title: alpha-Linolenic acid, Delta6-desaturase gene polymorphism, and the risk of nonfatal myocardial infarction.
abstract: BACKGROUND
  Delta(6)-Desaturase (FADS2) is the rate-limiting step in the polyunsaturated fatty acid (PUFA) biosynthetic pathway.
  
  
  OBJECTIVE
  The aim was to test whether the common deletion [T/-] in the promoter of FADS2 affects the PUFA biosynthetic pathway and consequently modifies the effect of alpha-linolenic acid (ALA) on myocardial infarction (MI).
  
  
  METHODS
  Case subjects (n =1694) with a first nonfatal acute MI were matched by age, sex, and area of residence to 1694 population-based control subjects in Costa Rica. PUFAs were quantified by gas-liquid chromatography from plasma and adipose tissue samples. Least-squares means from generalized linear models and odds ratios (ORs) and 95% CIs from multiple conditional logistic regression models were estimated.
  
  
  RESULTS
  The prevalence of the variant T/- allele was 48%. Eicosapentaenoic acid, gamma-linolenic acid, and arachidonic acid decreased in adipose tissue and plasma with increasing number of copies of the variant allele with a monotonic trend (P < 0.05 for all). Fasting plasma triacylglycerols by genotype were 2.08 mmol/L for TT, 2.16 mmol/L for T-, and 2.26 mmol/L for - - [ie, homozygous for the variant (deletion) allele] (P = 0.03). The FADS2 deletion was not associated with MI and did not significantly modify the association between adipose tissue ALA and the risk of MI.
  
  
  CONCLUSIONS
  The FADS2 deletion may prevent the conversion of ALA into very-long-chain PUFAs. However, this metabolic effect is not translated into an attenuated risk between ALA and MI among carriers of the variant. It is possible that, at current intakes of ALA, any potential defect in the transcription of the gene is masked by the availability of substrate. Further research in populations deficient in ALA intake is warranted.
authors.affiliation: Department of Community Health, Brown University, Providence, RI, USA. ana_baylin@brown.edu
authors.forename: Ana
authors.initials: A
authors.lastname: Baylin
authors.forename: Edward
authors.initials: E
authors.lastname: Ruiz-Narvaez
authors.forename: Peter
authors.initials: P
authors.lastname: Kraft
authors.forename: Hannia
authors.initials: H
authors.lastname: Campos
mesh_terms: D000368:Aged; D003364:Costa Rica / Q000453:epidemiology; D044943:Fatty Acid Desaturases; D005260:Female; D017353:Gene Deletion; D015971:Gene Expression Regulation, Enzymologic; D020022:Genetic Predisposition to Disease; D006801:Humans; D019787:Linoleic Acid / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000235:genetics* / Q000378:metabolism*; D011110:Polymorphism, Genetic / Q000235:genetics*; D011401:Promoter Regions, Genetic / Q000235:genetics; D012307:Risk Factors; D013230:Stearoyl-CoA Desaturase / Q000235:genetics*; D017962:alpha-Linolenic Acid / Q000378:metabolism*
chemical_list: D017962:alpha-Linolenic Acid; D019787:Linoleic Acid; D044943:Fatty Acid Desaturases; D013230:Stearoyl-CoA Desaturase; C533241:FADS2 protein, human