Although several new drugs are now available for the treatment of the exudative (wet) type of AMD, aside from cessation of smoking and a healthy diet of dark green leafy vegetables and fruits supplemented by zinc and anti-oxidant vitamins (Vitamins E, C, and beta carotene), very little is currently available to help patients with “dry” AMD to prevent progression to more serious stages of debilitating disease. Visit our page on Healthy Living to learn how patients with the dry form of AMD can potentially slow their disease. Taking the AREDS formula of anti-oxidants and zinc MAY be appropriate for some patients with the dry form of the disease. It is essential that you check with your doctor as this formula is not recommended for the early stages of the dry form of the disease.
The National Eye Institute’s Age-Related Eye Disease Study (AREDS) found that taking a specific high-dose formulation of antioxidants and zinc significantly reduces the risk of advanced AMD and its associated vision loss. Slowing AMD’s progression from the intermediate stage to the advanced stage will save the vision of many people.
People who should consider taking the combination of antioxidants plus zinc include those who are at high risk for developing advanced AMD. These people are defined as having either:
The doses used in the study were:
While most patients in the study experienced no serious side effects from the doses of zinc and antioxidants used, a few taking zinc alone had urinary tract problems that required hospitalization. Some patients taking large doses of antioxidants experienced some yellowing of the skin. Some supplements may interfere with each other or other medications. Smokers and former smokers should not take beta-carotene, as studies have shown a link between beta-carotene use and lung cancer among smokers. The long-term effects of taking large doses of these supplements are still unknown.
Again, before embarking on a vitamin supplement program, consult with your eye care professional and follow his or her dosage recommendations carefully.
In AREDS2, patients with either bilateral large drusen or large drusen in one eye and advanced AMD in the other will be given either high doses of lutein and zeaxanthin, both carotenoids, or omega-3 fatty acids or both, plus the original AREDS formulation for a total of six years.
The AREDS2 investigation will also compare the original AREDS formulation by comparing low zinc (25 mg) vs. high zinc (80 mg), and will also compare formulations with and without beta-carotene. As investigators note, the rational for adding lutein and zeaxanthin to the new formulation was based on observations that subjects in the original AREDS trial were less likely to progress to advanced AMD when they had high dietary levels of the two carotenoids. Results are due out in 2010.
Several companies are conducting research to explore how, or why, early, dry AMD converts to wet AMD or progresses to the late stages of the dry form – usually referred to as “geographic atrophy”. A few different pathways such as inflammation, and/or oxidative damage have been considered, mostly involving drusen.
Small drusen usually appear early in AMD and may not result in vision loss. However, the numbers and size of the drusen may increase along with concomitant other changes such as RPE cell pathology, causing AMD to progress with resulting vision loss. Linkage of these events to the appearance of wet AMD or progression to geographic atrophy is a key question and yet under investigation. One possibility is that the drusen debris buildup leads to a diminished blood supply to the RPE and photoreceptor cells, resulting in a diminished oxygen supply (hypoxia). In an attempt to compensate for this imbalance, new, abnormal blood vessels (neovascularization) could be formed, leading to wet AMD. Continuing research may lead to more effective antioxidants, anti-inflammatory agents, etc. which could halt or even reverse the progression of early, dry AMD to the more severe wet form or to the end stage dry form.
Researchers are also very interested in genetics as a link to AMD and as a factor in progression from dry to wet AMD. Researchers have now located particular genes whose mutations are associated with an increased risk for AMD. For example, one of these genes, known as Factor H, codes for a protein (complement factor H) which is a powerful inhibitor of inflammation. People who possess an alternate version of the gene produce an aberrant complement factor H, which fails to provide adequate suppression of the complement pathway of inflammation. This means that people with the defective gene are more vulnerable to certain inflammatory processes which can lead to the development of AMD.
However, this is an area which has ignited research interest, and the longer term future may be somewhat brighter for those with dry AMD.
Prophylactic laser treatment of drusen does not apparently affect the rate of vision loss over a five-year interval according to recently reported findings from the Complications of Age-Related Macular Degeneration Prevention Trial (CAPT). CAPT was designed to assess the safety and effectiveness of low-intensity laser treatment in preventing vision loss in patients with at least 10 large drusen in both eyes at study entry. During the study, patients received treatment in one eye only, the other eye was not treated. At the end of five years, 20.5 percent of both treated and observed eyes had visual acuity scores three lines worse than at study entry.
Another study (Laser to Drusen trial) confirmed that prophylactic laser of the fellow eye of patients with neovascular AMD is not beneficial.
