Journal Name:
Am. J. Clin. Nutr.
Article Title:
Does genetic variation in the {Delta}6-desaturase promoter modify the association between {alpha}-linolenic acid and the prevalence of metabolic syndrome?
Date Written:
2009
Volume:
89
Number:
NA
Page:
920
Author(s):
Truong, H.; Dibello, J.R.; Ruiz-Narvaez, E.; Kraft, P.; Campos, H.; Baylin, A.
Article:
The prevalence of the metabolic syndrome has been increasing worldwide. In the United States the prevalence for the period 1999–2002 was 34.5%. Several Latin American countries are experiencing an increasing prevalence of metabolic syndrome that is becoming closer to that in the United States. The collection of metabolic risk factors that define the metabolic syndrome include obesity, high blood pressure and plasma triglyceride concentrations, low HDL cholesterol, and impaired fasting glucose among others. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are associated with protection against components of the metabolic syndrome, but the role of alpha-linolenic acid (ALA), the metabolic precursor of EPA and DHA, has not been studied. The Delta (6)-desaturase enzyme converts ALA into EPA and DHA, and genetic variation in the Delta(6)-desaturase gene (FADS2) may affect this conversion.
In this study, the hypothesis that high ALA is associated with a lower prevalence of the metabolic syndrome and that genetic variation in FADS2 modifies this association was assessed. The subject group was 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.
High concentrations of adipose tissue ALA were associated with lower prevalence ratios (PR) of the metabolic syndrome compared with low ALA. Higher concentrations of adipose tissue ALA were associated with a lower PR among homozygote and heterozygote carriers of the FADS2 T allele, but not among homozygote carriers of the deletion variant allele.
Evidence about the direct effect of ALA on the metabolic syndrome is scarce (16). Significant correlations between ALA in plasma triacylglycerols and apolipoprotein B and LDL diameter were reported in a study performed among 97 white men. ALA was associated negatively with apolipoprotein B and positively with LDL diameter. The association between ALA and metabolic syndrome seen in this study may be due to the many protective properties of the metabolites of ALA, EPA and DHA.
Elevated ALA concentrations in adipose tissue are associated with lower prevalence of the metabolic syndrome. A higher prevalence of metabolic syndrome among those homozygous for this variant suggests that the potential protective properties of ALA may be due to its metabolism into EPA and DHA. The importance of this biosynthetic pathway emphasizes the role of EPA and DHA derived from dietary ALA among populations with low fish intake in attenuating the symptoms of the metabolic syndrome. Furthermore, the D6-desaturase is shared by both the omega 3 and the omega 6 metabolic pathways. A high ratio of dietary linoleic acid to ALA in the diet may decrease the efficacy of ALA regardless of the amount of its absolute consumption because the synthesis of ALA into EPA may be decreased in diets high in linoleic acid as a result of the competition for the D6-desaturase. It is also possible that ALA exerts protective effects on its own. 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. Future studies will be of special importance in those populations in which the intake of ALA and EPA and DHA from fish is low.
Back to New research paper