Evidence map›Paper›PMID 42309306›Full record

ArticleThe Journal of nutrition2026

Fish Consumption and Colorectal Neoplasms among Lynch Syndrome Carriers.

Marjolein T Bulbaai, Evertine Wesselink, Tanya M Bisseling, Jan Jacob Koornstra, Monique E van Leerdam, Loïc Le Marchand, Polly A Newcomb, N Jewel Samadder, Hanna Jm Schep-Wijnveen, Ellen Kampman and 1 more

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Article in The Journal of nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Marjolein T BulbaaiDivision of Human Nutrition and Health, Wageningen University & Research, Wageningen, The Netherlands. Electronic address: marjolein.bulbaai@wur.nl.
Evertine WesselinkDivision of Human Nutrition and Health, Wageningen University & Research, Wageningen, The Netherlands.
Tanya M BisselingDepartment of Gastroenterology, Radboud University Medical Center, Nijmegen, The Netherlands.
Jan Jacob KoornstraDepartment of Gastroenterology and Hepatology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Monique E van LeerdamDepartment of Gastroenterology and Hepatology, Leiden University Medical Center, Leiden, The Netherlands; The Netherlands Foundation for the Detection of Hereditary Tumors, Leiden, The Netherlands; Department of Gastrointestinal Oncology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Loïc Le MarchandPopulation Sciences in the Pacific (Epidemiology), University of Hawaii Cancer Center, Honolulu, HI, United States.
Polly A NewcombPublic Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, WA, United States; Department of Epidemiology, University of Washington, Seattle, WA, United States.
N Jewel SamadderDivision of Gastroenterology and Hepatology, Mayo Clinic, Scottsdale, AZ, United States.
Hanna Jm Schep-WijnveenDivision of Human Nutrition and Health, Wageningen University & Research, Wageningen, The Netherlands.
Ellen KampmanDivision of Human Nutrition and Health, Wageningen University & Research, Wageningen, The Netherlands.
Fränzel J van DuijnhovenDivision of Human Nutrition and Health, Wageningen University & Research, Wageningen, The Netherlands. Electronic address: franzel.vanduijnhoven@wur.nl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFish 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.

objectivesThe 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.

methodsData 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.

resultsDuring 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).

conclusionsTotal 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.

Indexed as

Colorectal NeoplasmsColorectal Neoplasms, Hereditary NonpolyposisDietFishesSeafoodAdultAnimalsAustraliaCohort StudiesFemaleGenetic Predisposition to DiseaseHumansMaleMiddle AgedNetherlandsProportional Hazards Modelscohort studycolorectal neoplasmfish intakeLynch syndromemismatch repair deficient

Identifiers

PMID42309306
PMCPMC13494212

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.