Age-related macular degeneration (AMD) is a progressive disease of the retina wherein the light-sensing cells in the central area of vision (the macula) stop working and eventually die. The disease is thought to be caused by a combination of genetic and environmental factors, and it is most common in people who are age sixty and over. A reasonable estimate of the total number of people in the United States affected by all stages of macular degeneration is set at more than 8 million.
AMD can be a confusing condition. With so many facets to its diagnosis, symptoms, pathology, and treatment, it is difficult to understand everything about it in a ten-minute session with one’s doctor. This, in tandem with misleading advertising and dishonest fund-raising schemes, can create an atmosphere in which misunderstandings and disappointments flourish. In an attempt to help clear the air, this presentation highlights the most common misconceptions, each followed by a straightforward discussion based upon current knowledge.
Misconception #1: “AMD causes blindness.”
At its worst, AMD will damage only the center of the retina at the back of the eye. This area, the macula, which is comprised mostly of cone cells for precise color and detail vision, makes up less than 5% of the total retina, but it is responsible for about 35% of the visual field. When the cone cells begin to degenerate from age and inflammation, an affected person will eventually find it difficult or impossible to read, drive, or recognize faces. The peripheral vision, however, is left untouched, so macular degeneration does not, by itself, lead to blindness. Unfortunately, the peripheral field is made up mostly of rod cells, which are not designed for detail vision. Peripheral vision is, therefore, good only for general mobility and limited reading with magnification, but it still offers a view of the world.
In spite of central vision loss, many affected people are able to use their remaining vision to move about with little or no assistance and lead independent, productive lives. The most successful of them have learned to use a wide variety of assistive devices such as magnifiers, special bioptic glasses, navigation software, and electronic readers to maximize their peripheral vision and other senses. The answer to living well with low vision is to take advantage of technology while learning and developing assistive living skills through a good rehabilitation program. The only way a person will become blind from AMD is by being unwilling to give such alternative skills a chance.
Misconception #2: “AMD is a growing epidemic.”
Recent research has found that the risk of developing AMD has been dramatically lessening over three generations. For that matter, Baby Boomers (people who were born between 1946 and 1964) may experience better retinal health over a longer period of time than the two previous generations. The Baby Boomers and the new Generation X populations are already seeing comparable declines in AMD incidence, attributed possibly to better environmental conditions, sanitation, nutrition, and prevention strategies.
That said, the number of people with visual impairment or blindness in the United States is still expected to double by the year 2050. This is due to the aging population increase, though, not by any dramatic escalation of the disease risks.
Misconception #3: “Wet and dry AMD are separate diseases.”
Dry AMD is distinguished by white or yellowish deposits of cellular debris (“drusen”) in the retina. Drusen are toxic to the retina, but they are usually carried away by the blood vessels before harm is done. Unfortunately that cleansing process is diminished in aging retinal cells, which can lead to macular degeneration and central vision loss.
About 10-15% of dry AMD cases progress to the “wet” form, in which immature blood vessels grow and leak into the retinas of people who are genetically prone to having an aggressive inflammatory response. Inflammation is the body’s way of trying to deliver nutrition to injured or diseased tissue. The process is beneficial to the rest of the body, but it can cause retinal scarring and blocking of central vision if not treated in time.
Wet AMD is, therefore, secondary to age-related macular degeneration, not a separate disease state. The commonly-used term “wet” further describes the type of macular degeneration involving errant blood vessels. Use of the term “dry”, therefore, is unnecessary unless a distinction needs to be made between the two conditions.
More about inflammation and AMD:
Misconception #4: “Reading in dim light will make AMD worse.”
“Turn on the light”, said Grandma. “You’re going to ruin your eyes.” She meant well, but her suggestion should have been simply, “Turn on the light. You’ll be able to see better.”
Eyes are damaged no more by reading in dim light than are ears by listening to soft music. Actually, the wearing demand on the sight cells increases as the light grows brighter, which may prove harmful to the vision of people with retinal deficiencies. The wisest approach would be to compromise between “enough light to see by” and “too much light.”
More about lighting:
Misconception #5: “Viewing cell phone, television, and computer screens damages the eyes.”
No scientific evidence has yet revealed that light from such devices causes eye damage. The sun and full spectrum lamps which imitate the sun are the two strongest and potentially most harmful sources of blue light. By comparison, blue light intensity from cell phones, television, and computer screens is much less than either of those sources.
Frankly, light of any color has the potential of harming the retina. When the sight cells are exposed to light, they expend energy, which is later replenished by darkness (eg. sleep)—something called the visual cycle. But if exposure to light is intense and prolonged, the cells may not recover sufficiently. That kind of abuse will obviously take a toll on the sight cells over time, but the body’s natural defenses help protect most people from light damage throughout their lives. These defenses include dark irises, yellowing lenses, eyebrows, eyelids, and the compulsions of squinting and blinking. Blue-eyed people, whose irises do not filter blue light, are slightly more at risk, but wearing amber or orange lenses under direct sunlight can make up that deficit.
Again, light from electronic device screens—100 time less than the sun—is simply not strong enough to cause concern. Warnings about using such technology should be viewed with a certain amount of healthy skepticism until well-supported evidence is presented. Meanwhile, instead of avoiding digital screens altogether, it may be prudent to simply follow sensible practices like limiting screen time, taking periodic breaks, and taking advantage of light-filtering options.
Misconception #6: “Cataract surgery causes AMD”
Most retinal surgeons say that there is minimal danger of retinal complications from such surgery in the hands of experienced practitioners. Recent research has shown that patients who have cataract surgery do not have a higher risk of progressing to more advanced forms of macular degeneration, when compared to those who do not have cataract surgery.
Cataracts are very common in older adults, and can develop in approximately 50% of people between the ages of 65-75. About 70% of people over the age of 75 have cataracts. Cataracts can be removed only by surgery, which is successful in about 90-95% of all cases. The surgery was previously known to cause retinal detachment in a small percentage of patients, but that risk is lessened now with extracapsular surgery, in which the posterior capsule of the natural lens is left in place to support the plastic replacement lens that is implanted during the operation.
Replacement of a clouded lens won’t restore vision lost from retinal disease, but it can significantly improve remaining vision and offer the examiner a clearer view of the retina. In light of the small risk, standard practice is to defer cataract surgery until vision loss from a cataract significantly reduces a patient’s quality of life. At that point, the benefit/risk ratio is sufficiently high to warrant the procedure.
More information about cataract surgery and AMD:
Misconception #7: “Stem cell replacement can cure AMD”
The media has been full of news about stem cell therapy as a future treatment for AMD. It is true that, in trials, stem cells are replacing the retinal pigment epithelium (RPE) layer that supports the sight cells (photoreceptors). And it is true that scientists are now beginning to replace damaged photoreceptor cells in animal models.
As exciting as the future of stem cell replacement is, however, it will not be a cure for AMD. Like a patch on a tire, it can restore vision for a time–maybe even until the end of life–but it does not address the underlying cause of the disease. The cure will more likely come from the field of gene replacement therapy, which is still several years down the road.
The day is fast-approaching when stem cell replacement will be available in the clinics. The possibility of actually restoring lost vision is exciting to think about, but it is important to remember that at this time, no stem cell treatments for any retinal diseases have been approved by the FDA for clinical use.
Find latest information about stem cell therapy at:
Misconception #8: “Anti-VEGF drugs for wet AMD will reverse vision loss.”
The anti-VEGF (antiangiogenic) drugs for treatment of wet AMD are designed only to block new blood vessel growth. The intent is not to restore vision, but to maintain current vision and prevent future damage. Some patients do see an improvement after initial injections, but that is mostly due to diminished swelling of the retina and/or gradual dissipation of collected blood.
While anti-VEGF drugs can effectively stop quick vision loss from uncontrolled blood vessels, most patients with wet AMD will continue to experience a gradual decline in vision over months and years until new treatments for geographic atrophy (advanced dry AMD) are available. Such treatments are now in trials.
Patients who notice a decrease in vision while undergoing treatment for wet AMD should, therefore, not be too quick to blame the drug. If there is no further sign of blood vessel growth, then the drug is doing its job. But in the rare instance that blood vessel growth continues in spite of the treatment, the doctor may suspect that the patient has become resistant and will probably recommend switching to one of the other compounds. This has been shown to be safe and effective.
Latest information about anti-VEGF treatments:
Antiangiogenic Drugs Are Stopping Neovascularization in Wet Macular Degeneration
Latest information about dry AMD research:
A Guide to Research in Dry AMD
Misconception #9: “Special glasses, eye exercises, electrical stimulation, acupuncture, and nutritional supplements can reverse AMD.”
Nothing has yet been developed that will reverse AMD. That would have to come from a cure for aging itself–a discovery that would turn the world of medical science upside down. Special prismatic lenses can redirect the wearer’s focus onto a healthier part of the retina. Magnification can enlarge an image to where it can be seen better peripherally. Eye exercises, electrical stimulation, and acupuncture can improve blood flow, temporarily improving visual acuity. And certain nutritional supplements can help to slow the progression of the disease. But once the retinal cells have begun to show the effects of aging, no lens, device, supplement, or treatment can restore their youth or—for that matter—the youth of any other cells in the human body.
Until an anti-aging pill is developed, if ever, the best that can be done to fix the damage caused by years of wear on the body is to replace its parts. And that is being done successfully in many cases. They can replace lungs, hearts, kidneys, livers, and even bones, but replacing brain tissue, which is exactly what the retina is, presents a formidable challenge. So until that challenge is met, Band-aid treatments and workarounds will have to do.
For more information about alternative and nutritional treatments for AMD, search by keywords in the Living Well With Low Vision Search Tool at:
Misconception #10: “Doctors don’t understand how patients see.”
When a doctor tells a patient that there is no change since the last visit, but the patient has been experiencing diminished vision during that time, it is not necessarily because the doctor does not understand. It is more likely that the patient has lost functional (everyday) vision that does not always show up in the imaging or on the acuity chart.
When the doctor says “no change” that usually refers to no apparent change in the anatomical structure of the eyeball, such as swelling or separation of the retina, vessel growth, fluid collection, cataract formation, or problems with the vitreous fluid. “No change” might also mean that the number of letters visible to the patient on the acuity chart matches the previous test.
So why does the patient report worsening of vision? The answer could be that contrast sensitivity and/or brightness acuity has lessened. These functions are just as important as how many letters one can see clearly on a chart, but they are not identifiable in photos or computer images. Without testing specifically for them, the doctor has no way to know that a patient’s everyday vision is being affected.
If a patient reports seeing worse when the doctor says there has been no change, that is when the patient might request a contrast sensitivity test and/or a brightness acuity test.
Misconception #11: “Nothing can be done”
By saying that nothing can be done about AMD, a doctor is saying that there is nothing medically that can be done other than anti-VEGF treatment for the wet form. AMD is incurable at this time, but hard-working researchers are close to providing answers. Meanwhile, there is much than can be done to maintain a person’s quality of life with visual impairment. Low vision rehabilitation can provide a strong foundation of knowledge and skills. Assistive devices and computer software programs equip low vision people with nearly every possible substitute for lost vision. Proper nutrition and health habits can slow the progression of the disease. And support organizations are ready to provide information and helpful social contact with others who share similar experiences.
Alot can be done for patients with eye diseases, but not solely in clinics. Living well with low vision requires looking outside of the limited box of medicine and recognizing all of the support, assistance, and opportunity that surrounds it. One good way to start is by visiting the resources at https://lowvision.preventblindness.org/resources/ or by calling 888-866-6148.
by Dan Roberts, Editor
Living Well With Low Vision