Hanseul Kim1, Marla Lipsyc-Sharf2, Xiaoyu Zong3, Xiaoyan Wang3, Jinhee Hur4, Mingyang Song5, Molin Wang6, Stephanie A Smith-Warner7, Charles Fuchs8, Shuji Ogino9, Kana Wu4, Andrew T Chan10, Yin Cao11, Kimmie Ng12, Edward L Giovannucci13. 1. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. 2. Department of Internal Medicine, Brigham and Women's Hospital, Boston, Massachusetts. 3. Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St Louis, Missouri. 4. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. 5. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts. 6. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. 7. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. 8. Yale Cancer Center, Smilow Cancer Hospital, New Haven, Connecticut. 9. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Program in MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; Cancer Immunology Program and Cancer Epidemiology Program, Dana-Farber Harvard Cancer Center, Boston, Massachusetts; Broad Institute of MIT and Harvard, Cambridge, Massachusetts. 10. Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; Broad Institute of MIT and Harvard, Cambridge, Massachusetts; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. 11. Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St Louis, Missouri; Alvin J. Siteman Cancer Center, Washington University School of Medicine, St. Louis, Missouri; Division of Gastroenterology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri. 12. Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts. 13. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. Electronic address: egiovann@hsph.harvard.edu.
Abstract
BACKGROUND & AIMS: Vitamin D has been implicated in colorectal cancer (CRC) pathogenesis, but it remains unknown whether total vitamin D intake is associated with early-onset CRC and precursors diagnosed before age 50. METHODS: We prospectively examined the association between total vitamin D intake and risks of early-onset CRC and precursors among women enrolled in the Nurses' Health Study II. Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for early-onset CRC were estimated with Cox proportional hazards model. Multivariable-adjusted odds ratios (ORs) and 95% CIs for early-onset conventional adenoma and serrated polyp were estimated with logistic regression model. RESULTS: We documented 111 incident cases of early-onset CRC during 1,250,560 person-years of follow-up (1991 to 2015). Higher total vitamin D intake was significantly associated with a reduced risk of early-onset CRC (HR for ≥450 IU/day vs <300 IU/day, 0.49; 95% CI, 0.26-0.93; P for trend = .01). The HR per 400 IU/day increase was 0.46 (95% CI, 0.26-0.83). The inverse association was significant and appeared more evident for dietary sources of vitamin D (HR per 400 IU/day increase, 0.34; 95% CI, 0.15-0.79) than supplemental vitamin D (HR per 400 IU/day increase, 0.77; 95% CI, 0.37-1.62). For CRC precursors, the ORs per 400 IU/day increase were 0.76 (95% CI, 0.65-0.88) for conventional adenoma (n = 1,439) and 0.85 (95% CI, 0.75-0.97) for serrated polyp (n = 1,878). CONCLUSIONS: In a cohort of younger women, higher total vitamin D intake was associated with decreased risks of early-onset CRC and precursors.
BACKGROUND & AIMS: Vitamin D has been implicated in colorectal cancer (CRC) pathogenesis, but it remains unknown whether total vitamin D intake is associated with early-onset CRC and precursors diagnosed before age 50. METHODS: We prospectively examined the association between total vitamin D intake and risks of early-onset CRC and precursors among women enrolled in the Nurses' Health Study II. Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for early-onset CRC were estimated with Cox proportional hazards model. Multivariable-adjusted odds ratios (ORs) and 95% CIs for early-onset conventional adenoma and serrated polyp were estimated with logistic regression model. RESULTS: We documented 111 incident cases of early-onset CRC during 1,250,560 person-years of follow-up (1991 to 2015). Higher total vitamin D intake was significantly associated with a reduced risk of early-onset CRC (HR for ≥450 IU/day vs <300 IU/day, 0.49; 95% CI, 0.26-0.93; P for trend = .01). The HR per 400 IU/day increase was 0.46 (95% CI, 0.26-0.83). The inverse association was significant and appeared more evident for dietary sources of vitamin D (HR per 400 IU/day increase, 0.34; 95% CI, 0.15-0.79) than supplemental vitamin D (HR per 400 IU/day increase, 0.77; 95% CI, 0.37-1.62). For CRC precursors, the ORs per 400 IU/day increase were 0.76 (95% CI, 0.65-0.88) for conventional adenoma (n = 1,439) and 0.85 (95% CI, 0.75-0.97) for serrated polyp (n = 1,878). CONCLUSIONS: In a cohort of younger women, higher total vitamin D intake was associated with decreased risks of early-onset CRC and precursors.
Authors: Changzheng Yuan; Donna Spiegelman; Eric B Rimm; Bernard A Rosner; Meir J Stampfer; Junaidah B Barnett; Jorge E Chavarro; Amy F Subar; Laura K Sampson; Walter C Willett Journal: Am J Epidemiol Date: 2017-04-01 Impact factor: 4.897
Authors: Rachel Pearlman; Wendy L Frankel; Benjamin Swanson; Weiqiang Zhao; Ahmet Yilmaz; Kristin Miller; Jason Bacher; Christopher Bigley; Lori Nelsen; Paul J Goodfellow; Richard M Goldberg; Electra Paskett; Peter G Shields; Jo L Freudenheim; Peter P Stanich; Ilene Lattimer; Mark Arnold; Sandya Liyanarachchi; Matthew Kalady; Brandie Heald; Carla Greenwood; Ian Paquette; Marla Prues; David J Draper; Carolyn Lindeman; J Philip Kuebler; Kelly Reynolds; Joanna M Brell; Amy A Shaper; Sameer Mahesh; Nicole Buie; Kisa Weeman; Kristin Shine; Mitchell Haut; Joan Edwards; Shyamal Bastola; Karen Wickham; Karamjit S Khanduja; Rosemary Zacks; Colin C Pritchard; Brian H Shirts; Angela Jacobson; Brian Allen; Albert de la Chapelle; Heather Hampel Journal: JAMA Oncol Date: 2017-04-01 Impact factor: 31.777
Authors: Vasiliki I Dimitrakopoulou; Konstantinos K Tsilidis; Philip C Haycock; Niki L Dimou; Kawthar Al-Dabhani; Richard M Martin; Sarah J Lewis; Marc J Gunter; Alison Mondul; Irene M Shui; Evropi Theodoratou; Katharina Nimptsch; Sara Lindström; Demetrius Albanes; Tilman Kühn; Timothy J Key; Ruth C Travis; Karani Santhanakrishnan Vimaleswaran; Peter Kraft; Brandon L Pierce; Joellen M Schildkraut Journal: BMJ Date: 2017-10-31