The document discusses how epigenetic modifications during fetal development, rather than genetic factors, may influence sexual development and orientation. Androgen signaling and sex-specific epigenetic marks set during ontogeny can influence sexually dimorphic traits by increasing androgen sensitivity in XY fetuses and decreasing it in XX fetuses. Some of these epigenetic marks, called SA-epi-marks, may escape erasure between generations and could pair with weaker in-sex marks in opposite-sex offspring, potentially feminizing XY children or masculinizing XX children and influencing sexual preference.

1. “Gay Gene”

2. Environmental Trigger?

7. Consequence of Epigenetically
Canalized Sexual Development
• Fetal androgen signaling
• Gene regulation via nongenetic changes in
DNA packaging (epigenetics)
• Androgen sensitivity in XX fetuses↓, in XY
fetuses ↑, caused by sex-specific epigenetic
modifications “epi-marks”

8. Epi-marks
• Influence some but not other sexually dimorphic
traits
• Vary in strength across individuals
• Produced during ontogeny
• Erased between generations
• Some escape erasure (SA-epi-marks)
• Steer development of the sexual phenotypes in a
gonad-discordant direction
feminizing XY offspring
masculinizing XX offspring

9. Homosexuality
Stronger-than-average SA-epi-marks
(influencing sexual preference) from an
opposite-sex parent
escape erasure and are then paired with a
weaker-than-average epi-marks produced in
opposite-sex offspring