Could diet be the cause of vision loss in seniors?

It’s possible that diets heavy in red meat and fatty foods may help spur a leading cause of vision loss in older Americans, according to new research.

A recent study found that people who ate a more typical Western diet were three times more likely to develop late-stage age-related macular degeneration.

“What you eat seems to be important to your vision, and whether or not you have vision loss later in life,” said study lead author Amy Millen. She’s an associate professor in the department of epidemiology and environmental health at the University at Buffalo’s School of Public Health and Health Professions, in Buffalo, N.Y.

“People know that diet influences cardiovascular risk and the risk of obesity, but the public may not know that diet can affect vision loss,” Millen said.

Age-related macular degeneration occurs when a part of the eye called the macula is damaged. Sometimes this happens when deposits called drusen grow on the macula. Or it can occur when new blood vessels continue to form and leak blood, scarring the macula, according to the American Academy of Ophthalmology.

Genetics and smoking are known risk factors for age-related macular degeneration.

This study included almost 1,300 people from a nationally representative sample. Most did not have macular degeneration. There were 117 who had early AMD, and 27 had late.

All of the study participants completed surveys about their diets twice during the 18-year study.

The researchers sorted the foods into 29 categories to measure the quality of the diet.

They found that people who ate a more Western diet were much more likely to develop late-stage AMD. Foods linked to a higher risk included:

  • Red and processed meats
  • Fats, such as margarine and butter
  • High-fat dairy
  • Fried foods.

In short the observational study showed a diet high in fatty foods, processed meats and refined grains makes the more severe form of macular degeneration more likely.

It is not known if you can make up for a lifetime of eating poorly. But a healthy diet — full of vegetables, especially dark, leafy greens, and fruits and fatty fish — contains important nutrients for eye health, including lutein and zeaxanthin.

The study was published in the December issue of the British Journal of Ophthalmology.

To read the original article click here (Fatty diet linked to leading cause of vision loss in seniors)

New hope for those affected by thyroid eye disease

The newly approved drug teprotumumab can offer hope to adults with thyroid eye disease, a rare and potentially blinding condition.

It’s the first treatment specifically approved for thyroid eye disease. The drug was approved Tuesday, January 11, 2020 by the U.S. Food and Drug Administration. It will be marketed under the brand name Tepezza.

“This may be a drug that offers a new approach and a paradigm shift,” said Dr. Raymond Douglas, lead author of a study the FDA considered when making its final decision. “Currently, we use supportive therapy for people with thyroid eye disease, but their quality of life is diminished by their symptoms.

“Teprotumumab was extraordinarily effective. We hope that people with thyroid eye disease won’t have to suffer as they have in the past. With treatment, they’re not going to be blind. They’re not going to be disfigured. They can even watch their kids playing soccer when it’s windy,” Douglas explained. Without treatment, wind could be too drying to the eyes.

Thyroid eye disease causes inflammation in the back of the eye causing the eyes to bulge. The swelling may also squeeze the optic nerve, causing vision problems, said Douglas, a professor of surgery in the division of ophthalmology at Cedars-Sinai Medical Center in Los Angeles.

Thyroid eye disease typically develops in people with an overactive thyroid gland caused by Graves’ disease. Redness, swelling and a gritty feeling in the eyes are also classic symptoms, the American Thyroid Association says. Other conditions that can occur include dry eyes or excessive tearing, double vision and sensitivity to light. The most noticeable symptom, however, is the bulging of the eyes, and it may be difficult to completely close the eyes.

Because thyroid eye disease is rare, the FDA gave this drug “orphan drug” status. This means companies are provided incentives to encourage the development of drugs for rare diseases. The medication was also given the FDA’s priority review, fast track and breakthrough therapy designations to assist the manufacturer in bringing the drug to market.

The drug’s approval was based on results of two studies that included 170 people with active thyroid disease. The drug was administered intravenously once every week for three weeks over a 21-week period. Douglas said the IV infusions take about an hour.

Teprotumumab started working after just two doses, Douglas said. After 24 weeks, 83 percent of people on the drug had a measurable reduction in eye bulge — more than 2 millimeters — versus just 10 percent of those on a placebo.

The overall response rate was 78 percent among those taking the drug compared to 7 percent of people taking a placebo. Quality of life was much higher for people taking the drug, the study found.

Douglas said treatment with the drug reversed double vision as well as surgery does.

Side effects were minimal and well-tolerated, according to Douglas. Some of the more common side effects included muscle cramps, nausea, hair loss and fatigue. The drug should not be used in pregnancy.

Learn more about thyroid eye disease from the American Thyroid Association.

 To read the original article, click here (New drug may stop blindness from thyroid eye disease)

Can cadavers help restore vision to the blind?

This may not be as far-fetched as it sounds. According to an article published Thursday, January 14, 2021 by Stem Cell Reports, retinal stem cells collected from human cadavers may offer a potential treatment for blindness.

When healthy retinal pigment epithelium cells were implanted under the macula of blind monkeys, at least some vision was restored without serious side effects, the study’s researchers from the Mount Sinai School of Medicine in New York City said. (The retinal pigment epithelium is a layer of pigmented cells in the retina and the macula is the central part of the retina.)

The transplanted cells (harvested from human cadavers) effectively took over the function of the monkeys’ natural retinal pigment epithelium, enabling them to see, according to the researchers.

The study’s co-author Timothy Blenkinsop, assistant professor of cell, developmental and regenerative biology at the Icahn School of Medicine at Mount Sinai, said this in a statement:

“We have demonstrated that [donor cells] at least partially replace function in the macula of a non-human primate, human cadaver donor-derived cells can be safely transplanted underneath the retina and replace host function, and therefore may be a promising source for rescuing vision in patients with retina diseases.”

Retinal pigment epithelium dysfunction can lead to eye disorders such as macular degeneration, causing vision loss and blindness, which affects about 200 million people worldwide.

Using cadaver donor eyes can help ensure donor cells match well with recipients, and can serve as a recurring source of human retinal pigment epithelium cells.

These retinal pigment epithelium “patches,” or small quantities of collected cells, transplanted under the primates’ maculas remained “stable and integrated” for at least three months, without serious side effects such as immune-system rejection or light sensitivity. This is quite encouraging.

Additionally, the transplanted cells worked well with the existing retinal pigment epithelium to support the existing photoreceptors in their eyes, which aids with light absorption, among other functions.

Transplantation of retinal pigment epithelium stem cells derived from human adult cadaver eyes could serve as a possible treatment for macular degeneration, the study suggests.

However, the researcher stress that additional research on this approach is necessary to explore whether stem cells derived from cadaver adult eyes can restore vision in human patients.

“The results of this study suggest human adult donor retinal pigment epithelium is safe to transplant, strengthening the argument for human clinical trials for treating retina disease,” Blenkinsop said.

To read the original article click here. (Retinal stem cells from cadavers may help restore vision in blind, study finds – UPI.com)

Could following the Mediterranean diet prevent blindness?

The evidence is in and it shows that a poor diet plays a big role in the development of age-related macular degeneration (AMD), a leading cause of blindness in the US.  A large collaboration of researchers from the EU investigated the connection between genes and lifestyle on the development of AMD has found that people who followed a Mediterranean diet cut their risk of late-stage AMD by 41% This research expanded on previous studies and suggests that such a diet is beneficial for everyone, whether you already have the disease or are at risk of developing it.

A Mediterranean diet emphasizes eating less meat and more fish, vegetables, fruits, legumes, unrefined grains, and olive oil. Previous research had linked it to a longer lifespan and a reduced incidence of heart disease and cognitive decline. Previous studies also showed following this diet can help with certain types of AMD, but only focused on different stages of the disease.

By combining this earlier research on AMD with the latest data, a clear picture emerges: Diet has the potential to prevent a blinding disease.

AMD is a degenerative eye disease. It causes loss of central vision, which is crucial for simple everyday activities, such as the ability to see faces, drive, read, and write. It’s a leading cause of vision loss among people age 50 and older, affecting 1.8 million Americans. By 2020, that number is expected to climb to nearly 3 million.

In this study, researchers analyzed food-frequency questionnaires from nearly 5,000 people who participated in two previous investigations — the Rotterdam Study, which evaluated disease risk in people age 55 and older, and the Alienor Study, which assessed the association between eye diseases and nutritional factors in people aged 73 and older. Patients in the Rotterdam study were examined and completed food questionnaires every five years over a 21-year period, while patients in the Alienor Study were seen every two years over a 4-year period. The researchers found that those who closely followed the diet were 41%  less likely to develop AMD compared with those who did not follow the diet.

They also found that none of the individual components of a Mediterranean diet on their own — fish, fruit, vegetables, etc. — lowered the risk of AMD. Rather, it was the entire pattern of eating a nutrient-rich diet that significantly reduced the risk of late AMD.

There are two kinds of AMD — dry and wet. The dry type affects about 80 to 90 percent of people with AMD. In dry AMD, small white or yellowish deposits, called drusen, form on the retina, causing it to deteriorate over time. In the wet form, blood vessels grow under the retina and leak. While there is an effective treatment available for the wet type, there is no treatment available for dry AMD.

So remember you are what you eat!

To read the original article in its entirety, click here. https://www.sciencedaily.com/releases/2018/10/181001101940.htm

Biomarkers could aid in early detection of glaucoma

Researchers bred mice in which the gene PTP-Meg2 (protein tyrosine phosphatase megakaryocyte 2) was mutated. As a result, the animals suffered from chronic intraocular pressure elevation. The research team successfully demonstrated that, in their model, the intraocular pressure elevation was associated with a loss of optic nerve fibers and retinal cells. They also observed that retinal cells were unable to function properly. They further discovered glial cells and certain components of the immune system showed a reaction in the animals’ optic nerve and retina. As both aspects may be relevant for neurodegeneration, specific and early intervention into these cellular mechanisms could inhibit glaucoma.

By making use of a genetic screening, the researchers identified new potential biomarkers for glaucoma, which in the future, may facilitate early detection. As a result, it will be possible to start therapy at an earlier stage, before the optic nerve and retina are damaged. The glaucoma-mouse model may, moreover, be used to test new therapy options. So far intraocular pressure was reduced and nerve cells were retained in the mice if they were given a drug that has been used to treat human patients.

With more than 60 million patients, Glaucoma is a leading cause of blindness worldwide. In Germany alone, there are one million patients — and the estimated number of unknown cases is likely to be much higher, due to the fact that symptoms often remain undetected during the early stage of the disease. In glaucoma patients, the optic nerve and the retinal nerve cells are damaged beyond repair.

To read the original article in its entirety, click here. https://www.sciencedaily.com/releases/2018/10/181025103308.htm

AMAZING: Congenital blindness reversed in mice!

Researchers funded by the National Eye Institute (NEI) have reversed congenital blindness in mice by changing supportive cells in the retina called Müller glia into rod photoreceptors. The findings advance efforts toward regenerative therapies for blinding diseases such as age-related macular degeneration and retinitis pigmentosa.

“This is the first report of scientists reprogramming Müller glia to become functional rod photoreceptors in the mammalian retina,” said Thomas N. Greenwell, Ph.D., NEI program director for retinal neuroscience. “Rods allow us to see in low light, but they may also help preserve cone photoreceptors, which are important for color vision and high visual acuity. Cones tend to die in later-stage eye diseases. If rods can be regenerated from inside the eye, this might be a strategy for treating diseases of the eye that affect photoreceptors.”

Photoreceptors are light-sensitive cells in the retina, located in the back of the eye, that signal the brain when activated. In mammals, including mice and humans, photoreceptors fail to regenerate on their own. Like most neurons, once mature they no longer divide.

Scientists have long studied the regenerative potential of Müller glia because in other species, such as zebrafish, they divide in response to injury and can turn into photoreceptors and other retinal neurons. The zebrafish can thus regain vision after severe retinal injury. In the lab, however, scientists can coax mammalian Müller glia to behave more like they do in the fish. But it requires injuring the tissue.

“From a practical standpoint, if you’re trying to regenerate the retina to restore a person’s vision, it is counterproductive to injure it first to activate the Müller glia,” said Bo Chen, Ph.D. “We wanted to see if we could program Müller glia to become rod photoreceptors in a living mouse without having to injure its retina,” said Chen, the study’s lead investigator.

In phase one of a two-phase reprogramming process Chen’s team spurred Müller glia in normal mice to divide by injecting their eyes with a gene to turn on a protein called beta-catenin. A few weeks later, in phase two, they injected the mice’s eyes with factors that encouraged the newly divided cells to develop into rod photoreceptors.

The researchers found that the newly formed rod photoreceptors looked structurally no different from real photoreceptors.  Additionally, synaptic structures that allow the rods to communicate with other types of neurons within the retina had also formed. To determine whether the Müller glia-derived rod photoreceptors were functional, they tested the treatment in mice with congenital blindness, which meant that they were born without functional rod photoreceptors.

In the treated mice that were born blind, Müller glia-derived rods developed just as effectively as they had in normal mice. Functionally, they confirmed that the newly formed rods were communicating with other types of retinal neurons across synapses. Furthermore, light responses recorded from retinal ganglion cells — neurons that carry signals from photoreceptors to the brain — and measurements of brain activity confirmed that the newly-formed rods were in fact integrating in the visual pathway circuitry, from the retina to the primary visual cortex in the brain.

Chen’s lab is conducting behavioral studies to determine whether the mice have gained the ability to perform visual tasks such as a water maze task. Chen also plans to see if the technique works on cultured human retinal tissue.

This is a fascinating development and one that we will definitely be following.

To read the original article in its entirety, click here. https://www.sciencedaily.com/releases/2018/08/180815130544.htm

Eye exams may one day predict Alzheimer’s

One day in the not too distant future, it may be possible to screen patients for Alzheimer’s disease using an eye exam.

By using technology similar to what is already found in many eye doctors’ offices, researchers at Washington University School of Medicine in St. Louis have detected evidence suggesting Alzheimer’s in older patients who had no symptoms of the disease.

“This technique has great potential to become a screening tool that helps decide who should undergo more expensive and invasive testing for Alzheimer’s disease prior to the appearance of clinical symptoms,” said the study’s first author, Bliss E. O’Bryhim, MD, PhD,. “Our hope is to use this technique to understand who is accumulating abnormal proteins in the brain that may lead them to develop Alzheimer’s.”

Substantial brain damage from Alzheimer’s disease can occur years before any symptoms such as memory loss and cognitive decline appear. Scientists estimate that Alzheimer’s-related plaques can build up in the brain two decades before the onset of symptoms, so researchers have been looking for ways to detect the disease sooner.

Physicians now use PET scans and lumbar punctures to help diagnose Alzheimer’s, but they are both expensive and invasive.

Previous studies that involved examining the eyes of people who had died from Alzheimer’s had reported that the eyes of such patients showed signs of thinning in the center of the retina and degradation of the optic nerve.

In the new study, the researchers used a noninvasive technique — called optical coherence tomography angiography — to examine the retinas in eyes of 30 study participants with an average age in the mid 70s, none of whom exhibited clinical symptoms of Alzheimer’s.

Those participants were patients in The Memory and Aging Project at Washington University’s Knight Alzheimer’s Disease Research Center

“In the patients with elevated levels of amyloid or tau, we detected significant thinning in the center of the retina,” said one of the researchers “All of us have a small area devoid of blood vessels in the center of our retinas that is responsible for our most precise vision. We found that this zone lacking blood vessels was significantly enlarged in people with preclinical Alzheimer’s disease.”

The eye test used in the study shines light into the eye, allowing a doctor to measure retinal thickness, as well as the thickness of fibers in the optic nerve. A form of that test often is currently available in some optometrist and most ophthalmologist’s offices. In fact, the Mettawa office of Visibly Better Eye Care has the OCT machine needed to perform this test, but as of yet they are not offering this service.

For purpose of this study, however, the researchers added a new component to the more common test: angiography, which allows doctors to distinguish red blood cells from other tissue in the retina.

“The angiography component allows us to look at blood-flow patterns,” said the other co-principal investigator said. “In the patients whose PET scans and cerebrospinal fluid showed preclinical Alzheimer’s, the area at the center of the retina without blood vessels was significantly larger, suggesting less blood flow.”

“The retina and central nervous system are so interconnected that changes in the brain could be reflected in cells in the retina.”

Of the patients studied, 17 had abnormal PET scans and/or lumbar punctures, and all of them also had retinal thinning and significant areas without blood vessels in the centers of their retinas. The retinas appeared normal in the patients whose PET scans and lumbar punctures were within the typical range.

“We know the pathology of Alzheimer’s disease starts to develop years before symptoms appear, but if we could use this eye test to notice when the pathology is beginning, it may be possible one day to start treatments sooner to delay further damage,” one of the researchers said.

To read the original article in its entirety, click here. https://www.sciencedaily.com/releases/2018/08/180823140921.htm

Eye infection in contact lens wearers due to poor hygiene can cause blindness

There are reports of an outbreak of a rare but essentially preventable eye infection that can cause blindness, identified in contact lens wearers in a new study led by UCL and Moorfields Eye Hospital researchers. The research team found a threefold increase in Acanthamoeba keratitis since 2011 in South-East England.

The findings showed that reusable contact lens wearers with the eye infection were more likely to have used an ineffective contact lens solution, have contaminated their lenses with water or reported poor contact lens hygiene. “This infection is still quite rare, usually affecting 2.5 in 100,000 contact lens users per year in South East England, but it’s largely preventable. This increase in cases highlights the need for contact lens users to be aware of the risks,” said the study’s lead author, Professor John Dart (UCL Institute of Ophthalmology and Moorfields Eye Hospital NHS Foundation Trust).

Acanthamoeba keratitis is an eye disease that causes the front surface of the eye, the cornea, to become painful and inflamed, due to infection by Acanthamoeba, a cyst-forming microorganism.

The most severely affected patients (a quarter of the total) have less than 25% of vision or become blind following the disease and face prolonged treatment. Overall 25% of people affected require corneal transplants to treat the disease or restore vision.

Anyone can be infected, but research shows that contact lens users face the highest risk, due to a combination of increased exposure to infection, for reasons not fully established, as a result of contact lens wear and contamination of lens cases.

Alongside these findings, they conducted a case-control study of people who wear reusable contact lenses on a daily basis (although the disease is also associated with disposable lenses), comparing those who had a diagnosis of Acanthamoeba keratitis to those who had come in to Moorfields A&E for any other reason, from 2011 to 2014.

The case-control study included 63 people with Acanthamoeba keratitis and 213 without. They all completed a questionnaire, from which the researchers found that the risk of developing the disease was more than three times greater amongst people with poor contact lens hygiene, people who did not always wash and dry their hands before handling their lenses, those who used a lens disinfectant product containing Oxipol (now phased out by the manufacturer), and for people who wore their contacts while in swimming pools or hot tubs. Showering and face washing while wearing contact lenses are also likely to be risk factors.

Acanthamoeba is more commonly found in the UK than in other countries, likely due to higher levels found in domestic (as opposed to mains) water supplies, so that water contamination of contact lenses is of particular concern in the UK.

The researchers say the current outbreak is unlikely to be due to any one of the identified risk factors in isolation.

“People who wear reusable contact lenses need to make sure they thoroughly wash and dry their hands before handling contact lenses, and avoid wearing them while swimming, face washing or bathing. Daily disposable lenses, which eliminate the need for contact lens cases or solutions, may be safer and we are currently analysing our data to establish the risk factors for these,” said Professor Dart.

To read to original article in its entirety, click here. https://www.sciencedaily.com/releases/2018/09/180921082952.htm

 

Human retinas grown in a dish show how color vision develops

Human retinas were grown from scratch by biologists at Johns Hopkins University to determine how cells that allow people to see color develop.

The research lays the foundation for researchers to develop therapies for eye diseases such as color blindness and macular degeneration.

“Everything we examine looks like a normal developing eye, just growing in a dish,” said Robert Johnston, a developmental biologist at Johns Hopkins. “You have a model system that you can manipulate without studying humans directly.”

Johnston’s lab explores what happens in the womb to turn a developing cell into a specific type of cell, an aspect of human biology that is largely unknown.

Johnston and his team focused on the cells that allow people to see blue, red and green — the three cone photoreceptors in the human eye.

Previously the majority of vision research has been on mice and fish, neither of these species has the dynamic daytime and color vision of humans. So Johnston’s team had to create the human eyes they needed — with stem cells.

“Trichromatic color vision delineates us from most other mammals,” said lead author Kiara Eldred, a Johns Hopkins graduate student. “Our research is really trying to figure out what pathways these cells take to give us that special color vision.”

Over several months, as the cells grew in the lab and became full-blown retinas, the team found the blue-detecting cells materialized first, followed by the red- and green-detecting ones. They found the key to the molecular switch was the ebb and flow of thyroid hormone. Important to note is the level of this hormone wasn’t controlled by the thyroid gland, which of course isn’t in the dish, but entirely by the eye itself.

“What’s exciting about this is our work establishes human organoids as a model system to study mechanisms of human development,” Johnston said. “What’s really pushing the limit here is that these organoids take nine months to develop just like a human baby. So what we’re really studying is fetal development.”

This groundbreaking work can lead to all sorts of applications is the vision deficiency arena.

To read the article in its entirety click here.  https://www.sciencedaily.com/releases/2018/10/181011143112.htm

A common Diabetes medication may actually help prevent development of Macular Degeneration, a common cause of blindness

According to an article published on October 29, 2018 by American Academy of Ophthalmology Researchers from Taiwan have shown that people with type-2 diabetes who were treated with Metformin showed a significantly lower rate of age-related macular degeneration (AMD).The study further suggests that the anti-inflammatory and anti-oxidative effects of metformin can protect against AMD while also controlling diabetes. The research was presented at AAO 2018, the 122nd Annual Meeting of the American Academy of Ophthalmology.

It has been long known that inflammation and oxidative stress play a key role in the development of both diabetes and AMD. Since metformin suppresses inflammation and oxidative stress, researchers in Taiwan theorized that it was possible that the diabetes drug could also protect against AMD, one of the leading causes of blindness in Americans over age 50, currently affecting about 2.1 million people in the United States alone.

The researchers used the Taiwan National Health Insurance Research Database, to collect data on all patients recently diagnosed with type 2 diabetes from January 2001 to December 2013, dividing them into two groups: Those who took metformin (45,524 patients) and those who did not (22,681 patients). After following both groups for 13 years, the researchers found that patients in the metformin group had a significantly lower risk of developing AMD. In fact, half as many patients in the metformin group had AMD compared to the control group.

“Our study is the first to reveal the protective effect of metformin on the development of AMD,” said lead investigator, Yu-Yen Chen, M.D. “While more study is required to determine just how metformin protects against the development of AMD, this is an exciting development for patients at risk.”

AMD is a degenerative disease that happens when part of the retina called the macula is damaged. It’s the part of the eye that delivers sharp, central vision needed to see objects straight ahead. Over time, the loss of central vision can interfere with everyday activities, such as the ability to drive, read, and see faces clearly.

Diabetes is a complex disease that can result from, genetics, environment, lifestyle factors, such as smoking and diet, and involve systemic diseases like heart disease. How the diabetes develops is not fully understood, but researchers have shown that oxidative stress and inflammation play a critical role in the development and progression of AMD. Drusen formation, the earliest clinical finding, has been shown to result from a localized inflammatory response.

The research on Metformin provides a hope that blindness need not be an eventuality for most people afflicted with diabetes.

Read Original Article:  https://www.sciencedaily.com/releases/2018/10/181029102836.htm