Background: Studies have shown an inverse association between use of glucosamine and chondroitin supplements and colorectal cancer risk. However, the association with the precursor lesion, colorectal adenoma and serrated polyp, has not been examined. Methods: Analyses include 43,163 persons from the Nurses' Health Study (NHS), Health Professionals Follow-up Study (HPFS), and NHS2 who reported on glucosamine/chondroitin use in 2002 and who subsequently underwent ≥1 lower gastrointestinal endoscopy. By 2012, 5,715 conventional (2,016 high-risk) adenomas were detected, as were 4,954 serrated polyps. Multivariable logistic regression for clustered data was used to calculate OR and 95% confidence intervals (CI). Results: Glucosamine/chondroitin use was inversely associated with high risk and any conventional adenoma in NHS and HPFS: in the pooled multivariable-adjusted model, glucosamine + chondroitin use at baseline was associated with a 26% (OR = 0.74; 95% CI, 0.60-0.90; Pheterogeneity = 0.23) and a 10% (OR = 0.90; 95% CI, 0.81-0.99; Pheterogeneity = 0.36) lower risk of high-risk adenoma and overall conventional adenoma, respectively. However, no association was observed in NHS2, a study of younger women (high-risk adenoma: OR = 1.09; 95% CI, 0.82- 1.45; overall conventional adenoma: OR = 1.00; 95% CI, 0.86- 1.17), and effect estimates pooled across all three studies were not significant (high-risk: OR = 0.83; 95% CI, 0.63-1.10; Pheterogeneity = 0.03; overall conventional adenoma: OR = 0.93; 95% CI, 0.85- 1.02; Pheterogeneity = 0.31). No associations were observed for serrated polyps. Conclusions: Glucosamine/chondroitin use was associated with lower risks of high-risk and overall conventional adenoma in older adults; however, this association did not hold in younger women, or for serrated polyps. Impact: Our study suggests that glucosamine and chondroitin may act on early colorectal carcinogenesis in older adults.
|Number of pages||9|
|Journal||Cancer Epidemiology Biomarkers and Prevention|
|Publication status||Published - 2020 Dec|
Bibliographical noteFunding Information:
The authors thank the participants and staff of the NHS and HPFS for their valuable contributions as well as the following state cancer registries for their help: AL, AZ, AR, CA, CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE, NH, NJ, NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA, WA, WY. The authors assume full responsibility for analyses and interpretation of these data. The Health Professionals Follow-up Study is supported by NIH U01 CA167552. The NHS was supported by NIH UM1 CA186107 and P01 CA87969. The NHS2 was supported by NIH U01 CA176726. This work was additionally supported by NIH grants: P30 CA008748 and R00 CA215314 to M. Song; R21 CA222940, R21 CA230873, and R03 CA197879 to K. Wu; and R03 CA212983 to E.D. Kantor. This work was also, in part, supported by Investigator Initiated Grants from the American Institute for Cancer Research (AICR) to K. Wu.
K. O’Connell reports grants from NIH R03 (R03 CA212983) during the conduct of the study. M. Du reports grants from NCI during the conduct of the study. K.D. Kantor reports grants from NCI (R03 CA212983 and P30 CA008748) during the conduct of the study. No potential conflicts of interest were disclosed by the other authors.
© 2020 American Association for Cancer Research.
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