Association between adolescent alcohol consumption and cigarette smoking with adult risk of breast cancer: A systematic review and meta-analysis.

The association between coffee consumption and esophageal cancer risk: a systematic review and meta-analysis of current observational evidence

Background Esophageal cancer remains a leading cause of cancer-related mortality worldwide, yet the association between coffee consumption—a ubiquitous dietary exposure—and its risk remains inconclusive. This meta-analysis systematically evaluates the association between coffee consumption and esophageal cancer risk, aiming to quantify the overall effect and explore potential heterogeneity. Methods A systematic search of PubMed, Cochrane Library, Embase, and Web of Science was conducted up to January 2026 for studies comparing coffee intake between esophageal cancer patients and healthy controls. Two reviewers independently extracted data. Pooled odds ratios (ORs) or hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using random- or fixed-effects models. Heterogeneity was assessed using the I2 statistic. Certainty of evidence was rated using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) framework. Results Across 22 included studies encompassing 1,775,988 participants (7,124 cases), neither cohort nor case-control studies demonstrated a significant association between coffee consumption and esophageal cancer risk. The pooled HR from cohort studies was 0.87 (95% CI: 0.74–1.03; I2=24.2%), while the pooled OR from case-control studies was 1.02 (95% CI: 0.77–1.35; I2=66.7%). Conclusions This meta-analysis found no statistically significant association between coffee consumption and esophageal cancer risk. The available evidence, of low certainty, does not support coffee as a major risk factor. Exploratory analyses on beverage temperature are inconclusive and require confirmation in prospective studies with standardized exposure assessment. This review was registered in PROSPERO (CRD42024562527).

Alcohol intake and risk of stomach cancer: a pooled analysis of 20 cohorts.

There was little evidence of an overall association between alcohol intake and stomach cancer risk, although modest positive associations were observed among never smokers and in Asian cohorts.

Meta-analysis/systematic review iScience Modifiable lifestyle factors and cancer risk in Latin America: A systematic review with meta-analysis

Alcohol amount, drinking patterns, and gastric cancer risk: a nationwide study using targeted maximum likelihood estimation.

It is suggested that alcohol consumption is associated with increased GC risk in a dose-response manner, and recommendations to limit alcohol consumption for cancer prevention are supported.

Association Between Dietary Total Fat and Cholesterol Intake and Pancreatic Cancer Risk: A Dose–Response Meta-Analysis of Cohort and Case-Control Studies

Dietary cholesterol and total fat intake were not associated with PC risk in cohort studies, whereas case–control studies suggested a positive association between cholesterol intake and PC risk.

Association between a combined lifestyle exposure index and age at pancreatic cancer diagnosis: a hospital-based retrospective study

Pancreatic cancer is a highly lethal malignancy, and its incidence is increasing among younger individuals. Although smoking, alcohol use, and unhealthy diet are established risk factors, the cumulative impact of multiple lifestyle exposures on age at diagnosis remains unclear. This study aimed to estimate the combined burden of lifestyle and environmental risks associated with the timing of pancreatic cancer diagnosis. We conducted a hospital-based retrospective case-only study including 134 patients diagnosed with pancreatic cancer between 2020 and 2025. Data on family history of pancreatic cancer, cigarette smoking, alcohol consumption, dietary patterns, exercise, and occupational chemical exposure were collected through structured interviews and medical record reviews. Cox proportional hazards models using age at diagnosis as the time scale were used to evaluate associations between exposures and earlier diagnosis. Lifestyle factors were integrated into a cumulative exposure index and analyzed using Cox models with adjustment for the remaining covariates. The mean age at diagnosis was 64.8 years. A significant difference in age at diagnosis was observed across smoking categories, with current smokers having the youngest mean age, whereas no significant difference was observed across alcohol consumption categories. Patients with triple exposure had the youngest mean age at diagnosis (55.5 years), followed by those with double (63.5 years), single (64.8 years), and no (69.0 years) exposures. Compared with no exposure, single, double, and triple exposures were associated with progressively higher hazards of earlier diagnosis (HR = 1.79, 95% CI: 1.14–2.81, p  = 0.011; HR = 2.97, 95% CI: 1.67–5.28, p  < 0.001; and HR = 6.66, 95% CI: 3.35–13.22, p  < 0.001, respectively). Our findings indicate a significant association between a higher combined exposure index and earlier age at pancreatic cancer diagnosis. This exposure–response gradient suggests that a greater accumulation of adverse lifestyle exposures corresponds to earlier age at diagnosis among affected patients. Not applicable.