The Role Of Free Radicals In Accelerated Aging and DNA Damage
Free Radicals and Accelerated Aging-While it remains unclear if it’s the most fundamental process involved in aging, excessive free-radical production is increasingly being regarded as a hallmark of aging. Free radicals (SEE QUICK DEFI¬NITION) damage cells, which causes the body’s organs and systems to lose functional capacity. Free-radical damage also impairs protein synthe¬sis, which is vital to tissue regeneration and repair. Although the body naturally produces certain free radical-neutralizing enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase, it may be unable to prevent all free-radical damage and this gradually causes organs to degenerate.
By lowering oxygen levels and creating acidic conditions in the body, free radicals produce a self-perpetuating cycle, since high acidity increas¬es free-radical production. Perhaps 80% of the chronically ill U.S. adult population has too much acid in their tissues and about 20% are severely acidic. People with acidosis of their tissues are more prone to develop chronic, degenerative diseases, such as heart disease, stroke, and arthritis. Excessive free-radical production has also been associated with loss of collagen in the body. Collagen is an essential component of the body’s musculoskeletal system; its loss results in tissues that are old and withered.
Free radicals damage the cell’s membrane, interfering with its abil¬ity to send and receive messages from other cells and to import neces¬sary nutrients while exporting waste products. Free radicals also dam¬age a cell’s nucleic acid, DNA, and mitochondria. Mitochondria are the cell’s power plant, furnishing the energy needed by cells and tis¬sues to properly function.” Deficits of energy cause greater fatigue and pain, and cause organs to function at a reduced capacity.
The process of free-radical damage and reduced energy produc¬tion occurs in a self-perpetuating cycle—impaired mitochondria pro¬duce less energy and increased levels of cell-damaging free radicals, which cause even more damage to the cell’s mitochondria. These sub¬tle changes show little outward effect until age 40 or so, when the exponential nature of the damage begins to take its toll and energy production declines below levels necessary for good health.
Studies indicate that many people with a shorter life span have higher than normal oxidative stress. Brain tissues from Alzheimer’s patients, for example, have unusually high levels of mitochondria! DNA damage. Tissue samples from individuals with heart disease reveal similar damage. Free-radical damage is most pronounced in oxygen-rich organs (eyes, brain, liver, heart, lungs, kidneys, and blood) and has been implicated in the following diseases: kidney disease, dia¬betes, pancreatitis, liver damage, inflammation of the gastrointestinal tract, lung diseases, eye diseases (macular degeneration, cataracts), nervous system disorders (Parkinson’s, Alzheimer’s, multiple sclerosis), diseases affecting red blood cells (malaria, sickle cell anemia, anemia), iron overload, and autoimmune diseases (rheumatoid arthritis, lupus, AIDS).
