In the course of normal human activity – energy production, detoxification of pollutants and immunologic defense mechanisms, free radicals are produced. These free radicals are unstable molecules that can extract an electron from a neighboring molecule, causing damage in the process. Unchecked free radical production accelerates the processes of human disease and aging. These free radicals are counter-balanced by the anti-oxidants present in our foods (and supplements).
Dietary antioxidants (such as proanthocyanidins found in blueberries and bioflavonoids found in citrus fruits), as well as the antioxidant enzymes, superoxide dismutase and glutathione peroxidase, provide critical protection against free radical damage. Oxidative stress results when this delicate pro-oxidant/antioxidant equilibrium is disrupted in favor of the pro-oxidant (free radical) state.
Evidence is accumulating that oxidative stress is involved in many disease processes, including:
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- Inflammatory Bowel Disease
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- Neurodegenerative diseases such as Parkinson’s and Alzheimer’s
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In a chain-like reaction, free radicals can cause cellular damage by oxidizing nucleic acids, proteins, and membrane lipids. Cellular mitochondria play an important role in aging and disease by being both a significant source of radicals and a primary site of free radical damage. Antioxidants blunt the production of compounds that create inflammation in the body.
To assess equilibrium between oxidative damage and antioxidant reserve, it is necessary to address the RESERVE capacity that provides protection; the ENZYMES that quench the free radicals; and evaluate the DAMAGE that free radical production has already caused.
A blood sample measures anti-oxidant reserve and enzyme function including: whole blood Glutathione, Total Antioxidant Capacity, and the enzymes Superoxide Dismutase and Glutathione Peroxidase. Additionally, blood markers of damage measure lipid peroxides (oxidative damage to cell membranes).
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