; nephropathy leading to renalfailure; peripheral neuropathy with riskof foot ulcers, amputations, and Charcotjoints; and autonomic neuropathy caus-ing gastrointestinal, genitourinary, and

cardiovascular symptoms and sexual dys-function. Patients with diabetes have anincreased incidence of atherosclerotic car-diovascular, peripheral arterial, and cere-brovascular disease. Hypertension andabnormalities of lipoprotein metabolismare often found in people with diabetes.

The vast majority of cases of diabetesfall into two broad etiopathogenetic cate-gories (discussed in greater detail below).In one category, type 1 diabetes, the causeis an absolute deficiency of insulin secre-tion. Individuals at increased risk of de-veloping this type of diabetes can often beidentified by serological evidence of anautoimmune pathologic process occurringin the pancreatic islets and by geneticmarkers. In the other, much more preva-lent category, type 2 diabetes, the cause is acombination of resistance to insulin actionand an inadequate compensatory insulinsecretory response. In the latter category, adegree of hyperglycemia sufficient to causepathologic and functional changes in var-ious target tissues, but without clinicalsymptoms, may be present for a longperiod of time before diabetes is detected.During this asymptomatic period, it ispossible to demonstrate an abnormality incarbohydrate metabolism by measurementof plasma glucose in the fasting state orafter a challenge with an oral glucose loador by A1C.

The degree of hyperglycemia (if any)may change over time, depending on theextent of the underlying disease process(Fig. 1). A disease process may be presentbut may not have progressed far enoughto cause hyperglycemia. The same diseaseprocess can cause impaired fasting glu-cose (IFG) and/or impaired glucose toler-ance (IGT) without fulfilling the criteriafor the diagnosis of diabetes. In some indi-viduals with diabetes, adequate glycemiccontrol can be achieved with weight reduc-tion, exercise, and/or oral glucose-lowering

agents. These individuals therefore donot require insulin. Other individualswho have some residual insulin secretionbut require exogenous insulin for ade-quate glycemic control can survive with-out it. Individuals with extensive b-celldestruction and therefore no residual in-sulin secretion require insulin for survival.The severity of the metabolic abnormalitycan progress, regress, or stay the same.Thus, the degree of hyperglycemia reflectsthe severity of the underlying metabolicprocess and its treatment more than thenature of the process itself.

CLASSIFICATION OFDIABETES MELLITUS ANDOTHER CATEGORIESOF GLUCOSEREGULATIONdAssigning a type ofdiabetes to an individual often dependson the circumstances present at the timeof diagnosis, and many diabetic individ-uals do not easily fit into a single class. Forexample, a person diagnosed with gesta-tional diabetes mellitus (GDM) may con-tinue to be hyperglycemic after deliveryand may be determined to have, in fact,type 2 diabetes. Alternatively, a personwho acquires diabetes because of largedoses of exogenous steroids may becomenormoglycemic once the glucocorticoidsare discontinued, but then may developdiabetes many years later after recurrentepisodes of pancreatitis. Another examplewould be a person treated with thiazideswho develops diabetes years later. Becausethiazides in themselves seldomcause severehyperglycemia, such individuals probablyhave type 2 diabetes that is exacerbated bythe drug. Thus, for the clinician andpatient,it is less important to label the particulartype of diabetes than it is to understand thepathogenesis of the hyperglycemia and totreat it effectively.

Type 1 diabetes (b-cell destruction,usually leading to absolute insulindeficiency)Immune-mediated diabetes. This formof diabetes, which accounts for only5–10% of those with diabetes, previouslyencompassed by the terms insulin-dependent diabetes or juvenile-onset di-abetes, results from a cellular-mediatedautoimmune destruction of the b-cells of


Updated Fall 2012.DOI: 10.2337/dc13-S067© 2013 by the American Diabetes Association. Readers may use this article as long as the work is properly






the pancreas. Markers of the immune de-struction of the b-cell include islet cell au-toantibodies, autoantibodies to insulin,autoantibodies toGAD (GAD65), and auto-antibodies to the tyrosine phosphatasesIA-2 and IA-2b. One and usually more ofthese autoantibodies are present in 85–90% of individuals when fasting hyper-glycemia is initially detected. Also, thedisease has strong HLA associations,with linkage to the DQA and DQB genes,and it is influenced by the DRB genes.These HLA-DR/DQ alleles can be eitherpredisposing or protective.

In this form of diabetes, the rate ofb-cell destruction is quite variable, beingrapid in some individuals (mainly infantsand children) and slow in others (mainlyadults). Some patients, particularly chil-dren and adolescents, may present withketoacidosis as the first manifestation ofthe disease. Others have modest fastinghyperglycemia that can rapidly changeto severe hyperglycemia and/or ketoaci-dosis in the presence of infection or otherstress. Still others, particularly adults,may retain residual b-cell function suffi-cient to prevent ketoacidosis for manyyears; such individuals eventually be-come dependent on insulin for survivaland are at risk for ketoacidosis. At thislatter stage of the disease, there is littleor no insulin secretion, as manifested bylow or undetectable levels of plasmaC-peptide. Immune-mediated diabetes

commonly occurs in childhood and ado-lescence, but it can occur at any age, evenin the 8th and 9th decades of life.

Autoimmune destruction of b-cellshas multiple genetic predispositions andis also related to environmental factorsthat are still poorly defined. Although pa-tients are rarely obese when they presentwith this type of diabetes, the presence ofobesity is not incompatible with the diag-nosis. These patients are also prone toother autoimmune disorders such asGraves’ disease, Hashimoto’s thyroiditis,Addison’s disease, vitiligo, celiac sprue,autoimmune hepatitis, myasthenia gravis,and pernicious anemia.Idiopathic diabetes. Some forms of type1 diabetes have no known etiologies.Some of these patients have permanentinsulinopenia and are prone to ketoaci-dosis, but have no evidence of autoim-munity. Although only a minority ofpatients with type 1 diabetes fall into thiscategory, of those who do, most are ofAfrican or Asian ancestry. Individualswith this form of diabetes suffer fromepisodic ketoacidosis and exhibit vary-ing degrees of insulin deficiency be-tween episodes. This form of diabetesis strongly inherited, lacks immunolog-ical evidence for b-cell autoimmunity,and is not HLA associated. An absoluterequirement for insulin replacementtherapy in affected patients may comeand go.

Type 2 diabetes (ranging frompredominantly insulin resistancewith relative insulin deficiency topredominantly an insulin secretorydefect with insulin resistance)This form of diabetes, which accounts for;90–95% of those with diabetes, previ-ously referred to as non–insulin-depen-dent diabetes, type 2 diabetes, or adult-onset diabetes, encompasses individualswho have insulin resistance and usuallyhave relative (rather than absolute) insu-lin deficiency At least initially, and oftenthroughout their lifetime, these individu-als do not need insulin treatment to sur-vive. There are probably many differentcauses of this form of diabetes. Althoughthe specific etiologies are not known, au-toimmune destruction of b-cells does notoccur, and patients do not have any of theother causes of diabetes listed above orbelow.

Most patients with this form of di-abetes are obese, and obesity itself causessome degree of insulin resistance. Patientswho are not obese by traditional weightcriteria may have an increased percentageof body fat distributed predominantly inthe abdominal region. Ketoacidosis sel-dom occurs spontaneously in this type ofdiabetes; when seen, it usually arises inassociation with the stress of anotherillness such as infection. This form ofdiabetes frequently goes undiagnosed formany years because the hyperglycemia

Figure 1dDisorders of glycemia: etiologic types and stages. *Even after presenting in ketoacidosis, these patients can briefly return to normo-glycemia without requiring continuous therapy (i.e., “honeymoon” remission); **in rare instances, patients in these categories (e.g., Vacor toxicity,type 1 diabetes presenting in pregnancy) may require insulin for survival.


Position Statement

develops gradually and at earlier stages isoften not severe enough for the patient tonotice any of the classic symptoms ofdiabetes. Nevertheless, such patients areat increased risk of developing macro-vascular and microvascular complica-tions. Whereas patients with this form ofdiabetes may have insulin levels thatappear normal or elevated, the higherblood glucose levels in these diabeticpatients would be expected to result ineven higher insulin values had their b-cellfunction been normal. Thus, insulin se-cretion is defective in these patients andinsufficient to compensate for insulin re-sistance. Insulin resistance may improvewith weight reduction and/or pharmaco-logical treatment of hyperglycemia but isseldom restored to normal. The risk ofdeveloping this form of diabetes increaseswith age, obesity, and lack of physical ac-tivity. It occurs more frequently in womenwith prior GDM and in individuals withhypertension or dyslipidemia, and its fre-quency varies in different racial/ethnic sub-groups. It is often associated with a stronggenetic predisposition, more so than is theautoimmune form of type 1 diabetes. How-ever, the genetics of this form of diabetesare complex and not fully defined.

Other specific types of diabetesGenetic defects of the b-cell. Severalforms of diabetes are associated withmonogenetic defects in b-cell function.These forms of diabetes are frequentlycharacterized by onset of hyperglycemiaat an early age (generally before age 25years). They are referred to as maturity-onset diabetes of the young (MODY) andare characterized by impaired insulin se-cretion with minimal or no defects in in-sulin action. They are inherited in anautosomal dominant pattern. Abnormali-ties at six genetic loci on different chro-mosomes have been identified to date.The most common form is associatedwith mutations on chromosome 12 in ahepatic transcription factor referred to ashepatocyte nuclear factor (HNF)-1a. Asecond form is associated with mutationsin the glucokinase gene on chromosome7p and results in a defective glucokinasemolecule. Glucokinase converts glucoseto glucose-6-phosphate, the metabolismof which, in turn, stimulates insulin secre-tion by the b-cell. Thus, glucokinaseserves as the “glucose sensor” for theb-cell. Because of defects in the glucoki-nase gene, increased plasma levels of glu-cose are necessary to elicit normal levelsof insulin secretion. The less common

forms result frommutations in other tran-scription factors, including HNF-4a,HNF-1b, insulin promoter factor (IPF)-1, and NeuroD1.

Diabetes diagnosed in the first 6months of life has been shown not to betypical autoimmune type 1 diabetes. Thisso-called neonatal diabetes can either betransient or permanent. The most com-mon genetic defect causing transientdisease is a defect on ZAC/HYAMI im-printing, whereas permanent neonataldiabetes is most commonly a defect in thegene encoding the Kir6.2 subunit of theb-cell KATP channel. Diagnosing the latterhas implications, since such children canbe well managed with sulfonylureas.

Point mutations in mitochondrialDNA have been found to be associatedwith diabetes and deafness The mostcommon mutation occurs at position3,243 in the tRNA leucine gene, leadingto an A-to-G transition. An identicallesion occurs in the MELAS syndrome(mitochondrial myopathy, encephalop-athy, lactic acidosis, and stroke-like syn-drome); however, diabetes is not partof this syndrome, suggesting differentphenotypic expressions of this geneticlesion.

Genetic abnormalities that result inthe inability to convert proinsulin to in-sulin have been identified in a few fami-lies, and such traits are inherited in anautosomal dominant pattern. The resul-tant glucose intolerance is mild. Similarly,the production of mutant insulin mole-cules with resultant impaired receptorbinding has also been identified in a fewfamilies and is associated with an autoso-mal inheritance and only mildly impairedor even normal glucose metabolism.Genetic defects in insulin action. Thereare unusual causes of diabetes that resultfrom genetically determined abnormali-ties of insulin action. The metabolic ab-normalities associated with mutations ofthe insulin receptor may range fromhyperinsulinemia and modest hyperglyce-mia to severe diabetes. Some individualswith these mutations may have acanthosisnigricans. Women may be virilized andhave enlarged, cystic ovaries. In the past,this syndrome was termed type A insulinresistance. Leprechaunism and the Rabson-Mendenhall syndrome are two pediatricsyndromes that have mutations in theinsulin receptor gene with subsequentalterations in insulin receptor functionand extreme insulin resistance. The formerhas characteristic facial features and isusually fatal in infancy, while the latter is

associated with abnormalities of teeth andnails and pineal gland hyperplasia.

Alterations in the structure and func-tion of the insulin receptor cannot bedemonstrated in patients with insulin-resistant lipoatrophic diabetes. Therefore,it is assumed that the lesion(s) must residein the postreceptor signal transductionpathways.Diseases of the exocrine pancreas. Anyprocess that diffusely injures the pancreascan cause diabetes. Acquired processesinclude pancreatitis, trauma, infection, pan-createctomy, and pancreatic carcinoma.With the exception of that caused bycancer, damage to the pancreas must beextensive for diabetes to occur; adreno-carcinomas that involve only a smallportion of the pancreas have been associ-ated with diabetes. This implies a mech-anism other than simple reduction inb-cell mass. If extensive enough, cystic fi-brosis and hemochromatosis will alsodamage b-cells and impair insulin secre-tion. Fibrocalculous pancreatopathy maybe accompanied by abdominal pain radi-ating to the back and pancreatic calcifica-tions identified on X-ray examination.Pancreatic fibrosis and calcium stonesin the exocrine ducts have been found atautopsy.Endocrinopathies. Several hormones(e.g., growth hormone, cortisol, gluca-gon, epinephrine) antagonize insulin ac-tion. Excess amounts of these hormones(e.g., acromegaly, Cushing’s syndrome,glucagonoma, pheochromocytoma, re-spectively) can cause diabetes. This gen-erally occurs in individuals withpreexisting defects in insulin secretion,and hyperglycemia typically resolveswhen the hormone excess is resolved.

Somatostatinomas, and aldostero-noma-induced hypokalemia, can causediabetes, at least in part, by inhibitinginsulin secretion. Hyperglycemia gener-ally resolves after successful removal ofthe tumor.Drug- or chemical-induced diabetes.Many drugs can impair insulin secretion.These drugs may not cause diabetes bythemselves, but they may precipitate di-abetes in individuals with insulin resis-tance. In such cases, the classification isunclear because the sequence or relativeimportance of b-cell dysfunction and in-sulin resistance is unknown. Certain tox-ins such as Vacor (a rat poison) andintravenous pentamidine can perma-nently destroy pancreatic b-cells. Suchdrug reactions fortunately are rare. Thereare also many drugs and hormones that


Position Statement

can impair insulin action. Examples in-clude nicotinic acid and glucocorticoids.Patients receiving a-interferon have beenreported to develop diabetes associatedwith islet cell antibodies and, in certaininstances, severe insulin deficiency. Thelist shown in Table 1 is not all-inclusive,but reflects the more commonly recog-nized drug-, hormone-, or toxin-inducedforms of diabetes.Infections. Certain viruses have been as-sociated with b-cell destruction. Diabetesoccurs in patients with congenital rubella,although most of these patients have HLAand immune markers characteristic of type1 diabetes. In addition, coxsackievirus B,cytomegalovirus, adenovirus, and mumpshave been implicated in inducing certaincases of the disease.Uncommon forms of immune-mediateddiabetes. In this category, there are twoknown conditions, and others are likelyto occur. The stiff-man syndrome is anautoimmune disorder of the central ner-vous system characterized by stiffness ofthe axial muscles with painful spasms.Patients usually have high titers of theGAD autoantibodies, and approximatelyone-third will develop diabetes.

Anti-insulin receptor antibodies cancause diabetes by binding to the insulinreceptor, thereby blocking the binding ofinsulin to its receptor in target tissues.However, in some cases, these antibodiescan act as an insulin agonist after binding tothe receptor and can thereby cause hypo-glycemia. Anti-insulin receptor antibodiesare occasionally found in patients withsystemic lupus erythematosus and otherautoimmune diseases. As in other states ofextreme insulin resistance, patients withanti-insulin receptor antibodies often haveacanthosis nigricans. In the past, this syn-dromewas termed type B insulin resistance.Other genetic syndromes sometimesassociated with diabetes. Many geneticsyndromes are accompanied by an in-creased incidence of diabetes. These in-clude the chromosomal abnormalities ofDown syndrome, Klinefelter syndrome,and Turner syndrome. Wolfram syn-drome is an autosomal recessive disordercharacterized by insulin-deficient diabe-tes and the absence of b-cells at autopsy.Additional manifestations include diabetesinsipidus, hypogonadism, optic atrophy,and neural deafness. Other syndromes arelisted in Table 1.

GDMFor many years, GDM has been defined asany degree of glucose intolerance with

Table 1dEtiologic classification of diabetes mellitus

I. Type 1 diabetes (b-cell destruction, usually leading to absolute insulin deficiency)A. Immune mediatedB. Idiopathic

II. Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiencyto a predominantly secretory defect with insulin resistance)

III. Other specific typesA. Genetic defects of b-cell function

1. MODY 3 (Chromosome 12, HNF-1a)2. MODY 1 (Chromosome 20, HNF-4a)3. MODY 2 (Chromosome 7, glucokinase)4. Other very rare forms of MODY (e.g., MODY 4: Chromosome 13, insulin promoter factor-1;

MODY 6: Chromosome 2, NeuroD1; MODY 7: Chromosome 9, carboxyl ester lipase)5. Transient neonatal diabetes (most commonly ZAC/HYAMI imprinting defect on 6q24)6. Permanent neonatal diabetes (most commonly KCNJ11 gene encoding Kir6.2 subunit of b-cell

KATP channel)7. Mitochondrial DNA8. Others

B. Genetic defects in insulin action1. Type A insulin resistance2. Leprechaunism3. Rabson-Mendenhall syndrome4. Lipoatrophic diabetes5. Others

C. Diseases of the exocrine pancreas1. Pancreatitis2. Trauma/pancreatectomy3. Neoplasia4. Cystic fibrosis5. Hemochromatosis6. Fibrocalculous pancreatopathy7. Others

D. Endocrinopathies1. Acromegaly2. Cushing’s syndrome3. Glucagonoma4. Pheochromocytoma5. Hyperthyroidism6. Somatostatinoma7. Aldosteronoma8. Others

E. Drug or chemical induced1. Vacor2. Pentamidine3. Nicotinic acid4. Glucocorticoids5. Thyroid hormone6. Diazoxide7. b-Adrenergic agonists8. Thiazides9. Dilantin

10. g-Interferon11. Others

F. Infections1. Congenital rubella2. Cytomegalovirus3. Others

G. Uncommon forms of immune-mediated diabetes1. “Stiff-man” syndrome2. Anti-insulin receptor antibodies3. Others

H. Other genetic syndromes sometimes associated with diabetes1. Down syndrome2. Klinefelter syndrome3. Turner syndrome4. Wolfram syndrome5. Friedreich ataxia6. Huntington chorea7. Laurence-Moon-Biedl syndrome8. Myotonic dystrophy9. Porphyria

10. Prader-Willi syndrome11. Others

IV. Gestational diabetes mellitus

Patients with any form of diabetes may require insulin treatment at some stage of their disease. Such use ofinsulin does not, of itself, classify the patient.


Position Statement

onset or first recognition during preg-nancy. Although most cases resolve withdelivery, the definition applied whetheror not the condition persisted after preg-nancy and did not exclude the possibilitythat unrecognized glucose intolerancemay have antedated or begun concomi-tantly with the pregnancy. This definitionfacilitated a uniform strategy for detectionand classification of GDM, but its limi-tations were recognized for many years.As the ongoing epidemic of obesity anddiabetes has led to more type 2 diabetes inwomen of childbearing age, the number ofpregnant womenwith undiagnosed type 2diabetes has increased.

After deliberations in 2008–2009, theInternational Association of Diabetes andPregnancy Study Groups (IADPSG), aninternational consensus group with rep-resentatives from multiple obstetrical anddiabetes organizations, including theAmerican Diabetes Association (ADA),recommended that high-risk womenfound to have diabetes at their initial pre-natal visit, using standard criteria (Table3), receive a diagnosis of overt, not gesta-tional, diabetes. Approximately 7% of allpregnancies (ranging from 1 to 14%, de-pending on the population studied andthe diagnostic tests employed) are com-plicated by GDM, resulting in more than200,000 cases annually.

CATEGORIES OF INCREASEDRISK FOR DIABETESdIn 1997 and2003, the Expert Committee on Diagno-sis and Classification of Diabetes Mellitus(1,2) recognized an intermediate group ofindividuals whose glucose levels do notmeet criteria for diabetes, yet are higherthan those considered normal. These peo-ple were defined as having impaired fast-ing glucose (IFG) [fasting plasma glucose(FPG) levels 100 mg/dl (5.6 mmol/l) to125mg/dl (6.9 mmol/l)], or impaired glu-cose tolerance (IGT) [2-h values in theoral glucose tolerance test (OGTT) of140 mg/dl (7.8 mmol/l) to 199 mg/dl(11.0 mmol/l)].

Individuals with IFG and/or IGT havebeen referred to as having prediabetes,indicating the relatively high risk for thefuture development of diabetes. IFG andIGT should not be viewed as clinicalentities in their own right but rather riskfactors for diabetes as well as cardiovas-cular disease. They can be observed asintermediate stages in any of the diseaseprocesses listed in Table 1. IFG and IGTare associated with obesity (especially ab-dominal or visceral obesity), dyslipidemia

with high triglycerides and/or low HDLcholesterol, and hypertension. Structuredlifestyle intervention, aimed at increasingphysical activity and producing 5–10%loss of body weight, and certain pharma-cological agents have been demonstratedto prevent or delay the development ofdiabetes in people with IGT; the potentialimpact of such interventions to reducemortality or the incidence of cardiovascu-lar disease has not been demonstrated todate. It should be noted that the 2003ADA Expert Committee report reducedthe lower FPG cut point to define IFGfrom 110 mg/dl (6.1 mmol/l) to 100 mg/dl(5.6 mmol/l), in part to ensure that prev-alence of IFG was similar to that of IGT.However, the World Health Organization(WHO) and many other diabetes organi-zations did not adopt this change in thedefinition of IFG.

As A1C is used more commonly todiagnose diabetes in individuals with riskfactors, it will also identify those at higherrisk for developing diabetes in the future.When recommending the use of the A1Cto diagnose diabetes in its 2009 report,the International Expert Committee (3)stressed the continuum of risk for diabe-tes with all glycemicmeasures and did notformally identify an equivalent intermedi-ate category for A1C. The group did notethat those with A1C levels above the lab-oratory “normal” range but below the di-agnostic cut point for diabetes (6.0 to,6.5%) are at very high risk of develop-ing diabetes. Indeed, incidence of diabe-tes in people with A1C levels in this rangeis more than 10 times that of people withlower levels (4–7). However, the 6.0 to,6.5% range fails to identify a substantialnumber of patients who have IFG and/orIGT. Prospective studies indicate thatpeople within the A1C range of 5.5–6.0% have a 5-year cumulative incidenceof diabetes that ranges from 12 to 25%(4–7), which is appreciably (three- toeightfold) higher than incidence in theU.S. population as a whole (8). Analysesof nationally representative data from theNational Health and Nutrition Examina-tion Survey (NHANES) indicate that theA1C value that most accurately identifiespeople with IFG or IGT falls between 5.5and 6.0%. In addition, linear regressionanalyses of these data indicate that amongthe nondiabetic adult population, an FPGof 110 mg/dl (6.1 mmol/l) correspondsto an A1C of 5.6%, while an FPG of 100mg/dl (5.6 mmol/l) corresponds to anA1C of 5.4% (R.T. Ackerman, personalcommunication). Finally, evidence from

the Diabetes Prevention Program (DPP),wherein the mean A1C was 5.9% (SD0.5%), indicates that preventive interven-tions are effective in groups of people withA1C levels both below and above 5.9%(9). For these reasons, the most appropri-ate A1C level above which to initiate pre-ventive interventions is likely to besomewhere in the range of 5.5–6%.

As was the case with FPG and 2-h PG,defining a lower limit of an intermediatecategory of A1C is somewhat arbitrary,as the risk of diabetes with any measureor surrogate of glycemia is a continuum,extending well into the normal ranges. Tomaximize equity and efficiency of pre-ventive interventions, such an A1C cutpoint should balance the costs of “falsenegatives” (failing to identify those whoare going to develop diabetes) againstthe costs of “false positives” (falsely iden-tifying and then spending intervention re-sources on those who were not going todevelop diabetes anyway).

As is the case with the glucose mea-sures, several prospective studies that usedA1C to predict the progression to diabetesdemonstrated a strong, continuous asso-ciation between A1C and subsequent di-abetes. In a systematic review of 44,203individuals from 16 cohort studies witha follow-up interval averaging 5.6 years(range 2.8–12 years), those with an A1Cbetween 5.5 and 6.0% had a substantiallyincreased risk of diabetes with 5-yearincidences ranging from 9 to 25%. AnA1C range of 6.0–6.5% had a 5-year riskof developing diabetes between 25 and50% and relative risk 20 times highercompared with an A1C of 5.0% (10). Ina community-based study of black andwhite adults without diabetes, baselineA1C was a stronger predictor of subse-quent diabetes and cardiovascular eventsthan was fasting glucose (11). Other anal-yses suggest that an A1C of 5.7% is asso-ciated with similar diabetes risk to thehigh-risk participants in the DPP (12).Hence, it is reasonable to consider anA1C range of 5.7–6.4% as identifying in-dividuals with high risk for future diabe-tes, to whom the term prediabetes may beapplied.

Individuals with an A1C of 5.7–6.4%should be informed of their increased riskfor diabetes as well as cardiovascular dis-ease and counseled about effective strate-gies, such as weight loss and physicalactivity, to lower their risks. As with glu-cose measurements, the continuum of riskis curvilinear, so that as A1C rises, the riskof diabetes rises disproportionately.


Position Statement

Accordingly, interventions should bemost intensive and follow-up should beparticularly vigilant for those with A1Clevels above 6.0%, who should be consid-ered to be at very high risk. However, justas an individual with a fasting glucose of98 mg/dl (5.4 mmol/l) may not be at neg-ligible risk for diabetes, individuals withA1C levels below 5.7% may still be atrisk, depending on level of A1C and pres-ence of other risk factors, such as obesityand family history.

Table 2 summarizes the categories ofincreased risk for diabetes. Evaluation ofpatients at risk should incorporate aglobal risk factor assessment for both di-abetes and cardiovascular disease. Screen-ing for and counseling about risk ofdiabetes should always be in the prag-matic context of the patient’s comorbidi-ties, life expectancy, personal capacity toengage in lifestyle change, and overallhealth goals.

DIAGNOSTIC CRITERIA FORDIABETES MELLITUSdFor deca-des, the diagnosis of diabetes has beenbased on glucose criteria, either the FPGor the 75-g OGTT. In 1997, the firstExpert Committee on the Diagnosis andClassification of Diabetes Mellitus revisedthe diagnostic criteria, using the observedassociation between FPG levels and pres-ence of retinopathy as the key factor withwhich to identify threshold glucose level.The Committee examined data from threecross-sectional epidemiologic studies thatassessed retinopathy with fundus pho-tography or direct ophthalmoscopy andmeasured glycemia as FPG, 2-h PG, andA1C. These studies demonstrated glyce-mic levels below which there was littleprevalent retinopathy and above whichthe prevalence of retinopathy increased inan apparently linear fashion. The decilesof the three measures at which retinopa-thy began to increase were the same foreach measure within each population.Moreover, the glycemic values above

which retinopathy increased were similaramong the populations. These analysesconfirmed the long-standing diagnostic 2-hPG value of $200 mg/dl (11.1 mmol/l).However, the older FPG diagnostic cutpoint of 140mg/dl (7.8mmol/l) was notedto identify far fewer individuals with dia-betes than the 2-h PG cut point. The FPGdiagnostic cut point was reduced to$126 mg/dl (7.0 mmol/l).

A1C is a widely used marker ofchronic glycemia, reflecting averageblood glucose levels over a 2- to 3-monthperiod of time. The test plays a critical rolein the management of the patient withdiabetes, since it correlates well with bothmicrovascular and, to a lesser extent,macrovascular complications and iswidely used as the standard biomarkerfor the adequacy of glycemic manage-ment. Prior Expert Committees have notrecommended use of the A1C for diag-nosis of diabetes, in part due to lack ofstandardization of the assay. However,A1C assays are now highly standardizedso that their results can be uniformlyapplied both temporally and across pop-ulations. In their recent report (3), an In-ternational Expert Committee, after anextensive review of both established andemerging epidemiological evidence, rec-ommended the use of the A1C test to di-agnose diabetes, with a threshold of$6.5%, and ADA affirms this decision.The diagnostic A1C cut point of 6.5% isassociated with an inflection point for ret-inopathy prevalence, as are the diagnosticthresholds for FPG and 2-h PG (3). Thediagnostic test should be performedusing a method that is certified by the Na-tional Glycohemoglobin StandardizationProgram (NGSP) and standardized ortraceable to the Diabetes Control andComplications Trial reference assay.Point-of-care A1C assays are not suffi-ciently accurate at this time to use for di-agnostic purposes.

There is an inherent logic to using amore chronic versus an acute marker ofdysglycemia, particularly since the A1C isalready widely familiar to clinicians as amarker of glycemic control. Moreover,the A1C has several advantages to theFPG, including greater convenience,since fasting is not required, evidence tosuggest greater preanalytical stability, andless day-to-day perturbations during pe-riods of stress and illness. These advan-tages, however, must be balanced bygreater cost, the limited availability ofA1C testing in certain regions of thedeveloping world, and the incomplete

correlation between A1C and averageglucose in certain individuals. In addi-tion, the A1C can be misleading in pa-tients with certain forms of anemia andhemoglobinopathies, which may alsohave unique ethnic or geographic distri-butions. For patients with a hemoglobin-opathy but normal red cell turnover, suchas sickle cell trait, an A1C assay withoutinterference from abnormal hemoglobinsshould be used (an updated list is avail-able at http://www.ngsp.org/interf.asp).For conditions with abnormal red cellturnover, such as anemias from hemolysisand iron deficiency, the diagnosis ofdiabetes must employ glucose criteriaexclusively.

The established glucose criteria forthe diagnosis of diabetes remain valid.These include the FPG and 2-h PG.Additionally, patients with severe hyper-glycemia such as those who present withsevere classic hyperglycemic symptomsor hyperglycemic crisis can continue to bediagnosed when a random (or casual)plasma glucose of $200 mg/dl (11.1mmol/l) is found. It is likely that in suchcases the health care professional wouldalso measure an A1C test as part of theinitial assessment of the severity of the di-abetes and that it would (in most cases) beabove the diagnostic cut point for diabe-tes. However, in rapidly evolving diabe-tes, such as the development of type 1diabetes in some children, A1C may notbe significantly elevated despite frankdiabetes.

Just as there is less than 100% con-cordance between the FPG and 2-h PGtests, there is not full concordance be-tween A1C and either glucose-basedtest. Analyses of NHANES data indicatethat, assuming universal screening of theundiagnosed, the A1C cut point of$6.5% identifies one-third fewer casesof undiagnosed diabetes than a fastingglucose cut point of $126 mg/dl (7.0mmol/l) (www.cdc.gov/diabetes/pubs/factsheet11/tables1_2.htm). However, inpractice, a large portion of the populationwith type 2 diabetes remains unaware oftheir condition. Thus, it is conceivablethat the lower sensitivity of A1C at thedesignated cut point will be offset by thetest’s greater practicality, and that widerapplication of a more convenient test(A1C) may actually increase the numberof diagnoses made.

Further research is needed to bettercharacterize those patients whose glyce-mic status might be categorized differ-ently by two different tests (e.g., FPG and

Table 2dCategories of increased risk fordiabetes (prediabetes)*

FPG 100mg/dl (5.6 mmol/l) to 125 mg/dl (6.9mmol/l) [IFG]

2-h PG in the 75-g OGTT 140 mg/dl (7.8mmol/l) to 199 mg/dl (11.0 mmol/l) [IGT]

A1C 5.7–6.4%*For all three tests, risk is continuous, extendingbelow the lower limit of the range and becomingdisproportionately greater at higher ends of therange.


Position Statement

http://www.ngsp.org/interf.asp

www.cdc.gov/diabetes/pubs/factsheet11/tables1_2.htm

www.cdc.gov/diabetes/pubs/factsheet11/tables1_2.htm

A1C), obtained in close temporal approx-imation. Such discordancemay arise frommeasurement variability, change overtime, or because A1C, FPG, and post-challenge glucose each measure differentphysiological processes. In the setting ofan elevated A1C but “nondiabetic” FPG,the likelihood of greater postprandial glu-cose levels or increased glycation ratesfor a given degree of hyperglycemia maybe present. In the opposite scenario (highFPG yet A1C below the diabetes cutpoint), augmented hepatic glucose pro-duction or reduced glycation rates maybe present.

As with most diagnostic tests, a testresult diagnostic of diabetes should berepeated to rule out laboratory error,unless the diagnosis is clear on clinicalgrounds, such as a patient with classicsymptoms of hyperglycemia or hypergly-cemic crisis. It is preferable that the sametest be repeated for confirmation, sincethere will be a greater likelihood of con-currence in this case. For example, if theA1C is 7.0% and a repeat result is 6.8%,the diagnosis of diabetes is confirmed.However, there are scenarios in which re-sults of two different tests (e.g., FPG andA1C) are available for the same patient. Inthis situation, if the two different tests areboth above the diagnostic thresholds, thediagnosis of diabetes is confirmed.

On the other hand, when two differ-ent tests are available in an individual andthe results are discordant, the test whoseresult is above the diagnostic cut pointshould be repeated, and the diagnosis ismade on the basis of the confirmed test.That is, if a patient meets the diabetescriterion of the A1C (two results $6.5%)but not the FPG (,126 mg/dl or 7.0mmol/l), or vice versa, that personshould be considered to have diabetes. Ad-mittedly, in most circumstance the

“nondiabetic” test is likely to be in a rangevery close to the threshold that defines di-abetes.

Since there is preanalytic and analyticvariability of all the tests, it is also possiblethat when a test whose result was abovethe diagnostic threshold is repeated, thesecond value will be below the diagnosticcut point. This is least likely for A1C,somewhat more likely for FPG, and mostlikely for the 2-h PG. Barring a laboratoryerror, such patients are likely to have testresults near the margins of the thresholdfor a diagnosis. The healthcare profes-sional might opt to follow the patientclosely and repeat the testing in 3–6months.

The decision about which test to useto assess a specific patient for diabetesshould be at the discretion of the healthcare professional, taking into account theavailability and practicality of testing anindividual patient or groups of patients.Perhaps more important than which di-agnostic test is used, is that the testing fordiabetes be performed when indicated.There is discouraging evidence indicatingthat many at-risk patients still do not re-ceive adequate testing and counseling forthis increasingly common disease, or for itsfrequently accompanying cardiovascularrisk factors. The current diagnostic criteriafor diabetes are summarized in Table 3.

Diagnosis of GDMGDM carries risks for the mother andneonate. The Hyperglycemia and AdversePregnancy Outcomes (HAPO) study(13), a large-scale (;25,000 pregnantwomen) multinational epidemiologicstudy, demonstrated that risk of adversematernal, fetal, and neonatal outcomescontinuously increased as a function ofmaternal glycemia at 24–28 weeks, evenwithin ranges previously considered

normal for pregnancy. For most compli-cations, there was no threshold for risk.These results have led to careful reconsid-eration of the diagnostic criteria for GDM.After deliberations in 2008–2009, theIADPSG, an international consensusgroup with representatives from multipleobstetrical and diabetes organizations, in-cluding ADA, developed revised recom-mendations for diagnosing GDM. Thegroup recommended that all women notknown to have diabetes undergo a 75-gOGTT at 24–28 weeks of gestation. Ad-ditionally, the group developed diagnos-tic cut points for the fasting, 1-h, and 2-hplasma glucose measurements that con-veyed an odds ratio for adverse outcomesof at least 1.75 compared with womenwith mean glucose levels in the HAPOstudy. Current screening and diagnosticstrategies, based on the IADPSG state-ment (14), are outlined in Table 4.

These new criteria will significantlyincrease the prevalence of GDM, primar-ily because only one abnormal value, nottwo, is sufficient to make the diagnosis.The ADA recognizes the anticipated sig-nificant increase in the incidence of GDMto be diagnosed by these criteria and issensitive to concerns about the “medical-ization” of pregnancies previously catego-rized as normal. These diagnostic criteriachanges are being made in the context ofworrisome worldwide increases in obe-sity and diabetes rates, with the intent ofoptimizing gestational outcomes forwomen and their babies.

Admittedly, there are few data fromrandomized clinical trials regarding ther-apeutic interventions in women who willnow be diagnosed with GDM based ononly one blood glucose value above thespecified cut points (in contrast to theolder criteria that stipulated at least two

Table 3dCriteria for the diagnosis of diabetes

A1C$6.5%. The test should be performed in a laboratory using a method that is NGSP certifiedand standardized to the DCCT assay.*

ORFPG $126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.*

OR2-h plasma glucose$200mg/dl (11.1mmol/l) during anOGTT. The test should be performed asdescribed by theWorld Health Organization, using a glucose load containing the equivalent of75 g anhydrous glucose dissolved in water.*

ORIn a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasmaglucose $200 mg/dl (11.1 mmol/l).

*In the absence of unequivocal hyperglycemia, criteria 1–3 should be confirmed by repeat testing.

Table 4dScreening for and diagnosis ofGDM

Perform a 75-g OGTT, with plasma glucosemeasurement fasting and at 1 and 2 h, at24–28 weeks of gestation in women notpreviously diagnosed with overt diabetes.

The OGTT should be performed in themorning after an overnight fast of at least8 h.

The diagnosis of GDM ismade when any of thefollowing plasma glucose values areexceeded:

c Fasting: $92 mg/dl (5.1 mmol/l)c 1 h: $180 mg/dl (10.0 mmol/l)c 2 h: $153 mg/dl (8.5 mmol/l)


Position Statement

abnormal values). Expected benefits totheir pregnancies and offspring is inferredfrom intervention trials that focused onwomen with more mild hyperglycemiathan identified using older GDM diag-nostic criteria and that found modestbenefits (15,16). The frequency of theirfollow-up and blood glucose monitoringis not yet clear but likely to be less inten-sive than women diagnosed by the oldercriteria. Additional well-designed clinicalstudies are needed to determine the op-timal intensity of monitoring and treat-ment of women with GDM diagnosedby the new criteria (that would nothave met the prior definition of GDM).It is important to note that 80–90% ofwomen in both of the mild GDM studies(whose glucose values overlapped withthe thresholds recommended herein)could be managed with lifestyle therapyalone.

References1. Expert Committee on the Diagnosis and

Classification of Diabetes Mellitus. Reportof the Expert Committee on the Diagnosisand Classification of Diabetes Mellitus.Diabetes Care 1997;20:1183–1197

2. Genuth S, Alberti KG, Bennett P, Buse J,DeFronzo R, Kahn R, Kitzmiller J, KnowlerWC, Lebovitz H, Lernmark A, Nathan D,Palmer J, Rizza R, Saudek C, Shaw J, SteffesM, Stern M, Tuomilehto J, Zimmet P, Ex-pert Committee on the Diagnosis andClassification of DiabetesMellitus. Follow-up report on the diagnosis of diabetesmellitus. Diabetes Care 2003;26:3160–3167

3. International Expert Committee. Inter-national Expert Committee report on the

role of the A1C assay in the diagnosis ofdiabetes. Diabetes Care 2009;32:1327–1334

4. Edelman D, Olsen MK, Dudley TK, HarrisAC, Oddone EZ. Utility of hemoglobinA1c in predicting diabetes risk. J Gen In-tern Med 2004;19:1175–1180

5. Pradhan AD, Rifai N, Buring JE, RidkerPM. Hemoglobin A1c predicts diabetesbut not cardiovascular disease in non-diabetic women. Am J Med 2007;120:720–727

6. Sato KK, Hayashi T, Harita N, Yoneda T,Nakamura Y, Endo G, Kambe H. Com-bined measurement of fasting plasmaglucose and A1C is effective for the pre-diction of type 2 diabetes: the KansaiHealthcare Study. Diabetes Care 2009;32:644–646

7. Shimazaki T, Kadowaki T, Ohyama Y,Ohe K, Kubota K. Hemoglobin A1c(HbA1c) predicts future drug treatmentfor diabetes mellitus: a follow-up studyusing routine clinical data in a Japaneseuniversity hospital. Translational Re-search 2007;149:196–204

8. Geiss LS, Pan L, Cadwell B, Gregg EW,Benjamin SM, Engelgau MM. Changes inincidence of diabetes in U.S. adults,1997–2003. Am J Prev Med 2006;30:371–377

9. Knowler WC, Barrett-Connor E, FowlerSE, Hamman RF, Lachin JM, Walker EA,Nathan DM, Diabetes Prevention ProgramResearch Group. Reduction in the in-cidence of type 2 diabetes with lifestyleintervention or metformin. N Engl J Med2002;346:393–403

10. Zhang X, Gregg EW, Williamson DF,Barker LE, Thomas W, Bullard KW,Imperatore G, Williams DE, Albright AL.A1C level and future risk of diabetes:a systematic review. Diabetes Care 2010;33:1665–1673

11. Selvin E, Steffes MW, Zhu H, MatsushitaK, Wagenknecht L, Pankow J, Coresh J,Brancati FL. Glycated hemoglobin, di-abetes, and cardiovascular risk in non-diabetic adults. N Engl J Med 2010;362:800–811

12. Ackermann RT, Cheng YJ, WilliamsonDF, Gregg EW. Identifying adults at highrisk for diabetes and cardiovascular dis-ease using hemoglobin A1c NationalHealth and Nutrition Examination Survey2005–2006. Am J Prev Med 2011;40:11–17

13. Metzger BE, Lowe LP, Dyer AR, TrimbleER, Chaovarindr U, Coustan DR, HaddenDR, McCance DR, Hod M, McIntyre HD,Oats JJ, Persson B, Rogers MS, Sacks DA.Hyperglycemia and adverse pregnancyoutcomes. N Engl J Med 2008;358:1991–2002

14. Metzger BE, Gabbe SG, Persson B,Buchanan TA, Catalano PA, Damm P,Dyer AR, Leiva A, Hod M, Kitzmiler JL,Lowe LP, McIntyre HD, Oats JJ, Omori Y,Schmidt MI. International Association ofDiabetes and Pregnancy Study Groupsrecommendations on the diagnosis andclassification of hyperglycemia in preg-nancy. Diabetes Care 2010;33:676–682

15. Landon MB, Spong CY, Thom E,Carpenter MW, Ramin SM, Casey B,Wapner RJ, Varner MW, Rouse DJ, ThorpJM, Jr., Sciscione A, Catalano P, Harper M,Saade G, Lain KY, Sorokin Y, PeacemanAM, Tolosa JE, Anderson GB. A multi-center, randomized trial of treatment formild gestational diabetes. N Engl J Med2009;361:1339–1348

16. Crowther CA, Hiller JE, Moss JR, McPheeAJ, Jeffries WS, Robinson JS. Effect oftreatment of gestational diabetes mellituson pregnancy outcomes. N Engl J Med2005;352:2477–2486


Position Statement

]Diabetes Care in the School andDayCareSettingAMERICAN DIABETES ASSOCIATION

D iabetes is one of the most commonchronic diseases of childhood (1).There are ;215,000 individu-

als ,20 years of age with diabetes inthe U.S. (2). The majority of these youngpeople attend school and/or some typeof day care and need knowledgeablestaff to provide a safe school environ-ment. Both parents and the health careteam should work together to provideschool systems and day care providerswith the information necessary to allowchildren with diabetes to participatefully and safely in the school experience(3,4).

DIABETES ANDTHE LAWdFederal laws that protectchildren with diabetes include Section504 of the Rehabilitation Act of 1973(5), the Individuals with Disabilities Edu-cation Act (originally the Education forAll Handicapped Children Act of 1975)(6), and the Americans with DisabilitiesAct (7). Under these laws, diabetes hasbeen considered to be a disability, and itis illegal for schools and/or day care cen-ters to discriminate against children withdisabilities. In addition, any school thatreceives federal funding or any facilityconsidered open to the public must rea-sonably accommodate the special needsof children with diabetes. Indeed, federallaw requires an individualized assessmentof any child with diabetes. The requiredaccommodations should be documentedin a written plan developed under the ap-plicable federal law such as a Section 504Plan or Individualized Education Pro-gram (IEP). The needs of a student withdiabetes should be provided for withinthe child’s usual school setting with aslittle disruption to the school’s and thechild’s routine as possible and allowing

the child full participation in all schoolactivities (8,9).

Despite these protections, children inthe school and day care setting still facediscrimination. For example, some daycare centers may refuse admission tochildren with diabetes, and children inthe classroom may not be provided theassistance necessary to monitor bloodglucose and administer insulin and maybe prohibited from eating needed snacks.The American Diabetes Association worksto ensure the safe and fair treatment ofchildren with diabetes in the school andday care setting (10–15) (www.diabetes.org/schooldiscrimination).

Diabetes care in schoolsAppropriate diabetes care in the school andday care setting is necessary for the child’simmediate safety, long-term well-being,and optimal academic performance. TheDiabetes Control and Complications Trialshowed a significant link between bloodglucose control and later development ofdiabetes complications, with improvedglycemic control decreasing the risk ofthese complications (16,17). To achieveglycemic control, a child must check bloodglucose frequently, monitor food intake,take medications, and engage in regularphysical activity. Insulin is usually takenin multiple daily injections or through aninfusion pump. Crucial to achieving glyce-mic control is an understanding of the ef-fects of physical activity, nutrition therapy,and insulin on blood glucose levels.

To facilitate the appropriate care ofthe student with diabetes, the schoolnurse as well as other school and day carepersonnel must have an understandingof diabetes and must be trained in itsmanagement and in the treatment of dia-betes emergencies (3,18,19,20,34,36).

Knowledgeable trained personnel are es-sential if the student is to avoid the imme-diate health risks of low blood glucose andto achieve the metabolic control requiredto decrease risks for later development ofdiabetes complications (3,20). Studieshave shown that the majority of schoolpersonnel have an inadequate under-standing of diabetes (21,22). Conse-quently, diabetes education must betargeted toward day care providers, teach-ers, and other school personnel who in-teract with the child, including schooladministrators, school nurses, coaches,health aides, bus drivers, secretaries, etc.(3,20). Current recommendations andup-to-date resources regarding appropri-ate care for children with diabetes in theschool are universally available to allschool personnel (3,23).

The purpose of this position statementis to provide recommendations for themanagement of children with diabetes inthe school and day care setting.

GENERAL GUIDELINES FORTHE CARE OF THE CHILD INTHE SCHOOL AND DAY CARESETTING

I. Diabetes Medical ManagementPlanAn individualized Diabetes Medical Man-agement Plan (DMMP) should be devel-oped by the student’s personal diabeteshealth care team with input from theparent/guardian. Inherent in this processare delineated responsibilities assumed byall parties, including the parent/guardian,the school personnel, and the student(3,24,25). These responsibilities are out-lined in this position statement. In addi-tion, the DMMP should be used as thebasis for the development of written edu-cation plans such as the Section 504 Planor the IEP. The DMMP should address thespecific needs of the child and providespecific instructions for each of the fol-lowing:


Originally approved 1998. Revised 2008.DOI: 10.2337/dc13-S075© 2013 by the American Diabetes Association. Readers may use this article as long as the work is properly




http://www.diabetes.org/schooldiscrimination

http://www.diabetes.org/schooldiscrimination



1. Blood glucose monitoring, includingthe frequency and circumstances re-quiring blood glucose checks, and useof continuous glucose monitoring ifutilized.

2. Insulin administration (if necessary),including doses/injection times pre-scribed for specific blood glucose val-ues and for carbohydrate intake, thestorage of insulin, and, when appro-priate, physician authorization of par-ent/guardian adjustments to insulindosage.

3. Meals and snacks, including food con-tent, amounts, and timing.

4. Symptoms and treatment of hypogly-cemia (low blood glucose), includingthe administration of glucagon if rec-ommended by the student’s treatingphysician.

5. Symptoms and treatment of hypergly-cemia (high blood glucose).

6. Checking for ketones and appropriateactions to take for abnormal ketonelevels, if requested by the student’shealth care provider.

7. Participation in physical activity.8. Emergency evacuation/school lock-

down instructions.

A sample DMMP (http://professional.diabetes.org/DMMP) may be accessedonline and customized for each individ-ual student. For detailed information onthe symptoms and treatment of hypogly-cemia and hyperglycemia, refer to Medi-cal Management of Type 1 Diabetes (26). Abrief description of diabetes targeted toschool and day care personnel is includedin the APPENDIX; it may be helpful to in-clude this information as an introductionto the DMMP.

II. Responsibilities of the variouscare providers

A. The parent/guardian should providethe school or day care provider withthe following:

1. All materials, equipment, insulin,and other medication necessary fordiabetes care tasks, including bloodglucose monitoring, insulin admin-istration (if needed), and urine orblood ketone monitoring. The par-ent/guardian is responsible for themaintenance of the blood glucosemonitoring equipment (i.e., cleaningand performing controlled testingper the manufacturer’s instructions)and must provide materials necessary

to ensure proper disposal of materials.A separate logbook should be kept atschool with the diabetes supplies forthe staff or student to record bloodglucose and ketone results; blood glu-cose values should be transmitted tothe parent/guardian for review as oftenas requested. Some studentsmaintain arecord of blood glucose results in me-ter memory rather than recording in alogbook, especially if the same meter isused at home and at school.

2. The DMMP completed and signed bythe student’s personal diabetes healthcare team.

3. Supplies to treat hypoglycemia, in-cluding a source of glucose and a glu-cagon emergency kit, if indicated inthe DMMP.

4. Information about diabetes and theperformance of diabetes-relatedtasks.

5. Emergency phone numbers for theparent/guardian and the diabeteshealth care team so that the schoolcan contact these individuals withdiabetes-related questions and/or dur-ing emergencies.

6. Information about the student’s meal/snack schedule. The parent shouldwork with the school during theteacher preparation period before thebeginning of the school year or beforethe student returns to school after di-agnosis to coordinate this schedulewith that of the other students as closelyas possible. For young children, in-structions should be given for whenfood is provided during school partiesand other activities.

7. In most locations, and increasingly, asigned release of confidentiality fromthe legal guardian will be required sothat the health care team can com-municate with the school. Copiesshould be retained both at the schooland in the health care professionals’offices.

B. The school or day care providershould provide the following:

1. Opportunities for the appropriatelevel of ongoing training and diabeteseducation for the school nurse.

2. Training for school personnel as fol-lows: level 1 training for all schoolstaff members, which includes a basicoverview of diabetes, typical needsof a student with diabetes, recogni-tion of hypoglycemia and hyper-glycemia, and who to contact for

help; level 2 training for school staffmembers who have responsibilityfor a student or students with di-abetes, which includes all contentfrom level 1 plus recognition andtreatment of hypoglycemia and hy-perglycemia and required accom-modations for those students; andlevel 3 training for a small group ofschool staff members who will per-form student-specific routine andemergency care tasks such as bloodglucose monitoring, insulin adminis-tration, and glucagon administrationwhen a school nurse is not availableto perform these tasks andwhichwillinclude level 1 and 2 training as well.

3. Immediate accessibility to the treat-ment of hypoglycemia by a knowl-edgeable adult. The student shouldremain supervised until appropriatetreatment has been administered,and the treatment should be availableas close to where the student is aspossible.

4. Accessibility to scheduled insulin attimes set out in the student’s DMMPas well as immediate accessibility totreatment for hyperglycemia includinginsulin administration as set out by thestudent’s DMMP.

5. A location in the school that providesprivacy during blood glucose moni-toring and insulin administration, ifdesired by the student and family, orpermission for the student to checkhis or her blood glucose level andtake appropriate action to treat hy-poglycemia in the classroom or any-where the student is in conjunctionwith a school activity, if indicated inthe student’s DMMP.

6. School nurse and back-up trainedschool personnel who can checkblood glucose and ketones and ad-minister insulin, glucagon, and othermedications as indicated by the stu-dent’s DMMP.

7. School nurse and back-up trainedschool personnel responsible for thestudent who will know the scheduleof the student’s meals and snacks andwork with the parent/guardian tocoordinate this schedule with that ofthe other students as closely as pos-sible. This individual will also notifythe parent/guardian in advance ofany expected changes in the schoolschedule that affect the student’smeal times or exercise routine andwill remind young children of snacktimes.


Position Statement

http://professional.diabetes.org/DMMP

http://professional.diabetes.org/DMMP

8. Permission for self-sufficient and ca-pable students to carry equipment,supplies, medication, and snacks; toperform diabetes management tasks;and to have cell phone access to reachparent/guardian and health careprovider.

9. Permission for the student to see theschool nurse and other trainedschool personnel upon request.

10. Permission for the student to eat asnack anywhere, including the class-room or the school bus, if necessary toprevent or treat hypoglycemia.

11. Permission to miss school withoutconsequences for illness and requiredmedical appointments to monitor thestudent’s diabetes management. Thisshould be an excused absence with adoctor’s note, if required by usualschool policy.

12. Permission for the student to use therestroom and have access to fluids(i.e., water) as necessary.

13. An appropriate location for insulinand/or glucagon storage, if neces-sary.

14. A plan for the disposal of sharpsbased upon an agreement with thestudent’s family, local ordinances,and Universal Precaution Standards.

15. Information on serving size and ca-loric, carbohydrate, and fat contentof foods served in the school (27).

The school nurse should be the key co-ordinator and provider of care and shouldcoordinate the training of an adequatenumber of school personnel as specifiedabove and ensure that if the school nurse isnot present at least one adult is presentwho is trained to perform these proce-dures in a timely manner while thestudent is at school, on field trips, par-ticipating in school-sponsored extracur-ricular activities, and on transportationprovided by the school or day carefacility. This is needed in order to enablefull participation in school activities(3,18,20). These school personnelneed not be health care professionals(3,9,20,28,33,35).

It is the school’s responsibility to pro-vide appropriate training of an adequate

number of school staff on diabetes-relatedtasks and in the treatment of diabetesemergencies. This training should be pro-vided by the school nurse or anotherqualified health care professional with ex-pertise in diabetes. Members of the stu-dent’s diabetes health care team shouldprovide school personnel and parents/guardians with educational materialsfrom the American Diabetes Associationand other sources targeted to school per-sonnel and/or parents. Table 1 includes alisting of appropriate resources.

III. Expectations of the student indiabetes careChildren and youth should be allowed toprovide their own diabetes care at schoolto the extent that is appropriate based onthe student’s development and his or herexperience with diabetes. The extent ofthe student’s ability to participate in di-abetes care should be agreed upon by theschool personnel, the parent/guardian,and the health care team, as necessary.The ages at which children are able toperform self-care tasks are variable anddepend on the individual, and a child’scapabilities and willingness to provideself-care should be respected (18).

1. Toddlers and preschool-aged children:unable to perform diabetes tasks in-dependently and will need an adult toprovide all aspects of diabetes care.Many of these younger children willhave difficulty in recognizing hypo-glycemia, so it is important that schoolpersonnel are able to recognize andprovide prompt treatment. However,children in this age range can usuallydetermine which finger to prick, canchoose an injection site, and are gen-erally cooperative.

2. Elementary school–aged children: de-pending on the length of diagnosisand level of maturity, may be able toperform their own blood glucosechecks, but usually will require su-pervision. Older elementary school–aged children are generally beginningto self-administer insulin with super-vision and understand the effect ofinsulin, physical activity, and nutritionon blood glucose levels. Unless thechild has hypoglycemic unawareness,he or she should usually be able to letan adult know when experiencing hy-poglycemia.

3. Middle school– and high school–agedchildren: usually able to provide self-care depending on the length of

Table 1dResources for teachers, child care providers, parents, and health professionals

Helping the Student with Diabetes Succeed: A Guide for School Personnel. National Diabetes EducationProgram, 2010. Available at http://ndep.nih.gov/publications/PublicationDetail.aspx?PubId=97#main

Diabetes Care Tasks at School: What Key Personnel Need to Know. Alexandria, VA, AmericanDiabetes Association, 2008. Available at http://shopdiabetes.org/58-diabetes-care-tasks-at-school-what-key-personnel-need-to-know-2010-edition.aspx

Your School & Your Rights: Protecting Children with Diabetes Against Discrimination in Schools andDay Care Centers. Alexandria, VA, American Diabetes Association, 2005 (brochure). Availableat http://www.diabetes.org/assets/pdfs/schools/your-school-your-right-2010.pdf*

Children with Diabetes: Information for School and Child Care Providers. Alexandria, VA, AmericanDiabetes Association, 2004 (brochure). Available at http://shopdiabetes.org/42-children-with-diabetes-information-for-school-and-child-care-providers.aspx*

ADA’s Safe at School campaign and information on how to keep children with diabetes safe atschool. Call 1-800-DIABETES and go to http://www.diabetes.org/living-with-diabetes/parents-and-kids/diabetes-care-at-school/

American Diabetes Association: Complete Guide to Diabetes. Alexandria, VA, American DiabetesAssociation, 2011. Available at http://www.shopdiabetes.org/551-American-Diabetes-Association-Complete-Guide-to-Diabetes-5th-Edition.aspx

American Diabetes Association: Guide to Raising a Child With Diabetes, 3rd ed. Alexandria, VA,American Diabetes Association, 2011. Available at http://www.shopdiabetes.org/548-ADA-Guide-to-Raising-a-Child-with-Diabetes-3rd-Edition.aspx

Clarke W: Advocating for the child with diabetes. Diabetes Spectrum 12:230–236, 1999School Discrimination Resources. Alexandria, VA, American Diabetes Association, 2006. Availableat http://www.diabetes.org/living-with-diabetes/know-your-rights/discrimination/school-discrimination/*

Every Day Wisdom: A Kit for Kids with Diabetes (and their parents). Alexandria, VA, AmericanDiabetes Association, 2000. Available at http://www.diabetes.org/living-with-diabetes/parents-and-kids/everyday-wisdom-kit-nov-dec-2012.html?loc=rightrail1_wisdomkit_evergreen

ADA’s Planet D, online information for children and youth with diabetes. Available at http://www.diabetes.org/living-with-diabetes/parents-and-kids/planet-d/

*Available in the American Diabetes Association’s Education Discrimination Packet by calling 1-800-DIABETES.


Position Statement

http://ndep.nih.gov/publications/PublicationDetail.aspx?PubId=97#main

http://shopdiabetes.org/58-diabetes-care-tasks-at-school-what-key-personnel-need-to-know-2010-edition.aspx

http://shopdiabetes.org/58-diabetes-care-tasks-at-school-what-key-personnel-need-to-know-2010-edition.aspx

http://www.diabetes.org/assets/pdfs/schools/your-school-your-right-2010.pdf

http://shopdiabetes.org/42-children-with-diabetes-information-for-school-and-child-care-providers.aspx

http://shopdiabetes.org/42-children-with-diabetes-information-for-school-and-child-care-providers.aspx

http://www.diabetes.org/living-with-diabetes/parents-and-kids/diabetes-care-at-school/

http://www.diabetes.org/living-with-diabetes/parents-and-kids/diabetes-care-at-school/

http://www.shopdiabetes.org/551-American-Diabetes-Association-Complete-Guide-to-Diabetes-5th-Edition.aspx

http://www.shopdiabetes.org/551-American-Diabetes-Association-Complete-Guide-to-Diabetes-5th-Edition.aspx

http://www.shopdiabetes.org/548-ADA-Guide-to-Raising-a-Child-with-Diabetes-3rd-Edition.aspx

http://www.shopdiabetes.org/548-ADA-Guide-to-Raising-a-Child-with-Diabetes-3rd-Edition.aspx

http://www.diabetes.org/living-with-diabetes/know-your-rights/discrimination/school-discrimination/

http://www.diabetes.org/living-with-diabetes/know-your-rights/discrimination/school-discrimination/

http://www.diabetes.org/living-with-diabetes/parents-and-kids/everyday-wisdom-kit-nov-dec-2012.html?loc=rightrail1_wisdomkit_evergreen

http://www.diabetes.org/living-with-diabetes/parents-and-kids/everyday-wisdom-kit-nov-dec-2012.html?loc=rightrail1_wisdomkit_evergreen

http://www.diabetes.org/living-with-diabetes/parents-and-kids/planet-d/

http://www.diabetes.org/living-with-diabetes/parents-and-kids/planet-d/

diagnosis and level of maturity butwill always need help when experi-encing severe hypoglycemia. Inde-pendence in older children should beencouraged to enable the child tomake his or her decisions about his orher own care.

Students’ competence and capabilityfor performing diabetes-related tasks areset out in the DMMP and then adapted tothe school setting by the school healthteam and the parent/guardian. At all ages,individuals with diabetes may requirehelp to perform a blood glucose checkwhen the blood glucose is low. In addi-tion, many individuals require a reminderto eat or drink during hypoglycemia andshould not be left unsupervised until suchtreatment has taken place and the bloodglucose value has returned to the normalrange. Ultimately, each person with di-abetes becomes responsible for all aspectsof routine care, and it is important forschool personnel to facilitate a student inreaching this goal. However, regardlessof a student’s ability to provide self-care,help will always be needed in the eventof a diabetes emergency.

MONITORING BLOODGLUCOSE IN THECLASSROOMdIt is best for a stu-dent with diabetes to monitor blood glu-cose levels and respond to the results asquickly and conveniently as possible.This is important to avoid medical prob-lems being worsened by a delay inmonitoring and treatment and to mini-mize educational problems caused bymissing instruction in the classroom.Accordingly, as stated earlier, a studentshould be permitted to monitor his orher blood glucose level and take appro-priate action to treat hypoglycemia andhyperglycemia in the classroom or any-where the student is in conjunctionwith a school activity, if preferred bythe student and indicated in the stu-dent’s DMMP (3,24). However, somestudents desire privacy for blood glu-cose monitoring and other diabetescare tasks, and this preference shouldalso be accommodated.

In summary, with proper planningand the education and training of schoolpersonnel, children and youth with di-abetes can fully participate in the schoolexperience. To this end, the family, thehealth care team, and the school shouldwork together to ensure a safe learningenvironment.

APPENDIX

Background information ondiabetes for school personnelDiabetes is a serious, chronic disease thatimpairs the body’s ability to use food.Insulin, a hormone produced by thepancreas, helps the body convert foodinto energy. In people with diabetes, ei-ther the pancreas does not make insulinor the body cannot use insulin properly.Without insulin, the body’s main energysourcedglucosedcannot be used as fuel.Rather, glucose builds up in the blood.Over many years, high blood glucoselevels can cause damage to the eyes, kid-neys, nerves, heart, and blood vessels.

The majority of school-aged youthwith diabetes have type 1 diabetes. Peoplewith type 1 diabetes do not produce in-sulin and must receive insulin througheither injections or an insulin pump. In-sulin taken in this manner does not curediabetes and may cause the student’sblood glucose level to become danger-ously low. Type 2 diabetes, the mostcommon form of the disease, typicallyafflicting obese adults, has been shown tobe increasing in youth. This may be dueto the increase in obesity and decrease inphysical activity in young people. Stu-dents with type 2 diabetes may be able tocontrol their disease through diet andexercise alone or may require oral medi-cations and/or insulin injections. Allpeople with type 1 and type 2 diabetesmust carefully balance food, medica-tions, and activity level to keep bloodglucose levels as close to normal as pos-sible.

Low blood glucose (hypoglycemia) isthe most common immediate healthproblem for students with diabetes. Itoccurs when the body gets too much in-sulin, too little food, a delayed meal, ormore than the usual amount of exercise.Symptoms of mild to moderate hypogly-cemia include tremors, sweating, light-headedness, irritability, confusion, anddrowsiness. In younger children othersymptoms may include inattention, fallingasleep at inappropriate times, unexplainedbehavior, and temper tantrums. A studentwith this degree of hypoglycemia willneed to ingest carbohydrates promptlyand may require assistance. Severe hypo-glycemia, which is rare, may lead to un-consciousness and convulsions and can belife-threatening if not treated promptlywith glucagon as per the student’s DMMP(18,24,29,30,31).

High blood glucose (hyperglycemia)occurs when the body gets too little insulin,too much food, or too little exercise; it mayalso be caused by stress or an illness suchas a cold. The most common symptomsof hyperglycemia are thirst, frequent uri-nation, and blurry vision. If untreatedover a period of days, hyperglycemia andinsufficient insulin can lead to a seriouscondition called diabetic ketoacidosis(DKA), which is characterized by nausea,vomiting, and a high level of ketones in theblood and urine. For students using insulininfusion pumps, lack of insulin supplymaylead to DKAmore rapidly. DKA can be life-threatening and thus requires immediatemedical attention (32).

AcknowledgmentsdThe American DiabetesAssociation thanks the members of the HealthCare Professional VolunteerWriting Group forthis updated statement: William Clarke, MD;Larry C. Deeb, MD; Paula Jameson, MSN,ARNP, CDE; Francine Kaufman, MD; Geor-geanna Klingensmith, MD; Desmond Schatz,MD; Janet H. Silverstein, MD; and Linda M.Siminerio, RN, PhD, CDE.

References1. American Diabetes Association: American

Diabetes Association Complete Guide to Di-abetes. 5th ed. Alexandria, VA, AmericanDiabetes Association, 2011

2. Centers for Disease Control and Pre-vention: National Diabetes Fact Sheet: Na-tional Estimates and General Informationon Diabetes and Prediabetes in the UnitedStates, 2011. Atlanta, GA, U.S. Departmentof Health andHuman Services, Centers forDisease Control and Prevention, 2011

3. National Institutes of Health: Helping theStudent with Diabetes Succeed: A Guide forSchool Personnel. Bethesda, MD, NationalDiabetes Education Program (NIH pub-lication no. 10-5217, revised September2010)

4. Nabors L, Troillett A, Nash T, Masiulis B:School nurse perceptions of barriers andsupports for children with diabetes. J SchHealth 75: 119–124, 2005

5. 504 of the Rehabilitation Act of 1973, 29U.S.C. 794, implementing regulations at35 CFR Part 104

6. Individuals with Disabilities EducationAct, 20 U.S.C. 1400 et seq., implementingregulations at 34 CRF Part 300

7. Title II of the Americans with DisabilitiesAct of 1990, 42 U.S.C. 12134 et seq., im-plementing regulations at 28 CFR Part 35

8. Rapp J: Students with diabetes in schools.In Inquiry & Analysis. Alexandria, VA,National School Boards Association Councilof School Attorneys, June 2005


Position Statement

9. Arent S, Kaufman F: Federal laws anddiabetes management at school. SchoolNurse News, November 2004

10. Jesi Stuthard and ADA v. KindercareLearning Centers, Inc. Case no. C2-96-0185 (USCD South Ohio 8/96)

11. Calvin Davis and ADA v. LaPetite Academy,Inc. Case no. CIV97-0083-PHX-SMM(USCD Arizona 1997)

12. Agreement, Loudoun County PublicSchools (VA) and the Office for CivilRights, United States Department of Ed-ucation (Complaint nos. 11-99-1003, 11-99-1064, 11-99-1069, 1999)

13. Henderson County (NC) Pub. Schls., Com-plaint no. 11-00-1008, 34 IDLER 43(OCR 2000)

14. Rapp J, Arent S, Dimmick B, Jackson C:Legal Rights of Students with Diabetes. 2nded. Alexandria, VA, American DiabetesAssociation,October 2005, updatedOctober2009. Available from http://www.diabetes.org/living-with-diabetes/know-your-rights/for-lawyers/education-materials-for-lawyers/legal-rights-of-students-with-diabetes.html

15. Greene MA: Diabetes legal advocacycomes of age. Diabetes Spectr 19: 171–179, 2006

16. Diabetes Control and Complications TrialResearch Group: Effect of intensive di-abetes treatment on the development andprogression of long-term complications ininsulin-dependent diabetes mellitus. NEngl J Med 329: 977–986, 1993

17. Diabetes Control and Complications TrialResearch Group: Effect of intensive di-abetes treatment on the development andprogression of long-term complications inadolescentswith insulin-dependent diabetesmellitus. J Pediatr 125: 177–188, 1994

18. American Diabetes Association: Care ofchildren and adolescents with type 1 di-abetes (Position Statement). Diabetes Care28: 186–212, 2005

19. Barrett JC, Goodwin DK, Kendrick O:Nursing, food service, and the child withdiabetes. J Sch Nurs 18: 150–156, 2002

20. Jameson P: Developing diabetes trainingprograms for school personnel. SchoolNurse News, September 2004

21. Wysocki T, Meinhold P, Cox DJ, ClarkeWL: Survey of diabetes professionalsregarding developmental charges in di-abetes self-care. Diabetes Care 13: 65–68,1990

22. Lindsey R, Jarrett L, Hillman K: Elemen-tary schoolteachers’ understanding of di-abetes. Diabetes Educ 13: 312–314, 1987

23. American Diabetes Association: DiabetesCare Tasks at School: What Key PersonnelNeed to Know. Alexandria, VA, AmericanDiabetes Association, 2008. Available fromhttp://www.diabetes.org/assets/pdfs/schools/forward2008.pdf

24. Jameson P: Helping students with di-abetes thrive in school. In On the Cut-ting Edge, American Dietetic Association’sDiabetes Care and Education PracticeGroup Newsletter. Summer 2006, p. 26–29

25. Owen S: Pediatric pumpsdbarriers andbreakthroughs. Pediatric Pumps 32 (Suppl.1), January/February 2006

26. American Diabetes Association: MedicalManagement of Type 1 Diabetes. 6th ed.Kaufman F, Ed. Alexandria, VA, AmericanDiabetes Association, 2012

27. Accommodating Children with Special DietaryNeeds in the School Nutrition Program:Guidance for School Food Service Staff.Washington, DC, U.S. Department of Ag-riculture Food and Nutrition Service, 2001

28. American Diabetes Association: Safe atSchool Campaign Statement of Principlesendorsed by American Academy of Pedi-atrics, American Association of ClinicalEndocrinologists, American Associationof Diabetes Educators, American Dia-betes Association, American Dietetic

Association, Children with Diabetes, Dis-ability Rights Education Defense Fund,Juvenile Diabetes Research Foundation,Lawson Wilkins Pediatric Endocrine Soci-ety, Pediatric Endocrine Nursing Society,Endocrine Society [article online]. Availablefrom http://www.diabetes.org/living-with-diabetes/parents-and-kids/diabetes-care-at-school/safe-at-school-statement-of.html

29. Evert A: Managing hypoglycemia in theschool setting. School Nurse News, No-vember 2005

30. Bulsara MD, Holman CD, David EA, JonesTW: The impact of a decade of changingtreatment on rates of severe hypoglycemiain a population-based cohort of childrenwith type 1 diabetes. Diabetes Care 27:2293–2298, 2004

31. Nabors L, Lehmkuhl H, Christos N,Andreone TF: Children with diabetes: per-ceptions of supports for self-managementat school. J Sch Health 73: 216–221,2003

32. Kaufman FR: Diabetes mellitus. PediatrRev 18: 383–392, 1997

33. Pediatric Endocrine Nursing Society:Children With Diabetes at School. Septem-ber 2005. Available from the PediatricEndocrinology Nursing Society, 7794Grow Dr., Pensacola, FL 32514

34. Committee on School Health, AmericanAcademy of Pediatrics Policy Statement:Guidance for the administration of medi-cation in school. Pediatrics 124: 1244–1251, 2009

35. Hellems MA, Clarke WL: Safe at school:a Virginia experience. Diabetes Care 30:1396–1398, 2007

36. American Medical Association: Report 4of the Council on Science and PublicHealth (A-08): Ensuring the Best In-SchoolCare for Children with Diabetes [articleonline], June 2008. Available from http://www.ama-assn.org/resources/doc/csaph/csaph4a08.pdf


Position Statement

http://www.diabetes.org/living-with-diabetes/know-your-rights/for-lawyers/education-materials-for-lawyers/legal-rights-of-students-with-diabetes.html





http://www.diabetes.org/assets/pdfs/schools/forward2008.pdf

http://www.diabetes.org/assets/pdfs/schools/forward2008.pdf

http://www.diabetes.org/living-with-diabetes/parents-and-kids/diabetes-care-at-school/safe-at-school-statement-of.html



http://www.ama-assn.org/resources/doc/csaph/csaph4a08.pdf



Diabetes and DrivingAMERICAN DIABETES ASSOCIATION

O f the nearly 19 million people in theU.S. with diagnosed diabetes (1), alarge percentage will seek or cur-

rently hold a license to drive. For many, adriver’s license is essential to work; takingcare of family; securing access to public andprivate facilities, services, and institutions;interacting with friends; attending classes;and/or performingmany other functions ofdaily life. Indeed, in many communitiesand areas of the U.S. the use of an automo-bile is the only (or the only feasible or af-fordable)means of transportation available.

There has been considerable debatewhether, and the extent to which, diabetesmay be a relevant factor in determiningdriver ability and eligibility for a license.This position statement addresses suchissues in light of current scientific andmedical evidence.

Sometimes people with a strong in-terest in road safety, including motor vehi-cle administrators, pedestrians, drivers,other road users, and employers, associateall diabetes with unsafe driving when infact most people with diabetes safely oper-ate motor vehicles without creating anymeaningful risk of injury to themselvesor others. When legitimate questions ariseabout the medical fitness of a person withdiabetes to drive, an individual assessment ofthat person’s diabetes managementdwithparticular emphasis on demonstrated abil-ity to detect and appropriately treat poten-tial hypoglycemiadis necessary in orderto determine any appropriate restrictions.The diagnosis of diabetes is not sufficientto make any judgments about individualdriver capacity.

This document provides an overviewof existing licensing rules for people withdiabetes, addresses the factors that impactdriving for this population, and identifiesgeneral guidelines for assessing driver fit-ness and determining appropriate licensingrestrictions.

LICENSINGREQUIREMENTSdPeople with dia-betes are currently subject to a great varietyof licensing requirements and restrictions.These licensing decisions occur at severalpoints and involve different levels andtypes of review, depending on the type ofdriving. Some states and local jurisdictionsimpose no special requirements for peoplewith diabetes. Other jurisdictions ask driv-ers with diabetes various questions abouttheir condition, including their manage-ment regimen and whether they have ex-perienced any diabetes-related problemsthat could affect their ability to safely oper-ate a motor vehicle. In some instances,answers to these questions result in restric-tions being placed on a person’s license, in-cluding restrictions on the type of vehicletheymay operate and/or where theymay op-erate that vehicle. In addition, the rules foroperating a commercial motor vehicle, andfor obtaining related license endorsements(such as rules restrictingoperationof a schoolbus or transport of passengers or hazardousmaterials) are quite different and in manyways more cumbersome for people with di-abetes, especially those who use insulin.

With the exception of commercialdriving in interstate commerce (Interstatecommercial driving is defined as trade,traffic or transportation in theUnited Statesbetween a place in a state and a placeoutside of such a state, between two placesin a state through another state or a placeoutside of the United States, or betweentwo places in a state as part of trade, trafficor transportation originating or terminat-ing outside the state or the United States[2]), which is subject to uniform federalregulation, both private and commercialdriving are subject to rules determined byindividual states. These rules vary widely,with each state taking its own approach todetermining medical fitness to drive andthe issuance of licenses. How diabetes is

identified,which people aremedically eval-uated, and what restrictions are placed onpeople who have experienced hypoglyce-mia or other problems related to diabetesall vary from state to state.

States identify drivers with diabetesin a number of ways. In at least 23 states,drivers are either asked directly if theyhave diabetes or are otherwise required toself-identify if they have diabetes. In otherstates drivers are asked some variation of aquestion about whether they have a con-dition that is likely to cause altered percep-tion or loss of consciousness while driving.In most states, when the answer to eitherquestion is yes, the driver is required tosubmit to a medical evaluation before heor she will be issued a license.

Medical evaluationDrivers whose medical conditions can leadto significantly impaired consciousness areevaluated for their fitness to continue todrive. For people with diabetes, this typi-cally occurswhen a person has experiencedhypoglycemia (3) behind the wheel, even ifthis did not result in a motor vehicle acci-dent. In some states this occurs as a resultof a policy to evaluate all people with di-abetes, even if there has been no triggeringevent. It can also occur when a person ex-periences severe hypoglycemia while notdriving and a physician reports the episodeto the licensing authority. In a handful ofstates, such reporting by physicians isman-datory. In most other states physicians arepermitted to make reports but are givendiscretion to determine when such reportsare necessary. Some states specify thatphysiciansmay voluntarily report those pa-tients who pose an imminent threat to pub-lic safety because they are driving againstmedical advice. Physicians and others re-quired to make reports to the licensing au-thority are usually providedwith immunityfrom civil and criminal actions resultingfrom the report.

When licensing authorities learnthat a driver has experienced an episodeof hypoglycemia that potentially affectedthe ability to drive, that driver is referredfor a medical evaluation and in manycases will lose driving privileges for a periodof time until cleared by the licensing au-thority. This period can range from 3 to 6months or longer. Some state laws allow forwaivers of the rules when the episode is aone-time event not likely to recur, for


Peer reviewed by the Professional Practice Committee, September 2011, and approved by the ExecutiveCommittee of the American Diabetes Association, November 2011.







example because of a change in medicationor episodes that occur only during sleep.

Medical evaluation procedures varyand range from a simple confirmation ofthe person’s diabetes from a physician to amore elaborate process involving a statemedical advisory board, hearings, andpresentation and assessment of medicalevidence. Some states convene medicaladvisory boards with nurses and physi-cians of different specialties who reviewand make recommendations concerningthe licensing of people with diabetes andother medical conditions. In other states,licensing decisions are made by adminis-trative staff with little or no medical train-ing and with little or no review by amedical review board or by a physicianor physicians with any relevant expertiseconcerning medical conditions presentedby individual applicants.

The medical evaluation process forcommercial drivers occurs at predeter-mined intervals, typically every 2 years.Unlike noncommercial licenses, theseregular evaluations are not linked toepisodes of severe hypoglycemia but arepart of an ongoing fitness evaluation forjobs requiring commercial driving. The fed-eral government has no diabetes-specificrestrictions for individuals who managetheir disease with diet, exercise, and/ororal medication. It offers an exemptionprogram for insulin-using interstate com-mercial drivers and issues medical certifi-cates to qualified drivers. Factors in thefederal commercial driving medical evalu-ation include a review of diabetes history,medications, hospitalizations, blood glu-cose history, and tests for various com-plications and an assessment of driverunderstanding of diabetes and willingnessto monitor their condition.

SCIENCE OF DIABETES ANDDRIVINGdHypoglycemia indicatingan impaired ability to drive, retinopathyor cataract formation impairing the visionneeded to operate a motor vehicle, andneuropathy affecting the ability to feel footpedals can each impact driving safety (4).However, the incidence of these conditionsis not sufficiently extensive to justify re-striction of driving privileges for all driverswith diabetes. Driving mishaps related todiabetes are relatively infrequent for mostdrivers with diabetes and occur at a lowerrate than mishaps of many other driverswith conditions that affect driving perfor-mance and that are tolerated by society.

However, just as there are some pa-tients with conditions that increase their

risk of incurring driving mishaps, such asunstable coronary heart disease, obstruc-tive sleep apnea, epilepsy, Parkinson’sdisease, or alcohol and substance abuse,there are also some drivers with diabetesthat have a higher risk for driving mis-haps. The challenges are to identify high-risk individuals and develop measures toassist them to lower their risk for drivingmishaps.

Understanding the risk of diabetesand drivingIn a recent Scottish study, only 62% ofhealth care professionals suggested thatinsulin-treated drivers should test theirblood glucose before driving; 13% of healthcare professionals thought it safe to drivewith blood glucose,72mg/dL (4mmol/L),and 8% did not know that impaired aware-ness of hypoglycemia might be a contrain-dication to driving (5). It is important thathealth care professionals be knowledgeableand take the lead in discussing risk reduc-tion for their patients at risk for hypoglyce-mia. In a large international study, nearlyhalf of drivers with type 1 diabetes andthree-quarters of those with type 2 diabeteshad never discussed driving guidelines withtheir physician (8).

A meta-analysis of 15 studies sug-gested that the relative risk of having amotor vehicle accident for people withdiabetes as a whole, i.e., without differen-tiating those with a significant risk fromthose with little or no risk, as comparedwith the general population ranges be-tween 1.126 and 1.19, a 12–19% in-creased risk (6). Some published studiesindicated that drivers with type 1 diabeteshave a slightly higher risk, with a relativerisk ratio of ;2 (7,8,9), but this was notconfirmed by other studies (10). Two stud-ies even suggested that there is no increasedrisk associated with insulin-treated diabe-tes (11,12), but the methodologies usedhave been criticized (13).

This increased risk of collisions mustbe interpreted in the light of society’s tol-erance of other and much higher–riskconditions. For example, 16-year-oldmales have 42 times more collisions than35- to 45-year-old women. If the heaviestcar collides with the lightest car, the driverof the latter is 20 times more likely to bekilled than the driver of the former. Themost dangerous rural highways are 9.2times more dangerous than the safest urbanhighways. Driving at 1:00 A.M. on Sunday is142 times more dangerous than driving at11:00 A.M. (7). Driverswith attention deficit/hyperactivity disorder have a relative risk

ratio of;4 (14), whereas those with sleepapnea have a relative risk of ;2.4 (15). Ifsociety tolerates these conditions, it wouldbe unjustified to restrict the driving priv-ileges of an entire class of individuals whoare at much lower risk, such as driverswith diabetes.

The most significant subgroup ofpersons with diabetes for whom a greaterdegree of restrictions is often applied isdrivers managing their diabetes with in-sulin. Yet, when the type of diabetes iscontrolled for, insulin therapy per se hasnot been found to be associated with in-creased driving risk (3,16,17). While im-paired awareness of hypoglycemia hasbeen found to relate to increased incidenceof motor vehicle crashes in some studies(12), it has not been found to be a relevantvariable in other studies (4,7,23). The sin-gle most significant factor associated withdriving collisions for drivers with diabetesappears to be a recent history of severe hy-poglycemia, regardless of the type of diabe-tes or the treatment used (1,3,18–21).

The American Diabetes AssociationWorkgroup on Hypoglycemia defined se-vere hypoglycemia as low blood glucoseresulting in neuroglycopenia that disruptscognitive motor function and requires theassistance of another to actively administercarbohydrate, glucagon, or other resuscita-tive actions (22). In a prospective multicen-ter study of 452 drivers with type 1 diabetesfollowed monthly for 12 months, 185 par-ticipants (41%) reported a total of 503 epi-sodes of moderate hypoglycemia (wherethe driver could still treat him/herself butcould no longer drive safely) and 23 partic-ipants (5%) reported 31 episodes of severehypoglycemia (where the driver was unableto treat him/herself) while driving (21).Conversely, the Diabetes Control andCom-plications Trial (DCCT) group reported 11motor vehicle accidents in 714 episodes ofsevere hypoglycemia, a rate of 1.5% (23).

The significant impact of moderatehypoglycemia while driving is supportedby multiple studies demonstrating thatmoderate hypoglycemia significantly andconsistently impairs driving safety (24–26)and judgment (27,28) as towhether to con-tinue to drive or to self-treat (29,30) undersuch metabolic conditions. In one study,25% of respondents thought it was safe todrive even when blood glucose was ,70mg/dL (3.9 mmol/L) (31).

While significant hyperglycemia mayimpair cognitive, motor, and perceptualfunctioning (32–35), there is only one re-port suggesting extreme hyperglycemiacan impact driving safety (36). Thus,


Position Statement

efforts to equate hyperglycemia with driv-ing impairment are currently not scientif-ically justified.

Individual differencesEighty percent of episodes of severe hy-poglycemia affect about 20% of peoplewith type 1 diabetes (37–39). Availabledata suggest that a small subgroup of driv-ers with type 1 diabetes account for themajority of hypoglycemia-related colli-sions (9,30,40). When 452 drivers withtype 1 diabetes were followed prospec-tively for a year, baseline reports of priorepisodes of mild symptomatic hypoglyce-mia while driving or severe hypoglycemiawhile driving, hypoglycemia-related driv-ing mishaps, or hypoglycemia-relatedcollisions were associated with a higherrisk of driving mishaps in the following12 months by 3, 6, 6, and 20%, respec-tively. Risk increased exponentially withadditional reported episodes: If individu-als had two episodes of severe hypoglyce-mia in the preceding 12 months their riskincreased to 12%, and two collisions inthe previous 2 years increased their riskby 40%. The strongest predictors in-volved a history of hypoglycemia whiledriving (21). Laboratory studies that com-pared drivers with type 1 diabetes whohad no history of hypoglycemia-relateddriving mishap in the past year to thosewho had more than one mishap foundthat those with a history of mishaps: 1)drove significantly worse during progres-sive mild hypoglycemia (70–50 mg/dL,3.9–2.8 mmol/L) but drove equally wellwhen blood glucose was normal (euglyce-mia); 2) had a lower epinephrine responsewhile driving during hypoglycemia, 3)were more insulin sensitive, and 4) demon-strated greater difficulties with workingmemory and information processing speedduring euglycemia and hypoglycemia(24,40,41). Thus, a history of mishapsshould be used as a basis for identifyinginsulin-managed drivers with elevatedrisk of future mishaps. Such individualsare appropriately subjected to additionalscreening requirements.

Four studies have demonstrated thatBlood Glucose Awareness Training(BGAT) reduces the occurrence of colli-sions and moving vehicle violations whileimproving judgment about whether todrive while hypoglycemic (42–45). BGATis an 8-week psycho-educational trainingprogram designed to assist individualswith type 1 diabetes to better anticipate,prevent, recognize, and treat extremeblood glucose events. This intervention

can be effectively delivered over the inter-net (46). Diabetes Driving (diabetesdriv-ing.com), a program funded by theNational Institutes of Health, is anotherinternet-based tool to help assess therisk of driving mishaps and assist high-risk drivers to avoid hypoglycemia whiledriving and to better detect and managehypoglycemia if it occurs while driving.

RECOMMENDATIONS

Identifying and evaluating diabetesin driversIndividuals whose diabetes poses a sig-nificantly elevated risk to safe drivingmust be identified and evaluated prior togetting behind the wheel. Because peoplewith diabetes are diverse in terms of thenature of their condition, the symptomsthey experience, and the measures theytake to manage their diabetes, it is impor-tant that identification and evaluation pro-cesses be appropriate, individualized, andbased not solely on a diagnosis of diabetesbut rather on concrete evidence of actualrisk. Laws that require all people withdiabetes (or all people with insulin-treateddiabetes) to be medically evaluated as acondition of licensure are ill advised be-cause they combine people with diabetesinto one group rather than identifyingthose drivers who may be at increased riskdue to potential difficulties in avoidinghypoglycemia or the presence of compli-cations. In addition, the logistics of regis-tering and evaluating millions of peoplewith diabetes who wish to drive presentsan enormous administrative and fiscal bur-den to licensing agencies. States that requiredrivers to identify diabetes should limitthe identification to reports of diabetes-related problems.

To identify potentially at-risk drivers, ashort questionnaire can be used to findthose drivers who may require furtherevaluation. The questionnaire should askwhether the driver has, within the past 12months, lost consciousness due to hypo-glycemia, experienced hypoglycemia thatrequired intervention from another per-son to treat or that interfered with driving,or experienced hypoglycemia that devel-oped without warning. The questionnaireshould also query about loss of visualacuity or peripheral vision and loss offeeling in the right foot. Inasmuch asobstructive sleep apnea is more commonin people with type 2 diabetes than in thenondiabetic population, patients shouldbe queried about falling asleep during theday. Any positive answer should trigger an

evaluation to determine whether restric-tions on the license or mechanical mod-ifications to the vehicle (e.g., handcontrols for people with an insensatefoot) are necessary to ensure public safety.It is ill-advised to determine risk fordriving mishaps based on a driver’s gly-cosylated hemoglobin because episodictransitions into hypoglycemia, not averageblood glucose, increases risk of drivingmishaps.

Evaluation of drivers with diabetesmust include an assessment by the treat-ing physician or another diabetes special-ist who can review recent diabetes historyand provide to the licensing agency arecommendation about whether thedriver has a condition that impairs hisor her ability to safely operate a motorvehicle. The treating physician or anotherphysician who is knowledgeable aboutdiabetes is the best source of informationconcerning the driver’s diabetes manage-ment and history. The input of such aphysician is essential to assess a person’sdiabetes management and determinewhether operation of a motor vehicle issafe and practicable. If questions ariseconcerning the safe driving ability of aperson with chronic complications of di-abetes (e.g., retinopathy or neuropathy),the individual should be referred to a spe-cialist with expertise in evaluating thediabetes-related problem for specific rec-ommendations.

Physicians should be requested toprovide the following information: 1)whether the driver has had an episode ofsevere hypoglycemia requiring interven-tion from another person within the pre-vious 2 years (and when this happened);2) whether there was an explanation forthe hypoglycemia; 3) whether the driver isat increased risk of severe hypoglycemia;4) whether the driver has the ability torecognize incipient hypoglycemia andknows how to take appropriate correctiveaction; 5) whether the driver provides ev-idence of sufficient self-monitoring ofblood glucose; 6) whether the driver hasany diabetes-related complications affect-ing safe driving that need further assess-ment; and 7) whether the driver has agood understanding of diabetes and itstreatment, has been educated on theavoidance of hypoglycemia while driving,and is willing to follow a suggested treat-ment plan.

When evaluating a driverwith a historyof severe hypoglycemia, impaired hypogly-cemia awareness, or a diabetes-related mo-tor vehicle accident, it is necessary to


Position Statement

http://diabetesdriving.com

http://diabetesdriving.com

investigate the reasons for the hypoglyce-mia and to determine whether it is afunction of the driver’s treatment regimenor lifestyle, a psychological reaction to themanagement of their diabetes, or the nor-mal course of diabetes. Appropriate clini-cal interventions should be instituted.

Licensing decisions followingevaluationDrivers with diabetes should only have alicense suspended or restricted if doing sois the only practical way to address anestablished safety risk. Licensing deci-sions should reflect deference to the pro-fessional judgment of the evaluatingphysician with regard to diabetes, whilealso balancing the licensing agency’s needto keep the roads and the public safe.States should have medical advisoryboards whose role is to assess potentialdriving risks based on continually up-dated medical information, to ensurethat licensing agency staff is prepared tohandle diabetes licensing issues, and tomake recommendations relevant to indi-vidual drivers. State medical advisoryboards should have representation byhealth care professionals with expertisein treating diabetes, in addition to the in-formation provided by the driver’s treatingphysician, prior to making licensing deci-sions for people with diabetes. Where themedical advisory board does not have apermanent member with expertise in di-abetes, such an expert should be consultedin cases involving restrictions on a driverwith diabetes.

As discussed above, a history of hy-poglycemia does not mean an individualcannot be a safe driver. Rather, whenthere is evidence of a history of severehypoglycemia, an appropriate evaluationshould be undertaken to determine thecause of the low blood glucose, the cir-cumstances of the episode, whether it wasan isolated incident, whether adjustmentto the insulin regimen may mitigate therisk, and the likelihood of such an episoderecurring. It is important that licensingdecisions take into consideration contrib-utory factors that may mitigate a potentialrisk, and that licensing agencies do notadopt a “one strike” approach to licensingpeople with diabetes. Drivers with diabe-tes must be individually assessed to deter-mine whether their diabetes poses a safetyrisk. The mere fact that a person’s diabeteshas come to the attention of the licensingagencydwhether by a report or becauseof an accidentdshould not itself pre-determine a licensing decision.

Generally, severe hypoglycemia thatoccurs during sleep should not disqualifya person from driving. Hypoglycemia thatoccurswhile theperson is not driving shouldbe examined to determine if it is indicativeof a larger problem or an event that is notlikely to recur while the person is behindthe wheel of a car (e.g., hypoglycemia thatoccurs during an intense bout of exercise).Some episodes of severe hypoglycemia canbe explained and corrected with the assis-tance of a diabetes health care professional,e.g., episodes that occur because of achange in medication. However, recurrentepisodes of severe hypoglycemia, definedas two or more episodes in a year, mayindicate that a person is not able to safelyoperate a motor vehicle.

States whose licensing rules lead to asuspension of a driver’s license followingan episode of hypoglycemia should allowfor waiver of these rules when the hypo-glycemia can be explained and addressedby the treating physician and is not likelyto recur. For example, waivers may be ap-propriate following hypoglycemia thathappens as a result of a change in medi-cation or during or concurrent with ill-ness or pregnancy. Licensing agenciesmay request documentation from thephysician attesting that the patient meetsthe conditions for a waiver (which mayinclude, among other requirements, edu-cation on diabetes management andavoidance of hypoglycemia).

Drivers with a suspended license be-cause of factors related to diabetes shouldbe eligible to have their driver’s license re-instated following a sufficient period oftime (usually no more than 6 months)upon advice from the treating physicianthat the driver has made appropriate ad-justments and is adhering to a regimenthat has resulted in correction of the prob-lems that led to the license suspension. Fol-lowing reinstatement of driving privileges,periodic follow-up evaluation is necessaryto ensure that the person remains safelyable to operate a motor vehicle.

People who experience progressiveimpairment of their awareness of hypo-glycemia should consult a health careprovider to determine whether it is safeto continue driving with proper measuresto avoid disruptive hypoglycemia (such astesting blood glucose before driving andat regular intervals in the course of ajourney lasting more than 30–60 min). Ifthe driver is able to make adjustments toimprove awareness or prevent disruptivehypoglycemia while driving, there shouldnot be license restrictions. Continuous

glucose monitoring may also be beneficial,particularly when noting the direction ofthe glucose trend. If this technology isused, the person using the device needsto appreciate that any action taken (e.g.,additional carbohydrate consumption)needs to be based on a blood glucose mea-surement.

The determination of which disquali-fied drivers should be reevaluated andwhen this should be done should bemadeon an individual basis considering factorssuch as the circumstances of the disqual-ifying event and changes in medicationand behavior that have been implementedby the driver. When an assessment deter-mines that the driver should be evaluatedat some point in the future, the driver’sphysician should be consulted to deter-mine the length of the reevaluation pe-riod. A driver with diabetes should notbe kept in an endless cycle of reevaluationif there is no longer a significantly ele-vated safety risk.

The determination of medical fitnessto drive should be a clinical one, weighingthe various factors noted above. Decisionsabout whether licensing restrictions arenecessary to ensure safety of the travelingpublic are ultimately determined by thelicensing agency, taking into account theclinical determination of medical fitness.

Physician reportingAlthough the concept behind mandatoryphysician reporting laws is to keep roadssafe by eliminating unacceptable riskfrom impaired driving, such laws havethe unintended consequence of discour-aging people with diabetes from discus-sing their condition frankly with aphysician when there is a problem thatneeds correction due to fear of losing theirlicense. Patients who are not candid withtheir physicians are likely to receive in-ferior treatment and therefore may expe-rience complications that present adriving risk. In addition to the negativeeffect that mandatory reporting has on thephysician-patient relationship, there isno evidence that mandatory physicianreporting reduces the crash rate or im-proves public safety (47).

Physicians should be permitted toexercise professional judgment in decid-ing whether and when to report a patientto the licensing agency for review ofdriving privileges. States that allow physi-cians to make such reports should focusonwhether the driver’s mental or physicalcondition impairs the patient’s ability toexercise safe control over a motor vehicle.


Position Statement

Reports based solely on a diagnosis of di-abetes, or tied to a characterization thatthe driver has a condition involving lapsesof consciousness, are too broad and donot adequately measure individual risk.Ultimately, reports must be left to the dis-cretion of the physician, using profes-sional judgment about whether thepatient poses a safety risk. Further, in or-der to protect the physician-patient rela-tionship and ensure the open and honestcommunication that ultimately promotessafety, it is important that physicians beimmunized from liability, both for mak-ing reports and not making reports.

Patient education and clinicalinterventionsIt is important that health care professio-nals be knowledgeable and take the lead indiscussing risk reduction for their patientsat risk for disruptive hypoglycemia. Thisstarts with health care professionals beingconversant with safe practices, particularlyfor those patients at increased risk fordiabetes-related incidents. Perhaps themost important aspect of encouraging peo-ple with diabetes to be safe drivers is forhealth care professionals who treat diabeticdrivers to provide education about drivingwith diabetes and potential risks associatedwith patients’ treatment regimens. Whenthat regimen includes the possibility of hy-poglycemia, education should include in-struction on avoiding and responding tohypoglycemia, discussion about the pa-tient’s vulnerability for driving mishaps,and ongoing learning to ensure that pa-tients have knowledge of when it is and isnot safe for them to drive. For example, therisks of driving under the influence of alco-hol are well known, but the delayed hypo-glycemic effects of even moderate alcoholintake are not, and alcohol exacerbates thecognitive impairment associated with hy-poglycemia (48). Inasmuch as hypoglyce-mia can be mistaken for intoxication, andboth increase the risk of motor vehicle ac-cidents, patients should be counseled totest glucose more frequently for severalhours after moderate alcohol intake.When a patient has complications of dia-betes, it is important for the physician todiscuss with the driver the effect of thosecomplications, if any, on driving ability.

Physicians and other health care pro-fessionals who treat people with diabetesshould regularly discuss the risk of drivingwith low blood glucose with their patients.Clinical visits should include review ofblood glucose logs and questions to thepatient about symptoms associated with

high or low blood glucose levels and whatthe patient did to treat those levels. Allow-ing health care professionals to exerciseprofessional judgment about the informa-tion they learn in these patient conversa-tions will encourage candid sharing ofinformation and lead to improved patienthealth and road safety.

Clinical interventions in response tohypoglycemia vary by individual but mayinclude strategies for the frequency andtiming of blood glucose monitoring,medication dosage changes, and estab-lishing more conservative glucose targetsif there is a history of severe hypo-glycemia. Certain people who have ahistory of severe hypoglycemia may beencouraged by their health care providerto use continuous glucose monitoringsystems that enable them to detect atrend toward hypoglycemia before glu-cose levels fall to a level that will affectsafe driving.

Of note, special care should be taken toprevent hypoglycemia while operating anyvehicle in driverswith type 1 diabetes and inthosewith type 2 diabeteswho are at risk fordeveloping hypoglycemia. They should beinstructed to always check blood glucosebefore getting behind the wheel and atregular intervals while driving for periodsof 1 h or greater. Consideration should begiven to factors that may predict a fall inblood glucose, including time of insulinadministration, timing of the last meal orfood ingestion, and exercise type, duration,intensity, and timing. Low blood glucosevalues should be treated immediately andappropriately, and the driver should notdrive until blood glucose is in a safelyacceptable range, usually after 30–60min because of delayed recovery of cog-nitive function.

People with diabetes who are at riskfor disruptive hypoglycemia should becounseled to: 1) always carry a blood glu-cose meter and appropriate snacks,including a quick-acting source of sugar(such as juice, nondiet soda, hard candy,or dextrose tablets) as well as snacks withcomplex carbohydrate, fat, and protein(e.g., cheese crackers), in their vehicle;2) never begin an extended drive withlow normal blood glucose (e.g., 70–90mg/dL) without prophylactic carbohy-drate consumption to avoid a fall in bloodglucose during the drive; 3) stop the ve-hicle as soon any of the symptoms of lowblood glucose are experienced and mea-sure and treat the blood glucose level; and4) not resume driving until their bloodglucose and cognition have recovered.

CONCLUSIONdIn summary, peoplewith diabetes should be assessed individ-ually, taking into account each individu-al’s medical history as well as the potentialrelated risks associated with driving.

AcknowledgmentsdThe American DiabetesAssociation thanks the members of the writinggroup for developing this statement: DanielLorber, MD, FACP, CDE (Chair); JohnAnderson, MD; Shereen Arent, JD; Daniel J.Cox, PhD, ABPP; Brian M. Frier, BSc, MD,FRCPE, FRCPG; Michael A. Greene, JD;John W. Griffin, Jr., JD; Gary Gross, JD;Katie Hathaway, JD; Irl Hirsch, MD; DanielB. Kohrman, JD; David G. Marrero, PhD;Thomas J. Songer, PhD; and Alan L. Yatvin, JD.

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Position Statement

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Position Statement

DiabetesManagement in CorrectionalInstitutionsAMERICAN DIABETES ASSOCIATION

A t any given time, over 2 million peo-ple are incarcerated in prisons andjails in the U.S (1). It is estimated

that nearly 80,000 of these inmates havediabetes, a prevalence of 4.8% (2). In ad-dition, many more people pass throughthe corrections system in a given year. In1998 alone, over 11 million people werereleased from prison to the community(1). The current estimated prevalence ofdiabetes in correctional institutions issomewhat lower than the overall U.S. prev-alence of diabetes, perhaps because the in-carcerated population is younger than thegeneral population. The prevalence of di-abetes and its related comorbidities andcomplications, however, will continue toincrease in the prison population as currentsentencing guidelines continue to increasethe number of aging prisoners and the in-cidence of diabetes in young people con-tinues to increase.

People with diabetes in correctionalfacilities should receive care that meetsnational standards. Correctional institu-tions have unique circumstances thatneed to be considered so that all standardsof care may be achieved (3). Correctionalinstitutions should have written policiesand procedures for the management ofdiabetes and for training of medical andcorrectional staff in diabetes care practices.These policies must take into considerationissues such as security needs, transfer fromone facility to another, and access to med-ical personnel and equipment, so that allappropriate levels of care are provided. Ide-ally, these policies should encourage or atleast allow patients to self-manage their di-abetes. Ultimately, diabetes management isdependent upon having access to neededmedical personnel and equipment. Ongo-ing diabetes therapy is important in orderto reduce the risk of later complications,including cardiovascular events, visualloss, renal failure, and amputation. Earlyidentification and intervention for people

with diabetes is also likely to reduceshort-term risks for acute complications re-quiring transfer out of the facility, thus im-proving security.

This document provides a general setof guidelines for diabetes care in correc-tional institutions. It is not designed to be adiabetes management manual. More de-tailed information on the management ofdiabetes and related disorders can be foundin the American Diabetes Association(ADA)Clinical Practice Recommendations,published each year in January as the firstsupplement to Diabetes Care, as well as the“Standards ofMedical Care in Diabetes” (4)contained therein. This discussion will fo-cus on those areas where the care of peoplewith diabetes in correctional facilities maydiffer, and specific recommendations aremade at the end of each section.

INTAKE MEDICALASSESSMENT

Reception screeningReception screening should emphasizepatient safety. In particular, rapid identi-fication of all insulin-treated persons withdiabetes is essential in order to identifythose at highest risk for hypo- and hyper-glycemia and diabetic ketoacidosis(DKA). All insulin-treated patients shouldhave a capillary blood glucose (CBG)determination within 1–2 h of arrival.Signs and symptoms of hypo- or hyper-glycemia can often be confused with in-toxication or withdrawal from drugs oralcohol. Individuals with diabetes exhib-iting signs and symptoms consistent withhypoglycemia, particularly altered mentalstatus, agitation, combativeness, and dia-phoresis, should have finger-stick bloodglucose levels measured immediately.

Intake screeningPatients with a diagnosis of diabetesshould have a complete medical history

and physical examination by a licensedhealth care provider with prescriptive au-thority in a timely manner. If one is notavailable on site, one should be consultedby those performing reception screening.The purposes of this history and physicalexamination are to determine the type ofdiabetes, current therapy, alcohol use, andbehavioral health issues, aswell as to screenfor the presence of diabetes-related com-plications. The evaluation should reviewthe previous treatment and the past historyof both glycemic control and diabetescomplications. It is essential that medica-tion and medical nutrition therapy (MNT)be continued without interruption uponentry into the correctional system, as ahiatus in either medication or appropriatenutritionmay lead to either severe hypo- orhyperglycemia that can rapidly progress toirreversible complications, even death.

Intake physical examination andlaboratoryAll potential elements of the initial med-ical evaluation are included in Table 7 ofthe ADA’s “Standards of Medical Care inDiabetes,” referred to hereafter as the“Standards of Care” (4). The essentialcomponents of the initial history andphysical examination are detailed in Fig.1. Referrals should be made immediatelyif the patient with diabetes is pregnant.

Recommendationsc Patients with a diagnosis of diabetesshould have a completemedical historyand undergo an intake physical exam-ination by a licensed health pro-fessional in a timely manner. (E)

c Insulin-treated patients should have aCBG determination within 1–2 h ofarrival. (E)

c Medications and MNT should be con-tinued without interruption upon entryinto the correctional environment. (E)

SCREENING FOR DIABETESdConsistent with the ADA Standards ofCare, patients should be evaluated fordiabetes risk factors at the intake physicaland at appropriate times thereafter. Thosewho are at high risk should be consideredfor blood glucose screening. If pregnant, arisk assessment for gestational diabetes


Originally approved 1989. Most recent revision, 2008.DOI: 10.2337/dc13-S086© 2013 by the American Diabetes Association. Readers may use this article as long as the work is properly






mellitus (GDM) should be undertaken atthe first prenatal visit. Patients with clin-ical characteristics consistent with a highrisk for GDM should undergo glucosetesting as soon as possible. High-riskwomen not found to have GDM at theinitial screening and average-risk womenshould be tested between 24 and 28weeks of gestation. For more detailedinformation on screening for both type 2and gestational diabetes, see the ADAPosition Statement “Screening for Type2 Diabetes” (5) and the Standards ofCare (4).

MANAGEMENT PLANdGlycemiccontrol is fundamental to the manage-ment of diabetes. A management plan toachieve normal or near-normal glycemiawith an A1C goal of ,7% should be de-veloped for diabetes management at thetime of initial medical evaluation. Goalsshould be individualized (4), and less strin-gent treatment goalsmay be appropriate forpatients with a history of severe hypoglyce-mia, patients with limited life expectancies,elderly adults, and individuals with co-morbid conditions (4). This plan shouldbe documented in the patient’s record

and communicated to all persons in-volved in his/her care, including securitystaff. Table 1, taken from the ADA Stand-ards of Care, provides a summary of rec-ommendations for setting glycemiccontrol goals for adults with diabetes.

People with diabetes should ideallyreceive medical care from a physician-coordinated team. Such teams include,but are not limited to, physicians, nurses,dietitians, and mental health professio-nals with expertise and a special interestin diabetes. It is essential in this collabo-rative and integrated team approach thatindividuals with diabetes assume asactive a role in their care as possible.Diabetes self-management education is anintegral component of care. Patient self-management should be emphasized, andthe plan should encourage the involve-ment of the patient in problem solving asmuch as possible.

It is helpful to house insulin-treatedpatients in a common unit, if this ispossible, safe, and consistent with pro-viding access to other programs at thecorrectional institution. Common hous-ing not only can facilitate mealtimes andmedication administration, but also po-

tentially provides an opportunity for di-abetes self-management education to bereinforced by fellow patients.

NUTRITION AND FOODSERVICESdNutrition counseling andmenu planning are an integral part of themultidisciplinary approach to diabetesmanagement in correctional facilities. Acombination of education, interdisciplin-ary communication, and monitoring foodintake aids patients in understandingtheir medical nutritional needs and canfacilitate diabetes control during and afterincarceration.

Nutrition counseling for patientswith diabetes is considered an essentialcomponent of diabetes self-management.People with diabetes should receive indi-vidualized MNT as needed to achievetreatment goals, preferably provided by aregistered dietitian familiar with the com-ponents of MNT for persons with diabetes.

Educating the patient, individually orin a group setting, about how carbohy-drates and food choices directly affectdiabetes control is the first step in facili-tating self-management. This educationenables the patient to identify better food

Figure 1dEssential components of the initial history and physical examination. Alb/Cr ratio, albumin-to-creatinine ratio; ALT, alanine amino-transferase; AST, aspartate aminotransferase.


Position Statement

selections from those available in thedining hall and commissary. Such anapproach is more realistic in a facilitywhere the patient has the opportunity tomake food choices.

The easiest and most cost-effectivemeans to facilitate good outcomes in pa-tients with diabetes is instituting a heart-healthy diet as the master menu (6). Thereshould be consistent carbohydrate contentat each meal, as well as a means to identifythe carbohydrate content of each food se-lection. Providing carbohydrate content offood selections and/or providing educationin assessing carbohydrate content enablespatients to meet the requirements of theirindividual MNT goals. Commissariesshould also help in dietary managementby offering healthy choices and listing thecarbohydrate content of foods.

The use of insulin or oral medicationsmay necessitate snacks in order to avoidhypoglycemia. These snacks are a part ofsuch patients’ medical treatment plansand should be prescribed bymedical staff.

Timing of meals and snacks must becoordinated with medication administra-tion as needed to minimize the risk ofhypoglycemia, as discussed more fully inthe MEDICATION section of this document.For further information, see the ADA Posi-tion Statement “Nutrition Recommenda-tions and Interventions for Diabetes” (7).

URGENT AND EMERGENCYISSUESdAll patients must have accessto prompt treatment of hypo- and hyper-glycemia. Correctional staff should betrained in the recognition and treatmentof hypo- and hyperglycemia, and appro-priate staff should be trained to adminis-ter glucagon. After such emergency care,patients should be referred for appropri-

ate medical care to minimize risk of futuredecompensation.

Institutions should implement a pol-icy requiring staff to notify a physician ofall CBG results outside of a specifiedrange, as determined by the treatingphysician (e.g., ,50 or .350 mg/dL).

HyperglycemiaSevere hyperglycemia in a person withdiabetes may be the result of intercurrentillness, missed or inadequate medication,or corticosteroid therapy. Correctionalinstitutions should have systems in placeto identify and refer to medical staff allpatients with consistently elevated bloodglucose as well as intercurrent illness.

The stress of illness in those with type1 diabetes frequently aggravates glycemiccontrol and necessitates more frequentmonitoring of blood glucose (e.g., every4–6 h). Marked hyperglycemia requirestemporary adjustment of the treatmentprogram and, if accompanied by ketosis,interaction with the diabetes care team.Adequate fluid and caloric intake mustbe ensured. Nausea or vomiting accom-panied with hyperglycemia may indicateDKA, a life-threatening condition that re-quires immediate medical care to preventcomplications and death. Correctional in-stitutions should identify patients withtype 1 diabetes who are at risk for DKA,particularly those with a prior history offrequent episodes of DKA. For further in-formation see “Hyperglycemic Crisis inDiabetes” (8).

HypoglycemiaHypoglycemia is defined as a blood glu-cose level,70 mg/dL. Severe hypoglyce-mia is a medical emergency defined ashypoglycemia requiring assistance of athird party and is often associated withmental status changes that may includeconfusion, incoherence, combativeness,somnolence, lethargy, seizures, or coma.Signs and symptoms of severe hypogly-cemia can be confused with intoxicationor withdrawal. Individuals with diabetesexhibiting signs and symptoms consistentwith hypoglycemia, particularly alteredmental status, agitation, and diaphoresis,should have their CBG levels checkedimmediately.

Security staff who supervise patientsat risk for hypoglycemia (i.e., those oninsulin or oral hypoglycemic agents)should be educated in the emergency re-sponse protocol for recognition and treat-ment of hypoglycemia. Every attemptshould be made to document CBG before

treatment. Patients must have immediateaccess to glucose tablets or other glucose-containing foods. Hypoglycemia can gen-erally be treated by the patient with oralcarbohydrates. If the patient cannot berelied on to keep hypoglycemia treatmenton his/her person, staff members shouldhave ready access to glucose tablets orequivalent. In general, 15–20 g oral glu-cose will be adequate to treat hypoglyce-mic events. CBG and treatment should berepeated at 15-min intervals until bloodglucose levels return to normal (.70 mg/dL).

Staff should have glucagon for intra-muscular injection or glucose for intra-venous infusion available to treat severehypoglycemia without requiring trans-port of the hypoglycemic patient to anoutside facility. Any episode of severehypoglycemia or recurrent episodes ofmild to moderate hypoglycemia requirereevaluation of the diabetes managementplan by the medical staff. In certain casesof unexplained or recurrent severe hypo-glycemia, it may be appropriate to admitthe patient to the medical unit for obser-vation and stabilization of diabetes man-agement.

Correctional institutions should havesystems in place to identify the patients atgreater risk for hypoglycemia (i.e., thoseon insulin or sulfonylurea therapy) and toensure the early detection and treatmentof hypoglycemia. If possible, patients atgreater risk of severe hypoglycemia (e.g.,those with a prior episode of severehypoglycemia) may be housed in unitscloser to the medical unit in order tominimize delay in treatment.

Recommendationsc Train correctional staff in the recogni-tion, treatment, and appropriate re-ferral for hypo- and hyperglycemia. (E)

c Train appropriate staff to administerglucagon. (E)

c Train staff to recognize symptoms andsigns of serious metabolic decompensa-tion, and immediately refer the patientfor appropriate medical care. (E)

c Institutions should implement a policyrequiring staff to notify a physician ofall CBG results outside of a specifiedrange, as determined by the treatingphysician (e.g.,,50 or.350 mg/dL).(E)

c Identify patients with type 1 diabeteswho are at high risk for DKA. (E)

MEDICATIONdFormularies shouldprovide access to usual and customary

Table 1dSummary of recommendations forglycemic, blood pressure, and lipid controlfor most adults with diabetes

A1C ,7.0%*

Blood pressure ,140/80 mmHg†

LipidsLDL cholesterol

,100 mg/dL(,2.6 mmol/L)‡

*More or less stringent glycemic goals may be ap-propriate for individual patients. Goals should beindividualized based on duration of diabetes, age/lifeexpectancy, comorbid conditions, known CVD oradvancedmicrovascular complications, hypoglycemiaunawareness, individual and patient considerations.†Based on patient characteristics and response totherapy, lower SBP targets may be appropriate. ‡Inindividuals with overt CVD, a lower LDL cholesterolgoal of,70 mg/dL (1.8 mmol/L), using a high doseof a statin, is an option.


Position Statement

oral medications and insulins necessary totreat diabetes and related conditions.While not every brand name of insulinand oral medication needs to be available,individual patient care requires access toshort-, medium-, and long-acting insulinsand the various classes of oral medica-tions (e.g., insulin secretagogues, bigua-nides, a-glucosidase inhibitors, andthiazolidinediones) necessary for currentdiabetes management.

Patients at all levels of custody shouldhave access to medication at dosing fre-quencies that are consistent with theirtreatment plan and medical direction. Iffeasible and consistent with security con-cerns, patients on multiple doses of short-acting oral medications should be placedin a “keep on person” program. In othersituations, patients should be permittedto self-inject insulin when consistentwith security needs. Medical departmentnurses should determine whether patientshave the necessary skill and responsible be-havior to be allowed self-administrationand the degree of supervision necessary.When needed, this skill should be a partof patient education. Reasonable syringecontrol systems should be established.

In the past, the recommendation thatregular insulin be injected 30–45 min be-fore meals presented a significant prob-lem when “lock downs” or otherdisruptions to the normal schedule ofmeals and medications occurred. Theuse of multiple-dose insulin regimens us-ing rapid-acting analogs can decrease thedisruption caused by such changes inschedule. Correctional institutionsshould have systems in place to ensurethat rapid-acting insulin analogs andoral agents are given immediately beforemeals if this is part of the patient’s medicalplan. It should be noted however thateven modest delays in meal consumptionwith these agents can be associated withhypoglycemia. If consistent access to foodwithin 10 min cannot be ensured, rapid-acting insulin analogs and oral agents areapproved for administration during orimmediately after meals. Should circum-stances arise that delay patient access toregular meals following medication ad-ministration, policies and proceduresmust be implemented to ensure the pa-tient receives appropriate nutrition toprevent hypoglycemia.

Both continuous subcutaneous insu-lin infusion and multiple daily insulininjection therapy (consisting of three ormore injections a day) can be effectivemeans of implementing intensive diabetes

management with the goal of achievingnear-normal levels of blood glucose (9).While the use of these modalities may bedifficult in correctional institutions, everyeffort should be made to continue multi-ple daily insulin injection or continuoussubcutaneous insulin infusion in peoplewho were using this therapy before incar-ceration or to institute these therapies asindicated in order to achieve blood glu-cose targets.

It is essential that transport of patientsfrom jails or prisons to off-site appoint-ments, such as medical visits or courtappearances, does not cause significantdisruption in medication or meal timing.Correctional institutions and police lock-ups should implement policies and pro-cedures to diminish the risk of hypo- andhyperglycemia by, for example, providingcarry-along meals and medication forpatients traveling to off-site appointmentsor changing the insulin regimen for thatday. The availability of prefilled insulin“pens” provides an alternative for off-siteinsulin delivery.

Recommendations

c Formularies should provide access tousual and customary oral medicationsand insulins to treat diabetes and re-lated conditions. (E)

c Patients should have access to medi-cation at dosing frequencies that areconsistent with their treatment planand medical direction. (E)

c Correctional institutions and policelock-ups should implement policiesand procedures to diminish the risk ofhypo- and hyperglycemia during off-site travel (e.g., court appearances). (E)

ROUTINE SCREENING FOR ANDMANAGEMENT OF DIABETESCOMPLICATIONSdAll patientswith a diagnosis of diabetes should re-ceive routine screening for diabetes-relatedcomplications, as detailed in the ADAStandards of Care (4). Interval chronicdisease clinics for persons with diabetesprovide an efficient mechanism to monitorpatients for complications of diabetes. Inthis way, appropriate referrals to consul-tant specialists, such as optometrists/ophthalmologists, nephrologists, andcardiologists, can be made on an as-neededbasis and interval laboratory testing canbe done.

The following complications shouldbe considered:

c Foot care: Recommendations for footcare for patients with diabetes and nohistory of an open foot lesion are de-scribed in the ADA Standards of Care.A comprehensive foot examination isrecommended annually for all patientswith diabetes to identify risk factorspredictive of ulcers and amputations.Persons with an insensate foot, an openfoot lesion, or a history of such a lesionshould be referred for evaluation by anappropriate licensed health professional(e.g., podiatrist or vascular surgeon).Special shoes should be provided asrecommended by licensed health pro-fessionals to aid healing of foot lesions andto prevent development of new lesions.

c Retinopathy: Annual retinal examina-tions by a licensed eye care professionalshould be performed for all patientswith diabetes, as recommended in theADA Standards of Care. Visual changesthat cannot be accounted for by acutechanges in glycemic control requireprompt evaluation by an eye care pro-fessional.

c Nephropathy: An annual spot urinetest for determination of microalbumin-to-creatinine ratio should be performed.The use of ACE inhibitors or angiotensinreceptor blockers is recommended forall patients with albuminuria. Bloodpressure should be controlled to ,140/80 mmHg.

c Cardiac: People with type 2 diabetesare at a particularly high risk of coro-nary artery disease. Cardiovasculardisease (CVD) risk factor managementis of demonstrated benefit in reducingthis complication in patients with di-abetes. Blood pressure should be mea-sured at every routine diabetes visit. Inadult patients, test for lipid disorders atleast annually and as needed to achievegoals with treatment. Use aspirin ther-apy (75–162 mg/day) in all adult pa-tients with diabetes and cardiovascularrisk factors or known macrovasculardisease. Current national standards foradults with diabetes call for treatmentof lipids to goals of LDL #100, HDL.40, triglycerides ,150 mg/dL, andblood pressure to a level of ,140/80mmHg.

MONITORING/TESTS OFGLYCEMIAdMonitoring of CBG is astrategy that allows caregivers and peoplewith diabetes to evaluate diabetes man-agement regimens. The frequency ofmonitoring will vary by patients’ glycemiccontrol and diabetes regimens. Patients


Position Statement

with type 1 diabetes are at risk for hypo-glycemia and should have their CBGmonitored three or more times daily. Pa-tients with type 2 diabetes on insulin needto monitor at least once daily and morefrequently based on their medical plan.Patients treated with oral agents shouldhave CBG monitored with sufficient fre-quency to facilitate the goals of glycemiccontrol, assuming that there is a programfor medical review of these data on anongoing basis to drive changes in medica-tions. Patients whose diabetes is poorlycontrolled or whose therapy is changingshould have more frequent monitoring.Unexplained hyperglycemia in a patientwith type 1 diabetes may suggest impend-ing DKA, and monitoring of ketonesshould therefore be performed.

Glycated hemoglobin (A1C) is a mea-sure of long-term (2- to 3-month) glyce-mic control. Perform the A1C test at leasttwo times a year in patients who aremeeting treatment goals (and who havestable glycemic control) and quarterly inpatients whose therapy has changed orwho are not meeting glycemic goals.

Discrepancies between CBGmonitor-ing results and A1C may indicate a he-moglobinopathy, hemolysis, or need forevaluation of CBG monitoring techniqueand equipment or initiation of morefrequent CBG monitoring to identifywhen glycemic excursions are occurringand which facet of the diabetes regimen ischanging.

In the correctional setting, policiesand procedures need to be developed andimplemented regarding CBG monitoringthat address the following:

c infection controlc education of staff and patientsc proper choice of meterc disposal of testing lancetsc quality control programsc access to health servicesc size of the blood samplec patient performance skillsc documentation and interpretation oftest results

c availability of test results for the healthcare provider (10)

Recommendationsc In the correctional setting, policies andprocedures need to be developed andimplemented to enable CBGmonitoringto occur at the frequency necessitated bythe individual patient’s glycemic controland diabetes regimen. (E)

c A1C should be checked every 3–6months. (E)

SELF-MANAGEMENTEDUCATIONdSelf-management ed-ucation is the cornerstone of treatmentfor all people with diabetes. The healthstaff must advocate for patients to partic-ipate in self-management as much aspossible. Individuals with diabetes wholearn self-management skills and makelifestyle changes can more effectivelymanage their diabetes and avoid or delaycomplications associated with diabetes.In the development of a diabetes self-management education program in thecorrectional environment, the unique cir-cumstances of the patient should beconsidered while still providing, to thegreatest extent possible, the elementsof the “National Standards for DiabetesSelf-Management Education and Sup-port” (11). A staged approach may beused depending on the needs assess-ment and the length of incarceration.Table 2 sets out the major componentsof diabetes self-management education.Survival skills should be addressed assoon as possible; other aspects of edu-cation may be provided as part of an on-going education program.

Ideally, self-management educationis coordinated by a certified diabeteseducator who works with the facility todevelop polices, procedures, and proto-cols to ensure that nationally recognizededucation guidelines are implemented.The educator is also able to identifypatients who need diabetes self-manage-ment education, including an assessmentof the patients’ medical, social, and di-abetes histories; diabetes knowledge,skills, and behaviors; and readiness tochange.

STAFF EDUCATIONdPolicies andprocedures should be implemented toensure that the health care staff hasadequate knowledge and skills to directthe management and education of per-sons with diabetes. The health care staffneeds to be involved in the developmentof the correctional officers’ training pro-gram. The staff education programshould be at a lay level. Training shouldbe offered at least biannually, and thecurriculum should cover the following:

c what diabetes isc signs and symptoms of diabetes

c risk factorsc signs and symptoms of, and emergencyresponse to, hypo- and hyperglycemia

c glucose monitoringc medicationsc exercisec nutrition issues including timing ofmeals and access to snacks

Recommendationsc Include diabetes in correctional staffeducation programs. (E)

ALCOHOL AND DRUGSdPatientswith diabetes who are withdrawing fromdrugs and alcohol need special consider-ation. This issue particularly affects initialpolice custody and jails. At an intakefacility, proper initial identification andassessment of these patients are critical.The presence of diabetes may complicatedetoxification. Patients in need of com-plicated detoxification should be referredto a facility equipped to deal with high-risk detoxification. Patients with diabetesshould be educated in the risks involvedwith smoking. All inmates should beadvised not to smoke. Assistance insmoking cessation should be providedas practical.

TRANSFER ANDDISCHARGEdPatients in jails may behoused for a short period of time beforebeing transferred or released, and it is notunusual for patients in prison to be trans-ferred within the system several timesduring their incarceration.One of themanychallenges that health care providers faceworking in the correctional system is howto best collect and communicate importanthealth care information in a timely mannerwhen a patient is in initial police custody, isjailed short term, or is transferred fromfacility to facility. The importance of thiscommunication becomes critical when thepatient has a chronic illness such as di-abetes.

Transferring a patient with diabetesfrom one correctional facility to anotherrequires a coordinated effort. Tofacilitate a thorough review of medicalinformation and completion of a trans-fer summary, it is critical for custodypersonnel to provide medical staff withsufficient notice before movement of thepatient.

Before the transfer, the health carestaff should review the patient’s medicalrecord and complete a medical transfersummary that includes the patient’s


Position Statement

current health care issues. At a mini-mum, the summary should include thefollowing:

c the patient’s current medicationschedule and dosages

c the date and time of the last medicationadministration

c any recent monitoring results (e.g.,CBG and A1C)

c other factors that indicate a need forimmediate treatment ormanagement atthe receiving facility (e.g., recent epi-sodes of hypoglycemia, history of se-vere hypoglycemia or frequent DKA,concurrent illnesses, presence of di-abetes complications)

c information on scheduled treatment/appointments if the receiving facility isresponsible for transporting the patientto that appointment

c name and telephone/fax number of acontact person at the transferring fa-cility who can provide additional in-formation, if needed

Themedical transfer summary, whichacts as a quick medical reference for thereceiving facility, should be transferredalong with the patient. To supplement theflow of information and to increase theprobability that medications are correctlyidentified at the receiving institution,sending institutions are encouraged toprovide each patient with a medicationcard to be carried by the patient thatcontains information concerning diagno-ses, medication names, dosages, and fre-quency. Diabetes supplies, includingdiabetes medication, should accompanythe patient.

The sending facility must be mindfulof the transfer time in order to provide thepatient with medication and food ifneeded. The transfer summary or medicalrecord should be reviewed by a health

care provider upon arrival at the receivinginstitution.

Planning for patients’ discharge fromprisons should include instruction in thelong-term complications of diabetes, thenecessary lifestyle changes and examina-tions required to prevent these complica-tions, and, if possible, where patients mayobtain regular follow-up medical care. Aquarterly meeting to educate patientswith upcoming discharges about commu-nity resources can be valuable. Invitingcommunity agencies to speak at thesemeetings and/or provide writtenmaterialscan help strengthen the community linkfor patients discharging from correctionalfacilities.

Discharge planning for the patientswith diabetes should begin 1 monthbefore discharge. During this time, ap-plication for appropriate entitlementsshould be initiated. Any gaps in thepatient’s knowledge of diabetes careneed to be identified and addressed. Itis helpful if the patient is given a di-rectory or list of community resourcesand if an appointment for follow-up carewith a community provider is made. Asupply of medication adequate to lastuntil the first postrelease medical ap-pointment should be provided to thepatient upon release. The patient shouldbe provided with a written summary ofhis/her current health care issues, in-cluding medications and doses, recentA1C values, etc.

Recommendationsc For all interinstitutional transfers,complete a medical transfer summaryto be transferred with the patient. (E)

c Diabetes supplies and medicationshould accompany the patient duringtransfer. (E)

c Begin discharge planning with ade-quate lead time to insure continuity of

care and facilitate entry into commu-nity diabetes care. (E)

SHARING OF MEDICALINFORMATION ANDRECORDSdPractical considerationsmay prohibit obtaining medical recordsfrom providers who treated the patientbefore arrest. Intake facilities should im-plement policies that 1) define the cir-cumstances under which prior medicalrecords are obtained (e.g., for patientswho have an extensive history of treat-ment for complications); 2) identify per-son(s) responsible for contacting the priorprovider; and 3) establish procedures fortracking requests.

Facilities that use outside medicalproviders should implement policiesand procedures for ensuring that keyinformation (e.g., test results, diagnoses,physicians’ orders, appointment dates) isreceived from the provider and incorpo-rated into the patient’s medical chart aftereach outside appointment. The proce-dure should include, at a minimum, ameans to highlight when key informationhas not been received and designation of aperson responsible for contacting theoutside provider for this information.

All medical charts should containCBG test results in a specified, readilyaccessible section and should be reviewedon a regular basis.

CHILDREN AND ADOLESCENTSWITH DIABETESdChildren andadolescents with diabetes present specialproblems in disease management, evenoutside the setting of a correctional in-stitution. Children and adolescents withdiabetes should have initial and follow-upcare with physicians who are experiencedin their care. Confinement increases thedifficulty in managing diabetes in chil-dren and adolescents, as it does in adultswith diabetes. Correctional authoritiesalso have different legal obligations forchildren and adolescents.

Nutrition and activityGrowing children and adolescents havegreater caloric/nutritional needs thanadults. The provision of an adequateamount of calories and nutrients foradolescents is critical to maintaininggood nutritional status. Physical activityshould be provided at the same time eachday. If increased physical activity occurs,additional CBG monitoring is necessaryand additional carbohydrate snacks maybe required.

Table 2dMajor components of diabetes self-management education

Survival skillsc hypo-/hyperglycemiac sick day managementc medicationc monitoringc foot care

Daily management issuesc disease processc nutritional managementc physical activityc medicationsc monitoringc acute complicationsc risk reductionc goal setting/problem solvingc psychosocial adjustmentc preconception care/pregnancy/gestationaldiabetes management


Position Statement

Medical management and follow-upChildren and adolescents who are incar-cerated for extended periods should havefollow-up visits at least every 3 monthswith individuals who are experienced inthe care of children and adolescents withdiabetes. Thyroid function tests and fast-ing lipid and microalbumin measure-ments should be performed according torecognized standards for children andadolescents (12) in order to monitor forautoimmune thyroid disease and compli-cations and comorbidities of diabetes.

Children and adolescents with diabe-tes exhibiting unusual behavior shouldhave their CBG checked at that time.Because children and adolescents arereported to have higher rates of nocturnalhypoglycemia (13), consideration shouldbe given regarding the use of episodicovernight blood glucose monitoring inthese patients. In particular, this shouldbe considered in children and adolescentswho have recently had their overnight in-sulin dose changed.

PREGNANCYdPregnancy in awoman with diabetes is by definition ahigh-risk pregnancy. Every effort shouldbe made to ensure that treatment of thepregnant woman with diabetes meetsaccepted standards (14,15). It should benoted that glycemic standards are morestringent, the details of dietary manage-ment are more complex and exacting, in-sulin is the only antidiabetic agentapproved for use in pregnancy, and anumber of medications used in the man-agement of diabetic comorbidities areknown to be teratogenic and must be dis-continued in the setting of pregnancy.

SUMMARY AND KEYPOINTSdPeople with diabetes shouldreceive care that meets national stand-ards. Being incarcerated does not changethese standards. Patients must have accessto medication and nutrition needed tomanage their disease. In patients who donot meet treatment targets, medical andbehavioral plans should be adjusted byhealth care professionals in collaboration

with the prison staff. It is critical forcorrectional institutions to identify par-ticularly high-risk patients in need ofmore intensive evaluation and therapy,including pregnant women, patients withadvanced complications, a history of re-peated severe hypoglycemia, or recurrentDKA.

A comprehensive, multidisciplinaryapproach to the care of people with di-abetes can be an effective mechanism toimprove overall health and delay or pre-vent the acute and chronic complicationsof this disease.

AcknowledgmentsdThe following membersof the American Diabetes Association/NationalCommission on Correctional Health CareJoint Working Group on Diabetes Guidelinesfor Correctional Institutions contributed tothe revision of this document: Daniel L.Lorber, MD, FACP, CDE (chair); R. ScottChavez, MPA, PA-C; Joanne Dorman, RN,CDE, CCHP-A; Lynda K. Fisher, MD;Stephanie Guerken, RD, CDE; Linda B. Haas,CDE, RN; Joan V. Hill, CDE, RD; David Ken-dall, MD; Michael Puisis, DO; Kathy Salo-mone, CDE, MSW, APRN; Ronald M.Shansky, MD, MPH; and Barbara Wakeen,RD, LD.

References1. National Commission on Correctional

Health Care: The Health Status of Soon-to-Be Released Inmates: A Report to Congress.Vol. 1. Chicago, NCCHC, 2002

2. Hornung CA, Greifinger RB, Gadre S: AProjection Model of the Prevalence of Se-lected Chronic Diseases in the Inmate Pop-ulation. Vol. 2. Chicago, NCCHC, 2002,p. 39–56

3. Puisis M: Challenges of improving qualityin the correctional setting. In ClinicalPractice in Correctional Medicine. St. Louis,MO, Mosby-Yearbook, 1998, p. 16–18

4. American Diabetes Association: Standardsof medical care in diabetesd2013 (Posi-tion Statement).Diabetes Care36 (Suppl. 1):S11–S66, 2013

5. American Diabetes Association: Screeningfor type 2 diabetes (Position Statement).Diabetes Care 27 (Suppl. 1):S11–S14,2004

6. Krauss RM, Eckel RH, Howard B, AppelLJ, Daniels SR, Deckelbaum RJ, ErdmanJW Jr, Kris-Etherton P, Goldberg IJ,Kotchen TA, Lichtenstein AH, Mitch WE,Mullis R, Robinson K, Wylie-Rosett J, StJeor S, Suttie J, Tribble DL, Bazzarre TL:American Heart Association DietaryGuidelines: revision 2000: a statementfor healthcare professionals from theNutrition Committee of the AmericanHeart Association. Stroke 31:2751–2766,2000

7. American Diabetes Association: Nutritionrecommendations and interventions fordiabetes (Position Statement). DiabetesCare 31 (Suppl. 1):S61–S78, 2008

8. American Diabetes Association: Hyper-glycemic crisis in diabetes (PositionStatement). Diabetes Care 27 (Suppl. 1):S94–S102, 2004

9. American Diabetes Association: Continu-ous subcutaneous insulin infusion (Posi-tion Statement). Diabetes Care 27 (Suppl.1):S110, 2004

10. American Diabetes Association: Tests ofglycemia in diabetes (Position Statement).Diabetes Care 27 (Suppl. 1):S91–S93,2004

11. Haas L, Maryniuk M, Beck J, Cox CE,Duker P, Edwards L, Fisher EB, Hanson L,Kent D, Kolb L, McLaughlin S, Orzeck E,Piette JD, Rhinehart AS, Rothman R,Sklaroff S, Tomky D, Youssef G, on be-half of the 2012 Standards Revision TaskForce: National standards for diabetesself-management education and support.DiabetesCare36 (Suppl. 1):S100–S108, 2013

12. International Society for Pediatric andAdolescent Diabetes: Consensus Guidelines2000: ISPAD Consensus Guidelines for theManagement of Type 1 Diabetes Mellitus inChildren and Adolescents. Zeist, Nether-lands, Medical Forum International, 2000,p. 116, 118

13. Kaufman FR, Austin J, Neinstein A, Jeng L,Halyorson M, Devoe DJ, PitukcheewanontP: Nocturnal hypoglycemia detected withthe continuous glucose monitoring systemin pediatric patients with type 1 diabetes.J Pediatr 141:625–630, 2002

14. American Diabetes Association: Gestationaldiabetes mellitus (Position Statement). Di-abetes Care 27 (Suppl. 1):S88–S90, 2004

15. Jovanovic L (Ed.): Medical Management ofPregnancy Complicated by Diabetes. 4th ed.Alexandria, VA, American Diabetes Asso-ciation, 2009


Position Statement

Diabetes and EmploymentAMERICAN DIABETES ASSOCIATION

A s of 2010, nearly 26 million Amer-icans have diabetes (1), most ofwhom are or wish to be participat-

ing members of the workforce. Diabetesusually has no impact on an individual’sability to do a particular job, and indeedan employer may not even know that agiven employee has diabetes. In 1984,the American Diabetes Associationadopted the following position on em-ployment:

Any person with diabetes, whether insulin[treated] or non–insulin [treated], should beeligible for any employment for which he/sheis otherwise qualified.

Questions are sometimes raised by em-ployers about the safety and effectivenessof individuals with diabetes in a given job.When such questions are legitimatelyraised, a person with diabetes shouldbe individually assessed to determinewhether or not that person can safelyand effectively perform the particularduties of the job in question. This docu-ment provides a general set of guidelinesfor evaluating individuals with diabetesfor employment, including how an as-sessment should be performed and whatchanges (accommodations) in the work-place may be needed for an individualwith diabetes.

I. EVALUATINGINDIVIDUALS WITHDIABETES FOREMPLOYMENTdIt was once com-mon practice to restrict individuals withdiabetes from certain jobs or classes ofemployment solely because of the diag-nosis of diabetes or the use of insulin,without regard to an individual’s abilitiesor circumstances. Such “blanket bans”are medically inappropriate and ignorethe many advancements in diabetes man-agement that range from the types of

medications used to the tools used toadminister them and to monitor bloodglucose levels.

Employment decisions should notbe based on generalizations or stereo-types regarding the effects of diabetes.The impact of diabetes and its manage-ment varies widely among individuals.Therefore, a proper assessment of in-dividual candidates for employment orcurrent employees must take this vari-ability into account.

In addition, federal and state lawsrequire employers to make decisionsthat are based on assessment of thecircumstances and capabilities of theindividual with diabetes for the particu-lar job in question (2,3). Application ofblanket policies to individuals with di-abetes results in people with diabetes be-ing denied employment for which theyare well qualified and fully capable ofperforming effectively and safely. Itshould be noted that, as a result ofamendments to the Americans with Dis-abilities Act, which became effective on1 January 2009, all persons with diabe-tes are considered to have a “disability”within the meaning of that law. This isbecause, among other reasons, diabetesconstitutes a substantial limitation onendocrine system functioningdthe Actwas amended to extend its coverage topersons with a substantial limitation in,among other things, a major bodilyfunction, such as the endocrine system.Therefore, persons with diabetes areprotected from discrimination in em-ployment and other areas. The amend-ments overturned a series of SupremeCourt decisions that had severely nar-rowed who was covered by the law andresulted in many people with diabetesand other chronic illnesses being deniedprotection from discrimination. Thissection provides an overview of the fac-tors relevant to a medically appropriate

individualized assessment of the candi-date or employee with diabetes.

Role of diabetes health careprofessionalsWhen questions arise about the medicalfitness of a person with diabetes for aparticular job, a health care professionalwith expertise in treating diabetes shouldperform an individualized assessment.The involvement of the diabetes healthcare professional should occur before anyadverse employment decision, such asfailure to hire or promote or termination.A health professional who is familiar withthe person with diabetes and who hasexpertise in treating diabetes is best ableto perform such an assessment. In somesituations and in complex cases, anendocrinologist or a physician who spe-cializes in treating diabetes or its compli-cations is the best qualified healthprofessional to assume this responsibility(4). The individual’s treating physician isgenerally the health care professionalwith the best knowledge of an individ-ual’s diabetes. Thus, even when the em-ployer utilizes its own physician toperform the evaluation, the opinions ofthe treating physician and other healthcare professionals with clinical expertisein diabetes should be sought out andcarefully considered. In situations wherethere is disagreement between the opin-ion of the employee’s treating physicianand that of the employer’s physician, theevaluation should be handed over to anindependent health care professionalwith significant clinical expertise indiabetes.

Individual assessmentA medical evaluation of an individualwith diabetes may occur only in limitedcircumstances (3). Employers may not in-quire about an individual’s health statusddirectly or indirectly and regardless ofthe type of jobdbefore making a job of-fer, but may require a medical examina-tion or make a medical inquiry once anoffer of employment has been extendedand before the individual begins the job.


Revised Fall 2009.DOI: 10.2337/dc13-S093© 2013 by the American Diabetes Association. Readers may use this article as long as the work is properly






The job offer may be conditioned on theresults of the medical inquiry or examina-tion. An employer may withdraw an offerfrom an applicant with diabetes only if itbecomes clear that he or she cannot do theessential functions of the job or wouldpose a direct threat (i.e., a significantrisk of substantial harm) to health orsafety and such threat could not be elim-inated with an accommodation (a work-place change that enables a worker with adisability to safely and effectively performjob duties). Another situation in whicha medical evaluation is permissible iswhen a problem potentially related tothe employee’s diabetes arises on the joband such problem could affect job perfor-mance and/or safety. In this situation, aphysician may be asked to evaluate theemployee’s fitness to remain on the joband/or his or her ability to safely performthe job.

Employers also may obtain medicalinformation about an employee when theemployee has requested an accomoda-tion and his or her disability or need foraccommodation is not obvious. An em-ployer should not rely on a medicalevaluation to deny an employment op-portunity to an individual with diabetesunless it is conducted by a health careprofessional with expertise in diabetes andbased on sufficient and appropriate med-ical data. The information sought andassessed must be properly limited to datarelevant to the individual’s diabetes andjob performance (3). The data needed willvary depending on the type of job and thereason for the evaluation, but an evalu-ation should never be made based onlyon one piece of data, such as a single bloodglucose result or A1C result. Since diabetesis a chronic disease in which health statusand management requirements naturallychange over time, it is inappropriatedand medically unnecessarydfor exam-iners to collect all past laboratory valuesor information regarding office visitswhether or not related to diabetes.Only medical information relevant toevaluating an individual’s current capac-ity for safe performance of the particularjob at issue should be collected. For ex-ample, in some circumstances a review ofan individual’s hypoglycemia historymaybe relevant to the evaluation and shouldbe collected.

Information about the individual’sdiabetes management (such as the currenttreatment regimen, medications, andblood glucose logs), job duties, andwork environment are all relevant factors

to be considered. Only health care profes-sionals tasked with such evaluationsshould have access to employee medicalinformation, and this information must bekept separate from personnel records (3).

Screening guidelinesA number of screening guidelines forevaluating individuals with diabetes invarious types of high risk jobs have beendeveloped in recent years. Examples in-clude the American College of Occupa-tional and Environmental Medicine’sNational Consensus Guideline for theMedical Evaluation of Law EnforcementOfficers, the National Fire ProtectionAssociation’s Standard on Comprehen-sive Occupational Medical Program forFire Departments, the U.S. Departmentof Transportation’s Federal Motor Car-rier Safety Administration’s DiabetesExemption Program, and the U.S. MarshallService and Federal Occupational HealthLaw Enforcement Program DiabetesProtocol.

Such guidelines and protocols can beuseful tools in making decisions aboutindividual candidates or employees ifthey are used in an objective way andbased on the latest scientific knowledgeabout diabetes and its management.These protocols should be regularly reeval-uated and updated to reflect changes indiabetes knowledge and evidence andshould be developed and reviewed byhealth care professionals with significantexperience in diabetes and its treatment.Individuals who do not meet the standardsset forth in such protocols should be giventhe opportunity to demonstrate excep-tional circumstances that would justifydeviating from the guidelines. Such guide-lines or protocols are not absolute criteriabut rather the framework for a thoroughindividualized assessment.

Recommendationsc People with diabetes should be in-dividually considered for employmentbased on the requirements of the spe-cific job and the individual’s medicalcondition, treatment regimen, andmedical history. (E)

c When questions arise about the medicalfitness of a person with diabetes for aparticular job, a health care professionalwith expertise in treating diabetesshould perform an individualized as-sessment; input from the treating phy-sician should always be included. (E)

c Employment evaluations should bebased on sufficient and appropriate

medical data and should never bemade based solely on one piece ofdata. (E)

c Screening guidelines and protocols canbe useful tools in making decisionsabout employment if they are used inan objective way and based on the latestscientific knowledge about diabetesand its management. (E)

II. EVALUATING THESAFETY RISK OFEMPLOYEES WITHDIABETESdEmployers who deny jobopportunities because they perceive allpeople with diabetes to be a safety riskdo so based on misconceptions, misin-formation, or a lack of current informationabout diabetes. The following guidelinesprovide information for evaluating an in-dividual with diabetes who works or seekstowork inwhatmaybe considered a safety-sensitive position.

Safety concernsThe first step in evaluating safety con-cerns is to determine whether the con-cerns are reasonable in light of the jobduties the individual must perform. Formost types of employment (such as jobsin an office, retail, or food service envi-ronment) there is no reason to believe thatthe individual’s diabetes will put employ-ees or the public at risk. In other types ofemployment (such as jobs where theindividual must carry a firearm or oper-ate dangerous machinery) the safety con-cern is whether the employee willbecome suddenly disoriented or inca-pacitated. Such episodes, which are usu-ally due to severely low blood glucose(hypoglycemia), occur only in peoplereceiving certain treatments such as in-sulin or secretagogues such as sulfonyl-ureas and even then occur infrequently.Workplace accommodations can bemade that are minimal yet effective inhelping the individual to manage his orher diabetes on the job and avoid severehypoglycemia.

HypoglycemiaHypoglycemia is defined as a bloodglucose level ,70 mg/dL (4,6). It is apotential side effect of some diabetestreatments, including insulin and sul-fonlyureas. It can usually be effectivelyself-treated by ingestion of glucose (carbo-hydrate) and is not often associated withloss of consciousness or a seizure. Severehypoglycemia, requiring the assistance ofanother person, is a medical emergency.


Position Statement

Symptoms of severe hypoglycemia mayinclude confusion or, rarely, seizure orloss of consciousness (6). Most individu-als with diabetes never experience an ep-isode of severe hypoglycemia becauseeither they are not on medication thatcauses it or they recognize the early warn-ing signs and can quickly self-treat theproblem by drinking or eating. Also,with self-monitoring of blood glucoselevels, most people with diabetes canmanage their condition in such a mannerthat there is minimal risk of incapacita-tion from hypoglycemia because mildlylow glucose levels can be easily detectedand treated (4,7).

A single episode of severe hypoglyce-mia should not per se disqualify an in-dividual from employment. Rather, anappropriate evaluation should be under-taken by a health care professional withexpertise in diabetes to determine thecause of the low blood glucose, the cir-cumstances of the episode, whether it wasan isolated incident, whether adjustmentto the insulin regimen may mitigate thisrisk, and the likelihood of such an episodehappening again. Some episodes of severehypoglycemia can be explained and cor-rected with the assistance of a diabeteshealth care professional.

However, recurrent episodes of se-vere hypoglycemia may indicate that anindividual may in fact not be able to safelyperform a job, particularly jobs or tasksinvolving significant risk of harm to em-ployees or the public, especially whenthese episodes cannot be explained. Theperson’s medical history and details ofany history of severe hypoglycemiashould be examined closely to determinewhether it is likely that such episodes willrecur on the job. In all cases, job dutiesshould be carefully examined to deter-mine whether there are ways to minimizethe risk of severe hypoglycemia (such asadjustment of the insulin regimen orproviding additional breaks to checkblood glucose levels).

HyperglycemiaIn contrast to hypoglycemia, high bloodglucose levels (hyperglycemia) can causelong-term complications over years or de-cades but does not normally lead to anyadverse effect on job performance. Thesymptoms of hyperglycemia generally de-velop over hours or days and do not occursuddenly. Therefore, hyperglycemia doesnot pose an immediate risk of sudden in-capacitation.While over years or decades,high blood glucose may cause long-term

complications to the nerves (neuropa-thy), eyes (retinopathy), kidneys (ne-phropathy), or heart, not all individualswith diabetes develop these long-termcomplications. Such complications be-come relevant in employment decisionsonly when they are established and in-terfere with the performance of the actualjob being considered. Evaluations shouldnot be based on speculation as to whatmight occur in the future. Job evaluationsshould take high blood glucose levels intoaccount only if they have already causedlong-term complications such as visualimpairment that interfere with perfor-mance of the specific job.

Aspects of a safety assessmentWhen an individual with diabetes isassessed for safety risk there are severalaspects that must be considered.Blood glucose test results. A singleblood glucose test result only gives infor-mation about an individual’s blood glucoselevel at one particular point in time. Be-cause blood glucose levels fluctuatethroughout the day (this is also true forpeople without diabetes), one test result isof no use in assessing the overall health of aperson with diabetes. The results of a seriesof self-monitored blood glucose measure-ments over a period of time, however, cangive valuable information about an indi-vidual’s diabetes health. Blood glucose re-cords should be assessed by a health careprofessional with expertise in diabetes (7).History of severe hypoglycemia. Of-ten, a key factor in assessing employmentsafety and risk is documentation of in-cidents of severe hypoglycemia. An in-dividual who has managed his or herdiabetes over an extended period of timewithout experiencing severe hypoglyce-mia is unlikely to experience this condi-tion in the future. Conversely, multipleincidents of severe hypoglycemia mayin some situations be disqualifying forhigh-risk occupations. However, thecircumstances of each incident shouldbe examined, as some incidents can beexplained due to changes in insulin dos-age, illness, or other factors and thus willbe unlikely to recur or have already beenaddressed by the individual throughchanges to his or her diabetes treatmentregimen or education.Hypoglycemia unawareness. Some in-dividuals over time lose the ability torecognize the early warning signs of hypo-glycemia. These individuals are at increasedrisk for a sudden episode of severe hypo-glycemia. Some of these individuals may

be able to lessen this risk with carefulchanges to their diabetes managementregimen (for example, more frequentblood glucose testing or frequent meals).Presence of diabetes-related complica-tions. Chronic complications that mayresult from long-term diabetes involve theblood vessels and nerves. These compli-cations may involve nerve (neuropathy),eye (retinopathy), kidney (nephropathy),and heart disease. In turn, these problemscan lead to amputation, blindness or othervision problems, including vision loss,kidney failure, stroke, or heart attack. Asthese complications could potentially affectjob performance and safety, such compli-cations should be evaluated by a specialistin the specific area related to the compli-cation. If complications are not present,their possible future development shouldnot be addressed, both because of lawsprohibiting such consideration and be-cause with medical monitoring and thera-pies, long-term complications can nowoften be avoided or delayed. Thus, manypeople with diabetes never develop any ofthese complications, and those that dogenerally develop them over a period ofyears.

Inappropriate assessmentsThe following tools and terms do notaccurately reflect the current state of di-abetes treatment and should be avoidedin an assessment of whether an individualwith diabetes is able to safely and effec-tively perform a particular job.Urine glucose tests. Urine glucose re-sults are no longer considered to be anappropriate and accurate methodologyfor assessing diabetes control (8). Beforethe mid-1970s, urine glucose tests werethe best available method of monitoringblood glucose levels. However, the urinetest is not a reliable or accurate indicatorof blood glucose levels and is a poor mea-sure of the individual’s current health sta-tus. Blood glucose monitoring is a moreaccurate and timely means to measureglycemic control. Urine glucose testsshould never be used to evaluate the em-ployability of a person with diabetes.A1C and estimated average glucose.Hemoglobin A1C (A1C) test results re-flect average glycemia over severalmonths and correlate with mean plasmaglucose levels (4). Estimated average glu-cose (eAG) is directly related to A1C andalso provides an individual with an esti-mate of average blood glucose over a pe-riod of time, but it uses the same valuesand units that are observed when using a


Position Statement

glucose meter or recording a fasting glu-cose value on a lab report (5). A1C/eAGvalues provide health care providers withimportant information about the effec-tiveness of an individual’s treatment regi-men (4) but are oftenmisused in assessingwhether an individual can safelyperform a job. Because they identifyonly averages and not whether the personhad severe extreme blood glucose read-ings, A1C/eAG results are of no value inpredicting short-term complications ofdiabetes and thus have no use in evaluat-ing individuals in employment situations.

The American Diabetes Associationrecommends that in most patients A1Clevels be kept below 7% (4), or eAG below154 mg/dL. This recommendation sets atarget in order to lessen the chances oflong-term complications of high bloodglucose levels but does not provide usefulinformation on whether the individual isat significant risk for hypoglycemia orsuboptimal job performance and is not ameasure of “compliance” with therapy.An A1C or eAG cut off score is not med-ically justified in employment evaluationsand should never be a determinative fac-tor in employment.“Uncontrolled” or “brittle” diabetes.Sometimes an individual’s diabetes is de-scribed as “uncontrolled,” “poorly con-trolled,” or “brittle.” These terms are notwell defined and are not relevant to jobevaluations. As such, giving an opinionon the level of “control” an individualhas over diabetes is not the same as assess-ing whether that individual is qualified toperform a particular job and can do sosafely. Such an individual assessment isthe only relevant evaluation.

Recommendationsc Evaluating the safety risk of employeeswith diabetes includes determiningwhether the concerns are reasonable inlight of the job duties the individualmust perform. (E)

c Most people with diabetes can managetheir condition in such a manner thatthere is no or minimal risk of incapaci-tation from hypoglycemia at work. Asingle episode of severe hypoglycemiashould not per se disqualify an individ-ual from employment, but an individualwith recurrent episodes of severe hypo-glycemia may be unable to safely per-form certain jobs, especially when thoseepisodes cannot be explained. (E)

c Hyperglycemia does not pose an imme-diate risk of sudden incapacitation onthe job, and long-term complications

are relevant in employment decisionsonly when they are established andinterfere with the performance of theactual job being considered. (E)

c Proper safety assessments should in-clude review of blood glucose test re-sults, history of severe hypoglycemia,presence of hypoglycemia unawareness,and presence of diabetes-related com-plications and should not include urineglucose or AIC/eAG tests or be basedon a general assessment of level of con-trol. (E)

III. ACCOMMODATINGEMPLOYEES WITHDIABETESdIndividuals with diabetesmay need certain changes or accommo-dations on the job in order to performtheir work responsibilities effectively andsafely. Federal and state laws require theprovision of “reasonable accommodations”to help an employee with diabetes to per-form the essential functions of the job (3).Additional lawsprovide for leave for an em-ployee to deal with his or hermedical needsor those of a family member (9). Althoughthere are some typical accommodationsthat many people with diabetes use, theneed for accommodations must be as-sessed on an individualized basis (2).

Accommodating daily diabetesmanagement needsMany of the accommodations that em-ployees with diabetes need on a day-to-day basis are those that allow them tomanage their diabetes in the workplace asthey would elsewhere. They are usuallysimple accommodations, can be providedwithout any cost to the employer, andshould cause little or no disruption in theworkplace. Most employers are requiredto provide accommodations unless thoseaccommodations would create an undueburden (3). Some accommodations thatmay be needed include the following.Testing blood glucose. Breaks may beneeded to allow an individual to testblood glucose levels when needed. Suchchecks only take minutes to complete.Some individuals use continuous glucosemonitors but will still need an opportu-nity to check blood glucose with a meter.Blood glucose can be checked whereverthe employee is without putting otheremployees at risk, and employers shouldnot limit where employees with diabetesare permitted to manage their diabetes.Some employees may prefer to have a pri-vate location for testing or other diabetes

care tasks that should be provided when-ever feasible.Administering insulin. Employees mayneed short breaks during the workday toadminister insulin when it is needed.Insulin can be safely administered wher-ever the employee happens to be. Theemployee may also need a place to storeinsulin and other supplies if work con-ditions (such as extreme temperatures)prevent the supplies from being carriedon the person (10).Food and drink. Employees may needaccess to food and/or beverages duringthe workday. This is particularly impor-tant in the event that the employee needsto quickly respond to low blood glucoselevels or maintain hydration if glucoselevels are high. Employees should bepermitted to consume food or beveragesas needed at their desk or work station(except in an extremely rare situation inwhich this would pose a hazard andcreate a safety issue, and if this is the case,an alternative site should be provided).Leave. Employees may need leave or aflexible work schedule to accommodatemedical appointments or other diabetescare needs. Occasionally, employees mayneed to miss work due to unanticipatedevents (severe hypoglycemic episode) orillness.Work schedules. Certain types of workschedules, such as rotating or split shifts,can make it especially difficult for someindividuals to manage diabetes effec-tively.

Accommodating complications ofdiabetesIn addition to accommodating the day-to-day management of diabetes in the work-place, for some individuals it is alsonecessary to seek modifications for long-term diabetes-related complications.Such people can remain productive em-ployees if appropriate accommodationsare implemented.

For example, an employee with di-abetic retinopathy or other vision impair-ments may benefit from using a big screencomputer or other visual aids, while anemployee with nerve pain may benefitfrom reduced walking distances or havingthe ability to sit down on the job. Indi-viduals with kidney problems may needto have flexibility to take time off work fordialysis treatment.

It is impossible to provide an exhaus-tive list of potential accommodations. Thekey message in accommodating an em-ployee with diabetes is to ensure that


Position Statement

accommodations are tailored to the in-dividual and effective in helping the in-dividual perform his or her job. Inputfrom health care professionals who spe-cialize in the particular complication, orfrom vocational rehabilitation specialistsor organizations, may help identify appro-priate accommodations.

Recommendationsc Individuals with diabetes may needaccommodations on the job in orderto perform their work responsibilitieseffectively and safely; these includeaccommodating daily diabetes needsand, when present, the complicationsof diabetes. All such accommodationsmust be tailored to the individual andeffective in helping the individual per-form his or her job. (E)

CONCLUSIONdIndividuals with di-abetes can and do serve as highly pro-ductive members of the workforce. Whilenot every individual with diabetes willbe qualified for, nor can perform, everyavailable job, reasonable accommoda-tions can readily be made that allow thevast majority of people with diabetes toeffectively perform the vast majority of

jobs. The therapies for, and effects of,diabetes vary greatly from person to per-son, so employers must consider eachperson’s capacities and needs on an in-dividual basis. People with diabetesshould always be evaluated individuallywith the assistance of experienced dia-betes health care professionals. The re-quirements of the specific job and theindividual’s ability to perform that job,with or without reasonable accommoda-tions, always need to be considered.

AcknowledgmentsdThe American DiabetesAssociation thanks the members of the vol-unteer writing group for this updated state-ment: John E. Anderson, MD; Michael A.Greene, JD; John W. Griffin, Jr., JD; Daniel B.Kohrman, JD; Daniel Lorber, MD, FACP, CDE;Christopher D. Saudek, MD; Desmond Schatz,MD; and Linda Siminerio, RN, PhD, CDE.


vention: National Diabetes Fact Sheet:General Information and National Estimateson Diabetes and Prediabetes in the U.S., 2011.Atlanta, GA,U.S.Department ofHealth andHuman Services, Centers for Disease Con-trol and Prevention, 2011

2. Equal Employment Opportunity Com-mission: Questions and Answers AboutDiabetes in the Workplace and theAmericans with Disabilities Act (ADA),Oct. 29, 2003. Available from http://www.eeoc.gov/facts/diabetes.html. Accessed 26May 2008

3. Americans with Disabilities Act of 1990,42 U.S.C. x12101 et seq.

4. American Diabetes Association: Standardsof medical care in diabetesd2013 (Posi-tion Statement). Diabetes Care 2013;36(Suppl. 1): S11–S66

5. Nathan DM, Kuenen J, Borg R, Zheng H,Schoenfeld D, Heine R: Translating theA1C assay into estimated average glucosevalues. Diabetes Care 31: 1473–1478, 2008

6. American Diabetes Association: Definingand reporting hypoglycemia in diabetes,a report from the American Diabetes As-sociation Workgroup on Hypoglycemia.Diabetes Care 28: 1245–1249, 2005

7. American Diabetes Association: Self-monitoring of blood glucose (ConsensusStatement). Diabetes Care 17: 81–86, 1994

8. American Diabetes Association: Tests ofglycemia in diabetes (Position Statement).Diabetes Care 27 (Suppl. 1): S91–S93,2004

9. FamilyMedical LeaveAct of 1993, 29U.S.C.x2601 et seq.

10. American Diabetes Association: Insulin ad-ministration (Position Statement). DiabetesCare 27 (Suppl. 1): S106–S109, 2004


Position Statement

http://www.eeoc.gov/facts/diabetes.html

http://www.eeoc.gov/facts/diabetes.html

Third-Party Reimbursement forDiabetesCare, Self-Management Education,and SuppliesAMERICAN DIABETES ASSOCIATION

D iabetes is a chronic disease that af-fects nearly 26 million Americans(1) and is characterized by serious,

costly, and often fatal complications. Thetotal cost of diagnosed diabetes in the U.S.in 2007 was estimated to be $174 billion(2). To prevent or delay costly diabetescomplications and to enable people withdiabetes to lead healthy, productive lives,appropriate medical care based on currentstandards of practice, self-managementeducation, and medication and suppliesmust be available to everyone with diabe-tes. This article is based on technical re-views titled “Diabetes Self-ManagementEducation” (3) and “National Standardsfor Diabetes Self-Management EducationPrograms” (4).

The goal of medical care for peoplewith diabetes is to optimize glycemic con-trol and minimize complications. The Di-abetes Control and Complications Trial(DCCT) demonstrated that treatment thatmaintains blood glucose levels near nor-mal in type 1 diabetes delays the onsetand reduces the progression of microvas-cular complications. The UK ProspectiveDiabetes Study (UKPDS) documentedthat optimal glycemic control can alsobenefit most individuals with type 2 dia-betes. To achieve optimal glucose control,the person with diabetes must be able toaccess health care providers who have ex-pertise in the field of diabetes. Treatmentplans must also include self-managementtraining and tools, regular and timely lab-oratory evaluations, medical nutritiontherapy, appropriately prescribed medi-cation(s), and regular self-monitoring ofblood glucose levels. The American Dia-betes Association position statement“Standards of Medical Care in Diabetes”

outlines appropriate medical care for peo-ple with diabetes (5).

An integral component of diabetescare is self-management education (in-patient and/or outpatient) delivered by aninterdisciplinary team. Self-managementtraining helps people with diabetes adjusttheir daily regimen to improve glycemiccontrol. Diabetes self-management edu-cation teaches individuals with diabetesto assess the interplay among medicalnutrition therapy, physical activity, emo-tional/physical stress, and medications,and then to respond appropriately andcontinually to those factors to achieve andmaintain optimal glucose control.

Today, self-management education isunderstood to be such a critical part ofdiabetes care that medical treatment of di-abeteswithout systematic self-managementeducation is regarded as inadequate. TheNational Standards for Diabetes Self-Management Education and Support estab-lish specific criteria against which diabeteseducation programs can be measured,and a quality assurance program has beendeveloped and subsequently revised (6).

Treatments and therapies that im-prove glycemic control and reduce thecomplications of diabetes will also signif-icantly reduce health care costs (7,8). Nu-merous studies have demonstrated thatself-management education leads to re-ductions in the costs associated with alltypes of diabetes. Participants in self-management education programs havebeen found to have decreased lower-extremity amputation rates, reducedmedication costs, and fewer emergencyroom visits and hospitalizations.

To achieve optimal glycemic control,thus achieving long-term reduction in

health care costs, individuals with dia-betes must have access to the integralcomponents of diabetes care, such ashealth care visits, diabetes supplies, self-management education, and diabetes med-ications. As such, insurers must reimbursefor diabetes-related medical treatment aswell as for self-management educationprograms that have met accepted stand-ards, such as the American Diabetes Asso-ciation’s National Standards for DiabetesSelf-Management Education and Support.Furthermore, third-party payers must alsoreimburse for medications and suppliesrelated to the daily care of diabetes. Thesesame standards should also apply to or-ganizations that purchase health care ben-efits for their members or employees, aswell as managed care organizations thatprovide services to participants.

It is recognized that the use of formu-laries, prior authorization, competitivebidding, and related provisions (hereafterreferred to as “controls”) can manage pro-vider practices and costs to the potentialbenefit of payors and patients. Social Se-curity Act Title XIX, section 1927, statesthat excluded medications should nothave “a significant clinically meaningfultherapeutic advantage in terms of safety,effectiveness or clinical outcomes of suchtreatment of such population.”A variety oflaws, regulations, and executive ordersalso provide guidance on the use of suchcontrols to oversee the purchase and useof durable medical equipment (hereafterreferred to as “equipment”) and single-use medical supplies (hereafter referredto as “supplies”) associated with the man-agement of diabetes.

Certain principles should guide thecreation and enforcement of controls inorder to insure that they meet the com-prehensive medical needs of people livingwith diabetes. A wide array of medicationsand supplies are correlated with improvedglycemic outcomes and a reduction in therisk of diabetes-related complications. Be-cause no single diabetes treatment regimenis appropriate for all people with diabetes,providers and patients should have accessto a broad array ofmedications and suppliesto develop an effective treatment modality.


The recommendations in this article are based on the evidence reviewed in the following publications: Diabetesself-management education (Technical Review). Diabetes Care 18:1204–1214, 1995, and National stand-ards for diabetes self-management education and support. Diabetes Care 35:2393–2401, 2012.

Approved 1995. Revised 2008.DOI: 10.2337/dc13-S098© 2013 by the American Diabetes Association. Readers may use this article as long as the work is properly






However, the Association also recognizesthat there may be a number of medica-tions and/or supplies within any givenclass. As such, any controls should ensurethat all classes of antidiabetic agents withunique mechanisms of action are avail-able to facilitate achieving glycemic goalsto reduce the risk of complications. Sim-ilar issues operate in the management oflipid disorders, hypertension, and othercardiovascular risk factors, as well as forother diabetes complications. Further-more, any controls should ensure thatall classes of equipment and suppliesdesigned for use with such equipment areavailable to facilitate achieving glycemicgoals to reduce the risk of complications.It is important to note that medical ad-vances are rapidly changing the landscapeof diabetes medications and supplies. Toensure that patients with diabetes haveaccess to beneficial updates in treatmentmodalities, systems of controls must em-ploy efficient mechanisms through whichto introduce and approve new products.

Though it can seem appropriate forcontrols to restrict certain items in chronicdisease management, particularly with acomplex disorder such as diabetes, itshould be recognized that adherence is amajor barrier to achieving targets. Anycontrols should take into account thehuge mental and physical burden that in-tensive disease management exerts uponpatients with diabetes. Protections shouldensure that patients with diabetes canreadily comply with therapy in the widely

variable circumstances encountered indaily life. These protections should guar-antee access to an acceptable range andall classes of antidiabetic medications,equipment, and supplies. Furthermore,fair and reasonable appeals processesshould ensure that diabetic patients andtheir medical care practitioners can obtainmedications, equipment, and suppliesthat are not contained within existentcontrols.

Diabetes management needs individu-alization in order for patients to reachglycemic targets. Because there is diversityin the manifestations of the disease and inthe impact of other medical conditionsupon diabetes, it is common that practi-tioners will need to uniquely tailor treat-ment for their patients. To reach diabetestreatment goals, practitioners shouldhave access to all classes of antidiabeticmedications, equipment, and supplieswithout undue controls. Without appro-priate safeguards, these controls couldconstitute an obstruction of effective care.

The value of self-management edu-cation and provision of diabetes supplieshas been acknowledged by the passageof the Balanced Budget Act of 1997 (9)and by stated medical policy on both di-abetes education and medical nutritiontherapy.

References1. Centers for Disease Control and Preven-

tion: National estimates and general

information on diabetes and prediabetes in theU.S., 2011. Atlanta, GA, U.S. Department ofHealth and Human Services, Centers forDisease Control and Prevention, 2011

2. American Diabetes Association: Economiccosts of diabetes in the U.S. in 2007. Di-abetes Care 31: 596–615, 2008

3. Clement S: Diabetes self-management ed-ucation (Technical Review). Diabetes Care18: 1204–1214, 1995

4. Funnell MM, Haas LB: National standardsfor diabetes self-management educationprograms (Technical Review). DiabetesCare 18: 100–116, 1995

5. American Diabetes Association: Standardsof medical care in diabetesd2013 (PositionStatement). Diabetes Care 36 (Suppl. 1):S11–S66, 2013

6. Haas L, Maryniuk M, Beck J, Cox CE,Duker P, Edwards L, Fisher EB, Hanson L,Kent D, Kolb L, McLaughlin S, Orzeck E,Piette JD, Rhinehart AS, Rothman R,Sklaroff S, Tomky D, Youssef G, on behalfof the 2012 Standards Revision TaskForce: National standards for diabetesself-management education and support.Diabetes Care 35: 2393–2401, 2012

7. Herman WH, Dasbach DJ, Songer TJ,Thompson DE, Crofford OB: Assessingthe impact of intensive insulin therapy onthe health care system.Diabetes Rev 2: 384–388, 1994

8. Wagner EH, Sandu N, Newton KM,McCullock DK, Ramsey SD, Grothaus LC:Effects of improved glycemic control onhealth care costs and utilization. JAMA 285:182–189, 2001

9. Balanced Budget Act of 1997. U.S. Govt.Printing Office, 1997, p. 115–116 (publ.no. 869-033-00034-1)


Position Statement

National Standards for DiabetesSelf-Management Education andSupportLINDA HAAS, PHC, RN, CDE (CHAIR)1

MELINDA MARYNIUK, MED, RD, CDE (CHAIR)2

JONI BECK, PHARMD, CDE, BC-ADM3

CARLA E. COX, PHD, RD, CDE, CSSD4

PAULINA DUKER, MPH, RN, BC-ADM, CDE5

LAURA EDWARDS, RN, MPA6

EDWIN B. FISHER, PHD7

LENITA HANSON, MD, CDE, FACE, FACP8

DANIEL KENT, PHARMD, BS, CDE9

LESLIE KOLB, RN, BSN, MBA10

SUE MCLAUGHLIN, BS, RD, CDE, CPT11

ERIC ORZECK, MD, FACE, CDE12

JOHN D. PIETTE, PHD13

ANDREW S. RHINEHART, MD, FACP, CDE14

RUSSELL ROTHMAN, MD, MPP15

SARA SKLAROFF16

DONNA TOMKY, MSN, RN, C-NP, CDE, FAADE17

GRETCHEN YOUSSEF, MS, RD, CDE18

ON BEHALF OF THE 2012 STANDARDSREVISION TASK FORCE

By the most recent estimates, 18.8mil-lion people in the U.S. have been di-agnosed with diabetes and an

additional 7 million are believed to be liv-ingwith undiagnosed diabetes. At the sametime, 79 million people are estimated tohave blood glucose levels in the range ofprediabetes or categories of increased riskfor diabetes. Thus, more than 100 millionAmericans are at risk for developing thedevastating complications of diabetes (1).

Diabetes self-management education(DSME) is a critical element of care for allpeople with diabetes and those at risk fordeveloping the disease. It is necessary inorder to prevent or delay the complicationsof diabetes (2–6) and has elements re-lated to lifestyle changes that are also es-sential for individuals with prediabetes aspart of efforts to prevent the disease (7,8).

The National Standards for Diabetes Self-Management Education are designedto define quality DSME and support andto assist diabetes educators in provid-ing evidence-based education and self-management support. The Standardsare applicable to educators in solo prac-tice as well as those in large multicenterprogramsdand everyone in between.There are many good models for the pro-vision of diabetes education and support.The Standards do not endorse any one ap-proach, but rather seek to delineate thecommonalities among effective and excel-lent self-management education strate-gies. These are the standards used inthe field for recognition and accred-itation. They also serve as a guide for non-accredited and nonrecognized providersand programs.

Because of the dynamic nature ofhealth care and diabetes-related research,the Standards are reviewed and revisedapproximately every 5 years by key stake-holders and experts within the diabeteseducation community. In the fall of2011, a Task Force was jointly convenedby the American Association of DiabetesEducators (AADE) and the American Di-abetes Association (ADA).Members of theTask Force included experts from theareas of public health, underserved pop-ulations including rural primary care andother rural health services, individualpractices, large urban specialty practices,and urban hospitals. They also includedindividualswith diabetes, diabetes research-ers, certified diabetes educators, registerednurses, registered dietitians, physicians,pharmacists, and a psychologist. The TaskForce was charged with reviewing thecurrent National Standards for DiabetesSelf-Management Education for their ap-propriateness, relevance, and scientific basisand updating them based on the availableevidence and expert consensus.

The Task Force made the decision tochange the name of the Standards fromthe National Standards for Diabetes Self-Management Education to the NationalStandards for Diabetes Self-ManagementEducation and Support. This name changeis intended to codify the significance ofongoing support for people with diabetesand those at risk for developing the disease,particularly to encourage behavior change,themaintenance of healthydiabetes-relatedbehaviors, and to address psychosocialconcerns. Given that self-managementdoes not stop when a patient leaves theeducator’s office, self-management supportmust be an ongoing process.

Although the term “diabetes” is usedpredominantly, the Standards should alsobe understood to apply to the educationand support of people with prediabetes.Currently, there are significant barriersto the provision of education and supportto those with prediabetes. And yet, thestrategies for supporting successful be-havior change and the healthy behaviorsrecommended for people with prediabe-tes are largely identical to those for


From the 1VA Puget Sound Health Care System Hospital and Specialty Medicine, Seattle, Washington; the2Joslin Diabetes Center, Boston, Massachusetts; 3Pediatric Diabetes and Endocrinology, The University ofOklahomaHealth Sciences Center College ofMedicine, Edmond,Oklahoma; the 4WesternMontana Clinic,Missoula, Montana; the 5Diabetes Education/Clinical Programs, American Diabetes Association, Alexan-dria, Virginia; the 6Center for Healthy North Carolina, Apex, North Carolina; 7Peers for Progress, AmericanAcademy of Family Physicians Foundation and Department of Health Behavior, Gillings School of GlobalPublic Health, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; 8UltracareEndocrine and Diabetes Consultants, Venice, Florida; the 9Group Health Central Specialty Clinic, Seattle,Washington; the 10Diabetes Education Accreditation Program, American Association of Diabetes Educators,Chicago, Illinois; 11On Site Health and Wellness, LLC, Omaha, Nebraska; 12Endocrinology Associates, MainMedical Plaza, Houston, Texas; the 13VA Center for Clinical Management Research and the University ofMichigan Health System, Ann Arbor, Michigan; 14Johnston Memorial Diabetes Care Center, Abingdon,Virginia; the 15Center for Health Services Research, Vanderbilt University Medical Center, Nashville, Ten-nessee; 16Technical Writer, Washington, DC; the 17Department of Endocrinology and Diabetes, ABQ HealthPartners, Albuquerque, New Mexico; and 18MedStar Diabetes Institute/MedStar Health, Washington, DC.

Corresponding authors: Linda Haas, [email protected], and Melinda Maryniuk, [email protected].

DOI: 10.2337/dc13-S100The previous version of this article “National Standards for Diabetes Self-Management Education” was pub-

lished in Diabetes Care 2007;30:1630–1637. This version received final approval in July 2012.© 2013 by the American Diabetes Association and the American Association of Diabetes Educators. Readers

may use this article as long as the work is properly cited, the use is educational and not for profit, and thework is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.


N A T I O N A L S T A N D A R D S

mailto:[email protected]

mailto:melinda.maryniuk@joslin<?tjl=20mm?><?tjl?>.harvard.edu

mailto:melinda.maryniuk@joslin<?tjl=20mm?><?tjl?>.harvard.edu


individuals with diabetes. As barriers tocare are overcome, providers of DSMEand diabetes self-management support(DSMS), given their training and experi-ence, are particularly well equipped to as-sist individuals with prediabetes indeveloping and maintaining behaviorsthat can prevent or delay the onset of di-abetes.

Many people with diabetes have orare at risk for developing comorbidities,including both diabetes-related compli-cations and conditions (e.g., heart dis-ease, lipid abnormalities, nerve damage,hypertension, and depression) and othermedical problems that may interfere withself-care (e.g., emphysema, arthritis, andalcoholism). In addition, the diagnosis,progression, and daily work of managingthe disease can take amajor emotional tollon people with diabetes that makes self-care even more difficult (9). The Stand-ards encourage providers of DSME andDSMS to address the entire panorama ofeach participant’s clinical profile. Regularcommunication among the members ofparticipant’s health care teams is essentialto ensure high-quality, effective educa-tion and support for people with diabetesand prediabetes.

In the course of its work on theStandards, the Task Force identified areasin which there is currently an insufficientamount of research. In particular, thereare three areas in which the Task Forcerecommends additional research:

1. What is the influence of organizationalstructure on the effectiveness of theprovision of DSME and DSMS?

2. What is the impact of using a struc-tured curriculum in DSME?

3. What training should be required forthose community, lay, or peer workerswithout training in health or diabeteswho are to participate in the provisionof DSME and to provide DSMS?

Finally, the Standards emphasize thatthe person with diabetes is at the centerof the entire diabetes education and sup-port process. It is the individuals withdiabetes who do the hard work of man-aging their condition, day in and day out.The educator’s role, first and foremost, isto make that work easier (10).

DEFINITIONSDSME: The ongoing process of facilitat-ing the knowledge, skill, and ability nec-essary for prediabetes and diabetes self-care.This process incorporates the needs, goals,

and life experiences of the person withdiabetes or prediabetes and is guided byevidence-based standards. The overall ob-jectives of DSME are to support informeddecision making, self-care behaviors, pro-blem solving, and active collaborationwith the health care team and to improveclinical outcomes, health status, and qual-ity of life.DSMS: Activities that assist the personwith prediabetes or diabetes in imple-menting and sustaining the behaviorsneeded to manage his or her conditionon an ongoing basis beyond or outside offormal self-management training. Thetype of support provided can be behav-ioral, educational, psychosocial, or clini-cal (11–15).

STANDARD 1

Internal structureThe provider(s) of DSME will document anorganizational structure, mission statement,and goals. For those providers workingwithin a larger organization, that organiza-tion will recognize and support qualityDSME as an integral component of diabetescare.

Documentation of an organizationalstructure, mission statement, and goalscan lead to efficient and effective pro-vision of DSME and DSMS. In the busi-ness literature, case studies and casereport investigations of successful man-agement strategies emphasize the impor-tance of clear goals and objectives,defined relationships and roles, and man-agerial support. Business and health pol-icy experts and organizations emphasizewritten commitments, policies, support,and the importance of outcomes report-ing to maintain ongoing support or com-mitment (16,17).

Documentation of an organizationalstructure that delineates channels of com-munication and represents institutionalcommitment to the educational entity iscritical for success. According to The JointCommission, this type of documentationis equally important for both small andlarge health care organizations (18).Health care and business experts over-whelmingly agree that documentationof the process of providing services is acritical factor in clear communicationand provides a solid basis from which todeliver quality diabetes education. In2010, The Joint Commission publishedthe Disease-Specific Care CertificationManual, which outlines standards andperformance measurements for chronic

care programs and disease managementservices, including “Supporting Self-Management” (18).

STANDARD 2

External inputThe provider(s) of DSME will seek ongoinginput from external stakeholders and expertsin order to promote program quality.

For both individual and group pro-viders of DSME andDSMS, external inputis vital to maintaining an up-to-date,effective program. Broad participation ofcommunity stakeholders, including indi-viduals with diabetes, health professio-nals, and community interest groups, willincrease the program’s knowledge of thelocal population and allow the provider tobetter serve the community. Often, but notalways, this external input is best achievedby the establishment of a formal advisoryboard. The DSME and DSMS provider(s)must have a documented plan for seekingoutside input and acting on it.

The goal of external input and dis-cussion in the program planning processis to foster ideas that will enhance thequality of the DSME and/or DSMS beingprovided, while building bridges to keystakeholders (19). The result is effective,dynamic DSME that is patient centered,more responsive to consumer-identifiedneeds and the needs of the community,more culturally relevant, and more ap-pealing to consumers (17,19,20).

STANDARD 3

AccessThe provider(s) of DSME will determine whoto serve, how best to deliver diabetes educa-tion to that population, and what resourcescan provide ongoing support for that popu-lation.

Currently, the majority of peoplewith diabetes and prediabetes do notreceive any structured diabetes education(19,20). While there are many barriers toDSME, one crucial issue is access (21).Providers of DSME can help address thisissue by:

c Clarifying the specific population to beserved. Understanding the community,service area, or regional demographics iscrucial to ensuring that as many peopleas possible are being reached, includingthose who do not frequently attendclinical appointments (9,17,22–24).

c Determining that population’s self-management education and support


National Standards

needs. Different individuals, their fam-ilies, and communities need differenttypes of education and support (25).The provider(s) of DSME and DSMSneeds to work to ensure that thenecessary education alternatives areavailable (25–27). This means under-standing the population’s demogra-phic characteristics, such as ethnic/cultural background, sex, and age, aswell as levels of formal education, lit-eracy, and numeracy (28–31). It mayalso entail identifying resources out-side of the provider’s practice that canassist in the ongoing support of theparticipant.

c Identifying access issues and workingto overcome them. It is essential todetermine factors that prevent in-dividuals with diabetes from receivingself-management education and sup-port. The assessment process includesthe identification of these barriers toaccess (32–34). These barriers may in-clude the socioeconomic or culturalfactors mentioned above, as well as, forexample, health insurance shortfallsand the lack of encouragement fromother health providers to seek diabeteseducation (35,36).

STANDARD 4

Program coordinationA coordinator will be designated to overseethe DSME program. The coordinator willhave oversight responsibility for the plan-ning, implementation, and evaluation of ed-ucation services.

Coordination is essential to ensurethat quality diabetes self-managementeducation and support is deliveredthrough an organized, systematic process(37,38). As the field of DSME continues toevolve, the coordinator plays a pivotalrole in ensuring accountability and conti-nuity in the education program (39–41).The coordinator’s role may be viewed asthat of coordinating the program (or ed-ucation process) and/or as supporting thecoordination of the many aspects of self-management in the continuum of diabe-tes and related conditions when feasible(42–49). This oversight includes design-ing an education program or service thathelps the participant access needed re-sources and assists him or her in navigat-ing the health care system (37,50–55).

The individual serving as the coordi-nator will have knowledge of the lifelongprocess of managing a chronic disease andfacilitating behavior change, in addition to

experience with program and/or clinicalmanagement (56–59). In some cases, par-ticularly in solo or other small practices, thecoordinator may also provide DSME and/or DSMS.

STANDARD 5

Instructional staffOne or more instructors will provideDSME and, when applicable, DSMS. Atleast one of the instructors responsible fordesigning and planning DSME and DSMSwill be a registered nurse, registered dieti-tian, or pharmacist with training and ex-perience pertinent to DSME, or anotherprofessional with certification in diabetescare and education, such as a CDE orBC-ADM. Other health workers can con-tribute to DSME and provide DSMS withappropriate training in diabetes and withsupervision and support.

Historically, nurses and dietitians werethe main providers of diabetes education(3,4,60–64). In recent years, the role of thediabetes educator has expanded to otherdisciplines, particularly pharmacists (65–67). Reviews comparing the effectivenessof different disciplines for education havenot identified clear differences in the qual-ity of services delivered by different profes-sionals (3–5). However, the literaturefavors the registered nurse, registered die-titian, and pharmacist serving both as thekey primary instructors for diabetes educa-tion and as members of the multidisciplin-ary team responsible for designing thecurriculum and assisting in the delivery ofDSME (1–7,68). Expert consensus sup-ports the need for specialized diabetesand educational training beyond academicpreparation for the primary instructors onthe diabetes team (69–72). Professionalsserving as instructors must document ap-propriate continuing education or compa-rable activities to ensure their continuingcompetence to serve in their instructional,training, and oversight roles (73).

Reflecting the evolving health careenvironment, a number of studies haveendorsed a multidisciplinary team ap-proach to diabetes care, education, andsupport. The disciplines that may be in-volved include, but are not limited to,physicians, psychologists and other men-tal health specialists, physical activityspecialists (including physical therapists,occupational therapists, and exercisephysiologists), optometrists, and podia-trists (68,74,75). More recently, healtheducators (e.g., Certified Health Educa-tion Specialists and Certified Medical

Assistants), case managers, lay healthand community workers (76–83), andpeer counselors or educators (84,85)have been shown to contribute effec-tively as part of the DSME team and inproviding DSMS. While DSME andDSMS are often provided within theframework of a collaborative and integratedteam approach, it is crucial that the indi-vidual with diabetes is viewed as central tothe team and that he or she takes an activerole.

Certification as a diabetes educator(CDE) by the National CertificationBoard for Diabetes Educators (NCBDE)is one way a health professional candemonstrate mastery of a specific bodyof knowledge, and this certification hasbecome an accepted credential in thediabetes community (86). An additionalcredential that indicates specialized train-ing beyond basic preparation is boardcertification in Advanced Diabetes Man-agement (BC-ADM) offered by the AADE,which is available for nurses, dietitians,pharmacists, physicians, and physicianassistants (68,74,87).

Individuals who serve as lay health andcommunity workers and peer counselorsor educators may contribute to the pro-vision of DSME instruction and provideDSMS if they have received training indiabetes management, the teaching of self-management skills, group facilitation, andemotional support. For these individuals, asystem must be in place that ensuressupervision of the services they provideby a diabetes educator or other health careprofessional and professional back-up toaddress clinical problems or questionsbeyond their training (88–90).

For services outside the expertise ofany provider(s) of DSME and DSMS, amechanism must be in place to ensurethat the individual with diabetes is con-nected with appropriately trained andcredentialed providers.

STANDARD 6

CurriculumA written curriculum reflecting current evi-dence and practice guidelines, with criteriafor evaluating outcomes, will serve as theframework for the provision of DSME. Theneeds of the individual participant will de-termine which parts of the curriculum will beprovided to that individual.

Individuals with prediabetes and di-abetes and their families and caregivershave much to learn to become effectiveself-managers of their condition. DSME


National Standards

can provide this education via an up-to-date, evidence-based, and flexible curric-ulum (8,91).

The curriculum is a coordinated set ofcourses and educational experiences. Italso specifies learning outcomes and ef-fective teaching strategies (92,93). Thecurriculum must be dynamic and reflectcurrent evidence and practice guidelines(93–97). Recent education research en-dorses the inclusion of practical problem-solving approaches, collaborative care,psychosocial issues, behavior change, andstrategies to sustain self-managementefforts (12,13,19,74,86,98–101).

The following core topics are com-monly part of the curriculum taught incomprehensive programs that havedemonstrated successful outcomes(2,3,5,91,102–104):

c Describing the diabetes disease processand treatment options

c Incorporating nutritional managementinto lifestyle

c Incorporating physical activity intolifestyle

c Using medication(s) safely and formaximum therapeutic effectiveness

c Monitoring blood glucose and otherparameters and interpreting and usingthe results for self-management de-cision making

c Preventing, detecting, and treatingacute complications

c Preventing, detecting, and treatingchronic complications

c Developing personal strategies to ad-dress psychosocial issues and concerns

c Developing personal strategies to pro-mote health and behavior change

While the content areas listed aboveprovide a solid outline for a diabeteseducation and support curriculum, it iscrucial that the content be tailored tomatch each individual’s needs and beadapted as necessary for age, type of di-abetes (including prediabetes and diabe-tes in pregnancy), cultural factors, healthliteracy and numeracy, and comorbidities(14,105–108). The content areas will beable to be adapted for all practice settings.

Approaches to education that are in-teractive and patient centered have beenshown to be effective (12,13,109–112). Alsocrucial is the development of action-orientedbehavioral goals and objectives (12–14,113). Creative, patient-centered, expe-rience-based delivery methodsdbeyondthemere acquisition of knowledgedare ef-fective for supporting informed decision

making and meaningful behavior changeand addressing psychosocial concerns(114,115).

STANDARD 7

IndividualizationThe diabetes self-management, education,and support needs of each participant willbe assessed by one or more instructors. Theparticipant and instructor(s) will then togetherdevelop an individualized education and sup-port plan focused on behavior change.

Research has demonstrated the im-portance of individualizing diabetes edu-cation to each participant’s needs (116).The assessment process is used to identifywhat those needs are and to facilitatethe selection of appropriate educationaland behavioral interventions and self-management support strategies, guidedby evidence (2,63,116–118). The assess-ment must garner information aboutthe individual’s medical history, age, cul-tural influences, health beliefs and atti-tudes, diabetes knowledge, diabetesself-management skills and behaviors,emotional response to diabetes, readinessto learn, literacy level (including healthliteracy and numeracy), physical limita-tions, family support, and financial status(11,106,108,117,119–128).

The education and support plan thatthe participant and instructor(s) developwill be rooted in evidence-based ap-proaches to effective health communica-tion and education while taking intoconsideration participant barriers, abili-ties, and expectations. The instructor willuse clear health communication principles,avoiding jargon, making information cul-turally relevant, using language- and literacy-appropriate education materials, and usinginterpreter services when indicated(107,129–131). Evidence-based commu-nication strategies such as collaborativegoal setting, motivational interviewing,cognitive behavior change strategies,problem solving, self-efficacy enhance-ment, and relapse prevention strategiesare also effective (101,132–134). Peri-odic reassessment can determine whetherthere is need for additional or differentinterventions and future reassessment(6,72,134–137). A variety of assessmentmodalities, including telephone follow-upand other information technologies (e.g.,Web based, text messaging, or automatedphone calls), may augment face-to-face as-sessments (72,87,138–141).

The assessment and education plan,intervention, and outcomes will be

documented in the education/health re-cord. Documentation of participant en-counters will guide the education process,provide evidence of communication amonginstructional staff and othermembers of theparticipant’s health care team, prevent du-plication of services, and demonstrate ad-herence to guidelines (117,135,142,143).Providing information to other membersof the participant’s health care teamthrough documentation of educationalobjectives and personal behavioral goalsincreases the likelihood that all the mem-bers will work in collaboration (86,143).Evidence suggests that the development ofstandardized procedures for documenta-tion, training health professionals to docu-ment appropriately, and the use ofstructured standardized forms based oncurrent practice guidelines can improvedocumentation and may ultimately im-prove quality of care (135,143–145).

STANDARD 8

Ongoing supportThe participant and instructor(s) will to-gether develop a personalized follow-upplan for ongoing self-management support.The participant’s outcomes and goals and theplan for ongoing self-management supportwill be communicated to other members ofthe health care team.

While DSME is necessary and effec-tive, it does not in itself guarantee alifetime of effective diabetes self-care(113). Initial improvements in partici-pants’ metabolic and other outcomeshave been found to diminish after ap-proximately 6 months (3). To sustainthe level of self-management needed toeffectively manage prediabetes and diabe-tes over the long term, most participantsneed ongoing DSMS (15).

The type of support provided can bebehavioral, educational, psychosocial, orclinical (11–14). A variety of strategies areavailable for providing DSMS both withinand outside the DSME organization. Somepatients benefit from working with a nursecase manager (6,86,146). Case manage-ment for DSMS can include remindersabout needed follow-up care and tests,medication management, education, be-havioral goal setting, psychosocial support,and connection to community resources.

The effectiveness of providing DSMSthrough disease management programs,trained peers and community healthworkers, community-based programs, in-formation technology, ongoing education,support groups, and medical nutrition


National Standards

therapy has also been established (7–11,86,88–90,142,147–150).

While the primary responsibility for di-abetes education belongs to the provider(s)of DSME, participants benefit by receiv-ing reinforcement of content and behav-ioral goals from their entire health careteam (135). Additionally, many patientsreceive DSMS through their primarycare provider. Thus, communicationamong the team regarding the patient’seducational outcomes, goals, and DSMSplan is essential to ensure that peoplewith diabetes receive support that meetstheir needs and is reinforced and con-sistent among the health care teammembers.

Because self-management takes placein participants’ daily lives and not in clin-ical or educational settings, patients willbe assisted to formulate a plan to findcommunity-based resources that maysupport their ongoing diabetes self-management. Ideally, DSME and DSMSproviders will work with participants toidentify such services and, when possi-ble, track those that have been effectivewith patients, while communicating withproviders of community-based resourcesin order to better integrate them intopatients’ overall care and ongoingsupport.

STANDARD 9

Patient progressThe provider(s) of DSME and DSMS willmonitor whether participants are achievingtheir personal diabetes self-managementgoals and other outcome(s) as a way to eval-uate the effectiveness of the educationalintervention(s), using appropriate measure-ment techniques.

Effective diabetes self-management canbe a significant contributor to long-term,positive health outcomes. The provider(s)of DSME and DSMS will assess each par-ticipant’s personal self-management goalsand his or her progress toward those goals(151,152).

The AADE Outcome Standards forDiabetes Education specify behaviorchange as the key outcome and provide auseful framework for assessment anddocumentation. The AADE7 lists sevenessential factors: physical activity, healthyeating, taking medication, monitoringblood glucose, diabetes self-care–relatedproblem solving, reducing risks of acuteand chronic complications, and psycho-social aspects of living with diabetes(93,153,154). Differences in behaviors,

health beliefs, and culture as well as theiremotional response to diabetes can have asignificant impact on how participantsunderstand their illness and engage inself-management. DSME providers whoaccount for these differences when collab-orating with participants on the design ofpersonalized DSME or DSMS programscan improve participant outcomes(147,148).

Assessments of participant outcomesmust occur at appropriate intervals. Theinterval depends on the nature of theoutcome itself and the time frame speci-fied based on the participant’s personalgoals. For some areas, the indicators,measures, and time frames will be basedon guidelines from professional organiza-tions or government agencies.

STANDARD 10

Quality improvementThe provider(s) of DSME will measure theeffectiveness of the education and supportand look for ways to improve any identifiedgaps in services or service quality using asystematic review of process and outcomedata.

Diabetes education must be respon-sive to advances in knowledge, treatmentstrategies, education strategies, and psy-chosocial interventions, as well as con-sumer trends and the changing healthcare environment. By measuring andmonitoring both process and outcomedata on an ongoing basis, providers ofDSME can identify areas of improvementand make adjustments in participant en-gagement strategies and program offer-ings accordingly.

The Institute for Healthcare Improve-ment suggests three fundamental questionsthat should be answered by an improve-ment process (149):

c What are we trying to accomplish?c How will we know a change is an im-provement?

c What changes can we make that willresult in an improvement?

Once areas for improvement are iden-tified, the DSME provider must designatetimelines and important milestones in-cluding data collection, analysis, andpresentation of results (150). Measuringboth processes and outcomes helps to en-sure that change is successful withoutcausing additional problems in the sys-tem. Outcome measures indicate the re-sult of a process (i.e., whether changes are

actually leading to improvement), whileprocess measures provide informationabout what caused those results(144,150). Processmeasures are often tar-geted to those processes that typically im-pact the most important outcomes.

AcknowledgmentsdNo potential conflicts ofinterest relevant to this article were reported.The Task Force acknowledges Paulina

Duker, ADA Staff Facilitator; Leslie Kolb,AADE Staff Facilitator; Karen Fitzner, PhD,meeting facilitator (FH Consultants, Chicago,Illinois); and Sara Sklaroff for technical writingassistance.


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60. Koproski J, Pretto Z, Poretsky L. Effectsof an intervention by a diabetes team inhospitalized patients with diabetes. Dia-betes Care 1997;20:1553–1555

61. Weinberger M, Kirkman MS, Samsa GP,et al. A nurse-coordinated interventionfor primary care patients with non-insulin-dependent diabetes mellitus: impact onglycemic control and health-relatedquality of life. J Gen Intern Med 1995;10:59–66

62. Spellbring AM. Nursing’s role in healthpromotion. An overview. Nurs ClinNorth Am 1991;26:805–814

63. Glasgow RE, Toobert DJ, Hampson SE,Brown JE, Lewinsohn PM, Donnelly J.Improving self-care among older pa-tients with type II diabetes: the “SixtySomething. . .” Study. Patient EducCouns 1992;19:61–74

64. Delahanty L, Simkins SW, Camelon K;The DCCT Research Group. Expandedrole of the dietitian in the DiabetesControl and Complications Trial: im-plications for clinical practice. J Am DietAssoc 1993;93:758–764, 767

65. Cranor CW, Bunting BA, ChristensenDB. The Asheville Project: long-termclinical and economic outcomes of acommunity pharmacy diabetes careprogram. J Am Pharm Assoc (Wash)2003;43:173–184

66. Garrett DG, Bluml BM. Patient self-management program for diabetes: first-year clinical, humanistic, and economicoutcomes. J Am Pharm Assoc (2003)2005;45:130–137

67. Shane-McWhorter L, Fermo JD,Bultemeier NC, Oderda GM. Nationalsurvey of pharmacist certified diabeteseducators. Pharmacotherapy 2002;22:1579–1593

68. Emerson S. Implementing diabetes self-management education in primary care.Diabetes Spectrum 2006;19:79–83

69. Anderson RM, Donnelly MB, DedrickRF, Gressard CP. The attitudes of nurses,dietitians, and physicians toward di-abetes. Diabetes Educ 1991;17:261–268

70. Lorenz RA, Bubb J, Davis D, et al.Changing behavior. Practical lessonsfrom the diabetes control and compli-cations trial. Diabetes Care 1996;19:648–652

71. Ockene JK, Ockene IS, Quirk ME, et al.Physician training for patient-centerednutrition counseling in a lipid inter-vention trial. Prev Med 1995;24:563–570

72. Leggett-Frazier N, Swanson MS, VincentPA, Pokorny ME, Engelke MK. Tele-phone communications between diabetesclients and nurse educators. DiabetesEduc 1997;23:287–293

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74. Piatt GA, Orchard TJ, Emerson S, et al.Translating the chronic care model intothe community: results from a random-ized controlled trial of a multifaceteddiabetes care intervention. Diabetes Care2006;29:811–817

75. Campbell EM, Redman S, Moffitt PS,Sanson-Fisher RW. The relative effec-tiveness of educational and behavioralinstruction programs for patients withNIDDM: a randomized trial. DiabetesEduc 1996;22:379–386

76. Satterfield D, Burd C, Valdez L, et al. The“In-Between People”: participation ofcommunity health representatives andlay health workers in diabetes pre-vention and care in American Indian andAlaska Native communities. HealthPromot Pract 2002;3:66–175

77. American Association of Diabetes Edu-cators. Community health workers po-sition statement [Internet], 2011. Availablefrom http://www.diabeteseducator.org/ProfessionalResources/position/position_statements.html. Accessed 26 June2012

78. American Public Health Association.Support for community health workers toincrease health access and to reduce healthinequities [Internet]. Available fromhttp://www.apha.org/advocacy/policy/policysearch/default.htm?id51393. Ac-cessed 26 June 2012

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84. Heisler M. Building Peer Support Pro-grams to Manage Chronic Disease: Seven


National Standards

http://www.diabeteseducator.org/ProfessionalResources/position/position_statements.html



http://www.apha.org/advocacy/policy/policysearch/default.htm?id=1393

http://www.apha.org/advocacy/policy/policysearch/default.htm?id=1393

Models for Success. Oakland, CA, Cal-ifornia Health Care Foundation, 2006

85. Long JA, Jahnle EC, Richardson DM,Loewenstein G, Volpp KG. Peer men-toring and financial incentives to im-prove glucose control in African Americanveterans: a randomized trial. Ann InternMed 2012;156:416–424

86. American Association of Diabetes Educa-tors. The Scope of Practice, Standards ofPractice, and Standards of ProfessionalPerformance for Diabetes Educators [In-ternet], 2011. Available from http://www.diabeteseducator.org/DiabetesEducation/position/Scope_x_Standards.html. Accessed26 June 2012

87. Valentine V, Kulkarni K, Hinnen D.Evolving roles: from diabetes educatorsto advanced diabetes managers. DiabetesEduc 2003;29:598–602, 604, 606

88. American Association of Diabetes Edu-cators. AADE guidelines for the practiceof diabetes self-management educationand training (DSME/T). Diabetes Educ2009;35(Suppl. 3):85S–107S

89. American Association of Diabetes Educa-tors. Competencies for diabetes educators:a companion document to the guidelinesfor the practice of diabetes education [In-ternet], 2011. Available from http://www.diabeteseducator.org/ProfessionalResources/position/competencies.html. Accessed 26June 2012

90. American Association of Diabetes Edu-cators. A sustainable model of diabetesself-management education/training in-volves a multi-level team that can includecommunity health workers [Internet], 2011.Available fromhttp://www.diabeteseducator.org/DiabetesEducation/position/White_Papers.html. Accessed 26 June 2012

91. Gillett M, Dallosso HM, Dixon S, et al.Delivering the diabetes education andself management for ongoing and newlydiagnosed (DESMOND) programme forpeople with newly diagnosed type 2 di-abetes: cost effectiveness analysis. BMJ2010;341:c4093

92. Redman BK. The Practice of Patient Educa-tion. 10th ed. St. Louis, MO, Mosby, 2007

93. Mulcahy K, Maryniuk M, Peeples M,et al. Diabetes self-management educa-tion core outcomes measures. DiabetesEduc 2003;29:768–770, 773–784, 787–768

94. Reader D, Splett P, Gunderson EP; Di-abetes Care and Education Dietetic Prac-tice Group. Impact of gestational diabetesmellitus nutrition practice guidelinesimplemented by registered dietitians onpregnancy outcomes. J Am Diet Assoc2006;106:1426–1433

95. Boucher JL, Evert A, Daly A, et al.American Dietetic Association revisedstandards of practice and standards ofprofessional performance for registereddietitians (generalist, specialty, and

advanced) in diabetes care. J Am DietAssoc 2011;111:156–166.e27

96. American Diabetes Association. Stand-ards of medical care in diabetesd2012.Diabetes Care 2012;35(Suppl. 1):S11–S63

97. Bantle JP, Wylie-Rosett J, Albright AL,et al.; American Diabetes Association.Nutrition recommendations and inter-ventions for diabetes: a position statementof the American Diabetes Association.Diabetes Care 2008;31(Suppl. 1):S61–S78

98. Wagner EH, Austin BT, Von Korff M.Organizing care for patients with chronicillness. Milbank Q 1996;74:511–544

99. Norris SL. Health-related quality of lifeamong adults with diabetes. Curr DiabRep 2005;5:124–130

100. Herman AA. Community health workersand integrated primary health care teamsin the 21st century. J Ambul Care Manage2011;34:354–361

101. Weinger K, Beverly EA, Lee Y, SitnokovL, Ganda OP, Caballero AE. The effectof a structured behavioral interventionon poorly controlled diabetes: a ran-domized controlled trial. Arch InternMed 2011;171:1990–1999

102. Norris SL, Zhang X, Avenell A, et al.Long-term effectiveness of lifestyle andbehavioral weight loss interventions inadults with type 2 diabetes: a meta-analysis. Am J Med 2004;117:762–774

103. Ellis SE, Speroff T, Dittus RS, Brown A,Pichert JW, Elasy TA. Diabetes patienteducation: a meta-analysis and meta-regression. Patient Educ Couns 2004;52:97–105

104. Armour TA, Norris SL, Jack L Jr, ZhangX, Fisher L. The effectiveness of familyinterventions in people with diabetesmellitus: a systematic review. DiabetMed 2005;22:1295–1305

105. Magee M, Bowling A, Copeland J, FokarA, Pasquale P, Youssef G. The ABCs ofdiabetes: diabetes self-managementeducation program for African Ameri-cans affects A1C, lipid-lowering agentprescriptions, and emergency depart-ment visits. Diabetes Educ 2011;37:95–103

106. Cavanaugh K, Huizinga MM, WallstonKA, et al. Association of numeracy anddiabetes control. Ann Intern Med 2008;148:737–746

107. Rothman RL, DeWalt DA, Malone R,et al. Influence of patient literacy on theeffectiveness of a primary care-baseddiabetes disease management program.JAMA 2004;292:1711–1716

108. Schillinger D, Grumbach K, Piette J, et al.Association of health literacywith diabetesoutcomes. JAMA 2002;288:475–482

109. Rubin RR, Peyrot M, Saudek CD. The ef-fect of a diabetes education program in-corporating coping skills, training on

emotional well-being, and diabetes self-efficacy. Diabetes Educ 1993;19:210–214

110. Trento M, Passera P, Borgo E, et al. A5-year randomized controlled study oflearning, problem solving ability, andquality of life modifications in peoplewith type 2 diabetes managed by groupcare. Diabetes Care 2004;27:670–675

111. Izquierdo RE, Knudson PE, Meyer S,Kearns J, Ploutz-SnyderR,WeinstockRS.Acomparison of diabetes education admin-istered through telemedicine versus inperson.DiabetesCare 2003;26:1002–1007

112. Garrett N, HagemanCM, Sibley SD, et al.The effectiveness of an interactive smallgroup diabetes intervention in improv-ing knowledge, feeling of control, andbehavior. Health Promot Pract 2005;6:320–328

113. Piette JD, Glasgow R. Strategies for im-proving behavioral health outcomesamong patients with diabetes: self-management, education. In Evidence-Based Diabetes Care. Gerstein HC,Haynes RB, Eds. Hamilton, Ontario,Canada, BC Decker, 2001, p. 207–251

114. Boren SA. AADE7 Self-care behaviors:systematic reviews. Diabetes Educ 2007;33:866, 871

115. American Association of Diabetes Edu-cators. AADE7 self-care behaviors, Ameri-can Association of Diabetes Educatorsposition statement [Internet], 2011. Avail-able from http://www.diabeteseducator.org/DiabetesEducation/position/position_statements.html. Accessed 26 June2012

116. American Association of Diabetes Educa-tors. AADE position statement. Individu-alization of diabetes self-managementeducation. Diabetes Educ 2007;33:45–49

117. Gilden JL, Hendryx M, Casia C, SinghSP. The effectiveness of diabetes educa-tion programs for older patients andtheir spouses. J Am Geriatr Soc 1989;37:1023–1030

118. Brown SA. Effects of educational inter-ventions in diabetes care: a meta-analysisof findings. Nurs Res 1988;37:223–230

119. Barlow J, Wright C, Sheasby J, Turner A,Hainsworth J. Self-management ap-proaches for people with chronic con-ditions: a review. Patient Educ Couns2002;48:177–187

120. Skinner TC, Cradock S, Arundel F, et al.Four theories and a philosophy: self-management education for individualsnewly diagnosed with type 2 diabetes.Diabetes Spectrum 2003;16:75–80

121. Brown SA, Hanis CL. Culturally com-petent diabetes education for MexicanAmericans: the Starr County Study. Dia-betes Educ 1999;25:226–236

122. Sarkisian CA, Brown AF, Norris KC,Wintz RL, Mangione CM. A systematicreview of diabetes self-care interventionsfor older, African American, or Latinoadults. Diabetes Educ 2003;29:467–479


National Standards

http://www.diabeteseducator.org/DiabetesEducation/position/Scope_x_Standards.html



http://www.diabeteseducator.org/ProfessionalResources/position/competencies.html



http://www.diabeteseducator.org/DiabetesEducation/position/White_Papers.html



http://www.diabeteseducator.org/DiabetesEducation/position/position_statements.html



123. Chodosh J, Morton SC, Mojica W, et al.Meta-analysis: chronic disease self-management programs for older adults.Ann Intern Med 2005;143:427–438

124. Anderson-Loftin W, Barnett S, Bunn P,Sullivan P,Hussey J, Tavakoli A. Soul foodlight: culturally competent diabetes edu-cation. Diabetes Educ 2005;31:555–563

125. Mensing CR, Norris SL. Group educa-tion in diabetes: effectiveness and im-plementation. Diabetes Spectrum 2003;16:96–103

126. Brown SA, Blozis SA, Kouzekanani K,Garcia AA, Winchell M, Hanis CL. Dos-age effects of diabetes self-managementeducation for Mexican Americans: theStarr County Border Health Initiative.Diabetes Care 2005;28:527–532

127. Hosey GM, FreemanWL, Stracqualursi F,Gohdes D. Designing and evaluating di-abetes education material for AmericanIndians. Diabetes Educ 1990;16:407–414

128. Thomson FJ, Masson EA. Can elderlypatients co-operate with routine foot care?Diabetes Spectrum 1995;8:218–219

129. HawthorneK, Robles Y,Cannings-JohnR,Edwards AG. Culturally appropriatehealth education for Type 2 diabetes inethnic minority groups: a systematic andnarrative review of randomized controlledtrials. Diabet Med 2010;27:613–623

130. Cavanaugh K,Wallston KA, GebretsadikT, et al. Addressing literacy and numer-acy to improve diabetes care: two ran-domized controlled trials. Diabetes Care2009;32:2149–2155

131. Doak CC, Doak LG, Root JH. TeachingPatients with Low Literacy Skills. Phila-delphia, PA, Lippincott, 2008

132. Schillinger D, Piette J, Grumbach K, et al.Closing the loop: physician communi-cation with diabetic patients who havelow health literacy. Arch Intern Med2003;163:83–90

133. Channon SJ, Huws-Thomas MV, RollnickS, et al. A multicenter randomized con-trolled trial ofmotivational interviewing inteenagers with diabetes. Diabetes Care2007;30:1390–1395

134. Naik AD, Palmer N, Petersen NJ, et al.Comparative effectiveness of goal set-ting in diabetes mellitus group clinics:

randomized clinical trial. Arch InternMed 2011;171:453–459

135. Glasgow RE, Funnell MM, Bonomi AE,Davis C, Beckham V, Wagner EH. Self-management aspects of the improvingchronic illness care breakthrough series:implementation with diabetes and heartfailure teams. Ann Behav Med 2002;24:80–87

136. Estey AL, Tan MH, Mann K. Follow-upintervention: its effect on compliancebehavior to a diabetes regimen. DiabetesEduc 1990;16:291–295

137. Beverly EA, Ganda OP, Ritholz MD, et al.Look who’s (not) talking: diabetic pa-tients’ willingness to discuss self-carewith physicians. Diabetes Care 2012;35:1466–1472

138. Mulvaney SA, Rothman RL, WallstonKA, Lybarger C, Dietrich MS. An Internet-based program to improve self-managementin adolescents with type 1 diabetes. Dia-betes Care 2010;33:602–604

139. Osborn CY, Mayberry LS, MulvaneySA, Hess R. Patient Web portals to im-prove diabetes outcomes: a systematicreview. Curr Diab Rep 2010;10:422–435

140. Mulvaney SA, Ritterband LM, Bosslet L.Mobile intervention design in diabetes:review and recommendations. Curr DiabRep 2011;11:486–493

141. Polonsky WH, Fisher L, Earles J, et al.Assessing psychosocial distress in diabetes:development of the diabetes distress scale.Diabetes Care 2005;28:626–631

142. Davis ED. Role of the diabetes nurseeducator in improving patient educa-tion. Diabetes Educ 1990;16:36–38

143. Glasgow RE, Davis CL, Funnell MM,Beck A. Implementing practical inter-ventions to support chronic illness self-management. Jt Comm J Qual Saf 2003;29:563–574

144. Daly A, Leontos C. Legislation for healthcare coverage for diabetes self-manage-ment training, equipment and supplies:past, present and future. Diabetes Spec-trum 1999;12:222–230

145. Grebe SK, Smith RB. Clinical audit andstandardised follow up improve qualityof documentation in diabetes care. N ZMed J 1995;108:339–342

146. Aubert RE, Herman WH, Waters J, et al.Nurse case management to improveglycemic control in diabetic patients ina health maintenance organization. Arandomized, controlled trial. Ann InternMed 1998;129:605–612

147. Anderson D, Christison-Lagay J. Di-abetes self-management in a communityhealth center: improving health behav-iors and clinical outcomes for un-deserved patients. Clin Diabetes 2008;26:22–27

148. Duncan I, Ahmed T, Li QE, et al. As-sessing the value of the diabetes educa-tor. Diabetes Educ 2011;37:638–657

149. Institute for Healthcare Improvement.Science of improvement: how to improve[Internet]. Available from http://www.ihi.org/knowledge/Pages/HowtoImprove/ScienceofImprovementHowtoImprove.aspx. Accessed 25 June 2012

150. The Joint Commission on Accreditationof Healthcare Organizations. Joint Com-mission Resources: Cost-Effective Perfor-mance Improvement in Ambulatory Care.Oakbrook Terrace, IL, Joint Commis-sion on Accreditation of Healthcare Or-ganizations, 2003

151. Glasgow RE, Peeples M, Skovlund SE.Where is the patient in diabetes perfor-mance measures? The case for includingpatient-centered and self-managementmeasures. Diabetes Care 2008;31:1046–1050

152. Beebe CA, Schmitt SS. Engaging patientsin education for self-management in anaccountable care environment. Clin Di-abetes 2011;29:123–126

153. American Association of Diabetes Edu-cators. Standards for outcomes mea-surement of diabetes self-managementeducation [Internet], 2011. Availablefrom http://www.diabeteseducator.org/ProfessionalResources/position/position_statements.html. Accessed 26 June 2012

154. American Association of Diabetes Educa-tors. Standards for outcomesmeasurementof diabetes self-management education,technical review [Internet], 2011. Availablefrom http://www.diabeteseducator.org/ProfessionalResources/position/position_statements.html. Accessed 26 June 2012


National Standards

http://www.ihi.org/knowledge/Pages/HowtoImprove/ScienceofImprovementHowtoImprove.aspx










Professional Practice Committee for the2013ClinicalPracticeRecommendationsCommittee members disclosed the following financial or other conflicts of interest covering the period 1 November 2011–31 October 2012.

Member Employment Research grant Other research support

Roger Austin, MS, RPH, CDE Henry Ford Health System,Sterling Heights, MI

None None

Nathaniel G. Clark, MD, RD Diabetes Center of Cape Cod,Hyannis, MA

None None

Cyrus V. Desouza, MD University of NebraskaMedical Center and Omaha VAMedical Center, Omaha, NE

REATA Research Trial#,Novo Nordisk#

None

Martha Funnell, MSN,RN, CDE

University of Michigan, AnnArbor, MI

None None

Allison B. Goldfine, MD Joslin Diabetes Center, Boston, MA NIDDK#, NHLBI# Research supplies from CaracoPharmaceuticals#, LifeScan#,Mercodia#, Nestle#, Amneal#

Richard Grant, MD, MPH Division of Research, KaiserPermanente, Oakland, CA

AHRQ#, NIDDK# None

James Lenhard, MD Christiana Care Health System,Wilmington, DE

NIH# None

Jennifer B. Marks, MD VA Diabetes Management Team,Miami, FL, and Diabetes ResearchInstitute, University of MiamiSchool of Medicine, Miami, FL

Lilly#, NIH#, Leona M. andHarry B. Helmsley CharitableTrust (T1D Exchange Clinic

Registry)#

NIDDK

Anthony L. McCall, MD, PhD University of Virginia,Charlottesville, VA

Aventis#, Eli Lilly#, NIDDK None

Janis R. McWilliams, RN, MSN,CDE, BC-ADM

Consultant, Pittsburgh, PA None None

R. Harsha Rao, MD University of Pittsburgh MedicalCenter, Pittsburgh, PA, and VAPittsburgh Healthcare System,

Pittsburgh, PA

None None

Andrew Rhinehart, MD,CDE, BC-ADM, FACP

Mountain States Health Alliance,Abingdon, VA

Diabetes Impact Grant#,Health Wagon Grant#

None

Henry Rodriguez, MD University of South Florida,Tampa, FL

NIH#, Bristol-Myers Squibb#,Daiichi Sankyo#, Novartis#,Merck#, Leona M. and HarryB. Helmsley Charitable Trust

(T1DExchange Clinic Registry)#

None

Debra L. Simmons, MD, MS University of Utah, VA Salt LakeCity, Salt Lake City, UT, andUniversity of Arkansas for

Medical Sciences and CentralArkansas Veterans Healthcare

System, Little Rock, AR

NHLBI#, Novo Nordisk# None

Patricia Urbanski,MEd, RD, LD, CDE

Consultant, Cloquet, MN None None

Carol Wysham, MD (Chair) Rockwood Clinic, Spokane, WA NIH#, Leona M. and Harry B.Helmsley Charitable Trust

(T1D Exchange Clinic Registry)#

None

Judy Fradkin, MD(Ex officio)

NIDDK, Bethesda, MD None None

Stephanie Dunbar, RD,MPH (Staff)

American Diabetes Association,Alexandria, VA

None None

Sue Kirkman, MD (Staff) American Diabetes Association,Alexandria, VA

None None

*$$10,000 per year from company to individual; #grant or contract is to university or other employer.


Member Speakers’ bureau/honoraria Ownership interest Consultant/advisory board Other

R.A. Johnson & JohnsonDiabetes Institute(wife Mary Austin)

None None None

N.G.C. Novo Nordisk, Amylin None None Clinical Diabetes, Editorial BoardC.V.D. None None Novo Nordisk, Takeda NoneM.F. None None Eli Lilly, Boehringer Ingelheim,

Halozyme Therapeutics,Merck Pharmaceutical,Bristol-Myers Squibb/AstraZeneca, UCLA

Center for Health PolicyResearch, Animas/LifeScanGlucose Meter, Bristol-Myers Squibb Nurse

Practitioner, Bayer HealthCare Diabetes Care, Novo

Nordisk Pen Devices

None

A.B.G. None Pending patents: JDP–106(SAZ–T2D), JDP–109

(SAZ–CUD), JDP–129 (SRF)

None Special Government Employee, FDA(invited participant for Endocrine and

Metabolic Advisory Committee)R.G. None None None NoneJ.L. Boehringer Ingelheim,

sanofi-aventisNone None Expert witness for variety of legal

firms. No cases involved in the last12 months concerned drugs, devices,

or pharmaceutical companiesJ.B.M. ADA, Diabetes Research

Institute FoundationNone Amgen None

A.L.M. None None None Clinical Science Chair, The EndocrineSociety Annual Meeting & Expo 2012

J.R.M. Roche (Creative CoachingWorkshop), VMS

(Steady Start EducatorNetwork), Healthy

Interactions

None None None

R.H.R. None Co-inventor of GENIE. Nocommercial agreementsor collaborations. (U.S.

patent applicationnumber 12464344 filed

by VA TechnologyTransfer Program, DC01-#145823-v1-066072-

0050 Automated Systemand Method of Diabetes

Control (Rao RH,Perreiah PL,

Cunningham CA,Inventors)

None None

A.R. Forest Laboratories*,Abbott Laboratories,

Eli Lilly, NovoNordisk*, sanofi-

aventis*, BoehringerIngelheim, Amylin

None sanofi-aventis*, Amylin Board Member and President, AppalachianDiabetes Foundation

H.R. Eli Lilly* None Eli Lilly*, Roche Diagnostics Diabetes Forecast, Associate EditorD.L.S. None None None NoneP.U. Eli Lilly None Eli Lilly, sanofi-aventis,

Halozyme Therapeutics,Medtronic

Clinical Diabetes, Editorial Board

C.W. Amylin Pharmaceuticals*,Eli Lilly*, Merck, Novo

Nordisk*, sanofi-aventis*, Boehringer

Ingelheim

None Amylin Pharmaceuticals*,Boehringer Ingelheim,Johnson & Johnson,

sanofi-aventis*

None

J.F. None None None NoneS.D. None None None None

S.K. None None None None


Professional Practice Committee

Systematic Reviews

A systematic review provides a scientificrationale for a position statement andundergoes critical peer review beforesubmission to the Professional PracticeCommittee for approval. Effective Janu-ary 2010, technical reports were re-placed with systematic reviews, forwhich a priori search and inclusion/exclusion criteria are developed and

published. Listed below are recentreviews.

Macronutrients, Food Groups, andEating Patterns in the Managementof Diabetes: A Systematic Review ofthe Literature, 2010Madelyn L.Wheeler, Stephanie A. Dunbar,Lindsay M. Jaacks, Wahida Karmally,Elizabeth J.Mayer-Davis, JudithWylie-Rosett,

and William S. Yancy Jr.Diabetes Care 35:434–445, 2012

Cost-Effectiveness of Interventionsto Prevent and Control DiabetesMellitus: A Systematic ReviewRui Li, Ping Zhang, Lawrence E. Barker,FarahM.Chowdhury, andXuanpingZhangDiabetes Care 33:1872–1894, 2010

care.diabetesjournals.org DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 e1

Consensus Reports

Effective January 2010, prior reports of the types listed below were renamed “consensus reports.” Listed below are recent consensusreports.

EXPERT COMMITTEE REPORTSInternational Expert Committee Re-port on the Role of the A1C Assay inthe Diagnosis of DiabetesInternational Expert CommitteeDiabetes Care 32:1327–1334, 2009

CONSENSUS REPORTSDiabetes in Older AdultsM. Sue Kirkman, Vanessa Jones Briscoe,Nathaniel Clark, Hermes Florez, Linda B.Haas, Jeffrey B. Halter, Elbert S. Huang,Mary T. Korytkowski, Medha N. Munshi,Peggy Soule Odegard, Richard E. Pratley,and Carrie S. SwiftDiabetes Care 35:2650–2664, 2012

The Charcot Foot in DiabetesLee C. Rogers, Robert G. Frykberg, DavidG. Armstrong, Andrew J.M. Boulton,Michael Edmonds, Georges Ha Van,Agnes Hartemann, Frances Game, WilliamJeffcoate, Alexandra Jirkovska, Edward Jude,Stephan Morbach, William B. Morrison,Michael Pinzur,Dario Pitocco, Lee Sanders,Dane K. Wukich, and Luigi UccioliDiabetes Care 34:2123–2129, 2011

Diabetes and CancerEdward Giovannucci, David M. Harlan,Michael C. Archer, RichardM. Bergenstal,Susan M. Gapstur, Laurel A. Habel, Mi-chael Pollak, Judith G. Regensteiner, andDouglas YeeDiabetes Care 33:1674–1685, 2010

AmericanAssociation of Clinical Endo-crinologists andAmericanDiabetes As-sociation Consensus Statement onInpatient Glycemic ControlEtie S. Moghissi, Mary T. Korytkowski,Monica DiNardo, Daniel Einhorn, Ri-chard Hellman, Irl B. Hirsch, Silvio E.Inzucchi, Faramarz Ismail-Beigi, M. SueKirkman, and Guillermo E. UmpierrezDiabetes Care 32:1119–1131, 2009

Hyperglycemic Crises in Adult Pa-tients With DiabetesAbbas E. Kitabchi, Guillermo E. Umpierrez,John M. Miles, and Joseph N. FisherDiabetes Care 32:1335–1343, 2009

How Do We Define Cure of Diabetes?John B. Buse, Sonia Caprio, William T.Cefalu, Antonio Ceriello, Stefano DelPrato, Silvio E. Inzucchi, SueMcLaughlin,Gordon L. Phillips II, R. Paul Robertson,Francesco Rubino, Richard Kahn, and M.Sue KirkmanDiabetes Care 32:2133–2135, 2009

Lipoprotein Management in PatientsWith Cardiometabolic Risk: Consen-sus Statement From the American Di-abetes Association and the AmericanCollege of Cardiology FoundationJohn D. Brunzell, Michael Davidson, CurtD. Furberg, Ronald B. Goldberg, BarbaraV. Howard, James H. Stein, and Joseph L.WitztumDiabetes Care 31:811–822, 2008

Managing Preexisting Diabetes forPregnancy: Summary of Evidenceand Consensus Recommendationsfor CareJohn L. Kitzmiller, Jennifer M. Block,Florence M. Brown, Patrick M. Catalano,Deborah L. Conway, Donald R. Coustan,Erica P. Gunderson, William H. Herman,Lisa D. Hoffman, Maribeth Inturrisi, LoisB. Jovanovic, Siri I. Kjos, Robert H. Knopp,Martin N. Montoro, Edward S. Ogata,Pathmaja Paramsothy, Diane M. Reader,Barak M. Rosenn, Alyce M. Thomas, andM. Sue KirkmanDiabetes Care 31:1060–1079, 2008

Influence of Race, Ethnicity, andCulture on Childhood Obesity: Implica-tions for Prevention and Treatment:A Consensus Statement of ShapingAmerica’s Health and the ObesitySocietySonia Caprio, Stephen R. Daniels, AdamDrewnowski, Francine R. Kaufman, Law-rence A. Palinkas, Arlan L. Rosenbloom,and Jeffrey B. SchwimmerDiabetes Care 31:2211–2221, 2008

Screening for Coronary ArteryDisease in Patients With DiabetesJeroen J. Bax, Lawrence H. Young,Robert L. Frye, Robert O. Bonow,Helmut O. Steinberg, and Eugene J.BarrettDiabetes Care 30:2729–2736, 2007

e2 DIABETES CARE, VOLUME 36, SUPPLEMENT 1, JANUARY 2013 care.diabetesjournals.org

Position Statements

A position statement is an official pointof view or belief of the ADA. Positionstatements are issued on scientific ormedical issues related to diabetes. Theymay be authored or unauthored and arepublished in ADA journals and otherscientific/medical publications as appro-priate. Position statements must be re-viewed and approved by the ProfessionalPractice Committee and, subsequently,by the Executive Committee of the Boardof Directors. ADA position statements aretypically based on a technical review orother review of published literature. Theyare reviewed on an annual basis and upda-ted as needed. In addition to those pub-lished in this supplement, listed below arerecent position statements.

Diabetes Management at Camps forChildren With DiabetesAmerican Diabetes AssociationDiabetes Care 35 (Suppl. 1):S72–S75,2012

Management of Hyperglycemia inType 2 Diabetes: A Patient-CenteredApproach. Position Statement of theAmerican Diabetes Association(ADA) and the European Associationfor the Study of Diabetes (EASD)Silvio E. Inzucchi, Richard M. Bergenstal,John B. Buse, Michaela Diamant, EleFerrannini, Michael Nauck, Anne L.Peters, Apostolos Tsapas, RichardWender, and David R. MatthewsDiabetes Care 35:1364–1379, 2012

Guidelines and Recommendations forLaboratory Analysis in the Diagnosisand Management of Diabetes MellitusDavid B. Sacks, Mark Arnold, George L.Bakris, David E. Bruns, Andrea RitaHorvath, M. Sue Kirkman, Ake Lernmark,Boyd E. Metzger, and David M. NathanDiabetes Care 34:e61–e99, 2011

Diabetes Care for Emerging Adults:Recommendations for TransitionFrom Pediatric to Adult DiabetesCare Systems. A Position Statementof the American DiabetesAssociation, With Representation bythe American College of OsteopathicFamily Physicians, the AmericanAcademy of Pediatrics, theAmerican Association of ClinicalEndocrinologists, the AmericanOsteopathic Association, theCenters for Disease Control andPrevention, Children with Diabetes,The Endocrine Society, theInternational Society for Pediatricand Adolescent Diabetes, JuvenileDiabetes Research FoundationInternational, the National DiabetesEducation Program, and thePediatric Endocrine Society (formerlyLawson Wilkins Pediatric EndocrineSociety)Anne Peters, Lori Laffel, and the AmericanDiabetes Association Transitions Work-ing GroupDiabetes Care 34:2477–2485, 2011

Aspirin for Primary Prevention ofCardiovascular Events in PeopleWith Diabetes: A Position Statementof the American DiabetesAssociation, a Scientific Statementof the American Heart Association,and an Expert Consensus Documentof the American College ofCardiology FoundationMichael Pignone, Mark J. Alberts, John A.Colwell, Mary Cushman, Silvio E. Inzuc-chi, Debabrata Mukherjee, Robert S.Rosenson, Craig D. Williams, Peter W.Wilson, and M. Sue KirkmanDiabetes Care 33:1395–1402, 2010

Exercise and Type 2 Diabetes.The American College of Sports

Medicine and the American DiabetesAssociation: Joint PositionStatementSheri R. Colberg, Ronald J. Sigal, Bo Fern-hall, Judith G. Regensteiner, Bryan J.Blissmer, Richard R. Rubin, Lisa Chasan-Taber, Ann L. Albright, and Barry BraunDiabetes Care 33:e147–e167, 2010

Clinical Care Guidelines for CysticFibrosis–Related Diabetes: APosition Statement of the AmericanDiabetes Association and a ClinicalPractice Guideline of the CysticFibrosis Foundation, Endorsed bythe Pediatric Endocrine SocietyAntoinette Moran, Carol Brunzell, RichardC. Cohen, Marcia Katz, Bruce C. Marshall,GaryOnady,KarenA.Robinson,KathrynA.Sabadosa, Arlene Stecenko, Bonnie Slovis,and the CFRD Guidelines CommitteeDiabetes Care 33:2697–2708, 2010

Intensive Glycemic Control and thePrevention of Cardiovascular Events:Implications of the ACCORD,ADVANCE, and VA Diabetes Trials.A Position Statement of theAmerican Diabetes Association anda Scientific Statement of theAmerican College of CardiologyFoundation and the American HeartAssociationJay S. Skyler, Richard Bergenstal, RobertO. Bonow, John Buse, Prakash Deedwania,Edwin A.M. Gale, Barbara V. Howard,M. Sue Kirkman, Mikhail Kosiborod, PeterReaven, and Robert S. SherwinDiabetes Care 32:187–192, 2009

Nutrition Recommendations andInterventions for Diabetes: A PositionStatement of the American DiabetesAssociationAmerican Diabetes AssociationDiabetes Care 31 (Suppl. 1):S61–S78, 2008

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Scientific Statements

A scientific statement is a scholarly syn-opsis of a topic related to diabetes, whichmay ormay not contain clinical or researchrecommendations. Any recommenda-tions included represent the officialpoint of view or belief of the ADA.Work Group Reports and Task ForceReports fall into this category. Scientificstatements must be reviewed and ap-proved by the Professional PracticeCommittee and, subsequently, by theExecutive Committee of the Board ofDirectors. Listed below are recent scien-tific statements.

Nonnutritive Sweeteners: CurrentUse and Health Perspectives. AScientific Statement From the

American Heart Association and theAmerican Diabetes AssociationChristopher Gardner, Judith Wylie-Rosett, Samuel S. Gidding, Lyn M. Steffen,Rachel K. Johnson, Diane Reader, andAlice H. Lichtenstein, on behalf of theAmerican Heart Association NutritionCommittee of the Council on Nutrition,Physical Activity and Metabolism, Coun-cil on Arteriosclerosis, Thrombosis andVascular Biology, Council on Cardiovas-cular Disease in the Young, and theAmerican Diabetes AssociationDiabetes Care 35:1798–1808, 2012

Comprehensive Foot Examinationand Risk Assessment: A Report of theTask Force of the Foot Care Interest

Group of the American DiabetesAssociation, With Endorsement bythe American Association of ClinicalEndocrinologistsAndrew J.M. Boulton,DavidG.Armstrong,Stephen F. Albert, Robert G. Frykberg,Richard Hellman, M. Sue Kirkman,Lawrence A. Lavery, Joseph W. LeMaster,Joseph L. Mills, Sr., Michael J. Mueller,Peter Sheehan, and Dane K. WukichDiabetes Care 31:1679–1685, 2008

American Diabetes AssociationStatement on Emergency andDisaster Preparedness: A Report ofthe Disaster Response Task ForceThe Disaster Response Task ForceDiabetes Care 30:2395–2398, 2007

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