Oxidation of different molecules in our body can be responsible for a whole host of diseases - coronary artery disease, cancer, Alzheimer's, Parkinson's, cataracts, and many more...

Oxidative damage may play an important role in cardiovascular diseases

There is abundant evidence that individuals whose diets contain 5 or more portions of antioxidant-rich fruits and vegetables are protected against cardiovascular disease. Studies also suggest that having high blood levels of vitamin E decreases your risk of having a heart attack. How do antioxidants protect you from heart disease? It has been proposed that oxidation of the proteins that carry lipids throughout the body, the lipoproteins, may be the first step in a cascade of events leading to the formation of blood clots in key arteries in your heart, brain and peripheral blood vessels. These oxidized lipoproteins appear to cause damage to the lining of the wall of an artery, which is followed in turn by lipid accumulation, plaque formation, narrowing of the artery wall and clot formation.

Oxidative damage can cause serious neurodegenerative diseases

Oxidative damage appears to play an important role in three diseases that affect the aging brain: Alzheimer's and Parkinson's diseases, and Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease).

In Alzheimer's disease there is an accumulation in the brain of a protein fragment called beta amyloid. This protein is believed to be the major culprit in the formation of the plaques in the brains of Alzheimer victims. Recent research ¹ suggests that one of the ways that beta amyloid produces injury and destroys brain cells in this disease is through oxidative damage. Antioxidants, such as Vitamin E and selegiline (Deprenyl) have been given to Alzheimer patients and have resulted in a slight retardation of the progression of the disease. However, these results, like those obtained with prescription drugs, have only small effects and are certainly not a cure for this terrible condition.

Oxidative damage may play an even greater role in Parkinson's disease. In 1973, two brothers were seen by a neurologist in a hospital in San Jose, California with symptoms that resembled Parkinson's disease. What puzzled the doctor was the age of these two patients - they were in their twenties! He had never seen a case of Parkinson's disease in someone that young. He questioned them about their recent activities and learned that they had tried some designer drugs. One of these designer drugs, MTPT, was sent to the National Institutes of Health where it was injected into experimental animals. These animals soon developed the characteristics of Parkinson's disease. MTPT, a potent oxidizer, appeared to specifically attack the part of the brain that is most affected in Parkinson's disease. Using these experimental animals ² , scientists were able to come up with a drug, selegiline (Deprenyl) that prevented the oxidative damage by MTPT and protected the exposed animals from developing Parkinson's disease. Selegiline is now being used with limited success in Parkinson victims.

In families that have a hereditary form of Amyotrophic Lateral Sclerosis (ALS), Lou Gehrig's disease, scientists have found that the gene for superoxide dysmutase, the main cellular antioxidant enzyme, has mutated. This evidence strongly suggests that an altered superoxide dysmutase causes ALS in these families, perhaps by lowering antioxidant activity.

Oxidative damage may cause several other diseases

Scientific studies have also linked oxidation to many other diseases and disorders including cancer, diabetes, chronic obstructive pulmonary disease, macular degeneration and osteoarthritis. One disease that we will all get if we live long enough is a cataract. A recent nutritional study of over 75,000 women showed that cataracts were significantly less frequent in women who used a vitamin C supplement for 10 or more years, when compared with women who never used vitamin C supplements ³ In the same study, higher blood levels of vitamins C and E were related to a lower risk of cataracts.

Information provided in this article is for informational purposes and is not meant to substitute for the advice furnished by your own physician or other medical professional. This content should not be utilized for diagnosing or treating a health problem or disease, or prescribing any medication. Before taking any health product, you should read carefully all product packaging. If you have or suspect that you have a medical problem, promptly contact your health care provider. Information and statements regarding dietary supplements have not been evaluated by the Food and Drug Administration and are not intended to diagnose, treat, cure, or prevent any disease.

Links

• Click here to read all the articles in this "Oxidative Damage" series
• The Inner Layer of Your Aging Blood Vessels is a Battlefield
• Can antioxidants prevent cell damage, disease and aging?

Footnotes

1.

Oxidative injury in diseases of the central nervous system: focus on Alzheimer's disease. D. Pratico, N. Delanty, Am J Med, 2000, vol. 109, pp. 577--585

2.

Neuroprotective strategies in Parkinson's disease using the models of 6-hydroxydopamine and MPTP. E. Grunblatt, S. Mandel, MB. Youdim, Ann N Y Acad Sci, 2000, vol. 899, pp. 262--273

3.

Long-term nutrient intake and early age-related nuclear lens opacities.  , Arch Ophthalmol, 2001, vol. 119, pp. 1009--1019