Professional Documents
Culture Documents
Practical Exercises
© IAH 2007
1
The DET
©©
IAH 2007
IAH 2007 2
The objective of this course is to be able to locate the current status of the patient
on the DET, starting from the patient’s 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.
2
Disease Evolution
©©
IAH 2007
IAH 2007 3
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.
3
Health Evolution
©©
IAH 2007
IAH 2007 4
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 doesn’t 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 body’s mechanisms biotherapeutically and not try to suppress them.
The latter could possibly mean that we would be acting against the body’s own
purposeful defense mechanisms, something that is to be avoided at all costs.
4
Decision Tree
©©
IAH 2007
IAH 2007 5
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 patient’s 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).
5
Decision Tree
©©
IAH 2007
IAH 2007 6
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.
6
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
©©
IAH 2007
IAH 2007 7
In the decision tree we start from the worst case scenario to the best.
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.
7
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
©©
IAH 2007
IAH 2007 8
8
Practical exercises on placing the
patient on the DET
© IAH 2007
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.
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.
9
Practical exercise on location on the DET
• Acute Tonsillitis
©©
IAH 2007
IAH 2007 10
10
Practical exercise on location on the DET
• Arthrosis
©©
IAH 2007
IAH 2007 11
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 organism’s reaction is a trial to compensate instead of a trial
to regulate.
11
Practical exercise on location on the DET
• Crohn’s disease,
morbus Crohn
©©
IAH 2007
IAH 2007 12
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 body’s 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.
12
Practical exercise on location on the DET
• Lymph oedema
©©
IAH 2007
IAH 2007 13
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
body’s 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.
13
Practical exercise on location on the DET
• Hypersalivation
©©
IAH 2007
IAH 2007 14
14
Practical exercise on location on the DET
• Hayfever
©©
IAH 2007
IAH 2007 15
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.
15
Practical exercise on location on the DET
©©
IAH 2007
IAH 2007 16
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.
16
Practical exercise on location on the DET
• Gouty tophi
©©
IAH 2007
IAH 2007 17
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.
17
Practical exercise on location on the DET
• Warts
©©
IAH 2007
IAH 2007 18
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.
18
Practical exercise on location on the DET
• Ovarian cysts
©©
IAH 2007
IAH 2007 19
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.
19
Practical exercise on location on the DET
• Acute cystitis
©©
IAH 2007
IAH 2007 20
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.
20
Practical Exercises on Disease
Evolution and Health Evolution
© IAH 2007
The following exercises are to recognize disease evolution and health evolution in
the patient’s history.
21
Case 1: Benign Inguinal Lymphadenopathy
©©
IAH 2007
IAH 2007 22
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”.
22
Allopathic Treatment
©©
IAH 2007
IAH 2007 23
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.
23
Biotherapeutic Approach
(Exclusion of malignancy is always mandatory, legally and ethically)
©©
IAH 2007
IAH 2007 24
24
Antihomotoxic Therapy
• 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
©©
IAH 2007
IAH 2007 25
* 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
25
Case 2: Trigeminal Neuropathy
Diagnosis:
• MRI showed moderately dilated looping vessel
• Compressing T.N. at the level of its cranial exit
©©
IAH 2007
IAH 2007 26
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.
26
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
©©
IAH 2007
IAH 2007 27
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.
27
Possible Therapeutic Approaches
©©
IAH 2007
IAH 2007 28
Surgery: Risks are too high, and in this Pt. it was not indicated (yet)
28
Biotherapeutic Approach
• Physiopathology:
Most compatible with “hyper-excitation of afferent sensory
nerves and subsequent generation of paroxysmal ectopic action
potentials secondary to vascular compression” (Harrison’s
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
©©
IAH 2007
IAH 2007 29
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!
29
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
©©
IAH 2007
IAH 2007 30
Points if injections – (on the affected Left side of face, for this particular Pt)
BL-2, St-2, St-6, St-7
Mental Foramen
30
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
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.
31
Home Therapy
• Arnica-Heel drops
• Gelsemium-Homaccord drops
• Aesculus compositum drops
• Lymphomyosot drops
©©
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.
33
Practical Exercises on
Antihomotoxic Treatment Plan
© 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
©©
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
©©
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
©©
IAH 2007
IAH 2007 37
37
Disease progression on the DET
Dedifferentiation
Lymphodermal
©©
IAH 2007
IAH 2007 38
38
Planning treatment: Dedifferentiation,
Lymphodermal
Dedifferentiation
Lymphodermal
©©
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
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)
40
Basic Advanced
Detoxification and Detoxification and
Drainage Drainage
Liver Nux vomica- Hepar compositum
Homaccord
Use for 12 weeks Use first for 6 weeks then basic for 12 weeks
©©
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
©©
IAH 2007
IAH 2007 42
42
Course
©©
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
© IAH 2007
46
Case with Crohn’s disease and “Leaky Gut”
©©
IAH 2007
IAH 2007 47
This boy was unfortunate to get Crohn’s 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.
©©
IAH 2007
IAH 2007 48
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 Crohn’s.
Worrying was the one episode of obstruction, as these has a tendency to recur.
49
Relevant clinical examination
©©
IAH 2007
IAH 2007 50
50
Relevant conventional lab
©©
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
©©
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.
52
On colonoscopy
©©
IAH 2007
IAH 2007 53
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
55
©©
IAH 2007
IAH 2007 56
56
©©
IAH 2007
IAH 2007 57
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 Crohn’s 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 Crohn’s.
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
59
Planning treatment: Degeneration,
Mucodermal digestive
Degeneration
©©
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
©©
IAH 2007
IAH 2007 62
The four R concept gives a good regime to restore the gut permeability.
62
Immune resuscitation
©©
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
©©
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
©©
IAH 2007
IAH 2007 65
65
Reinoculate
• Probiotics
• Live strain
• Cold chain
• DDS, Rhasemosus, Bifidus
• Bulgaricus has no immunomodulatory properties
©©
IAH 2007
IAH 2007 66
66
Course
©©
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
©©
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
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