Cases of herpes zoster ophthalmicus tripled in 12-year time span, highest among older adults
Michigan Medicine – University of Michigan
Images of the mouse retina with a fluorescent fluid tracer. Diseased blood vessels allow the tracer to permeate nearby tissues. Vessels treated with AXT107 do not allow fluids to escape and exhibit clean crisp borders with surrounding tissue.
Credit: Alexsander Popel
Millions of Americans are progressively losing their sight as cells in their eyes deteriorate, but a new therapy developed by researchers at the University of California, Berkeley, could help prolong useful vision and delay total blindness.
The treatment — involving either a drug or gene therapy — works by reducing the noise generated by nerve cells in the eye, which can interfere with vision much the way tinnitus interferes with hearing. UC Berkeley neurobiologists have already shown that this approach improves vision in mice with a genetic condition, retinitis pigmentosa, that slowly leaves them blind.
Reducing this noise should bring images more sharply into view for people with retinitis pigmentosa and other types of retinal degeneration, including the most common form, age-related macular degeneration.
“This isn’t a cure for these diseases, but a treatment that may help people see better. This won’t put back the photoreceptors that have died, but maybe give people an extra few years of useful vision with the ones that are left,” said neuroscientist Richard Kramer, a professor of molecular and cell biology at UC Berkeley. “It makes the retina work as well as it possibly can, given what it has to work with. You would maybe make low vision not quite so low.”
Kramer’s lab is testing drug candidates that already exist, he said, though no one suspected that these drugs might improve low vision. He anticipates that the new discovery will send drug developers back to the shelf to retest these drugs, which interfere with cell receptors for retinoic acid. Many such drug candidates were created by pharmaceutical companies in the failed hope that they would slow the development of cancer.
“There has been a lot of excitement about emerging technologies that address blinding diseases at the end stage, after all of the photoreceptors are lost, but the number of people who are candidates for such heroic measures is relatively small,” Kramer said. “There are many more people with impaired vision — people who have lost most, but not all, of their photoreceptors. They can’t drive anymore, perhaps they can’t read or recognize faces, all they have left is a blurry perception of the world. Our experiments introduce a new strategy for improving vision in these people.”
Kramer and his UC Berkeley colleagues reported their results this week in the journal Neuron.
‘Ringing in the eyes’
WordResearchers have known for years that the retinal ganglion cells, the cells that connect directly with the vision center in the brain, generate lots of static as the light-sensitive cells — the photoreceptors — begin to die. This happens in inherited diseases such as retinitis pigmentosa, which afflicts about one in 4,000 people worldwide, but it may also occur in the much larger group of older people with age-related macular degeneration, a disease that affects the crucial part of the retina needed for precise vision. The sharp edges of an image are drowned in such static, and the brain is unable to interpret what’s seen.
Kramer focused on the role of retinoic acid after he heard that it was linked to other eye changes resulting from retinal degeneration. The dying photoreceptors — the rods, sensitive to dim light, and the cones, needed for color vision — are packed with proteins called opsins. Each opsin combines with a molecule of retinaldehyde, to form a light-sensitive protein called rhodopsin.
“There are 100 million rods in the human retina, and each rod has 100 million of these sensors, each one sequestering retinaldehyde,” he said. “When you start losing all those rods, all that retinaldehyde is now freely available to get turned into other things, including retinoic acid.”
Kramer and his team found that retinoid acid — well-known as a signal for growth and development of embryos — floods the retina, stimulating the retinal ganglion cells to make more retinoic acid receptors. It’s these receptors that make ganglion cells hyperactive, creating a constant buzz of activity that submerges the visual scene and prevents the brain from picking out the signal from noise.
“When we inhibit the receptor for retinoic acid, we reverse the process and shut off the hyperactivity. People who are losing their hearing often get tinnitus, or ringing in the ears, which only makes matters worse. Our findings suggest that retinoic acid is doing something similar in retinal degeneration — essentially causing ‘ringing in the eyes,'” Kramer said. “By inhibiting the retinoic acid receptor, we can decrease the noise and unmask the signal.”
The researchers sought out drugs known to block the receptor and showed that treated mice could see better, behaving much like mice with normal vision. They also tried gene therapy, inserting into ganglion cells a gene for a defective retinoic acid receptor. When expressed, the defective receptor bullied out the normal receptor in the cells and quieted their hyperactivity. Mice treated with gene therapy also behaved more like normal, sighted mice.
Ongoing experiments suggest that the brain, too, responds differently once the receptor is blocked, showing activity closer to normal.
While Kramer continues experiments to determine how retinoic acid makes the ganglion cells become hyperactive and how effective the inhibitors are at various stages of retinal degeneration, he is hopeful that the research community will join the effort to repurpose drugs originally developed for cancer into therapies for improving human vision.
It’s a new year, and many of us are looking to make positive changes in our lives.
The best way to do that is not by making resolutions, but by creating habits that will stick for the long term. If you want to run a marathon, form the habit of running. If you want to write a novel, form the writing habit. If you want to be more mindful, form the habit of meditation.
Of course, that’s easier said than done — just form new habits, no problem! So, in this guide, I’m going to lay out the key steps to forming the habits that will change your life.
Steps to Creating a Habit
Pick a positive habit. I recommend you find new, positive habits to form, rather than starting with quitting a bad habit. If you want to quit eating junk food … focus instead on creating the habit of eating more vegetables. Good positive habits to start with: meditation, reading, writing, exercise, eating vegetables, journaling, flossing.
One habit at a time. We all have a list of a dozen habits we’d like to change — and all right now! But in my experience, the more habits you do at once, the less likely your chances of success. Even one habit at a time takes focus and energy! Trust me on this: doing one habit at a time is the best strategy, by far, for any but the best habit masters.
Small steps are successful. People underestimate the importance of this, but along with one habit at a time, it’s probably the most important thing you can do to ensure success. Start really small. Meditate for 2 minutes a day the first week (increase by 2-3 minutes a week only if you’re consistent the previous week). Start running for 5-10 minutes a day, not 30 minutes. Eat a small serving of vegetables for one meal, don’t try to change your entire diet at once. Start as small as you can and increase in small steps, only as long as you stay consistent. Small steps allow your mind to adjust gradually and are the best method by far.
Set up reminders. The thing that trips people up in the beginning is remembering to do the habit. Don’t let yourself forget! Set up visual reminders around where you want to remember (ex: in the kitchen, for the veggies habit, or a note on your bathroom mirror for flossing), along with digital reminders on your phone and calendar.
Set up accountability. How will you hold yourself to this habit change when you feel like quitting? Accountability. Join a community or small team to hold yourself accountable.
Find reward in the doing. You won’t stick to any change for long if you really hate doing it. Instead, find some pleasure in the doing of the habit. For example, if you go running, don’t think of it as torture, but as a way to enjoy the outdoors, to feel your body moving, to feel alive. Bring mindfulness to each moment of doing the habit and find gratitude and joy as you do it. The habit will become the reward, and you’ll look forward to this nice oasis of mindfulness.
Try to be as consistent as possible. The more consistent you are, the better. Resist putting off the habit and make it your policy to just get started when you have said you’ll do it, rather than indulging in the old pattern of, “I’ll do it later.” That’s an old habit that you want to retrain by doing it immediately.
Review & adjust regularly. I like to review how I did with my habits at the end of each day, before I sleep. It helps me get better and better at habits. But at the minimum, review once a week (and do a check-in with your accountability team) and adjust as needed. For example, if you forgot to do the habit, adjust by creating new reminders. If you aren’t consistent, maybe set up a challenge with your team so that you pay them $10 each day you miss (for example). Adjusting each week means you’ll get better and better at doing this habit. If you fall down, keep coming back.
Research shows that losing weight can help prevent or delay the onset of diabetes. While best practice for weight loss often includes decreasing or eliminating calories from alcohol, few studies examine whether people who undergo weight loss treatment report changes in alcohol intake and whether alcohol influences their weight loss.
A new study from the University of Pennsylvania School of Nursing (Penn Nursing) suggests that alcohol consumption may attenuate long-term weight loss in adults with Type 2 diabetes.
In the study, close to 5,000 people who were overweight and had diabetes were followed for four years. One group participated in Intensive Lifestyle Intervention (ILI) and the other in a control group consisting of diabetes support and education. Data showed that participants in the ILI group who abstained from alcohol consumption over the four-year period lost more weight than those who drank any amount during the intervention. Results from the study also showed that heavy drinkers in the ILI group were less likely to have clinically significant weight loss over the four years.
“This study indicates that while alcohol consumption is not associated with short-term weight loss during a lifestyle intervention, it is associated with worse long-term weight loss in participants with overweight or obesity and Type 2 diabetes,” says lead investigator Ariana M. Chao, PhD, CRNP, Assistant Professor of Nursing in the Department of Biobehavioral Health Sciences. “Patients with Type 2 diabetes who are trying to lose weight should be encouraged to limit alcohol consumption.”
Summer birth and hours spent playing computer games are linked to a heightened risk of developing nearsightedness (myopia) in childhood, indicates a twin study, published online in the British Journal of Ophthalmology.
Myopia is defined as a refractive error, meaning that the eye can’t focus light properly. The result is that close objects look clear, but distant ones appear blurred.
It can be corrected with prescription glasses, laser surgery, or contact lenses, but the condition is linked to a heightened risk of visual impairment and sight loss in later life.
And it is becoming increasingly common: 4.758 billion people worldwide are likely to be affected by 2050, up from 1.950 billion in 2010.
Genes are thought to have a role, but they don’t fully explain the rising prevalence. And given the rapid development of the eyes in early life, the researchers wanted to explore potential contributory environmental factors across the life course.
They studied 1991 twins whose age was 16.7 years, on average. The twins were all born between 1994 and 1996 in the UK and taking part in the long-term Twins Early Development Study (TEDS).
Opticians provided information from their eye tests about myopia, and the researchers analyzed demographic, social, economic, educational and behavioral factors in the twin pairs from when these children were 2,3,4,7,8,10,12,14, and 16 years old, to capture critical stages of child and eye development.
Parents and teachers filled in comprehensive questionnaires and the twins did web-based assessments to provide a wide range of background and potentially relevant information on factors that might have influenced early life development.
The average age at which children with myopia started wearing glasses to correct the condition was 11. Around one in 20 (5.4%) had a ‘lazy eye’ (amblyopia) and a similar proportion (nearly 4.5%) had a squint. Overall, one in four (26%) of the twins was myopic.
The factors most strongly associated with the development of myopia across the various time points were the mother’s educational attainment (university or postgraduate level), hours spent playing computer games, and being born during the summer.
Hours spent playing computer games may not just be linked to close working, but also to less time outdoors- a factor that has previously been linked to heightened myopia risk.
Educational level has also been linked to myopia, and as children in the UK, born in the summer months, will start school at a younger age than those born during the winter months, the researchers suggest that this earlier close work may speed up eye growth which is responsible for near-sightedness.
Higher levels of household income and measures of intelligence, particularly verbal dexterity scores, were associated with heightened risk, but to a lesser extent.
Fertility treatment seemed to afford protection against myopia and was associated with a 25-30 per cent lower risk. The researchers speculate that children born as a result of fertility treatment are often born smaller and slightly more premature, and may have some level of developmental delay, which might account for shorter eye length and less myopia.
This is an observational study, and as such, can’t establish cause, say the researchers, highlighting that future research may be able to look at the interplay between genetic susceptibility and environmental influences.
In a linked editorial, Drs Mohamed Dirani, Jonathan Crowston, and Tien Wong, of, respectively, the Singapore National Eye Centre, Centre for Eye Research, Melbourne, Australia, and the Department of Surgery, University of Melbourne, point out that environmental factors are now thought to have a greater role than genetic ones.
They add that the study involved data gathered before the explosion in digital media.
“The rapid adoption of smart devices in children adds a new dimension to how we define and quantify near-work activity,” they write…The role of smart devices, quantified as device screen time (DST) must also be investigated.”
As children start using these devices at an increasingly younger age. “The increased DST resulting from gaming, social media, and digital entertainment has led to a rise in sedentary behavior, poor diet and a lack of outdoor activity,” they suggest.
They conclude- “The use and misuse of smart devices, particularly in our pediatric populations, must be closely monitored to address the emerging phenomenon of digital myopia”
Story Source: Materials provided by BMJ. Note: Content may be edited for style and length.