leaky gut. pdf

2015 Online Review Course

Important Schematics and Anchor Slides

Biotransformation&Elimination(e.g.,Toxicity,Detoxification)

Energy(e.g.,EnergyRegulation,MitochondrialFunction)

Communication(e.g.,Endocrine,Neurotransmitters,

Immunemessengers)

Defense&Repair(e.g.,Immune,Inflammation,

Infection/Microbiota)

StructuralIntegrity(e.g.,fromSubcellularMembranesto

MusculoskeletalStructure)

Assimilation(e.g.,Digestion,Absorption,Microbiota/GI,Respiration)

Antecedents(PredisposingFactorsGenetic/Environmental)

TriggeringEvents(Activators)

Exercise&Movement

PersonalizingLifestyleFactorsNutrition&Hydration

PhysiologyandFunction:OrganizingthePatientsClinicalImbalances

Mediators/Perpetuators(Contributors)

Spiritual

e.g.,meaning&purpose,relationshipwithsomething

greater

e.g., cognitivefunction,perceptualpatterns

e.g., emotionalregulation,grief,

sadness,anger,etc.

Sleep&Relaxation

Name:____________________________Date:___________CC:_____________________________________ Copyright2011InstituteforFunctionalMedicine

Stress&Resilience Relationships&Networks

Transport(e.g.,Cardiovascular,LymphaticSystem)

RetellingthePatientsStory

2012 The Institute for Functional Medicine2013 The Institute for Functional Medicine

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CurrentConcerns

Antecedents

TriggersorTriggeringEvents

Signs,SymptomsorDiseasesReported

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2012 The Institute for Functional Medicine2013 The Institute for Functional Medicine2013 The Institute for Functional Medicine

Functional MedicineOperating System

2012 The Institute for Functional Medicine2013 The Institute for Functional Medicine2013 The Institute for Functional Medicine

OO TT TTGG

Gather Oneself & InformationOrganize on Timeline & MatrixTell the Patients StoryOrder of your PrioritiesInitiate Assessment and CareTrack Progress

OO II

2014 The Institute for Functional Medicine

THE PRINCIPLES: A SCIENCE BASED FIELD OF HEALTHCARE

Biochemical individuality based on genetic and environmental uniqueness

Patient centered versus disease centered Dynamic balance of internal and external factors Web-like interconnections of physiological

factors Health as a positive vitality not merely the

absence of disease Promotion of organ reserve healthspan


Key differences between Conventional and Functional Medicine

The Conventional Model Differential diagnosis:

reductionism Eliminating confounding

variables Naming and blaming Confirmatory laboratory

and imaging tests Symptom suppression

The Functional Model Etiologic and causative

evaluation: patterns and connections

Including all variables New lenses and cognitive

organization Testing: causes and

mechanisms Removing causes and

restoring normal function


ClinicalExpertise

EvidenceBasedClinicalPractice


Definitions:Antecedents, Triggers, and Mediators

Antecedents are factors, genetic or acquired, that predispose individual to an illness or pattern

Triggers are factors that provoke the symptoms and signs of illness

Mediators/mediation are factors, biochemical or psychosocial, that contribute to pathological changes and dysfunctional responses


Patient Centered Care

Organizing the C

linical Imbalances


Key functional roles of the Gut:

Digestion/AbsorptionIntestinal PermeabilityGut Microbiota/DysbiosisInflammation/ImmuneNervous System


The 5R Approach What does this patient need to have Removed?

What does this patient need to have Replaced?

What does this patient need to support and/or to re-establish a healthy balance of microflora; that is, does he/she require pre- or probiotic Reinoculation?

What does this patient require to support healing and Repairof the GI epithelial barrier and the biofilm?

What does this patient need to do to Rebalance their lifestyle; that is, are there things to modify in their attitude, diet, and lifestyle to promote a healthier way of living?


AlteredIntestinal

Permeability

Poor Dietary Choices

Stress & Emotions

Infection

Lectins

Systemic Disease

Toxic Exposure

Food Allergy

Malnutrition

Dysbiosis

Toxic Overload

Elevated TotalToxic & AntigenicBurden

Low Stomach Acid

Systemic Disease

Pathophysiology


Triggers:nutrientinsufficiency,medication,dysbiosis,parasite,foodreaction,surgery,etc

Portalandsystemicoverload

Bacterial/yeast/protozoa/toxintranslocation

DistantSignsandSymptoms:Systemicillness

DisturbanceofGIflora

Increasedmucosalpermeability

Foodproteintranslocation

Immunologicallymediatedreactions(andperpetuation)

DisruptionofEpithelialTightJunctionsAndMucosalBarrier


IFM Food Reaction Definitions Food allergy: IgE-mediated type 1

hypersensitivity Food sensitivity: IgG-mediated type 3 delayed

hypersensitivity Food intolerance: Non-immunological reaction

to food (e.g. lactose intolerance)


MechanismsofImmuneandNonImmuneMediatedReactionstoFood

Immunemediated NonImmunemediated(Intolerance)

IgEmediatedreactions

Otherimmunereactions

Toxic(occurringin

anyindividual)

Nontoxic(individualsusceptibility)

Latephase

IgAmediated

Tcellmediated

IgG,Immunecomplexes

Enzymatic(e.g.lactoseintolerance)

Pharmacologic(e.g.vasoactiveamines)

Other(e.g.additiveintolerance

ImmediatePhase


Gut Permeability and Food Allergies

Clinical & Experimental AllergyVolume 41, Issue 1, pages 20-28, 11 NOV 2010


Labs


Symptom Characteristics:IgE vs. IgGIgE IgG

ALLERGY SENSITIVITYOnset Rapid (minutes) Delayed (hours)

Duration Brief (hours) Prolonged (days)

Mechanism Mast Cell Circulating Complexes

Quantity of Food Tiny Dose Dependent

Food Any (uncommon) Common Foods

Patient Awareness Often Rarely

Persistence of Lifelong Months After EliminationAntibody


The Celiac Iceberg

The celiac iceberg represents all persons genetically susceptible to celiac disease because of a positive celiac-associated antibody test. The majority of such persons have latent celiac disease. The tip of the iceberg represents the minority of persons who present with classic celiac disease.


Clinical & Experimental Allergy, 2011 (41) 2028.

1

4

32

56

7


Figure 3 | Proposed causes of dysbiosis of the microbiota. We propose that the composition of the microbiota can shape a healthy immune response or predispose to disease.

Nature Reviews in Immunology Vol 9 May 2009 | 313


Prevent infections(systemic and GI)

Regulate local and systemicimmune function

Metabolic pathway nutrients: glycemic control, cholesterol, amino acids

Enhance nutrient utilization

Regulate bowel motility

Regulate appetite(leptin, ghrelin)

Regulate inflammation(local and systemic)

Prevent neoplastic changes

Support mucosalbarrier

Probiotics and Prebiotics: Exploring the Mutually Beneficial Effects of Bacteria and

their Substrates in the Human Host

Prebiotics andProbiotics


Cancer

Arthritis

AtherosclerosisAlzheimers

Colitis

Psoriasis

Infection

Diabetes

Chronic inflammation plays a role in MOST disease conditions

Eczema

Inflammation


NFB bindstoDNAleading

activationof..

Leukotrienes Prostaglandins

NFB Activated

InflammatoryTrigger

CyclooxygenaseLipoxygenase

TNF,IL1,IL6

BiologicsRituximabEtanercept,

Etc.


TissueFactorPAI1

ICAMS,VCAMsSelectin,MIP

iNOS

NFB bindstoDNAleading

totranslationalactivationof..

CyclooxygenaseLipoxygenase

TNF,IL1,IL6OxidativeStress

DietaryComponentsVitamins,Minerals,EssentialFattyAcids,

nonessentialnutrients,Phytochemicals

PPARs NRf2


The Inflammatory Process: A Physiologic Algorithm

Antecedents:

Inflammatory Response (itis)


TriggersStressToxinsFood

InfectionsNutrient Insufficiencies

ThyroidHashimotosThyroiditisGraves Disease

SkinEczemaPsoriasisSclerodermaVitiligo

GI TractCeliacCrohn's DiseaseUlceratic Colitis

NervesPeripheral NeuropathyDiabetic Neuropathy

LungsAsthmaWegnersGranulomatosis

BloodLeukemiaLupusHemolyticDysglycemia

MusclesFibromyalgiaMuscular Dystrophy

BonesRheumatoid ArthritisAnkylosing SpondylitisPolymyalgia Rheumatica

BrainMultiple SclerosisAutismGuillain-Barre SyndromePsychological


Leaky Barriers: A Common Antecedent for Chronic Inflammatory Disease


Spectrum of virulence

poliomyelitis in a child0.1-1% of infections are clinically apparent

rubella50% of infections are clinically apparent

rabies100% of infections are clinically apparent

Asymptomatic Infections: The Iceberg Concept

asymptomatic Carrier/health

classical clinical disease

less acute/obviousdisease

Acute infections = obvious infections

Dysbiotic infections = chronic immune activation

Most people probably have some dysbiosis, but many tolerate it

for better or for worse.


CysteinylLeukotrienes

Cyclooxygenases(COX1,COX2)

Lipoxygenase

HPETE(hydroxyperoxyeicosatetraenoicacid)

LeukotrieneA4

LeukotrieneC4

LeukotrieneD4

LeukotrieneE4Prostacylcin(PGI2)

Thromboxane(TXA2)

Thromboxane(TXA2)

PGD2

PGE2

PGF2

LTB4

H2O

6ketoPGF1

(endothelium) (platelets)

Glutamicacid

Arachidonic Acid CascadeArachidonicacid(AA)

20:4n6

ProstaglandinH2 (PGH2)

Prostacyclinsynthase

Thromboxanesynthase

PGDSynthase

PGESynthase

GlutathioneStransferase

LipoxinsF2Isoprostanes


Baselinenutritionaldeficiency

Increasedbaseline

oxidativestressImpaired

immunefunctionImpairedmucosaldefenses

Increasedsusceptibilityto

infection

Exacerbationofnutritiondeficiencies,

tissuedepletion

Facilitatedviralmutation

Directmucosaldamage

Exacerbationofoxidativestress

Anorexia,reducedfoodintake,and

increasedmetabolicandrepairneeds

Increasedfrequency,severity,anddurationof

infection

Facilitatedviral

replication


Production

Sensitivity

Transport

Detoxification

Production/synthesis and secretion of the hormone

Transport/conversion/distribution/ interaction with other hormones

Cellular sensitivity to the hormone signal

Detoxification/excretion of the hormone


DHEASulfateSO4

O

DiHydroTestosterone

OH

O

CH3

CH3

17 hydroxysteroiddehydrogenase Aromatase

11 hydroxysteroiddehydrogenase1&2 Cytochrome3A4

CytochromeP450scc 18hydroxydehydrogenase 17hydroxylase Cytochrome1A1

18hydroxylase 21hydroxylase 11 hydroxylase Cytochrome1B1

17,20lyase 3 hydroxysteroiddehydrogenase,

Isomerase

CatecholOMethylTransferase(COMT)

Sulfatase(SO4)Sulfotransferase(+SO4)5 reductase

EstroneSulfate

16Hydroxyestrone

O

HO

OH

2HydroxyestroneHO

HO

O

4HydroxyestroneHO

HO

O

2MethoxyestroneHO

H3CO

O

4MethoxyestroneHO

OCH3

O

Estriol

OH

HO

OH

Cholesterol

PregnenoloneHO

O

Progesterone

O

O

11deoxycorticosterone

OOH

O

Corticosterone

HOO

OH

O

18OHcorticosterone

HOHO

O

OOH

Aldosterone

OHOHO

O

O

17OHpregnenoloneHO

OHO

17OHprogesteroneO

OHO

11deoxycortisol

OHO

OH

O

Cortisol

HO OHO

OH

O

Cortisone

OH

OHO

O

O

DHEAHO

O OH

SO4

Androstenedione

O

O

Testosterone

OH

OEstradiol

HO

OH

EstroneHO

O

Ster id genic Pathways


HO

Cholesterol

Pregnenolone

O

HO

Progesterone

O

O

11-deoxycorticosterone

OOH

O

Corticosterone

HO OOH

O

18-OH-corticosterone

HOHO

O

OOH

Aldosterone

OHO OOH

O

17-OH-pregnenoloneHO

OHO

17-OH-progesteroneO

OHO

11-deoxycortisol

OHO

OH

O

Cortisol

OHO

OH

O

OHO

OH

OCortisone

DHEAHO

O

Androstenedione

O

O

Testosterone

OH

OEstradiol

HO

OH

EstroneHO

O

Cortisol Steal


Primary Effects

(cellular events regulated by primary mediators)

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Secondary Outcomes

(waist-hip ratio, blood pressure, cholesterol, glucose)

Tertiary Outcomes

(cardiovascular disease, severe cognitive decline, diabetes, hypertension, cancer)

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(insulin, immune capacity, glucose tolerance)

Repeated Hits Prolonged Response Inadequate Response

Stress RecoveryRe

s

p

o

n

s

e

Lack of Adaptation


FactorsthatAffectThyroidFunction

Factorsthatcontributetoproperproductionofthyroidhormones Nutrients:iron,iodine,

tyrosine,zinc,seleniumvitaminE,B2,B3,B6,C,D

Factorsthatinhibitproperproductionofthyroidhormones Stress Infection,trauma,radiation,

medications Fluoride(antagonisttoiodine) Toxins:pesticides,mercury,

cadmium,lead Autoimmunedisease:Celiac

FactorsthatincreaseconversionofT4toT3 Selenium Zinc

Factorsthatimprovecellularsensitivitytothyroidhormones VitaminA Exercise ZincCell

FactorsthatincreaseconversionofT4toRT3 Stress Trauma Lowcaloriediet Inflammation

(cytokines,etc.) Toxins Infections Liver/kidney

dysfunction Certainmedications

T3RT3T3andRT3competeforbindingsites

Nucleus/Mitochondria

T4


T4

T3 RT3

D35-deiodinase

(Se Independent)

D1 (and D2)5-deiodinase

(Se Dependent)

T2 (inactive)

D35-deiodinase

(Se Independent)

D1 5-deiodinase

(Se Dependent)

T2 (inactive)Peeters, RP et. al. Reduced Activation and Increased Inactivation of Thyroid Hormone in Tissues of

Critically Ill Patients J Clin Endocrinol Metab. 2005 Oct;90(10):5613-20.


Stress signal to thecerebral cortex

Visceralbrain

NeurohypothalamusACh

Acute stress

Adrenalmedulla

Sympatheticnervoussystem Epinephrine

release

Chronicstress

Endocrinehypothalamus

CRH Anteriorpituitary

CRHPOMC

-Lipotropin

ACTH

-Endorphin

Adrenalcortex

Cortisolrelease

PNMTinduction

Neuroendocrine Pathways Associated with the Stress Response

Corticotrophinvia Gs

Estrogen Production/Metabolism(the estrogen factory in the breast)

DHEA Androstenediol

Androstenedione Testosterone

AromArom

Estrone Estradiol

STSSULT STSSULT

E1SE2S

DHEAS AdiolS

17HSD1

17HSD2

17HSD5

STS STS

3HSDisomerase

17HSD

17HSD2

17HSD6,2

3HSDisomerase

17HSD217HSD1


Macronutrients ATP

ATPPool

ProteinFat Carbs

oxidationTCACycle

ETC


LipoicAcid

Magnesium


Oxidative Stress Exposure to Medications Exposure to Heavy Metals Exposure to Chemicals Exposure to PCBs Exposure to Pesticides

Causes of 2o Mitochondrial Dysfunction


How Does Body Protect From ROS?1. Enzymes

Catalase (Fe)Superoxide dismutase-SOD (Zn, Cu, Mn)Glutathione peroxidase (Se) and glutathione

reductase2. Dietary Anti-Oxidants

Vitamin C for aqueous compartmentsVitamin E for lipid compartmentsCarotenoids, flavonoids, etc.

3. Endogenous Anti-Oxidant MoleculesGlutathione, cysteine, CoQ10, lipoic acid, uric acid, cholesterol.


Regulation of Cognitive Function

NeurogenesisNeuroprotection

Synaptic Plasiticity

Sedentary LifestyleDiabetes, ObesityHigh cholesterol

Exercise

Adaptive Cellular Stress

ResponsesBDNFIGFsHSPsUCPs

MnSODHO-1

Oxidative StressInflammation

Impaired Synaptic PlasticityImpaired Neurognesis

Neurodegeneration

Cognitive ImpairmentDisease Progression

Cognitive ImpairmentDisease Progression

Adapted from: Stranahan and Mattson, 2011

Caloric Restriction

Mild Oxidative Stress

PGC-1


Caloric restriction Physical exercise

DHAMental exercise

BDNF


Treatment:

Get adequate nutrition Stay cool and hydrate Prevent infections Supplements:

CoQ-10 Omega-3 Fatty Acids

Exercise (physical & mental) Avoid toxins

a TO DO list to support your mitochondrial function


AnthropometricsScreening Exam Vitals

Blood Pressure Height and Weight Pulse Ox

Body Mass Index Waist to Hip Ratio

Waist Circumference Hip Circumference

Waist to Height Ratio Bioelectrical Impedance Analysis


Body SDefining Body Composition

Pattern Recognition

overfatOVER VAT

overfatOVER VAT

overfatOVER SAT

overfatOVER SAT

OVER WeightOVER Weight

GynoidObesityGynoidObesity

AndroidObesityAndroidObesity


NO

NO

Increased WC?

Possible High Muscle

Mass or Athlete

NO

Increased BIA Fat%?

YES

Abnormal High BMI?

YES

Dx:OverFatYESYES

NO

Gut/Detox/HPATG dysfunctions?

Assessing Body Composition

YES

NO YES

IdealSkinny Fat or Metabolically

Obese

NO

Increased WHR?

TLCNx/ Rx

Increased WC or WHR?

YES

Increased BIA Fat%?

NO

Increased WHR?

Increased BIA Fat%?

Metabolically Obese

(OverVAT)

YESNO

Gynoid Obesity/overSAT

Gynoid Obesity/overSAT

Possible High Muscle Mass

or Large Skeletal Frame

Increased BIA Fat%?

Dx:Overweight/Obese

Android Obesity(OverVAT)

MetSyn?

Dx:OverVAT

YES

YES


Role of ROS on Hypertension and Hyperlipidemia and Atherosclerosis

A-II

AT1 Receptor

NAD(P)H Oxidase

CytokinesGrowth Factors

O2 (Superoxide Anion)Ox LDL Inactivates NO

Upregulates

LOX-1Endothelial

Receptor for Ox LDLHypertension

Foam CellsFatty Streaks

HypertrophyProliferationED

Atherosclerosis


InsulinResistance

Chronic Stress

Genetic propensity

Elevated Fasting and PP

Insulin & Glucose

Visceral Adiposity

Lack of ExerciseSmoking

High Glycemic Diet

Inflammation

Antecedents, Triggers and MediatorsAntecedents, Triggers and Mediators

Sleep


Treatments that Change Risk Differentially

statins

statin + ezetimibe

low fat diet

Lipid-RichDISORDERS

omega 3 fatty acids fibrates niacin exercise low glycemic impact diet

Triglyceride-RichDISORDERS

METABOLICCARDIOCOMPREHENSIVE RISK REDUCTION


The Road to Diabetes: Insulin Resistance and Hyperinsulinemia

Overproductionof FFAs

by adipose cells

Glucose toxicity leading to further impaired insulin secretion

Inability to suppress hepatic glucose

production

Stimulates gluconeogenesisIncreases muscle insulin resistance

Impairs insulin secretion

Increased muscle cellresistance toinsulin action

Elevated serumglucose

Elevated serumglucose Elevated serum glucose


Type 2 Diabetes

Hypertension

Dyslipidemia

Cardiovascular Disease

Osteoporosis

Obesity

PCOSNASH

Cognitive Decline / Alzheimer's Disease

Sarcopenia

Erectile Dysfunction

Sleep Apnea

Clinical Consequences of CardioMetSynClinical Consequences of CardioMetSyn

CardioMetSynCardioMetSyn


Communicate this


Inflammatory elements Inconsistent behaviors Imbalanced fats High glycemic impact

Standard American Diet

Healthy foods Phytonutrient dense Balanced diet

Core Food Plan Foods tailored to a

clinical condition Detox and Cleansing Elimination/Allergies CARDIOMETABOLIC

Modified Therapeutic Intervention

Clinical Use of Food as Medicine


Basic Toxicology

Exposure

Assimilation

Retention

Toxicity

2014 The Institute for Functional MedicineFrom. Larry Needham, PhD: CDC NCEH Presentation (2004)


Periodontal Disease

Root Canals Mercury Amalgams

Mixed Metal/Base Metal

Crowns

Orthodontic Appliances

Dental Implants

Genetics Epigenetics Lifestyle Quality of Care

InflammationOxidative

StressImmune

Dysregulation


TOTAL TOXIC LOADequals

Total Toxic Exposure minus

Ability to Detoxify and

Excrete Toxins


KnownEffects

The Limits of Certainty and Under-recognition of Toxic Threats

THE UNKNOWN

UNKNOWN

WHATWEKNOW

WHATWEDONTKNOW

Long latency effects


Thereiswidevariationinindividualsensitivitytotoxicantexposure.Thismeansthatinalargepopulationwithwidespreadexposures,evenwhenthedosageisacceptableonaverage,manypeoplewillstillbehurt.Asignificantmarginofsafetyisrequiredtopreventsuchinjuries.From:InHarmsWay:ToxicThreatstoChildDevelopment.GreaterBostonPSR


heavymetals(Pb,Hg,As,Cd)

polycyclicaromatichydrocarbons

(PAH)

phthalates(i.e.plasticizers)

phenols(BPA,triclosan)

organochloride(OC)pesticides

organophosphate(OP)pesticides

polychlorinateddibenzodioxins

(PCDDs)&furans (PCDFs)

polychlorinatedbiphenyls(PCBs)

polybrominateddiphenyl ethers

(PBDEs)

polyfluorinatedcompounds(PFCs)


Pattern Recognition

Undernourished

Reduce Exposures

Ensure a Safe Detox

2014 The Institute for Functional MedicineLiska;ExploreMarch2006,Vol 2,No2,pg125


Types of Reactions

Phase ICytochromeP450enzymes:

OxidationReductionHydrolysis

Parent Compound

Water-Soluble

Compound

Phase IIGlucuronosyl TransferaseSulfotransferasesAminoAcidConjugationGlutathioneConjugationAcetylation

ActivatedIntermediate


The Role of Nutritional Factors in Liver Detoxification

FreeRadicals

Toxins Conjugated MetabolitesToxic

IntermediatesPhase I Phase II

Phase INutritional Support

AntioxidantsVitamin & Mineral Cofactors

Phase IINutritional Support

Conjugating AgentsVitamin & Mineral Cofactors

XenobioticsEndotoxins

Non-Polar, Lipophilic Poorly Excreted

Cytochrome P-450Mixed Oxidase System

Secondary Tissue Damage

EnzymaticConjugation

Less ToxicPolar

Water-solubleReadily Excreted


Oxidation, reduction, or hydrolysis Introduce or expose a functional group on

the parent compound Rendering parent more polar May activate inert compounds

(e.g. pro-drugs & pro-carcinogens)

Phase I Reactions


Phase II Reactions

Covalent linkage between parent compound and a polar (water-soluble) moiety

Phase II Products are generally: Metabolically Inactive Prepared for elimination (via bile or urine)


Imbalanced Detoxification

Phase ICYP P450

Phase IIConjugation

Damage to DNA, RNA, Proteins

Reactive Intermediate

Non-Polar Xenobiotic

InertWater-Soluble

Metabolite


PhysicalExam&ConventionalLabs

Intake&MedicalHistory

KeyQuestionnaires

KnownToxicExposures:Occupational,Lifestyle,Residential,Medical?

ToxicitySigns/Symptoms?NutritionalDeficiencies?Detox&Elim.Capacity?

ToxicDamage

Nutritional&

Assimilation

BodyBurden

EnvironmentalExposures PatientSensitivityLevel

MSQTEQ

ReviewofFindings&InterventionProgram

FUNCTIONALLABTESTS(ifindicated)

GeneticSusceptibility


Physical Exam & Conventional Labs

Intake & Medical History

Key Questionnaires

Known Toxic Exposures: Obtain a Historical Implant

List of the Entire Body what was used and how did it work

Ask about periodontal disease

Root Canals if present 3D cone beam evaluation to screen for infection

Oral soft and hard tissue exam: Look for red, puffy swollen gums

around crowns; note any mucosal lesions on cheeks and tongue

Salivary pH ideal is 6.8+ Oral galvanism Ammeter is

best, chew strip of Aluminum foil (1x 2) as alternative

Mercury chew test for patients with Amalgams

Environmental Exposures Patient Sensitivity Level

MSQTEQ


Food Plays a Role in All Phases of Detoxification

ToxinsIn

PhaseISupport

PhaseIProtection

PhaseIISupport

ToxinsOut

FOOD


Phase I Nutrients and Food Sources on the Detox Food Plan

ToxinsIn

PhaseISupport

PhaseIProtection

PhaseIISupport

ToxinsOut

Nutrient FoodSourcesRiboflavin(vitaminB2) Soybeans,spinach,tempeh,crimini mushrooms,eggs,asparagus,almonds,

turkeyNiacin(vitaminB3) Tuna,chicken,turkey,salmon,lamb,beef,sardines,brownricePyridoxine(vitaminB6) Tuna,turkey,beef,chicken,salmon,sweetpotato,potato,sunflowerseeds,

spinach,bananaFolicacid Lentils,pintobeans,garbanzobeans,blackbeans,navybeans,turnip

greens,broccoliVitaminB12 Choosemethylcobalamin forsupplementalsource,sardines,salmon,tuna,

cod,lambbeefGlutathione Undenatured wheyprotein,asparagus,curcumin,broccoli,avocado,

spinach,garlic,foodshighinvitaminC(e.g.,citrusfruits)andselenium(e.g.,Brazilnuts)

Branchedchainaminoacids

Wheyprotein,chicken,fish,eggs

Flavonoids Virtuallyallplantfoods,includingapples,apricots,blueberries,pears,raspberries,strawberries,blackbeans,cabbage,onions,parsley,pintobeans,andtomatoes

Phospholipids Soy,sunflowerseeds,eggs


Antioxidant Nutrients and Phytonutrients that Protect Against Overproduction of Phase I Metabolites

Nutrient FoodSourcesCarotenes(vitaminA) Essentiallyallred,orange,yellow,andgreenplantfoodsAscorbicacid(vitaminC) AllwillbehigherinvitaminCifuncooked:Bellpeppers,papaya,citrusfruits,broccoli,

Brusselssprouts,strawberries,kiwiTocopherols (vitaminE) Sunflowerseeds,almonds,spinach,Swisschard,avocado,turnipgreens,asparagus,

mustardgreensSelenium Brazilnuts,tuna,sardines,salmon,turkey,cod,chicken,lamb,beefCopper Sesameseeds,cashews,soybeans,mushrooms(shiitake),sunflowerseeds,tempeh,

garbanzobeans,lentils,walnuts,limabeansZinc Beef,lamb,sesameseeds,pumpkinseeds,lentils,garbanzobeans,cashews,quinoa,

turkeyManganese Cloves,(glutenfree)oats,brownrice,garbanzobeans,spinach,pineapple,pumpkin

seeds,tempeh,soybeansCoenzymeQ10 Meat,poultry,fishThiols Chives,daikonradishes,garlic,leeks,onions,scallions,shallotsFlavonoids Virtuallyallplantfoods,includingapples,apricots,blueberries,pears,raspberries,

strawberries,blackbeans,cabbage,onions,parsley,pintobeans,andtomatoesSilymarin Milkthistle(herb),artichokesPycnogenol Smallamountsinthepeels,skins,orseedsofgrapes,blueberries,cherries,andplums

ToxinsIn

PhaseISupport

PhaseIProtection

PhaseIISupport

ToxinsOut


Nutrients for Phase II Conjugation Pathways

Nutrient FoodSources

Glycine Beef,chicken,lamb

Taurine Fish,meat

Glutamine Beef,chicken,fish,eggs,cabbage,beets,beans,spinach,andparsley

Nacetylcysteine Mosthighproteinfoods(e.g.,chicken),garlic,cruciferousvegetables

Cysteine Beef,chicken,lamb,fish

Methionine Eggwhite/wholeegg,sesameseeds,Brazilnuts,soyprotein,chicken,tuna,beef,chickpea,almonds,pintobeans,lentils,brownrice

ToxinsIn

PhaseISupport

PhaseIProtection

PhaseIISupport

ToxinsOut


Sequencing a Detox Program

REMOVE DetoxFoods

PotentialTherapeuticInterventions

Nutraceuticals&BotanicalsMedical/FunctionalFoodLiquidFastingChelationTherapyHydrotherapyHomeopathicDrainage

1 2 3Reduce Toxin ExposureInclude Dietary Changes

ReduceorRemoveAlcohol&CaffeineArtificialSweetenersFats&SugarHighAllergenFoodsEnvironmentalToxicantsToxicHabitsStressors

MayIncludeVegetablesCitrusProteinGoodOilsFiberWaterHerb

4 Maintenance Therapeutic Interventions & Monitoring TherapyTherapeuticIntervention Maintenance

MayIncludeMVM/EFAsBowelSupportKidneySupportLiverSupport


Methylation: Interconnections with Folate

Folate CycleMethionine Cycle

Transsulfuration

NeurotransmitterUrea Cancers

ASCVD

Adverse DrugEnvironmental

Reactions

DepressionAnxietySchizophrenia

PeriphVascdiseaseAsthma

neuropathies

DementiasCNS PathologiesAutism Spectrum

leaky gut. pdf

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