title: Fatty acids in the de novo lipogenesis pathway and risk of coronary heart disease: the Cardiovascular Health Study.
abstract: BACKGROUND
  De novo lipogenesis (DNL) is an endogenous pathway whereby carbohydrates and proteins are converted to fatty acids. DNL could affect coronary heart disease (CHD) or sudden cardiac arrest (SCA) via generation of specific fatty acids. Whether these fatty acids are prospectively associated with SCA or other CHD events is unknown.
  
  
  OBJECTIVE
  The objective was to investigate the relations of 4 fatty acids in the DNL pathway-palmitic acid (16:0), palmitoleic acid (16:1n-7), 7-hexadecenoic acid (16:1n-9), and cis-vaccenic acid (18:1n-7)-with incident CHD, including fatal CHD, nonfatal myocardial infarction (NFMI), and SCA.
  
  
  METHODS
  A community-based prospective study was conducted in 2890 men and women aged ≥65 y, who were free of known CHD at baseline and who were followed from 1992 to 2006. Cardiovascular disease risk factors and plasma phospholipid fatty acids were measured at baseline by using standardized methods. Incident CHD was ascertained prospectively and was centrally adjudicated by using medical records. Risk was assessed by using multivariable-adjusted Cox proportional hazards.
  
  
  RESULTS
  During 29,835 person-years of follow-up, 631 CHD and 71 SCA events occurred. Both 18:1n-7 and 16:1n-9 were associated with a higher risk of SCA [multivariable-adjusted hazard ratio (95% CI) for the interquintile range: 7.63 (2.58, 22.6) for 18:1n-7 and 2.30 (1.16, 4.55) for 16:1n-9] but not of total CHD, fatal CHD, or NFMI. In secondary analyses censored to mid-follow-up (7 y) to minimize the effects of changes in concentrations over time, 16:1n-9 was also associated with a significantly higher risk of total CHD (2.11; 1.76, 2.54), including a higher risk of CHD death, NFMI, and SCA; 16:0 and 16:1n-7 were not associated with clinical CHD outcomes.
  
  
  CONCLUSIONS
  Higher plasma phospholipid 18:1n-7 and 16:1n-9 concentrations were prospectively associated with an elevated risk of SCA but not of other CHD events, except in secondary analyses.
authors.affiliation: Division of Cardiovascular Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. jasonwu@hsph.harvard.edu
authors.forename: Jason H Y
authors.initials: JH
authors.lastname: Wu
authors.forename: Rozenn N
authors.initials: RN
authors.lastname: Lemaitre
authors.forename: Fumiaki
authors.initials: F
authors.lastname: Imamura
authors.forename: Irena B
authors.initials: IB
authors.lastname: King
authors.forename: Xiaoling
authors.initials: X
authors.lastname: Song
authors.forename: Donna
authors.initials: D
authors.lastname: Spiegelman
authors.forename: David S
authors.initials: DS
authors.lastname: Siscovick
authors.forename: Dariush
authors.initials: D
authors.lastname: Mozaffarian
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015331:Cohort Studies; D003327:Coronary Disease / Q000209:etiology*; D016757:Death, Sudden, Cardiac / Q000209:etiology; D004032:Diet; D005227:Fatty Acids / Q000378:metabolism*; D005260:Female; D006801:Humans; D050155:Lipogenesis; D008297:Male; D010743:Phospholipids / Q000097:blood; D016016:Proportional Hazards Models; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D005227:Fatty Acids; D010743:Phospholipids