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American Journal of Epidemiology Vol. 150, No. 9: 910-918
Copyright © 1999 by The Johns Hopkins University School of Hygiene and Public Health
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Effects of Similarities in Lifestyle Habits on Familial Aggregation of High Density Lipoprotein and Low Density Lipoprotein Cholesterol: The NHLBI Family Heart Study
1Section of Preventive Medicine and Epidemiology, Evans Department of Medicine, Boston University School of Medicine Boston, MA
2Division of Epidemiology and Clinical Applications, National Heart, Lung, and Blood Institute Bethesda, MD
3Cardiovascular Genetics Research Clinic, Department of Internal Medicine, University of Utah School of Medicine Salt Lake City, UT
4Division of Biostatistics, Washington University School of Medicine St. Louis, MO
5Deceased
It is generally assumed that familial aggregation of lipids relates to both genetic and shared environmental factors. To determine the degree to which familial similarities in lifestyle habits explain familial aggregation of high density lipoprotein (HDL) and low density lipoprotein (LDL) cholesterol, the authors analyzed 1994–1996 data from 2,284 US adult participants in the National Heart, Lung, and Blood Institute Family Heart Study. For men and women, respectively, HDL cholesterol correlated with alcohol consumption (r= 0.27, p < 0.001; r = 0.21, p < 0.001), exercise (r = 0.06, p = 0.05; r = 0.10, p = 0.002), and smoking (r = –0.09, p = 0.005; r = –0.13, p < 0.001). There was strong familial aggregation of HDL cholesterol (parent-child, r = 0.32; sibling-sibling, r = 0.29), but less than 10% was explained by lifestyle habits. For LDL cholesterol, weak correlations were found for intake of total fat (r = 0.06, p = 0.07) and fruits/vegetables (r = –0.09, p = 0.005) among men and for smoking (r = 0.10, p = 0.002) among women. LDL cholesterol correlated strongly among family members (parent-child, r = 0.24; sibling-sibling, r = 0.31), but essentially none of this aggregation related to the lifestyle factors studied. This study suggests that lifestyle factors have little effect on the familial aggregation of HDL and LDL cholesterol. Am J Epidemiol 1999;150:910-18.
cholesterol; coronary disease; genetics; medical; risk factors
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