The Journal of the National Cancer Institute last week published a study revealing that a certain mutation increases the risk of thromboembolism in women taking tamoxifen (a treatment for breast cancer). The authors of the study including Judy E. Garber, M.D. of the Dana-Farber Cancer Institute conducted research on 412 women who received tamoxifen in the time period of 1999 to 2005.
Differences in genotypes in part explain why men are affected differently than women by diseases like cardiovascular diseases and myocardial infarction. But there are a lot more examples.
Caucasians and African-Americans have a similar prevalence of early age-related macular degeneration. However, the progression to the late form of this disease is very rare for African-Americans and common in Caucasians.(1)
Similarly, infantile hemangiomas of the skin are commonly seen in Caucasians but are rare in African-Americans.(2)
Certain breast cancers in young black women are less common but usually much more lethal than in young white women, even when socioeconomic factors are taken into account.(3, 4)
Among cigarette smokers, African Americans and Native Hawaiians are more susceptible to lung cancer than whites, Japanese Americans, and Latinos. (5)
Breast cancer is now treated based on the genotype of the patient and the tumor. It seems like every week another study links a gene mutation to a disease.
And humans are not the only ones that have been studied.
It has long been noted that different strains of mice respond differently to chemicals and so forth. We now know that the deletion of a gene in one strain of mice may be result in death, whereas deletion of exactly the same gene in a different strain will have no effect. (6-8)
The above should give reasonable people some insight into why testing on mice or other animals is not going to predict human response.
In a Newsweek piece on primate experimentation, Michael Conn PhD of the Oregon Health & Science University is quoted:
"There is a degree of truth to the argument that animals are not a good model for humans," says Conn . . . "But it's also true that adults are not the best model for children and men are not the best model for women. The only perfect model for you is you, but obviously we can't test every substance on every individual." (9)
Actually we can. Gene-based testing easily allows this. As more and more genes are linked with diseases and drug reactions, this is exactly how all testing will be done. But for the time being, even though gene-based testing is not available for avery drug and disease, animal testing is not predictive hence should not be used for such purposes or sold to society based on the myth that it can predict human response. Such practices have more in common with religion than science.
There is at present no hard evidence to show the value of more extensive and more prolonged laboratory testing as a method of reducing eventual risk in human patients. In other words the predictive value of studies carried out in animals is uncertain. The statutory bodies such as the Committee on Safety of Medicines which require these tests do so largely as an act of faith rather than on hard scientific grounds. With thalidomide, for example, it is only possible to produce specific deformities in a very small number of species of animal. In this particular case, therefore, it is unlikely that specific tests in pregnant animals would have given the necessary warning: the right species would probably never have been used. Even more strikingly, the practolol adverse reactions have not been reproducible in any species of animal except man. [(10) p29] (Emphasis added.)
All the other animal models — including those of inflammation, vascular disease, nervous system diseases and so on — represent nothing more than an extraordinary, and in most cases irrational, leap of faith. We have a human disease, and we have an animal model which in some vague and almost certainly superficial way reflects the human disease. We operate on the unjustified assumption that the two are congruent, and then we spend vast amounts of money trying to investigate the animal model, often without bothering to test our assumptions by constantly referring back to the original disease in humans. (6) (Emphasis added.)
Today the subject and practice of toxicology has become exalted to the eminence and influence of a religion. It is, moreover, an established form of worship, actively supported by the State. It has its creeds and its commandments, and its hierarchy of high-priests, worshippers, adherents and novitiates. Again, like a religion, it relies on faith then reason. (11) (Emphasis added.)
Using animal models as predictive models for humans whether in drug testing or disease research is a purely religious act, an example of a purposeless fetishtic performance of ritual in accordance with the religion of pseudoscientists. Today, defending the use of animals as predictive models denies evolution and makes a complete mockery out of the scientific method.
Society has better ways of learning about diseases and drugs.
1. Z. Gregor, L. Joffe, Br J Ophthalmol 62, 547 (Aug, 1978).
2. D. S. Cheung, M. L. Warman, J. B. Mulliken, Ann Plast Surg 38, 269 (Mar, 1997).
3. University of North Carolina School of Medicine. Press release. June 6, 2006.
4. J. Couzin, Science 315, 173 (Jan 12, 2007).
5. C. A. Haiman et al., N Engl J Med 354, 333 (Jan 26, 2006).
6. D. F. Horrobin, Nat Rev Drug Discov 2, 151 (Feb, 2003).
7. H. Pearson, Nature 415, 8 (Jan 3, 2002).
8. D. W. Threadgill et al., Science 269, 230 (Jul 14, 1995).
9. J. Interlandi. (Newsweek, 2009), vol. 2009.
10. G. A. Teeling-Smith, Question of Balance: the Benefits and Risks of Pharmaceutical Innovation. (Office of Health Economics, London, 1980).
11. New Scientist 134, 29-33 (May 2, 1992).