Animal Aid

In this first main section of the Bred to Suffer report, we look at physical/chemical manipulation in medical research, including cancer, AIDS, epilepsy and diabetes research.

Heart disease

The most common cause of heart disease in people is atherosclerosis (cholesterol deposition on artery walls). This leads to bottlenecks in blood flow, thereby restricting oxygen supply, raising blood pressure and, ultimately, culminating in a heart attack.

Dogs are often the model of choice for research into heart disease although 'it is virtually impossible to produce atherosclerosis in a dog' even when vast amounts of cholesterol and saturated fat are added to their diet. (5)(6) or blocked by plastic plugs. The most obvious cure for the condition in humans is to lower cholesterol levels but this would clearly have no effect in such a model, which is therefore of no real relevance.

Of course, a great deal of heart disease is avoidable and the money spent on such expensive treatments as bypass surgery would be far more profitably invested in strategies such as health and nutrition education. According to the National Heart Forum, if current knowledge were to be put into policy action, death and disability from avoidable coronary heart disease among people under 65 could be virtually eliminated. 'Inaction now creates a public health time bomb for future generations.' (7)

Artificial strokes are induced in cats by blocking arteries in their brains, (8) which clearly gives no useful insight into the cause of a stroke.

The damage caused by a stroke can be reduced if treatment is received quickly enough. All the currently accepted treatments, such as anti-clotting medications, have been identified in people, while animal experiments have an abysmal record of predicting useful treatments. Researchers at the Mayo clinic concluded that 'over-reliance upon such animal models may impede rather than advance scientific progress in the treatment of this disease'. (9)

Again, prevention is far more valuable than cure, and most strokes could be avoided by improvements in diet and exercise. In fact, it has been calculated that the incidence of strokes could be cut by 39% through a daily reduction of 3 grams of salt in an individual's diet. (10)

But, even in supposedly equivalent cancers, there are major differences between species that invalidate the models. In fact, it is true to say that the lack of success in finding treatments for cancer in humans is because the research effort has been concentrated in animals. Thomas E. Wagner, senior scientist at Ohio University's Edison Biotechnology Institute, remarked: 'God knows we've cured mice of all sorts of tumours. But that isn't medical research.' (11) And according to Dr Albert Sabin, developer of the polio vaccine, 'Giving cancer to laboratory animals has not and will not help us to understand the disease or to treat those persons suffering from it... Laboratory cancers have nothing in common with natural human cancers'. (12)

When it comes to curing these experimental tumours, the animal models turn out to be of little value. For every 30-40 drugs effective in treating mice with cancer, only one is effective in people. (13) This problem is inherent in all research using animals because 'for the great majority of disease entities, the animal models either do not exist or are really very poor'. (14)

Animal responses to carcinogens are so different from ours that it took 50 years to induce lung cancer in laboratory animals forced to breathe tobacco smoke, (15) thus delaying the health warning to humans and resulting in millions more unnecessary deaths. The following words from Dr Irwin Bross, former director of the largest cancer research institute in the world - the Sloan-Kettering, say it all: 'While conflicting animal results have often delayed and hampered advances in the war on cancer, they have never produced a single substantial advance either in the prevention or treatment of human cancer.' (16)

Tens of thousands of primates and other animals, notably cats, have been consumed in AIDS research over the past 20 years. This is despite the fact that infecting animals, even chimpanzees, with HIV does not produce an equivalent disease to human AIDS. The immune systems of different primate species are so diverse that data from one species does not even translate to another species, much less to humans. 'SIV in monkeys is not the same as HIV in humans.' (17) This has long been recognised by many in the research community and by AIDS activists, who have campaigned hard against futile vaccine research in monkeys. Leading AIDS researcher Dr Mark Feinberg puts it thus, 'What good does it do you to test something [a vaccine] in a monkey? You find five or six years from now that it works in the monkey, and then you test it in humans and you realise that humans behave totally differently from monkeys, so you've wasted five years.' (18)

Everything we know about HIV and AIDS has been learned from studying people with the disease, through epidemiology and in vitro research on human blood cells, which is where the virus operates and, therefore, where it needs to be studied. 'It is now clear... that a strategy for an effective HIV vaccine can be devised only with a thorough understanding of the biology of HIV and the immunopathogenesis of AIDS.' (19)

According to Dr Ray Greek, President of Americans For Medical Advancement, 'Far too frequently animal models have been used to develop vaccines that are effective in laboratory animals but are ineffective or worse, harmful, in humans. AIDS is a terrible illness, and research money and personnel need to be directed toward methodologies that are viable. Using an archaic methodology like animal models to combat a 21st century disease is more than foolish, it is immoral.' (20)

For example, scientists at the Kennedy Institute of Rheumatology in London operated on beagles to induce surgically symptoms of osteoarthritis, which was then allowed to develop for six months until the dogs were killed for analysis of their cartilage. (21) Even one of the scientists conducting the research acknowledged that animal cartilage differs from human cartilage in important ways and that studying human surgical specimens is preferable. (22) There is no shortage of these!

Rodent 'models' of the disease are produced by injecting the animals with a chemical called streptozotocin, which damages the insulin-producing cells in their pancreas. But 'diabetic' rats and mice bear little relation to humans with diabetes, in that they do not require insulin to survive. Some 'models' do not even have raised levels of glucose in their blood - a hallmark of the human disease. Regardless, many researchers are studying numerous animal 'models', even while acknowledging that 'they differ markedly from the human disease'. (23)

The more common Type 2 diabetes usually affects overweight people in later life. Dramatic improvements in their condition can be made through dietary control and exercise, which can also significantly reduce the chances of getting the disease in the first place. Its incidence is projected to double in the next ten years, so the need for preventive strategies is urgent. Sadly, research into these important factors has been neglected in favour of the search for treatments effective in animals. One such medication, Rezulin, was launched on to the market in 1997 after its success in treating 'diabetic' animals, only to be withdrawn three years later when it was found to cause liver failure and had killed 391 people. (24)

Despite these technological advances, animal models of ageing and associated neurological disorders are a large and rapidly growing area of research worldwide, even though many experts agree that 'there is no successful animal model of Alzheimer's Disease'. (25) The experiments are particularly crude and barbaric.

At Cambridge University, marmosets were repeatedly injected into the brain with destructive, seizure-causing chemicals. Then they were injected with drugs that made them spin uncontrollably in their cages, up to 300 times in an hour. The researchers claim their intention was to advance treatment of Huntington's Disease, even while admitting that the brain damage they inflicted 'did not replicate the pathology or the symptoms of Huntington's Disease'. (26)

Recent epidemiological studies suggest a link between Alzheimer's disease and consumption of dairy products. (27) Other research shows a link between garden pesticide usage and Parkinson's disease. (28) Surely, these are the types of enquiry we should be pursuing, rather than generating spurious data in animals.

If researchers believe animals are capable of experiencing the same kind of complex emotional stresses as people, they should not be experimenting on them in the first place. Yet this is indeed the basic premise of such wilfully cruel experiments as separating young animals, including primates, (29) from their mothers at an early age. The deliberate intent is to cause them stress and induce symptoms of schizophrenia and other disorders for further study. Schizophrenia manifests as speech disturbances, delusions and hallucinations. How can these problems be diagnosed in animals?

Many animals, particularly monkeys, have been deliberately brain-damaged over the years to monitor the effects on their behaviour and mental state. Many psychology researchers themselves have asked questions such as 'is the infliction of so much pain and terror warrantable?' (30) Such callous 'research' can clearly have little relevance for humans, plenty of whom are suffering these various disorders and who could reveal an abundance of information for study if they were only asked.

Monkeys at Oxford University were brain- damaged to assess the effect on their emotion and motivation. This was measured by depriving them of food and then placing food in front of them, but out of reach. The animals resorted to biting their own limbs. (31)

Others had parts of their brains' visual cortex removed and were then tested at various times for their visual abilities over the next nine years, until they had all died. (32)

In fact, there is a range of pain assessment tests employed in laboratories that would not be out of place in a medieval torture chamber. These include the 'mouse writhing test', induced by injecting acetic acid into the stomach; the 'tail-clip assay'; the 'paw-licking response' to wounds induced by injections of formalin; the 'rat tail-flick response' to intense heat; the 'hot-plate response'; and, of course, electric-shock avoidance responses. Scientists in Japan are investigating pain transmission in cats by administering electric shocks to their canine tooth pulp and recording the impulses generated in the spinal column. (33)

Scientists have devised around 50 methods to induce epileptic fits in mice, rats, baboons and other animals. These include the use of electric shocks, chemical treatments and exposure to flashing strobe lights. At Porton Down, guinea-pigs had holes drilled in their heads and electrodes and probes implanted into their brains, in order to monitor cerebrospinal fluid and electrical activity during the course of chemically-induced seizures. (34) Yet, even according to epilepsy researchers themselves, 'none of the models is fully trustworthy as an imitation of clinical epilepsy'. (35)

The director of a leading epilepsy research facility in Europe said, 'As a scientist, I am of the opinion that animal experiments bring no progress in the diagnosis and therapy of epilepsies. I have a well-founded suspicion that similar facts apply in other areas of medicine'. (36)

Cats and monkeys have had their eyelids stitched shut, their optic nerves or optic lobes of the brain removed, polystyrene beads injected into their eyes, and have been reared in total darkness. Concerning a series of such experiments using two species of macaque monkey, in whom the results were quite different, the British Institute of Medical Ethics concluded that 'neither can serve as an animal model for human myopia, because there is no way to decide which, if either, mechanism is similar to the human'. (37) Similarly, a group of American researchers showed that 'the feline visual system is a poor analogue to the human one'. (38)

All of the 'disease models' described above are created in a crude and artificial manner that renders them invalid for comparison with the naturally occurring disorder in humans. Indeed, the Medical Research Modernisation Committee analysed ten animal models of human illness and found 'little, if any, contribution towards the treatment of patients'. (39) It seems so obvious that complex human disorders require sophisticated models based on human anatomy, physiology and biochemistry. It is surely equally obvious that the maimed and broken animals described in this report do not fulfil that requirement.

In the second main section of the Bred to Suffer report, we look at transgenic animal disease models and expose the massive failure rate as well as the ethical, moral and religious concerns.

References

5. WC Roberts, American Journal of Cardiology, 1990 Vol 66 p896
6. SCU Marsch et al, Anaesthetics and Analgesics, 1996 Vol 82 p695-701
7. See National Heart Forum website at www.heartforum.org.uk/young
8. AJ Strong et al, Cerebral Blood Flow and Metabolism, 1996 Vol 16 p367-77
9. DO Wiebers et al, Stroke, 1990 Vol 21 p1-3
10. MR Law et al, British Medical Journal, April 6th 1991 p819-24
11. The Colombus Despatch, March 20th, 1998 (in Sacred Cows and Golden Geese: the Human Cost of Experiments on Animals, CR Greek, MD and JS Greek, DVM, Continuum 2002, p142)
12. As quoted in Vivisection Unveiled, Jon Carpenter Publishing, 1997, p47
13. DJ Galloway, Cancer Surveys, 1989 Vol 8 p169-88
14. C Dollery in Risk-benefit Analysis in Drug Research, ed Cavalla, 1981 p87
15. The Lancet, June 25th 1977 p1348-49
16. Testimony before US Congress, 1981 (in Sacred Cows and Golden Geese, op cit)
17. S Bende, The Scientist, 16th August 1999, Vol 13 (16) p7
18. Atlanta Journal Constitution, 21st September 1997
19. NL Letvin, New England Journal of Medicine, 1994, Vol 329 (19) p1400-1405
20. Monkeying around with their lives, and ours... NAVS USA newsletter 2001, www.navs.org
21. Carney et al, Matrix, 1992 Vol 12 137-147
22. MT Bayliss, Recent Advances in the use of in vitro Techniques, HRT Conference, 1987
23. JH McNeill, (Ed) Experimental Models of Diabetes, CRC Press, 1999 p95
24. Los Angeles Times, 20th December 2000
25. Journal of the American Medical Association, 1997 Vol 277 p813-17
26. AL Kendall et al, Brain 2000 Vol 123, Part 7, p1442-58
27. HC Hendrie at al, Journal of the American Medical Association, 16th Feb 2001 Vol 285 p739-47
28. New Scientist, 11th November 2000 Vol 168: 2264 p16
29. Medical Research Modernisation Committee, Aping Science (www.mrmcmed.org/ape.html)
30. A Heim, as quoted in The Cruel Deception, R Sharpe, Thorsons, 1988 p209
31. Stern and Passingham, Behavioural Brain Research, 1996 Vol75 p179-93
32. Johnson and Cowey, Experimental Brain Research 2000, Vol 132, 2 p269-75
33. Kiguchi et al, Clinical and Experimental Pharmacology and Physiology, 2000 Vol 28 (3) p169-75
34. J.Bourne and P. Fosbraey, Journal of Neuroscience Methods, 2000 Vol 99 p85-90
35. RS Fisher, Brain Research Reviews, 1989 Vol 14 p245-78
36. M Bernhard Rambeck, speech at International Conference in Zurich, 25th April 1987
37. Institute of Medical Ethics Bulletin, 1985 Vol 4 p1-2
38. SR Kaufman et al, Perspectives on Medical Research, 1993 Vol 4 p39-51
39. Medical Research Modernisation Committee; A Critical Look at Animal Research, New York 1990