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The etiology of most chronic human diseases (such as asthma, atherosclerosis, and cancer) is complex, involving a mix of genetic and environmental factors interacting with each other over hours, days, months, or years. Until recently, however, the disciplines of environmental sciences and genetics have proceeded independently; investigators in the former discipline have focused primarily on adverse conditions and diseases that are etiologically driven by environmental factors (such as benzene-induced leukemia), and those in the latter field have been finding genetic factors for highly heritable conditions (such as cystic fibrosis). Progress is now being made in identifying common genetic variations that contribute to complex diseases such as age-related macular degeneration (1, 2), type 2 diabetes (3, 4), and prostate cancer (5). However, the best opportunity to reduce risk in genetically susceptible people for the foreseeable future will not be to re-engineer their genes, but to modify their environment. The successful dietary treatment of phenyl-ketonuria is a clear example.
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Schwartz et al. (2007) studied this question.
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