Putting aside the political BS with "Don't Say Gay" bills, puppy play gimps, drag shows, and Screwdolph…
At what age are children developmentally capable of understanding the complexities of genetic predisposition, environmental, and en-utero developmental factors that affect human sexuality?
It has to be well past elementary school.
https://royalsocietypublishing.org/doi/10.1098/rspb.2019.2907
https://www.science.org/doi/10.1126/science.aat7693
At what age are children developmentally capable of understanding the complexities of genetic predisposition, environmental, and en-utero developmental factors that affect human sexuality?
It has to be well past elementary school.
https://royalsocietypublishing.org/doi/10.1098/rspb.2019.2907
Quote:
The fraternal birth order effect (FBOE) is the finding that older brothers increase the probability of homosexuality in later-born males,1 and the female fecundity effect (FFE) is the finding that the mothers of homosexual males produce more offspring than the mothers of heterosexual males.2 There is a considerable amount of empirical evidence for the reproducibility of the FBOE [25] and the FFE [68]. Each effect relates to a specific biological theory of the aetiology of homosexuality in malesan immunological theory, in the case of the FBOE [9,10], and a genetic theory, in the case of the FFE [11].
The maternal immune hypothesis (MIH) is the hypothesis that the FBOE reflects the progressive immunization of some mothers to male-specific antigens and the consequent effects of anti-male antibodies on sexual differentiation in the brain in male fetuses. According to this hypothesis, cells (or cell fragments) from male fetuses enter the maternal circulation during childbirth or perhaps earlier in pregnancy. These cells include substances that occur primarily on the surfaces of male brain cells, for example, the Y-linked membrane proteins NLGN4Y and PCDH11Y. The mother's immune system recognizes these male-specific molecules as foreign and produces antibodies to them. In subsequent male pregnancies, her antibodies cross the placental barrier and enter the fetal brain. Once in the brain, these antibodies bind to male-specific molecules on the surface of neurons and prevent these neurons from 'wiring-up' in a fully male-typical pattern. In consequence, the individual will later be attracted to men rather than to women. There has only been one laboratory test of the MIH, but its results were consistent with the hypothesis. This test found higher concentrations of anti-NLGN4Y antibody in the sera of mothers of homosexual men, especially those with older brothers, compared with the concentrations for mothers of heterosexual control subjects [10].
The FFE is a prediction of the balancing selection hypothesis (BSH). The BSH is an attempt to reconcile the findings from behaviour genetics and molecular genetics that homosexuality in men is partially heritable with the finding that homosexual men produce far fewer offspring than do their heterosexual counterparts. If both these findings are trueand there is no particular reason to doubt eitherthen the number of people who carry genes predisposing to homosexuality should be declining and the prevalence of homosexuality in the male population should be decreasing. Such a decrease, however, is not evident. The BSH resolves this seeming conundrum by proposing that the same genes that predispose to homosexuality in some males also increase fecundity in their heterosexual relatives, especially female relatives; this is the predicted FFE. Because of the FFE, the family's total number of descendants and the number of individuals carrying 'gay genes' remain constant. The FFE compensates for the low fertility of homosexual men.
https://www.science.org/doi/10.1126/science.aat7693
Quote:
In the discovery samples (UK Biobank and 23andMe), five autosomal loci were significantly associated with same-sex sexual behavior. Follow-up of these loci suggested links to biological pathways that involve sex hormone regulation and olfaction. Three of the loci were significant in a meta-analysis of smaller, independent replication samples.
Although only a few loci passed the stringent statistical corrections for genome-wide multiple testing and were replicated in other samples, our analyses show that many loci underlie same-sex sexual behavior in both sexes. In aggregate, all tested genetic variants accounted for 8 to 25% of variation in male and female same-sex sexual behavior, and the genetic influences were positively but imperfectly correlated between the sexes [genetic correlation coefficient (rg) = 0.63; 95% confidence intervals, 0.48 to 0.78]. These aggregate genetic influences partly overlapped with those on a variety of other traits, including externalizing behaviors such as smoking, cannabis use, risk-taking, and the personality trait "openness to experience." Additional analyses suggested that sexual behavior, attraction, identity, and fantasies are influenced by a similar set of genetic variants (rg > 0.83); however, the genetic effects that differentiate heterosexual from same-sex sexual behavior are not the same as those that differ among nonheterosexuals with lower versus higher proportions of same-sex partners, which suggests that there is no single continuum from opposite-sex to same-sex preference.
