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QUESTIONS
LOOKING FOR ANSWERS
(This
text may be consulted any time by clicking on the question index
in the right upper corner.)
This
is a small sample of questions among which you will certainly find
more than one having crossed your mind. To
vary, we will quickly view following fields:
SOME
NON-MALIGNANT AFFECTIONS
Why
do we get eczema, sciatic neuralgia or that painful inflammation of
the shoulder called scapulohumeral periarthritis? The simple fact
of being affected already seems a mystery but other, even so legitimate,
add to it. First of all concerning the importance of the affection:
why an eczema, a sciatica or a periarthritis of the shoulder lasting
a few days, weeks, months or years; or relapsing at so diverse rates?
Then – when tissues spreading over the whole body are concerned –
an even so sharp question arises as to its localisation: why eczema
(or a furuncle, a wart, etc…) in the face, on the thorax, on the thigh
or on the foot?Why
a sciatica or a periarthritis of the right or the left shoulder?
Why
do bronchitis, peptic ulcers or myocardial infarctions much more often
affect men than women? One may have different reasons to cough: secretions
of a cold running down in the back of the throat, pharyngitis, laryngitis,
tracheitis, bronchitis, pneumonia, etc… Do you know a lot of men who,
during their cold, loose their voice, meaning an affection of the
larynx? Men and women have a bladder, why is cystitis so seldom seen
in men, when, in women it is so current? Why are women much more affected
by thyroid diseases (and more in particular of the "cold nodes"
i.e. the non-functional one’s), by phlebitis or by rectal lesions?
A
little enigma: why do people considered "insane" – and here,
I think in particular, of autists – almost never develop diseases
anymore; and why do the few getting out of it start becoming ill again
as do the others? This fact is well known by the psychiatrists.

Decades
of research did not respond to the elementary questions: why does
it, one day, invade us, and why that organ? We will go more fully
into the details of the conception of this disease and, to take over
the expression of a French cancerologist, using "a medieval approach:
that of the devil". But let us linger over one terrifying characteristic
of the "malignant" tumour. This one, in contrast to the
non-malignant tumours, has the property to spread. This means that,
considered as the original tumour, the primary tumour or "the
mother tumour", enables cells to evade from it forming, in turn,
secondary tumours or "daughter tumours" also called metastases.
This phenomenon is able to lead to generalised cancer.
If
you have had cancer some years ago and if a new tumour localisation
is discovered, they might very well speak ex cathedra of metastases.
What comes to explaining a hazardous phenomenon (the daughter tumour)
as a consequence of another phenomenon (the mother tumour) itself
not understood. At this stage, an assault of questions arises before
this concept of metastasis, a concept that is one of the intangible
foundations of cancerology. Why does a cancer develop metastases in
one diseased and not in another one? Why metastases at that particular
period: at the moment of the discovery of the original tumour, six
months, two years or ten years later? Why an eventual excellent health
during years separating cancer from its metastases? Why metastases
in that organ and not in another one? Why such a variation in the
evolution of those metastases? How can a metastasising cell transform
itself since one can, supposedly, detect a difference in structure
between the original tumour and the secondary tumour? Let us illustrate
this last question, which is a little more complex, by means of an
example. One speaks of metastases in the brain following a lung cancer.
The lung cells, however, have a pavemented structure (hence the term
epithelioma in the medical jargon) and all samples of the tumour cells
of the brain only show cells of a glial nature, being a totally different
structure. By which miracle can a cancerous cell change structure
during its migration?

Leukaemia
is described as of form of bone marrow cancer. The bone marrow is
responsible for the making of blood. Thus the marrow can enormously
multiply the blood corpuscles circulation in the blood vessels. The
"malignant" blood cells are especially the white corpuscles
or leukocytes, hence the term leukaemia (from the Greek leukos meaning
white). This peculiar type of cancer adds to the incomprehension of
the cancerous phenomenon and raises additional questions (next to
all the others proper to every cancer: why its appearance, its evolution,
etc…). The malignant cells being spread within the blood in this case,
why are there not infinitely more cases of metastases than in other
cancers? On the contrary, there are almost none. Why does this cancer
evolve – and is treated and followed up accordingly – following such
a peculiar scenario: one always speaks of "remission" when
the treatment has reduced the leukocyte count, while awaiting a subsequent
"relapse"? Why is the situation alarming when the leukocyte
count lies between 50 or 100,000 (norm: between 4 and 10,000) while
the entirely normal physiological variations of the erythrocytes or
red corpuscles lie between 4 and 5.8… million? Or else, what can be
the danger of having 100 or 200,000 leukocytes more when the total
variation of all our corpuscles may near 2,000,000? We will explain
the origin and the precise mechanism of what is called leukaemia.

Let
us resume the essential content of this diagnosis: a degenerescence
of the nervous system through sclerosis of the medullary sheath. The
affection is of an unknown origin, incurable, evolving by upsurges
the frequency of which being so whimsical and variable that the spectre
of crutches and of the wheelchair within a delay depending on the
classification in more or less severe forms is hanging around. This
classification results … from the extent of the symptoms observed.
Answering some essential questions would radically change this dark
situation. Why does one start a multiple sclerosis? What sets off
an upsurge? Why is cortisone often effective but might as well worsen
the symptoms? Why is the evolution very often worsened after the diagnosis?
This latter fact is much easier to establish as diagnosis has been
put long after the first outbreaks.

Here
again, the diagnosis is so heavy that we will dedicate an entire chapter
to it in the second part of this booklet. Fifteen years of intensive
research did not succeed in giving answers to some key problems calling
into question again the basis of this acquired immunodeficiency theory.
Why does long-term survival stretch proportionally with the time rolling
by since the description of this affection with such a pessimistic
prognosis? In the same sense: what are the reasons to survive it rather
than to die from it? What provokes the passage from a simple asymptomatic
seropositivity to the declared disease? Why this opportunistic infection
rather than another? Or why, for instance, a Kaposi tumour and why
at this localisation on the body ?

Why
do we find peptic ulcers almost exclusively at the exit of the stomach
(antrum and pylorus, next to the localisation at the duodenum, one
speaks then of duodenal ulcer) and not within the largest part of
the stomach being the bottom and the large flexure? Why is this largest
part the place for large cauliflower-like tumours, which do not occur
at the exit of the stomach where, however more seldom, the tumours
have a flat and ulcerated aspect? And why ulcers where there is less
acid and not at the bottom where there is more? If the peptic ulcer
is commonly recognised as being a psychosomatic disease, then why
does stress limit itself to the provocation of ulcerous lesions (i.e.
destruction of substance) when a lesion, considered more severe, such
as stomach cancer has nothing to do with an even stronger stress?
Did the cells find a way to immediately preserve themselves
against too strong stress in order only to be disturbed within the
narrow frame of a few so-called psychosomatic affections; and thus
not in a too severe manner and for a limited stress?
Breast
cancer is always considered more or less hormone dependent (i.e. that
may be encouraged by female hormones), the proof is that a woman should
not use contraceptives anymore and that she often sees her intervention
completed by an anti-hormone substance such as tamoxifen. But then,
which is the incriminated hormonal influence in breast cancer with
a woman in her menopause since ten or twenty years?
Why
is a woman threatened by osteoporosis in her menopause when her hormonal
decrease should be compensated by an external administration? And
why a man, having a fortiori much less female hormones, is he not
threatened by the same risk? There was, though, never established
that the good bone density of man was depending on his own male hormones.
It is even the opposite when "bone metastasis" of his prostate
cancer is diagnosed. Female… hormones are then proposed to him. It
is true that the logic in this case is to fight the cells issuing
from a cancer, considered to be hormone dependent. But the facts remain
disconcerting: these bone metastases of prostate cancer express themselves
by decalcification phenomena, by destruction of bone tissue and testosterone
does not protect from these lesions. Finally, the basic question remains:
why this difference in relation between both sexes as far as their
respective hormone levels and their bone pathology are concerned?

From
the therapeutic point of view, one may ask oneself why two persons
presenting an affection having the same intensity will have to be
treated in very varying time intervals. For example, why will one
cystitis be cured after one pack of antibiotics while another will
require two or four because a relapse occurs at each treatment arrest?
Or else, a lumbago will be cured in one treatment at the specialist
in osteopathy who, for another patient, will have to perform some
ten manipulations in four or six weeks. But this links to the question
of the intensity of the affection in general. Another question is
sharper however: how can diseases be treated with an equal success
rate by so different means i.e. drugs from the classical pharmacopoeia,
homeopathic remedies, acupuncture needles, and even magnetism or a
placebo? Could these methods have something in common? The answer
is very important since it would largely contribute to throw a light
on the recovery mechanism.

The
problem of contagion in infectious disease also entails a swarm of
questions out of which we will only pick a few representative one’s
representative for the lack of explanation of this phenomenon.
Why
is an affection as banal as a cough described as being far more contagious
than much more severe infections such as bronchitis, hepatitis or
tuberculosis? In the latter example, one may work for over twenty
years in a sanatorium where one lives in an environment very rich
in tubercle bacillus without getting it whereas one finds cases of
tuberculosis without any kind of favourable environment.
We
are literally full of milliards of germs inside a large number of
our organs, some of which, such as the intestinal germs, are even
essential for our lives. So on our skin, in our throat and our urinary
passages live respectively staphylococcus, streptococcus and colon
bacillus. When an infection declares in one of these organs (furuncle,
angina, cystitis,…), we find, most of the time, those same microbes
in a much larger number; and it is them we are fighting by means of
antibiotics or antiseptics. Why these microbes, being fully normally
part of us, do they proliferate and become harmful? I do state here
that I am referring to our microbes and not to those prevailing in
far away regions such as Africa or Asia.
Why
are all persons in contact with infected persons not contaminated?
And when they are, why such a difference in the extent of the infection
they are going to develop?
In
an infection, considered very severe, such as A.I.D.S., how is it
possible that numerous and unprotected sexual intercourse may be compatible
with such diverging fate for each partner: one may die from A.I.D.S.,
while the other might even never be seropositive?
Trying
to explain contagion, or the absence of it, a very sophisticated defence
system is referred to which is the subject of numerous studies, called
the immune system. If this immune system is the answer
to infection, how are such strange situations possible then? Bed-ridden
patients or patients weakened by end-stage cancer or another severe
disease stay months without getting any other affection (e.g. a whole
winter) while, during the same period, persons in excellent health
cumulate two angina’s, a cold and the traditional influenza? In which
of both groups would we expect to find the best immune system?
How
explain the daring experience realised around 1900 by Metchenikoff
in France and Pottenkoffer in Germany? Those researchers and their
teams ingested cultures of germs taken from patients deceased from
cholera. One really found large quantities of germs (cholera vibrio)
in their excrements, but none of them developed the disease!
The
mystery of contagion can be resumed by means of two questions: what
is the real relation between the immune system and the infectious
disease? Does a reliable criterion exist to define not a simple risk,
but the reality of an eventual contagion?

The
immune system, described as our defence system against our lifelong
microbial enemies, its properties and pathologies still give rise
to lots of questions.
Allergy
is considered as an unsettlement of this system leading to an excess
of substances – such as histamine, hence the recourse to antihistaminics
– generating the most varying disorders. These biological modifications
are well described but the question lies elsewhere. Animal
hairs, aliments, pollen, acarids and other various elements have never
changed over thousands of years; they are part of nature and are harmless
for most of us. Allergy though starts and reproduces itself at a precise
and personal time in our life. Change may consequently only be inherent
to ourselves: what made us allergic one day and to that very element?
What
is worse: why can this defence system come to round on our own organs
and destroy them? This is the extensive field of the so-called autoimmune
diseases, in full expansion. If it is recognised as a disease
of the immune system, what is the origin of this sudden change of
nature leading to self-destruction? And why the self-destruction
of that organ rather than another one?
Why
did vaccines never succeed in decreasing the incidence of the diseases
they were conceived for? (I have this information from the WHO official
curves but also by having studied them before the start of the
vaccinations.)

RISK
FACTORS AND STATISTICS
In
the absence of a precise cause for a disease, medicine often uses
two elements that are not explanations but influencing agents: the
"risk factors" and the statistics. Both elements are, however,
themselves sources to questions. As far as the risk factor concept
is concerned, let us take the so widespread case of breast cancer.
A woman having, for instance, her mother, her aunt and one of her
sisters affected by this tumour is considered at high risk. Hence,
prescription of repeated examinations, the consecutive concern and
even at present projects of anti-hormonal substance intake (such as
tamoxifen) merely preventively. But the right question is: what is
the reliable risk criterion as this woman, and her other sisters,
will not necessarily develop the same cancer?
As
to the use of statistics, the case of lung cancer is so well known
that it is often called the smoker’s cancer. Whatever the statistics
the interpretation of which is known to be determining, the real question
for the patient is to know according to which criterion he will be.
Will he be situated among the 60 or 70 % risk – and in this eventuality,
to him, it is 100 % - or among the 40 or 30 % escaping from it, what,
in fact, comes to 0 %. Another way to put the question: why
so much lung cancers with non-smokers and so much smokers who will
never have this cancer? By means of a rigorous explanation of the
disease, we will see that all breast or lung cancer cases have a respective
launch factor; and this whatever the family antecedents or smoking
habits.

Epidemiology
studies the different factors interfering with the appearance of the
diseases: age categories, geographical distribution, socio-economic
conditions, etc… But these findings are essentially of a statistical
nature and do not explain the observations raised.
In
our western societies, why such a raise in incidence of breast cancer,
while the uterine cervix cancer is regressing? As to A.I.D.S.: why
does only a negligible percentage of contaminated (para) medicals
develop the disease afterwards? Within the large variety of symptoms
attributed to this disease, why the very different prevalence of those
symptoms according to the regions of the world, the "risk groups"
and the life style?
Epidemiology
only leads to concrete questions: why is such a pathology prevailing
in this age category; why a more important frequency in that region,
etc…?

SYNTHESIS
AND CONCLUSIONS
One
could lengthen the list of "why" (how many did you count
up to now?) proportionally to all the health problems. One could wonder
about all the diseases, starting from a cold, a tendinitis or a haemorrhoid
up to the most severe cases of metastasised cancers or very invalidating
multiple sclerosis through psoriasis, polyarthritis, asthma, diabetes,
infarction … or megalomania. One
could screen the coherence and the foundation of all the theories,
hypotheses, risk factors and others. But it would only lead to a book
of questions whereas, on the contrary, the object of this small work
is to lay the bases of a tool allowing to obtain answers.
The
explanation is important and the patients wish to receive it. A non-malignant
affection – next to its symptoms – already creates a feeling of discomfort:
why did one "catch" the cold or the influenza of a person
and not one of the other persons who, however, visited him? Why now,
while one was much more tired a few months ago? How long will the
rheumatism last they promised to relieve but about the duration of
which they could not give an answer? With dramatic diagnoses, most
often anxiety adds to the treatments. One had already enough suffered
some years ago from that cancer for which one had had a hard treatment.
And now metastases are discovered elsewhere. What is all one has endured
been good for if everything starts again and worsens? And nobody can
say if this time bomb is not going to strike again later.
Understand
the origin of their disease, the nature and the evolution of its manifestations
enables them to better tackle and manage their affection. The disease
does not faint for all that but the need to find a sense to what one
is living in that period of physical suffering is as imperative, if
not more, as this usual search for a sense that is a general characteristic
of a human being. We will see that the comprehension of disease may
replace its fatality by working on its process, what considerable
raises the assets and the hope before what only seemed to a strike
of fate.
Let
us remain humble: the explanatory system developed here will give
a good answer to all questions in this introduction but it is not
an exhaustive answer to the problem of suffering and death. This "search"
– as all the important interrogations of life (the classics "what
are we", "where do we come from", "where are we
going", "what free will", etc…) – largely goes beyond
the frame of our intention that is not meant to be an essay on philosophy
nor on metaphysics. Our goal will be reached if the reader finds in
it all the help conveyed by liberating informations.

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