Social Science & Medicine

The impact of early childhood adversity on adult cognitive performance: The mediating roles of childhood cognitive ability and educational attainment

Study in peoplePopulations
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Abstract

Unraveling the complex mechanisms by which environmental exposures across the lifespan impact cognition are necessary to uncover pathways to successful aging. While it is known that greater childhood adversity is related to worse adult cognition, the specific pathways through which adversity influences distinct cognitive domains remain unresolved. This study examined the differential roles of childhood general cognitive ability (GCA) and educational attainment in mediating the impact of childhood adversity on adult cognitive performance. Data from the New England Family Study (N = 679), a longitudinal prenatal cohort, were utilized. Childhood adversity scores (birth to age 7) were constructed using prospective assessments of family dysfunction, social determinants of health, and parenting behaviors. Childhood GCA (age 7) was quantified based upon performance on the Wechsler Intelligence Scale for Children. Adult (Mean age = 33.5) measures of semantic memory, episodic memory, perceptual reasoning, and executive function/processing speed were derived using latent factor analysis. A survey-weighted structural equation model was employed to examine childhood GCA and educational attainment as serial mediators of adversity on adult cognition jointly across domains. Childhood GCA was a significant mediator of the relationship between adversity and adult cognition but mediated a greater proportion of the total adversity effect for perceptual reasoning than semantic memory. While educational attainment emerged as an additional mediator of adversity for each domain, pathways through education accounted for a greater proportion of the total indirect effect for executive function/processing speed than perceptual reasoning. These findings identify two early life pathways through which childhood adversity may impact risk for cognitive aging by influencing peak levels of cognition in adulthood.