Abstract

Greater psychosocial risk in childhood and adolescence predicts poorer cardiometabolic outcomes in adulthood. We assessed whether the timing of psychosocial risk from infancy through adolescence predicts cardiometabolic outcomes in young adulthood. Young adults and their mothers participated in a longitudinal study beginning in infancy in Santiago, Chile (N = 1040). At infancy, 5 years, 10 years, and adolescence, mothers reported on depressive symptoms, stressful experiences, support for child development in the home, father absence, parental education, and socioeconomic status (SES) to create a psychosocial risk composite at each time point. Young adults (52.1% female; 21-27 years) provided fasting serum samples and participated in anthropometric and blood pressure (BP) assessments, including a dual-energy X-ray absorptiometry (DXA) scan for measuring body fat. Greater infant psychosocial risk was associated with a greater young adult metabolic syndrome score (β = 0.07, 95% confidence intervals (CI): 0.01 to 0.13, p = 0.02), a higher body mass index and waist circumference composite (β = 0.08, 95% CI: 0.03 to 0.13, p = 0.002), and a higher body fat (DXA) composite (β = 0.07, 95% CI: 0.01 to 0.12, p = 0.02). No psychosocial risk measure from any time point was associated with BP. Infant psychosocial risk predicted cardiometabolic outcomes in young adulthood better than psychosocial risk at 5 years, 10 years, or adolescence, mean of psychosocial risk from infancy through adolescence, and maximum of psychosocial risk at any one time. Consistent with the Developmental Origins of Health and Disease model, findings suggest that infancy is a sensitive period for psychosocial risk leading to poorer cardiometabolic outcomes in young adulthood.

Highlights

  • Greater psychosocial risk in childhood and adolescence predicts poorer cardiometabolic outcomes in adulthood

  • Greater infant psychosocial risk was associated with a higher body mass index (BMI) and waist circumference composite (β = 0.08, 95% confidence intervals (CI): 0.03 to 0.13, p = 0.002) and higher body fat (DXA) composite (β = 0.07, 95% CI: 0.01 to 0.12, p = 0.023) (Table 3)

  • Infant psychosocial risk was not associated with the blood pressure (BP) composite, and this path was excluded from the final model

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Summary

Introduction

Greater psychosocial risk in childhood and adolescence predicts poorer cardiometabolic outcomes in adulthood. Another study found that psychosocial stressors before age 12 years were correlated with elevated chronic disease risk in adulthood (Slopen, Non, Williams, Roberts, & Albert, 2014) These prospective studies suggest that experiencing high psychosocial risk before age 12 years may be associated with poor adult cardiometabolic outcomes. These effects may be partially mediated through early life programming of the sympathetic nervous system, hypothalamic–pituitary–adrenal (HPA) axis, immune system, and epigenetics, as well as through changes in behavior (Nusslock & Miller, 2016; Reynolds, 2013; Suglia et al, 2020)

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