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An Eye to the Future

May 2004

By Dean S. Cunningham, MD, PhD

LE Magazine May 2004
An Eye to the Future
By Dean S. Cunningham, MD, PhD

“I would give anything to read the newspaper again,” laments my otherwise healthy 68-year-old patient with recent onset macular degeneration, a condition she had never heard of before. Her physical disability in turn has led to clinical depression, characterized by frequent crying spells, hypersomnia, reclusiveness, and hopelessness. Despite the prevalence of eye disorders in people over the age of 50, relatively few such adults have heard of the major disorders, know what they are or what causes them, understand their paralyzing impact, or know what can be done to prevent them.

I recently surveyed 50 adults between the ages of 35 and 50 and was surprised to learn that while 92% had heard of cataracts, fewer than 15% could describe what one is. Only 4% had heard of diabetic retinopathy and none could describe the condition. While 34% had heard of glaucoma, a mere 4% knew what glaucoma is. Finally, just 8% had heard of macular degeneration and only one person out of 50 knew what it was.

Prevention of disease requires awareness, basic knowledge, and a plan. In this article, I will review the anatomy of the eye, briefly describe how we see, and outline the four major eye diseases for which we all are at risk: cataracts, diabetic retinopathy, glaucoma, and macular degeneration. You will learn what these conditions are, what causes them, and the simple steps you can and should take now to prevent them.

Scope of the Problem
Diseases of the eye that result in loss of vision affect nearly one of two people in the US over the age of 75. Prevalence rates for cataracts, glaucoma, and macular degeneration are seemingly stable, affecting 3-4% of the adult population. Although a risk of 3-4% may seem miniscule and insignificant to the healthy young adult, a prevalence rate of 3-4% for the entire population equates to a 33-50% age-specific prevalence rate as one lives beyond 65 years of age.

The prevalence of diabetic retinopathy is on the rise. Some 8-9% of US adults are diabetic and therefore at risk for diabetic retinopathy. Currently, 2.5% of the US population has permanent visual loss due to diabetic retinopathy. Because of the obesity epidemic, however, it is projected that as many as one-third of today’s children will be diabetic as adults. Should this projection hold up, the percentage of the population facing permanent visual loss due to diabetic retinopathy could conceivably triple or quadruple.

Cataracts are the leading cause of blindness worldwide, affecting up to 40% of people over 75. Cataract formation is ubiquitous, beginning in all adults over the age of 30.

A cataract develops when proteins aggregate in the lens of the eye with progressive opacification, thus admitting less light. Cataracts are described according to their location (nuclear, cortical, capsular, or subcapsular) and characterized as congenital, immature, mature, or hypermature. Cataracts are painless and the loss of vision is generally gradual but progressive.

While the etiology leading to the development of cataracts remains unknown, some well-established risk factors predispose one to cataract formation. These include age (being over 30), ocular trauma, concomitant ocular disease, diabetes and/or uncontrolled hyperglycemia, hypertension, hypocalcemia, chronic steroid use, sunlight overexposure, tobacco abuse, alcohol abuse, genetic factors (Native Americans, African-Americans, women, and individuals with dark irises are at higher risk), diets deficient in antioxidants, and increased ex-posure to oxidative stress.

Oxidative stress occurs as free radicals accumulate as both endogenous by-products (from dietary intake and its breakdown/oxidation) and exogenous by-products (from environmental factors). A free radical has an unpaired electron and is therefore a highly reactive, unstable molecule. Because the free radical is compelled to complete its electron pair, it will in essence “steal” an electron from a cell membrane or strand of DNA, rendering the donor structurally altered and possibly damaged.

Antioxidants contained in the food we eat and the supplements we take are our bodies’ defense against free radicals. Compared to a cohort of matched individuals without cataracts, individuals with cataracts have been shown to have lower levels of the antioxidants glutathione and superoxide dismutase, and higher levels of thiobarbituric acid reactive substances, a marker for free radical damage.1

There is wide agreement that diets rich in beta-carotene (a nontoxic, water-soluble precursor of vitamin A) and vitamin C may significantly reduce one’s risk of cataract formation.2,3 By contrast, no definitive evidence exists to suggest that vitamin E prevents or slows the progression of cataracts.4 This may be due in part to the lipophilic and hydrophobic properties of vitamin E within the vitreous humor.

Application of eye drops containing carnosine or N-acetylcarnosine has a favorable impact on existing cataracts, presumably as both a quencher of oxygen free radical species and an inhibitor of glycation, in which sugars bind to excessive protein to form advanced glycation end-products.5-7 Because N-acetylcarnosine is more lipid soluble than its parent compound, carnosine, its potential is indeed more promising. Alpha lipoic acid, a uniquely fat- and water-soluble antioxidant, also may be beneficial in preventing cataracts. Protective eyewear should always be used to block ultraviolet radiation and prevent traumatic eye injury.