Frequently Asked Questions

AMD is a common eye disease associated with aging that gradually destroys sharp, central vision. The retina is the very thin tissue that lines the back of the eye and contains the light-sensing cells that send visual signals to the brain. Sharp, clear, 'straight ahead' vision is processed by the macula, which is the central part of the retina. When the macula is damaged, many daily activities such as driving, reading and recognizing faces become increasingly difficult.

There are two forms of AMD, dry and wet. If dry AMD reaches the advanced stages, there is no treatment currently available that will prevent vision loss. However, a specific high-dose formula of antioxidants and zinc may delay or prevent intermediate dry AMD from progressing to the advanced stage.

The wet form of AMD can be treated with Lucentis® (or Avastin®), Macugen®, photodynamic therapy and laser photocoagulation.

• Lucentis (ranibizumab injection), approved by the U.S. Food and Drug Administration (FDA) in 2006, is an antibody fragment that binds to and inhibits the biologic activity of human vascular endothelial growth factor (VEGF). VEGF is a protein believed to play a critical role in the formation of new, abnormal leaky blood vessels, which can damage the macula (area of the eye responsible for central vision). Lucentis is injected into the vitreous portion of the eye (the clear jelly-like substance that fills the eye from the lens back to the retina). Since VEGF is continually produced in AMD, ongoing, routine administration of Lucentis is required. Lucentis can prevent further vision loss in most patients and improve the vision of some. Avastin is manufactured by the same pharmaceutical company, Genentech, Inc., that makes Lucentis. It is a blood vessel growth inhibitor used to treat colorectal cancer, but is not approved for AMD. However, physicians have successfully used small doses of Avastin as an AMD therapy by injecting it into the eye at regular intervals over the course of months or a year.
  
  
• Macugen (pegaptanib sodium injection), approved by the FDA in 2004, blocks vascular endothelial growth factor (VEGF), a protein that promotes blood vessel growth. In clinical trials, patients receiving Macugen were less likely to progress to legal blindness and experience severe vision loss. Macugen is injected into the vitreous portion of the eye (the clear jelly-like substance that fills the eye from the lens back to the retina). Macugen is routinely administered since VEGF is continually produced in AMD.
  
  
• Photodynamic therapy (PDT) was approved by the FDA in 2000 as a treatment for wet AMD. In PDT, Visudyne®, a light-sensitive drug, is injected into a vein in the arm. The drug enters the bloodstream and is absorbed by the abnormal blood vessels growing underneath the macula. A low-intensity, non-thermal (“cold”) laser is then directed at the retina for a little over a minute. This activates the Visudyne allowing it to destroy the abnormal vessels and inhibit new growth. The cold laser does not damage the retina or other cell layers that overlie the abnormal vessels. PDT may help to stabilize vision, but it will not restore lost vision and is not likely to improve vision. Treatments are typically administered every 3 months and as many times as needed to prevent re-growth of the abnormal vessels (potentially 6-7 treatments over 2-3 years). One treatment normally takes about 20 minutes and is relatively painless. PDT is most effective in treating predominantly classic, subfoveal AMD in which the blood vessel growth and leakage borders are well defined and occur under the center of the fovea (small region at the center of the macula that is dense in light-sensitive cells and provides the sharpest vision). Other light-sensitive drugs are being evaluated. Researchers are also studying the use of verteporfin in combination with other therapies.
  
  
• In photocoagulation, the first treatment that was used for wet AMD, a laser is focused on the abnormal blood vessels growing beneath the retina to seal or destroy leaking blood vessels and potentially prevent further vision loss. While photocoagulation can decrease the chances of moderate to severe vision loss, it does not restore lost vision, so early treatment is critical. It is not possible to treat those with “subfoveal” AMD in which the abnormal blood vessels are located under the fovea, in the center of the macula. Almost 90% of AMD is subfoveal, so only a small percentage of patients are candidates for this procedure. Photocoagulation laser surgery can be performed on an outpatient basis. The patient remains awake during the entire process. Eye drops are used to numb the eye and dilate the pupil, then a high-energy laser is focused on the abnormal blood vessels. The laser heats and destroys the abnormal blood vessels and prevents them from leaking. This can help prevent or slow further damage. However, it can also scar parts of the macula and result in some central vision loss. In addition, the blood vessel leakage may reoccur, and it is not always possible to repeat photocoagulation treatment.

For those with permanent vision loss, there are a variety of low vision aids and coping strategies that can improve the quality of life. The "Resources" section of this website includes information on low vision aids and organizations.

Age-related macular degeneration (AMD) is a major cause of visual impairment in the U.S. Approximately 1.8 million Americans age 40 and older have advanced AMD, and another 7.3 million people with intermediate AMD are at substantial risk for vision loss. The government estimates that by 2020 there will be 2.9 million people with advanced AMD.

There are two forms of AMD: dry and wet. It is possible for a person to suffer from both forms, for AMD to affect one or both eyes, and for the disease to progress slowly or rapidly. Dry AMD may advance and cause loss of vision without turning into the wet form of the disease. However, it is also possible for early-stage dry AMD to change into the wet form of the disease.

Dry macular degeneration is the most common type of AMD. This form, in which the photosensitive cells of the macula slowly break down, is diagnosed in 85-90 percent of cases. Yellow deposits called drusen (extracellular waste products from metabolism) form and accumulate under the retina between the retinal pigmented epithelium (RPE) layer and the Bruch's membrane, which supports the retina. Drusen are often found in the eyes of older people, but an increase in the size and number of these deposits is frequently the first sign of macular degeneration. Over time, drusen are associated with deterioration of the macula and the death of RPE and photoreceptor cells, resulting in a blurring or spotty loss of clear, straight-ahead vision.

Wet macular degeneration occurs when abnormal blood vessels grow behind the macula as RPE and photoreceptor cells die. The Bruch’s membrane begins to break down, usually near drusen deposits, and new blood vessels grow. This growth is called neovascularization. These vessels are very fragile and can leak fluid and blood, resulting in scarring of the macula and the potential for rapid, severe damage. Straight-ahead vision can become distorted or lost entirely in a short period of time, sometimes within days or weeks. Wet macular degeneration accounts for approximately 10 percent of the cases, but it results in 90 percent of the cases of legal blindness. All wet AMD is considered advanced.

To help diagnose AMD, an eye care professional will perform a dilated eye exam to view the retina and optic nerve for damage, a visual acuity test to measure sight from various distances and a fundoscopy to examine the back of the eye. If wet AMD is suspected, fluorescein angiography, in which dye is used to detect leaking blood vessels, may also be performed. The patient might be asked to look at Amsler grid; if the straight lines on the grid appear wavy or distorted, AMD may be developing.

Researchers continue to explore environmental, genetic and dietary factors that may contribute to developing AMD. New treatment strategies are also being explored, including retinal cell transplants, drugs to prevent or slow down the progress of the disease, radiation therapy, gene therapies, a computer chip implanted in the retina (may help simulate vision) and agents to prevent the growth of new blood vessels under the macula.

All wet AMD is considered advanced; however, the dry form of AMD has three stages:

• Early AMD - patients have several small drusen or a few medium-sized drusen. There is no vision loss or symptoms at this stage.
• Intermediate AMD - patients have many medium-sized drusen or one or more large drusen. Some people may need more light for tasks such as reading. A blurry spot may appear in the center of the visual field.
• Advanced AMD - patients exhibit a large number of drusen deposits and a breakdown of RPE and photoreceptor (light sensitive) cells and supporting tissue in the retina. A large blurry spot occurs in the center of the visual field and can become larger and darker, eventually causing a complete loss of central vision.

Some limited studies appear to indicate that eating a diet high in carotenoids, antioxidant vitamins (such C and E), and omega-3 fatty acids may reduce the risk of developing age-related macular degeneration (AMD); however, more research is required before definitive statements can be made.

Carotenoids are compounds that are found in plants, which have been associated with protection not only from macular degeneration, but from cancer, heart disease, diabetes, and a number of other medical conditions. Dark green, yellow and orange fruits and vegetables, especially those high in the carotenoids known as lutein and zeaxanthin, appear to provide the best protection for AMD. Lutein and zeaxanthin are the primary pigments in the macula and are thought to protect the retina from ultraviolet light.

Lutein is found in spinach, collard greens, kale, broccoli, papaya, oranges, kiwi, mango, green beans, peaches, sweet potatoes, lima beans, squash, red grapes, and green bell pepper.  Yellow corn, honeydew melon, squash, oranges, mango, kale, apricots, peaches, and orange bell pepper are good sources of zeaxanthin.

Foods abundant in vitamin C include green peppers, citrus fruits, tomatoes, broccoli, strawberries, yams, leafy greens, and cantaloupe.

Vitamin E is found in eggs, fortified cereals, fruit, wheat germ, green leafy vegetables, nuts/nut oils, vegetable oils, and whole grains.

Wild salmon, sardines, walnuts, and flaxseed oil are good sources of omega-3 fatty acids.