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The process of bio-medical discovery:
An historial perspective”

Dr Brandon Reines
Vet. Medicine, Graduate of Tufts University, Boston
Speech delivered at the International Scientific Congress, London, April 1991

It so happens that I became a medical historian in a rather roundabout way: I had always been very fond of animals and had been looking for an animal welfare issue that would hold my interest. When I entered veterinary school and began to learn more about medical science, I became more and more suspicious of the claims that had been made about the importance of animal experimentation to medical progress. I had grown rather tired of the empty ethical debates, carried on without any scientific background or context, about whether it is right or wrong to use a mouse in an experiment. I wanted to know whether animal experiments were actually useful for their intended purpose, and, if so, why they were useful. This led me to study the literature in the history and philosophy of science as well as to analyse a great deal of historical case material in order to understand how and why animals were being used in medical experiments.

What I found flatly contradicts the government party line, that animal experimentation has led to virtually every major advance in the last hundred years. On the contrary, I found that animal experiments had in fact misled biomedical science time and time again; I found that they are not a means for generating biomedical discoveries. I also found that most major medical discoveries are achieved by doctors and surgeons who study human patients during life and at autopsy. The animal experiments are usually performed in order to convince sceptical colleagues of the validity of a discovery already made in the clinical context.

In my thesis of biomedical discovery, the initial stage in discovery is the generation of a ‘clinical hypothesis’, and this initial clinical hypothesis derives from an anomalous clinical observation. For instance, in the early part of this century surgeons began to observe an odd form of lung cancer in men who smoked cigarettes. That anomalous observation led them to the clinical hypothesis that cigarette smoking causes lung cancer. In the late 1940s epidemiologists in the US and UK undertook large human population studies to determine if the initial clinical hypothesis was correct. Based on this human data, it was, by 1950, clear that cigarettes cause lung cancer in human beings. However, public-health action against cigarette smoking was stalled for many years because researchers were unable to reproduce lung cancer in laboratory animals by blowing smoke down their windpipes. They tried smoke on guinea-pigs, rats, mice and other animals but were unable to induce lung tumours. So the tobacco companies could argue that cigarettes were perfectly harmless.

Once I had gained confidence in my thesis of biomedical discovery, by testing it against case material in physiology, pathology, therapeutics and prophylaxis, I decided that it was time to attempt my magnum opus: to try to understand how, in the 1840s, Claude Bernard managed to convince the medical world that animal experimentation is reliable as a means of biomedical discovery and testing. Bernard, the father of modern laboratory medical research, wrote An Introduction to the Study of Experimental Medicine, and it is the Bible of modern medical research.

By analysing Bernard’s book and by going over every passage with care, I deduced that he had deliberately misattributed biomedical discovery in general, and his own discoveries in particular, to animal experimentation. He did this in an extremely subtle but highly effective way. I have, in fact, worked out how Claude Bernard was able to misattribute his own medical discoveries to animal experimentation. By writing An Introduction, he was able to pass on his fraudulent account of biomedical discovery to his successors in the animal laboratory.

Modern animal researchers have followed Bernard’s erroneous rules to the tee. The main idea is: always claim to have made your discovery “by accident”. This allows the animal researcher to assert absolute priority of discovery. It is a way for him to claim that his discovery was not actually inspired by clinical observations – although it invariably was inspired by clinical studies. Bernard always claimed that his discoveries were “born by chance”. We now know that this is nonsense. Discoveries are no more made by chance than are rockets built by chance. In Bernard’s case, he always made his discoveries by reading the human pathological literature. For example, his first major discovery was that the pancreatic juice breaks up fat. He claimed to have made the discovery by an accidental observation made during a rabbit experiment. In fact, the American historian Fred Holmes examined Bernard’s notebooks in search of proof that the celebrated animal experiment had taken place. There is absolutely no evidence that Bernard ever did the experiment! He apparently made it up to assert his own priority in the discovery.

As I argue in the April 1991 issue of The Journal of Medicine and Philosophy, Bernard had actually made the discovery by reading about an “experiment of Nature” – a human case in which the pancreatic duct had been blocked by cancer. The patient had extremely fatty stools throughout life because the pancreatic juice could not get into his intestine. Many similar case studies had been reported during the 1830s, but Bernard claimed to have made his discovery in the apocryphal rabbit experiment of 1848 – many years after the initial clinical studies. I call Bernard’s tactic “chronological inversion”. He contends that animal studies lead to human studies, when in fact the opposite is the case: human autopsy studies are the actual source of inspiration and lead to attempts to “confirm” the clinical hypothesis in animals. Because the animal laboratory produces such varied results, you can “prove” almost any hypothesis you wish. The animal researcher who wants to plagiarise a discovery can always do so by claiming that he is the first to “prove” the discovery which before had been only “dimly suspected” on the basis of human autopsy studies.

I feel that Claude Bernard’s distorted account of biomedical discovery has had an extremely negative overall impact on the course of biomedical progress. There are three primary impacts. 1) First, widespread “interadditional plagiarism”, which means that animal researchers have been plagiarising physician investigators for many years by claiming to have “confirmed” what the physicians “merely hypothesised”. People who make such claims know nothing about how hypotheses are actually tested in a biomedical context. 2) The second impact is that many of the major medical breakthroughs of the 20th century were delayed by as much as 50 years – I will discuss this later. 3) Finally, and perhaps worst of all, Bernard’s account hinders the acceptance of major new biomedical theories which are based upon human clinical evidence and not on animal experiments.

I suggested at the outset that the cigarette-cancer hypothesis was not taken seriously during the 1950s because it was based upon human clinical evidence and not on animal studies. Since animal experiments are so much more dramatic than clinical studies – for example, in the case of smoking baboons – they were used to “sell” the idea that cigarettes cause lung cancer in human beings. Unfortunately, researchers were unable to duplicate the human “experiment” until the late 1960s. At that time, researchers finally succeeded in inducing a form of lung tumour in dogs by blowing smoke into their lungs. It had taken some 17 years to eventually find the “right” experimental set-up to reproduce roughly the human experience.
Another case in which animal experiments badly retarded the advance of medical progress is bypass surgery. While widely touted as a breakthrough by animal research, bypass surgery was actually held back by many years because of misleading animal experiments. Nevertheless, the animal researcher Alexis Carrel is generally considered the founder of bypass surgery. It was, in fact, not Carrel but the French clinical investigator Jean Kunlin who pioneered bypass surgery in 1949 without any prior animal experiments. Kunlin was actually building on 200 years of clinical investigation of a rare “experiment of Nature” called arteriovenous aneurysm (AA). Patients with AA have veins that pulsate like arteries, and the veins hold up as if they are arteries. So, based on long studies of the veins of AA patients, doctors prior to Carrel’s time concluded that human veins can withstand the relatively high blood pressure in the arterial system. Kunlin was aware of the clinical studies and decided to use a segment of the patient’s own vein to bypass an arterial obstruction. It worked very well. Unfortunately, American researchers then tried putting the vein grafts into the arterial system of dogs. And what happened? The vein grafts ballooned into aneurysms. An illustration of this was presented at the 1952 American College of Surgeons’ annual convention, and it created quite a stir. Such experimental results scared most American surgeons away from using the patient’s own vein as bypass graft material – which was eventually shown to be the best way to do bypass surgery of the leg and heart. Thus, misleading animal experiments actually delayed the development of bypass surgery by many years.

The development of kidney transplantation was also delayed for many years by misleading dog experiments. In the late 1940s and early 1950s, the leading dog experimenters in Britain, Simonsen and Dempster, argued that kidney transplants could not possibly work in human beings as the rejection reaction would be too violent. In fact, however, American surgeons in Boston, led by David Hume, decided to try such transplants in people, because they reasoned that patients in severe kidney failure seemed to have natural immunosuppression, so they would be likely to tolerate an implant better than healthy dogs. The team at Peter Bent Brigham ignored the animal data and tried the transplants in patients, and the procedure worked for as long as six months – more than 10 times as long as it had worked in dogs.

Another example of how animal experimentation can delay medical progress comes from the case of the polio vaccine. While that triumph is widely attributed to animal experimentation, in fact misleading monkey experiments actually delayed application of the polio vaccine by more than 30 years. Simon Flexner, who performed the monkey experiments in 1911, was the head of the Rockefeller Institute for Medical Research, so his opinion held enormous weight. Flexner had blown the polio virus into the monkeys’ noses and, on that basis, concluded that polio is by and large a disease of the human brain and spinal cord. If you blow a virus into the nose, it will head straight for the brain. Because, therefore, the virus could only go directly into the brain, he was forcing Nature to answer his question in the way he wanted. In fact, from studies of children with polio, it was discovered that polio is largely a disease of the intestinal tract – the virus does not usually go to the spinal cord to cause paralysis. Once researchers realised that the polio virus would grow in the intestine in human beings, they reasoned that the virus could be grown in intestinal tissue in the test tube. That breakthrough allowed the cultivation of enough virus to be used for a mass-produced vaccine. It was John Enders and his team at Harvard who first grew polio in tissue culture. That development made the monkey studies of polio completely obsolete. But the monkey studies had delayed the polio vaccine by 30 years.

As I mentioned earlier, Claude Bernard’s distorted account of biomedical discovery has led to widespread plagiarism of physician investigators by animal researchers. A classic case is that of Philip Levine, who actually discovered the so-called “rhesus factor” of blood cells but whose work was plagiarised by a monkey researcher. Levine made his discovery by studying a woman named Mary Seno in a New York City hospital. Seno had had a severe immunological reaction both to her unborn foetus (which was born dead) and to her husband’s transfused blood. On that basis, Levine deduced that Seno’s husband and foetus must have had an unnamed blood factor on the surface of their blood cells which she lacked. Unfortunately, however, when Levine published the case in 1939, he did not name the blood factor – and of course “he who names it claims it”. That allowed the rhesus-monkey researchers to come along and attempt to duplicate Mary Seno’s experience in monkeys. While they in fact failed to find the identical blood factor in monkeys, they named Levine’s blood factor the “rhesus” or “Rh” factor of blood. So Levine’s clinical discovery was plagiarised by monkey researchers.

I predict that it will become more and more difficult for clinical investigators to win acceptance for new medical theories. The reason is that the theories are becoming more and more complicated, and it is becoming harder and harder to “confirm”, or more accurately “dramatise”, a clinical hypothesis with an animal experiment. In such an experiment you can yank out an organ or laser-beam a tissue, but you can’t test complex medical theories. There are currently several major medical discoveries that are being resisted because they cannot be “proven” by animal experiments, although they are solidly grounded in clinical evidence. One example is the discovery that low-level radiation of a father or mother can cause leukaemia in offspring – even if the radiation is delivered prior to conception. This finding cannot be proven in animal experiments. Another example is a bold new theory of disease called the Mutagenic Theory of Chronic Diseases. The brain-child of Irwin D J Bross, this theory holds that most cancer and heart disease is actually caused by environmental damage to human DNA. But it cannot be “proven” in animal experiments, and so – like the cigarette-cancer theory – it is steadfastly resisted by the biomedical establishment.

I hope this talk has clarified the reasons that I thought it necessary to understand the process of biomedical discovery and to lay to rest the notion that Claude Bernard’s vivisectional method is a scientific method.

Thank you for your attention.

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