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| Cataracts and Antioxidants |
CALCIUM: ANOTHER WEIGHT LOSS STRATEGY CALCIUM AND VIT D SUPPLEMENTATION PMS - PROPER MULTIPLE SUPPLEMENTATION CATARACTS AND ANTIOXIDANTS CHELATION & MINERAL BIOAVAILABILITY MAGNESIUM: ARE YOU "MARGINALLY" DEFICIENT? MAGNESIUM: THE MEDICINAL MINERAL "TIS THE SEASON TO BE STRESSED" VEGETARIANISM: A 90'S APPROACH TO A HEALTHIER LIFESTYLE SHOULD YOU TAKE EXTRA VITAMINS MACULAR DEGENERATION STUDY SUPPORTS SUPPLEMENTATION WHAT DO HEART DISEASE, STROKES AND ALZHEIMER'S HAVE IN COMMON? 3 B VITAMINS
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The eyes lens is a clear, gelatin-like substance consisting of long fiber cells of protein and water. Inside the lens, there are no blood vessels or cell nuclei to prevent the passage of light through the lens to the retina, the light sensitive tissue at the back of the eye. Cataracts
and Oxidation To generate energy, cells remove electrons from sugars (i.e. burn the sugars) and add these electrons to oxygen. This forms highly reactive compounds; unstable and electrically charged in such a way as to combine quickly with other elements. When oxygen finally combines with hydrogen, it forms a stable compound - water. A molecule with an unpaired electron must either acquire an additional electron from some other molecule or get rid of the odd one. As oxygen combines, recombines and electrons are exchanged, other unstable molecules are generated, containing unpaired electrons. These normal metabolic processes generate oxygen "fragments" or free radicals, including the hydroxyl radical and singlet oxygen. These free radicals are unstable, volatile, and eventually damage DNA proteins, carbohydrates and lipids. Peroxidation, free radical damage and "oxidative stress" are synonymous. Cataracts occur in diabetics because excess sugar migrates into the eye's lens. Here, the excess sugar is converted into sorbitol, an odorless crystalline alcohol. This results in osmotic changes and oxidative stress. Free radicals are also generated by ultraviolet light. When these events occur, the len's cells form light-scattering globules. These milky balls produce opaque cataracts. Antioxidants Vitamin C. As early as 1935 investigators reported that there is very little vitamin C in the aqueous humor of cataractous eyes and that the patients with cataractous eyes and that the patients with cataracts often have a low level of vitamin C in the blood plasma. Monjukowa and Fradkin reported that the low concentration of vitamin C in the lens preceded the formation of the cataract and concluded that low vitamin C is the cause, not the consequence of cataract formation. They suggested that in old age there is a decreased permeability of the eye to vitamin C and suggested that it might be overcome by a high intake of the vitamin. In 1984, Verma et al. concluded from their studies that vitamins C and E are important for the prevention of senile cataracts. In another study (1991), researchers at the University of Western Ontario compared 174 patients with cataracts to a control group of 175 subjects cataract-free. Results showed that the cataract-free group consumed more supplemental vitamin C and E then did the group with cataracts. Antioxidant supplementation was associated with a 50% reduction in the incidence of cataracts. Vitamin E. Vitamin E compounds (tocopherals) are major lipid-soluble antioxidants responsible for protecting polyunsaturated fatty acids from lipid peroxidation. The tocopherals protect lipids by scavenging peroxyl radicals. Vitamin E is derived from natural (from vegetable oils) and synthetic (from turpentine or petroleum product sources. The natural form of vitamin E has a higher biological value (effectiveness) and is absorbed at least two times better than synthetic vitamin E. There are several forms of vitamin E:
In a 1990 study, isolated liver cells were exposed to an oxygen-rich environment and cell injury and death were observed within hours of incubation. Oxygen-induced injury was preceded by lipid peroxidation and rapid depletion of cellular alpha tocopherol levels. While treatment with alpha tocopherol increased cellular levels of this vitamin 20 fold, the added vitamin E did not protect the cells from oxygen damage. In contrast, liver cells included with alpha tocopherol succinate (TS) contained both alpha tocopherol and TS and were completely protected against the toxic effects of oxygen, including the formation of lipid peroxides. The results of this study indicate that TS protects the cells against free radical damage by increasing cellular concentrations of TS, not by increased levels of tocopherol alone. And, alpha tocopherol succinate might provide the unique cytoprotective capabilities that intercede in the cellular events that otherwise result in oxygen toxicity. Thus, vitamin E succinate might be the most powerful and effective source of the vitamin. In a 1988 study, vitamin E added to a diabetic rat's diet resulted in reduction of diabetes-induced leakage of gamma crystalline - a major protein of the lens - into the vitreous humor. Although the succinate form of vitamin E produced similar results, the synthetic forms of vitamin E did not protect significantly. According to Dr. Trevithick, who conducted the study, synthetic vitamin E esters may not be equally effective as natural vitamin E, even though the same number of vitamin units is given. (Synthetic vitamin E is identified by the prefix "dl", such as dl-alpha tocopherol, dl-alpha tocopheryl succinate, etc.) A study conducted at the Stony Brook SUNY (1991) found that older people who consume plenty of vitamins through a healthy diet or by taking daily supplements are 37% less likely to have cataracts. The study was based on 1,380 people aged 40 to 79 who were treated at two Boston hospitals. Intakes of riboflavin, vitamin C, E and carotene were found to be linked to lower risk for four different types of cataracts. Niacin, thiamin and iron were also associated with reduced risk. In Summary Copyright
© January-February, 1992 |
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