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-Linolenic acid, ⁶-desaturase gene polymorphism, and the risk of nonfatal myocardial infarction^1,2,3

¹ From the Department of Community Health, Brown University, Providence, RI (AB), the Departments of Nutrition (ER-N and HC) and Epidemiology (PK), Harvard School of Public Health, Harvard University, Boston, MA; and the Centro Centroamericano de población, Universidad de Costa Rica, San Pedro de Montes de Oca, Costa Rica (HC)

Background: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 -linolenic acid (ALA) on myocardial infarction (MI).

Design: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, -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.

Key Words: Myocardial infarction • genetics • diet • fatty acids • epidemiology

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