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September 1995
Animal Experimentation: A Critical Evaluation

By Marjorie Cramer, M.D., F.A.C.S.


The moral case against vivisection has been well documented, but as Marjorie Cramer argues, there is a scientific case to be made.

While animal experimenters routinely credit animal experimentation for increased longevity in this century, many medical historians have argued otherwise. John and Sonja McKinlay rejected the notion that medical intervention has played a substantial role in the improvement of human health, estimating that at most 3.5% of the total decline in mortality since 1900 could be ascribed to medical measures.

Prior to this century, human clinical investigation enjoyed academic prestige. However, for several reasons, in the 20th century animal experimentation has assumed pre-eminence over human clinical investigation. This is related in part to the appearance of “control” in the laboratory setting, but it also reflects laboratory researchers’ political victory over clinical researchers in the pursuit of scarce research funds.

For largely extrascientific reasons, researchers tend to regard human clinical investigation as less “scientific” than laboratory (particularly animal) experiments. This has had unfortunate consequences. For example, even though a clear correlation between cigarette smoking and lung cancer had been observed long before the Surgeon General’s 1967 health warnings, researchers attempted to “prove” the relationship in animals. Repeated failures prompted leading scientists to reject the clear human evidence that cigarette smoking causes lung cancer in humans. This tragically delayed cancer warnings for years, and many doctors even urged patients to smoke to avoid weight gain. Similarly, while human data suggested a causal relationship between asbestos exposure and the malignant tumor, mesothelioma, animal studies did not, and this delayed workplace precautions.

Unsound in theory, animal modeling is also unsound in practice. Animal experimenters claim that the study of whole, integrated, metabolizing, living systems is essential to scientific progress. But, mice, rats, and other animals differ from humans in anatomy, physiology, biochemistry, and metabolism, and this undermines efforts to extrapolate data from one species to another. Animal experimenters, of course, recognize this and in published articles always advise other scientists to use caution when extrapolating experimental results to humans. When addressing the general public, however, they typically talk of needing to test in “the living organism” or doing experiments on “the brain,” as if all animals were the same except for differences in size.

To illustrate the poor correlation of test results between species, carcinogenicity assays in rats and mice yield the same results only 70% of the time. Similarly, of the 19 known human oral carcinogens, only seven have been shown to cause cancer in animals using the standard National Cancer Institute protocol. Studies to assess birth defects are notoriously unreliable, and many substances commonly used by humans such as aspirin, insulin, epinephrine, and certain antibiotics, cause malformations in animals. Thalidomide is a teratogen in a few species but not in most. Indeed, toxicologist R.W. Smithells has concluded: “The extensive animal reproductive studies to which all new drugs are now subjected are more in the nature of a public relations exercise than a serious contribution to drug safety.”

In the area of product testing, the LD50 test (in which substances are administered to animals in order to determine the dose that kills 50%) and the Draize test (in which substances are placed into the eyes of unanesthetized animals) are scientifically unsound. Animal tests for carcinogens are notoriously unreliable: an international study in 1981 demonstrated that in vitro cell and tissue culture tests are more sensitive and more accurate than animal tests.

Animal experimenters, exploiting the general public’s ignorance of medical history and the process of medical discovery, have convinced most people that animal experimentation is required for medical progress. The public is largely unaware of what happens behind the locked, well-guarded laboratory doors. Experimenters typically paint a rosy picture, assuring the public that animals are treated humanely in laboratories. However, all animal experimentation involves suffering — often from the experimental manipulations themselves, always from confinement, social deprivation, and other aspects of the unnatural and stressful laboratory environment. Animal experimenters seem to be relatively indifferent to the plight of individual animals in laboratories and fail to appreciate animal suffering. Evidently, experimenters become desensitized to animal suffering, or perhaps those who are most sensitive are likely to choose research careers that do not involve harming animals.

The Myths of Polio & Diabetes

Animal experimentation advocates routinely credit this method for the most dramatic medical breakthroughs of this century, such as poliomyelitis (polio) control and diabetes treatments. Their interpretation is overly revisionist.

The symptoms and mode of transmission of polio were described in 1840 by Jacob von Heine. In the early 1900s, animal experiments suggested inaccurately that transmission of the virus was via the nose rather than by mouth, as we know from human studies. Inspired by misleading animal data, in 1937 clinicians used a nasal spray to prevent polio in children. Of course, this was useless, and many children lost their sense of smell. Similarly, in 1910 and 1914, animal studies gave false leads when researchers attempted to immunize people by using intraspinal injections of serum from immunized monkeys. The project was a failure and, in 1931, controlled human studies showed that such passive immunization was ineffective. Later, in 1984, Albert Sabin said: “the work on prevention [of polio] was long delayed by an erroneous conception of the nature of the human disease based on misleading experimental models of disease in monkeys.”

In 1934, a vaccine made from infected monkey spinal cords resulted in the paralysis of 12 children and the death of six. The Salk vaccine was developed in 1954 using killed human polio virus grown in monkey kidney cells and tested on live monkeys. This vaccine caused many cases of polio, some resulting in death. Similarly, the Sabin live vaccine, developed in 1954, was also initially grown in monkey tissues and tested on live monkeys resulting in many cases of paralytic polio. Later vaccines derived from human cell culture proved to be effective and less expensive than the vaccines from monkey tissue and avoided completely the serious danger of animal virus contamination. There is now a laboratory method of determining safety that does not require live animal testing. Had efforts been made to develop vaccines from human cell lines earlier, instead of expending effort in animal studies, progress might have been made faster and human illness and deaths avoided.

As with polio, progress in the diagnosis and treatment of diabetes mellitus (diabetes) derived from clinical observation of human patents. In 1788, Thomas Cawley’s autopsy of a diabetic patient demonstrated the association of diabetes with pancreatic disease. Subsequent autopsy studies confirmed this relationship and eventually identified the islets of Langerhans as the specific sites of the disease. In spite of this, many scientists were convinced by Claude Bernard’s animal experiments that liver damage causes diabetes.

Animal studies argued against implicating the pancreas, as experimenters repeatedly failed to induce diabetes in animals by removing the pancreas. We now know that it is necessary to remove the entire pancreas in order to create diabetes by this means, and this is difficult. Finally, in 1889, von Mering and Minkowski succeeded at this task, but their diabetic dogs merely dramatized the already recognized clinical observation that pancreatic disease underlies diabetes.

In 1921, Frederick Grant Banting and Charles Best, in experiments that again dramatized human clinical findings, isolated a crude extract from a dog and used it to treat a diabetic dog whose pancreas had been surgically removed. The dog extract was a failure in treating human diabetic patients. In 1922, James Bertram Collip isolated human insulin from ox pancreas and used it to treat human patients. Today, of course, synthetic human insulin has replaced animal derived insulin. It is impossible to know whether or not insulin would have been available sooner or later if efforts had been made to develop it from human cadavers rather than from the slaughterhouse. Therefore, as reservoirs of insulin, animals have been useful for diabetic therapy, but animals experiments were not necessary for the discoveries that led to insulin treatment. — M.C.

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