A large prospective cohort analysis published in Gastro Hep Advances reports that daily consumption of sugar-sweetened beverages is associated with a 2.45-fold higher risk of stomach cancer compared with little or no consumption. The study, led by Andrew T. Chan of Massachusetts General Hospital, pooled data from the Nurses' Health Study and the Health Professionals Follow-up Study, encompassing 112,284 participants followed for 36 years (1986–2022). During that period, 278 incident stomach cancer cases were documented.
Participants completed repeated food-frequency questionnaires and provided lifestyle and medical-history updates. A serving was defined as 237 ml (8 oz) of a sugar-sweetened soda, punch, lemonade or sports drink. The primary comparison was between participants who consumed at least one serving per day and those who consumed less than one serving per month.
The adjusted hazard ratio for stomach cancer in the daily-consumption group was 2.45 (95% confidence interval not supplied in the source). The association was stronger in women (approximately threefold) than in men (approximately twofold). The authors did not provide a definitive explanation for the sex difference, noting that hormonal and metabolic factors warrant further study.
No statistically significant association was observed between artificially sweetened beverage intake and stomach cancer risk in this analysis.
Gastroenterologist Sergey Danilov emphasized that the study is observational and therefore establishes correlation, not causation. He noted that sugar drives metabolic disturbances that may systemically weaken the body, but direct carcinogenic action requires confirmation in clinical trials. Internist Anna Kuznetsova added that excess sugar is a proven driver of inflammatory processes and that insulin resistance linked to overweight indirectly creates a favorable environment for gastrointestinal pathologies, making dietary correction a key preventive element.
The authors acknowledge that Helicobacter pylori infection status — a major established risk factor for gastric cancer — could not be fully accounted for. Complete family-history data were also unavailable for all participants. The biological mechanism, whether through insulin resistance, DNA damage, microbiome alteration or another pathway, remains to be elucidated.
Important: This article is for general information and does not replace medical advice. Do not start, stop, or change treatment without a qualified clinician.
Source: This article was adapted from an original Russian-language publication by Pravda.Ru.
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