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IJE Advance Access originally published online on November 22, 2005
International Journal of Epidemiology 2006 35(2):222-224; doi:10.1093/ije/dyi231
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Published by Oxford University Press on behalf of the International Epidemiological Association © The Author 2005; all rights reserved.

Commentary

Commentary: Vitamin D and colorectal cancer—twenty-five years later

Edward Giovannucci1,2,3

1 Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
2 Department of Nutrition, Harvard School of Public Health, Boston, MA 02115, USA.
3 Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA.

Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, 181 Longwood Avenue, Boston, MA 02115, USA. E-mail: edward.giovannucci@channing.harvard.edu

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In 1980, Garland and Garland hypothesized that vitamin D status accounted for the inverse association between UV-B radiation exposure and risk of colon cancer.1 The title of their article was posed as a question, ‘do sunlight and vitamin D reduce the likelihood of colon cancer?’ At the time, essentially nothing was known about the biology of vitamin D and colon cancer, and epidemiological data were sparse. Largely stimulated by this article, substantial research in this area has been conducted over the past 25 years. The biological underpinnings of this hypothesis have become quite strong; colorectal cells contain vitamin D receptors, and express 1-alpha-hydroxylase, and are thus able to convert 25(OH) vitamin D into 1,25(OH)2 vitamin D. Activation of these receptors by 1,25(OH)2D induces differentiation and inhibits proliferation, invasiveness, angiogenesis, and metastatic potential. The biological basis of . . . [Full Text of this Article]


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