AbstractsPsychology

Evidence suggests that early life stress increases risk for cardiovascular disease in adulthood. However, less is known about how early life experiences propagate risk into adulthood. The current study examines a potentially critical mediator of the relationship between early life stress and disease outcomes, namely poor sleep. Early life stress was hypothesized to contribute to poor sleep, as well as to other physiological health risk indicators (i.e., BP and BMI), by affecting adult psychosocial functioning. Further, poor sleep was examined as a mediator between adult psychosocial functioning and BP and BMI. An online sample and a university population sample completed measures of early life stress (i.e., a measure of childhood socioeconomic status and the risky family questionnaire), along with measures of adult psychosocial functioning and sleep quality. The university sample also participated in a 6-night actigraphy assessment to obtain objective sleep measurements. Results indicated that adult psychosocial functioning mediated the relationship between family risk in childhood and poorer subjective sleep quality for both sample populations. However, in the university sample, family risk also demonstrated a direct effect with respect to poorer subjective sleep quality, as well with respect to a latent factor reflecting physical restlessness and wakefulness during the sleep period. Family risk also demonstrated an indirect relationship with sleep length, largely via relationships with social support. Results did not suggest that family risk was associated with adult BP or BMI. However, in the university sample, social support, perceived stress, and negative affect were found to be significant predictors of BMI, and social support was found to be predictive of BP indices. Hypotheses examining sleep as a mediator of the relationship between psychosocial variables and BP and BMI were not well supported. Overall, results suggest that an adverse early childhood environment is a potentially important determinant of adult psychosocial and sleep functioning, which in turn may increase disease risk.