Explore the vast range of titles available.

PurposeTo provide evidence of the relationship of Mediterranean diet (MD) on incidence/mortality for cardiovascular disease (CVD), coronary/ischemic heart disease (CHD)/acute myocardial infarction (AMI) and stroke (ischemic/hemorrhagic) by sex, geographic region, study design and type of MD score (MDS).MethodsWe performed a systematic review and meta-analysis of observational studies. Pooled relative risks (RRs) were calculated using random-effects models.ResultsWe identified 29 articles. The RR for the highest versus the lowest category of the MDS was 0.81 (95% CI 0.74–0.88) for the 11 studies that considered unspecified CVD, consistent across all strata. The corresponding pooled RR for CHD/AMI risk was 0.70 (95% CI 0.62–0.80), based on 11 studies. The inverse relationship was consistent across strata of study design, end point (incidence and mortality), sex, geographic area, and the MDS used. The overall RR for the six studies that considered unspecified stroke was 0.73 (95% CI 0.59–0.91) for the highest versus the lowest category of the MDS. The corresponding values were 0.82 (95% CI 0.73–0.92) for ischemic (five studies) and 1.01 (95% CI 0.74–1.37) for hemorrhagic stroke (four studies).ConclusionsOur findings indicate and further quantify that MD exerts a protective effect on the risk of CVD. This inverse association includes CHD and ischemic stroke, but apparently not hemorrhagic stroke.

We reviewed available evidence on coffee drinking and the risk of all cancers and selected cancers updated to May 2016. Coffee consumption is not associated with overall cancer risk. A meta-analysis reported a pooled relative risk (RR) for an increment of 1 cup of coffee/day of 1.00 [95% confidence interval (CI): 0.99–1.01] for all cancers. Coffee drinking is associated with a reduced risk of liver cancer. A meta-analysis of cohort studies found an RR for an increment of consumption of 1 cup/day of 0.85 (95% CI: 0.81–0.90) for liver cancer and a favorable effect on liver enzymes and cirrhosis. Another meta-analysis showed an inverse relation for endometrial cancer risk, with an RR of 0.92 (95% CI: 0.88–0.96) for an increment of 1 cup/day. A possible decreased risk was found in some studies for oral/pharyngeal cancer and for advanced prostate cancer. Although data are mixed, overall, there seems to be some favorable effect of coffee drinking on colorectal cancer in case–control studies, in the absence of a consistent relation in cohort studies. For bladder cancer, the results are not consistent; however, any possible direct association is not dose and duration related, and might depend on a residual confounding effect of smoking. A few studies suggest an increased risk of childhood leukemia after maternal coffee drinking during pregnancy, but data are limited and inconsistent. Although the results of studies are mixed, the overall evidence suggests no association of coffee intake with cancers of the stomach, pancreas, lung, breast, ovary, and prostate overall. Data are limited, with RR close to unity for other neoplasms, including those of the esophagus, small intestine, gallbladder and biliary tract, skin, kidney, brain, thyroid, as well as for soft tissue sarcoma and lymphohematopoietic cancer.

An inverse association has been reported between coffee drinking and the risk of hepatocellular carcinoma (HCC) and chronic liver disease (CLD), but its magnitude is still unclear. Thus, we carried out a systematic review and meta-analysis of prospective cohort studies that investigated the association between coffee consumption and the risk of HCC or CLD. We separately estimated the relative risk (RR) of the two conditions, for regular, low, and high consumption compared with no or occasional coffee consumption; we also calculated the summary RR for an increment of one cup of coffee per day. Twelve studies on HCC (3414 cases) and six studies on CLD (1463 cases) were identified. The summary RRs for HCC were 0.66 [95% confidence interval (CI): 0.55–0.78] for regular, 0.78 (95% CI: 0.66–0.91) for low, and 0.50 (95% CI: 0.43–0.58) for high coffee consumption, respectively. The summary RR for an increment of one cup per day was 0.85 (95% CI: 0.81–0.90). The summary RRs for CLD were 0.62 (95% CI: 0.47–0.82) for regular, 0.72 (95% CI: 0.59–0.88) for low, 0.35 (95% CI: 0.22–0.56) for high, and 0.74 (95% CI: 0.65–0.83) for an increment of one cup per day. The present meta-analysis provides a precise quantification of the inverse relation between coffee consumption and the risk of HCC, and adds evidence to the presence of an even stronger negative association with CLD.

Both observational studies and randomized trials have shown that a diet rich in antioxidants can reduce systemic inflammation and oxidative stress, two conditions that, together with obesity and smoking, are established risk factors for stroke. However, the association between antioxidant intake and risk for stroke is poorly understood, particularly when studying possible interaction with sex. We investigated the relationship of nonenzymatic antioxidant capacity (NEAC) on risk for stroke in a large Swedish prospective cohort. The cohort study included 34 555 men and women from the Swedish National March Cohort. NEAC was assessed using a detailed food frequency questionnaire, collected at baseline. We achieved complete follow-up from enrollment in 1997 through 2010 by record linkage to nationwide registers. We identified 1186 incident cases of a first stroke, of which 860 were ischemic, 201 hemorrhagic, and 125 unspecified. We used multivariable Cox proportional hazards models to estimate adjusted hazard ratios (HR) with 95% confidence intervals (CIs). Compared with women in the lowest quartile of NEAC, women in the highest quartile had a 27% lower incidence of total stroke (HR, 0.73; 95% CI, 0.53–0.99; Ptrend = 0.03) and 35% lower incidence of ischemic stroke (HR, 0.65; 95% CI, 0.43–0.99; Ptrend = 0.01). Among men, the relationship between NEAC and risk for stroke was not statistically significant and all HRs were close to unity. Findings from the present study suggest that dietary antioxidant capacity from different foods and beverages is inversely associated with risk for stroke, more specifically ischemic stroke, in women. •Dietary nonenzymatic antioxidant capacity (NEAC) is a measure of the overall antioxidant capacity of diet.•Dietary NEAC takes into account synergistic interactions among dietary antioxidants.•The relationship between dietary NEAC and risk for stroke has not been extensively explored.•High levels of dietary NEAC are associated with a decreased risk for ischemic stroke in women.

Several prospective studies considered the relation between coffee consumption and mortality. Most studies, however, were underpowered to detect an association, since they included relatively few deaths. To obtain quantitative overall estimates, we combined all published data from prospective studies on the relation of coffee with mortality for all causes, all cancers, cardiovascular disease (CVD), coronary/ischemic heart disease (CHD/IHD) and stroke. A bibliography search, updated to January 2013, was carried out in PubMed and Embase to identify prospective observational studies providing quantitative estimates on mortality from all causes, cancer, CVD, CHD/IHD or stroke in relation to coffee consumption. A systematic review and meta-analysis was conducted to estimate overall relative risks (RR) and 95 % confidence intervals (CI) using random-effects models. The pooled RRs of all cause mortality for the study-specific highest versus low (≤ 1 cup/day) coffee drinking categories were 0.88 (95 % CI 0.84-0.93) based on all the 23 studies, and 0.87 (95 % CI 0.82-0.93) for the 19 smoking adjusting studies. The combined RRs for CVD mortality were 0.89 (95 % CI 0.77-1.02, 17 smoking adjusting studies) for the highest versus low drinking and 0.98 (95 % CI 0.95-1.00, 16 studies) for the increment of 1 cup/day. Compared with low drinking, the RRs for the highest consumption of coffee were 0.95 (95 % CI 0.78-1.15, 12 smoking adjusting studies) for CHDflHD, 0.95 (95 % CI 0.70-1.29, 6 studies) for stroke, and 1.03 (95 % CI 0.97-1.10, 10 studies) for all cancers. This meta-analysis provides quantitative evidence that coffee intake is inversely related to all cause and, probably, CVD mortality.

A meta-analysis of case-control studies on coffee consumption and colorectal cancer risk was conducted. Twenty-four eligible studies published before May 2010 were identified, including a total of 14,846 cases of colorectal, colon or rectal cancer. Compared to non/occasional drinkers, the odds ratios (OR) for drinkers were 0.83 (95% CI 0.73-0.95) for colorectal, 0.93 (95% CI 0.81-1.07) for colon and 0.98 (95% CI 0.85-1.13) for rectal cancer, with significant heterogeneity among studies; the corresponding ORs for the increment of 1 cup/day were 0.94 (95% CI 0.91-0.98), 0.95 (95% CI 0.92-0.98), and 0.97 (95% CI 0.95-0.99). For the highest coffee drinkers, the ORs were 0.70 (95% CI 0.60-0.81) for colorectal cancer, 0.75 (95% CI 0.64-0.88) for colon cancer and 0.87 (95% CI 0.75-1.00) for rectal cancer, when compared to non/low drinkers. The results of this meta-analysis of case-control studies suggest a moderate favorable effect of coffee consumption on colorectal cancer risk. The reduced risk was consistent across study design (hospital vs. population based), geographic area, and various confounding factors considered. It may reflect a real protection but also partly or largely be due to reverse causation, i.e. decreased coffee consumption among cases following the onset of bowel symptoms.

The aim of this study was to investigate the relation between bladder cancer risk and the use of selected drugs for cardiovascular disease (CVD) prevention, such as aspirin, statins, and calcium channel blockers (CCBs). We analyzed data from a multicentric case–control study carried out in Italy between 2003 and 2014, including 690 bladder cancer cases and 665 hospital controls. Odds ratios (ORs) of bladder cancer and corresponding 95% confidence intervals (CIs) were estimated using unconditional multiple logistic regression models. The ORs for bladder cancer were 1.21 (95% CI: 0.87–1.68) for regular use of aspirin, 0.72 (95% CI: 0.54–0.97) for use of any CCBs, and 1.32 (95% CI: 0.87–1.99) for use of any statins. A slight inverse association was found with duration of use of CCBs, whereas no consistent association was found with duration of use, age at first use, and frequency for aspirin and statin use, or with indication of use for aspirin (as an analgesic or, for CVD prevention). No significant association was found for various combinations of drugs or for all drugs combined (OR=1.23, 95% CI: 0.31–4.85). Our data indicate the lack of a relevant association between the use of selected drugs for CVD prevention and bladder cancer risk, although suggest a potential favorable role for CCBs.

The literature from 1990 to 2003 on the relation between coffee, decaffeinated coffee, tea and colorectal cancer risk has been reviewed. For the relation with coffee, three cohort (517 total cases) and nine case-control studies (7555 cases) analysed colon cancer; three cohort (307 cases) and four case-control studies (2704 cases) rectal cancer; six case-control studies (854 cases) colorectal cancer. For colon cancer most case-control studies found risk estimates below unity; the results are less clear for cohort studies. No relation emerged for rectal cancer. A meta-analysis, including five cohort and twelve case-control studies, reported a pooled relative risk of 0.76 (significant). Any methodological artefact is unlikely to account for the consistent inverse association in different countries and settings. Plausible biological explanations include coffee-related reductions of cholesterol, bile acids and neutral sterol secretion in the colon; antimutagenic properties of selected coffee components; increased colonic motility. Decaffeinated coffee was not related to either colon or rectal cancer in three case-control studies. No overall association between tea and either colon or rectal cancer risk emerged in seven cohort (1756 total cases of colon, 759 of rectal and 60 of colorectal cancer) and 12 case-control studies (8058 cases of colon, 4865 of rectal, 604 of colorectal cancer).

ObjectivesThe aims of this study were to estimate the occurrence of pregnancy-associated cancer overall and by site, to evaluate if the risk increases over time, and to investigate some major determinants.MethodsThis is a population-based linkage study using the regional hospital discharge forms [Scheda di Dimissione Ospedaliera (SDO)] database of Lombardy, Italy, a region with 10 million inhabitants. All resident women with a SDO reporting a birth or abortion between 2001 and 2012 were identified. Pregnancy-associated cancers were defined as a cancer occurring during pregnancy or within 12 months after pregnancy and were identified by selecting all SDOs reporting a first diagnosis of cancer. Risk of developing a pregnancy-related cancer was calculated as the ratio of the number of pregnancy-related cancers to the total number of pregnancies. The effect of potential predictors on the risk was estimated using a logistic regression model, and odds ratios (OR) were estimated.ResultsDuring the period 2001–2012, the risk of pregnancy-related cancer was 122.9 per 100,000 pregnancies. The most common cancers were breast cancer (479 cases, 39.9/100,000 pregnancies), thyroid cancer (186 cases, 15.5/100,000), and lymphomas (157 cases, 13.1/100,000). Skin cancer accounted for 177 cases (14.8/100,000), half of which were melanomas. The risk of developing a pregnancy-related cancer increased significantly with age, from 60 of 100,000 for women less than 30 years old to 265 of 100,000 for women aged more than 40 years. Italian women had a higher risk than foreign ones (OR, 1.6), and the pregnancy outcome was more frequently an abortion (OR, 1.2), whereas no trend in risk was observed with calendar year (P = 0.249).ConclusionsThis study confirms previously reported incidence estimates but does not show increases over time.

To evaluate the association between alcohol consumption and endometrial cancer risk, we analyzed data from a hospital-based case-control study, conducted in Italy between 1992 and 2006, on 454 endometrial cancer cases and 908 controls, and performed a meta-analysis updated to October 2009. Compared to never alcohol drinkers, the odds ratio was 1.03 (95% confidence interval, CI, 0.76-1.41) for ≤7, 1.27 (95% CI 0.86-1.87) for 8-14, and 1.19 (95% CI 0.80-1.77) for ≥15 drinks/week, with no trend in risk. No association emerged for wine, beer, and spirit consumption analyzed separately. The meta-analysis included 20 case-control and seven cohort studies, for a total of 13,120 cases. Compared to non/low drinkers, the pooled relative risks for drinkers were 0.90 (95% CI 0.80-1.01) for case-control studies, 1.01 (95% CI 0.90-1.14) for cohort studies, and 0.95 (95% CI 0.88-1.03) overall, with no heterogeneity between study design (p = 0.156). The overall estimate for heavy versus non/low drinkers was 1.12 (95% CI 0.87-1.45). The results were consistent according to selected study characteristics, including geographic area, definition of alcohol drinkers, and type of controls in case-control studies. Our findings provide evidence that alcohol drinking is not associated with endometrial cancer risk, although a weak positive association for very high drinkers cannot be excluded.