The association between childhood emotional functioning and adulthood inflammation is modified by early-life socioeconomic status.

OBJECTIVE

Identifying interrelationships among childhood social disadvantage, emotional functioning and adult health may help illustrate how health disparities may become embedded early in life, yet few have considered how these factors are associated. We examined whether the association of child emotional functioning and adult health risk was modified by child socioeconomic status (CSES), or whether child emotional functioning mediated the association of CSES and adult health risk.

METHOD

We studied 430 adult offspring (mean age 42 years) of Collaborative Perinatal Project participants, a cohort of pregnant women enrolled in 1959-1966 (Broman, Nichols, & Kennedy, 1975; Niswander & Gordon, 1972). Child emotional functioning was assessed by psychologist ratings at age 7 and included inappropriate self regulation (ISR) and distress proneness. CSES measures included parental education, household income, and parental occupation. Adult health risk was measured by the inflammatory marker C-reactive protein (CRP). Hypotheses were tested with multiple linear regression. Effect modification was evaluated via interaction terms and stratification of fully adjusted models by CSES. Mediation by child emotional functioning was evaluated via coefficient changes.

RESULTS

There was no evidence that child emotional functioning mediated the association of CSES and CRP. Significant interactions were observed for ISR and low income (b = 1.67, SE = 0.70, p < .05), and distress proneness and low (b = 3.14, SE = 1.47, p < .05) and middle (b = 3.52, SE = 1.46, p < .05) income. Stratified models indicated that associations of child emotion with CRP varied significantly by level of parental education, household income and occupation.

CONCLUSION

The highest levels of adult inflammation were observed among those with childhood emotional problems who were also exposed to low socioeconomic status as children. This study suggests adulthood disparities in CRP may have developmental origins in childhood adversity.