title: Vitamin E dietary supplementation significantly affects multiple risk factors for cardiovascular disease in baboons.
abstract: BACKGROUND
  Oxidative stress is a widely accepted risk factor for cardiovascular disease (CVD), but the CVD benefit of dietary antioxidants, such as vitamin E, is controversial.
  
  
  OBJECTIVE
  Therefore, we have investigated, in the baboon model, the effects of dietary vitamin E supplementation on risk factors for CVD.
  
  
  METHODS
  Pedigreed baboons (n = 251) were fed 2 atherogenic diets, high in fat and cholesterol, that differed in vitamin E concentrations. After 7 wk on each diet, blood samples were taken, and a panel of CVD risk factor traits (ie, indicators of lipoprotein metabolism and oxidative stress) were measured.
  
  
  RESULTS
  Vitamin E supplementation caused significantly higher total antioxidant status (TAS) and lower oxidized LDL as expected. In addition, vitamin E caused 2 paradoxical effects on HDL metabolism: higher apolipoprotein A-I (apo A-I) concentrations and lower HDL sizes. We calculated a difference (Delta) variable for each trait as the value on the high-vitamin E diet minus that on the low-vitamin E diet and determined that several HDL concentration Delta variables were significantly correlated with Delta TAS, but only one, Delta apo A-I, was independently correlated. Genetic analyses showed that 2 Delta variables, Delta paraoxonase and Delta HDL(2), were significantly heritable, but that neither Delta TAS nor Delta apo A-I were heritable.
  
  
  CONCLUSIONS
  Thus, our data show that dietary vitamin E improves TAS and LDL quality. They also show 2 apparently paradoxical effects on HDL metabolism: lower HDL(2), which is mediated by genes, and higher apo A-I, which is not. These effects have contrasting associations with CVD risk and may help account for the mixed results from clinical trials of dietary vitamin E.
authors.affiliation: Department of Genetics and the Southwest National Primate Research Center, Southwest Foundation for Biomedical Research, San Antonio, TX 78245-0549, USA. david@sfbrgenetics.org
authors.forename: David L
authors.initials: DL
authors.lastname: Rainwater
authors.forename: Michael C
authors.initials: MC
authors.lastname: Mahaney
authors.forename: John L
authors.initials: JL
authors.lastname: VandeBerg
authors.forename: Xing Li
authors.initials: XL
authors.lastname: Wang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage* / Q000494:pharmacology; D002318:Cardiovascular Diseases / Q000097:blood* / Q000453:epidemiology*; D018592:Cross-Over Studies; D004036:Diet, Atherogenic; D019587:Dietary Supplements; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D006801:Humans; D050356:Lipid Metabolism / Q000187:drug effects* / Q000235:genetics; D008074:Lipoproteins / Q000097:blood; D018384:Oxidative Stress / Q000187:drug effects*; D010215:Papio; D015995:Prevalence; D012307:Risk Factors; D014810:Vitamin E / Q000008:administration & dosage* / Q000494:pharmacology