Nutrient-dependent pheromone controlled behavioral epigenetics
April 10, 2013 | James Kohl
Comment by Ed Yong on Power failure: why small sample size undermines the reliability of neuroscience [subscription required]
Excerpt: “Statistical power refers to the odds that a study will find an effect—say, whether antipsychotic drugs affect schizophrenia symptoms, or whether impulsivity is linked to addiction—assuming those effects exist.”
My comment: Now that behavioral epigenetics has detailed gene x environment interactions at the molecular level of adaptive evolution in species from microbes to man, it’s time to look at study design and results in the context of what we’ve already learned from animal models. For example, nutrient-dependent amino acid substitutions show up in phenotypical traits of pheromone controlled reproductive fitness. Selection is for pheromones that signal hormone-dependent reproductive fitness in vertebrates and invertebrates.
Although statistical analyses can be used to link mutations to nutrient-dependent pheromone-controlled adaptive evolution, the statistical analyses do not address Darwin’s “conditions of existence,” which are nutrient-dependent and pheromone-controlled. Thus, mutations theory tells us about missense mutations and nonsense mutations that somehow result in adaptive variations or disease, with no mention of how the epigenetic landscape becomes the physical landscape of DNA (e.g., via chromatin modifications which are important to learning and memory).
Consistent use of a model for how olfactory/pheromonal input epigenetically effects phenotypic traits that include behavior might provide a framework for evaluation of study results from different disciplines and bring us closer to placing what seem like disparate findings into their ‘proper’ context. The proper context has not changed from ‘conditions of existence,’ which are nutrient-dependent and pheromone-controlled. Proper context is not statistically determined; it’s the result of adaptive evolution. For example: “In light of other evidence that histone and chromatin modifications are important in both cognition and memory disorders49,50, it is tempting to speculate that Aβ-induced abnormalities in the formation and repair of DSBs similar to those we identified in hAPP mice and neuronal cultures may contribute to Alzheimer’s disease–related neurological deficits (Supplementary Fig. 8).” Mouse models of nutrient-dependent pheromone-controlled adaptive evolution have established the fact that conserved molecular mechanisms for learning and memory can be found in all species and that “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.” — Kohl (2012)