Macular degeneration (aka age-related macular degeneration) is a condition that causes blurred, limited, or no vision in the center of the eye’s visual field.
Macular degeneration is an eye disease that results in irreversible impairments in visual function. The disease results from the progressive accumulation of damage to a part of the eye called the macula, a photoreceptor-dense area responsible for central vision.
Macular degeneration is classified into one of three stages: early, intermediate, or late. Signs and symptoms vary according to stage.
Early stage: Plaque deposits known as drusen accumulate in the retina. Eyesight is typically unaffected.
Intermediate stage: Drusen grow larger in size. Blurring of central vision and difficulty seeing in low light may occur, but most people experience no noticeable symptoms.
Late/Advanced stage: Drusen grow even larger in size. At this stage most people experience visual symptoms such as blurred vision, loss of color perception, difficulty seeing in low light, and central blindness.
Additionally, the late stage is further classified as either dry (a.k.a. geographic atrophy) or wet/neovascular macular degeneration. Wet/neovascular macular degeneration differs from the dry form in that it features abnormal blood vessel growth in the back of the eye. This form is less common, but much more likely to result in blindness.
The main method of diagnosing macular degeneration is a dilated fundus examination, in which the back of the eye (the fundus) is examined for the presence of drusen and certain pigmentation abnormalities. If macular degeneration is present, additional tests (e.g., optical coherence tomography, fluorescein angiography) are required to either diagnose or rule out wet/neovascular macular degeneration. Ophthalmological examinations are also used to assess visual function and eyesight changes.
There is no cure for macular degeneration, meaning treatment is focused on preventing or slowing progression. This involves avoiding risk factors that make the disease worse, like smoking. In the case of wet/neovascular macular degeneration, disease progression can be slowed with drugs called VEGF inhibitors, which are injected into the eye.
Several supplements, often in combination, have been tested for their effect on macular degeneration, including vitamin C, vitamin E, zinc, lutein, and zeaxanthin. Notably, one large clinical trial found that supplementation with lutein and zeaxanthin slowed disease progression among people with intermediate stage macular degeneration.
A Mediterranean dietary pattern has been linked to a lower risk of the disease and slower disease progression. Among individual foods, eating more fish is associated with a lower risk of developing macular degeneration, while eating more red meat tends to be associated with a higher risk. Foods rich in lutein and zeaxanthin (like green vegetables and eggs) may also help reduce the risk of developing late stage macular degeneration.
In rare cases, photodynamic therapy may be used to slow the progression of specific types of wet/neovascular macular degeneration. The procedure involves administering a drug and exposing the eye to a type of light that “activates” the drug.
Macular degeneration is caused by damage to the macula, which is the area of the retina with the highest concentration of photoreceptor cells, and thus a key factor in eyesight. The exact cause of this damage is not well understood, but it may be related to inflammation, the accumulation of lipofuscin (a type of particle arising from cell damage), oxidative stress, and reduced autophagy (a process that eliminates dysfunctional cellular material).
Aging is one of the most well-established and strongest risk factors for macular degeneration. Other risk factors include smoking, moderate-to-heavy alcohol consumption, type 2 diabetes, limited physical activity, and a lighter colored iris (e.g., blue vs. brown).
Finally, genetics can have a significant impact on the risk of macular degeneration. Two genes (CFH and ARMS2) seem especially important, as common variations in these genes can significantly increase a person’s risk of developing the disease.