By Debora Yost
Plant caroteinoids such as lutein and zeaxanthin were long ago shown to help prevent macular degeneration. But is there more that can be done to protect against this epidemic of blindness?
George W. Rozakis, MD is a Cornell-trained biomedical engineer specializing in laser eye surgery and lens implants. A pioneer in the field of LASIK surgery,1 Dr. Rozakis is now vigorously involved in anti-aging medical research.
Dr. Rozakis is focusing on a potential breakthrough in treating macular degeneration, a condition that gradually destroys central vision. Also called age-related macular degeneration, it is the leading cause of blindness in people aged 65 and older.
Dr. Rozakis believes that restoring the correct balance of natural hormones that decline with age can retard and possibly even reverse the progression of macular degeneration. To investigate this hypothesis, he is setting up a long-term study and is currently seeking subjects to participate in the trial.
Hormones and Your Vision
The hormonal link with macular degeneration began to evolve when Dr. Rozakis met another medical pioneer, Sergey A. Dzugan, MD, PhD, during a conference in Chicago four years ago. Dr. Dzugan is a cardiovascular surgeon and internationally known expert in anti-aging and hormonal medicine.
“Dr. Dzugan has done numerous studies2-4 and written numerous articles on the association between low hormone levels and multiple disease states, including the problem of atherosclerosis and cholesterol elevation,” says Dr. Rozakis. “As an ophthalmologist I was impressed by the evidence that restoring and optimizing levels of key hormones improve brain function, largely because the retina is part of the brain. For example, there is very impressive literature that testosterone slows down the progression of Alzheimer’s disease.5 Pregnenolone is extremely important for the brain and nervous system, as are progesterone and estrogens. Women whose progesterone levels drop develop negative personality changes.6 In animal models, pregnenolone and DHEA have been shown to profoundly stimulate the healing of neurologic injury.7-9 Women who enter into menopause at a young age develop macular degeneration, presumably because of the absence of estrogens.10,11 Blocking estrogens with the anti-cancer drug tamoxifen is harmful to the retina.12 This leads us to wonder if optimal hormonal health also positively impacts ocular health.”
“When an article appeared in the American Journal of Ophthalmology indicating that DHEA, or dehydroepiandrosterone, is exceptionally low in macular degeneration patients,13 I was shocked and excited,” says Dr. Rozakis. This finding provided a major clue that hormonal imbalance was part of the problem of macular degeneration.
“DHEA is like the Grand Central Station of hormone chemistry,” says Dr. Rozakis. “When DHEA levels drop, it strongly implies that levels of other hormones such as pregnenolone, estrogens, and testosterone are out of balance or suboptimal.” All of these hormones make the body thrive—they give us virility, fertility, and help us act and react quicker. Since the retina contains hormone receptors, hormones must be part of the biophysiology of vision itself.
Cardiovascular Link
Low DHEA levels in macular degeneration could also explain its association with heart disease, as it is known that macular degeneration is an independent risk factor for stroke and coronary artery disease. In a study conducted by Australian scientists,14 macular degeneration predicted a five-fold higher risk of cardiovascular mortality and a 10-fold higher risk of stroke mortality. After controlling for traditional cardiovascular risk factors, age-related macular degeneration predicted a doubling of cardiovascular mortality. Since hormone deficiency has been linked with both heart disease and eye disorders,13,15 it is a prime suspect that links the heart to the eye.
Further examination of the literature reveals a major review article from Italy that explains the importance of hormones to the retina.16 In this article, it is shown that the retina is able to attempt to make its own hormones, just like the brain. “The article also indicates that many of the hormones we use in anti-aging programs have a role in the retina, such as pregnenolone, DHEA, testosterone, estrogens, and progesterone. Few ophthalmologists and optometrists are aware of this relationship. This was the smoking gun that led to our hypothesis,” Dr. Rozakis notes.
Macular Degeneration and Cholesterol
A good theory needs to connect all the dots. Dr. Rozakis explains that one challenge in shaping his theory was explaining the presence of “drusen” or spots that appear in the retina in patients with macular degeneration. Many consider these spots to be “degradation products.”
Recently, Goldis Malek, PhD, and others17-19 found that cholesterol was present in those spots. This led some people to think that cholesterol-lowering agents, such as statins, might help macular degeneration—but they do not. In fact, there is concern that statins actually increase the risk of dry macular degeneration advancing to the neovascular form of the disease, whereby tiny blood vessels in the eye begin to bleed.20
Dr. Rozakis notes, “To Dr. Dzugan and me, the presence of cholesterol in the macula was the key piece of data that integrated everything. The presence of cholesterol in the macula suggests that the retina is trying to make hormones—but that it can’t. So, the body’s accumulation of cholesterol and drusen worsen.” He continues, “The macula can’t get the hormones it needs from the blood because there aren’t much there. As a result, if the macula is having trouble converting cholesterol into hormones, drusen form, and this results in the drusen we see in macular degeneration. Why the macula stops making hormones is unknown, but it is associated with aging. We can speculate that it happens because the enzymes which do the conversion decrease or are down-regulated with aging.”
“This same ‘story’ of cholesterol and hormones plays itself out in the body as a whole,” says Dr. Rozakis. “We do know that the adrenal gland, which produces DHEA, loses the ability to manufacture hormones as we age. As Dr. Dzugan published, this hormonal decline stimulates the liver to produce more cholesterol in an attempt to create more hormones.3 This is why restoring hormones to their normal levels causes the liver to produce less cholesterol. That same paradigm may be happening in the macula. This is the basis of our hypothesis. The goal therefore must be to provide the retina the hormones it needs through supplementation.”
Reviewing the Evidence
There is already evidence to support the notion that DHEA protects the eyes against oxidative damage21 and that the hormone pregnenolone improves electrical activity in the retina, as measured by the electroretinogram (ERG).22,23 There is also evidence to support the use of melatonin in the treatment of macular degeneration.24,25
The theory that optimizing hormones may help promote macular health is based on these scientific facts:
1.The macula, which is located in the center of the retina, uses hormones to function.16
2.The normal macula has the unique ability to make its own hormones.26
3.The bloodstream of patients with macular degeneration is deficient in hormones.11,13
4.Drusen—the tiny yellow abnormalities that appear behind the macula in individuals with macular degeneration—contain cholesterol.17-19
5.Age-related macular degeneration is related to cardiovascular mortality.14
Dr. Rozakis speculates that the solution for treating macular degeneration is to measure and restore age-depleted hormones to optimal levels so that the macula can absorb the hormones it needs from the blood. “Hopefully restoring hormones to their normal levels in the bloodstream will cause the macula to stop absorbing cholesterol and, as a result, drusen formation will hopefully decline,” says Dr. Rozakis. “We certainly need a better understanding of the pathophysiology of this blinding disease.”27
A Higher Level of Natural Treatment
Dr. Rozakis sees hormone restoration as a strategy to improve on existing studies showing that certain nutrients can reduce the progression of age-related macular degeneration. The long-term Age-Related Eye Disease Study (AREDS), conducted by the National Eye Institute, found that supplementing the anti-oxidants beta-carotene, vitamin C, vitamin E, and the mineral zinc reduced the risk of developing advanced states of macular degeneration in more than 4,700 high-risk patients aged 55 to 80 who were enrolled in the study.28
The specific amounts of nutrients used by the study researchers were:
*500 mg of vitamin C
*400 IU of vitamin E
*15 mg of beta-carotene
*80 mg of zinc
*2 mg of copper.
The copper, administered as cupric oxide, was included in the formula to prevent copper-deficiency anemia, which is associated with high zinc intake.
As a result of the AREDS trial, many ophthalmologists are recommending supplements containing the study’s recommended dosages for patients with or at a high risk for age-related macular degeneration.
Dr. Rozakis is currently developing his own study to test his theory concerning the relationship between low levels of DHEA and macular degeneration. “Our study is going to focus on overall hormonal balance and will include the supplements used in the AREDS study as well,” says Dr. Rozakis. “Our goal is to do everything we can to stop macular degeneration. The fact that hormones are much more powerful than vitamins holds hope that the results will be significant.”
If you have any questions on the scientific content of this article, please contact a Life Extension Health Advisor at 1-800-226-2370.
Saturday, December 27, 2008
Tuesday, December 16, 2008
Macular Degeneration Can Disappear with Natural Therapies
Filed Under Dr. Zoltan Rona (MD) |
Macular degeneration is the leading cause of visual loss in Europeans and North Americans over the age of 50. It is thought to be the direct result of free radical damage to the macula, a small area located at the centre of the retina. The macula is responsible for fine vision.
Patient Profile:
A 79-year-old woman recently consulted me because a top expert in eye diseases diagnosed her as having macular degeneration. She was told that nothing could be done and, to quote the specialist, “You are going to go blind.”
As it turns out, this was not only discouraging for my patient, but a completely wrong prediction.
Here’s the advice I gave this patient:
Diet
• Eat more legumes, which have a cleansing effect due to their high content of sulphur-containing amino acids.
• Consume more fresh fruits and vegetables, especially yellow vegetables.
• Berries are wonderful—particularly blueberries because of their high content of anthocyanidins.
• Cherries are valuable because they offer carotenes, flavonoids, and vitamins E and C.
• Carotenoids—lutein and zeaxanthin—are most strongly associated with reduced risk of macular degeneration. The best sources are spinach, kale, and collard greens.
Supplements
None of these natural supplements have any serious side effects. Take the following antioxidant supplements each day:
• Beta-carotene: 100,000 IU
• Green powder: Choose an enzymatically active green “superfood” powder. Green products are high in carotenoids. Take 1 tablespoon in 15 ml of water or juice.
• Vitamin C: 2,000 mg three times daily
• Pycnogenol: 300 mg (from either pine bark extract or grape seed extract)
• Coenzyme Q10: 100 mg three times daily
• Vitamin E: 400 IU three times daily
• Selenium: 600 mcg
• Zinc chelate or citrate: 100 mg. Several published studies support the use of zinc supplements to help reverse numerous eye disorders including macular degeneration.
Botanicals
Research reveals that the following botanical medicines also show impressive results with macular degeneration:
• Ginkgo biloba extract: 250 mg
• Bilberry extract: 80 mg twice daily (25% anthocyanidin content). Bilberry is used in Europe for cataracts, macular degeneration, retinitis pigmentosa, and diabetic retinopathy. It can also prevent further damage from glaucoma by working as an antioxidant in the eyes. Its anthocyanidins increase vitamin C levels (a critical nutrient for healthy eyes) within the cells and decrease capillary fragility.
Result
A six-month follow-up visit to the eye specialist showed complete clearing of this patient’s macular degeneration.
Dr. Zoltan Rona
Friday, December 12, 2008
Macular degeneration patients treated with cancer drug show problems
Last Updated: Friday, December 5, 2008 | 10:21 AM ET
The Canadian Press
The colon cancer drug Avastin is used off-label to treat wet AMD. (CBC)Public health authorities in Canada are investigating a spike in cases of eye inflammation among patients being treated for macular degeneration with the cancer drug Avastin.
First noticed in British Columbia, there appears to be a rise in cases in other parts of the country as well. And now authorities are trying to draw the potential problem to the attention of the global public health community in the hopes of seeing if it is being observed elsewhere.
The problem is believed to stem from a particular lot of the drug that was distributed widely around the world, though not to the United States. The lot number is B3002B028.
The drug's manufacturer, the Swiss pharmaceutical firm Roche, is co-operating with Health Canada and the British Columbia Centre for Disease Control, which was alerted to the problem by ophthalmologists.
The situation puts Roche in an awkward position. Avastin (bevacizumab) is a colon cancer drug; it is not approved for use as a treatment age-related macular degeneration.
And Roche doesn't want to encourage the off-label use of the drug by ophthalmologists who have embraced it as a much cheaper alternative to a similar drug, Lucentis, which has been approved as a treatment for macular degeneration.
"Absolutely we do not recommend this," said Samantha Ouimet, a spokesperson for Roche Canada. "They're taking it out of its [original] packaging, repackaging it and injecting it into people's eyes. This comes in a bag and it's meant for intravenous use for people with cancer."
Ouimet said the company is in discussions with Health Canada. But it is reluctant to put out an advisory warning people not to use the drug as a treatment for age-related macular degeneration when the drug was never approved for this purpose.
Any statement could be seen as promoting the off-label use, Ouimet said.
"Is it a delicate situation? Absolutely."
B.C. cluster investigated
Ophthamologists in British Columbia started noticing a problem in October. Under two per cent of people treated for age-related macular degeneration with Avastin will develop acute intra-ocular inflammation. But between Oct. 3 and Oct. 27, the rates were much higher.
The BC CDC was called in to help investigate the cluster of cases, and concluded the rate of inflammation among patients treated with Avastin from the lot in question was almost 10 times higher than the normal rate. The lot is no longer in use there.
Dr. David Patrick, the centre's director of epidemiology services, submitted a report on the investigation to ProMED, an electronic reporting system that sends out alerts about outbreaks to a mailing list of public health officials, scientists and other interested parties around the world.
No problems reported in other countries
Patrick said the team investigating the issue sent out feelers to ophthamologists in about a half-dozen other Canadian centres and has heard back that others too have noticed an increase in cases of inflammation after use.
The inflammation causes cloudy vision, but appears to clear up over time, he said.
Ouimet said there have been no reports of problems from other countries — and no reports of adverse reactions in cancer patients who received treatments from the same lot.
"We have reviewed all the analytical release data for the lot in question. And all the best parameters were within the limits for use in oncology," she said.
"So we found no deviations in the manufacturing process. All the environmental testing was fully compliant. We've revisited the batch. It is safe … for its indicated purpose."
Patrick said scientists at the University of British Columbia are studying vials of the drug, but haven't found anything usual.
"On the initial go-through they haven't determined a chemical difference between the implicated lot and another one. But there may well be further work with that," he said.
Tuesday, December 9, 2008
Treatment of Macular Degeneration Looks Promising After New Study
It may now be possible to trigger the regeneration of inner nerve cells in a damaged mammalian retina, according to researchers from The University of Washington.
Writing about their findings in the Proceedings of the National Academy of Sciences, the researchers revealed that they studied a particular retinal cell called the Muller glia.
"This type of cell exists in all the retinas of all vertebrates, so the cellular source for regeneration is present in the human retina," said lead researcher Tom Reh, a professor of Biological Structure at the university.
He said that developing certain methods to re-generate such cells might lead to new treatments for vision loss from retina-damaging diseases, like macular degeneration.
The researchers pointed out that cold-blooded vertebrates like fish have a remarkable ability to regenerate their retinas after damage, while Birds that are warm-blooded have some limited ability to regenerate retinal nerve cells after exposure to nerve toxins.
While fish can generate all types of retinal nerve cells, the researcher said, chicks produce only a few types of retinal nerve cell replacements, and few receptors for detecting light.
After a baby's eyes pass a certain developmental stage, Muller glia cells generally stop dividing.
According to the researchers, damage to retinal cells in both fish and birds prompts the specialized Muller glia cells to start dividing again, and to increase their options by becoming a more general type of cell called a progenitor cell. They say that such progenitor cells can then turn into any of several types of specialized nerve cells.
The researchers say that mammals have an even more limited Muller glia cell response to injury, compared to birds. They suggest that in an injured mouse or rat retina, the cells may react and become larger, but few start dividing again.
The team points out that several research groups have tried to stimulate the Muller glia cells to grow in lab dishes and in lab animals by injecting cell growth factors or factors that re-activate certain genes that were silenced after embryonic development.
Observations made during such studies suggested that the Muller glia cells could be artificially stimulated to start dividing again, and to show light-detecting receptors.
However, all those studies had failed to detect any regenerated inner retina nerve cells, except when the Muller glia cells were genetically modified with genes that specifically promote the formation of amacrine cells, which act as intermediaries in transmitting nerve signals.
"This was puzzling, because in chicks amacrine cells are the primary retinal cells that are regenerated after injury," Reh said.
With a view to resolving the discrepancy between what was detected in chicks and not detected in rodents, the researchers carried out a systematic analysis of the response to injury in the mouse retina, and the effects of specific growth factor stimulation on the proliferation of Muller glia cells.
They injected a substance into the retina to eliminate ganglion cells, a type of nerve cell found near the surface of the retina, and amacrine cells. Then by injecting the eye with epidermal growth factor (EGF), fibroblast growth factor 1 (FGF1) or a combination of FGF1 and insulin, they were able to stimulate the Muller glia cells to re-start their dividing engines and begin to proliferate across the retina.
The proliferating Muller glia cells first transformed into unspecialised cells, something that the researchers were able to detect by checking for chemical markers that indicate progenitor cells.
Soon some of the general cells changed into amacrine cells, and the researchers detected their presence by checking for chemicals produced only by amacrine cells.
The researchers observed that many of the progenitor cells arising from the dividing Muller glia cells died within the first week after their production, but those that managed to turn into amacrine cells survived for at least 30 days.
"It's not clear why this occurs, but some speculate that nerve cells have to make stable connections with other cells to survive," the researchers wrote.
Source-ANI
Writing about their findings in the Proceedings of the National Academy of Sciences, the researchers revealed that they studied a particular retinal cell called the Muller glia.
"This type of cell exists in all the retinas of all vertebrates, so the cellular source for regeneration is present in the human retina," said lead researcher Tom Reh, a professor of Biological Structure at the university.
He said that developing certain methods to re-generate such cells might lead to new treatments for vision loss from retina-damaging diseases, like macular degeneration.
The researchers pointed out that cold-blooded vertebrates like fish have a remarkable ability to regenerate their retinas after damage, while Birds that are warm-blooded have some limited ability to regenerate retinal nerve cells after exposure to nerve toxins.
While fish can generate all types of retinal nerve cells, the researcher said, chicks produce only a few types of retinal nerve cell replacements, and few receptors for detecting light.
After a baby's eyes pass a certain developmental stage, Muller glia cells generally stop dividing.
According to the researchers, damage to retinal cells in both fish and birds prompts the specialized Muller glia cells to start dividing again, and to increase their options by becoming a more general type of cell called a progenitor cell. They say that such progenitor cells can then turn into any of several types of specialized nerve cells.
The researchers say that mammals have an even more limited Muller glia cell response to injury, compared to birds. They suggest that in an injured mouse or rat retina, the cells may react and become larger, but few start dividing again.
The team points out that several research groups have tried to stimulate the Muller glia cells to grow in lab dishes and in lab animals by injecting cell growth factors or factors that re-activate certain genes that were silenced after embryonic development.
Observations made during such studies suggested that the Muller glia cells could be artificially stimulated to start dividing again, and to show light-detecting receptors.
However, all those studies had failed to detect any regenerated inner retina nerve cells, except when the Muller glia cells were genetically modified with genes that specifically promote the formation of amacrine cells, which act as intermediaries in transmitting nerve signals.
"This was puzzling, because in chicks amacrine cells are the primary retinal cells that are regenerated after injury," Reh said.
With a view to resolving the discrepancy between what was detected in chicks and not detected in rodents, the researchers carried out a systematic analysis of the response to injury in the mouse retina, and the effects of specific growth factor stimulation on the proliferation of Muller glia cells.
They injected a substance into the retina to eliminate ganglion cells, a type of nerve cell found near the surface of the retina, and amacrine cells. Then by injecting the eye with epidermal growth factor (EGF), fibroblast growth factor 1 (FGF1) or a combination of FGF1 and insulin, they were able to stimulate the Muller glia cells to re-start their dividing engines and begin to proliferate across the retina.
The proliferating Muller glia cells first transformed into unspecialised cells, something that the researchers were able to detect by checking for chemical markers that indicate progenitor cells.
Soon some of the general cells changed into amacrine cells, and the researchers detected their presence by checking for chemicals produced only by amacrine cells.
The researchers observed that many of the progenitor cells arising from the dividing Muller glia cells died within the first week after their production, but those that managed to turn into amacrine cells survived for at least 30 days.
"It's not clear why this occurs, but some speculate that nerve cells have to make stable connections with other cells to survive," the researchers wrote.
Source-ANI
Sunday, December 7, 2008
Osiris completes enrollment in Phase III GVHD trial
Dec 05, 2008 (Datamonitor via COMTEX)
Osiris Therapeutics, a stem cell therapeutic company, has completed patient enrollment in its Phase III pivotal trial evaluating Prochymal for the treatment of steroid-refractory acute graft versus host disease.
This double-blinded, placebo controlled trial will assess safety and efficacy of Prochymal over a six-month period. A total of 244 patients were enrolled at 72 leading bone marrow transplant centers across the US, Canada, the UK, Spain, Italy, Australia, Germany and Switzerland.
In total, 168 patients were treated in the US, 31 in Canada, 27 in Europe, and 18 in Australia. A total of 27 pediatric patients were enrolled. The last patient is expected to complete the trial by May 29, 2009.
Prochymal is a proprietary formulation of adult mesenchymal stem cells designed to provide therapeutic benefit by controlling inflammation, promoting tissue regeneration, and preventing scar formation.
Osiris and Genzyme have previously announced a strategic alliance for the development and commercialization of Prochymal. Under the terms of the agreement, Osiris will commercialize Prochymal in the US and Canada, and Genzyme will commercialize the treatment in all other countries.
Moya Daniels, study director for the steroid-refractory graft versus host disease (GVHD) program at Osiris, said: "On behalf of everyone at Osiris, I would like to offer our sincere appreciation to the patients, their families, and all of the outstanding healthcare professionals who participated in this historic event. We look forward with great anticipation to the results of this landmark stem cell trial and the opportunity to make a positive difference in the care of transplant patients everywhere."
Osiris Therapeutics, a stem cell therapeutic company, has completed patient enrollment in its Phase III pivotal trial evaluating Prochymal for the treatment of steroid-refractory acute graft versus host disease.
This double-blinded, placebo controlled trial will assess safety and efficacy of Prochymal over a six-month period. A total of 244 patients were enrolled at 72 leading bone marrow transplant centers across the US, Canada, the UK, Spain, Italy, Australia, Germany and Switzerland.
In total, 168 patients were treated in the US, 31 in Canada, 27 in Europe, and 18 in Australia. A total of 27 pediatric patients were enrolled. The last patient is expected to complete the trial by May 29, 2009.
Prochymal is a proprietary formulation of adult mesenchymal stem cells designed to provide therapeutic benefit by controlling inflammation, promoting tissue regeneration, and preventing scar formation.
Osiris and Genzyme have previously announced a strategic alliance for the development and commercialization of Prochymal. Under the terms of the agreement, Osiris will commercialize Prochymal in the US and Canada, and Genzyme will commercialize the treatment in all other countries.
Moya Daniels, study director for the steroid-refractory graft versus host disease (GVHD) program at Osiris, said: "On behalf of everyone at Osiris, I would like to offer our sincere appreciation to the patients, their families, and all of the outstanding healthcare professionals who participated in this historic event. We look forward with great anticipation to the results of this landmark stem cell trial and the opportunity to make a positive difference in the care of transplant patients everywhere."
Saturday, November 22, 2008
Reversing Destructive Eye Diseases Maybe Just a Supplement Away
Dr. Brian Lewy- Dr. Jay Stockman
Americans have pursued a never ending search for nutrients, and supplements in an effort to improve ocular health and prevent eye diseases. While many advertized items have little or no actual benefit, there are some that have been shown to be helpful, and efficacious. Over the last half century research has started to embrace these supplements as beneficial to our health, and their impact on one’s general well being.
Understanding the aging, and physiological processes offers a pathway to the benefits of these nutrients. Cataracts, Macular Degeneration, dry eyes and other age related disorders are but a few of the considerations that these neutricuticals are targeted to address. A study conducted by West and associates concluded that there are some supplements that are very helpful and when taken properly will prevent damage and even do some repair.
Research conducted by the Age Related Eye Disease Study ( AREDS) found that individuals who took antioxidant combinations of 500 IU Vit C, 400 IU Vit E, 15 mg of beta carotene and Zinc for approximately 6 years had a 17%-21% lower rate of Age Related Macular Degeneration(ARMD) progression as compared to individuals in the placebo group. Patients who took Zinc or antioxidants alone also showed a decrease in the progression of ARMD, but not to the extend as the first group. No benefit was shown with the folks who took Vit E alone. In addition, participants who took Lutein for 18-20 weeks demonstrated higher plasma levels, and increased macular pigment density. This would counter the ARMD damage and improve visual quality.
The West and associate study found no benefit at all in preventing, improving or reversing the damage caused by Cataracts or Diabetic Retinopathy. Herbal remedies, antioxidants, and all vitamins were found to be useless with regard to these two conditions.
Unlike cataracts, Glaucoma has been shown to be aided by the use of supplements. Cannabinoids have demonstrated an ability to lower the intraocular pressure, thereby lowering the visual devastations of Glaucoma. The problem with this supplement is obtaining an accepted method of administration that is regulated, dose reproducible and legal. Additional studies have shown that Ginkgo Biloba has improved the visual fields of normal tension glaucoma patients with as little as four weeks of use. The reason is believed to be the vasodilating affect of this supplement. Bringing more blood, and oxygen to the starved retinal tissue. Bilberry has not been clinically demonstrated to aid glaucoma patients in any way.
While additional studies must be conducted to asses all the benefits of these, and other nutritional supplements, it is clear that some do help. Furthermore, of equal importance is the drug interaction of supplements with both each other and prescription medicines. Many herbs, drugs and supplements can and do increase/ decrease the affect of other substances when present at the same time. Care must always be taken and warnings displayed. In all cases, one must consult with their health care professionals as to what supplements can be safely used.
Americans have pursued a never ending search for nutrients, and supplements in an effort to improve ocular health and prevent eye diseases. While many advertized items have little or no actual benefit, there are some that have been shown to be helpful, and efficacious. Over the last half century research has started to embrace these supplements as beneficial to our health, and their impact on one’s general well being.
Understanding the aging, and physiological processes offers a pathway to the benefits of these nutrients. Cataracts, Macular Degeneration, dry eyes and other age related disorders are but a few of the considerations that these neutricuticals are targeted to address. A study conducted by West and associates concluded that there are some supplements that are very helpful and when taken properly will prevent damage and even do some repair.
Research conducted by the Age Related Eye Disease Study ( AREDS) found that individuals who took antioxidant combinations of 500 IU Vit C, 400 IU Vit E, 15 mg of beta carotene and Zinc for approximately 6 years had a 17%-21% lower rate of Age Related Macular Degeneration(ARMD) progression as compared to individuals in the placebo group. Patients who took Zinc or antioxidants alone also showed a decrease in the progression of ARMD, but not to the extend as the first group. No benefit was shown with the folks who took Vit E alone. In addition, participants who took Lutein for 18-20 weeks demonstrated higher plasma levels, and increased macular pigment density. This would counter the ARMD damage and improve visual quality.
The West and associate study found no benefit at all in preventing, improving or reversing the damage caused by Cataracts or Diabetic Retinopathy. Herbal remedies, antioxidants, and all vitamins were found to be useless with regard to these two conditions.
Unlike cataracts, Glaucoma has been shown to be aided by the use of supplements. Cannabinoids have demonstrated an ability to lower the intraocular pressure, thereby lowering the visual devastations of Glaucoma. The problem with this supplement is obtaining an accepted method of administration that is regulated, dose reproducible and legal. Additional studies have shown that Ginkgo Biloba has improved the visual fields of normal tension glaucoma patients with as little as four weeks of use. The reason is believed to be the vasodilating affect of this supplement. Bringing more blood, and oxygen to the starved retinal tissue. Bilberry has not been clinically demonstrated to aid glaucoma patients in any way.
While additional studies must be conducted to asses all the benefits of these, and other nutritional supplements, it is clear that some do help. Furthermore, of equal importance is the drug interaction of supplements with both each other and prescription medicines. Many herbs, drugs and supplements can and do increase/ decrease the affect of other substances when present at the same time. Care must always be taken and warnings displayed. In all cases, one must consult with their health care professionals as to what supplements can be safely used.
Spotting eye disease sooner
Roxanne Stein
BACKGROUND: Macular degeneration is the age-related degenerative process of the macula. The macula is the area of the retina that is responsible for fine visual acuity. Macular degeneration can make it difficult or impossible to read and recognize faces and it's a major cause of blindness in the elderly. Age-related macular degeneration (AMD) begins with characteristic yellow deposits in the macula, called drusen. 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.
There are two forms of AMD -- wet and dry. Central geographic atrophy, the dry form of AMD, results from atrophy to the retinal pigment epithelial layer below the retina, which can lead to blindness through loss of photoreceptors (rods and cones) in the central part of the eye. Neovascular or exudative AMD, the wet form of AMD, causes vision loss due to abnormal blood vessel growth in the choriocapillaries, ultimately leading to blood and protein leakage below the macula. Bleeding, leaking and scarring from these blood vessels can eventually cause irreversible damage to the photoreceptors and rapid vision loss if left untreated.
DIAGNOSING: The traditional way to diagnose macular degeneration has been with the Amsler Grid Test. The Amsler Grid is a pattern of intersecting lines, identical to a piece of graph paper, with a black dot in the center. A person with normal vision can fixate on the dot while still seeing the grid patterns. A person with macular degeneration will see part of the grid missing, or some of the grid lines will appear to be bent or unevenly spaced.
A new test called prospective hyperacuity perimetry, or PHP, is able to detect the change from dry to wet AMD. The computerized test is more accurate because it has a higher sensitivity level. It will detect a change from dry macular degeneration to the wet form faster or at an earlier stage than traditional testing. PHP testing works by showing a series of linear dots in a pattern and it tests the entire 14 degrees of the macular fields. It tests small portions at a time in a prearranged sequence. The patient is asked to detect if any of the dots arranged in a line are out of space. The PHP test also incorporates some dot sequences that really are out of order, allowing it to test a patient's reliability in answering. A computer records the data and can detect even the smallest changes in a patient's macula over time.
BACKGROUND: Macular degeneration is the age-related degenerative process of the macula. The macula is the area of the retina that is responsible for fine visual acuity. Macular degeneration can make it difficult or impossible to read and recognize faces and it's a major cause of blindness in the elderly. Age-related macular degeneration (AMD) begins with characteristic yellow deposits in the macula, called drusen. 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.
There are two forms of AMD -- wet and dry. Central geographic atrophy, the dry form of AMD, results from atrophy to the retinal pigment epithelial layer below the retina, which can lead to blindness through loss of photoreceptors (rods and cones) in the central part of the eye. Neovascular or exudative AMD, the wet form of AMD, causes vision loss due to abnormal blood vessel growth in the choriocapillaries, ultimately leading to blood and protein leakage below the macula. Bleeding, leaking and scarring from these blood vessels can eventually cause irreversible damage to the photoreceptors and rapid vision loss if left untreated.
DIAGNOSING: The traditional way to diagnose macular degeneration has been with the Amsler Grid Test. The Amsler Grid is a pattern of intersecting lines, identical to a piece of graph paper, with a black dot in the center. A person with normal vision can fixate on the dot while still seeing the grid patterns. A person with macular degeneration will see part of the grid missing, or some of the grid lines will appear to be bent or unevenly spaced.
A new test called prospective hyperacuity perimetry, or PHP, is able to detect the change from dry to wet AMD. The computerized test is more accurate because it has a higher sensitivity level. It will detect a change from dry macular degeneration to the wet form faster or at an earlier stage than traditional testing. PHP testing works by showing a series of linear dots in a pattern and it tests the entire 14 degrees of the macular fields. It tests small portions at a time in a prearranged sequence. The patient is asked to detect if any of the dots arranged in a line are out of space. The PHP test also incorporates some dot sequences that really are out of order, allowing it to test a patient's reliability in answering. A computer records the data and can detect even the smallest changes in a patient's macula over time.
Ophthotech Enrolls First Patient in a Phase I Complement (Anti-C5) Inhibitor Trial for Macular Degeneration
ARC1905 Represents Second Compound in Clinical Development
PRINCETON, NJ and NEW YORK, NY--(Marketwire - October 27, 2008) - Ophthotech Corp. ("Ophthotech"), a privately held biopharmaceutical company focused on developing ophthalmic therapies for back-of-the-eye diseases, announced today the enrollment of its first patient in a complement inhibition trial for the treatment of age-related macular degeneration (AMD). This Phase I trial will assess the safety and tolerability of ARC1905, an anti-C5 complement factor aptamer, in combination with an anti-VEGF agent.
Dr. Donald J. D'Amico, Professor and Chairman, Department of Ophthalmology, Weill Cornell Medical College, New York-Presbyterian Hospital, and a member of Ophthotech's Scientific Advisory Board, said, "Multiple lines of evidence now point to a fundamental problem with inflammation and complement activation in patients with high susceptibility to develop AMD. Intervention in the complement pathway is the single most promising target for new therapeutic and preventive strategies for AMD."
"Preclinical and human genetic linkage studies strongly support the significant role of complement-mediated inflammation in both dry and wet AMD," said Samir Patel, M.D., President and Chief Executive Officer of Ophthotech. "We believe that anti-C5 aptamer blockade represents a potential breakthrough therapy for both wet and dry forms of AMD."
Published studies in Science, the New England Journal of Medicine and other leading journals suggest that abnormalities involving the complement pathway may be responsible for the majority of cases of dry and wet forms of AMD in the western world.
ARC1905 represents one of three compounds that Ophthotech is developing to treat AMD. Additional molecular entities include E10030, an anti-PDGF aptamer currently in a Phase I study, and volociximab, an anti-angiogenic monoclonal antibody targeting the alpha5beta1 integrin, which is on track to commence clinical trials in the near future.
About ARC1905
Anti-C5 aptamer ARC1905 inhibits C5, a central component of the complement cascade, which plays multiple roles in innate immunity and inflammatory diseases. Inhibition of this key step in the complement cascade at the level of C5 prevents the formation of key terminal fragments (C5a and C5b-9) regardless of which pathway (alternate, classical or lectin) induced their generation. The C5a fragment is an important inflammatory activator inducing vascular permeability, recruitment and activation of phagocytes. C5b-9 is involved in the formation of membrane attack complex (MAC: C5b-9), which initiates cell lysis. By inhibiting these C5-mediated inflammatory and MAC activities, therapeutic benefit may be achieved in both dry and wet AMD. In August 2007, Ophthotech licensed worldwide rights to all ophthalmic uses of Archemix's proprietary aptamers (ARC186 and ARC1905) targeting the C5 component of the complement cascade.
About E10030
E10030, currently being investigated in a Phase I trial, is an aptamer-based compound directed against PDGF-B. Pharmacology studies indicate that E10030 binds to PDGF-B with high specificity and affinity and inhibits the functions of PDGF-B both in vitro and in vivo. In preclinical studies, E10030 demonstrated the potential to regress neovascularization when used in combination with a VEGF-A inhibitor. In experiments involving models of ocular vascularization, concurrent inhibition of PDGF-B and VEGF-A signaling was superior to inhibition of the VEGF-A pathway alone.
About Volociximab (M200)
Volociximab is a monoclonal antibody targeting alpha5beta1 integrin, a key protein involved in the formation of new blood vessels, a process known as angiogenesis. alpha5beta1 integrin is a critical survival factor for proliferating endothelial cells involved in angiogenesis. Inhibition of alpha5beta1 integrin has demonstrated potent anti-angiogenic effects in multiple pre-clinical models of angiogenesis.
About AMD
AMD is the leading cause of blindness for people over the age of 50 in the United States and Europe. There are two forms of the disease, namely "dry" and "wet" AMD. The "wet" form is characterized by the growth of new blood vessels into the central region of the retina. These new vessels cause severe visual loss due to retinal damage caused by subsequent leakage and scar formation. Anti-VEGF therapies and photodynamic therapies have been approved for "wet" AMD. "Dry" AMD accounts for up to 90 percent of all cases of AMD. There is no approved therapy for "dry" AMD, which afflicts 8 million patients in the United States and an additional 8 million in Europe. Visual loss in "dry" AMD is typically not as severe as "wet" AMD, however, over time, "dry" AMD can progress to the wet form of the disease.
About Ophthotech
Ophthotech Corp. is a privately held biopharmaceutical company focused on developing and commercializing therapies for back-of-the-eye diseases. Ophthotech plans to develop a pipeline of compounds with strong scientific foundations for the treatment of AMD and bring them to market in an accelerated manner. In August of 2007, Ophthotech announced a Series A venture financing and two separate in-licensing deals with Archemix Corp. and Eyetech, Inc., which recently spun out of (OSI) Eyetech. A third in-license from Biogen Idec and PDL BioPharma was announced in January of 2008. Ophthotech's venture investors include SV Life Sciences, HBM BioVentures and Novo A/S. For more information, please visit www.ophthotech.com.
PRINCETON, NJ and NEW YORK, NY--(Marketwire - October 27, 2008) - Ophthotech Corp. ("Ophthotech"), a privately held biopharmaceutical company focused on developing ophthalmic therapies for back-of-the-eye diseases, announced today the enrollment of its first patient in a complement inhibition trial for the treatment of age-related macular degeneration (AMD). This Phase I trial will assess the safety and tolerability of ARC1905, an anti-C5 complement factor aptamer, in combination with an anti-VEGF agent.
Dr. Donald J. D'Amico, Professor and Chairman, Department of Ophthalmology, Weill Cornell Medical College, New York-Presbyterian Hospital, and a member of Ophthotech's Scientific Advisory Board, said, "Multiple lines of evidence now point to a fundamental problem with inflammation and complement activation in patients with high susceptibility to develop AMD. Intervention in the complement pathway is the single most promising target for new therapeutic and preventive strategies for AMD."
"Preclinical and human genetic linkage studies strongly support the significant role of complement-mediated inflammation in both dry and wet AMD," said Samir Patel, M.D., President and Chief Executive Officer of Ophthotech. "We believe that anti-C5 aptamer blockade represents a potential breakthrough therapy for both wet and dry forms of AMD."
Published studies in Science, the New England Journal of Medicine and other leading journals suggest that abnormalities involving the complement pathway may be responsible for the majority of cases of dry and wet forms of AMD in the western world.
ARC1905 represents one of three compounds that Ophthotech is developing to treat AMD. Additional molecular entities include E10030, an anti-PDGF aptamer currently in a Phase I study, and volociximab, an anti-angiogenic monoclonal antibody targeting the alpha5beta1 integrin, which is on track to commence clinical trials in the near future.
About ARC1905
Anti-C5 aptamer ARC1905 inhibits C5, a central component of the complement cascade, which plays multiple roles in innate immunity and inflammatory diseases. Inhibition of this key step in the complement cascade at the level of C5 prevents the formation of key terminal fragments (C5a and C5b-9) regardless of which pathway (alternate, classical or lectin) induced their generation. The C5a fragment is an important inflammatory activator inducing vascular permeability, recruitment and activation of phagocytes. C5b-9 is involved in the formation of membrane attack complex (MAC: C5b-9), which initiates cell lysis. By inhibiting these C5-mediated inflammatory and MAC activities, therapeutic benefit may be achieved in both dry and wet AMD. In August 2007, Ophthotech licensed worldwide rights to all ophthalmic uses of Archemix's proprietary aptamers (ARC186 and ARC1905) targeting the C5 component of the complement cascade.
About E10030
E10030, currently being investigated in a Phase I trial, is an aptamer-based compound directed against PDGF-B. Pharmacology studies indicate that E10030 binds to PDGF-B with high specificity and affinity and inhibits the functions of PDGF-B both in vitro and in vivo. In preclinical studies, E10030 demonstrated the potential to regress neovascularization when used in combination with a VEGF-A inhibitor. In experiments involving models of ocular vascularization, concurrent inhibition of PDGF-B and VEGF-A signaling was superior to inhibition of the VEGF-A pathway alone.
About Volociximab (M200)
Volociximab is a monoclonal antibody targeting alpha5beta1 integrin, a key protein involved in the formation of new blood vessels, a process known as angiogenesis. alpha5beta1 integrin is a critical survival factor for proliferating endothelial cells involved in angiogenesis. Inhibition of alpha5beta1 integrin has demonstrated potent anti-angiogenic effects in multiple pre-clinical models of angiogenesis.
About AMD
AMD is the leading cause of blindness for people over the age of 50 in the United States and Europe. There are two forms of the disease, namely "dry" and "wet" AMD. The "wet" form is characterized by the growth of new blood vessels into the central region of the retina. These new vessels cause severe visual loss due to retinal damage caused by subsequent leakage and scar formation. Anti-VEGF therapies and photodynamic therapies have been approved for "wet" AMD. "Dry" AMD accounts for up to 90 percent of all cases of AMD. There is no approved therapy for "dry" AMD, which afflicts 8 million patients in the United States and an additional 8 million in Europe. Visual loss in "dry" AMD is typically not as severe as "wet" AMD, however, over time, "dry" AMD can progress to the wet form of the disease.
About Ophthotech
Ophthotech Corp. is a privately held biopharmaceutical company focused on developing and commercializing therapies for back-of-the-eye diseases. Ophthotech plans to develop a pipeline of compounds with strong scientific foundations for the treatment of AMD and bring them to market in an accelerated manner. In August of 2007, Ophthotech announced a Series A venture financing and two separate in-licensing deals with Archemix Corp. and Eyetech, Inc., which recently spun out of (OSI) Eyetech. A third in-license from Biogen Idec and PDL BioPharma was announced in January of 2008. Ophthotech's venture investors include SV Life Sciences, HBM BioVentures and Novo A/S. For more information, please visit www.ophthotech.com.
Using Bifocal Reading Glasses
Telescopic glasses are among the latest of the numerous low vision aids used to help people in dealing with macular degeneration symptoms. While there is no cure for age related macular degeneration (AMD), there are macular degeneration treatments available that can assist such patients in maximizing what sight they do have; telescopic glasses are possibly among the most effective, both in terms of cost and effectiveness.
In some ways, these remarkable devices – also known as bioptics - are similar to bifocal reading glasses. They essentially work the same way; patients utilize these macular degeneration devices by tilting their heads forward. These particular macular degeneration devices are different however in their construction. Unlike bifocal reading glasses, which integrate two different prescriptions into single lenses, telescopic glasses actually consist of miniature telescopes that sit atop the frames.
The marvelous aspect of telescopic glasses – also known as bioptics - is the fact that they can be adjusted in the same way as many full-sized telescopes. As low vision aids for the relief of macular degeneration symptoms, telescopic glasses can be adjusted for a variety of activities requiring far, mid-range and near vision.
In fact, some states actually allow those who cannot pass the eye test for driving to operate a motor vehicle as long as bioptics are used. While there are usually restrictions, the use of telescopic glasses can help the patient to regain some measure of independence. These low vision aids are of great help in seeing road signs and other objects on the highway.
Telescopic glasses are like regular glasses, and if you plan on driving with them, you’ll need an optometrist’s prescription. Even if you’re not planning to operate an automobile (and admittedly, this is not appropriate for everyone – or even very many – people with macular degeneration symptoms), the use of these remarkable low vision aids can greatly add to your quality of life.
With the use of bioptics, people who use such macular degeneration devices can once again enjoy watching television and motion pictures, engage in artistic pursuits such as sculpture and painting or music requiring reading, and engage in their favorite sports.
Of course, because macular degeneration symptoms affect one’s central vision and because different activities in life require different kinds of vision, there is no one single solution. Bioptics are only one part of a comprehensive solution that will most likely require several different types of macular degeneration devices. Only your optometrist can advise you as to which of these prosthetic devices can be of most good in helping your particular case.
In some ways, these remarkable devices – also known as bioptics - are similar to bifocal reading glasses. They essentially work the same way; patients utilize these macular degeneration devices by tilting their heads forward. These particular macular degeneration devices are different however in their construction. Unlike bifocal reading glasses, which integrate two different prescriptions into single lenses, telescopic glasses actually consist of miniature telescopes that sit atop the frames.
The marvelous aspect of telescopic glasses – also known as bioptics - is the fact that they can be adjusted in the same way as many full-sized telescopes. As low vision aids for the relief of macular degeneration symptoms, telescopic glasses can be adjusted for a variety of activities requiring far, mid-range and near vision.
In fact, some states actually allow those who cannot pass the eye test for driving to operate a motor vehicle as long as bioptics are used. While there are usually restrictions, the use of telescopic glasses can help the patient to regain some measure of independence. These low vision aids are of great help in seeing road signs and other objects on the highway.
Telescopic glasses are like regular glasses, and if you plan on driving with them, you’ll need an optometrist’s prescription. Even if you’re not planning to operate an automobile (and admittedly, this is not appropriate for everyone – or even very many – people with macular degeneration symptoms), the use of these remarkable low vision aids can greatly add to your quality of life.
With the use of bioptics, people who use such macular degeneration devices can once again enjoy watching television and motion pictures, engage in artistic pursuits such as sculpture and painting or music requiring reading, and engage in their favorite sports.
Of course, because macular degeneration symptoms affect one’s central vision and because different activities in life require different kinds of vision, there is no one single solution. Bioptics are only one part of a comprehensive solution that will most likely require several different types of macular degeneration devices. Only your optometrist can advise you as to which of these prosthetic devices can be of most good in helping your particular case.
Friday, November 21, 2008
Medical Treatment
- Antioxidants: Deficiencies in antioxidants (specifically zinc and vitamins A, C, and E) have been noted in some people with age-related macular degeneration. Antioxidants may protect against age-related macular degeneration by preventing free radicals or unstable oxygen from damaging the retina.
- Laser treatment: Clinical trials have demonstrated the value of laser treatment for some people with the wet form.
- Laser treatment may stop or lessen vision loss in early stages of the disease.
- A laser beam destroys existing blood vessels and may stop the growth of new ones.
- A scar forms after the laser treatment. This produces a permanent loss of vision in that area of the retina, sacrificed in order to preserve the rest of the eye layer.
- Vision usually does not improve after laser treatment. It works in about half the cases, and only a small number of people meet the criteria for laser treatment. Its limitations have prompted a search for other forms of therapy.
- Laser treatment may stop or lessen vision loss in early stages of the disease.
- Photodynamic therapy: In April 2000, the U.S. Food and Drug Administration (FDA) approved this treatment. A light-activated drug called verteporfin (Visudyne) is given intravenously and uses a laser to close the abnormal vessels while leaving the retina intact. You may need several treatments over one to two years because closed blood vessels can reopen within the treated area. Because Verteporfin is activated by light, exposure to sunlight must be avoided for five days after treatment.
- Antioxidants: Deficiencies in antioxidants have been noted in some people with age-related macular degeneration. Antioxidants may protect against age-related macular degeneration by preventing free radicals or unstable oxygen from damaging the retina.
- A variety of drugs that block vascular endothelial growth factor (VEGF) are being evaluated as a treatment option.
No one has found a treatment of or a cure for the dry form of age-related macular degeneration.
The wet form of age-related macular degeneration is more likely than the dry form to cause significant vision loss. Different treatments of the wet form are available and may help decrease the amount of vision that is lost.
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