Dr. Edward Boshnick
Snapper Creek Professional Center
7800 SW 87 Ave Suite B-270
Miami, Florida 33173
Macular degeneration is a progressive eye condition affecting 15 million Americans and millions more
around the world. The disease attacks the macula of the retina (the back of the eye) where the sharpest
vision occurs. Although it rarely results in complete blindness, it robs the individual of all but the
outermost, peripheral vision leaving only dim images as black holes at the center of vision.
There are several types of macular degeneration, but the fastest growing form is age-related macular
degeneration (AMD). AMD is the number one cause of vision loss and legal blindness in adults over the
age of 60 in the U.S. Although it rarely causes blindness, age-related macular degeneration robs those
affected of their sharp central vision and can dim contrast sensitivity and color perception. AMD
destroys clear "straight ahead" central vision necessary for reading, driving, identifying faces,
watching T.V., doing fine detailed work, safely navigating stairs, and performing other daily tasks
that we take for granted. Peripheral vision may not be affected and it is possible that the individual
affected may be able to "see out of the corner of the eye." However, the impact to those affected by
AMD can be devastating as their visual world gradually diminishes into a vague blur making ordinary
daily activities extremely difficult if not impossible.
There is no cure for AMD but new treatments are available. The most effective treatments involve the use
of low vision lenses. Training and special new technologies can promote independence and a return to
There are two types of age-related macular degeneration. One form is known as the "wet" type and the
other form as the "dry" form. It is possible to experience both forms at the same time in one or both
eyes. It is not uncommon for a patient with the "dry" form to develop the "wet" form later. The onset
and progression of either type do not follow any particular pattern. In some cases, progression is very
slow while in others deterioration can be very rapid.
Dry AMD is the most common form affecting 90% of the people who have the condition. In the dry form,
there is a breakdown or thinning of the retinal pigment epithelial cells (RPE) in the macula. The RPE
cells are important to the health of the retina. They are light sensitive and contain hundreds of
thousands of photoreceptors. The death or degeneration of these cells is called atrophy which is why
dry AMD is often referred to as atrophic AMD. It is characterized by the presence of drusen (dots of
yellow crystalline deposits that develop within the macula) and thinning of the macula. Generally,
the damage caused by the dry form is not as severe as that of the wet form. Unfortunately, there is no
proven cure or treatment.
Wet AMD is the more severe form of this disease. Although it affects only 10% of those who have the
condition, it accounts for 90% of the blindness caused by this disease. With this type, the membrane
underlying the retina thickens and then breaks. The oxygen supply to the macula is disrupted and the
body responds by growing new abnormal blood vessels. These blood vessels begin to grow through the
breaks in the membrane behind the retina towards the macula often raising the retina. To visualize this,
imagine the roots of a tree growing and spreading until they actually uproot a sidewalk. Then imagine
rainwater seeping up throughout the cracks. These abnormal blood vessels (the "roots") tend to be very
fragile. They often grow, lead or breed causing scarring of the macula. This damage to the macula
results in rapid central vision loss. Once this vision is destroyed, it cannot be restored.
Most patients report that their first sign of AMD was the rapid onset of prolonged, distorted vision.
Straight lines like telephone wires and door frames appear to be wavy. A certain percentage of patients
with wet AMD can benefit from laser treatment if the blood vessel leak is caught early enough. Both
traditional photocoagulation laser and new photodynamic therapy (using a photosensitive drug and a cold
laser) can be effective in certain cases. A new drug, Macugen, is delivered by injection to the eye. It
is designed to stop the growth of new blood vessels in the wet macular degeneration.
As new treatments become available, details about their effectiveness will appear on this website.
Related Websites: www.myvisiontest.com
- Aging: Approximately 10% of patients 66 to 74 years of age will have findings of macular degeneration. The prevalence increases to 30% in patients 75 to 85 years of age.
- Smoking: The only environmental exposure clearly associated with macular degeneration is tobacco smoking. Exposure to cigarette smoke more than doubles the risk of macular degeneration.
- Family history: The lifetime risk of developing late-stage macular degeneration is 50% for people who have a relative with macular degeneration vs. 12% for people who do not have relatives with macular degeneration, i.e. a four fold higher risk.
- Macular degeneration gene: The genes for the complement system proteins factor H (CFH) and factor B (CFB) have been determined to be strongly associated with a person's risk for developing macular degeneration. CFH is involved in inhibiting the inflammatory response mediated via C3b (and the Alternative Pathway of complement) both by acting as a cofactor for cleavage of C3b to its inactive form, C3bi, and by weakening the active complex that forms between C3b and factor B. C-reactive protein and polyanionic surface markers such as glycosaminoglycans normally enhance the ability of factor H to inhibit complement . But the mutation in CFH(Tyr402His) reduces the affinity of CFH for CRP and probably also alters the ability of factor H to recognize specific glycosaminoglycans. This change results in reduced ability of CFH to regulate complement on critical surfaces such as the specialized membrane at the back of the eye and leads to increased inflammatory response within the macula. In two 2006 studies at Yale Department of Epidemiology and Public Health and the Department of Ophthalmology and Visual Sciences, Moran Eye Center at the University of Utah School of Medicine, another gene that has implications for the disease, called HTRA1 (encoding a secreted serine protease), was identified. 
- Hypertension: Also known as high blood pressure.
- Cardiovascular status - high cholesterol, obesity.
- High fat intake is associated with an increased risk of macular degeneration in both women and men. Fat provides about 42% of the food energy in the average American diet. A diet that derives closer to 20-25% of total food energy from fat is probably healthier. Reducing fat intake to this level means cutting down greatly on consumption of red meats and dairy products such as milk, cheese, and butter. Eating more cold-water fish (at least twice weekly), rather than red meats and eating any type of nuts may help macular degeneration patients.
- Oxidative stress: It has been proposed that age related accumulation of low molecular weight, phototoxic, pro-oxidant melanin oligomers within lysosomes in the retinal pigment epithelium may be partly responsible for decreasing the digestive rate of photoreceptor outer rod segments (POS) by the RPE. A decrease in the digestive rate of POS has been shown to be associated with lipofuscin formation - a classic sign associated with macular degeneration.
- Race Macular degeneration is more likely to be found in whites than in blacks.
- Exposure to sunlight especially blue light. There is conflicting evidence as to whether exposure to sunlight contributes to the development of macular degeneration. A recent study in the British Journal of Ophthalmology on 446 subjects found that it does not. High energy visible light (HEV) has been implicated as a cause of age-related macular degeneration.
- ^ http://news.bbc.co.uk/2/hi/health/4217010.stm
- ^ Yang Z, Camp NJ, Sun H, Tong Z, Gibbs D, Cameron DJ, Chen H, Zhao Y, Pearson E, Li X, Chien J, Dewan A, Harmon J, Bernstein PS, Shridhar V, Zabriskie NA, Hoh J, Howes K, Zhang K. "A variant of the HTRA1 gene increases susceptibility to age-related macular degeneration." Science. 2006 Nov 10;314(5801):992-3. PMID 17053109.
- ^ Dewan A, Liu M, Hartman S, Zhang SS, Liu DT, Zhao C, Tam PO, Chan WM, Lam DS, Snyder M, Barnstable C, Pang CP, Hoh J. "A variant of the HTRA1 gene increases susceptibility to age-related macular degeneration". Science. 2006 Nov 10;314(5801):989-92. PMID 17053108
- ^ Macular degeneration Types and Risk Factors
- ^ "Melanin aggregation and polymerization: possible implications in age related macular degeneration." Ophthalmic Research, 2005; volume 37: pages 136-141.
- ^ Age-Related Eye Disease Study Research Group. "Risk factors associated with age-related macular degeneration. A case-control study in the age-related eye disease study: Age-Related Eye Disease Study Report Number 3." Ophthalmology. 2000 Dec;107(12):2224-32. PMID 11097601.
- ^ Clemons TE, Milton RC, Klein R, Seddon JM, Ferris FL 3rd; Age-Related Eye Disease Study Research Group. "Risk factors for the incidence of Advanced Age-Related Macular Degeneration in the Age-Related Eye Disease Study (AREDS) AREDS report no. 19." Ophthalmology. 2005 Apr;112(4):533-9. PMID 15808240.
- ^ Khan, JC; Shahid H, Thurlby DA, Bradley M, Clayton DG, Moore AT, Bird AC, Yates JR, Genetic Factors in AMD Study (Jan 2006). "Age related macular degeneration and sun exposure, iris colour, and skin sensitivity to sunlight". The British Journal of Ophthalmology 90 (1): 29-32. PMID 16361662. Retrieved on 2006-10-23.
- ^ Glazer-Hockstein, C; Dunaief JL (Jan 2006). "Could blue light-blocking lenses decrease the risk of age-related macular degeneration?". Retina 26 (1): 1-4. PMID 16395131. Retrieved on 2006-10-23.
- ^ Margrain, TH; Boulton M, Marshall J, Sliney DH (Sep 2004). "Do blue light filters confer protection against age-related macular degeneration?". Progress in Retinal and Eye Research 23 (5): 523-31. PMID 15302349. Retrieved on 2006-10-23.
>> What is PRK?