title: Niacin administration significantly reduces oxidative stress in patients with hypercholesterolemia and low levels of high-density lipoprotein cholesterol.
abstract: Oxidative stress has been implicated in the pathogenesis of cardiovascular disorders, including atherosclerosis. In pharmacological doses, niacin (vitamin B3) was proven to reduce total cholesterol, triglyceride, very-low-density lipoprotein, and low-density lipoprotein levels, and to increase high-density lipoprotein (HDL) levels. The aim of this study was to evaluate the effect of niacin treatment in patients with low levels of HDL cholesterol (HDL-C; <40 mg%) on their lipid profile and oxidative stress status. Seventeen patients with hypercholesterolemia and low HDL-C and 8 healthy control subjects were enrolled in the study. The patients were treated with niacin for 12 weeks. Lipid profile, oxidative stress and C-reactive protein (CRP) levels were determined at the time of enrollment, and 2 and 12 weeks after initiation of niacin treatment. Subjects with lower HDL-C levels exhibited higher oxidative stress compared with subjects with normal HDL-C levels. Niacin treatment in hypercholesterolemic patients caused a significant increase in HDL-C and apolipoprotein A1 levels, and a decrease in triglyceride levels. Niacin also significantly reduced oxidative stress, as measured by a significant decrease in the serum content of thiobarbituric acid reactive substances, lipid peroxides and paraoxonase activity, compared with the levels before treatment. Although serum CRP levels were not affected by niacin treatment, a correlation between CRP and HDL levels was obtained when computing the results. Niacin treatment in hypercholesterolemic patients with low HDL levels caused a significant decrease in their oxidative stress status. These results indicate an additional beneficial effect of niacin beyond its ability to affect the lipid profile.
authors.affiliation: Internal Medicine E Department, Rappaport Family Institute for Research in the Medical Sciences, Rambam Medical Center, Haifa, Israel. s_hamoud@rambam.health.gov.il
authors.forename: Shadi
authors.initials: S
authors.lastname: Hamoud
authors.forename: Marielle
authors.initials: M
authors.lastname: Kaplan
authors.forename: Edna
authors.initials: E
authors.lastname: Meilin
authors.forename: Ahmad
authors.initials: A
authors.lastname: Hassan
authors.forename: Rafael
authors.initials: R
authors.lastname: Torgovicky
authors.forename: Raanan
authors.initials: R
authors.lastname: Cohen
authors.forename: Tony
authors.initials: T
authors.lastname: Hayek
mesh_terms: D016632:Apolipoprotein A-I / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood*; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood* / Q000188:drug therapy; D000960:Hypolipidemic Agents / Q000008:administration & dosage*; D008054:Lipid Peroxides / Q000097:blood; D008297:Male; D008875:Middle Aged; D009525:Niacin / Q000008:administration & dosage*; D018384:Oxidative Stress / Q000187:drug effects*; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis / Q000378:metabolism; D014280:Triglycerides / Q000097:blood
chemical_list: C505693:APOA1 protein, human; D016632:Apolipoprotein A-I; D008076:Cholesterol, HDL; D000960:Hypolipidemic Agents; D008054:Lipid Peroxides; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; D009525:Niacin; D002097:C-Reactive Protein