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1 From the Fred Hutchinson Cancer Research Center and Nutritional Sciences Program, Department of Epidemiology, University of Washington, Seattle, WA. 2 Presented at the symposium, "Fifth International Congress on Vegetarian Nutrition," held in Loma Linda, CA, March 4–6, 2008. 3 Supported by US NCI grants R01CA070913 and R01CA097366 and the Fred Hutchinson Cancer Research Center. 4 Reprints not available. Address correspondence to JW Lampe, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, M4-B402, PO Box 19024, Seattle, WA 98109. E-mail: jlampe{at}fhcrc.org.
ABSTRACT
Genetic differences in taste preference, food tolerance, and phytochemical absorption and metabolism all potentially influence the effect of plant-based diets on cancer risk. Diet is a mixture of carcinogens, mutagens, and protective agents, many of which are metabolized by biotransformation enzymes. Genetic polymorphisms that alter protein expression or enzyme function can modify risk. Genotypes associated with more favorable handling of carcinogens may be associated with less favorable handling of phytochemicals. For example, glutathione S-transferases detoxify polycyclic aromatic hydrocarbons and metabolize isothiocyanates, which are chemopreventive compounds in cruciferous vegetables. A polymorphism in the GSTM1 gene results in lack of GSTM1-1 protein. Pharmacokinetic studies suggest that lack of GSTM1 enzyme is associated with more rapid excretion of the isothiocyanate sulforaphane; therefore, individuals who have this genetic variation may derive less benefit from consuming cruciferous vegetables. Flavonoids are conjugated with glucuronide and sulfate and are excreted in urine and bile. Polymorphisms in UDP-glucuronosyltransferases and sulfotransferases may contribute to variability in phytochemical clearance and efficacy. Genetic polymorphisms in enzymes that metabolize phytochemicals may account in part for variation in disease risk and also have to be considered in the context of other aspects of human genetics, gut bacterial genetics, and environmental exposures.
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