title: ApoE genotype does not predict lipid response to changes in dietary saturated fatty acids in a heterogeneous normolipidemic population. The DELTA Research Group. Dietary Effects on Lipoproteins and Thrombogenic Activity.
abstract: Recent studies have suggested that variations in apoE genotypes may influence the magnitude of plasma lipid changes in response to dietary interventions. We examined the ability of apoE genotype to predict plasma lipid response to reductions in percent of calories from total fat (TF) and saturated fat (SF) in a normolipidemic study population (n = 103) heterogeneous with respect to age, gender, race, and menopausal status. Three diets, an average American diet (34.3% TF, 15.0% SF), an AHA Step 1 diet (28.6% TF, 9.0% SF), and a low saturated fat (Low-Sat) diet (25.3% TF, 6.1% SF) were each fed for a period of 8 weeks in a three-way crossover design. Cholesterol was kept constant at 275 mg/d; monounsaturated and polyunsaturated fat were kept constant at approximately 13% and 6.5% of calories, respectively. Fasting lipid levels were measured during each of the final 4 weeks of each diet period. Participants were grouped by apoE genotype: E2 (E2/2, E2/3, E2/4); E3 (E3/3); E4 (E3/4, E4/4). Relative to the average American diet, both the Step 1 and Low-Sat diets significantly reduced total cholesterol, LDL cholesterol, and HDL cholesterol in all three apoE genotype groups. No evidence of a significant diet by genotype interaction, however, could be identified for any of the measured lipid and lipoprotein end points. Additional analysis of the data within individual population subgroup (men and women, blacks and whites) likewise provided no evidence of a significant diet by genotype interaction. Thus, in a heterogeneous, normolipidemic study population, apoE genotype does not predict the magnitude of lipid response to reductions in dietary saturated fat.
authors.affiliation: Pennington Biomedical Research Center, Baton Rouge, LA 70808-4124, USA. lefevrm@mhs.pbrc.edu
authors.forename: M
authors.initials: M
authors.lastname: Lefevre
authors.forename: H N
authors.initials: HN
authors.lastname: Ginsberg
authors.forename: P M
authors.initials: PM
authors.lastname: Kris-Etherton
authors.forename: P J
authors.initials: PJ
authors.lastname: Elmer
authors.forename: P W
authors.initials: PW
authors.lastname: Stewart
authors.forename: A
authors.initials: A
authors.lastname: Ershow
authors.forename: T A
authors.initials: TA
authors.lastname: Pearson
authors.forename: P S
authors.initials: PS
authors.lastname: Roheim
authors.forename: R
authors.initials: R
authors.lastname: Ramakrishnan
authors.forename: J
authors.initials: J
authors.lastname: Derr
authors.forename: D J
authors.initials: DJ
authors.lastname: Gordon
authors.forename: R
authors.initials: R
authors.lastname: Reed
mesh_terms: D000328:Adult; D000368:Aged; D001057:Apolipoproteins E / Q000235:genetics*; D015992:Body Mass Index; D002791:Cholesterol, Dietary / Q000494:pharmacology; D015331:Cohort Studies; D004032:Diet; D004040:Dietary Carbohydrates / Q000494:pharmacology; D004041:Dietary Fats / Q000494:pharmacology*; D002149:Energy Intake; D005227:Fatty Acids / Q000494:pharmacology*; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic
chemical_list: D001057:Apolipoproteins E; D002791:Cholesterol, Dietary; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D005227:Fatty Acids; D008055:Lipids