The aim of this study was to systematically review all evidence evaluating obesity as a prognostic factor for PC mortality. Cohort and case-control studies reporting mortality among PC patients stratified by body mass index (BMI) were included. The risk of mortality among obese patients (BMI ≥ 30) was compared with the risk for normal weight (BMI < 25) patients, pooling individual hazard ratios (HR) in random-effects meta-analyses. Reasons for heterogeneity were assessed in subgroup analyses. Dose-response associations for BMI per 5 kg/m² change were assessed. Among 7278 citations, 59 studies (280,199 patients) met inclusion criteria. Obesity was associated with increased PC-specific mortality (HR: 1.19, 95% CI: 1.10–1.28, I²: 44.4%) and all-cause mortality (HR: 1.09, 95% CI: 1.00–1.18, I²: 43.9%). There was a 9% increase (95% CI: 5–12%, I²: 39.4%) in PC-specific mortality and 3% increase (95% CI: 1–5%, I²: 24.3%) in all-cause mortality per 5 kg/m² increase in BMI. In analyses restricted to the higher quality subgroup (NOS ≥ 8), obesity was associated with increased PC-specific mortality (HR: 1.24, 95% CI: 1.14–1.35, I²: 0.0%) and maintained the dose-response relationship (HR: 1.11 per 5 kg/m² increase in BMI, 95% CI: 1.07–1.15, I²: 26.6%). Obesity had a moderate, consistent, temporal, and dose-response association with PC mortality. Weight control programs may have a role in improving PC survival.

Background: Inverse associations of the Mediterranean diet (MedDiet) and physical activity with cardiovascular disease have been previously reported. We investigated the individual and combined contributions of both to this inverse association in a Mediterranean cohort. Design: We used data from 19,536 participants from a prospective cohort of Spanish university graduates, the ‘Seguimiento Universidad de Navarra’ (SUN) cohort, followed up between December 1999 and December 2016. Methods: Adherence to the MedDiet was obtained from a 136-item validated food-frequency questionnaire and categorized in tertiles using four previously reported dietary scores. A validated questionnaire assessed the physical activity levels according to volume, intensity and frequency. Results: Participants were followed up during a median time of 10.4 years. Compared with the lowest category of adherence to the MedDiet (≤3 in the Mediterranean Diet Score), higher adherence (6–9 points) was strongly inversely associated with cardiovascular disease (multivariable adjusted hazard ratio = 0.33; 95% confidence interval (CI) 0.20–0.55). Also, engaging in an active lifestyle (6–8 points in an eight-item score) compared with low activity (<2 points) was associated with a reduced risk of incident cardiovascular disease (hazard ratio = 0.43; 95% CI 0.20–0.90). Greater adherence to the MedDiet and engaging in high levels of active lifestyle showed a 75% relatively reduced risk of cardiovascular disease (hazard ratio = 0.25; 95% CI 0.13–0.48). Conclusions: The combined effect of adherence to the MedDiet and adopting an active lifestyle showed a synergistic inverse association with cardiovascular disease risk.

The aim of this study was to assess the association between alcohol intake and premature mortality (younger than 65 years) and to explore the effect of potential alcohol underreporting by heavy drinkers. We followed-up 20 272 university graduates. Four categories of alcohol intake were considered (abstainer, light, moderate and heavy consumption). Repeated measurements of alcohol intake and updated information on confounders were used in time-dependent Cox models. Potential underreporting of alcohol intake by some heavy drinkers (likely misclassified as light or moderate drinkers) was explicitly addressed in an attempt to correct potential underreporting by using indirect information. During 12·3 years of median follow-up (interquartile range: 6·8–15·0), 226 participants died before their 65th birthday. A higher risk of early mortality was found for the highest category of alcohol intake (≥50 g/d) in comparison with abstention (multivariable-adjusted hazard ratio (HR) = 2·82, 95 % CI 1·38, 5·79). In analyses of alcohol as a continuous variable, the multivariable-adjusted HR was 1·17 (95 % CI 1·08, 1·26), for each 10 g/d of alcohol. This harmful linear association was present both in uncorrected models and in models corrected for potential underreporting. No significant inverse association between light or moderate alcohol intake and premature mortality was observed, even after correcting for potential misclassification. Alcohol intake exhibited a harmful linear dose–response association with premature mortality (<65 years) in this young and highly educated Mediterranean cohort. Our attempts to correct for potential misclassification did not substantially change these results.