Age-Related Macular Degeneration – Nutrition Based Approaches

By Paul E. Lemanski, MD, MS, FACP

Editor’s Note: This is the 125th in a series on optimal diet and lifestyle to help prevent and treat disease. Any planned change in diet, exercise or treatment should be discussed with and approved by your personal physician before implementation. The help of a registered dietitian in the implementation of dietary changes is strongly recommended.

Medicines are a mainstay of American life and the healthcare system not only because they are perceived to work by the individuals taking them, but also because their benefit may be shown by the objective assessment of scientific study. Clinical research trials have shown that some of the medicines of Western science may reduce the risk of Type 2 diabetes, heart attacks, strokes, cardiovascular death and even some cancers.

In the first 124 installments of the Non-Medicated Life, a healthy diet and lifestyle have been shown to accomplish naturally for the majority of individuals most of the benefits of medications in the prevention and treatment of the chronic medical conditions mentioned above. This may also be true for the number one cause of blindness in the developed world: Age-Related Macular Degeneration.

To understand AMD and how to help prevent and treat it first requires a description of eye anatomy. The eyeball is a spherical structure consisting of four major parts moving front to back: 1) the cornea, the eye’s clear front surface which begins to bend and focus light, 2) the iris which imparts eye color and controls the amount of light to enter the eye through the pupil, 3) the lens which further helps focus light upon, and 4) the retina the inner lining at the back of the eye where an image is formed. The retina contains specialized photoreceptor cells called rods and cones that are stimulated by light to produce nerve impulses that travel through the optic nerve to the brain producing vision. At the center of the retina is a yellow pigmented area producing high visual resolution called the macula and at the center of the macula is the fovea, an area devoid of and thus unobstructed by retinal blood vessels resulting in ultra-sharp central vision.

When eyes are open the rods and cones of the retina are continuously being stimulated by light to produce the changing images we call vision. This continuously changing light stimulation requires a large amount of energy contained in molecules called adenosine tri-phosphate or ATP. ATP is produced in structures called mitochondria, which are the oxidative furnaces of the cell, burning glucose and fatty acids to produce energy. Indeed, the rods and cones of the retina have some of the highest concentrations of mitochondria in all body tissues and as such are at risk for damage from excessive oxidative stress when not mitigated by protective antioxidants. The damage caused to the macula by uncontrolled oxidative stress is felt to be the central mechanism for AMD. Moreover, free radical formation from exposure to ultraviolet light/blue light (from sunlight) may cause further oxidative stress.

The clinical hallmark of AMD is progressive loss of central vision resulting in the severe loss of visual acuity, ability to read, ability to drive, and ultimately to functional blindness. AMD comes in two primary forms: 1) dry AMD which makes up 85-90% of all cases. It occurs when the macula slowly thins with age. Yellow deposits called drusen build up under the retina and gradually cause central vision loss. 2) wet AMD. It is less common, but more severe and rapid in onset. Wet AMD occurs when abnormal blood vessels grow under the retina. These vessels may leak blood or fluid which quickly may damage the macula leading to severe and rapid loss of central vision. Significantly, dry AMD may progress to wet AMD. 

The question arises: if excessive oxidative stress causes AMD can high doses of antioxidants slow disease progression or possibly arrest progression. In the 1990s the Age-Related Eye Disease Study looked to establish risk factors for AMD as well as cataract formation and then attempted to determine if certain antioxidant vitamins and minerals could affect disease progression. The original AREDS completed in 2001 found that a formulation containing vitamin C, vitamin E, beta-carotene, zinc and copper reduced the risk of progression in people with moderate or advanced AMD. 

The follow up AREDS-2 in 2013 further refined the formulation with the removal of beta carotene, replacing it with the antioxidant pigments lutein, zeaxanthin, and omega-3 fatty acids. This formulation proved safer especially for smokers for whom beta-carotene could possibly increase the risk for lung cancer but still achieved a marked slowing of disease progression from moderate AMD to advanced AMD.

The AREDS-2 nutritional formulation has now become the standard treatment for slowing progression of AMD. Such supplements, however, have not been found effective in preventing AMD. Indeed, the Harvard’s Physician Health Study-2 found individuals with multivitamin supplementation had higher rates of macular degeneration than those without supplementation. To attempt to prevent AMD, it appears that the safest route is to increase consumption of foods containing antioxidant pigments rather than to take supplements. The two primary antioxidant pigments to protect the retina from damage from both oxidative damage and UV/blue light damage are lutein and zeaxanthin. Identifying foods containing these pigments and including these foods in your daily diet may help prevent not only AMD but other oxidation mediated disease processes.

At the top of the list of foods containing lutein and zeaxanthin are green leafy vegetables including kale, collard greens, and spinach, as well as yellow vegetables such as corn. Literally, a cup of corn per day or half cup of spinach per day can increase these protective macular carotenoid pigments within one month. Since lutein and zeaxanthin are fat soluble, healthy fats such as those contained in walnuts and avocados can markedly increase absorption. In a randomized trial participants who consumed one avocado per day for six months resulted in 26% increase in macular pigment density compared to baseline. Orange bell peppers and Goji berries contain large amounts of these macular pigments. It is certainly possible – and enjoyable – to have a daily lunch or dinner salad with baby kale or spinach, topped with sliced orange bell peppers, avocado, walnuts, Goji berries, olive oil and vinegar.

Other lifestyle changes that can help reduce the risk of AMD include smoking cessation, a reduction in meat consumption, a reduction in cholesterol intake, and a reduction in saturated fat intake. Increased intake of the spice saffron (20 mg per day) can increase visual acuity in adults with mild to moderate AMD. Finally, the use of sunglasses to reduce UV/blue light (from sunlight) may also help to reduce photooxidative stress on the retina and macula.

In summary, nutritional approaches to slow progression of established AMD have been proved in the AREDS and AREDS-2 studies. The formulation of a supplement with the antioxidant macular pigments lutein, zeaxanthin, along with antioxidant vitamin C, vitamin E, zinc and copper has been shown to slow progression of AMD. Maximizing the intake of foods containing antioxidant macular pigments is preferred over supplements in the primary prevention of AMD. Smoking cessation, restricting saturated fat and cholesterol, and protecting eyes from UV/blue light through the use of appropriate sunglasses may also help prevent AMD and reduce progression in established AMD.

Paul E. Lemanski, MD, MS, FACP (plemanski3@gmail.com) is a board-certified internist practicing internal medicine and lifestyle medicine in Albany. Paul has a master’s degree in human nutrition, he’s an assistant clinical professor of medicine at Albany Medical College, and a fellow of the American College of Physicians.