title: Lipid profiles reflecting high and low risk for coronary heart disease: contribution of apolipoprotein E polymorphism and lifestyle.
abstract: To elucidate the role of modifiable factors and the apolipoprotein E polymorphism in explaining lipid profiles reflecting low, average and high risk for coronary heart disease, we selected subjects from a large population-based study. Subjects with low total cholesterol (TC) (< 15th percentile) and high HDL-cholesterol levels (> 85th percentile) were randomly selected (n = 99) and represent subjects with a low risk lipid profile. Additionally, 95 subjects with total and HDL-cholesterol levels in the 15% around the population-median (median risk lipid profile) and 100 subjects with high TC (> 85th percentile) and low HDL-cholesterol levels (< 15th percentile) (high risk lipid profile) were selected. Compared with E3/3 subjects, the likelihood for a low risk lipid profile was considerably higher (odds ratio 14.3; 2.6-79) in female, but not in male E2-carriers (1.5; 0.3-6.7). Smoking and alcohol consumption were independently associated with a low risk lipid profile in both genders, physical inactivity only in women. The odds ratio for a high risk lipid profile was elevated in male E4-carriers (4.9; 1.1-23) only. In addition to the E4 isoform, smoking and physical inactivity, overweight was the main determinant for a high risk lipid profile (odds ratio 16.8; 3.4-82). Male overweight E4-carriers had a 50 times higher likelihood of a high risk lipid profile than E3/3 men of normal weight. In women, only overweight was independently associated with a high risk lipid profile. Our results suggest that both modifiable factors and the apolipoprotein E polymorphism contribute to a lipid profile, reflecting low, average and high risk for coronary heart disease, but effects may be gender-specific.
authors.affiliation: Department of Chronic Disease and Environmental Epidemiology, National Institute of Public Health and the Environment, Bilthoven, The Netherlands. JMA.Boer@rivm.nl
authors.forename: J M
authors.initials: JM
authors.lastname: Boer
authors.forename: E J
authors.initials: EJ
authors.lastname: Feskens
authors.forename: E G
authors.initials: EG
authors.lastname: Schouten
authors.forename: L M
authors.initials: LM
authors.lastname: Havekes
authors.forename: J C
authors.initials: JC
authors.lastname: Seidell
authors.forename: D
authors.initials: D
authors.lastname: Kromhout
mesh_terms: D000328:Adult; D000483:Alleles; D001057:Apolipoproteins E / Q000235:genetics*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000209:etiology* / Q000235:genetics; D005260:Female; D006801:Humans; D008019:Life Style; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D010641:Phenotype; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008055:Lipids; D002784:Cholesterol