Similarity of Anti-Vaccination and Anti-Animal-Testing Arguments

While reading Edzard Ernst’s fantastic blog I came across a list of “common anti-vaccination tropes” that originated in a 2012 paper by A. Kata.

Ernst anti-vaccination animal testing

What’s interesting is that nearly every argument could be used by an animal rights activist if you simply switch the word “vaccination” to “medicine”. So:

1. I am not anti-medicine, I am pro-safe-medicine.
This is a common attack on animal research, as they claim that they want medicines, but don’t believe animal research helps. This is often conflated with the idea that side effects only exist because  a drug was developed using animal research (as if other chemicals, discovered other ways, would not have side effects). This is silly – all chemicals have side effects, all can be overdosed on, even water.

2. Medicines are toxic
The nuttier end of the animal rights movement sometimes try to reject all animal researched medicines as toxic – since only “natural” or “herbal” remedies will work. I have heard it claimed (multiple times) that homeopathy or herbal remedies can cure cancer or AIDS (see Ernst’s blog). Similar points about adverse drug reactions as mentioned above also apply to this point.

3. Medicines should be 100% safe
Neither animal research, nor human clinical trials can guarantee 100% safety. We all have slight genetic differences. Penicillin may have saved million upon millions of lives, but some people will still have violent, and sometimes fatal, allergic reactions to it. Some people are even allergic to sunlight, you cannot have a 100% safe solution. Sometimes we know how dangerous a treatment is, but we still go ahead with it because it’s better than the alternative (e.g. Chemotherapy to treat cancer).

4. You cannot prove that medicines are safe
Animal research is not designed to say that a drug is safe for mass consumption. It is designed to show that it is safe enough to go to early stage clinical trials in humans. These trials are there to determine if drugs are safe for larger trials.

5. Medicine did not save us
Sadly, no medicines are 100% perfect. Nonetheless saying they don’t always work is far from saying they never work. Certainly homeopathy and other “natural” remedies don’t achieve the success rates of proper medicines.

6 Medicines are not natural.
Firstly, many are (e.g. Aspirin was originally a willow bark extract). Secondly, why does it matter? In the words of Tim Minchin:

“Alternative Medicine”, I continue “Has either not been proved to work, or been proved not to work. You know what they call alternative medicine that’s been proved to work? Medicine.

7. I am an expert in my own child
The first and only one on the list that can’t cross the anti-vaccination, anti-animal-research bridge.

8. Galileo was persecuted too
Otherwise known as “Just because animal research is supported by most of the scientific community doesn’t mean you’re wrong”. No, it doesn’t – but it’s a pretty big hint.

9. Science has been wrong before
Yup, it’s been right a lot too. Especially on things with lots of evidence – see entire history of modern medicine.

10. So many people simply cannot be wrong
Blow me down, Dr. Greek, Dr. Hansen, Dr. Menache, Dr. Vlasak, couldn’t all be wrong? Surely it must be the 93% of scientists who believe animal research is essential who are wrong!! This ridiculous argument usually joins the great scientific conspiracy against animals.

11. You must be in the pocket of BIG PHARMA
Again the great conspiracy rears its ugly head – read this great post dispelling that idea.

12. I do not believe that the problems after medication occur coincidentally
This would apply to animal research insofar that it is one of the side effect comments dealt with above. For vaccines this takes a specific turn of blaming autism on vaccines – an idea thoroughly discredited.

Ernst also makes the point that those against vaccines tend to be in favour of “alternative medicine”. So we can see the crossover between the anti-proper-medicine, anti-vaccination, and anti-animal-research movements.



9 thoughts on “Similarity of Anti-Vaccination and Anti-Animal-Testing Arguments

  1. do you know how much money and time was wasted on experimenting on cats with feline HIV as an analogue to human HIV? It wasn’t until the late 90’s that a consensus was formed that rejected this approach. It took even longer for the primate model to be debunked. It was only through activists that stood up and insisted drugs be tried by those in hospices that any progress was made. While not true of all diseases, and I am not an absolutist, your assumption that it is more reasonable to be the opposite of what animal rights say is a little juvenile and anti-science. Scientists don’t write like Op-Ed writers like you, they examine the data with a disinterested approach.

    1. Tim, you are very misinformed.

      Firstly, feline HIV (FIV) was never a very widely used model for HIV drug and vaccine development, as most researchers focussed on SIV that is more similar to HIV, and more recently on HIV in GM mice, there was never a consensus to reject it and FIV research has continued, see

      Secondly, far from being debunked non-human primate models of HIV play a crucial role in the development of vaccines against HIV, as we have discussed on this blog and a recent review published in Annual Review of Medicine expands on this to highlight this critical role played by non-human primate studies in the development of AIDS vaccines

      Animal studies also played a key role in identifying and developing the drugs that are used in HAART and in preventing mother -to-child transmission and in post-exposure prophylaxis

      It is tue that one particular non-human primate model of AIDS – the SHIV model (especially SHIV 89.6p) – turned out to be not stringent enough, a problem that several researchers had warned about due to differences in its coreceptor specificity and infection course, and is not used so much now, but more stringent SIV models remain very important to HIV research

  2. You’re basically using animal rights activists as an excuse to avoid a discussion on the importance of developing alternatives to reduce the need for animal testing and speeding up the testing stage. That’s cute.

    1. Not in the least – Nowhere have I suggested that scientists shouldn’t embrace the 3Rs of replacement, refinement and reduction. I think they are important. However, most of the “alternatives” we develop turn into complementary methods – working alongside the use of animals and replacing little bits of it. We are nowhere near blanked replacement methods.

  3. You simply cannot use an animal model as a predictive tool when the human disease doesn’t exist at all in the animal specie: this is a waste of money, resources and is slowing medical progress in a way not acceptable anymore. Just an example, in a thousand that exist:

    “Animal models of Alzheimer’s disease and drug development”
    B. Laurijssens, F. Aujard, A. Rahman,
    Drug Discovery Today, April 2012

    “Animal disease models are considered important in the development of drugs for Alzheimer’s disease. This brief review will discuss possible reasons why their success in identifying efficacious treatments has been limited, and will provide some thoughts on the role of animal experimentation in drug development. Specifically, none of the current models of Alzheimer’s disease have either construct or predictive validity, and no model probably ever will.”

    Please, stop supporting bad science.

    1. Dogs develop Alzheimer type disease, so do old monkeys and old bears. they are a minority (like humans!) and we only know about it because they are or ahve been in care in zoos or human companions, with the luxury of care, daily meals and protection from predators. In the wild, animals developing such bad diseases would not survive past the early stages. even a prodromal stage would probably be enough to make you easy prey. And yes, human and animal diseases are different but the basic physiological principles of how cells live and die are the same. We can learn a lot of why and how it happens from animals, one step at a time, if not yet how to stop it. And yes, there are bad scientists, as much as bad mechanics and bad writers and bad everything. But the majority does the job that keeps people alive and healthier and has given you a life expectancy of >70 yrs as opposed to 40 yrs old, a couple centuries ago!

      1. Very few species spontaneously develop Alzheimer-like disease (of course different from the human one), and quite often the “animal model” is not provided by animals that spontaneously develop the disease, yet the disease will be induced with chemicals or genetical mutations: that is NOT Alzheimer; that is bad science, that is a waste of money and effort, that is an insult to human patients that suffer and are waiting for a cure.

    2. Here we see Antonio using one of the most popular tactics that anti-vivisectionists (and for that matter anti-vaccination campaigners, creationists, AGW delialists and sundry anti-science folk) like to use: Quote mangling.

      The full abstarct of the paper by Laurijssens he quotes (available at is:

      “Animal disease models are considered important in the development of drugs for Alzheimer’s disease. This brief review will discuss possible reasons why their success in identifying efficacious treatments has been limited, and will provide some thoughts on the role of animal experimentation in drug development. Specifically, none of the current models of Alzheimer’s disease have either construct or predictive validity, and no model probably ever will. Clearly, specific animal experiments contribute to our understanding of the disease and generate hypotheses. Ultimately, however, the hypothesis can only be tested in human patients and only with the proper tools. These tools are a pharmacologically active intervention (in humans) and a clinical trial suited to evaluate the mechanism of action. Integration of knowledge in quantitative (sub) models is considered important if not essential in this process.”

      So in fact despite their limitations the authors see the animal models as being very important to the development of new therapies.

      Rather ironically given Antonio’s first statement the article itself has a section devoted to naturally occuring animal models of alzheimers, the first paragraph of which reads:

      “Natural models

      Several animals including polar bears, dogs, cats, goats and sheep and some non-human primates spontaneously develop some AD-related neuropathological features [4]. The few animal models reviewed in this section either show major AD-related neuropathology or are in close phylogenetic proximity to humans. In recent years dogs have been considered as a useful animal model for AD due to the close proximity of canine and human brain aging. Dogs develop extensive Aβ and diffuse plaque deposition and the extent of Aβ deposition correlates with the decline of some measures of cognitive function in the absence of neurofibrillary tangles (NFTs). Moreover, the amino acid sequence of Aβ is fully conserved between dogs and humans [5]. Because of spontaneous age-related Aβ deposition and relative ease of cognitive function assessment, aged dogs were used to evaluate interventions with the aim of reduction of Aβ load and subsequent cognitive improvement (Table 1).”

      The review goes on the value and limitations of different animal models of Alzheimer’s disease and how they have contributed to our understanding of the disease, and to analyse the use of animal models in developing therapies for Alzheimer’s disease and how it can be optimized, before reaching its conclusion:


      The value of many of the so-called animal models for AD lies not in the fact that they attempt to replicate the full spectrum of the human disease, but in that they could help us, together with clinical data, to generate hypotheses and understand the complex physiology relevant to the human disease. In that sense, they are not really animal models of disease but ‘just’ animal experiments. These experiments, then, need to address specific questions that allow the construction of the hypotheses for the whole or parts of a quantitative human disease model. The conceptual human model is where interventions should be evaluated: for example, target selection, dosing regimen and timing, biomarker and clinical endpoint selection and safety. Integration of information and ideas into a quantitative conceptual (sub) model of human disease and pharmacology is therefore considered essential.

      For drug development, whereas there is likely to remain great uncertainty around target selection and the associated hypotheses, it is crucial to identify a pharmacologically active dosing regimen to test in patients. Then a negative clinical patient study, although disappointing, will at least increase our knowledge regarding the disease.”

      Very different from what Antonio would have us believe the paper claims!

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