Premium
Association between the dietary inflammatory index (DII) and telomere length and C‐reactive protein from the National Health and Nutrition Examination Survey‐1999–2002
Author(s) -
Shivappa Nitin,
Wirth Michael D.,
Hurley Thomas G.,
Hébert James R.
Publication year - 2017
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201600630
Subject(s) - national health and nutrition examination survey , quartile , medicine , c reactive protein , telomere , confidence interval , calorie , biomarker , inflammation , immunology , environmental health , biology , population , dna , biochemistry , genetics
Scope Leukocyte telomere length (LTL) is an important biomarker of aging. This study examined whether inflammatory potential of diet, as measured by the Dietary Inflammatory Index TM (DII) has an impact on telomere shortening in the National Health and Nutrition Examination Survey (NHANES). We also carried out validation of the DII with C‐reactive protein (CRP). Methods and results Data came from NHANES 1999–2002. LTL and CRP were assayed from leukocyte DNA and serum specimens, respectively. The DII was calculated from food intakes assessed using 24‐h dietary recalls and expressed per 1000 calories consumed. Associations were examined using survey‐based multivariable linear regression for log‐transformed LTL. After multivariable adjustment, higher DII scores (i.e. relatively more pro inflammatory) were associated with shorter LTL both when used as continuous ( b = –0.003; 95% confidence interval [CI] = –0.005, –0.0002) and as quartiles ( b DIIquartile4vs1 = –0.013; 95% CI = –0.025, –0.001; P trend = .03). In this same sample the DII also was associated with CRP ≥3 mg/L (OR DIIcontinuous = 1.10; 95% CI = 1.06, 1.16). Conclusion In these NHANES data there was an association between DII and LTL. This study also provided a successful construct validation of the DII using CRP in a nationally representative sample. These results are consistent with the hypothesis that diet‐associated inflammation determines LTL.