NEED WE RECOVER THE CLINICAL IDEA
OF AN INDIVIDUAL RESISTANCE TO ILLNESSES?
Renato Cocchi, a neurologist and a medical
psychologist.
Summary.
The author started from the idea that the
illness is always a compromise between an offence ability and a resistence
ability. He pointed out the making up of the notion of "individual
ground" as the emphasing of the current non specific resistance ability of
a peculiar biological organism, to both external and internalstress of any
origin. As it was already done in past for the struggle against the TB by the
sanatoriums, it is possible to modulate the non specific resistance of a body,
by already available means.
Key words: individual ground, illnesses,
individual resistance, clinical variable, stress, modulation, synergy.
Drug modulation of stress answers.
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Every illness is always a compromise between
an offence ability (the causal agent ) and a resistance ability very personal,
in a given moment of the biological cycle of that living body. For what
concerns the man, this latest is what the old clinicians called "the
individual ground" (IG), and it has been a variable on which in past they
acted in an empirical way, but with good success.
If, as I wrote, the illness is even a
compromise between two variables, not having the means to act on the offensive
agent, they did face, in the exemplary case of the TB on the IG, by increasing
what, in even farther times, they termed "vis medicatrix naturae, alias
"the natural ability of the body to cure itself."
The antitubercular sanatoriums, when we lack
sulphamidics and antibiotics, were a splendid example, by now forgotten, of
this clinical-therapeutic intuition. Pure air, sum, excellent diet, hygiene,
calm and sociability could strengthen the weakened organism of the TB
individual to the point to make inactive even imposing pulmonary caverns. It
not even did succeed so well, but surely in most cases this approach gained
evident improvements.
The first sulphamides marketed, then
antibiotics (streptomycin) and later on chemotherapeutics (isoniazid), moved
the application point of the therapy, from the "IG" to the pathogenic
agent with great therapeutic advantages and above all with a drastic reduction
of the costs. The sanatoriums, already exhibited pride of many county
administrations, decaied and they were first closed, then, in part, "recycled
".
This prevailing and by now nearly exclusive
change of therapeutic perspective involved an ample series of changes, and not
only in the physician-patient relationship, and in the physician way of
thinking. Who, as I, started the profession when these changes were not still
absolute, or had Teachers with the old way to think, and not still adapted to
the new, could realize, retrospectively, what was happening. The later coming
colleagues can, instead, being convinced that it has always gone as today, and
that this is the only possible way.
To exemplify roughly it was the time where
we moved from a medicine where "the clinical eye" (the intuition )
was still a value much appreciated, even if not exclusive, to a medicine where
the diagnosis was coming out by confirmations and exclusions always more tied
to the laboratory or to other investigation means as less subjective.
In facts, in this direction we had to go
however. It was instead the seeking and the imposing drugs development that
brought radical followings.
The need of clinical testing of the new
drugs obliged rigorous statistical methods and, first, the pairing of the not
interesting variables. For a dragging effect, even the clinic passed from the
natural scientific method (what was the exclusive base of the astronomy, till
the first artificial satellite appeared), now called as anecdotal, to the
experimental scientific method.
This last becomes such a forced imperative,
to the point that most physicians are wrongly convinced that scientific method
and experimental scientific method are synonymous.
One of its perverse effects was the dogma of
the monotherapy, derived from the experimental necessity of the elimination of
the variables, already a dogma much verbally established but then, fortunately,
not always applied in the clinical practice. Even if appreciable as a caution,
rationally it has poor logics, because it presupposes, in the animal and human
bodies, a series of linear cause and effect relationships, each of them as
independent from the others.
From a geographical point of view a value
move happened and then of intellectual influence. The clinical medicine of the
Mediterranean countries was supplanted from the scientific medicine of the
Anglo-Saxon and Scandinavian countries, that had greater facility in fitting
this new perspective. We skip, even if not it should to do it, the problem of
the capitals for research and that of the interests of the multinational drug
industries.
Unfortunately the problem of the ability of
individual resistance continued to interfere in the scientific trials.
Researchers tried to reduce this variable weigh with statistical means: Paired
control groups, random choice, double blind, crossover and multi-centric
experimentations. To the end, if it sharpened the technique of clinical
validation of drugs, both new or again tested old ones, it did not resolve the
result of the single case, because this is last not a smaller rate, but always
equal to 100%.
The "peripheral" dissatisfaction
unchanged, and drugs that, in pre-marketed phases would have to give guarantees
of success, in the clinical practice, mainly in outpatients', did not show the
scheduled effectiveness.
A further attempt to solution was, first,
the introduction of "guidelines protocol" proposed from excellence
centers. In this case, the sharing of a protocol rather than of an other was
left to much subjective decisions and based, to the best, on the criterion of
the " clear fame", a characteristic that, today, is enough easy to
manipulate with an unprejudiced use of mass media.
More aseptic are the principles of the
Evidence Based Medicine (EBM), which builds on the statistic of the
publications on a topic, by choosing which respect the rules of the
experimental scientific method.
They approved, as evidence based, the
results common to all these papers, and suitable as probable those as common to
most of them.
A general and uncritical acceptance of the
EBM seems me impossible for many reasons.
Among them:
a. Not all the medicine is already Evidence Based,
but for this it has to be enough to wait.
b. Who are doing only the EBM would have
even decided, perhaps with poor or null awareness, to become always less a
clinician, and less that never a researcher. This is a possible perspective,
which however, eventually, would bring to an exact distinction between
physicians who research and those who limit themselves to apply. These lasts,
inevitably, would be replaced by the computer.
c. Any illness that would not have its clear
frame into the EBM would have to have an exam in a research centre.
d. The problem of the IG, still a time would
become so cut out of.
As for to the IG, we may think that there
would be nothing of serious, if it were not that, in facts, the physicians
already pay attention to it, at least in two rough but essential distinctions.
The therapy with the same drug in children
and in elderly persons, requires different dosing, and, as an initial approach,
lower than that usually prescribed in adults, because the reduced resistance of
children and elderly people.
The null care for the individual resistance,
as the other pole of the illness, drives to two therapeutic always more
frequent approaches:
1. The insistence on the causing agent
involves the dosing increase, with always threaten risks of side effects (as
reactions creditable to different IG, and dose-dependent).
2. By not systematically acting even on the
individual resistance, which it is possible and already somehow it is doing in
all the hospitals, does not allow a reduction of the drug or drugs or specific
treatments.
What is then the individual resistance,
which, evidently, varies with the age? A quite simple thing: It is the ability
of answering to the stress, considering the field of the stress well more ample
than the current triviality (external stress, primarily of
psychological-relational or social origin).
About stress I suggested, in a previous
paper, the following operational definition.
We term stress a set of relations linking external or internal
stressors of physical, chemical, biological / metabolic, and psychological /
social origin to nonspecific reactions of a living organism. These reactions
come out from the homeostasis' modification elicited by the stressor or
stressors, and act as a common final pathway. Stress reactions can be due from
external stressors or internal stressors or both and depend on individually set
genetic and acquired abilities [1].
This stress idea, which I had for a long
time clear and published [2], was specified by the Loo [3] who affirmed that
". . . today it is guilty if we do not consider an illness as the sum of
three factors:
1. The causal agent;
2. The specific answer of the body;
3. The not specific answer of the body,
which is an answer of stress to the current illness situation, an answer that
will be different in every subject, and it will depend from constitutional,
hereditary and acquired, features."
According to Mortola, [4] who affirmed that
no one symptom of the premenstrual syndrome has directly anything to do with
the progesterone, I have pointed out the premenstrual syndrome as a
paradigmatic example of internal metabolic stress.
The cyclical fall of the progesterone, which
is a physiological fact in the fertile woman, modifies the homeostasis and
elicits non specific symptoms, which are stress symptoms [5]. The premenstrual
syndrome doesn't strike all the women: About 10%, more resistant, do not suffer
from it [4].
I gave satisfaction to a curiosity of mine:
On one hundred drugs selected in alphabetical order, with planned exclusions to
not have interferences, I found again, as side effects, 13 on 19 symptoms of
the premenstrual syndrome.
For the trouble of the sleep, one drug could
give, as side effect, either the insomnia either the sleepiness, a
demonstration that such effect doesn't cannot be directly linked to the drug as
the same.
Recently I treated a premenstrual syndrome
as rebellious to the tried therapies, with an antistress drug therapy, with a
good success, as for the first eight months of therapy.
The reaction of the body to the stress
initially involves the retroactive GABA-glutamate pathway [8], two
neurotransmitters much interconnected, because the GABA derives from the
glutamate, and the glutamate has, as precursors, the glucose (through the
Krebs' cycle) and the glutamine.
When in the hospital the physician does a
glucose phleboclysis to a patient, he does already a "restaurating"
therapy because an antistress one.
However the body can look to defend by
itself from the stress by increasing the glucose introduction (greediness for
sweet things, a neurophysiological mechanism of compensation). Since the other
glutamate and GABA precursor is the glutamine, by prescribing glutamine it has
to get a reduction of the greediness for sweet things. I did so with a positive
result and I published it [10].
This is one among behaviour and
symptoms that can supply information on the brain neurotransmitters and help to
understand the neurochemical balance or unbalance of the single patient, who
will have symptoms of a deficit [11] or of excess, or mixed ones.
At the end of these brief considerations on
the possible IG rediscovery as the ability to answer to the stress, I believe
that this will be a common clinical perspective, independent from the EBM,
because it concerns both the evaluation and the modulation of non specific
resistance of a person.
As I think, this will allow the
recuperation:
- of the patient, as whole suffering
biological body;
- of the physician-patient relationship,
well beyond of too sectoral psychology, with unjustified pretensions of
explaining all;
- of the physician as who does sharpen his
diagnostic ability in the single case (the current illness of this patient);
- of the therapy (contemporary action on the
morbid cause and on the individual resistance both specific and non specific
being the last one more easily modulated).
It not seems me of having written
extraordinary things, because, however, something is already done since long
time, even if a reflection on a such way of acting remains still much modest.
References.
[1] Cocchi R .: Drug therapy of
pseudodementia as modulation of stress reactions. Three cases It. J. Intellect.
Impair. 1996, 9: 173-180.
[2] Cocchi R.: Psychopharmacotherapy of
anxiety in the first years of life. Agressology 1981, 22, "D":5-8
[3] Loo P., Loo H.: Le stress permanent.
Masson, Paris, 1986.
[4] Mortola J.F.: The premenstrual syndrome.
Curr. Ther. Endocrinol. Metabolism. 1997, 6: 251-256.
[5] Cocchi R. Pre-menstrual syndrome as the
paradigm of an internal biochemical stress. Melbourne, 1998.
www.stress-cocchi.net/Speculation3.htm
[6] Cocchi R. Unwanted effects of drugs and
premenstrual syndrome. Melbourne, 1998, www.stress-cocchi.net/Drugs4.htm
[7] Cocchi R.: The case history of a
32-years-old woman with premenstrual syndrome by now rebellious to usual
therapies, improved with antistress drugs.
www.stress-cocchi.net/premestrual.htm.
[8] Horger B.A., Roth R.H.: Stress and
central amino acid system. In: Friedman M.J., Charney D.S., Deutch A.Y. (eds):
Neurobiological and clinical consequences of Stress: From normal adaptation to
PTSD. Lippincott-Raven, Philadelphia 1995: 61-81.
[9] Ward H.K., Thank C.M., Bradford H.F.:
Glutamine and glucose as precursors of transmitter amino acids: Ex vivo
studies. J. Neurochem. 1983, 40: 855-860.
[10] Cocchi R.: Greediness for sweet things
in children as a symptom of antidepressive homeostatic compensation: 41 cases.
Acta Paedopsychiat. 1980, 45: 293-300.
[11] Cocchi R.: Hypo-A-Gaba-erge Depression
bei Kindern. Klinisches Bild und mit neurochemis-ches Mechanismen Verbundene
Symptome. In: Friese H.-J., Trott G.-E. (hrsg): Depression in Kindheit und in
Jugend. Huber, Bern 1988: 126-133.
Posted on Internet in August 2003. Copyright by Renato Cocchi,
2003.
Author's address: dr. Renato Cocchi, via
Rabbeno, 3
42100 Reggio Emilia (Italy).
renatococchi@libero.it