The impact of adult SEP on later life ability may be exaggerated when not accounting for the stability of individual differences in cognitive ability and measurement error in test scores.
BackgroundThe mechanisms underlying the association of parental socioeconomic position with later life allostatic load remain unclear. The present study aims to examine potential pathways underlying this association: personality, social relations, intelligence and education.MethodsThe study comprised 361 members of the Copenhagen Perinatal Cohort who participated in two subsequent follow-ups: the Prenatal Development Project (mean age 27 years) and the Copenhagen Aging and Midlife Biobank study (mean age 50 years). Allostatic load was based on 14 biomarkers representing the inflammatory, metabolic and cardiovascular system measured at midlife. Information on potential mediators was collected in young adulthood, and their role in the association of parental socioeconomic position with midlife allostatic load were examined in linear regression path analyses.ResultsParental socioeconomic position at one year was inversely associated with midlife allostatic load (β = − 0.238, p < .001). No mediation effects were found for personality or social relations. In a model including intelligence and education, a significant indirect effect was found for education (β = − 0.151, p < .001). A significant direct effect remained (β = − 0.111, p = .040).ConclusionsParental socioeconomic position was inversely associated with allostatic load in midlife. Results suggest that part of this association was mediated by education. A better understanding of the non-cognitive pathways related to education is an important prerequisite for the development of effective intervention strategies.Electronic supplementary materialThe online version of this article (10.1186/s12889-018-5956-x) contains supplementary material, which is available to authorized users.
Objective: The aim was to estimate the effects of ponderal index at birth and body mass index (BMI) in early adulthood on C-reactive protein (CRP) and interleukin-6 (IL-6) and to quantify the effects through subsequent measures of body size. In a subanalysis, the contributions of maternal BMI to the inflammatory status of offspring were investigated. Methods: The study was based on 2,986 Danish males from the Copenhagen Aging and Midlife Biobank. Path analysis was employed to estimate direct and indirect effects. Results: A 10% higher maternal BMI was associated with 7% higher CRP and 3% higher IL-6 among offspring. A 10% higher ponderal index at birth was associated with 4% lower CRP in late midlife; this effect was only partially mediated by later growth. A 10% higher BMI in early adulthood was associated with 8% higher CRP and 4% higher IL-6 in late midlife. The findings suggest that weight gain in adulthood is associated with low-grade inflammation in late midlife. Conclusions: Ponderal index at birth is associated with CRP in later life independently of adult BMI. The findings additionally suggest that preventing weight gain in early adulthood would be beneficial for inflammatory status in later life.
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