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Biomedical
Therapy
J o urnal o f
Volume 2, Number 1 ) 2008
Integrating Homeopathy
and Conventional Medicine
Metabolic
Syndrome
• An “Incurable” Diabetic Foot Ulcer
• Suis-Organ Products in Antihomotoxic Medicine
)
Contents
I n Fo c u s
Metabolic Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
W h a t E l s e I s N e w ? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
From the Practice
An “Incurable” Diabetic Foot Ulcer . . . . . . . . . . . . . . . . . . . . . .10
Immediate Intervention Required! . . . . . . . . . . . . . . . . . . . . . . 12
Around the Globe
ACAM Fall Meeting in Phoenix . . . . . . . . . . . . . . . . . . . . . . . . .15
Re f r e s h Yo u r H o m o t ox i c o l o g y
Citric Acid Cycle Catalysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .16
M a r ke t i n g Yo u r P r a c t i c e
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
Re s e a r c h H i g h l i g h t s
Emotional Stabilization
Through Homeopathic Medication . . . . . . . . . . . . . . . . . . . . .26
C r o s s w o r d P u z z l e . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .27
)
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Published by/Verlegt durch: International Academy for Homotoxicology GmbH, Bahnackerstraße 16,
76532 Baden-Baden, Germany, e-mail: [email protected]
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
M
etabolic 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 me­
di­cine 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 me­
tabolic syndrome is now better understood, but as we see from Professor Michael Kirkman’s com­pre­hen­
sive 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
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
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
) I n Fo c u s
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)
Epidemiologic key factors
relating to metabolic syndrome
“Structure Is an Expression of Function.”
Introduction
)
4
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 be­
tween the two key determinant pro­
jections (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 sig­
naling, protein expression, gene expression, and free radical formation.
These may be relevant to associat­ed pathophysiological factors (pro­
thrombotic 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 defi­
ciency. Hence, vasoconstriction, prothrombotic, pro­in­flammatory, and
pro-oxidant states ensue.1(p741),2
Abdominal obesity
• men
• women
Triglycerides
HDL cholesterol
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
• men
• women
< 40 mg/dL
< 50 mg/dL
Blood pressure
≥ 130/≥ 85 mm Hg
Fasting glucose
≥ 110 mg/dL
Diagnosis of metabolic syndrome is made when 3 or more of the above risk determinants
are present
Table 1: ATP III criteria for diagnosing metabolic syndrome
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
) I n Fo c u s
Table 2: Effects of adipocytokines
Promotes weight gain and inflammation
Promotes weight loss
IL-6: causes insulin resistance,
proinflammatory cytokine
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 depolar­
ized, 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 cas­cade
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).
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
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 adi­pogenesis and is affected by
the leptin secreted by mature adi­
pocytes. 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
) I n Fo c u s
Abdominal obesity, recognized by
increased waist circumference, is
a risk factor for developing metabolic
syndrome.
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, naturopa­
thic, 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
)
6
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
end­products [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 Recke­
weg’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,
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
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.)
) I n Fo c u s
Elevated blood pressure is one of
the components that characterize
metabolic syndrome.
Adjuvant nutritional therapy
Recommended texts for homotoxicologists
(relevant to paper)
On a microbiological level, the intake of probiotics will help to overcome gut microbial dysfunction.
Immunonutrition products (especial­
ly 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 anti­
oxidants (free radical scavengers)
and so-called “cleansers,” e.g., spirulina (an alga that provides a full range of amino acids).
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.
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.|
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.
)
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
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
artificial food colorings
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.
Soda: Is just one a day too
much for your heart?
Does TV make children
smart?
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.
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.
Circulation 2007;116:480-488
)
8
The Lancet
2007;370(9598):1560-1567
Arch Pediatr Adolesc Med
2007;161:473-479
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
) What Else Is New?
Educational aid or electronic baby­
A happy partner-
parents let their infants and toddlers
prevent the
sitter? A recent US survey shows that
watch television on a regular basis.
ship helps to
development
of CHD.
Live hard,
die young
Marital discord is bad
for the heart
Love handles
are hereditary
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.
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.
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.
Arch Intern Med
2007;167(18):1951-1957
Science 2007;316(5826):889-894
J Epidemiol Community Health
2007;61:896-901
F O R P RO F E S S I ONA L U S E ON LY
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products or ingredients referred to for informational purposes only, is not intended to be a recommendation with respect to the use of or benefits derived from the
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articles in this journal.
The purpose of the Journal of Biomedical Therapy is to share worldwide scientific information about successful protocols from orthodox and complementary practitioners. The intent of the scientific information contained in this journal is not to “dispense recipes” but to provide practitioners with “practice information” for a better
understanding of the possibilities and limits of complementary and integrative therapies.
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Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
)
9
) From the Practice
An “Incurable” Diabetic Foot Ulcer
By Ulrike Keim, MD
Specialist in internal medicine
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.
T
he 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.
) 10
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
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
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
) From the Practice
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.
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
Unless otherwise noted, dosages refer to the
daily amount of medication (taken orally).
1
Visceral
obesity
Insulin resistance
Beta-cell dysfunction
Hyperglycemia
Oxidative stress
Inflammatory
cytokines
increase
Non-enzymatic glycosylation
Glutathione level
decreased in
peripheral nerve
Thickening
of basement
membrane
Disturbance of blood flow
in the perineurium
and endoneurium
Impaired lymphatic
function
Edema in the nerve sheaths
Colloid osmotic
pressure increases
Matrix
edema
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
Figure 2: Pathological cascade
leading to polyneuropathy
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
) From the Practice
Immediate Intervention Required!
Prophylaxis in a Male Patient With
Early-Stage Metabolic Syndrome
By Ulrike Keim, MD
Specialist in internal medicine
Treatment model
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.
T
)
12
his 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
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
Aci­dum 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
Endurance sports such as bicycling and swimming are most effective; Nordic walking is the best of all.
1
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
Photo by Ann Murray, University of Florida/IFAS Center
for Aquatic and Invasive Plants. Used with permission.
) From the Practice
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 DetoxKit (ingredients: Lymphomyosot,
Berberis-Homaccord, and Nux vo­
mica-Homaccord). Lymphomyosot
has cleansing effects on matrix metabolism, Berberis-Homaccord detoxifies the organism via the kidneys
and urinary tract, and Nux vomicaHomaccord 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.
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
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
• 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])
)
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
13
) From the Practice
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.
Detoxification
Syzygium
compositum
Improving
circulation
Citric acid cycle
Figure 1: Basic treatment concept for metabolic syndrome
) 14
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
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.|
) Around the Globe
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.
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.|
It is probably the largest and oldest organization of this
kind in the USA.
T
he 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
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
) 15
) Re f r e s h Yo u r H o m o t ox i c o l o g y
Citric Acid Cycle Catalysts
By Ivo Bianchi, MD
Therapeutic approaches
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.
A
n 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.
16
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
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.
) Re f r e s h Yo u r H o m o t ox i c o l o g y
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 phenyl­
alanine. 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
neo­plasia 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.
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
)
17
) M a r k e t i n g Yo u r P r a c t i c e
Practical Tips
for Improving Your Marketing Strategy
By Marc Deschler
Marketing specialist
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.
B
) 18
ut 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?
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
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.
) M a r k e t i n g Yo u r P r a c t i c e
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.
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.
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 appoint­
ment, 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
) Specialized Applications
Individualized Infusion Therapy
in Metabolic Syndrome
By Ulrike Keim, MD
Specialist in internal medicine
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.
I
n 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
20
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
In metabolic syndrome, late
damage is due to deposition of
the following homotoxins:
• glucose
• free oxygen radicals
• sorbitol
• advanced glycation end
products
• inflammatory mediators
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 accom­­pa­nied 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.
) Specialized Applications
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
AGEs (advanced glycation end products)
Polyol pathway
Auto-oxidation pathway
Glucose
Protein kinase pathway PKC
Oxygen radical pathway
Expression of inflammation
mediators NF-kB
NO-reduction
Figure 1: Pathological pathways triggered by elevated blood glucose levels
1Please 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.
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
)
21
) Specialized Applications
Infusion protocols in metabolic syndrome
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
Infusion for metabolic
syndrome with high blood
pressure (adjuvant)
• Melilotus-Homaccord
• Rauwolfia compositum
• Arteria suis-Injeel
• Traumeel
• Lymphomyosot
Infusion for metabolic
syndrome with pancreatic
insufficiency
• Pankreas suis-Injeel
• Acidum DL-malicum-Injeel
• Momordica compositum
• Traumeel
• Lymphomyosot
) 22
Infusion for metabolic
syndrome with mild to
moderate circulatory
disturbances
• Circulo-Injeel
• Placenta compositum
• Vertigoheel
• Traumeel
• Lymphomyosot
• Cerebrum compositum
(in cerebral circulatory
disturbances)
Infusion for metabolic
syndrome with
polyneuropathy
• Lymphomyosot
• Vitamin B6
• Vitamin B12
• Traumeel
• Vertigoheel
• Selenium
• Vitamin C
(administered as a separate
infusion)
Infusion for metabolic
syndrome with hyper­
homocysteinemia
• Vitamin B6
• Vitamin B12
• Folic acid
• Traumeel
• Vertigoheel
• Circulo-Injeel
• Cerebrum compositum
(for cerebral circulatory
disorders)
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
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
D
organ support, followed by a long
period of drainage with the DetoxKit.) 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
etoxification 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
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
Advanced organ
support
Hepar comp.
Solidago comp.
Alternative
products
Hepeel
Reneel
Galium-Heel/
Lymphomyosot
For cellular
detoxification,
add:
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Note
Dosage
Lymph
Skin
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Gut
Gallbladder
Connective
tissue
Hepar comp.
Thyreoidea comp.
Nux vomicaHomaccord
Leber-Galle
Tropfen
Pulsatilla comp.
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Respiratory
tract
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
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
Basic detoxification and drainage
Detox-Kit
Detox-Kit
Detox-Kit
For cellular
detoxification,
add:
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Skin
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Gut
Gallbladder
Connective
tissue
Detox-Kit
ChelidoniumHomaccord
Detox-Kit
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Coenzyme comp./
Ubichinon comp.
(or Ubicoenzyme)
Note
In very obese patients, continue with Thyreoidea compositum/Pulsatilla compositum for 12 weeks longer.
Dosage
Ampoules: In general, 3-1 times weekly 1 ampoule i.m., s.c., i.d. Drops: In general, 10 drops 3 times daily
Table 1: Detox protocol for metabolic syndrome
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
) 23
) 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)
)
T
he 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
24
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
) 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 disin-
fection. 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
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
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. BadenBaden, Germany: Aurelia Verlag, 1991.
2. Reckeweg H-H. Homotoxikologie – Ganzheitsschau einer Synthese der Medizin. 6th ed. BadenBaden, Germany: Aurelia Verlag, 1986: 616.
) 25
) Re s e a r c h H i g h l i g h t s
Emotional Stabilization
Through Homeopathic Medication
Neurexan reduces the psychological strain of stress
I
n a randomized, placebo-controlled double-blind study, neurophysiological methods were used to
determine the effects of Neurexan
on patients’ psychophysiological
con­dition. The administration of
Neurexan was found to help them
to cope better with acute stress situations.
The homeopathic combination me­
dication 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.
The passionflower (Passiflora incar-
Reference:
nata) has anxiolytic properties and is
) 26
used for the treatment of nervousness
and insomnia.
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
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. |
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.
) C r o s s w o r d P u z z l e 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:
[email protected] 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:
D etox ification
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 1
) 27
IAH Abbreviated
Course
An e-learning course leading to
certification in homotoxicology
from the International Academy for
Homotoxicology in just 40 hours.
1 Access the IAH website at www.iah-online.com. Select your language.
2 Click on Login and register.
3 Go to Education Program.
4 Click on The IAH abbreviated course.
5 When you have finished the course, click on Examination.
After completing it successfully, you will receive your
certificate by mail.
For MDs and licensed healthcare practitioners only
www.iah-online.com
Free of charge