16. Human Sexual Behavior II

What this lecture covers

This lecture continues directly from the previous one, finishing the discussion of pheromonal releasing stimuli before working further back through the course's "march to the left" framework: acute environmental effects, hormone levels over weeks to months, perinatal hormone exposure, genetics, and finally evolutionary biology. It answers questions like whether human sexual behavior tracks the menstrual cycle, whether testosterone causes male sexual behavior or merely modulates it, and how early hormonal and social environments shape adult sexual behavior and identity.

The second half turns to evolutionary explanations, using bonobo chimpanzees to challenge simple reproduction-only models of sex, and surveys male strategies to control female reproduction, female counter-strategies such as hidden ovulation, and alternative male mating tactics ranging from affiliative "nice guy" strategies in baboons to coercive strategies in orangutans. After this lecture, you can explain why testosterone's role in sexual behavior is modulatory rather than strictly causal, and why simple linear-access models of primate mating have been replaced by more nuanced pictures involving female choice.

Key ideas

• Pheromone-hormone dependency: generating and perceiving sexually meaningful pheromones requires intact gonadal hormones in both sexes; pheromones can accelerate puberty, alter testosterone or sperm production, or affect ovulation, depending on species and context.
• Coolidge effect: sexual interest that has waned with a familiar partner is restored by introducing a novel one, observed across many species including humans.
• Organizational vs. activational hormone effects: perinatal hormone exposure organizes brain circuits in a largely permanent way, while hormones later in life have temporary, activational effects on behavior.
• Testosterone as modulator, not trigger: castration reduces male sexual behavior but never to zero, replacement works similarly across a wide range of physiological doses, and only supra-physiological levels increase behavior further—testosterone lowers the threshold for arousal rather than causing it outright.
• Alpha-fetoprotein: a fetal-specific protein that neutralizes circulating estrogen, explaining why female fetuses are not accidentally masculinized by maternal estrogen while male brains are organized through testosterone's local conversion to estrogen.
• Heritability of sexual orientation: twin studies show higher concordance in identical twins than fraternal twins or other siblings, suggesting a genetic contribution, though Dean Hamer's "gay gene" marker was never replicated.
• Bonobo sexuality: bonobos use frequent, largely non-reproductive sex to manage social tension and cohesion, challenging strict reproduction-only models of sexual selection.
• Female choice and alternative mating strategies: linear-access models where dominant males automatically win mating access have been replaced by evidence of active female choice, "nice guy" affiliative strategies in baboons, and coercive strategies such as rape in low-ranking orangutans.

Walkthrough

Pheromones and cross-sex physiological effects (0:04)

The lecture picks up the pheromone discussion from the prior class, covering effects like the Wellesley effect (cycle synchronization among females), pheromone-induced delays or accelerations of puberty, and dominance-dependent testosterone or sperm-production changes in males exposed to rival pheromones. Sapolsky describes classic examples including inducible ovulation in pigs and a famous anonymous field-researcher's self-tracked beard-growth study as an indirect measure of testosterone response to social contact.

Non-olfactory releasers and acute environmental effects (13:12)

He briefly covers gustatory and auditory sexual releasers in other species, then turns to acute human factors: thought itself as the primary human releaser, fear and extreme stress suppressing libido, and the variable effects of acute stress. The Coolidge effect is introduced here as a releaser that transcends any single sensory modality, illustrated by an anecdote involving Calvin Coolidge and breeding roosters.

Menstrual cycle and hormone effects on sexual behavior (18:15)

The lecture reviews a classic 1970s study finding modest increases in reported female sexual activity and orgasm likelihood around ovulation, with a secondary rise near menstruation attributed to lower fear of pregnancy. It notes this effect is harder to replicate for behavior than for arousal, and explains supporting mechanisms: estrogen increasing progesterone receptor expression, boosting oxytocin synthesis, lowering tactile thresholds, and heightening olfactory sensitivity to male pheromones near ovulation.

Testosterone's causal versus modulatory role (27:28)

Using castration-and-replacement experiments, Sapolsky shows that testosterone is necessary for a normal range of male sexual behavior but that behavior never drops to zero after castration (with more pre-castration experience predicting more residual behavior), and that replacement across a wide physiological dose range produces roughly the same effect. Only supra-physiological doses, as seen with anabolic steroid abuse, increase behavior further. The conclusion: testosterone sensitizes and lowers the threshold for arousal rather than directly causing it.

Perinatal organization and early experience (37:38)

The lecture distinguishes organizational (early, lasting) from activational (later, temporary) hormone effects, using primate isolation studies to show early social experience shapes when and in what context sexual behavior occurs, not the fixed action patterns themselves. It covers congenital adrenal hyperplasia and prenatal DES exposure as sources of human prenatal androgenization, the confound of resulting genital surgeries in those studies, and the biochemical puzzle of testosterone acting through conversion to estrogen in the brain, resolved by alpha-fetoprotein protecting female fetuses. The testicular feminization case is used to show that social sex assignment can outweigh even organizational hormone effects on gender identity.

Genetics of sexual orientation (1:05:56)

Sapolsky reviews twin-study evidence for heritability (roughly 50% concordance in identical twins versus 22% in fraternal twins and 9% in other siblings) and critically examines Dean Hamer's widely publicized "gay gene" marker finding, noting its inconsistent location across twin pairs and lack of subsequent replication, in contrast to LeVay's more consistently replicated brain-structure finding from the earlier lecture.

Evolutionary biology of sexual behavior and bonobos (1:12:03)

The lecture challenges simple "sex is for reproduction" evolutionary models using bonobo chimpanzees, who show minimal sexual dimorphism, low aggression, female-based social dominance, and extensive non-reproductive sex used for social cohesion and tension reduction, contrasting sharply with more aggressive, male-dominated chimpanzee societies.

Male control strategies, female counter-strategies, and alternative tactics (1:19:07)

The closing section surveys the cost asymmetry between sperm and eggs driving female selectivity, male attempts to control female reproduction (mate guarding, copulatory plugs, chastity belts, chemical suppression of female attractiveness in some fly species), and female counter-strategies such as hidden ovulation and pseudo-estrus. It then replaces the older linear-access model of primate mating with evidence of active female choice, describing baboon "nice guy" affiliative strategies documented by Barbara Smuts and coercive alternative strategies such as rape among low-ranking orangutans, as documented by Biruté Galdikas.

Before you watch

• Watch the previous lecture (15. Human Sexual Behavior I), since this lecture continues directly from its discussion of pheromones and limbic/hormonal circuitry.
• Recall the earlier lecture's coverage of testosterone, estrogen and receptor biology, referenced here when explaining organizational hormone effects.
• Be familiar with basic evolutionary biology concepts such as gene copies and sexual selection, introduced earlier in the course.

Check your understanding

1. Why does castration reduce but never eliminate male sexual behavior, and what does the dose-response pattern of testosterone replacement suggest about its role?
2. What problem does alpha-fetoprotein solve during fetal brain development, and why does it matter that testosterone's effects in the brain depend on conversion to estrogen?
3. Why is Dean Hamer's "gay gene" marker considered weaker evidence than LeVay's brain-structure finding discussed in the prior lecture?
4. How does bonobo behavior complicate the idea that sexual behavior evolved purely to maximize reproduction?
5. What is the difference between the "nice guy" affiliative mating strategy documented in baboons and the coercive strategy documented in orangutans, and what does each suggest about alternatives to male-male competition?