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Vivisection or Science - cont'd
That a drug may do no good matters little, at the most it could be considered fraudulent. Almost always, moreover, it has a certain efficacy all the same, as it pleases a lot of people hysterically anxious to consume medicines.
What one should worry about is that it should not be harmful, that is, not poisonous.*
For this reason toxicity tests are carried out on animals, but differences between species, as those indicated in the preceding pages, are not taken into account.
Still less is another factor taken into account:
toxicity tests are almost always carried out on healthy animals whereas the medicine is given to a sick person. But the illness by itself modifies the metabolism of drugs. For instance, fever renders many drugs more toxic: diseases of the liver diminish the capacity of the liver to neutralise dangerous substances; many kidney diseases slow down the elimination of foreign substances like medicines and the products of their degradation.
Immunopathies depress reaction to allergens. A congenital dismetabolism, recognised or hidden, can render toxic a substance which normally is harmless. All these conditions do not exist in the experimental animal or they exist under different aspects and with different consequences.
The majority of human diseases do not afflict any of the most known animals. Then how can one demonstrate in the animal the efficacy of a drug intended for a particular human illness?
If the illness does not normally afflict the animal we have to produce it artificially.
That is relatively easy in the case of infectious diseases, but it is only apparently easy because there are many pitfalls.
* "Toxic" is anything that shortens life or impairs its quality. The concept of toxicity is, however, closely linked to quantity or "dose". Many drugs like digitalis, strophanthin, atropine, are not toxic, on the contrary are beneficial, if they are used in very small doses.
On the other hand, any substance, even the most necessary for life, is harmful in excessive doses. Oxygen, for example, when breathed in at a pressure of more than 20 atmospheres kills in a few minutes. Natural foods (proteins, carbohydrates, fats) consumed in too great amounts lead to obesity and so are "toxic". Obesity does, in fact, shorten life.
Apart from dosage, toxicity is linked to time. For example, hydrocyanic acid (prussic acid) kills in a few seconds; arsenic (according to dose) in a few hours or months; tobacco smoke in years.
Thus we distinguish between acute toxicity and chronic toxicity.
The main pitfall lies in the fact that each animal species reacts differently to the same infection. Here are some examples: monkeys are habitual carriers of the "simian B virus"* which can from time to time cause irritation of the mucus membranes similar to the harmless herpes labialis (cold sore) in man. But the same virus infecting man (from the bite of a monkey or by contamination of a wound by saliva) causes a serious, often fatal illness.
Smallpox virus and yellow fever virus do not affect any known animal.
The rabbit is more susceptible to bovine Mycobacterium tuberculosis than to human Mycobacterium tuberculosis; the guinea-pig reacts in the opposite way. But in neither the guinea-pig nor the rabbit has tuberculosis characteristics comparable with tuberculosis in man.
Mycobacterium leprae (or Hansen's bacillus) is unable to flourish, apart from in man, in only one other animal species, the armadillo, in which it does not, however, arise spontaneously.
The BCG strain of Mycobacterium Tuberculosis of the bovine variety is used, thanks to its relative harmlessness, as a vaccine against tuberculosis. Inoculated into golden hamsters (Microcetus auratus) it causes generalised tuberculosis, with death following in 10-14 months.
Treponema pallidum causes syphilis only in human beings. Inoculated into monkeys it brings about an acute illness which is quite different from that caused in man.
Actinomyces bovis causes a skin disease in cattle, and in human beings an often serious illness of the internal organs. In laboratory animals** it can be cultured only with difficulty and under particular conditions.
The majority of other mycoses (fungal infections) do not give rise to spontaneous diseases in the most common laboratory animals. In order that they should, they must first be inoculated into very sensitive organs like the peritoneum or hyporeactive ones like the central nervous system.
Nocardia, Blastomyces dermatitidis, Balstomyces braziliensis, Coccidioides immitis (very pathogenic for man), Histoplasma capsulatum, Criptococcus neoformans, Geotrichum candidum, Sporotrichum Schenkii, and the Mucorales behaves in this way.
No animal is known to be susceptible to Chromoblastomycosis which is due to various species of fungi, among them being Hormodendrum compactum and Phialifora verrucosa.
* Only in the baboon has the simian B virus never been found.
** The term "laboratory animal" is vague. Any animal can be a laboratory animal, but the choice is made according to practicality and cost rather than according to "scientific" criteria.
If we should find out that the animal with bio-chemical reactions most similar to those of man is, let us suppose, the rhinoceros, would the bulky pachiderm become the most common laboratory animal?
In reality laboratory animals serve ends quite other than scientific ones: they must be easily obtainable, cost little, be easily handled and, if possible, not bite.
Disturbing differences are found in the reaction of many mammals to parasitic metazoans. And what is one to make of the way in which these parasites choose a different host for each phase of their development?
The following is one example among many:
Dicrocoelium dendriticum*, the liver fluke, in its adult stage lives in the intestine of a herbivore (and occasionally of man).
The eggs pass out with excrement into water and are taken in by a snail in which, after two metamorphoses, they become larvae ("cercarie"). The cercarie are deposited on grass where they are eaten by an ant. In the ant they undergo further development to become metacercarie. The ant is eaten with grass by a herbivore (and occasionally by man). In the herbivore (or man) it becomes an adult animal and the cycle begins again.
As is seen, the liver fluke Dicrocoelium specialises in its adult form in living in certain kinds of hosts while its larve (cercarie, metacercarie) are adapted to living in other kinds.
So, Dicrocoelium provides us with a free lesson in the fact that one animal is not worth another, since each animal becomes the wet-nurse at only one stage of its development.
Even fleas are able to distinguish differences between animals. The human flea is Pulex irritans, but the cat flea is Ctenocephalides felis and the dog flea is Ctenocephalides canis. These two latter kinds of flea bite people only occasionally and by mistake.
Hitherto we have considered infectious and parasitic diseases. By inoculating pathogenic agents in animals, the researcher tries to obtain a model of human disease. Illusion or mystification? When we take the wrong road, we avoid looking back in order not to see the truth that could transform us into a statue of salt. And so, having created in an animal an infectious disease which is not the same as that of the human being, the experimenter starts trying out drugs which are supposed to cure it. At this point, the errors multiply in geometric progression, forming an inverted pyramid which cannot stand upright.
The error of studying an artificially created disease is compounded by treating it with a drug which, in all probability, in the animal will be metabolised in a different way than in man. Indeed, different to the point that the animal could die before the infection kills it, just as occurs with penicillin in guinea-pigs.** Besides, it is different because drugs used to combat the infection do not function alone but in synergy with the natural defences.
* Dicrocoelium dendriticum is common in Eastern Europe, in Russia, less so in Africa, in Asia, in North and South America. The adult worm is 5-15 millimetres long and 1.5-2.5 millimetres wide.
** Statement by Sir Howard Florey, (61) joint Nobel Prize winner with Fleming and Chain for the discovery of penicillin: "It was by good luck that in the initial toxicity tests we used mice because if we had used guinea-pigs we would have concluded that penicillin is toxic."
For example, the majority of antibiotics not only stop the multiplication of certain bacteria but also stimulate phagocytosis, that is, the capacity of certain cells (leucocytes, macrophages) to attack and destroy micro-organisms by "eating them up".
However, this capacity for natural defence varies according to different species. An indication of this is given by the different proportions in which different phagocytic cells are found in the blood and in the tissue liquids of different animals and the lack of certain cells in some species. For example, fish and other animals still lower down the evolutionary scale do not possess polymorphonucleate leucocytes and their defence against infection is undertaken by mononucleate cells analogous to monocytes and macrophages of mammals.
In the struggle against infection antibodies are associated with
leucocytes:
natural antibodies, which are inherited;
acquired antibodies, which are formed as a result of contact
with micro-organisms or with aggressive substances called "antigens".
The presence of acquired antibodies is shown by a hyperactivity which serves to eliminate or neutralise the foreign substance. Beyond certain limits allergies arise in the form of genuine illnesses like bronchial asthma, hay fever, allergic rhinitis and conjunctivitis, nettle rash, erythema nodosum and eczemas.
In animals, too, contact with antigens causes, as in man, the development of antibodies.*
However, it is not possible, even with the most ingenious methods, to reproduce in animals allergies similar to those which afflict so many people.
Why?
Is not different behaviour always an expression of more profound biochemical, nervous and psychic differences?
From infections which do not attack animals or do so in a different way than in man, and from immunological phenomena which in animals are never similar to allergic illness found in man, we turn now to another area in which animals differ from man, the "collagenopathies".
The collagenopathies comprise a wide range of manifestations: from rare but fatal diseases like Lupus erythematosus sistemicus or Wegener's granuloma to the most varied diseases which affect the quality of life more than its length, like arteriosclerosis and osteoarthritis.
Old age itself is seen by some as a collagenose disease, because in elderly people collagenous tissue is always "altered" when compared to that of the young.
* It is even suspected that, in humans, allergies to certain drugs may in some cases be due to eating the meat of animals treated with those drugs. This would explain, for example, the allergic reaction to penicillin in certain individuals who claim never to have been treated with penicillin; (but couldn't they have forgotten about it?).
Collagenous tissue exists virtually everywhere in the organism. It is like, in a cloth, the weft, without which it would be impossible to weave the warp. When it changes, the functional capacity of all the organs and all the tissues is impaired.
If it were possible to avoid the ageing of collagen we would be able (so it is said) to prolong life.
So experimental models have to be found.
How can one build, for example, the model for "arteriosclerosis"?
With dogs, fed on a high cholesterol diet or on a diet deficient in cholesterol, or a high lipidic diet or a lipid-deficient diet, or overfed to the point of making the liver burst, or underfed to the point of starvation; dogs made into alcoholics or poisoned with tobacco, dogs overfed with vitamins or deprived of vitamins.
But what do they expect? An arteriosclerotic dog? Such dogs already exist: let it get old and it will get arteriosclerosis just like anyone else.
Those who believe they can understand arteriosclerosis in humans through animal experiments will feel rather annoyed, if not downright indignant, when they examine the bio-chemical characteristics of arteriosclerosis. They look for those dietary factors which cause or favour the development of the disease. They blame diet so obstinately that it makes one think of some hypochondriac seeking revenge on a gourmet.
Eat, eat, and soon you will regret it! Perhaps they are not entirely wrong. If, however, they try to disentangle the confusion analysing the animals, well, here is what they find.
The main culprit, cholesterin, in man is principally esterified by oleic and by stearic acid; in the rat, mainly by arachidonic acid, an essential fatty acid.
A diet containing few calories is good for man but worsens natural arteriosclerosis in rabbits.
The atheromes (degenerative fatty deposits on the walls of the arteries) in man contain high levels of cholesterol and other lipids. The naturally occurring atheromes in the cat and in the rat contain relatively low levels.
The foam-like cells (cells laden with lipids) of human atheromas are altered smooth muscle cells; the foam-like cells of the atheromas of the guinea-pig are monocytes (a third kind of white blood corpuscle with rounded cell nucleus) which have fagocytized lipids.
Compounds which attract particular attention in the study of arteriosclerosis are the lipoproteins, but in humans the VLDL* and the LDL** predominate, while in the majority of primates prevail the HDL.*** It is easy to understand how the above mentioned (and other) differences would frustrate anyone seeking the explanation for human arteriosclerosis in the arteries of animals.
* Very Low Density Lipoproteins
** Low Density Lipoproteins
*** High Density Lipoproteins
Animals also make fools of us when, by using certain drugs to treat arteriosclerosis, we seek to prolong our own life by shortening theirs.
One of these drugs is Clofibrate, which in some animals, apart from being completely harmless, reduces the amount of cholesterol in the blood by about 20%: a resounding success which enabled the drug to be sold by the ton. But how does it actually work in humans?
In humans it not only reduces very slightly the cholesterolemia, but also increases the incidence of heart attacks, damages the liver, the gall bladder and gall duct, sometimes with fatal results.* Truly a splendid success!
Then there are those suffering from osteoarthritis. Why do our
joints become so grotesquely (and painfully) deformed?
Dogs, cats, sheep, pigs - let us attempt to mimic our lamenesses
on these animals. How can we do it?
Joints beaten with hammer blows, injected with irritating liquids, subjected to ionizing radiation, brutally dislocated.**
What can't be done, when one wants to cause harm? One thing, however, is incomprehensible: that the vivisectors should have such a poor understanding of biology, such a crude conception of life, that they cannot realize that these tortures cause nothing more than fractures, haemorrhages, thromboses, contusions and inflammation. All but an acceptable model of human osteoarthrosis which is a local manifestation of a generalised illness of the collagen.
Nevertheless, the tortures continue. Why? Because the number of animals used in the study of arthrosis is in direct proportion to the amount of anti-arthritic drugs, and to the profits deriving from them.
* In Italy, drugs containing clofibrate were withdrawn from sale in 1979.
** In the Institute of Clinical Orthopedics and Traumatology of the University of Rome, during a lecture, Professor Giorgio Monticelli bent the backs of some dogs in front of the horrified students to illustrate how the vertebral column snaps when it passes a certain angle.
Our indignation is aroused less on account of the miserable victim of such dreadful sadism than on account of the students who were indeed "horrified" but did nothing to stop it.
Copyright © 1991 by Hans Ruesch Foundation
Excerpted from Prof. Croce's book Vivisection or Science - A Choice to Make (CIVIS, 1991).
For further information or to purchase the book contact Hans Ruesch Foundation/CIVIS - POB 152, via Motta 51, CH-6900 Massagno/Lugano, Switzerland - or Campaign Against Fraudulent Medical Research (CAFMR) - P.O. Box 234, Lawson, New South Wales 2783, Australia; Phone +61 (0)2-4758-6822. www.pnc.com.au/~cafmr