dc.contributor.author | McCullough, ML | |
dc.contributor.author | Zoltick, ES | |
dc.contributor.author | Weinstein, SJ | |
dc.contributor.author | Fedirko, V | |
dc.contributor.author | Wang, M | |
dc.contributor.author | Cook, NR | |
dc.contributor.author | Eliassen, AH | |
dc.contributor.author | Zeleniuch-Jacquotte, A | |
dc.contributor.author | Agnoli, C | |
dc.contributor.author | Albanes, D | |
dc.contributor.author | Barnett, MJ | |
dc.contributor.author | Buring, JE | |
dc.contributor.author | Campbell, PT | |
dc.contributor.author | Clendenen, TV | |
dc.contributor.author | Freedman, ND | |
dc.contributor.author | Gapstur, SM | |
dc.contributor.author | Giovannucci, EL | |
dc.contributor.author | Goodman, GG | |
dc.contributor.author | Haiman, CA | |
dc.contributor.author | Ho, GYF | |
dc.contributor.author | Horst, RL | |
dc.contributor.author | Hou, T | |
dc.contributor.author | Huang, W-Y | |
dc.contributor.author | Jenab, M | |
dc.contributor.author | Jones, ME | |
dc.contributor.author | Joshu, CE | |
dc.contributor.author | Krogh, V | |
dc.contributor.author | Lee, I-M | |
dc.contributor.author | Lee, JE | |
dc.contributor.author | Männistö, S | |
dc.contributor.author | Le Marchand, L | |
dc.contributor.author | Mondul, AM | |
dc.contributor.author | Neuhouser, ML | |
dc.contributor.author | Platz, EA | |
dc.contributor.author | Purdue, MP | |
dc.contributor.author | Riboli, E | |
dc.contributor.author | Robsahm, TE | |
dc.contributor.author | Rohan, TE | |
dc.contributor.author | Sasazuki, S | |
dc.contributor.author | Schoemaker, MJ | |
dc.contributor.author | Sieri, S | |
dc.contributor.author | Stampfer, MJ | |
dc.contributor.author | Swerdlow, AJ | |
dc.contributor.author | Thomson, CA | |
dc.contributor.author | Tretli, S | |
dc.contributor.author | Tsugane, S | |
dc.contributor.author | Ursin, G | |
dc.contributor.author | Visvanathan, K | |
dc.contributor.author | White, KK | |
dc.contributor.author | Wu, K | |
dc.contributor.author | Yaun, S-S | |
dc.contributor.author | Zhang, X | |
dc.contributor.author | Willett, WC | |
dc.contributor.author | Gail, MH | |
dc.contributor.author | Ziegler, RG | |
dc.contributor.author | Smith-Warner, SA | |
dc.date.accessioned | 2018-07-05T08:57:48Z | |
dc.date.accessioned | 2018-07-11T14:17:53Z | |
dc.date.issued | 2019-02-01 | |
dc.identifier.citation | Journal of the National Cancer Institute, 2019, 111 (2), pp. 158 - 169 | |
dc.identifier.issn | 0027-8874 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/2041 | |
dc.identifier.eissn | 1460-2105 | |
dc.identifier.doi | 10.1093/jnci/djy087 | |
dc.description.abstract | BACKGROUND: Experimental and epidemiological studies suggest a protective role for vitamin D in colorectal carcinogenesis, but evidence is inconclusive. Circulating 25-hydroxyvitamin D (25(OH)D) concentrations that minimize risk are unknown. Current Institute of Medicine (IOM) vitamin D guidance is based solely on bone health. METHODS: We pooled participant-level data from 17 cohorts, comprising 5706 colorectal cancer case participants and 7107 control participants with a wide range of circulating 25(OH)D concentrations. For 30.1% of participants, 25(OH)D was newly measured. Previously measured 25(OH)D was calibrated to the same assay to permit estimating risk by absolute concentrations. Study-specific relative risks (RRs) for prediagnostic season-standardized 25(OH)D concentrations were calculated using conditional logistic regression and pooled using random effects models. RESULTS: Compared with the lower range of sufficiency for bone health (50-<62.5 nmol/L), deficient 25(OH)D (<30 nmol/L) was associated with 31% higher colorectal cancer risk (RR = 1.31, 95% confidence interval [CI] = 1.05 to 1.62); 25(OH)D above sufficiency (75-<87.5 and 87.5-<100 nmol/L) was associated with 19% (RR = 0.81, 95% CI = 0.67 to 0.99) and 27% (RR = 0.73, 95% CI = 0.59 to 0.91) lower risk, respectively. At 25(OH)D of 100 nmol/L or greater, risk did not continue to decline and was not statistically significantly reduced (RR = 0.91, 95% CI = 0.67 to 1.24, 3.5% of control participants). Associations were minimally affected when adjusting for body mass index, physical activity, or other risk factors. For each 25 nmol/L increment in circulating 25(OH)D, colorectal cancer risk was 19% lower in women (RR = 0.81, 95% CI = 0.75 to 0.87) and 7% lower in men (RR = 0.93, 95% CI = 0.86 to 1.00) (two-sided Pheterogeneity by sex = .008). Associations were inverse in all subgroups, including colorectal subsite, geographic region, and season of blood collection. CONCLUSIONS: Higher circulating 25(OH)D was related to a statistically significant, substantially lower colorectal cancer risk in women and non-statistically significant lower risk in men. Optimal 25(OH)D concentrations for colorectal cancer risk reduction, 75-100 nmol/L, appear higher than current IOM recommendations. | |
dc.format | Print | |
dc.format.extent | 158 - 169 | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | OXFORD UNIV PRESS INC | |
dc.relation.replaces | https://repository.icr.ac.uk/handle/internal/1983 | |
dc.relation.replaces | internal/1983 | |
dc.rights.uri | https://www.rioxx.net/licenses/all-rights-reserved | |
dc.subject | Humans | |
dc.subject | Colorectal Neoplasms | |
dc.subject | Vitamin D Deficiency | |
dc.subject | Vitamins | |
dc.subject | Vitamin D | |
dc.subject | Prognosis | |
dc.subject | Risk Factors | |
dc.subject | Case-Control Studies | |
dc.subject | Follow-Up Studies | |
dc.subject | Prospective Studies | |
dc.subject | Aged | |
dc.subject | Middle Aged | |
dc.subject | International Agencies | |
dc.subject | Female | |
dc.subject | Male | |
dc.title | Circulating Vitamin D and Colorectal Cancer Risk: An International Pooling Project of 17 Cohorts. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2018-04-16 | |
rioxxterms.versionofrecord | 10.1093/jnci/djy087 | |
rioxxterms.licenseref.uri | https://www.rioxx.net/licenses/all-rights-reserved | |
rioxxterms.licenseref.startdate | 2019-02 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | Journal of the National Cancer Institute | |
pubs.issue | 2 | |
pubs.notes | Not known | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research/Aetiological Epidemiology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Genetics and Epidemiology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Genetics and Epidemiology/Aetiological Epidemiology | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research/Aetiological Epidemiology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Genetics and Epidemiology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Genetics and Epidemiology/Aetiological Epidemiology | |
pubs.publication-status | Published | |
pubs.volume | 111 | |
pubs.embargo.terms | Not known | |
icr.researchteam | Aetiological Epidemiology | |
dc.contributor.icrauthor | Jones, Michael | |
dc.contributor.icrauthor | Schoemaker, Minouk | |
dc.contributor.icrauthor | Swerdlow, Anthony | |