Epigenetic effects underlie sexual preferences III

Can Epigenetics Explain Homosexuality?  By Sabrina Richards January 1, 2013

Scientists propose a new model for how homosexuality develops, but observers say it will be difficult to test.

Excerpt: “It’s a very provocative, very interesting new twist that is plausible,” said Margaret McCarthy, a neuroscientist at the University of Maryland who studies how hormones influence brain development and was not involved in producing the model. But, she cautioned, so far the theory “is not supported by any data.”

My comment: Taken together, all data on hormone-organized and hormone-activated brain development and behavior in every species with a central nervous system conclusively proves that sexual orientation is nutrient chemical-dependent and pheromone-controlled. It is the nutrient chemicals and the pheromones that epigenetically effect the gene, cell, tissue, organ, organ system pathway of invertebrates and vertebrates, which links sensory input from their ever-changing environment to hormone-organized and hormone-activated behavior.

A new model for cause and effect was established in 1996, in From fertilization to adult sexual behavior.  “Research has established the broad mammalian developmental plan that genes on the sex chromosomes influence gonad development which determines gonadal hormone production (or its absence) leading to modification of the genitalia and simultaneously biasing the nervous system to organize adult sexual behavior. This might be considered the “gonad to hormones to behavior” model. It is clear, however, that although this model generally works well it is incomplete. The model does not account for behavioral influences attributed to the environment or to genetic but nongonadal or hormonal factors. In this essay we probe those areas of sexual development that are neither differentiated by hormones nor activated by them. The concept of the environment used for our discussion is very broad; it incorporates considerations of both the molar and the molecular levels.” (Diamond, Binstock, and Kohl)

Our 1996 addition to a decades-old model was restated, in part, 15 years later in 2011: Reframing sexual differentiation of the brain “In the twentieth century, the dominant model of sexual differentiation stated that genetic sex (XX versus XY) causes differentiation of the gonads, which then secrete gonadal hormones that act directly on tissues to induce sex differences in function. This serial model of sexual differentiation was simple, unifying and seductive. Recent evidence, however, indicates that the linear model is incorrect and that sex differences arise in response to diverse sex-specific signals originating from inherent differences in the genome and involve cellular mechanisms that are specific to individual tissues or brain regions.” (McCarthy and Arnold)

Data from research on pheromones somehow went missing from the reiteration of Diamond, Binstock, and Kohl (1996) by McCarthy and Arnold (2011).  Lest others continue to miss this, I will add…

Pheromones are sex-specific signals that originate from inherent sex differences in the genome. They epigenetically effect the cellular mechanisms that are specific to individual tissues and brain regions via the gene, cell, tissue, organ, organ system pathway. That pathway links both food odors and social odors (i.e., pheromones) to the development of brain-directed behavior. It links food odors and pheromones to directly to alterations in gonadotropin releasing hormone (GnRH) and its downstream affects on vertebrate behavior, or via the downstream effects of juvenile hormone (JH) on invertebrate behavior.

“Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus (Runge and Zakian, 1996; Wu and Haber, 1995).” — also from Diamond, Binstock and Kohl (1996)

The epigenetic modifications are nutrient chemical-dependent and pheromone-controlled, which leads to another conclusion:  “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.” If not for some very obvious politics in the science of human sexuality, more people would have been aware, since 1996, that epigenetics explains both homosexuality and heterosexuality. Indeed, it is ridiculous for researchers to attempt to use one model for homosexuality and another for heterosexuality. It is equally ridiculous to claim that one model is a theory unsupported by data.  Heterosexual orientation is nutrient chemical-dependent and pheromone-controlled in every species on the planet. How did an epigenetic explanation of homosexuality become someone’s “new” model that McCarthy thinks is a theory that “is not supported by any data.”? Is there a theory of heterosexuality that is supported by data, or is the model for the development of food preferences and development of sexual preferences from species of microbes to man supported equally well by the same data?

Author: James Kohl

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