title: Childhood family psychosocial environment and coronary heart disease risk.
abstract: 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).
authors.affiliation: Departmentof Community Health, Center for Population Health and ClinicalEpidemiology, Brown University, 121 S Main St, Providence, RI 02906, USA. eric.loucks@brown.edu
authors.forename: Eric B
authors.initials: EB
authors.lastname: Loucks
authors.forename: Nisha D
authors.initials: ND
authors.lastname: Almeida
authors.forename: Shelley E
authors.initials: SE
authors.lastname: Taylor
authors.forename: Karen A
authors.initials: KA
authors.lastname: Matthews
mesh_terms: D000328:Adult; D002648:Child; D003327:Coronary Disease / Q000209:etiology* / Q000523:psychology; D004522:Educational Status; D005190:Family / Q000523:psychology*; D005260:Female; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D011584:Psychology; D012044:Regression Analysis; D012307:Risk Factors; D012737:Sex Factors; D012959:Socioeconomic Factors; D011795:Surveys and Questionnaires; D014481:United States