Blindness Prevention and Treatment-Free Glaucoma Treatment

The leading causes of blindness in the U.S are diabetic related eye complications, glaucoma, and macular degeneration. Cataracts are generally listed as the number one cause but this is somewhat misleading.

Cataracts effect in excess of 20 million people but most cataracts are treatable with modern surgical techniques and artificial lens implants. The complication rate is low. While some cataracts may be inoperable due to other health problems, most can be successfully removed. Many cases of blindness attributed to cataracts are actually due to preexisting retinal problems such as macular degeneration and advanced glaucoma. If the retina is not healthy to start with, removing the cataract will not restore vision, and the low level of vision categorized as blindness is actually not due to cataracts. The cost of cataract surgery is a barrier to treatment to the uninsured and can account for some of the large numbers of blindness attributed to cataracts.

Next to cataracts, diabetic complications in the eye do result in blindness in over 4 million people. With the current increase in obesity in our culture, especially in youth, this is a serious concern for the future. Most diabetes related blindness is due to changes in the blood vessels in the retina that causes microanuysms, bleeding, proliferation of fragile new blood vessels, and detachments of the retinal tissue. There is a correlation with how many years the diabetes has been present and how well the blood sugar has been controlled. Early treatment of retinal complications is a proven method of greatly lowering the incidence of blindness.

Glaucoma also is responsible for several million cases of blindness. Glaucoma has traditionally been thought of as high pressure in the eye. Today it is gradually becoming viewed as a circulatory problems to the optic nerve and a neurodegenerative disease, where the death of the nerves are a vital part of the disease. This will greatly alter our treatment regimins at some point in the future as we transition to using drugs to protect the nerve health and increase blood circulation.

All three of these conditions are primarily a condition of aging and as the population ages the incidence is increasing. All three are also highly likely to prove amendable to lifestlye and nutritional intervetion at early stages.

Protection of the lens in the eye from UV exposure and enrichment of the diet with food and nutriional supplements containing lutein and zeaxanthin appears to show promise. Eating a diet with a low glycemic index (limiting refined sugars, eating complex carbohydrates like whole grains, and lost of vegetables) also will probably be shown to reduce cataracts. Finally, like the other leading causes of blindness, reducing obesity will reduce cataract fomration. While vitaimin E and C have been shown in recent studies not to reduce cataract formation. I do not beleive this will prove to be true with repeated studies. I do beleive antioxidants will be shown over time to be useful but it may be true in the context of whole foods and balanced diets, not in the form of supplementation.

Macualr degeneration has it’s proven formula manufactured by Bausc & Lomb under the name of Preservision which was shown in the initial Age Related Eye Disease Study (A.R.E.D.S.)  to slow the progression of the mild form of macualr degeneration to the severe form. The supplements in the original formula are:

PRESERVISION
Vitamin A (beta-carotene)
Vitamin C  (ascorbic acid )
Vitamin E (dl-Alpha Tocopheryl Acetate)
zinc oxide
copper cupric oxide

While a studies have shown an increase in lung cancer in smokers taking Vitamin A (beta-carotene) supplements, this is not a clear cut finding and may be proven wrong in the future. Currently supplements are being made both with and without Vitamin A. The exciting new news on the macular degeneration front is Age Related Eye Disease Study 2 -, which is testing the addition of lutein and zeaxanthin. Omega 3 fatty acids are also currently being looked at as a preventative supllements for macualr degeneration. Oxidative damage is presumably a major factor in macualr degeneration but it, like every other disease is usually not a simple one fix all type of propostition. Focusing on lifestlye prevention and nutrition and not late miracle  cures should be a large part of our research expenditures.

It is still incredibly important to remember that many cases of all three of these conditions are due to genetic, environmental,coexisting health conditions, social, and mental health conditions out of our hands; and to place the blame or burden on an individual for their own illness is one of the cruelest and narcissistic attitudes we can take. On the other hand, we are enterning a new era where we can offer new forms of advice and interventions at an early age.

Glaucoma is at an earlier stage where we know less. While we will address individuals supplements and conditions in laters articles, for now a few peices of the clue. Vitamin C  loweres eye pressure in some people due to osmotic pressure.  Ginko may increase blood flow to the optice nerve. Forskolin comes from a plant named Coleus forskohlii and it has been  used to lower intraocular pressure.

You can alter your lifestlye and nutrition and in conjunction with your prevetative eye exams from your family eye doctor thier is a good chance you can expect a lifetime of healthy eyesight. Fortunatly, most vision insurance plans, including Vision Service Plan and Medicare are recognizing the need for annual eye check ups for theses diseases.

As a final note, we feel so strongly about preventing blindness, if you have lost your job the last 12 months and are unisured we will work with you to manage your glaucoama for free for the remaider of the year if we feel we can help your case.

The National Eye Institute does love it’s acronyms. CATT is one of the more recent ones-the comparison of AMD Treatments Trials. Translated that means there is going to be a study on the two drugs already being widely used to treat macular degeneration, one of the top leading causes of blindness.

Lucentis was actually approved by the U.S. Food and Drug Administration  in June of 2006 for the treatment of advanced macular degeneration based on clinical studies. Avastin is a drug similar to Lucentis not approved for use in the eye but it has become the treatment of choice in many offices due to the feeling  that it is more efficacious and requires less frequent injections. This is more than a minor consideration since many people have a high level of fear for injections involving their eye and less frequent injections may translate to much higher compliance with treatment schedules. Lucentis and Avastin are both made by Genentech, Inc.

Macular degeneration is at an epidemic proportion with over 2 million Americans visually compromised. It is unfortunate that the clinical trials are coming after the drug has entered the mainstream, hopefully in the future we can have a voluntary mechanism to help translate off label use of drugs into the first layer of clinical trials when advantages become apparent early on as they have in this case.

Neither drug should be looked at as a miracle cure. Mostly there has been a slowing of progression of the wet form of macular degeneration and a small improvement in vision in about a third of the patients. Time will tell whether there is a real or perceived difference between the two drugs.

Annual preventative eye health check ups with your eye doctor are vital to early detection and treatment of conditions like macular degeneration, glaucoma, and cataracts.

Out of This World Eyecare

Fascinating information from out for this world on new directions in eyecare from the NEI:

NEI Press Release

NATIONAL INSTITUTES OF HEALTH
National Eye Institute

For Immediate Release Thursday, January 8, 2009

From Outer Space to the Eye Clinic: New Cataract Early Detection Technique
Patients and Astronauts Benefit from NEI-NASA Collaboration

A compact fiber-optic probe developed for the space program has now proven valuable for patients in the clinic as the first non-invasive early detection device for cataracts, the leading cause of vision loss worldwide.

Researchers from the National Eye Institute (NEI), part of the National Institutes of Health, and the National Aeronautics and Space Administration (NASA) collaborated to develop a simple, safe eye test for measuring a protein related to cataract formation. If subtle protein changes can be detected before a cataract develops, people may be able to reduce their cataract risk by making simple lifestyle changes, such as decreasing sun exposure, quitting smoking, stopping certain medications and controlling diabetes.

“By the time the eye’s lens appears cloudy from a cataract, it is too late to reverse or medically treat this process,” said Manuel B. Datiles III, M.D., NEI medical officer and lead author of the clinical study. “This technology can detect the earliest damage to lens proteins, triggering an early warning for cataract formation and blindness.”

The new device is based on a laser light technique called dynamic light scattering (DLS). It was initially developed to analyze the growth of protein crystals in a zero-gravity space environment. NASA’s Rafat R. Ansari, Ph.D., senior scientist at the John H. Glenn Research Center and co-author of the study, brought the technology’s possible clinical applications to the attention of NEI vision researchers when he learned that his father’s cataracts were caused by changes in lens proteins.

Several proteins are involved in cataract formation, but one known as alpha-crystallin serves as the eye’s own anti-cataract molecule. Alpha-crystallin binds to other proteins when they become damaged, thus preventing them from bunching together to form a cataract. However, humans are born with a fixed amount of alpha-crystallin, so if the supply becomes depleted due to radiation exposure, smoking, diabetes or other causes, a cataract can result.

“We have shown that this non-invasive technology that was developed for the space program can now be used to look at the early signs of protein damage due to oxidative stress, a key process involved in many medical conditions, including age-related cataract and diabetes, as well as neurodegenerative diseases such as Alzheimer’s and Parkinson’s,” said NASA’s Dr. Ansari. “By understanding the role of protein changes in cataract formation, we can use the lens not just to look at eye disease, but also as a window into the whole body.”

The recent NEI-NASA clinical trial, reported in the December 2008 Archives of Ophthalmology, looked at 380 eyes of people aged 7 to 86 who had lenses ranging from clear to severe cloudiness from cataract. Researchers used the DLS device to shine a low-power laser light through the lenses. They had previously determined alpha-crystallin’s light-scattering ability, which was then used to detect and measure the amount of alpha-crystallin in the lenses.

They found that as cloudiness increased, alpha-crystallin in the lenses decreased. Alpha-crystallin amounts also decreased as the participants’ ages increased, even when the lenses were still transparent. These age-related, pre-cataract changes would remain undetected by currently available imaging tools.

“This research is a prime example of two government agencies sharing scientific information for the benefit of the American people,” said NEI director Paul A. Sieving, M.D., Ph.D. “At an individual level, this device could be used to study the effectiveness of anti-cataract therapies or the tendency of certain medications to cause cataract formation.”

The DLS technique will now assist vision scientists in looking at long-term lens changes due to aging, smoking, diabetes, LASIK surgery, eye drops for treating glaucoma, and surgical removal of the vitreous gel within the eye, a procedure known to cause cataracts within six months to one year. It may also help in the early diagnosis of Alzheimer’s disease, in which an abnormal protein may be found in the lens. In addition, NASA researchers will continue to use the device to look at the impact of long-term space travel on the visual system.

“During a three year mission to Mars, astronauts will experience increased exposure to space radiation that can cause cataracts and other problems,” Dr. Ansari explained. “In the absence of proper countermeasures, this may pose a risk for NASA. This technology could help us understand the mechanism for cataract formation so we can work to develop effective countermeasures to mitigate the risk and prevent it in astronauts.”

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Macular Degeneration and Vitamin D-Update

Melanocytes are specialized cells that contain the pigment found in our hair skin, eyes, and other area of the body. The eye has melanocytes in the iris, retina, and the choroidal layer under the retina that supplies it with blood. Underneath the retina is a layer of cells referred to as the retinal pigmented epithelium. These cells interact with the photoreceptor cells, the rods and cones that register light you see and turn it into electrical impulses. Melanin is the pigment and it comes in two different forms. In the retina, melanin acts as an antioxidant to help protect the tissue from free radicals that can damage the cellular DNA.

Various detrimental influences can reduce this protective function and may even cause it to accelerate damage from free radicals. Ultraviolet exposure, blue visible light, and high levels of oxidative stress can cause cell damage and increase the rate of cell death. An article by Meyskens FL, Farmer P, Fruehauf JP  suggested that this may be a contributory factor in macular degeneration and choroidal melanomas.

Melanocytes also populate our skin where they protect the underlying levels from ultraviolet damage. UV-B exposure is an essential step in producing the active form of  vitamin D. Darker skinned intervals have more UV screening and subsequently are more at risk for low levels of vitamin D. When you wear highly protective sunscreen the same effect occurs, lower levels of UV are absorbed by the skin and the proactive form of Vitamin D does not get its needed UV-B exposure to form. It is a very narrow band of UV-B that is needed, not the entire spectrum.

Vitamin D degeneration is related to multiple forms of cancer and other health problems. Macular degeneration may have an association with lowered vitamin D. One possibility is the overall reduction in UVB on the skin from sunscreen, living indoors, and poor dietary habits results in systemic changes in vitamin D levels that precipitates cellular changes in the retina unrelated to the melanin in the eye. Another possibility is lowered systemic levels of vitamin D resulting in decreased melanin production in the retina. This could lead to an overload to the pigmented epithelial cells from oxidative stress and UV exposure inside the eye, degrading the functional capacity of the melanin to protect the retina.
The irony is UV exposure is a risk factor for cataracts and macular degeneration and we are always encouraging eye protection against UV (and rightfully so given today’s evidence). With the known association of skin cancer and UV exposure it is not prudent to drop recommendation for sunscreen and limiting sun exposure.

At some point there will be better answers. For now, some mild daily exposure to UV with eyewear that includes UV protection is something you should discuss with your eye doctor and dermatologist or family physician. Vitamin D supplementation during winter months and in geographic locations that get limited sunlight should also be considered with your healthcare providers.  Perhaps sunscreen lotions will be developed that allow the narrow band of UV-B needed to pass through in the future.  Many people have vision insurance coverage like Vision Service Plan that provides coverage for eyeglasses. Even if your prescription is minor, having protection against UV and visible blue light is good preventative medicine if you spend time outdoors. And if you spend six months on a submarine or live underground you should examine your options-and maybe see a psychologist!

Reference:
Meyskens FL, Farmer P, Fruehauf JP (June 2001). “Redox regulation in human melanocytes and melanoma”. Pigment cell research / sponsored by the European Society for Pigment Cell Research and the International Pigment Cell Society 14 (3): 148-54. doi:10.1034/j.1600-0749.2001.140303.x. PMID 11434561.