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. 2011 May;73(4):295-303.
doi: 10.1097/PSY.0b013e31821534f6. Epub 2011 May 2.

Emotional functioning at age 7 years is associated with C-reactive protein in middle adulthood

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Emotional functioning at age 7 years is associated with C-reactive protein in middle adulthood

Allison A Appleton et al. Psychosom Med. 2011 May.

Abstract

Objective: Few have considered whether and how child emotional functioning is associated with inflammation later in life. Therefore, we evaluated whether child emotional functioning at age 7 years is associated with C-reactive protein (CRP), an indicator of systemic inflammation, in middle adulthood.

Methods: We studied adult offspring (mean age 42.2 years) of participants in the National Collaborative Perinatal Project, a national cohort of pregnant women enrolled between 1959 and 1966. Three measures of child emotional functioning were derived from psychologist ratings of child behavior at age 7 years: inappropriate self-regulation (ISR), distress proneness, and behavioral inhibition. Multiple linear regression models were fit to investigate the association between childhood emotional functioning and adulthood CRP and also to evaluate potential mediators of this association. Model n's were from 400 for Model 1 to 379 for Model 4 depending on covariates included and missing data on those covariates.

Results: Children with high ISR and distress proneness at age 7 years had significantly higher CRP as adults (ISR: β = 0.86; standard error [SE] = 0.28; p = .002; distress proneness: β = 1.23; SE = 0.57; p = .03). In contrast, children with high levels of behavioral inhibition had lower CRP as adults (β = -0.58; SE = 0.38; p = .04). Furthermore, there was evidence that associations of ISR and distress proneness with CRP may be mediated in part by adulthood body mass index (Sobel significance tests of mediation: ISR: p = .003; distress proneness: p = .07).

Conclusions: Findings suggest that poor childhood emotional functioning is associated with inflammation in adulthood. These results suggest a potential childhood origin of adult inflammatory risk.

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