Age related macular degeneration is a medical condition that usually affects older adults that result in a loss of vision in the center of the visual field (the macula) because of damage to the retina. It occurs in “dry” and “wet” forms. It is a major cause of visual impairment in older adults (>50 years). Macular degeneration can make it difficult or impossible to read or recognize faces, although enough peripheral vision remains to allow other activities of daily life.
The inner layer of the eye is the retina, which contains nerves that communicate sight; behind the retina is the choroid, which contains the blood supply to all three layers of the eye, including the macula (the central part of the retina that surrounds the optic disc). In the dry (nonexudative) form, cellular debris called drusen accumulates between the retina and the choroid, and the retina can become detached. In the wet (exudative) form, which are more severe, blood vessels grow up from the choroid behind the retina, and the retina can become detached. It can be treated with laser coagulation, and with medication that stops and sometimes reverses the growth of blood vessels.
Although some macular dystrophies affecting younger individuals are sometimes referred to as macular degeneration, the term generally refers to age-related macular degeneration (AMD or ARMD).
Age-related macular degeneration begins with characteristic yellow deposits in the macula (central area of the retina, which provides detailed central vision) called drusen between the retinal pigment epithelium and the underlying choroid. Most people with these early changes (referred to as age-related maculopathy) have good vision. People with drusen can go on to develop advanced AMD. The risk is considerably higher when the drusen are large and numerous and associated with disturbance in the pigmented cell layer under the macula. Recent research suggests that large and soft drusen are related to elevated cholesterol deposits and may respond to cholesterol-lowering agents.
Central geographic atrophy, the “dry” form of advanced AMD, results from atrophy to the retinal pigment epithelial layer below the retina, which causes vision loss through loss of photoreceptors (rods and cones) in the central part of the eye. No medical or surgical treatment is available for this condition, however vitamin supplements with high doses of antioxidants, lutein and zeaxanthin, have been suggested by the National Eye Institute and others to slow the progression of dry macular degeneration and, in some patients, improve vision.
Beta-carotene was not protective.
Neovascular or exudative AMD, the “wet” form of advanced AMD, causes vision loss due to abnormal blood vessel growth (choroidal neovascularization) in the choriocapillaris, through Bruch's membrane, ultimately leading to blood and protein leakage below the macula. Bleeding, leaking, and scarring from these blood vessels eventually causing irreversible damage to the photoreceptors and rapid vision loss if left untreated.
Until recently, no effective treatments were known for wet macular degeneration. However, new drugs, called anti-angiogenics or anti-VEGF (anti-Vascular Endothelial Growth Factor) agents, can cause regression of the abnormal blood vessels and improvement of vision when injected directly into the vitreous humor of the eye. The injections have to be repeated on a monthly or bi-monthly basis. Examples of these agents include ranibizumab (trade name Lucentis), bevacizumab (trade name Avastin, a close chemical relative of ranibizumab) and pegaptanib (trade name Macugen). The FDA approves only ranibizumab and pegaptanib for AMD as of April 2007. Bevacizumab is not approved for intra-ocular use, but is approved for other systemic indications. Pegaptanib (Macugen) has benefits in neovascular AMD and has approval for such use. Worldwide, bevacizumab has been used extensively despite its "off label" status. The cost of ranibizumab (Lucentis) is approximately (US $2000) per treatment while the cost of bevacizumab (Avastin) is approximately (US $150) per treatment. Genentech makes both drugs. In the UK, NICE institute issued guidelines for the treatment of wet AMD in the NHS. NICE only approved use of ranibizumab (trade name Lucentis) for wet AMD in the NHS in England. NHS hospitals and Primary Care Trusts in England are required to follow NICE guidance. Only about ten percent of patients suffering from macular degeneration have the wet type.
Signs and symptoms:
Exudative changes: hemorrhages in the eye, hard exudates, subretinal/sub-RPE/intraretinal fluid
Atrophy: incipient and geographic
Visual acuity drastically decreasing (two levels or more) ex: 20/20 to 20/80.
Preferential hyper acuity perimetry changes (for wet AMD)
Blurred vision: Those with nonexudative macular degeneration may be asymptomatic or notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss.
Central scotomas (shadows or missing areas of vision)
Distorted vision (i.e., metamorphopsia) - A grid of straight lines appears wavy and parts of the grid may appear blank. Patients often first notice this when looking at mini-blinds in their home.
Trouble-discerning colors: specifically dark ones from dark ones and light ones from light ones.
Slow recovery of visual function after exposure to bright light
A loss in contrast sensitivity:
Macular degeneration by itself will not lead to total blindness. For that matter, only a very small number of people with visual impairment are totally blind. In almost all cases, some vision remains. Other complicating conditions may possibly lead to such an acute condition (severe stroke or trauma, untreated glaucoma, etc.), but few macular degeneration patients experience total visual loss. The area of the macula comprises only about (2.1%) of the retina, and the remaining (97.9%) (The peripheral field) remains unaffected by the disease. Interestingly, even though the macula provides such a small fraction of the visual field, almost half of the visual cortex is devoted to processing macular information.
The loss of central vision profoundly affects visual functioning. It is not possible, for example, to read without central vision. Pictures that attempt to depict the central visual loss of macular degeneration with a black spot do not really do justice to the devastating nature of the visual loss. This can be demonstrated by printing letters six inches high on a piece of paper and attempting to identify them while looking straight ahead and holding the paper slightly to the side. Most people find this difficult to do.
There is a loss of contrast sensitivity, so that contours, shadows, and color vision are less vivid. The loss in contrast sensitivity can be quickly and easily measured by a contrast sensitivity test performed either at home or by an eye specialist.
Epiretinal membrane or macular pucker or leaking blood vessels in the eye can cause similar symptoms with a very different etiology and different treatment.
Some evidence supports a reduction in the risk of age-related macular degeneration with increasing intake of two carotenoids: lutein and zeaxanthin
Consuming omega-3 fatty acids (docosahexaenoic acid and eicosapentaenoic acid) has been correlated with a reduced progression of early ARMD, and in conjunction with low glycemic index foods, with reduced progression of advanced ARMD
Symptoms of macular degeneration include:
Straight lines start to appear distorted, or the center of vision becomes distorted
Dark, blurry areas or white out appears in the center of vision
Diminished or changed color perception
If you experience any of these symptoms, see an ophthalmologist as soon as possible.
Wet AMD can be treated with laser surgery, photodynamic therapy, and injections into the eye. None of these treatments is a cure for wet AMD. The disease and loss of vision may progress despite treatment.Laser surgery: This procedure uses a laser to destroy the fragile, leaky blood vessels. A high-energy beam of light is aimed directly onto the new blood vessels and destroys them, preventing further loss of vision. However, laser treatment may also destroy some surrounding healthy tissue and some vision. Only a small percentage of people with wet AMD can be treated with laser surgery. Laser surgery is more effective if the leaky blood vessels have developed away from the fovea, the central part of the macula. Laser surgery is performed in a doctor's office or eye clinic.
The risk of new blood vessels developing after laser treatment is high. Repeated treatments may be necessary. In some cases, vision loss may progress despite repeated treatments.
Photodynamic therapy: A drug called verteporfin is injected into your arm. It travels throughout the body, including the new blood vessels in your eye. The drug tends to "stick" to the surface of new blood vessels. Next, a light is shined into your eye for about 90 seconds. The light activates the drug. The activated drug destroys the new blood vessels and leads to a slower rate of vision decline. Unlike laser surgery, this drug does not destroy surrounding healthy tissue. Because the drug is activated by light, you must avoid exposing your skin or eyes to direct sunlight or bright indoor light for five days after treatment.
Photodynamic therapy is relatively painless. It takes about 20 minutes and can be performed in a doctor's office.
Photodynamic therapy slows the rate of vision loss. It does not stop vision loss or restore vision in eyes already damaged by advanced AMD. Treatment results often are temporary. You may need to be treated again.
Injections: Wet AMD can now be treated with new drugs that are injected into the eye (anti-VEGF therapy). Abnormally high levels of a specific growth factor occur in eyes with wet AMD and promote the growth of abnormal new blood vessels. This drug treatment blocks the effects of the growth factor.
You will need multiple injections that may be given as often as monthly. The eye is numbed before each injection. After the injection, you will remain in the doctor's office for a while and your eye will be monitored. This drug treatment can help slow down vision loss from AMD and in some cases improve sight.
How is dry AMD treated?
Once dry AMD reaches the advanced stage, no form of treatment can prevent vision loss. However, treatment can delay and possibly prevent intermediate AMD from progressing to the advanced stage, in which vision loss occurs.
The National Eye Institute's Age-Related Eye Disease Study (AREDS) found that taking a specific high-dose formulation of antioxidants and zinc significantly reduces the risk of advanced AMD and its associated vision loss. Slowing AMD's progression from the intermediate stage to the advanced stage will save the vision of many people.
Age-Related Eye Disease Study (AREDS):
What is the dosage of the AREDS formulation?
The specific daily amounts of antioxidants and zinc used by the study researchers were 500 milligrams of vitamin C, 400 International Units of vitamin E, 15 milligrams of beta-carotene (often labeled as equivalent to 25,000 International Units of vitamin A), 80 milligrams of zinc as zinc oxide, and two milligrams of copper as cupric oxide. Copper was added to the AREDS formulation containing zinc to prevent copper deficiency anemia, a condition associated with high levels of zinc intake.
Who should take the AREDS formulation?
People who are at high risk for developing advanced AMD should consider taking the formulation. You are at high risk for developing advanced AMD if you have either:
1. Intermediate AMD in one or both eyes.
2. Advanced AMD (dry or wet) in one eye but not the other eye.
Your eye care professional can tell you if you have AMD, its stage, and your risk for developing the advanced form. The AREDS formulation is not a cure for AMD. It will not restore vision already lost from the disease. However, it may delay the onset of advanced AMD. It may help people who are at high risk for developing advanced AMD keep their vision.
There is no apparent need for those diagnosed with early stage AMD to take the AREDS formulation. The study did not find that the formulation provided a benefit to those with early stage AMD. If you have early stage AMD, a comprehensive dilated eye exam every year can help determine if the disease is progressing. If early stage AMD progresses to the intermediate stage, discuss taking the formulation with your doctor.
The high levels of vitamins and minerals are difficult to achieve from diet alone. However, previous studies have suggested that people who have diets rich in green leafy vegetables have a lower risk of developing AMD. The formulation's levels of antioxidants and zinc are considerably higher than the amounts in any daily multivitamin.
For example, people with osteoporosis need to be particularly concerned about taking vitamin D, which is not in the AREDS formulation.
How can I take care of my vision now that I have AMD?
If you have dry AMD, you should have a comprehensive dilated eye exam at least once a year. Your eye care professional can monitor your condition and check for other eye diseases. In addition, if you have intermediate AMD in one or both eyes, or advanced AMD in one eye only, your doctor may suggest that you take the AREDS formulation containing the high levels of antioxidants and zinc.
Because dry AMD can turn into wet AMD at any time, you should get an Amsler grid from your eye care professional. Use the grid every day to evaluate your vision for signs of wet AMD. This quick test works best for people who still have good central vision.
Amsler Grid Test:
The Amsler Grid Test is one of the simplest and most effective methods for patients to monitor the health of the macula. The Amsler Grid is, in essence, a pattern of intersecting lines (identical to graph paper) with a black dot in the middle. The central black dot is used for fixation (a place for the eye to stare at). With normal vision, all lines surrounding the black dot will look straight and evenly spaced with no missing or odd-looking areas when fixating on the grid's central black dot. When there is disease affecting the macula, as in macular degeneration, the lines can look bent, distorted and/or missing.
If you have wet AMD and your doctor advises treatment, do not wait. After laser surgery or photodynamic therapy, you will need frequent eye exams to detect any recurrence of leaking blood vessels.
If you have lost some sight from AMD, do not be afraid to use your eyes for reading, watching TV, and other routine activities. Normal use of your eyes will not cause further damage to your vision.
Anti-angiogenesis drugs. These medications block the development of new blood vessels and leakage from the abnormal vessels within the eye that cause wet macular degeneration. This treatment has been a major change in the treatment of this condition and many patients have actually regained vision that was lost. The treatment may need to be repeated during follow-up visits.
Smoking, high blood pressure, high cholesterol, obesity, and being Caucasian are also risk factors for macular degeneration. Unfortunately, even after macular degeneration treatment, the condition can recur.
The National Eye Institute is conducting and supporting a number of studies to learn more about AMD. For example, scientists are:
Studying the possibility of transplanting healthy cells into a diseased retina.
Evaluating families with a history of AMD to understand genetic and hereditary factors that may cause the disease.
Macular degeneration can advance to legal blindness and inability to drive. It can also result in difficulty or inability to read or see faces.
Adaptive devices can help people read. These include magnifying glasses, special eyeglass lenses, and computer screen readers such as JAWS for Windows.
A desktop unit consisting of a closed-circuit television (CCTV) camera, monitor and a movable XY table is easy to use. The camera is aimed at a book and enables the user to zoom in and magnify the printed material to the right size
Squinting achieves the same result, as it also reduces the surrounding bright light. Individuals who find it impossible to read normal text can extend their ability to read by many years, with this simple adjustment.
Because peripheral vision is not affected, people with macular degeneration can learn to use their remaining vision to continue most activities.
Cannabinoids Help MD Symptoms:
- Cannabinoids reduce ocular pressure
- Cannabinoids inhibit VEGF growth
- Cannabinoids are anti-inflammatory Amsler Grid
- Cannabinoids are anti-angiogenesis
- Cannabinoids protects cells
- Cannabinoids have anti-aging properties
- Cannabinoids are neuro-protective
- Cannabinoids protect cells
- Cannabinoids lower blood pressure
- Cannabinoids protect retina cells
- Cannabinoids relieve depression
Best Strains: Cannabis hybrids (possibly Sativa dominant)
Purple Kush, Hawaiian Sativa, Silver Haze, Killer Queen, Burmese Pure, Kali Mist, Herijuana x TrainWreck, Northern Lights x Cinderella 99, Blue Moon Rocks
1. Thompson, Dennis. "New Treatments Hold Hope for Failing Eyes". Yahoo! News. September 27, 2009.
2. de Jong PT (2006). "Age-related macular degeneration".N Engl J Med. 355 (14): 1474–1485.doi:10.1056/NEJMra062326. PMID 17021323.
3. Ch. 25, Disorders of the Eye, Jonathan C. Horton, in Harrison's Principles of Internal Medicine, 16th ed.
4. a b Tan JS, Wang JJ, Flood V, Rochtchina E, Smith W, Mitchell P. (February 2008). "Dietary antioxidants and the long-term incidence of age-related macular degeneration: the Blue Mountain Eye Study". Ophthalmology. 115 (2): 334–41. doi:10.1016/j.ophtha.2007.03.083.PMID 17664009.
5. "Eye Conditions: Macular Degeneration". lasiksurgerycost.net. Retrieved 2011-02-18.
6. "Clinical effectiveness and cost–utility of photodynamic therapy for wet age-related macular degeneration: a systematic review and economic evaluation". Hta.ac.uk. Retrieved 2011-01-11.
7. [dead link]
8. "Preferential Hyperacuity Perimetry (PHP) as an Adjunct Diagnostic Tool to Funduscopy in Age–related Macular Degeneration - Ophthalmology Technology Spotlight". Medcompare. Retrieved 2011-01-11.
9. Roberts, DL (September 2006). "The First Year--Age Related Macular Degeneration". (Marlowe & Company): 100.
10. Roberts, DL (September 2006). "The First Year--Age Related Macular Degeneration". (Marlowe & Company): 20.
11. Zimbardo, Philip (2010). "Honoring Elliot Aronson". In Gonzales, Marti Hope; Tavris, Carol; Aronson, Joshua. The scientist and the humanist: A Festschrift in honor of Elliot Aronson. New York: Psychology Press. pp. 15–18.ISBN 9781848728677
12. McNulty, Jennifer. "UCSC Professor Emeritus Elliot Aronson receives lifetime achievement award from the Association for Psychological Science". UC Santa Cruz. Retrieved 7 July 2010.
13. a b AgingEye Times (2009-05-19). "Macular Degeneration types and risk factors". Agingeye.net. Retrieved 2011-01-11.
14. Hirschler, Ben (2008-10-07). "Gene discovery may help hunt for blindness cure". Reuters. Retrieved 2008-10-07.[dead link]
15. Yang Z, Camp NJ, Sun H, Tong Z, Gibbs D, Cameron DJ, Chen H, Zhao Y, Pearson E et al. (Nov 2006). "A variant of the HTRA1 gene increases susceptibility to age-related macular degeneration". Science 314 (5801): 992–3.doi:10.1126/science.1133811. PMID 17053109