Age-Related Macular Degeneration

What is AMD?

When given a checklist to rank their greatest health-related fears, most adults didn’t choose cancer or heart disease as number one. Of more than ten thousand people surveyed during an international study conducted by India’s Prasad Eye Institute, over ninety percent chose blindness (Giridhar, 2002). In a survey commissioned by Pfizer, twice as many respondents feared blindness as premature death (Pfizer, 2008).  But mere fear of something doesn’t make it go away. Taking action, though, could.

Age-related macular degeneration, or AMD, is a degenerative disease of the retina (the thin layer of nerve cells lining the back of the eyeball) that causes progressive loss of central vision, where the macula interprets details. Photoreceptor cells in the macula convert light into electrical messages that are transferred to the brain by the optic nerve.  If these cells degenerate, central vision does likewise. Risk for macular degeneration increases with age, and is the most common cause of vision loss in those over sixty.  It’s estimated that eight million people in the United States over age fifty-five have one or both eyes affected by intermediate AMD (Bressler, 2003). Because life expectancy has increased, the number of AMD cases is likely to rise to three million by 2020 (Friedman, 2004), thus becoming a major public health problem.

There are two types of AMD: dry and wet. The dry form accounts for more than 90% of all cases, and is characterized by yellowish-whitish deposits, called drusen, that accumulate behind the macula. Drusen are composed of the glycoprotein and glycolipid waste products of the photoreceptor cells, and they interfere with the blood supply to those cells.  In dry AMD, vision loss is gradual over the course of many years, often affecting only one eye. The wet form of AMD is identified by the appearance of newly created abnormal blood vessels growing under the macula. Unfortunately, these vessels leak, bleed and scar the macula, distorting or destroying central vision. Because the blood and fluid lift the macula out of position at the back of the eye, damage occurs rapidly. Wet AMD is the leading cause of irreversible legal blindness.

What Are The Risk Factors?

Age and race are common factors. As Caucasians age from their 60s to their late 70s, the risk changes from about 2% to almost 30%. No such increase is seen in other populations. Smoking reduces the amount of oxygen that reaches the eye—and other organs—and precludes the use of nutritional interventions that may prevent AMD in the first place. It’s been discovered that certain supplements related to vitamin A are causative of respiratory disease among smokers, including cancer. As with many diseases, family history plays a role, as well as a gene labeled CFH, compliment factor H, which is probably implicated in more than half the AMD cases in the United States (Chakravarthy, 2010) (Klein, 2005).

What Are The Symptoms?

The need for increasingly bright illumination (especially for close work), difficulty in adapting to lower levels of illumination (as when entering a dimly lit restaurant), increasing blurriness of printed material, reduced intensity of bright colors, and a blurred or blind spot combined with a loss of central visual sharpness are signs of dry AMD. Wet AMD may present as crookedness or waviness of lines known to be straight, a street sign that is out of focus, objects appearing farther away than they actually are, and a decrease in central vision, among others. Because a good eye can compensate for one affected by AMD, symptoms might not be noticed right away.

Pupil dilation by your eye doctor will enable him or her to see your retina through a tool called a slit lamp, which allows examination through a kind of microscope. The doctor will look for drusen and for other suspicious features. Because new blood vessels beneath the retina are hard to see, the doctor will look for other signs of wet AMD that may include bleeding, fluid behind the retina or elevation of the retina. Should these be identified, further evaluation is probably needed.

How About Treatment?

Lifestyle changes (and medications) can alter the progress of dry AMD. Antioxidant deficiencies, notably of zinc, and vitamins A, C, and E, have been noted in age-related macular degeneration (Age-Related Eye Disease Study Group, 2001). These substances prevent free radicals and unstable oxygen from damaging the retina, and are commonly found in leafy greens, colorful vegetables (oranges, yellows and purples), and fruits. A person diagnosed with AMD should look at diet anyway, so why not take the preventive route? Do it now. Lowering intake of animal fats and getting a little exercise to drop a few pounds is part of the regimen.

Early in this century the Dutch conducted a review of work that started in the 1990’s, examining an over-55 population of middle-class suburbanites who had at least one risk factor for AMD. Of almost six thousand at-risk subjects, all of whom had supplied a comprehensive dietary inventory, fewer than ten percent experienced incident AMD after an 8-year follow-up. It was noted that those with the highest intakes of all four antioxidant compounds (Zn, A, C, E) had a significant reduction in risk of disease (vanLeeuwen, 2005).

An earlier British study acknowledged the protective function of vitamins A, C, and E, concurrently citing the role of zinc in retinal metabolism and that of selenium as anti-oxidative. High serum levels of carotenoids, the yellow to red pigments in plants that are concentrated in the retina, are associated with reduced risk of AMD. A serendipitous discovery in this elderly group, though not directly related to its goal, found that the essential omega-6 fat, gamma-linolenic acid (GLA), helps in dry eye conditions. The value of the omega-3 fats in retinal development is reiterated (Brown, 1998).

Harvard investigations found that omega-3 fats from fish oil and fish consumption reduced risk for AMD, especially among smokers (Seddon, 2006), whose additional risks include uncontrolled cholesterol and diabetes (Tomany, 2004). Most recently, investigators at the University of Alberta found DHA, the omega-3 that partners with EPA in fish and fish oil, able to block the accumulation of toxic molecules behind the retina (Dornstauder, 2012). Keep in mind that DHA must be balanced with EPA, at a ratio of approximately 3:1, EPA:DHA. The reason? Alone, or in unbalanced supplementation, DHA can be excitatory, despite its known connection to eye and brain health.

A randomized trial recounted by Harvard Medical School says that markers of inflammation provide an environment conducive to AMD. Homocysteine and C-reactive protein are analytes that can be mitigated by the judicious use of vitamins B12, B6, and folic acid, all of which are related to the reduced incidence of coronary episodes. Together, these supplements proved effective in reducing incidence of AMD in a considerably large group enrolled in a women’s cardiovascular study (Christen, 2009).  That these markers are implicated in eye-related pathologies had been established earlier (Seddon, 2004).

Getting antioxidants from foods is held by traditional medicine to be the best route, but this may be a misguided stance. The general food supply has been denigrated by less-than-stellar corporate farming practices that use chemical soil enhancers and biocides that linger on food surfaces. Dousing stored seeds with pesticides that eventually appear in the stems, leaves, roots, and fruits of plants, followed by sloppy storage and shipping practices negate the veracity of obtaining all the nutrition we need from our food. It’s bad enough that much food lacks nutrition, but it’s an insult that our livers have to detoxify it, too. Add all this to what happens in a careless kitchen and we can establish the need for supplementation.

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*These statements have not been evaluated by the FDA. These products are not intended to treat, diagnose, cure, or prevent any disease.