As I explained in my blog about the claim that animal-based research informs scientists about humans, animal modelers want to say that there is a one-to-one correlation between animal models and humans but the facts prevent the more honest among them from making this claim. At least explicitly. At least some of the time. What many say instead is that animal models inform them about what a drug or disease process will do in humans while never defining inform. Or, they say that discoveries in animals could lead to cures. By so stating, they give themselves an out when accused of claiming that animal models can predict human response to drugs and disease or when the animal model-based discovery does not pan out. However, overall the press releases and other statements by animal modelers and their representatives do indicate that the animal model community as a whole wants society to believe that what happens in an animal is what will happen in a human.
From a pamplet by Understanding Animal Research published in 2009:
Animals are important here [in drug testing] because researchers need to know about side-effects, how the chemical passes through the body and what dose is needed . . . A big development in recent years has been in genetics. By studying humans and mice, which share more than 90 per cent of our genes, scientists are discovering which genes do what and what happens when they wrong. Genes can be altered, and genetically-modified (GM) animals are used increasingly to study disease, to develop conventional treatments and to test new treatments for diseases like cystic fibrosis and muscular dystrophy.1
Clearly, the above is equating what happens in animals when exposed to a drug to what we can expect from humans when exposed to the same drug. It is also saying that similarities among genes are why these predictions are possible. This notion is demonstrably false. (See Animal Models in Light of Evolution for more.)
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Tibetian Terrier dogs could play key role in developing therapy for early-onset Parkinson’s. (Emphasis added.)
Indeed they could. Anything is possible. But the history of using animals for research forces us to expect they will not. The press release continues:
University of Missouri researchers believe both man and animal will benefit from their discovery that the same gene mutation found in Tibetan Terrier dogs can also be found in a fatal human neurological disorder related to Parkinson’s disease . . . The disease in Tibetian Terriers is called adult-onset neuronal ceroid-lipofuscinosis (NCL). Within the dogs’ cells in the brain and eye, material that should be “recycled” builds up and interferes with nerve cell function. Due to this buildup, around the age of five years old, the dog begins to exhibit dementia, impaired visual behavior, loss of coordination, and shows unwarranted aggression . . .
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There is no doubt that studying a disease of Tibetan Terriers in Tibetan Terriers will lead to more knowledge about the disease in Tibetan Terriers. It is entirely another question whether what researchers learn from Tibetan Terriers will apply humans. The press release continues:
While there are many forms of NCL in humans, the symptoms of NCL are similar in people and dogs, and the disease is ultimately fatal for both. Utilizing the canine genome map and DNA samples from dogs diagnosed with NCL, the researchers were able to pinpoint the specific gene that causes NCL. The mutation they discovered in dogs, however, causes a hereditary form of Parkinson’s disease in humans.
So, despite the fact that the mutation causes different diseases, studying dogs will result in cures for humans?
This suggests that the recycling that goes awry in NCL may also be involved in degenerative diseases like Parkinson’s . . . “Dogs and people suffer from the same diseases, and it’s much easier to discover gene issues in dogs because of the unique genetics of pure-bred dogs,” O’Brien said.
The best way to find what genes cause which diseases in humans is by studying humans and human genomes. The press release continues:
“Because we have a medical school and veterinary school near each other, we can find the genes in the dog and then find out if they cause a similar disease in people.”
I am not clear on why school proximity is important here but I am clear, based an understanding of complex systems and evolution, that what happens in dogs has a low probability of predicting what will happen in humans. The article referred to in the press release was published in Neurobiology of Disease.2
Polybrominated diphenyl ethers (PBDEs) are chemicals that have been widely used as flame retardants and are now classified as persistent organic pollutants. Health concerns in humans have arisen based primarily on studies with laboratory animals exposed to high levels of PBDEs . . . It is unclear what impact PBDEs have on human health as people are typically not exposed to the high concentrations of PBDE compounds that have detrimental neurological and endocrine effects in laboratory animals. There is a need to determine the impact of low doses of PBDEs in laboratory animals which approach the levels that humans are exposed to in daily life, and in addition to determine the effects of these compounds in offspring exposed during critical developmental periods . . . (Emphasis added.)
This need is based on the invalid premise that we can extrapolate between species.
Dr. Blake, who led the endocrine studies [on animals] remarked, "Our thyroid findings, taken together with previous work with high doses of penta-BDEs, indicate that these compounds may have biphasic effects depending on exposure levels where low dose exposures may increase thyroid hormone concentrations and higher PBDE doses may decrease them. In addition, the physiological status of the animal (i.e., pregnant versus non-pregnant) may determine if the thyroid hormone levels are affected. These studies could potentially be critical to understanding the effects of PBDE accumulation in the tissues of pregnant women. They also emphasize the potential importance of reducing exposure to PBDEs in homes and the environment and regulating the import of manufactured items that contain PBDEs." (Emphasis added.)
Yes, they could. They could also lead to a solution to world hunger but the odds are against it. The way one can determine the probability of such things is by studying the relevant science, like evolution and complex systems, and then putting past studies of animals into that context. When one does undertake those studies, one finds that the probability is low indeed.
Also from ScienceDaily, Studies of Marine Animals Aim to Help Prevent Rejection of Transplanted Organs: “Studies of the small sea squirt may ultimately help solve the problem of rejection of organ and bone marrow transplants in humans, according to scientists at UC Santa Barbara.” (Emphasis added.) Yes, they might. They also might yield absolutely nothing of relevance for human medicine. Indeed, that is far more probable.
An April 28, 2001 article, Study: Monkey memory parallels humans' from the UPI stated:
A finding that monkeys can reproduce simple shapes from memory help us understand the evolution of memory and other cognitive abilities, U.S. researchers say. Scientists at the Yerkes National Primate Research Center at Emory University said identifying this recall ability in monkeys could be applied to better diagnosing and treating memory impairments in humans. "We believe we have found a new method for testing animals that opens a whole new window into the world of non-human memory research," researcher Ben Basile said. "For the first time, monkeys can actually show us what they recollect, and their test results are directly comparable to human tests" . . . "Our observations of recall in Old World monkeys suggest it may have been adaptive in primates long before humans evolved, and that it does not depend on language or anything else that is uniquely human," Basile said . . . "With this type of information, we are moving closer to better diagnosing and developing treatments for memory impairments in humans," he said. (Emphasis added.)
Once again, anything is possible but not everything is probable. The scientific article3 referred to can be accessed here. It certainly appears that human memory and monkey memory are similar. Indeed such would be expected from current understanding of evolution. However, such similarities must be considered in light of the fact that they are occurring in complex systems and hence small differences will greatly influence perturbations to the system for example in the form of disease and drugs. Furthermore, the genetic similarities animal modelers are so fond of throwing into discussions are least common in the brain.
Even scientists that are attempting to be honest seem unable to confine themselves to the facts. The following is in Nasal aerosol flu treatment 'shows promise', from the BBC, 22 April 2011:
Inhaling a protein that boosts the immune system could help in the fight against flu, tests on mice suggest. US experts found it reduced symptoms and prevented death despite "lethal" doses of flu. Writing in the American Journal of Respiratory and Critical Care Medicine, they say the nasal aerosol treatment has "great potential". A UK flu expert said the work could be useful in directing research, even if it was not directly transferable . . . Professor John Oxford, a virologist based at Queen Mary, University of London, said it was "cutting edge" research. But he added: "Transferring it into humans can be quite difficult. We don't know the sort of problems that could occur if you start meddling with the immune system, as we saw with the Northwick Park trial [in which six men became seriously ill after taking a drug which was meant to "retune" the immune system]. "So first we'll see how it pans out in mice, then see how it can possibly apply to humans. "But it could also help our understanding of the pathology of flu."
I understand why animal modelers seize upon every new discovery in animals and herald it as the next cure. They have to. If they waited for actual cures from animal studies they would be out of funding and jobs. So it was no surprise to see all the hype (and here) about the current AIDS vaccine that has worked well in monkeys. Of course, there have been a lot of AIDS vaccines that worked well in monkeys but failed in humans. Now, that does not mean this one will fail. Indeed, I hope it does prevent AIDS in humans. But the probability is low and there are better options for seeking vaccines and treatments for AIDS. Sadly, these facts will not stop vivisection activists from spinning this monkey research as a victory for the animal model. The vivisection activist will also take this opportunity to accuse those who accept the facts of evolution, science in general, and the empirical evidence as being misanthropes. As always, when they don’t have the facts to back up their claims, they attack character.
1. Understanding Animal Research. Where do medicines come from. London, 2009.
2. Farias, F.H.G., et al. A truncating mutation in ATP13A2 is responsible for adult-onset neuronal ceroid lipofuscinosis in Tibetan terriers. Neurobiology of Disease 42, 468-474 (2011).
3. Basile, B.M. & Hampton, R.R. Monkeys Recall and Reproduce Simple Shapes from Memory. Current biology : CB (2011).