Objective Sugar-sweetened beverage (SSB) consumption had substantially increased across successive US birth cohorts until 2000, and adolescents and young adults under age 50 years have the highest consumption. However, the link between SSBs and early-onset colorectal cancer (EO-CRC) remains unexamined.
Design In the Nurses’ Health Study II (1991–2015), we prospectively investigated the association of SSB intake in adulthood and adolescence with EO-CRC risk among 95 464 women who had reported adulthood beverage intake using validated food frequency questionnaires (FFQs) every 4 years. A subset of 41 272 participants reported beverage intake at age 13–18 years using a validated high school-FFQ in 1998. Cox proportional hazards models were used to estimate relative risks (RRs) with 95% CIs.
Results We documented 109 EO-CRC cases. Compared with individuals who consumed <1 serving/week of SSBs in adulthood, women who consumed ≥2 servings/day had a more than doubled risk of EO-CRC (RR 2.18; 95% CI 1.10 to 4.35; ptrend=0.02), with a 16% higher risk (RR 1.16; 95% CI 1.00 to 1.36) per serving/day increase. Each serving/day increment of SSB intake at age 13–18 years was associated with a 32% higher risk of EO-CRC (RR 1.32; 95% CI 1.00 to 1.75). Replacing each serving/day of adulthood SSB intake with that of artificially sweetened beverages, coffee, reduced fat milk or total milk was associated with a 17%–36% lower risk of EO-CRC.
Conclusion Higher SSB intake in adulthood and adolescence was associated with a higher risk of EO-CRC among women. Reduction of SSB consumption among adolescents and young adults may serve as a potential strategy to alleviate the growing burden of EO-CRC.
- colorectal cancer
- dietary - colon cancer
- gastrointestinal cancer
- cancer epidemiology
Data availability statement
No additional data are available.
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KW, EG and YC contributed equally.
Contributors JH and YC had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. KW, EG and YC contributed equally. Concept and design: JH, EG and YC. Acquisition, analysis or interpretation of data: JH, KNg, SO, JAM, ATC, WCW, KW, EG and YC. Drafting of the manuscript: JH and YC. Critical revision of the manuscript for important intellectual content: all authors. Statistical analysis: JH. Obtained funding: KNg, SO, ATC, WCW, KW, EG and YC. Administrative, technical or material support: KW, EG and YC. Supervision: EG and YC.
Funding This work was supported by grants U01 CA176726 (WCW), R01 CA205406 (KNg), R21 CA230873 (SO, KW), R01 CA151993 (SO), R35 CA197735 (SO), R35 CA253185 (ATC), R03 CA197879 (KW), R21 CA222940 (KW), R37 CA246175 (YC) and K07 CA218377 (YC) from the National Institutes of Health. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. EO is supported by T32 CA009621. KNg is supported in part by Department of Defense CA160344 and the Project P Fund. ATC is the Stuart and Suzanne Steele MGH Research Scholar. KW is supported in part by an Investigator Initiated Grant from the American Institute for Cancer Research.
Competing interests KNg has received institutional research funding from Pharmavite, Revolution Medicines and Evergrande Group, has served on an advisory board for Seattle Genetics and Array BioPharma and served as a consultant to X-Biotix Therapeutics. JAM has received institutional research funding from Boston Biomedical, has served as an advisor/consultant to Ignyta and COTA Healthcare and served on a grant review panel for the National Comprehensive Cancer Network funded by Taiho Pharmaceutical. ATC previously served as a consultant for Bayer Pharma, Pfizer and Boehringer Ingelheim for topics unrelated to this work.
Provenance and peer review Not commissioned; externally peer reviewed.
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