"Age-related Macular Degeneration: Answers to All Your Questions"
Transcript of Teleconference with Adam S. Wenick, MD, PhD
January 27, 2016
1:00 – 2:00 p.m. EST
Please note: This Chat was edited for clarity and brevity.
GUY EAKIN: Hello everyone, welcome to our monthly BrightFocus Chat, presented by the BrightFocus Foundation. My name is Guy Eakin; I am the Vice President for Scientific Affairs for BrightFocus. Happy New Year. And thanks for joining us for the first Chat of the year 2016.
With the New Year, we are going to try something new and dedicate the entire Chat to answering questions that you have submitted, both for this Chat as well as some of the questions that were submitted during previous Chats that we were not able to get to on the call. Of course, you can still submit questions during today’s call, and I will be providing that information shortly and will be repeating it throughout the call.
With that, I’d like to welcome our featured speaker to the call today. We have Dr. Adam Wenick, who is an MD, PhD at the Johns Hopkins Wilmer Eye Institute, so he’s active in research as well as patient care there.
So, Dr. Wenick, welcome to the Chat. We are so glad you agreed to join us for the topic and so grateful for the friendship of you and your colleagues. Why don’t you say a little bit about what you do in your professional life, and we will take it from there.
ADAM WENICK: Well thank you, and thank you for having me, Guy. I’m an assistant professor of ophthalmology and primarily see patients in the clinic, but I do have some research time. I see patients with any retinal disorder, but one of the most common conditions is age-related macular degeneration (AMD) just because, as our population is getting older, we do see more and more age-related diseases such as this. We—both myself and my colleagues—are doing some exciting research at Johns Hopkins: kind of later stages of research with medications that are almost ready to be in clinical use, as well as to the really early stages of understanding why macular degeneration happens.
GUY EAKIN: Well thank you so much, we certainly appreciate everything you’re doing for the community and your participation on our call today. So the challenge ahead of us is that we have this Chat every month, and we have them on a specific topic usually, and we always collect some extra questions that are important questions but not quite on the topic of the Chat of that month. So we have a surplus of questions that we want to address today, as well as some people who are going to be calling in and asking questions that are new. But let’s get right into it. And I want to ask, let’s do a little bit of background: so in your view, what defines AMD and, with that background, the first question we have is Sue from Michigan asking, is it hereditary?
ADAM WENICK: Right, so I think the most important thing in the beginning—and I do this with any patient of mine that comes in, either with AMD or a suspected diagnosis of this—is to just understand the terminology, because that’s where I think a lot of the confusion comes in. So the macula first of all is not a specific disease. There are a number of conditions, such as epiretinal membrane and macular hole, that affect the macula, but they are not this condition, age-related macular degeneration, which is often shortened to macular degeneration. There are other conditions that can be thought of as macular degeneration in a generic sense.
So what I consider age-related macular degeneration is a condition characterized by the buildup of material called drusen underneath the retina. We think of these as a byproduct of normal vision, and if you look at anyone over the age of 40, we see a couple of these little deposits under the retina. When more of them or larger ones accumulate than a certain amount, that’s when we call it this condition, age-related macular degeneration. So anyone under 50 might have a problem with the macula, but it’s not this specific condition, and if these deposits under the retina are not present, again, it’s a different condition that could affect that part of the retina.
The macula is the part of the retina that controls our fine vision for driving, reading, threading a needle, or anything else that requires us to see in fine detail. Symptoms can occur from anything affecting that part of the retina without it being age-related macular degeneration, and that would be a blurring and a loss of central vision. In terms of genetics, there is a genetic component to it. It’s not as strong an association as inherited diseases, such as cystic fibrosis for instance, where if both parents have a copy that one in four children could have this condition, but family history does increase the risk by about 50 percent that you could have the condition.
GUY EAKIN: Thank you. We are going to be breaking the disease down into some component parts. For the clinician, you may have some different words, but in the patient community we will be talking about what we might refer to as wet and dry forms of the disease, and one of the most frequent topics is about that wet form. So let’s start with a question from Sandy from Florida, who would like to know if patients ever see reversal of symptoms after receiving treatment for wet macular degeneration.
ADAM WENICK: That’s a very good question. When we are getting into these questions on treatment of wet macular degeneration, I think the other important thing to frame is just what to expect with treatment. So this question gets to that, and I’ll expand to that a bit further. The treatments that we have now are dramatically better than anything we had 10 years ago, so that’s the most important thing. We do need to think of it as a treatment, though, and not a cure—so repeated treatments, which are injections, don’t mean that things are going badly. That’s par for the course: just as someone with diabetes needs to take insulin to keep the blood sugar under control, with wet macular degeneration, often continued injections are needed.
In terms of treatments, about 1 in 3 patients in the landmark studies looking at these medications saw improvement in vision, and that was just defined as reading on the eye chart that improved more than 3 lines on the eye chart in the doctor’s office. About 1 in 3 got better; a greater number had improved than otherwise. There can be improvement in symptoms such as distortion as well, which are common with the condition. Larger numbers of patients just don’t show any further decline, so a small number do see improvement—or not even small but a sizable minority see improvement, but if no improvements are happening, it still means that the treatment could be working as expected.
GUY EAKIN: That gets into a conversation about the course of treatment and the maintenance of those injections. James from Illinois, who just got started on Lucentis, had a question about the protocols that the eye provider is using and was asking about monthly doses versus the as-needed. So maybe the doctor just gives an injection any time that they feel that the patient looks like they would benefit from one. So what does that mean, and what is the research out there telling us about that monthly dosing, or what might be called PRN dosing, which is the physician’s way of describing the as-needed?
ADAM WENICK: The idea behind monthly dosing, to begin with, came from the early-phase trials in humans as well as experiments in animals—and this was for ranibizumab, Lucentis initially, which was the first of these to be approved for use in the eye. For the first very effective one, it lasted about a month in the eye, so at the beginning of the trials—they were called MARINA and ANCHOR (all of our trials in ophthalmology tend to have acronyms that are somewhat related to each other)—the idea was to see what the best-case scenario was for these treatments. So in the original trials that lasted for 2 years, patients were treated every single month, regardless of what was going on with the retina, for a 2-year period.
Now, when we try to put this into practice, for a number of reasons it can become difficult. Either it’s inconvenient to come in that often, it’s not pleasant to get these injections—though most people are happy to get them if they are helping—but for a number of reasons, we’ve tried to decrease the treatment burden that’s there.
The very first thing that was tried, they were given every 3 months—again, regardless of what was going on with the retina—and in that experiment things really didn’t go well. Patients had a greater decline in vision if they were just given every 3 months. So the next thing that was tried, and many of us had been doing this in our practice anyway, was to look at treating when we saw evidence that there was active leaking from blood vessels on the types of pictures in the office. We all thought this was working well, and that was actually validated in another clinical trial that was at least very close, that treating as needed when we saw disease activity was as good as treating every month. That still requires monthly or close to monthly visits, but not necessarily an injection on every single visit.
The average patient undergoing treatment like this who is on an as-needed basis rather than getting one every month ends up getting about 8 injections a year, so that’s still quite a few. And again, some people need 2 or 3, some people still need 1 every month, but treating that way seems to be as effective.
GUY EAKIN: Well along that theme, Bernice from California is wondering—you mentioned Lucentis, but there is a group of anti-VEGF treatments—Lucentis, Eylea, Avastin—how do these differ from one another? I know that some of those differences are along the timing of the dosing.
ADAM WENICK: The most important thing about all of these is that they are all very, very effective. The differences between them require studies with thousands of patients to see a little difference. They are all highly effective. At a molecular level, they can be somewhat different; the most similar to each other are Lucentis and Avastin, which are made by the same company. Avastin is actually a colon cancer drug that’s not approved by the FDA for use in the eye, but it was the first in this class of medications that was around. The company—Genentech—that makes this modifies things a little bit for use in the eye, and that was the drug, Lucentis, that was used in the clinical trials, and it was through the clinical trials that it gained approval.
We have data on the comparison between those from a clinical study called CATT, Comparative Anti-VEGF Treatment Trials. Again, anti-VEGF is this class of medicines. VEGF is a molecule in the body and in the eye that induces new blood vessel growth; in this study, there was no significant difference seen when Avastin or Lucentis was given every month. It wasn’t clear that Avastin was as good, or maybe not quite as good when it was given in an as-needed regimen. I think for most patients it’s probably similar, but it’s a little bit more of a gray area there.
Eylea is the newest of these medicines, and again, it blocks that same factor. It was compared in a trial to Lucentis, and it was compared to Lucentis given every month and then different regimens with the Eylea, so either given every month or given three doses and then given every 8 weeks. Those results seemed to be fairly equivalent. Eylea does have a longer half-life, meaning it does last a little bit longer in the eye. The 8-week treatment schedule isn’t necessarily the best for every patient, so if there’s a lot of fluid at the 4-week point, in my view it’s better to treat it. And if we look at the number of treatments per year with an as-needed Lucentis regimen versus the every 8 weeks, after the initial 3 weeks we still end up with that around 8 injections a year. There are small differences. They all work quite well.
GUY EAKIN: We are certainly glad to have each of them. Let’s move on to the next question. Marilyn from New Hampshire is concerned about, in her case, some scar tissue that’s forming after injection. She is asking how to balance those risks that come with those medications versus the benefit of the medications. So what are the side effects that we might see from repeated injections? Can we have too many injections? How do we manage our expectations about what’s going to happen with these drugs?
ADAM WENICK: Differentiating types of scar tissue I think will help answer this question. My impression from how she’s worded the question is that perhaps at the site of injection it is becoming a little more uncomfortable. Some patients do note that, other patients can have repeated injections, and now that we’ve had these treatments for 7 or 8 years, some patients have gotten 50, 60 more injections and don’t seem to have more problems with further injections. There’s also scar tissue that can form underneath and affecting the retina that these treatments do nothing but decrease the incidence of that scar tissue. The scar tissue that can steal vision away will increase without treatment.
In terms of how effective they are, again, over a 2-year period, about 90 percent of people keep their vision, and about a third of people get some improvement. This is the best data we have, actually treating frequently, so every month or whenever we see the littlest bit of fluid. The data that we have going out more than 2 years—we have some data out to 7 years—becomes less clear because fewer patients that were well-studied were followed out that long. What we see at 7 years is that about 40 percent of people continue to do very well and about 30 percent of people become legally blind, but people that did well actually had far more injections than the ones that didn’t do well. It’s not clear if that’s because of more frequent injections or what made the difference, or if the patients that didn’t do well stopped getting the injections because it was felt that they wouldn’t be helpful anymore.
The only concern about frequent injections that’s been raised is that there’s maybe an increased risk of atrophy or loss of retinal tissue—which can also lead to decreased vision—with these treatments. I think the jury is still out on whether that’s a real concern or not. Even if it is a real concern, the alternative—which is not treating—tends to take vision away faster, so really, more treatments seem to be better. There are the rare complications, such as infection in the eye or retinal detachment, which also have to be considerations. By far people do better with continued treatments.
GUY EAKIN: I’m sure some specifics are a conversation to have with your eye care provider.
Let’s complement what we’ve been talking about so far by moving on to the dry form of the disease, and this is the more common form: it’s perhaps affecting as many as 9 million people in the U.S. The wet form is a bit rarer, certainly severe, but, you know, 2 million people, so that’s a sense of scale. We have a question from Carol from Ohio who says that she has soft drusen in both eyes and has been warned about that dry AMD turning into wet in the future. How long does that take? Is there a specific timeframe that people should be concerned about?
ADAM WENICK: A lot of this has to do with the individual appearance of that person’s eye. If we look at all the risk factors for vision loss for macular degeneration—if you look at smoking, which is clearly a risk factor, genetics, age is obviously a risk factor—by far the most important risk factor is the appearance of the retina.
The other important thing to know is that most patients who have drusen never end up with vision loss. It is because so many people that have the condition, there are a lot of people that have the forms of it—either advanced dry macular degeneration or wet macular degeneration—that do lead to vision loss.
There was an NIH-sponsored study called the Age-Related Eye Disease Study, or AREDS, and people will see this on some of the eye vitamins, those letters, and that is what it stands for. From that, looking at patients at the beginning of the study and then seeing who developed either vision loss from dry macular degeneration or who developed wet macular degeneration, it was based on whether there were pigment changes in the retina and based on whether—what we would consider to be large drusen. We base the size of drusen on how they look on our exam, and that is something that your eye doctor should be able to tell you. They should be able to look in the eye and say, “This is what I see,” and the scale is called the AREDS Simple Scale for Risk. That can range anywhere from a 1-percent risk over 5 years of getting macular degeneration to a 50-percent or greater risk, based on how the back of the eye looks. That is a very important thing to talk to your eye care provider about.
GUY EAKIN: I want to take a moment—certainly that AREDS Simple Scale for Risk might be something that is a little hard for people to remember. We will have a large print transcript of this and all of our other Chats available.
One of the questions that came in from two people, both from California—Ruth and Darlene are asking a question about risk. In this case, they have AMD in one eye and were asking about the risk of it progressing to the other healthy eye. What can you tell them about the chances of that happening over time?
ADAM WENICK: Again, having wet macular degeneration in one eye is a risk factor that will increase the risk of getting it in the other eye. Still, the most important factor is what that other eye looks like. The increase in risk from having it in one eye is about a twofold change. If the other eye really does not look that affected, the risk remains quite low. However, if there are changes that would put you farther along in that Simple Scale, the risk could be significant. That is certainly important to watch more closely. See someone every 6 months and have them look at that eye to make sure that wet macular degeneration isn’t developing and, again, asking your eye care provider what that other eye looks like. Does it look similar to the other one before I got wet? Or does it really look much milder?
GUY EAKIN: You hinted here at monitoring the progression of the disease. You can certainly do that at home. Joanne from Florida is asking, “If I notice distortion on my Amsler grid, what does that mean? Is all hope lost then?” I think we started to get into the treatments, but maybe the question is, what do you do when you do notice changes in an Amsler grid? Are there other technologies beyond the Amsler grid that we can use for at-home monitoring of the disease?
ADAM WENICK: There are a number of ways to monitor things in between visits. Some type of monitoring should definitely be done. We are still trying to figure out what the best thing is to tell patients. With any type of monitoring—and I will go through some of the older and newer options—the most important thing is, if there is a change, to be seen quickly. Now, quickly doesn’t mean to be seen at 4 in the morning if you notice it at 12:00 at night. We usually say within a week. If we catch people within a week of developing wet macular degeneration, which would be one concern with distortion on the grid, earlier treatment is better. We have great evidence that people do much better the earlier we can treat things.
Distortion can be caused by a number of things. The most concerning thing would be wet macular degeneration, but even a progression of the material—the drusen under the retina—can lead to these symptoms. We wouldn’t do anything differently if drusen were causing the symptoms, because we don’t have treatment for drusen per se, but it is very important to make sure it is not wet macular degeneration that has developed, which we do have very effective treatments for. In addition to the Amsler grid, which is often recommended—and for those of you who don’t know what it is, it looks like a piece of graph paper that you look at to see if any lines are missing or bent or twisted, and you look with each eye separately. Sometimes the Amsler grid itself either misses things or can find things that aren’t really there. I personally don’t recommend it that often. I find some people drive themselves crazy looking at it. I do recommend just that people look at one eye separately and either read or look at a picture or tile floor and see if anything looks different.
Some newer technologies coming out that have been shown to be effective—there is a home monitoring device called Foresee. It was actually validated in a clinical trial to pick up macular degeneration sooner. That is one thing that could be discussed with your doctors to see if they know more about that or if it is available through them. It doesn’t work for everyone. Some patients, their eyes are such that they can’t use it, but it may pick things up earlier and lead to better outcomes.
GUY EAKIN: Okay, well, it’s about time to move on. We have many questions coming through about nutrition and about all of the vitamin supplements. As an example, we have Melanie from Colorado asking a simple question, “How important are the eye vitamins, and do you need to take a name brand?” So what can you tell us about the role of supplementation and the need in preserving your vision?
ADAM WENICK: The best data we have on this come from the AREDS Study. Patients in this study that had drusen and various degrees of drusen were either given supplements or not. We will get into which supplements we recommend, but they were only effective in patients that had a large number of these drusen. So even in the early stages of macular degeneration there wasn’t any benefit from these vitamin supplements. Part of that is that they are not actually designed to improve them. Taking them will not actually make your vision better. They don’t slow down the accumulation of the drusen material or the progression of dry macular degeneration either, but they seem to decrease the risk of developing wet macular degeneration. It does so by about 25 percent.
If we go back to the Simple Scale, and if you are at the end of the spectrum where risk is at about 1 percent and decreasing that to slightly less than 1 percent, it is maybe not so important to be taking them. However, if you are at the other end of the spectrum where the risk is at 50 percent or greater, then that is a significant change in the amount of vision loss that is likely by taking these supplements.
The original study looked at a combination of beta-carotene, which is a form of Vitamin A, and then Vitamins C and E, zinc, and copper—which is present to prevent lack of absorption from zinc—and that was the original formulation. For patients with at least intermediate dry macular degeneration, there is a benefit to taking those supplements. For people over the age of 50, or younger than 50 who don’t have the actual disease or don’t have an advanced stage of the disease, there is no proven benefit to any of these. So that was the original formulation.
In a later study, called the AREDS2, the addition of two other carotenoids called lutein and zeaxanthin, which are found in high levels in green leafy vegetables, were also added to that or used rather than the other form of Vitamin A, the beta-carotene. There was no added benefit of taking them both together, and the lutein and zeaxanthin seemed to do at least as well as the beta-carotene with fewer side effects. One concern with beta-carotene, especially in patients who are current smokers and perhaps with people who used to smoke, is there is a slightly increased risk of lung cancer. One important point with the supplements is if you smoke, you should not have the beta-carotene in the supplements.
The other thing looked at in the AREDS2 study—and I think this gets to another question that someone had sent in—is fish oil. From some dietary studies, asking people with and without the disease what they ate and that fish oil might be helpful, we actually found it wasn’t helpful when it was given in pill form in the study. They can be effective by reducing the risk of wet macular degeneration, but the only ones we have evidence for are the exact formula that was in this study.
Patients come in bewildered about all of the different choices that they have. What I tend to do is print up the version of what was actually used in the study. I tell them, I know that PreserVision, the AREDS2 formula that Bausch + Lomb makes, is what was tested in the study. Some people say, “Well do I have to get these?” And I say, no, you don’t have to get these, but you have to get something that has these ingredients in it. If you find another company that has exactly this, these amounts, that’s fine. If it’s something different, well, it may be effective, but we just don’t know. It hasn’t been looked at.
GUY EAKIN: For anyone curious, we would be happy to share with you that formula for the AREDS2 vitamins. There was a news article out, an academic publication, a couple months ago saying that you do need to be careful, that some of the vitamins, even though the label says AREDS, they may not have the exact AREDS formulation. So I think that definitely you should check the label, and we would be happy to give you something to compare against.
ADAM WENICK: I think that the other thing that’s helpful is to bring what you’re taking in with you to your appointments, because I’ll also have people come in and they say, “Oh, is this ok?” Just having that bottle there with you with the ingredients makes it so much easier to know what you are actually taking.
GUY EAKIN: Wonderful advice. So we do get just tons and tons and tons of questions about other supplements and some of the things you covered a bit, but maybe could we ask a question—I think you’ve identified what we know about supplementations for AMD specifically, but are there nutrients or supplements or general dietary practices that would be beneficial just to overall eye health as opposed to specifically for macular degeneration?
ADAM WENICK: We actually don’t have a tremendous amount of data on this. A number of supplements are recommended—again, just for people over 50—some of the companies recommend certain supplements. We don’t have great evidence for this, and the vast majority of the things that are good for the eye can be obtained in sufficient amounts just with a well-balanced diet. We think occasional fish and green leafy vegetables—unless there’s a reason because of medication interactions, such as Coumadin, that you can’t have green leafy vegetables—most of these things that are good for general eye health are plenty abundant in green leafy vegetables, such as kale, spinach, collards, mustard greens, things like that. That’s really the only recommendation that we have for general eye health.
GUY EAKIN: Well we always have a group of questions coming in about clinical trials that are going on, and one of them that’s near and dear to our heart, there was a report about the possibility of L-Dopa being useful for macular degeneration. Now, that was a study that was published from a review of medical records, and it hasn’t gone to clinical trials yet, but if there’s anything you would like to say about L-Dopa, I would love to hear it. In general, what’s the role of a clinical trial, and how does a patient get into a clinical trial or find out about them?
ADAM WENICK: In terms of the L-Dopa study, what was done there was very interesting and very exciting, but always before we actually begin treating patients with anything, we like to do well-controlled trials where some patients are getting medicine and others aren’t, or some patients are getting one medicine and some patients are getting a different medicine to know (1) if it’s effective and (2) that we aren’t doing harm by any of these things. So clinical trials have really been critical to all of the current treatments that we have now, and they continue to be critical as new treatments are developed. And there are a number of things in the pipeline that, if we have time, we can go through what some of these are.
GUY EAKIN: Maybe give us an example of one or two, if you have time.
ADAM WENICK: The very first thing is to see an eye doctor to see exactly what you have. Many of these trials, it depends on exactly what version of the condition that you have. If we know what you have, then you can go to either an academic center, or many private practices are involved in some of these later-stage clinical trials. There are plenty of ways to get into some of them.
I think the very next thing on the horizon—it’s somewhat lower-hanging fruit—is for wet macular degeneration, which is just having things that last longer, so rather than needing this monthly—or as-needed but potentially as often as every month—we may have some treatments soon. There are some phase 3 medicines that may last as long as 3 months. There is another implantable device that’s in an earlier-stage trial that could also give a much longer duration of action. That’s exciting, that even if the final outcome isn’t better, that we might be able to see patients every 3 or 6 months, or even longer, rather than monthly with monthly treatments.
Wet macular degeneration is caused by growth of blood vessels that shouldn’t be growing or leaking, and many of the other new treatments for wet macular degeneration focus on other factors, so VEGF, which is what all of the current medicines target, is just one part of why abnormal blood vessels grow.
There are other phase 3 trials that target platelet-derived growth factor, which is another important factor that could potentially—in addition to the current treatments—give better results.
Turning to the dry side of things, there is a medicine that modulates the part of the immune system that’s also injected into the eye—it’s called lampalizumab—that’s in a phase 3 or final stage trial that may slow down the progression of geographic atrophy, which is the loss of retinal tissue that causes loss of vision and advanced dry macular degeneration, and that’s an ongoing trial.
One of the very exciting things, but really in its infancy, that I get asked about are stem cells. Stem cells now are being used not to replace the retinal cells themselves. The retina is the light-sensitive layer that does the seeing, but one of the tissues affected in macular degeneration is the retinal pigment epithelium cells, which are underneath the retina; they support and keep the retina healthy. They both need to be working well for the retina to work. Stem cells are actually affected likely sooner than the retinal cells in macular degeneration. Those could possibly be replaced after they’ve died. If this does work, we will just see the slowing down of the process. If we look at the 5, 10, 15 year horizon, there is some hope that some of these treatments could be restorative as well.
GUY EAKIN: We are moving on. We have talked a fair amount about medicine, nutrition, and behavior. We just conversed about clinical trials. There are certainly some resources like clinicaltrials.gov that are online that can help you find out what clinical trials might be recruiting in your area. If you call into BrightFocus, we would be happy to explain some of those, how to navigate that website, if you should need that help. But there’s a great question that came from Bari from Maryland. Bari is saying that the mindset with the majority of patients diagnosed with age-related macular degeneration is that they’ve been told that nothing more can be done beyond those medicines and the things we’ve talked about today. He says he’s pleased to say that, in his life, he’s found wonderful options that are available so that people can experience enhanced vision with new technology or other options and just have a better quality of life outside of modifying the actual disease. He’s asking about how we can be more proactive in informing patients that options exist.
What I’m hearing in Bari’s question are some references to what we might call low vision services, and we certainly feature experts in that field on these chats. Dr. Wenick, how does low vision therapy feature into the advice that you give patients?
ADAM WENICK: I think it’s really critical. I’m practicing in the D.C. area, and we often see patients who have gone to not one but several other doctors. I’m always disheartened when someone comes in and is told, “Well, they told me there’s nothing else they could do,” because that’s far from the truth.
It’s true that I may not be able to do anything to make the retina work better, but that doesn’t mean that there’s not something that can make people see and function better. Going to a low vision specialist is a critical step in the door to really learn about the different things. They have a tremendous amount of experience from their training, and they pick up tips that other patients have told them that work for them, really just learning the best way to get the most out of the vision, either from magnifiers or new technologies with text recognition that will read the words back to you. For instance, in the grocery store you could shine it at a word and it whispers the price to you or what the label says.
Losing vision from macular degeneration doesn’t have to be the end of your life and doesn’t even have to be the end of what you can do to see; there are many options out there. I find that one of the most important things that we can do for patients—and low vision therapy also is not just for people who are legally blind—anyone whose vision is less than perfect from any eye disease. A lot can be done to improve things. I think in a lot of ways the name “low vision” is an unfortunate name and doesn’t have to be thought of that way. I tell my patients it’s like seeing a physical therapist—that if your surgeon gives you a knee replacement, you need to learn how to use that knee that again, and the physical therapist can help you do that.
GUY EAKIN: So I heard in that last statement that perhaps the way to find out about low vision therapy services in your community would be through a referral through your eye care provider.
ADAM WENICK: I think that’s one of the easiest ways. I think also you can just either go online or have someone help you, and you can search for one. I think you could even find it in the phone book. The term is “low vision.”
GUY EAKIN: I’d like to make a comment that this is part of BrightFocus’ mission—to build awareness about different services that exist—so, some of the technologies that you described, we have quite an extensive body of information on our own website. And, of course, if you would rather not communicate through a computer—many people prefer just to pick up the phone—you can always call us at 1-800-437-2423.
Thank you certainly to Dr. Adam Wenick from the Johns Hopkins Wilmer Institute for taking the time for speaking with us today, and thank you to everyone who joined us on the call and asked all these questions. Within about a week we will post a recording and a transcript of the call on our website. You can also listen to and download our past chats on iTunes or SoundCloud. Our next chat will have the topic of “Tips for Maximizing Doctor Visits,” and that will be on February 24, 2016. We encourage anyone to register now and to submit questions in advance. If you were registered for this call, we will also be sending you a reminder email about the next call.
You can always call BrightFocus at 1-800-437-2423 or find any of our resources at our website, www.brightfocus.org. So again, thank you to Dr. Adam Wenick for taking the time to talking to us today, and thank you to everyone who joined the call.
The information provided in this transcription is a public service of BrightFocus Foundation and is not intended to constitute medical advice. Please consult your physician for personalized medical, dietary, and/or exercise advice. Any medications or supplements should be taken only under medical supervision. BrightFocus Foundation does not endorse any medical products or therapies.
Useful Resources and Key Terms
BrightFocus Foundation: 1-800-437-2423 or visit us at www.brightfocus.org. Available resources include:
Clinical trials information: www.clinicaltrials.gov.
Possible treatments discussed
- Anti-VEGF therapies (Lucentis, Eylea, Avastin)
- L-Dopa, a drug for Parkinson's disease that seems to reduce the incidence of AMD in Parkinson's patients
- Adult stem cells
- AREDS and AREDS2 vitamins
This content was last updated on: August 8, 2016