J Nutr 2017 01 26;147(1):78-85. Epub 2016 Oct 26.
Molecular Epidemiology Research Group, Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany;
Background: High consumption of red and processed meats has been linked to higher chronic disease risk. It has been hypothesized that inflammation markers may mediate part of this association. Most previous studies on the association of red meat intake with circulating inflammation markers used C-reactive protein (CRP) but rarely other markers, and not all differentiated between processed meat and unprocessed red meat.
Objective: We investigated the cross-sectional association of processed meat and unprocessed red meat consumption with plasma concentrations of CRP, interleukin 6 (IL-6), tumor necrosis factor (TNF)-α, soluble TNF receptor (sTNF-R) 1, and sTNF-R2 in German adults.
Methods: Inflammation markers were quantified in the plasma of 553 adults (233 men and 320 women) aged 18-80 y within the cross-sectional Bavarian Food Consumption Survey II. Dietary intake was estimated from three 24-h dietary recalls. The association between red meat consumption and inflammation markers was analyzed with the use of multivariable-adjusted linear regression.
Results: Processed meat consumption was borderline significantly associated with higher IL-6 [relative difference per 50-g increment: 5% (95% CI: -1%, 10%)] but not with CRP (2%; 95% CI: -6%, 10%), and it was inversely associated with total TNF-α (-3%; 95% CI: -6%, -1%), sTNF-R1 (-3%; 95% CI: -4%, -1%), and sTNF-R2 (-2%; 95% CI: -4%, 0%) concentrations. Unprocessed red meat consumption was not associated with CRP (-5%; 95% CI: -15%, 5%) or IL-6 (-1%; 95% CI: -9%, 7%) but was inversely associated with sTNF-R1 (-3%; 95% CI: -5%, -1%) and sTNF-R2 (-4%; 95% CI: -7%, -2%).
Conclusions: Our results suggest an inverse association between both processed meat and unprocessed red meat with inflammation markers of the TNF pathway in Bavarian adults but no association with CRP. Further research on the role of TNF pathway markers in chronic inflammation is warranted.