The question “Is homosexuality biologically based?” is more complicated than a simple yes-or-no choice between biology and environment. Contemporary research does not support the idea that sexual orientation is produced by one gene, one hormone, one brain structure, or one childhood experience. Instead, the evidence points toward a multifactorial developmental process in which genetic influences, prenatal biology, neurodevelopment, and other factors contribute in different ways across individuals. Biological influence is therefore substantial, but biological influence is not the same as biological determinism.
This distinction also matters conceptually. Sexual orientation refers to patterns of sexual and romantic attraction, but studies do not always measure the same thing. Some examine identity, others behavior, attraction, physiological response, or partnership history. These dimensions overlap but are not identical. Research results can therefore differ depending on how orientation is defined and measured, a limitation emphasized in major reviews of biological research on sexual orientation (Mustanski et al., 2002). A 2020 review by Bogaert and Skorska concluded that genetics, prenatal hormones, neural correlates, and the fraternal birth-order effect provide substantial evidence for biological influences, while also emphasizing major unanswered questions about mechanisms and sex differences.
Genetic Evidence
Twin and family studies have long suggested that sexual orientation is partly heritable. Identical twins tend to resemble one another in sexual orientation more than fraternal twins do, but concordance is far from complete. This pattern is exactly what would be expected for a complex trait influenced by genetics without being genetically predetermined. If one gene or fixed genetic program controlled sexual orientation, identical twins would show much higher concordance than they actually do.
Large genome-wide association studies have strengthened this conclusion while rejecting older “gay gene” narratives. Ganna and colleagues (2019) analyzed genetic data from nearly half a million people and identified several variants associated with same-sex sexual behavior. However, each individual variant had a very small effect, and the combined genetic information could not meaningfully predict an individual’s sexual behavior. The findings support a highly polygenic model in which many genetic variants contribute tiny influences rather than one decisive gene.
This is common in behavioral traits. Height, educational attainment, personality, depression risk, and many other complex characteristics are influenced by large numbers of genetic variants interacting with development and environment. Sexual orientation appears to fit this broader pattern. Genetic influence helps explain population-level variation but does not function as a diagnostic test or personal predictor.
The large GWAS also illustrates a measurement limitation. It examined same-sex sexual behavior rather than every component of sexual orientation. Behavior can be influenced by opportunity, culture, partnership history, disclosure, and identity. A genetic association with behavior should therefore not be treated as a complete biological explanation of attraction or identity.
Recent reviews continue to describe sexual orientation as multifactorial. Alagha and colleagues (2025) reviewed genetic, neurological, biological, and environmental research and concluded that no single pathway explains homosexuality. Their review also stresses that the literature is heterogeneous, heavily concentrated in Western populations, and affected by differences in study design and measurement.
Prenatal Development
Prenatal biology provides another important line of evidence. The developing nervous system is influenced by sex hormones during critical periods, and research in animals demonstrates that early hormonal environments can alter later patterns of sexual behavior and partner preference. Translating animal findings directly to humans is difficult, but several human observations are consistent with prenatal hormonal influence.
Studies involving congenital adrenal hyperplasia have been particularly informative. Females with this condition can experience unusually high prenatal androgen exposure. On average, they show higher rates of male-typical play behavior and somewhat higher rates of nonheterosexual attraction than comparison groups. These findings do not mean prenatal hormones determine orientation, but they support the idea that prenatal hormonal exposure can influence later sexual development.
The fraternal birth-order effect provides another biological clue in some gay men. Research has repeatedly found that, on average, the probability of male homosexuality increases with the number of older biological brothers born to the same mother. The effect does not explain most gay men and is not observed in the same way among women. It has nevertheless been replicated often enough to become one of the better-established epidemiological findings in this field.
One proposed explanation is the maternal immune hypothesis. During successive male pregnancies, some mothers may develop immune responses to male-specific proteins, potentially influencing aspects of fetal neurodevelopment in later male pregnancies. Evidence supporting this hypothesis exists, but the mechanism remains under investigation and should not be presented as proven for every case (Bogaert & Skorska, 2020).
Prenatal-development research is important because it challenges theories that treat sexual orientation as simply learned through imitation, parenting style, or deliberate choice. At the same time, biological development is itself complex. Genes influence hormone systems, maternal physiology interacts with fetal development, and developmental outcomes can vary even among people with similar biological exposures.
Brain Research
Researchers have also examined possible differences in brain structure and function associated with sexual orientation. Simon LeVay’s 1991 study of the anterior hypothalamus became one of the best-known early examples (LeVay, 1991). He reported an average group difference in one hypothalamic region between homosexual and heterosexual men. The study was historically important but had major limitations, including small sample size, postmortem design, medical differences among subjects, and the inability to determine whether the observed difference preceded or followed other biological or experiential factors.
Later neuroimaging research has reported group-level differences in responses to sexually relevant stimuli, connectivity, anatomy, and functional activation. However, these findings do not identify a single “homosexual brain.” Brain characteristics overlap substantially across groups, and observed correlations do not establish causation. Experience can also influence the brain, making it difficult to determine whether every neural difference is a cause, consequence, or correlate of sexual orientation.
Wang, Wu, and Sun’s 2019 review integrated research on hormonal, genetic, neural, maternal-immune, and environmental influences (Wang et al., 2019). Their central conclusion was not that one brain region explains orientation, but that sexual orientation is a complex developmental trait involving multiple interacting systems. The review also noted that mechanisms may differ between males and females and that findings from one sex should not automatically be generalized to the other.
This caution is especially important because earlier scientific literature often interpreted group differences through stereotypes about masculinity and femininity. Modern research needs to separate sexual orientation from gender expression, personality, and gender identity. A gay man is not biologically equivalent to a heterosexual woman, and a lesbian woman is not simply a masculinized version of a heterosexual man. Biological research is most useful when it avoids these simplistic models.
Beyond Nature and Nurture
The traditional “nature versus nurture” framework is too crude for contemporary developmental science. Genes are expressed through biological systems that develop in particular environments. Prenatal hormones are themselves influenced by genes and maternal physiology. Social context affects whether people recognize, describe, or disclose their attractions, even if it does not create those attractions in a simple causal way.
Environmental influence also needs careful definition. In behavioral science, “environment” can include prenatal conditions, maternal immune processes, nutrition, exposure to hormones, family structure, culture, peer relationships, and life experience. Treating every non-genetic influence as evidence that sexual orientation is socially taught is therefore incorrect.
The strongest current evidence does not support older claims that homosexuality results from defective parenting, absent fathers, domineering mothers, seduction, or social recruitment. Nor does the scientific literature support a simple model in which people can deliberately select their orientation. Research on sexual fluidity shows that attractions and identities can change for some individuals, particularly over longer periods, but fluidity is not equivalent to voluntary control.
The scientific history of this subject also requires caution because research has sometimes been shaped by social prejudice. Earlier medical systems classified homosexuality as pathology, while later research sometimes searched for biological explanations partly to counter moral stigma. Science should not be used to decide whether a group deserves equal dignity. A trait does not need to be genetically fixed in order for people experiencing it to deserve ethical treatment.
The evidence available today therefore supports a qualified conclusion. Sexual orientation has important biological influences, including genetic and prenatal-developmental contributions. There is no single biological cause, and current evidence cannot predict an individual’s orientation from genes, hormones, birth order, or brain imaging. Different mechanisms may contribute in different people, and substantial uncertainty remains about how those mechanisms interact.
Modern research has moved beyond the older question of whether homosexuality is purely “natural” or purely “learned.” The more accurate scientific model is developmental and multifactorial. Biology clearly matters, but it operates through complex pathways rather than one deterministic mechanism. The continuing challenge is to understand those pathways without reducing human sexuality to a single gene, brain structure, social experience, or political argument.
References
Alagha, M., Antoun, F., Bacha, C., El Nabbout, T., & El Khoury, N. B. (2025). Biological, genetic, neurological and environmental influences on homosexuality—a narrative review. Frontiers in Behavioral Neuroscience, 19, 1574713. https://doi.org/10.3389/fnbeh.2025.1574713
Bogaert, A. F., & Skorska, M. N. (2020). A short review of biological research on the development of sexual orientation. Hormones and Behavior, 119, 104659. https://doi.org/10.1016/j.yhbeh.2019.104659
Ganna, A., Verweij, K. J. H., Nivard, M. G., et al. (2019). Large-scale GWAS reveals insights into the genetic architecture of same-sex sexual behavior. Science, 365(6456), eaat7693.
LeVay, S. (1991). A difference in hypothalamic structure between heterosexual and homosexual men. Science, 253(5023), 1034–1037.
Mustanski, B. S., Chivers, M. L., & Bailey, J. M. (2002). A critical review of recent biological research on human sexual orientation. Annual Review of Sex Research, 13(1), 89–140.
Wang, Y., Wu, H., & Sun, Z. S. (2019). The biological basis of sexual orientation: How hormonal, genetic, and environmental factors influence to whom we are sexually attracted. Frontiers in Neuroendocrinology, 55, 100798. https://doi.org/10.1016/j.yfrne.2019.100798
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