The reason why this and other GWAS analyses of complex diseases and traits are unable to detect strong individual signals—and why there has been much concern about the “missing heritability” 39—is probably because the individual effects of common SNPs are too small to pass the stringent genome-wide significance level. This suggests that human intelligence and perhaps other complex traits are highly polygenic, and that very large sample sizes are required to detect such small individual effects, if the same experimental design is used which relies on LD between common SNPs and causal variants. These findings are consistent with the recently reported results for other complex traits, including schizophrenia33 and human height28. If genetic variation that is not captured through LD with common SNPs is due to rare variants with large effect sizes, then other experimental designs such as those employing exome or whole genome resequencing may facilitate the identification of genes and/or gene variants that are associated with human intelligence.
