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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).
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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.
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( 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.