The goal of healthy aging is to prolong the ‘healthspan’ of the individual, to optimize vitality and to minimize illness and suffering from age related diseases. With this goal in mind, researchers have discovered physiological processes that appear to be related to the basic biology of aging.
One of the most important disruptions at the cellular level with aging is the loss of mitochondrial function. Mitochondria are the organelles found in large numbers in most cells. An important function of mitochondria is to take nutrients in the cell and turn those nutrients into ATP. This ATP is the energy that fuels the cell and regulates cellular metabolism, allowing the cell to properly carry out its various functions. A decline in mitochondrial function and activity has been associated with aging.
Another physiological disruption of aging is the decreased ability of the cell to respond to toxicological and oxidative stresses of everyday living. This can lead to damage of DNA making chronic diseases and cancer more likely to occur. There is solid evidence that accumulated DNA damage is directly related to disorders of aging, including metabolic disorders such as diabetes and neurological disorders such as Alzheimer’s. The central nervous system is particularly susceptible to oxidative damage.
Researchers at Linus Pauling Institute’s Healthy Aging Program are seeking to identify the mechanism of action of two nutrients that are considered “age essential”, Lipoic Acid (LP) and Acetyl-L-Carnitine (ALCAR) to address these aging processes. Feeding old rats LP significantly increased cellular ascorbic acid (vitamin C) and glutathione, two important cellular antioxidants. It was also noted that LP upregulated Phase II detoxification enzymes which decrease markedly with age. This phase of detoxification is critical to the removal of toxins created by everyday biological processes and toxins that come from the outside, such as chemicals like pesticides.
LP also was found to improve cellular stress-response mechanisms by activating a transcription factor called Nrf2. The Nrf2 can then bind to DNA sequences called the Antioxidant Response Element (ARE) which is found in over 200 genes that are involved in protecting cells against oxidative and toxic challenges.
In addition, it was also found that when both ALCAR and LP were fed to old rats, many markers of mitochondrial decay improved markedly. Improving mitochondrial function may be a significant key to healthy aging, as mitochondrial dysfunction negatively affects generation of cellular energy, dysregulates cellular calcium levels, increases oxidative stress and decreases tissue regeneration.
LP and ALCAR appear to have a synergistic affect on markers of aging at the cellular level. Our gratitude extends to the Linus Pauling Institute and other members of the orthomolecular community for the important work they are doing to promote an understanding of the physiology of healthy aging.
The Mitochondrial Basis of Aging, NCBI- NIH ncbi.nlm.nih.gov>pmc
Linus Pauling Institute, Stress Response and Mitochondrial Decay, Tory M Hagen, PhD
Mitochondrial Aging and Metabolism: The Importance of a Good Relationship in the Central Nervous System DOI:10.5772/intechopen.76652