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The free radical theory of aging Scientists studying aging have decided that we age because our cells and the DNA that contains our genetic code sustain damage by an onslaught of highly reactive chemical species they refer to a free radicals. These loose cannons in the body are the result of normal metabolic processes, making oxygen a double edged sword. We cannot live without it, but oxygen also generates these damaging chemical species that create havoc with our cells and cause us to age. A mitochondria is like a tiny furnace contained in each cell in the body. Mitochondria generate energy inside each cell by burning food in the presence of oxygen. This is why cells that are fully oxygenated have a higher level of energy. But again, oxygen can be both friend and foe. This firing process ends up subjecting the mitochondria themselves to high levels of free radical damage. As we age, mitochondria become so damaged by these free radicals that they lose their ability to function efficiently. The result is continually diminishing cellular energy and even more aging. And as our cells lose energy, we become subject to degenerative diseases. Researchers look for a way to halt mitochondrial deterioration The study, reported in the October issue of Neurochemical Research, took place at the University of California. Researchers investigated mitochondrial decay and oxidative damage by examining the activity of the mitochrondria in the brains of young and old rats, as well as old rats fed with R-alpha lipoic acid plus acetyl L-carnitine (LA/ALC). The brain mitochondria of the old rats, compared with that of the young rats, had significantly lower levels of naturally present antioxidants and superoxide dismutase (SOD) activity. They also had more oxidative damage to fats and proteins, and overall decreased activity. Feeding LA/ALC to the old rats partially restored age-associated mitochondrial dysfunction to the levels had by the young rats. These results document that mitochrondia decay plays an important role in brain aging. They also document that a combination of nutrients targeting mitochrondria can ameliorate mitochondrial decay by preventing oxidative damage. Interest in LA/ALC has been increasing since researchers at the Linus Pauling Institute at Oregon State University found that activity, energy and cognition could be improved by adding the compounds to the diet. Lead researcher Tory Hagen says that after just a month, older rats on the supplement were about twice as active as older rats not supplemented, whose activity was minimal. Supplementation with LA/ALC has also been shown to improve both spatial and temporal memory. Pictures of the brain cells of supplemented old rats show less decay. Apparently, compounds such as LA/ALC can either mask or reverse metabolic problems caused by cellular aging and the natural oxidative process. Human trials are now underway to determine whether the LA/ALC combo can give people a way to enhance energy and cognitive function well into old age. If in fact they can, the numbers of people afflicted with degenerative diseases could be significantly decreased, and the older years could really become the golden time pictured in ads for retirement accounts. The University of California has patented the LA/ALC combo as a way to enhance metabolism and alleviate oxidative stress. Juvenon, a company founded by Ames and Hagen have licensed the patent from the university, and introduced their first version of the combo. Fortunately, both R-alpha-lipoic acid and acetyl L carnitine are readily available as separate, non-patented items that can be taken in tandem. Researchers recommend LA/ALC for prevention of Parkinson's Disease Researchers in China are also climbing on the LA/ALC bandwagon. The Journal of Cellular and Molecular Medicine, June edition, reported a study to evaluate the preventative effects of LA/ALC on the mitochondra in a human cellular model of Parkinson's Disease. The researchers found a 4-week pretreatment with LA/ALC effectively protected various human neuroblastoma cells against rotenone-induced mitochrondrial dysfunction and oxidative damage. When combined, LA and ALC worked at 100 to 1000 fold lower concentrations than they each did individually. They also found that the pretreatment with LA/ALC increased mitochondrial biogenesis and decreased production of reactive oxygen species. They reported that LA/ALC might be an effective and safe prevention strategy for Parkinson's Disease. Source for information about Tory Hagen and Bruce Ames is Can Acetyl L-Carnitine and alpha-lipoic acid really turn back the clock? The Facts About Fitness. About the authorBarbara is a school psychologist, a published author in the area of personal finance, a breast cancer survivor using "alternative" treatments, a born existentialist, and a student of nature and all things natural.Related CounterThink Cartoons:
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