Supplemental Material can be found at: http://jn.nutrition.org/content/suppl/2013/10/10/jn.113.18094 3.DCSupplemental.html
The Journal of Nutrition Nutritional Epidemiology
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 Modifier1–3 Chantal Julia,4–8* Mathilde Touvier,4–7 Nathalie Meunier,9 Isabelle Papet,10,11 Pilar Galan,4–7 Serge Hercberg,4–8 and Emmanuelle Kesse-Guyot4–7 4 Inserm (National Institute of Health and Medical Research), U557 Nutritional Epidemiology Unit, Bobigny, France; 5INRA, U1125, Bobigny, France; 6CNAM, Nutritional Epidemiology Unit, Bobigny, France; 7Universit´e Paris 13, Sorbonne Paris Cit´e, Nutritional Epidemiology Unit, Bobigny, France; 8Department of Public Health, Avicenne Hospital, Bobigny, France; 9CHU Clermont-Ferrand, Unit´e dÕExploration en Nutrition, Clermont-Ferrand, France; 10Clermont Universit´e, Universit´e d’Auvergne, Unit´e de Nutrition Humaine, Clermont-Ferrand, France; and 11INRA, UNH, CRNH Auvergne, Clermont-Ferrand, France
Although n–3 (v-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% CI 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 [a-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)] and n–6 PUFA [linoleic acid (18:2n–6) + arachidonic acid (20:4n–6)] and elevated CRP (OR for tertile 3 vs. tertile 1 of intake: 0.41; 95% CI: 0.21, 0.77; P-trend 5 0.01; and OR 0.38; 95% CI: 0.21, 0.70; P-trend 5 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. This trial was registered at clinicaltrials.gov as NCT00272428.
J. Nutr. 143: 1760–1766, 2013.
Introduction Low-grade inflammation has been recognized as an underlying process for several chronic diseases, including cancer and cardiovascular diseases (1–3). Identification of modifiable risk factors for low-grade inflammation could therefore contribute 1
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. 2 Author disclosures: C. Julia, M. Touvier, N. Meunier, I. Papet, P. Galan, S. Hercberg, E. Kesse-Guyot, no conflicts of interest. 3 Supplemental Table 1 is available from the ‘‘Online Supporting Material’’ link in the online posting of the article and from the same link in the online table of contents at http://jn.nutrition.org. * To whom correspondence should be addressed: E-mail:
[email protected]. univ-paris13.fr.
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to understanding and preventing the early stages of chronic diseases. PUFAs are of utmost interest, because they are precursors for several pro- or anti-inflammatory mediators, including eicosanoids (4–6). The main substrate for eicosanoid production is arachidonic acid (AA12; 20:4n–6), but n–3 PUFAs have been identified as alternate sources of production for eicosanoids with lesser inflammatory power (6). They are also precursors for mediators involved in the resolution of inflammation, protectins and resolvins (7). Several studies have investigated relationships between n–3 PUFAs and inflammation, suggesting a protective effect against Abbreviations used: AA, arachidonic acid; ALA, a-linolenic acid; CRP, C-reactive protein; DPA, docosapentaenoic acid; LA, linoleic acid.
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ã 2013 American Society for Nutrition. Manuscript received June 12, 2013. Initial review completed July 2, 2013. Revision accepted August 8, 2013. First published online September 11, 2013; doi:10.3945/jn.113.180943.
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Abstract
Participants and Methods Study population. The study population was selected from participants in the SU.VI.MAX study. Individuals not taking any supplements were included in 1994–1995 in a randomized, double-blind, placebo-controlled primary prevention trial designed to evaluate the effect of a planned 8-y supplementation in antioxidant vitamins and minerals at nutritional doses on the incidence of cardiovascular disease and cancer (17). In 2007–2009, individuals were offered to enroll in an additional follow-up study, the SU.VI.MAX2 study (18). Both the SU.VI.MAX and the SU.VI.MAX2 studies were approved by the Ethics Committee for Studies with Human Subjects of Paris– Cochin Hospital (706 and 2364, respectively) and the Comit´e National Informatique et Libert´e (334641 and 907094, respectively). All individuals gave written informed consent to participate in the study. Individuals having had CRP measurements and with CRP values
