#Old gay men fuck me full
An interaction between the immune mechanisms discussed here and the endocrine or genetic mechanisms is less obvious, but not inconceivable.Īlternatively, perhaps the prenatal/perinatal biological factors do not by themselves determine sexual orientation but interact with specific aspects of the postnatal environment to reveal their full effect. A mutation of this gene in males could thus modify testosterone action during brain development, although such an interaction still raises a number of questions ( 14). A gay orientation in males has been linked to the terminal Xq28 region of the X chromosome ( 8, 9), and this region contains a gene coding for protein MAGE-11 (melanoma-associated antigen), which is a coactivator of the androgen receptor ( 13).
The endocrine and genetic mechanisms can easily be seen as interacting for example, if a genetic mutation or variant affects the secretion or action of sex steroids in the brain. Either the diverse biological mechanisms (hormonal, genetic, and immune) each explain a fraction of the cases and homosexuality is a multifactorial phenotype that can have multiple independent origins, or these different mechanisms interact and complement each other to control a phenotype that is otherwise essentially homogeneous.
Whether a unifying theory can be derived from the available experimental evidence thus remains unclear and will require additional investigations. Similarly, the other biological mechanisms implicated in the control of sexual orientation, the effects of early steroid hormones, and genetic background, also explain only a fraction of the cases of male homosexuality ( 6). present direct biochemical evidence indicating that the increased incidence of homosexuality in males with older brothers results from a progressive immunization of the mother against a malespecific cell-adhesion proteinhad a gay son had unknowingly miscarried male embryos previously ( 12). While FBO represents the best-documented biological influence on sexual orientation, the underlying mechanisms had remained completely speculative so far. ( 3), homosexuality in males has been consistently and repeatedly linked to the presence of older brothers born to the same mother, the FBO effect ( 1, 2, 12). Third, and directly relevant to Bogaert et al. Recent publications also suggest that epigenetic mechanisms could be involved ( 10) but the specifics have so far remained elusive ( 11). Second, there is strong evidence, from studies of family trees and of monozygotic and dizygotic twins, of a genetic component to the control of sexual orientation, even if attempts to identify the specific genes involved have met so far with little success ( 5, 8, 9). Additionally, numerous epidemiological studies have shown that gay men and lesbians display a partial sex-reversal of morphological, physiological, and behavioral/cognitive traits that are sexually differentiated, and in many cases known to develop under the early influence of sex steroids ( 6). Endocrine pathologies that modify the embryonic hormonal environment are associated with increased incidence of homosexuality. Correlative studies suggest that these mechanisms are also at play in humans. First, work in a variety of animal models has shown that sexual partner preference can be experimentally modified by perinatal treatments with sex steroids: masculinization following exposure to testosterone or its estrogenic metabolites, and feminization in the (relative) absence of these steroids during a critical period of development. Three types of biological mechanisms have been identified in this context ( 4– 7). This study provides the first data-based explanation for the FBO effect and adds a significant chapter to growing evidence indicating that sexual orientation is heavily influenced by prenatal biological mechanisms rather than by unidentified factors in socialization. ( 3) present direct biochemical evidence indicating that the increased incidence of homosexuality in males with older brothers results from a progressive immunization of the mother against a male-specific cell-adhesion protein that plays a key role in cell–cell interactions, specifically in the process of synapse formation, during development called neuroligin 4 Y-linked, or NLGN4Y. Despite this compelling evidence, a mechanism to account for the effect remained elusive. This startling phenomenon was confirmed in multiple studies based on independent populations totaling over 10,000 subjects, and a meta-analysis indicated that between 15% and 29% of gay men owe their sexual orientation to this effect ( 2).
Their first investigation indicated that each older brother increased the probability of being gay by about 33% ( 1). Twenty years ago, Ray Blanchard and Anthony Bogaert demonstrated that the probability of a boy growing up to be gay increases for each older brother born to the same mother, the so-called fraternal birth order (FBO) effect.