Many studies have explored the relationship between coffee—one of the most commonly consumed beverages today—and obesity. Despite inconsistent results, the relationship has not been systematically summarized. Thus, we conducted a meta-analysis by compiling data from 12 epidemiologic studies identified from PubMed and Embase through February 2019. The included studies assessed obesity by body mass index (BMI, a measure of overall adiposity) or waist circumference (WC, a measure of central adiposity); analyzed the measure as a continuous outcome or binary outcome. Using random effects model, weighted mean difference (WMD) and 95% confidence interval (CI) were obtained for continuous outcomes; summary relative risk (RR) and 95% CI for the highest vs. lowest categories of coffee intake were estimated for binary outcome. For BMI, WMD was −0.08 (95% CI −0.14, −0.02); RR was 1.49 (95% CI 0.97, 2.29). For WC, WMD was −0.27 (95% CI −0.51, −0.02) and RR was 1.07 (95% CI 0.84, 1.36). In subgroup analysis by sex, evidence for an inverse association was more evident in men, specifically for continuous outcome, with WMD −0.05 (95% CI −0.09, −0.02) for BMI and −0.21 (95% CI −0.35, −0.08) for WC. Our meta-analysis suggests that higher coffee intake might be modestly associated with reduced adiposity, particularly in men.

Alcohol is widely consumed and is known as a major risk factor for several types of cancers. Yet, it is unclear whether alcohol consumption is associated with the risk of prostate cancer (PCa) or not. We conducted linear and non-linear dose–response meta-analyses of cohort studies on alcohol consumption and PCa risk by types of alcohol (total, wine, beer, and liquor) and PCa (non-aggressive and aggressive). Pubmed and Embase were searched through April 2020 to identify relevant studies. Summary relative risk (RR) and 95% confidence interval (CI) were estimated using a random-effects model. For non-aggressive PCa, by alcohol type, the risk increased linearly with liquor (RR per 14 g/day intake (alcohol content in standard drink) being 1.04 (95% CI = 1.02–1.06, I² = 0%, three studies) and non-linearly with beer (P_{non-linearity} = 0.045, four studies), with increased risk observed in the lower range (RR = 1.03, 95% CI = 1.01–1.05; 14 g/day), with 1.05 (95% CI = 1.01–1.08) at 28 g/day. Wine was not significantly associated with the risk of non-aggressive PCa. For aggressive PCa, a non-linear relationship of diverse shapes was indicated for all types of alcohol in the sensitivity analysis. Compared to non-drinking, a significant positive association was more apparent at lower dose for liquor (RR = 1.12, 95% CI = 1.04–1.20 at 14 g/day; RR = 1.16, 95% CI = 1.03–1.31 at 28 g/day; P_{non-linearity} = 0.005, three studies) but at higher doses for wine (RR = 1.02, 95% CI = 0.90–1.16 at 28 g/day, RR = 1.35, 95% CI = 1.08–1.67 at 56 g/day; P_{non-linearity} = 0.01, four studies). In contrast, decreased risks were indicated at lower doses of beer (RR = 0.85, 95% CI = 0.79–0.92 at 14 g/day; RR = 0.79, 95% CI = 0.70–0.90 at 28 g/day, P_{non-linearity} < 0.001, four studies). Total alcohol consumption was not associated with both types of PCa. In this study, we found heterogeneous associations between alcohol intake and PCa by types of alcohol and PCa.

Previous studies have suggested a “cholesterol-lowering effect” of preclinical pancreatic cancer, suggesting lower total cholesterol as a potential diagnostic marker. Leveraging repeated measurements of total cholesterol, this study aims to examine the temporal association of total cholesterol and pancreatic cancer incidence. We conducted a nested case-control study based on a Korean National Health Insurance Service–Health Screening Cohort, including 215 pancreatic cancer cases and 645 controls matched on age and sex. Conditional logistic regression was applied to estimate the odds ratio (OR) and 95% confidence interval (CI) for the associations of pancreatic cancer incidence with total cholesterol levels across different time windows over 11 years before pancreatic cancer diagnosis (recent, mid, distant). We found that, compared to participants with total cholesterol < 200 mg/dL in the recent 3 years prior to diagnosis, those having total cholesterol ≥ 240 mg/dL showed a significantly lower pancreatic cancer incidence (OR = 0.50 (0.27–0.93)). No significant association was found in relation to total cholesterol measured in the mid and distant past. When changes in total cholesterol over the three time periods were analyzed, compared with those with total cholesterol levels consistently below 240 mg/dL over the entire period, the OR of pancreatic cancer was 0.45 (0.20–1.03) for participants with recent-onset hypercholesterolemia, 1.89 (0.95–3.75) for recent-resolved hypercholesterolemia, and 0.71 (0.30–1.66) for consistent hypercholesterolemia. In conclusion, while high total cholesterol in the recent past may indicate a lower pancreatic cancer incidence, a recent decrease in total cholesterol may suggest an elevated incidence of pancreatic cancer.