Copyright © 1995 by Jack Challem, The Nutrition Reporter™
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Researchers increasingly believe that the aging process ultimately begins in the mitochondria, thread-like "organs" found in each cell of the body. Mitochondria are the cell's energy factories, where much of the cell's work is actually performed and 85 percent of all oxygen is consumed.
Of course, wherever there's oxygen, there are also free radicals stripping away electrons from healthy molecules-and aging cells.
In a provocative paper in the Proceedings of the National Academy of Sciences of the USA (Nov. 8, 1994;91:10771-8), respected biochemist and molecular biologist Bruce Ames, PhD, of the University of California, Berkeley, explored some of the causes of aging-and how the amino acid carnitine and antioxidant nutrients likely slow down or turn back the aging process.
Free radicals, or oxidants, are produced as a consequence of normal energy-producing reactions, infection-fighting, and detoxification reactions in the body, as well as by air pollution and cigarette smoke.
"Accumulation of such damage may contribute to aging and age-associated degenerative diseases," Ames wrote. "The continuous threat of oxidant damage to the cell, tissue, and organism as a whole is underscored by the existence of an impressive array of cellular defenses that have evolved to battle these reactive oxidants. However, these defenses are not perfect..."
One of the key mitochondrial defenses is cardiolipin, essential for membrane permeability. By maintaining the flexibility of membranes, cardiolipin allows smaller molecules to pass through to the mitochondria. One of these small molecules is coenzyme Q10, a nutrient that stimulates the mitochondria's production of adenosine triphophate (ATP) and energy.
However, cardiolipin levels in heart, liver, and brain cells decrease as a result of oxidation and aging.
As it turns out, carnitine promotes cardiolipin synthesis. "Acetyl-L-carnitine (ALCAR) fed to old rats increases the amount of cardiolipin to levels similar to that of young rats, suggesting that ALCAR administration may improve cellular bioenergetics in the aged rat," Ames explained.
Numerous studies have supported the thesis that low levels of carnitine in the mitochondria contribute to aging. "A rapidly growing body of evidence suggests that the apparent age-related deficits in mitochondrial function can be slowed or reversed by ALCAR, a normal component of the inner mitochondrial membrane that serves as a precursor for acetyl-CoA (needed to synthesize fatty acids) as well as the neurotransmitter acetylcholine." ALCAR is converted to L-carnitine, which is stored in the mitochondrial membrane and can be converted back to ALCAR.
In addition, Ames pointed out that "excitatory" amino acids, such as glutamate, are often toxic to neurons and have been implicated in a large number of neurological diseases, including Parkinson's and Alzheimer's diseases.
However, he added, several nutrients-mostly antioxidants- protect against neural toxicity. Among them are ALCAR, glutathione and oxidized glutathione, vitamin B3, and CoQ10. These substances prevent the depletion of ATP, a situation that makes neurons susceptible to the damaging effects of excitatory amino acids.
"Clinical studies in elderly humans indicate that various dietary antioxidants such as glutathione, beta-carotene, and alpha-tocopherol (vitamin E) improve cell-mediated immunity," concluded Ames. "Increasing the intracellular anti-oxidant levels, improving mitochondrial function, and decreasing oxidant-induced membrane rigidity could all be mechanisms by which dietary antioxidants serve to boost cell-mediated immunity."
This article originally appeared in The Nutrition Reporter™ newsletter. The information provided by Jack Challem and The Nutrition Reporter™ newsletter is strictly educational and not intended as medical advice. For diagnosis and treatment, consult your physician.