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No responsibility

The vested interest groups want society to believe that animal studies translate directly into human treatments and cures. For example:

A June 24, 20011 press release from McMaster University:

McMaster researchers from three disciplines are deploying thousands of tiny worms and a homegrown invention to test drugs in a collaborative bid to defeat Parkinson's Disease. . . . The McMaster team will use a device that was created by its engineers, compounds from its medical researchers and modified worms prepared by its biologists for the Parkinson's project – one they hope will create new knowledge about the disease and become a model for future research in other areas. "This could have direct application to human health and welfare," said Ram Mishra, a professor in the Department of Psychiatry and Neuroscience who studies nervous system degeneration. "It's a simple model, but it can answer very complex questions." The McMaster team will use a new device created at the university to assess the effects of more than 500 compounds on nematodes – tiny worms that are almost invisible to the naked eye, but which share more than 50 per cent of their DNA in common with humans. . . . Parkinson's affects the brain's dopamine neurons. Humans have billions of such neurons, but nematodes have only eight. But of the eight genes linked to Parkinson's in humans, nematodes have all eight, making them model test subjects. (Emphasis added.)

From a June 28, 2011 press release from Oregon Health & Science University:

OHSU researchers discover MS-like disease in monkeys

Findings could lead to major advance in MS research in humans

Researchers at Oregon Health & Science University have discovered a naturally occurring disease in monkeys that is very much like multiple sclerosis in humans — a discovery that could have a major impact on efforts to understand the cause of multiple sclerosis. The disease that the researchers discovered in monkeys at OHSU’s Oregon National Primate Research Center is associated with a herpes virus that could give significant clues into how multiple sclerosis develops in humans. MS researchers have long believed that a type of herpes virus may trigger multiple sclerosis in people who are genetically susceptible to the disease. . . . “These findings could have a huge impact on our understanding of MS and could be a landmark in someday developing more effective treatments for the disease, or even methods to prevent the onset of MS,” said Scott Wong, Ph.D., senior author of the study and a scientist at the Vaccine and Gene Therapy Institute and the Oregon National Primate Research Center. (Emphasis added.)

David Pruce, pharmacist and Interim (as of June 11, 2011) Chief Executive of Understanding Animal Research, in an interview on the BBC:

. . . at the end of the day you have to get to a stage where you need to see what the medicine does in a whole animal or in a whole person and what we want as patients is to know that a medicine when it comes on the market is absolutely safe. So at the moment yes we still do need to use animals.

From a June 29, 2011 press release from North Carolina State University:

A team of North Carolina State University researchers has discovered more about how a gene connected to the production of new brain cells in adults does its job. Their findings could pave the way to new therapies for brain injury or disease. . . . However, further experiments with newly developed genetically modified mice unexpectedly revealed that a fraction of Foxj1-expressing cells actually functioned as stem cells. But they only did so until the mouse reached the age equivalent of a human toddler, not throughout adulthood. In addition, the number of neurons generated by these cells was much lower than expected, which led to more questions about its function. (Emphasis added.)

Daniel Foggo and Hannah Kent-Martin writing in The Sunday Times, 10 July 2011, quote a vice-president of Harlan (a beagle breeder in the UK) as saying: “Right now many medicines can only be developed with the use of animal testing.”

All of the above is just another way of saying that animals can predict human response—the very thing I accuse animal modelers of saying and that basic researchers vehemently deny is ever the case, in their research or anytime animal models are used.

I learned long ago not to believe every new cure or treatment that came down the road, even those that have been tested in clinical trials. Animal modelers want to claim as a success every new treatment that was in any way associated with animal models, even if the association has nothing to do with the actual discovery or if the supposed breakthrough proves to be a failure later on. Further, the animal modeler refuses to take responsibility for the myriad failures. Recent examples include:

The drug aspirin was compared to a new drug called terutroban for prevention of stroke or transient ischemic attack (TIA). (Bousser et al. 2011)Previous studies on animal models had shown terutroban was as, if not more, effective than aspirin for preventing such events. Furthermore, animal studies also revealed that terutroban had other beneficial effects on blood vessels.(Gelosa et al. 2010; Gelosa et al. 2011; Wong et al. 2010; Chamorro 2009). None of this was the case in the large human trial.

Turner, writing in Nature 2011:

Man's best friend bears a heavy burden in the pharmaceutical industry. Every year, tens of thousands of dogs are subjects in drug-toxicity studies in Europe and the United States, even though many scientists think that they are poor predictors of drug effects in humans. (Turner 2011)

Other sensational failures include the failure to link smoking to heart disease and cancer, to link asbestosis to cancer, and the failure to predict drug reactions both good and adverse. Penicillin stayed on the shelf for over a decade because the rabbits Fleming tested it on lead him to believe it would be ineffective in humans. Scientists were misled about HIV enters the human cell because of studies on monkeys. The polio vaccine was delayed by decades because the way monkeys responded turned out to be very different from the way humans reacted. The cardiopulmonary bypass machine killed the first patients it was used on and it was only after human data was used that the machine turned was safe. Studying strokes and brain hemorrhage in animals has led to multiple medical treatments that worked in animals but that resulted in harm to human patients. HIV vaccines that protected monkeys have actually increased the risk of contracting HIV in the volunteers that took the vaccine. The flip side of all this is the fact that society has also lost cures and treatments because scientists believed the results from animals. 

Even Robert Weinberg, of Massachusetts Institute of Technology (a big fan of mine :-) ), was quoted by Leaf in Fortune magazine as saying:

Weinberg explains. “And it’s been well known for more than a decade, maybe two decades, that many of these preclinical human cancer models have very little predictive power in terms of how actual human beings—actual human tumors inside patients—will respond . . . preclinical models of human cancer, in large part, stink . . . hundreds of millions of dollars are being wasted every year by drug companies using these [animal] models. (Leaf 2004)

Needless to say, Weinberg is none-the-less a big defender of mouse research.

The reasons animals fail to predict human response have been covered in this blog many times. I will give just one example of one reason—complexity.

Since humans and other animals are complex systems, they exhibit the properties of robustness and nonlinearity. The nonlinearity aspect is demonstrated by a finding that mutations in just one gene can remove the fissures and convolutions from the human brain. These physical properties increase the surface area of the brain which some interpret as allowing humans to think rationally and abstractly. By analyzing humans, scientists discovered that mutations in the gene laminin gamma3 (LAMC3) were associated with brains that lack the fissures and convolutions. Such physical traits are not seen in mammals like rodents but are seen to a degree in apes and dolphins. Gunel, a coauthor of the study stated: "Although the same gene is present in lower organisms with smooth brains such as mice, somehow over time, it has evolved to gain novel functions that are fundamental for human occipital cortex formation and its mutation leads to the loss of surface convolutions, a hallmark of the human brain." The article can found in Nature Genetics.


Bousser, M. G., P. Amarenco, A. Chamorro, M. Fisher, I. Ford, K. M. Fox, M. G. Hennerici, H. P. Mattle, P. M. Rothwell, A. de Cordoue, and M. D. Fratacci. 2011. Terutroban versus aspirin in patients with cerebral ischaemic events (PERFORM): a randomised, double-blind, parallel-group trial. Lancet 377 (9782):2013-22.

Chamorro, A. 2009. TP receptor antagonism: a new concept in atherothrombosis and stroke prevention. Cerebrovascular diseases 27 Suppl 3:20-7.

Gelosa, P., R. Ballerio, C. Banfi, E. Nobili, A. Gianella, A. Pignieri, M. Brioschi, U. Guerrini, L. Castiglioni, V. Blanc-Guillemaud, L. Lerond, E. Tremoli, and L. Sironi. 2010. Terutroban, a thromboxane/prostaglandin endoperoxide receptor antagonist, increases survival in stroke-prone rats by preventing systemic inflammation and endothelial dysfunction: comparison with aspirin and rosuvastatin. The Journal of pharmacology and experimental therapeutics 334 (1):199-205.

Gelosa, P., G. Sevin, A. Pignieri, S. Budelli, L. Castiglioni, V. Blanc-Guillemaud, L. Lerond, E. Tremoli, and L. Sironi. 2011. Terutroban, a thromboxane/prostaglandin endoperoxide receptor antagonist, prevents hypertensive vascular hypertrophy and fibrosis. American journal of physiology. Heart and circulatory physiology 300 (3):H762-8.

Leaf, C. 2004. Why we are losing the war on cancer. Fortune (March 9):77-92.

Turner, M. 2011. Call to curb lab tests on dogs. Nature 474 (7353):551.

Wong, E. S., R. Y. Man, P. M. Vanhoutte, and K. F. Ng. 2010. Dexmedetomidine induces both relaxations and contractions, via different {alpha}2-adrenoceptor subtypes, in the isolated mesenteric artery and aorta of the rat. The Journal of pharmacology and experimental therapeutics 335 (3):659-64.


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