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Inflammation, a risk factor for cardiovascular disease, is associated with low plasma levels of antioxidant vitamins. In addition to vitamins, other antioxidants modulate the synthesis of inflammatory markers in vitro and contribute to the total antioxidant capacity (TAC) of a diet. However, the relationship between dietary TAC and markers of inflammation has never been evaluated in vivo. We investigated the relationship between dietary TAC and markers of systemic (high-sensitivity C-reactive protein (hs-CRP), leucocytes) and vascular (soluble intercellular cell adhesion molecule-1) inflammation in 243 nondiabetic subjects. General Linear Model (GLM) analysis showed a significant (P¼0·005) inverse relationship between hs-CRP and quartiles of energyadjusted dietary TAC, even when recognized modulating factors of inflammation, namely alcohol, fibre, vitamin C, a-tocopherol, b-carotene, BMI, waist circumference, HDL-cholesterol, hypertension, insulin sensitivity and plasma b-carotene, were included in the model as covariates (P¼0·004). The relationship was stronger for subjects with hypertension (P¼0·013 v. P¼ 0·109 for normotensive individuals). Among dietary factors, TAC was significantly higher (5·3 (SD 3·0) v. 4·9 (SD 2·7) mmol Trolox/d; P¼0·026) in subjects with low plasma hs-CRP (range: 0·0-4·1 mg/l) than in subjects with high plasma hs-CRP (range: 4·2-27·8 mg/l). We conclude that dietary TAC is inversely and independently correlated with plasma concentrations of hs-CRP and this could be one of the mechanisms explaining the protective effects against CVD of antioxidant-rich foods such as fruits, whole cereals and red wine. This could be of particular significance for subjects with high blood pressure.

Selecting foods according to their TAC markedly affects antioxidant intake and modulates hepatic contribution to systemic inflammation without affecting traditional markers of antioxidant status.

The total antioxidant capacity (TAC) of the diet may be an important tool to monitor the protective effect of plant foods in epidemiological studies. We developed a semi-quantitative FFQ for the assessment of dietary TAC by 3 different assays, i.e., Trolox equivalent antioxidant capacity (TEAC), total radical-trapping antioxidant parameter (TRAP) and ferric reducing-antioxidant power (FRAP). The FFQ consists of 53 questions about the major sources of dietary TAC in Northern Italy and was validated against a 3-d weighed food record (3D-WR) in 285 individuals (159 males and 126 females) aged 35-88 y and living in the province of Parma (Italy). Plasma TAC was also evaluated in a subgroup of subjects using the TEAC and FRAP assays. The FFQ was associated with 3D-WR (quadratic-weighted kappa = 0.49 for TEAC, 0.53 for TRAP, and 0.49 for FRAP; P < 0.0001) and proved reasonably accurate to classify individuals into quartiles of TAC intake. The FFQ had a good repeatability when readministered after 1 y in 55 subjects (quadratic-weighted kappa for intertertile agreement = 0.66 for TEAC, 0.70 for TRAP and 0.68 for FRAP; P < 0.0001). With both dietary instruments, the main contributors to TAC intake were coffee and tea in women and alcoholic beverages in men, followed by fruits and vegetables in both sexes. Plasma TAC and dietary TAC were not associated. In conclusion, our FFQ has the potential for being used to rank subjects on the basis of their antioxidant intake as determined by dietary TAC in large epidemiological studies. The FFQ should be validated in external populations before being used for research purposes.

High-GI dietary habits are associated with HG-LS, particularly in insulin-resistant subjects. Dietary advice on the quality of carbohydrate sources therefore may be a complementary tool for preventing or treating LS of metabolic origin.

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Insulin deficiency induces an increase in blood glucose levels that, in long run, becomes toxic for many organs and systems. Microangiopathy and derangements in the immune function are known consequences of hyperglycemia, but the way in which these systemic alterations may affect pulmonary function has been scarcely investigated. Although confirmation from large clinical trials is still to come, the diabetic disease seems to hit the pulmonary microcirculation as any other organ by increasing vessel wall thickness and impairing gas exchange, which leads to a measurable loss of function and respiratory efficiency. In addition, a diabetic lung is more susceptible to low respiratory tract infections by atypical microorganisms and more likely to host severe episodes of pneumonia than a normal, non-diabetic lung. This is a review of current knowledge on the impact of diabetes mellitus in lung health. We have paid special attention to the role of metabolic control in preventing damage to the lung by sustained hyperglycemia.