The Journal of nutrition · 2026
Fish Consumption and Colorectal Neoplasms among Lynch Syndrome Carriers.
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Bulbaai Marjolein T, Wesselink Evertine, Bisseling Tanya M, Koornstra Jan Jacob, van Leerdam Monique E, Le Marchand Loïc, Newcomb Polly A, Samadder N Jewel, Schep-Wijnveen Hanna Jm, Kampman Ellen, van Duijnhoven Fränzel J
Аннотация
BACKGROUND: Fish intake may exert antineoplastic effects, potentially through omega-3 fatty acids. However, its role in the development of colorectal neoplasms (CRNs) among individuals with Lynch syndrome (LS), a genetic predisposition to colorectal cancer, remains unclear.
OBJECTIVES: The aim of this study was to examine the association between fish intake and CRN risk among LS carriers, overall and across subgroups defined by nonsteroidal anti-inflammatory drug/aspirin use, sex, geographical region, CRN history, and pathogenic variant type, and to examine associations between fish types and CRN risk.
METHODS: Data from 1816 confirmed LS carriers in the GEOLynch cohort (The Netherlands) and the Colon Cancer Family Registry (Australia, Canada, and the United States) were used. Information on fish intake was collected at inclusion using food frequency questionnaires. CRNs included adenoma, serrated lesions, and colorectal cancer. Multivariable Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) across sex-specific quartiles and per 10 g/d of total fish intake. Associations for specific fish types were assessed per 5 g/d increase.
RESULTS: During a median follow-up time of 7.0 y (IQR range: 2.8-13.6), 742 (40.9%) participants developed a CRN. The CRN risk was similar in individuals in the highest quartile of fish intake compared with the lowest quartile (HR 1.03; 95% CI: 0.81, 1.32). No association was observed for every 10 g/d increment in fish intake (HR: 1.0; 95% CI: 0.95, 1.05) and across subgroups. However, a 5 g/d increase in canned fish appeared to increase the risk of CRNs (HR: 1.06; 95% CI: 1.01, 1.10).
CONCLUSIONS: Total fish intake does not appear to influence the development of CRNs in individuals with LS, whereas the influence of canned fish intake on CRN risk should be further investigated.
OBJECTIVES: The aim of this study was to examine the association between fish intake and CRN risk among LS carriers, overall and across subgroups defined by nonsteroidal anti-inflammatory drug/aspirin use, sex, geographical region, CRN history, and pathogenic variant type, and to examine associations between fish types and CRN risk.
METHODS: Data from 1816 confirmed LS carriers in the GEOLynch cohort (The Netherlands) and the Colon Cancer Family Registry (Australia, Canada, and the United States) were used. Information on fish intake was collected at inclusion using food frequency questionnaires. CRNs included adenoma, serrated lesions, and colorectal cancer. Multivariable Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) across sex-specific quartiles and per 10 g/d of total fish intake. Associations for specific fish types were assessed per 5 g/d increase.
RESULTS: During a median follow-up time of 7.0 y (IQR range: 2.8-13.6), 742 (40.9%) participants developed a CRN. The CRN risk was similar in individuals in the highest quartile of fish intake compared with the lowest quartile (HR 1.03; 95% CI: 0.81, 1.32). No association was observed for every 10 g/d increment in fish intake (HR: 1.0; 95% CI: 0.95, 1.05) and across subgroups. However, a 5 g/d increase in canned fish appeared to increase the risk of CRNs (HR: 1.06; 95% CI: 1.01, 1.10).
CONCLUSIONS: Total fish intake does not appear to influence the development of CRNs in individuals with LS, whereas the influence of canned fish intake on CRN risk should be further investigated.