title: Dietary alpha-linolenic acid reduces inflammatory and lipid cardiovascular risk factors in hypercholesterolemic men and women.
abstract: Alpha-linolenic acid (ALA) reduces cardiovascular disease (CVD) risk, possibly by favorably changing vascular inflammation and endothelial dysfunction. Inflammatory markers and lipids and lipoproteins were assessed in hypercholesterolemic subjects (n = 23) fed 2 diets low in saturated fat and cholesterol, and high in PUFA varying in ALA (ALA Diet) and linoleic acid (LA Diet) compared with an average American diet (AAD). The ALA Diet provided 17% energy from PUFA (10.5% LA; 6.5% ALA); the LA Diet provided 16.4% energy from PUFA (12.6% LA; 3.6% ALA); and the AAD provided 8.7% energy from PUFA (7.7% LA; 0.8% ALA). The ALA Diet decreased C-reactive protein (CRP, P < 0.01), whereas the LA Diet tended to decrease CRP (P = 0.08). Although the 2 high-PUFA diets similarly decreased intercellular cell adhesion molecule-1 vs. AAD (-19.1% by the ALA Diet, P < 0.01; -11.0% by the LA Diet, P < 0.01), the ALA Diet decreased vascular cell adhesion molecule-1 (VCAM-1, -15.6% vs. -3.1%, P < 0.01) and E-selectin (-14.6% vs. -8.1%, P < 0.01) more than the LA Diet. Changes in CRP and VCAM-1 were inversely associated with changes in serum eicosapentaenoic acid (EPA) (r = -0.496, P = 0.016; r = -0.418, P = 0.047), or EPA plus docosapentaenoic acid (r = -0.409, P = 0.053; r = -0.357, P = 0.091) after subjects consumed the ALA Diet. The 2 high-PUFA diets decreased serum total cholesterol, LDL cholesterol and triglycerides similarly (P < 0.05); the ALA Diet decreased HDL cholesterol and apolipoprotein AI compared with the AAD (P < 0.05). ALA appears to decrease CVD risk by inhibiting vascular inflammation and endothelial activation beyond its lipid-lowering effects.
authors.affiliation: Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA.
authors.forename: Guixiang
authors.initials: G
authors.lastname: Zhao
authors.forename: Terry D
authors.initials: TD
authors.lastname: Etherton
authors.forename: Keith R
authors.initials: KR
authors.lastname: Martin
authors.forename: Sheila G
authors.initials: SG
authors.lastname: West
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Gillies
authors.forename: Penny M
authors.initials: PM
authors.lastname: Kris-Etherton
mesh_terms: D000328:Adult; D000368:Aged; D016632:Apolipoprotein A-I / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000097:blood / Q000517:prevention & control*; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D008076:Cholesterol, HDL / Q000097:blood; D004032:Diet; D018752:Diet, Fat-Restricted; D004041:Dietary Fats / Q000008:administration & dosage; D019040:E-Selectin / Q000097:blood; D015118:Eicosapentaenoic Acid / Q000097:blood; D002149:Energy Intake; D015525:Fatty Acids, Omega-3 / Q000097:blood; D005231:Fatty Acids, Unsaturated / Q000097:blood; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications*; D007249:Inflammation / Q000517:prevention & control*; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D017962:alpha-Linolenic Acid / Q000008:administration & dosage*
chemical_list: D016632:Apolipoprotein A-I; D002791:Cholesterol, Dietary; D008076:Cholesterol, HDL; D004041:Dietary Fats; D019040:E-Selectin; D015525:Fatty Acids, Omega-3; D005231:Fatty Acids, Unsaturated; D008055:Lipids; D019010:Vascular Cell Adhesion Molecule-1; D017962:alpha-Linolenic Acid; D002097:C-Reactive Protein; D015118:Eicosapentaenoic Acid; C026219:docosapentaenoic acid