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-Tierney, Donna K. Arnett, Kari E. North, James S. Pankow, Steven C. Hunt, R. Curtis Ellison, J. Michael Gaziano, Luc Djoussé

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Background: We sought to examine whether 4 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 4 carrier status available. We used generalized estimating equations to examine the interaction between BMI and 4 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. Results: 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 4 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 4 allele (p-value for trend < 0.0001). There was no evidence for an interaction between BMI and 4 status on HDL(p-value 0.39). Conclusion: Our findings do not support an interaction between 4 allele status and BMI on HDL.

Original languageEnglish (US)
Article number167
JournalLipids in Health and Disease
Volume10
DOIs
StatePublished - 2011

Bibliographical note

Funding Information:
The NHLBI FHS is a multicenter, population-based study that includes probands recruited from three parent studies: the Framingham Heart Study (Framingham, MA), the Atherosclerosis Risk in Communities Study (Forsythe County, NC and Minneapolis, MN), and the Utah Family Health Tree (Salt Lake City, UT). Between 1993 and 1995, 2,000 randomly selected participants and 2,000 with family histories of CHD enrolled in the 3 parent studies were mailed invitations to provide information regarding the health of themselves, their parents, their children, and their siblings. Of these, 3,150 returned responses, and family members of these responders were contacted. From the 22,908 persons who provided information, 588 families were randomly selected and an additional 657 with high family risk scores were also selected. Family risk score was calculated by comparing the actual incidence of CHD to the age-and sex-adjusted expected incidence of CHD within a family. Enrollees underwent study examinations during which height, weight and blood pressure were documented, and 12-hour fasting blood samples were taken on which lipids and other parameters were measured, and from which DNA was stored. Genotyping for the APOE allele was performed on a selection of FHS participants. More detailed description of the methods of the NHLBI FHS have been described previously [17]. The FHS is supported by the National Heart, Lung, and Blood Institute (NHLBI) (grant numbers U01 HL56563, U01 HL56564, U01

Funding Information:
The FHS is supported by the National Heart, Lung, and Blood Institute (NHLBI) (grant numbers U01 HL56563, U01 HL56564, U01 HL56565, U01

Keywords

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

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