Scheie Eye Institute, University of Pennsylvania
Smoking is the largest modifiable risk factor for age-related macular degeneration. Learn why smoking damages the retina, and explore a number of steps you can take to protect your vision.
Many studies have determined that smoking significantly increases the risk of AMD, and some research has shown that the risk is at least double that of non-smokers. Since smoking is an addiction, it is very hard to stop. The information that smoking significantly and irrefutably increases risk of vision loss from AMD should help increase motivation.
Both current smokers and past smokers are at increased risk of developing AMD, but it’s likely that stopping now will decrease the risk. Cigarette smoke contains a mixture of chemicals, absorbed through the lungs. Some of these are oxidants, which can damage the retina when they travel through the bloodstream. Experimental mice exposed to cigarette smoke develop retinal degeneration that looks similar to AMD. Retinal cells grown in plastic dishes can be harmed or killed by cigarette smoke extract. The cigarette smoke irritates the cells, causing them to activate the immune system, which causes harmful inflammation.
Recently, an arm of the immune system called the complement cascade has been strongly implicated in macular degeneration. Cigarette smoke can activate the complement cascade in retinal cells. Also, people with certain DNA sequence changes in their complement genes are particularly susceptible to cigarette smoke-induced AMD.
This begs the question of whether people with AMD, or with a family history of AMD, should have genetic testing. This is probably premature, since stopping smoking will decrease everyone’s risk for AMD, not just those with complement-risk genes. Within the next few years, a treatment for dry AMD called lampalizumab, may be shown to work best in people with certain complement-risk genes. If so, it would be helpful to have genetic testing at that point.
Cigarette smoking increases the risk of lung cancer. Surprisingly, the risk is even higher among people taking high levels of beta-carotene (about 20 milligrams per day). This is why AMD patients who are smokers are told to use the “smokers’ formula” AREDS vitamins. The original AREDS formulation contained 15 milligrams of beta-carotene. Recently, the AREDS2 study showed that replacing the beta-carotene with related carotenoids called lutein and zeaxanthin worked just as well, if not better, than the formula containing beta-carotene. Currently, there is no evidence that lutein and zeaxanthin increase the risk of lung cancer in smokers. Therefore, it is recommended that all AMD patients with a certain number of drusen (small white spots in the retina visible to an ophthalmologist or on retinal photographs), take AREDS2 formula vitamins twice a day.
Other behaviors that can decrease AMD risk include eating a diet rich in fruits and vegetables, especially spinach, and fatty fish (salmon, sardines, mackerel, or tuna) twice a week. There is evidence that high intake of red meat increases risk, so avoid eating meat every day. A high glycemic index diet with lots of simple sugars also increases risk. White rice and pasta, white bread, and foods with large amounts of sugar or high fructose corn syrup, such as sodas, cakes and cookies contain carbohydrates that raise the glycemic index. These simple carbohydrates quickly convert into blood sugar (glucose), resulting in a rapid rise and subsequent fall in a person's glucose level.
Repeated exposure to bright visible light is damaging to the retina and may be a risk factor for age-related macular degeneration (AMD) and other retinal diseases. The right type of sunglasses may decrease risk.
Regardless of whether you have AMD or have an affected family member, avoid smoking and do your very best to quit if you are currently smoking. Get help from a smoking cessation program or your doctor. Otherwise, you may find yourself unable to read or drive as a result of late-stage AMD.
Joshua Dunaief, MD, received his BA magna cum laude in Biology from Harvard (1987), MD/PhD from Columbia College of Physicians and Surgeons (1996), completed ophthalmology residency at the Wilmer Eye Institute, Johns Hopkins in 2000, and medical retina fellowship at Scheie Eye Institute, University of Pennsylvania in 2004.
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