Péter Przemyslaw Ujma, Kristof Kovacs
J. Intell. 2020, 8(3), 27; https://doi.org/10.3390/jintelligence8030027
(This article belongs to the Special Issue Discussing the Mitochondrial Functioning Theory of General Intelligence)
In two recent reviews (Geary 2018, 2019), Geary attributed a substantial role in generating individual differences in the general factor of intelligence, g, to mitochondrial functioning. While understanding the appeal of reducing a complex psychological phenomenon to an elementary biological cause and providing a new lease to Spearman’s theory of g as mental energy, we find the evidence supporting the theory to be rough-and-ready, indirect, or even contradictory. In particular, the theory lacks specificity in describing the causal path from mitochondria to g in two respects: (1) it would imply that genetic effects on g would exert their effect on mitochondria, which is at odds with current genetic evidence; (2) if g reflects variation in mitochondrial functioning and thus differences in g loadings necessarily indicate differences in the extent to which performance on a test depends on mitochondrial functioning, then the theory fails to account for why the effect of mitochondrial functioning on performance is greater in tests that have higher across-domain correlations.
First, the theory is contradicted by genetic studies of g. Cognitive ability is strongly heritable: based on quantitative genetic studies, in childhood around 50%, and in adulthood up to 80% of individual differences in cognitive ability or IQ scores can be ascribed to genetic differences (Plomin and Deary 2015; Polderman et al. 2015). Most studies use simple sum scores or first unrotated principal components of multiple cognitive tests as the dependent variable in quantitative genetic studies. However, when cognitive ability is decomposed to its hierarchical factor structure, g usually turns out to be even more heritable, while in less general abilities, genetic factors play a progressively weaker and environmental variables a progressively stronger role (Shikishima et al. 2009; Panizzon et al. 2014).
Quantitative genetic studies remain agnostic about the nature of the genetic determinants of a trait. However, recent large-scale genome-wide association studies (GWASs) revealed a large number of single nucleotide polymorphisms (SNPs) associated with cognitive ability (Lam et al. 2017; Savage et al. 2017; Trampush et al. 2017; Zabaneh et al. 2017; Davies et al. 2018; Hill et al. 2018). Even larger studies investigating the genetic correlates of educational attainment (Rietveld et al. 2013; Okbay et al. 2016; Lee et al. 2018) also found genetic variants which predicted cognitive ability. GWAS-derived polygenic scores currently predict up to 10% of cognitive performance (Lee et al. 2018; Allegrini et al. 2019). Within-family studies indicate that this effect size may be inflated due to population stratification, but a substantial proportion is still retained (Selzam et al. 2019). The functional interpretation of these genetic variants is not simple, because (1) many SNP hits are in intergenic regions with an unknown function, and (2) SNP hits are not necessarily causal for g; it is very likely that they are merely in linkage disequilibrium with truly functional variants in neighboring genomic regions. Still, multiple attempts have been made to at least approximately interpret the biological function of g-associated SNPs. These studies have unequivocally shown that g-associated genetic variants are primarily expressed in the brain, in specific brain regions and specific cell types, and they are implicated in very specific cellular functions, none of which concern mitochondria (Lam et al. 2017; Sniekers et al. 2017; Davies et al. 2018; Hill et al. 2018; Lee et al. 2018; Savage et al. 2018; Coleman et al. 2019). (…)