title: Dietary intake of trans fatty acids and systemic inflammation in women.
abstract: BACKGROUND
  trans Fatty acid (TFA) intake predicts risks of coronary artery disease and diabetes. Systemic inflammation may be involved in the pathogenesis of such conditions; however, relations between TFA intake and systemic inflammation are not well established.
  
  
  OBJECTIVE
  We investigated the relations between TFA intake and inflammatory markers.
  
  
  METHODS
  In 823 generally healthy women in the Nurses' Health Study I and II, concentrations of soluble tumor necrosis factor alpha receptors 1 and 2 (sTNF-R1, sTNF-R2), interleukin 6 (IL-6), and C-reactive protein (CRP) were measured. Usual dietary intakes assessed from 2 semiquantitative food-frequency questionnaires were averaged for each subject.
  
  
  RESULTS
  In age-adjusted analyses, TFA intake was positively associated with sTNF-R1 and sTNF-R2 (P for trend < 0.001 for each): sTNF-R1 and sTNF-R2 concentrations were 10% (+108 pg/mL; 95% CI: 50, 167 pg/mL) and 12% (+258 pg/mL; 138, 377 pg/mL) higher, respectively, in the highest intake quintile than in the lowest. These associations were not appreciably altered by adjustment for body mass index, smoking, physical activity, aspirin and nonsteroidal antiinflammatory drug use, alcohol consumption, and intakes of saturated fat, protein, n-6 and n-3 fatty acids, fiber, and total energy. Adjustment for serum lipid concentrations partly attenuated these associations, which suggests that they may be partly mediated by effects of TFAs on serum lipids. TFA intake was not associated with IL-6 or CRP concentrations overall but was positively associated with IL-6 and CRP in women with higher body mass index (P for interaction = 0.03 for each).
  
  
  CONCLUSIONS
  TFA intake is positively associated with markers of systemic inflammation in women. Further investigation of the influences of TFAs on inflammation and of implications for coronary disease, diabetes, and other conditions is warranted.
authors.affiliation: Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. darymd@hotmail.com
authors.forename: Dariush
authors.initials: D
authors.lastname: Mozaffarian
authors.forename: Tobias
authors.initials: T
authors.lastname: Pischon
authors.forename: Susan E
authors.initials: SE
authors.lastname: Hankinson
authors.forename: Nader
authors.initials: N
authors.lastname: Rifai
authors.forename: Kaumudi
authors.initials: K
authors.lastname: Joshipura
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; D015415:Biomarkers; D016207:Cytokines / Q000097:blood; D004041:Dietary Fats / Q000008:administration & dosage / Q000009:adverse effects*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000209:etiology*; D016014:Linear Models; D008875:Middle Aged; D011446:Prospective Studies; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood*; D044242:Trans Fatty Acids / Q000008:administration & dosage / Q000009:adverse effects*
chemical_list: D015415:Biomarkers; D016207:Cytokines; D004041:Dietary Fats; D018124:Receptors, Tumor Necrosis Factor; D044242:Trans Fatty Acids