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cron-web.org Calorie Restriction with Optimum Nutrition Forum
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A1CR Site Admin
Joined: 18 Jan 2006 Posts: 559
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Posted: Mon Mar 06, 2006 10:53 pm Post subject: Interview With Dr. Denham Harman |
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Here is a segment from an interview-based article, ''The Free-Radical Theory of Aging: Part I and II: How it all began''. It features free-radical-theory-of-aging guru Denham Harman:
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Passwater: It seems so obvious today, but it wasn't until your paper appeared in the Journal of the American Geriatrics Society that the suggestion was made that the mitochondrion might serve as the biologic clock. The inner membrane permeability of the mitochondrion is highly selective as to what can pass through it, yet the mitochondrion is where most of the oxygen reactions occur. Thus, most of the free-radical damage may occur in the mitochondria, where it is not subject to modification from the outside because of the difficulties in getting antioxidants into the mitochondria in sufficient quantity or concentrations to do anything. It was a very fortunate deduction because today a great deal of work is going on in the field of mitochondria and aging.
The mitochondria are the "energy factories" in our cells that convert our food components into by-products and energy. In the digestive process, food is broken-down into smaller components which are then absorbed and transported by the blood to nourish the cells. Still, the digested food components are complex organic molecules. The mitochondria in our cells can further degrade these complex molecules into simpler products, ultimately producing the waste products carbon dioxide and water. In this process, mitochondria produce adenosine triphosphate (ATP), which becomes a source of energy for the body. ATP is much like a charged battery, and adenosine diphosphate (ADP) is analogous to a discharged battery. The free energy is stored in the phosphate bonds of these high-energy phosphates. When the body needs energy to drive a biochemical reaction, it usually involves ATP going to ADP somewhere in the process. The mitochondria recharge ADP back into ATP.
When we eat a lot or exercise, we increase the energy reactions in the mitochondria and the oxygen that is needed in those reactions. How much we eat helps determine how much oxygen is consumed in the mitochondria. Thus, the more we eat, the more we increase our need for antioxidant protection. Let's discuss what happens when we reduce these reactions? Hasn't it been shown that maximum lifespan can be increased by decreasing free radical production by the mitochondria by decreasing food intake?
Harman: Decreasing caloric consumption can indeed increase maximum life span. Decreasing the caloric intake of rats decreased body weight and oxygen consumption by 40 percent, increased average life expectancy at birth by 40 percent, and increased maximum life span by 49 percent. I believe these effects are caused by the lowered oxygen utilization; one to three percent of the oxygen we use is diverted to the superoxide radical and hydrogen peroxide. In essence, by decreasing caloric intake we decrease our exposure to internal radiation.
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Passwater: Earlier you mentioned that eating less food reduces oxygen consumption and the load on the mitochondria. There is good evidence that calorie restriction -- cutting calorie intake by 30% or so while maintaining high micronutrient levels -- slows aging. Calorie restriction seems to lower the levels of undesirable sugar-damaged proteins called Advanced Glycosylation End-products (AGE).
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The full article is available at this site:
http://www.healthy.net/scr/interview.asp?Id=174 |
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