Human pheromones, nutrition, DNA, epigenetics
Posted on July 30, 2012 by James Kohl.
My comment: Now that others are talking about the epigenetic effects of nutrient chemicals, it should not be long before more people realize that the epigenetic effects of pheromones are equally important to adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction, as I detailed in Kohl (2012).
The clearest common link across the molecular biology of species from microbes to man is the conservation of gonadotropin releasing hormone (GnRH), and diversification of its receptor. In our species, as in other mammals, the measure of luteinizing hormone (LH) reflects sex differences in brain development and their link to GnRH-directed neuroendocrine and neuroimmune system development as is important to consider in autism spectrum disorders, and every other aspect of genetically predisposed brain development. See also our pioneering work: From fertilization to adult sexual behavior. Diamond M, Binstock T, Kohl JV. Horm Behav. 1996 Dec;30(4):333-53.
Proceeding from the quote above “You are what you eat.” –> The metabolism of nutrient chemicals (what you eat) determines the pheromone production that tells others who and what you are, as exemplified in the honeybee model organism (and in yeasts). What the queen bee eats determines her pheromone production and everything else about the interaction in the colony, including the neuroanatomy of the worker bees’ brains.
Video (10.21 minutes) Dana Dolonoy
Did those who say that diet may influence the DNA of future generations not get my memo? Of course there are transgenerational epigenetic effects of diet (and pheromones). They are responsible for adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction – as occurs with speciation from microbes to man.
The transgenerational epigenetic effects of diet and pheromones cause speciation. A new nutrient source in an existing ecological niche causes diet-driven changes in intracellular signaling and stochastic gene expression. The changes in gene expression are linked to the metabolism of the new nutrient and to changes in pheromones and in chemical (e.g., olfactory or odor receptors).
Substantial changes in diet result in substantial changes in species-specific pheromones that signal reproductive fitness. Natural selection for a well-nourished conspecific that is reproductively fit is ensured via the epigenetic effects of nutrient chemicals and pheromones. Had Darwin’s followers known anything about genetics they might have figured out the the changing beaks of finches were caused by the epigenetic changes of nutrient chemicals and that even subtle changes in the beaks were accompanied by changes in pheromones that controlled reproduction — so that different species with different beaks could evolve to maximize their reproductive potential in a new ecological niche. As it turns out, now we know that nutrient chemicals and pheromones are responsible for evolution. What we don’t know is why so many people think that random mutations cause adaptive evolution. Is there a model for that? If so, is there a pattern comparable to the one recognized as the design in biology of 1) ecological, 2) social, 3) neurogenic, and 4) socio-cognitive niche construction? How could random mutations be responsible for such an obvious complex sequence of receptor-mediated events?
Retired medical laboratory scientist
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