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Cornelia M. Ulrich, MS, PhD; John D. Potter, MD, PhD

JAMA. 2007;297:2408-2409.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

A large number of epidemiological studies have shown that a higher intake of folate, as well as higher intakes of vegetables and fruit, is associated with a decreased risk of colorectal polyps and cancer.¹ These results have been corroborated by animal experiments,² and biological mechanisms underlying these associations have been proposed³: folate functions as a source of carbon moieties in the synthesis of nucleotides that are essential for DNA replication and repair. Folate deficiency leads to mutations and chromosomal damage—effects that are also central to the efficacy of antifolate chemotherapeutic agents (eg, methotrexate). In addition, folate status is important for the provision of S-adenosylmethionine, the universal methyl donor, involved in normal and pathological methylation of DNA. Disturbances in DNA methylation are relevant in carcinogenesis⁴; however, the role of folate in these epigenetic changes is not yet understood.

. . . [Full Text of this Article]

Author Affiliations: Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Wash.

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