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A response from the authors of the article "Virus C hepatitis and Type 2 diabetes: A cohort study in Southern Italy" in 2013 issue, is presented.

OBJECTIVES:The relationship between hepatitis C virus (HCV) infection and type 2 diabetes mellitus (DM 2) is still uncertain. The objective of this study was to evaluate the association between HCV infection, measured as positivity to anti-HCV antibodies, and the incidence of DM 2 in a cohort of subjects sampled from the general population and followed up for 20 years.METHODS:At baseline, the cohort consisted of a random sample of 2,472 subjects (72% response rate, age range 30-69 years) from the electoral register of a town in Southern Italy. The cohort subjects were examined three times: in 1985 (M1), in 1992 (M2), and in 2005 (M3). At M1, M2, and M3, each participant filled in a questionnaire and had a blood sample taken to measure blood glucose and other serum variables including glutamic pyruvic alanine aminotransferase (ALT). Anti-HCV antibodies were analyzed with standard techniques at M1 and M2. Diabetes type 2 diagnosis was a history of diabetes and/or serum glucose ≥126 mg/dl and/or treatment with insulin or hypoglycemic drugs. Logistic regression was used for multivariable data analysis.RESULTS:Diabetes prevalence was higher in subjects with positive anti-HCV antibodies at M1 and M2, and diabetes incidence was higher in subjects with baseline positive anti-HCV antibodies at M1-M2 and lower at M2-M3. In multivariable models, controlling for gender, age, and body mass index (BMI), there was no association between incident cases of diabetes and positive anti-HCV antibodies at baseline, either at M1-M2 (odds ratio (OR) 0.73, 95% confidence interval (CI) 0.43-1.22) or at M2-M3 (0.65, 0.41-1.04). HCV was associated with DM 2 only in subjects with elevated ALT (OR 0.58, 95% CI 0.31-1.08, if ALT normal; OR 1.47, 95% CI 1-2.16, if ALT elevated, controlling for age, gender, and BMI).CONCLUSIONS:Our findings, in a cohort study at population level, support an association between the presence of anti-HCV antibodies at baseline and a higher incidence of type 2 diabetes in the following 20 years only in subjects with elevated ALT. [ABSTRACT FROM AUTHOR]

Background: Higher Dietary Inflammatory Index (DII®) scores are associated with increased morbidity and mortality. However, little is known about the effects of DII on mortality in Mediterranean countries. Therefore, in the present study, we aimed to investigate the potential association between DII scores and overall, cancer and cardiovascular disease (CVD) mortality in people living in a Mediterranean area. Methods: DII scores were calculated using a validated food‐frequency questionnaire. DII scores were then categorised into tertiles. Mortality was ascertained via death certificates. The association between DII scores with overall and cause‐specific mortality was assessed via a multivariable Cox's regression analysis and reported as hazard ratios (HRs) with their 95% confidence intervals (CIs). Results: The study included 1565 participants (mean age 65.5 years; females 44.7%). After a median follow‐up of 12 years (2005–2017), 366 (23.4%) participants died. After adjusting for 17 potential confounders, people with higher DII scores had an increased risk of death compared to those in the lowest (most anti‐inflammatory) tertile (HR = 1.38; 95% CI = 1.04–1.82 for the second tertile; HR = 1.38; 95% CI = 1.03–1.86 for the third tertile). Each 1 SD increase in DII score increased the risk of death by 13%. No association was found between DII scores and cancer or CVD death when considered separately. Conclusions: Higher DII scores were associated with a significantly higher mortality risk, whereas the association with cause‐specific mortality was less clear. These findings highlight the potential importance of diet in modulating inflammation and preventing death. [ABSTRACT FROM AUTHOR]

Context:Endocannabinoids control food intake via both central and peripheral mechanisms, and cannabinoid type-1 receptor (CB1) modulates lipogenesis in primary adipocyte cell cultures and in animal models of obesity.Objectives:We aimed to evaluate, at the population level, the frequency of a genetic polymorphism of CB1 and to study its correlation with body mass index.Design, setting and participants:Healthy subjects from a population survey carried out in southern Italy examined in 1992–1993 and older than 65 years (n=419, M=237, F=182) were divided into quintiles by body mass index (BMI). Two hundred and ten subjects were randomly sampled from the first, third and fifth quintile of BMI (BMI, respectively: 16.2–23.8=normal, 26.7–28.4=overweight, 31.6–49.7=obese) to reach a total of 70 per quintile. Their serum and white cells from the biological bank were used to measure the genotype and the blood variables for the study.Measurements:Anthropometric parameters, blood pressure, serum glucose and lipid levels were measured with standard methods; genotyping for the CB1 1359G/A polymorphism was performed using multiplex PCR. Statistical methods included χ2 for trend, binomial and multinomial multiple logistic regression to model BMI on the genotype, controlling for potential confounders.Results:We found a clear trend of increasing relative frequency of the CB1 wild-type genotype with the increase of BMI (P=0.03) and, using a multiple logistic regression model, wild-type genotype, female gender, age, glycaemia and triglycerides were directly associated with both overweight (third quintile of BMI) and obesity (fifth quintile of BMI).Conclusions:Although performed in a limited number of subjects, our results show that the presence of the CB1 polymorphic allele was significantly associated with a lower BMI.International Journal of Obesity (2007) 31, 908–912; doi:10.1038/sj.ijo.0803510; published online 12 December 2006 [ABSTRACT FROM AUTHOR]