The following is a collection of arguments that have been made against the use of animals in research. We have attempted to provide responses to these statements with factual and reliable information.
- Research on animals is irrelevant to people because findings from animal experiments cannot be transmitted to humans.
- Animal research is not necessary because there are alternatives.
- The agent TGN1412 never showed detrimental side-effects in animal tests, but human probands nearly died of it.
- Again and again, drugs have to be taken off the market, e.g. Baycol, because they produce strong side effects in humans, even after being found safe in animals.
- We would not have beneficial medicine, e.g. penicillin, if we had relied on the current drug discovery procedure.
- Insulin causes congenital malformations in guinea pigs but not in humans.
- Despite animal testing we still do not have a cure for cancer.
- Aspirin is toxic to animals but not to humans.
- 25 years of research on monkeys has brought no vaccine or cure for AIDS.
- Animal tests are the wrong way to go – you can see that when a cure for Alzheimer’s works in mice but not in humans.
- Animal testing is inexpensive and an easy way to make a profit.
- Cosmetic products are tested on animals.
- Some animal studies are not for medical purposes but rather for the scientists to explore their own curiosity.
- Although many Nobel Prizes were awarded to the field of physiology or medicine, only 45% of those winners conducted research using animals.
- Drug tests on animals are useless, case in point Thalidomide.
- 9 out of 10 drugs tested on animals are not suitable for humans, proving that results from animal tests are not transferable.
Research on animals is irrelevant to people because findings from animal experiments cannot be transmitted to humans.
This is an incorrect statement as the relevance of animal experiments to humans has been seen all throughout the history of medicine. Many of the most important medical advances of the last 100+ years are directly attributable to animal experiments. Examples include everything from antibiotics, insulin for diabetics and blood transfusions to the basic knowledge that bacteria may cause diseases. The European Commission concluded in 2015 a detailed report stating that these advances would have been impossible without the results obtained by means of animal experiments. All vertebrates (mammals, birds, reptiles, amphibians and fish) have descended from one common ancestor, which is why they share the same basic biological principles. We all have the same organs (heart, lungs, liver, etc.) that function in similar manners and are controlled via the bloodstream and nervous system. This similarity goes so far that you can even use different animal hormones for treating sick people, where they have the same effect (e.g. insulin from pigs and cows, salmon calcitonin, oxytocin and vasopressin from pigs). Even animals that are only distantly related to us show many similarities. For example, human cells are similar to those of insects. Thus, the hedgehog-signaling pathway, for cell-to-cell communication during development, was first studied in fruit flies. The decryption of this mechanism led – among other things – to the development of the skin cancer treatment, vismodegib. Through basic research of system functions and anatomy we know which animals are similar enough to humans for different purposes of study. Of course, there are still many differences between species. However, in some cases, this can be of particular interest. Transferability to humans is not a requirement for relevance. If we, for example, were to better understand why the naked mole rat is resistant to cancer or why Axolotl promotes tissue regeneration, then completely new human therapies could arise.
Animal research is not necessary because there are alternatives.
Most scientists would be delighted if this statement was true, especially because animal experiments are extremely complex, expensive and lengthy. Nevertheless, for the animal experiments currently carried out in Germany there are no non-animal alternatives. This is a legal requirement (Animal Welfare Act §7a (2) 2). Alternative methods, such as cell cultures, computer models and imaging techniques are interesting for scientists not only because they replace animal experiments. They are also seen as complementary approaches to animal research that can provide more detailed information. Accordingly, such methods are routinely used. They are also constantly evolving and increasingly replacing animal experimentation. To understand many biological and medical issues we also need such insights, which up to now, can only be reached by means of animal experiments. See: Alternatives to Animal Testing.
The agent TGN1412 never showed detrimental side- effects in animal tests, but human probands nearly died of it.
In 2006, the monoclonal antibody TGN1412 was first administered to human volunteers in a clinical study at Northwick Park Hospital, London. Shortly thereafter, a powerful immune reaction occurred that put six participants in danger of dying. All of them survived, but their immune system was affected. One man also lost his toes and fingertips due to this accident. The incident occurred despite the mandatory testing for toxicity that had taken place beforehand. So is TGN1412 evidence that animal testing is incapable of protecting us from toxic substances?
All new drugs are first tested with usually healthy volunteers (phase 1 study), before being administered to a larger group of patients. To best protect participants from accidents, toxicity testing must make use of the most significant methods available. Today’s methods are very effective, as demonstrated by the fact that accidents like the one involving TGN1412 are exceedingly rare – after all, Great Britain alone sees about 200 such phase 1 studies each year. Not unlike a safety belt or net, however, even the best methods cannot guarantee 100% safety. Before its use in humans, TGN1412 was tested on animals (monkeys and rats) as well as in a culture of human cells. None of these three testing systems produced any warning signs pointing to the detrimental effects of the agent. So cell cultures, too, failed as a security measure in this case.
Through extensive study of the mechanisms involved we now know the reasons for the powerful immune reaction observed in the study. TGN1412 activates cells of the immune system (so-called regulatory T-cells), which are capable of excessive inflammations and defensive reactions. This made TGN1412 a likely candidate for treating autoimmune diseases like rheumatism and multiple sclerosis. Besides regulatory T-cells, TGN1412, to a lesser degree, also activates another type of T cells: effector memory cells, which promote inflammation. Effector memory cells are created throughout our whole lifetime against every pathogen that is exposed to the body. Overactivation of this kind of cells led to the dangerous immune reaction in the six participants mentioned above.
The rodents used for testing had been kept very clean and they were quite young, so that they basically had not produced any natural effector memory cells yet. Thus, TGN1412 only activated regulatory T-cells while the effect on effector memory cells remained undiscovered.
The drug was also tested in macaques, which have a receptor for TGN1412 just like humans. However, the receptor is not carried on their effector memory cells. That is why TGN1412 does not lead to the release of inflammation-promoting substances in macaques.
The additional testing in cell cultures was done on immune cells that had been isolated from human blood. Later, it was found that these cells enter a ‘state of rest’ while in the bloodstream, as they lack certain signals that they normally receive in body tissue. They no longer reacted to signals like that of TGN1412. This newfound knowledge has led to the development of an improved in vitro test, which dependably predicts T-cell reaction to TGN1412.
Indeed further work was done on TGN1412 itself. Understanding the underlying mechanisms led to the development of a dosage that avoids the immune system’s overreaction without losing its therapeutic efficacy. The latest studies on patients suffering from rheumatoid arthritis have shown promising results. The case of TGN1412 has also led to various improvements in phase 1 testing, lowering the overall risk for participants. Moreover, the case demonstrates the importance of basic research in medicine. Only a detailed and encompassing understanding of physiological mechanisms allows us to choose suitable species for animal drug testing, or, ideally, to develop appropriate animal-free testing methods – as has happened in this case.
Again and again, drugs have to be taken off the market, e.g. Baycol, because they produce strong side effects in humans, even after being found safe in animals.
In August 2001, Bayer took its cholesterol-lowering drug Baycol (Lipobay) off the market. Hundreds of patients had suffered from muscle damage after taking Baycol. But is this proof that animal experiments do not protect us against side effects? No, because in actuality a drug is not officially approved by law until it has successfully been tested in humans. Before a new drug is approved it is first tested on animals for toxicity. Thereafter, it is administered in clinical trials of different groups of human volunteers. These studies will determine whether the drug works as hoped and how often side effects occur. Only with good results from these studies is a drug approved. The toxicity test on animals serves to protect the subjects during clinical trials. The clinical tests on humans in turn protect the patient. Any severe side effects that occur after a drug has become publicly available were largely unnoticed by participants during the clinical trials. For example, a rare side effect may become visible only in very large groups or populations. It is estimated that the muscle damage after taking Baycol occurred in about 400 out of 700,000 patients (0.06%) in the United States. Finding these severe side effects was made even more difficult by the fact that, in most cases, they occurred only after concurrent use of another drug, Gemfibrozil. If animal testing of candidate drugs was substituted with less meaningful non-animal methods, we would pose a greater risk to human volunteers during clinical trials. However, the risk of rarely occurring side effects and interactions, as in the case of Baycol, would not change. It is estimated from the results of the human clinical trials, not the toxicity testing- however it is done.
We would not have beneficial medicine, such as penicillin, if we had relied on the current drug discovery procedure.
To answer this we first need to know about the current drug discovery procedure. It is a legal requirement that potential new drugs are tested on animals for toxicity before they are administered to people. In some cases, it may be that a species tolerates a toxic substance better than humans. Thus, to minimise the risk for human volunteers, the toxicity in two different animal species that are not closely related to each other is examined- mostly rats and pigs, but sometimes dogs or monkeys. The goal of toxicity tests is not to find out whether a substance is toxic, for each drug is toxic at a high enough dose. Rather the goal is to identify the specific kind of problems that are to be expected and at what doses these problems begin (e.g. liver damage or high blood pressure). If the expected medical benefit is outweighed by the side effects occurring during animal testing, then the compound is not tested further. Penicillin would not have failed during this procedure. The rumour comes from the fact that penicillin in high doses, similar to other antibiotics, is harmful to guinea pigs and hamsters. Penicillin works by killing bacteria, however in these animals, the drug was fighting bacteria they needed to survive. Specifically, penicillin kills Gram-positive bacteria. Now guinea pigs and hamsters have the rare peculiarity that their intestinal flora consists mainly of Gram-positive bacteria. Thus, if penicillin was tested on them they could have potentially died from inflammation and diarrhoea caused by the loss of their natural bacteria. For this reason, no one would even think of wanting to test a new antibiotic on hamsters. Through basic research we know a lot of such peculiarities in different animal species. This knowledge helps us to handle scientific issues and for selecting a suitable animal for toxicity tests. If there was no animal testing we would not have penicillin today. In 1940, Florey and Chain made history with an experiment involving eight mice. All mice were injected with a lethal dose of infectious bacteria (streptococci) and four of them were also given penicillin. These four survived. This discovery is regarded as one of the most important in medical history. It has saved the lives of millions of people and animals (and still does).
Insulin causes congenital malformations in guinea pigs but not in humans.
All mammals, guinea pigs included, produce insulin. An excessive administration of insulin in pregnant animals harm the foetus. This is due to the insulin-induced low blood sugar levels. It is likely that the same damage in humans could also occur, however, to test this would not be ethically justifiable. Nevertheless, the isolation of insulin and the recognition of its lifesaving effect in diabetic patients date back to animal testing. Across different species, the insulin compound is so similar that it can be isolated from pigs to treat these patients. For this achievement Banting and Mcleod received the Nobel Prize for Medicine in 1923.
Despite animal testing we still do not have a cure for cancer.
The life expectancy for a cancer patient has been continuously growing for decades (see figure below). According to the German Cancer Research Center, this development can be attributed to constantly improving therapeutic techniques. Not only are there better early detection methods and more health awareness but also more effective cancer treatments. Furthermore, such treatments would not have been possible without animal experiments.
These improvements are particularly apparent for breast cancer. For instance, in eight out of ten cases, breast cancer is estrogen-sensitive, i.e. the hormone estrogen induces growth. This concept was first understood through research on rats, and further research using both animal and human tissues led to the development of an estrogen receptor antagonist, Tamoxifen, into a breast cancer drug. During the 1990s, Tamoxifen was introduced as a large-scale therapeutic measure, reducing the mortality of breast cancer patients by approximately 30%. Hundreds of thousands of women owe their lives to this drug.
The next breakthrough in treating breast cancer was the immunotherapy compound Herceptin, which is effective against an especially aggressive kind of breast cancer. The basis of this therapy was the discovery of oncogenes, or genes that influence cancer generation. J. Michael Bishop and Harold E. Varmus, who discovered these genes in chickens and other animals, were awarded the Nobel Prize for Medicine or Physiology in 1989. Based on this work, research on rats and mice revealed that the oncogene “neu” promotes cancer generation. When the role of this gene (known as “Her-2” in humans) was investigated in cancer patients, it turned out to be overactive in about 25% of breast cancer patients. The resulting hypothesis was that blocking Her-2/neu using monoclonal antibodies should combat the cancer. This hypothesis was confirmed in a mouse model for this kind of breast cancer. These studies on mice led to the development of Herceptin, which has been approved in Europe for extreme cases in 2000, and as a supplemental therapeutic measure since 2006.
The fact that we can manufacture monoclonal antibodies, such as Herceptin, is due to basic research, partly performed on animals. Niels Kai Jerne, César Milstein and Georges J. F. Köhler were awarded the Nobel Prize for Medicine or Physiology in 1984 for this research.
Another example for the application of antibodies in cancer therapy (e.g. cancer immunotherapy) can be found in the Fact Check on animal models. Herceptin is also considered groundbreaking for the development of personalised medicine, where drugs are individually tailored to a patient’s genetic characteristics.
Thus, the statement that we have no cure for cancer misses the point. Although we cannot cure every cancer, we have better treatments for more and more kinds of cancer today – a development we owe to research on animals.
Figure: Mortality rates for cancer (age-standardized using European standards). Mortality rates have declined steadily since 1995. The earliest year for which reliable data on cancer exists for Germany (a), including breast cancer (b). For the UK, these data are available as far back as 1971 (c). It is apparent that the decline in mortality due to breast cancer began during the 1990s. Besides better early detection methods, this is due to the introduction of Tamoxifen as an adjuvant therapy. The data shown here were retrieved from the GEKID and Cancer Research UK (July 2015).
Aspirin is toxic to animals but not to humans.
Toxicity of aspirin was observed for cats and rats at doses that correspond to about 40-50 pills per day in humans (250-300 mg/kg). At this dose aspirin is just as toxic to humans as it is to other mammals. The same applies to the harmfulness of high doses during pregnancy. Fortunately, the effective dose of aspirin is many times lower, so that we can use it as a drug. It is sometimes speculated that it would be difficult to put aspirin on the market today. However, this is due to today’s very stringent regulations for approval. Aspirin, just like many other over-the-counter drugs, can have quite severe side effects. The reason is not that aspirin is particularly toxic in animals. On the contrary, aspirin is a common drug in veterinary medicine. As for other drugs, the recommended dose varies between species because many animals excrete drugs at different rates.
25 years of research on monkeys has brought no vaccine or cure for HIV/AIDS.
HIV is difficult to come to terms with, as it outwits the body’s immune system. It is correct to say that there is no effective vaccine at this time. However, animal tests have helped in recent decades with the development of HIV drugs that prolong the lives of millions of people, and thus keep HIV from becoming an automatic death sentence, as it was in the 1980s. The HIV virus was first identified during animal experiments, and these experiments were necessary to develop new diagnostic methods. Even though science at the moment is unable to cure AIDS, the development of diagnostics and treatments would not have been possible if not for research on animals. Figure: Diagnoses and mortality due to HIV/AIDS in the U.S. After introducing protease inhibitors in 1995, mortality rates declined (dashed black line) by 64%, from 50,000 to approximately 18,000 per year (source).
Animal tests are the wrong way to go – you can see that when a cure for Alzheimer’s works in mice but not in humans.
Through the examination of deceased patients we know that there are deposits of proteins, better known as plaques, in the brain. These plaques are mainly composed of the protein amyloid beta. To test whether amyloid beta could be the cause of Alzheimer’s, transgenic mice were bred. The genes which actually trigger the disease were inserted into transgenic mice. All of these mice produced amyloid beta in their brains, and consequently exhibited disease related changes, such as learning and memory disorders. This supports the amyloid hypothesis for the development of Alzheimer’s disease. Using these mice has been instrumental in developing various substances that prevent the formation of amyloid beta plaques. Treatment of the mice with these substances showed a recovered sense of memory. In simplified terms, they were “cured of Alzheimer’s.”
When these substances were tested in patients with advanced Alzheimer’s disease there was, disappointingly, no improvement of symptoms. It is considered possible that the formation of plaques must be prevented early during the disease’s progression, e.g. before the brain is too badly damaged. Another hypothesis would be that the fight against amyloid beta is simply not sufficient to prevent Alzheimer’s. Proponents of the so-called tau hypothesis lean toward the latter.
In an ongoing clinical trial, Alzheimer’s patients were administered the anti-amyloid drug Aducanumab in the earliest possible stage. This study shows very promising initial success (as of July 2015).
It should be noted that the amyloid hypothesis was developed from studies on human subjects, not animals. But the causal effects of amyloid beta was first established in mouse models. Without these experiments, we would be in the dark about the actual role played by the amyloid beta protein: whether it impairs memory, whether it has nothing to do with the disease, or whether it might even be a defense mechanism against Alzheimer’s, thus having positive effects. Furthermore, without these animals models, we would not have been able to develop substances that prevent the formation of amyloid beta plaques.
Animal models also assist researchers in establishing early biomarkers – a prerequisite for the development of preventive treatments for high-risk patients. Animal-free in vitro cell culture models may help to understand cellular mechanisms and to make the screening process for potential drugs more efficient. Nevertheless, they cannot completely replace animal models. In vitro cell cultures, for example, have no memory to be impaired by disease. Environmental factors, such as sleep deprivation, and their effect on the progression of the disease cannot be studied in cell cultures either. Significant progress in the understanding of the disease and the development of improved treatments has already been made. A shift away from animal testing at this time, however, would bring the bulk of this promising research to a standstill.
Other mouse models are used to study the role of tau and inflammatory processes in the development of Alzheimer’s. Additionally, these animal models are also used to investigate the onset of the disease. See also Fact Check on Animal Models.
Animal testing is inexpensive and an easy way to make a profit.
If scientists were anxious to make a profit rather than to establish new knowledge, animal testing would certainly be the last method to use. Animal experiments are not only morally burdensome, but also lengthy, complex and more expensive than other methods. Additional finances accrue from the strict legal regulations on animal testing for scientific purposes and the related application and evaluation procedures. The high cost can be attributed to the many employees who work around the clock for the welfare of the animals as well as their food, accommodation and medical care.
Cosmetic products are tested on animals.
Since March 11, 2013 Europe banned the sale of cosmetics that have been tested on animals (Regulation (EC) no. 1223/2009, Article 18, German Animal Welfare Act, §7a, (4)). The tests themselves are, of course, also banned.
Some animal studies are not for medical purposes but rather for the scientists to explore their own curiosity.
This statement refers to basic research, to which applied research and development, whether in medicine or technology, largely depends upon. The better we understand a disease, the more sophisticated our treatments can be. Without knowledge of a healthy organ system we cannot fully understand a disease. Without knowledge of the physiology of an animal we cannot understand what factors could threaten the survival of its kind. At the time basic research is performed, we can only vaguely or not at all predict how the results will one day be useful. However, it is evident from our past that basic research has helped us prepare for health and environmental threats. For example, hygiene methods, such as normal hand washing and the sterilisation of an operating room prior to surgery, is dependent on the germ theory – basic research of Louis Pasteur. The decoding of the structure of DNA– basic research by James Watson, Francis Crick and Rosalind Franklin – was the precondition, among other things, that therapeutic insulin or somatropin growth hormone no longer needed to be extracted from pigs or deceased humans. Instead, they are produced by genetically modified yeast or bacteria. The importance of basic research is also recognised by the German legislature, which explicitly permits animal experiments for this purpose. See also FAQs on Basic Research.
Although many Nobel Prizes were awarded to the field of physiology or medicine, only 45% of those winners conducted research on animals.
This statement suggests that 55% of the Nobel Laureates in physiology or medicine would not approve of animal experiments. However, this does not reflect the truth. In fact, this statistic was originally collected by Andrew Blake, a member of the group, Patients Voice for Medical Advance, which supports medical research. Blake had surveyed all 71, then living, Nobel Laureates in physiology or medicine, and asked them whether they considered animal experiments necessary. Out of 71 laureates only 39 had provided an answer. Thirty-two laureates said that animal testing was crucial for their own research. Although these 32 participants correspond to 45% of all living Nobel Laureates they were actually 82% of the participants in the survey! In addition, 100% of the participants agreed that animal experiments were important for the discovery and development of physiology and medicine (and still are). The false interpretation of these numbers goes back to the Anti-Vivisection Newsletter (VIN Issue 2). The fact that more than half of the Nobel Prize winners who completed a survey being conducted by a small, relatively unknown patient association shows how important they take the issue of animal testing. In May 2015, 16 European Nobel Prize winners turned in an open letter to the European Commission. They called this a matter of urgency: to support the continuation of animal experiments as long as they cannot be fully replaced by non-animal methods.
Drug tests on animals are useless, case in point Thalidomide.
In fact, Thalidomide is a particularly striking example of the need for drug testing on animals. The real scandal of this tragedy was that Thalidomide had been approved for pregnant women, without ever having been tested on pregnant animals. The harmfulness of Thalidomide for embryonic development went by unnoticed in adult animals as well as adult humans during studies prior to clinical approval. In an effort to find the cause of this damaging effect on development, this dramatic side effect is now demonstrated in several animal species (mice, rats, hamsters, rabbits, baboons, and marmosets). In rats and mice, the damage was so big that the foetuses died before birth. If Thalidomide had been originally tested on pregnant animals, the malformations or the reduced number of pups would have immediately led to the disapproval of the drug. Nowadays, it is a legal requirement that drugs for pregnant women are tested on pregnant animals first. To date, this regulation has prevented a repeated case of Thalidomide. Concerning alternative tests, there is currently no existing animal-free method to pregnancy. There is no suitable in vitro model for human embryonic development, and since we still do not fully understand the harmful effects of Thalidomide, it would not be possible to predict the side effects in a computer model. Up
9 out of 10 drugs tested on animals are not suitable for humans, proving that results from animal tests are not transferable.
This requires first that you know how drugs are developed. First, basic research identifies (by using non-animal methods and animal experiments) a point at which a drug could begin to take effect, such as a mechanism a pathogen uses to escape the immune system. Then, a substance is found that intervenes at this point in the system. Following, this substance is tested on animals, mainly for drug toxicity. If these tests show no strong toxicity, the substance has undergone the “preclinical phase” and is tested on healthy people (Phase 1). Phase 1 tests for side effects in humans, including ones that were difficult to see in animals, such as headaches. Only after that is the substance tested on a small group of patients (Phase 2). If the drug displays no significant side effects and produces the desired effect, it is tested on a large group of patients, mainly to discover rarer side effects (Phase 3). In each of these stages of drug development many substances are filtered out, for example because they do not have the desired effect or because of excessive side effects. It is true that less than 1 in 10 (6%) of the substances that successfully pass toxicity testing will result in an approved drug. However, the situation is similar with the substances that successfully pass the first phase involving humans (phase 1). Of those, only 1 of 7 (14%) will result in an approved drug. If you were to conclude from these numbers that the results from animals do not translate to humans, you would also have to conclude that the results from humans do not translate to humans. Both conclusions, of course, are false, as each drug development phase focuses on different characteristics of the substances. The toxicity tests on animals in drug development serve to protect the healthy volunteers in Phase 1. To administer untested experimental substances on humans would be unethical. Promising new methods, such as organ chips, could greatly reduce the number of animals required, and henceforth, the cost of toxicity tests in the future. During the discovery of starting points for potential new drugs, as in basic research, the use of alternatives to animal testing are implemented wherever possible. This is ensured by legal regulation. Animal experiments are approved only if a scientific question cannot be answered using an animal-free method.