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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