Intakes of PUFAs Were Inversely Associated with Plasma C-Reactive Protein 12 Years Later in a Middle-Aged Population with Vitamin E Intake as an Effect Modifier

Supported by Agence Nationale de la Recherche (ANR-05-PNRA-010). Because French public research is independent, the sponsors were not involved in analysis or interpretation of the findings. Amer soc nutrition-asn Bethesda

anglais. Although n-3 (omega-3) polyunsaturated fatty acids (PUFAs) are considered anti-inflammatory components, the role of dietary n-6 PUFAs in inflammation remains controversial. Some mechanistic evidence suggests vitamin E as a potential effect modifier in the relationship between PUFAs and inflammation. Our objectives were to evaluate the long-term associations between dietary intakes of PUFAs and elevated plasma C-reactive protein (CRP) and to investigate potential effect modification by vitamin E. Individuals in the placebo group of the SU.VI.MAX trial who had available CRP measurements in 2007-2009 were included in the study (n = 843). Dietary intakes of n-3 PUFAs, n-6 PUFAs, and vitamin E were assessed in 1994-1996 with at least 6 dietary records. The logistic regression OR for elevated CRP (>3 mg/L) and 95% Cl were estimated for individual PUFAs and for total n-3 and n-6 PUFA intakes. Models were adjusted for sociodemographical, lifestyle, anthropometric, and dietary variables. Interactions with vitamin E intakes were also assessed. Inverse associations were observed between intakes of total n-3 PUFAs la-linolenic acid (ALA; 18:3n-3), ALA + eicosapentaenoic acid (EPA; 20:5n-3), EPA + docosapentaenoic acid (DPA; 22:5n-3), DPA + docosahexaenoic acid (DHA; 22:6n-3)1 and n-6 PUFA [linoleic acid (18:2n-6) + arachidonic acid (20:4n-6)1 and elevated CRP (OR for tertile 3 vs. tertile 1 of intake 0.41; 95% CI: 0.21, 0.77; P-trend = 0.01; and OR 0.38; 95% CI: 0.21, 0.70; P-trend = 0.002, respectively). Stratification on vitamin E intakes showed that inverse associations between dietary n-3 and n-6 PUFA intakes and elevated CRP were substantial only in individuals with low intakes of vitamin E. Our results supported the contention that intakes of both n-3 and n-6 PUFAs are inversely associated with plasma CRP concentrations. Vitamin E is a potential effect modifier and should therefore be taken into account in such investigations.