Abstract

ObjectivesWe evaluated whether higher (i.e., pro-inflammatory) Dietary Inflammatory Index (DII) scores were associated with increased concentrations of inflammatory markers in the community-based Framingham Heart Study (FHS) Offspring Cohort. MethodsWe studied 1978 participants (age 61 [SD, 9] years, 53.9% women) from the Offspring cohort who completed a validated 126-item Food Frequency Questionnaire (FFQ) at exam 7 (1998–2001) and at least one of exams 5 (1991–1995) or exam 6 (1995–1998), and on whom inflammatory markers were measured at exam 7. We created a DII score based on the published scoring algorithm by Shivappa et al. 2014, (developed from previous studies linking individual dietary factors to six inflammatory markers); a cumulative DII score was calculated by averaging across a maximum of three FFQs. We used linear regression models to test associations between the cumulative DII score and natural log-transformed concentrations of adiponectin, cluster of differentiation 40 (CD40), C-reactive protein (CRP), fibrinogen, intracellular adhesion molecule (ICAM), interleukin (IL)-6, IL-18, resistin, and TNF-α. ResultsHigher DII scores were independently associated with higher mean concentrations of four inflammatory markers after adjustment for demographic, clinical, and lifestyle covariates (β± SE, CRP 0.14 mg/L ± 0.04; P < 0.0001, IL-6 0.07 pg/mL ± 0.02; P < 0.003, resistin 0.04 ng/mL ± 0.02 ng/mL; P = 0.01). Exclusion of individuals who smoke currently did not change the results. Additionally, we observed that body mass index had a partially mediating effect on all relationships except the relationships with TNF-α. Further, we observed no significant interactions between higher DII scores and sex in their associations with each inflammatory marker. ConclusionsHigher DII scores were associated with higher concentrations of four out of nine inflammatory markers. Our results suggest that anti-inflammatory diets, which correlate with low DII scores may lower systemic chronic inflammation, a process that plays an important role in the development and progression of chronic disease. Funding SourcesASPEN Rhoads Research Foundation and NIH.

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