The relationship between biology and sexual orientation is a subject of research. A simple and singular determinant for sexual orientation has not been conclusively demonstrated; various studies point to different, even conflicting positions, but scientists hypothesize that a combination of genetic, hormonal and social factors determine sexual orientation.[1][2] Biological theories for explaining the causes of sexual orientation are more popular,[1] and biological factors may involve a complex interplay of genetic factors and the early uterine environment.[3] These factors, which may be related to the development of a heterosexual, homosexual, bisexual or asexual orientation, include genes, prenatal hormones, and brain structure.
A number of twin studies have attempted to compare the relative importance of genetics and environment in the determination of sexual orientation. In a 1991 study, Bailey and Pillard found that 52% of monozygotic (MZ) brothers and 22% of the dizygotic (DZ) twins were concordant for homosexuality.[4] 'MZ' indicates identical twins with the same sets of genes and 'DZ' indicates fraternal twins where genes are mixed to an extent similar to that of non-twin siblings. In 2000 Bailey, Dunne and Martin studied a larger sample of 4,901 Australian twins but reported less than half the level of concordance.[5] They found 20% concordance in the male identical or MZ twins and 24% concordance for the female identical or MZ twins. Self reported zygosity, sexual attraction, fantasy and behaviours were assessed by questionnaire and zygosity was serologically checked when in doubt. A meta-study by Hershberger (2001)[6] compares the results of eight different twin studies: among those, all but two showed MZ twins having much higher concordance of sexual orientation than DZ twins, suggesting a non-negligible genetic component.
Bearman and Brckner (2002) criticized early studies of concentrating on small, select samples[7] and non-representative selection of their subjects.[8] They studied 289 pairs of identical twins (monozygotic or from one fertilized egg) and 495 pairs of fraternal twins (dizygotic or from two fertilized eggs) and found concordance rates for same-sex attraction of only 7.7% for male identical twins and 5.3% for females, a pattern which they say "does not suggest genetic influence independent of social context."[7]
A 2010 study of all adult twins in Sweden (more than 7,600 twins)[9] found that same-sex behavior was explained by both heritable factors and individual-specific environmental sources (such as prenatal environment, experience with illness and trauma, as well as peer groups, and sexual experiences), while influences of shared-environment variables such as familial environment and societal attitudes had a weaker, but significant effect. Women showed a statistically non-significant trend to weaker influence of hereditary effects, while men showed no effect of shared environmental effects. The use of all adult twins in Sweden was designed to address the criticism of volunteer studies, in which a potential bias towards participation by gay twins may influence the results;
Biometric modeling revealed that, in men, genetic effects explained .34.39 of the variance [of sexual orientation], the shared environment .00, and the individual-specific environment .61.66 of the variance. Corresponding estimates among women were .18.19 for genetic factors, .16.17 for shared environmental, and .64.66 for unique environmental factors. Although wide confidence intervals suggest cautious interpretation, the results are consistent with moderate, primarily genetic, familial effects, and moderate to large effects of the nonshared environment (social and biological) on same-sex sexual behavior.[9]
Twin studies have received a number of criticisms including self-selection bias where homosexuals with gay siblings are more likely to volunteer for studies. Nonetheless, it is possible to conclude that, given the difference in sexuality in so many sets of identical twins, sexual orientation cannot be attributed solely to genetic factors.[10]
Another issue is the recent finding that even monozygotic twins can be different and there is a mechanism which might account for monozygotic twins being discordant for homosexuality. Gringas and Chen (2001) describe a number of mechanisms which can lead to differences between monozygotic twins, the most relevant here being chorionicity and amniocity.[11]Dichorionic twins potentially have different hormonal environments because they receive maternal blood from separate placenta, and this could result in different levels of brain masculinisation. Monoamniotic twins share a hormonal environment, but can suffer from the 'twin to twin transfusion syndrome' in which one twin is "relatively stuffed with blood and the other exsanguinated".[12]
Chromosome linkage studies of sexual orientation have indicated the presence of multiple contributing genetic factors throughout the genome. In 1993 Dean Hamer and colleagues published findings from a linkage analysis of a sample of 76 gay brothers and their families.[13] Hamer et al. found that the gay men had more gay male uncles and cousins on the maternal side of the family than on the paternal side. Gay brothers who showed this maternal pedigree were then tested for X chromosome linkage, using twenty-two markers on the X chromosome to test for similar alleles. In another finding, thirty-three of the forty sibling pairs tested were found to have similar alleles in the distal region of Xq28, which was significantly higher than the expected rates of 50% for fraternal brothers. This was popularly dubbed the "gay gene" in the media, causing significant controversy. Sanders et al. in 1998 reported on their similar study, in which they found that 13% of uncles of gay brothers on the maternal side were homosexual, compared with 6% on the paternal side.[14]
A later analysis by Hu et al. replicated and refined the earlier findings. This study revealed that 67% of gay brothers in a new saturated sample shared a marker on the X chromosome at Xq28.[15] Two other studies (Bailey et al., 1999; McKnight and Malcolm, 2000) failed to find a preponderance of gay relatives in the maternal line of homosexual men.[14] One study by Rice et al. in 1999 failed to replicate the Xq28 linkage results.[16] Meta-analysis of all available linkage data indicates a significant link to Xq28, but also indicates that additional genes must be present to account for the full heritability of sexual orientation.[citation needed]
Mustanski et al. (2005) performed a full-genome scan (instead of just an X chromosome scan) on individuals and families previously reported on in Hamer et al. (1993) and Hu et al. (1995), as well as additional new subjects.[17] With the larger sample set and complete genome scan, the study found somewhat reduced linkage for Xq28 than reported by Hamer et al. However, they did find other markers with a likelihood score falling just short of significance at 7q36 and likelihood scores approaching significance at 8p12 and 10q26. Interestingly, 10q26 showed highly significant maternal loading, thus further supporting the previous family studies.
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