Genomics, Nutrition & Inflammation
Friday, May 04, 2007
Our genes are formed from microscopic double-strands of deoxyribonucleic acid (DNA). They are dependent on adequate nutrition for their structure and activity. By appropriately switching on and off (this is called transcription in the genome research world) our genes direct the behavior of our body's 60 trillion cells. Many genetic researchers consider our genes to be the Rosetta stone of health and disease.
When we feed our genes with optimal amounts of the full spectrum of nutrients they enable us to live a long life with a lower risk of disease. When we allow our genes to live in a nutritionally deficient environment, they send mixed up messages that accelerate our body's aging process and increase the risk and progression of degenerative diseases, including cancer, heart disease, Alzheimer's, Parkinson's and eye diseases.
How does this really happen? The information in our genes is written in yet another language we need to become comfortable with: the chemical language of DNA. The letters in the DNA alphabet are sequences of molecules called nucleotides. Each letter is constructed around one of four substances called DNA bases: adenine (A), cytosine (C), guanine (G), and thymine (T).
Different arrangements of these four nucleotides spell different words in DNA language. In his new book, Feed Your Genes Right, Jack Challem, the veteran nutrition expert journalist, used the following example to explain this language, "TACGACCTGA describes the genes that instruct our cells to make specific enzymes and proteins. These enzymes, in turn, catalyze a host of other biochemical reactions, and the proteins form the structure of hormones and tissue."
All of this amazing activity is dependent on nutrients. The DNA in the proteins we consume is broken down and reconstructed into our own distinctive DNA. Vitamins B3 and B6 are needed for thymine synthesis, folic acid for guanine and adenine, and B3 for cytosine. When we are deficient in any of these particular nutrients DNA cannot be properly synthesized and its instructions cannot be carried out.
The discovery of this exciting science led to a new area of research called nutragenomics - the promising cost effective nutrition approach to modulation of the risk of diseases of aging associated with gene expression, including the interleukin 1 (IL-1) proteins that are inherited together in a small set of patterns and linked to the inflammatory process now associated with degenerative disease, including degenerative diseases of the eye.
DNA Damage and Antioxidants
Unfortunately, our DNA is easily damaged. Most of this damage is caused by free radical molecules, 'according to Denham Harman, M.D., Ph.D., of the University of Nebraska, Omaha. Bruce Ames, PhD, the famous molecular biology and biochemistry department chair at UC Berkeley and the inventor of the Ames Test for carcinogens suggests that free radicals are naturally formed as a byproduct of burning food for energy.
Dr. Harman and other free radical researchers also suggest that free radicals are formed by infections, ultraviolet sunlight, cigarette smoke, and internal and external pollutants. They all agree that free radicals delete sections of DNA, rearrange it, or cut it into pieces, and the end result is analogous to typographical errors that distort DNA's instructions and no doubt, influence longevity. Large numbers of studies now suggest that supplemental antioxidants reduce the rate of DNA damage and slow age-related damage to cells.
DNA damage also takes place during normal cell division. When a cell divides in a nutrient deficient body, it replicates its DNA, but not perfectly. Cell division messages are sent by our individual DNA through ribonucleic acid (RNA). RNA message errors happen in nutrient deficient environments during each cell division in the same way misspellings used to happen when we retyped a written page. As the number of DNA errors increases, instructions for normal cell functions become more garbled. Fortunately for us, DNA that lives in a nutrient rich environment has the remarkable ability to proofread itself and to send RNA messages to correct many errors before they become permanent.
DNA Repair and Nutrients
Research conducted by Bruce Ames, PhD and presented in the Proceedings of the National Academy of Sciences, suggested that breaks in a single strand of DNA can usually be repaired by specific nutrients if they are readily available. For example, low intake of folic acid interferes with the production of thymine, one of DNA's four bases. When cells cannot make thymine, they replace it in our DNA with uracil. But when normal DNA repair enzymes scan the DNA, they remove the uracil and that leaves breaks in cellular DNA that could have been prevented by adequate amounts of folic acid. Unfortunately, a deficiency of folic acid is suggested to lead to large numbers of uracil deposits in DNA - so many deposits, in fact, that they dramatically increase the risk of double-strand DNA breaks. Double-strand breaks are not as easily repaired and are more likely to result in permanent damage to DNA and death.
Given the large amount of time, money and scientific effort devoted to the completion of the human genome project, and given the tremendous amount of scientific knowledge we now have as a result of that project, we find it most unfortunate that the AREDs2 study formulation does not include any of the B vitamins associated with the most basic DNA production and repair. These nutrients are vital to those patients who suffer from degenerative eye disease.
Measuring Ring for Toric IOLs G33762
Micronutrient deficiencies, A major cause of DNA damage. Ames BN. Ann NY Acad Sci 1999;889:87 87-106 [ abstract]
Nutrition and developmental biology - implications for public health. Stover PJ, Garza C. Nutr Rev 2006 May;64: 560-71 [ abstract]
Genetic aspect of nutrition and toxicology: report of a workshop Archer MC, Clarkson TW, Strain JJ, J Am Coll Nutr. 2001 Apr;20: 119-28 [ abstract]
High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme binding affinity (increased K(m): relevance to genetic disease and polymorphisma. Ames BN, Elson-Schwab I, Silver EA, Am J Clin Nutr 2002 Apr;75(4):616-58 [ abstract]
Interleukin 1 genetics, inflammatory mechanisms, and nutrigenetic opportunities to modulate diseases of aging. Kornman KS. Am J Clin Nutr. 2006 Feb;83(2):4755-4835 [ abstract]
Folate deficiency and ionizing radiation cause DNA breaks in primary human lymphocytes: a comparison. Courtemanche C, Huang AC, et al. FASEB J. 2004 Jan;18(1):209-11 [ abstract]
Feed Your Genes Right. Eat to Turn Off Disease Causing Genes and Slow Down Aging. Jack Challem, with forward by Kilmer McCully, MD John Whiley and Sons 2005 [ purchase here]