Los errores de la experimentación animal

La experimentación animal, además de haber producido un infinito dolor y muerte a millones de víctimas inocentes[1], es un fraude científico[2], pues los resultados científicos de la experimentación animal no son extrapolables y precisan de una posterior experimentación por parte de los consumidores, pudiéndoles causar graves daños en su salud e incluso la muerte. Para muestra, aquí se dejan unos ejemplos (pendientes de ser traducidos al español):



experiments indicated that FK506, an anti-rejection drug, was too toxic
for human use.[1][2] However, when used on human liver transplant
patients, the results were found to be ‘promising’.[3] [1] R. Allison, Journal of the American Medical Association, 4 April 1990, p.1766.
[2] R. Y. Calne, et al, Lancet, 22 July 1989, p.227.
[3] J. Neuberger, Hepatology, vol. 13, pp.1259-1260.


Committee of Official Enquiry into the incidence of leukaemia in
children near the Sellafield nuclear plant, declared the plant was not
the cause; this decision was based on animal testing.[1] However, later
research did support the view that the plant was responsible.[2] [1] E. Millstone, in Animal Experiments: The Consensus Changes, ed. G. Langley (Macmillan, 1989).
[2] M. J. Gardner, et al, British Medical Journal, 17 February 1990, pp.423-429.


life-threatening symptoms were observed when this drug, for migraine,
was tested on animals[1], and the British Medical Journal acknowledged
that it had not been possible to produce fibrotic lesions in laboratory
animals[2]. And yet the British National Formulary (1993), found it
necessary to warn that the drug should only be administered to humans by
trained medical staff as it had been found that the drug had serious
side-effects which arose from fibrous tissue (retroperitoneal fibrosis)
and these included heart failure.

[1] R. Heywood in Animal Toxicity Studies: Their Relevance For Man, eds. C. E. Lumley and S. R. Walker (Quay Pub: 1990).
[2] K. A. Misch, British Medical Journal, May 18 1974, pp.365- 366.


an arthritis drug, was withdrawn globally in 1987 after reports of
kidney problems and pain.[1] Those who reported these problems had to
have their kidneys monitored for two years after they stopped using the
drug.[2] And yet it was reported: ‘In animal studies, Suprofen has been
shown to have an excellent safety profile. No significant effects were
observed on cardiac, renal [kidney] or central nervous system…in
several species.[3] [1] Drug Withdrawal from Sale, C. Spriet-Pourra and M. Auriche (PJB Publications, 1988).
[2] FDA Drug Review: Postapproval Risks, 1976-1985 (US General Accounting Office, April 1990).
[3] A. Yeardon, et al, Pharmacology, 1983, vol. 27, Suppl. 1, pp.87-94.


the twentieth century, alcohol was considered to be poisonous for the
liver.[1] This view changed after experiments on animals,[1][2] and in
1934, animal testing concluded that there was no evidence for alcohol
causing cirrhosis.[3][4] Alcohol is of course today
considered to be a liver toxin, but some still question this in view of
the difficulty in inducing cirrhosis in laboratory animals.[5] In
addition to this, alcohol appears to be more harmful to the circulatory
system of human beings than animals. For example, excessive consumption
raises the blood pressure in alcoholics, and yet this is not usually the
case with rats.[6] Furthermore, alcohol is able to
damage the human heart but studies involving various animals who were
given ‘large amounts’ of alcohol found that none suffered heart
failure.[6] Animal experiments also showed that Librium
could assist in dealing with withdrawal although as some animals died,
it also suggested there was a lethal side-effect.[7] In fact clinical
tests carried out at an earlier time had already revealed that Librium
was effective,[8] and it continues to be used in relation to alcohol

[1] H. J. Zimmerman, Alcoholism: Clinical and Experimental Research, 1986, vol. 10, pp.3-15.
[2] C. S. Lieber and L. M. DeCarli, Journal of Hepatology, 1991, vol. 12. pp.394-401.
[3] V. H. Moon, Archives of Pathology, 1934, vol. 18, pp.381- 424.
[4] As [2].
[5] R. F. Derr, et al, Journal of Hepatology, 1990, vol. 10, pp.381-386.
[6] J. V. Jones, et al, Journal of Hypertension, 1988, vol. 6, pp.419-422.
[7] D. B. Goldstein, Journal of Pharmacology and Experimental Therapeutics, 1972, vol. 183, pp.14-22.
[8] G. Sereny and H. Kalant, British Medical Journal, 9 January 1965, pp.92-97.


1986, the British Parliament’s Agriculture Committee instigated a
review into pesticides. Despite the general faith placed in animal
experiments, the Committee was forced to concede that ‘similar tests in
different animal species often yield quite different results’.[1] One
example was the organophosphate pesticide dipterex which caused nerve
damage in human beings but not in animals.[2] One physician member of
the National Poisons Unit advised the Committee that one documented case
of human poisoning was worth 20,000 animal experiments.[1] In
view of the findings, the Committee declared: ‘It cannot be
satisfactory to rely on animals so much as a means of testing and, as
other forms of testing becomes available, we recommend that they be
adopted…we are satisfied from the evidence that we have received that
animal testing can produce misleading results’.

[1] Special Report of the House of Commons Agriculture Committee, rep. FRAME News, 1987, No. 16, p.2.
[2] A. N. Worden, in Animals and Alternatives in Toxicity Testing, eds. M. Balls, et al (Academic Press, 1983).


some seventy years, researchers were unable to connect arsenic with
cancer due to being unable to verify the suspicion with animal
experiments. Although arsenic had been connected with cancer as early as
1809, a report published in 1947 stated that the many animal
experiments which had been conducted had only produced ‘doubtful
results’.[1] Experiments continued after this date and
even by 1969, researchers acknowledged that while it was believed there
was a connection between cancer and arsenic, animal experiments had not
offered any supporting evidence for this.[2] In 1977, a report yet again
said that animal experiments had not produced supporting evidence of a
link.[3] It was not until the end of the 1980s that researchers were
finally able to produce the cancer in animals – nearly 200 years after
the link had first been suggested.

[1] O.Neubauer, British Journal of Cancer, 1947, vol. 1, pp.192- 251.
[2] A. M. Lee and J. F. Fraumeni Jr., Journal of the National Cancer Institute, 1969, vol. 42, pp.1045-1052.
[3] F. W. Sunderman Jr., in Advances in Modern Technology, vol. 2, eds. R. A. Goyer and M. A. Mehlman (Wiley, 1977).


Benzene was widely used, e.g., for the manufacture of detergents,
pharmaceuticals, etc., there was concern as there appeared to be a link
with cancer. Animal experimentation did not support this view,[1] and
some fourteen animal trials failed to show any connection between
benzene and cancer.[2] Therefore workers were put at considerable risk
in view of there being no ‘evidence’ of a link. It was not until the
late 1980s, after dosing animals with benzene that cancer was induced.

[1] L. B. Lave, The American Statistician, 1982, vol. 36, pp.260-261.
[2] D. M. De Marini, et al, in Benchmarks: Alternative Methods in
Toxicology, ed. M. A. Mehlman (Princeton Scientific Publishing, 1989).


while primarily known as an agricultural insecticide, it is also used
in different forms, in a diluted amount, for lice and similar
afflictions. However these can cause serious eye irritation,[1] and the
British National Formulary 1993, warns that eye contact should be
avoided. And yet in rabbits, when a far more concentrated solution was
used, the effects were minimal. Additionally, exposure to lindane dust
caused no problem to rabbits, but caused irritation to the eyes and
respiratory systems of some people.[1] [1] W. M. Grant, Toxicology of the Eye, 2nd edn (Charles Thomas, 1974).


considerable animal testing, this product was used as a treatment for
obesity but after human usage it was noted that some patients were
developing cataracts. Attempts were then made to replicate this in rats,
rabbits, guinea pigs, and dogs, and yet none of the experiments
produced any change to the lens of the eye.[1] A summary of the
experimentation stated: ‘All attempts to produce experimental cataracts
in laboratory animals by various and repeated doses of dinitrophenol
have been unsuccessful’.[2] It was only later that an experiment
accidentally discovered that birds dosed with dinitrophenol developed
cataracts.[1] A similar situation arose with triparanol
intended to reduce cholesterol levels. While the cataracts noticed in
humans could be induced in rats and dogs (after very high doses) they
could not be in rabbits and monkeys.[3] The product was withdrawn.

[1] B. H. Robbins, Journal of Pharmacology, 1944, vol. 80, pp.264-269.
[2] Rep. in ref [1].
[3] W. M. Grant, Toxicology of the Eye, 2nd edn (Charles Thomas, 1974).


product is used for ophthalmic surgery when dealing with cataracts.
While recommended for human use,[1] it is harmful to a rabbit’s eye,
resulting in severe swelling of the cornea and sometimes causing
perforation.[1] It is stated: ‘The rabbit cornea appears to differ
significantly from the human cornea in its reaction to
a-chymotrypsin’.[2] [1] British National Formulary, No.26 (BMA and The Royal Pharmaceutical Society of G.B., 1993).
[2] Morton Grant, Toxicology of the Eye, (1974).

Corticosteroids: Shock

idea for this medication arose after animal experiments when the
survival rate of animals improved after being given the treatment just
before, or after, shock.[1][2] Corticosteroids were then prescribed for
people who required treatment for septic shock, which can often result
in heart, respiratory and kidney failure.
However when
The Drug and Therapeutic Bulletin analysed the trials it reported that:
‘high-dose corticosteroids are ineffective for the prevention or
treatment of shock associated with sepsis. They do not improve outcome,
and make secondary infection worse. They may harm patients with impaired
renal [kidney] function’.[1] In fact, one trial found that
corticosteroids not only failed, but actually appeared to increase death
among patients.[3] [1] Drug and Therapeutics Bulletin, 1990, vol. 28, pp.74-75.
[2] S. G. Hershey, in Anaesthesiology, Proceedings of the VI World Congress
of Anaesthesiology, Mexico City, April 1976, eds. E. Hulsz, et al
(Excerpta Medica, 1977).
[3] R. C. Bone, et al. New England Journal of Medicine, 10 September 1987, pp.653-658.


chemical (produced by nerve endings) was believed, after experiments
with dogs, to dilate the coronary arteries. However when used with
humans, it was found to narrow the blood vessels which can result in
heart spasm.[1] Another body chemical, bradykinin, relaxes blood vessels
in human brain tissue but contracts them in dogs.[2] [1]S. Kalser, Journal of Physiology, 1985, vol. 358, pp.509-526.
[2]K. Schror and R. Verheggen, Trends in Pharmacological Sciences, 1988, vol. 9, pp.71-74.

Leukotrienes (LT).

leukotrienes known as LTC4 and LTD4, constrict blood vessels in the
skin of the guinea pig, but dilate corresponding issue originating from
human beings and pigs.[1] [1]P.J. Piper, et al, Annals of the New York Academy of Sciences, 1988, vol. 524, pp.133-141.

Prostaglandins (PG).

are a family of substances in human seminal fluid. In the heart tissue
from cats and rabbits, PGE1 has no effect on contractile force or heart
rate, and yet in rats, guinea pigs and chickens, it increases them.[1] Because
of such anomalies, some pharmacologists concede that the extrapolation
from animals to humans is often invalid and acknowledge the increased
interest in using tissue from human beings to overcome those
restrictions which arise when using animal tissue.[2] [1]S. Bergstrom, et al, Pharmacological Review, 1968, vol. 20, pp.1-48.
[2]Trends in Pharmacological Sciences, 1987, vol. 8, pp.289-290.


experiments during the 1960s indicated that clonidine might be useful
in treating migraine (Experiments with cats showed that the drug
affected those processes believed to cause headaches). The drug was
therefore introduced in 1969, but later research indicated that it was
largely useless.[1].
However after being used as a
nasal decongestant, it was discovered that clonidine could be effective
when used to treat high blood pressure.[2]. However serious side-effects
were then noted. Furthermore, attempts to replicate the condition in
dogs and cats only provided inconsistent results,[3] and in the case of
testing with rats, there were even more difficulties and
disagreements.[4] The Drug and Therapeutic Bulletin therefore deems
clonidine to be obsolete for the treatment of high blood pressure.[5] [1]Drugs and Therapeutics Bulletin, 1990, vol. 28, pp.79-80.
S. Niles in Clinical Pharmacology: Basic Principles in Therapeutics,
2nd edn, eds, K. L. Melmon and H. F. Morrelli (MacMillan, 1978).
[3]L. Hansson, et al, American Heart Journal, 1973, vol. 85, pp.605-610.
[4]M. J. M. C. Thoolen, et al, General Pharmacology, 1981, vol. 12, pp.303-308.
[5]Drug and Therapeutics Bulletin, 1984, vol. 22, pp.42-43.


the 1960s, at least 3,500 young asthma sufferers died after using
isoprenaline aerosol inhalers.[1] Fatalities occurred when the aerosol
delivered 0.4mg of isoprenaline per spray.[2][3] Attempts
to replicate the same effects in laboratory animals were problematic
and the New York Food and Drug Research Laboratory was forced to admit:
‘Intensive toxicological studies with rats, guinea pigs, dogs and
monkeys at dosage levels far in excess of current commercial metered
dose vials…have not elicited similar adverse effects’.[4] It was only
after artificially reducing the oxygen in the animals’ tissue that
vivisectors were able to increase the toxic effects of isoprenaline.[5] [1]W. H. Inman, Monitoring for Drug Safety, ed. W. H. Inman (MTP Press, 1980).
[2]P. D. Stolley, American Review of Respiratory Diseases, 1972, vol. 105, pp.883-890.
[3]P. D. Stolley and R. Schimmar, Lancet, 27 October 1979, p.896.
[4]S. Carson, et al, Pharmacologist, 1971, vol. 18, p.272.
[5]British Medical Journal, 25 November 1972, pp.443-444.


the early 1950s, kidney damage associated with the prolonged use of
combination painkillers was noted. Despite animal experiments, the
reason for the damage could not be ascertained. It transpired that the
animal experiments only served to further confuse the issue as while
phenacetin was thought to be responsible, the damage could not be
reproduced in the animals.[1] Furthermore, the experiments suggested it
was the aspirin component that was causing the damage,[2] as aspirin,
unlike phenacetin, readily induces kidney damage in laboratory animals.
was only when human studies took place that it was realized that
phenacetin was the cause,[3] leading to it being withdrawn in 1980 (when
there was also the suspicion that it caused cancer).
An analysis concluded that if the research had only used animals the effects would not have been suspected or predicted.[1] [1]I. Rosner, CRC Critical Reviews in Toxicology, 1976, vol. 4, pp.351-352.
[2]British Medical Journal, 17 October 1970, pp.125-126.
[3]K. G. Koutsaimanis and H. E. de Wardener, British Medical Journal, 17 October 1970, pp.131-134.


the 1960s there was an epidemic of drug-induced disease in Japan,
related to clioquinol, the principal ingredient of Ciba- Geigy’s
antidiarrhoea drugs Enterovioform and Mexaform. It is believed that
between 10,000 and 30,000 people fell victim to SMON (subacute
myelo-optic neuropathy) which produced numbness, paralysis and eye
problems including the loss of sight.[1] In 1970, the drug was banned in
Japan, and fifteen years later, it was withdrawn globally.
all the serious problems caused by the drug, those experiments carried
out on animals, which included rats, cats, beagles and rabbits, revealed
‘no evidence that clioquinol is neurotoxic’.[2] Although
there have been claims to have produced toxicity from clioquinol in
mongrel dogs,[3] it has also been noted that different species yield
different results, e.g., monkeys, hens, cocks and mice were only mildly
affected even after they were given high doses while it was discovered
that beagle dogs were 3-4 times less sensitive to clioquinol than

[1]Lancet, 5 March 1977, p.534.
[2]R. Hess, et al, Lancet, 26 August 1972, pp.424-425.
[3]J. Tateishi, et al, Lancet, 10 June 1972, pp.1289-1290.

Oral Contraception.

of the pill have shown that of the side-effects which can occur, the
most serious is that of problems with the circulatory system, i.e.,
blood clots, strokes and heart disease. By 1980 the CSM (Committee on
Safety on Medicines) had received reports of over 400 deaths,[1] and
further studies showed that some women using the pill had raised blood
pressure. However none of these problems had been identified during
animal experiments;[2] in fact the oral conceptive had produced the
opposite effect (i.e., making it more difficult for the blood to clot)
in some species.[3] Prof. Briggs of Deakin University,
Australia, noted: ‘At multiples of the human dose no adverse effect on
blood clotting was found in mice, rats, dogs, or non-human primates.
Indeed, far from accelerating blood coagulation, high doses of
oestrogens in rats and dogs prolonged clotting times. In sum, there is
no appropriate animal model for the coagulation changes in women using
oral contraceptives’.[4] In 1972 the CSM described how the tests which
had been conducted on some 13,000 animals revealed that there was a
connection between high doses of oral contraceptives and cancer.[5] And
yet the rats and mice were so prone to cancer that even those who were
not dosed with the oral contraceptive (‘the control animals’) developed
high levels of disease; lung and liver tumours were found in 25% and 23%
of the control mice, and adrenal, pituitary and breast tumours were
found in 26%, 30% and 99% of the control rats.
view of this, the British Medical Journal stated: ‘It is difficult to
see how experiments on strains of animals so exceedingly liable to
develop tumours of these various kinds can throw any useful light on the
carcinogenity of any compound for man’.[5] Thus, it is those women who have used the pill who have really been the ‘guinea pigs’ for the drug.

[1]G. R. Venning, British Medical Journal, 22 January 1983, pp.289-292.
[2]R. Heywood, in Animal Toxicity Studies: Their Relevance for Man, eds, C. E. Lumley and S. R. Walker (Quay Publishing, 1990).
[3]R. Heywood and P. F. Wadsworth in Pharmacology of Estrogens, ed. R. R. Chaudhury (Pergamon Press, 1981).
[4]M. H. Briggs in Biomedical Research Involving Animals, eds. Z. Bankowski and N. Howard-Jones (CIOMS, 1984).
[5]British Medical Journal, 28 October 1972, p.190.


experiments indicated that chloramphenicol, an anti-biotic, was safe
although it was equally clear that the drug produced side- effects in
humans. Due to the serious side-effects, the drug was withdrawn in
France.[1] In 1952 American physicians discovered that
chloramphenicol affected the nerve cells and they related how one
patient had almost became blind and could only walk with great pain
after taking chloramphenicol for just five months. This was only one of
many reported cases when chloramphenicol produced optical and peripheral
neuritis, and yet animal experimentation showed that the drug was
virtually free of side-effects, even after prolonged use.[2] A
far more serious side-effect was the fact that chloramphenicol caused
aplastic anaemia, an often fatal blood disease. Once again, animal
experimentation did not provide any indication of this occurring and the
British Medical Journal noted that chloramphenicol resulted in nothing
worse than transient anaemia in dogs when injected for long periods:
furthermore, no problems occurred when administered by mouth.[3] It is now known that chloramphenicol is deadly by test-tube studies with human bone marrow cells.[4] [1]C. Spriet-Pourra and M. Auriche, Drug Withdrawal From Sale, (PJB Publications, 1988).
[2]I. Wallenstein and J. Snyder, Annals of Internal Medicine 1952, vol. 26, pp.1526-1528.
[3]British Medical Journal, 19 July 1952, pp.136-138.
[4]G, M. I. Gyte and J. R. B. Williams, ATLA, 1985, vol. 13, pp.38-47.


was introduced in 1956 and viewed as a considerable advance in
anaesthesia. However it was soon found to be harmful to the liver and
within five years there were over three hundred reported cases of
‘halothane hepatitis’. The effects were sometimes fatal and nearly two
hundred deaths in Britain were attributed to halothane.[1] And
yet animal experimentation had not provided any evidence of liver
damage,[2] and despite many animal experiments and different ‘animal
models’, the significance of their application to human beings was
considered ‘doubtful’.[3] Even by 1986, when Britain’s
Committee on Safety of Medicine increased the warnings about liver
toxicity,[4]. it was still unclear whether the same results could be
induced in animals.[5] [1]British Medical Journal, 5 April 1986, pp.949.
[2]Anaesthesiology, 1963, vol. 24, pp.1990-110.
[3]D. C. Ray and G. B. Drummond, British Journal of Anaesthesia, 1991, vol. 67, pp.84-99.
[4]Scrip, 2 October 1987, p.2.
[5]C. E. Blogg, British Medical Journal, 28 June 1986, pp.1691-1692.


product was believed to produce cancer as cancer arose when it was
tested on certain strains of laboratory mice, an animal widely used when
seeking to assess the risk-element of chemical substances. When the
dose was very high, cancer also arose in rats.
In view
of the results of the animal experimentation, America’s National
Institute of Occupational Safety and Health (NIOSH) classified butadiene
as a carciinogen.
And yet when humans who worked with
butadiene were monitored, no extra cancer arose. In fact the number of
deaths from cancer was less than the national average.[1] An editorial
in Science therefore called for a review of the methodology which was
used when considering the risk.

[1]P. H. Abelson, Science, 19 June 1992, p.1609.


to animal experimentation, it was believed that pneumoconiosis, a lung
disease suffered by miners, was caused by silica rather than coal dust.
Therefore mines, in which there was no exposure to silica, were viewed
as being safe. Believing the problem was understood, there was no
information about miners’ pneumoconiosis until the early 1960s.[1] As
noted by the British Medical Journal, the idea that coal dust was safe
arose from animal experimentation,[2] which not only absolved coal dust,
but made silica the most likely culprit.[3] Nonetheless, the findings
from the animal experimentation were shown to be suspect when miners,
who only worked with pure coal dust or carbon, were found to have
developed pneumoconiosis.[1][2] Thus it was shown that coal dust caused
pneumoconiosis without any silica being present.
results of the animal experimentation was further weakened when coal
dust, collected from a mine where the incidence of pneumoconiosis was
high, was found to be harmless to laboratory rats.[2] Naturally there is
the question of how much serious illness was suffered by miners, and
many deaths occurred, due to the incorrect information gleaned from
animal experimentation.

[1]W. K. C. Morgan, in Occupational Lung Diseases, eds. W. K. C. Morgan and A. Seaton (Saunders, 1982).
[2]British Medical Journal, 17 January 1953, pp.144-146.
U. Gardner, Journal of the American Medical Association, 19 November
1938, pp.1925-1936. Chronic Pulmonary Disease in South Wales III
Experimental Studies, MRC special report series no. 250 (HMSO, 1945).


a skin condition, arises in many people when they come into contact
with nickel compounds.[1] In fact nickel is considered to be the most
common cause of dermatitis in women; in some cases it can result in
severe eczema and disability.[2] And yet in most animal
testing, nickel is not found to be a skin sensitizer,[3] and, for
example, the draize test on guinea pigs suggests that nickel does not
produce an allergic reaction. Even in the two most widely used forms of
animal testing, nickel produces no response (the Buehler test) or only a
moderate response (the Maximization test).

[1]Medical Toxicology, eds. M J. Ellenhorn and D. G. Barceloux (Elsevier, 1988).
[2]Textbook of Dermatology, vol. 1, 5th edn, eds. R. H. Champion, et al (Blackwell Scientific Publications, 1992).
[3]P. A. Botham et al, Food and Chemical Toxicology, 1991, vol. 29, pp.275-286.


using monkeys in malaria research led to the suggestion that coma in
humans was caused by an increased amount of protein in the
cerebro-spinal fluid, and this could be resolved by using steriods.[1] But in contrast to the animal experiments, it was ascertained that
humans were not assisted by steroids when in a coma and if anything they
were harmful.[2] It was found that the time of coma
was lengthened by some sixteen hours and serious complications, e.g.,
pneumonia, urinary tract infections, convulsions, etc., also occurred
more often in those patients using steroids. Later research reported
‘that the monkey model may simply not be relevant’.[1] [1]Lancet, 2 May 1987, p.1016.
[2]D. A. Warrell, et al, New England Journal of Medicine, 11 February 1982, pp.313-319.


drug, an antidepressant, can produce potentially fatal blood disorders
and the British National Formulary recommends that people using the drug
have full blood counts every 4 weeks in the first months of usage.[1] By 1988, the World Health Organisation had over 300 reports relating to
white cell disorders.
Despite these problems, the
animal experimentation which had been conducted had not predicted these
effects,[2] although later test tube studies with human tissue did allow
the effects to be observed.[3] [1]British National Formulary, No. 26 (BMA and the Royal Pharmaceutical Society of GB, 1993).
[2]H. M. Clink, British Journal of Clinical Pharmacology, 1983, vol. 15, pp.2915-2935.
[3]P. Roberts, Drug Metabolism and Disposition, 1991, vol. 19, pp.841-843.

Caged ball valve.

are preferred in cardiac experiments which include tests to develop an
artificial mitral valve although these valves are known to produce fatal
blood clots in the dogs.[1] Because of this, many surgeons have been
deterred from carrying out human trials.[2] To overcome
the blood clots which occur, two experimental surgeons decided on a
‘caged ball’ valve,[3] as other devices proved fatal to those dogs on
which they had been tested. Of the 7 dogs that received the caged ball
valve, 6 died within 17 days and only one survived and this was for a
few months. Despite this failure in dogs, the device was much more
successful in clinical trials where blood clotting was not a problem.[4] The surgeons concluded: ‘The marked propensity of the dog to thrombotic
occlusion [blood clotting] …from a mitral prosthesis is not shared by
the human being’.[5] The surgeons intended
carrying out further experiments with their caged ball valve on animals
but as it invariably resulted in the death of the animals, the surgeons
had to produce a different valve made specially for use in the dogs. One
would have thought this would have been sufficient to indicate animal
experimentation was of no value in respect of human health, but they
continued and found that while the different valve did not kill so many
dogs so quickly, nearly 80% died in 46 days. The surgeons admitted that
‘the species differences’ forced them to design one type of valve for
use in humans and another type for use in the laboratory animals.[5] Finally, the successful clinical use of another design of mitral valve
replacement gave further proof that animal experimentation is of no use
as none of the dogs used in the preclinical testing survived more than
40 hours.[6] [1]A. V. Doumanian and F. H. Ellis, Journal of Thoracic and Cardiovascular Surgery, 1961, vol. 41, pp.683-695.
[2]G. H. A. Clowes, jr., Annals of Surgery, 1961, vol. 154, p.740.
[3]A. Starr, American College of Surgeons, Surgical Forum, 1960, vol. 11, pp.258-260.
[4]A. Starr and M. L. Edwards, Annals of Surgery, 1961, vol. 154, pp.726-740.
[5]A. Starr and M. L. Edwards, Journal of Thoracic and Cardiovascular Surgery, 1961, vol. 42, pp.673-682.
[6]N. S. Braunwald, et al, Journal of Thoracic and Cardiovascular Surgery, 1960, vol. 40, pp.1-11.


an anti-inflammatory drug used for arthritis, was considered an
improvement on other anti-inflammatory preparations as it did not damage
the stomach, a major problem with this type of drug. It was advertised
as providing ‘gastric protection’, being based on animal
experimentation. However this claim could not be confirmed by clinical
trials and as a consequence, Roussel, the manufacturer, was fined twenty
thousand pounds for misleading advertising. The Lancet described how
expert witnesses for both sides ‘agreed that animal data could not
safely be extrapolated to man’.[1] [1]J. Collier and A. Herxheimer, Lancet, 10 January 1987, pp.113-114.


diuretic product was tested on animals and no harmful effects were
detected.[1] After being introduced in 1979, it had to be withdrawn in
America the following year when over 300 cases of liver damage were
reported, which included 24 deaths.[1] Development of the drug was
cancelled in many countries including Britain.[2] [1]S. Takagi, et al, Toxicology Letters, 1991, vol. 55, pp.287-293.
[2]C. Spriet-Pourra and M. Auriche, Drug Withdrawal From Sale (PJB Publications, 1988).


a treatment for angina, was originally marketed in France in the 1970s.
When it became linked to liver damage, it was withdrawn in Britain
while other countries did not licence it at all. In fact some considered
that it should never have been licensed.[1] The animal
experimentation conducted did not indicate the danger,[2] and even when
high doses were administered to several different species for up to two
years, there was no indication that the drug affected the liver.[3] The
company responsible for marketing perhexiline said: ‘there has been an
inordinate amount of animal work done…At this point we simply have
been unable to induce hepatic [liver] damage in any species’.[4] [1]D. G. McDevitt and A. M. MacConnachie, in Meyler’s Side Effects of Drugs, 11th edn., ed. M. N. G. Dukes (Elsevier, 1988).
[2]C. T. Eason, et al, Regulatory Toxicology and Pharmacology, 1990, vol. 11, pp,288-307.
[3]J. W. Newberne, Postgraduate Medical Journal, 1973, vol. 49, April Suppl., pp.125-129.
[4]Ibid., p.130.


is included in a number of cough and cold remedies, and is also used as
an inhalent when conditions such as bronchitus and sinusitis arise. It
is also used as a ointment. If it comes into contact with the eye it
will produce burning sensation which can last up to thirty minutes
although there are no after-effects. In stark contrast, menthol causes
severe damage to the eye of the rabbit.[1] [1]W. M. Grant, Toxicology of the Eye (Charles Thomas, 1974).

Selenium disulphide (Selsun).

view of this product being successful as an antidandruff shampoo, it
was suggested that it might be of assistance for blepharitis, a painful
and similar condition of the eyelids. Trials were then conducted in
which a preparation with 0.5% selenium disulphide was applied to the lid
margins. It was noted that if it came into contact with the
conjunctivita there was irritation, and one patient developed
conjunctivitis.[1] And yet animal experiments showed that: ‘Selenium
disulphide 0.5% ophthalmic ointment is nontoxic to rabbit corneas or
conjunctivitas’.[2] [1]G. C. Bahn, Southern Medical Journal, 1954, vol. 47, pp.749-752.
[2]J. W. Rosenthal and H. Adler, Southern Medical Journal, March 1962, p.318.

Domestic and cosmetic products.

discovered that while coconut soap had a negligible effect on human
skin, it causes skin irritation in rabbits. Pine oil cleaner also
produced a ‘moderate’ reaction in rabbits and guinea pigs, whereas it
only had a slight effect on human skin. Other substances have been found
to have different effects on animals and humans, e,g., high and low
carbonate detergents, phosphate detergents, enzyme detergents, sodium
carbonate and lemon juice all had an insignificant effect on human skin
while causing irritation in animals. Overall, only 6 of the 24 products
tested on animals and humans had the same effect on humans, rabbits and
guinea pigs. The report concluded: ‘Neither the rabbit nor the guinea
pig provides an accurate model for human skin. The skin responses of
these animals differ in both degree and in kind from those found in
human skin’.[1] Similar findings arose with cosmetic
ingredients. Researchers at the New Jersey Warner Lambert Research
Institute observed that: ‘Animal skin is entirely differently from human
skin and that there may be no correlation between the mildness of a raw
material on a rabbit’s back and its safety during use on a human face’.
They offer the example of isopropyl myristate which is deemed safe for
human use but causes irritation in rabbits.[2] [1]G. A. Nixon, et al, Toxicology and Applied Pharmacology, 1975, vol. 31, pp.481-490.
[2]M. M. Rieger and G. W. Battista, Journal of the Society of Cosmetic Chemists, 1964, vol. 15, pp.161-172.


is used to treat nausea and vomiting, particularly those instances
caused by anti-cancer treatment. The injectable form was withdrawn
globally in 1986,[1] due to hazardous heart rhythm disturbances.
However, this danger was not predicted by animal experimentation.[2] Dogs, the animal often used to test effects on the heart, were given 70
times the recommended human dosage, and yet no changes in the
electrocardiogram occurred.[3] [1]C. Spriet-Pourra and M. Auriche Drug Withdrawal From Sale (PJB Publications, 1988).
Heywood, in Animal Toxicity Studies: Their Relevance For Man, eds. C.
E. Lumley and S. R. Walker (Quay Publications, 1990).
[3]R. N. Brogden, et al, Drugs, 1982, vol. 24, pp.360-400.


is a natural constituent of human sebum, the substance formed by
sebaceous glands surrounding the root of the hair; this keeps the skin
lubricated and supple. It is extensively and safely used in
cosmetics.[1] However, when used on the skin of rabbits and guinea pigs,
it produces loss of hair, the very opposite of what occurs in human
beings.[2] [1]M. M. Rieger and G. W. Battista, Journal of the Society of Cosmetic Chemists, 1964, vol. 15, pp.161-172.
[2]B. Boughton, et al, Journal of Investigative Dermatology, 1955, vol. 24, pp.179-189.


product, a treatment for angina, was removed from the American market
in 1988,[1] in view of it causing ventricular tachycardia, i.e., the
heart beats abnormally fast and patients can faint. In stark contrast to
this, animal experimentation revealed that prenylamine reduced the
heart rate by up to 25% in cats, rabbits and guinea-pigs.[2] [1]C. Spriet-Pourra and M. Auriche, Drug Withdrawal From Sale, (PJB Publications, 1988).
[2]H. Obianwu, Ata Pharmacology et Toxicology, 1967, vol. 25, pp.127-140.


had to be issued to ophthalmologists against the prolonged use of this
product when treating glaucoma,[1] as it was noted that the tear passage
became permanently obstructed in over 70% of those patients who used it
for more than three months.
And yet those who
conducted the animal experimentation related to this product (on rats,
guinea pigs and rabbits) declared it ‘entirely safe’ and worthy of
clinical trial.[2] [1]R. N. Shaffer and W. L. Ridgway, American Journal of Opthalmology, 1951, vol. 34, pp.718-720.
[2]A. Myerson and W. Thau, Archives of Opthalmology, 1940, vol. 24, pp.758-760.

Phenylbutazone (Butazolidine).

was once widely used to treat arthritis, but was withdrawn in several
countries and restricted in others, due to reports of aplastic anaemia
(an often fatal blood disease caused by damage to the bone marrow)
arising.[1] Animal testing had indicated phenylbutazone
to be a safe medication with no side effects even when ten times the
dosage recommended for humans was administered to the animals.[2] The
animal testing had certainly not suggested phenylbutazone would have a
harmful effect on the bone marrow,[3] and a year after marketing,
researchers said ‘there have been no published reports of serious
effects…on the hemopoietic [blood forming] system…in the
experimental animal’.[4] Noteworthy is the fact that
later research involving test tube experiments using human bone marrow
cell showed the dangers could be identified.[5] It has
been estimated that phenylbutazone and oxyphenbutazone (a closely
related drug that has also caused aplastic anaemia which was withdrawn
in 1985), have been responsible for 10,000 deaths worldwide.[6] [1]C. Spriet-Pourra and M. Auriche, Drug Withdrawal From Sale, (PJB Publications, 1988).
[2]C. Hinz and I. M. Gaines, Journal of the American Medical Association, 1953, vol. 151, pp.38-39.
[3]R. Heywood in Animal Toxicity Studies: Their Relevance For Man, eds. C. E. Lumley and S. R. Walker (Quay Publishing, 1990).
[4]O. Steinbrocker, et al, Journal of the American Medical Association, 15 November 1952, pp.1087-1091.
[5]C. S. Smith, et al, Biochemical Pharmacology, 1977, vol. 26, pp.847-852.
[6]Estimate by Dr. Sidney Wolfe, in Lancet, 11 February 1984, p.353.


from chloroform were regularly reported in the second half of the
nineteenth century; it was believed that it caused respiratory failure
but this could be minimized by careful administration and monitoring.
Regrettably animal experimentation supported the idea that chloroform
affected respiration rather than the heart.[1] Launder
Brunton, in a communication to the Lancet,[2] summarized the results
from the Second Commission: ‘four hundred and ninety dogs, horses,
goats, cats and rabbits used. Results most instructive. Danger from
chloroform is asphyxia or overdose: none whatever heart direct’. With
this confirmation, from animal experimentation, that chloroform did not
stop the heart, anaesthetists continued to use chloroform.
1893, clinical observations completely contradicted the previous
findings and showed that heart failure is the most common cause of death
from chloroform.[1] [1]K. B. Thomas, Proceedings of the Royal Society of Medicine, 1974, vol. 67, pp.723-730.
[2]Lancet, 7 December 1889, p.1183.

Anaemia and iron.

patients suffer iron deficiency, physicians prefer that they take iron
by mouth, but if this is unsuccessful, iron is injected.[1] Due to
animal experimentation, this option could have easily been discarded.
Experiments which involved anaemia being induced in animals by iron
deficiency or by repeated haemorrhage led the experimenters to conclude
that injecting iron had no therapeutic value.[2] Fortunately, non-animal
studies proved that human patients could be treated by iron injection.
sorbitol is one type of injectable iron that could have been rejected
for a different reason. Administration to rats and rabbits caused cancer
at the injection site but once again non-animal trials showed that
there was no hazard to human patients.[3] [1]British National Formulary, no.276 (BMA and Royal Pharmaceutical Society of GB, 1993).
[2]G. N. Burger and L. J. Witts, Proceedings of the Royal Society of Medicine, 1934, vol. 27, pp.447-455.
[3]M. Weatherall, Nature, 1 April 1982, pp.387-390.

Spinal injuries.

the previous century, vivisectors attempted to develop an animal that
would mimic spinal cord injuries (SCI) in humans.[1] One method used to
achieve such injuries was dropping weights onto the spinal cord of
cats.*** Through this, it was intended to devise therapies for SCI.
Despite all the suffering experienced by laboratory animals, virtually
no treatments were developed that work in human patients.[1] In
1988, Dennis Maiman of the Dept. of Neurosurgery at the Medical College
of Wisconsin, said: ‘In the last two decades at least 22 agents have
been found to be therapeutic in experimental SCI. Unfortunately, to date
none of these have been proven effective in clinical SCI’.[1] In 1990
clinical trials showed that high doses of steroids could be beneficial.
While this was subjected to animal testing, the fact remains that the
testing was not only unnecessary but the animals gave inconsistent
results, with some tests indicating the therapy would not work.[2] [1]D. Maiman, Journal of the American Paraplegia Society, 1988, vol. 11, pp.23-25.
[2]S. R. Kaufman, Perspectives on Medical Research, 1990, vol. 2, pp.1-12.


vivisectors tested psicofuranine for an anti-cancer treatment, the rats
and mice used gave contradictory evidence.[1] The drug was effective
against tumours in rats but had no effect on three different cancers in
Physicians were also unable to properly assess
the drug against human cancer as it caused severe side-effects in early
human trials. It was found that the drug damaged the heart and yet no
cardiac toxicity was found in the mice, rats, dogs or monkeys used in
the testing.[1] Although clinical study of
psicofuranine was abandoned, animal experiments continued in an attempt
to reproduce the heart ailments in humans. Yet again, no cardiac
toxicity could be observed even when the animals (dogs and monkeys),
were given up to 10 times the dose that would be harmful to humans.[1] [1]C. G. Smith, et al, Journal of International Medical Research, 1973, vol. 1, pp.489-503.


clinical trials, sparsomycin, an anti-cancer drug, was found to produce
eye damage. And yet while sparsomycin was highly toxic in several
animal species (as would be expected for an anti-cancer drug), no
specific effect on the eye was found.[1] After the eye
damage was reported, vivisectors sought to induce the condition in rats
and monkeys, but these attempts were unsuccessful even though the rats
were dosed every day for two weeks with up to 300 times the amount that
was found to harm humans.[1] No retinal toxicity was noted in additional
animal tests and the drug was abandoned.

[1]C. G. Smith et al, Journal of International Medical Research, 1973, vol. 1, pp.489-503.

Corticosteroids: the unborn.

involving pregnant mice and rabbits indicate that corticosteroids are
very dangerous to the unborn human child. In the case of mice, cortisone
produces cleft palate in up to 100% of the offspring of some
species.[1] And in the case of rabbits, corticosteroids affect the heart
and they can also cause severe growth retardation in the uterus, and
death of the foetus. In stark contrast, rats and monkeys are very
tolerant to corticosteroids in pregnancy.[2] Researchers
have noted the ‘very wide species variation’,[2] and despite the
results of animal testing, cortisone is not considered harmful to human
babies.[1] [1]R. M. Ward and T. P. Green, Pharmacology and Therapeutics, 1988, vol. 36, pp.326.
K. Sidhu in Drugs and Pregnancy: Human Teratogenesis and Related
Problems, ed. D. F. Hawkins (Churchill Livingstone, 1983).


was originally manufactured for the treatment of tuberculosis, but was
subsequently used as an anti-depressant. Although it was considered
‘harmless’ on the basis of animal tests,[1] iproniazid produced fatal
cases of liver damage in humans, and the drug was eventually
abandoned.[2] [1]J. Boyer in Clinical
Pharmacology: Basic Principles in Therapeutics, 2nd edn., eds. K. I.
Melmon and H. F. Morrelli (Macmillan, 1978).


was first introduced as a sedative by the German drug company Chemie
Grünenthal in 1957, and by the Distillers company in Britain a year
later. Although animals could tolerate massive doses without
ill-effect,[1] thalidomide was soon found to cause peripheral neuritis
in human patients.
William McBride, an Australian
obstetrician, was alerted to thalidomide’s most notorious side-effect
after seeing three babies born with very unusual birth defects.
Regrettably, his warnings to the medical profession were delayed because
he attempted to confirm his suspicions by experiments on mice and
guinea pigs, both of which were resistant to the drug.[2] It was only
after he saw more human cases, did McBride publish his findings.
it was not specifically tested for birth defects before it was
marketed, subsequent experiments revealed ‘extreme variability in
species’ susceptibility to thalidomide’.[3] For example, mice could
safely tolerate eight thousand times the dose which was found harmful to
human babies.[4] In his book, Drugs as Teratogens,
Schardein writes: ‘In approximately ten strains of rats, fifteen strains
of mice, eleven breeds of rabbits, two breeds of dogs, three strains of
hamsters, eight species of primates, and in other such varied species
as cats, armadillos, guinea pigs, swine and ferrets, in which
thalidomide had been tested, teratogenic effects [birth defects] have
been induced only occasionally’.
Scientists eventually
found that birth defects similar to those occurring in humans could be
induced in certain types of rabbit and primate. Nonetheless, New Zealand
white rabbits had to be dosed with three hundred times the amount that
was dangerous to humans.[5] The thalidomide tragedy
prompted additional extensive testing of drugs and chemicals in pregnant
animals, but some scientists believe that: ‘Animal malformations seldom
correlate with those of humans’.[6] Additionally, ‘No animal model has
been found which responds satisfactorily to all known teratologic agents
in humans to permit reliable screening of substances for their
teratologic potential. Careful surveillance, reporting and prospective
study…remain the mainstays for detection of adverse effects following
foetal drug exposure’.[6] [1]R. D. Mann, Modern Drug Use, an Enquiry on Historical Principles (MTP Press, 1984).
[2]The Sunday Times ‘Insight’ Team: Suffer the Children: the Story of Thalidomide, (Andre Deutsche, 1979).
[3]T. H. Shepard, Catalogue of Teratogenic Agents (John Hopkins Press, 1976).
[4]S. K. Keller and M. L. Smith, Teratogenesis, Carcinogenesis and Mutagenesis, 1982, vol. 2, pp.361-374.
Zealand White rabbits were sensitive to doses of 150mg/Kg of
thalidomide (ref. 6), while the dangerous human dose was 0.5mg/Kg (ref.
[6]R. M. Ward and T. P. Green, Pharmacology and Therapeutics, 1988, vol. 36, p.326.


drug was produced for the treatment of cancer without side- effects on
the heart. After beagles, on whom the drug was tested , ‘failed to
demonstrate cardiac failure’,[1] researchers believed that it was safe.
However in clinical trials, a number of patients suffered side-effects
including heart failure; more widespread use of the drug confirmed that
cardiac toxicity was a major problem with the drug.
from over three thousand patients who were given the drug included
nearly a hundred reports of cardiac side-effect with twenty- nine of
heart failure.[2] A recent study indicated that 20% of patients develop
cardiotoxicity after using mitoxantrone.[3] [1]R. Stuart Harris, et al, Lancet. 28 July 1984, pp.219- 220.
[2]Martindale: The Extra Pharmacopoeia, 29th edn., ed. J. E. F. Reynolds (Pharmaceutical Press, 1989).
[3]A. Stanley and G. Blackledge, Side Effects of Drugs, Annual 15, eds. M. N. G. Dukes and J. K. Aronson (Elsevier, 1991).


was introduced during the 1960s for the treatment of peptic ulcers.
Before being marketed it was tested on animals and the tests indicated
that carbenoxalone was safe and there were no harmful effects.[1] When
vivisectors realized that humans metabolized carbenoxalone differently
to rats, mice and rabbits, further experiments were carried out on
monkeys, but yet again, there was no evidence of toxicity.[1] When
carbenoxalone began to be used by human patients, salt and water
retention occurred and this led to high blood pressure, swelling, weight
gain, muscle weakness and heart failure. The British National Formulary
advises other drugs are preferred and if carbenoxalone is used,
treatment must be carefully monitored.[2] [1]C. T. Eason, et al, Regulatory Toxicology and Pharmacology, 1990, vol. 11, pp.288-307.
[2]British National Formulary, no.26 (BMA and the Royal Pharmaceutical Society of G.B., 1993).


the antibiotic clindamycin was given to rats and dogs every day for a
year, it was found that the animals could tolerate twelve times the
recommended human dose.[1] However, Britain’s Committee
on the Safety of Medicines was forced to warn the medical profession
about the dangers of clindamycin, one of which was the sometimes-fatal
intestinal disease, pseudomembraneous colitis. By 1980, 36 deaths had
been reported.[2] Although the problem can occur with other antibiotics,
it is more frequently seen with clindamycin and the British National
Formulary warns that patients should stop using clindamycin immediately
if side-effects develop.

[1]The British
National Formulary (No. 26, 1993) says the maximum oral dose for severe
infections is 450mg every six hours, i.e., 25mg/kg for a person weighing
70 kg taking 4 doses in 24 hours. Rats and dogs could tolerate more
than 300mg/kg (J. E. Gray, et al, Toxicology and Applied Pharmacology,
1972, vol. 21, pp.516- 531).
[2]G. R. Venning, British Medical Journal, 15 January 1983, pp.199-202.

Leukaemia treatment.

decades, in an attempt to find a treatment for leukemia, tens of
thousands of chemicals have been used in mice which have been given
leukaemia. This has proved highly ineffective. One scientist has
estimated that for every 30-40 drugs that are effective in treating mice
with cancer, only one will work with humans.[1]. During the 1980s,
researchers admitted that the American NCI (National Cancer Institute)
was failing to identify promising new treatments.[2][3] A
new strategy involves test tube studies rather than mice, at least for
the preliminary experiments. Drugs that appear to be promising are then
tested on animals so the prospect of misleading results is still very
much there.[4] [1]D. D. Von Hoff, Journal of the American Medical Association, 10 August 1979, p.503.
[2]R. Kolberg, Journal of NIH Research, 1990, vol. 2, pp.82- 84.
[3]A. Pihl, International Journal of Cancer, 1986, vol. 37, pp.1-5.
[4]S. E. Salmon, Cloning of Human Tumor Stem Cells (Alan Liss, 1980).

Pronethalol and Propranolol.

first agents used as beta-blockers, for the treatment of heart
conditions, were pronethalol and propranolol. While pronethalol was
found to be safe and effective with laboratory animals, but failed the
clinical tests, propranolol appeared to be toxic in numerous animal
experiments, and yet it is widely used in clinical practice, i.e.,
treating humans.
Pronethalol was ‘well tolerated’ by
rats and dogs in prolonged toxicity tests at high doses except for
occasional effects on the central nervous system.[1] In complete
contrast, clinical trials revealed an unacceptable number of
side-effects,[2] including heart failure – a hazard not predicted by the
animal experiments which had been conducted.[1] Shortly after,
long-term tests in a particular strain of laboratory mouse produced
cancer of the thymous gland but no carcinogenic effects were ever found
in rats, guinea pigs, dogs, monkeys or other types of mouse.[1] Pronethalol
was promptly replaced by propranolol but tests in rats, dogs and mice
resulted in further development being jeopardized.[3] Moderate to high
doses caused rats to collapse and dogs to vomit severely.[1] Deaths also
occurred in mice shortly after dosing. When the amount of the drug was
reduced to the dosage that would be used by humans, propranolol was said
to be ‘well tolerated’, although even then, some of the rats still had
heart lesions.[1] [1]M. Cruickshank, et al, Safety Testing of New Drugs, eds. D. R. Lawrence, et al (Academic Press, 1984).
[2]W. Sneader, Drug Discovery: The Evolution of Modern Medicine (Wiley, 1985).
[3]D. R, Laurence, et al, eds., Safety Testing of New Drugs (Academic Press, 1984).

Librium and Valium.

were the first of a new type of tranquillizing drug which appeared in
the 1960s. Soon after their introduction, the medical profession became
aware of cases of dependence although it was nevertheless believed that
high doses were necessary.[1] At the usual therapeutic doses, dependence
was thought to be uncommon and not a serious problem and this idea
prevailed for some twenty years as laboratory research confirmed it:
‘animal experiments…do not indicate the potential for the development
in the human of dependence at therapeutic dosage levels’.[2] At
the same time it is also known that ‘animal studies…do not predict
clinical dependence potential reliability’,[3] and careful human
observations revealed that tranquillizers could in fact induce
dependence at ordinary doses. By the mid-1980s, some 500,000 people in
Britain alone were addicted to this treatment.[4] [1]H. Peturrson and M. Lader, Dependence on Tranquillizers (OUP, 1984).
[2]J. Marks, The Benzodiazepines (MTP Press, 1978).
[3]Drug and Therapeutics Bulletin, 1989, vol. 27,28.
[4]The Benzodiazepines in Current Clinical Practice, eds., H. Freeman and Y. Rue (Royal Society of Medicine Services, 1987).


the early 1970s, doctors became aware of women who, while using ‘the
pill’, became pregnant.[1] Of 88 women who used oral contraceptives in
addition to the antituberculous drug rifampicin, 75% suffered
disturbances to their menstrual cycle and 5 became pregnant. The British
National Formulary (1993) advised doctors who prescribed rifampicin to
recommend to patients that they use additional means of contraception.
was discovered that rifampicin accelerates the breakdown of other
medicines,[2] and in these cases it had stimulated the patient’s liver
to metabolize/breakdown the pill. Another example was methadone where
rifampicin led to withdrawal symptoms by reducing the amount of the
drug. In one case, a patient rejected a kidney graft because rifampicin
reduced the dose of the immunosuppresive drug which had been given.
peculiar effects had not been predicted by animal experimentation.[3] After the discovery of the effects in humans, further animal
experimentation was conducted but this proved contradictory. For
example. the drug’s action could not be reproduced in rats.[4] In mice
however, prolonged treatment with rifampicin did stimulate the liver’s
metabolic processes; however a single dose had the opposite effect of
slowing down metabolism.[4] If rifampicin had been tested on human liver
tissue rather than on live animals, it is likely the problems would
have been predicted.[5] [1]Reported in J. P. Mumford, British Medical Journal, 11 May 1974, pp.333-334.
[2]H. Meyer, et al, in Meyer’s Side Effect of Drugs, 11th edn., ed. M. N. G. Dukes (Elsevier, 1988).
[3]E. Nieschlag, Pharmacology and Therapeutics, 1979, vol. 5, pp.407-409.
[4]D. Pessayre and P. Mazel, Biochemical Pharmacology, 1976, vol. 25, pp.943-949.
[5]A. M. Jezequel, et al, Gut, 1971, vol. 12, pp.984-987.


was developed during the 1960s as an oral contraceptive. However, while
it prevented ovulation and terminated pregnancy in rats,[1] it
stimulated ovulation in women and became listed as a treatment for
infertility.[2] It is used also in breast cancer
therapy as it blocks the action of oestrogen in breast tissue. In
monkeys, and rats at low doses, it also acts as an anti-oestrogen, but
in mice, dogs, and rats at high doses, it has the opposite effect,
behaving like an oestrogen.[1] Due to the different results of animal
experimentation, it was admitted that ‘significant species variation has
been observed in target tissue response to oestrogens and
anti-oestrogens making it hazardous to predict therapeutic activity in
the human by extrapolation of effects in experimental animals’.[3] Other
conflicting results from animal testing has occurred, e.g., taxoxifen
produces liver tumours in rats but not in mice,[4] and does not appear
to do so in humans. Due to the conflicting results the two leading
British cancer charities disagreed over taxoxifen and the Medical
Research Council withdrew its support and decided to initiate new tests.
The Imperial Cancer Research fund said: ‘We are going to be in a
position where the animal rights people are going to be saying to us:
‘you ignore animal data when you choose to’.'[5] Yet
further doubts arose through a subsequent study which suggested an
increased risk of womb cancer among the breast cancer patients being
tested with the drug. However overall, the drug is said to have few
side-effects and according to the manufacturer, the main reason to stop
taking the drug is if nausea and vomiting begin.[1] This comes as a
surprise as it had been noted: ‘None of the toxicological studies
produced any evidence of vomiting even though high doses were used in
dogs which we consider to be a predictive species for vomiting in

[1]M. J. Tucker, Safety Testing of New Drugs, eds. D. R. Laurence, et al (Academic Press, 1984).
[2]British National Formulary, No. 26 (BMA and the Royal Pharmaceutical Company of GB, 1993).
[3]P. K. Devi, in Pharmacology of Estrogens, ed. R. R. Chaudhury (Pergamon Press, 1981).
[4]I. N. White, et al, Biochemical Pharmacology, 1993, vol. 45, pp.21-30.
[5]P. Brown, New Scientist, 21 March 1992, p.9.


drugs are widely used in medicine although they have many side-effects.
It is admitted that there are ‘remarkable differences in susceptibility
to glucocorticosteroids between various species’ with animals
classified as steroid-resistant or steroid-sensitive.[1] In
mice, a single dose of cortisone produces a 90% decrease in the thymus
(an organ that plays a crucial role in immunity). In contrast, the same
dose of cortisone given to a guinea-pig every day for a week, only
produces a 37% decrease. Furthermore, the same effect is difficult to
achieve in other species.[1] Much of the research on
corticosteroids have been carried out on steroid-sensitive animals
(e.g., mice, rats, rabbits, and hamsters) whereas human beings fall into
the steroid-resistant category.[1] Researchers at the University of
Dundee acknowledged: ‘the mode of action of these drugs is very
complicated, so it is regrettable that most of the extensive literature
on animal experimental work is irrelevant to human therapeutics since
many species respond in a very different manner from man’.[2] [1]H. N. Claman, New England Journal of Medicine, 24 August 1972, pp.388-397.
[2]J. S. Beck and M. C. K. Browning, Journal of the Royal Society of Medicine, 1983, vol. 76, pp.473-479.


1956, the British medical profession drew attention to a link between
X-rays during pregnancy and subsequent childhood cancers.[1] Within a
short time, similar findings were reported in respect of American
children. And yet for a quarter of a century, scientists doubted that
X-rays could cause such cancer and cited animal experimentation to argue
that the foetus is not particularly sensitive to radiation.[2] In
fact, compared with other species, the human foetus is more susceptible
to the carcinogenic effects of X-rays,[2] and this was confirmed during
the 1980s.[3] [1]A. M. Stewart, et al, Lancet, 1 September 1956. p.447; British Medical Journal, 28 June 1958, pp.1495-1508.
[2]E. B. Harvey, et al, New England Journal of Medicine, 28 February 1985, pp.541-545.
G. Knox, et al, Journal of the Society of Radiological Protection,
1987, vol 7, pp.3-15; E. A. Gilman, et al, Journal of the Society of
Radiological Protection, 1988, vol. 8, p.308.


is used in a wide range of consumer products, e.g., solid fuel,
antifreeze, paint remover and varnishes. It is also consumed as a heap
alternative to alcohol.
Although methanol is a highly
poisonous, potentially lethal substance, this was not realized for some
years.[1] Laboratory animals such as rats and mice are resistant to its
effects,[2] and animal experiments in the early part of the twentieth
century gave the impression that methanol was only marginally toxic, and
far less poisonous than alcohol.[3] In reality,
methanol is ten times more toxic; a single dose of methanol can result
in temporary or permanent blindness in human beings.[4] However, this
does not occur in rats, mice, dogs, cats, rabbits or chickens.[3] It was
only in the 1960s and again in the next decade that the actual symptoms
of methanol poisoning were induced in monkeys.[2] As
is obvious from the above, animal experimentation was both highly
misleading and dangerous. Some good treatment results were obtained in
the earlier part of the twentieth century by using bicarbonate to treat
human poisoning, but the results were undermined by animal
experimentation. In 1955 an analysis stated: ‘It is indeed deplorable
that about thirty years before the good effects of this treatment became
commonly known…it seems that the authors of medical textbooks have
paid more attention to the results of animal experimentation than to
clinical observations’.[3] The treatment not only failed in animals but
actually proved fatal, prompting some researchers to advise against
using it.
Another method involves administering alcohol
to reduce the toxicity of methanol. While this is effective in human
beings, animal tests suggested that this practice would increase the
danger of methanol. Once again, animal experimentation discouraged using
this method of treating human poisoning.[3] [1]M. J. Ellenhorn and D. G. Barceloux, Medical Toxicology: Diagnosis and Treatment of Human Poisoning (Elsevier, 1988).
[2]T. R. Tephly, Life Sciences, 1991, vol. 48, pp.1031- 1041.
[3]O. Roe, Pharmacological Reviews, 1955, vol. 7, pp.399- 412.
[4]P. Wingate, Medical Encyclopedia, (Penguin, 1983).


the 1960s, physicians in Switzerland became aware of a sudden rise in
obstructive pulmonary hypertension, a dangerous lung disease. The cause
was traced to the drug aminorex which had been used for treating
obesity.[1] The drug was found to cause chest pains, difficulty in
breathing, fainting, heart problems and in some cases, death.[2] The
deadly side-effects of this drug had not been predicted by the animal
experimentation which had been conducted.[3]. In view of its dangers,
the drug was withdrawn in 1968.
Animal experimentation
continued after withdrawal and even then, long administration to rats
failed to induce the disease.[2] In dogs, the drug increased lung
pressure,[1] but its relevance to the human condition is unclear since
later analysis concluded that: ‘pulmonary hypertension cannot by induced
in experimental animals even with aminorex’.[4] [1]F. Follath, et al, British Medical Journal, 30 January 1971, pp.265-266.
[2]E. H. Ellinwood and W. J. K. Rockwell in Meyler’s Side Effects of Drugs, 11th edn, ed. M. N. G. Dukes (Elsevier, 1988).
[3]A. D. Dayan in Risk-Benefit Analysis in Drug Research, ed. J. F. Cavalla (MTP Press, 1981).
[4]P. H. Connell in Side Effects of Drugs Annual – 3, ed. M. N. G. Dukes (Excerpta Medica, 1979).

Diethylstilbestrol (DES).

the basis of what animal experimentation revealed, the synthetic
oestrogen Diethylstilbestrol (DES) was suggested as a means by which
miscarriage could be avoided.[1] Although no proper clinical, i.e.,
human, trials were conducted,[2] the procedure became widely accepted
and to 1971, up to 3 million pregnant women in America alone were given
However, DES was found to be ineffective; in 1953
trials had shown that DES did not work,[3] although this study failed to
report that DES increased abortion, neonatal deaths and premature
deaths, a conclusion that could have been made from the available
data.[4] Thus, DES was not only ineffective, it was
dangerous and in 1971, researchers discovered how dangerous it was when
they traced a link between exposure to DES and a previously rare form of
vaginal and cervical cancer in the daughters of those women who had
taken the drug while pregnant.[5] Nearly six hundred cases were
reported,[6] and DES proved to be a biological time-bomb as its
side-effects continued to appear in the sons and daughters of women who
took the drug.
Although, in 1938, it was found that DES
caused breast cancer in male mice, this information was of no value as
the cancer-causing potential of other oestrogens varied according to the
strain of mouse used.[7] Furthermore, the consensus among vivisectors
at the time was that oestrogens did not produce cancer,[7] rather they
gave male mice mammary glands and therefore made them susceptible to the
same cancer-causing factors that arose in female animals. In fact, a
summary of the animal data found ‘only meagre evidence’ that oestrogens
caused cancer of the cervix.[7] It was not until the
1970s that it became clear that in contrast to the majority of animal
experiments, DES was a potent cause of cervical cancer in women.

[1]Health Action International, ‘Problem Drugs’ pack, 13 May 1986.
[2]D. Brahams, Lancet, 15 October 1988, p.916.
[3]W. J. Dieckmann, et al, American Journal of Obstetrics and Gynaecology, 1953, vol. 66, pp.1062-1081.
[4]Y. Brackbill and H. W. Berendes, Lancet, 2 September 1978, p.520.
[5]A. L. Herbst, et al, New England Journal of Medicine, 22 April 1971, pp.878-881.
[6]C. Vanchieri, Journal of the National Cancer Institute, 1992, vol. 84, pp.565-566.
[7]S. Peller, Cancer in Man (Macmillan, 1952).


the basis of experiments with dogs, the narcotic analgesic pethidine
was considered to be non-addictive.[1] This error was not realized
because in dogs, the drug was metabolized (broken down) much more
quickly, resulting in less exposure to the drug. In fact, dogs
metabolize pethidine six times faster than humans.[2] Such
differences in metabolism are the rule rather than the exception;[2,3] a
former director of Wellcome Research Laboratories admitted that ‘every
species has its own metabolic pattern, and no two species are likely to
metabolize a drug identically’.[4] [1]B. Brodie, Pharmacologist, 1964, vol. 6, pp.12- 26.
[2]R. Levine, Pharmacology, Drug Actions and Reactions (Little, Brown and Co, 1978).
[3]G. Zbinden, Advances in Pharmacology, 1963, vol. 2, pp.1-112.
[4]M. Weatherall, Nature, 1 April 1982, pp.387-390.

Digoxin and Digitoxin.

heart drugs are pure substances extracted from digitalis, the value of
which in treating heart failure and cardiac arrhythmias originated from
the studies of human patients;[1,2] (despite its value, care must be
taken over high doses which can be toxic). Fortunately the drugs did not
derive from animal experiments as the doses which were considered safe
for rats, guinea-pigs, dogs and cats can in fact kill human beings.[3] Digoxin’s lethal dose is now more accurately determined by test-tube
studies using human cells.[4] Animal experimentation
also indicated that digitalis raised the blood pressure and as a result
of this, the drug was widely considered to be dangerous for certain
patients and should not be prescribed to them. Fortunately, studies, not
using animals, showed this to be false and digitalis can be, and is
used for the treatment of human patients with great benefit.[2] [1]W. Sneader, Drug Discovery: The Evolution of Modern Medicine (Wiley, 1985).
[2]T. Lewis, Clinical Science (Shaw and Sons Ltd, 1934).
[3]G. T. Okita, Federation Proceedings, 1967, vol. 26, pp.1125-1130.
[4]R. Jover, et al, Toxicology In Vitro, 1992, vol. 6, pp.47-52.


are not only used in domestic and industrial settings, i.e.,
experimentation which sought to increase the penetration of therapeutic
drugs across the cornea used a number of dilute detergents which were
assessed in the eyes of human volunteers. Although these were deemed
‘generally harmless to rabbit eyes’, some caused pain and irritation in
the human volunteers.
For example, Brij 58 resulted in
‘alarming’ changes to the surface of the human eye, accompanied by
discomfort and impaired vision.[1] And yet in rabbits, Brij 58 is
designated a ‘non-irritant’.[2] A 3% solution of a
similar product called Brij 35 produced delayed irritation in volunteers
but was once again non- irritating to the rabbit eye, and this was even
when undiluted.[1] Another detergent, dupanol, caused immediate severe
pain in human subjects,[1] but was deemed to only have moderate effects
in the eyes of rabbits.[3] [1]R. J. Marsh and D. M. Maurice, Experimental Eye Research, 1971, vol. 11, pp.43-48.
[2]M. Cornelis, et al, ATLA, 1991, vol. 19, pp.324- 326.
[3L.W. Hazelton, Proceedings of the Scientific Section of the T.G.A, 1952, vol. 17, pp.509.

Cancer treatment.

cancer patients suffered unnecessarily when it was believed that large
doses of anticancer drugs were necessary for efficient treatment. It was
held that to reduce the tumour size, chemotherapy also had to be
toxic.[1] This idea was based on animal
experimentation,[1,2] even though there were early warning signs that
patients survived longer when treated with comparatively non-toxic
doses, despite the drug having a smaller effect on the tumour size.[3] Studies
in the 1960s concluded that toxicity was not necessary and could be
counterproductive.[2] In 1976, cancer specialists in London found that
the data from animal experimentation, on which the high dose concept was
based, are not necessarily valid for human patients,[1] and argued that
‘alternative methods of improving the selectivity of cancer
chemotherapy must be explored’.

[1]M. H. N.Tattersall and J. S. Tobias, Lancet, 13 November 1976, pp.1073-1074.
[2]I. D. Bross, Perspectives on Animal Research, 1989, vol. 1, pp.83-108.
[3]M. A. Schneiderman and M. J. Krant, Cancer, Chemotherapy Reports, 1966, vol. 50, pp.107-112.


fact that even chimpanzees do not develop AIDS when infected with HIV
naturally casts doubts on whether animal experimentation concerned with
AIDS can have any possible value.[1] Some AIDS researchers appear to
have grasped this fact as vaccines which failed to protect chimpanzees
from HIV were nevertheless tried in human trials.[2] Animal
experimentation has the potential to be dangerous as the failure to
induce AIDS in laboratory animals has led some to argue that HIV is not
the cause of AIDS.[3] There is a further danger by
producing an ‘animal model’ of AIDS as this may simply produce an animal
version of AIDS and could also promote hazardous changes in the manner
in which AIDS is spread.

[1]P. Newmark, Nature, 19 October 1989, pp.566-567.
[2]A. S. Fauci and P. J. Fischinger, Public Health Reports, 1988, vol. 103, pp.203-236.
[3]New Scientist, 3 March 1988, p.34.
[4]J. Marx, Science, 16 February 1990, p.809. P. Lusso, et al, Science, 16 February 1990, pp.848-852.


is successfully used for the treatment of cardiovascular and kidney
disease in human beings. However, in mice it causes massive liver damage
and similar effects have been found in rats and hamsters.[1] And yet
liver toxicity is not a major problem for human patients.[2] The harmful
effects in mice have been traced to a breakdown product of furosemide
which is not found to any serious extent in the human body.[3] Fortunately the adverse effects in mice were reported after the safety
in people had been established.[3] If it had been otherwise, the drug
may have never been introduced.
A comparison of human
and animal test data shows that the case of furosemide is not an
isolated instance. At most, only one out of every four side-effects
produced by animal tests actually occurs in human beings.[4] Consequently animal testing leads to the rejection of medicines which
are potentially valuable for treating human illnesses.

[1]R. M. Walker and T. F. McElligott Journal of Pathology, 1981, vol. 135, pp.301-314.
[2]M. N. G. Dukes in Meyler’s Side Effects of Drugs, 11th edition, ed. M. N. G. Dukes (Elsevier, 1988).
[3]M. Weatherall, Nature, 1 April 1982, pp.387-390.
[4]A. P. Fletcher, Journal of the Royal Society of Medicine, 1978, vol. 71, pp.693-698.


is used to prevent the rejection of transplanted organs: while hailed
as a major advance over existing drugs, side- effects are common and
sometimes dangerous. The most serious hazard is kidney damage,[1] an
effect that was not predicted by the initial animal experimentation.[2] And yet kidney toxicity has been reported in almost 80% of kidney
transplant patients receiving the drug.[2] Some heart transplant
patients who were treated with cyclosporin required dialysis because
their kidneys failed.[3] Subsequent animal experiments
showed that only extremely high doses of cyclosporin could induce kidney
toxicity in rats,[1] although dogs and rhesus monkeys were still
unaffected.[2] Researchers believe that: ‘…failure to produce renal
dysfunction [kidney damage] experimentally that is similar to that seen
clinically may result from species differences in metabolism’.[2] Although
cyclosporin can prevent the rejection of transplanted organs in both
animals and human beings, an early review of the drug found sufficient
variation in experimental results to indicate: ‘the immunosuppressive
effects of cyclosporin have…differed considerably between species,
limiting any direct inference that may be made regarding use in human
organ transplantation…'[1] [1]D. J. Cohen, et al, Annals of Internal Medicine, 1984, vol. 101, pp.667-682.
[2]W. M. Bennett and J. P. Pulliam, Annals of Internal Medicine, 1983, vol. 99, pp.851-854.
[3]Lancet, 22 February 1986, pp.419-420.


September 1987, the antidepressant zimelidine (Zelmid) was withdrawn
worldwide after potentially serious side-effects, including nerve
damage, leading to the loss of sensation or paralysis.[1] Some
patients experienced hypersensitivity reactions such as fever, joint
pains and liver problems. The drug had been introduced only a year
earlier but Britain’s Committee on Safety of Medicine had received over
300 reports of adverse reactions, 60 of which were serious; there were 7
deaths.[2] And yet prolonged testing in rats and dogs
showed no evidence of toxicity even when they were given five times the
human dose.[3] [1]B. Blackwell in Side Effects of Drugs Annual, vol. 8, eds M. N. G. Dukes and J. Elis (Elsevier, 1984).
[2]R. D. Mann, Modern Drug Use; An Inquiry on Historical Principles (MTP Press, 1984).
[3]R. C. Heel, et al, Drugs, 1982, vol. 24, pp.169- 206.



1984 a Milan poison control centre reported 32 patients suffering
severe neurological side-effects following an overdose with zipeprol, a
cough suppressant.[1] Symptoms included seizures and comas. Animal
testing had given no warning of severe neurological problems despite
higher doses being given to the animals that were used.[2] [1] C. Moroni, et al, Lancet, 7 January 1984, p.45.
[2] D. Cosnier, et al, Drug Research, 1976, vol. 26, pp.848-854. G. Rispat, et al, Drug Research, 1976, vol. 26, pp.523-530.


was submitted for clinical (i.e., human) trials as an antiasthmatic
after being tested on mice, rats, hamsters, rabbits, ferrets, squirrel
monkeys, cynomolgus monkeys, stump- tail monkeys and baboons. Despite
giving the animals doses many times greater than would be taken by
humans, no harmful effects were noted, including the liver.[1] However,
20% of patients participating in the trial developed symptoms of liver
damage, which prevented any further development of the drug.[2] Subsequent tests showed that liver toxicity could only be induced in
dogs.[1,2] [1]D. V. Parke, in Animals and Alternatives in Toxicity Testing, eds., M. Balls, et al (Academic Press, 1983).
[2]C. T. Easton, et al, Regulatory Toxicology and Pharmacology, 1990, vol.11 pp.288-307.

Fenclozic acid.

clinical trials (i.e., on humans), ICI’s anti-arthritic drug fenclozic
acid produced jaundice in some patients. This was unexpected as testing
which was undertaken on rats, mice, dogs and monkeys had given no hint
of liver problems.[1] Not content with these results, there were further
experiments with rabbits, guinea pigs, ferrets, cats, pigs, horses,
neonatal rats and mice, along with a different strain of rat: yet again,
no evidence of liver damage could be found.[1] The ICI
researcher commented: ‘the quite unexpected onset of jaundice in a few
patients caused withdrawal of the drug from humans and initiated a vast
programme of experimental work. This search for hepatotoxicity [liver
damage] in different species or any indication of its likelihood has so
far been unrewarding [in other words, unsuccessful].

[1]S. J. Alcock, Proceedings of the European Society for the Study of Drug Toxicity, 1971, vol. 12, pp.184-190.


1985, Britain’s Committee on Safety of Medicines issued a warning about
serious liver damage associated with the antifungal drug ketoconazole
(Nizeral).[1] The Committee referred to 82 cases, with 5 deaths. The
warnings followed a similar action by the American FDA in 1982.[2] Despite this, no evidence of liver toxicity was found in the animal testing.[3] [1]Lancet, 12 January 1985, p.121.
[2]C. B. M. Tester-Dalderup in Meyler’s Side-Effects of Drugs, 11th edn, ed. M. N. G. Dukes (Elsevier, 1988).
[3]J. K. Heiberg and E. Svejgaard, British Medical Journal, 26 September 1981, p.825.


the early part of the previous century there was interest in the
possibility that a lack of food during childhood might interfere with
the development of the brain. Regrettably almost of the research was
carried out on animals which showed that starving baby or adult rats had
no effect on the brain. The issue was abandoned and not revived until
the late 1950s when children with histories of undernutrition were found
to persistently underachieve.[1] Researchers then
realized that the earlier animal testing had not taken ‘brain growth
spurt’ into account, this being the time of fastest growth when the
brain is most vunerable. Additionally, the timing varies between the
different species, i.e., in human babies the brain growth spurt begins
during the final period of pregnancy and lasts for about a year, whereas
in guinea pigs, it occurs almost wholly during the foetal period, and
yet in rats, it occurs during the first three weeks after being born.[2] Despite
the number of starving humans in the world today, there appears to be
no shortage of funds for vivisectors who claim to be researching early
life undernutrition in animals.

[1]J. Dobbing in Early Nuitrition and Later Behaviour, ed. J. Dobbing (Academic Press, 1987).
[2]J. Dobbing and J. L. Smart, British Medical Bulletin, 1974, vol. 30, pp.154-168.


(Practolol), marketed during the 1970s, was said to be ‘particularly
notable for the thoroughness with which its toxicity was studied in
animals, to the satisfaction of the regulatory authorities’.[1] In
time, serious effects began to be noted, i.e., skin, eye and abdominal
disorders. In some cases, patients suffered blindness; sclerosing
peritonitis also occurred, resulting in 23 deaths being reported.[2] The
manufacturers (ICI) paid compensation to over 1000 victims.[3] The
side-effects of the drug (for the treatment of heart conditions) were
not predicted by the animal testing that was conducted. Moreover,
subsequent to the drug being withdrawn from the market in 1976, it has
not been possible to replicate the side- effects in laboratory
animals.[1] [1]M. Weatherall, Nature, 1 April 1982, pp.387-390.
[2]G. R. Venning, British Medical Journal, 15 January 1983, pp.199-202. 22 January 1983, pp.289-292.
[3]A Question of Balance, Office of Health Economics, 1980.
[4]F. H. Gross and W. H. Inman, Drug Monitoring (Academic Press, 1977).

Cortisone: the eye.

of the principal side-effects of treating the eye with steroids is
glaucoma (high pressure arises within the eye which can lead to loss of
sight). And yet when corticosteroids were used in ophthalmology, the
animal testing conducted indicated that cortisone did not affect the
pressure within the eye.[1] Later attempts to induce
glaucoma in monkeys and rabbits were either difficult or impossible.[2] One group of researchers admitted to: ‘the differing response of the eye
of man and animals to repeated topical [surface] application of
corticosteroids’. They added ‘Such a procedure is without effect on
tension of the eye of many experimental mammals, but increases tension
in the human eye’.[3] Another side-effect of using
steroid treatment which is difficult to replicate in the laboratory
animal is the cataract. While slight changes in the lens of the rabbit’s
eye have been produced – after repeated high doses – they do not mimic
the severity of the condition as found in humans.[2] [1]L. H. Leopold, et al, American Journal of Ophthalmology, 1951, vol. 34, pp.361-371.
[2]W. M. Grant, Toxicology of the Eye, 2nd edn (Charles Thomas, 1974).
[3]B. Ballantyne and D. W. Swanston in Current Approaches in Toxicology, ed. B. Ballantyne (Wright and Sons, 1977).

Talcum powder.

experiments, using vast amounts of talcum powder, were conducted on
animals, these suggested that using talcum powder presented no danger.
In 1977 hamsters were exposed to high grade cosmetic talc at nearly two
thousand times the amount that babies would encounter, and yet there was
no damage to the lungs.[1] Another experiment in the same year involved
rats being forced to breathe talc at doses nearly six thousand times
the amount used in infant care; despite the amount used, there was only a
slight effect on the lungs.[1] However, subsequent to
this time the medical profession had to issue warnings about using talc,
e.g. in 1991 physicians at one hospital in Southern England warned that
inhaling babies’ talcum powder could be fatal.[2] Eight deaths were
attributed to inhalation of talc.

[1]Lancet, 25 June 1977, pp.1348-1349.
[2]P. W. Pairaudean, et al, British Medical Journal, 18 May 1991, pp.1200-1201.

CS Gas.

experimentation was responsible for providing incorrect and dangerous
information about CS gas. When CR was applied to a rabbit’s eye, only
‘minor transient changes’ occurred in respect of pressure in the eye.
However, when a smaller amount was applied to a human eye, this resulted
in a 40% increase in pressure in 5 minutes – while in rabbits, this
only produced a 3% rise after 10 minutes.[1] Tests
found that human beings are 18 times more sensitive to CS than rabbits,
and 90 times more sensitive to CR, another irritant.[2] Tests
involving application to the skin showed CR was a more potent irritant
than CS and yet the very opposite was found when tested on rodents.[3] The research also determined that VAN, another sensory irritant, was
less potent than CR which, once again, was the very opposite when tested
on animals.

[1]B. Ballantyne, et al, in Current Approaches in Toxicology, ed. B. Ballantyne (Wright and Sons, 1977).
[2]D. W. Swanston in Animals and Alternatives in Toxicity Testing, eds. M. Balls, et al (Academic Press, 1983).
[3]R. W. Foster, et al, Pain, 1986, vol. 25, pp.269-278.


of the water supply is considered to be a primary reason for the
decline in dental decay. The adding of fluoride to the water supply does
not appear to have caused any health problems.[1] However,
experimentation involving rats gave some indication that it might cause
cancer,[2] and yet after an intensive study, the American DHHS (Dept.
of Health and Human Services) reported that it had not found any
evidence of fluoride causing cancer. Tests involving animals have also
suggested other detrimental effects, but the DHHS reported that
different species react divergently to fluoride and this made it
difficult to apply to humans.[3] [1]E.g., R. Peto and R. Doll, The Causes of Cancer (OUP, 1981).
[2]Journal of NIH Research, 1991, vol. 3, p.46.
[3]C. Anderson, Nature, 28 February 1991, p.732.


is obtained from the tonka bean, having been used for many years, in
consumer items and as a therapeutic agent. However, in the 1950s, there
were questions concerning its safety due to animal experimentation that
resulted in liver damage in rats. Because of this, coumarin was
prohibited as a food flavouring agent.[1] Later
research revealed there was a considerable variation in reactions by
different species, e.g. although dogs suffered liver toxicity (as rats),
there were only slight effects in baboons.[2] Furthermore those amounts
which damaged the liver of rats were harmless to gerbils.[3] The
nonsense of vivisection was further demonstrated when it was found that
different strains of the same species reacted differently to coumarin.
who receive coumarin, even in high doses, for therapeutic reasons,
rarely experience liver toxicity,[1] and rats and dogs are therefore now
viewed as unreliable models for testing the substance as they
metabolize it in totally different ways.[1,2,3] [1]J.H. Fentum, et al, Toxicology, 1992, vol. 71, pp.129- 136.
[2]J. G. Evans, et al, Food and Cosmetic Toxicology, 1979, vol. 17, pp.187-193.
[3]W. Endell and G. Seidsel, Agents and Actions, 1978, vol. 8, pp.299-302.


for those people who worked with formaldehyde arose after it was
discovered that the substance caused cancer in rats.[1] Despite this,
epidemiological studies did not give any indication of cancer arising in
such people: additionally, monitoring of workers also found no evidence
of this danger.
In fact the rats had been forced to
breathe high doses – 7-15 times the amount that workers inhaled –
resulting in formaldehyde causing tissue damage and cancers in them.

[1]P. Grasso, Journal of the Royal Society of Medicine, 1989, vol. 82, pp.470-473.

Epilepsy models.

have produced numerous methods of producing fits in laboratory animals;
the reason for this is because no particular method is wholly
trustworthy.[1] After suggestions that high amounts of
aspartame could cause seizures in some people, the London Institute of
Psychiatry conducted experiments, sponsored by Nutrasweet Company and
the Wellcome Trust, which involved flashing lights to produce fits in
photosensitive baboons. In fact aspartame had no effect on the baboons
although conflicting evidence has arisen in other animals. For example
aspartame enhances chemically-induced convulsions in mice, but has no
effect on electric-shock-induced or sound-induced seizures in these
animals.[2] Similar variations are found with different
species. Although the drug THIP reduced convulsions in mice and
baboons, it was ineffective when used with epileptic patients.[3] [1]R. S. Fisher, Research Reviews, 1989, vol. 14, pp.245- 278.
[2]B. S. Meldrum, et al, Epilepsy Research, 1989, vol. 4, pp.107.
[3]Lancet, 26 January 1985, pp.198-200.

Glass Fibre.

made from glass wool were produced for decades with animal testing
suggesting no health risk. Experiments involving rats, guinea pigs,
rabbits and monkeys who were forced to breathe in glass wool fibres
showed no damage to lungs.[1] Subsequent tests during
the 1980s confirmed ‘an increase in lung tumours or mesothelioma has not
been observed following long-term inhalation studies in several animal
species including rats, hamsters, guinea pigs, mice, monkeys and
baboons, exposed to glass fibres, glass wool or mineral wool’.[2] Those
experiments when rats developed cancer were dismissed as having no
relevance for human health. This was due to the fibres being implanted
into the membrane of the animal’s lung which is in contrast to how
humans become exposed, i.e., through breathing; additionally, rats are
known to develop cancer when solid substances are implanted in their
bodies.[1] However, in 1991 the American Occupational
Safety and Health administration declared that products made of glass
fibre were a potential cancer risk.[3] This was after studies involving
people working with glass fibre showed an increased risk of lung cancer.
In Occupational Lung Disorders, Raymond Parkes notes that ‘the
production of malignant tumours in animals by direct implantation
experiments is unlikely to have any relevance to human exposure’.

[1]Rep. in R. Parkes, Occupational Lung Disorders (Butterworths, 1982).
[2]C. S. Wheeler, Toxicology and Industrial Health, 1990, vol. 6, pp.293-307.
from G. F. Scannell, assistant secretary for OSH, Washington DC, to
Richard Munson, Chairman of Victims of Fibreglass, 6 May 1991. The
Guardian, 20 July 1991.


the 1960s, women who used the steroid Depo-Provera to deal with
premature labour found that there was a delay in returning to fertility
after their babies were born. Because of this, there was an
investigation as to whether it could be used as a contraceptive.[1] When
tested on beagle dogs there was a range of serious side- effects
including abnormal growths, breast cancer and death from pyometra (pus
building up in the uterus), and yet none of these side-effects occurred
in women who used Depo-Provera.[2] Researchers could only say that these
side-effects were due to the physiological differences between human
beings and dogs.[1] In fact high doses of Depo-Provera
can cause cancer in monkeys but the relevance of this is questioned as
the tumours arise from a type of cell not found in women. Ironically,
the type of cancer produced in monkeys is actually successfully treated
by Depo- Provera in women.[1] In 1991, the Lancet
called for certain countries to ‘reassess’ their existing policies on
Depo-Provera as they might be depriving women of a ‘reliable, effective
and safe method of contraception’.[2] Shortly afterwards, the American
FDA then approved Depo-Provera as a long-acting contraceptive for women
to use.

[1]Bulletin of the World Health Organisation, 1982, vol. 60, pp.199-210.
[2]Lancet, 5 October 1991, pp.856-857.


the late 1930s researchers discovered that the inhalation of metallic
aluminium prevented silicosis in rabbits.[1] Consequently, this was used
as a means of treating and preventing silicosis in workers,[2] who had
to pass through an aluminium dusting chamber in which they inhaled the
In the following decade, studies revealed the
process did not work and the Industrial Pulmonary Disease Committee of
Britain’s Medical Research Council advised against this procedure being
used.[3] In fact the ‘treatment’ had considerable
dangers. While large amounts of aluminium were found to be harmless to
animals,[4], lung damage and cancer were reported amongst those working
with aluminium.[5] Further studies have shown that Canadian workers who
inhaled aluminium powder to prevent silicosis, have symptoms that agree
with the idea that aluminium may produce Alzheimer’s Disease.[6] [1]J. J. Denny, et al, Canadian Medical Association Journal, 1939, vol. 40, p.213.
[2]W. R. Parkes, Occupational Lung Disorders, (Butterworths, 1982).
[3]M. C. S. Kennedy, British Journal of Industrial Medicine, 1956, vol. 13, pp.211-223.
[4]L. U. Gardner, et al, Journal of Industrial Hygiene and Toxicology, 1944, vol. 26, pp.211-223.
[5]M. J. Ellenhorn and D. G. Barceloux, Medical Toxicology (Elsevier, 1988).
[6]Lord Walton of Detchant, Journal of the Royal Society of Medicine, 1992, vol. 85, pp.69-70.

Diet and cancer.

of people of different nationalities have revealed that the consumption
of too much fat, particularly saturated fat, can lead to cancer of the
colon. In contrast, animal experimentation, while confirming excessive
fat can be dangerous, indicate that it is not saturated but
polyunsaturated fat which is responsible.[1] Clinical
(i.e., human) studies have also shown that a high fibre diet is
preferable for health but when tested on animals, there have been
conflicting results: some tests have indicated a higher risk of cancer,
whereas others suggest a lower risk.[2] Additionally, studies have shown
diets which are high in animal protein are hazardous,[3] and yet animal
testing indicates this protein is of no relevance.[2] Human
studies confirm that diets which include fruit and vegetables offer
protection against colon cancer. However, the natural substances which
fruit and vegetables have evolved to ensure protection against
predators, actually produce cancer when administered to mice and
rats.[4] [1]J. L. Freudenheim and S. Graham, Epidemiologic Reviews, 1989, vol. 11, pp.229-235.
[2]D. Galloway, Cancer Surveys, 1989, vol. 8, pp.169- 188.
[3]B. Armstrong and R. Doll, International Journal of Cancer, 1975, vol. 15, pp.617-631.
[4]P. H. Abelson, Science, 21 September 1990, p.1357.


Prednisone is a useful drug for treating leukaemia and other cancers
which occur in human beings, it does not work in respect of animal
tumours, and this includes two types of leukaemia in mice.[1] Prednisone
is even more effectual when used with other anti- cancer medications
although yet again animal experimentation provided spurious results,
i.e., of six combinations which showed an improvement in health, only
one of these was predicted by animal testing.[1] The
background of Prednisone provides further examples of animal testing
delaying effective medicine. When researchers claimed they could cure
human cancer with adrenal gland extracts in the 1930s, the result was
animal testing which was negative and the treatment was therefore
jettisoned.[2] It was only later when researchers confirmed that adrenal
extracts could be useful in combating some cancers that human trials
led to such analogues as Prednisone.

[1]R. J. Johnson and A. Goldin, Cancer Treatment Reviews, 1975, vol. 2, pp.1-31.
[2]B. Reines, Cancer Research on Animals: Impact and Alternatives, (Chicago: NAVS, 1986).


the fanciful claims made by pro-vivisectionists that polio is an
example of how vivisection can combat human illness, the reality is that
animal experimentation delayed a proper insight of polio for many
years.[1] In 1908 there was the announcement that the
polio virus had been discovered. Tissue from an infected human resulted
in spinal cord disease when injected into monkeys; the animals died with
one developing paralysis in both legs. However, negative results had
arisen with rabbits, guinea pigs, and mice and it was little more than
chance that the researchers had selected Old World monkeys which are
susceptible to the disease: if they had used New World monkeys they
would have had different results from the experimentation as these
monkeys are resistant to the disease.
Believing that a
replica of the human form was now available, researchers concentrated on
artificially inducing the disease in monkeys; these experiments gave
support for the view that the poliovirus entered the system through the
nose and it only attacked the CNS (Central Nervous System].[1,2] And
yet in 1907, a study of human cases had revealed that poliomyelitis was
not wholly a disease of the CNS, and the gastrointestinal tract was the
most likely route of the infection[1]. By 1912, other studies confirmed
the intestinal tract as the means by which infection entered the body.
because animal experimentation dominated research, most researchers, up
to 1937, rejected the view that polio was an intestinal disease. The
fact of whether the virus entered the body through the mouth or the nose
was of course of major importance as the route dictated the best action
to prevent its spread. In 1937, a nasal spray which prevented infection
in monkeys was produced; not surprisingly it failed, also sometimes
having a lasting side-effect, when it was used by human beings.[1] It
was only after the idea of the nasal route of infection, based on
animal testing, was rejected and it was recognized that the polio virus
entered the mouth and first resided in the intestines that a vaccine,
orally administered could be produced. A solution was further delayed
when monkeys were then used in time-consuming and expensive testing for
the presence of the virus; tissue was inoculated into monkeys who were
then examined for spinal cord damage. Progress was made when in 1949,
Enders, Weller and Robins showed that the polio virus could be grown in
human tissue culture; in this environment changes in infected cells,
produced by the virus, could be monitored by microscope. If this
alternative had been adopted an at earlier stage, there can be no doubt
that progress would have been quicker, and both animal and human
suffering would have been far less. However, valuable time was wasted
through vivisectors asserting that the virus could only grow in the CNS,
and the ‘monkey model’ of polio delaying the tissue culture development
which was crucial to discovering a vaccine.[1,3] [1]J. R. Paul, A History of Poliomyelitis (Yale University Press, 1971).
[2]H. F. Dowling, Fighting Infection (Harvard University Press, 1977.
[3]A Critical Look at Animal Research (Medical Research Modernization Committee, New York, 1990).


animals, i.e., guinea pigs and hamsters, are especially sensitive to
the negative effects of anti-biotic treatment. Ampicillin, Amoxycillin
and Oxytetracycline are anti- biotics widely used by human beings but
they are deemed ‘toxic’ and therefore inappropriate for guinea pigs and
hamsters.[1] In the case of the Erythromycin, the usual human dose will
kill a hamster.[2] In Drug Development: From Laboratory
to Clinic, Dr Walter Sneader noted that if guinea pigs had been used
when penicillin was first tested, this valuable treatment would have
almost certainly been abandoned as these animals are hypersensitive to
penicillin. Florey, one of the scientists who carried out animal testing
after Fleming’s discovery of penicillin , admitted: ‘If we had used
guinea pigs exclusively, we should have said that pencillin was toxic,
and we probably should not have proceeded to try and overcome the
difficulties of producing the substance for…man’.[3] Thus, this is yet
another example of how different animals provide different results in
testing, and once again shows that the use of animals can, and does,
impede medical progress.

[1]A. A. Tuffery (ed.), Laboratory Animals – An Introduction for New Experimenters, (Wiley, 1987).
single minimum recommended dose of erythromycin is 250-500mg every 6
hours, i.e., 3.5-7.0 mg/kg for a 70kg person. The lethal dose for
hamsters is 3.5mg/kg.
[3]H. Florey, Conquest, January 1953.


the first decade of the last century, epidemiology had identified a
number of causes of cancer.[1] One of the earliest observations was that
of Potts, an English surgeon who in the eighteenth century identified
soot as a carcinogen in chimney sweeps. However, attempts to replicate
his findings in animals failed,[2] although in 1918 researchers in Japan
announced that cancer could be produced – on the ear of a rabbit by
continually painting it with tar.
Progress was delayed
by a dependence upon animals: the British epidemiologist Sir Richard
Doll observes that human observational data was often dismissed because
it was felt that success would be found in the laboratory.[1] When
studies correctly reported that people who consumed high large amounts
of fruit and vegetable were less likely to develop cancer,[3] little
attention was given.[1] Due to the lack of human
epidemiological data, erroneous ideas arising from animal
experimentation abounded; although only 5% of Western cancers are
connected to viral infections,[4], e.g., some scientists believed that
most, possibly all cases, were caused by viruses, an idea which arose
from animal testing. One animal researcher even claimed that women
should not breast feed their babies because, as in mice, a virus caused
breast cancer which could be acquired in the mother’s milk.[5] After
the Second World War, there was a greater interest in epidemiology with
the realization that smoking caused lung cancer. In the years following
there has been a greater awareness that the vast majority of instances
of cancer can be prevented. Noteworthy is the 1980 US Congress Office of
Technology Assessment Report on the causes of cancer which relied more
far more on epidemiology than laboratory testing as these ‘cannot
provide reliable risk assessment’.[4] Sadly, the curse
of cancer is still very much with us and is likely to continue as long
as animal experimentation is used in attempts to find the solution.

[1]R. Doll, Cancer, 1980, vol. 45, pp.2475-2485.
[2]W. H. Woglom, Archives of Pathology, 1926, vol. 2, pp.533-576.
[3]P. Stocks and M. N. Karn, Annals of Eugenics, 1933, vol. 5, pp.237-280.
[4]R. Peto and R. Doll, The Causes of Cancer (OUP, 1981).
[5]J. Furth, Bulletin of the New York Academy of Medicine, 1964, vol. 40, pp.421-431.


(Oraflex in America), to treat arthritis, was withdrawn in August 1982
after reports of deaths and serious liver damage after people had used
the drug.[1] Since 1980, when it first appeared in the UK, there were
some 3,500 reports of adverse effects with 61 deaths, mainly involving
the elderly.[2] Researchers declared Opren was a drug
where the injuries could not be predicted from animal
experimentation,[3] and Dista, which marketed Opren in Britain
acknowledged that after Opren was studied for a year using rhesus
monkeys, ‘there were no apparent adverse effects on survival’.

[1]E. M. B. Sorensen, Toxicology Letters, 1986, vol. 34, pp.277-286.
[2]British Medical Journal, 14 August 1982, pp.459- 460.
[3]C. T. Eason, et al, Regulatory Toxicology and Pharmacology, 190, vol. 11, pp.288-307.

Stroke treatment.

on rabbits, dogs, gerbils and monkeys suggested that the use of
barbiturates could offer protection against the effects of a stroke,[1] and yet in humans, barbiturates were found to offer little or no
protection.[2] In fact between 1978 and 1988, some 25 drugs which were
found to be useful in treating animals with artificially-induced stokes
did not come into general use.[2] Some researchers have
argued that an over-reliance on animal models may impede progress in
treating the disease,[2] and Mayo Clinic researchers also acknowledged
‘the answers to many of our questions regarding the underlying
pathophysiology and treatment of stroke do not lie with continued
attempt to model the human situation perfectly in animals, but rather
with the development of techniques to enable the study of…living
humans’.[2] [1]Stroke, vol. 6, pp.28-33,
1974, vol. 5, pp.107, 1972, vol. 3, pp.726-732, Neurology, 1975, vol.
425, pp.870-874, Annals of Neurology, 1979, vol. 5, pp.59-64.
[2]D. O. Wiebers, et al, Stroke, 1990, vol. 21, pp.1-3.


new test, developed by Glaxo, raised concerns about Omeprazole, an
ulcer treatment produced by Astra, in respect of causing stomach cancer.
The test involves dosing rats with a drug/substance and then removing
tissue which is analysed for effects on the DNA. Interference with DNA
is deemed to be a possible first step to cancer.
test showed that Omeprazole damaged the DNA while it also showed that
Ranitidine (Zantac), Glaxo’s own anti-ulcer drug, did not.[1] Because of
the test result, Glaxo ended the comparative trials of Ranititide and
Omeprazole which the Lancet commented would almost certainly affect
prescription.[2] Astra responded by claiming that
Glaxo’s testing method was ‘scientifically unsound’ and the results had
‘no clinical consequences’.[3] Astra went on to say that its own tests
showed that after administering Omeprazole to rats for up to 2 years, to
mice for 18 months, and to dogs for 12 months, there was ‘no evidence
for a direct carcinogenic potential in the stomach or elsewhere’ – the
very opposite of Glaxo’s conclusion after its animal testing.

[1]B. Burlinson, et al, Lancet, 17 February 1990, p.419.
[2]Lancet, 17 February 1990, p.386.
[3]L. Ekman, et al, Lancet, 17 February 1990, pp.419- 420.

Encainide and Flecainide.

study conducted in America discovered that two drugs which were
designed to prevent irregular heart beats could cause certain types of
patients to have heart attacks. CAST (Cardiac Arrhythmia Suppression
Trial) commenced in 1987 but was concluded within two years after
physicians discovered that more deaths occurred in those patients using
encainide and flecainide than those who received a placebo (a dummy
pill).[1] These findings led to estimates that
nationally, some 3000 people may have prematurely died after using these
drugs,[2] and yet animal testing had indicated that encainide and
flecainide were safe and effective.[3] [1]CAST Investigators, New England Journal of Medicine, 10 August 1989, pp.406-412.
[2]Dr. J. Morganroth reported in Washingon Times, 26 July 1989.
B. Holmes and R. C. Heel, Drugs, 1985, vol. 29, pp.1-33. Encainide: D.
C. Harrison, et al, American Heart Journal, 1980, vol. 1090,
pp.1046-1054, and J. E. Byrne et al, Journal of Pharmacology and
Experimental Therapeutics, 1977, vol. 200, pp.147-154.

Olive Oil.

oil has been used without any noticeable ill-effect on the human body
for thousands of years.[1] And yet testing undertaken at New York
University showed that olive oil had a harmful effect when it was
applied to the skin of rats, e.g., swelling.[2] [1]M. M. Rieger and G. W. Battista, Journal of the Society of Cosmetic chemists, 1964, vol. 15, pp.161-172.
[2]E. O. Butcher, Journal of Investigative Dermatology, 1951, vol. 16, pp.85-90.

Skin tests.

and guinea-pigs are frequently used in respect of assessing irritancy;
this is despite the fact that these animals do not provide accurate
results. For example, animal experiments indicate that hypochlorite
bleach is safe for human usage as it only results in ‘slight visible
irritation’ in rabbits and guinea pigs.[1] In reality, in humans, it
causes severe skin reactions.

[1]G. A. Nixon, et al, Toxicology and Applied Pharmacology, 1975, vol. 31, pp.481-490.

Cancer and smoking.

1954, the results of an investigation into smoking was published; this
showed that the likelihood of developing lung cancer increased in
accordance with the number of cigarettes which were smoked.[1] By this
time, a number of other reports had also been published asserting much
the same thing. However researchers continued to argue that claiming
lung cancer and smoking were linked was unwarranted due to the disease
not being produced in laboratory animals.[2] In 1956,
the British Empire Cancer Campaign (the forerunner to the Cancer
Research Campaign) advised that during two years of experimentation with
mice, rabbits and other animals which involved them being exposed to
tobacco derivatives by inhalation, feeding, injection and skin painting,
none had developed cancer.[3] Consequently, due to the
negative results of the animal experimentation, health warnings about
the dangers of smoking were delayed for several years: further
experimentation showed that it was either difficult or impossible to
induce lung cancer in animals using the inhalation method.[4] [1]R. Doll and A. B. Hill, British Medical Journal, 26 June 1954, pp.1451-1455.
[2]Reported in S. Peller, Quantitative Research in Human Biology (J. Wright and Sons, 1967).
[3]Reported in E. Northrup, Science Looks at Smoking (Conrad-McCann, 1957).
[4]Lancet, 25 June 1977, pp.1348-1349. See also F. T. Gross, et al, Health Physics, 1989, vol. 56, p.256.


1907, the lung disease asbestosis (caused by breathing in asbestos) was
recognised. Although research into this condition, using animals,
commenced in 1925, most of the results were contradictory. For example,
in 1930 on the basis of the animal testing conducted, researchers
designated the chrysotile, amosite and crocidolite forms of asbestos as
harmless .[1] And yet others determined that while chrysotile caused
lung damage in guinea pigs, it did not do so in rabbits.[2] Researchers
using animals then reported that injuries caused by asbestos began to
heal when the animals were removed from the asbestos-dust
environment.[2] This is in stark contrast to humans when asbestosis
advances even after the person is no longer exposed. It was only later
that animal researchers were able to mimic this feature in animals.[3] Concern
grew when it was announced that there was a link between asbestos and
lung cancer, and yet attempts to induce cancer in animals were
unsuccessful. Because of this, even though there was considerable
evidence of the link from asbestos workers, there was doubt about the
carcinogenic effect of asbestos until the 1960s.[4,5] It was only then
that researchers could mimic the condition in animals.
Annals of the New York Academy of Sciences says that before this: ‘a
large literature on experimental studies has failed to furnish any
definite evidence for induction of malignant tumours in animals exposed
to various varieties and preparations of asbestos’.[6] [1]Reported in L. U. Gardner, Journal of the American Medical Association, 19 November 1938, pp.1925-1936.
C. Wagner, British Journal of Industrial Medicine, 1963, vol. 20,
[3]J. C. Wagner, et al, British Journal of Cancer, 1974, vol.
29,. pp.252-269.
[4]P. E. Enterline in Epidemiology and Health Risk Assessment, ed. L. Gordis (OUP, 1988).
[5]P. E. Enterline. American Review of Respiratory Diseases, 1978, vol. 118, pp.975-978.
[6]W. E. Smith, et al, Annals of the New York Academy of Sciences, 1965, vol. 132, pp.456-488.


anti-inflammatory medication became available in Britain during the
mid-1960s but had to be withdrawn within two years after deaths
occurred; the primary cause being liver damage.
happened despite ‘extensive’ animal testing in which mice, rats and dogs
were used; these showed no indication of liver damage (apart from a
slight effect in rats exposed to a lethal dose).[1] Dr
M. F. Cuthbert of the British Department of Health and Social Security’s
Medicine Division admitted: ‘Evidence of liver damage is sometimes
detected in animal studies of non-steroidal anti- inflammatory drugs,
but usually no such evidence is forthcoming even in circumstances when a
drug is eventually shown to be hepatotoxic [liver-damaging] to man’.[1] [1]M. F. Cuthbert, Current Approaches in Toxicology, ed. B. Ballantyne (Wright and Sons, 1977).

Fialuridine (FIAU).

at America’s National Institutes of Health of a new drug to combat
hepatitis B were halted in the Summer of 1993 after complications and
deaths occurred among those involved in the trials. Although fialuridine
was supposed to improve the condition of persons suffering from liver
disease, many of those who had prolonged treatment experienced a
deterioration in their health; some died from liver failure.[1] And
yet the drug was found to be safe in animal experiments,[1] reducing
the amount of the virus in the preferred animal model used; tests for
toxicity were also conducted in mice, rats and rhesus monkeys. Indeed
one of the principal investigators asked: ‘Why didn’t the animal
toxicity studies show any abnormality at all due to the drug?’.[2] In fact the metabolism of anti-viral drugs is considered to be very different in animals and humans.[3].

[1]N. Touchette, The Journal of NIH Research, 1993. 5, pp.33-55.
[2]J. Hoofnagle, reported in [1].
[3]C. Macilwain, Nature, 22 July 1993, p.275.

Hytrin (Abbott Laboratories Ltd)

Containing terazosin as terazosin hydrochloride.
Use: Hytrin is indicated in the treatment of mild to moderate hypertension.
warnings etc: Carcinogenicity: Hytrin has been shown to produce tumours
in male rats when administered at a high dose over a long period of
time. No such occurrences were seem in a similar study in mice. The
relevance of these findings with respect to the clinical use of the drug
in man is unknown.

Losec (Astra Pharmaceuticals Ltd)

Contains omeprazole as enteric-coated granules.
Treatment of reflux oesophagitis. Treatment of duodenal and benign
gastric ulcers including those complicating NSAID therapy.
warnings, etc: Animal toxicology: Gastric ECL-cell hyperplasia and
carcinoids, localised to the oxyntic mucosa, have been observed in
life-long studies in rats. These changes have been related to sustained
hypergastrinaemia secondary to acid inhibition, and not from a direct
effect of any individual drug. No treatment related mucosal changes have
been observed in patients treated continuously for periods up to 5

Dtic-dome (Bayer plc)

Active ingredient: 5-(3,3-dimethyl-1-triazeno) imidazole-4-carboxamide prepared as the citrate salt (dacarbazine).
Use: metastatic malignant melanoma, sarcoma, Hodgkin’s disease.
warnings, etc: Studies have demonstrated this agent to have a
carcinogenic and teratogenic effect when used on animals.

Ridaura Tiltab tablets (Bencard)

Containing 3 mg auranofin.
In the management of adults with active progressive rheumatoid
arthritis only when non-steroidal anti-inflammatory drugs have been
found to be inadequate alone to control the disease, i.e. when
second-line therapy is required.
warnings, etc: Gold has been shown to be carcinogenic in rodents
although there was no evidence of carcinogenicity in 7 year dog studies.

Bezalip (Boehringer Mannheim UK (Pharmaceuticals) Ltd)

Contains bezafibrate.
Use: In hyperlipidaemias of Type 11a, 11b, 111, 1V and V.
warnings, etc: Warnings: The chronic administration of a high dose of
bezafibrate to rats was associated with hepatic tumour formation in
females. This dosage was in the order of 30 to 40 times the human
dosage. No such effect was apparent at reduced intake levels
approximating more closely to the lipid-lowering dosage in humans.
note: Drug companies often excuse animal results by claiming that the
dosage used in animal tests was far higher than that used in human
beings. If such studies are irrelevant because of the high dosage then
why do them?)

Spiroctan (Boehringer Mannheim UK)

Contains spironolactone
Spiroctan is recommended for the treatment of congestive cardiac
failure, cirrhosis with ascites and oedema, malignant ascites, nephrotic
syndrome and also for diagnosis and treatment of primary
Contra-indications, warnings, etc:
Carcinogenicity: Spironolactone has been shown to produce tumours in
rats when administered at high doses over a long period of time. The
significance of these findings with respect to clinical use is not

Bicnu (Bristol-Myers Pharmaceuticals)

Contains a 30 ml vial containing 100 mg carmustine and a 5 ml vial containing 3 ml sterile ethanol diluent.
BiCNU is indicated as palliative therapy as a single agent or in
established combination therapy with other approved chemotherapeutic
agents in the following:
1. Brain tumours – Glioblastoma, brainstem glioma, medulloblastoma, astrocytoma, ependymoma, and metastatic brain tumours.
2. Multiple myeloma – in combination with prednisone.
Hodgkin’s Disease – As secondary therapy in combination with other
approved drugs in patients who relapse while being treated with primary
therapy, or who fail to respond to primary therapy.
4. Non-Hodgkin’s lymphomas – As secondary therapy as above.
warnings, etc: BiCNU is carcinogenic in rats and mice, producing a
marked increase in tumour incidence in doses approximating those
employed clinically.

Apresoline (Ciba Laboratories)

Contains Hydralazine Hydrochloride.
Use: Hypertension
warnings etc: Warnings: Hydralazine, in lifetime carcinogenicity
studies, caused, towards the end of the experiments, small but
statistically significant increases in lung tumours in mice and in
hepatic and testicular tumours in rats. These tumours also occur
spontaneously with fairly high frequency in aged rodents.
due consideration of these animal and in-vitro toxicological findings,
hydralazine in therapeutic doses does not appear to bear a risk that
would necessitate a limitation of its administration. Many years of
clinical experience have not suggested that human cancer is associated
with hydralazine use.

Tolectin 200/400 Mg capsules (Cilag Ltd)

Contains tolmetin sodium dihydrate.
Use: Rheumatoid arthritis,; osteoarthritis; ankylosing spondylitis; peri-articular disorders such as fibrositis and bursitis.
warnings, etc: Renal papillary necrosis has occurred in animals after
long term administration although there has been no evidence of renal
toxicity in clinical trials.

Chendol 125, and Chendol 250 (CP Pharmaceuticals)

Contains chenodeoxycholic acid.
For dissolution of radiolucent cholesterol-rich gallstones in
functioning gall bladders. It has a particular place where surgery is
contra-indicated or those patients anxious to avoid surgery.
warnings, etc: Precautions: Chenodeoxycholic acid, given in long term
studies at doses of 600 mg/kg/day to rats and 1000 mg/kg/day to mice,
induced malignant liver cell tumours in female rats and male mice. The
clinical significance of these findings is not known.

Normax (Evans Medical Ltd)

Contains danthron docusate sodium.
Constipation in geriatric practice. Analgesic-induced constipation in
terminally ill patients of all ages. Constipation in cardiac failure and
coronary thrombosis (conditions in which defaecation must be free of
Contra-indications, warnings, etc:
Precautions: In experimental animals, danthron has been associated with
adenocarcinomas in the bowel and tumours in the liver.

Farlutal (Farmitalia Carlo Erba Ltd)

Contains medroxyprogesterone acetate.
Palliative treatment of hormone-sensitive malignancies. Farlutal has
been successfully used to produce regressions in breast, endometrial,
prostatic and renal cell carcinoma.
warnings, etc: Precautions: It should be noted that long term
administration of medroxyprogesterone acetate to beagle dogs has
resulted in the development of mammary nodules which were occasionally
found to be malignant. The relevance of these findings to humans has,
however, not been established.

Pharmorubicin rapid dissolution (Farmitalia Carlo Erba Ltd)

Contains epirubicin hydrochloride with lactose and hydroxybenzoate.
Use: Antimitotic and cytotoxic.
warnings, etc: Like most other anticancer agents, epirubicin has shown
mutagenic and carcinogenic properties in animals.

Zavedos (Farmitalia Carlo Erba Ltd)

Contains idarubicin hydrochloride with lactose.
Use: Antimitotic and cytotoxic agent.
warnings, etc: Warnings: Like most other cytotoxic agents, idarubicin
has mutagenic properties and it is carcinogenic in rats.

Tegretol (Geigy Pharmaceutical)

Active ingredient: Carbamazepine.
Use: Epilepsy generalised tonic-clonic and partial seizures.
warnings, etc: Precautions: In rats treated with carbamazepine for two
years, the incidence of tumours of the liver was found to be increased.
There is, however, no evidence to indicate that this observation has any
significant bearing on the therapeutic use of the drug.

Grisovin tablets (Glaxo Laboratories Ltd)

Contain griseofulvin.
The treatment of fungal infections of the skin, scalp, hair or nails
where topical therapy is considered inappropriate or has failed.
warnings etc: Precautions: Long term administration of high doses of
griseofulvin with food has been reported to induce hepatomas in mice and
thyroid tumours in rats but not hamsters. The clinical significance of
these findings is not known.

Lasilactone capsules (Hoechst)

Contain Frusemide and Spironolactone.
In the treatment of resistant oedema where this is associated with
secondary hyperaldosteronism; conditions include chronic congestive
cardiac failure and hepatic cirrhosis.
warnings, etc: Carcinogenicity: Spironolactone has been shown to
produce tumours in rats when administered at high doses over a long
period of time. The significance of these findings with respect to
clinical use is not certain.

Atromid (ICI Pharmaceuticals)

Contains Clofibrate.
Use: In the treatment of severe hyperlipoproteinaemia where full investigation has been performed to define the abnormality.
warnings, etc: Clofibrate has been shown to produce liver tumours in
rats and mice. The liver changes found in rodents have not been seen in
other species, including sub-human primates and man. The relevance of
this finding to man has not been established.

Nolvadex, Nolvadex – D, and Nolvadex – Forte tablets (ICI Pharmaceuticals)

Containing Tamoxifen Citrate.
Use: The treatment of breast cancer and the treatment of anovulatory infertility.
warnings, etc: Gonadal tumours in mice and liver tumours in rats
receiving tamoxifen have been reported in long-term studies. The
clinical relevance of these findings has not been established.

Zoladex (ICI Pharmaceuticals)

Containing goserelin acetate.
1. Prostate cancer.
2. Advanced breast cancer in pre- and peri-menopausal women suitable for hormonal manipulation.
3. Endometriosis.
warnings, etc: General: Following long-term repeated dosing with
Zoladex, an increased incidence of benign pituitary tumours has been
observed in male rats. Whilst this finding is similar to that previously
noted in this species following surgical castration, any relevance to
man has not been established.
In mice, long term
repeated dosing with multiples of the human dose produced histological
changes in some regions of the digestive system manifested by pancreatic
islet cell hyperplasia and a benign proliferative condition in the
pyloric region of the stomach, also reported as a spontaneous lesion in
this species. The clinical relevance of these findings is unknown.

Novantrone injection (Lederle Laboratories)

Contains mitozantrone hydrochloride.
For the treatment of advanced breast cancer, non-Hodgkin’s lymphoma and
adult acute non-lymphocytic leukaemia. Novantrone has also been used in
the palliation of non-resectable primary hepatocellular carcinoma.
warnings, etc: Warnings: Novantrone is mutagenic in vitro and in vivo
in the rat. In the same species there was a possible association between
administration of the drug and development of malignant neoplasia. The
carcinogenic potential in man is unknown.

Prostap SR (Lederle Laboratories)

Contains leuprorelin acetate.
In the treatment of advanced prostatic cancer and the management of
endometriosis, including pain relief and reduction of endometriotic
Contra-indications, warnings, etc: Warnings:
Men: Whilst the development pituitary adenomas has been noted in chronic
toxicity studies at high doses in some animal species, this has not
been observed in long term clinical studies with Prostap.

Thiotepa (Lederle Laboratories)

Contains Thiotepa (N,N’,N» triethylenethiophosphoramide)
A polyfunctional alkylating agent used alone or in combination with
other cytotoxic drugs, hormones, radiotherapy or surgery in the
treatment of neoplastic diseases.
warnings, etc: Thiotepa has been reported to possess mutagenic activity
on the basis of bacterial, plant and mammalian mutagenicity tests. It
has also been reported to be carcinogenic in mice and rats. These
effects are consistent with its activity as an alkylating agent. The
carcinogenic potential in humans has not been clearly established.

Celace (Eli Lilly and Co Ltd)

Contains pergolide base.
Use: Adjunctive treatment to levodopa in the management of the signs and symptoms of Parkinson’s disease.
warnings, etc: Carcinogenesis, mutagenesis and impairment of fertility:
Two year carcinogenicity studies in mice and rats used doses up to 340
and 12 times the maximum human oral dose (6 mg or 6000 micrograms/day
equivalent to 120 micrograms/kg/day). A low incidence of uterine
neoplasms occurred in both rats and mice. Endometrial adenomas and
carcinomas were observed in rats. Endometrial sarcomas were observed in
mice. These occurrences are probably attributable to the high
oestrogen/progesterone ratio, which would occur in rodents as a result
of the prolactin-inhibiting action of pergolide mesylate.
endocrine mechanisms are not present in humans. However, there are no
human data with pergolide to substantiate this conclusion concerning the
lack of potential for human risk.
Mutagenic potential
was evaluated in a battery of tests. A weak response was noted in one
test but the other 3 tests were negative. The relevance to humans is

Seconal Sodium (Eli Lilly and Co Ltd)

Contains Secobarbitone Sodium.
Use: For the short-term treatment of severe, intractable insomnia.
warnings, etc Carcinogenesis: Animal data show that phenobarbitone can
be carcinogenic after lifetime administration.

Sodium Amytal Injections (Eli Lilly and Co Ltd)

Contains Amylobarbitone Sodium.
May be used parenterally to control status epilepticus, but it is not
the barbiturate of choice in the routine treatment of grand mal
Contra-indications, warnings, etc:
Carcinogenesis: Animal data show that phenobarbitone can be carcinogenic
after lifetime administration.

Destolit (Marion Merrell Dow Ltd)

Contains ursodeoxycholic acid.
For the dissolution of radiolucent (i.e. non-radio opaque) cholesterol
gallstones in patients with a functioning gallbladder.
warnings, etc: A product of this class has been found to be
carcinogenic in animals. The relevance of these findings to the clinical
use of ursodeoxycholic acid has not been established.

Sabril tablets (Marion Merrell Dow Ltd)

Contains vigabatrin.
Use: For the treatment of epilepsy which is not satisfactorily controlled by other antiepileptic drugs.
warnings, etc: Warning: Animal safety studies indicate that vigabatrin
causes intramyelinic oedema in the brain white matter tracts. Currently
there is no evidence to suggest that this effect occurs in man.

Dolobid (Thomas Morson Pharmaceuticals)

Contains Diflunisal.
Use: For the relief of pain and also inflammation associated with osteoarthritis and rheumatoid arthritis.
warnings, etc: Precautions: In rats and dogs, high oral doses of
diflunisal (50-200 mg/kg/day) as with aspirin, produced similar
pathological changes (gastro-intestinal ulceration and renal papillary
oedema). These dosages are approximately 3 to 12 times the maximum
dosages recommended in man.

Ortho dienoestrol cream (Ortho)

Contains Dienoestrol.
Atrophic vaginitis and kraurosis vulvae in post menopausal women, and
for the treatment of pruritus vulvae and dyspareunia when associated
with the atrophic vaginal epithelium.
warnings, etc: Long term continuous administration of natural and
synthetic oestrogens in certain animal species increases the frequency
of carcinomas of the breast, cervix, vagina and liver. There is now
evidence that oestrogens increase the risk of carcinoma of the
endometrium in humans.
At the present time there is no
satisfactory evidence that oestrogens given to post-menopausal women
increase the risk of cancer of the breast, although a recent long-term
follow up of a single physician has raised this possibility. However,
because of animal data there is a need for caution in prescribing
oestrogens for women with a strong family history of breast cancer or
who have breast nodules, fibrocystic disease, or abnormal mammograms.
Note: Do oestrogens only increase the risk of cancer in female animals
who have a strong family history of breast cancer, or who have breast
nodules, fibrocystic disease or abnormal mammograms?).

Retin-a Lotion, Gel, Cream (Ortho)

Contains Tretinoin.
Use: For topical application in the treatment of acne vulgaris in which comedones, papules and pustules predominate.
warnings, etc: Recent studies in mice treated with the active
ingredient (tretinoin) of Retin-A and exposed to artificial sunlight
suggest that tretinoin may speed up the appearance of sunlight induced
skin tumours. Laboratory mice treated with tretinoin but not exposed to
sunlight did not develop skin tumours. The significance of these studies
as related to human beings is unknown. High oral doses of tretinoin
(retinoic acid), like Vitamin A, are teratogenic in animals.

Lopid (Parke-Davis Research Laboratories)

Contains gemfibrozil and polysorbate 80 PhEur.
For the primary prevention of coronary heart disease in men between
40-55 years of age and with hyperlipidaemias who have not responded to
diet and other appropriate measures.
warnings, etc: Precautions: Long-term toxicity studies in rats and mice
were carried out at one and ten times the human dose on a weight for
weight basis. In male rats receiving ten times the human dose, there was
a significant increase in incidence of benign liver nodules and liver
carcinomas. Male rats receiving a dose equivalent to the human dose had
no statistically significant increase in the incidence of liver
carcinomas. At all dose levels, there were no statistically significant
differences from controls in the incidence of liver tumours in female
rats, or in mice of either sex.
Electron microscopy
demonstrated a marked hepatic peroxisome proliferation following Lopid
administration to the male rat. Similar changes have been sought but not
found in the human liver at up to 27 months continuous gemfibrozil
therapy. Male rats had a dose-related increase of benign Leydig cell
tumours. Subcapsular bilateral cataracts occurred in 10%, and unilateral
cataracts in 6.3% of the high dose males.

Mithracin (Pfizer Ltd)

Contains plicamycin, mannitol and disodium phosphate.
Use: For the treatment of refractory hypercalcaemia associated with a variety of neoplasms.
warnings, etc: Warnings: Antineoplastic and cytotoxic agents have been
shown to be mutagenic and carcinogenic in animals and possibly man.
limited animal and in vitro mutagenicity studies have been carried out
with plicamycin; the possibility that plicamycin has similar effects to
other antineoplastic cytotoxic agents should be borne in mind.

Calcitare (Rhone-Poulenc Rorer Ltd)

Contains Calcitonin (Pork).
Use: For short term treatment in:
i) Paget’s disease of bone
ii) Hypercalcaemia.
warnings, etc: A species and strain-specific dose-related increase of
pituitary adenomas has been observed in long term toxicity studies in
the rat. As the significance of these findings to man is uncertain, long
term use is not recommended.

Calsynar (Rhone-Poulenc Rorer Ltd)

Contains synthetic Salmon Chloride. The solution also contains Sodium Chloride, Sodium Acetate, Acetic Acid and Phenol.
Use: For the short term treatment of:
a) Paget’s disease of bone.
b) Advancing osteolytic hypercalcaemia of malignancy.
c) Pain associated with advanced metastatic bone cancer.
d) Postmenopausal osteoporosis.
warnings, etc: Precautions: Rat carcinogenicity studies have shown a
dose related excess of pituitary tumours. As the significance of this
finding is uncertain, long term use is not recommended.

Roaccutane (Roche Products Ltd)

Contains isotretinoin.
For the treatment of cystic and conglobate acne and severe acne which
has failed to respond to an adequate course of a systemic antimicrobial
Contra-indications, warnings, etc: Precautions:
At the completion of a lifespan study in rats there was an increased
incidence of phaeochromocytoma in animals given isotretinoin at dosages
of 32 and 8 mg/kg/day, but not 2 mg/kg/day. Since rats are particularly
prone to develop this tumour type, the significance of this finding for
use of Roaccutane in man is uncertain; nevertheless, repeated courses of
treatment are not normally recommended.

Negram (Sanofi Winthrop)

Contains Nalidixic Acid.
Use: For the treatment of acute or chronic infections.
warnings, etc: Nalidixic acid has been shown to induce lesions in
weight-bearing joints of young animals. The relevance of this to man is

Androcur (Schering Health Care)

Contains cyproterone acetate.
Use: Control of libido in severe hypersexuality and/or sexual deviation in the adult male.
warnings, etc: Warnings/side-effects: Cyproterone acetate has been
found to cause liver abnormalities in animals, including the development
of tumours.

Cyprostat (Schering Health Care)

Contains cyproterone acetate.
Use: Palliative treatment of prostatic carcinoma.
warnings, etc: Cyproterone acetate has been found to cause liver
abnormalities in animals, including the development of tumours.

Dianette (Schering Health Care)

Contains anti-androgen cyproterone acetate and oestrogen ethinyloestradiol.
In women only: (i)severe acne, refractory to prolonged oral antibiotic
therapy and (ii)idiopathic hirsutism of mild to moderate degree.
warnings, etc: Warnings: Like many other steroids, cyproterone acetate,
when given in very high doses and for the majority of the animal’s
life-span, has been found to cause an increase in the incidence of
tumours, including carcinoma, in the liver of rats. The relevance of
this finding to humans is unknown. Dianette has been shown to have good
liver tolerance in women given prolonged treatment.

Aldactide (Searle)

Contains Spironolactone and Hydroflumethiazide.
Use: Congestive cardiac failure.
warnings, etc – Warnings: Carcinogenicity: Spironolactone has been
shown to produce tumours in rats when administered at high doses over a
long period of time. The significance of these findings with respect to
clinical use is not certain.

Cytotec (Searle)

Contains misprostol
for the healing of duodenal ulcer and gastric ulcer including those
induced by non steroidal anti inflammatory drugs (NSAID) in arthritic
patients at risk, whilst continuing their NSAID therapy.
information: Cytotec in multiples of the recommended therapeutic dose
in animals has produced gastric mucosal hyperplasia. This characteristic
response of E prostaglandins reverts to normal on discontinuation of
the compound. In patients, histological examination of gastric biopsies
taken before and after treatment with misoprostol after up to one year’s
duration have shown no adverse tissue response attributable to

Napratec (Searle)

Contains Naproxen and Cytotec (containing misoprostol)
Naproxen is indicated for the treatment of rheumatoid arthritis,
osteoarthritis (degenerative arthritis) and ankylosing spondylitis.
Cytotec is indicated for the prophylaxis of nonsteroidal
anti-inflammatory drug induced gastroduodenal ulceration.
information: Cytotec in multiples of the recommended therapeutic dose
in animals has produced gastric mucosal hyperplasia. This characteristic
response of E prostaglandins reverts to normal on discontinuation of
the compound. In patients, histological examination of gastric biopsies
taken before and after treatment with misoprostol after up to one year’s
duration have shown no adverse tissue response attributable to

Dolmatil tablets (E. R. Squibb and Sons Ltd)

Contains sulpiride (and hydrated silica, lactose, magnesium stearate, methyl cellulose, potato starch, talc).
Use: Acute and chronic schizophrenia.
warnings, etc: Warnings: In long term animal studies with neuroleptic
drugs, including sulpiride, an increased incidence of various endocrine
tumours (some of which have occasionally been malignant) has been seen
in some but not all strains of rats and mice studied. The significance
of these findings to man is not known; there is no evidence of an
association between Dolmatil use and tumour risk in man.

Chenofalk (Thames Laboratories Ltd)

Contains chenodeoxycholic acid (CDCA). (And gluten).
Use: Dissolution of radiolucent gallstones measuring up to 15 mm diameter.
warnings, etc: Warnings: Chenodeoxycholic acid given in long-term
studies at doses of 600 mg/kg/day to rats and 1000 mg/kg/day to mice,
induced malignant liver cell tumours in female rats and benign liver
cell tumours in female rats and male mice. The clinical significance of
these findings is not known.

Ursofalk (Thames Laboratories Ltd)

Contains ursodeoxycholic acid (UDCA) and gluten.
Use: Dissolution of radiolucent gallstones measuring up to 15 mm diameter.
warnings, etc: A product of this class has been found to be
carcinogenic in animals. The relevance of these findings to the clinical
use of UDCA has not been established.

Sulpitil (Tillotts Laboratories)

Contains sulpiride.
Use: For the treatment of acute and chronic schizophrenia.
warnings, etc: Warnings and precautions: In long term animal studies
with neuroleptic drugs, including sulpiride, an increased incidence of
various endocrine tumours, some of which have occasionally been
malignant, has been seen in some, but not all, strains of rats and mice
studied. The significance of these findings to man is not known. There
is no current evidence of an association between neuroleptic use and
tumour risk in man.

Depo-Provera (Upjohn Ltd)

Contains medroxyprogesterone acetate.
Use: Progestogen: for the treatment of endometriosis.
warnings, etc: Warnings, precautions, side-effects: Endometrial tumours
have developed in monkeys given fifty times the human contraceptive
dose but the relevance of this to man has not been established.

Hemabate Sterile Solution (Upjohn Ltd)

Contains carboprost as the tromethamine salt.
Treatment of post-partum haemorrhage due to uterine atony and
refractory to conventional methods of treatment with oxytocic agents and
ergometrine used either alone or in combination.
warnings, etc: Precautions: Animal studies lasting several weeks at
high doses have shown that prostaglandins of the E and F series can
induce proliferation of bone.

Prostin E2 (Upjohn Ltd)

Contains dinoprostone.
Use: Oxytocic agent.
For the induction of labour when there are no foetal or maternal contra-indications.
warnings, etc: Precautions: Animal studies lasting several weeks at
high doses have shown that prostaglandins of the E and F series can
induce proliferation of bone.

Myleran tablets (Wellcome Medical Division)

Contains Busulphan.
Use: For the palliative treatment of the chronic phase of chronic granulocytic leukaemia.
warnings, etc: Precautions: Busulphan has been shown to be mutagenic in
various systems, including bacteria, fungi, Drosophila and cultured
mouse lymphoma cells. In vivo cytogenetic studies in rodents have shown
an increased incidence of chromosome abberations in both germ cells and
somatic cells after busulphan treatment.
NB. Busulphan interferes with spermatogenesis in experimental animals.

Retrovir capsules and syrup (Wellcome Medical Division)

Contains zidovudine.
Use: For the management of patients with advanced HIV disease.
warnings, etc: Mutagenicity: Zidovudine was weakly mutagenic in a mouse
lymphoma cell assay and was positive in an in vitro cell transformation
assay. Clastogenic effects (chromosome damage) were observed in an in
vitro study in human lymphocytes and in in- vivo oral repeat dose
micronucleus studies in rats and mice. An in vivo cytogenetic study in
rats did not show chromosomal damage. The clinical significance of these
findings is unclear.
Carcinogenicity: Zidovudine was
administered orally at three dosage levels to separate groups of mice
and rats (60 females and 60 males in each group). Initial single daily
doses were 30, 60 and 120 mg/kg/day and 80, 220 and 600 mg/kg/day in
mice and rats respectively. The doses in mice were reduced to 20, 30 and
40 mg/kg/day after Day 90 because of treatment-related anaemia, whereas
in rats only the high dose was reduced (to 450 and then 300 mg/kg/day
on Days 91 and 279, respectively).
In mice, seven
late-appearing (after 19 months) vaginal neoplasms (5 squamous cell
carcinomas, one squamous cell papilloma and one squamous cell polyp)
occurred at the highest dose. One late-appearing squamous cell papilloma
occurred in the vagina of a middle-dose animal. No vaginal tumours were
found at the lowest dose.
In rats, two late-appearing
(after 20 months) vaginal squamous cell carcinomas occurred in animals
given the highest dose. No vaginal tumours occurred at the middle or low
doses in rats.
The predictive value of rodent
carcinogenicity studies for humans is uncertain and thus the clinical
significance of these findings is unclear.

In addition to the general warnings I have recorded above
there are many drug companies which warn doctors not to give specific
products to patients who are pregnant. These companies invariably report
having performed experiments on pregnant animals but then often go on
to admit (something like): ‘the relevance of these studies to human
beings is not known’. It is difficult to avoid asking the question: ‘Why
do the studies if the relevance is not known?’ As can be seen from the
above, a huge number of drug companies seem to be doing animal tests
without knowing their relevance to human patients.

other occasions drug companies report that animal experiments have
shown that their drugs cause problems – but that human experience
suggests that the drug is entirely safe so the animal experiments can be
safely ignored! Animal experiments provide answers for all seasons. It
is not surprising that drug companies love them.

some of the examples which follow drug companies seem uncertain about
the significance of the animal experiments which have been done. If the
relevance of the animal experiments is not known or the experiments
cannot be relied upon then why on earth does anyone do them? Just as
puzzling are the many instances where drug companies state that animal
experiments have not indicated that there will be any problems if their
drugs are given to pregnant women – but still advise doctors against
giving those drugs to pregnant women.

short sections are intended only to illustrate the point I want to make
and are not intended to provide useful information about the drugs

Dr Vernon Coleman.


– PARTE 1: Extracts from Science on Trial: The Human Cost of Animal Experiments, by Dr Robert Sharpe (Awareness, 1994)
– PARTE 2: Extracts from Betrayal of Trust, by Dr Vernon Coleman: European Medical Journal.

Ambas partes fueron extraidas en 2009/2010 de la siguiete web: The errors of vivesection, que ya no está online.


– prescriptiondrugs.procon.org – 35 FDA-Approved Prescription Drugs Later Pulled from the Market

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