Open Access Open Badges Research

Apolipoprotein ε4 polymorphism does not modify the association between body mass index and high-density lipoprotein cholesterol: a cross-sectional cohort study

Catherine R Rahilly-Tierney134*, Donna K Arnett5, Kari E North6, James S Pankow7, Steven C Hunt8, R Curtis Ellison9, J Michael Gaziano1234 and Luc Djoussé1234

Author Affiliations

1 Massachusetts Veterans Epidemiology and Information Research Center (MAVERIC), Boston VA Healthcare, Boston, Massachusetts, USA

2 Geriatric Research Education and Clinical Centers (GRECC), Boston VA Healthcare, Boston, Massachusetts, USA

3 Division of Aging, Brigham & Women's Hospital, Boston, Massachusetts, USA

4 Harvard Medical School, Boston, Massachusetts, USA

5 Department of Epidemiology, University of Alabama at Birmingham School of Public Health, Birmingham, Alabama, USA

6 Carolina Center for Genome Science, University of North Carolina Gillings School of Global Public Heatlh, Chapel Hill, North Carolina, USA

7 Division of Epidemiology & Community Health, University of Minnesota School of Public Health, Minneapolis, Minnesota, USA

8 Cardiovascular Genetics Division, University of Utah, Salt Lake City, Utah, USA

9 Section of Preventive Medicine & Epidemiology, Boston University School of Medicine, Boston, Massachusetts, USA

For all author emails, please log on.

Lipids in Health and Disease 2011, 10:167  doi:10.1186/1476-511X-10-167

Published: 23 September 2011



We sought to examine whether ε4 carrier status modifies the relation between body mass index (BMI) and HDL. The National Heart, Lung, and Blood Institute Family Heart Study included 657 families with high family risk scores for coronary heart disease and 588 randomly selected families of probands in the Framingham, Atherosclerosis Risk in Communities, and Utah Family Health Tree studies. We selected 1402 subjects who had ε4 carrier status available. We used generalized estimating equations to examine the interaction between BMI and ε4 allele carrier status on HDL after adjusting for age, gender, smoking, alcohol intake, mono- and poly-unsaturated fat intake, exercise, comorbidities, LDL, and family cluster.


The mean (standard deviation) age of included subjects was 56.4(11.0) years and 47% were male. Adjusted means of HDL for normal, overweight, and obese BMI categories were 51.2(± 0.97), 45.0(± 0.75), and 41.6(± 0.93), respectively, among 397 ε4 carriers (p for trend < 0.0001) and 53.6(± 0.62), 51.3(± 0.49), and 45.0(± 0.62), respectively, among 1005 non-carriers of the ε4 allele (p-value for trend < 0.0001). There was no evidence for an interaction between BMI and ε4 status on HDL(p-value 0.39).


Our findings do not support an interaction between ε4 allele status and BMI on HDL.

HDL cholesterol; body mass index; genetic epidemiology; apolipoproteins; lipid metabolism; adiposity