Circulation. 2003;108:155-160
Published online before print June 23, 2003, doi: 10.1161/01.CIR.0000079224.46084.C2
Published online before print June 23, 2003, doi: 10.1161/01.CIR.0000079224.46084.C2
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(Circulation. 2003;108:155.)
© 2003 American Heart Association, Inc.
Clinical Investigation and Reports |
Habitual Dietary Intake of n-3 and n-6 Fatty Acids in Relation to Inflammatory Markers Among US Men and Women
From the Departments of Nutrition and Epidemiology, Harvard School of Public Health (T.P., S.E.H., G.S.H., W.C.W., E.B.R.), Boston, Mass; Channing Laboratory, Harvard Medical School and Brigham & Women’s Hospital (S.E.H., W.C.W., E.B.R.) and Department of Laboratory Medicine, Children’s Hospital and Department of Pathology, Harvard Medical School (N.R.), Boston, Mass; and Franz-Volhard-Clinic, Charité, Humboldt-University (T.P.), Berlin, Germany.
Correspondence to Tobias Pischon, MD, MPH, Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115. E-mail tpischon{at}hsph.harvard.edu
Background— Polyunsaturated fatty acid intake favorably affects chronic inflammatory-related diseases such as cardiovascular disease; however, high intake of n-6 fatty acids may attenuate the known beneficial effects of n-3 fatty acids.
Methods and Results— We investigated habitual dietary n-3 fatty acid intake and its interaction with n-6 fatty acids in relation to the plasma inflammatory markers C-reactive protein, interleukin 6, and soluble tumor necrosis factor receptors 1 and 2 (sTNF-R1 and R2) among 405 healthy men and 454 healthy women. After adjustment for other predictors of inflammation, intake of the n-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) was inversely associated with plasma levels of sTNF-R1 and sTNF-R2 (P=0.03 and P<0.001, respectively) and somewhat less so for C-reactive protein (P=0.08). n-3 
-linolenic acid and n-6 cis-linoleic acid were not significantly related to the inflammatory markers. We found little if any association between n-3 fatty acid (EPA+DHA) intake and tumor necrosis factor receptors among participants with low intake of n-6 but a strong inverse association among those with high n-6 intake (P=0.04 and 0.002 for interaction of n-3 with n-6 on sTNF-R1 and sTNF-R2, respectively).
Conclusions— These results suggest that n-6 fatty acids do not inhibit the antiinflammatory effects of n-3 fatty acids and that the combination of both types of fatty acids is associated with the lowest levels of inflammation. The inhibition of inflammatory cytokines may be one possible mechanism for the observed beneficial effects of these fatty acids on chronic inflammatory-related diseases.
Key Words: fatty acids • inflammation • nutrition • risk factors
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