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Genetic and Environmental Effects on Same-sex Sexual Behavior: A Population Study of Twins in Sweden

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There is still uncertainty about the relative importance of genes and environments on human sexual orientation. One reason is that previous studies employed self-selected, opportunistic, or small population-based samples. We used data from a truly population-based 2005-2006 survey of all adult twins (20-47 years) in Sweden to conduct the largest twin study of same-sex sexual behavior attempted so far. We performed biometric modeling with data on any and total number of lifetime same-sex sexual partners, respectively. The analyses were conducted separately by sex. Twin resemblance was moderate for the 3,826 studied monozygotic and dizygotic same-sex twin pairs. Biometric modeling revealed that, in men, genetic effects explained .34-.39 of the variance, 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.
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ORIGINAL PAPER
Genetic and Environmental Effects on Same-sex Sexual Behavior:
A Population Study of Twins in Sweden
Niklas La
˚
ngstro
¨
m Æ Qazi Rahman Æ Eva Carlstro
¨
m Æ
Paul Lichtenstein
Received: 8 October 2007 / Revised: 29 February 2008 / Accepted: 19 April 2008 / Published online: 7 June 2008
Ó Springer Science+Business Media, LLC 2008
Abstract There is still uncertainty about the relative
importance of genes and environments on human sexual ori-
entation. One reason is that previous studies employed self-
selected, opportunistic, or small population-based samples.
We used data from a truly population-based 2005–2006 sur-
vey of all adult twins (20–47 years) in Sweden to conduct the
largest twin study of same-sex sexual behavior attempted so
far. We performed biometric modeling with data on any and
total number of lifetime same-sex sexual partners, respec-
tively. The analyses were conducted separately by sex. Twin
resemblance was moderate for the 3,826 studied monozygotic
and dizygotic same-sex twin pairs. Biometric modeling
revealed that, in men, genetic effects explained .34–.39 of the
variance, 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 bio-
logical) on same-sex sexual behavior.
Keywords Sexual behavior Sexual orientation
Population survey Twin study
Introduction
The prevalence of same-sex (or homosexual) sexual behavior
varies over time and geographical region; population-based
surveys suggest lifetime estimates of 3–20% for men and 2–
9% in women (Caceres, Konda, Pecheny, Chatterjee, & Ly-
erla, 2006; Sell, Wells, & Wypij, 1995). The origin of same-
sex sexual behavior is of obvious interest to theories regarding
the development of sexual preferences (Rahman, 2005).
However, the issue is also important for professionals con-
cerned with sexual health in general and the psychological
health of non-heterosexual populations. Same-sex behavior
remains a substantial correlate of sexually transmitted infec-
tions in men and is also associated with increased risk of
physical and psychiatric morbidity among both men and
women in the general population (Cochran & Mays, 2000;
Sandfort, Bakker, Schellevis, & Vanwesenbeeck, 2006;Sand-
fort, de Graaf, Bijl, & Schnabel, 2001).
Twin studies can be used to study the relative importance
of genetic and environmental origins of same-sex behavior.
Early studies reported significant familial aggregation—due
to genetic and environmental factors—of behavioral (i.e.,
same-sex sexual experiences) and psychological (i.e., sexual
attraction) components of sexual orientation (Bailey &
Pillard, 1991; Bailey, Pillard, Neale, & Agyei, 1993). The
inheritance pattern is still unclear. Family pedigree studies
of male homosexual behavior have suggested that mater-
nally inherited factors might be involved (Camperio-Ciani,
N. La
˚
ngstro
¨
m(&)
Centre for Violence Prevention, Karolinska Institutet,
P.O. Box 23000, 104 35 Stockholm, Sweden
e-mail: niklas.langstrom@ki.se
Q. Rahman
School of Biological Sciences, Queen Mary-University
of London, London, UK
Q. Rahman
Institute of Psychiatry, King’s College-University of London,
London, UK
E. Carlstro
¨
m P. Lichtenstein
Department of Medical Epidemiology and Biostatistics,
Karolinska Institutet, Stockholm, Sweden
123
Arch Sex Behav (2010) 39:75–80
DOI 10.1007/s10508-008-9386-1
Corna, & Capiluppi, 2004; Hamer, Hu, Magnuson, Hu, &
Pattatucci, 1993; Hu et al., 1995; Rahman et al., 2007), but
Bailey et al. (1999) failed to replicate maternal inheritance
with data from a large pedigree study. Moreover, two linkage
studies reported DNA marker loci for male homosexuality
on the X chromosome (Hamer et al., 1993; Hu et al., 1995)
whereas another study found no such linkage (Rice, Ander-
son, Risch, & Ebers, 1999; Sanders et al., 1998). Finally, one
genome-wide scan reported several new autosomal markers
for male sexual orientation (Mustanski et al., 2005).
Nonetheless, the conclusions of previous studies (twin,
pedigree, and molecular genetic work) are limited by their
reliance on self-selected volunteers (e.g., through advertise-
ments in gay and lesbian publications) and associated ascer-
tainment biases. To our knowledge, only two studies of same-
sex behavior were population-based and both reported lower
concordance rates than previously found in self-selected
samples (Bailey, Dunne, & Martin, 2000; Kendler, Thornton,
Gilman, & Kessler, 2000). One of these reports also suggested
that the etiological pathways towards same-sex behavior are
different for men and women (Bailey et al., 2000). However,
these two studies require confirmation in larger population-
level samples given low statistical power due to the skewed
distribution of same-sex sexuality. Therefore, we undertook
the largest ever population-based twin study to estimate the
influence of genetic and environmental effects on same-sex
sexual behavior.
Method
Participants
Data were from the Swedish Twin Registry, the largest
population register of twin births in the world (Lichtenstein
et al., 2006). All twin pairs born in Sweden 1959–1985
where both siblings were alive and living in the country were
invited to participate in the Swedish Twin Study of Adults:
Genes and Environments (STAGE); 21,481 men and 21,607
women were eligible for the web-based survey conducted in
2005–2006. Non-responders were approached with up to
three reminders. They could also choose a telephone inter-
view supplemented with a self-administered written
questionnaire for sensitive topics such as traumatic events
and sexuality. The STAGE screens for major psychiatric and
physical morbidity, health-related experiences, and behav-
iors, including trauma, substance misuse, and sexuality. The
overall response rate was 59.6%; 11,229 men (53.2%) and
14,096 women (65.9%) participated (M = 33.7 years, SD =
7.7, range = 20–47). By definition (being born in Sweden),
no respondents were first generation immigrants. Sixty-four
percent were married/cohabiting, 5% had a stable partner
they were not living with, 27% were single, and 4% were
separated/divorced, widowed or did not answer. With respect
to the highest education completed (or currently attending),
5% responded elementary school, 41% high school, 12%
vocational education, military college or other, and 42%
college/university.
Measures
The STAGE survey included no direct question about self-
defined sexual orientation. Actual partnered sexual behavior
was assessed with two items: lifetime number of opposite-sex
and same-sex individuals, respectively, that the respondent
had ever ‘been sexually together with.’ We deliberately
attempted to use a more gender- and sexual orientation-
neutral definition rather than ‘‘sexual intercourse.’’ Respon-
ses for lifetime number of same-sex individuals were
obtained from 7,231 men (64.4% of survey respondents) and
10,676 women (75.7%). From this, we constructed the two
variables any lifetime same-sex partner and total number of
lifetime same-sex partners (divided into seven categories to
minimize the impact of outliers; 0, 1, 2, 3–5, 6–10, 11–20, and
21 or more partners) based on prior work (Kirk, Bailey,
Dunne, & Martin, 2000).
Zygosity was established using standard physical simi-
larity questions previously validated through genotyping
(98% correct classification; Lichtenstein et al., 2006). For
7,335 individuals, their twin siblings did not participate and
121 twin pairs were not possible to classify regarding
zygosity. After we had excluded 1,339 opposite-sex dizy-
gotic (DZ) twin pairs from further analysis, the final sample
comprised 7,652 individuals with known zygosity where
both twins had responded to sexuality items; 2,320 mono-
zygotic (MZ) pairs (807 male and 1,513 female) and 1,506
DZ same-sex pairs (517 male and 989 female). The Regional
Ethics Committee in Stockholm, Sweden provided ethical
approval.
Procedure
Twin resemblance was assessed using probandwise con-
cordance (i.e., the proportion of twins reporting same-sex
sexual behavior given the same behavior in the co-twin) and
tetra- or polychoric correlations for the liability to express
same-sex sexual behavior. Liability is assumed to be a con-
tinuous and normally distributed latent tendency for a certain
phenotype resulting from numerous etiological components.
Individuals who exceed a theoretical threshold on this latent
distribution would exhibit same-sex sexual behavior.
To study the sources of individual differences, we used
univariate twin modeling based on contingency tables for
same-sex sexual behavior between twins in MZ and DZ
pairs. We tested a model where observed phenotypic vari-
ance was assumed to result from the sum of additive genetic
76 Arch Sex Behav (2010) 39:75–80
123
effects, shared or familial environmental effects, and unique
environmental effects. The model was fitted with maximum
likelihood estimation using the Mx structural modeling
program (Neale, 1999). Since same-sex behavior may have
different etiology in men and women (Bailey et al., 2000),
we included only same-sex twin pairs in the model-fitting
analyses.
Results
Fewer men (407/7,231; 5.6%) than women (835/10,676;
7.8%) reported any lifetime same-sex sexual partner, v
2
(1) =
32.11, p \ .001. The average number of same-sex sexual
partners among those reporting any such partner was 12.86 in
men and 3.53 in women, Wilcoxon rank sum test = 8.75,
p \ .001. A weak negative correlation between any lifetime
same-sex partner and age was found in women, rho =-.05,
p \ .001, but not in men, rho = .01, p = .24.
Table 1 shows twin resemblance and estimates of genetic
and environmental influences on same-sex behavior for both
men and women. Twin resemblance for the two measures
was moderate overall, but higher upon direct comparison in
monozygotic than in dizygotic twins for both sexes
(Table 1). In men, the full twin model suggested heritability
estimates of 39% for any lifetime same-sex partner (95% CI:
00–59%) and 34% for total number of same-sex partners
(95% CI: 00–53%) whereas unique environmental factors
accounted for 61% (95% CI: 41–85%) and 66% (95% CI:
47–87%), respectively (Table 1). No shared environmental
effects were found among men. For women, 18–19% of
same-sex sexual behaviors were explained by genetic fac-
tors and 64–66% by unique environmental factors. Shared
environmental effects were weak at 16–17%.
Discussion
In the largest twin sample studied so far, we found familial
clustering of same-sex sexual behavior in both men and
women. Our results support the notion that same-sex behav-
ior arises not only from heritable but also from individual-
specific environmental sources. Further, although not sta-
tistically significant, hereditary effects appeared weaker in
women and of the same magnitude as those of the shared
environment.
This is the first study assessing same-sex behavior in a
truly population-based Scandinavian register of twins, thus
avoiding the problems of volunteer self-selection, known to
introduce bias towards monozygotic twin pairs concordant
for specific traits (Bailey et al., 2000; Kendler & Eaves,
1989). This study also had greater statistical power and high
response rates relative to prior research. However, it was
inevitably limited by the fact that same-sex behavior was
relatively rare. With the unexpectedly low familial effects,
the twin method has restricted power to detect statistically
significant influences. For example, with 4% prevalence and
a sample size of 2,000 twin pairs, there was 25% power to
detect a heritability of 20% at the 5% level (assuming that
shared environmental effects explain 15% and unique
environmental effects 65%). To achieve 80% power to
detect significant genetic effects with these assumptions,
Table 1 Behaviorally measured same-sex sexual orientation in 20- to 47-year-old Swedish twins separated by sex
Twin group Twin resemblance Model fitting parameter estimate (95% con-
fidence interval)
Number
of pairs
Number of
concordant pairs
Number of
discordant pairs
Probandwise
concordance
Correlation
in liability
a
Genetic Shared
environment
Unique
environment
Any lifetime same-sex partner
b
Males Monozygotic 807 7 64 .18 .39 .39 (.00–.59) .00 (.00–.46) .61 (.41–.85)
Dizygotic 517 3 50 .11 .19
Females Monozygotic 1,513 26 188 .22 .36 .19 (.00–.49) .17 (.00–.42) .64 (.51–.78)
Dizygotic 989 13 127 .17 .27
Total number of same-sex partners
c
Males Monozygotic 807 2 69 .05 .40 .34 (.00–.53) .00 (.00–.39) .66 (.47–.87)
Dizygotic 517 0 53 .00 .17
Females Monozygotic 1,513 12 202 .11 .38 .18 (.11–.45) .16 (.00–.39) .66 (.55–.78)
Dizygotic 989 5 135 .07 .25
a
Tetrachoric correlation for Any lifetime same-sex partner, polychoric correlation for Total number of same-sex partners
b
Prevalences were 4.8% for monozygotic male twins, 5.4% for dizygotic male twins, 7.9% for monozygotic female twins, and 7.7% for dizygotic
female twins, v
2
(3) = 21.48, p \ .001
c
Divided into seven ordinal categories; 0, 1, 2, 3–5, 6–10, 11–20, and 21+ partners
Arch Sex Behav (2010) 39:75–80 77
123
Table 2 Demographic and methodological characteristics and major findings of three population-based twin studies of sexual orientation
Variable Study
Bailey et al. (2000) Kendler et al. (2000)La
˚
ngstro
¨
m et al. (present study)
Country of origin Australia USA Sweden
Type of sample Volunteer register of twins National household sample
Relatives or twins provided co-twin
contact information
National population register
Definition used for sexual
orientation
Mean of sexual attraction and fantasies,
both rated on 7-point Kinsey scales,
and divided into three ordinal categories
Self-reported sexual orientation with
response options heterosexual,
homosexual or bisexual attraction
Any lifetime same-sex sexual
partner Lifetime number of
same-sex partners
Year(s) of data collection 1992 1995–1996 2005–2006
Overall response rate (%) 53.8 60.0 59.6
Age range of overall sample (years) 17–50 25–74 20–47
Overall sample size (individuals in
same-sex pairs with complete data)
a
3,076 1,128 7,652
No. of male twins in same-sex pairs
with complete data
988 Not specified 2,648
No. of female twins in same-sex pairs
with complete data
2,088 Not specified 5,004
Summary of parameter estimates
Genetic .45 for men (95% CI: .00–.71)
.08 for women (95% CI: .00–.67)
.62 with no information on 95% CIs or sex
differences
.34–.39 for men (95% CIs: .00–.59)
.18–.19 for women (95% CIs: .00–.49)
considering both measures
Shared environment .00 for men (95% CI: .00–.41)
.41 for women (95% CI: .00–.64)
.05 with no information on 95% CIs or sex
differences
.00 for men (95% CIs: .00–.46)
.16–.17 for women (95% CIs: .00–.42)
considering both measures
Unique environment .55 for men (95% CI: .18–.85)
.50 for women (95% CI: .30–.69)
.33 with no information on 95% CIs or sex
differences
.61–.66 for men (95% CIs: .41–.87)
.64–.66 for women (95% CIs: .51–.78)
considering both measures
a
Reflects the total number of individuals included in model fitting analyses, although sample sizes varied somewhat within each study depending on the analysis performed
78 Arch Sex Behav (2010) 39:75–80
123
one would need to increase the sample size 5-fold (i.e.,
include approximately 10,000 monozygotic and dizygotic
same-sex twin pairs with complete data). Consequently,
though familial effects certainly are important for same-sex
behavior, the exact magnitude of genetic and environmental
contributions to these effects should be interpreted cau-
tiously. Moreover, the sensitivity of the topic should be borne
in mind although this study was conducted in a sexually
liberal Scandinavian country. Even if very large twin sam-
ples are approached, the number of pairs where both twins
choose to reveal same-sex behavior will remain limited.
Furthermore, while this study focused on same-sex sexual
behavior, assessment of sexual attraction or fantasies and
even romantic attractions would more fully capture the
complexity of sexual orientation. However, both behavioral
measures of sexual orientation (any same-sex sexual partner
and total number of same-sex partners) correlated strongly
with self-reported same-sex sexual attraction (r = .70–.75)
upon cross-validation in a contemporary referred sample
(n = 555) of age-matched adult men in Toronto, Canada
(data available upon request).
There are only two other published population based twin
studies of same-sex behavior, from Australia (Bailey et al.,
2000; Kirk et al., 2000) and the U.S. (Kendler et al., 2000).
Table 2 provides a comparison of demographic and meth-
odological characteristics and major findings of these two
studies and the present one. Our results of genetic and unique
environmental effects largely agreed with the estimates
found by Bailey et al. (2000), but less so with those reported
by Kendler et al. (2000). Unfortunately, the latter study did
not report sex-separated analyses. The concordance rates
found by us were lower than in studies using opportunistic or
otherwise non-representative samples of non-heterosexual
individuals (Bailey & Pillard, 1991; Bailey et al., 1993).
Although our results are not inconsistent with relatively large
heritabilities, this suggests cautious interpretation of data
from non-representative sampling of individuals from sexual
minorities.
Our data indicated that genetic influences on any lifetime
same-sex partner and total number of same-sex partners were
weaker in women than in men. This disagrees with the greater
genetic influences on number of same-sex partners in women
found by Kirk et al. (2000), using different complex genetic
models. In contrast, our finding does concur with the results
obtained when the same group conducted less complex uni-
variate modeling using essentially the same data (Bailey
et al., 2000, summarized in Table 2).We did notperform sex-
limitation tests in our model fitting because these would not
be statistically powerful even in our large sample. Also, the
large confidence intervals warrant careful interpretation.
Nevertheless, our findings for women (suggestive of weaker
but equal genetic and shared environmental effects and
higher levels of same-sex behavior compared to men) are
congruent withobservations thatfemale sexual attraction and
behavior are more flexible in response to shared environ-
mental factors contrasted to that of men (Baumeister, 2000;
Lippa, 2006; Rahman, 2005).
It has been suggested that individual differences in heter-
osexual and homosexual behavior result from unique environ-
mental factors such as prenatal exposure to sex hormones,
progressive maternal immunization to sex-specific proteins,
or neurodevelopmental instability (Rahman, 2005). Although
the unique environmental variance component also includes
measurement error, the present results support the notion that
the individual-specific environment does indeed influence
sexual preference.
In conclusion, although confidence intervals were wide,
we believe this study provides the most unbiased estimates
presented so far of genetic and non-genetic contributions to
same-sex sexual behavior. The results should inform further
research on this complex trait.
Acknowledgments We are grateful to Dr. Ray Blanchard who
generously provided validation data from men referred to the Kurt
Freund Laboratory at the Centre for Addiction and Mental Health in
Toronto, Ontario. The Swedish Twin Registry is supported by unre-
stricted grants from the Swedish Department of Higher Education, the
Swedish Research Council, and AstraZeneca. Niklas La
˚
ngstro
¨
mis
supported by the Swedish Research Council-Medicine.
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... Male sexual orientation is moderately heritable (30 ~ 40% heritability) and appears multifactorial, with evidence of multiple genetic and environmental contributions via family, twin, and segregation analyses (Alanko et al., 2010;Bailey & Bell, 1993;Bailey & Benishay, 1993;Bailey & Pillard, 1991;Bailey et al., , 1999Bailey et al., , 2000Buhrich et al., 1991;Hamer et al., 1993;Heston & Shields, 1968;Kallmann, 1952;Kendler et al., 2000;King & McDonald, 1992;Kirk et al., 2000;Langström et al., 2010;Pattatucci & Hamer, 1995;Pillard & Weinrich, 1986;Santtila et al., 2008;Schwartz et al., 2010;Whitam et al., 1993). Genome-wide linkage studies (GWLS) of homosexual brother pairs have been applied to the trait (Mustanski et al., 2005;Ramagopalan et al., 2010;Sanders et al., 2015), with the largest GWLS sample finding genome-wide significant linkage to the pericentromeric region of chromosome 8 (LOD = 4.08) and strong support for the previously reported linkage to Xq28 (LOD = 2.99) (Sanders et al., 2015). ...
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... Why are some people sexually attracted to people of the same sex? Several large scale twin studies have addressed the question of samesex attraction in recent years, including: Bailey (2000), 32 Långström (2010) 33 and Bur r i (2011). 34 Again, they h a ve e x p l o r e d t h e influences of genes, family and unique life experiences. ...
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Homosexuality has been a constant throughout human evolution and civilization, and yet, science has been slow to look at the causes of sexual preferences.
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Sex, in case you did not notice, is an important part of the human condition. And just as people differ in their personality characteristics, so too do they differ in their sexual behaviors, attitudes, and preferences. In this chapter, we will begin by identifying some important aspects of sexuality and examining their relations with personality. We will then examine several important issues concerning the nature of these sexuality dimensions, including their biological bases, their genetic and environmental origins, and their evolutionary function.
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• Homosexual female probands with monozygotic cotwins, dizygotic cotwins, or adoptive sisters were recruited using homophile publications. Sexual orientation of relatives was assessed either by asking relatives directly, or, when this was impossible, by asking the probands. Of the relatives whose sexual orientation could be confidently rated, 34 (48%) of 71 monozygotic cotwins, six (16%) of 37 dizygotic cotwins, and two (6%) of 35 adoptive sisters were homosexual. Probands also reported 10(14%) nontwin biologic sisters to be homosexual, although those sisters were not contacted to confirm their orientations. Heritabilities were significant using a wide range of assumptions about both the base rate of homosexuality in the population and ascertainment bias. The likelihood that a monozygotic cotwin would also be homosexual was unrelated to measured characteristics of the proband such as self-reported history of childhood gender nonconformity. Concordant monozygotic twins reported similar levels of childhood gender nonconformity.
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This study, following Camperio-Ciani, Corna, and Capiluppi [(2004), Proceedings of the Royal Society of London, Series B, Biological Sciences, 271, 2217–2221] aimed to examine the familial history of male homosexuality, and test the so-called “fertile female” hypothesis for this trait in a contemporary British sample. Using a comparative survey design, we found that white (comprising those of Anglo-European descent) and non-white (comprising ethnic “Blacks, “South Asians,” “East Asians,” “Hispanics,” and “Others”) homosexual men (n=147) had a significant excess of maternal but not paternal line male homosexual relatives compared to heterosexual men (n=155). We also found significantly elevated fecundity of maternal aunts of white homosexual men compared to white heterosexual men, whereas non-white heterosexual men showed elevated fecundities of almost every class of relative compared to non-white homosexual men. No significant excess of older brothers was found in homosexual compared to heterosexual men, irrespective of ethnic grouping. These data were discussed in relation to possible population-related factors in evolutionary explanations for human male homosexuality.
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Homosexual female probands with monozygotic cotwins, dizygotic cotwins, or adoptive sisters were recruited using homophile publications. Sexual orientation of relatives was assessed either by asking relatives directly, or, when this was impossible, by asking the probands. Of the relatives whose sexual orientation could be confidently rated, 34 (48%) of 71 monozygotic cotwins, six (16%) of 37 dizygotic cotwins, and two (6%) of 35 adoptive sisters were homosexual. Probands also reported 10 (14%) nontwin biologic sisters to be homosexual, although those sisters were not contacted to confirm their orientations. Heritabilities were significant using a wide range of assumptions about both the base rate of homosexuality in the population and ascertainment bias. The likelihood that a monozygotic cotwin would also be homosexual was unrelated to measured characteristics of the proband such as self-reported history of childhood gender nonconformity. Concordant monozygotic twins reported similar levels of childhood gender nonconformity.
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The Darwinian paradox of male homosexuality in humans is examined, i.e. if male homosexuality has a genetic component and homosexuals reproduce less than heterosexuals, then why is this trait maintained in the population? In a sample of 98 homosexual and 100 heterosexual men and their relatives (a total of over 4600 individuals), we found that female maternal relatives of homosexuals have higher fecundity than female maternal relatives of heterosexuals and that this difference is not found in female paternal relatives. The study confirms previous reports, in particular that homosexuals have more maternal than paternal male homosexual relatives, that homosexual males are more often later-born than first-born and that they have more older brothers than older sisters. We discuss the findings and their implications for current research on male homosexuality.
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Homosexual male probands with monozygotic cotwins, dizygotic cotwins, or adoptive brothers were recruited using homophile publications. Sexual orientation of relatives was assessed either by asking relatives directly, or when this was impossible, asking the probands. Of the relatives whose sexual orientation could be rated, 52% (29/56) of monozygotic cotwins, 22% (12/54) of dizygotic cotwins, and 11% (6/57) of adoptive brothers were homosexual. Heritabilities were substantial under a wide range of assumptions about the population base rate of homosexuality and ascertainment bias. However, the rate of homosexuality among nontwin biological siblings, as reported by probands, 9.2% (13/142), was significantly lower than would be predicted by a simple genetic hypothesis and other published reports. A proband's self-reported history of childhood gender non-conformity did not predict homosexuality in relatives in any of the three subsamples. Thus, childhood gender nonconformity does not appear to be an indicator of genetic loading for homosexuality. Cotwins from concordant monozygotic pairs were very similar for childhood gender nonconformity.
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Several lines of evidence have implicated genetic factors in homosexuality. The most compelling observation has been the report of genetic linkage of male homosexuality to microsatellite markers on the X chromosome. This observation warranted further study and confirmation. Sharing of alleles at position Xq28 was studied in 52 gay male sibling pairs from Canadian families. Four markers at Xq28 were analyzed (DXS1113, BGN, Factor 8, and DXS1108). Allele and haplotype sharing for these markers was not increased over expectation. These results do not support an X-linked gene underlying male homosexuality.
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Background It has been suggested that homosexuality is associated with psychiatric morbidity. This study examined differences between heterosexually and homosexually active subjects in 12-month and lifetime prevalence of DSM-III-R mood, anxiety, and substance use disorders in a representative sample of the Dutch population (N = 7076; aged 18-64 years). Methods Data were collected in face-to-face interviews, using the Composite International Diagnostic Interview. Classification as heterosexual or homosexual was based on reported sexual behavior in the preceding year. Five thousand nine hundred ninety-eight (84.8%) of the total sample could be classified: 2.8% of 2878 men and 1.4% of 3120 women had had same-sex partners. Differences in prevalence rates were tested by logistic regression analyses, controlling for demographics. Results Psychiatric disorders were more prevalent among homosexually active people compared with heterosexually active people. Homosexual men had a higher 12-month prevalence of mood disorders (odds ratio [OR] = 2.93; 95% confidence interval [CI] = 1.54-5.57) and anxiety disorders (OR = 2.61; 95% CI = 1.44-4.74) than heterosexual men. Homosexual women had a higher 12-month prevalence of substance use disorders (OR = 4.05; 95% CI = 1.56-10.47) than heterosexual women. Lifetime prevalence rates reflect identical differences, except for mood disorders, which were more frequently observed in homosexual than in heterosexual women (OR = 2.41; 95% CI = 1.26-4.63). The proportion of persons with 1 or more diagnoses differed only between homosexual and heterosexual women (lifetime OR = 2.61; 95% CI = 1.31-5.19). More homosexual than heterosexual persons had 2 or more disorders during their lifetimes (homosexual men: OR = 2.70; 95% CI = 1.66-4.41; homosexual women: OR = 2.09; 95% CI = 1.07-4.09). Conclusion The findings support the assumption that people with same-sex sexual behavior are at greater risk for psychiatric disorders.
This report examines the impact of two major kinds of unequal ascertainment on the estimation of true probandwise concordance (Cpbt ) in twin studies: 1) concordance-dependent – where the ascertainment rate differs in affected members of concordant vs discordant pairs, and 2) non-independent – where ascertainment rates differ in affected members of concordant pairs where the cotwin has vs has not been ascertained. Concordance-dependent ascertainment is easily modeled algebraically; non-independent ascertainment is more complex and we here propose a model based on survival analysis. Overall, concordance-dependent ascertainment produces greater bias in estimates of probandwise concordance than does non-independent ascertainment. The bias introduced by concordance-dependent ascertainment is greatest when Cpbt is low and/or when the ascertainment rate for twins in concordant pairs is low. The bias introduced by non-independent ascertainment is greatest when Cpbt is high and/or when the ascertainment probability for an affected twin in a concordant pair where the cotwin has already been ascertained approaches unity. The impact of concordance-dependent and non-independent ascertainment on estimates of heritability and common environment is examined. Correction terms to estimate Cpbt in the presence of concordance-dependent and/or non-independent ascertainment are presented.