The role of miscarriage and sororal birth order in male same-sex orientation: Theoretical predictions and empirical data

This study explores the proximal and biological mechanisms underlying male same-sex orientation, with a focus on the Fraternal Birth Order Effect (FBOE), a robust phenomenon whereby same-sex oriented men tend to have more older brothers than the population average, and its relationship with the Sororal Birth Order Effect (SBOE), whereby older sisters also appear to influence sexual orientation, albeit less consistently. The Maternal Immune Hypothesis (MIH), which posits that maternal immune responses to male-specific antigens accumulate across successive male pregnancies, provides a compelling proximal explanation for the FBOE, but it fails to fully account for the SBOE and other birth order patterns, such as the elevated prevalence of same-sex orientation among only-children compared to firstborns in larger sibships. Through explicit modelling of the MIH, our simulations reveal that the correlation between the number of older brothers and sisters generates a spurious SBOE, which disappears when controlling for older brothers. However, this control becomes insufficient when miscarriages are included in the simulations. Additionally, the increased prevalence of same-sex orientation among only-children, relative to firstborns with siblings, only emerges when miscarriages are incorporated into the model. Empirical analyses across eight diverse populations (Indonesia, France, French Polynesia, Greece, Canada, Czech Republic, Samoa, Iran) confirm the presence of an overall significant FBOE and, critically, an overall significant SBOE even after controlling for the number of older brothers. The higher frequency of same-sex orientation men among only-children, compared to firstborns in larger sibships, supports a possible role of miscarriage for this SBOE. However, the estimated miscarriage rates (37% - 58%) explaining the observed SBOE slightly exceeds reported rates (30% - 45%) which conservatively include early pregnancy losses. This possibly suggests that additional mechanisms contribute to a spurious SBOE or that a genuine SBOE coexists with the FBOE. Limitations of this study are discussed, as well as whether the MIH framework can be extended to accommodate these findings, or if alternative explanations are needed to resolve these discrepancies.