Metabolic Syndrome - International Academy of Homotoxicology

d 2.00 • US $ 2.00 • CAN $ 3.00 

Journal of 

Biomedical 

Therapy 

Volume 2, Number 1 ) 2008 

Integrating Homeopathy 

and Conventional Medicine 

Metabolic 

Syndrome 

• An “Incurable” Diabetic Foot Ulcer 

• Suis-Organ Products in Antihomotoxic Medicine

) 

Contents 

In Focus 

Metabolic Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 

What Else Is New? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 

Fr o m t h e P ra c t i c e 

An “Incurable” Diabetic Foot Ulcer . . . . . . . . . . . . . . . . . . . . . . 10 

Immediate Intervention Required! . . . . . . . . . . . . . . . . . . . . . . 12 

Around the Globe 

ACAM Fall Meeting in Phoenix . . . . . . . . . . . . . . . . . . . . . . . . . 15 

Refresh Your Homotoxicology 

Citric Acid Cycle Catalysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 

Marketing Your Practice 

Practical Tips for Improving Your Marketing Strategy . . . . . . 18 

Specialized Applications 

Individualized Infusion Therapy 

in Metabolic Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 

Practical Protocols 

Detoxification and Drainage in Metabolic Syndrome . . . . . . 23 

Making of ... 

Suis-Organ Products in Antihomotoxic Medicine . . . . . . . . . 24 

Research Highlights 

Emotional Stabilization 

Through Homeopathic Medication . . . . . . . . . . . . . . . . . . . . . 26 

Crossword Puzzle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 

Cover photograph © Ashe/Fotolia.de 

) 2 

Published by/Verlegt durch: International Academy for Homotoxicology GmbH, Bahnackerstraße 16, 

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Editor in charge/verantwortlicher Redakteur: Dr. Alta A. Smit 

Print/Druck: Konkordia GmbH, Eisenbahnstraße 31, 77815 Bühl, Germany 

© 2008 International Academy for Homotoxicology GmbH, Baden-Baden, Germany

) 

A Challenge for the Future: 

Fighting Metabolic Syndrome 

Dr. Alta A. Smit 

Metabolic syndrome has come 

a long way since its beginnings 

as Syndrome X (so called because 

its pathophysiology was not 

totally clear). The syndrome was described 

as early as 1946 by a French 

physician in Marseille, but the link 

between insulin resistance and cardiovascular 

disease did not become 

commonplace in cardiovascular medi 

cine until after the Banting Award 

address by Gerald M. Reaven in early 

spring of 1988, when metabolic 

syndrome emerged as a pattern of 

inflammatory disease with devastating 

consequences if left untreated. 

Modern articles have examined the 

connections among leptin resistance, 

insulin resistance, and the age-old 

genetic patterns of maintenance and 

adaptive metabolism that ensure the 

survival of our species. 

In the normal maintenance pattern 

of fat burning, which ensures the 

optimum environment for reproduction 

of the species, leptin is relatively 

low and insulin levels are normal. 

Under stressful conditions, our genetic 

make-up triggers the so-called 

adaptive response and a different 

pattern of fat utilization sets in, 

namely, storage in anticipation of a 

time when the species will again be 

able to reproduce. If the adaptive response 

persists for too long, resistance 

to both insulin and leptin develops 

as the body protects the cells 

from their effects. The brain interprets 

this situation as leptin or insulin 

deficiency, and levels rise even 

further, resulting in true leptin and 

insulin resistance. 

In the maintenance response to dietary 

carbohydrate and fat, no fat is 

deposited. Our stressful modern 

lifestyle, however, constantly triggers 

the adaptive response of storing 

food for the future. As a result, fat 

accumulates, especially around the 

midriff. Switching the prevailing 

pattern from the adaptive response 

back to the maintenance mode of fat 

burning is a major challenge for the 

future. 

Clearly, the pathophysiology of metabolic 

syndrome is now better understood, 

but as we see from Professor 

Michael Kirkman’s com pre hensive 

focus article, it remains a complex 

and multifactorial disease. As 

in all such conditions, bioregulatory 

therapy can play an important role, 

since it also addresses sequelae of 

metabolic syndrome such as tissue 

acidosis and chronic inflammation. 

Dr. Ulrike Keim is one of the leading 

homotoxicological experts on 

this syndrome, so we asked her to 

write about some of her cases and 

protocols. She expands on this practical 

aspect by sharing her experience 

with i.v. therapy, which is an 

important component of treatment 

in many acute and chronic diseases, 

especially in cases of metabolic syndrome. 

Free radical formation and loss of 

mitochondrial function are major 

factors in all chronic diseases. Two 

preparation groups – the catalysts 

and the suis-organ preparations – 

play special roles in the homotoxicological 

approach to metabolic 

syndrome. Dr. Ivo Bianchi, a worldrenowned 

expert on homotoxicology, 

has studied the catalysts in depth 

and has a wealth of experience in 

using these compounds in his practice. 

His short article in the section 

“Refresh Your Homotoxicology” 

puts the use of the catalyst combination 

Coenzyme compositum in context. 

Finally, Dr. Erich Reinhart 

presents the first of two articles in a 

series on manufacturing the suis-organ 

preparations and ensuring their 

quality. 

Alta A. Smit, MD 

References: 

1. Reaven GM. Syndrome X: A Short History. 

The Ochsner Journal 2001;3(3): 

124-125. 

2. Chilton FH III. The role of natural 

bioactives for the prevention and treatment 

of chronic human diseases. Lecture 

given at: ACAM Fall 2007 Conference; 

November 14-18, 2007; Phoenix, AZ. 

) 3 

Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1

) In Focus 

Metabolic Syndrome 

By Prof. Michael F. Kirkman, MD 

Chartered Biologist (Institute of Biology, London) 

Fellow Royal Institute of Public Health (London) 

Principal, Academy of Homotoxicology and Bio-Regulatory Medicine (States of Jersey) 

Director of Academic Affairs, The Society for Homotoxicology and Antihomotoxic Therapy (Great Britain) 

“Structure Is an Expression of Function.” 

Epidemiologic key factors 

relating to metabolic syndrome 

) 4 

Introduction 

The term “metabolic syndrome” denotes 

a constellation of cardiovascular 

risk factors related to insulin resistance 

and obesity with a visceral 

fat pattern. 1(p741),2 Definitions have 

varied, but the basic elements are 

well validated and include insulin 

resistance, inflammation, and immunologic 

dysfunction with increased 

oxidative stress preceding the accepted 

characteristics of hypertension, 

atherogenic dyslipidemia (high 

triglycerides, low HDL, high LDL), 

obesity (increased waist circumference, 

BMI, and waist-hip ratio), 

together with elevated fasting blood 

sugar level, glucose intolerance, hyperglycemia, 

and a prothrombotic 

state (see Table 1). 

Although the exact criteria vary between 

the two key determinant projections 

(National Cholesterol Education 

Programme – Adult Treatment 

Panel III [NCEP ATP III] and World 

Health Organization [WHO]), the 

criteria correlate closely. 

Interestingly, the WHO includes microalbuminuria 

(overnight urinary 

albumin excretion rate > 20 μg/ 

min), which the author believes is 

significant in relation to the inflammation/oxidative 

stress element and 

the fact that glucotoxicity and lipotoxicity 

induce changes in cell signaling, 

protein expression, gene expression, 

and free radical formation. 

These may be relevant to associated 

pathophysiological factors (prothrombotic 

components, vascular 

endothelial dysfunction, and accelerated 

athero-embolic conditions) 

and are undoubtedly related to an 

imbalance in vascular endothelial 

mediators, which results in excess 

angiotensin II and nitric oxide deficiency. 

Hence, vasoconstriction, prothrombotic, 

pro in flammatory, and 

pro-oxidant states ensue. 1(p741),2 

Abdominal obesity 

Triglycerides 

HDL cholesterol 

Blood pressure 

Fasting glucose 

• men 

• women 

• men 

• women 

Table 1: ATP III criteria for diagnosing metabolic syndrome 

Here we first need to mention the 

genetic predisposition of an individual. 

Gestational diabetes is a risk 

factor, and so may be bottle feeding. 

Lifestyle factors also play a role in 

this context. To begin with dietary 

habits, the consumption of white 

sugar (Professor Yudkin’s “pure, 

white, and deadly”) and other high 

calorie foods, especially refined carbohydrates 

and those of high glycemic 

index, stand paramount. Reduced 

physical activity, particularly 

in adolescence, and an imbalanced 

microbial gut flora will also contribute 

to the development of metabolic 

syndrome. 

Minor factors seem to be elevated 

homocysteine levels (> 5 μg/L), ab- 

> 102 cm (40 in) 

> 88 cm (35 in) 

≥ 150 mg/dL 

< 40 mg/dL 

< 50 mg/dL 

≥ 130/≥ 85 mm Hg 

≥ 110 mg/dL 

Diagnosis of metabolic syndrome is made when 3 or more of the above risk determinants 

are present 


) In Focus 

Table 2: Effects of adipocytokines 

Promotes weight gain and inflammation 

IL-6: causes insulin resistance, 

proinflammatory cytokine 

Promotes weight loss 

Adiponectin: important insulin sensitizer 

IL-1: proinflammatory cytokine 

Leptin: major (down-) regulator of 

food intake and appetite 

TNF-α: increased in obesity, 

modulates insulin sensitivity 

Resistin: modulates insulin sensitivity 

Non-esterified fatty acids (NEFA): 

cause insulin resistance 

normalities in autonomic nervous 

system regulation (affecting somatostatin 

function in relation to beta 

cells in the pancreatic islets, perhaps 

also delta and alpha cells), and low 

C2 reactive protein function. 1(p742) 

To confirm the diagnosis of metabolic 

syndrome, 3 or more of the 

ATP III criteria must be present (see 

Table 1). 

Pathophysiology 

This brings us to the key player in 

metabolic syndrome – insulin and 

its receptors. Insulin (a small protein 

in the form of two chains with 

disulphide bonds, with a molecular 

weight around 6000 daltons) is synthesized 

in the pancreatic beta cells. 

The cytoskeletal ribosomes manufacture 

preproinsulin from insulin 

MRNA. The “pre” is enzymatically 

cleaved off, leaving the proinsulin to 

move into secretory granules in the 

Golgi apparatus for storage. During 

the secretory process, the connecting 

C-peptide is split off by specific 

endopeptidases. Equimolar quantities 

of insulin and C-peptide (a risk 

factor marker) are released into the 

circulation, on occasion of glucose 

entry via specialized glucose transporter 

proteins (GLUT-2). Potassium 

channels in the beta-cell membrane 

are closed (glucose metabolism 

ATP), the membrane thus depolarized, 

and calcium channels opened, 

leading to calcium-dependent exocytosis 

of insulin-rich granules. 

The insulin receptor on cell surfaces 

is a glycoprotein that includes the 

insulin binding site where a cas cade 

response is initiated, resulting in 

increased transport of glucose into 

the cell (GLUT-4). Insulin is subsequently 

degraded, and the receptor 

is recycled to the cell surface. 3 

In relation to the process above, insulin 

resistance is probably multifactorial, 

i.e., influenced by a continuum 

of factors including diet, exercise, 

body weight, toxic hypertriglyceridemia, 

decreased HDL cholesterol, 

obesity, and hypertension, together 

with various multi-endocrine and 

inflammatory factors, which will be 

discussed next. 

It has recently been discovered that 

subclinical inflammatory changes 

are characteristic of both type 2 diabetes 

and obesity. Unknown abnormalities 

reduce the effect of insulin 

signaling within the cell, producing 

not only insulin resistance (high intracellular 

triglyceride is a possible 

factor) but also (as a result) beta-cell 

stress and strain due to high output 

failure. (The author suspects that 

release of NF-kB plays a role here 

triggered by the release of reactive 

oxygen species.) Proinflammatory 

cytokines, especially TNF-a and 

IL-6, are elevated in both diabetes 

2 and obesity, and the raised C-reactive 

protein levels are associated 

with raised fibrinogen and PAI-1 

levels (again, possibly the effect of 

NF-kB). 

Two key endocrine organs are involved 

in the process: endocrineadipose 

tissue and the endocrineskeleton. 

Yes, the skeleton is an 

endocrine organ that regulates 

blood sugar! In higher eukaryotes, 

including humans, adipose tissue is 

the main energy reservoir – there 

may be evolutionary connotations 

here –, and its primary purpose is 

to store triacylglycerol in periods 

of energy excess and mobilize it 

during energy shortage. Transcriptional 

activation of adipocyte genes 

(PRARg) is involved in directing 

adipocyte-specific gene expression 

and adi pogenesis and is affected by 

the leptin secreted by mature adipocytes. 

Leptin is a recently discovered 

hormone that seems to regulate 

body fat mass by binding to its receptor 

in the hypothalamus (energy 

balance and homeostasis). 4 

Adipose tissue produces many adipocytokines, 

including inflammatory 

mediators and hormones that cause 

low grade chronic inflammation and 

other endocrine and metabolic dysregulatory 

effects, thus resulting in 

insulin resistance and cardiovascular 

risks (see Table 2). 

The insulin resistance produces an 

imbalance of the mitogen-activated 

protein kinase (MAPK) at the level 

of insulin receptors and the phosphatidylinositol 

3-kinase (PI3-K) 

pathways. The PI3-K is an antiatherogenic 

pathway and the 

MAPK proatherogen. 1(p743),5 ) 5 


) In Focus 

Abdominal obesity, recognized by 

increased waist circumference, is 

a risk factor for developing metabolic 

syndrome. 

© iStockphoto.com 

) 6 

Various other mediators are sourced 

from adipocytes, 1(p743),4 but two key 

ones need discussion here. First, 

adipose tissue-specific secretory 

factor (ADSF/resistin) plays a role 

in insulin resistance to affect adipogenesis, 

thereby linking obesity to 

diabetes. Second, the peroxisome 

proliferator-activated receptors 

(PPARa and g) are involved not 

only in insulin resistance and glucose 

and lipid metabolisms but also 

in inflammation (again, through 

NF-kB), aging, and atherosclerosis 

and its complications. 4 

Surprisingly, the skeleton is also involved 

in this process. It is now 

known that the osteocalcin produced 

by cells in bone “increases 

both the secretion and sensitivity 

of insulin, in addition to boosting 

the number of insulin-producing 

cells and reducing stores of fat.” 6 

Let us now move on to discuss antihomotoxic, 

integrated, naturopathic, 

holistic management of insulin 

resistance. This paper will leave 

aside regular exercise (aerobic and 

resistance) and dietary and lifestyle 

engineering (including cognitive 

behavior therapy) to concentrate 

on homotoxicology and nutritional 

engineering. 

Clinical relevance 

The net effect of insulin resistance 

on the organism is the accumulation 

of insulin and glucose in the tissues, 

which have detrimental effects 

through a number of pathways. 

Elevated blood glucose levels lead to 

activation of the polyol pathway (resulting 

in toxic sorbitol), auto-oxidation 

pathway (resulting in crosslinking 

via advanced glycation 

end products [AGEs]), protein kinase 

pathway (resulting in expression of 

inflammatory mediators such as the 

transcription factor NF-kB), and 

oxygen radical pathway (resulting in 

NO reduction and tissue damage as 

well as the activation of NF-kB). 

The end result of these pathways is 

chronic inflammation, tissue destruction, 

and an interference in cellular 

processes. 

Antihomotoxic approach to 

metabolic syndrome 

Where does homotoxicology fit into 

this picture? Hans-Heinrich Reckeweg’s 

unique intellectual synthesis 

and system of medicine seems to fit 

metabolic syndrome like a glove, 

and his antihomotoxic therapy appears 

to have all the necessary bioregulatory 

and integrated holistic 

facets for successful management of 

this condition. 

Dr. Alta Smit’s detailed protocols, as 

outlined in the Journal of Biomedical 

Therapy, stand paramount. 7 This 

author, however, believes that because 

the helenalin in Arnica “douses” 

NF-kB, Traumeel should be added 

to the initial treatment protocols, 

which consist of the pillars of treatment 

for regulating the biological 

terrain (through detox and drainage, 

cellular activation, organ regeneration, 

immunostimulation, and immunomodulation). 

The above analysis 

of metabolic syndrome supports 

the use of these medications, especially 

in the protocols for weeks 

7-12. I would add Pankreas suis 

(also included in Hepar compositum) 

and (in view of associated autonomic 

nervous system dysregulatory 

states) perhaps also Ypsiloheel 

and in particular Ginseng compositum 

as a PNETI rebalancer that simultaneously 

reduces gluco- and lipotoxicity. 

(The author is currently 

undertaking a practice-based study 

of Ginseng compositum for the annual 

seminar of the Society for Homotoxicology 

and Antihomotoxic 

Therapy in Great Britain.) 


) In Focus 

Elevated blood pressure is one of 

the components that characterize 

metabolic syndrome. 

© iStockphoto.com/Maxim Tupikov 

Adjuvant nutritional therapy 

On a microbiological level, the intake 

of probiotics will help to overcome 

gut microbial dysfunction. 

Immunonutrition products (especially 

trace elements such as selenium, 

zinc, chromium, and manganese) 

and functional foods also support 

medicinal treatment. Last but not 

least, I would like to mention antioxidants 

(free radical scavengers) 

and so-called “cleansers,” e.g., spirulina 

(an alga that provides a full range 

of amino acids). 

Conclusion 

In conclusion, now that biomedical 

pathophysiological research is beginning 

to explain conditions such 

as metabolic syndrome, it is becoming 

more important to adopt Dr. 

Reckeweg’s integrated, holistic approaches 

and to incorporate concepts 

such as the living matrix, 

structural/functional interconnectedness, 

and bioinformational transmission 

into our prophylactic and 

therapeutic endeavours.| 

Recommended texts for homotoxicologists 

(relevant to paper) 

1. Jänig W. The Integrative Action of the 

Autonomic Nervous System. Neurobiology 

of Homeostasis. Cambridge: Cambridge 

University Press; 2007. 

2. Jones DS, Quinn S. Textbook of Functional 

Medicine. Gig Harbor, WA: Institute for 

Functional Medicine; 2005 (especially 

Section VII, Chapter 37, Metabolic 

Syndrome). 

3. Oschman J. Energy Medicine in Therapeutics 

and Human Performance. Amsterdam, 

the Netherlands: Butterworth-Heinemann; 

2003. 

References: 

1. Jones DS, Quinn S. Textbook of Functional 

Medicine. Gig Harbor, WA: Institute 

for Functional Medicine; 2005. 

2. Laaksonen DE, Lakka HM, Niskanen 

LK, Kaplan GA, Salonen JT, Lakka TA. 

Metabolic syndrome and development 

of diabetes mellitus: application and 

validation of recently suggested definitions 

of the metabolic syndrome in a 

prospective cohort study. Am J Epidemiol 

2002;156:1070-1077. 

3. Shepherd PR, Kahn BB. Glucose transporters 

and insulin action. New Engl J 

Med 1999;341:248-257. 

4. Kim KH, Lee K, Moon YS, Sul HS. 

A cysteine-rich adipose tissue-specific 

secretory factor inhibits adipocyte 

differentiation. J Biol Chem 

2001;276(14):11252-11256. 

5. Xu H, Barnes GT, Yang Q, Tan G, 

Yang D, Chou CJ, Sole J, Nichols A, 

Ross JS, Tartaglia LA, Chen H. Chronic 

inflammation in fat plays a crucial 

role in the development of obesityrelated 

insulin resistance. J Clin Invest 

2003;112:1821-1830. 

6. Lee NK, Sowa H, Hinoi E, Ferron M, 

Ahn JD, Confavreux C, Dacquin R, 

Mee PJ, McKee MD, Jung DY, Zhang 

Z, Kim JK, Mauvais-Jarvis F, Ducy P, 

Karsenty G. Endocrine regulation of 

energy metabolism by the skeleton. Cell 

2007;130(3):456-469. 

7. Smit A. Metabolic syndrome and diabetes 

type II: adjuvant treatment. J Biomed 

Ther 2004;Fall:5-6. 

Physical activity and healthy, 

low-calorie food can help to prevent 

the development of metabolic 

syndrome. 

) 7 


) What Else Is New? 

New scientific findings suggest 

that artificial food colors and 

additives (AFCAs) are associated 

with increased hyperactivity in 

children. 

More evidence on 

Soda: Is just one a day too 

much for your heart? 

Does TV make children 

smart? 

artificial food colorings 

) 8 

and hyperactivity 

A randomized, double-blinded, placebo-controlled 

clinical trial published 

in The Lancet presents additional 

evidence that artificial food 

colors and additives (AFCAs) in the 

diet cause hyperactivity in children. 

The 153 3-year-old children and 

144 8/9-year-olds included in the 

study consumed either a placebo 

mix or test drinks containing sodium 

benzoate preservatives plus one 

of two AFCA mixes (A or B). To assess 

hyperactivity levels in both age 

groups, the researchers used aggregated 

z-scores of observed behaviors 

and ratings by parents and 

teachers. In addition, the 8/9-yearolds 

took a computerized test of attention. 

Compared with placebo, mix A had 

statistically significant adverse effects 

on 3-year-olds, whereas mix B 

did not. The 8/9-year-olds showed 

statistically significant adverse effects 

from both mixes. The authors 

concluded that artificial food colors 

and/or sodium benzoate preservatives 

in the diet result in increased 

hyperactivity in 3-year-old and 

8/9-year-old children in the general 

population. 

The Lancet 

2007;370(9598):1560-1567 

Increased consumption of sugary 

drinks, already linked to obesity and 

diabetes among children and teens 

and to high blood pressure in adults, 

may also increase the risk of metabolic 

syndrome, which in turn increases 

chances of developing heart 

disease and/or diabetes. A new 

study published in the July 31 2007 

issue of the American Heart Association’s 

journal Circulation found that 

the prevalence of metabolic syndrome 

was 44 to 48 percent higher 

among people who drank as little as 

one soda a day, either diet or regular, 

as compared to those who drank 

less than one. 

The study did not determine whether 

soda consumption constitutes a 

true risk factor in itself or is simply 

a marker for other behaviors that 

promote metabolic syndrome. People 

who drink soda habitually also 

tend to consume more total calories 

and high-fat foods, smoke more, 

and exercise less than people who 

do not. Sodas may also displace 

healthier beverages in the diet or encourage 

a sweet tooth. 

Needless to say, the soda industry 

took issue with the findings. 

Circulation 2007;116:480-488 

Child psychologists and pediatricians 

advise beginning early with 

normal social interactions with other 

toddlers, using normal language 

(not baby talk) with babies and toddlers, 

and finding playful ways to 

introduce children to logical processes. 

But parents don’t always have 

a lot of time to spend talking to their 

babies, keeping them occupied, or 

reading to them on a regular basis. 

That’s why parents in the USA are 

increasingly using television, with 

its special children’s programs, as an 

educational aid. A recent study explored 

this topic, asking whether 

TV promotes child development or 

whether parents simply permit TV 

watching for egotistical reasons. 

In a telephone survey, 40 percent of 

parents admitted to allowing their 

three-month-old babies to watch 

television on a regular basis. According 

to the same survey, 90 percent 

of two-year-olds spend 1.5 

hours a day in front of the TV. The 

respondents said they believed television 

would help their children develop 

language skills, but they also 

admitted that they used television to 

keep kids entertained and as an 

electronic babysitter. 

Arch Pediatr Adolesc Med 

2007;161:473-479 


) What Else Is New? 

Educational aid or electronic babysitter? 

A recent US survey shows that 

parents let their infants and toddlers 

watch television on a regular basis. 

A happy partnership 

helps to 

prevent the 

development 

of CHD. 

Live hard, 

die young 

Mortality rates of rock and pop stars 

are significantly higher (more than 

1.7 times) than rates for their age 

peers in the general population. The 

average age of death for pop musicians 

is unusually low: 42 years in 

North America and only 32 years in 

Europe, according to the findings of 

an epidemiological study. The most 

frequent causes of death are drugs 

(31%), cancer (20%), accidents 

(16%), and suicide (9%). In later life, 

when stars are no longer in the spotlight, 

their mortality rates begin to 

return to population levels. Even 

then, however, drug and alcohol 

abuse remain significant causes of 

death. Of particular concern is the 

fact that rock stars are serving as 

poor role models for teens, who 

need to be encouraged not to imitate 

the lifestyles of their idols. 

J Epidemiol Community Health 

2007;61:896-901 

Marital discord is bad 

for the heart 

An unhappy marriage puts heart 

health at risk. A study followed 

9,011 British subjects for 12 years. 

Most of them (8,499) did not have 

heart disease when the study began. 

During the observation period, 589 

developed coronary heart disease. In 

analysis of the participants’ living 

situations, unhappy partnerships 

emerged as an independent risk factor. 

Arch Intern Med 

2007;167(18):1951-1957 

Love handles 

are hereditary 

For the first time, scientists have 

identified a specific gene on chromosome 

16 that is instrumental in 

increasing body mass index and is 

involved in the development of diabetes 

mellitus. This variant of the 

FTO (fat mass and obesity associated) 

gene is a reproducible variant in 

the first intron. The association with 

excess weight was found in several 

cohorts with a total of 38,759 participants. 

Individuals with a homozygous 

risk allele were 1.67 times 

more likely to become obese and averaged 

3 kg heavier. The connection 

is first observed around age six and 

is independent of gender and ethnicity. 

In the future, individuals predisposed 

to obesity will be able to 

take preventive measures early in 

life. 

Science 2007;316(5826):889-894 

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) 9 


) From the Practice 

An “Incurable” Diabetic Foot Ulcer 

By Ulrike Keim, MD 

Specialist in internal medicine 

) 10 

I met this patient’s wife first, when she approached me after 

a diabetes education day in Bonn, Germany. She reported that 

her husband had recently been released from the hospital, 

where he had spent almost a year due to a diabetic ulcer on 

the sole of his foot. 

The ulcer had not healed, the 

condition of his foot had not 

changed in a year, and the open 

wound was considered incurable. 

I asked the couple to come see me in 

my office. The patient was very unhappy 

because he had been told to 

spend most of the day lying down 

and not to put any weight on that 

foot. He almost never left the house 

anymore. His wife described him as 

a “closet depressive,” and he was becoming 

increasingly forgetful. 

While hospitalized, he had not been 

allowed to put any weight on the 

foot at all. Whenever he was not lying 

in bed, he wore a special shoe 

that kept the weight off the forefoot. 

Medical history 

This 76-year-old patient had a 

twenty-year history of metabolic 

syndrome, type 2 diabetes, hypertension, 

and hyperuricemia. Diabetic 

nephropathy had developed, 

along with motor, sensory, and autonomic 

polyneuropathy. The patient 

no longer had any sensation of 

touch or pain in his feet, lower legs, 

or thighs. He was constantly dizzy 

and unsteady on his feet and had 

become very forgetful. His hospital 

records showed that he also had 

coronary heart disease with cardiac 

insufficiency (NYHA II). I ordered 

lab tests that revealed elevated levels 

of free radicals and hyperhomocysteinemia. 

Laboratory parameter Results 4/2003 Results 10/2003 Reference values 

HbA1c 6.1% 6.1% < 6.1% 

Creatinine 3.4 mg/dL 2.9 mg/dL < 1.1 mg/dL 

Urea 134 mg/dL 100 mg/dL < 71 mg/dL 

Homocysteine 23 11 < 9 

Oxidative stress 580 180 < 200 

Diabetic foot ulcer 

The wound was 3 cm in diameter, 

clean, and clearly delineated (see 

Figure 1). It was not deep and there 

was no bone involvement. When examining 

a patient with diabetic foot 

syndrome, vibration sensation testing 

with a 128 Hz tuning fork is 

obligatory. 

The patient had no vibration sensation 

in his feet and could not distinguish 

between cold and warm or 

pointed and dull. His feet were pale 

(with some livid discoloration) and 

slightly edematous. The foot pulses 

were not palpable. An MRI showed 

complete closure of the distal arteries 

of the lower legs. 

The patient’s blood sugar levels were 

good, with fasting levels between 

90 mg/dL and 120 mg/dL and 

postprandial levels between 120 

mg/dL und 140 mg/dL, with only 

a few “maverick” readings up to 180 

mg/dL (see Table 1). 

What to do? 

The patient presented with multifactorial, 

pathological metabolic processes 

accompanied by significant 

late damage. During his almost yearlong 

hospitalization, the causes of 

the foot ulcer had not been adequately 

treated and therapeutic measures 

had addressed only the ulcer 

itself. Successful wound healing requires 

treatment of the triggering 

Table 1: Lab test results 



factors, in this case impaired microcirculation 

and diabetic polyneuropathy. 

Figure 2 shows the pathological 

cascade that leads to polyneuropathy. 

Clearly, this patient needed 

therapeutic intervention on several 

different levels: 

1. A combination of fast-acting and 

long-acting insulins effectively controlled 

his blood sugar, thus his dosages 

were not changed. 

2. The patient’s endogenous antioxidant 

capacity and free radical 

loads were out of balance, resulting 

in increased oxidative stress and 

subsequent metabolic inflammation. 

Intervention, therefore, had to include 

both antioxidant and anti-inflammatory 

therapy. 

3. The patient had received no prior 

treatment for his macro- and microcirculatory 

disorders. The goal 

here was to achieve vasodilation of 

the small blood vessels and normalization 

of homocysteine levels as a 

discrete risk factor for atherosclerosis. 

4. The overall therapeutic goal was 

to reduce matrix edema. 

5. Therapy for the wound itself. 

Inflammatory 

cytokines 

increase 

Visceral 

obesity 

Oxidative stress 

Glutathione level 

decreased in 

peripheral nerve 

Disturbance of blood flow 

in the perineurium 

and endoneurium 

Hyperglycemia 

Edema in the nerve sheaths 

Treatment Concept 

Antioxidants 1 

• 600 mg vitamin E 

• 300 μg selenium 

• 20 mg zinc 

• 500 mg vitamin C 

Normalization of 

elevated homocysteine 

• 50 mg vitamin B6 

• 1 mg vitamin B12 

• 5 mg folic acid 

Antihomotoxic treatment 

• For organ strengthening in coronary 

heart disease with cardiac 

insufficiency: Cor compositum 

twice weekly, i.v. 

• To improve macrocirculation: Circulo-Injeel 

twice weekly, i.v. 

• To improve cerebral microcirculation: 

Cerebrum compositum twice 

weekly, i.v. 

• To improve systemic microcirculation: 

Vertigoheel 2 tablets 3 times 

a day for 8 weeks, then 2 tablets 2 

times a day 

1 

Unless otherwise noted, dosages refer to the 

daily amount of medication (taken orally). 

Insulin resistance 

Beta-cell dysfunction 

Non-enzymatic glycosylation 

Thickening 

of basement 

membrane 

Impaired lymphatic 

function 

Colloid osmotic 

pressure increases 

Figure 1: Diabetic foot ulcer 

• To reduce matrix edema: Lymphomyosot 

1 tablet 3 times a day; 

Ubichinon compositum and Coenzyme 

compositum injected together, 

once weekly, i.m. 

• To reduce inflammation: Traumeel 

1 tablet 3 times a day 

• Wound therapy: daily treatment of 

the wound with Traumeel ampoules, 

dry bandage 

Under this treatment regimen, the 

wound grew smaller and flatter from 

week to week. After five months, it 

had completely closed. The patient’s 

subjective symptoms were significantly 

reduced, and his quality of 

life had improved considerably. He 

was already able to go for short 

walks again, and even under this 

stress the ulcer did not break open 

again. Objective criteria (lab results) 

also showed improvement over the 

initial findings. 

His wife reported that he was responding 

better to minor exertion, 

did not get out of breath as quickly, 

and was no longer so forgetful 

(which she especially appreciated). 

He was able to concentrate much 

better during his daily rummikub 

games. Antihomotoxic therapy addressed 

the causes of the ulcer by 

improving microcirculation and reducing 

matrix edema, which then 

allowed the wound to heal.| 

) 11 

Matrix 

edema 

Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1 

Figure 2: Pathological cascade 

leading to polyneuropathy


Immediate Intervention Required! 

Prophylaxis in a Male Patient With 

Early-Stage Metabolic Syndrome 



) 12 

Previously, Mr. B. E. had visited my office only occasionally, 

during the spring allergy season, when he suffered from 

bronchial asthma. In February 2007, however, he reported 

having been hospitalized for a week for treatment of sudden 

deafness and tinnitus in his left ear. Cortisone treatment 

and rheological infusion therapy had restored his hearing, 

but the tinnitus continued to bother him. Overall, he felt 

unmotivated and physically weak. 

This 63-year-old patient was 

overweight, with a body-mass 

index of thirty and a waist circumference 

of 104 cm (41 in). His liver 

was palpably fatty and soft to the 

touch. Other findings were unremarkable; 

his pulse was regular and 

his reflexes normal. Lab test results 

were indicative of early-stage metabolic 

syndrome bordering on type 2 

diabetes (see Table 1). 

Four major interventional studies 

conducted in recent years all came 

to the same conclusions on how development 

of type 2 diabetes can be 

prevented in cases of metabolic syndrome 

such as this one (see Table 

2). 

After nutritional counseling, the 

patient changed his eating habits 

significantly, reducing his consumption 

of animal fats in particular. Mr. 

B.E. was well aware that he stood at 

the crossroads: Either he would have 

to adopt a more health-conscious 

lifestyle and undergo holistic homeopathic 

treatment, or the metabolic 

syndrome would develop into 

full-fledged type 2 diabetes. Due to 

the “demands of his job,” as the patient 

put it, he was unable to implement 

the recommended exercise 

program. 1 

In addition to advising lifestyle 

changes, I developed a treatment 

program for the patient that focused 

on his microcirculatory disorders 

(which were already pronounced) 

and the following risk factors: 

• hypercholesterolemia 

• hypertriglyceridemia 

• excess weight 

• borderline erythrocyte 

and hematocrit values 

• impaired glucose tolerance 

Treatment model 

Mr. B.E. received the following basic 

treatment for metabolic syndrome 

(see also Figure 1): 

1. Syzygium compositum is the 

basic medication in antihomotoxic 

treatment of metabolic syndrome, 

especially in elderly and debilitated 

patients. Its main ingredient is the 

seed of the jambul or black plum 

(Syzygium cumini), which grows in 

Malaysia, India, and the tropical 

parts of China. It has been known 

since the nineteenth century for its 

ability to reduce blood sugar. Syzygium 

compositum’s other ingredients, 

selected for their complementary 

effects, include: 

• Acidum phosphoricum and 

Aci dum sulfuricum, for their 

strengthening effects in debility 

• Hepar suis and Pankreas suis, 

for their organ-strengthening 

effects 

• Strychnos ignatii, for its benefits 

in states of psychological stress 

and worry 

1 

Endurance sports such as bicycling and swimming are most effective; Nordic walking is the best of all. 



Photo by Ann Murray, University of Florida/IFAS Center 

for Aquatic and Invasive Plants. Used with permission. 

The jambul or black plum 

(Syzygium cumini) is the main 

ingredient of Syzygium compositum. 

2. Detoxification: 

The patient was accustomed to a 

fatty diet and frequent alcohol consumption 

and had a stressful job. 

The need for detox therapy was urgent. 

I recommended Heel’s Detox- 

Kit (ingredients: Lymphomyosot, 

Berberis-Homaccord, and Nux vomica-Homaccord). 

Lymphomyosot 

has cleansing effects on matrix metabolism, 

Berberis-Homaccord detoxifies 

the organism via the kidneys 

and urinary tract, and Nux vomica- 

Homaccord detoxifies the digestive 

system and the liver. Because of obvious 

liver involvement, I supplemented 

this detox program with one 

tablet of Hepeel three times a day to 

enhance liver detoxification. 

Laboratory parameter Results 2/2007 Results 6/2007 Reference range 

Fasting blood sugar 130 mg/dL 84 mg/dL < 110 mg/dL 

HbA1c 6.5% 5.6% < 6.5% 

Total cholesterol 346 mg/dL 171 mg/dL < 200 mg/dL 

HDL cholesterol 39 mg/dL 38 mg/dL > 35 mg/dL 

LDL cholesterol 241 mg/dL 114 mg/dL < 150 mg/dL 

LDL/HDL quotient 6.1 3.0 < 3.0 

Triglycerides 378 mg/dL 214 mg/dL < 200 mg/dL 

Erythrocytes 6.0/pL 5.7/pL 4.4-5.9/pL 

Hematocrit 51% 47% 42-52% 

Table 1: Lab test results 

3. Improving circulation: 

Because the patient’s blood was too 

viscous, blood-letting was performed 

at weekly intervals. The cubital vein 

was punctured and approximately 

100 ml of blood allowed to flow 

freely into a cup. This procedure was 

followed by infusion of the following 

antihomotoxic medications to 

promote circulation: 

• Circulo-Injeel 

• Vertigoheel 

• Placenta compositum 

• 7% reduction in weight 

• Increasing activity to 150 minutes a week @ 30 minutes a day, 5 times a week 

• Increasing fiber intake to 15 grams/1000 kcal 

• Reducing fat intake to 30% of calories 

• Reducing saturated fats to a maximum of 10% 

Successful implementation of 2 of these points prevents 23% of diabetes cases; 

achieving all 5 prevents almost 100%. 

Table 2: Measures to prevent the development of type 2 diabetes 

(Source: Consensus paper of the German Ministry of Health and Social Security 

[BmGS]) 

) 13 



Figure 2: 

The citric acid cycle 

Bloodletting was performed five 

times and infusion ten times, at one 

infusion per week. On days when he 

did not receive infusion therapy, the 

patient took two tablets of Vertigoheel 

three times a day to improve 

microcirculation. 

4. To activate blocked cell and 

enzyme functions and to improve 

metabolism, the acids and salts of 

the citric acid (Krebs) cycle were 

added to the infusion three times at 

two-week intervals (see Figure 2). 

Already after three weeks, the patient 

was free of tinnitus symptoms. 

By the end of four weeks, he had 

completely changed his diet and lost 

four kilograms. Further treatment 

with Syzygium compositum improved 

his glucose tolerance and 

psychological state. Upon conclusion 

of the series of infusions, the 

patient felt very well and no longer 

reported any feeling of weakness. 

As Table 1 shows, his lab test results 

also improved. 

Although symptom-free, the patient 

continues to take the following 

medications, which I prescribed to 

prevent metabolic syndrome and 

type 2 diabetes and to improve microcirculaton: 

• 1 tablet Lymphomyosot 

3 times a day 

• 10 drops Syzygium compositum 

3 times a day 

• 2 tablets Vertigoheel 

3 times a day 

• 1 tablet Hepeel 

3 times a day 

We arranged to repeat the course of 

infusions once a year.| 

Detoxification 

Improving 

circulation 

Syzygium 

compositum 

Citric acid cycle 

Figure 1: Basic treatment concept for metabolic syndrome 

) 14 


) A r o u n d t h e G l o b e 

ACAM Fall Meeting in Phoenix 

By Rüdiger Schneider, PhD 

The acronym “ACAM” stands for the American College for 

Advancement in Medicine. This non-profit medical society 

is dedicated to educating physicians and other healthcare 

professionals on the latest findings and emerging procedures 

in preventive/nutritional medicine, especially as related to 

the practice of complementary and alternative medicine. 

It is probably the largest and oldest organization of this 

kind in the USA. 

Worldwide, there are very few large 

conferences on alternative, complementary, 

and integrative medicine, 

which makes it all the more important 

to take advantage of such venues 

for sharing the latest scientific 

findings with the CAM community. 

The reaction of participants in the 

2007 ACAM conference speaks for 

itself.| 

The ACAM meets twice yearly, 

in spring and in fall. The 2007 

fall meeting, on “Integrative Medicine: 

Advancing Science and Clinical 

Practice,” took place from November 

16-18 in Phoenix, Arizona. 

Most of the approximately 300-400 

attendees were naturopathic physicians 

(NDs) or MDs specializing in 

natural medicine/CAM. Plenary 

session lectures dealt with the latest 

clinical and empirical findings and 

developments in alternative medicine. 

The topics covered included 

inflammation in the brain, the NO/ 

ONOO-cycle, treatment of IBD, 

pain neutralization techniques, evidence-based 

nutrition, and detoxification 

treatments. 

In a one-day pre-conference workshop 

on detoxification and drainage 

that was attended by about forty 

people, Dr. Alta A. Smit, the editor 

of this journal, presented detailed 

theoretical and practical approaches 

to proper detoxification and drainage, 

including easy-to-use guidelines 

that cover the entire process, 

beginning with assessing the patient’s 

toxic status and concluding 

with how to use the Detox-Kit and 

other Heel products for basic detoxification 

and drainage and advanced 

organ support. Judging by 

the spontaneous applause, this approach 

was received with great interest 

and enthusiasm. (See the previous 

issue of this journal for more 

information on detoxification and 

drainage.) 

Heel Inc.’s booth at the 

ACAM 2007 fall meeting 

) 15 


) Refresh Your Homotoxicology 

Citric Acid Cycle Catalysts 

By Ivo Bianchi, MD 

) 16 

The contribution of homotoxicology to the progress of 

medicine has been pivotal because it links homeopathic 

concepts and laws to modern scientific knowledge. 

Dr. Reckeweg’s starting point was the study of homeopathic 

materia medica, but he enriched and added to it in various 

ways and on various levels. 

An original and essential contribution 

resulted from the great 

attention paid to the study of the 

cell, which Reckeweg defined as the 

primary and fundamental element in 

which disease originates. An energy 

deficiency in the cell causes it to 

dysfunction, and an individual cell 

dysfunction is the start of a more 

complex pathology, which inevitably 

becomes an organic disorder. 

When it enters a crisis, the cellular 

energy plant (i.e., the mitochondrion) 

begins to lack energy for any 

biochemical cellular process; in particular, 

the proteins, enzymes, and 

cytokines which are fundamental to 

the life of a specialized cell are not 

synthesized. 

A cell that is lacking energy reduces 

its function to a minimum, uses large 

quantities of glucose via a metabolic 

route that does not require oxygen, 

pollutes the surrounding connective 

tissue, and progressively assumes the 

characteristics of a neoplastic cell. 

This whole sequence of events 

which leads from normal physiology 

to dysfunction, to degeneration, and 

eventually to neoplasia, is initiated 

in the mitochondrion and, more 

specifically, in that sequence of oxidative 

reactions involved in pyruvic 

acid catabolism and ATP production. 

It is clear how important it is to 

keep this sequence of key biochemical 

reactions as efficient as possible 

for both the catabolic and anabolic 

aspects of cell function. 

Patients with chronic degenerative 

diseases, which are those we encounter 

most frequently today in 

our natural medicine clinics, primarily 

need specific, selective stimulation 

of the citric acid cycle. Treatment 

with intermediary catalysts in 

a dilute, dynamized form offers an 

exceptional therapeutic opportunity 

in this domain. 

Therapeutic approaches 

The patient is assessed and, if this 

shows that he is in one of the cellular 

phases of the homotoxicology 

table, total stimulation of the citric 

acid cycle must be carried out, either 

by the administration of Coenzyme 

compositum or the individual catalysts 

if they are available. 

If we consider that the organism often 

uses the building blocks of the 

citric acid cycle via many other metabolic 

pathways, it is clear that deficiencies 

of substances at various levels 

will tend to block the cycle once 

again. It is therefore useful to start 

therapy to support the citric acid 

cycle with Coenzyme compositum, 

at the rate of one ampoule sublingually 

or by injection 1 to 3 times 

weekly. Children, in whom the citric 

acid cycle has presumably not 

reached a block as in adults or in 

chronically ill patients, can obviously 

start directly with the catalysts 

providing energy and a reactive 

stimulus to the organism. 

Although this is the best general 

strategy for using the citric acid cycle 

catalysts, it is also useful to be 

familiar with the role and consequently 

the clinical indications of 

the individual catalysts, which we 

summarize below. 


) Refresh Your Homotoxicology 

Natrium pyruvicum 

This is the next product in glucose 

metabolism. If the metabolism and 

the use of this metabolite are not 

stimulated, it tends to accumulate in 

the cytoplasm, where it is used anaerobically 

and induces tissue acidosis. 

Citric acid 

This is the first stage in the citric 

acid cycle and represents a basic 

building block not only in the production 

of energy at this level, but 

also in the synthesis of essential fatty 

acids fundamental to the nerve 

structures of the organism. 

Cis-Aconitic acid 

This is a metabolite which forms 

very fleetingly. A lack of its regulation 

leads to general problems of tissue 

hyperreactivity. 

Alpha-Ketoglutaric acid 

This is a fundamental stage in the 

citric acid cycle, but it is also a fundamental 

metabolite in the synthesis 

of some biological amines important 

for the functioning of nerve tissue, 

such as glutamic acid and glutamine. 

If the cycle is blocked at this point, 

it causes changes in neuromuscular 

function. 

Succinic acid 

This is the substance used in the innermost 

part of the mitochondrion 

to trigger oxidative phosphorylation, 

the peak stage of energy production 

in the cell. Blocking of this 

metabolic pathway leads to damage 

to tissues, particularly those with a 

high energy requirement such as hematopoietic 

tissue in particular. 

Fumaric acid 

This is a key stage not only in the 

citric acid cycle but also for a whole 

series of metabolites involved in the 

synthesis of fundamental amino acids, 

including tyrosine and phenylalanine. 

Blockage of the cycle at this 

point causes disturbances of lipid 

metabolism. 

DL-Malic acid 

Blocking of the citric acid cycle at 

this point prevents the correct use of 

Natrium pyruvicum. Such a blockage 

is typical in individuals with senile 

diabetes and causes many of the 

tissue and primary cell problems 

that occur in this disease. 

Natrium oxalaceticum 

This is a key metabolite for triggering 

the citric acid cycle through its 

reaction with acetyl CoA. A disturbance 

of this metabolic stage leads 

to a general weakening of organic 

reactivity, making the individual 

prone to disease and parenchymal 

toxin accumulation. It should also 

be noted that Natrium oxalaceticum 

is a precursor of aspartic acid, which 

is involved in the urea cycle and thus 

in the production of nitric oxide, a 

substance which is vital to the circulatory 

system. 

Barium oxalsuccinicum 

This is not a citric acid cycle catalyst 

but a salt originally believed by 

Reckeweg to activate cell reactivity 

in the elderly and in individuals in a 

degenerative phase. 

In severe or chronic cases, an intensive 

stimulation of the individual 

components of the citric acid cycle 

catalysts may be beneficial. In my 

practice, I use the so-called “Sammelpackung” 

(combination pack) of 

the citric acid cycle catalysts to 

achieve this. 

In this, the 10 ampoules of the single 

pack of catalysts are administered 

at the same time, without placing 

too much importance on the 

route of administration. If possible, 

the 10 ampoules should be placed 

in a small infusion of 100 cc, which 

should be administered over about 

30 minutes. Intramuscular administration 

of the 10 ampoules is, however, 

also effective, and a good effect 

can likewise be obtained by the sublingual 

route. The administration of 

the 7 citric acid cycle catalysts, the 

reactive stimulus salt Barium oxalsuccinicum, 

and the trace elements 

magnesium, manganese, and phosphorus, 

all in a dilute, dynamized 

form, gives this mitochondrial metabolic 

cycle a remarkable reactive 

stimulus. 

This “rekindling” or stimulation 

should be repeated every 2 to 3 

weeks in very elderly patients or 

those with metabolic dysfunction or 

neo plasia because various toxic 

problems other than metabolic problems 

tend to re-block the citric acid 

cycle. Patients who are not in a 

clearly degenerative phase will, 

however, need this therapeutic 

application only every 3 to 6 

months.| 

The mitochondrion provides cellular 

energy through a series of biochemical 

reactions called “citric acid cycle.” In 

patients with chronic degenerative 

diseases, intermediary catalysts are 

successfully used to stimulate this 

process. 

) 17 


) Marketing Your Practice 

Practical Tips 

for Improving Your Marketing Strategy 

By Marc Deschler 

Marketing specialist 

) 18 

Practitioners often mentally equate marketing with 

advertising, but in fact marketing serves multiple goals: 

tapping into the market, winning over patients, market 

protection, and patient loyalty. It is important to know 

that just under 70 percent of patients in a practice are 

there because of the practitioner’s personal charisma, 

making that a good foundation for marketing when 

fostering patient loyalty is your goal. 

But before you even begin to 

think about new and improved 

marketing behavior, first evaluate 

the current state of your practice. 

Get clear on your current status by 

answering the following questions: 

1. Why do patients come to us in 

particular? Is it the location? Absence 

of competition? (Not likely!) 

Are we exceptionally friendly? 

2. Which patients come to us? 

What is their age, gender, social 

class? 

3. Why don’t other patient groups 

come to us? 

4. What do we do differently, better, 

or worse than other practices in 

the area? 

5. How do our patients feel in our 

office? Welcomed and well treated, 

or rushed through and out of 

place? 

6. What do we offer? Is there anything 

we offer that patients are especially 

happy about, or anything they 

almost never take advantage of? 

7. What do we do well and gladly, 

and what do we do less well or only 

reluctantly? 

8. Is there anything special about 

our patient service, any particular 

offerings or support services? 

9. Do our patients know the full 

range of what we offer? Do we make 

them aware of it only in passing, or 

do we provide printed information? 

Answer these questions yourself and 

then ask your patients to answer 

some of them. Determine where you 

stand now and base your future 

marketing efforts on an adequate 

understanding of your current status. 

Handling complaints 

How your practice handles complaints 

is important in developing 

patient loyalty. Wouldn’t you know 

it – patients who complain but get 

satisfaction are six times more loyal 

than patients who never have a 

problem with you, so when a patient 

does complain, your complaints 

management needs to be excellent. 

Keep in mind the following points 

for working things out with those 

problem patients: 

1. Listen, listen, and listen some 

more. Let the patient “let off steam,” 

even if he or she says the same 

thing several times. 


) Marketing Your Practice 

When a patient complains, listen 

carefully and make sure you understand 

why he or she is angry. If possible, let the 

patient offer a solution. 

© iStockphoto.com/Marcin Balcerzak 

2. Ask questions and more questions. 

From his/her point of view, 

the patient is certainly right, and 

you need to understand why he/ 

she is angry. (Understanding is not 

the same as acknowledging that 

you’re at fault.) 

3. Solutions: Let the patient solve 

the problem. If you can accept a solution 

he/she offers, the issue simply 

evaporates. If you can’t, suggest 

one or more possible compromises. 

4. The most important thing is to 

follow through with everything 

you promise, or else your effort will 

be wasted. 

5. Check with the patient again to 

make sure that everything has been 

resolved to his/her satisfaction. 

Marketing in the 

waiting room 

Actively marketing your practice is 

especially important in your waiting 

room because you’re not there to 

make a good impression yourself. 

© iStockphoto.com/Ivonne Wierink 

You can, however, use your waiting 

room as a learning opportunity for 

your patients. Instead of standardissue 

furniture, get together with a 

local supplier and arrange to test 

balance ball chairs, or demonstrate 

how to adjust a desk chair for back 

support. Provide related handouts 

so your patients can see how to use 

ergonomic devices as they try them 

out on the spot. Videos for patients 

to watch while waiting are also instructive, 

but not all patients want to 

be inundated with medical information, 

so make sure there’s a corner 

where they can get away from it. 

Having ordinary TV programming 

available is more problematic because 

the patients have to agree on 

what to watch. 

There’s nothing worse than sitting 

around in an oppressive atmosphere 

waiting for your name to be called. 

Whether to have the radio on or a 

CD of relaxing music playing in the 

background depends on your patients’ 

tastes. If you resort to canned 

music, don’t forget to change it at 

least once a month so it doesn’t become 

too monotonous for everyone. 

If patients have to wait for their appointment, 

their waiting time should be as 

pleasant as possible. There is nothing 

worse than sitting in an oppressive 

atmosphere. 

Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1 

When choosing reading material for 

your waiting room, don’t just opt 

for the standard subscriptions or put 

out your own back issues. Maybe 

you’d be happy with the Financial 

Times, but how would it go over 

with your target group? Instead, ask 

yourself what issues you’d like your 

patients to raise with you, and select 

material that addresses topics you 

want to discuss. For example, many 

women’s magazines regularly include 

articles on medical topics, so 

you need to be prepared to answer 

questions about them. Under no circumstances, 

however, do your medical 

journals belong in the waiting 

room! 

Offering hot and cold drink service 

also has a place in the perfect waiting 

room. If drinks are available, 

make sure there’s a sign telling patients 

that they can help themselves 

free of charge. Make sure someone is 

assigned to ensure a constant supply 

(and let in a bit of fresh air at the 

same time, if needed). 

If you have a bulletin board, check it 

regularly to make sure that the information 

posted is up-to-date and 

of interest. 

It’s not always possible to avoid 

making patients wait for their appointments, 

but when it happens, 

their waiting time should be as productive 

and pleasant as possible. 

That’s also part of good office ambiance.| 

) 19

) S p e c i a l i z e d A p p l i c a t i o n s 

Individualized Infusion Therapy 

in Metabolic Syndrome 



Metabolic syndrome is a multifactorial problem. 

A paradigm shift is required in order to understand the 

metabolic processes involved and treat our patients with 

metabolic syndrome holistically. The old glucose-centered 

view no longer reflects the reality of well-researched 

metabolic processes. 

In metabolic syndrome, late 

damage is due to deposition of 

the following homotoxins: 

• glucose 

• free oxygen radicals 

• sorbitol 

• advanced glycation end 

products 

• inflammatory mediators 

In metabolic syndrome, the pathological 

cascade is initiated by the 

triad of visceral adiposity with associated 

dyslipidemia, hyperglycemia 

with beta-cell dysfunction, and 

insulin resistance. As the pathology 

progresses, we see increased free 

radical formation, reduced bioavailability 

of NO, release of inflammatory 

cytokines, and accumulation of 

toxins in the matrix. The end results 

of this pathophysiological interaction 

are endothelial dysfunction 

with micro- and macrocirculatory 

disturbances and diabetic polyneuropathy. 

The toxic byproducts of 

this pathological cascade constitute 

homotoxins in the sense of modern 

homeopathy and Hans-Heinrich 

Reckeweg’s theory of disease. The 

effects of homotoxins are first felt in 

the early stages of glucose intolerance, 

even before metabolic syndrome 

is diagnosed. Elevated glucose 

levels lead to four pathological 

“pathways”: 

1. the polyol pathway: sorbitol develops 

and accumulates around 

nerve endings 

2. the auto-oxidation pathway: advanced 

glycation end products develop 

3. the protein kinase pathway: inflammatory 

mediators such as NFkB 

und TNF-α are expressed 

4. the free radical pathway: reduction 

of NO occurs 

The antihomotoxic therapeutic approach 

is to reduce the damaging 

effects of homotoxins. According to 

Reckeweg’s six-phase table, in diabetes 

deposition of homotoxins occurs 

first, followed later by impregnation 

and degeneration accom pa nied by 

the characteristic late damage. 

In planning infusion therapy for 

prophylaxis and treatment of metabolic 

syndrome and its late damage, 

the following questions should be 

considered: 

• Which toxins are present? 

• What is the patient’s phase on 

the six-phase table? 

• What is the patient’s clinical 

status? 

In some cases, extensive lab tests 

may also be helpful. For example, 

knowing the patient’s homocysteine 

level and free radical loads (e.g., lipid 

peroxidase) can be valuable. 

) 20 



Intravenous therapy is an important 

component of treatment in many acute 

and chronic diseases, especially in cases 

of metabolic syndrome. 

Treatment concept 

I recommend twice-yearly infusion 

therapy for my patients – ideally, 

twice-weekly infusions (to a total of 

ten) each spring and fall. Lymphomyosot 

is the basic medication. Its 

constituents act on four different 

levels: on the lymphatic, respiratory, 

and digestive systems and on the 

urinary tract. Infusion therapy 

should be preceded by approximately 

two weeks of oral treatment with 

Lymphomyosot at the standard dosage 

of 1 tablet 3 times a day or 15 

drops 3 times a day. In multimorbid 

or severely debilitated patients, better 

tolerance is achieved by reducing 

the dosage to 8 to 10 drops 3 times 

a day. 

In patients with metabolic syndrome, 

both visceral adipose tissue 

and the interaction of free radicals 

and advanced glycation end products 

contribute to metabolic inflammation 

(which can be corroborated 

by ultrasensitive CRP measurements, 

among other tests). To reduce inflammation, 

I often add Traumeel 

(antihomotoxic medicine’s most important 

anti-inflammatory) to the 

infusions. As a component of the 

citric acid (Krebs) cycle, dl-malic 

acid has notable metabolism-stabilizing 

effects in metabolic syndrome. 

Below are several examples of timetested 

infusions with special emphases. 

1 The products Coenzyme compositum 

and Ubichinon compositum 

are not registered for intravenous 

use in most countries and should 

therefore be administered either i.m. 

or s.c. after every infusion. 

Toxic sorbitol 

Polyol pathway 

Protein kinase pathway PKC 

Expression of inflammation 

mediators NF-kB 

Glucose 

AGEs (advanced glycation end products) 

Auto-oxidation pathway 

Oxygen radical pathway 

NO-reduction 

© iStockphoto.com/Wa Li 

Figure 1: Pathological pathways triggered by elevated blood glucose levels 

1 Please note that some of the medications listed may not be available for injection in a few countries. It is the practitioner’s responsibility to use the medications as 

directed in the product information. 

) 21 



Infusion protocols in metabolic syndrome 

) 22 

Infusion for metabolic 

syndrome/obesity 

• Graphites-Injeel (Ed. note: 

or Graphites-Homaccord) 

• Hepar compositum 

• Nux vomica-Injeel (Ed. note: 

or Nux vomica-Homaccord) 

• Lymphomyosot 

• Traumeel 

• Acidum DL-malicum-Injeel 


syndrome with high blood 

pressure (adjuvant) 

• Melilotus-Homaccord 

• Rauwolfia compositum 

• Arteria suis-Injeel 

• Traumeel 



syndrome with pancreatic 

insufficiency 

• Pankreas suis-Injeel 

• Acidum DL-malicum-Injeel 

• Momordica compositum 

• Traumeel 



syndrome with mild to 

moderate circulatory 

disturbances 


• Placenta compositum 


• Traumeel 


• Cerebrum compositum 

(in cerebral circulatory 

disturbances) 


syndrome with 

polyneuropathy 


• Vitamin B 6 


• Traumeel 


• Selenium 

• Vitamin C 

(administered as a separate 

infusion) 


syndrome with hyperhomocysteinemia 



• Folic acid 

• Traumeel 



• Cerebrum compositum 

(for cerebral circulatory 

disorders) 

If the catalysts of the citric acid 

(Krebs) cycle are available, patients 

will derive great benefit (in the form 

of improved metabolism) from yearly 

or twice-yearly infusions of these 

catalysts (see case study on page 12 

and the article on citric acid cycle 

catalysts on page 16 of this journal). 

Ideally, the catalyst infusions should 

be administered every two weeks 

and in alternation with any of the 

infusions listed above, to a total of 

three citric acid cycle infusions, after 

which the basic infusions can be 

continued without the interspersed 

catalyst infusions. 

The patients’ subjective wellbeing is 

greatly enhanced by these treatments, 

and objective signs such as 

blood pressure, blood sugar levels, 

and cholesterol levels also improve. 

For all of these reasons, patients usually 

return without being reminded 

for their next annual infusion series 

and recommend the infusions to 

relatives and friends.| 


) Practical Protocols 

Detoxification and Drainage 

in Metabolic Syndrome 

By Bruce H. Shelton, MD, MD(h), DiHom 

Detoxification is an important 

component in the basic treatment 

of metabolic syndrome patients. 

Individuals with central obesity 

are a high risk group, not only 

because of the inflammatory potential 

of fatty tissue but also because 

fatty tissue is a reservoir for toxins 

(see BT 2/2007, page 13). For this 

reason, these patients need fairly 

gradual detoxification with adequate 

support of the organs of detoxification 

and drainage. (Esthetic mesotherapy 

in particular mobilizes fat 

tissue, releasing stored toxins, so 

these patients always need advanced 

organ support, followed by a long 

period of drainage with the Detox- 

Kit.) We seek a delicate balance in 

treating patients with metabolic 

syndrome: Weight loss is imperative 

because inflammatory fatty tissue 

poses a risk to the entire organism, 

but mobilizing fat releases dangerous 

toxins, which may exacerbate 

the pathology. 

For these patients, Thyreoidea compositum 

is a good choice because of 

its metabolic, immunologic, and organ-strengthening 

properties. Fatty 

tissue (simply another form of connective 

tissue) is supported by the 

Funiculus umbilicalis suis in the 

product. In patients who develop 

central obesity as a consequence of 

stress or extraneous cortisone use, 

Pulsatilla compositum is especially 

useful and can replace the Thyreoidea 

compositum. The catalysts are 

mandatory in these conditions. 

Many of these patients develop gallstones 

during rapid breakdown of 

fatty tissue. Patients at high risk (especially 

fair-skinned females over 

40 years of age) can be supported by 

adding Chelidonium-Homaccord to 

the Detox-Kit during the drainage 

phase. (See protocol in Table 1.)| 

Disease-specific treatment Strumeel and/or Syzygium compositum, Cralonin, Barijodeel 

Followed by detoxification treatment: Always do advanced organ support first 

Weeks 1-6 or until point count is < 100 

Liver 

Urinary tract/ 

Kidney 

Lymph Skin Gut Gallbladder Connective 

tissue 

Respiratory 

tract 

Advanced organ 

support 

Hepar comp. Solidago comp. Hepar comp. Thyreoidea comp. 

Alternative 

products 

Hepeel Reneel Galium-Heel/ 

Lymphomyosot 

Nux vomica- 

Homaccord 

Leber-Galle 

Tropfen 

Pulsatilla comp. 

For cellular 

detoxification, 

add: 

Coenzyme comp./ 

Ubichinon comp. 

(or Ubicoenzyme) 






















Note 

Dosage 

The metabolically active medications Hepar compositum and Coenzyme compositum can also be injected into ST 36 (0.5 cc of the mixture into the AP point). 

Ampoules: In general, 3-1 times weekly 1 ampoule i.m., s.c., i.d. Drops: In general, 10 drops 3 times daily 

After six weeks or when point count < 100: Basic detoxification and drainage 

Liver 

Urinary tract/ 

Kidney 

Lymph Skin Gut Gallbladder Connective 

tissue 

Basic detoxification 

and drainage 

Detox-Kit Detox-Kit Detox-Kit Detox-Kit Chelidonium- 

Homaccord 

Detox-Kit 

For cellular 

detoxification, 

add: 






















Note 

Dosage 

In very obese patients, continue with Thyreoidea compositum/Pulsatilla compositum for 12 weeks longer. 

Ampoules: In general, 3-1 times weekly 1 ampoule i.m., s.c., i.d. Drops: In general, 10 drops 3 times daily 

) 23 

Table 1: Detox protocol for metabolic syndrome 


) Making of ... 

Suis-Organ Products in 

Antihomotoxic Medicine 

Part 1: Breeding and Raising the Donor Pigs 

By Erich Reinhart, DVM 

Therapy with animal endocrine extracts is widespread, even 

in conventional medicine, but some countries, including 

Germany and France, have a long history of more extensive 

use of animal organ derivatives for therapeutic purposes. 

Organotherapeutic medicines in this broader sense may be 

derived from organs, cells, cell fractions, organ extracts, 

enzymes, or any combination of the above. 1(p102-103) 

) 24 

The suis-organ products used in 

antihomotoxic therapy are homeopathically 

prepared (i.e., diluted 

and potentized) organ tissues produced 

from raw materials derived 

from healthy pigs and manufactured 

according to Regulations 42a (oral 

and external medications) or 42b 

(parenteral medications) of the German 

Homeopathic Pharmacopeia 

(HAB), as applicable. The designation 

“suis” (Latin, “pig”) indicates the 

origin of the raw materials. Suis-organ 

products expand the classical 

homeopathic repertory to cover 

functional organ disorders and degenerative 

organ damage (for more 

information about the rationale behind 

and use of suis-organ medications 

in antihomotoxic medicine, 

see BT 2/2007, pp. 16-17). According 

to Schmid, “Organ preparations 

are medicinal products which 

contain several, or all, tissue components 

of an organ. In addition to the 

differentiated cellular constituents – 

e.g., liver cells, kidney cells, cerebrum 

cells, blood cells, bone marrow 

cells, and thymus cells – these preparations 

also contain connective 

vascular tissue and ground substance 

(stromata).” 1(pp102) 

Ideal donor animal 

Pig tissues are the obvious choice in 

view of the many chemical, biological, 

physiological, and morphological 

similarities between this species 

and the human organism – similarities 

that have even led to attempts to 


) Making of ... 

Left: 

The fodder of the donor pigs consists of 

cereal groats, organically-grown soy 

groats, and minerals. 

Right: 

Proper cleaning and disinfecting of the 

animals’ stalls are effected according to 

the requirements of the Ministry of 

Agriculture’s hygiene regulations. 

substitute pig organs for scarce human 

organs in transplantation medicine. 

From the homeopathic perspective, 

a pig-derived potentized 

organ product can be considered a 

“simile” of the homologous human 

organ(s). For this reason, stronger 

effects are being attributed to pig 

organ preparations than to products 

derived from cattle or sheep. 2 

Breeding and husbandry 

Pigs destined to supply the raw materials 

for homeopathic organ extracts 

for antihomotoxic medications 

are provided by a breeding operation 

that is certified to be free of 

specific pathogens and under constant 

veterinary oversight to ensure 

compliance with all applicable hygiene 

regulations of the German 

Federal Ministry of Agriculture. The 

brood sows all come from the same 

breeding line. The future donor pigs 

stay with their mother until they are 

six weeks old, and her milk is their 

primary food until they are weaned. 

After weaning, the litter stays together 

and the piglets are raised 

separately from other pigs to prevent 

the stress and fights for dominance 

that may ensue if new animals 

are introduced into the group. The 

animals’ stalls are cleaned and disinfected 

before occupancy. The breeding 

operation must abide by all of 

the Ministry of Agriculture’s hygiene 

regulations applicable to hog 

rearing, including requirements for 

proper cleaning and effective disinfection. 

Non-employees must wear 

either disposable outer garments or 

protective clothing provided by the 

company, and their shoes must be 

cleaned and disinfected before entering 

the stall areas. 

The pigs’ fodder consists entirely of 

plant materials (cereal groats) grown 

on the farm itself, supplemented 

with purchased protein (soy groats) 

and minerals. The soy groats are organically 

grown to ensure that this 

critical feedstuff is free of genetically 

engineered products. Feeding of 

food scraps or animal by-product 

meals from mammals is both legally 

and contractually forbidden. In addition 

to monitoring by the state 

Animal Health Service for compliance 

with all health directives applicable 

to animal breeding operations, 

the animals are checked both at regular 

intervals and as needed by the 

company’s veterinarian. They are 

also examined by the district veterinary 

officer before shipping out. 

Safety measures 

Ensuring the microbiological safety 

of the final products involves an extensive 

checklist of procedures. Suitable 

sample tissues are selected for 

testing for the zoonotic pathogens 

most common in pigs. In southern 

Germany, where the pigs are raised, 

Salmonella spp., Campylobacter 

spp., and Yersinia spp. are the most 

relevant. Tests for these and other 

pathogens must be negative if the 

animal’s tissues are to be used in 

manufacturing suis-organ medicines. 

Separate records of test results are 

kept for each animal. Also available 

for reference are two files of materials 

from groups of experts. These 

files list and discuss all diseases 

known to occur in pigs, describe 

which of these diseases might theoretically 

occur in the geographical 

area and under the conditions in 

which the donor pigs were raised, 

and explain the measures to be taken 

to eliminate the possibility of using 

animals infected with these (theoretically 

possible) diseases. 

The above-mentioned standards of 

livestock husbandry, feeding, and 

hygiene along with the combination 

of clinical, microbiological, and serological 

tests (some of which exceed 

government requirements) 

minimize the risk of using organs 

contaminated with hog-borne 

zoonotic pathogens and maximize 

the safety of the final organ products.| 

References: 

1. Schmid F (ed). Biological Medicine. Baden- 

Baden, Germany: Aurelia Verlag, 1991. 

2. Reckeweg H-H. Homotoxikologie – Ganzheitsschau 

einer Synthese der Medizin. 6th ed. Baden- 

Baden, Germany: Aurelia Verlag, 1986: 616. 

) 25 


) Research Highlights 

Emotional Stabilization 

Through Homeopathic Medication 

Neurexan reduces the psychological strain of stress 

In a randomized, placebo-controlled 

double-blind study, neurophysiological 

methods were used to 

determine the effects of Neurexan 

on patients’ psychophysiological 

con dition. The administration of 

Neurexan was found to help them 

to cope better with acute stress situations. 

The homeopathic combination medication 

Neurexan consists of the 

components passionflower (Passiflora 

incarnata), oats (Avena sativa), 

caffeine (Coffea arabica), and zinc 

salts (Zincum isovalerianicum) in 

homeopathic dosages. The literature 

contains a number of references 

to the tension-relieving, anxiolytic 

properties of the passionflower. 

Exposure to a stressful situation 

To investigate the effect of Neurexan 

during mental strain, a total of 30 

persons took part in a study in which 

a stress situation was created. To assess 

their clinical condition, initial 

and final examinations were performed 

in which, in addition to a 

standardized clinical case history 

and a physical examination, an ECG 

was recorded, blood and urine samples 

were taken, and an alcohol test 

was performed. 

The healthy male and female volunteers, 

who were between 30 and 60 

years of age, underwent a test in 

which they had to solve mathematical 

problems. If they solved the 

problems well, volunteers received a 

reward (increase in volunteer remuneration); 

if they did badly, they received 

a “punishment” (loss of remuneration). 

During the study, either 

active medication or a placebo was 

used in a single dose of 4 tablets in 

each case. EEGs of the study participants 

were recorded. The recordings 

were repeated hourly until four 

hours after the administration of the 

tablets. 

It is assumed that different emotional 

moods are shown by statistically 

significant changes in the electrical 

activity of the brain. Six frequency 

ranges (delta, theta, alpha, alpha 2, 

beta 1, and beta 2) were therefore 

defined for the analysis of the quantitative 

EEG and color-coded. 

Sharp rises in the beta waves are observed 

mainly during cognitive tasks 

and powerful emotional events such 

as the mentally stressful situations 

that were part of the study design. 

During the study there was a clear 

reduction in spectral output in the 

beta frequency band in the Neurexan 

group. After just one hour, a significant 

difference was seen between 

the Neurexan group and the placebo 

group, which intensified in the second 

and third hours. The reduced 

rise in the beta waves is a sign of the 

lesser subjective strain in the active 

medication group and is evidence of 

emotional stabilization. 

The test substances were very well 

tolerated. In a few cases the volunteers 

complained of tiredness. 

Conclusion 

The single dose of 4 tablets of Neurexan 

produces statistically significant 

changes in electrical brain activity 

compared to placebo. This is 

interpreted as evidence of a more 

balanced mood, which makes it 

possible to cope better with psychological 

strain in stressful situations 

without mental functions being 

impaired. | 

) 26 

The passionflower (Passiflora incarnata) 

has anxiolytic properties and is 

used for the treatment of nervousness 

and insomnia. 

Reference: 

Dimpfel W. Psychophysiological effects of Neurexan 

® on stress-induced electropsychograms. A 

double-blind, randomized, placebo-controlled 

study in human volunteers. Paper presented at: 

2nd World Conference of Stress; August 23-26, 

2007; Budapest, Hungary. 


) Crossword Puzzle Re s e a r c h 

Highlights 

Solve the puzzle and win! 

Here’s how it works: Complete the 

crossword puzzle and enter the letters 

from the numbered boxes in the 

blanks to make a word. Then e-mail 

your solution to: 

journal@iah-online.com to enter it 

in our drawing before August 31, 

2008. Ten lucky winners will receive 

copies of the book “Biological 

Medicine in Geriatrics” (Ingo Füsgen, 

Hartmut Heine, and Werner 

Frase, eds.). Please remember to include 

your complete mailing address. 

Results of the drawing are 

final. Good luck! 

Solution to last issue’s puzzle: 

Detoxification 

) 27 


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