The Creation of an Antioxidant Arsenal
Martha Reid, ND

We are in an exciting epoch of health care in which patients are becoming more responsible for their well-being, an era in which disease prevention and the promotion of optimal health are of primary importance. Many individuals now recognize that a lifetime of vibrant health is held within their lifestyle, of which diet has a predominant role. Over the past several decades, researchers have plied the abundant waters of nutritional medicine, discovering an amazing array of knowledge about the healing power of food. Perhaps the most notable development of the past 50 years is the discovery of antioxidants and their ability to neutralize free radicals and prevent disease. Free radicals and antioxidants have virtually become household terms, yet what do they really mean, and how do they affect health and disease? This essay discusses the connection between free radicals and disease and how antioxidants found in whole foods are the key to reducing oxidative stress (free radical damage) and preventing disease. Equipped with this knowledge, individuals can use their diet as a means to prevent disease and promote optimal health and longevity.

As the earth’s atmosphere evolved, so did aerobic metabolism, as well as the paradox that would affect all aerobic creatures, namely, the absolute necessity of oxygen for survival and its innate toxic effects that can cause cellular damage and cell death. In aerobic respiration, oxygen creates toxic metabolites known as free radicals.1-3 A free radical is an extremely unstable highly reactive molecular species owing to the fact that it contains unpaired electrons in its outer shells. This results in inherent instability. To create balance, the molecule must find an electron to fill its half-empty orbital and does so by “stealing” an electron from a weaker molecule, much in the same way that a dominant child steals a toy from a younger sibling. This causes instability in the newly victimized molecule, which then goes on to steal an electron from a molecule weaker than itself, resulting in the propagation of chain reactions that are highly damaging to cellular structure and function. In the chemical world, the loss of an electron is known as oxidation, while the gain of one is called reduction. Although deleterious, free radical reactions are a common and necessary component of all biologic systems: they are involved in aerobic metabolism, are essential to a multitude of biochemical processes within the body, and are a means for host defense against pathogenic microbes.

Harman, a researcher at the University of Nebraska Medical Center, Omaha, proposed in the 1950s the free radical theory of aging, which postulated that an accumulation of free radicals within tissues causes cellular damage and results in aging over time.1,2 It was not until later that his work was expanded to look at free radicals as a cause of degenerative disease. Today, numerous scientific investigations have been performed linking free radical–induced tissue damage to diseases such as cardiovascular disease, arthritis, neurodegenerative diseases, diabetes mellitus, and various forms of cancer.4

All forms of stress, including physical, chemical, environmental, and even emotional, can trigger free radical reactions.2,5 The mechanisms by which free radical damage occurs are diverse, complex, and not fully understood, yet what is known represents a hornet’s nest of pathologic processes and disease manifestations. For example, free radicals are capable of damaging cellular membranes and organelles through the oxidation of cholesterol and polyunsaturated fatty acids embedded within cell membranes. This causes cross-linking of membrane proteins, resulting in loss of membrane function. An influx of sodium and calcium ions into the cell triggers numerous intracellular events, resulting in further insult. Damage to the mitochondrial membrane affects the energy production mechanisms of the cell, resulting in insufficient energy to maintain enzymatic activities, transport systems, ion-pumping mechanisms, and even the production of enzymes needed to trigger apoptotic pathways. Necrosis occurs, resulting in increased inflammation and other pathologic processes. Damaged DNA and intracellular proteins result in mutations that may eventually become neoplastic.2,5 With just this basic outline, one sees how free radical damage can culminate in degenerative disease processes. Thankfully, Mother Nature in her infinite wisdom evolved a powerful defense to combat free radical damage in the antioxidant arsenal of whole foods.

Antioxidants are molecules such as vitamins (mainly A, C, and E), minerals (selenium, zinc, copper, and manganese), certain amino acids, and phytonutrients (plant nutrients) capable of preventing oxidation of other molecules by giving electrons to quench free radicals. This inhibits the initial generation of free radicals and limits the intensity of their chain reactions. These potent radical quenchers are abundant in plant foods and evolved in concert with aerobic metabolism as a means of protecting plants from the toxic effects of atmospheric oxygen and other ongoing environmental challenges such as UV radiation, toxins, and pollution.2,4,6

Over the past several decades, an abundance of research has elucidated the synergistic nature of antioxidants: they work together to provide protection, each depending on the others to help support optimal function, and create greater protection as a whole than they do as individual parts.4 A prime example of this is almonds and their ability to prevent oxidation of cholesterol. Their skins contain more than 20 different flavonoids, while their core is high in vitamin E.4 If the skins alone are eaten, they provide an 18% increase in the resistance of cholesterol to oxidation; eaten whole, they provide almost 53% resistance to oxidation. This demonstrates the synergistic nature of the antioxidant network and the importance of consuming an array of nutrients rather than attempting to supplement one’s diet with single entities.

Although vast amounts of research have been performed in this arena, there is much that we have yet to learn about the nutrient value of plants and how they affect our health. There are thousands of phytonutrient antioxidants yet to be discovered; some researchers estimate that up to 40,000 phytonutrients may one day be cataloged and their actions on the body understood.4 For me, how to tap this antioxidant arsenal and what it means for health represent the most exciting areas of nutritional research. As our science becomes more advanced, our understanding of the truth becomes simpler that the whole is greater than the sum of its parts.

 

References

1. Harman D. Aging: a theory based on free radicals and radiation chemistry. J Gerontol. 1956;11(3):298-300.

2. Levine & Parris. 1985.

3. McKee T, McKee J. Biochemistry: The Molecular Basis of Life. 3rd ed. New York, NY: McGraw-Hill Publishers; 2003.

4. Mateljan G. The World’s Healthiest Foods. USA: George Mateljan; 2007.

5. Robbins. 2005.

6. Mahan K, Escott-Stump S. Krause’s Food, Nutrition & Diet Therapy. 11th ed. San Diego, CA: Elsevier Inc; 2004.

 

Background Reading

Ashock B. The aging paradox: free radical theory of aging. Exp Gerontol. 1999; 34(3):293-303.

Bruckdorfer K. Antioxidants and cardiovascular disease. Proc Nutr Soc. 67(2):214-222.

de Grey AD. A proposed refinement of the mitochondrial free radical theory of aging. Bioessays. 1997;19(2):161-166.

Halliwell B. The wanderings of a free radical. Free Radic Biol Med. 2009;46(5):531-542.

Kumar V, Abbas A, Fausto N. Robbins and Cotran Pathological Basis of Disease. 7th ed. San Diego, CA: Elsevier Inc; 2005.

Muller FL, Lustgarten MS, Jang Y, Richardson A, Van Remmen H. Trends in oxidative aging theories. Free Radic Biol Med. 2007;43(4):477-503.

Priebe MG, van Binsbergen JJ, de Vos R, Vonk RJ. Whole grain foods for the prevention of type 2 diabetes mellitus. Cochrane Database Syst Rev. 2009;(1):CD006061.

Singal P, Khapner N, Palace V, Kumar D. The role of oxidative stress in the genesis of heart disease. Cardiovasc Res. 1998;40(3):426-432.

 

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