Pheromones, GnRH, and brain development
Posted on April 19, 2013 by James Kohl.
Effects of peripubertal gonadotropin-releasing hormone agonist on brain development in sheep—A magnetic resonance imaging study exemplifies some of the latest research on molecular mechanisms of adaptive evolution. It also links the latest research to the central focus of my model of nutrient-dependent pheromone-controlled adaptive evolution. The link is via epigenetic effects of food odors and pheromones on gonadotropin-releasing hormone (GnRH).
GnRH is the biological core of mammalian reproductive sexual behavior. Nuruddin et al., may be the first in several years to put GnRH in its proper place, which is upstream from everything else involved in behavioral development. They write:
“GnRH is a decapeptide neurohormone that plays a key role in the reproductive axis, ultimately modulating therelease of gonadal steroid hormones. Its receptor (GnRHR) has been found in various brain regions, including the frontal cortex, the olfactory bulb and the limbic system (Albertson et al., 2008; Skinner et al., 2009; Chu et al., 2010; Rosati et al., 2011; Schang et al., 2011). Importantly, not all of these brain regions have roles in the control of reproductive function, suggesting that GnRH is involved in other processes and,as such, may modulate sex differences in emotional processing and cognitive functions.”
In the context above, you may think in terms of GnRH-dependent ecological, social, neurogenic, and socio-cognitive niche construction in mammals. When others realize it is GnRH that controls androgen secretion, like testosterone secretion, and controls oxytocin secretion as well as estrogen secretion, they may also begin to realize why attempts to link hormones to behavior without first linking sensory input to GnRH and other hormones is a ridiculous waste of time.
Those attempts lead to horrid misrepresentations of cause and effect in the context ofDarwinian natural selection. Selection is for nutrients that metabolize to pheromones that control reproduction. There’s a model for that, sans mutations theory! It’s the model I’ve been detailing since its first presentation in 1992.
Retired medical laboratory scientist
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