Detail the parts of the scientific method discussed in your article and comparing that information to what was reported in the news story.

8/30/2019
No “gay gene” — New study says no single gene drives sexual behavior; A complex mix of genetic and other influences answer the ques…
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Is there a “gay gene”? Major new study says no
BY DENNIS THOMPSON
A U G U S T 2 9 , 2 0 1 9 / 8 : 3 3 P M / H E A LT H D AY
There’s no such thing as a single “gay gene” that drives a person’s sexual behavior, concludes the
largest genetic study ever conducted on the issue. Instead, a person’s attraction to those of the
same sex is shaped by a complex mix of genetic and environmental in uences, similar to what’s
seen in most other human traits, researchers report.
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8/30/2019
No “gay gene” — New study says no single gene drives sexual behavior; A complex mix of genetic and other influences answer the ques…
“This is a natural and normal part of variation in our species,” said researcher Ben Neale, director
of genetics with the Stanley Center for Psychiatric Research at the Broad Institute of MIT and
Harvard. “That should also support the position that we shouldn’t try and develop gay cures. That’s
not in anyone’s interest.”
The international study focused on the genetic pro les of nearly 480,000 people from the United
States and the United Kingdom, a group approximately 100 times larger than any previous study of
the link between genetics and same-sex attraction, said lead researcher Andrea Ganna, a research
fellow with the Massachusetts General Hospital’s Analytical and Translational Genetic Unit.
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The research team discovered ve speci c genetic variants that were signi cantly associated with
same-sex behavior, but when combined these variants explained less than 1% of any person’s
attraction to their own gender, Ganna said.
Overall, genetics account for between 8% and 25% of a person’s same-sex attraction, taking into
account the thousands of genetic traits ultimately involved in shaping a person’s sexual desires,
Neale said.
“It’s e ectively impossible to predict an individual’s sexual behavior from their genome,” Neale
said. “Genetics is less than half of this story for sexual behavior, but it’s still a very important
contributing factor. These ndings reinforce the importance of diversity as a key aspect of sexual
behavior.”
GLAAD, the world’s largest LGBTQ advocacy group, said the results show that sexual orientation is
just another normal piece of the human experience.
“This new study provides even more evidence that that being gay or lesbian is a natural part of
https://www.cbsnews.com/news/no-gay-gene-new-study-no-single-gene-drives-sexual-behavior-complex-mix-of-genetic-and-other-influences-2019-0…
2/20
8/30/2019
No “gay gene” — New study says no single gene drives sexual behavior; A complex mix of genetic and other influences answer the ques…
human life, a conclusion that has been drawn by researchers and scientists time and again,” said
GLAAD Chief Programs O cer Zeke Stokes. “The identities of LGBTQ people are not up for debate.
This new research also recon rms the long-established understanding that there is no conclusive
degree to which nature or nurture in uence how a gay or lesbian person behaves.”
The results also call into question the Kinsey Scale, a long-utilized rating scale of sexual attraction
developed in part by sex researcher Alfred Kinsey, Ganna said.
“We discovered that the Kinsey Scale, which really places individuals on a continuum from
basically exclusively opposite-sex partners to exclusively same-sex partners, is really an
oversimpli cation of the diversity of sexual behavior in humans,” Ganna said.
“That can’t be a single line,” Neale added. “The results are not consistent with that being a single
line, but they don’t actually tell us what those other dimensions are” that shape human desire.
Researchers are now considering whether a person’s attraction to men and to women should be
considered separate from each other, with the two characteristics shaping the person’s overall
sexual identity and desires, Ganna said.
The ndings were published Aug. 29 in the journal Science.
The results did show that genetic variation has a stronger in uence on same-sex sexual behavior in
men than in women, possibly demonstrating the complexity of women’s sexuality, said Melinda
Mills, a professor of sociolo y at Oxford University who wrote an editorial accompanying the new
study.
“This re ects voices from the LGBTQ+ (lesbian, gay, bisexual, transgender, queer+) community
arguing that a range of sexualities exist,” Mills wrote. “Sexuality is dynamic, with the ability to
express and realize sexual preferences, and is thus also shaped and regulated by cultural, political,
social, legal and religious structures.”
The ve speci c genes related to same-sex desire cropped up in odd places, the researchers noted.
https://www.cbsnews.com/news/no-gay-gene-new-study-no-single-gene-drives-sexual-behavior-complex-mix-of-genetic-and-other-influences-2019-0…
3/20
8/30/2019
No “gay gene” — New study says no single gene drives sexual behavior; A complex mix of genetic and other influences answer the ques…
For example, one was located in a stretch of DNA that contains several genes related to the sense of
smell, Ganna said.
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“We know that smell has a strong tie to sexual attraction, but its links to sexual behaviors are not
clear,” he said.
Another gene was associated with male baldness, which is closely linked to how the body regulates
sex hormones and might suggest a relationship between hormone regulation and same-sex desire,
Ganna said.
Despite their overall small e ect, “these genetic variants could hint at some biological pathways
that may be involved in same-sex sexual behavior,” Ganna said.
First published on August 29, 2019 / 2:58 PM
© 2019 HealthDay. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed.
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4/20
R ES E A RC H
RESEARCH ARTICLE SUMMARY

HUMAN GENETICS
Large-scale GWAS reveals insights
into the genetic architecture of
same-sex sexual behavior
Andrea Ganna, Karin J. H. Verweij, Michel G. Nivard, Robert Maier, Robbee Wedow,
Alexander S. Busch, Abdel Abdellaoui, Shengru Guo, J. Fah Sathirapongsasuti,
23andMe Research Team, Paul Lichtenstein, Sebastian Lundström, Niklas Långström,
Adam Auton, Kathleen Mullan Harris, Gary W. Beecham, Eden R. Martin,
Alan R. Sanders, John R. B. Perry, Benjamin M. Neale, Brendan P. Zietsch*
RATIONALE: For the first time, new large-
scale datasets afford sufficient statistical
power to identify genetic variants associated
with same-sex sexual behavior (ever versus
never had a same-sex partner), estimate the
proportion of variation in the trait accounted
for by all variants in aggregate, estimate the
genetic correlation of same-sex sexual behavior with other traits, and probe the biology
and complexity of the trait. To these ends, we
performed genome-wide association discovery analyses on 477,522 individuals from the
United Kingdom and United States, replication analyses in 15,142 individuals from
the United States and Sweden, and followup analyses using different aspects of sexual
preference.
RESULTS: In the discovery samples (UK
Biobank and 23andMe), five autosomal loci
were significantly associated with same-sex

CONCLUSION: Same-sex sexual be-
Phenotypic complexity and heterogeneity
Same-sex sexual behavior
N. of individuals
23andMe
(N=68,527)
UK Biobank
(N=408,995)
Same-sex sexual
behavior
Exclusively
heterosexual
Bisexual
Proportion same-sex
partners among
non-heterosexuals
vs
Exclusively
same-sex
Exclusively
heterosexual
Combined
Female-specific
Male-specific
Bisexual
Exclusively
same-sex
Log 10 (P value)
Genetic
architecture
vs
Sex
differences
Biological
processes
Chromosome
Genetic
correlations
Replication in 3
independent studies
0.3 0.5 0.7 0.9
Communication to lay audience
A genome-wide association study (GWAS) of same-sex sexual behavior reveals five loci and high
polygenicity. Follow-up analyses show potential biological pathways; show genetic correlations with
various traits; and indicate that sexual preference is a complex, heterogeneous phenotype.
Ganna et al., Science 365, 882 (2019)
30 August 2019
havior is influenced by not one or a
few genes but many. Overlap with
genetic influences on other traits provides insights into the underlying biology of same-sex sexual behavior,
and analysis of different aspects of
sexual preference underscore its
complexity and call into question
the validity of bipolar continuum
measures such as the Kinsey scale.
Nevertheless, many uncertainties remain to be explored, including how
sociocultural influences on sexual preference might interact with genetic
influences. To help communicate our
study to the broader public, we organized workshops in which representatives of the public, activists, and
researchers discussed the rationale, results, and implications of our study.

The list of author affiliations is available in the
full article online.
*Corresponding author.
Email: zietsch@psy.uq.edu.au
Cite this article as A. Ganna et al., Science
365, eaat7693 (2019). DOI: 10.1126/science.
aat7693
1 of 1
Downloaded from http://science.sciencemag.org/ on August 30, 2019
INTRODUCTION: Across human societies and
in both sexes, some 2 to 10% of individuals
report engaging in sex with same-sex partners, either exclusively or in addition to sex
with opposite-sex partners. Twin and family
studies have shown that same-sex sexual behavior is partly genetically influenced, but
previous searches for the specific genes involved have been underpowered to detect effect sizes realistic for complex traits.
sexual behavior. Follow-up of these loci suggested links to biological pathways that involve
sex hormone regulation and olfaction. Three of
the loci were significant in a meta-analysis
of smaller, independent replication samples.
Although only a few loci passed the stringent
statistical corrections for genome-wide multiple testing and were replicated in other samples, our analyses show that many loci underlie
same-sex sexual behavior in both sexes. In
aggregate, all tested genetic variants accounted
for 8 to 25% of variation in male and female
same-sex sexual behavior, and the genetic
influences were positively
ON OUR WEBSITE
but imperfectly correlated between the sexes
Read the full article
[genetic correlation coat http://dx.doi.
efficient (rg) = 0.63; 95%
org/10.1126/
science.aat7693
confidence intervals, 0.48
…………………………………………..
to 0.78]. These aggregate
genetic influences partly overlapped with
those on a variety of other traits, including
externalizing behaviors such as smoking,
cannabis use, risk-taking, and the personality
trait “openness to experience.” Additional
analyses suggested that sexual behavior, attraction, identity, and fantasies are influenced
by a similar set of genetic variants (rg > 0.83);
however, the genetic effects that differentiate
heterosexual from same-sex sexual behavior
are not the same as those that differ among
nonheterosexuals with lower versus higher
proportions of same-sex partners, which suggests that there is no single continuum from
opposite-sex to same-sex preference.
R ES E A RC H
RESEARCH ARTICLE

in the United States, and replications were performed in three other smaller studies. This study
is part of a preregistered research plan (Open
Science Framework; https://osf.io/357tn), and we
explain our deviations from that plan in (14).
HUMAN GENETICS
Large-scale GWAS reveals insights
into the genetic architecture of
same-sex sexual behavior
Andrea Ganna1,2,3,4*, Karin J. H. Verweij5*, Michel G. Nivard6, Robert Maier1,2,3,
Robbee Wedow1,3,7,8,9,10,11, Alexander S. Busch12,13,14, Abdel Abdellaoui5, Shengru Guo15,
J. Fah Sathirapongsasuti16, 23andMe Research Team16, Paul Lichtenstein4,
Sebastian Lundström17, Niklas Långström4, Adam Auton16, Kathleen Mullan Harris18,19,
Gary W. Beecham15, Eden R. Martin15, Alan R. Sanders20,21, John R. B. Perry12†,
Benjamin M. Neale1,2,3†, Brendan P. Zietsch22†‡
A
cross human societies and in both sexes,
some 2 to 10% of individuals report engaging in sex with same-sex partners,
either exclusively or in addition to sex with
opposite-sex partners (1–4). The biological
factors that contribute to sexual preference are
largely unknown (5), but genetic influences are
suggested by the observation that same-sex sexual behavior appears to run in families (6) and is
concordant more often in genetically identical
(monozygotic) twin pairs than in fraternal twin
pairs or siblings (7).
With respect to genetic influences, several
questions arise. First, what genes are involved
and what biological processes do they affect?
Previous reports of genetic variants associated
with sexual orientation (8–10) were based on
relatively small samples and did not meet current standards of genome-wide significance
(P < 5 × 10−8). Identification of robustly associated variants could enable exploration of the biological pathways and processes involved in development of same-sex sexual behavior. One hypothesis suggests that sex hormones are involved (11–13), but little direct genetic or biological evidence is available. Second, to what extent are genetic influences the same or different for females and males; behavior, attraction, and identity; and heterosexuality and different same-sex sexual behaviors (such as bisexuality)? In order to identify genetic variants associated with same-sex sexual behavior and explore its genetic architecture and underlying biology, we performed a genome-wide association study (GWAS) of same-sex sexual behavior. Analyses were conducted in the UK Biobank from the United Kingdom and a cohort of research participants from 23andMe, predominantly located The UK Biobank study comprises a sample of ~500,000 genotyped UK residents aged 40 to 70 years (tables S1 and S2) (14). Our primary phenotype of interest is a binary, self-reported measure of whether respondents had ever had sex with someone of the same sex (here termed “nonheterosexuals”) or had not (here termed “heterosexuals”) (Box 1). In the UK Biobank sample, 4.1% of males and 2.8% of females reported ever having had sex with someone of the same sex (tables S1 and S2), with higher rates among younger participants (Fig. 1A). This binary phenotype follows from previous work proposing that sexual preference is taxonic rather than dimensional in structure, with individuals reporting exclusively oppositesex preference differing from individuals reporting any same-sex preference (15). However, the binary variable also collapses rich and multifaceted diversity among nonheterosexual individuals (15), so we explored finer-scaled measurements and some of the complexities of the phenotype, although intricacies of the social and cultural influences on sexuality made it impossible to fully explore this complexity. The 23andMe sample comprised 23andMe customers who consented to participate in research and chose to complete a survey about sexual orientation (from many possible survey topics). Individuals who engage in same-sex sexual behavior may be more likely to self-select the sexual orientation survey, which would explain the unusually high proportion of individuals who had had samesex sexual partners in this sample (18.9%) (table S3) (14). We also performed replication analyses in three smaller datasets (14): (i) Molecular Genetic Study of Sexual Orientation (MGSOSO) (n = 2308 U.S. adult males), in which respondents were asked about their sexual identity; (ii) Add Health (n = 4755 U.S. young adults), in which respondents were asked whether they ever had same-sex intercourse and whether they were romantically attracted to the same sex; and (iii) Child and Adolescent Twin Study in Sweden (CATSS) (n = 8093 Swedish adolescents), in which 1 Analytic and Translational Genetics Unit, Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA. 2Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. 3Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. 4Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. 5Department of Psychiatry, Amsterdam University Medical Centers (UMC), location AMC, University of Amsterdam, Meibergdreef 5, 1105 AZ Amsterdam, Netherlands. 6Department of Biological Psychology, Vrije Universiteit Amsterdam, 1081 BT, Amsterdam, Netherlands. 7Department of Sociology, Harvard University, Cambridge, MA 02138, USA. 8Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA. 9Department of Sociology, University of Colorado, Boulder, CO 80309-0483, USA. 10 Health and Society Program and Population Program, Institute of Behavioral Science, University of Colorado, Boulder, CO 80309-0483, USA. 11Institute for Behavioral Genetics, University of Colorado, Boulder, CO 80309-0483, USA. 12Medical Research Council (MRC) Epidemiology Unit, University of Cambridge School of Clinical Medicine, Institute of Metabolic Science, Cambridge Biomedical Campus, Cambridge, UK. 13Department of Growth and Reproduction, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. 14International Center for Research and Research Training in Endocrine Disruption of Male Reproduction and Child Health (EDMaRC), Rigshospitalet, Copenhagen, Denmark. 15Department of Human Genetics, University of Miami, Miami, FL 33136, USA. 1623andMe, Mountain View, CA 94041, USA. 17Centre for Ethics, Law and Mental Health, Gillberg Neuropsychiatry Centre, University of Gothenburg, Sweden. 18Carolina Population Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27516, USA. 19Department of Sociology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. 20Department of Psychiatry and Behavioral Sciences, NorthShore University HealthSystem Research Institute, Evanston, IL 60201, USA. 21Department of Psychiatry and Behavioral Neuroscience, University of Chicago, Chicago, IL 60637, USA. 22Centre for Psychology and Evolution, School of Psychology, University of Queensland, St. Lucia, Brisbane QLD 4072, Australia. *These authors contributed equally to this work. †These authors contributed equally to this work. ‡Corresponding author. Email: zietsch@psy.uq.edu.au Ganna et al., Science 365, eaat7693 (2019) 30 August 2019 1 of 8 Downloaded from http://science.sciencemag.org/ on August 30, 2019 Twin and family studies have shown that same-sex sexual behavior is partly genetically influenced, but previous searches for specific genes involved have been underpowered. We performed a genome-wide association study (GWAS) on 477,522 individuals, revealing five loci significantly associated with same-sex sexual behavior. In aggregate, all tested genetic variants accounted for 8 to 25% of variation in same-sex sexual behavior, only partially overlapped between males and females, and do not allow meaningful prediction of an individual’s sexual behavior. Comparing these GWAS results with those for the proportion of same-sex to total number of sexual partners among nonheterosexuals suggests that there is no single continuum from opposite-sex to same-sex sexual behavior. Overall, our findings provide insights into the genetics underlying same-sex sexual behavior and underscore the complexity of sexuality. Phenotypic characterization R ES E A RC H | R E S EA R C H A R T I C LE Box 1. Phenotype and sample definition and limitations. Fig. 1. Descriptive statistics regarding same-sex sexual behavior in the UK Biobank. (A) The percentage of participants in the UK Biobank who reported having had at least one same-sex sexual partner (y axis) increased with participants’ year of birth (x axis). (B) Among participants reporting at least one same-sex partner, those with a greater proportion of same-sex partners (x axis) have a larger reproductive disadvantage (lower birth-year adjusted number of children) (y axis). Vertical bars represent 95% CIs. Ganna et al., Science 365, eaat7693 (2019) 30 August 2019 Genetic architecture of same-sex sexual behavior We first assessed whether same-sex sexual behavior clustered in families in a manner consistent with genetic influences on the phenotype. Among pairs of individuals in the UK Biobank related at full cousin or closer [as identified by genomic similarity (14); n pairs = 106,979], more closely related individuals were more likely to be concordant in terms of same-sex sexual behavior. By modeling the correspondence of relatedness among individuals and the similarity of their sexual behavior, we estimated broad-sense heritability—the percentage of variation in a trait attributable to genetic variation—at 32.4% [95% confidence intervals (CIs), 10.6 to 54.3] (table S4). This estimate is consistent with previous estimates from smaller twin studies (7). To identify genetic variants [largely singlenucleotide polymorphisms (SNPs)] associated with same-sex sexual behavior, we performed a GWAS in the UK Biobank study (n = 408,995 individuals) (14). To increase power and generalizability of our results, we also performed a GWAS in the cohort from 23andMe using an equivalent variable (individuals who reported having had sex with “Other sex only” versus the other options on a seven-point scale regarding participants’ sexual partners) (n = 68,527 individuals, of which 12,933 reported same-sex sexual behavior) (table S3) (14). We estimated the genetic correlation (16) between different heritable traits to determine the degree of consistency of genetic influences on same-sex sexual behavior in the two studies, which was high [genetic correlation coefficient (rg) = 0.87; 95% CIs, 0.67 to 1.06] (table S5) (14). Genetic correlations between same-sex sexual behavior and 28 different traits were largely similar in the UK Biobank and 23andMe (fig. S2) (14), although a few differences were observed; for example, in females, the genetic correlations between samesex sexual behavior and anorexia were in opposite directions in the UK Biobank (rg = –0.36; 95% CIs, –0.60 and –0.09) and 23andMe data (rg = 0.36; 95% CIs, 0.08 to 0.65; Wald test P value for differences = 0.0001). Overall, these results indicate that the genetic influences on same-sex sexual behavior in the two samples is similar, although there is some suggestion of phenotypic heterogeneity. We meta-analyzed the two sample sets using MTAG (17), which models 2 of 8 Downloaded from http://science.sciencemag.org/ on August 30, 2019 In this study, we use the term “same-sex sexual behavior,” which is defined as having ever had sex with someone of the same sex. Detailed descriptions of the variables used in the different cohorts can be found in the supplementary materials (14). To aid in readability throughout the manuscript, in some places we refer to individuals who have ever had sex with someone of the same sex as “nonheterosexuals,” whereas we refer to individuals who have never had sex with someone of the same sex as “heterosexuals.” We acknowledge that the grouping phrase “nonheterosexuals” has the potential to present messages of othering (that is, undesirable marginalization of another person or group on the basis of their sexual expression)—by defining an “outgroup” in reference to an “ingroup” and implying that “nonheterosexual behavior” may have a negative connotation, whereas “heterosexual behavior” may have a positive one. We wish to make clear that our choice of language is not meant to forward messages of othering on the basis of sexual behavior. Throughout this manuscript, we use the terms “female” and “male” rather than “woman” and “man.” This is because our analyses and results relate to biologically defined sex, not to gender. As is common in genetic analyses, we dropped individuals from our study whose biological sex and self-identified sex/gender did not match. This is an important limitation of our analyses because the analyses do not include transgender persons, intersex persons, and other important persons and groups within the queer community. We hope that this limitation will be addressed in future work. participants reported the degree of attraction to the same versus opposite sex. We observed in the UK Biobank that individuals who reported same-sex sexual behavior had on average fewer offspring than those of individuals who engaged exclusively in heterosexual behavior, even for individuals reporting only a minority of same-sex partners (Fig. 1B). This reduction in number of children is comparable with or greater than for other traits that have been linked to lower fertility rates (fig. S1) (14). This reproductive deficit raises questions about the evolutionary maintenance of the trait, but we do not address these here. R ES E A RC H | R E S EA R C H A R T I C LE their genetic correlation to determine the metaanalytic weights, yielding a total sample size of 477,522 individuals (26,827 individuals reporting same-sex sexual behavior). After standard quality control checks (table S6) (14), we identified two genome-wide significant signals for same-sex sexual behavior (rs1111497512q21.31 and rs10261857-7q31.2) (Fig. 2 and tables S7 and S8). We discuss these SNPs further in the section “In-silico follow-up of GWAS results.” To assess differences in effects between females and males, we also performed sex-specific analyses. These results suggested only a partially shared genetic architecture across the sexes; the acrosssex genetic correlation was 0.63 (95% CIs, 0.48 to 0.78) (table S9). This is noteworthy given that most other studied traits show much higher across-sex genetic correlations, often close to 1 (18–21). Through the sex-specific analyses, we identified two additional signals in males (rs28371400-15q21.3 and rs34730029-11q12.1), which showed no significant association in females, and one in females (rs13135637-4p14), which showed no significant association in males. Overall, three of the SNPs replicated at a nominal P value in the meta-analyzed replication datasets (Wald test P = 0.027 for rs34730029, P = 0.003 for rs28371400, and P = 0.006 for rs11114975) (table S10), despite the much smaller sample size (MGSOSO, Add Health, and CATSS; total sample size = 15,156 individuals, effective sample size = 4887 individuals). The SNPs that reached genome-wide significance had very small effects (odds ratios ~1.1) (table S7). For example, in the UK Biobank, males with a GT genotype at the rs34730029 locus had 0.4% higher prevalence of same-sex sexual behavior than those with a TT genotype (4.0 versus 3.6%). Nevertheless, the contribution of all Ganna et al., Science 365, eaat7693 (2019) Fig. 3. SNP-based versus family-based heritability estimates for same-sex sexual behavior compared with a variety of other traits. Heritability, h2; same-sex sexual behavior, red dot; other traits, gray dots. The estimates for all traits are provided in table S23. Horizontal bars represent 95% CIs for the SNP-based estimate, and vertical bars represent 95% CIs for the family-based estimate. Dashed and solid lines represent the observed (obtained by linear regression) and expected relationship between family-based and SNP-based heritability, respectively. measured common SNPs in aggregate (SNPbased heritability) was estimated to be 8 to 25% (95% CIs, 5 to 30%) of variation in female and male same-sex sexual behavior, in which the range reflects differing estimates by using different analysis methods or prevalence assumptions (table S11) (14). The discrepancy between the variance captured by the significant SNPs and all common SNPs suggests that same-sex 30 August 2019 sexual behavior, like most complex human traits, is influenced by the small, additive effects of very many genetic variants, most of which cannot be detected at the current sample size (22). Consistent with this interpretation, we show that the contribution of each chromosome to heritability is broadly proportional to its size (fig. S3) (14). In contrast to linkage studies that found substantial association of sexual 3 of 8 Downloaded from http://science.sciencemag.org/ on August 30, 2019 Fig. 2. Manhattan plot for a GWAS of same-sex sexual behavior. Diamonds (red) represent genome-wide significant signals from analysis of males and females combined, and triangles represent genome-wide significant signals that are female (pointing up, blue) or male (pointing down, green) specific. R ES E A RC H | R E S EA R C H A R T I C LE crepancy, including, but not limited to, variants not captured by genotyping arrays, nonadditive genetic effects, and phenotypic heterogeneity. In silico follow-up of GWAS results orientation with variants on the X-chromosome (8, 23), we found no excess of signal (and no individual genome-wide significant loci) on the X-chromosome (fig. S4). To test whether these aggregate estimates of genetic effects correlate with sexuality in other samples, we constructed polygenic scores for same-sex sexual behavior (14, 24). These polygenic scores were significantly associated with sexual identity in MGSOSO (Wald test, P = 0.001) and same-sex attraction in the Add Health (P = 0.017) and CATSS (P = 3.5 × 10−6) studies (tables S12, S13, and S14). In CATSS, polygenic scores were also significantly associated with sexual attraction in participants at age 15 years (P = 6.4 × 10−5), suggesting that at least some of the genetic influences on same-sex sexual behavior manifest early in sexual development. The purpose of these analyses is to further characterize the genetic influences on same-sex sexual behavior and not Ganna et al., Science 365, eaat7693 (2019) to predict same-sex sexual behavior on the individual level. In all cases, the variance explained by the polygenic scores was extremely low (

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