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Dr. Denham Harman & aging

Townsend Letter for Doctors and Patients,  Dec, 2005  by Jule Klotter

When Denham Harman, MD, PhD, first introduced his theory that free radical reactions were responsible for the deterioration associated with aging in 1955, the idea was dismissed as "too simple to explain such a complex process as aging." In a two-part interview with Richard Passwater, Harman explains that US Navy research on free radical damage caused by radiation exposure, prompted his theory that aging results from free radical activity that occurs in the body. As a former researcher at Shell Development Company, and then as a resident in internal medicine and research associate at the Donner Laboratory of Medical Physics (University of California-Berkeley) in 1954, Harman had the background in radiation chemistry and biology to understand that free radical reactions, which result during radiation exposure, naturally occur in the human body, given the cells' constant exposure to oxygen. At that time, evidence of free radical activity in biological systems was scarce; it had just been found in yeast by St. Louis researchers. Dietary antioxidants were known to provide protection against radiation exposure. By 1957, Harman showed that the same compounds extended the median life span of mice undergoing normal aging. Antioxidants did not, however, increase maximum life expectancy--the "biological clock."

In 1972, Harman modified his theory of aging by proposing that free radical damage to the mitochondria determines maximum life span. The maximum life span for humans is 115-120 years. Most oxygen reactions (which produce free radicals) occur in the mitochondria, but the mitochondrial inner membrane is very selective and will not readily admit most antioxidants. However, researchers have identified a few antioxidants that protect mitochondria. Coenzyme Q-10 slows mitochondria deterioration without interfering with ATP production. The antioxidants alpha-lipoic acid and acetyl carnitine can actually reverse mitochondrial aging in young animals.

Controlling energy output is another way to reduce mitochondrial aging. Free radical damage to mitochondria increases and decreases according to how much we eat and how intensely we exercise. Oxygen consumption increases as food intake and exercise increases. In the Passwater interview, Harman tells about rat experiments in which decreasing caloric intake resulted in "decreased body weight and oxygen consumption by 40%, increased average life expectancy at birth by 40%, and increased maximum life span by 49%.... In essence, by decreasing caloric intake we decrease our exposure to internal radiation."

Harman, who was the subject of a CBS News report in June 2003, at age 87, told Passwater that he takes 200 milligrams of vitamin E per day; ten milligrams of coenzyme Q-10 with each meal; one yeast tablet containing 50 micrograms of selenium twice a day, and a multivitamin. "There are other things involved in living a long life," he says. "These include keeping your weight down at a level compatible with a sense of well-being, getting a moderate amount of exercise, little or no smoking, and minimal alcohol." At the time of the CBS News report, he was still researching aging--without pay--at the University of Nebraska Medical Center from 7 am to 3 pm, five days a week. He "officially" retired from his teaching position at age 70. "If you don't stay busy," he says, "you die. I don't want to die right now."

Associated Press. Finding the Fountain of Youth. 13 June 2003 (Accessed www.cbsnews.com on 8 September 2005)

Colman, John. Denham Harman--A Pioneer in Gerontology and Anti-aging Research. Life Extension July 2004

Passwater RA, PhD. The Free-Radical Theory of Aging: Part I--How It All Began (Interview with Dr. Denham Harman) (Accessed at www.healthy.net on 8 September 2005)

Passwater RA, PhD. The Free-Radical Theory of Aging: Part II--Calorie Restriction, Free Radicals and New Research. (Accessed at www.healthy.net on 7 September 2005)

COPYRIGHT 2005 The Townsend Letter Group
COPYRIGHT 2005 Gale Group