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More Spin and A Little Honesty

I have said many times that while basic research using animal models can reveal facts regarding the material universe, those facts will probably not lead to medical advances. This presents a problem for basic researchers using animal models as they are under pressure from funders to actually produce something useful. In order to obtain grants, they therefore lie and say that whatever they are doing is going to cure some terrible disease. Most in society don’t know any better so the public does not hound the funding agencies demanding change and the status quo continues. We provided some examples of NIH grant proposals that demonstrated this type of malfeasance in our book Animal Models in Light of Evolution. Here are some more recent examples.

An August 27, 2012 press release from the Journal of Clinical Investigation announced: “New model of muscular dystrophy provides insight into disease development.” The press release continued:

In order to develop treatments for this disease [muscular dystrophy], it is important to have an animal model that accurately reflects the course of the disease in humans. In this issue of the Journal of Clinical Investigation, researchers at the University of Iowa report the development of a mouse model of Fukuyama's muscular dystrophy that copies the pathology seen in the human form of the disease.

Researchers at the University of Iowa removed the gene fukutin from mice and discovered that “fukutin disrupts important modifications of dystrophin that prevent the muscle cells from attaching to the [extracellular matrix].”

There are myriad problems with this but I will confine myself to just three. Genes have different functions in different species and even different strains of the same species. Finding a gene that performs function X in a mouse does not mean it will do the same in humans. Second, even if the same genes performs the same function that does not imply the same ultimate result as modifier genes can profoundly impact the final outcome. Third, put the same gene in different complex system—different species—and all the properties of complex system will then come into play. One simply cannot blindly extrapolate between complex systems and one certainly cannot expect a cure to a disease as complex as muscular dystrophy from a gene discovery in a mouse.

A press release from the Genetics Society of America states: “Scientists use worms to unearth cancer drug targets.” Mark Johnston, Ph.D., Editor-in-Chief of the journal Genetics stated: “This research is important because it offers possible new ways to shut down the genetic machinery that contributes to cancer growth and progression. The causes of cancer are complex and varied, so we must approach this disease from many angles. Using simple 'model organisms,' such as nematode worms to find new drug targets, is becoming an increasingly important and effective strategy.” The article (Polley and Fay 2012) was published in the journal Genetics. I have often said that studying worms and other less complex organisms like flies can reveal fundamentals about life and as such can be justified without appealing to “future cures.” But claiming you are going to cure cancer with such research is beyond the pale. It will, however, make it easier to obtain grant money and fool the alumni into thinking the university is cutting edge and deserves more in donations.

Along those lines, Dr Rachael Dunlop of the University of Technology, Sydney, Australia explained to a audience at TAM 2012 that a university in Australia was teaching anatomy to chiropractic students. When a group of scientists confronted the department they explained that the money from teaching the chiropractic students was going to fund their research hence they would not stop teaching even though they agreed that chiropractic was not science-based. [(TAM 2012)begins at 18 minutes 40 seconds into the video.] If a vivisection activist states that university researchers are above reproach and would never do something “just for the money,” ask him about university’s across America embracing complimentary and alternative medicine for the money.

An August 9, 2012 press release from Wake Forest University informed us that: Hormone in fruit flies sheds light on diabetes cure, weight-loss drug for humans. Braco et al (Braco et al. 2012) discovered that by turning off AMP-activated kinase in the brains of fruit flies, cells decreased their release of sugar. The press release states:

"Since fruit flies and humans share 30 percent of the same genes and our brains are essentially wired the same way, it suggests that this discovery could inform metabolic research in general and diabetes research specifically," said Johnson, the study's principal investigator. "The basic biophysical, biochemical makeup is the same. The difference in complexity is in the number of cells. Why flies are so simple is that they have approximately 100,000 neurons versus the approximately 11 billion in humans."

Well, that's getting pretty close to saying we should study stars in order to cure diabetes since humans are composed of stardust. Sharing 30% of genes is insignificant in terms of disease pathophysiology. We share around 98% with chimps but they do not contract AIDS or many other diseases that kill humans. And our brains are very different from those in fruit flies. Our brains are even different from the brains of chimps. Based on the activity of gene expression in human brains, Konopka et al suggest that an increase in complexity, not just size, separates human brains from those of chimpanzees. Their research revealed an increase in gene expression for genes involved in plasticity – “the ability of the brain to process information and adapt.” They also discovered “more connections among gene networks that featured FOXP1 and FOXP2,” genes involved in speech and language.(UCLA 2012; Konopka et al. 2012)

But the press release continues:

Medical advances as a result of this research might include:

Diabetes research . . .

Weight-loss drugs: An "exercise drug" would turn on all AMP-activated kinase in the body and trick the body into thinking it was exercising. "Exercise stimulates AMP-activated kinase, so manipulation of this molecule may lead to getting the benefits of exercise without exercising,"

For me, that one is the clincher. Promising weight loss without exercise is the sine qua non of charlatanism. Animal modelers have now stooped to the lowest of the low. Next thing you know we will be seeing them on late night TV promising that for the low, low price of $19.95 they will someday send to you a drug that will cause weight loss regardless of what you eat and without exercise. Just send that check today and expect the drug “soon.” Given that Johnson is quoted, one cannot blame this on the university’s PR department.

Apropos, Gorski commenting on studies (Woloshin et al. 2009; Schwartz et al. 2012) that show that press releases exaggerate research findings stated the following:

Specifically, the results support the hypothesis that university press offices are prone to exaggeration, particularly with respect to animal studies and their relevance to human health and disease, although press releases about human studies exaggerated 18% of the time compared to 41% of the time for animal studies. Again, this seems to make intuitive sense, because in order to “sell” animal research results it is necessary to sell its relevance to human disease. Most lay people aren’t that interested in novel and fascinating biological findings in basic science that can’t be readily translated into humans; so it’s not surprising that university press offices might stretch a bit to draw relevance where there is little or none.(Gorski 2012) (Emphasis added.)

Which is consistent with Freeman and St Johnston writing in Dis Model Mech 2008:

Many scientists who work on model organisms, including both of us, have been known to contrive a connection to human disease to boost a grant or paper. It’s fair: after all, the parallels are genuine, but the connection is often rather indirect. DMM is about something quite different. This new journal is aimed at people who set out with an explicit goal to investigate human disease using model organisms. (Freeman and St Johnston 2008)

And with Hicks:

What motivates a lot of biomedical scientists is using animal models to generate novel and new ideas.  However, what has happened -- and Dr. Greek is entirely correct -- is that to sell the idea, quote, unquote, sell it, I would -- I would agree that many biomedical scientists can be accused of over promising and under delivering.  But the over promising is what's required or the -- or is what they have to define why are you doing this research and how's it going to directly benefit humans.

In other words, it is OK to lie to get grant money because animal modelers are not subject to the same rules as the rest of us. Maybe that is why Gorski et al will not defend their position in public.


Braco, Jason T., Emily L. Gillespie, Gregory E. Alberto, Jay E. Brenman, and Erik C. Johnson. 2012. Energy-dependent Modulation of Glucagon-like Signaling in Drosophila via the AMP-activated Protein Kinase. Genetics.

Freeman, Matthew, and Daniel St Johnston. 2008. Wherefore DMM? Disease Models & Mechanisms 1 (1):6-7.

Gorski, David. 2012. Related by coincidence only? University and medical journal press releases versus journal articles. Science-Based Medicine, August 20 2012 [cited August 20 2012]. Available from

Konopka, Genevieve, Tara Friedrich, Jeremy Davis-Turak, Kellen Winden, Michael†C Oldham, Fuying Gao, Leslie Chen, Guang-Zhong Wang, Rui Luo, Todd†M Preuss, and Daniel†H Geschwind. 2012. Human-Specific Transcriptional Networks in the Brain. Neuron 75 (4):601-617.

Polley, Stanley R. G., and David S. Fay. 2012. A Network of Genes Antagonistic to the LIN-35 Retinoblastoma Protein of Caenorhabditis elegans. Genetics.

Schwartz, Lisa M, Steven Woloshin, Alice Andrews, and Therese A Stukel. 2012. Influence of medical journal press releases on the quality of associated newspaper coverage: retrospective cohort study. BMJ 344.

TAM. 2012. The Truth About Alternative Medicine. YouTube 2012 [cited August 25 2012]. Available from

UCLA. 2012. More sophisticated wiring, not just bigger brain, helped humans evolve beyond chimps, geneticists find. ScienceDaily, August 22 2012 [cited August 22 2012]. Available from

Woloshin, S., L. M. Schwartz, S. L. Casella, A. T. Kennedy, and R. J. Larson. 2009. Press releases by academic medical centers: not so academic? Annals of internal medicine 150 (9):613-8.


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