Romina di Giuseppe

Alcohol consumption and cardiovascular risk: mechanisms of action and epidemiologic perspectives.

An inverse association between moderate alcohol intake and cardiovascular risk, in particular coronary disease and ischemic stroke, has been demonstrated in many epidemiologic studies. In addition, several not primarily vascular diseases are also known to occur less frequently in moderate drinkers than in nondrinkers, whereas excess drinking is unquestionably harmful. As a consequence, strong concern exists on the possibility that at any dosage the benefit of alcohol could overcome its harmful effects. Alcohol affects several biochemical factors that have potential cardioprotective benefits, including lipids, platelet aggregation, fibrinogen, tissue-plasminogen activator, plasminogen-activator inhibitor and omega-3 fatty acids. Wine possibly acts through mechanisms that might provide additional cardiovascular benefits. Mechanisms supporting the protective effect of moderate alcohol intake against cardiovascular disease, and epidemiologic evidence concerning the relationship between alcohol dosing and vascular and all-cause mortality are discussed in this review.

Association of proinflammatory diet with low-grade inflammation: results from the Moli-sani study

OBJECTIVES The association between diet and inflammation is well documented. Yet, no evidence exists on the relationship between the inflammatory potential of the diet and low-grade inflammation (LGI) as measured by a composite score of plasma and cellular biomarkers. The aim of this study was to assess the association between the Dietary Inflammatory Index (DII®) and LGI in a large population-based cohort. METHODS Cross-sectional analyses were conducted on data from 20 823 adults (age ≥35 y; 48% male) without acute inflammation, who were recruited within the general population of the Moli-sani study from 2005 to 2010. LGI was measured by using a composite score (INFLA-score) including platelet and leukocyte counts, the granulocyte to lymphocyte ratio, and C-reactive protein. DII scores were computed based on dietary intake assessed by the EPIC food frequency questionnaire. Multivariable linear regression models were fit to produce adjusted regression coefficients and 95% confidence intervals (CIs). RESULTS Higher DII scores were associated with increased LGI (β = 0.131; 95% CI, 0.089-0.174 for the highest versus lowest quintile of DII) after adjusting for age, sex, lifestyle, prevalence of chronic diseases, and health conditions. A higher DII score also was positively associated with each single biomarker of inflammation included in the INFLA-score, unhealthy behaviors (smoking, sedentary lifestyle), and insulin. CONCLUSIONS Higher DII scores, indicating greater inflammatory potential of the diet, were directly associated with LGI, as measured by a composite score of plasma and cellular biomarkers of inflammation. These findings are consistent with the contributing role of diet-mediated inflammation in increasing risk for inflammation-related chronic diseases.