title: Plasma folate, but not homocysteine, is associated with Apolipoprotein A1 levels in a non-fortified population.
abstract: BACKGROUND
  Elevated total plasma homocysteine (tHcy) in humans is associated with cardiovascular disease but prevention trials have failed to confirm causality. Reported reasons for this association have been that homocysteine and its major genetic determinant methylenetetrahydrofolate reductase (MTHFR) may have an effect on HDL and Apolipoprotein (Apo) A1 levels. We wanted to study if tHcy and its major determinants were correlated with Apo A1 levels in a large population without folate fortification.
  
  
  METHODS
  This study was a prospective incident nested case-referent study within the Northern Sweden Health and Disease Study Cohort (NSHDSC), including 545 cases with first myocardial infarction and 1054 matched referents, median age at inclusion was 59 years. Univariate and multiple regression analyzes was used to study the associations between apolipoproteins Apo A1 and B, tHcy, folate and vitamin B12 in plasma as well as MTHFR polymorphisms 677C>T and 1298A>C.
  
  
  RESULTS
  Apo A1 and Apo B were strongly associated with the risk of a first myocardial infarction. tHcy was not associated with Apo A1 levels. Instead, folate had an independent positive association with Apo A1 levels in univariate and multiple regression models. The associations were seen in all men and women, among referents but not among cases. MTHFR polymorphisms had no clear effect on Apo A1 levels.
  
  
  CONCLUSIONS
  Analyzing over 1500 subjects we found an independent positive association between plasma folate (major dietary determinant of tHcy) and Apo A1 levels among those who later did not develop a first myocardial infarction. No association was seen between tHcy and Apo A1.
authors.affiliation: Department of Medical Biosciences, Clinical Chemistry, Umeå University, 90185 Umeå, Sweden. elisabet.soderstrom@medbio.umu.se
authors.forename: Elisabet
authors.initials: E
authors.lastname: Söderström
authors.forename: Mats
authors.initials: M
authors.lastname: Eliasson
authors.forename: Owe
authors.initials: O
authors.lastname: Johnson
authors.forename: Göran
authors.initials: G
authors.lastname: Hallmans
authors.forename: Lars
authors.initials: L
authors.lastname: Weinehall
authors.forename: Jan-Håkan
authors.initials: JH
authors.lastname: Jansson
authors.forename: Johan
authors.initials: J
authors.lastname: Hultdin
mesh_terms: D000328:Adult; D016632:Apolipoprotein A-I / Q000097:blood*; D001055:Apolipoproteins B / Q000097:blood* / Q000235:genetics / Q000378:metabolism; D005260:Female; D005492:Folic Acid / Q000097:blood* / Q000235:genetics; D056726:Genetic Association Studies; D005828:Genetics, Population; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000097:blood / Q000235:genetics*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000473:pathology; D011110:Polymorphism, Genetic; D012307:Risk Factors; D014805:Vitamin B 12 / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D006710:Homocysteine; D005492:Folic Acid; C573423:MTHFR protein, human; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D014805:Vitamin B 12