Society for the Scientific Study of Sexuality, Tampa, FL
Nov 8-11. Poster A-18 (Scheduled for presentation Nov 9)
Background:A detailed model 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 (Kohl, 2012). That model is used to exemplify the effects of olfactory/pheromonal conditioning, which alters genetically predisposed, nutrient chemical -dependent, hormone-driven mammalian behavior and choices for pheromones that control reproduction via their effects on luteinizing hormone (Kohl, 1992).
Model: In this diagrammatic representation of the model [soon to be linked here], nutrient chemicals are metabolized to pheromones that condition behavior in precisely the same way that food odors condition behavior associated with food preferences. The epigenetic effects of olfactory/pheromonal input calibrate and standardize molecular mechanisms for genetically predisposed receptor-mediated changes in intracellular signaling and stochastic gene expression in gonadotropin releasing hormone (GnRH) neurosecretory neurons of brain tissue. For example: glucose (Roland & Moenter, 2011) and pheromones alter the secretion of GnRH and luteinizing hormone (LH). Parenthetically, a form of GnRH that is also linked to sexual orientation appears to control the feedback loops of developmental processes required for nutrient chemical ingestion, movement, reproduction, and the diversification of species from microbes to man.
Additional Considerations (not shown): The honeybee is an invertebrate model of adaptively evolved social behavior. The concept that is extended is the epigenetic tweaking of immense gene networks in superorganisms that solve problems through the exchange and the selective cancellation and modification of signals. In the context of what has also been referred to as “biological embedding,” olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans. It is now clearer how an environmental drive evolved from that of nutrient chemical ingestion in unicellular organisms to that of socialization in insects. It is also clear that, in mammals, food odors and pheromones cause changes in hormones such as LH, which has developmental affects on sexual behavior in nutrient chemical-dependent reproductively fit individuals across species of vertebrates.
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).
Conclusions: 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. 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.