title: Lowering dietary saturated fat and total fat reduces the oxidative susceptibility of LDL in healthy men and women.
abstract: The present study examined the effects of reducing dietary total fat and saturated fat (SFA) on LDL oxidative susceptibility in 27 healthy men and women (age 24-65 y). Each subject consumed each of three diets for 8 wk: an average American diet (AAD, 34% energy from fat, 15% from SFA), a Step-1 diet (29% fat, 9% SFA) and a very low SFA diet (Low-Sat, 25% fat, 6% SFA). In vitro LDL oxidation was assessed by copper-mediated oxidation, as measured by the kinetics of conjugated diene formation and lipid peroxide formation. Compared with the AAD, plasma LDL-cholesterol (LDL-C) and HDL cholesterol levels were 8% lower (P: = 0.16 and P: = 0.11, respectively), in subjects when they consumed the Step-1 diet and 11% (P: < 0.03) and 14% (P: < 0.057) lower, respectively, when they consumed the Low-Sat diet. Conjugated diene production and oxidation rate were 7% (P: < 0. 05) and 9% (P: < 0.05) lower, respectively. The reduction of lipid peroxide formation was 9% (P: < 0.05) in subjects when they consumed the Low-Sat diet vs. the AAD. In addition, lipid peroxide and conjugated diene formation were positively correlated with plasma total and LDL-C and apolipoprotein B (apo B) levels (r = 0.5-0.6, P: < 0.001), suggesting that quantity of LDL is an important determinant of oxidative modification. Furthermore, at the same level of apo B or LDL-C, LDL from subjects when they consumed either Step-1 or Low-Sat diets was less susceptible (P: < 0.05) to oxidation than those when they consumed the AAD, suggesting that qualitative changes also affect LDL oxidative susceptibility. Therefore, the benefits of lowering dietary SFA may extend beyond decreasing LDL-C levels and include favorable qualitative changes in LDL that further decrease risk of coronary heart disease.
authors.affiliation: Graduate Program in Nutrition, Department of Dairy and Animal Science, The Pennsylvania State University, University Park, PA 16802, USA.
authors.forename: S
authors.initials: S
authors.lastname: Yu-Poth
authors.forename: T D
authors.initials: TD
authors.lastname: Etherton
authors.forename: C C
authors.initials: CC
authors.lastname: Reddy
authors.forename: T A
authors.initials: TA
authors.lastname: Pearson
authors.forename: R
authors.initials: R
authors.lastname: Reed
authors.forename: G
authors.initials: G
authors.lastname: Zhao
authors.forename: S
authors.initials: S
authors.lastname: Jonnalagadda
authors.forename: Y
authors.initials: Y
authors.lastname: Wan
authors.forename: P M
authors.initials: PM
authors.lastname: Kris-Etherton
mesh_terms: D000328:Adult; D000368:Aged; D001055:Apolipoproteins B / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D018592:Cross-Over Studies; D004041:Dietary Fats / Q000008:administration & dosage / Q000494:pharmacology*; D004311:Double-Blind Method; D005227:Fatty Acids / Q000008:administration & dosage / Q000494:pharmacology; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage / Q000494:pharmacology; D005260:Female; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects*; D008077:Lipoproteins, LDL / Q000097:blood / Q000378:metabolism*; D008297:Male; D008875:Middle Aged
chemical_list: D001055:Apolipoproteins B; D008078:Cholesterol, LDL; D004041:Dietary Fats; D005227:Fatty Acids; D005231:Fatty Acids, Unsaturated; D008077:Lipoproteins, LDL