Dr. Grossman’s Blog

FRIDAY, Aug. 29 (HealthDay News) — Eating plenty of antioxidant-rich food such as blueberries, artichokes and pecans may help protect against macular degeneration, the leading cause of age-related blindness in the United States and other developed countries.

U.S. researchers found that antioxidants disrupt a link between two processes in the retina that, in combination, contribute to macular degeneration. Antioxidants also extend the lifetime of irreplaceable photoreceptors and other retinal cells.

The “destructive synergy” that causes macular degeneration occurs when a buildup of a compound called A2E disrupts energy production in mitochondria, the “power plants” in cells, the researchers said. The lack of energy interferes with daily cleaning and maintenance of photoreceptors and another type of retinal cell. This leads to more buildup of A2E and a continuing cycle that results in the destruction of the vital visual cells that can’t be replaced.

Experiments using visual cells from humans, rats and cows showed that antioxidants could completely counter the damage caused by this process, said the researchers from Brigham Young University and Weill Medical College of Cornell University.

“The implication is that people at risk of macular degeneration could help prevent the disease by consuming antioxidants,” study author Heidi Vollmer-Snarr, a Brigham Young chemist, said in a university news release.

The study was published online in the Journal of Biological Chemistry.

“This work by Dr. Vollmer-Snarr and colleagues ties these two damaging processes together and demonstrates the harm they cause in combination is much more than would be expected,” Dr. Paul Bernstein, of the University of Utah’s Moran Eye Center, said in the news release. “This new knowledge,” added Bernstein, who wasn’t involved in the study, “suggests the possibility of interventions which could prove to be powerful ways to prevent or delay age-related macular degeneration.”

For more related studies, go to the “Research” section as www.naturaleyecare.com

A combination of exposure to blue light from sunlight and inadequate levels of antioxidants in the blood contribute to the development of some forms of the eye disease age-related macular degeneration (AMD), say researchers.

Astrid E. Fletcher, PhD, of the London School of Hygiene & Tropical Medicine, and colleagues measured levels of vitamin C and E, the carotenoids lutein and zeaxanthin, and zinc, in the blood of 4,753 seniors with an average age of 73.2 years. The participants were also questioned about sun exposure, and had photographs taken of their retinas.

Results showed that of the 4,400 participants with complete data, 2% had neovascular AMD, an advanced form of the disease, and 50% had early-stage AMD. Overall, there was no link between blue light exposure and neovascular AMD or early-stage AMD. However, participants with a history of blue light exposure and low blood levels of zeaxanthin, vitamin E, and vitamin C were found to be 3.7-times more likely to develop neovascular AMD.

The researchers conclude: Our results suggest that people in the general population should use ocular protection and follow dietary recommendations for the key antioxidant nutrients.

 Posted in Nutrition, Sensory on Thu October 16, 2008

Fletcher AE, Bentham GC, Agnew M.Sunlight Exposure, Antioxidants, and Age-Related Macular Degeneration. Arch Ophthalmol. 2008;126:1396-1403. 

For more related studies, see the “Research” section at www.naturaleyecare.com

Hemianopia is a blindness in one half of the visual field due to damage of the optic pathways in the brain. This damage can result from brain injuries caused by stroke, tumor or trauma.  A patient with hemianopia may be unaware of what he or she cannot see and may frequently bump into walls, trip over objects or walk into people on the side in which the visual field is missing.

Prism eyeglasses were invented by Dr. Eli Peli of the Schepens Eye Research Institute, an affiliate of Harvard Medical School, to assist patients with hemianopia.  Dr. Peli attached small high power prisms on the top and bottom of one spectacle lens, leaving the center of the lens untouched. The prisms pull in images missing from the visual field above and below the line of sight on the side of the vision loss.  The prisms alert the patient to the presence of a potential obstacle, so that the patient can then move his/her head and eyes to examine the prism-captured image directly through the clear center of the lens.

In the trial, 32 of 43 participants (74%) who were fitted with prism glasses continued wearing the glasses at week six; at 12 months, 20 (47%) were still wearing the spectacles eight hours daily and rating them as “very helpful” for obstacle avoidance.

A larger study is currently underway to evaluate a newer model of the eyeglasses. 

SOURCE: “Community-Based Trial of a Peripheral Prism Visual Field Expansion Device for Hemianopia”, Bowers, et al, Archives of Ophthalmology, 2008, vol. 126, no5, pp. 657-664.

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).

Last month Archives of Ophthalmology published a meta analysis on omega-3 fatty acid and fish intake and its effect on the prevention of age-related macular degeneration (AMD).

This study identified 274 abstracts, 3 prospective cohort, 3 case-control, and 3 cross-sectional studies.

Using quantitative methods, a high dietary intake of omega-3 fatty acids was associated with a 38% reduction in the risk of late AMD. Fish intake (2x per week) was associated with reduced risk of early and late AMD.

More omega-3 and AMD specific studies need to be conducted to further investigate omega-3¹s effect on AMD.

Ref: Arch Ophthalmol. 2008;126(6):826-833.

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

Research shows bilberry extract helps fight against macular degeneration and cataracts in lab rats

Cataracts and macular degeneration are the major cause of vision deterioration in the elderly. A study by Russian scientists shows that taking bilberry supplements may help ward off these diseases.

Researchers used a particular strain of lab rats (OXYS rats) capable of reproducing many of the key features of human age-related cataracts and macular degeneration. From 1.5 to 3 months, these rats were given either a control diet or a diet supplemented with bilberry extract.

At 3 months, more then 70% of the rats in the control group had cataract and macular degeneration. Rats in the group given bilberry extract had no impairments in the lenses and retina.

Bilberry is also known as European blueberry, and is closely related to North American wild and cultivated blueberries and huckleberries. Bilberry is known to be a potent antioxidant and has been shown to help other vision problems such as glaucoma. (Read more about bilberry and glaucoma).

Results suggest that long-term supplementation with bilberry extract is effective in prevention of macular degeneration and cataract.

Read more research on cataracts and macular degeneration

Learn about natural bilberry supplements

Source: “Dietary supplementation with bilberry extract prevents macular degeneration and cataracts in senesce-accelerated OXYS rats”, Fursova et al, Adv Gerontol, 2005; 16: 76-9.

Antioxidants not only help prevent some eye diseases, they may also help limit progression of the diseases

It’s known that taking antioxidants helps delay the onset of some eye diseases associated with aging, such as cataract. Now researchers believe that antioxidants can be effective if damage to retinal tissue has already set in.

Researchers at the University of Maryland School of Medicine studied the effects of reactive oxygen species (ROS)-induced damage to retinal tissue. An increase in ROS levels can result in significant damage to cell structures — a situation known as oxidative stress. Oxidative stress is a significant risk factor in the development of many eye diseases associated with aging.

Since the formation of cataract is a well-defined progressive disease, believed to be related to a continued generation of ROS in the aqueous humor, the researchers hypothesized that even a late start with an appropriate antioxidant could halt the process and delay cataract development and vision impairment.

The results? Adding pyruvate – known to be an effective ROS scavenger — to lens cultures after lenses had sustained 50% damage was significantly effective in preventing progress.

Pyruvate can be found in foods such as red apples, and to a lesser extent, in dark beer and some cheeses.

Learn more about antioxidants

Read more about antioxidants and their importance in maintaining healthy vision

SOURCE:  “Oxidative damage to lens in culture: reversibility by pyruvate and ethyl pyruvate”, Varma, et al, Ophthalmologica, 2008; 222 (3):194-198.

Study could lead to new therapies to help improve sight following trauma or stroke

Neuroscientists studying the mind’s ability to process images have completed the first empirical study to demonstrate how nerve cells in the visual cortex adapt to changing images. 

In the study, researchers at the University of Texas Health Science Center measured the effects of visual stimulation on the responses of multiple neurons whose electrical activity was measured simultaneously in animals. They examined the responses of a population of cells in visual cortex to dynamic stimuli (movie sequences displayed on a video monitor).

Results showed that brief exposure or adaptation to a fixed stimulus caused changes in the degree of cooperation between individual neurons and improved the efficiency with which the population of cells encoded information.

“Our perception of the environment relies on the capacity of neural networks to adapt rapidly to changes in incoming stimuli,” wrote senior author Valentin Dragoi.  “It is increasingly being realized that the neural code is adaptive, that is, sensory neurons change their responses and selectivity in a dynamic manner to match the changes in input stimuli.” The neural code is the set of rules that converts electrical impulses in the brain into thoughts, memories and decisions.

“Right now, we don’t know the causes of brain illnesses such as Alzheimer’s disease or disorders caused by trauma,” Dragoi said. “However, it is our belief that understanding not only how individual neurons work, but how they cooperate with their neighbors to impact the functions of the brain involved in diseases may help develop better diagnostic tools and therapies to improve visual function following trauma, stroke or disease, or even prevent brain disorder.”

SOURCE:  “Populations Of Brain Cells Adapt To Changing Images,” Dragoi, et al., Nature 452, 220-224 (13 March 2008).

Homocysteine, an amino acid believed to contribute to heart attack, stroke and dementia, may also play a role in retinal damage and vision loss.  Homocysteine levels rise when folic acid levels drop, a common problem for Americans whose diets are often poor in folate-rich fruits, tomatoes, vegetables and grains.

Dr. Sylvia Smith, cell biologist at Medical College of Georgia (MCG), and Dr. Vadivel Ganapathy, chair of the MCG Department of Biochemistry and Molecular Biology are studying the consequence of slightly elevated homocysteine on the retina under a $1.8 million grant from the National Institutes of Health.  They want to learn the impact of elevated homocysteine levels on the extensive blood vessel and neuronal network of the retina; their preliminary evidence suggests that it isn’t good.

“You don’t have to be a cell biologist to see that there is a problem in this retina. It’s terribly disrupted,” Dr. Smith says, looking at images of a fragmented 10-layer retina exposed to high levels of homocysteine.  A healthy retina is “beautifully” organized, horizontally and vertically, she says.

Folate and vitamin B12 convert homocysteine to methionine, an amino acid essential to protein synthesis.  Dr. Ganapathy notes that people need only about 1 microgram per day of vitamin B12, which comes from microorganisms common in animals’ gastrointestinal tract. Strict vegetarians are typically the only Americans who have problems with B12 deficiency, he says. People need about 400 micrograms of folate daily. Pregnant women as well as those trying to become pregnant need at least double that.

Researchers are studying a mouse model with a slightly elevated homocysteine level that simulates a low-folate diet in humans; a version of the mouse that also has diabetes, which goes along with cardiovascular disease and retinopathy; and a second model of the rare genetic defect that results in extraordinarily high homocysteine levels.  These mice will be put on diets that elevate and lower folate levels, so that resultant homocysteine levels and the impact on the retina can be studied.

Researchers hypothesize that sustained elevation will compromise retinal function and degrade the once well-stratified tissue; in pilot studies, the researchers have shown that diabetes exacerbates this problem.

SOURCE:  Medical College of Georgia, “Impact of elevated homocysteine levels on vision under study,” Oct. 15, 2007.

Researchers at the University of Pennsylvania School of Medicine have created the first animal model of age-related macular degeneration (AMD) caused by a mutation known to produce disease in people.

AMD is the most common cause of vision loss in elderly people, affecting more than 10 million people in the U.S. and about 50 million world-wide. Because AMD develops late in life (patients typically show symptoms of AMD after age 60), it is a difficult condition to investigate.

Although some forms of AMD are inherited, one type is thought to be caused by a mutation in the Efemp1 gene. Researchers introduced the disease-causing mutation into the Efemp1 gene of mice. These Efemp1-mutant mice develop the same basal deposits as people with AMD.

It is believed that these mice will provide a means to study how basal deposits form and what they are made of. The mice can also be used to test potential treatments to prevent basal deposit formation.

“To better develop treatments for preventing the progression of AMD, we need to understand the real biochemical details of how AMD occurs,” says lead author Eric A. Pierce, MD, PhD, Associate Professor of Ophthalmology at Penn’s K.M Kirby Center for Molecular Ophthalmology. “To do that, we need a model, and now we have one.”

Learn more about age-related macular degeneration (AMD)

Read other studies about macular degeneration

SOURCE: Model To Study Age-related Macular Degeneration Could Pave Way For Better Treatment, Pierce et al, University of Pennsylvania School of Medicine (2007, October 10).