ABSTRACT
SCOPE: A study is conducted to determine the anti-inflammatory effects of cocoa and polyphenol-rich cocoa fractions in the dextran sulfate sodium (DSS)-induced mouse model of acute colonic inflammation. METHODS AND RESULTS: Male C57BL/6J mice are treated with dietary cocoa powder, an extractable cocoa polyphenol fraction, or a non-extractable cocoa polyphenol fraction for 2 weeks prior to treatment with 2.5% DSS in the drinking water for 7 days to induce colonic inflammation. Cocoa treatment continues during the DSS period. Cocoa and/or cocoa fractions exacerbate DSS-induced weight loss and fail to mitigate DSS-induced colon shortening but do improve splenomegaly. Cocoa/cocoa fraction treatment fails to mitigate DSS-induced mRNA and protein markers of inflammation. Principal component analysis shows overlap between cocoa or cocoa fraction-treated mice and DSS-induced controls, but separation from mice not treated with DSS. CONCLUSION: The results suggest cocoa and cocoa polyphenols may not be useful in mitigating acute colonic inflammation.
Subject(s)
Cacao , Colitis , Colon , Dextran Sulfate , Mice, Inbred C57BL , Polyphenols , Animals , Male , Polyphenols/pharmacology , Polyphenols/analysis , Colitis/chemically induced , Colitis/drug therapy , Colitis/diet therapy , Cacao/chemistry , Colon/drug effects , Colon/pathology , Colon/metabolism , Mice , Disease Models, Animal , Anti-Inflammatory Agents/pharmacology , Inflammation/drug therapyABSTRACT
Obesity causes inflammation which may lead to development of co-morbidities like cardiovascular diseases. Cocoa is a popular food ingredient that has been shown to mitigate obesity and inflammation in preclinical models. Cocoa typically undergoes fermentation and roasting prior to consumption, which can affect the polyphenol content in cocoa. The aim of this study was to compare the effect of fermentation and roasting protocols on the ability of cocoa to mitigate obesity, gut barrier dysfunction, and chronic inflammation in high fat (HF)-fed, obese C57BL/6J mice. We found that treatment of mice with 80 mg/g dietary cocoa powder for 8 weeks reduced rate of body weight gain in both male and female mice (46-57%), regardless of fermentation and roasting protocol. Colonic length was increased (11-24%) and gut permeability was reduced (48-79%) by cocoa supplementation. Analysis of the cecal microbiome showed that cocoa, regardless of fermentation and roasting protocol, reduced the ratio of Firmicutes to Bacteroidetes. Multivariate statistical analysis of markers of inflammation and body weight data showed sex differences in the effect of both the HF diet as well as cocoa supplementation. Based on this data there was strong protective efficacy from cocoa supplementation especially for the more processed cocoa samples. Overall, this study shows that anti-obesity and anti-inflammatory efficacy of cocoa is resilient to changes in polyphenol content and composition induced by fermentation or roasting. Further, this study shows that although cocoa has beneficial effects in both males and females, there are significant sex differences.
Subject(s)
Cacao , Chocolate , Food Ingredients , Animals , Anti-Inflammatory Agents/pharmacology , Anti-Inflammatory Agents/therapeutic use , Body Weight , Diet, High-Fat/adverse effects , Disease Models, Animal , Inflammation , Male , Mice , Mice, Inbred C57BL , Mice, Obese , Obesity , Polyphenols/pharmacologyABSTRACT
Sub-optimal diet and physical activity (PA) levels have been associated with increased risk of cardiovascular disease (CVD) mortality. The relationship between pre-cancer diagnosis diet quality and PA level on CVD mortality risk in cancer survivors is unclear. We examined the association between pre-cancer diagnosis diet quality and leisure-time PA and their interaction on CVD mortality in cancer survivors. Diet quality was characterized by the Alternative Mediterranean Diet Index (aMED). Leisure-time PA was converted to a metabolic equivalent of task hours per week (MET-h/wk). During a median of 6.3 years of follow-up of 18,533 female cancer survivors, we identified 915 CVD deaths. aMED score was not associated with CVD mortality. PA level was inversely associated with CVD mortality (HRQ1-Q4 = 0.74; 95% CI: 0.61-0.88; Ptrend = 0.0014). Compared to cancer survivors with the lowest pre-diagnosis aMED score and PA level, cancer survivors with higher aMED scores and higher MET-hrs/wk were at a 33% lower risk of CVD mortality (HR = 0.67; 95% CI: 0.52-0.87). Overall, this study shows PA to be a strong predictor of CVD mortality in female cancer survivors. Our observations support the importance of PA throughout the lifecycle in lowering CVD mortality risk.