Concluding sentence: “Interest in the gene determined the fate of the population genetics article, and resulted in a large number of citations to an unlikely candidate article.”
How does the social environment ‘get into the mind’? Epigenetics at the intersection of social and psychiatric epidemiology
Excerpt 1) “… increased DNA methylation at the SLC6A4 locus thus provides an additional example of how epigenetic processes may mediate social exposures in a manner salient to psychopathology.”
Excerpt 2) “These data confirm that nutritional intake — a process with clear social environmental contributions — can affect epigenetic processes, which have been associated with schizophrenia.”
My comment: The biological facts reported in the article excerpts attest to the need to understand the importance of nutritional epigenetics for comparison to the concluding sentence from the article about population genetics. For example, “Vitamin D-mediated production of serotonin may be critical for the production of serotonergic signals during neurodevelopment. This indirectly links vitamin D to the development of the brain and changes in the brain associated with skull architecture and brain development throughout adulthood because serotonin plays a critical role in regulating a variety of brain functions, which include social behavior.” — Kohl (under review)
Nutrient uptake clearly enables the metabolism of nutrients to species-specific social odors called pheromones that may epigenetically effect serotonin and brain development via the conserved molecular mechanisms associated with the epigenetic effects of:
1) food odors;
2) nutrient uptake and
3) the pheromone-controlled physiology of reproduction in species from microbes to man.
The epigenetic link from SLC6A4 polymorphism to schizophrenia may be as simple as that. Ecological variation in the availability of specific nutrients probably determines whether or not human populations ecologically adapt. Some individuals may not. However, it seems futile to try to find a mutation in cell types that may somehow cause a mental disorder in individuals that appear to be maladapted. It would be easier to trace a genetic predisposition and nutritional deficiency to cause and effect — not in human populations, or individual humans — but via the use of animal models.
However, when ecological variation leads to ecological adaptations, population geneticists tend to dismiss across species examples of ecological factors. When ecological variation appears to result in diseases and disorders, population geneticists attribute the diseases and disorders to mutation-driven evolution. The conserved molecular mechanisms of biophysically constrained cause and effect are removed as if psychiatry research had somehow become a branch of social science.
Nearly all social scientists are more likely to place the biologically based cause and effect manifested in diseases and disorders into the context of population genetics and constraint-breaking mutations. Most biologists and all psychiatrists should not do that. Parenthetically, it is okay for a few biologists to set a bad example, nonetheless. Someone must exemplify ignorance and arrogance so that others may recognize the difference in biologically plausible approaches.
No experimental evidence suggests that mutations, which perturb protein folding, are beneficial. However, the obviousness of biophysically constrained protein folding is only reassuring to those who are familiar with the basic principles of biology and levels of biological organization that link the sensory environment to behavior in species from microbes to man.
The obviousness of biophysical constraints can only disturb those who tout theories of mutation-induced SLC6A4 polymorphism that automagically include beneficial affects of polymorphisms on typical behavior. Those touting theories have begun to realize their theories are nothing more than pseudoscientific nonsense framed in the ridiculous context of mutation-driven evolution of human populations.