Authors
Ha Thi Thao Mai, Nilufar Mirzaeva, Do Tung Dac, Tran Tin Nghia, Mai Anh Thi Nguyen, J Luis Espinoza
Published in
Molecular nutrition & food research. Volume 70. Issue 19. Pages e70617.
Abstract
Hyperglycemia and altered carbohydrate metabolism may promote pancreatic cancer cell survival and proliferation. This narrative review critically evaluates epidemiological evidence on whether sugar-sweetened beverage (SSB) consumption is associated with pancreatic cancer risk and examines potential biological mechanisms involving glucose and fructose metabolism, oncogenic KRAS signaling, and metabolic reprogramming.
Earlier pooled analyses and a 2019 meta-analysis found no significant overall association between SSB consumption and pancreatic cancer risk. However, three subsequent studies, including a large prospective cohort from Taiwan and case-control studies from the United States and Jordan, reported positive associations in selected high-consumption groups. Differences in beverage definitions, dietary assessment methods, residual confounding, and study populations complicate comparisons. Mechanistic studies provide biological plausibility, suggesting that glucose and fructose metabolism and KRAS-driven metabolic reprogramming may enhance glycolysis, anabolic metabolism, nutrient acquisition, and cancer cell survival.
Evidence linking SSB consumption to pancreatic cancer remains inconsistent and insufficient to establish causality. Future research should standardize beverage definitions, distinguish SSBs from artificially sweetened beverages and fruit juices, use repeated dietary assessments, control metabolic and lifestyle confounders, include diverse populations, and integrate epidemiological data with metabolic and molecular biomarkers.
PMID:
42806724
Bibliographic data and abstract were imported from PubMed on 29 Sep 2026.
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