FIGURE 2.

Gene–environment interactions and health. Graphically depicted are the results of the study by Cole and colleagues⁵³, who found that a single nucleotide polymorphism in the human IL6 promoter alters the likelihood of threat-activated GATA1 transcription factors to bind to DNA to stimulate IL6 transcription. Individuals homozygous for the GATA1-sensitive G allele have high binding affinity, which enables stress-induced GATA1 activity to upregulate IL6 gene expression, leading to greater inflammatory activity, a higher likelihood of developing diseases of aging, and elevated mortality risk in the context of social adversity. In contrast, those with the C allele at this locus have low binding affinity for GATA1, meaning that the biochemical social adversity signals do not efficiently stimulate IL6 gene expression. As such, C allele carriers at this locus experience standard levels of inflammation, prevalence of diseases of aging, and mortality risk under both socially favorable and socially adverse conditions.