Why Vivisection Is of No Use to Humans
Many people believe that Vivisection provides "safe" drugs and/or cosmetics for Humans when in actual fact, they could not be further from the truth. An animal model only side-tracks real medical progress and the extrapolation of results from animal models harms human patients, indirectly by delaying life-saving discoveries, and directly by endangering human lives. Certainly when we compare a dog to a human
for example, we initially appear to have much in common. Both man and dog have legs, eyes, nose, hair, digestive
system etc… If we are so similar, why then do we send Veterinarian students and Medical students to separate institutions? The answer is clearer when we examine each species at a cellular level. On a cellular level, dogs and humans diverge dramatically. And it is on a cellular level that most of today's research is done. Cellular differences determine such things as incidence, clinical manifestation and prognosis of diseases, response to therapy and susceptibility to toxins.
For example: Most of us have come to grips with the idea that smoking causes cancer, at least in man. Dogs are however extremely resistant to the cancer causing effects of cigarette smoke(Right).
The tobacco companies were able to hide behind science's inability to reproduce the obvious in dogs for many, many years and used such research to "prove" that smoking was not unhealthy.
Cancer is naturally something that provokes a strong response as it now strikes so many people. Because it creates so much fear and distress, whenever vivisectors seek to justify their butchering, the stock response is that 'We must experiment on animals to find the cure for cancer'. However, after so much time, after so many animals have been slaughtered in 'cancer research', and after so much money has been given to cancer research, one naturally wonders why so many people continue to be afflicted by, and die from cancer. In fact this is hardly surprising in view of the animals used in this pseudo-research. When vivisectors induce cancer in laboratory animals (primarily mice and rats), the cancer-causing substance gives different results, not only from species to species, but also from one strain to another of the same species. For example:
- In the mouse strain C3HF, urethane gives rise to hepatomas, tumours of the reticuloendothelium and lung tumours. And yet in the mouse strain C57B1, urethane causes lymphomas of the thymus. However, in humans, urethane is a good remedy in treating leukaemia.
- Dimethyl-benzo-alpha-anthracene causes lymphomas in mice of the 'Swiss' strain, but produces bronchial adenomas (benign tumours) in the 'Strong A' strain of mice; in other mouse strains, it produces liver tumours (but only in the males).
- Benzol and arsenic, both carcinogenic in humans, are not so in any of the rodent species used for experiments. 2-naphthyl is carcinogenic for the human bladder, but does not cause any form of cancer in mice.
- Benzidine causes bladder cancer in human beings, but in mice it causes a neuroma of the acoustic nerve and intestinal and liver cancer.
- Carbon tetrachloride (CCl4) produces liver cancer in the mouse but causes cirrhosis of the liver in rats.
- 4-amino-diphenyl causes bladder cancer in humans and yet in the mouse it results in mammary cancer.
- Chloroform (CHCl3) gives rise to liver cancer in the females of various strains of mice, but not in the males.
- Isonicotine hydrazine (INH), or isoniazid, causes adenomas (benign) and bronchial adenocarcinomas (malignant) in different strains of mice, but nothing similar has been found in human beings despite being used for treating TB over the last forty years.
Despite the fact that most of this knowledge came from studying people, vast amounts of money are still spent each year by scientists trying to find a disease “model.” The tools they research include cats, monkeys, chimpanzees, rabbits, guinea pigs, and mice. Although Chimpanzees can be infected with HIV, they never develop AIDS or AIDS related illnesses like cancer. They do not even carry the HIV virus in all the body fluids that AIDS patients do despite the fact that they share 98% of our genetic make-up. While there are an estimated 10 000 new infections everyday, and to date approximately 6 million people have died from AIDS – Governments and the Medical community are more enthusiastic about
infecting animals who may never light the way for a cure.
Pro-animal experiment contingencies always site the development of insulin as support for continued animal testing. They assert, with justification, that without insulin harvested from slaughterhouses many diabetics would have lost their lives. Whereas it is true that animals have figured largely in the history of diabetic research and therapy, their use has not been necessary and furthermore has not always advanced science.
Diabetes is a very serious disease, even today affecting millions of people. It
is a leading cause of blindness, amputation, kidney failure and premature death. Although the clinical signs of human diabetes have been known since the first century AD, not until the late eighteenth century did physicians associate the disease with characteristic changes in the pancreas seen at autopsy. As this was difficult to reproduce in animals, many scientists disputed the pancreas’ role in the disease.Nearly a century later, in 1869, scientists identified insulin-producing pancreatic cells that malfunction in diabetic patients. Other human pancreatic conditions, such as pancreatic cancer and pancreatitis (inflammation of the pancreas) were seen to produce diabetic symptoms, reinforcing the disease’s link with the pancreas.
Animal experimenters continued to interrupt the nicely progressing course of knowledge regarding the pancreas and diabetes. When they removed pancreases from dogs, cats, and pigs, sure enough, the animals did become diabetic. However, the animals’ symptoms led to conjecture that diabetes was a liver disease, linking sugar transport to the liver and glycogen. These animal studies threw diabetes research off track for many years.
In 1882, a physician named Dr. Marie noted the association between acromegaly, a pituitary disorder, and sugar in the urine, thus connecting sugar metabolism and the pituitary gland. Another doctor, Atkinson, published data in 1938 that revealed 32.8 per cent of all acromegalic patients suffered from diabetes. Bouchardat published similar findings in 1908. For some reason, the scientist who reproduced this in dogs, Bernardo Houssay, ended up winning the Nobel Prize in 1947. Obviously, it is hardly fair to say dogs were responsible for his kudo, since knowledge predated Houssay’s experiments and any number of human-based methods would have produced the same findings.
In the early 1920s two scientists, John Macleod and Frederick Banting, isolated insulin by extracting it from a dog. For this they received a Nobel Prize. Macleod admitted that their contribution was not the discovery of insulin, but rather reproducing in the dog lab what had already been demonstrated in man. They were not obliged to extract insulin from dogs, because certainly there was ample tissue from humans. They merely did so because it was convenient. In that same year Banting and another experimenter, named Best, gave dog insulin to a human patient with disastrous results. Note what scientists said about the dog experiments in 1922,
The production of insulin originated in a wrongly conceived, wrongly conducted, and wrongly interpreted series of experiments.
Banting, Best and other scientists modified the process using in vitro techniques and later mass-produced insulin from pigs and cattle by reaping insulin in slaughterhouses.
In coming years scientists continued to refine the animal-derived substance. Though it is true that beef and pork insulin saved lives, it also created an allergic reaction in some patients. Beef insulin has three amino acids that differ from human amino acids while pork insulin has only one. Whereas this sounds negligible, it takes very little amino acid discrepancy to undermine health. (Only one deviant amino acid is enough to produces certain life threatening diseases, such as cystic fibrosis or sickle cell anemia.) Injecting animal-derived insulin also presented the sizable danger of transmitting viruses that cross from one species to another. Had researchers then recognized these potentialities as well as the gulf of differences between humans and farm animals, scientists would have hastened to develop human insulin more quickly .
The ability to treat patients suffering from diabetes without giving them insulin injections was discoveF by chance on humans. Today, the administration of oral anti-hyperglycemics, which arose from serendipity and self-experimentation, eliminates the need for insulin injections in many patients.
Diabetes is still stunningly enigmatic, in large part due to our continued reliance on the animal model. Most clinicians believe that strict glucose control though insulin injections offers advantages over a less regimented treatment plan. However, insulin is a treatment not a cure for diabetes. The exact biochemical process through which insulin regulates blood sugar is not yet known.
Polio first broke out around 1835, with victims rapidly becoming paralyzed and dying. In 1840, an orthopedic surgeon wrote that the spinal cord was the seat of infection, a hypothesis that was proven twenty-three years later.
In 1908, scientists suggested that a virus was responsible, a virus that might be eradicated with a vaccine. In developing a vaccine, it is very important to determine how the infection enters the body and takes hold. You cannot interrupt its contagion unless you determine its path. Pathologists discovered the poliovirus in human intestines as early as 1912, which suggested it might enter humans through the digestive track.
Meanwhile researchers successfully infected animals with polio. This "triumph" winded up postponing the development of an efficacious vaccine by decades. As it turned out, our close relatives the monkeys contracted polio nasally (not through the digestive system), and the virus moved directly from the nose to the brain. Incredibly, the scientists working on the vaccine chose to ignore the human digestive data in favor of the monkey data!
The pro-animal experimenters are not incorrect when they claim that a polio vaccine derived from animal experiments because in 1934, a polio vaccine manufactured from monkey tissue was released. What they fail to mention is that it resulted in twelve people being paralyzed and six deaths. In 1937, animal experiments led scientists to spray zinc sulfate and picric acid alum into children’s noses, reasoning that if the human transmission route was via the nasal mucosa as it was in monkeys, this would kill the virus in the nose. The only result was that some children permanently lost their sense of smell. In 1941, thirty years after the original animal experiments, Dr. Albert Sabin worked with autopsy findings to demonstrate that the human nasal mucosa did not have virus. What he did find was that the virus was confined to the gastrointestinal tract, as had been determined nearly thirty years prior. Years later, Dr. Sabin recalled the folly of the monkey models for polio:
Paralytic polio could be dealt with only by preventing the irreversible destruction of the large number of motor nerve cells, and the work on prevention was long delayed by the erroneous conception of the nature of the human disease based on misleading experimental models of the disease in monkeys.In 1949, John Enders grew the virus in tissue culture. This paved the way for vaccine. For this achievement he won the Nobel Prize in Physiology or Medicine in 1954.
The vaccine could have been produced from non-animal tissue, however manufacturers opted for monkey kidney tissue instead. The older animal-based vaccine contained live virus, causing 204 people to contract polio, and eleven documented deaths.
The polio vaccine is now grown in human diploid-cell culture instead of in animal tissue.
Courtesy Americans for Medical Advancement
A principle called Karnofsky’s Law states that any substance can be teratogenic (cause birth defects) if given to the right species, at the right stage in development, in the right dose. Even common table salt and water are teratogens in some species if given at a vulnerable time in ample enou
gh amount. In other words, all medications can cause birth defects in some creature. An immense amount of experimentation supports this rule. Data also supports the fact that not all species are equally susceptible to teratogenic influences by any given chemical. Likewise, an agent that is teratogenic in some species may have little or no teratogenic effect in others. According to a respected treatise on birth defects, “because substances cross the placental membrane by a number of mechanisms, some differences in species reactivity to teratogens may be due to accessibility of the drug to the embryo.” Of over 1,200 tested chemicals that cause birth defects in animals, only thirty cause them in humans, according to the New England Journal of Medicine. Articles in many other publications repeat these conclusions.
Many safe and useful drugs have been shown to cause birth defects in lab animals:
- Lovastatin
- Chondroitin sulfate
- Acetazolamide
- Dichlorphenamide
- Ethoxzolamide
- Methazolamide
- Furosemide
- Clonidine
- Diazoxide
- Hydralazine
- Reserpine
- Guanabenz
- Diltiazem
- Nifedipine
- Codeine,LI> Hydrocodone
- Hydromorphone
- Meperidine (Demerol)
- Morphine,
- Oxymorphone
- Phenazocine
- Propoxyphene
- Colchicine
- Allopurinol
- Aspirin
- Acetaminophen Other non-steroidal anti-inflammatory drugs
- Enflurane
- Ether
- Halothane
- Isoflurane
- Nitrous oxide
- Sevoflurane
- Procaine
- Corticosteroids
- Ampicillin
- Cephalothin
- Chloramphenicol
- Erythromycin
- Many antibiotics, antifungal medications and antiviral medications
- Antiparasitics
- Anthelmintics
- Antimalarials
- Anti-hyperglycemics
- Insulin
- Thyroxine
- Triiodothyroacetic acid
- Methylthiouracil
- Propylthiouracil
- Aminophylline
After epidemiology or clinical observation links drugs to birth defects, animals can usually, though not always, be found to demonstrate that effect. Researchers have not been successful in reproducing birth defects in other animals for the following drugs that are teratogenic in humans: Captopril, Enalapril , Minoxidil, some calcium channel blockers, Warfarin. The popular lab animal, the rat, has been shown to get birth defects from almost every chemical that causes birth defects in humans. This is meaningless though. If chemicals that harm rat offspring do not cause birth defects in humans, the rat tests are not predictive.
What is teratogenicity testing good for and why does it continue? As Dr. Hawkins, professor of Obstetrics, pointed out,
The great majority of perinatal toxicological studies seems to be intended to convey medico-legal protection to the pharmaceutical houses and political protection to the official regulatory bodies, rather than produce information that might be of value in human therapeutics.
Just as Karnofsky postulated, if researchers try hard enough they may eventually inflict birth defects on some animal species with a substance that is teratogenic in humans. But to what purpose? Animal experiments that are not predictive are of no value. They just use up money that might otherwise fund research of real medical value. There is no sense in “validating” something that is already known from human data.
Courtesy Americans for Medical Advancement
then tried them out on humans. Only after completely blinding several humans, did they finally correct the procedure. The field of neurosurgery offers another example. Extracranial-intracranial (EC-IC) bypass procedures for inoperable carotid artery disease were tested and perfected on dogs and rabbits. Neurosurgeons performed thousands of EC-ICs before it was discovered the operation did more harm than good. More patients died or suffered strokes because of the operation than were saved as a result of it. Transplantation surgeries are much the same story. Hundreds and hundreds of cats, dogs, pigs and primates have been sacrificed as surgeons tried to fashion surgeries that lift organs from one creature to another. No matter the number of practice surgeries on animals, the first humans operations fail. Carrying the animal data over to the human body always proves duplicitous. Only conducting procedures on humans provides dependable techniques. Courtesy Americans for Medical Advancement
According to PCRM (The Physicians Committee for Responsible Medicine) president Neal D. Barnard, M.D. “There is never a need for practicing surgery in animals. Surgical skill relies on knowing human anatomy, not dog anatomy. Training on animals teaches students the wrong anatomical landmarks and the wrong 'feel.'
Courtesy Liberation Magazine
Vivisection exists because the industry has become so engraved in our society. Egos are on the line. Scientists who have devoted their entire lives to animal experimentation are reluctant to admit that those methods were useless, much less dangerous. Simply put, animal experimentation continues because it is highly profitable. All the following constituencies make money: scientists, physicians, hospitals, regulation agency bureaucrats, pharmaceutical companies, medical conglomerates, politicians, animal farmers and vendors, lawyers, reporters, and news media, to name a few. Many companies support Vivisection in order to secure themselves against litigation too. Think asbestos. Think tobacco. None of these constituencies can afford for the public to lose confidence in the idea that animal testing protects them. The Fact that 68% of drug related deaths last year were as a result of legal drugs; that animal testing is less than 30% accurate – flipping a coin is 50% accurate!; that 61% of birth defects are caused by drugs passed safe in animal tests; and that one in six patients in hospital are there because of treatment they have taken are just some of the reason why Vivisection makes no sense. Charity funds continue to funnel into wasteful experiments that are of no use to the consumer who supports them. Animal experimentation is a kind of "white coat welfare." But the animal testing machine, now large and in perpetual motion, will be difficult to stop, but not impossible. We can start by not purchasing products known to be tested until such time the companies that produce them change their testing methods.
