Nutrition at the Molecular Level

It has been only a few years since the human genome was sequenced, and what we learned through this processs has radically altered our understanding of human genetics. As a general rule, scientists thought that each gene contained the information needed to produce one protein, a key element used in nearly every bodily process. And, given the complexity of humans compared with other animals and with plants, it was estimated that the human genome would have 100,000 genes or more that coded for proteins. In fact, the human genome has only about 30,000 genes that code for proteins; at least 98% of the genome does not code for proteins at all.

It turns out that most of our DNA is the software involved in determining how and when 30,000 genes are expressed. Regulation of this expression can be affected by environmental, nutritional, and other factors. These changes to the genome by external factors, called epigenetic changes, can have significant effects on a wide variety of molecular processes.

For example, one of the most important nutritional factors modulating gene expression is folic acid: a lack of folic acid has been linked to an increased risk of heart disease and cancer. Folic acid, which is found in dark green leafy vegetables such as spinach and green lettuce, participates in a pathway leading to the stabilization of DNA. Early man evolved on a rich plant-based diet, so our metabolism came to depend upon a rich supply of folic acid to assist in multiple processes protecting against disease. However, as humans began to migrate out of agricultural lands, the ability to grow enough green plant food to provide adequate folic acid was reduced. As a result, it is believed that changes occurred in the genome of individuals to conserve folic acid for DNA integrity while sacrificing its other roles in metabolism — ultimately contributing to an increased risk of heart disease and cancer.

If this sounds far fetched, consider the Agouti mouse. This type of mouse has been specially bred to make a mutated protein called the Agouti protein. The protein disrupts the brain’s ability to signal that the stomach is full and control appetite, so the mice eat to excess and become obese. At the same time, the Agouti protein interferes with the action of another protein that turns the coats of the mice brown. Because of these genetic changes, the Agouti mouse has a yellow coat, as well as a lifetime increased risk of diabetes and some forms of cancer. However, if you supplement the diet of a pregnant Agouti mouse with folic acid and other similar compounds, the yellow-coated mother will give birth to a lean brown mouse with no increased risk of disease. The addition of folic acid silenced the expression of the abnormal Agouti gene — no Agouti protein is produced, and the mouse is born normal.

Similarly, in the development of human prostate cancers, the tumor silences production of a protein called GSTP1, which plays a critical role in defending DNA against mutation caused by oxidation in the prostate. It is believed that the on-off switch for this protein is mediated by epigenetic changes similar to that which allows folic acid to mediate the change in the Agouti mouse, enabling a healthy brown mouse to be born from a diabetic yellow mouse.

The mere existence of these and other epigenetic changes demonstrates that your DNA is not set in stone. It is a living part of the cells in your body and its software code can be influenced by nutritional and environmental factors. In fact, it is estimated that only 30% of processes normally associated with aging are dictated by genes, while 70% are under your personal control — through diet, exercise, and other lifestyle behaviors.

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