Homosexualität und Biologie

Ein interessanter Artikel fasst die Forschung zur Homosexualität zusammen:

Homosexuality is a common occurrence in humans and other species. It is a complex, universal phenomenon whose genetic and evolutionary basis is poorly understood. Despite great progress in the sciences, our understanding of the determinants of sexual orientation and, more specifically, of male homosexuality, is incomplete. In this paper, we have reviewed the biological causes of male homosexuality, which may provide clues for further research in this field, as provable biological or genetic differences between heterosexuals and homosexuals that weren’t caused by their behaviour
haven’t been found.

Quelle: The biochemistry of male homosexuality

Das war schon häufig hier Thema:

Dennoch finde ich solche Übersichtsartikel immer sehr interessant, weil sie immer neue Punkte aufzeigen:

On certain experiments conducted on animals and specifically guinea pigs, Phoenix and colleagues (1959) showed that testosterone, when administered
during sensitive periods of development , has a masculinizing action on neuronal tissue involved in mating behaviour. This organizing effect of sex hormones in males and females seems to hold true for most mammalian species (Ward & Ward 1985).

Das Tierstudien zu den gleichen Ergebnissen kommen finde ich sehr aussagekräftig.

Auch interessantes findet sich zur Fraternal birth order:

According to this hypothesis, the causal mechanism is purely biological (Blanchard 2001, Blanchard & Bogaert 1996, Bogaert 2006). This hypothesis
runs as follows: The fraternal birth order effect may be triggered when foetal cells (or cell fragments) enter the maternal circulation, an event especially
common during childbirth. If these cells are from a male foetus, they may include substances that only occur in, or on the surfaces of, male cells. The
mother’s immune system recognises these malespecific molecules as foreign and starts producing antibodies to them. Following maternal immunisation, maternal anti-male antibodies are available to cross the placental barrier and enter the brain of a male foetus.
These antibodies somehow divert the sexual differentiation of the foetal brain from the male-typical pathway, so that the individual will later be attracted to men rather than women. The probability -or strengthof maternal immunisation increases with each male
foetus, therefore the probability of homosexuality increases with each older brother.
Also, the maternal immune hypothesis is consistent with biological data relevant with the effect of prenatal hormones on sexual orientation (Gladue et al.
1984, LeVay 1991, Swaab & Hofman 1990). Substances that are produced solely by males and are capable of provoking immune responses in females are referred to as ‘‘male-specific antigens’’. These could be large molecules like proteins or, in some cases, peptides. The maternal immune hypothesis cannot be true unless male-specific antigens exist, unless there is some reason to believe that they might play a role in sexual differentiation in the brain, and
unless it is possible that they could be inactivated by antibodies without producing gross abnormalities. All
three things do appear to be true or possible.

Research has shown that genes on the human Y-chromosome collectively encode at least 27 distinct male-specific proteins or protein families (Skaletsky et al. 2003). Three of these proteins are expressed in the foetal brain, and two of the three are relatively good examples of candidate antigens for the hypothesis because they encode cell-surface proteins, which might be accessible to antibodies. The first is protocadherin
11 Y-linked (PCDH11Y, also known as PCDH22 and PCDHY; Blanco et al. 2000), and the second is neuroligin 4 Y-linked (NLGN4Y; Jamain et al. 2003).
Both the protocadherin and neuroligin families of proteins are cell adhesion molecules, thought to play an essential role in specific cell-cell interactions during embryonic brain development. Blanco et al. (2000) suggested that PCDH11Y might have gained a malespecific function in brain morphogenesis, with behavioural consequences. Speaking in a similar but broader vein, Skaletsky et al. (2003) indicated that Ychromosome genes (besides SRY, the testisdetermining gene) could be related to sex-dimorphic differences in behaviour and cognition as well as to differences in anatomy and physiology. Finally, it does appear possible that some male-specific proteins could be inactivated without obvious phenotypic consequences, because there are lineages of men who lack the encoding genes altogether (Jobling et al. 2007). Such deleted genes include two expressed in foetal brain, PCDH11Y and TBL1YΗ. The maternal immune hypothesis does not challenge the long-standing theory that sexual orientation in men is primarily driven by prenatal testosterone (e.g., Ellis & Ames 1987). It proposes, rather, that sexual orientation development in the human male brain depends on two systems: a main system driven by testosterone, and a supplementary system driven by malespecific proteins under direct genetic control. The similar view that brain sexual differentiation is directly influenced by sex chromosome genes as well as by gonadal secretions has been advanced by other authors
(e.g., Arnold 2004). If it is true that male-specific proteins represent a kind of back-up or booster system, then antibodies that inactivate them would increase the odds of homosexuality

Auch interessant fand ich diese Stelle:

For example, Archer and Mehdikhani (2003) proposed that sexual selection has produced greater variability in male mating strategies, leading to
greater male variability in a number of psychological traits, including physical aggressiveness and preferences for various mate characteristics, such as looks, resources, and youth. Miller (2000) applied this reasoning to masculine and feminine personality traits, proposing that men may be more variable on such traits than women are, because such variation provides men with differing, complementary mating strategies
(e.g., one man could be attractive to mates because he is dominant, sexy, and virile, whereas another could be attractive because he is kind, committed, and interpersonally perceptive). Increased male variance on gender-related traits could occasionally produce extreme outcomes, including male homosexuality. Male homosexuality is, in fact, more common than female homosexuality (Diamond 1993, Laumann et al. 1994).

Und zu den evolutionären Überlegungen:

It would be expected that natural selection would eliminate a genetic factor that favors the existence of homosexuality. This Darwinian paradox, became
the focus of many researches, but remains unsolved. Some mechanisms assume that genes inducing homosexuality provide superior fitness in heterozygous conditions. For example, men heterozygous for a homosexual gene may have higher success in attracting women and/or their sperm may have a competitive advantage over that of other men (Hutchinson 1959, Kirsch & Weinrich 1991, MacIntyre & Estep 1993,Miller 2000, Weinrich 1987, Wilson 1975). Furthermore, Muscarella (2000) as well as Bobrow & Bailey (2001), showed that homosexual men don’t act as helpers/facilitators and don’t offer more emotional or financial support to their siblings than heterosexual men.

An other mechanism, which was briefly mentioned by Hammer & Copeland (1994; see also McKnight 1997; Pillard & Bailey 1998) but that has never been rigorously explored previously is a sexually antagonistic selection (Arnqvist & Rowe 2005, Rice 1984, Rice & Holland 1997), under which alleles that decrease fitness of one sex are maintained in the population because they increase the fitness of the other sex. The potential importance of this mechanism is highlighted by recent data which indicate that female maternal relatives of homosexuals (Camperio-Ciani et al. 2004) or relatives of gay men for both maternal and paternal lines (King et al. 2005) have increased fecundity.

In dem Artikel sind aus meiner Sicht noch viele andere interessante Stellen. Es lohnt sich ihn ganz zu lesen.