Disease Evolution Table (DET)

Practical Exercises

IAH AC DET Practical Exercises

IAH 2007

As mentioned in detail before (IAH AC Introduction to Homotoxicology) the

Disease Evolution Table (DET) is an instrument to evaluate the evolution of the
disease status of the patient. A disease is not a static but a dynamic
phenomenon, often the result of a merging between the genetic entity of the
patient and his environmental contacts. Main trigger for a disease is the
homotoxin and its intoxicating status. In this not only the presence of the
homotoxin is important but also its influence on the bodys own systems.

The location of the homotoxin, its biochemical interactions with regulation

systems in the body, its influence on the transmission of steering messengers
(mediators) and even more important on the functioning of the cell, are all to be
taken in consideration.

If micro-organisms are present the determination of the triggering homotoxin is

obvious. More difficult is to point the homotoxin when laboratorium tests are
negative and clinical examination (symptoms) and patients history are the only
points of reference. By the type of clinical symptoms, even when the homotoxins
are not known, classification on the DET is possible and conclusions for therapy
plan can be drawn. To do this a general decision tree is used. Other tests known
in complementary medicine might help to confirm the diagnostic results of a
homotoxic approach of the patient.

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 The DET

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The objective of this course is to be able to locate the current status of the patient
on the DET, starting from the patients history, his current clinical data, the
decision tree and the homotoxicologic interpretation of all this.

We should keep in mind that the current status often already is the result of an
evolution on the table and that our treatment will also often result in an evolution.
Essential in this is the direction in movement on the two axes of the table. In this
we have to be able to recognise a Disease Evolution and a Health Evolution if
appearing. False interpretations of an evolution will mostly result in false
therapeutic measures, maybe even damaging the patient on the long term.

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 Disease Evolution

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Disease evolution
The progress of a disease in time, whereby the movement is from a left-hand phase to a right-
hand phase in the Disease Evolution Table, is called disease evolution. For the patient this means
a worsening of the situation, as the homotoxins are tending towards a deposition phase, possibly
from extracellular to intracellular, instead of being processed and eliminated. Again we want to put
an accent on the fact that not the topographic position of the homotoxin is crucial, but the effect it
has. In a disease evolution the effects of intoxication will move from the left to the right on the
table, and from the top to the bottom.
Disease evolution induces chronic conditions. Often a suppressive treatment is behind this
evolution. When an acute condition is treated suppressively, the homotoxins might condense or
bound into the extra cellular matrix. After some time the toxins might disturb interactive regulation
processes at the level of the ECM, intrude into the cell or disturb the cell function from outside and
interfere with cell to matrix and cell to cell communication, leading to cellular disease and even
genotoxicity which results in cancer.
If, for example, eczema is suppressed (e.g. by using a corticoid ointment locally), the homotoxins
that cause the eczema the eczema is the biologically efficient defense against homotoxins
expressed at the level of the skin will be moved by the body to an alternative elimination
channel. This may be over the BBRS, the blood circulation or the lymphatic system. If these
homotoxins are deposited in the bronchial cells with the intention of eliminating them via the
respiratory tract, they will affect the respiratory system and can, for example cause bronchial
asthma.
Disease evolution can last for decades. This means that years of apparent health can lie between
two phases of disease. This is because the deposition phases nearly always pass unnoticed.
Many apparently innocent illnesses such as flu, viral childhood diseases, herpes labialis, etc. are
more serious in homotoxicological terms than apparently severe, acute inflammatory diseases in
traditional medicine, such as arthritis, nephritis or purulent inflammation of the bladder. The first
group is, after all, viral and so immediately crosses the cellular wall, causing intracellular
intoxication that involves a very real risk of irreparable cellular damage. The second group
includes all phases of inflammation, which may be accompanied by pain and appear more serious
but in which the intoxication is between the cells. The intracellular structures are in no danger of
damage unless there are complications.

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 Health Evolution

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Health Evolution
Diseases that move from right to left on the Disease Evolution Table are called
health evolutions. The former terminology was regressive vicariation. This
terminology is removed due to the etymological origin that doesnt say anything
about what essentially is going on in the body. Health evolutions occur in a
recovering body and serve only one purpose : elimination.
The patient referred to above, with his bronchial asthma, who has no further
attacks after a while but who does develop eczema, is undergoing health
evolution. The homotoxins are evolving from deeper tissues to the surface. The
homotoxicologist will try to treat the eczema biotherapeutically, so that the
defense mechanisms are encouraged locally in the ECM and the homotoxins are
rendered harmless and eliminated.
Health evolution is not always more pleasant for the patient than the existing
condition. Arthritis is more painful than arthrosis, eczema is visible, asthma is not
always apparent, diarrhoea following chronic constipation may be a blessing in
homotoxicological terms, but hell for the patient.
It is therefore essential to provide the patient with adequate support, to motivate
and to explain why the reaction and elimination phases are so important. In any
case, suppressive treatment of the symptoms resulting from health evolution is
absolutely contra-indicated for the reasons already explained. We need to
support the bodys mechanisms biotherapeutically and not try to suppress them.
The latter could possibly mean that we would be acting against the bodys own
purposeful defense mechanisms, something that is to be avoided at all costs.

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 Decision Tree

How to locate a patient on the Disease Evolution Table

What is his evolution?
What are the consequences for the treatment plan?

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The decision tree is an instrument to help us defining where the current position
of the patient is on the table. We start first from a clinical examination of the
patient, add to this the information we get from objective and subjective
complaints of the patient, his patients history and the outcome of the decision
tree to define the location of the patient and the consequences for the treatment
plan (according to the 3 pillars of antihomotoxic treatment if needed and the
choice of the right type of preparations to treat).

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 Decision Tree

Features Phase characteristics Therapy

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We first will have to look at the features the patient is presenting, compare them
to the characteristics of the phases of the Disease Evolution Table and pull out of
this conclusions for the structure of our therapy. Not all the phases will be treated
in the same way and therefore this decision tree is made.

We start with the analyses of the worst case scenario, compare the features and
findings with the phase characteristics, locate the patient on the table and
conclude our therapy plan.

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 Yes:
Chromosomal damage, Malignancy present
Treatment
atypical cells, Pre-malignancy present
frank malignancy
PPG, MPG;
NO CPG, ORPG

Yes:
Tissue destruction Degeneration present Treatment

PPG, MPG;
CPG, ORPG
NO

Enzyme damage,
functional damage, Yes:
Functional disturbance
exacerbations with Treatment
on
periods of normality
a tissue level
PPG, MPG;
CPG, ORPG

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In the decision tree we start from the worst case scenario to the best.

First we look from a pure conventional medical approach if there is malignancy or

pre-malignancy present. At the level of the cell this means that there is
chromosomal damage, that there might be atypical cells or pure frank
malignancy. If this is the case we are in the dedifferentiation phase and the
treatment will be the full 3 pillars of homotoxicology which are 1. drainage and
detoxification, 2. immunomodulation and 3. cell and organ support. These 3
pillars are filled in with medications containing plant preparation groups (PPG),
mineral preparation groups (MPG), catalysts preparation groups (CPG) and
organ preparation groups (ORPG).

If no malignancy is present we go down the tree to the next phase and look if
degeneration is present. Clinically we will find tissue destruction. If this is the
case we are in the degeneration phase and again the 3 pillar approach is
necessary as beside the ECM treatment the defense system needs to regain his
regulation capabilities and cell support and organ support should compensate for
the cell damage.

If also no degeneration is present we will search for a functional disturbance on a

tissue level. We might discover enzyme damage, functional damage,
exacerbations with periods of normality. If this is the case the patient is in the
impregnation phase and the 3 pillars of homotocicological treatment should be
involved in the therapy protocol.

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 Tissues aggregated in Yes:
abnormal benign growths Deposition present Treatment
or substances have
aggregated into
deposition PPG, MPG
NO

Yes:
Inflammatory process
Acute inflammation present Treatment
a once off process

PPG, MPG
NO

Increased secretion
of a normal physiological Yes:
Increased excretion
process in view Treatment
of fluids,
of a homotoxin
neurotransmitters
PPG, MPG

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If no enzyme damage or tissue damage is present we will look if deposition is

present. Clinically we might find tissues aggregated in abnormal benign growths
or substances that have aggregated into deposition. If this is the case the patient
is in deposition phase and needs to be treated with the 2 first pillars (drainage
and detoxification on one hand and immunomodulation on the other hand. No
organ preparation groups or catalysts preparation groups are used.

If there is no deposition we look after acute inflammation. Clinically we should find

a once off process of inflammation. If this is the case the patient is in the
inflammation phase. Also here the first two pillars of homotoxicological treatment
are needed.

If no inflammation is present but we see increased excretion of fluids,

neurotransmitters or other body own substances the patient deals with an
excretion phase. In this case mostly the first pillar of homotoxicological treatment
will do (drainage should be sufficient to support the patient). In some cases
immunomodulation might be interesting to speed up the process of cleanse and
to avoid reccurence.

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 Practical exercises on placing the
patient on the DET

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On the following slides we will make some exercises to be able to locate on the
Disease Evolution Table. Compare the clinical diagnosis (symptoms) with the
characteristics of each phase and locate the patient.

It is a good idea to use the IAH AC Introduction to Homotoxicology lecture to find

out the characteristics of the phases on the DET.

The disease or clinical data are on the slide, the determination and solution are in
the text under the slide. Try to solve the case and than check if your
determination logic is right in the text under the slide.

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 Practical exercise on location on the DET

Acute Tonsillitis

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Clinically, we see all the characteristics of an inflammation: redness, pain,

swelling, warmth and function loss of the affected tissue (swallowing, eating,
etc). The complaints are acute and not recurrent after a period of latency. It is
not a tonsil hypertrophy but a clearly localized manifestation of defense: a pure
inflammation on the lymphodermal level as the tonsil is part of the lymphatic
system.

Acute tonsillitis is an inflammation phase.

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 Practical exercise on location on the DET

Arthrosis

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An arthrosis is the chronic degeneration of the cartilage of a joint. In time

metalloproteinases damage the cartilage surface. Synovial cells might be in
dysfunction producing less hyaluronic acid. Chondrocytes might become less in
number, become deficient in producing the cartilage structure (repairing the
damage). We should not get confused by the fact that a reactivated arthrosis
has inflammatory symptoms as this should be seen as a trial of the organism to
create a health evolution over inflammation (which is SECONDARY!!!). We could
than speak of an arthritis on an arthrosis.

Main points are the degeneration of tissue (cartilage or even subchondral bone in
stage 4), the deficient repairing over synovial cells and chondrocytes, the
presence of endogenous homotoxins (metalloproteinases, abrasion parts of the
cartilage,) and the chronicity. If time goes by, there is a spontaneous worsening
of the case and the organisms reaction is a trial to compensate instead of a trial
to regulate.

This patient definitely is at the right side of the Regulation/Compensation division,

has intra-cellular dysfunction/damage and shows tissue loss.

Arthrosis is a degeneration phase on cavodermal level.

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 Practical exercise on location on the DET

Crohns disease,
morbus Crohn

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Crohns disease shows great inflammatory symptoms, especially if endoscopy is

used. There is definitely pain (boring pains to heavy cramps), redness, swelling.
The warmth sensation can be replaced by a burning heat sensation.

Although in some cases with periods of latency between two severe inflammatory
periods (which would more likely point to an impregnation phase) we should not
forget that morbus Crohn is an auto-immune disease where the bodys own
defense is directing itself against proper tissues (in this case in the digestive
tract). What we see is chronicity, degeneration and loss of proper tissue. Cell
death is present (due to the destruction and elimination of proper cells by
deficient cellular defense).

Morbus Crohn shows a specific Human Leukocyte Antigen HLA B27 that is also
present in morbus Bechterev and psoriasis. In this way, the 3 variations of the
same disease can appear in the DET. Psoriasis in the ectoderm, morbus Crohn
in the endoderm and morbus Becherev (ankylosing spondylitis) in the mesoderm.
In practice we sometimes see a morbus Crohn evoluting (disease evolution) to a
morbus Bechterev. In fact all 3 of the diseases mentioned are degeneration
phases in different tissues and embryonic layers.

Morbus Crohn is a degeneration phase at endodermal, mucodermal, digestive

level.

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 Practical exercise on location on the DET

Lymph oedema

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Lymph oedema can be acute or chronic, primary or secondary. What we see

clinically is a soft swelling due to lymph liquid storage (impaired lymph transport).

Differentiation with venous stasis is important. Venous stasis will give also a
swelling but with more tension. Pressing on it with the finger will tension the skin
immediately in venous stasis. In lymphatic oedema, we see for many seconds a
dip in the skin where it was pressed on with the finger.

The swelling is not due to proliferation of cells (tumor). The stasis is due to the
bodys own liquid. There is an impaired drainage of the lymph (obstruction or not).
The situation is in stage 1 and 2 reversible, which is the objective of our
treatment.

Lymphoedema is a mesodermal, mesenchymal, lymphodermal deposition phase.

There is accumulation or stasis of substances that under normal conditions would
have been drained away. Inflammations seen in lymphoedema are secondary
due to the stasis of the liquid and the homotoxins contained in it.

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 Practical exercise on location on the DET

Hypersalivation

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Hypersalivation is an increased secretion of saliva without any signs of

inflammation or other clinical symptoms. It can be primary or secondary. Although
not completely healthy, the situation of the patient is clinically without any reason
to treat. In most cases of hypersalivation the symptom disappears by itself after a
few hours or days.

Hypersalivation is an ectodermal, orodermal excretion phase

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 Practical exercise on location on the DET

Hayfever

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Hayfever is a form of allergic rhinites. Depending on the trigger, it is mainly

seasonable, TH-2 and IgE mediated. Like all allergic reactions the clinical
sympoms appear with the presence of the allergen in the organism.

Hayfever has indeed all the characteristics of an inflammatory pathway but there
are some mayor differences with an acute inflammation:

- There are periods of latency were no symptoms are seen (no or less allergens)
- The reaction of defense is not in proportion to the danger of the homotoxin (not
appropriate or overdone reaction)
- There is a tendency to spontaneous aggravation with each renewed contact
- There is a tendency to generalisation to trigger-like allergens

Due to its tendency to compensate (and not regulate), the periods of latency and
the chronicity, hayfever is an ectodermal, orodermal impregnation phase.

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 Practical exercise on location on the DET

Non Hodgkins lymphoma

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Non-Hodgkin lymphoma (NHL) is a cancer of lymphoid tissue. It is sometimes

just called lymphoma. Although clinically there is swelling and we could think in
the direction of a deposition phase, the reason for the swelling is of main
importance here. In NHL lymph tissue cells are dividing without control, creating a
malign tumor. Natural killer cells are not able to eliminate the fast growing and
deviated cells.

A cancer cell is a proper cell that has lost his tissue peculiarities, becomes
omnipotent. In fact, a cancer cell is the opposite of a differentiated cell. That is
why we talk about dedifferentiating cells. All cancers belong to the
dedifferentiation phase, also the lymphoma.

New and uncontrolled cell growth is the main characteristic.

Non-Hodgkin lymphoma is a mesodermal, mesenchymal, lymphodermal

dedifferentiation phase.

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 Practical exercise on location on the DET

Gouty tophi

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Gouty tophi are one of the clinical signs of gout. Gouty tophi are depositions of
uric acid with mainly calcium at the level of generally small articulations (finger
and toes). Although inflammation can be highly expressed at these tophi
locations, this is secondary, mainly meant to eliminate through inflammation, the
deposition. In fact, we can state that the inflammation on the tophi is an attempt
towards the health evolution of the organism.

The gouty tophi of themselves are pure molecular depositions of uric acid crystals
bound with mostly calcium and should thus be seen as a deposition of
endogenous homotoxins.

In an early stage, these tophi are reversible.

Gouty tophi are mesodermal, mesenchymal, cavodermal deposition phases.

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 Practical exercise on location on the DET

Warts

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Warts are caused by human papilloma virus infections. The cause is thus a virus
and this should be seen as an exogenous homotoxin.

Main characteristic of viral infections is that the virus changes the intra-cellular
encoding of the host cell. Therefore, we should see a virus always as an intra-
cellular intoxication which brings warts location on the DET at the right side of
the Regulation/Compensation Division.

Wrats will mainly appear as long as the defense against the virus remains weak.
On the other hand, a weakened virus and stronger or enhanced defense system
can eliminate the homotoxin (virus) and establish a nearly healthy state again
(warts gone). In many patients we see a latent state of the virus causing
recurrence of warts. That is why the crypto therapy and operative elimination of
the warts is not a causal therapy as the recurrence, only depends on the activity
of the virus itself, not on the number of cells in the warts!

Due to the viral cause and the often latency periods between recurrence warts
are ectodermal, epidermal impregnation phases.

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 Practical exercise on location on the DET

Ovarian cysts

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An ovarian cyst is any collection of fluid within the ovary. Some of these, called
functional cysts, are part of the normal process of menstruation. Any ovarian
follicle that is larger than about two centimeters is termed an ovarian cyst.

From the definition above we know that it is about a collection or storage of liquid
on a location were there should be no collection at all. The deposition of liquid
and the size of the cyst can be so big that it starts disturbing the normal
functioning of the surrounding tissue.

The liquid stored can be seen as endogenous homotoxins. The storage is out of
the living cells, in the ECM, like a water-bag. The deposition can disappear by
itself (what often happens). This brings the location on the left hand side of the
DET. As it is a deposition, no inflammation (initially) or hyperexcretion it is a
deposition phase.

Ovarian cysts are mesodermal germinodermal (female) deposition phases.

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 Practical exercise on location on the DET

Acute cystitis

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Acute cystitis is an inflammation of the inner wall (mucosa) of the urinary bladder.
The symptoms are frequent urge to urinate, often with little release of urine,
during and after urination burning pain in the bladder and even urethra.
Cystoscopy would show an inflamed bladder, red, swollen. In some cases fever
may be present.

Although often isolated, an inflammation of the bladder can retrograde upwards to

a syndrome of nephritis, which is more severe.

Cystitis is a common inflammation, more frequent in females than in males.

Micro-organisms are often the trigger for the inflammation.

All characteristics of an acute inflammation are present, there is no deposition

and no intra-cellular damage.

Acute cystitis therefore is an endodermal, mucodermal, urogenital inflammation

phase.

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 Practical Exercises on Disease
Evolution and Health Evolution

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To recognize the evolutions in disease in the patients history and to be able to

locate them on the DET is important in antihomotoxic treatment. Treatment plans
do often take into account the evolution of the patients condition and we have to
be aware that old diseases might reappear in health evolution. Avoiding
reappearance is possible by including the right preparations in the therapy plan.

The following exercises are to recognize disease evolution and health evolution in
the patients history.

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 Case 1: Benign Inguinal Lymphadenopathy

Pt: 29 y.o. female, married, normal life-style

Presentation:
4-5 swollen inguinal lymph nodes, bilaterally
no other relevant data from medical history
first noticed about 8 months before, recurrences every
1-2 months
diagnosed in hospital as benign but no etiology identified
Diagnosis:
Benign Inguinal Lymphadenopathy (cause unknown)

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Case:
A 29 years old female was referred with the diagnosis of Bilateral Benign
Inguinal Lymphadenopathy of unknown origin.

Medical History:
About 8 months before the Pt. had noticed a gradual (over 5-6 days) increase of
small lumps (as described by pt) on both of her inguinal areas. Pt. refers that
these swellings were almost uniform, and without great discomfort, no red skin,
and no fever and/or other symptoms. She saw her family physician who directed
her to a specialized diagnostic center for an evaluation. After various diagnostic
procedures, including biopsy, malignancy was excluded and some form of
infectious origin was suspected but not identified.
An apparently healthy female, married and mother of 2 children (2 and 6 y.o.)
with no personal or family history of malignancy and/or lymphadenopathy.
Apparently normal family life and lifestyle. Upon a detailed medical history review
the only possible connection that could be made was in reference to the fact that
the Pt. recalled using an anti-perspirant stick (she did not recall the name) daily
for several months before the appearance of the swellings.

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 Allopathic Treatment

Treatment: (2 wk cycle during recurrences)

Large-spectrum antibiotics
NSAIDs
Results:
Only initially, some reduction
Recurrences continued (prescribed medication had little or
no effect)

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Patient was sent home with a therapeutic prescription of antibiotics and a NSAID.
After the prescribed treatment some improvement was noted but the lymph
nodes did not return to completely normal size. She had periodic recurrences
about every month and a half, and without any relationship with the menstrual
cycles. Pt. repeated the therapy prescribed but the effects were never constant,
occasionally it was effective in reducing the size and the discomfort. The Pt. was
tired of taking antibiotics and wanted to try another approach.

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 Biotherapeutic Approach
(Exclusion of malignancy is always mandatory, legally and ethically)

DET-Phase: Deposition, Lymphodermal Tissue

Therapeutic Rationale:
Symptomatic
Detox & Drainage
Immunomodulation
What preparations?
Lymphomyosot for its specific tropism for lymphoid tissue
Apis an anti-oedematous action
Traumeel modulates as an anti-inflammatory agent that
provides a physiological inflammatory regulation finalized to
natural healing

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Deposition: - Matrix Phase Left of Regulation/Compensation Division

Rationale of Treatment: Provide physiological stimulation for lymphatic tissue to
react to or mobilize homotoxins to be drained to detoxifying organs Reduce
oedema by stimulating drainage Modulate an inflammatory reaction that tends
towards a natural healing process

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 Antihomotoxic Therapy

Lymphomyosot drops + Apis-Homaccord drops

+ Traumeel drops
8-10 drops of each 3x/day for 4-5 weeks
+
Traumeel ointment
Local applications 4x/day

Results:
2 weeks about 50% reduction of swelling
4 weeks almost completely normal
Recurrences at 4 and 10 months (same treatment)
After 2 years, no recurrences

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Since malignancy had been excluded, it was attempted a homotoxicological

approach with the intention of influencing/restoring a physiological
filtration/drainage of the involved lymph nodes with a simple prescription for 4-5
weeks: Traumeel ointment (local applications 4x/day)

* Special attention being given morning before getting up and night when in bed
by gently massaging the ointment for a few minutes over each side and with
maneuvers (taught to the patient) that would facilitate lymphatic drainage towards
the physiological flow of the lymph

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 Case 2: Trigeminal Neuropathy

Patient: S.S. 58 years old female suffering from

chronic left trigeminal neuropathy
duration of about 3 years
attacks 2-3 a month

Diagnosis:
MRI showed moderately dilated looping vessel
Compressing T.N. at the level of its cranial exit

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Case:
A 58 y.o. female suffering from chronic episodic left Trigeminal neuralgia referred
by her physician for acupuncture (or whatever alternative might have worked) in
order not to increase the dosage of Neurontin (concerned about side-effects) as
continuously requested by the patient.

Medical History:
About 3 years before, while sailing with friends on a cool October morning, the
Pt. vividly recalled the development of a sudden and strange headache that
during the rest of the day gradually increased, but especially during that night
becoming intolerable and accompanied with left-sided hyperesthesia of the scalp
with a small soft lump developing behind her head on the left at the base of the
skull.

The pain slowly subsided towards early morning, but the lump persisted for
several weeks. The day after she had consulted her physician who had no
explanation for what had happened but scheduled the Pt. for an MRI.

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 Allopathic Treatment

Neurontin (gabapentin)
300 mg 3x/day
Lately had to be increased to 400 mg 3x/day

Physician referral
Concerned about side-effects of Neurontin

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The Pt had been diagnosed as suffering from Trigeminal neuralgia and was
prescribed Neurontin (gabapentin) 300 mg 3x/day. Lately increased to 400 mg,
but the Pt. was still requesting a further increase in dosage.

The physician (friend of the family) concerned about side-effects, was open to
other solutions and referred the Pt. to my office.

Even though the day of the visit it was a sunny and warm day, the Pt.
arrives to the office with head scarf protecting her face and neck to avoid
any form of draft that might trigger an attack.

Pt. refers that recently even brushing her teeth had become a problem, fearing
that it would initiate another attack and her medication was always taken on
schedule.

She had heard about acupuncture and wanted to see if it could help her
condition.

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 Possible Therapeutic Approaches

Surgical vascular decompression (high risks for more

damages)
Allopathic drugs may help in blocking pain sensations
Acupuncture may help to desensitize the nerve
Neuraltherapy may help in preventing generation of action
potentials
Homeopathy may help in controlling the pain perception
Homotoxicology may help by addressing directly the
physiopathology
Some combination of the above?

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Possible Therapeutic Approaches

Surgery: Risks are too high, and in this Pt. it was not indicated (yet)

Allopathic: Rx Neurontin 300 mg 3x/day (gabapentin = anticonvulsant,

w/unknown mechanism of action, but helps to control pain, especially initially
toxic side-effects of concern)

TCM: Acupuncture generally successful in keeping the symptoms under control,

but requires in- office long-term therapy that the Pt. may be reluctant to accept.

Neuraltherapy: Sometimes provides good results, but the local anaesthetics

could only reduce the generation of the action potentials and no other action on
the nerve fibers and on the blood vessel.

Homotoxicology: only discipline offering preparations with direct tropism on

tissues involved
BEST Results: A combination of the theories and practices of the above.

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 Biotherapeutic Approach

DET-Phase: Impregnation, Hemodermal / Neurodermal

Physiopathology:
Most compatible with hyper-excitation of afferent sensory
nerves and subsequent generation of paroxysmal ectopic action
potentials secondary to vascular compression (Harrisons
Principles of Internal Medicine)

Therapeutic Rationale:
Biotherapeutic approach would attempt
to influence the vascular dilation
to reduce nerve irritation / trauma
to minimise generation of action potentials

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For the sake of the patient we must always look in many directions in order to
provide what the patient expects of us. To be healed, even if we have to
resort to disciplines that we are not immersed in!

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 Bio-Meso-Therapeutic Injections
Protocol A (facial affected side)

Medications:
Procaine 3% (1 ml)
1 Spigelon vial
Materials & Method:
Mix contents in a single 5-cc syringe
Use meso needles (least painful = 4 mm x 27 g)
Inject small volume of mixture into mesoderm at specified
points
Points of Injection:
Mental foramen
Facial acupoints: BL-2, St-2, St-6, St-7
Frequency: Week 1 & 2 , 2x/wk

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Protocol A (Facial): Week 1 & 2 (2x/wk)

FACE- Meso-therapeutic injections (s.c. using meso needles 4 mm x 27 g)

with a cocktail of
Procaine 3% ( 1 ml )
1 Spigelon vial ( 1.1 ml )
(Total liquid = 2.2 ml to inject in 5 points)

Points if injections (on the affected Left side of face, for this particular Pt)
BL-2, St-2, St-6, St-7
Mental Foramen

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 Bio-Meso-Therapeutic Injections
Protocol B (general body acupoints)

Medications:
1 Silicia-Injeel ampule
1 Funiculus umbilicus suis-Injeel ampule
Materials & Method:
Mix contents of both ampules in 5-cc syringe
Use meso needles (least painful = 4 mm x 27 g)
Inject small volume of mixed liquids into mesoderm at
specified points
Points of Injection: St-25, St-36 (bilaterally)
Frequency: ADD to Protocol A (facial) at weeks 3 & 4, 2 x/wk,
therefore for weeks 3 & 4 do Protocol A + Protocol B

IAH 2007
IAH 2007 31

Protocol B (other body acupoints) * Add to Protocol A (Face)

Silicia-Injeel + Funiculus umbilicus suis-Injeel

(As mesotherapy, bilaterally at St-36 & St-25, acupoints that traditionally in TCM
represent the major acupoints of constitutional strengthening)

Actually, the application of moxa at these 4 points before the cold winter
months has had for centuries in China the function of vaccinations in
strengthening the immune system.

Therefore: For weeks 3 & 4 (2x/wk)

Protocol A (Face) + Protocol B (other body acupoints)

31
 Home Therapy

Long term therapy:

8-10 drops of each 3x/day (2 months cycles with 1 wk rest)

Arnica-Heel drops
Gelsemium-Homaccord drops
Aesculus compositum drops
Lymphomyosot drops

In case of eminent attack or during an attack:

Add Spigelon tablets (sublingually, every 15 minutes for up to
2 hours)

IAH 2007
IAH 2007 32

The home therapy includes also whatever prescription medications the Pt. may
be taking.

32
 Maintenance

In Office:
Every 2-3 months, repeat Protocol A + B (1 treatment/wk for
4 weeks)
Home:
Continue home therapy, 1 week rest per month
Results
After 1 month Pt was able to reduce dosage of Neurontin
After a few months frequency of attacks reduced
After 1 year, no prescription medication
Following 2 years had 2-3 tolerable recurrences

IAH 2007
IAH 2007 33

Maintenance:
4-week cycle - 1 treatment /week (Protocol A+B), every 2-3 months
Home medications continues - taking 1 week rest per month.

- Following few months attacks reduced in frequency (from 3-4/month to 1-

2/month) and in intensity.
- After 1 year Pt. was gradually taken off prescription medication
- After about 2 years, Pt. had practically stopped considering it as a problem but
continued faithfully her 4-5 yearly appointments and home medications (in this
period had 2-3 tolerable recurrences)

33
 Practical Exercises on
Antihomotoxic Treatment Plan

Case 3 case with residual lymphoma

IAH 2007

After the location on the DET and the determination of the type of evolution (if it
can be pointed), a treatment plan has to be set up. For the choices of the
medications we refer to the lecture IAH AC The Treatment Plan.

34
 Case study

Mrs TP 60 yr old Female

Diagnosis: Inoperable lymphoma in inaccessible
position (behind inferior vena cava in hepatic region)
Only intra-abdominal lymphatic metastases
Had 3 cycles of chemotherapy with intrathecal protection
Was on high doses of corticosteroid

IAH 2007
IAH 2007 35

The patient was a relatively vital lady, who had a tumor which was not quite in
remisssion, but slowly growing. Despite chemotherapy the tumor was not
shrinking further and was slowly growing. Due to its anatomical location, this was
inoperable. Of note though is that she was never really detoxified after the
chemotherapy.

35
 Case study

Came to me 6 months after her last chemotherapy

Was in remission, tumor had a small amount of growth on CT
and oncologist was observing

IAH 2007
IAH 2007 36

This patient was relatively well with a good dynamis, so that one can aggressively
manipulte regulation.
This is not so in other cancer cases, where the patient is often debilitated, and
where regulation should be a slow process.

36
 Patient profile and relevant history

Happily married, 2 well adjusted children

Time urgent perfectionist
Grew up on a grain farm
Crops were sprayed, she played in the fields during those times
Had very few childhood diseases
Had flu vaccines every year till one year got very sick from
vaccine
Lived in an area with very high EMF irradiation
Sleep with many electronics in the bedroom

IAH 2007
IAH 2007 37

Of note in the history was three tings:

1. Her time urgency perfectionism. This will result in a constant stress situation
with the resultant secretion of cortisol. This will put her in a Th2 rigidity over
time and cause cellular immune dysfunction, which predispose towards
cancer.
2. 2. The few childhood infections
The immune system trains itself with acute banal infections,, the question
is now being asked, if we deprive a developing immune system of
childhood diseases, whether we actually increase the risk for diseases
on the right side of the regulation division, thus towards CID (Cellular
Immune Deficiency) and autoimmunity.
The patients suffering from cancer rarely get acute banal infections, often
getting stuck in a TH2 rigidity, as seen in regulation rigidity.
3. The large chemical load she got due to pesticides.

37
 Disease progression on the DET

Dedifferentiation

Lymphodermal

IAH 2007
IAH 2007 38

This disease is thus in the dedifferentiation pphase in the Lymphodermal tissue

layer.
This is a cellular Phase and will need aggressive regulation.
Fortunately in this patient it was possible.

38
 Planning treatment: Dedifferentiation,
Lymphodermal
Dedifferentiation

Detoxification Immuno- Organ

+ + Regulation
and Drainage Modulation

Lymphodermal

PPG + MPG + CPG + ORPG

IAH 2007
IAH 2007 39

In making a treatment plan we will follow the algorithm which was discussed
above.
Once we know that the patient is in the dedifferentiation phase, we ned to use all
the pharmacological groups as well as all the pillars.

39
 Residual Lymphoma

Basic preparation
Engystol given one month
Basic 3 weeks rest then 1 month
again

Detoxification Advanced Detox

Support
regulation
Immunomodulation Tonsilla compositum

Cellular activation
Ubichinon compositum
organ strengthening

IAH 2007
IAH 2007 40

Engystol N is a good basic preparation in this case. It will stimulate a TH1 state,
and the sulfur gives reactivity.
It is used with breaks in between in tablet form ( 1 tid)

The Advanced and basic detox is discussed in the next slide.

Tonsilla is an especially good medication here, as it will strengthen the immune
system, but also the glandular system.
It further regulates the adrenal gland as well.
It is thus both an immunomodulator and a tissue preparation.

The catalyst of choice her is Ubichinon comp.

It has a number of anti neoplastic preparations in it ,such as conium, which is
especially important here. It also has a deep cleansing action. The other two
catalysts are incorporated into the detox regimes.

40
 Basic Advanced
Detoxification and Detoxification and
Drainage Drainage
Liver Nux vomica- Hepar compositum
Homaccord

Kidney Berberis-Homaccord Solidago compositum

Matrix Galium-Heel Thyreoidea compositum

Cell Coenzyme compositum Glyoxal compositum

Use for 12 weeks Use first for 6 weeks then basic for 12 weeks

Mucosa Lymphomyosot Mucosa compositum

IAH 2007
IAH 2007 41

To get the body to free itself of toxins we need to do two things: Support the organs which
metabolise harmful substances, support the function of the organs which store toxins, such as the
matrix, and lastly we also have to stimulate elimination from these organs.
It is important to note that once stored toxins are released they often have not completed their
metabolism, and therefore still need to be made water soluble in the liver before getting excreted
in the kidney and other organs.
If the stored toxins are released too rapidly all at once, or the liver and other metabolising and
elimination organs are overloaded or not functioning properly, the released toxins will diffuse into
the blood, but cannot be excreted. They will thus circulate in the blood stream till they found a
compartment where the concentration is less than in the blood and then diffuse into this
compartment. The crux is that in this way toxins are merely shifted from point A to B.
This is not such a problem in well persons or patients with mild toxicity, but patients with severe
toxicity it may have repercussions, such as heavy metals now entering the brain where it is
extremely difficult to remove them.
Especially in patients where the organs of elimination is not functioning properly or burdened by
disease or with other toxins (such as seen in patients on chemotherapy), this needs to be
considered. In these patients we need to support the organs of detoxification and elimination first
before we actually drain the tissues.
It is also important to note that the process of detoxification and drainage puts a severe burden on
the body, and thus in the very frail and sick patients it can put another burden on the body and in
these patients detoxification should be done as a later event, when the patient has received other
medications to support the body. Detoxification and drainage also needs energy, and therefore the
catalysts are a standard addition to more strenuous detoxification programmes. Apart from the
fact that they also play a role in cellular detoxification.

41
Conclusion: General principles of detoxification in
cancer patients

Should be a slow process

Combined with lifestyle changes (see part 2)
Beware of toxins flowing too quickly out of matrix
In all cancer patients, we should assume the toxins to be on a
cellular level
Support thus before drainage, need to restore the matrix and the
autoregulatory system (see part two)

IAH 2007
IAH 2007 42

42
 Course

After about 9 weeks into the therapy, the patient developed

acute appendicitis
Fever of 42 degrees Celsius
Surgery for appendicitis
On CT-abdo 2 months later almost total tumor regression with
calcification
Patient completed the detox and one course of
immunomodulation treatment, was still in remission after two
years after the treatment

IAH 2007
IAH 2007 43

This is indeed a good thing. The patient was worried that her disease has
recurred, and she waited a few hours before contacting me, thus she had a long
and protracted fever.
In the olden days physicians use to give heir cancer patients malaria and
tuberculosis to try and induce fever, and a reaction of the cellular immune
system.
As seen in this patient she had an excellent result after this, with almost complete
remission of the tumor.
We do not see such strong reaction in all patients, but as mentioned before, her
dynamis was quite good, and the reaction confirms this.

43
 Health progression on the DET

Dedifferentiation
Inflammation

Lymphodermal

IAH 2007
IAH 2007 44

She thus moved into health progression on a horizontal line in the same tissues.
Again in other patients they move up on the vertical axis as well.
The important thing is though that she is now regulating.

44
 Planning treatment after shift in disease:
Inflammation, Lympohodermal
Inflammation

Detoxificaton Immuno-
+ modulation
and Drainage

Lymphodermal

PPG + MPG
Traumeel and Lymphomyosot

IAH 2007
IAH 2007 45

During the acute episode, I supported her with Traumeel and Lymphomyosot in
hospital after her appendectomy, once she was well again, we continues the 3
pillar regime till it was completed.

45
Case: Gastroenterology

Case with Crohns disease

IAH 2007

46
 Case with Crohns disease and Leaky Gut

Master. T.R. 15 year old schoolboy

Diagnosed with Crohns disease 2 years ago
At the time parents got divorced
He now lives 6 months with his mother and 6 months with the
father
Unhappy in himself
Has few friends

IAH 2007
IAH 2007 47

This boy was unfortunate to get Crohns at such a young age, as he was still
growing.
In these cases the social problems around this is very demanding, apart from the
fact that his growth will be stunted due to the cortisone.
He was thus doubly unhappy.

47
 Clinical history cont.

Eat a diet rich in junk food

Mother bought him some commercial vitamins and minerals, but
he is not taking them
Childhood history:
Had numerous antibiotics for URTIs
Vaccinations as per schedule
Had chicken pox as a child
Unhappy childhood, was shifted from school to school
Several episodes where he was treated for parasites

IAH 2007
IAH 2007 48

When enquiring about risk factors the following stands out:

1. Lots of antibiotics: Risk of dysbiosis
2. Constant stress: leaky gut
3. Measles vaccine: reports of this causing Crohns in susceptible individuals in
later life

48
 Mr TR

Clinical presentation:
Still has six watery bloody stools a day despite being on
corticosteroids (Oral and as enema)
Joint pain with some nail changes
No iritis
No biliary involvement
One episode of obstruction, which was treated conservatively
without surgery

IAH 2007
IAH 2007 49

The patient has several signs of disease elsewhere, but they were due to his
malnutrition, not extra abdominal manifestations of the Crohns.
Worrying was the one episode of obstruction, as these has a tendency to recur.

49
 Relevant clinical examination

Patient was clinically anaemic

Blood pressure low to normal, but orthostatic hypotension
Abdomen: slight distention with tenderness in the right iliac fossa
Ridges on nails with pitting
Obvious matrix toxicity with severe tenderness of Spleen 6,
liver 3 Kidney 2

IAH 2007
IAH 2007 50

He displayed signs of malnutrition and deficiency. This patient was more

debilitated than the cancer patient above.

50
 Relevant conventional lab

Full blood count

Iron deficiency anaemia Hb 10 g/dl
CRP 38
WCC within normal limits

IAH 2007
IAH 2007 51

Iron deficiency anemia as well as a very high CRP, a sign of infection. Normal
value is less than 1.

51
 Conventional treatment

Corticosteroids 30 mg p.o. and as an enema, when severe

Also on Sulphasalazine 600 mg bid
Had one trial of Cyclosporin, had to be stopped due to bone
marrow suppression

IAH 2007
IAH 2007 52

Despite a stringent allopathic treatment for IBD, he was still not in remission.
Especially the oral corticosteroids are very worrying at his age.

He was on chemotherapy which had to be stopped due to side effects.

52
 On colonoscopy

IAH 2007
IAH 2007 53

On his colonoscopy he had the typical cobblestone appearance of Crohns and

intense inflammation of the small bowel.

53
 Gut milieu
Luminal contents and pH

Bacteria

Immunity:
Barriers
Strains important

IAH 2007
IAH 2007 54

The symbiotic bacteria also have a very specific function on the immunity.
By exerting a low grade antigen load, they are also able to induce Th3 cells,
apart from the fact that they have a host of other functions, notably
contributing to the mucosal health. The concept of mucosal distress
syndrome is also being recognized more and more in modern
immunological texts.
They furthermore contribute to the barrier function of the gut, as a passive barrier,
and by providing fuel for the mucosal cells, in order to keep the tight junction
shut.

54

IAH 2007
IAH 2007 55

Due to the severity of this patients syndrome, a CDSA or comprehensive

diagnostic stool analysis was done.
This showed good digestion, some malabsorbtion, but severe dysbiosis (see next
slide)

55

IAH 2007
IAH 2007 56

The dysbiosis index was off the chart (right bottom).

The patient had severe infection with pathogenic bacteria , Notably Proteus ,
Klebsiella and Aeromonas as well as with Candida.

56

IAH 2007
IAH 2007 57

Due to severe dysregulation, an amino acid panel was done as well.

The low levels of certain amino acids reflects the stress on the regulatory system
where they act as co factors, repair mechanisms and anti oxidants.

57

IAH 2007
IAH 2007 58

Most patient s with Crohns has a leaky gut syndrome. Even unaffected family
members will have a higher incidence of leaky gut,
The wide open mucosa will allow food particles and toxins to enter uninhibited.
Patients with IBD are thought to have an abnormal immune response in the gut
as well. Instead of a tolerant TH 1response, they mount a TH1 response.
This cause a cascade of event, which is discussed more in depth in the lecture
on gastroenterology.
The chronic vicious cycle between inflammation , tissue breakdown and defective
repair mechanisms will allow for the typical result we see with Crohns.
One major objective of therapy thus is to repair the gut lining and to establish
normal permeability

58
 Disease progression on the DET

Degeneration

Endodermal
Mucodermal
Digestive

IAH 2007
IAH 2007 59

On the DET we see a disease in the degeneration phase, in the mucodermal

digestive layer.

59
 Planning treatment: Degeneration,
Mucodermal digestive

Degeneration

Detoxification Immuno- Organ

+ + regulation
and Drainage modulation
Endodermal
Mucodermal
Digestive

PPG + MPG + CPG +ORPG

IAH 2007
IAH 2007 60

On the right side of the regulation division, these patients need a comprehensive
approach with all three pillars plus supportive therapy.

60

IAH 2007
IAH 2007 61

The two basic preparations, namely Podophyllum comp and also Diarrheel, will
support the watery bloody stools and reduce cramping and bleeding.
This can be given in an acute dose form if necessary.

The three pillars follow first the advanced supportive detox and drainage follow by
the basic.
The organ support and immune modulation will be Mucosa compositum, and also
further Tonsilla.
In this boy the Tonsilla was also important to support his adrenal gland after the
withdrawal of the of the cortisone.

61
 Mucosal support

Four pillars of mucosal support

Remove all noxious factors
Food
Homotoxins
Replace all factors mucosa need
Nutrients
ENERGY (Catalysts)
Repair
Mucosa compositum, functional food
Reinoculate good bacteria

IAH 2007
IAH 2007 62

The four R concept gives a good regime to restore the gut permeability.

62
 Immune resuscitation

Increase CMI ( TH1) Increase Th3

Tuberculinum Probiotics
Astralagus membranaceus Sterols / sterolins
Colostrum
Microdose preparations
Decrease the TH1
Traumeel (SLIT)
Traumeel (also increase Th2)
Corticosteroids Suis-organ extracts in dilution
Immunosupressants
Sulphasalazine

IAH 2007
IAH 2007 63

Immune resuscitation in this case is aimed in down regulating the TH1 pathway
and up regulating the TH3 tolerance.
This is best achieved in this case with suis organs such as Mucosa compositum.
This needs to be given orally to induce oral tolerance.

63
 Remove

Minimal rotation diet (Beware of the elimination diets)

Antibacterial treatment
Hydrastis Canadensis
Artemisia
Juglans
Garlic

IAH 2007
IAH 2007 64

To remove the pathogenic bacteria, a natural antibiotic regime was used. It must
be kept in mind that the Phytos in this regime may be toxic in the long run, and
therefore should not be used for longer than three weeks at a time.

64
 Replace

Amino acids, especially Glutamine

Functional foods have it all
Inulin (FOS)
Vitamins and minerals

IAH 2007
IAH 2007 65

The replacement of nutrient are especially important.

The amino acid glutamine, is one of the main fuel sources for the mucosa cell
and is of utmost importance.

65
 Reinoculate

Probiotics
Live strain
Cold chain
DDS, Rhasemosus, Bifidus
Bulgaricus has no immunomodulatory properties

IAH 2007
IAH 2007 66

Probiotic need to be live, as we need the products of their metabolism. Certain

strains are also more immune active.( see lecture on gastroenterology)

66
 Course

The patient was weaned of the oral corticosteroid over a period

of 12 weeks at the same time of regulation
After remove phase felt dramatically better
Mood improved
Developed a common cold with a laryngitis after he was off the
cortisone (was put on Phosphor-Homaccord and Naso-Heel see
below)
Stools down to two watery stools per day with no blood
Had one relapse during stress period

IAH 2007
IAH 2007 67

This patient regulated over the Orodermal tissue, into an acute inflammatory
phase. However, one such episode is probably not enough to keep the patient
ton the left side of the regulation division, and the therapy should be continues, till
a few of these acute regulatory phenomena are observed.

67
 Course

After 12 weeks another cycle of regulation was done

Sulfasalazine was reduced to 200 mg bid
Patient then immigrated to London. I lost contact, but had one
email from mother to tell me he was continuing to do well.
I referred him to a colleague in England

IAH 2007
IAH 2007 68

Sometimes, if patients are on the right of the regulation division, we only achieve
a reduction of the suppressive medication.
In a young boy like this, when one treats all the concomitant symptoms, one
should see normalization to health.
It is thus worthwhile in patients like this to continue therapy, even if it is
intermittent, till full remission has occurred.
In his case it will be much easier as he is off the cortisone, and as the co factors
for regulation has been replaced (amino acids vitamins etc) and the gut has been
sanitized.
At some stage the body will take over the regulatory process.
The aim is to manipulate the system to cross the regulation division time and time
again to the left, till it can do so itself

68
 Health progression on the DET

Inflammation Degeneration

Ectodermal
Orodermal

Endodermal
Mucodermal
Digestive

IAH 2007
IAH 2007 69

On the DET we see a disease in the degeneration phase, in the mucodermal

digestive layer.

69
 Planning treatment: Inflammation,
orodermal

Phosphor-Homaccord, Naso-Heel
Endodermal
Mucodermal
Digestive

PPG + MPG

IAH 2007
IAH 2007 70

This patient was already excreting and the laryngitis was mild.
Supportive therapy was all which was needed at this stage.
After this episode, go back to the three pillars

70