Cognitive Connie
Behavioural Genetics
Why do people differ so dramatically from one another — in personality, intelligence, mental health, and behaviour — even when raised in apparently similar environments? Behavioural genetics is the scientific discipline that attempts to answer this question by disentangling the contributions of genetic differences, shared family environment, and unique individual experience to individual variation.
Key figures
Francis Galton
Victorian polymath who pioneered the scientific study of individual differences and coined "nature vs nurture." Conducted early twin studies and proposed that eminent ability was heritable. His later advocacy of eugenics represents a historically important cautionary tale about misapplied genetics.
Thomas Bouchard
Psychologist at University of Minnesota who led the Minnesota Study of Twins Reared Apart (MISTRA) — the most extensive study of MZ twins raised in separate families. MISTRA data reported surprisingly high heritability for personality, IQ, occupational interests, and attitudes, substantially influencing the field.
Robert Plomin
Behavioural geneticist at King's College London and one of the field's most prolific researchers. Articulated the "non-shared environment paradox" — that siblings reared together are nearly as different as strangers for most personality traits. Pioneer in applying molecular genetics to behavioural phenotypes.
Sandra Scarr
Developmental behavioural geneticist who, with Kathleen McCartney, described the three types of gene-environment correlation (passive, evocative, active) and argued that genetic predispositions increasingly shape environments across development.
Avshalom Caspi
Personality and clinical psychologist (Duke University and King's College London) whose longitudinal Dunedin cohort studies produced landmark GxE findings: MAOA × maltreatment (2002) and 5-HTTLPR × stress (2003), demonstrating that genetic risk operates through environmental mediation.
Key concepts
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.
Test your knowledge
Frequently asked questions
Does high heritability mean a trait cannot be changed by intervention?+
No — this is one of the most common misunderstandings in behavioural genetics. High heritability estimates the sources of variation within a population under current environmental conditions; it says nothing about what would happen if environments changed dramatically. Height has heritability of ~80% in Western populations, yet average heights increased by ~10 cm across the 20th century due to improved nutrition and healthcare. Phenylketonuria (PKU) is essentially 100% heritable, yet is completely preventable by a dietary intervention (phenylalanine restriction). Reading disability is ~60–70% heritable, yet is highly responsive to intensive phonics instruction. Heritability and malleability are orthogonal.
What is the "missing heritability" problem in genomics?+
Twin studies suggest high heritability for many traits (IQ ~60–80%, height ~80%, schizophrenia ~80%). But genome-wide association studies (GWAS) — looking for individual gene variants associated with these traits — typically find many variants each with tiny effects that together explain only a fraction of the twin-estimated heritability. This gap is "missing heritability." Possible explanations include: rare variants not captured by standard GWAS arrays; gene-gene interactions (epistasis) not modelled; copy number variations; epigenetic effects not measured by standard genomics; and possibly twin-method heritability overestimation due to violated assumptions. Increasingly large GWAS (UK Biobank, hundreds of thousands of participants) are recovering more heritability through polygenic scores, but the gap has not fully closed.
How do behavioural geneticists control for gene-environment correlation in twin studies?+
Gene-environment correlation (rGE) is a significant challenge in twin methodology. If genetically similar twins also end up in more similar environments (because their genotype influences their environmental exposures — active rGE), this inflates heritability estimates. Twin researchers address this through: (1) Comparing MZ twins raised apart vs together — differences between these groups estimate the effect of shared environment independent of genetics. (2) Using measured environments as phenotypes and examining their heritability directly (showing that even environmental measures like "stressful life events" are partly heritable). (3) Multivariate genetic analyses that simultaneously model genetic and environmental paths. (4) Molecular genetic controls: comparing twin-method heritability to GWAS-based heritability (which does not assume random environmental distribution).
Sources
Last reviewed July 2025- 1.
Plomin, R., DeFries, J. C., Knopik, V. S., & Neiderhiser, J. M. (2016). Top 10 replicated findings from behavioral genetics. Perspectives on Psychological Science, 11(1), 3–23.
+About this source
Concise summary of the most robust and replicated findings across five decades of behavioural genetics research.
- 2.
Bouchard, T. J., & McGue, M. (1981). Familial studies of intelligence: A review. Science, 212(4498), 1055–1059.
+About this source
Classic review of IQ heritability across kinship pairs, establishing the ~50% heritability of intelligence.
- 3.
Caspi, A., McClay, J., Moffitt, T. E., Mill, J., Martin, J., Craig, I. W., … Poulton, R. (2002). Role of genotype in the cycle of violence in maltreated children. Science, 297(5582), 851–854.
+About this source
Landmark GxE study showing that MAOA genotype moderates the effect of childhood maltreatment on antisocial behaviour.