Human Pheromones: Epigenetic Effects on Hormones and Their Affects on Behavior
Posted on November 15, 2012 by James Kohl.
Until now, behavioral epigenetics needed to connect all its levels of analysis and provide “… at least one slam-dunk demonstration of all the links in a chain from behavior to neural activity to gene expression and back out again.” When I learned that others thought this demonstration still was needed, I brought my 1992 model current by incorporating the latest perspectives from neuroscience. One month after the 2012 annual meeting of the Society for Neuroscience, my detailed model now explains how chemical ecology drives adaptive evolution via 1) ecological niche construction, 2) social niche construction, 3) neurogenic niche construction, and 4) socio-cognitive niche construction in accord with my previously published work: see (Kohl, 2012).
I used my updated 1992 model to exemplify the effects of olfactory/pheromonal conditioning. The model now shows that food odors and pheromones alter genetically predisposed, nutrient chemical-dependent, hormone-driven mammalian behavior and choices for pheromones that control reproduction via their effects on luteinizing hormone (Kohl, unpublished). For example, clink on the link below to view my poster presentation from November 9, 2012. It represents two decades of neuroscientific progress.
This poster was submitted to the F1000 poster site on Tuesday 11/13/12, and receipt of the submission was confirmed by “Alla” in an email response to me on 11/16/12, which states:
Hi James, Your poster submission is currently being processed. Your poster will appear on the F1000 Posters website very soon. Regards, Alla
As is indicated in the poster text (provided at the link above): This model of systems biology represents the conservation of bottom-up organization and top-down activation via:
1. Nutrient-dependent stress-induced and social stress-induced intracellular changes in the homeostatic balance of microRNA(miRNA) and messenger RNA (mRNA);
2. Intermolecular changes in DNA (genes);
3. Non-random experience-dependent stochastic variations in de novo gene expression for odor receptors;
4. The required gene-cell-tissue-organ-organ system pathway that links sensory input directly to gene activation in neurosecretory cells of the brain;
5. The required reciprocity that links gene expression to behavior that alters gene expression (i.e., from genes to behavior and back).
Additional support for this model can be found in: Evolution of the human-specific microRNA miR-941, an open access article. Published on
Across species comparisons of epigenetic effects on genetically predisposed nutrient-dependent and hormone-driven invertebrate and vertebrate social and sexual behavior indicate that human pheromones also alter the development of the brain and behavior via the same molecular mechanisms that are responsible for invertebrate foraging and social behaviors exemplified in the honeybee model organism. Obviously, those molecular mechanisms must be conserved across all species for adaptive evolution of the human brain and human behavior to occur (e.g., via properly timed reproductive sexual behavior of mammals).
Note: In mammals, LH secretion is the measurable proxy for genetically predisposed differences in hypothalamic GnRH pulse frequency and amplitude and the downstream effects of GnRH on the HPG and HPA axes that provide feedback to the GnRH neuronal system, which is the central regulator of genetically predisposed nutrient chemical-dependent individual survival and pheromone-dependent species survival. What this means is that LH is the link between sex and the sense of smell, as indicated in the title of my 1992 presentation: Luteinizing Hormone: The link between sex and the sense of smell? The question mark in the title indicated that in 1992 I was not quite sure of what is now perfectly clear due to neuroscientific progress that epigenetically links olfactory/pheromonal input directly to all the links in a chain from behavior to neural activity to gene expression and back out again.
During the past two decades, my model has gone virtually unrecognized by all but a few distinguished colleagues, and the model has been repeatedly attacked by those who have not distinguished themselves via any efforts to make neuroscientific progress. The antagonism is to be expected, but I now expect it to end with discussion of whatever I have missed that should be included in the model, or whatever other model anyone think better represents the conservation of the molecular biology of adaptive evolution across species from microbes to man.
Retired medical laboratory scientist
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