title: Effects of dietary components on high-density lipoprotein measures in a cohort of 1,566 participants.
abstract: BACKGROUND
  Recent data suggest that an increased level of high-density lipoprotein cholesterol (HDL-C) is not causally protective against heart disease, shifting focus to other sub-phenotypes of HDL. Prior work on the effects of dietary intakes has focused largely on HDL-C. The goal of this study was to identify the dietary intakes that affect HDL-related measures: HDL-C, HDL-2, HDL-3, and apoA1 using data from a carotid artery disease case-control cohort.
  
  
  METHODS
  A subset of 1,566 participants with extensive lipid phenotype data completed the Harvard Standardized Food Frequency Questionnaire to determine their daily micronutrient intake over the past year. Stepwise linear regression was used to separately evaluate the effects of dietary covariates on adjusted levels of HDL-C, HDL-2, HDL-3, and apoA1.
  
  
  RESULTS
  Dietary folate intake was positively associated with HDL-C (p = 0.007), HDL-2 (p = 0.0011), HDL-3 (p = 0.0022), and apoA1 (p = 0.001). Alcohol intake and myristic acid (14:0), a saturated fat, were each significantly associated with increased levels of all HDL-related measures studied. Dietary carbohydrate and iron intake were significantly associated with decreased levels of all HDL-related measures. Magnesium intake was positively associated with HDL-C, HDL-2, and HDL-3 levels, but not apoA1 levels, while vitamin C was only associated with apoA1 levels. Dietary fiber and protein intake were both associated with HDL-3 levels alone.
  
  
  CONCLUSIONS
  This study is the first to report that dietary folate intake is associated with HDL-C, HDL-2, HDL-3, and apoA1 levels in humans. We further identify numerous dietary intake associations with apoA1, HDL-2, and HDL-3 levels. Given the shifting focus away from HDL-C, these data will prove valuable for future epidemiologic investigation of the role of diet and multiple HDL phenotypes in heart disease.
authors.affiliation: Department of Medicine, Division of Medical Genetics, University of Washington School of Medicine, Box 357720, Seattle, WA 98195-7720 USA ; Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA USA.
authors.forename: Daniel Seung
authors.initials: DS
authors.lastname: Kim
authors.affiliation: Department of Medicine, Division of Medical Genetics, University of Washington School of Medicine, Box 357720, Seattle, WA 98195-7720 USA.
authors.forename: Amber A
authors.initials: AA
authors.lastname: Burt
authors.affiliation: Department of Medicine, Division of Medical Genetics, University of Washington School of Medicine, Box 357720, Seattle, WA 98195-7720 USA.
authors.forename: Jane E
authors.initials: JE
authors.lastname: Ranchalis
authors.affiliation: Department of Medicine, Division of Medical Genetics, University of Washington School of Medicine, Box 357720, Seattle, WA 98195-7720 USA.
authors.forename: Leah E
authors.initials: LE
authors.lastname: Jarvik
authors.affiliation: Department of General Medicine, Virginia Mason Medical Center, Seattle, WA USA.
authors.forename: Jason F
authors.initials: JF
authors.lastname: Eintracht
authors.affiliation: Department of Medicine, Division of Medical Genetics, University of Washington School of Medicine, Box 357720, Seattle, WA 98195-7720 USA ; Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA USA.
authors.forename: Clement E
authors.initials: CE
authors.lastname: Furlong
authors.affiliation: Department of Medicine, Division of Medical Genetics, University of Washington School of Medicine, Box 357720, Seattle, WA 98195-7720 USA ; Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA USA.
authors.forename: Gail P
authors.initials: GP
authors.lastname: Jarvik
keywords: Alcohol; Apolipoprotein A1; Cardiovascular disease; Fatty acids; Folate; Food frequency questionnaire; HDL; HDL subfractions; HDL-2; HDL-3; HDL-C; Magnesium