It recently came to my attention that there are researchers who think that hormones are solely responsible for sex differences in behavior. Indeed, this is probably what many people were taught based on the only knowledge that was available until the latter part of the last century. Prenatal testosterone, secreted from the testes, was touted as the key to what makes a male a male, and the makings of a male took place largely in the third trimester of human gestation. I don’t know how many of today’s medical practitioners and medical researchers are under that mistaken impression, but I do know that, in 1993, a large audience of medical practitioners was told that they would need to learn about molecular biology by the co-discoverer of the Sry gene. Therefore, in the human-ethology discussion group under the thread Genes, Hormones, and Behavior, I have attempted to clarify the fact that genetically directed organization of the testes and ovaries involves many genes and molecular mechanisms.
I have detailed genetically programmed mammalian sexual differentiation in the Journal of Psychology and Human Sexuality and clearly, it’s not just Sry (the gene that was reported to make a male of a female). It is also becoming clearer that the required molecular mechanisms that make males different than females impact prenatal GnRH pulse generation before sexual differentiation of the gonads (and testosterone production). Thus, even the embryonic environment in the mammalian womb impacts sexual differentiation throughout gestation, just as does the postnatal social environment throughout life. The effects occur via the same molecular mechanisms that ultimately effect GnRH pulsatility — as we tentatively detailed 15 years ago in Hormones and Behavior.
In this regard, my focus has been the role of pheromones in postnatal sexual differentiation. Since 1996 it has become clear that GnRH pulsatility links genetic nature and social-environmental nurture. Thus, any focus on sex steroid hormones without knowledge of the molecular mechanisms involved in their prenatal or postnatal regulation continues to be ridiculously misleading. For example, when someone indicates that genetic mechanisms are not responsible for prenatal brain organizational effects of testosterone, as did the human-ethology group’s moderator , it becomes clearer that they either intend to be misleading; need to clarify what they said, or that they lack the knowledge required to comment and should be asking questions.
Sadly, this is now even more the case than it has been at any time since ethologists somehow determined that sex differences in hormones were solely responsible for the sex differences in behavior that they observed. Given the apparent truth of their observations, they seem to expect that correlating visual input with changes in levels of testosterone is meaningful in the absence of knowledge about molecular biological events. However, given the discovery of Sry, in the early 1990’s, and other discoveries of the molecular mechanisms responsible for sex differences, it is now these molecular biological events that give ethological meaning to the relationships between genes, hormones, and behavior via the scientific study of animal behavior.
Ignoring the molecular biology of sex differences leads to claims that humans are primarily visual creatures, which can then be supported by correlative evidence (sans cause) that adolescent males mark their territory with visual signals, not odors. And claims of our diminished olfactory acuity and specificity can be made by comparing us to canines. That’s the pervasive nonsense we have all seen in discussions on the human-ethology group, although some may not see it as nonsense.
Meanwhile, “Genes underlying isolated GnRH deficiency have been shown to be important for the specification and proliferation of GnRH neurons (16, 17), their migration to the hypothalamus during embryonic development (18–22), the regulation of GnRH secretion (23–25), and the response of pituitary gonadotropes to GnRH stimulation (26).” Abstract Here
And a recent review “…updates the list of candidate proteins and pathways involved in GnRH neuronal migration and highlights those shown to be involved in human disorders of GnRH deficiency.” Abstract Here
These articles, as does my 2007 review, cite the existing supporting scientific literature that establishes the validity of my mammalian model, and makes discussion of visually perceived aspects of human physical attraction, like sinusoidal edges of fertile females, a ridiculous waste of my time with regard to the scientific study of animal behavior.
It is obvious that olfactory/pheromonal input conditions the hormone responses causally associated with animal behavior. It is also obvious, that animal behavior is so thoroughly conditioned that once conditioning has occurred olfactory/pheromonal input is no longer required to elicit the same behavioral hormone-directed behavioral response. Other sensory input may elicit the same effects on hormones and affects on behavior, but only after responses are conditioned. This is what molecular biology shows, and what cannot be simply observed.
Clearly, “In the final analysis, there is an ongoing need to account for the influence of hormones in the context of underlying genetic circumstances and null hormone conditions.” Abstract Here — as we indicated in 1996. If others are allowed to take the influence out of context, by ignoring the underlying genetic circumstances or null hormone conditions, they will continue to misrepresent what is known about the molecular mechanisms that are required for sexual differentiation, both prenatally and postnatally.
It is equally clear that in the human-ethology group there will be no accounting for the molecular mechanisms of behavior detailed in the articles linked above, and no accounting for how any non-olfactory/pheromonal stimuli from the environment establish their relative salience in humans. As the moderator of the group, has said: “There is another principle in science that says, “observation trumps theory.”
I’m familiar with explanations of behavior that involve genes and hormones, and don’t know of any scientific principle that supports observation over theory when it comes to molecular mechanisms, which cannot be directly observed.