Higher UPF intake was associated with increased digestive system cancer risk, with relatively consistent evidence for colorectal and colon cancers, and dose–response analyses suggested an exposure–response gradient.
Abstract
Background Ultra-processed food (UPF) intake has been associated with digestive system cancer risk, but evidence remains scattered across cancer sites, study designs, and exposure metrics. This systematic review and meta-analysis evaluated associations between UPF intake and digestive system cancer risk overall and by cancer site. We further examined UPF subcategories and dose–response relationships. Methods We systematically searched PubMed, Embase, Web of Science, and the Cochrane Library for English-language cohort and case–control studies published from database inception to May 1, 2026. Hazard ratios (HRs) from cohort studies and odds ratios (ORs) from case–control studies were pooled separately with their corresponding 95% confidence intervals (CIs) using random-effects models. Additional analyses were conducted to investigate site-specific digestive system cancers, UPF subcategories, and dose–response relationships, alongside subgroup, sensitivity, meta-regression, and publication bias assessments. The study protocol was registered in PROSPERO (CRD420261404299). Results A total of nine prospective cohort studies and five case–control studies were included. The main pooled estimates showed a 12% higher risk in cohort studies (HR = 1.12, 95% CI: 1.05–1.20; I2 = 37.6%) and 42% higher odds in case–control studies (OR = 1.42, 95% CI: 1.25–1.60; I2 = 26.7%). Site-specific analyses showed relatively consistent positive associations for colorectal and colon cancer outcomes. Among UPF subcategories, ultra-processed meat/protein products were associated with higher digestive system cancer risk (HR = 1.33, 95% CI: 1.15–1.53). In dose–response analyses using UPF weight share as the primary exposure metric, each 10-percentage-point increase in UPF intake was associated with a 6% higher risk (HR = 1.06, 95% CI: 1.01–1.10), with evidence of non-linearity, although no reliable threshold could be identified. Supplementary analyses based on g/day showed a consistent direction of association. Sensitivity analyses supported the stability of the main findings, and no clear evidence of publication bias was observed. Conclusion Higher UPF intake was associated with increased digestive system cancer risk, with relatively consistent evidence for colorectal and colon cancers. Ultra-processed meat/protein products may be a relevant contributing subcategory, and dose–response analyses suggested an exposure–response gradient. Because evidence came mainly from observational studies and dose–response data were limited, findings require confirmation in high-quality prospective studies. Systematic Review Registration https://www.crd.york.ac.uk/PROSPERO/view/CRD420261404299, identifier PROSPERO (CRD420261404299).
Evidence on the association between ultra-processed food (UPF) consumption and cancer risk is inconsistent, and systematic reviews (SRs) and meta-analyses (MAs) are fragmented across different cancer types and study populations. A comprehensive synthesis is needed to evaluate the robustness of the evidence. We therefore conducted an umbrella review (UR) of SRs and MAs to synthesize the available evidence on the association between UPF consumption and the risk of various cancers. PubMed, Embase, Web of Science, and Cochrane Library were systematically searched from inception to January 15, 2026. Seven MAs and one SR were included. The methodological quality of the included reviews was assessed using AMSTAR 2, and the certainty of evidence was evaluated using the GRADE framework. UPF consumption may be associated with increased risks of overall cancer, colorectal cancer, breast cancer, and gastric cancer. Subgroup analyses indicated that age, region, dietary assessment methods, and study design may contribute to differences in the observed associations. According to the GRADE assessment, two associations were rated as low certainty, while eight were rated as very low certainty. The AMSTAR 2 assessment showed that three reviews were of low methodological quality and four were of very low quality. Overall, this umbrella review suggests that UPF consumption may be associated with an increased risk of several cancers, although the overall certainty of the evidence remains low. Further high-quality prospective studies using standardized methods to assess UPF consumption are needed to strengthen the evidence base and inform public health recommendations.
Jianfang Bao, Xuan Cheng, Yijia Yin et al.· Journal of Food Science· 0 citations
Background Previous studies suggest red and processed meat consumption may increase the risk of pancreatic cancer (PC); however, there is no consensus regarding the associations. A systematic review and meta-analysis were therefore performed to explore the relationship between red and processed meats and PC risk. Methods We searched PubMed, EMBASE, and Web of Science for articles up to April 13, 2026, using random-effects models to calculate relative risks (RRs) and 95% CIs, restricted cubic splines for dose-response relationship, and subgroup/meta-regression for heterogeneity. This systematic review was prospectively registered on PROSPERO (registration number: CRD42022384026; https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=384026). Results Sixteen articles with 1,959,527 participants and 8,856 PC cases were included. There was a 16% increased risk of PC found in the highest versus lowest red meat consumption levels (RR = 1.16, 95% CI: 1.02–1.31). A linear association was observed between red (P non-linear = 0.656) and processed meats (P non-linear = 0.857) and PC risk, with a 10% increase in the risk of PC for each additional 100 g/d of red meat consumption (RR = 1.10, 95% CI: 1.00–1.21). For processed meat products, no significant association with PC risk was found. Conclusion This finding indicates that increased red meat consumption may elevate the PC risk; therefore, daily red meat intake is recommended to be controlled. No evidence links processed meat to PC risk.
Yina Lu, Minqi Gu, Yang Zhao et al.· Frontiers in Nutrition· 1 citation
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.
Syed O. Ahmad, M. Umair, U. Ali et al.· Nutrients· 0 citations
Pancreatic cancer has a poor prognosis and limited preventive strategies. Magnesium is a biologically important micronutrient involved in metabolic regulation, genomic stability, and inflammation, but evidence linking magnesium intake to pancreatic cancer risk is inconsistent. We conducted a systematic review and meta-analysis to evaluate the association between dietary magnesium intake and pancreatic cancer risk.
A systematic search of major electronic databases was conducted from inception to September 2025 in accordance with PRISMA guidelines. Prospective cohort and case–control studies assessing dietary magnesium intake and pancreatic cancer risk were included. Summary relative risks (RRs) and 95% confidence intervals (CIs) comparing highest versus lowest intake categories were pooled using random-effects models. Heterogeneity was assessed using the I² statistic. Subgroup, sensitivity, and publication bias analyses were performed. Study quality was evaluated using the Newcastle–Ottawa Scale.
Nine observational studies (four cohort and five case–control) were included, comprising over 650,000 participants and approximately 2,400 pancreatic cancer cases. Higher magnesium intake was associated with a significantly lower risk of pancreatic cancer (pooled RR = 0.62, 95% CI: 0.45–0.85). Heterogeneity was substantial (I² = 74%), with stronger associations observed in case–control studies. Sensitivity analyses confirmed the robustness of the findings, and no significant publication bias was detected.
Higher dietary magnesium intake is associated with a reduced risk of pancreatic cancer. Although heterogeneity and potential biases warrant cautious interpretation, 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
Background Numerous epidemiological studies have suggested a potential association between the antioxidant capacity of the diet and the risk of breast cancer. Yet, these studies have yielded inconclusive results. We therefore conducted a systematic review and dose-response meta-analysis of observational studies to ascertain the association between dietary total antioxidant capacity (TAC) and breast cancer risk. Methods We systematically searched PubMed, Embase, Scopus, ISI Web of Science and China National Knowledge Infrastructure (CNKI) from database inception to May 2026, using predefined keywords to identify the relevant articles. Random-effects or fixed-effects models were used to pool relative risks (RRs) with corresponding 95% confidence intervals (CIs), as appropriate. Heterogeneity across studies was estimated using Cochran's Q test and the I2 statistics. Results Nine observational studies (seven case-control and two cohort studies), encompassing 33,981 participants, were included in the meta-analysis. Higher dietary TAC intake was significantly associated with a lower risk of breast cancer (RR = 0.86; 95%CI: 0.76–0.98; P = 0.022). Conversely, each standard deviation increment in dietary TAC intake was not associated with the risk of breast cancer (RR = 0.98; 95%CI: 0.94–1.02, P = 0.295). Also, the dose-response analysis showed a linear inverse association between dietary TAC and risk of breast cancer (RR = 0.988; 95%CI: 0.981–0.995, Pdose−response=0.001, Pnonlinearity = 0.546). The results of subgroup analyses showed a significant inverse association between dietary TAC and breast cancer in cohort studies, with low heterogeneity (P = 0.174; I2 = 18.9%). Conclusions This study indicates that higher dietary TAC intake is associated with a reduced risk of breast cancer. Further well-designed longitudinal studies are warranted to confirm these findings.
Jianying Zhou, Haiyan Jin, Jing Shan et al.· Frontiers in Nutrition· 0 citations
