lymphomyosot aids conventional therapy in diabetic peripherial neuropathy 2003

FORTBILDUNG UND PRAXISFÜR DEN HAUSARZT

Reprint

Diabetic Peripheral Neuropathy

Adjuvant Homeopathic TreatmentEnhances the Effects of ConventionalTherapy

Alois Eiber, Peter Klein, Michael Weiser

AbstractContext: This study compares the efficacy of a combi-nation therapy consisting of alpha-lipoic (α-lipoic)acid plus Lymphomyosot (a homeopathic combina-tion medication for treating edema in the extracellularmatrix) to α-lipoic acid monotherapy in the treatmentof diabetic peripheral neuropathy.Patient population: 269 type II diabetics withperipheral neuropathy and residual sensation intoes/foot/ankle.Methods: Multicenter, open-label prospective cohortstudy (add-on design).Results: Statistically significant differences betweentreatments were seen in favor of the Lympho-myosot/α-lipoic acid combination therapy withregard to the following subjective criteria: light touch

(monofilament), numbness, paresthesia, nocturnalspontaneous pain, and reduction in palpable edema inthe foot/ankle. The combination therapy also pro-duced more rapid improvement in symptoms, andphysicians’ overall ratings of its efficacy were higher.No adverse drug events were reported for either treat-ment group.Conclusion: Adding Lymphomyosot to α-lipoic acidtherapy for diabetic peripheral neuropathy results instatistically significant and clinically relevant improve-ments in sensation and palpable edema in comparisonto α-lipoic acid monotherapy.

Keywords: Lymphomyosot, α-lipoic acid, diabeticneuropathy, homeopathy

P R O S P E C T I V E C O H O R T S T U D Y

Der Allgemeinarzt 2003;25(8):610-42

Introduction

In Germany alone, diabetic periph-eral neuropathy (DPN) results in ap-proximately 25,000 foot amputationsper year. As early as 1989, the WorldHealth Organization’s St. VincentDeclaration called for halving thisamputation rate within tenyears. This goal is still farfrom being accomplished.1, 2

The WHO and the Interna-tional Diabetes Federationpredict a doubling in annual-ly reported new diabetescases by 2025.1, 3 The numberof patients with diabetic footlesions is also expected tocontinue to increase sharply,since at least one in three dia-betics is affected by DPN.4

Neuropathic/neuroischemiccauses account for 85-90% ofcases of diabetic foot syn-drome, and 45-60% of casesare assumed to be purelyneuropathic in origin.5, 6 Typ-ical symptoms of diabetic neuro-pathy include burning, stabbing pain (“burning feet”), paresthesia,hyperesthesia, and numbness. Othercharacteristics include nocturnal exacerbation of pain and im-provement in symptoms while walk-ing.2, 3, 6

Clinical monitoring of foot sensitivi-ty to temperature, pain, movementand touch is very important. Defi-ciencies in or loss of these types ofsensations indicate the developmentof complications such as neuropathicfoot ulcers, edema, osteoarthropa-thy, Charcot’s joint, and os-teomyelitis.4

In the purely neuropathic diabeticfoot, peripheral neuropathy is thesole cause of foot lesions. Ratherthan inadequate perfusion, the pri-mary manifestation is severe damageto the sympathetic nerves of the vas-cular walls, which results in periph-eral vasodilation and opening of thearteriovenous anastomosis with sub-sequent hyperperfusion and possibleswelling of the foot.7 Characteristicwarning signs such as temperature

sensitivity and pain duringweight-bearing activities are not pro-nounced.3 The foot appears rosy andwarm with good perfusion.8 Re-duced sensitivity to pain preventspatients from noticing foot injuriesand infections, which tend to healpoorly in diabetics, and inflamma-

tion may go unnoticed and untreateduntil it is severe.9 Foot ulcers maynot heal, and necrosis may eventual-ly lead to loss of the limb.2

The primary approach to treating thecause of diabetic peripheral neuropa-thy is to eliminate hyperglycemia asan etiological factor by normalizingsugar metabolism to the greatest ex-tent possible.4 Alpha-lipoic acid is afrequently prescribed treatment forDPN. Administered either intra-venously or orally, α-lipoic acid re-duces neuropathic symptoms/defi-cits. Through reduction of free radi-cals, it relieves oxidative stress andincreases glucose utilization, whichin turn reduces levels of nonenzy-matic glycosylation products. Theresulting improvement in energyavailability leads to improved nerveresponse and reduces vascular dys-function.10 Adjuvant therapies in-cluding physical therapy, bal-neotherapy, relaxation therapy, tran-scutaneous electrical nerve stimula-tion (TENS) and acupuncture mayoffer additional symptomatic relieffrom pain.4 Platelet derived growth

factor (PDGF) in the form of therecombinant drug beclapermin is atreatment that has recently becomeavailable for severe cases.6, 11

In spite of all therapeutic efforts,however, the amputation rate amongpatients with diabetic foot syndromeis not declining worldwide.1, 2, 7, 12 As

a result, the search is on foralternative and adjuvantmeasures. The antihomotoxicapproach aims at optimizinglymphatic functioning inorder to improve nutritionand waste removal on thecellular level.8, 13 Antihomo-toxic medicine pays particu-lar attention to the extracel-lular matrix as the transit areabetween capillaries and thecells (including neurons andtheir axons) that they supplywith nutrients.13 In diabetes,the detrimental effects ofconstant excess glucose causethe matrix to respond withinflammatory and edematous

changes.14 These changes are evidenton ultrasound and angiographic im-ages even in early-stage diabetic neu-ropathy, before vascular damage isdetected.8

Lymphomyosot (N) (drops, tablets,or injection solution), manufacturedby Biologische Heilmittel HeelGmbH of Baden-Baden, Germany,is a homeopathic combination med-ication containing components ofplant, animal, and mineral originprocessed in accordance with theregulations of the German homeo-pathic pharmacopoeia. The drugportraits of its constituents suggestapplications in a number of patholo-gies (such as edema, susceptibility toinfection, swollen glands, hypertro-phy of the tonsils, tonsillitis, andperfusion disorders) in which ede-matous disorders of the extracellularmatrix play a direct or indirect role.15

The therapeutic efficacy of Lym-phomyosot has been confirmed bymultiple clinical studies.15-20 Further-more, in an observational study of 90type II diabetics, Dietz showed thatLymphomyosot improved clinical

Absence of sensation of pain is the decisive factor in the patho-genesis of the most serious types of diabetic foot lesions, includinggangrene, and amputation of toes.


3Der Allgemeinarzt 2003;25(8):610-4

symptoms of diabetic neuropathy bystimulating lymph flow.8 After Lym-phomyosot therapy, edema was re-duced and sensation improved in amajority of patients. Based on thesestudies, the current multicenter,prospective, open-label cohort studywas designed to systematically ex-amine a larger patient population inorder to determine whether a com-bination therapy of α-lipoic acidplus Lymphomyosot is superior toα-lipoic acid alone in its effect onsymptom severity in diabetic neu-ropathy.

Results

Medical historyWith regard to demographic para-meters and vital signs, there were no

obvious differences between the twogroups at the beginning of the study.Furthermore, no statistically signifi-cant differences between groupswere found with regard to averageduration of the diabetic illness, typeof diabetes therapy prescribed todate (oral antidiabetic medications,diet, insulin), or the presence of gen-eral risk factors such as hypertensionand obesity. Significantly, diabetesmanagement in both groups wasrated only “satisfactory” by thephysicians at the beginning of thestudy, and reduced compliance isalso reflected in slightly elevatedmean HbA1c levels in both groups(Group A: 7.2%; Group B: 7.4%;see Table 1).

Analysis of data on the patients’history of DPN and skin lesions also

revealed no significant differencesbetween Group A and Group B withregard to these criteria. Detailedclinical assessments of peripheralneuropathy revealed that the pre-dominant symptoms in both groupswere: pain sensitivity (pinprick),sensitivity to light touch (monofila-ment), numbness, paresthesia, and(nocturnal) spontaneous pain. Thesymptom “palpable edema in thefoot/ankle” occurred in a significant-ly higher percentage of patients inGroup B (see Table 2).In both groups, as expected, diabetesmellitus was accompanied by a num-ber of concomitant illnesses, mostcommonly endocrine/metabolic/nutritional disorders, circulatorydisorders, or diseases of the muscu-loskeletal system and connectivetissue.

Tab. 1: Demographic data, vital signs, blood test results, and characterization of patients’ type II diabetes at the beginning of the study.(1Fisher’s exact test, 2variance analysis, *multiple listings possible, SD = standard deviation).

Criteria Group A: Group B:α-lipoic acid α-lipoic acid +(N = 114) Lymphomyosot (N = 155) Statistics

Gender (f/m, %) 58/42 53/47 P = 0.42 1

Age (mean ± SD, in years) 65 ± 9.9 64 ± 12.0 P = 0.66 2

Weight (mean ± SD, in kg) 81 ±13.1 80 ±14.8 P = 0.72 2

Systolic blood pressure (mean ± SD, mmHg, seated) 145 ± 14.6 145 ± 16.9 P = 0.94 2

Diastolic blood pressure (mean ± SD, mmHg, seated) 86 ± 9.1 85 ± 8.6 P = 0.28 2

Pulse (mean ± SD, beats/min, seated) 76 ± 8.8 75 ± 10.4 P = 0.36 2

Fasting blood sugar (mean ± SD, mmol/l) 148 ± 39.4 151 ± 44.0 P = 0.54 2

HbA1c (mean ± SD, %) 7.2 ± 1.1 7.4 ± 1.2 P = 0.10 2

Duration of diabetes (mean ± SD, in months) 101 ± 72.1 108 ± 75.4 P = 0.45 1

Diabetes management (mean ± SD) 2.8 2.7 P = 0.97 1

Scale: very good (1), good (2), satisfactory (3)

Type of diabetes therapy* (%)

•oral antidiabetic medication 83.3 75.5 P = 0.12 2

•diet 40.4 44.5 P = 0.50 2

• insulin 20.2 29.0 P = 0.10 2

•other 3.5 2.6

Risk factors* (type and frequency, %)

• total 97.4 94.2 P = 0.21 2

• hypertension 71.9 65.8• obesity 53.5 51.6• fatty liver 26.3 21.9• hyperlipidemia 61.4 53.5• gout 18.4 13.5• nicotine/alcohol 23.7 20.6• medications 7.9 7.7• other 4.4 0.0

TreatmentThe type of treatment for DPN was left to the discretion of each patient’sphysician and took individual cir-cumstances into account. 43% of pa-tients in Group A and 49% inGroup B were prescribed 300 to 600mg per day of oral α-lipoic acidwhile 43% of Group A and 37% ofGroup B were prescribed the sameoral dosage preceded by two to fourweeks of intravenous therapy (also300 to 600 mg per day).The majority of the 155 patients whoreceived adjuvant Lymphomyosot(oral only) were prescribed the stan-dard dosage of three tablets or 15drops three times a day.Average duration of therapy was 184days for Group A and 182 days forGroup B.

Target criteria

Neuropathic symptomsOver the course of therapy, bothtreatment groups experienced obvi-ous improvements in subjectivesymptoms. With regard to the targetcriteria sensitivity to touch (monofil-ament), numbness, paresthesia, and(nocturnal) spontaneous pain, how-ever, findings revealed statisticallysignificant advantages to administer-

ing α-lipoic acid in combinationwith Lymphomyosot. Especiallytelling are the results with regard tothe criterion “palpable edema in thefoot/ankle.” At the beginning of thestudy, 49 patients (46%) in Group Aand 88 patients (63%) in Group Bhad palpable edema in the feet/an-kles (P<0.01). Edema was reduced(in comparison to initial examinationfindings) in only 18% of the patientsin Group A who experienced thatsymptom. In contrast, 47% of thepatients with edema in Group B (ad-juvant Lymphomyosot) experiencedimprovement (P<0.001) (see Figure).Statistical analysis of the criterion“onset of improvement in symp-toms” (a measure of general state ofhealth) revealed significantly morerapid onset of efficacy in Group B(adjuvant Lymphomyosot) (Ptotal

<0.0058). In the first two months,improvement in neuropathic symp-toms occurred in only 24% of thepatients in Group A in comparisonto 37% in Group B.

Blood test resultsIn both groups, scores for “overalldiabetes management” improvedfrom “satisfactory” to “good” overthe course of the study (from 2.8/2.7at the beginning of the study to



MethodsProcedureThe participating physicians (47 family practitionersand/or internists, some specializing in diabetes care)were recruited by Heel GmbH of Baden-Baden. Med-ical histories and clinical data on a total of 269 pa-tients ranging in age from 20 to 94 years wererecorded using standardized questionnaires. Eachphysician reported on several patients treated exclu-sively with α-lipoic acid (Group A, n = 114) as wellas several others treated with a combination of α-lipoic acid and Lymphomyosot (Group B, n = 155),with a maximum of six patients per physician. Thetype of treatment each patient received (i.e., with orwithout adjuvant Lymphomyosot therapy) was left tothe physician’s discretion. For both groups, durationof treatment was six months. Data were compiled onpatients/treatments and target criteria (see categoriesbelow) during initial, interim (after three months), andexit examinations.

PatientsInclusion criteria• Diabetes mellitus type II (for medical history data,

see below)• Confirmed diagnosis of diabetic peripheral neuro-

pathy (for medical history data, see below)

Exclusion criteria• Total absence of sensation in toes/foot/ankle• Known intolerance reactions to Lymphomyosot

and/or α-lipoic acid

Demographics/vital signs• Age (in years)• Gender (f/m)• Height (in cm)• Weight (in kg)• Blood pressure (seated, in mmHg)• Pulse (seated, beats per minute)

Medical history: Type II diabetes• Duration of diabetic illness (months)• Overall diabetes management (very good, good,

satisfactory, unsatisfactory)• Type of diabetic therapy (oral antidiabetic medica-

tions, diet, insulin, other)• Risk factors (no/yes; for list, see Table 1)• Fasting blood sugar (mmol/l)• HbA1c (%) (Scale: <6.5 very good, 6.5-7.0 good,

7.1-8.0 satisfactory, >8.0 unsatisfactory)• Concomitant illnesses/therapies

Medical history: Peripheralneuropathy/skin lesions• Duration of illness (months)• Patient status (ongoing care/returning/first time

treated) • Extent of the neuropathy (toes only/foot/foot &

ankle)• Ulcers/gangrene (no/yes, size in cm: <0.5, 0.5-

1.5, >1.5)• Other skin lesions (no/yes, type: fissures, eczema)• Pale/livid skin discoloration (no/yes, scale: slight,

moderate, severe)

0 10 20 30 40 50 60 70 80

Edema foot/ankle (EE)

Edema foot/ankle (IE)

Reduction in pain during movement (EE)

Reduction in pain during movement (IE)

(Nocturnal) spontaneous pain (EE)

(Nocturnal) spontaneous pain (IE)

Paresthesia (EE)

Paresthesia (IE)

Numbness (EE)

Numbness (IE)

Light touch (monofilament) (EE)

Light touch (monofilament) (IE)

Sensitivity to pain (pinprick) (EE)

Sensitivity to pain (pinprick) (IE)

% of patients demonstrating improvement

Alpha-lipoic acid (n=114)

Lymphomyosot + alpha-lipoic acid (n=155)

Fig.: Efficacy of treatment: Percentage of patients demonstrating improvement in target criteriaas compared to entrance examination findings (IE = interim examination, EE = exit examina-tion, * P<0.05)



2.3/2.2 at the end for Groups A andB respectively. At the same time, av-erage blood sugar levels dropped(from 148/151 mmol/l at the begin-ning of the study to 133/131 mmol/lat the end), as did mean HbA1c lev-els (from 7.2%/7.4% at the begin-ning of the study to 6.7%/6.8% atthe end for Groups A and B respec-tively, Pgroup comparison >0.05 in eachcase).

Evaluation of therapyThe superiority of the combinedtherapy is also reflected in ratings ofthe therapeutic results. In Group B,a significantly (Ptotal <0.0018) largernumber of patients achieved “verygood” or “good” results (70% ofGroup B vs. 46% of Group A). Sim-ilarly, the treatment failure rate ingroup A, at 16%, was four times ashigh as in Group B.

TolerabilityNo adverse drug events occurred ineither of the treatment groups dur-ing the course of the study. In bothgroups, the physicians rated patienttolerance of therapy as either “verygood” or “good” in over 98% ofcases.

Compliance/dropoutsThe two treatment groups did notdiffer significantly with regard to pa-tient compliance. In both groups,compliance was rated either “verygood” or “good” in over 90% ofcases.A total of 10 patients (four fromGroup A and six from Group B) ter-minated treatment prematurely. Rea-sons given were: inadequate efficacyof the therapy (three cases) and per-sonal reasons (seven cases).

DiscussionThe causes of loss of sensation in di-abetic foot syndrome include func-tional disorders of the autonomicnervous system. Poorly controlleddiabetes, in particular, promotesdenervation because the constantexcess glucose flooding the extra-cellular matrix leads to nonenzymat-

ic glycosylation processes that ob-struct transit between blood/lymphvessels and peripheral nerves.14, 21

Reduced matrix permeability leadsto reduced lymph evacuation. Inearly-stage peripheral neuropathy,the resulting edema can be detectedby means of sonography, NMR im-aging, or body tissue measurements.Vascular damage can be detectedwith the help of color Dopplersonography and angiography.8 Thesignificance of edema in the develop-ment of diabetic foot syndrome isunderlined by the observation thatarterial and venous vascular damageis already evident in moderateedema; in severe chronic edema, in-creasingly serious vascular sclerosiswith lumen constriction becomes ev-ident.8 Edema – specifically, extracel-lular edema – plays a crucial role indiabetes mellitus because it is associ-ated not only with pronounced tis-sue degeneration (including diabeticfoot syndrome) but also with peri-pheral neuropathy.Consequently, treating the perineur-al matrix edema that accompaniesperipheral neuropathy improves theefficacy of measures to prevent andtreat diabetic foot syndrome. Severalstudies have already demonstratedthat the homeopathic combinationmedication Lymphomyosot effec-tively “flushes out” edema.15-20 Thecurrent study revealed decreases inpalpable edema in only 18% (n = 49)of patients treated with α-lipoic acidalone but in 47% (n = 88) of thosereceiving adjuvant Lymphomyosot.In the development of diabetic neu-ropathy, thickening of the basalmembranes of the capillaries inmyelin sheaths of peripheral nervesplays an important role because ithinders tissue fluid drainage andleads to overburdening of lymphvessels.13 In addition, nonenzymaticglycosylation products in the matrixcreate an inflammatory situation, in-cluding formation of free radicals.The consequences are functionalbreakdowns of the affected nervesand/or slowed neural transmission.Alpha-lipoic acid, which is used to

• Mycosis (no/yes, location: skin, interdigital,toenails)

• Anhidrosis (no/yes, scale: mild, moderate, severe)• Pressure points/calluses (no/yes, scale: mild, mod-

erate, severe)• Reduced joint mobility (no/yes, scale: mild,

moderate, severe)• Paresthesia at rest (no/yes, scale: mild, moderate,

severe)

Treatment prescribed for neuropathy

• Dosage and duration of therapy with Lym-phomyosot (oral only) and/or α-lipoic acid (i.v.,oral, or parenteral)

• Other therapies (pharmaceutical/nonpharmaceuti-cal)

Target criteria

• Severity of neuropathic disorders:1. sensitivity to pain (pinprick) (not felt/felt, scale:

sharp, dull)2. light touch (monofilament) (not felt/felt, scale:

faint sensation, significant sensation, pronouncedsensation)

3. numbness (no/yes, scale: mild, moderate, se-vere)

4. paresthesia (prickling) (no/yes, scale: mild, mod-erate, severe)

5. (nocturnal) spontaneous pain (no/yes, scale:mild, moderate, severe)

6. reduction in pain during movement (no/yes,scale: slight, significant)

• Palpable edema in the foot/ankle (no/yes)• Onset of improvement in neuropathic symptoms

(scale: <1 month, 1-2 months, 2-3 months, 3-6months, no improvement)

• Overall assessment of results of therapy (scale: verygood, good, fair, no success, symptoms worsened)

• Overall assessment of patient compliance (scale:very good, good, fair, poor)

• Tolerability (overall assessment of therapy in termsof adverse effects) (scale: very good, good, fair,poor)

• Premature termination of therapy

Statistical analysis

Data compiled on patients/therapies were analyzedusing exploratory statistical methods; absolute andpercentage frequencies were calculated and graphed.Differences in treatment effects were calculated with95% confidence intervals. The patients’ demographicdata and medical histories were compared (usingANOVA/Fisher’s exact test) to test for comparabilityof the treatment groups at commencement of therapy.Distribution of background characteristics in the twotreatment groups was described using statistical pa-rameters and absolute and relative frequencies. Thelogistic regression (propensity score) method wasused to test for possible interactions between back-ground characteristics (structural variables) and treat-ments prescribed. Because patients with similarpropensity scores exhibit similar distribution of back-ground characteristics, comparisons within propen-sity score classes can reduce the influence of unequaldistribution of these characteristics on treatment re-sults.



deactivate free radicals in diabeticperipheral neuropathy, is a sulfur-containing fatty-acid. An easily oxi-dized compound, it assumesimportant biological functions inredox reactions, including catalyticfunctions in energy metabolism andantioxidant functions in hydrophilicand lipophilic cell compartments.The efficacy of α-lipoic acid intreating DPN has been debated foryears.22 The ALADIN study dem-onstrated that clinical symptoms ofperipheral neuropathy can be signi-ficantly reduced by a three-weekcourse of intravenous α-lipoic acid(600 mg/day) in comparison to

placebo.23 The ALADIN II studyfound that 24 months of α-lipoicacid therapy, when administered as acombination of five intravenousdoses followed by oral adminis-tration of 600 mg per day, producedsignificant improvements in sensoryneural transmission speed incomparison to placebo.24 TheALADIN III study, however, foundthat three weeks of intravenous α-lipoic acid therapy followed by sixmonths of oral therapy (both with600 mg of α-lipoic acid per day) wasnot significantly more effective thanplacebo in reducing neuropathicsymptoms.10

The purpose of the present studywas to investigate whether acombination therapy of Lym-phomyosot plus α-lipoic acid issuperior to α-lipoic acid alone intreating diabetic peripheral neuro-pathy. In this exploratory approach,no special requirements were im-posed regarding the dosage of α-lipoic acid or its method of adminis-tration (i.v., injection, oral). The de-cision to limit the treatment periodto six months takes the etiology ofperipheral neuropathy into accountand aligns the study with compara-ble clinical investigations.10

The results of this study confirm

Tab. 2: Characterization of diabetic neuropathy and/or skin lesions at the beginning of treatment (1Fishers exact test, 2 variance analysis, SD = standard deviation).

Criteria Group A: Group B: Statistics α-lipoic acid α-lipoic acid +(N = 114) Lymphomyosot

(N = 155)

Duration of symptoms (mean ± SD, in months) 28 ± 27.8 31 ± 28.2 P = 0.31 1

Patient status (%)•patients in ongoing care 27.2 33.5•returning patients 28.1 31.0• first-time patients 44.7 34.2 P = 0.08 2

•not given 0.0 1.3

Extent of neuropathy (%)• toes only 28.9 16.8 P = 0.02 2

• foot 34.9 42.6 P = 0.16 2

• foot/ankle 37.7 41.9 P = 0.49 2

•other/not given 0.9 0.6

Findings, neuropathy (% of patients exhibiting symptom)

•ulcer/gangrene 5.3 6.5 P = 0.68 2

•other skin lesions (fissures, eczema) 20.2 25.2 P = 0.34 2

•pale/livid skin discoloration 37.7 42.6 P = 0.42 2

•mycosis 32.5 34.8 P = 0.68 2

•anhidrosis 29.0 25.2 P = 0.49 2

•pressure points / calluses 47.4 45.2 P = 0.72 2

• reduced joint mobility 50.9 51.0 P = 0.99 2

•paresthesia at rest 86.0 87.7 P = 0.67 2

•pain (pinprick) not felt or felt as dull pain 50.0 54.2 P = 0.73 2

• light touch (monofilament) not felt or felt only slightly 75.4 79.4 P = 0.30 2

•numbness 90.4 89.7 P = 0.83 1

•paresthesia 93.0 96.8 P = 0.64 1

• (nocturnal) spontaneous pain 72.8 72.9 P = 0.99 2

•pain does not decrease with movement 36.8 40.7 P = 0.53 2

•palpable edema in the foot/ankle 45.6 62.6 P = 0.01 2

•A. tibialis posterior not palpable 7.9 11.6 P = 0.32 2

•A. pedis dorsalis not palpable 9.6 10.3 P = 0.86 2

•Achilles tendon reflex not present 15.8 17.4 P = 0.72 2

•patellar reflex not present 15.8 17.4 P = 0.80 2



that improving the cell matrix milieuthrough adjuvant use of Lym-phomyosot improves the prospectsof success in treating diabeticperipheral neuropathy. In otherwords, a combination therapy thatincludes this homeopathic medica-tion has advantages over treatmentwith α-lipoic acid alone.During the average six-monthtreatment period, the target criteriasensitivity to touch (monofilament),numbness, paresthesia, (nocturnal)spontaneous pain, and edema in thefoot/ankle showed significantlygreater improvement under thecombination protocol than with α-lipoic acid alone. In addition, im-provements occurred significantlyearly (after one to two months oftreatment). This “enhancing” pro-perty of Lymphomyosot is alsoreflected in assessments of therapeu-tic results. In the group receivingcombination therapy with Lympho-myosot, results of therapy wererated “very good” or “good” in 70%of cases in comparison to only 47%of cases treated with α-lipoic acidalone.It is not known how much influencethe severity of the patients’ neuro-pathy (toes only, foot, foot/ankle)had on overall results, especiallysince Group A included a signifi-cantly higher percentage of patientswith symptoms limited to the toes.In such patients in particular, thepossibility of clinical confirmation ofdocumented subjective symptoms islimited and symptomatic improve-ments are difficult to differentiate.(For this reason, statistical analysisthat separates out these patients iscurrently in progress.)The effect of the confounder“diabetes management” – in otherwords, of lower blood sugar levels –on improvements in symptoms isalso not known. For purposes ofanswering the question posed by thisstudy, however, this issue isirrelevant because if the effect ofimproved diabetes management isassumed to be not one-sided (i.e., tohave had the same size effect in both

groups), it has no influence on anyassessment of treatment effects or ofhow they differed between thegroups (α-lipoic acid alone vs. α-lipoic acid plus Lymphomyosot).Independent of these questions, theresults of the present study givediabetics reason to hope that theirunpleasant and painful symptomscan be reduced and their quality oflife enhanced. Adding the homeo-pathic medication Lymphomyosotto their therapeutic regimen cancontribute significantly to theprophylaxis of lesions of varioustypes. Persistent sensory deficits inthe feet and/or ankles due to diabeticperipheral neuropathy often allowseemingly minor injuries to go unde-tected by the patient. In combinationwith the delayed wound healingcommon in diabetics, such injuriescan quickly develop into chronicinfections that can lead to ulceration,gangrene, and even the loss of thelimb.2, 9

In this context, Lymphomyosot’sexcellent tolerability should beemphasized. The fact that thishomeopathic medication has nocounterindications, side effects, orknown drug interactions makes itsuitable for long-term use. Incontrast, the allopathic medicationsused for symptomatic relief ofdiabetic neuropathy (such as tri-cyclic antidepressants and anticon-vulsants) have been linked to seriousside effects that limit their long-termuse. (These side effects include anti-cholinergic effects such as cardiacdysrhythmias, changes in bloodpressure, tremors, dry mouth, exces-sive perspiration, and urinationdisorders. Monoamine oxidase inhi-bitors are also associated with sleepdisorders, nausea, headache, andblood pressure changes; serotoninuptake inhibitors have been linked toheadache, nausea, and vertigo.)

ConclusionsThis study’s findings indicate thatthe addition of the homeopathiccombination medication Lym-

phomyosot enhances the effect of α-lipoic acid therapy. The mechanismon which this effect is based is stillunknown, but it is conceivable thatLymphomyosot’s plant ingredients(including pine, yellow gentian, andhorsetail) support the action of α-lipoic acid by trapping free radicals.25

It is also possible that Lym-phomyosot, an alkaline product, im-proves α-lipoic acid utilization bycounteracting tissue acidosis.Further studies are needed to answerthese questions.

For the authors: Dr. Michael WeiserInstitute for Antihomotoxic Medicineand Ground Regulation ResearchBahnackerstr. 1676532 Baden-BadenGermany



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