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Aging


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Introduction
Aging is a process, not a disease. We cannot stop the aging process, but an impressive body of scientific research is teaching us that individuals have a great deal of control over their immune system and their own aging process. How long you live really depends on how you live.(1, 2)

To date, we have not developed the scientific breakthroughs that will enable us to extend the potential, maximum human life span, which is estimated to be approximately 120 years.(3) However, there are many things that people can do to improve their immune system and their aging process, which will enable them to live in relatively good health significantly longer than the current average life span for humans.

Average life expectancy at birth is a rough measure of the span of healthy, productive life--the functional life span. In the developed countries average life expectancies at birth now range from 76-79 years, which is far less than the estimated 120-year maximum potential human life span.

Aging is the accumulation of changes that increase the risk of illness and death. Aging changes can be attributed to development, genetic defects, the environment, disease, and the inborn aging process.(4) Inborn aging processes become the major risk factors for disease and death after age 28 in the developed countries.

Free radicals: The free radical theory of aging, which was first presented by Denham Harman, M.D., in 1956,(5) postulated that aging changes were caused by free radical reactions. In a recently published paper, Dr. Harman acknowledged that there is a growing scientific consensus, largely based on the results of measures to minimize more-or-less random endogenous free radical reactions, that such reactions are a major cause of aging, possibly the only one.(6)

Normally electrons exist in pairs. Throughout nature, things are held together by chemical bonds, which are pairs of electrons. Free radicals are molecules that have lost an electron. Thus, a free radical is defined as a molecule that has a free, or unpaired electron, which is one of the most unstable, highly reactive conditions known. At the cellular level, a free radical will violently tear an electron away from whatever is close by to regain its own electron pair status. However, in stealing an electron from somewhere else in the body, something else gets damaged. It may be a cell wall, an enzyme, or part of the DNA. Thus, gradual, ongoing free radical activity is what damages tissues, organs, and all other parts of the body including the immune system.(7, 8)

One of the most important things to understand about free radicals is that they are self-generating, self-perpetuating chain reactions.(9) This means that one unchecked free radical may actually generate many thousands of damaging events at the cellular level.(10)

Slowing down the aging process: There are some significant things people can do to enhance their immune systems and slow down the rate of free radical aging damage. In addition to learning about and understanding the concept of free radicals, it is important to take steps to minimize one's exposure to free radicals. There is a wide range of substances in the environment that can generate free radicals if or when we are exposed to them. A partial listing includes ionizing radiation (x-rays), ultraviolet light (a sunburn, 11) traces of pesticides and insecticides that occur in our water and food supplies, heavy metal toxins such as lead and mercury, and many more.

In addition to external exposure from the environment, free radicals are also generated internally in our bodies. Oxygen reacting with unsaturated fatty acids in cell walls and cellular membranes creates a free radical process known as lipid peroxidation.(12)

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Footnotes
1 Troen BR. The biology of aging. Mt Sinai J Med. Jan2003;70(1):3-22.
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2 Weisburger JH. Lifestyle, health and disease prevention: the underlying mechanisms. Eur J Cancer Prev. Aug2002;11(Suppl 2):S1-7.
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3 Finch CE, Pike MC. Maximum life span predictions from the Gompertz mortality model. J Gerontol A Biol Sci Med Sci. May1996;51(3):B183-94.
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4 Christensen K, Vaupel JW. Determinants of longevity: genetic, environmental and medical factors. J Intern Med. Dec1996;240(6):333-41.
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5 Harman D. Aging: A theory based on free radical and radiation chemistry. J Gerontol. 1956;11:298-300.
6 Harman D. Extending functional life span. Exp Gerontol. Jan1998;33(1-2):95-112.
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7 Kilgore KS, Lucchesi BR. Reperfusion injury after myocardial infarction: the role of free radicals and the inflammatory response. Clin Biochem. Oct1993;26(5):359-70.
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8 Piccolo G, Banfi P, Azan G, et al. Biological markers of oxidative stress in mitochondrial myopathies with progressive external ophthalmoplegia. J Neurol Sci. Sep1991;105(1):57-60.
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9 Shigenaga MK, Hagen TM, Ames BN. Oxidative damage and mitochondrial decay in aging. Proc Natl Acad Sci U S A. Nov1994;91(23):10771-8.
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10 Mylonas C, Kouretas D. Lipid peroxidation and tissue damage. In Vivo. May1999;13(3):295-309.
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11 Schallreuter KU, Wood JM. Free radical reduction in the human epidermis. Free Radic Biol Med. 1989;6(5):519-32.
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12 North JA, et al. Cell fatty acid composition affects free radical formation during lipid peroxidation. Am J Physiol. Jul1994;267(1 Pt 1):C177-88.
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