Chen Yuan1,2, Hee-Kyung Joh3,4,5, Qiao-Li Wang1, Yin Zhang1,2,6, Stephanie A Smith-Warner2,5, Molin Wang2,6,7, Mingyang Song2,8,9, Yin Cao10,11,12, Xuehong Zhang5,6, Emilie S Zoltick13, Jinhee Hur5,14, Andrew T Chan6,8,9,15,16, Jeffrey A Meyerhardt4, Shuji Ogino2,16,17,18, Kimmie Ng1, Edward L Giovannucci2,5,6, Kana Wu5. 1. Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA. 2. Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, MA, USA. 3. Department of Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea. 4. Department of Family Medicine, Seoul National University Hospital, Seoul, Republic of Korea. 5. Department of Nutrition, Harvard TH Chan School of Public Health, Boston, MA, USA. 6. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 7. Department of Biostatistics, Harvard TH Chan School of Public Health, Boston, MA, USA. 8. Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 9. Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 10. Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St. Louis, MO, USA. 11. Alvin J Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO, USA. 12. Division of Gastroenterology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA. 13. Department of Population Medicine, Harvard Pilgrim Health Care Institute and Harvard Medical School, Boston, MA, USA. 14. Department of Food Science and Biotechnology, Sungkyunkwan University, Suwon, Republic of Korea. 15. Department of Immunology and Infectious Diseases, Harvard TH Chan School of Public Health, Boston, MA, USA. 16. Broad Institute of MIT and Harvard, Cambridge, MA, USA. 17. Program in Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 18. Cancer Immunology and Cancer Epidemiology Programs, Dana-Farber Harvard Cancer Center, Boston, MA, USA.
Abstract
BACKGROUND: Recent preclinical research strongly suggests that dietary sugars can enhance colorectal tumorigenesis by direct action, particularly in the proximal colon that unabsorbed fructose reaches. OBJECTIVES: We aimed to examine long-term consumption of sugar-sweetened beverages (SSBs) and total fructose in relation to incidence and mortality of colorectal cancer (CRC) by anatomic subsite. METHODS: We followed 121,111 participants from 2 prospective US cohort studies, the Nurses' Health Study (1984-2014) and Health Professionals Follow-Up Study (1986-2014), for incident CRC and related death. Cox proportional hazards regression was used to compute HRs and 95% CIs. RESULTS: During follow-up, we documented 2733 incident cases of CRC with a known anatomic location, of whom 901 died from CRC. Positive associations of SSB and total fructose intakes with cancer incidence and mortality were observed in the proximal colon but not in the distal colon or rectum (Pheterogeneity ≤ 0.03). SSB consumption was associated with a statistically significant increase in the incidence of proximal colon cancer (HR per 1-serving/d increment: 1.18; 95% CI: 1.03, 1.34; Ptrend = 0.02) and a more pronounced elevation in the mortality of proximal colon cancer (HR: 1.39; 95% CI: 1.13, 1.72; Ptrend = 0.002). Similarly, total fructose intake was associated with increased incidence and mortality of proximal colon cancer (HRs per 25-g/d increment: 1.18; 95% CI: 1.03, 1.35; and 1.42; 95% CI: 1.12, 1.79, respectively). Moreover, SSB and total fructose intakes during the most recent 10 y, rather than those from a more distant period, were associated with increased incidence of proximal colon cancer. CONCLUSIONS: SSB and total fructose consumption were associated with increased incidence and mortality of proximal colon cancer, particularly during later stages of tumorigenesis.
BACKGROUND: Recent preclinical research strongly suggests that dietary sugars can enhance colorectal tumorigenesis by direct action, particularly in the proximal colon that unabsorbed fructose reaches. OBJECTIVES: We aimed to examine long-term consumption of sugar-sweetened beverages (SSBs) and total fructose in relation to incidence and mortality of colorectal cancer (CRC) by anatomic subsite. METHODS: We followed 121,111 participants from 2 prospective US cohort studies, the Nurses' Health Study (1984-2014) and Health Professionals Follow-Up Study (1986-2014), for incident CRC and related death. Cox proportional hazards regression was used to compute HRs and 95% CIs. RESULTS: During follow-up, we documented 2733 incident cases of CRC with a known anatomic location, of whom 901 died from CRC. Positive associations of SSB and total fructose intakes with cancer incidence and mortality were observed in the proximal colon but not in the distal colon or rectum (Pheterogeneity ≤ 0.03). SSB consumption was associated with a statistically significant increase in the incidence of proximal colon cancer (HR per 1-serving/d increment: 1.18; 95% CI: 1.03, 1.34; Ptrend = 0.02) and a more pronounced elevation in the mortality of proximal colon cancer (HR: 1.39; 95% CI: 1.13, 1.72; Ptrend = 0.002). Similarly, total fructose intake was associated with increased incidence and mortality of proximal colon cancer (HRs per 25-g/d increment: 1.18; 95% CI: 1.03, 1.35; and 1.42; 95% CI: 1.12, 1.79, respectively). Moreover, SSB and total fructose intakes during the most recent 10 y, rather than those from a more distant period, were associated with increased incidence of proximal colon cancer. CONCLUSIONS: SSB and total fructose consumption were associated with increased incidence and mortality of proximal colon cancer, particularly during later stages of tumorigenesis.
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