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Speaking Lies For Research So Funding Can Continue

On October 28, 2013, Tom Holder, of Speaking for Research, and I were interviewed on BBC Radio Humberside. My interview can be accessed here and Holder’s here. I was interviewed first and Holder was interviewed some time later. The purpose of the interviews was to briefly discuss the use of Beagles in research and testing as a company called B&K Universal is requesting permission to open a breeding facility in East Yorkshire in the UK. I want to analyze Holder’s statements from his interview as they reveal two important details. 1. All of his arguments have been refuted before. 2. Despite this, Holder and other vivisection activists continue to use these arguments. This speaks volumes regarding his position. This is also why a properly moderated debate is needed on the use of animal in research and testing.

The BBC asked Holder: “It’s [animal testing] out of date though isn’t it, we’ve seen modern scientists have said their animal testing completely out of date . . . you can’t actually predict the human response, completely too vague.” Holder replied: “Well certainly that is not the scientific consensus . . .”

Actually it is. As I have pointed out in many blogs and articles, including There is Consensus on Prediction, the consensus among scientists that work in areas associated with drug development and disease research is that animal models have no predictive value. If by “scientific consensus,” Holder means scientists that use animal models and thus have a vested interest in animal models, then he is most certainly correct. In reality, “scientific consensus” does not mean that and Holder is demonstrably wrong. (For actual quotes from scientists, see There is Consensus on Prediction.)

Holder continues: “animal research is hugely expensive so there is a strong drive to replace the use of animals where ever possible, . . .”

Wrong again. Clinical research is expensive; animal testing and research is relatively cheap. According to DiMasi et al. (DiMasi, Hansen et al. 2003), the expected cost of a new chemical entity in drug development breaks down as follows (in 2000 US dollars).

  • Phase I                                    $15.2
  • Phase II                                   $16.7 million
  • Phase III                                  $27.1 million
  • Long-term animal tests        $1.6 million

This means long-term animal testing amounts to <3% of the development cost that begins with clinical trials. This estimate does not include initial chemistry testing (nonanimal) and acute toxicity and efficacy testing (animal) but these are also cheap compared to clinical trials.(Paul, Mytelka et al. 2010, Allison 2012) The following is from Drug Discovery & Development: “The major costs incurred by a drug company are for clinical trials and marketing. The amount of money spent on initial discovery and development is only about 2 to 5% of the total cost of getting the drug to market.” (Unknown 2002) And, according to Roy (Roy 2012), 90% of total drug development cost occurs during Phase III clinical trials. Failing late is the major problem in drug development and this is because of the failure of animal models.(Mullane and Williams 2012) Animal testing and animal-based research are cheap in the short-term but costly in the long-term. Catherine Shaffer, Contributing Editor to Drug Discovery & Development states:

Drug development is an extremely costly endeavor. Estimates of the total expense of advancing a new drug from the chemistry stage to the market are as high as $2 billion. Much of that cost is attributable to drug failures late in development, after huge investments have been made. Drugs are equally likely to fail at that stage for safety reasons, as for a lack of efficacy [both of which use animal models to evaluate], which is often well-established by the time large trials are launched. (Shaffer 2012)

Basic research with animals is also cheap compared to clinical trials and clinical research in general. However, universities profit from animal-based research.

Holder continues: “and there are promising technologies . . . being developed, but there’s no sign of a blanket replacement at present . . .”

As I have stated many times, society does not need to wait for blanket replacements/predictive technologies before abandoning useless technologies and methods. Think how insane it would sound to hear someone say that we cannot abandon treating schizophrenia with trephination (cutting a hole in the skull) because we do not have a cure for schizophrenia yet. The reason medicine abandoned trephination was because it was ineffective, not because we discovered a cure for, or found a better method of treating, schizophrenia.

Holder continues:

so it’s important to understand that the cell cultures and computer models are currently used in conjunction with animal research rather than necessarily as just a straight alternative and all these tools are used to build up an understanding of human and animal physiology and the pathologies which affect us.

This is somewhat true but is also largely the reason most drugs fail late. Pharma does not have the technologies it needs for drug development. Currently, in vitro and in silico cannot do everything necessary to being a drug to market. They are successful at some things and this is what separates them from animal models. But again, regardless of the other options, continuing to reply on a methodology that is known to fail is not good for business nor is it good science. Cell cultures and computer models are effective as far as they go but they cannot predict efficacy and safety in humans. Pharms need technology that will do this. And when they find it, it will be human-based, not animal-based. Clinging to animal-based testing is a sign of poor science not a lack of options.

The BBC then asks: “Why is it unavoidable in some cases, why do we have to still use animals?” Holder replies:

Well, simply because we don’t have another, um method so, you can get so far using computer models or cell cultures, MRI scans, a whole host of other techniques but ultimately at some point you need to move a novel chemical into a whole organism or you need a whole organism to understand whatever it is that you’re doing. I mean there’s no other way of studying for instance genetics, accurately, without having the ability to breed animals and to be able to knock in or knock out genes, to understand what it is that they do.

Again, even if there were no other methods for developing drugs, smart people would nevertheless refrain from relying on Ouija boards, drawing names of drugs out of a hat, or using other methodologies with no predictive value. Here, Holder reverts back to the intact system’s argument: you need an intact, living, whole organism. The intact systems argument basically states that scientists need an intact, living system to test drugs on because humans are intact living systems and cannot be wholly represented by in vitro and in silico models. This is true in what it confirms but wrong in what it denies. Animals and humans are both intact living systems. However, because animals are living, intact systems that are differently complex from humans, they cannot be successfully used to determine what a second living, intact complex system e.g., humans are going to do either. Empirical evidence supports this. (For more on this see the blogs:

More Misrepresentations, Fallacies, and Other Lies. Part II and

Vivisection Or Death: Part III, No Other Options.

Our books Animal Models in Light of Evolution and FAQs About the Use of Animals in Science: A handbook for the scientifically perplexed also discuss the intact systems argument.)

This leads to Trans-Species Modeling Theory and what animals can be used to model and what they can not. Animal models will never be capable of providing predictive value for humans when the questions concern higher levels of organization. Animal models can be successfully used when perturbations occur at lower levels of organization or to determine the general function of gross morphology. (See above 2 links for more.)

In terms of the genetics Holder mentions, many if not most scientists, that are not financially linked to animal models, currently maintain that genetically modified animals offer little of value in determining a gene’s role in humans. Horrobin states:

Second, consistent phenotypes are rarely obtained by modification of the same gene even in mice. The disruption of a gene in one strain of mice may be lethal, whereas disruption of exactly the same gene in another strain of mice may have no detectable phenotypic effect. If this is true of the impact on one gene of the rest of the mouse genome, how much more is it likely to be true of the impact of the rest of the genes in the human genome? (Horrobin 2003)

van Regenmortel states:

Furthermore, disruption of the same gene can have diverse effects in different strains of mice (Pearson 2002). Such findings question the wisdom of extrapolating data that are obtained in mice to other species. In fact, there is little reason to assume that experiments with genetically modified mice will necessarily provide insights into the complex gene interactions that occur in humans (Horrobin, 2003). (Van Regenmortel 2004)

Pearson states:

It was Terry Magnuson of the University of North Carolina at Chapel Hill who opened many mouse geneticists’ eyes to the influence of the rest of the genome on knockout experiments. In 1995, his team disabled the gene for the epidermal growth-factor receptor. In one mouse strain, CF-1, the knockout embryos perished at around the time of implantation in the uterus. But in the CD-1 strain, they survived for up to three weeks after birth (Threadgill, Dlugosz et al. 1995). “From that time on, everyone started paying much more attention to the genetic background,” says Magnuson. (Pearson 2002)

Threadgill et al. state:

Gene targeting was used to create a null allele at the epidermal growth factor receptor locus (Egfr). The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities. (Threadgill, Dlugosz et al. 1995)

Nijhout states:

The importance of context is also illustrated by studies of the effects of “knockouts” of specific genes in mice, a method that completely eliminates the function of a gene’s product. For example, knockout of a retinoblastoma-related gene causes severe abnormalities and embryonic death in one strain of mice, but the same mutation in another strain has no effect. The mutant mice are viable and become fertile adults, as shown by Michael Rudnicki (LeCouter, Kablar et al. 1998)and his colleagues at McMaster University. (Nijhout 2003)

All of the above should be placed in the context of the success scientists are having by studying genomes and specific genes in humans.

Holder then goes on to explain that animals are needed to ensure safety for human participating in drug development studies; namely Phase I human clinical trials. Vivisection activists oscillate on who is being protected by safety studies in animals. Some claim, like Holder, that only humans participating in Phase I are offered some protection from animal studies but other claim that the population as whole, when taking the new drug, is protected by animal studies. The more reality-based answer is Holder’s but his answer fails nonetheless.

The "one incident" Holder is referring to was a huge failure and humans were severely harmed. However, society has no way of knowing whether other such trials likewise harmed humans: the data is proprietary and Pharma does not want nasty things that make them look bad released to the media. We do now from data collected during drug trials in India that, according to India's Tribune newspaper, at least 1725 people died in drug trials between 2007 and 2011. Based on known trans-species toxicity testing data, we have no reason to believe that animal models offer any protection to humans in Phase I trials.

B&K Universal actually made claims about medical research on their actual planning application.

The presence of a vibrant life sciences industry in the UK should help to enhance opportunities for patients to participate in clinical trials, known to help improve patient care and provide early access to new treatments. A strong life sciences industry is dependent on our world leading research base. Use of animals is a small but important part of biomedical research for example to further understanding of basic mechanisms of health and disease and provide new targets for treatment of diseases such as dementia. Research involving animals is also necessary in agricultural science, where developments are required to prove they are safe for the environment, wildlife and humans. (Emphasis added.)

Note that B&K is explicitly stating what I have pointed out many times before regarding the ways animal models are used in drug development. Animals are used to identify targets for drug intervention, usually in research at universities, and this is why drugs fail in efficacy. Animals are also used to identify adverse drug reactions in the form of toxicity testing and this is why the drugs fail in safety both from the perspective of allowing dangerous drugs to the market and stopping otherwise good drugs because of bogus safety concerns. Safety and efficacy make up the two main reasons drug fail late and both rely on animal-based testing.

The statements and positions from B&K and Holder can and have been scientifically refuted. In some cases the claim has been refuted many times. I have noted the same claims being used in debates, articles, lectures, and op-ed pieces. The reality that these claims are make-believe never seems to achieve the level of public consciousness. There could be many reasons for this. Perhaps society as a whole simply does not understand enough science to appreciate when a claim has been refuted. Perhaps the fact that the media is biased, reflected by the different amounts of time allowed for the two interviews or the people frequently asked to represent the pro-science, anti-vivisection position, influences society away from the scientific facts. Regardless, society needs a way to separate fact from fiction and determine the reality of what animal models offer. Society needs a widely available, properly moderated, debate.

I will be writing more about this.


Allison, M. (2012). "Reinventing clinical trials." Nat Biotech 30(1): 41-49.

DiMasi, J. A., R. W. Hansen and H. G. Grabowski (2003). "The price of innovation: new estimates of drug development costs." J Health Econ 22(2): 151-185.

Horrobin, D. F. (2003). "Modern biomedical research: an internally self-consistent universe with little contact with medical reality?" Nat Rev Drug Discov 2(2): 151-154.

LeCouter, J. E., B. Kablar, P. F. Whyte, C. Ying and M. A. Rudnicki (1998). "Strain-dependent embryonic lethality in mice lacking the retinoblastoma-related p130 gene." Development 125(23): 4669-4679.

Mullane, K. and M. Williams (2012). "Translational semantics and infrastructure: another search for the emperor's new clothes?" Drug Discovery Today 17(9-10): 459-468.

Nijhout, H. F. (2003). "The Importance of Context in Genetics." American Scientist 91(5): 416-423. 

Paul, S. M., D. S. Mytelka, C. T. Dunwiddie, C. C. Persinger, B. H. Munos, S. R. Lindborg and A. L. Schacht (2010). "How to improve R&D productivity: the pharmaceutical industry's grand challenge." Nat Rev Drug Discov 9(3): 203-214.

Pearson, H. (2002). "Surviving a knockout blow." Nature 415(6867): 8-9.

Roy, A. S. A. (2012). Stifling New Cures: The True Cost of Lengthy Clinical Drug Trials. Project FDA Report. New York, Manhattan Institute for Policy Research. 5.

Shaffer, C. (2012, January 1, 2012). "Safety Through Sequencing." Drug Discovery & Development Retrieved January 30, 2012, from

Threadgill, D. W., A. A. Dlugosz, L. A. Hansen, T. Tennenbaum, U. Lichti, D. Yee, C. LaMantia, T. Mourton, K. Herrup, R. C. Harris and et al. (1995). "Targeted disruption of mouse EGF receptor: effect of genetic background on mutant phenotype." Science 269(5221): 230-234.

Unknown (2002). Drug Discovery & Development(November): 35. 

Van Regenmortel, M. (2004). "Reductionism and complexity in molecular biology. Scientists now have the tools to unravel biological complexity and overcome the limitations of reductionism." EMBO Rep 5(11): 1016-1020.


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