- Heritability (h²)
- The proportion of observed variance in a trait in a specific population attributable to genetic differences between individuals. A population statistic, not a statement about any individual. Does not imply immutability — high heritability is compatible with large environmental effects on trait levels (e.g., height is ~80% heritable yet nutrition dramatically changed average heights across the 20th century).
- Monozygotic (MZ) twins
- Twins arising from a single fertilised egg that split into two embryos — genetically identical (~100% DNA shared). If MZ twins raised apart resemble each other, this implicates genetic influence. Used to establish upper bounds on heritability and to separate genetic from shared environmental effects.
- Dizygotic (DZ) twins
- Twins arising from two separately fertilised eggs — genetically similar to ordinary siblings (~50% DNA shared). The MZ–DZ comparison is the foundation of the classical twin method: traits more similar in MZ than DZ pairs imply genetic influence; similarity equal in both implicates shared environment.
- Concordance rate
- For categorical traits (disorders): the percentage of co-twins sharing a trait given that one twin (the proband) has it. Higher MZ than DZ concordance suggests genetic influence. Schizophrenia: MZ ~48%, DZ ~17%. Not 100% even for MZ twins, demonstrating environmental contribution.
- Shared environment (c²)
- Environmental factors that make family members similar to each other — shared home, parenting style, neighbourhood, school. Surprisingly, for most adult personality traits, c² is near zero: siblings reared together in the same family are nearly as different from each other as unrelated individuals.
- Non-shared environment (e²)
- Unique individual experiences that make family members different from each other — different friends, teachers, accidents, illnesses, birth-order effects. Includes measurement error. For most personality traits in adults, non-shared environment accounts for ~40–60% of variance along with genetic factors.
- Gene-environment correlation (rGE)
- The tendency for genetic predispositions to correlate with environmental exposures. Three types (Scarr & McCartney, 1983): passive (parents provide both genes and correlated environment), evocative (genotype elicits particular reactions from others), and active/niche-picking (individuals seek environments matching their genetic predispositions — increases with age).
- Gene-environment interaction (GxE)
- When the effect of a genotype on a phenotype depends on the environment, or vice versa. Neither genetics alone nor environment alone predicts the outcome — their combination does. Classic example: Caspi et al. (2002) MAOA × childhood maltreatment → antisocial behaviour; Caspi et al. (2003) 5-HTTLPR × life stress → depression.
- Diathesis-stress model
- A GxE model in which a pre-existing vulnerability (diathesis — genetic or biological) combines with environmental stress to produce disorder. Neither the diathesis alone nor the stress alone is typically sufficient. Predicts that genetically at-risk individuals will develop disorders only when exposed to sufficient environmental adversity.
- Differential susceptibility
- Belsky's extension of diathesis-stress: some genotypes confer heightened sensitivity to environmental quality in both directions — these individuals do worse in adverse environments AND better in supportive environments. The "orchid and dandelion" hypothesis: orchid children wilt under adversity but bloom spectacularly in nurturing conditions.