A Chinese woman was attempting to make a traditional healing liquor from scratch, but after the long process was finally complete, it literally came back to bite her.
Shejiu is liquor made by pickling a venomous snake in a bottle of alcohol. The venom in the snake is neutralized from the process, and practitioners of Chinese medicine say that it has healing properties.
The woman suffers from chronic joint pain, so in order to relieve her symptoms, she frequently takes shots of the shejiu. One day, as the woman opened the top to pour out more alcohol, the snake, which had been pickling in the jar for three months, jump out and attacked her. The venomous snake bit the woman on her finger.
“Before the shejiu could have any effect on me I was sent to the hospital for a snake bite,” said the woman.
The woman was released from the hospital not long after she was bit, and the snake was later killed.
John Ericson wrote an article titled The Price of Killing Off Animal Testing, which was published by Newsweek.com on February 20, 2014.
Ericson begins by stating that: “Each year, more than 25 million animals are used for scientific research in the U.S. More than 90 percent of those are mice . . .” The actual numbers are unknown but a more realistic estimate would be over 100 million. Even a former editor of Scientific American stated that around 100 million genetically modified mice were used annually in the US. (Mukerjee 2004) So anyone or any organization that claims less than that is clearly biased or uninformed.
Ericson goes on to paint a very black and white picture of animal-based research and testing. He cites the American Association for the Advancement of Science (AAAS) as supporting it and quotes Frankie Trull of the Foundation for Biomedical Research (FBR), as saying the usual: “An immediate end to animal research in the U.S. would be a death sentence for millions of people around the world . . . If you've ever taken antibiotics, had a vaccine, had chemotherapy, an MRI, a blood transfusion, dialysis, an organ transplant, bypass surgery or joint replacement, you have been the beneficiary of research that started with lab animals.” Although these claims are widespread they is also unsupported by a critical examination of the scientific literature along with currently known facts regarding species differences. Moreover it is an example of the fallacy post hoc ergo propter hoc. (See The Strengths and Limits of Animal Models as Illustrated by the Discovery and Development of Antibacterials and Are animal models predictive for humans? for a refutation of some of the above claims. See Trans-Species Modeling Theory for why animals are very poor models for humans.)
Ericson goes on to describe why the elimination of animal-based research would be a blow to “research on neurodegenerative disease” like Alzheimer's disease (AD). This is an odd choice for an example since research with animal models has misled researchers studying AD more often than not. (For example, see Evidence Supports TSMT. See Trans-Species Modeling Theory for a detailed examination of this claim as related to amyotrophic lateral sclerosis (ALS).)
I wrote the following in the comments section of the article:
Animal-based research and testing originated during a time when creationism was accepted as the norm. Under that paradigm, animals and humans were thought to be more alike than different. Today we know better. Animal testing is a failure from a scientific perspective and animal-based research results in something medically useful only a tiny fraction of the time. For more on why animal experimentation is scientifically nonviable see http://www.futuremedicine.com/doi/pdfplus/10.2217/pme.11.89
The reason animal models fail to be of predictive value for human response to drugs and disease lies in evolution and genetic variability. This variability exists even within the same species, for example monozygotic twins. An article in Developmental Cell by Spector and Mélanie Eckersley-Maslin et al., (Eckersley-Maslin et al. 2014) reveals new reasons for this. A team from Cold Springs Harbor conducted research, which revealed that “some cells activate only one of their two gene copies during development, altering protein yields and raising new questions.” We have one copy of each gene from each parent. Usually both of these copies are activated. But in some cases it appears that only one copy is activated either in development or later. “Random monoallelic gene expression cuts the amount of a protein by half, suggesting that this type of variability may have significant implications for disease.” The researchers found that “monoallelic gene expression is truly a random process.” Spector stated: “It is not deterministic in any way . . . This significant amount of flexibility and randomness in gene expression is important for adaptation as a species evolves, but it is unclear how it functions in organisms today.”
The above differences in genetic make-up are in addition to differences in mutations like single nucleotide polymorphisms (SNPs) and copy number variants (CNVs) and differences in gene regulation and expression, among many others. Just one such difference between species could account for why a disease affects one species differently from another or why one drug affects one human differently from another. Species are defined by thousands of such differences and this is why we can eat chocolate but dogs should not.
The failures of animal modeling are best demonstrated by intra-human variation. A February 26, 2014, Mayo Clinic press release announces: Mayo Clinic Discovers African-Americans Respond Better to Rubella Vaccine. Scientists compared vaccine responses from Somali Americans and Caucasians and discovered that Somali Americans developed “twice the antibody response to rubella.” A non-Somali, African-American cohort also saw a high response and Hispanic Americans exhibited a low response as did Caucasians.(Haralambieva et al. 2014) Dr. Poland, the chair of a Safety Evaluation Committee for non-rubella vaccine trials being conducted by Merck Research Laboratories stated: “The significance of the findings is that in the future we may be able to create vaccines for specific groups or even individuals based on their genomic and other characteristics . . . That may mean adjusting doses for some or being able to treat larger populations with the same vaccine if the dosage is less.”
Vivisection activists should be concerned that the practice they are defending is based on a creation model of life. But they’re not.
(Photo from CDC and Wikiperia Commons http://en.wikipedia.org/wiki/File:Rubella_virus_TEM_B82-0203_lores.jpg)
Eckersley-Maslin, MÈlanie†A, David Thybert, Jan†H Bergmann, John†C Marioni, Paul Flicek, and David†L Spector. 2014. "Random Monoallelic Gene Expression Increases upon Embryonic Stem Cell Differentiation." Developmental cell 28 (4):351-365. http://linkinghub.elsevier.com/retrieve/pii/S1534580714000586
Haralambieva, I. H., H. M. Salk, N. D. Lambert, I. G. Ovsyannikova, R. B. Kennedy, N. D. Warner, V. S. Pankratz, and G. A. Poland. 2014. "Associations between race, sex and immune response variations to rubella vaccination in two independent cohorts." Vaccine. doi: 10.1016/j.vaccine.2014.01.090.
Mukerjee, Madhusree. 2004. "Book Review of Speaking for the Animals " Scientific American August:96-7.
Weverton Silva, 10, was called a medical miracle after he was impaled with a 2 foot long metal spike and survived.
The young boy was picking guava fruits on Saturday in the Brazilian city of Macae when he fell from the tree. He landed on an iron bar, which punctured the left side of his body under his armpit and emerged near his right ear.
The bar missed all of Silva’s vital organs and his basic arterial routes. It was removed in one piece after five hours of surgery.
“It is difficult to arrive at a hospital with such a situation and survive,” Dr. Rodrigo Chicralla said. “I think it was just God.”
Silva was discharged on Sunday.
Apple’s merger and acquisitions chief Adrian Perica and Tesla Motor’s chief executive Elon Musk met last year, suggesting that the iPhone maker may expand its business to electric cars.
Considering Apple has announced plans to better integrate iOS into car dashboard screens and has partnered with Ferrari, it seems likely that the Silicon Valley giant would be interested in Tesla.
The meeting was reported Sunday by The San Francisco Chronicle, which cited an anonymous source. The paper also noted that Apple is interested in medical devices, specifically those that can predict heart attacks.
Apple’s interest in electric cars and medical devices signal that the company wants to expand and take risks beyond the iPad and iPhone, as Wall Street analysts have speculated in the past.
Adnaan Ahmad, an investment bank analyst in Germany, wrote an open letter to Apple CEO Tim Cook in October suggesting that Apple buy Tesla. He argued that the electric car industry could provide long-term revenue growth unlike smartphones and tablets.
“I know this is radical and potentially 'transformative',” Ahmad wrote, “but this would radically alter Apple's growth profile.”
Neither Tesla nor Apple have commented on the alleged merger.
A son and husband teamed up Sunday morning to leave a heartwarming snow message on the roof of a Chicago hospital parking garage.
“HI MOM GOD BLESS U!” the message, written in snow, reads from a room at Rush University Medical Center.
Tim Hart and his 14-year-old son Will wrote the message for Hart’s wife, who is fighting leukemia.
After finishing the message, Will called his mother and asked her to look out the window. With the help of a nurse, Sharon Hart got out of bed and saw the message outside.
“It was uplifting and it was a proud mom moment to think that my 14-year-old son would do this,” Sharon Hart said.
The message could be seen from 70 hospital rooms across four floors, encouraging both medical staff and patients.
Angela Washek, a nurse at the medical center, said that it was nice to see the good side of health care.
Azra Raza, M.D. Professor of Medicine, Director of the MDS Center, at Columbia University recently wrote the following regarding mouse models of cancer. Azra was answering the question: “What Scientific Idea Is Ready For Retirement?”
An obvious truth that is either being ignored or going unaddressed in cancer research is that mouse models do not mimic human disease well and are essentially worthless for drug development. We cured acute leukemia in mice in 1977 with drugs that we are still using in exactly the same dose and duration today in humans with dreadful results. . . . there are no appropriate mouse models which can mimic the human situation.
Raza quotes Robert Weinberg of the Whitehead Institute at MIT, as stating that the reason people continue to use mouse models are: "Two reasons. First, there's no other model with which to replace that poor mouse. Second, the FDA has created inertia because it continues to recognize these models as the gold standard for predicting the utility of drugs." (See here for more on the comments of Robert Weinberg. I will also address some of his comments on the FAQs section of the new website.) Weinberg’s first reason is fallacious as there are many times when doing nothing is preferred to the status quo of doing something. For example, doing research that is misleading is worse than doing no research at all. Weinberg’s second reason, while true is just an excuse to maintain the status quo. Scientists do not have to use models that do not work just because someone in a different department of the federal government suggests they use mouse models.
But Raza adds a third reason that is more to the point:
There is a third reason related more to the frailties of human nature. Too many eminent laboratories and illustrious researchers have devoted entire lives to studying malignant diseases in mouse models and they are the ones reviewing each other's grants and deciding where the NIH money gets spent. They are not prepared to accept that mouse models are basically valueless for most of cancer therapeutics.
Sound familiar? I wonder if David Gorski MD, PhD agrees with her? (You can read her entire essay at http://www.edge.org/responses/what-scientific-idea-is-ready-for-retirement.) Furthermore, I wonder if any scientists will speak out and support her in this position? I doubt it. Growing a spine could result in their colleagues talking behind their back or the university speaking sternly to them about their tenured position and being a team player. I cannot imagine anyone asking a full professor to endure that kind of horror just to save the lives of few billion human patients.
Raza’s position is consistent with a December 19, 2013 press release from Jackson Laboratory that announced the response to cocaine and methamphetamine differs between 2 substrains of the commonly used Black 6 mouse. The C57BL/6J mice appeared to have a weaker response to the drugs than the C57BL/6N mice. The reason appears to be a single nucleotide polymorphism (SNP) in the gene Cyfip2. The press release states that: “This means that researchers should be very cautious when comparing behavioral data from studies using 6J and 6N strains.” (For more see reference .)
As I have stated many times, when strains of mice differ in their response to drugs and disease and monozygotic human twins do the same, trans-species extrapolation is not going to have any predictive value. (See Trans-Species Modeling Theory for more.) But it will be a hard to convince people of this when they have a vested interest in animal models. And by vested interest I do not just mean a financial interest.
Recently Universities and Science Minister of the UK, David Willetts stated: “Animals are only used when there are no suitable alternatives. But the results we get from research can transform lives and pave the way for new and ground-breaking medical advances.” Needless to say the Science Minister provided no references for this claim and refuses to support a proper debate as I outlined here or even consider the notion that vested interest groups might lie. Willetts supports the status quo as long as he benefits. Moreover, as I have also stated, there are no alternatives to something that is not viable in the first place. There are no alternatives to using animals as predictive models for human response to drugs and disease.
Interestingly, in the same article that Willets was quoted in, Minister Norman Baker was quoted as saying that “the scientific case for developing new techniques that do not involve animals is ‘as strong as the moral one.’ ”
Raza is not the first to point out that mouse models have failed. The list of scientists who have stated more or less the same thing in science journals is long. Despite this, nothing seems to be changing. Perhaps that is because society seems to be under the impression that all scientists support the use of animals as predictive models in drug and disease research. As long as the vested interest groups get to phrase the survey questions, can buy advertising space, have the support of the media, and refuse to debate specific questions in the presence of unbiased experts, this will not change. Must be nice to have that kind of job security.
1. Kumar, V.; Kim, K.; Joseph, C.; Kourrich, S.; Yoo, S.-H.; Huang, H.C.; Vitaterna, M.H.; Pardo-Manuel de Villena, F.; Churchill, G.; Bonci, A.; Takahashi, J.S. C57BL/6N Mutation in Cytoplasmic FMRP interacting protein 2 Regulates Cocaine Response. Science 2013, 342, 1508-1512. http://www.sciencemag.org/content/342/6165/1508.abstract
Continued from part I.
Magee also points out, correctly, that almost every study we quote also states that animal models are invaluable for medical science to continue. We have addressed this many times including in Animal Models in Light of Evolution (p27):
The FACTS of species differences relevant to the prediction issue are not in question. What is at issue are the INTERPRETATIONS authors place on the facts they refer to. We are justified in citing facts (and quoting researchers who do so) while rejecting interpretations. We cite many examples of the same phenomenon (species difference) to establish that it is a more or less agreed fact. Our point is not to get involved in an endless ding-dong about examples but to suggest that there are other well-established ways to deal with what we see (i.e. evolutionary biology). It matters not to us that those referring to the facts of species differences are also ardent advocates of animal experimentation. What matters are the facts, along with consideration of alternative hypotheses about their significance. We will offer some alternative hypotheses about the significance of the facts we uncover. Science, after all, is as much driven by disputes about the meaning and significance of facts as it is about the facts themselves. We have nothing to apologize for in this regard. (Capitals in original but bold added.)
Since most of the people we quote or cite are themselves animal modelers, it would be a shock if they did not say something positive about their research method. They are entitled to this, but we are also allowed to interpret the very impressive data they present as revealing that animal models have very little predictive value at higher levels of organization such as where drugs and diseases act and to explain why we think our interpretation of the data is correct. Statements against interest, on the other hand, are impressive on their own merit and such statements abound from animal modelers.
Magee also seems to have only minimal understanding of complexity science: “Arguing that animal models are not predictive because life is complex, when there hasn’t been a single death during a phase 1 clinical trial in the UK in over 30 years (and only one serious incident, due to human error), is a bit like arguing that airplanes can’t fly whilst being seated on an airplane at 30,000 feet.” Three points: 1. Data on who has died in Phase I trials is proprietary and any death-based lawsuits are probably settled out of court. Arguments from ignorance (we do not know how many people die in Phase I clinical trials) are not valid. 2. It does appear that in India, where many Phase I trials are done, they have a reasonably high death rate from clinical trials in general. For more on the problems of using animals to determine dose for first in man see . 3. Magee is clearly stating that animal studies are used to confirm safety for first-in-man Phase I clinical trials. This means Magee thinks they have predictive value and are used to predict human response, which is somewhat contrary to earlier statements by Magee. But, many vivisection activists have stated this is true for first in man trials. However, many others claim that animal studies are performed so that all people receiving the drug will be safer. It takes different data to support or negate these claims and vivisection activists rarely provide data. Magee’s reference to first-in-man deaths in the UK being an example of where no data is provided.
Magee goes on, and I have ignored many previous claims, but my main issue with the essay is the same issue I have with almost every critique of the work Shanks and I have published. Our main message has always been some version of the following. From Animal Models in Light of Evolution (p24):
The purpose of this book is to address the ability, or lack thereof, of animals to predict human response and to see what other roles they may have in research and testing. We will argue that claims concerning the great utility of animals as predictive models of human biomedical phenomena are unsupported by evidence and are compromised by both methodological issues and issues arising from basic biological theory.
From Animal Models in Light of Evolution (p358):
Our position can be summarized as follows: Living complex systems belonging to different species, largely as a result of the operation of evolutionary mechanisms over long periods of time, manifest different responses to the same stimuli due to: (1) differences with respect to genes present; (2) differences with respect to mutations in the same gene (where one species has an ortholog of a gene found in another); (3) differences with respect to proteins and protein activity; (4) differences with respect to gene regulation; (5) differences in gene expression; (6) differences in protein-protein interactions; (7) differences in genetic networks; (8) differences with respect to organismal organization (humans and rats may be intact systems, but may be differently intact); (9) differences in environmental exposures; and last but not least; (10) differences with respect to evolutionary histories. These are some of the important reasons why members of one species often respond differently to drugs and toxins, and experience different diseases. Immense empirical evidence supports this position.
Many other such quotes could be produced from all of our writings. I have recently formulated this message into Trans-Specia Modeling Theory (TSMT):
While trans-species extrapolation is possible when perturbations concern lower levels of organization or when studying morphology and function on the gross level, one evolved, complex system will not be of predictive value for another when the perturbation affects higher levels of organization.
All of the above are concise explanations of a very complicated, trans-disciplinary position. I am always amused when I see critiques of the position from people that obviously do not know what some of the words and concepts even mean. If people want to criticize our position, they must first be familiar with it and only one critique  has revealed even minimal familiarity. For my response to that criticism see . (I am hoping that author will continue our dialogue.)
There are some that have read and understood the books and articles. Compare their interpretation with what I stated above and with what Magee and others have claimed was the position of the book. Rachel A. Ankeny of the Department of History & Politics at the University of Adelaide, Adelaide, Australia offers a reasonable review of Animal Models in Light of Evolution:
Nonetheless, the authors do an admirable job of situating their discussions against the backdrop of relevant theories and information from evolution theory and systems biology, while at the same distancing their arguments from claims about animal ethics or rights, the typical domain where debates about the validity of animal models have previously occurred. Perhaps most importantly, they do not attempt to take their conclusions too far, and grant that nonhuman animals can be used for some forms of basic biological research where prediction for human health is not the main goal.  (Emphasis added.)
Lewis Wolpert also appears to understand the main point of Animal Models in Light of Evolution when he reviews the book:
Animal Models in the Light of Evolution provides persuasive evidence that animal models should be used with great caution when applying the results to human diseases. Mice and other model animals are both similar and different, in their biology, to humans. It is rather technical and not easy reading. [That’s the truth!] . . . Arguments from evolution are used to show the fundamental differences between, for example, rats and humans, as the organisms are too complex for information about one to be applied to the other. The authors discuss this complexity in terms of dynamical systems theory and its mathematical basis and question the possible similarity of such systems in different mammals. Quite small changes can have significant effects. They use such views to raise doubt on just how much genes contribute to an organism's form and function, but their arguments are themselves complex and hard to follow, and there is no persuasive evidence. It is no mystery that mice can differ significantly from humans in their response to drugs.
I could take exception to some of the comments in the above two reviews but at least the two reviewers understood the basis for our position. Comments like the above from Magee miss the big picture either from ignorance or malice.
Wolpert is right—our position is technical, requires trans-disciplinary education, and is not easy. Moreover, it is unpopular as the hierarchy of academia will change dramatically as will salaries. I have presented posters at the largest conferences in evolutionary biology and complex systems. The attendees walk by, read the poster, say they agree with me and ask why I am at their meeting as everyone already knows all this. After all, they say, no one uses animals as surrogate humans in biomedical research anyone. They are only used for basic research. I show them a few grant applications that claim the research project will directly cure humans and they are aghast. So, I ask them to sign a petition that states the following scientists agree with TSMT. They refuse and then they all say the same thing. “No. I agree with you but I would lose my job. My university will not allow us to voice opposition to something that brings in money to the university.” Needless to say, I do not have any of that on tape. But the experts in the two fields on which our position is based agree with us while the basic researchers that use animals use fallacy after fallacy along with obfuscation to try and confuse society and justify their research. They never address our position or the issues that arise out of it. Suffice it to say Magee is not an exception to that rule.
I am happy to correct mistakes made in any of our books or articles and actually appreciate them being pointed out. But I will in the future resist responding to people who are the equivalent of young earth creationists in that they simply do not have enough appreciation of the science to understand why their questions and comments are not even wrong. In the future, if someone wants to engage me in a discussion of TSMT please demonstrate that you at least understand what we are saying by explaining it in your first or second paragraph. Only then will I comment on your issues.
Essays like Magee’s and Gorski’s recent post are why I have also changed my criteria for debates. The recent Bill Nye debate notwithstanding, most science debates would benefit from the rules I list here. I would also suggest the same concepts be employed in debates in the scientific literature. That being said, I welcome the opportunity to engage in a fair and proper debate either in the scientific literature or in a public forum. Once again, I am not holding my breath waiting for a response.
9. Greek R, Hansen LA: Questions regarding the predictive value of one evolved complex adaptive system for a second: exemplified by the SOD1 mouse Progress in Biophysics and Molecular Biology 2013:http://dx.doi.org/10.1016/j.pbiomolbio.2013.1006.1002. http://www.sciencedirect.com/science/article/pii/S0079610713000539
10. Shanks N, Greek R: Animal Models in Light of Evolution. Boca Raton: Brown Walker; 2009.
11. Greek R, Rice MJ: Animal models and conserved processes. Theoretical Biology and Medical Modelling 2012, 9(40). http://www.tbiomed.com/content/9/1/40/abstract
58. Shelley C: Why test animals to treat humans? On the validity of animal models. Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences 2010, 41(3):292-299. http://www.sciencedirect.com/science/article/B6VHP-50NH66T-3/2/adf77c24c844a88e0c8b93547272a7b9
59. Greek R, Shanks N: Complex systems, evolution, and animal models. Stud Hist Philos Biol Biomed Sci 2011, 42(4):542-544. http://www.ncbi.nlm.nih.gov/pubmed/22035727
60. Ankeny RA: Book Review: Animal Models in Light of Evolution. Q Rev Biol 2011, 86(September):223-224.
61. Wolpert, Lewis. 2010. Review of "Animal Models in the Light of Evolution" by Niall Shanks, Ph.D., and C. Ray Greek, M.D. Philosophy, Ethics, and Humanities in Medicine. doi: 10.1186/1747-5341-5-12. http://www.peh-med.com/content/5/1/12
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  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 . 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  “
 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.:
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. The JPMA study is also described in another Lumley book in yet another chapter by Igarashi. 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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Before I begin, allow me to once again explain that while I think the writers at Science-Based Medicine are flat wrong regarding their assessment of my position on animal models (or not even wrong as most of the positions that they criticize they attribute to me while these statements and positions are actually mythical or at least not from me), on the whole I agree with Science-Based Medicine and their positions on Evidence-Based Medicine, CAM, vaccines, and so forth. I find it sad that some of the SBM bloggers appear to have little knowledge of critical thinking but even they usually nail down difficult medical topics very effectively. On the whole, Science-Based Medicine offers something of value to society!
On February 3, 2014, David Gorski, MD, PhD wrote a roughly 4600-word essay titled: Animal rights activism: Petitions aren’t science. I encourage everyone to read the entire essay, as there are themes, specifics, and especially tone that I will be unable to reproduce or address.
Dr Gorski’s essay revolves around the fact that a group in the UK is sending him messages regarding a political measure in the UK called an Early Day Motion (EDM), specifically EDM 263 put forth by For Life On Earth (FLOE).
As a prelude, however, let me point out that I won’t be dealing (much) with the morality of animal research, mainly because I believe that whether or not animal research is morally acceptable is not primarily a scientific question. Science can inform the consideration of the question of animal research, but in the end it’s a moral question. That is not to say that science is irrelevant, because part of the consideration of the moral question of whether and when it is acceptable to use animals in research is the issue of how much value to science animal research brings. How utilitarian you want to be considering this question is something that can be discussed . . . (Emphasis added.)
I agree with this! One might say that this is exactly what I have been addressing over the last few decades.
But here come the straw man arguments. Gorski continues:
but animal rights activists often invoke an extreme negative version of a utilitarian argument in that they try to portray as animal research as not just useless (i.e., providing no useful scientific information), but even as harmful or providing misleading or mistaken scientific conclusions. If that is the case, then it’s a no-brainer that animal research cannot be justified ever because in that case it would cause suffering to animals but provide no benefit in terms of scientific advancements that could lead to improved medical care.
Some of the above is exactly what some nonscientists in the animal rights movement say and I have chastised them for it repeatedly. But some of Gorski’s criticisms appear to be based on false assumptions about the value of animal-based research or are just made up out of whole cloth. Regardless, Gorski continues:
Unfortunately, as I documented six years ago, animal rights activists have a distressing tendency to use truly bad arguments to do everything they can to paint animal research as useless or even harmful to the science of medicine. These arguments tend to fall into one or more of three categories:
Animal research doesn’t teach us anything of value or even misleads us (i.e., it is bad science).
Animal research does not predict human physiology or response to disease, or animals are “just too different from humans to give reliable results” (i.e., it is bad science).
There are better ways of getting the information that do not use animals (i.e., there is better science available than using animals.)
Yep, those are what some animal rightists say. My position however, is and has always been the following.
1. Animal-based research has and can continue to help us learn a lot about the material universe in the form of anatomy and physiology of animals (animals being all members of the Animal Kingdom). This is a tautology IMO.
2. However, animal-based research does not offer predictive value for human responses to perturbations that occur at, or involve, higher levels of organization.
3. But in terms of responses on the gross level of human physiology and anatomy, animals and humans share a lot of properties and a lot of facts regarding humans and animals were or could have been learned using animals. The history is tricky and some claims made by vivisection activists are simply false but their greater claim (if they know the difference)—that such breakthroughs could have been made with animals—is true.
4. There are better ways of getting the information that do not use animals (i.e., there is better science available than using animals.)
5. But in some areas we have no predictive modalities at all—animal or in vitro or in silico. In these areas, we should consider human-based research. But perseverating that “animal-based research is all we have so we must use it” is like saying “sacrificing children for a good corn harvest is all we have so must use it.” Such statements fail both morally and scientifically. In science before we make statements like that we need actual data and numbers—studies that looked at the number of tons produced at the corn harvest when children were sacrificed and when they were not. We need numbers in terms of success rates when animals were used and when they were not. Were the animals necessary or merely sufficient? Are the historical explanations for the development of, say heart surgery, actually consistent with what happened or even what could have happened and again, were the animals used necessary or sufficient. These questions lie within the realm of philosophy of science and the answers shed light on what works and what doesn’t. In my experience, this area of science has been ignored and demeaned to the detriment of society. (But I don’t have any meta-analyses on this.)
On to the main part of the blog.
Like the case with many holding dubious scientific beliefs whom many would consider cranks, one favorite tool to promote their agenda is “public debate.” I’ve seen it many times myself. For example, I’ve had HIV denialists and antivaccine activists challenge me to “live” public debates over their favorite topics.
Contrast this with the following from Dr Steven Novella who wrote: “During a live debate we can see how the candidates think and what they know and believe about scientific issues. They can also be pushed on specific points if they give evasive answers.”
Gorski maintains that: “They [cranks and nonscientists] seem to think that science is decided in public debates and view the quite understandable reluctance among scientists like myself and skeptics to engage cranks in such spectacles as ‘cowardice’.” Sadly, Gorski is correct on some of this in at least some cases and Gorski is more or less spot on when he continues stating:
It is not, but cranks continue to labor under the delusion that science is somehow decided in such forums, which are a variant of a sort of argumentum ad populum, in which something is argued to be true because it is popular or, in a debate, an argument is thought to be closer to the truth because it is more popular. Science doesn’t work that way. It is decided on evidence presented at scientific conferences and in peer-reviewed journals, where the real scientific debate plays out until it is temporarily settled and scientists come to a provisional consensus. That provisional consensus, of course, is always subject to change as new observations, data, and experimental results come to light, but it takes observations, data, and experimental results to change the consensus, not “live public debates.”
Popularity does not equal truth! How about that? Gorski misses the boat on some of the above, however. First of all, the above is how “normal science” works. It is not how paradigm shifts occur nor how really big changes in science sometimes occur. Moreover, Gorski creates a straw man in stating: “Such ‘live public debates’ have only one purpose: To sway public opinion to a viewpoint not supported by science, in the process elevating pseudoscience or the unproven to the same plain as the scientific consensus as a scientifically viable “alternative,” no more, no less.” If that were the purpose why would Novella endorse and participate in them? Unless, maybe, those debates, when properly conducted allowed each side to make previously unaddressed points? A proper debate would take a long time but it could also end general public acceptance of a lot of nonsense.
My purpose in debates is to prove that my position is correct. In an effort to do that, I have suggested rules for debates, which I will present momentarily. Such rules eliminate or penalize many things, such as snarky comments that are directed at the opponent and do not inform on the science. I for example, do not write ~5000 word essays filled with vituperative hyperbole, no real content, that contain many examples of the fallacy of equivocation along with other fallacies, and illustrate essentially no critical thinking. But if someone did have that as his modus operandi, a proper debate might present challenges for him and not accepting an invitation to such a debate might result in his being called a coward.
Gorski continues: “The fact is, pseudoscientists, pseudohistorians, and cranks desperately want to debate accepted experts in the field in which they apply their crankery.” Such is not the case for me. I tried the debate thing for over a decade and was very frustrated at the results, in part, for the same reasons that underlie Gorski’s comments and for the following.
1. The audience cannot follow the science and hence has no idea who is spouting nonsense. By audience I mean both nonscientists and scientists whose discipline lies outside the area in contention. For example, do not ask me to be an expert in a debate regarding quantum gravity. I know nothing about it, hence as an “expert” or audience member I would be clueless regarding who was right and who was wrong.
2. There are no referees / experts that both parties agree on and whom can be asked to settle matters of dispute in their area of expertise. There is no effort to find and educate such experts in the form of making sure they have the material that will enable them to understand both sides of the argument and render a judgment. This can be easily remedied by each side providing a small number of articles or position paper for the experts to read and understand prior to the debate. Not all experts would be expected to comment on every point in the debate—just the salient points in his or her area of expertise.
Currently, I don’t do debates as, without the list of debate requirement’s below being fulfilled, I just do not see any reason to leave the lovely weather of southern California, interact with the airline industry, risk encountering pro-vivisection extremists that will threaten and harass me, listen to the campus police say that if there is any kind of disturbance they will Taser me first (regardless of which side started the disturbance, yep, those campus cops know which side their bread is buttered on), and so forth. Flying from one hostile encounter to another when there exists no standard to judge outcome has not worked out well for me and others like me (think evolutionists debating creationists).
I would be happy to participate in a debate that includes the following.
1. The subject of the debate will be: Resolved: Animal models have no predictive value for human response to drugs and disease. (This is our issue despite the purposeful misrepresentations by Dr Gorski and others.) If anyone requests a second debate on the role of animals in basic research, AFMA will be happy to participate but only after the prediction issue has been addressed. AFMA is willing to have the basic research debate first if our opponent stipulates to the fact that animal models offer no predictive value for human response to drugs and disease. Thirdly, AFMA will debate specific historical breakthroughs that the pro-vivisection activists claim as one-shot arguments that prove everything they say is right (for example the Blalock-Taussig procedure was developed and could only have been developed by Blalock experimenting on dogs at Johns Hopkins). AFMA does not really have such historical debates in our mission, because they are immaterial to the prediction problem, but we can do it provided the predictive issue is debated first. And finally, the speaker or speakers on the opposite side must be recognized by the vivisection community as a world renowned expert on the topic being debated. I have debated many times only to hear from the vivisection community that the other guy (who lost) was not really an expert in all this. Funny how he seems to get a lot of his verbiage on animal models published in the scientific literature and endorsed by various science societies.
2. In term of judges and a moderator, the below are necessary:
a. Someone from the media, a university’s law school, business school, medical school, a science department, or any other person agreed upon by both participants will moderate the debate.
b. A panel of judges will be present. They may come from academia or industry. The judges should include experts from the fields of clinical medicine, complexity/chaos theory, philosophy of science, evolutionary biology, clinical research, drug development, the meaning of predictive value, and the differences between applied and basic research. Both debaters must agree on each of the judges.
c. A position paper or papers, complete with references, will be presented to the judges by each participant. The judges are expected to verify that the references state or imply what the presenter was claiming (in each judge’s area of expertise) in order for the paper and concept to be allowed in as evidence. The position paper would then function as the presenter’s official position and the presenter must adhere to the facts in the paper during his portion of the debate. Allusions, by the presenter, to areas outside the topic or his respective position paper would not be allowed in the formal portion of the debate. Any false claims or mistakes discovered in the position papers will be acknowledged by the moderator prior to the debate. This allows the audience to see where the presenters started in terms of their claims and facts.
d. Basic principles of science will also have to be agreed on, as will the basics of critical thinking. Disagreements regarding the principles of critical thinking and science that occurred during the negotiation process must be acknowledged by the moderator prior to the debate. This will encourage all parties to play fair, as their requests will be matter of record.
e. A Q&A from the judges and moderator will follow the debate, after which, or during which, the judges and moderator will comment on the positions of the presenters. The judges are expected to point out errors of logic or errors of fact in their area of expertise as well as remark on whether the presenter proved his position or disproved the opponent’s position.
f. The above guidelines are designed, in part, to ensure that both presenters are adhering to current science and not misrepresenting areas of science that the audience may not be familiar with. (This is similar to the fact checking that happens after presidential debates but allows the fact checking to be done pre-debate, by the judges, and thus affect what is presented.) The position paper will allow the judges to confirm the principles and facts in the paper and rule accordingly on disagreements involving those facts. It will also encourage the presenters to make sure their facts are current. If such a situation creates degenerates into one side not accepting the views of the experts the debate moderator will acknowledge this and explain that such is why one side is not participating in the debate.
g. Moreover, if one side consistently breaking the rules or attempts to Gish Gallop or use examples that the experts have not allowed, his presentation must be in the form of a pre-recorded video.
3. The moderator will inform the audience before the debate begins that there are time limits being imposed on the participants and that interruptions or harassment of the presenters will be met with expulsion from the debate.
4. A clock with a timer function must be clearly visible to the presenters. The moderator will start and stop the clock, enforce the time limits, and stop a presenter who exceeds his time limit unless the opposite side agrees to grant more time.
5. Each participant will be provided a microphone, lectern and access to a projector by the host institution and will be allowed to use audio-visual equipment during the formal presentation as well as the Q&A period. A maximum of two projectors must be available to be used by a presenter. A white board and stand should also be available for each side.
6. Each presenter may hand out printed materials before and after the debate.
7. The debate will last no less than 2 and no more than 3 hours. Each side will initially receive a total of 45 minutes. AFMA will present first, as the pro side of the resolution, and speak for 40 minutes, followed by the other party speaking for 40 minutes. After this each side will be given a 5-minute rebuttal. A break will be then be given, after which the Q&A will occur.
8. Neither side will be allowed to interrupt the other. If one side does interrupt or harass the other, the moderator must award 5 minutes or more for the other side to speak on whatever aspect of the topic he wishes. The added time will be added to the rebuttal time or be available immediately if the interruption is after the formal debate.
Properly moderated and judged debates would be a welcome addition to many controversies in society. On to the remainder of the blog.
As I have repeatedly stated, I have no formal arrangement with FLOE. What they say and what positions they take appear to mimic some of mine but I doubt dead scientists who are lauded by various people today are challenged to prove that the dead have no influence on the websites of the living or that living scientists are constantly asked to correct what their fans say about certain aspects of science. There are a lot of people in the world and some of them like to “help” their heroes get out what they perceive the message to be regardless of whether or not the heroes ever asked for such a thing. The sensible thing to do would be to ask the scientist to clarify his position and then attack that rather than attacking second hand claims. And therein we come to the rub.
Despite publishing numerous books, book articles, and journal articles describing my position (most in PubMed-indexed journals but some in newer, peer-reviewed journals that are not currently eligible for indexing in PubMed) [1-25] no one has actually addressed the position. People like Gorski have offered it for derision among his followers who have belittled it even though they were belittling a straw man, and ignored corrections from the person that actually wrote the article. Now, none of this means I am right. Poor critiquing skills do not mean that what Gorski is critiquing is in fact correct. On the other hand, when people write thousands and thousands of words and never actually address the heart of the position, I am forced to think that maybe there is more going on here than first meets the eye.
Steven Novella, MD, neurologist at Yale stated on the February 1, 2014 podcast The Skeptics’ Guide to the Universe (beginning at 37:28): “Animal models for medical research are still essential. . . . For the foreseeable future medical progress is absolutely dependent upon animal models and doing animal research . . .” I challenged an earlier version of that statement made by Dr Novella when discussing the role of animal models, stating: “Mouse and other animal models are essential to biomedical research. The goal is to find a specific animal model of a human disease and then conduct preliminary research on the animal model in order to determine which research is promising enough to study in humans (Novella, 2013a).”
Hansen and I replied:
Indeed, that is the goal. Implied in this goal is the notion that animal models are, or can be, of predictive value for humans in terms of responses to drugs and disease. However, as we have shown, such a notion is simply without support. Anecdotes offer nothing in terms of PPV and NPV, and correlations that are only revealed retrospectively do not qualify as being of predictive value. Thus the claim that animal models are essential to biomedical research is a case of begging the question. Nevertheless, most defenses of animal models begin just this way. 
Our article continues:
. . . Novella continues: “It turns out that the SOD1 mouse is an excellent animal model for SOD1 FALS in humans. This is not surprising considering that it is the same mutation. However, the SOD1 mouse model of ALS is much less predictive for sporadic ALS. Most of the drugs that look promising in the SOD1 model have not shown a significant clinical effect in humans with sporadic ALS (only one drug has actually made it through FDA approval: riluzole)” (Novella, 2013a). Novella, a neurologist who treats ALS, is arguably in a reasonable position to judge the value of an animal model. However, as we should anticipate from the section on evolution, mutations do not result in the same outcomes across species lines. For example, mutations that cause phenylketonuria and Sanfilippo syndrome in humans are normal in macaque monkeys (Gibbs et al., 2007 and Holmes, 2007). As we stated, even strains of the same species vary in their response to seemingly potent perturbations such as knocking out a gene. Combine this with convergent evolution and we see no reason to suspect conservation of gene function across species. Conservation does happen (Greek and Rice, 2012), but there seems to be no standard method for determining it without comparative studies. Thus again we can only establish validity in retrospect. 
I suggest you read the entire article on the SOD1 mouse in order to understand Trans-Species Modeling Theory (TSMT) and for examples of how vivisection activists respond to our position. In fairness to them, I do not think they actually understand our position—they have not read it. Commenting on a position that you have not read is not a good thing for anyone, but it is especially poor form for people who are self-professed critical thinkers.
When I was a child in the Deep South, being raised by fundamentalist Christians, we did not understand much of anything about evolution. The language the few scientists spoke that we heard and the phrases they threw at us might as well have been Martian. Not much changed even though I majored in science (it was at a Bible college). But the two things that poor, uneducated Christian creationists can spot a mile away are inconsistency and just flat out avoiding the argument. They may not see that their being unable to answer the evolutionists’ argument is really important, but that’s because they do not have a clue what the evolutionists are saying. Of course they can’t answer them.
But when they see scientist number 1 attacking scientist number 2 tooth and nail and saying the exact same things about scientist number 2’s position that he was saying about creation, AND when scientist number 1 is shown to be WRONG, that is all the creationist needs to completely discount evolution. We heard the same verbiage and the same angry tone from the same guy both about how stupid we creationists were and how stupid his opponent in some science controversy was. But then he lost that argument to scientist number 2. Think anybody in that community ever believed anything scientist number 1 said about creation and evolution ever again?
Discussing animal-based research on podcasts or blogging about it on the Internet is what I call “blogging without consequences.” No matter how wrong you are, no harm will come to you or your reputation. In part because no one will actually read and understand the literature on the topic and even if they do they will probably just bandwagon along as no one wants to be called a crank. Not be a crank, no one wants to be called a crank.
So if your name is Gorski or Novella and you are just damn certain you are right, you should jump on that debate format listed above. Everything to protect you is in place. Top name referees (I can offer some names I guarantee we will all agree on, if you wish) that will judge the merits of the arguments in their areas of expertise, solid rules that eliminate misquoting, avoiding the argument, various fallacies, as well as the Gish Gallop (and more can be added). WOW! Now what’s missing guys?
But if you do the debate and these experts/referees actually come out and agree with me? What then? Hmmmm. Better not risk it.
Photos courtesy http://skepticdenialism.blogspot.com/2011/01/f-u-brian-deer-steven-novella-david.html
1. Greek R, Greek J: Evolution and animal models. Comp Med 2002, 52(6):499-500; author reply 500.
2. Greek R, Pound P: Animal studies and HIV research. BMJ 2002, 324(7331):236-237.
3. Greek R: Letter. Dogs, Genes and Drugs. American Scientist 2008, 96(1):4.
4. Shanks N, Greek R: Experimental use of nonhuman primates is not a simple problem. Nature Medicine 2008, 14(10):807-808.
5. Greek J, Shanks N: Thoughts on animal models for human disease and treatment. JAVMA 2009, 235(4):363.
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Father Of 15-Year-Old Held At Boston Children's Hosptial Claims "Progress Is Being Made" In Custody Battle
Lou Pelletier, the father of a 15-year-old currently being held by the Massachusetts Department of Children and Families at Boston Children’s Hospital, claimed today that “progress is being made” in he and his wife Linda’s efforts to regain custody of their daughter Justina.
Justina’s case is a strange and complicated story of government intervention and hospital influence over a family’s medical decisions.
Last February, Justina was diagnosed at Tufts Medical Center in Boston with a rare genetic disease called mitochondrial disorder. According to the West Hartford News, the Pelletiers arranged for Justina to receive treatment for the disorder at Boston Children’s Hospital. Doctors at that hospital, however, claimed that mitochondrial disorder does not exist. Instead, they diagnosed her with somatoform disorder, a mental illness that leads to the manifestation of physical symptoms such as gastrointestinal pain.
When the Pelletiers attempted to remove Justina from Boston Children’s Hospital and transfer her back to Tuft’s, the Massachusetts Department of Children and Families refused to allow them, accusing them of medical child abuse. Despite protests from the Pelletiers as well as the general public, the girl has been held in the psychiatric ward of the hospital, called Bader 5, ever since.
The Pelletiers had a hearing regarding their daughter at a juvenile court today, but they were unable to comment on the hearing’s outcome due to a judge’s gag order on the case.
According to the West Hartford Patch, however, sources close to the family claimed that Justina is soon to be scheduled to be transferred back to Tufts Medical Center, the hospital where she originally received the diagnosis of mitochondrial disorder.
No official report of Justina’s release from Bader 5 has been confirmed, but her transferral to Tuft’s would signify one small victory for a family entangled in a series of lengthy and complex legal and medical battles.