Association Between Dietary Total Fat and Cholesterol Intake and Pancreatic Cancer Risk: A Dose–Response Meta-Analysis of Cohort and Case-Control Studies
Aug 2026· Nutrients· Vol 18· 0 citations· 56 references
Medicine
TL;DR
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.
Abstract
Background: Pancreatic cancer (PC) is a highly lethal malignancy with a poor prognosis. Dietary total fat and cholesterol intake have been suggested as potential modifiable risk factors, but the evidence remains inconsistent. This study aimed to systematically evaluate the association between dietary total fat and cholesterol intake and PC risk. Methods: A comprehensive literature search was conducted in PubMed, Scopus, Google Scholar, and Web of Science from database inception to May 2026. Cohort and case–control studies reporting relative risks (RRs), odds ratios (ORs), or hazard ratios (HRs) for the association between dietary total fat or cholesterol intake and PC risk were included. Pooled effect size (ES) and 95% confidence intervals (CIs) were calculated using random-effects models. Results: Twenty-five studies (17 case–control and 8 cohort studies) were included, most of which were of high quality. Cohort studies showed no association of dietary cholesterol (ES: 1.02; 95% CI: 0.87–1.20) or total fat intake (ES: 1.00; 95% CI: 0.84–1.20) with PC risk. In case–control studies, high cholesterol intake was associated with increased PC risk (ES: 1.63; 95% CI: 1.32–2.01), whereas total fat intake was not (ES: 1.18; 95% CI: 0.85–1.65). In cohort studies, dose–response analyses showed no significant associations between cholesterol or total fat intake and PC. In case–control studies, each 100 mg/day increase in cholesterol intake was associated with a 13% higher risk of PC, whereas no significant dose–response association was observed for total fat intake. Subgroup and sensitivity analyses supported these findings, and no publication bias was detected. Conclusions: 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. Further prospective studies are needed to clarify these associations.
Breast cancer remains the most commonly diagnosed malignancy among women worldwide. Although dietary fatty acids have been widely investigated, the relationship between polyunsaturated fatty acids intake and breast cancer risk remains unclear. This study aimed to conduct a systematic review and meta-analysis of cohort studies to elucidate the association between higher dietary intake of omega-3 (ω-3) and omega-6 (ω-6) fatty acids and breast cancer risk. A systematic search of major databases was conducted up to January 2026 to identify eligible cohort studies. Random-effects models were used to pool multivariable-adjusted effect sizes (ESs). Heterogeneity was assessed using the I2 statistic, and publication bias was evaluated using Begg's and Egger's tests. Sixteen studies on ω-3 and 18 on ω-6 were included. ω-3 intake was not significantly associated with breast cancer risk (ES: 0.97; 95% CI: 0.92-1.02; p = 0.248; I2 = 10.2%). ω-6 intake also demonstrated no significant overall effect (ES: 1.03; 95% CI: 0.97-1.10; p = 0.384; I2 = 43.9%). Subgroup analyses revealed regional variability, with American studies showing a significant, small inverse association with ω-6 intake (ES: 0.95; 95% CI: 0.92-0.98; p = 0.002). Sensitivity analyses confirmed the robustness of findings, and funnel plots indicated no substantial publication bias. This meta-analysis found no significant association between higher dietary intake of ω-3 or ω-6 and the risk of breast cancer.
Mehdi Karimi, Shirin Maghboulian, O. Asbaghi et al.· Lipids· 0 citations
BACKGROUND
Pancreatic cancer is relatively rare but remains one of the most lethal tumors. Identifying modifiable risk factors is a crucial step to reduce disease burden. Evidence suggests a potential role of type 2 diabetes mellitus in its pathogenesis.
OBJECTIVE
To examine the association between dietary patterns related to diabetes and pancreatic cancer risk in a European population.
METHODS
A total of 367,395 participants from the European Prospective Investigation into Cancer and Nutrition study were included. After a median follow-up of 14.9 years, 926 incident cases were identified. The Diabetes Risk Reduction Diet (DRRD), the Empirical Dietary Index for Hyperinsulinemia (EDIH) and the Empirical Dietary Index for Insulin Resistance (EDIR) were estimated from food frequency questionnaires at recruitment. Hazard ratios (HRs) and 95% confidence intervals (CI) for the association between dietary patterns and pancreatic cancer were calculated using multivariable Cox proportional hazards regression models, adjusted for relevant confounders.
RESULTS
Adherence to DRRD showed no association with risk of pancreatic cancer (HRT3vsT1 = 0.94, 95% CI 0.79-1.12). Higher adherence to EDIH was associated with a borderline 19% increased pancreatic cancer risk (HRT3vsT1 = 1.19, 95% CI 0.99-1.44). No significant associations were observed in relation to EDIR. No heterogeneity was observed among the subgroups.
CONCLUSIONS
Higher adherence to a hyperinsulinemic dietary pattern may contribute to the risk of developing pancreatic cancer in our population. Further research is warranted to elucidate the potential role of dietary factors in cancer risk prevention.
L.F. Torres-Laiton, W. Balcerzak, R. Zamora et al.· Journal of NutriLife· 0 citations
A possible protective role for magnesium is supported and potential biases warrant cautious interpretation, and these findings support a possible protective role for magnesium and highlight the need for further large prospective studies.
Essam Rama, Yusef Ibraheem, David Wong et al.· British Journal of Surgery· 0 citations
This study indicates that higher dietary TAC intake is associated with a reduced risk of breast cancer, and well-designed longitudinal studies are warranted to confirm these findings.
Jianying Zhou, Hai-Yan Jin, Shan Jing et al.· Frontiers in Nutrition· 0 citations
Depression is a leading cause of global disability, and identifying modifiable lifestyle factors is a public health priority. We conducted a systematic review and dose-response meta-analysis of prospective cohort studies examining the association between fruit and vegetable intake and incident depression. PubMed, Web of Science, Scopus, Embase, and Google Scholar were searched through November 2025. Data on study characteristics, dietary assessment, outcomes, effect estimates, and covariates were independently extracted by two reviewers. Random-effects models were used to calculate pooled relative risks (RRs), and linear and non-linear dose-response relationships were assessed. Heterogeneity was evaluated using I2, and evidence certainty was rated with GRADE. Thirteen cohorts with 385,449 participants and 26,592 depression cases were included. Highest versus lowest combined fruit and vegetable intake was associated with a 37% lower risk of depression (RR: 0.63; 95% CI: 0.50, 0.80). Each 200 g/day increase corresponded to a 16% risk reduction (RR: 0.84; 95% CI: 0.74-0.94). Separate analyses showed that fruit and vegetable intake reduced depression risk by 16% and 12%, respectively, with a non-linear dose-response for vegetables. These findings indicate that higher consumption of fruits and vegetables is associated with lower depression risk, supporting dietary strategies as a potential approach for mental health prevention. However, given the observational nature of the included studies, these results should be interpreted with caution, as residual confounding may partially account for the observed associations. Registration: This study was registered at PROSPERO (CRD420261279998).
Nazanin Zamanian, Kimia Torabinasab, Mohammadreza Moradi Baniasadi et al.· Journal of Affective Disorde...· 0 citations
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).
