After the age of 50, the most common cause of blindness worldwide is macular degeneration, which causes loss of vision at the center of focus while peripheral vision, around the outer edges of the field of vision, remains relatively clear. Both forms of the disorder, wet or dry, result in the same visual symptoms. Limited to mostly older people, a juvenile form of the disease occurs, too.
Without actually resulting in total loss of vision, except in rare cases, macular degeneration causes enough vision loss that the patient cannot read, identify people in photographs, enjoy watching television or movies, or drive safely. In many cases, the disorder stems from genetic origins (especially where juvenile macular degeneration is involved) but continued research indicates lifestyle choices can play a role in slowing onset or progression of the disease, where genetic factors are less influential.
Wet macular degeneration, also called exudative age-related macular degeneration (AMD), occurs when blood vessels grow abnormally in the area behind the retina. These abnormal blood vessels eventually leak proteins and blood into the vitreous humor, the gel-like substance that fills the eyeball. When this leakage obstructs the macula (the center of the field of vision), AMD begins. If not treated, wet AMD can cause rapid loss of vision as the eye’s photoreceptors (the eye’s rods and cones) become damaged irreversibly.
Dry (non-exudative) AMD occurs when the layer beneath the retina atrophies (withers) enough to destroy photoreceptors in the central vision area. Advanced AMD is associated with yellow deposits collecting in the macula. Called drusen, these deposits are similar to the plaque deposits associated with atherosclerosis and Alzheimer’s disease.
Symptoms of AMD include a blurring of the vision although the blurring may not seem associated with just the center of the vision at first. When vision loss is rapid, wet AMD is most often developing. The macula forms about 35% of the field of vision so most AMD patients retain about 65% of the field of vision. Unfortunately, that 65% is around the outside, not the center, of vision.
Other symptoms include shadows or areas of vision that seem to be missing (central scotomas) and distortion of vision is especially noticeable when looking at a grid of straight lines. The straight lines may appear wavy or have gaps. This symptom is most often noticed first when looking at the mini-blinds in one’s own home.
Color is affected, too. Distinguishing one dark color from another or one light color from another become particularly difficult with the onset of AMD. Contrast sensitivity is frequently noted, making everything appear fuzzy, and AMD patients are often slow to recover clear vision after exposure to bright lighting or sunlight.
While little can be done at this time to offset the effects of genetic factors, lifestyle choices thought to improve AMD or delay its onset include successful management of high blood pressure, maintenance of cardiovascular health (reduce cholesterol counts and avoid excess pounds), and limit fat in the diet to no more than 25% of total caloric intake (the average American diet is 42% fat). The disorder is more common in older white people than in those of color.
Oxidative stress is thought to play a role in the development of AMD and certain antioxidants are thought to be beneficial, including high doses of beta-carotene, vitamins C and E, and zinc. Two nutrients from eggs and green vegetables (lutein and zeaxanthin) are thought to have preventive effects. A diet rich in cold-water fish and nuts is thought to be beneficial, too.
The drugs Lucentis, Avastin, and Macugen are currently being used to treat AMD. Treatment involves monthly or bi-monthly injections directly into the eye. Lucentis costs about $3,000 per injection and Avastin about $150 per treatment (although it is not FDA-approved for this condition). Some drugs commonly prescribed for controlling cholesterol are used, too, as a means of controlling the drusen accumulations in the eye.