The Adaptation Diet by Charles A. Moss M.D

Author:Charles A. Moss M.D. [Moss, Charles A., M.D.]
Language: eng
Format: epub
ISBN: 978-1-58394-628-2
Publisher: North Atlantic Books
Published: 2013-05-06T16:00:00+00:00

Figure 1: Nutritional and Toxic Influences on Epigenetic Methylation Pathways (from Su et al. Frontiers in Genetics. Jan 9, 2012)

Diet, Environment, and the Epigenome

A striking example of the effect of diet on genetic expression comes from the world of bees. Despite having the same genetics, honeybees grow up to be either workers or queen bees based on whether they are fed royal jelly or beebread as larvae. Studies of honeybees have shown that the key effect of the different foods is in methylation of the DNA, which controls the activity of multiple genes.

In humans, epigenetic effects also include methylation and histone modification, which impact gene expression and tremendously influence the risk for cancer, diabetes, obesity, heart disease, and neurodegenerative disorders, as well as affect the health and function of the brain and other vital organs. In situations where dietary deficiency or toxic exposures have led to global hypomethylation (too few methyl groups throughout the genome), there is a marked increase in cancerous cells. Hypomethylation often results from inadequate methylators in the diet, including folic acid, B12, betaine, and methionine, leading to excess activity of genes like oncogenes, increasing cancerous changes and abnormal cell function. On the other hand, triggers for hypermethylation, including toxins like arsenic and PCBs, alcohol, aging, or maternal protein deficiency, also increase risk for cancer and other diseases.

The Agouti gene in a strain of mice has been used to identify the impact of diet and toxins on epigenetic effects in pregnancy and their impact on future generations. These mice have multiple genes that control the color of the coat in the offspring. One of the genes, the Agouti gene, has several versions leading to different coats, ranging from brown to yellow. One version of the gene, called Avy, will express a yellow coat in the offspring if there is inadequate methylation. In addition to the mouse pup having a yellow coat, there is a greater risk for obesity, diabetes, and cancer and a shortened life span. If the Avy gene is switched off through adequate methylation, the mouse is brown or black in color and has fewer health problems.

Even though the DNA sequence of the Agouti gene does not change, the health and color of the mice are remarkably different based on how much methylation occurs at this gene location, providing researchers with a tremendous tool in assessing the impact of diet and toxins on the epigenome. What determines methylation in these animals and in general is primarily diet and environment. Diets rich in methylating nutrients, such as folic acid, betaine, choline, and B12, or with added genistein, a phytoestrogen from soy, will influence the color of the offspring dramatically, leading to more pure Agouti (brown) and healthier offspring.

On the other hand, exposure of a pregnant mouse to bisphenol A (BPA), an estrogen-like contaminant in food and water (used to make polycarbonate plastics found in water bottles, plastic containers, and tin cans), will increase the yellow coat frequency in the mouse’s offspring. (Bisphenol A is one of several chemicals termed endocrine disruptors because of their hormone-like effect.

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