In this consensus report by a diverse group of academics who conduct and/or are concerned about social and behavioral genomics (SBG) research, the authors recount the often-ugly history of scientific attempts to understand the genetic contributions to human behaviors and social outcomes. They then describe what the current science-including genomewide association studies and polygenic indexes-can and cannot tell us, as well as its risks and potential benefits. They conclude with a discussion of responsible behavior in the context of SBG research. SBG research that compares individuals within a group according to a "sensitive" phenotype requires extra attention to responsible conduct and to responsible communication about the research and its findings. SBG research (1) on sensitive phenotypes that (2) compares two or more groups defined by (a) race, (b) ethnicity, or (c) genetic ancestry (where genetic ancestry could easily be misunderstood as race or ethnicity) requires a compelling justification to be conducted, funded, or published. All authors agree that this justification at least requires a convincing argument that a study's design could yield scientifically valid results; some authors would additionally require the study to have a socially favorable risk-benefit profile.

Risky behaviors, such as substance use and unprotected sex, are associated with various physical and mental health problems. Recent genome‐wide association studies indicated that variation in the cell adhesion molecule 2 (CADM2) gene plays a role in risky behaviors and self‐control. In this phenome‐wide scan for risky behavior, it was tested if underlying common vulnerability could be (partly) explained by pleiotropic effects of this gene and how large the effects were. Single nucleotide polymorphism (SNP)‐level and gene‐level association tests within four samples (25 and Up, Spit for Science, Netherlands Twin Register, and UK Biobank and meta‐analyses over all samples (combined sample of 362,018 participants) were conducted to test associations between CADM2, substance‐ and sex‐related risk behaviors, and various measures related to self‐control. We found significant associations between the CADM2 gene, various risky behaviors, and different measures of self‐control. The largest effect sizes were found for cannabis use, sensation seeking, and disinhibition. Effect sizes ranged from 0.01% to 0.26% for single top SNPs and from 0.07% to 3.02% for independent top SNPs together, with sufficient power observed only in the larger samples and meta‐analyses. In the largest cohort, we found indications that risk‐taking proneness mediated the association between CADM2 and latent factors for lifetime smoking and regular alcohol use. This study extends earlier findings that CADM2 plays a role in risky behaviors and self‐control. It also provides insight into gene‐level effect sizes and demonstrates the feasibility of testing mediation. These findings present a good starting point for investigating biological etiological pathways underlying risky behaviors.

Sex differences in brain and behavior of animals including humans result from an interaction between biological and environmental influences. This is also true for the differences between men and women concerning sexual orientation. Sexual differentiation is mediated by three groups of biological mechanisms: early actions of sex steroids, more direct actions of sex-specific genes not mediated by gonadal sex steroids and epigenetic mechanisms. Differential interactions with parents and conspecifics have additionally long-term influences on behavior. This presentation reviews available evidence indicating that these different mechanisms play a significant role in the control of sexual partner preference in animals and humans, in other words the homosexual versus heterosexual orientation. Clinical and epidemiological studies of phenotypically selected populations indicate that early actions of hormones and genetic factors clearly contribute to the determination of sexual orientation. The maternal embryonic environment also modifies the incidence of male homosexuality via immunological mechanisms. The relative contribution of each of these mechanisms remains however to be determined.

Sexual conflict likely plays a crucial role in the origin and maintenance of homosexuality in our species. Although environmental factors are known to affect human homosexual (HS) preference, sibling concordances and population patterns related to HS indicate that genetic components are also influencing this trait in humans. We argue that multilocus, partially X-linked genetic factors undergoing sexually antagonistic selection that promote maternal female fecundity at the cost of occasional male offspring homosexuality are the best candidates capable of explaining the frequency, familial clustering, and pedigree asymmetries observed in HS male proband families. This establishes male HS as a paradigmatic example of sexual conflict in human biology. HS in females, on the other hand, is currently a more elusive phenomenon from both the empirical and theoretical standpoints because of its fluidity and marked environmental influence. Genetic and epigenetic mechanisms, the latter involving sexually antagonistic components, have been hypothesized for the propagation and maintenance of female HS in the population. However, further data are needed to truly clarify the evolutionary dynamics of this trait.

Humans develop relatively stable attractions to sexual partners during maturation and present a spectrum of sexual orientation from homosexuality to heterosexuality encompassing varying degrees of bisexuality, with some individuals also displaying asexuality. Sexual orientation represents a basic life phenomenon for humans. However, the molecular mechanisms underlying these diverse traits of sexual orientation remain highly controversial. In this review, we systematically discuss recent advancements in sexual orientation research, including those related to measurements and associated brain regions. Current findings regarding sexual orientation modulation by hormonal, genetic, maternal immune system, and environmental factors are summarized in both human and model systems. We also emphasize that future studies should recognize the differences between males and females and pay more attention to minor traits and the epigenetic regulation of sexual orientation. A comprehensive view of sexual orientation may promote our understanding of the biological basis of sex, and that of human reproduction, and evolution.

A genetic study of male sexual orientation. 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.

Does the homosexuality of parents affect the sexual orientation or experiences of their children? Seventeen of 5,182 randomly obtained adults from six U.S. cities answered questionnaires indicating that they had a homosexual parent. Parental homosexuality may be related to findings that: (1) 5 of the 17 reported sexual relations with their parents; (2) a disproportionate fraction reported sexual relations with other caretakers and relatives; and (3) a disproportionate fraction: (a) claimed a less than exclusively heterosexual orientation (47%); (b) indicated gender dissatisfaction; and (c) reported that their first sexual experience was homosexual. Of 1,388 consecutive obituaries in a major homosexual newspaper, 87 of the gays who died had children and registered a median age of death of 47 (the 1,267 without children had a median age of death of 38); 10 lesbians did and 24 did not have children. We estimate that less than 1% of parents are bisexual or homosexual and that < 7% of gays and about a third of lesbians are parents.