Why Animal Research is Poor Science
Did it delay new treatments for HIV?
Animal tests are not always a reliable indicator of how drugs will affect humans
Government enthusiasm for animal research is misplaced. Vivisection is scientifically flawed. It may have seriously delayed the development of new treatments for HIV
Deputy Prime Minister John Prescott says animal research is vital for the future of the British pharmaceutical industry. Arguing that investment, jobs and medical breakthroughs depend on it, he overturned an independent planning inquiry's refusal to give permission for a new primate research centre at Cambridge University.
Prescott's backing for vivisection is supported by the science minister Lord Sainsbury, and a by coalition of powerful drug companies, including GlaxoSmithKline, AstraZeneca and Pfizer. They argue that without these experiments Britain will lose its competitive edge in the development of new medical treatments.
The government is determined to ensure the expansion of animal research, not just in Cambridge but also in a new lab in Oxford. Responding to protests that have the halted the laboratory's construction, Home Secretary David Blunkett has outlined new legislation to crack down on "animal rights extremists." These new laws are far more draconian than the statutes against animal abusers. When it comes to acts of violence, Blunkett seems more concerned about the harassment of a handful of researchers than the industrial-scale infliction of pain, suffering and death on over two million living, feeling animals, including nearly 4,000 non-human primates last year.
According to John Prescott and Lord Sainsbury there is no alternative. Animal research is vital for medical progress. But are they right?
Even some scientists are concerned that vivisection is based on the dubious premise that laboratory animals provide accurate models of human diseases and treatments.
They point out that drug therapies can have vastly different effects on different species. Strychnine, for example, kills people but not monkeys, and Belladonna is deadly to humans yet harmless to rabbits. Research findings in other species cannot therefore be automatically transposed to people.
We have witnessed many times the tragic consequences of blind faith in animal testing. The anti-rheumatic drug Opren killed 76 people and caused serious illness to 3,500 others, despite having been declared safe after seven years of animal research.
Likewise, thousands of people with heart trouble suffered adversely after taking the animal-vetted drug, Eraldin. Since then, further experimentation has failed to find a single species that reacts to Eraldin in the same way as humans.
Undeterred, the big pharmaceutical corporations have cynically exploited public fears concerning life-threatening diseases like cancer and HIV to demand more money for animal experiments and to oppose animal welfare legislation restricting their activities.
The battle against HIV provides a classic example of the pitfalls of vivisection. Protease inhibitor drugs have made a major contribution to cutting the death rate; enabling many people with the virus to maintain a more or less normal life. HIV infection has been transformed from a death sentence into a manageable condition.
The initial development of these highly effective anti-HIV therapies was, it appears, seriously compromised by reliance on animal testing. In possibly one of the biggest medical scandals of recent times, there was a four-year delay in the clinical trials of protease inhibitor treatments. This may have contributed to the needless deaths of tens of thousands of people world-wide.
In 1989 researchers at the pharmaceutical giant Merck, Sharpe and Dohme (MSD) were working on a promising protease drug. Development was going well until the scientists decided to test the new therapy on dogs and rats. They all died.
According the MSD's former Vice-President of Worldwide Basic Research, Bennett M Shapiro, the company "stopped development" of its most promising protease inhibitor after it produced "severe side effects" in laboratory animals.
MSD presumed the drug would have the same lethal effect on humans, believing animal experiments provide an accurate model of how protease drugs affect people. The result? Research on a potentially life-saving treatment was halted in 1989, and clinical trials of a new protease drug, Crixivan, did not start until 1993.
This delay is confirmed by one of MSD's senior researchers, Emilio Emini. Documenting the history of protease research for Washington Post Magazine, investigative reporter Stephen Fried exposed how reliance on animal data caused MSD to abandon its first protease inhibitor:
"It did not take long for the drug to crash. 'This is not going to work', the toxicologist said when he bought Emini the news about the eight dying dogs. The rats weren't doing any better. Merck's drug had the nasty habit of shutting off the bile flow to the liver. Emini felt that if the animal test results were that severe, it was 'unethical to even do the study on humans.So there went four years.'"
We do not know whether this original protease drug would have had adverse effects on people with HIV. Drugs causing liver failure in other animals are not necessarily fatal for humans. This first protease inhibitor might have been a lifesaver, like the subsequent generation of protease drugs. But MSD concluded that what kills dogs and rats will also kill people. Development was axed, and vast numbers of people with HIV continued to die.
Did MSD act wisely? Perhaps not. There are huge physiological differences between human and non-human animals. Drugs that are harmful to one species can be beneficial to others. Penicillin, for example, is deadly to guinea pigs but cures many human infections. If Penicillin had been initially tested only on guinea pigs, it might have been discarded and the world would have been deprived of the single most important medical treatment ever invented.
MSD admits that animal studies were not used in the primary research that led to the invention of the follow-up protease inhibitor, Crixivan. Based on the knowledge that HIV is a uniquely human disease, MSD scientists focused on studying the structure of HIV and its interaction with human cells. Designed on computers, the protease drug was safety-tested using non-animal methods.
According to Shapiro: "Animal tests were neither needed, nor used, to explore the ability of protease inhibitors to block the growth of the Aids virus.the target action was already well understood and could be evaluated before the clinical trials using computers, cell culture and biochemical assays."
This looks like a tacit admission that animal studies were not scientifically necessary for the development of protease drugs, and that for the purposes of primary research non-animal methods were able to provide reliable data.
It was only when MSD decided to further test the new drug on dogs and rats that they ran into trouble. All died of liver failure.
As we now know, there are protease inhibitors that do not have the same fatal consequences for humans. On the contrary, they have dramatically improved the lives of people with HIV.
These setbacks in the development of anti-HIV treatments highlight the scientific flaws of animal-based medical research. Vivisection can produce inaccurate data that is inapplicable to humans.
Instead of backing the expansion of animal labs, John Prescott and Lord Sainsbury might help medical science more effectively by funding the development of alternatives - including cell, tissue and organ banks for testing the toxicity of new drugs, and virtual reality supercomputers to simulate the workings of the human body and the effects of innovative therapies.
A majority of the diseases we suffer are unique to our species. Cures are most likely to be found by studying the physiology of human beings, not other animals.
An edited version of this article appeared in the New Statesman on 9 August 2004.
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