Dr. Grossman’s Blog

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A new clinical trial seeks to find alternative ways to treat glaucoma, specifically investigating how to help those who’ve been told that no more can be done.  This trial is operating under the hyopothesis that “state-of-the-art low vision aids in patients with advanced glaucomatous visual loss will provide an improvement in visual tasks and thereby an improvement in quality of life.”  Researchers want to study how low vision rehabilitation can help those suffering from glaucoma.  Source: http://clinicaltrialsfeeds.org/clinical-trials/show/NCT01262209

We believe that is is possible to both prevent and treat glaucoma naturally.  Visit our website for tips and information on dealing with glaucoma.

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One risk factor for glaucoma is central corneal thickness.

Researchers looking at ethnic populations in Singapore have identified the genes that affect collagen growth, which in turn affects central corneal thickness.  Knowing how these specific genes work can help provide insight into the cause and progression of glaucoma.

Source: http://hmg.oxfordjournals.org/content/early/2010/11/23/hmg.ddq511.abstract

Learn more about how to prevent and treat glaucoma naturally at our website.

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Recent research has shown that glaucoma may not originate in the retina itself, but at the other end of the optic nerve located back in the middle of the brain.  In a study of rodents published in PNAS, it was found that the problem may stem from the nerve’s inability to transport impulses.  The scientists from Vanderbilt University and University of Washington say that this transport deficit seems related to the subject’s age and is not necessarily related in increased ocular pressure.  Locating glaucoma’s cause in the nerve rather than the retina may lead to new breakthroughs in glaucoma detection and therapy.

Source: http://www.pnas.org/content/107/11/5196.abstract

Learn more about who is at risk for glaucoma and how to prevent the eye disease known as “the silent thief.”

In glaucoma, cells in the optic nerve die, preventing the brain from understanding what patients see.

Scientists have long believed that there is a link between a gene named WDR36 and glaucoma, but have been unable to determine what the gene does and why some people with variations of the gene get glaucoma while others don’t.

University of Alberta geneticist, Dr. Michael Walter, has published results of a new study which help to explain this link. 

“Our results suggest that glaucoma is polygenetic, which means there have to be changes in several different genes in order for WDR36 to cause the disease,” said Walter, a professor and chair of the Department of Medical Genetics in the Faculty of Medicine & Dentistry.  This finding helps explain why only some people who have WDR36 gene variations get glaucoma.

“Only 10 per cent of glaucoma cases are caused by known genes, so the genes involved in this polygenetic interaction may help to explain the other 90 per cent,” said Walter, who is also a professor in the Department of Ophthalmology.

The WDR36 gene normally helps make ribosomes, specialized molecules that make the proteins necessary to keep the cell functioning.  Dr. Walter suspects that changes to WDR36 will affect ribosome production, and in turn affect the cell’s ability to function.

In addition to this mutation, changes also have to happen to the STI1 gene, which normally packages the proteins produced by WDR36′s ribosomes.  Glaucoma occurs when WDR36 isn’t producing ribosomes properly and STI1 isn’t packaging those proteins properly.  Both mutations must be present to cause the disease.

This DNA detective work may have a tangible impact on preventing and treating glaucoma, as it may help doctors learn to treat the disease rather than just the symptoms.

Learn more about glaucoma

SOURCE:  “Genetic Sleuth Solves Glaucoma Mystery”, University of Alberta Express News, March 20, 2009, http://www.expressnews.ualberta.ca/article.cfm?id=10052.

The findings provide hope for treating blindness caused by optic-nerve damage, but
also look promising for spurring similar regeneration in the spinal cord and brain.
Researchers said Monday a newly discovered growth factor could hold the key to regenerating damaged optic nerves — and more. The research team at Children’s Hospital in Boston say they have found a naturally occurring, previously unrecognized growth factor that stimulates regeneration in injured optic nerves.
The findings provide hope for treating blindness caused by optic-nerve damage, but
also look promising for spurring similar regeneration in the spinal cord and brain,
they said.

The growth factor is called oncomodulin and when it was added to retinal nerve cells
in the lab, with known growth-promoting factors already present, the growth of axons
– or cells in the optic nerves — nearly doubled.

No other growth factor was as potent, the researchers said.

More Nerve Regeneration

In live rats with optic-nerve injury, oncomodulin released from tiny sustained-release
capsules increased nerve regeneration five- to seven-fold when given along with
a drug that helps cells respond to oncomodulin, the team said.

Oncomodulin also appears to switch on a variety of genes associated with axon growth,
the researchers said.

“Out of the blue, we found a molecule that causes more nerve regeneration than
anything else ever studied,” said one of the study investigators. We expect
this to spur further research into what else oncomodulin is doing in the nervous
system and elsewhere.

The data are published in the May 14 online edition of Nature Neuroscience.

For more related research, go to www.naturaleyecare.com (see “Research” section).

A study by Alcon Research Ltd. and the University of Iowa suggests that increased expression of the protein sFRP-1, an inhibitor of cell signaling through WNT proteins, may be responsible for elevated IOP in individuals with glaucoma.

Glaucoma is a major cause of visual impairment and blindness throughout the world. An important risk factor for the disease is an increase in the intraocular pressure (IOP). IOP, the fluid pressure in the eye, is determined by the rate of production of the clear fluid in the eye and the rate at which this fluid flows out of the eye. Although it is thought that impaired outflow of fluid from the eye causes the increased IOP in individuals with glaucoma, the exact molecular mechanisms of the disease are not fully understood.

Researchers found increased expression of sFRP-1 in eye tissue from patients with glaucoma; when they treated donor human eyes with sFRP-1 ex vivo, these eye tissues had less outflow of fluids compared to untreated eyes. The sFRP-1-treated donor eyes also had reduced expression of a WNT-related protein.

To further support this relationship, mice manipulated to express sFRP-1 in the eye displayed increased IOP. When a downstream suppressor of WNT signaling was inhibited, the problem was resolved.

The authors believe that restoring WNT signaling might provide a new method for treating patients with glaucoma in the future.

Read more about glaucoma, including information on lifestyle choices and nutrition for maintaining healthy vision.

SOURCE: “Increased expression of the WNT antagonist sFRP-1 in glaucoma elevates intraocular pressure”, Wang, et al, Journal of Clinical Investigation, 118(3): 1056-1064 (2008).

New study shows that supplementing with bilberry can helps lower intraocular pressure (IOP). Uncontrolled high IOP is the major cause of vision loss for those with glaucoma.

In a study performed by researchers from the University of Chieti-Pescara in San Valentino, Italy, thirty-eight subjects with IOP were either given bilberry and French maritime pine bark (20 subjects) or were not treated (18 subjects)¹. The visual acuity, IOP, and ocular blood flow were measured at two, three, and six months. After two months of supplementation the mean IOP decreased. No side effects were observed and ocular blood flow improved. An improved ocular blood flow may contribute to the prevention of glaucoma. The results of this study indicate that bilberry and pine bark may represent a safe preventative intervention for lowering the risk for developing symptomatic glaucoma by controlling IOP and improving ocular blood flow. This helps to support research for other preventative nutritional approaches to major eye health, such as cataract, age-related macular degeneration, and retinopathy.

For more information on nutrition and glaucoma, go to www.naturaleyecare.com

A research study shows that people with open-angle glaucoma (POAG) had significantly higher levels of homocysteine (Hcy) levels in their tear fluids. Patients with open-angle glaucoma who also had dry eye disease had significantly higher Hcy levels both in tear fluid and plasma than POAG patients without dry eye disease.

SOURCE: Roedl JB, Bleich S, Schlotzer-Schrehardt U, et al. Increased homocysteine levels in tear fluid of patients with primary open-angle glaucoma. Ophthalmic Res 2008;40(5):249-56

Editor’s Note: People with elevated homocysteine levels are more likely to have strokes, Alzheimer’s disease and dementia, kidney disease, diseases of the eye, erectile dysfunction, and, especially, heart disease (De Bree A et al 2002).

Homocysteine level is affected by a number of influences, including lifestyle, dietary choices, and genetics. As we age, our ability to absorb nutrients decreases. As a result, less of the important B vitamins are available to help metabolize homocysteine. Homocysteine level is also increased by certain pharmaceuticals, an aging metabolism, smoking, drinking too much alcohol or coffee, lack of exercise, obesity, and stress.

Supplementation of certain B vitamins can help reduce homocysteine levels including folic acid, and Vitamins B6 amd B12. To varying degrees, folic acid and vitamin B12 increase the remethylation of homocysteine back into SAMe. Vitamin B6 is necessary for the conversion of homocysteine into glutathione along the transsulfuration pathway.

See more glaucoma research