Diet–Gene Interactions

Authored by: Carolyn D. Berdanier

Handbook of Nutrition and Food

Print publication date:  July  2013
Online publication date:  April  2016

Print ISBN: 9781466505711
eBook ISBN: 9781466505728
Adobe ISBN:

10.1201/b15294-66

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Abstract

It has long been understood that humans as well as other creatures can vary in their health status. In part, this variation is attributable to variation in the environment and in part is due to variation in the genetic heritage of the individual. A well-nourished individual is far more likely to be healthy than is a poorly nourished individual, yet people do develop unhealthy conditions due in part to their genetic heritage. There is a large list of disorders that are attributable to mutations in specific genes in the metabolic pathways. 1 4 For the most part, these disorders are infrequent. Some of them are manageable with appropriate dietary maneuvers. Table 60.1 lists a number of these disorders and associated mutation(s). This is a partial list, and not all of the genetic diseases are listed. For some of the disorders, there is more than one mutation associated with the disease. For example, there are a number of genetic mutations in the code for red cell glucose-6-phosphate dehydrogenase. The code is carried as a recessive trait on the X chromosome, and thus only males are affected. These mutations are usually silent. That is, the male, having a defective red cell glucose-6-phosphate dehydrogenase, does not know he has the problem unless his cells are tested or unless he is given a drug such as quinine or one of the sulfur antibiotics that increases the oxidation of NADPH+H+. When this happens, NADPH+H+ is depleted and is not available to reduce oxidized glutathione. In turn, the red cell ruptures (hemolytic anemia). In almost all cases, the affected male has sufficient enzyme activity to meet the normal demands for NADPH+H+. It is only when stressed by these drugs that a problem develops.

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