Lecture 6: Behavioral Genetics I

What this lecture covers

This lecture opens the course's third disciplinary approach to behavior: behavior genetics, the attempt to infer a genetic basis for traits by comparing individuals with different degrees of shared genes and shared environment. It works through the field's classical tools, twin studies and adoption studies, in order, showing how each was built to control for a confound the previous method missed, and how each still falls short.

The second half of the lecture pivots to what the field largely ignored: that environment does not begin at birth. Using examples ranging from rat litters to the Dutch Hunger Winter, it shows how prenatal conditions can produce heritable-looking, sometimes multigenerational, differences that have nothing to do with DNA sequence. By the end, you can explain why classic behavior-genetics findings, including some famous ones, are less clean than they first appear, and why researchers now have to rule out prenatal and epigenetic explanations before claiming a trait is genetic. The lecture sets up the next lecture's move to finding actual genes and gene-environment interactions.

Key ideas

• Shared traits vs. shared genes: traits running in families can reflect shared environment as much as shared genes, since the two tend to correlate.
• Monozygotic vs. dizygotic twin studies: comparing identical and fraternal twins raised together aims to control for environment while varying genetic relatedness, but identical twins are treated more similarly than fraternal twins, confounding the comparison.
• Adoption studies: comparing adopted individuals to biological versus adoptive parents aims to separate genes from environment, but adoption placements are typically non-random and matched for similar traits.
• Twins separated at birth: the strongest classical design, pairing identical genes with different environments, still suffers from non-random placement and small sample sizes.
• Prenatal environment: conditions shared with the mother before birth, hormones, nutrients, stress, even sounds, can shape lifelong traits and are often mistaken for genetic inheritance.
• Non-Mendelian (epigenetic) inheritance: effects like the multigenerational consequences of the Dutch Hunger Winter show that a trait can be inherited across generations without any change in DNA sequence.
• Indirect genetic effects: a trait can appear heritable because a genuinely inherited physical trait (such as height or feather color) changes how others treat the individual, which then shapes behavior.

Walkthrough

From shared traits to twin studies (5:07)

The lecture starts with the field's crudest tool: assuming any universal or family-shared trait is genetic. It moves quickly to the standard rebuttal that genes and environment both run in families, then to the classical fix, comparing identical (monozygotic) and fraternal (dizygotic) twins raised together, on the logic that any extra similarity in identical twins must come from their extra shared genes. The lecture immediately undercuts this by showing that identical twins are treated more alike than fraternal twins, and that even identical twins differ in prenatal environment depending on whether they shared a placenta (monochorionic) or not, which measurably affects outcomes like IQ similarity.

The math gene study and gender differences (14:09)

The lecture examines a widely publicized 1980s study by Benbow and Stanley claiming a math skills gap between boys and girls at a stage before differentiated schooling, framed as evidence of a genetic "math gene." It shows that even by one hour after birth, infant boys and girls are handled differently, and that by elementary school, teachers call on and praise boys and girls unequally for the same math answers, undermining the study's core assumption of identical environments.

Adoption studies and the schizophrenia landmark (22:14)

The lecture details Seymour Kety's large-scale Danish adoption study, which found that adoptees with a schizophrenic biological parent had roughly nine times the population base rate of schizophrenia, versus about three times for those raised by (but not biologically related to) a schizophrenic adoptive parent, with a nonadditive synergy when both were present. This became the founding evidence for a heritable component to a psychiatric disorder, but the lecture immediately raises its confounds: shared time with the biological mother before adoption, unaccounted prenatal effects, uncertain paternity, and the fact that adoption agencies deliberately match children to adoptive families with similar traits.

Twins separated at birth and its limits (36:30)

Identical twins separated at birth and raised apart, studied most extensively by Thomas Bouchard, are presented as the field's strongest design, since genes are fixed while environments differ. Early, colorful anecdotes about long-separated twins sharing odd habits gave way to more rigorous findings: roughly 50% heritability estimates for IQ, introversion/extraversion, and aggression. The lecture notes the same non-random-placement problem still applies, along with small sample sizes, and introduces the deeper theme that all these methods assume "environment begins at birth," an assumption the rest of the lecture dismantles.

Prenatal environment as a hidden variable (44:42)

The lecture presents a series of findings showing how prenatal conditions shape lifelong traits: fetal rats' hormone exposure depends on the sex of neighboring littermates; human puberty timing depends on maternal age; prenatal maternal stress produces smaller brains and higher lifelong glucocorticoid levels in offspring, an effect (the "grandmother effect") that persists for several generations. The Dutch Hunger Winter is used as the central case study: third-trimester fetuses during the 1944 Nazi-imposed famine developed a "thrifty phenotype," metabolically programmed for scarcity, leading to sharply higher adult rates of obesity, diabetes, and metabolic syndrome, an effect later observed even in their grandchildren. Related studies show prenatal exposure to phytoestrogens raising later breast cancer risk, and prenatal learning, such as rat fetuses developing flavor preferences and human newborns preferring a story read aloud repeatedly during the third trimester.

Asymmetric parental inheritance and Lamarckian effects (1:09:02)

The lecture explains why comparing similarity with biological mothers versus fathers, long used to estimate prenatal effects, is itself unreliable: mitochondrial DNA is inherited only from the mother, imprinted genes function differently depending on the parent of origin, and only the egg supplies the transcription factors and cellular machinery present at fertilization. This last point opens the door to a form of Lamarckian, non-genetic inheritance: an environmental toxin that disables a transcription factor in an egg can silence a gene's expression for generations, without altering the gene's DNA sequence at all.

Indirect genetic effects and epigenetic mothering (1:21:07)

Drawing on Judith Rich Harris's concept of indirect genetic effects, the lecture shows that some "heritable" behavioral traits are mediated by an inherited physical trait that changes how others treat the individual, as with introversion/extraversion (mediated by height and attractiveness), social rank in birds (mediated by feather coloring), and political affiliation (mediated by tolerance for ambiguity, not a directly inherited preference). The lecture closes with Michael Meaney's work on rat maternal licking and grooming: variation in natural mothering style produces lasting differences in offspring brain development and stress hormone levels, transmitted to the next generation through epigenetic changes (not DNA sequence changes) in access to genes for stress and hormone receptors, and shown to be reversible through cross-fostering.

Before you watch

• Watch the two prior lectures on molecular genetics in this course, since this lecture assumes familiarity with promoters, transcription factors and epigenetic mechanisms like methylation.
• Recall the discussion of imprinted genes from earlier in the course, since it is used here to explain asymmetric maternal versus paternal inheritance.

Check your understanding

1. Why does comparing monozygotic and dizygotic twins raised together fail to cleanly separate genetic from environmental influence?
2. What confounds undermine Kety's Danish adoption study of schizophrenia, despite its careful design?
3. How did the Dutch Hunger Winter demonstrate that prenatal environment can produce effects that look inherited across multiple generations?
4. Why is mitochondrial DNA inheritance an example of unequal genetic contribution from each parent?
5. Give an example from the lecture of an "indirect genetic effect," where an inherited trait causes a behavioral outcome without directly coding for that behavior.