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Does genetic variation in the ⁶-desaturase promoter modify the association between -linolenic acid and the prevalence of metabolic syndrome?

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

² Supported by grant HL081549 from the National Institutes of Health.

³ Reprints not available. Address correspondence to A Baylin, Department of Community Health, Brown University, 121 South Main Street, 2nd Floor, Box G-S121, Providence, RI 02903. E-mail: ana_baylin{at}brown.edu.

Background: Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are associated with protection against components of the metabolic syndrome, but the role of -linolenic acid (ALA), the metabolic precursor of EPA and DHA, has not been studied. The ⁶-desaturase enzyme converts ALA into EPA and DHA, and genetic variation in the ⁶-desaturase gene (FADS2) may affect this conversion.

Objectives: We hypothesize that high ALA is associated with a lower prevalence of the metabolic syndrome and that genetic variation in FADS2 modifies this association.

Design: We studied 1815 Costa Rican adults. Adipose tissue ALA was used as a biomarker of intake, and metabolic syndrome was identified with the definition from the National Cholesterol Education Program, Adult Treatment Panel III. Prevalence ratios (PRs) and 95% CIs were estimated from binomial regression models, and the likelihood ratio was used to test for effect modification.

Results: High concentrations of adipose tissue ALA were associated with lower PRs of the metabolic syndrome compared with low ALA (0.81; 95% CI: 0.66, 1.00, for the comparison between the highest and the lowest quintiles; P for trend < 0.02). Higher concentrations of adipose tissue ALA were associated with a lower PR among homozygote (0.67; 95% CI: 0.53, 0.86) and heterozygote (0.84; 95% CI: 0.72, 0.99) carriers of the FADS2 T allele, but not among homozygote carriers of the deletion variant allele (0.99; 95% CI: 0.78, 1.27; P for interaction: 0.08).

Conclusions: Elevated ALA concentrations in adipose tissue are associated with lower prevalence of the metabolic syndrome. A lack of association among homozygote carriers of the FADS2 deletion allele suggests that this association may be due in part to the conversion of ALA into EPA.