Of Mice and Men: Nutrition Miscommunication

Happy National Nutrition Month! I use this bully pulpit often to decry the persistent plague of rampant – and often nefarious – nutrition miscommunication. After 25 years on this soapbox, I’m sure many think I should just give it a rest. But how can I when releases labeled, “America’s most widely consumed oil causes genetic changes in the brain” come over the electronic transom? And this from a university, not some sensationalist tabloid.

In fairness, the lead of the release was marginally more honest, “Soybean oil linked to metabolic and neurological changes in mice.” (The actual title of the study as published in the prominent academic journal, Endocrinology, was the more sober, “Dysregulation of Hypothalamic Gene Expression and the Oxytocinergic System by Soybean Oil Diets in Male Mice.”) But the release dove deeper into the abyss of irresponsible misinformation with the grossly inaccurate declaration about soybean oil that, “In all likelihood, it is not healthy for humans.”

Using rodents in metabolic studies, and applying the results to humans, is an extremely dicey prospect. While it has been a standard to use Mickey and his cousins in research, scores of analyses and studies have demonstrated many inherent flaws in the model. Too many for a short editorial, but here’s the gist:

Multiple factors impact experimental animals, including environmental conditions (lighting, air, water, stress), the food they eat (i.e. energy dense high-fat diets), and the species and condition of the mice themselves. And there’s a more acute factor when considering the mouse model: Mice eat each other’s feces.

Rodents have unique microbiomes and metabolic responses, which also impacts results. (All animals do, including people; for my graduate research I did feeding studies on human volunteers and individual variation in the first two runs completely confounded results.) This study used an inbred strain of genetically modified mice reportedly extremely sensitive to environmental assaults; prone to atherosclerosis, addiction, and other diseases; and highly susceptible to genetic drift.

Writing in the Journal of the Royal Society of Medicine, Michael Bracken, PhD, cited a host of other weaknesses in such studies, including: small experimental groups with inadequate statistical power; confounding influences from laboratory techniques that might go unrecognized or unreported; and selection of outcome measures as surrogates or precursors of disease that are of uncertain relevance to humans.

Bracken also pointed out the “variable duration of follow-up, which may not correspond to disease latency in humans.” In other words, a one-off, limited-
duration experiment (on mice or men) does not account for the possibility that any changes are transitory and could resolve once the body resets its balance of energy, metabolism, and chemistry.

Nutrition science is a gray area and, as communicators and developers navigate the “better for you” products field, credible, relevant science must be at the foundation of our efforts.

PS: to Dr. Kantha Shelke: Thanks for the title!