Abstract 41: Omega-6 Fatty Acid Biomarkers and Incident Type 2 Diabetes: A Pooled Analysis of 20 Cohort Studies

Abstract

Background: Emerging evidence suggests that dietary omega-6 polyunsaturated fatty acids (n-6 PUFA) plays a role in the primary prevention of type 2 diabetes (T2D). Aims: To evaluate the relation between blood and adipose tissue levels of n-6 PUFA and incident T2D, including n-6 linoleic acid (LA), the major dietary PUFA abundant in vegetable oils, and n-6 arachidonic acid (AA), a key precursor of endogenous metabolites that modulate glucose metabolism and inflammation. Methods: A global consortium of 20 prospective cohort studies identified by February 2016. Each study measured LA and AA at study baseline among adults>18y without prevalent T2D, and assessed the association of n-6 PUFA biomarkers and T2D risk prospectively using individual-level data, using a pre-specified analytic plan and harmonized exposures, covariates, and effect modifiers. Findings were centrally pooled using fixed-effects meta-analysis. Results: 39,740 men and women from 10 countries were included (range of cohort means, age, 49-76y, and BMI, 25.0-28.1kg/m 2 ), with 4,347 incident cases of T2D observed during follow-up. In continuous multivariate-adjusted analyses, higher LA was associated with 36% lower risk of T2D (RR,0.64, 95% CI,0.59-0.71, P<0.001, I 2 =49%, Figure 1A ) per interquintile range. Similar inverse associations were observed for LA measured in different fractions, and in sensitivity analysis using random effects model. Levels of AA were not associated with T2D risk overall and in studies grouped by different biomarker fractions except total plasma (per interquintile RR=0.74, 95% CI=0.62-0.88, P<0.001, Figure 1B ). The relations of LA and AA with T2D were not significantly modified by age, BMI, sex, race, aspirin use, n-3 PUFA biomarker, or FADS genetic variants ( P ≥ 0.13 for each). Conclusion: Higher blood and adipose tissue LA levels, biomarkers of the major dietary PUFA, were associated with lower risk of T2D among free-living populations worldwide. There was little evidence that AA levels were appreciably associated with risk of T2D.