Realized and potential neutralization of mutant genes in man by nutritional selection.
Inborn errors of metabolism are examples of monogenic disease in man that, more often than not, impair adaptation. Appropriate modification of the nutritional environment has been used in several instances to offset the phenotypic effects of the mutant allele, with resultant relaxation of selection. Despite an impressive, if brief, record of its efficacy, nutritional treatment of inborn errors of metabolism remains suboptimal in the absence of relevant and superior food technology and well-established systems for its application to the patient. Some of the more commonly encountered multifactorial diseases are likely to yield in the future to the type of genetic analysis that has been effective for monogenic disease. Delineation of various monogenic subsets in a multifactorial disease profile may permit the application of specific treatment to persons in the universal population at particular risk with the disease. Coronary heart disease is an example of a major disease burden now undergoing such delineation, which may benefit from the assignment of specific nutritional and pharmacological treatment for particular forms of the disease.
D005818:Genetic Engineering; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications / Q000178:diet therapy / Q000235:genetics; D008661:Metabolism, Inborn Errors / Q000178:diet therapy*; D009203:Myocardial Infarction / Q000150:complications / Q000517:prevention & control*; D010661:Phenylketonurias / Q000178:diet therapy