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Childhood Family Psychosocial Environment and Coronary Heart Disease Risk

Loucks, Eric B. PhD; Almeida, Nisha D. MSc; Taylor, Shelley E. PhD; Matthews, Karen A. PhD

doi: 10.1097/PSY.0b013e318228c820
Original Articles
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Objective: Little is known about whether the childhood family psychosocial environment affects coronary heart disease (CHD). Study objectives were to evaluate associations of childhood family psychosocial environment (termed "risky families"; characterized by cold, unaffectionate interactions, conflict, aggression, neglect, and/or low nurturance) with calculated risk for CHD.

Methods: Study participants included 3554 participants of the Coronary Artery Risk Development in Young Adults Study, aged 33 to 45 years. Childhood family psychosocial environment was measured using a risky family questionnaire via self-report. Ten-year CHD risk was calculated using the validated Framingham risk algorithm.

Results: In a multivariable-adjusted regression analysis adjusted for age, race/ethnicity, and childhood socioeconomic position, a 1-unit (range, 0-21) increase in risky family score was associated with 1.0% (95% confidence interval = 0.4%-1.7%) and 1.0% (95% confidence interval = 0.2%-1.8%) higher CHD risk in women and men, respectively. Multiple mediation analyses suggested significant indirect effects of education, income, depressive symptomatology, and anger-out expression in women and education in men, indicating that these may be mediating mechanisms between childhood psychosocial environment and CHD risk. Of the modifiable Framingham algorithm components, smoking (in women and men) and high-density lipoprotein (in women) were the factors most strongly associated with risky family score.

Conclusions: Childhood family psychosocial environment was positively associated with the calculated 10-year CHD risk. Mechanisms may include the potential negative impact of childhood family psychosocial environment on later-life socioeconomic position (e.g., education in men and women) and/or psychosocial functioning (e.g., depression and anger-out expression in women), which may in turn lead to higher CHD risk, particularly through smoking (in men and women) and low level of high-density lipoprotein cholesterol (in women).

CHD = coronary heart disease; SEP = socioeconomic position; CARDIA = Coronary Artery Risk Development in Young Adults; HDL = high-density lipoprotein; CES-D = Center for Epidemiologic Studies Depression scale; CV = Coefficient of variation

From the Department of Community Health (E.B.L.), Center for Population Health and Clinical Epidemiology, and Department of Epidemiology (N.D.A.), Biostatistics and Occupational Health, McGill University, Montreal, Canada; Department of Psychology (S.E.T.), University of California, Los Angeles, California; and Departments of Psychiatry, Psychology, and Epidemiology (K.A.M.), University of Pittsburgh, Pittsburgh, Pennsylvania.

Address correspondence and reprint requests to Eric B. Loucks, PhD, Department of Community Health, Center for Population Health and Clinical Epidemiology, Brown University, 121 S Main St, Providence, RI 02906. E-mail: eric.loucks@brown.edu

This work was performed without financial support from a funding agency.

The views and interpretations expressed in this article do not necessarily reflect the views of the National Heart, Lung, and Blood Institute.

Received for publication September 8, 2010; revision received May 30, 2011.

Copyright © 2011 by American Psychosomatic Society
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