Animal Rights

Response To More Comments From Disingenuous People. Part I

| by Dr Ray Greek

Chris Magee posted an essay regarding yours truly on the Speaking of Research website on February 4, 2014. I encourage all to read it before reading this response, which exists in 2 parts. I will analyze sections of the essay here. Titled “Animal Testing and Greek Mythology,” Magee begins by stating: “Ray Greek has been held up by the animal rights community as a standard bearer for the “animal research doesn’t work” movement. While his arguments appear credible at first glance, they quickly fail under scientific scrutiny. In this post we take a broad look at the arguments made in his key work, Animal Models in the Light of Evolution.” (Emphasis in the original.) Perhaps this introduction is from Holder; it is not clear from the post.

Why Shanks’ and my position would be described this way by anyone is perplexing. We consistently have stated that animal models offer limited predictive value at higher levels of organization while simultaneously acknowledging that seven out of nine ways animals are used in science and research are scientifically viable. To reduce our position to “animal research doesn’t work,” is rather disingenuous. (See almost any article, book, or book chapter we have published in the last 5-10 years for verification of this.) So to begin with, Magee (or Holder) is setting up a straw man here.

Magee continues: “However, the modern era has been marked by the rise of pseudoscience which argues from a perspective that animal research is ineffective, rather than immoral. It is often underpinned with an assertion that there are “modern alternatives” that should be used instead, if only scientists would take off their blinkers!”

I have gone on record many times stating that the term alternatives is not used by vivisectors or animal activists in the form the dictionary endorses. I am the least alternatives proponent in this controversy. There are alternatives to some animal uses but not when animals are used as a predictive modality. The reason for my position is the following. Most animal-based research and tests for drug development simply do not give data that can be applied to humans. See almost any of our articles from the last 5 years for references. Therefore, there can be no alternative to a method that does not work in the first place. There is no alternative to the Carter-Strong faster than light (FTL) engine because that engine does not exist. Moreover, FTL travel is impossible. So, if Magee is looking for someone who harps on alternatives, and many animal activists do, I am not that person. I am anti-alternatives if such a sweeping generalization is worth anything.

Magee then accuses Greek et al. of quoting out of context, but with little to support this claim. AFMA will actually address the specific instance Magee raises in our FAQs section of the new website. The website revision update should be ready by Spring.

Magee then discusses what our position is as opposed to what some animal activists say our position is. I do not see how plainly expressing our position and then having it misinterpreted is our fault. We used pretty straightforward language in our books. I stand behind every word Shanks and I published. Magee even acknowledges the limited scope of our position in quoting the following from Animal Models in Light of Evolution: “We are primarily concerned with the practise of using animals as predictive models of human and biomedical phenomena. […] [However], there can be no doubt that studies of animals have contributed greatly to our scientific understanding of life, and there is little doubt that these studies will continue to illuminate these matters in the future”

I find it interesting that while David Gorski MD, PhD states that there are far to many types of vivisection to place them in categories, Magee complains that animal activists have taken our clearly demarcated, and accepted, categories and generalized them. 1. Some animal activists have done this. 2. But Magee should be just as condemning of Gorski et al. who takes our position in exactly the opposite direction from the animal activists but ends up in the same place. This is one reason it is difficult to argue with vivisection activists—they make contradictory, often completely opposite, claims and act triumphant if I do not address their claims. They really need a formal process for deciding what they believe this week, but I doubt their politics will allow this. In the meantime, I will just keep pointing out the inconsistencies. (For example see below for claims regarding animals and first-in-man studies.)

Magee states: “Of course, animal models in most cases aren’t being used to “predict” anything.” Numerous quotes from vivisectors refute this (see [1-9] for examples). Animal models are being widely used as predictive modalities. If there is any controversy surrounding this read the grant application that led to a specific paper. Almost every animal-based research grant proposal says this animal model can predict what will happen in humans if not in those exact words. See the appendix 3 in reference [10] for examples.

Magee writes: “Where animals are used in drug testing it is to suggest that an effect observed in animals may also be observed in humans. When an effect is observed across multiple mammalian species, the probability of it also having that effect in humans can be sufficiently high to allow the compound to proceed to human trials.” This is not the reality of animal-based research. Species and even strains reveal opposite reactions to the same drug or disease. Rarely do we see the same effect across species lines. There are exceptions, see reference [11]. But even then important effects may or may not be seen in humans. That is why animal models have little predictive value—essentially no predictive value—for real life situations. The reality is that when a serious adverse effect is observed in even one species, there is a high probability the drug will not be further developed. There are dramatic instances of lone scientists ignoring the company policy and developing the drug anyway only to discover that the side effects were in fact minimal and or that the main effect was good but unanticipated. There are also instances of scientists simply ignoring the bad results from one species and showing the FDA the good results from another. Even Pharma says animal testing and use in drug development has failed. I have over 100 references for this and I only peruse a limited number of journals. I suggest anyone interested read my past blogs and articles for more.

Magee then accuses us of cherry picking data and not understanding probability.

Elsewhere, AMLE’S companion “FAQs about the use of animals in science” (FAQ) quotes heavily from “Animal Toxicity Studies: their relevance for man”, an out-of-print book of essays from 1990 in which a selection of toxicologists consider how toxicology models could be improved. Greek gleefully cherry-picks from their examples, which are necessarily focused upon examples where the models of the day weren’t working well. Nonetheless he regularly ignores the overriding points that they make – that animal research remains important and that the animal models need improving not removing. Greek is happy to support his case with quotes such as:

“In one small series in which the toxicity in clinical trials led to the termination of drug development it was found that in 16/24 cases toxicity was not predicted in animals [49] “

[49] Lumley C: Clinical toxicity: could it have been predicted? Premarketing experience. In Animal Toxicity Studies: Their Relevance for Man. Edited by Lumley C, Walker, S: Quay; 1990: 49-56.

This appears on Page 53 of his FAQ (and his marketing excerpt of the book), but curiously does not appear in either the chapter of the book quoted, nor anywhere else in Lumley’s (et al.) book.

I searched for the above quote and it is NOT in the Lumley and Walker book in any form that I can find. I then searched my notes for the reason that I used that reference. I found the exact reference in Olson et al 2000.[12]:

Clinical toxicity data for more diverse types of drugs have also been the subject of several workshops and overviews (Lawrence et al., 1984; Fletcher, 1987; Lumley and Walker, 1990; Parkinson et al., 1994). In one small series in which the toxicity in clinical trials led to the termination of drug development, it was found that in 16/24 (67%) cases the toxicity was not predicted in animals (Lumley, 1990). In another analysis, 39/91 (43%) clinical toxicities (from 64 marketed drugs) were not predicted from animal studies (Igarashi, 1994). This latter publication forms part of the largest data set known to us, that of the Japanese Pharmaceutical Manufacturers Association (JPMA, 1994). This was derived from the literature (as distinct from questionnaire-derived data) and refers to data from 139 drugs approved in Japan from 1987 to 1991.

I should have referenced the Olson study as what we said was apparently a direct quote from Olson et al. My bad!! I wrote (actually typed it out on the computer) the FAQs book (we collaborated on both) while Shanks did the same for the Animal Models . . . book (the mistakes and typos in that one are his, although we both proofed both of the books dozens of times). The JPMA reference in Olson et al. above is also in Lumley and Walker but the 16/24 figure is not there, or at least I could not find it. I have also seen the 16/24 figure in other sources that also referenced Lumley and Walker. For example, Lumley and Walker is also referenced for the 16/24 figure in the book: Adverse Drug Reactions (2009 Springer) by Jack Uetrecht. With that many people referencing the Lumley chapter, there must be a reason (or everyone copied Olson et al.).

But the original source appears to be in the JPMA article discussed by another author, Igarashi, in the Lumley and Walker book.[13] The JPMA study is also described in another Lumley book in yet another chapter by Igarashi.[14]  But, the JPMA article is in Japanese, which is why I think most people have incorrectly referenced Lumley and Walker as the study is described there by Igarashi. Translations of the JPMA article have been made. I lost mine apparently (I’m looking for it). But the 16/24 figure is in the literature and appears to be a viable translation from Japanese. The JPMA study is also frequently quoted as being one of the most well done studies of the past.

In any event, as the Olson et al. study appears to be the original source for the error and as it predates our books and articles, we clearly did not fabricate the figure. It appears to have come from or been associated with the Japanese study but it may have been referenced in the Japanese study or come from somewhere else entirely. I will see what else I can find regarding the origin.

I thank Magee for pointing this out! I make mistakes and am happy to correct them. There are probably another ten or so similar mistakes in the reference section of the FAQs book alone. But the mistake does not invalidate the general concept or even the data (the JPMA studies) the figure apparently came from. The only thing wrong about the 16/24 figure was how I referenced it both directly and indirectly. Moreover, there are many well-referenced examples of animal models having really poor predictive value. See the numerous references below ([15-57]). One thing Shanks and I argued about was the use of examples. He wanted one and no more and I wanted ten so if situations like this arose we were not dependent on that one example. I gave in to him more often than not. But in my blogs and articles I now list many examples and references for this very reason.

Again, the 16/24 figure was just an example. There are many studies and examples where the authors found the PPV of animal studies to be minimal. Anyone who has read my articles should be familiar with this. Scores of scientists involved with drug development echo this, as I also pointed out in our books and articles. There is scientific consensus on the very low predictive values for animal models.[15-57] This appears to be controversial only in the basic research community that uses animal models. If anyone wants to compare quotes from head-to-head comparative studies and or the data from all such studies available, I will win. But examples and even studies are not as powerful as theory, which is what Shanks and I really focus on.

Continued in part II.


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