title: Habitual dietary intake of n-3 and n-6 fatty acids in relation to inflammatory markers among US men and women.
abstract: 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.
  
  
  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 alpha-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.
authors.affiliation: Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave, Boston, Mass 02115, USA. tpischon@hsph.harvard.edu
authors.forename: Tobias
authors.initials: T
authors.lastname: Pischon
authors.forename: Susan E
authors.initials: SE
authors.lastname: Hankinson
authors.forename: Gökhan S
authors.initials: GS
authors.lastname: Hotamisligil
authors.forename: Nader
authors.initials: N
authors.lastname: Rifai
authors.forename: Walter C
authors.initials: WC
authors.lastname: Willett
authors.forename: Eric B
authors.initials: EB
authors.lastname: Rimm
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000097:blood; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D015777:Eicosanoids / Q000096:biosynthesis; D002149:Energy Intake; D015525:Fatty Acids, Omega-3 / Q000378:metabolism*; D043371:Fatty Acids, Omega-6; D005231:Fatty Acids, Unsaturated / Q000378:metabolism*; D005247:Feeding Behavior; D005260:Female; D005500:Follow-Up Studies; D006282:Health Personnel / Q000706:statistics & numerical data; D006801:Humans; D007249:Inflammation / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012016:Reference Values; D012737:Sex Factors; D011795:Surveys and Questionnaires; D014481:United States
chemical_list: D015703:Antigens, CD; D015415:Biomarkers; D015777:Eicosanoids; D015525:Fatty Acids, Omega-3; D043371:Fatty Acids, Omega-6; D005231:Fatty Acids, Unsaturated; D015850:Interleukin-6; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D002097:C-Reactive Protein