How to help prevent cataract
Cataracts can occur by common environmentally-induced changes in lens proteins that are caused by exposure to excessive sunshine or radiation that lead to the formation of super-oxide radicals in the eye. But environmentally-induced changes aren’t the only factors. Consider these issues:
• Preventable excess exposure to solar UV radiation (particularly UV-B) on sunny days is a major risk factor for spicular (spoke-like) cortical cataract. Spicules start behind the iris, especially behind darker irides, due to heat transfer from the iris to the crystalline lens.
• Microwave effects are recently identified and less-understood risk factors. Exposure to a few mW at 1 GHz over 36 hours affects the optical function of the lens. Self-recovery occurs if the exposure is interrupted, but microscopic changes remain.
• An increased prevalence of nuclear cataracts has been associated in recent studies with other modifiable factors, especially smoking and marked obesity. A study of 1,808 women found that a healthy diet was “the strongest modifiable predictor of low prevalence of nuclear cataract among numerous risk factors.”
• Patients with diabetes tend to develop precocious metabolic cataract, typically posterior sub-capsular cataract (PSC) or cortical cataract. Dietary intervention that normalizes blood glucose control can provide prophylactic benefits. Supplements of chromium/glucose tolerance factor (GTF) and cinnamon powder, along with a low glycemic-index diet, can help control blood sugar and diabetes.
• Myopia has been reported to be a non-modifiable risk factor associated with nuclear cataract. Nuclear sclerosis is also known to cause a myopic shift in the crystalline lens. However, myopia has not been shown to cause nuclear cataract.
• Brown eyes are another non-modifiable risk factor for increased incidence of nuclear lens changes. Dark brown iris pigment increases the risk for spicules of vacuoles in the cortical layer—hidden from sunlight by the iris—by transmitting heat from the iris to the lens cortex in adults over 20 years of age.
• Medications known to cause cataract include corticosteroids, thiazides, loop diuretics, some anti-psychotics, phenothiazine tranquilizers, mercurials and other known toxins. Minimizing dosages of such medications or finding appropriate alternatives can help prevent onset of the disease.
As is the case with environmentally-induced changes in lens proteins, common dietary-induced changes in lens proteins also lead to the formation of super-oxide radicals in the eye. These radicals can be defused by appropriate food antioxidants, which are as important as supplements, offering the added benefit of enzymes and bioflavinoids in raw foods that are not found in most supplements.
Nobel Laureate Albert Szent-Gyorgi, the co-discoverer of vitamin C, first wrote about the beneficial, electrical nature of vitamin C in 1930. Other early pioneers of the theory that free radicals lead to cataract formation include:
• The Bhuyans, primarily using animal models in New York.
• Taylor and associates who showed that decreased carotenoids were associated with PSC and cortical cataract.
• Knekt and associates who showed that low serum concentrations of the antioxidant vitamins alpha tocopherol (vitamin E) and beta carotene are risk factors for end-stage senile cataract.
Additional studies found beneficial effects for the following antioxidants:
• Vitamins D and C.
• Lutein and zeaxanthin.
Researchers have documented that H2O2 accumulation in the aqueous humor of the anterior chamber actually promotes the formation of cataract. As long as our bodies have reserves of selenium, however, we can synthesize glutathione peroxidase (GSH.Px) to convert the H2O2 into harmless H2O, quite important in preventing cataract.
The GSH.Px also helps defuse organic mercury, unless the body is overwhelmed by too much mercury in the presence of too little selenium. Catalase, glucose-6-phosphate dehydrogenase, and glutathione reductase are also part of the armamentarium we use to neutralize the effects of excessive oxidants.