Macular Degeneration (ARMD / AMD)

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Macular Degeneration (AMD, ARMD) is the gradual breakdown of the macula cells, a small yellowish part of the eye near the retina's center. This is your central vision, the point where your vision is most exact. The deterioration weakens your ability to read, write, drive, and recognize faces, which are all activities requiring healthy central vision. Peripheral, or side vision isn't damaged. Take the Amsler Test.

Self Help & Tips

Blindness is not inevitable for people who have ARMD. There is a large amount of peer review research showing ARMD to be a nutritional and lifestyle responsive eye disease, and that you can stabilize and possibly even improve your vision with healthy lifestyle choices.

Macular Degeneration

Most people with ARMD have dry macular degeneration. In dry macular degeneration tiny, yellow drusens develop. Drusens are accumulations of fatty, yellow material that form in the macula and people with ARMD have more and larger drusens than what is common with aging. They are thought to be comprised of waste proteins and lipids (oily material) that begin to accumulate due to poor circulation and waste-flushing in the eye. Antioxidants are important for the normal waste-clearing process. The drusen slowly crowd, distort, or break the cells in the macula leading to deterioration and resulting in blurred vision. Because drusen also include immune-system regulating molecules, it is thought that they are part of the immune system.3

The second type of macular degeneration is the "wet" form, (also known as choroidal neovascularization) in which new blood vessels begin to develop near the macula, causing fast and serious vision loss. Wet macular degeneration can result from progression of dry macular degeneration, left untreated, and affects about 10% of macular degeneration patients.


  • Lines look distorted or wavy. (try the amsler test) In more developed AMD, the amsler grid can look quite distorted
  • Shapes look blurred, fuzzy, or hazy
  • Colors appear more dim and less distinct
  • Words are hard to read because they are blurred
  • Blank or dark areas hide the center area of your vision
  • The center of vision looks foggy or cloudy


blurry vision with macular degeneration
  • Heredity is a risk factor.
  • Free radicals can damage the eyes. They are formed when the blue and ultraviolet sunlight passes through the crystalline lens of the eye. Free radicals also result as natural metabolism byproducts. These chemical are highly reactive and cause oxidation. The result is destabilization of healthy macula cells in the eyes.
  • Smoking, chronic fatigue and a weak immune system hasten damage from free radicals.
  • Poor digestion and nutritional deficiencies - People with ARMD are often deficient in a number of nutrients that are essential to eye health such as lutein, essential fatty acids, zeaxanthin, taurine, antioxidants, zinc, bioflavonoids, selenium, and vitamin B-complex.
  • Systemic inflammation, indicated by high levels of c-reactive protein has been tied to increased macular degeneration risk.2

Who is at Risk?

  • Smokers - smoking increases the risk of AMD by 200-300%
  • Women
  • Adult diabetics
  • Those with a family history of AMD
  • People with high blood pressure
  • People who have difficulty absorbing nutrients which are needed for the healthy macula, especially lutein and zeaxanthin.

Retina-damaging drugs:

Also see a list of harmful drugs tied to macular degeneration.

  • Plaquenil (hydroxychloroquine sulfate), often prescribed for rheumatoid arthritis, has been found to cause permanent damage to the retinal.
  • Chloridine (Catapres), for high blood pressure
  • NSAIDS (non-steroidal, anti-inflammatory drugs) side effects from regular use include retinal hemorrhages. This group includes ibuprofen, aspirin1, ibuprofen, ketoprofen, flurbiprofen, and naproxen sodium. In addition acetaminophen (Tylenol), though not an NSAID, can harm vision.

Conventional Treatment

See Complementary treatment

Doctors now acknowledge that at least the AREDs formulations can be helpful as macular degeneration supplements. Sometimes laser surgery is the recommended treatment, but it may not completely repair a leaking blood vessel without permanently damaging nerve fibers passing through the retina. The National Eye Institute reports that macular degeneration treatment using laser technology can make vision worse, and benefits towards slowing progress of the condition not appear until at more than a year following surgery.

Photodynamic Therapy (PVT) is a generally less damaging procedure to seal blood vessels in the eye than traditional laser treatments.

Antiangiogenesis drugs such as Macugen can be injected into the retina for wet macular degeneration; they help prevent the body from growing new, leak-prone blood vessels in the retina. Lucentis and Avastin are considered more effective injection treatment strategies. Research suggests that the best results are using a combination of Lucentis and PVT to help stabilize wet macular degeneration.

In the future bone marrow stem cell injections or optogenetics may be used to treat conditions like AMD.

Drugs can have potentially serious side effects, so the benefits of going on these therapies have to be evaluated with your eye doctor and family.

The best cure is prevention. You can use complementary medicine to address underlying causes of AMD, along with conventional medicine to alleviate acute event damage. Since less than 1% of those with ARMD are legally blind, most people are able to benefit greatly from prevention.

Related Conditions

Studies and Information

See research on macular degeneration vitamins and supplements.


1. The Association of Aspirin Use With Age-Related Macular Degeneration; Gerald Liew, PhD, et al; JAMA Internal Medicine, Feb 25, 2013, Vol 173, No. 4
2. C-Reactive Protein and the Incidence of Macular Degeneration, Vinod P. Mitta, MD, MPH; et al, JAMA Ophthalmol. 2013;():1-7
3. "An integrated hypothesis that considers drusen ... macular degeneration", Hageman GS, et al, Progressive Retina Eye Res., November 2001, 20(6), p 705-32