Heritability of Cognitive Ability - Findings from Twin Studies
Behavioral genetics twin studies estimate genetic contributions to individual differences in cognitive ability. Comparing similarity between monozygotic twins (100% shared genes) and dizygotic twins (50% shared genes) yields heritability estimates. General intelligence (g factor) heritability is estimated at approximately 0.60-0.80 in adults. Individual differences in reaction time and working memory capacity are also thought to have a genetic component. However, heritability is not 'the proportion of an individual's ability determined by genes' but 'the proportion of individual differences in a population explained by genetic differences.' This distinction is crucial. Heritability of 0.60 does not mean '60% of your reaction speed is genetically determined' but rather '60% of differences in people's reaction speeds are attributable to genetic differences.' At the individual level, there is room for change through the environment.
Gene Groups Involved in Processing Speed
Cognitive ability is a polygenic trait where thousands of genes have tiny effects, not a single-gene determination. GWAS (Genome-Wide Association Studies) have identified hundreds of loci associated with cognitive ability, but individual effect sizes are extremely small. For processing speed, genes involved in myelination (MBP, PLP1, etc.) are notable. Myelin sheath thickness and uniformity influence nerve conduction velocity, which is thought to partially explain individual differences in processing speed. Additionally, dopamine system genes (COMT, DRD2) affect prefrontal cortex functional efficiency, contributing to working memory and executive function individual differences. The COMT Val158Met polymorphism shows Val/Val types having faster dopamine degradation (thought to give higher flexibility but lower stability) and Met/Met types having slower degradation (thought to give higher stability but vulnerability to anxiety); the stability-flexibility contrast comes from a 2004 hypothesis by Bilder et al.
Age-Dependent Heritability and the Wilson Effect
Cognitive ability heritability increases with age, a counterintuitive phenomenon. In twin data analyzed by Haworth et al. (2010), heritability rose from 0.41 at age 9 to 0.66 at age 17, and Bouchard (2013) reports that it levels off at about 0.80 around ages 18-20. Called the 'Wilson Effect,' this is interpreted as individuals increasingly selecting environments matching their genetic predispositions with age (active gene-environment correlation). Children with genetic predisposition for fast reactions are drawn to games and sports, which further train reaction speed. Conversely, genetically slower children avoid such activities, reducing training opportunities. Consequently, genetic differences can be amplified through environmental selection. This finding does not mean 'give up if genetically disadvantaged.' Rather, it suggests that intentionally placing oneself in training environments can break the negative spiral of gene-environment correlation.
Genetic Limits and the Boundary of Trainability
Genetics sets a 'ceiling,' but many people likely haven't reached it. The physiological lower limit of reaction time is thought to be approximately 100ms (physical minimum for nerve conduction and muscle contraction), but the general population averages longer, with room to shorten it through training. Thus, large room for training improvement exists before reaching genetic ceilings. At elite athlete or professional gamer levels, genetic predisposition is thought to become prominent, but in typical performance improvement contexts, training volume and quality are also likely to matter a great deal. Even low initial scores can improve with appropriate training. Initial scores reflect 'current state' only, not 'genetic limits.'
Epigenetics and Environmental Regulation of Gene Expression
Genes are not fixed blueprints but have expression regulated by environment. Epigenetics (DNA methylation, histone modification) changes gene activity without altering DNA sequence. Exercise promotes demethylation of the BDNF gene promoter region, increasing BDNF expression. Adequate sleep maintains synaptic plasticity gene expression; sleep deprivation suppresses these genes. Chronic stress methylates hippocampal glucocorticoid receptor genes, altering stress response sensitivity. Thus, lifestyle habits change how genes are 'read,' regulating cognitive ability expression levels. Even with identical genes, those who exercise, sleep adequately, and manage stress tend to express higher cognitive ability than those who don't. MyRank scores measure phenotype (gene × environment result), not genotype, and phenotype can improve as the environment is adjusted.