British Journal of Nutrition. 2011;106(Suppl 3):S5-78
Low grade inflammation is a characteristic of the obese state, and adipose tissue releases many inflammatory mediators. The source of these mediators within adipose tissue is not clear, but infiltrating macrophages seem to be especially important, although adipocytes themselves play a role. Obese people have higher circulating concentrations of many inflammatory markers than lean people do and these are believed to play a role in causing insulin resistance and other metabolic disturbances. Blood concentrations of inflammatory markers are lowered following weight loss. In the hours following the consumption of a meal there is an elevation in the concentrations of inflammatory mediators in the bloodstream which is exaggerated in obese subjects and in type 2 diabetics. Both high glucose and high fat meals may induce post-prandial inflammation and this is exaggerated by a high meal content of advanced glycated end-products (AGEs) and partly ablated by inclusion of certain antioxidants or antioxidant containing foods within the meal. Healthy eating patterns are associated with lower circulating concentrations of inflammatory markers. Among the components of a healthy diet, whole grains, vegetables and fruits, and fish are all associated with lower inflammation. AGEs are associated with enhanced oxidative stress and inflammation. Saturated fatty acids and trans monounsaturated fatty acids are pro-inflammatory, while polyunsaturated fatty acids (PUFAs), especially long chain n-3 PUFAs are anti-inflammatory. Hyperglycaemia induces both post-prandial and chronic low grade inflammation. Vitamin C, vitamin E and carotenoids decrease the circulating concentrations of inflammatory markers. Potential mechanisms are described and research gaps, which limit our understanding of the interaction between diet and post-prandial and chronic low grade inflammation, are identified.