Biology and sexual orientation

The relationship between biology and sexual orientation is a topic of sustained scientific inquiry. Although no single deterministic cause has been identified, researchers widely agree that sexual orientation arises from a complex interplay of genetic, hormonal, neurodevelopmental, and environmental influences. Contemporary science views sexual orientation as a multidimensional trait, shaped predominantly by biological processes that occur before birth, with comparatively little support for postnatal socialisation as a determining factor, especially in males. This multidisciplinary research includes genetics, prenatal endocrinology, neuroanatomy, evolutionary biology, and epigenetics.

Overview of Biological Influences

Most researchers favour biological explanations for sexual orientation, proposing that crucial influences occur during fetal development. These include genetic predispositions, variations in prenatal hormone levels, maternal immune responses, and structural differences within the brain. While heterosexuality can be interpreted through evolutionary pressures favouring reproductive success, homosexuality requires alternative explanations such as kin selection, inclusive fitness, antagonistic pleiotropy, or non-adaptive developmental pathways.
Scientists distinguish between biological predispositions and deterministic mechanisms. Evidence strongly indicates that genes and prenatal conditions shape sexual orientation, but these interactions are complex rather than strictly predetermining.

Fetal Development and Prenatal Hormonal Effects

One of the most influential hypotheses concerns the impact of prenatal hormones on the developing brain. In early development, the fetal brain follows a default template often described as female-typical. Masculinisation occurs when testes—triggered by activation of the SRY gene on the Y chromosome—produce testosterone, which enters target cells and influences brain differentiation.
Two key hypothalamic structures have been studied in relation to sexual orientation:

• INAH3 (third interstitial nucleus of the anterior hypothalamus)
• BSTc (bed nucleus of the stria terminalis, central subdivision)

Exposure to sufficient levels of testosterone around 12 weeks post-conception appears to contribute to typical male-typical sexual attraction patterns. If INAH3 receives lower levels of testosterone, or if cells respond differently to androgen signals, its development may shift towards a female-typical pattern. Studies suggest:

• Gay men may have INAH3 structures with higher cell density and developmental features differing from heterosexual men.
• Lesbians often display more male-typical digit ratios on the right hand (a marker of prenatal androgen exposure), a finding replicated across cultures.
• Controlled animal experiments consistently show that manipulating prenatal hormone exposure can induce lasting shifts in sex-typical behaviour.

In females, elevated prenatal testosterone exposure may enlarge INAH3 beyond typical female size, increasing the likelihood of same-sex attraction.

Maternal Immune Response and the Fraternal Birth Order Effect

One of the most robust findings in the field is the fraternal birth order effect, which describes the observation that later-born sons are statistically more likely to be gay. This is explained through maternal immune responses:

• Male fetal cells enter the maternal bloodstream during pregnancy.
• The mother may generate antibodies against proteins encoded on the Y chromosome.
• These antibodies can affect the brain masculinisation of subsequent male fetuses.

A 2017 biochemical study found higher levels of anti-NLGN4Y antibodies in mothers of gay sons, particularly those with older brothers. This mechanism is estimated to account for 15–29% of gay men, providing one of the clearest biological pathways identified to date.

Evidence Against Socialisation Theories

Socialisation-based theories were influential in the twentieth century but lack empirical support. Medical interventions in which infant boys were reassigned as girls after accidental genital injury demonstrated that upbringing could not override prenatal brain organisation. All documented cases showed the individuals adopting male gender identities and heterosexual orientation towards women, reinforcing the primacy of prenatal hormonal effects in male sexual orientation.

Neuroanatomy and Brain Structure

Neuroanatomical studies contribute further evidence for biological influences:

• The sexually dimorphic nucleus of the preoptic area (SDN-POA) differs between sexes and in animals correlates with sexual preference.
• Initial dissection studies by Simon LeVay reported that INAH3 in gay men was smaller and shifted towards female-typical size, a finding later replicated.
• In sheep, long-term studies show that 6–8% of rams display lifelong homosexual preference, correlated with a smaller and more feminised form of the ovine sexually dimorphic nucleus (oSDN).
• Brain imaging by Ivanka Savic demonstrated hemisphere size differences:
  • Straight men: right hemisphere larger than left
  • Straight women: hemispheres equal
  • Gay men: hemispheres equal (female-typical)
  • Lesbians: right hemisphere slightly larger (male-typical)

These findings support the hypothesis of sex-atypical brain lateralisation in sexual minorities.

Genetic and Epigenetic Contributions

Genetic studies have not identified a single “gay gene”; instead, many genes each contribute a small influence. Modern research suggests:

• Sexual orientation may emerge from polygenic influences, similar to many complex human traits.
• Epigenetic mechanisms appear to play a significant role.
• A prominent model proposed by William R. Rice posits “epimarks” that regulate testosterone sensitivity during development.
• These epimarks normally prevent intersex development but may sometimes persist across generations, affecting sexual preference in offspring.

This model may account for why identical twins, who share nearly all their genes, can differ in sexual orientation.

Evolutionary Perspectives

The existence of exclusive homosexuality across multiple species—including humans—requires evolutionary explanation. Several theories have been proposed:

• Kin selection: individuals who do not reproduce may still increase genetic fitness by supporting relatives.
• Antagonistic pleiotropy: genes increasing fertility in one sex may predispose the other to homosexuality.
• Heterozygote advantage: genetic variants harmful in homozygous form may offer advantages in heterozygotes.
• Spandrel hypothesis: homosexuality may arise as a by-product of other adaptive traits.

These models aim to reconcile stable prevalence rates of homosexuality with evolutionary processes.

Prenatal Thyroid Theory

A more recent proposal identifies a possible link between maternal thyroid dysfunction and developmental variations in gender identity or same-sex attraction. Early clinical observations suggested a correlation between maternal thyroid disease during pregnancy and later atypical gender-related behaviours in offspring. This prenatal thyroid model remains preliminary but highlights potential endocrine pathways beyond sex hormones.

Multidimensional Models of Sexual Orientation

Current scientific consensus holds that sexual orientation is influenced by:

• Genetic predispositions
• Prenatal hormonal environment
• Maternal immune effects
• Neurodevelopmental differentiation
• Epigenetic regulation

Postnatal social environment is considered a weak or negligible determinant of sexual orientation, particularly for males.
Although the exact mechanisms remain under investigation, contemporary models emphasise the integrated nature of biological development. Sexual orientation is therefore understood not as a fixed genetic outcome, nor as a product of social learning, but as the result of intertwined biological processes shaping brain development and later behavioural patterns.