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| Formato: | Artículo Open Access |
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Wiley
2025
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| Acceso en línea: | https://acamh.onlinelibrary.wiley.com/doi/10.1111/jcpp.70022 |
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- Parental income and psychiatric disorders from age 10 to 40: a genetically informative population study Hans Fredrik Sunde Espen Moen Eilertsen Jonas Minet Kinge Thomas H. Kleppesto Magnus Nordmo Avshalom Caspi Terrie E. Moffitt Fartein Ask Torvik Journal of Child Psychology and Psychiatry Background Lower parental income is associated with more psychiatric disorders among offspring, but it is unclear if this association reflects effects of parental income (social causation) or shared risk factors (social selection). Prior research finds contradictory results, which may be due to age differences between the studied offspring. Methods Here, we studied psychiatric disorders in the entire Norwegian population aged 10 to 40 years between 2006 and 2018 ( N = 2,468,503). By linking tax registries to administrative health registries, we described prevalence rates by age, sex, and parental income rank. Next, we grouped observations into age groups (adolescence, ages 10–20 years; early adulthood, 21–30 years; adulthood, 30–40 years) and applied kinship‐based models with extended families of twins and siblings to decompose the parent–offspring correlation into phenotypic transmission, passive genetic transmission, and passive environmental transmission. Results We found that lower parental income rank was associated with higher prevalence of nearly all psychiatric disorders, except for eating disorders, for both men and women at all ages from 10 to 40 years. Comparing the top with the bottom paternal income quartile, the prevalence ratio of any psychiatric disorder was 0.47 among 10‐year‐olds and decreased to 0.72 among 40‐year‐olds. The parent–offspring correlation was −.15 in adolescence, −.10 in early adulthood, and −.06 in adulthood. The kinship‐based models indicated that phenotypic transmission could account for 39% of the parent–offspring correlation among adolescents ( p < .001), but with no significant contribution in early adulthood ( p = .181) or adulthood ( p = .737). Passive genetic and environmental transmission contributed to the parent–offspring correlation in all age groups (all p 's < .001). Conclusions Our findings are consistent with a significant role of social causation during adolescence, while social selection could fully explain the parent–offspring correlation in adulthood. 10.1111/jcpp.70022 http://onlinelibrary.wiley.com/termsAndConditions#vor