ArticlePsychological medicine2026
The long reach of childhood income inequality: a multinational twin study of gene-environment interplay on adult depressive symptoms.
Article in Psychological medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundLiving in a country with a large gap between high and low earners has been linked to poor health, including depression. Less studied is gene-by-environment interplay with income inequality as the environmental exposure. Here, we examine the association between childhood exposure to inequality and individual differences in adult depressive symptoms, testing for moderation of genetic influences by inequality using polygenic indices for major depressive disorder, as well as twin models.
methodsThe research participants were 69,924 members of twin studies from four developed countries, born between 1893 and 1979, aged 22-103 years at depressive symptom assessment. Genotyping was available for 6,256 participants. Income inequality was operationalized as share of income accruing to the top 1% for each country when the participants were between age 5 and 15 years.
resultsChildhood income inequality was associated with depressive symptom scores in adulthood, adjusting for covariates. Each 1% rise in inequality was associated with 0.295 higher depressive symptoms (scaled on T-score units). In genetic analyses, interaction effects showed that men who faced more inequality as children and had higher genetic risk for depression reported modestly higher depressive symptoms compared to other men. For women, both genetic risk and inequality mattered, with each independently associated with depressive symptoms. Twin models showed that inequality moderated genetic variance underlying depressive symptoms; heritability of depressive symptoms was higher where exposure to income inequality was higher.
conclusionsFindings illustrate the long reach of childhood exposure to income inequality and suggest that advantaged environments may help protect against the effects of deleterious genes.
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