What You Need to Know about Wet Age-Related Macular Degeneration

BrightFocus Foundation
What You Need to Know about Wet AMD
Transcript of Teleconference
June 24, 2015
1:00 – 2:00 p.m. EDT

Please note: BrightFocus Chats may be edited for clarity and brevity.

GUY EAKIN: Hello, everyone, and welcome to our monthly BrightFocus Chat, presented by the BrightFocus Foundation . My name is Guy Eakin; I’m the Vice President for Scientific Affairs at BrightFocus. Today we are delighted to talk again with Dr. Michael Gorin, who is an ophthalmologist at UCLA, who is devoted to research and clinical care of hereditary retinal disorders, and we know that age-related macular degeneration (AMD) is a condition that is certainly influenced by genetics. Dr. Gorin is also part of the BrightFocus family as a previously funded researcher who studied the genetics of AMD and is also a volunteer reviewer for a grants, and, as I alluded to earlier, now twice a speaker on this chat program, having served as a speaker on our very first BrightFocus chat. So Dr. Gorin thank you so much for joining us again today.

MICHAEL GORIN: Oh it’s my pleasure, it’s an honor to be able to address so many people and answer their concerns and questions.

GUY EAKIN: I thank you for joining us, and before we get on the call, I’d like to mention that if you have any questions you’d like to ask Dr. Gorin, just press *3 to submit your question to an operator, and if for any reason you’re disconnected from the call there is a number to call back in: that number is 877-229-8493 and you’ll be asked to punch in an ID code, that would be 112435. Again, that ID code is 112435 and the phone number is 877-229-8493. So, Dr. Gorin—as you probably recalled, we host these chats on a monthly basis and the topics vary. We will cover clinical topics like we are today, as well as chats about research and living with low vision, but no matter the topic, we always receive questions about today’s topic, which is wet macular degeneration. We receive lots of questions about what are the current treatment options, about the progression from dry to wet macular degeneration, and about predicting the future of our own health as well as predicting the future of what’s coming down the pipes in terms of research. We are tremendously happy to see you back and we hope we will bring your understanding of the disease to everyone who is listening. So before we get into that long list of questions that people have submitted, would you provide us with a basic description of what wet macular degeneration is, and is that even a good description of it, wet macular degeneration?

MICHAEL GORIN: Well it is a very commonly used term, and there are other terms that professionals use to describe that form of age-related macular degeneration. Let’s take a step back and I’ll get us to understand that distinction. So, age-related macular degeneration used to—unfortunately—have the poor name of senile macular degeneration, but we dropped that, because people who have this have no reason to believe they have a senile process. But age-related macular degeneration is associated with getting older, but not necessarily present in everyone who is aging, and it represents a degenerative process in the back of the eye that affects the function of the retina, which is essential for you to detect light and send a signal to the brain so you can have informed vision.

We understand a great deal more in recent years because of the genetics studies that have been done. We know that there is a component of inflammation that goes on in the back of the eye that triggers the formation of deposits and damage to the cells that take care of the retina. This layer of cells—that take care of the retina—is called the pigment epithelium, and they can build up deposits of proteins and lipids, and you will hear your doctor refer to them as bruising. This material is actually sort of an inflammatory focus, a little bit like having an athermanous plaque in a blood vessel. So, over time, what happens is that there is cumulative damage that occurs, and for some people their macular degeneration may simply be the accumulation of more of these deposits and damage, and that’s all they go to. But for a group of patients, it can diverge into two different paths of progression. One is where the cells that care for the retina begin to die and you start getting areas of atrophy—that is, cell loss—and on those areas of cell loss, you lose areas of vision. And that’s called atrophic, or advanced dry macular degeneration. That’s usually slower, but it can be very problematic for people, because it can create little holes in their vision and ultimately, if those holes get larger and coalesce, one can lose central vision from that. The second pathway—and by the way, they are not mutually exclusive, some people can have both of these things going on—is because of the damage to the cells underneath the retina, it triggers the formation of a blood vessel, either a blood vessel underneath the retina or sometimes even in the retina. That blood vessel is an abnormal growth; it’s not a tumor or a cancer, but it’s a blood vessel that’s stimulated to grow, and it unfortunately leaks and can bleed, and because of that leakage and bleeding, you get the term “wet,” because the fluid is leaking into the retina. Over time, that accumulation of blood and fluid disrupts not only the architecture of the cells, but can lead to fairly rapid vision loss. So, wet macular degeneration treatments at this stage are really focused on trying to prevent the ongoing growth and leakage of these abnormal blood vessels. The treatments do not stop the underlining degenerative process or the causes of macular degeneration in the first place. A person who is having successful treatment of the wet form of macular degeneration is really not having their macular degeneration stopped. The treatment is blocking and limiting the amount of damage that occurs.

Now, we will talk—I guess in a few minutes—about the treatments for wet macular degeneration. For right now, all the treatments are focused on stopping these abnormal blood vessels from growing. In the old days, before we had the injections that we talk about now, and the medications, we used to try to use laser to essentially cauterize these abnormal vessels, kind of like using a flame thrower to destroy the weeds in your driveway, but obviously we’ve come a long way. Now, we can preserve a lot more vision with the treatments we have. I will stop at this point.

GUY EAKIN: I think you’re leading right into the topic that we get so many questions on: What are the current treatments? So many of the people on the line have been receiving treatments for a while, and they have been receiving what their eye care provider has prescribed, but could you tell us what are the most common treatments for the age-related and wet forms of macular degeneration and how they might differ from one another?

MICHAEL GORIN: First of all, the only basic treatment that we have for age-related macular degeneration itself are the AREDS supplements—these are the vitamin and nutrient supplements that were tested by the Age-Related Eye Disease Study (AREDS) that was funded by the National Eye Institute. They had two studies: an AREDS study and AREDS2. Those supplements are the only thing that we know of right now that can slow, but not stop, the progression of underlining age-related macular degeneration. There are companies working on therapies to try to get at the fundamental processes that go on, but there’s nothing really out there yet. But we are optimistic.

Turning to wet macular degeneration, again, all of the treatments are designed to prevent the growth and leakage of the abnormal blood vessels in or under the retina. All of the drugs currently in use are targeted against a specific molecule that is released by the cells as the degeneration process occurs. That molecule that is released is called vascular endothelial growth factor, and it is actually used by the body to stimulate the growth of blood vessels under many circumstances—so it’s not just limited to the eye, it can be used in other tissues as well. Whenever you have an injury and blood vessels have to grow back into that tissue, that factor is released by the tissue in order to stimulate blood vessels to grow. In fact, the discovery of drugs to block that molecule are the result of the work of a scientist who really was focused on using it to stop cancer growth, because cancers, as they grow, have to have a blood supply to feed the cancer or tumor as it enlarges. The scientist developed drugs to essentially prevent that, and that’s where the drug came from that we are using. So, there are currently three major drugs that we are using that we inject into the eye that act as an inhibitor of vascular endothelial growth factor (VEGF). They are Avastin—I’m giving you the brand names, not the generics, which I find are very hard to pronounce, to be honest with you—Lucentis, and Eylea. All of these drugs work basically by very similar mechanisms, binding that particular factor. Now, anybody who knows biology can tell you that nothing happens with just a single molecule being released; any time tissues are stimulated or injured, multiple factors are released and the same thing occurs as the stimulus for blood vessels to grow in wet macular degeneration. So there are other factors, but there is no question that the VEGF is the biggest one and the most important. There are companies that are working on drugs that attack other molecules along those pathways that stimulate vessels to grow, and so we are hoping that in the next few years we will see additional medications available for people where simply attacking one molecule is insufficient.

Now, what are the differences between Avastin, Lucentis, and Eylea, are they identical? Not exactly. Avastin was originally created specifically for the treatment of cancers and it was given systematically—that is, given as an intravenous infusion of drug to go throughout the whole body to inhibit the growth or vessels associated with a person’s cancer, and it’s used for that. When we use it for the eye, we take one of those dosages, and the pharmacy divides it up into smaller dosages that we then use for individual patients. This is when you’ve heard about compounding pharmacies and things like this—these are places that are dividing up these large doses of Avastin into smaller doses necessary to be used in the eye. Because of the pricing by pharmaceutical companies, the actual cost of the small dose of Avastin necessary to treat the eye is very small, on the order of $20-$40, and that’s why Avastin is so much cheaper. It’s not an inferior drug, it was made to be sold in an amount for a charge of several thousand dollars for a single dose for a cancer patient.

Lucentis was developed by the same company, Genentech, but it’s engineered slightly different. The molecule has slightly different components and binds a little bit differently, but overall, multiple studies have found no difference in the effectiveness of Avastin versus Lucentis. There have been efforts to try to show that one may be safer than the other, but quite frankly, I have not found that evidence terribly compelling. There are patients who come to me sometimes that say that Lucentis—which was developed specifically for the eye—they think it may be safer, and so they prefer it. In my opinion, there is really no difference. And the effectiveness of the two drugs is about the same.

Eylea is called the VEGF trap, and it’s a little bit different than Avastin and Lucentis because it’s not an antibody that’s been engineered, but a molecule that’s meant to mimic the receptor for VEGF. So it binds differently, but very strongly, and it binds to more of the forms of VEGF, hence it seems to be not only a bit more potent but lasts longer in the eye, which is why you will see doctors who will use Eylea in patients who fail Avastin or Lucentis, or if they feel that they want to extend the time between treatments. Currently, the recommendations for Eylea are to use it monthly for several cycles—like three—and then to go to up to 2 months. Personally, I don’t use it that way, but many doctors do, and the reason for that is the feeling that it can last a bit longer. There are companies that are working on delivery forms of these drugs to allow one to not have to have an injection every month, and ideally, one would like to see it for at least a 6 month period before you need to be re-treated again. This is being achieved by a number of approaches, including eye drops that might substitute for the injections.

There are also people working on implantable reservoirs that could be refilled—you fill the little chamber up with the drug and it sits there and releases it at a slow, regular rate over a number of months and then gets refilled again. And finally, there are people who are working on a gene therapy approach, where, essentially, they inject into the cells of the retina a virus that contains a molecule that can make a molecule like the drug, and it’s continuously manufactured in the eye for a long period of time, thus achieving essentially long term inhibition of VEGF. Those are some of the things being developed to try and get longer term action.

GUY EAKIN: Well, I was going to say, one of the questions that comes in all the time—we have it coming in again from a couple of different people right now—is about the actual injection process and the questions about the safety of that, how long the injections occur, what is the long term safety of having a needle in your eye injecting these drugs, and what’s the long term safety of the drugs themselves. Do you have any opinion?

MICHAEL GORIN: First of all, I think that those concerns are very understandable, and they are something you should always discuss with your doctor. Most of us believe that these injections and the medications are very safe. I have patients who I have treated with many, many injections over many months, over years, who have tolerated it well. There are potential risks and complications, some people get elevated pressure in the eye from repeated injections, and we are not quite sure why some people do and some people don’t, but that then has to be treated as a new and separate problem.

There are some people who can get bleeding—bleeding on the outside of the eye is not a big deal—which often occurs with these injections, and the little blood vessels on the surface of the eye can bleed. You look terrible, but it’s nothing to worry about. Some people get bleeding in the eye, and usually those are people who have low pressure in the eye when they start—maybe they are an advanced glaucoma patient. Our biggest fear is inflammation or infection in the eye after the injection, and this is why our techniques are developed to minimize the chance of that. There is no way of completely eliminating the possibility of that occurring in somebody, but the steps that most of us have taken have reduced that to a really, really low level. And we try to make sure that all of our patients understand what the early symptoms are, and if they are getting inflammation or infection in the eye to come in so we can promptly diagnose it and treat it.

You’ve asked a question of how long people need injections, and is there a limit on how many people can have. I have people who have had over 50 injections in one eye and they’ve tolerated it well. You might think they would get scarring at the injection site, but we have not seen that as a serious problem, and we do not see them necessarily becoming resistant to the drug. There have been concerns about an increased risk of heart attacks and strokes—quite frankly, we just analyzed the maximum amount of health insurance data about this, and it’s really not all that clear. The people who are at greatest risk for these drugs increasing their risk of heart attack and stroke are people who have already had a heart attack and a stroke. The drugs themselves may increase the risk slightly in most people who are vulnerable, but in general, again, it can be done very safely. I injected a gentleman yesterday who is 103 and he tolerated it very well. He’s been getting injections since he was in his 90s and we’ve been able to preserve sight in his one good eye fairly effectively over the last 8 or 10 years. The original studies showed that patients benefited the most by getting monthly injections over a 2 year period.

Obviously, we have all reached a point of exhaustion, both patients and doctors, so we are all looking for ways of reducing the number of injections that we do without compromising vision, so you will find that your doctor may use a variety of strategies to reduce the total number of injections that you may have to have. I have a particular way that I do it, but others use a treat and extend approach, where once the person shows no activity of their new vessels, those abnormal vessels, they will do an injection and extend the period longer and longer between injections up to a period of 3 months so that the person has no more than four injections in the year. My preference is to inject the person to the point where there is no activity of that vessel, then continue injections for another 2-month period, and if I can show that after 2 months again there is still no activity, I actually stop injections for a period of time and see if the person remains stable. I’ve had some patients go 3 to 5 years without requiring another injection with no loss of vision, while other people only after a few months will start to have a recurrence of the vessel activity and then we start injections again.

GUY EAKIN: Dr. Gorin, this is actually quite interesting. We just had a caller dial in a question. Meryl from Ohio asked a question about PRN, and if there is a difference from AREDS to it? It sounds like PRN is the medical abbreviation for essentially what you’re describing—when we see that acronym, what are we seeing?

MICHAEL GORIN: PRN stands for “as needed,” and I don’t actually follow that exactly, because what I found—if you stop injecting the minute a person doesn’t show any leakage, the risk of the vessel coming back is extremely high. So, what happens is you can find yourself in a position of being chased. The doctor sees you and there’s no leakage, so he says, “Ok, no injection now, come back in a few weeks,” and the person comes back in a few weeks and now there’s leakage, the doctor gives an injection and says come back in a month, person comes back in a month they look dry, he says no injection, then they come back a few weeks later and there’s fluid again, he gives another injection. And what this means is that during that time, the person is constantly getting re-accumulation of fluid for periods of time; ultimately, that causes damage and there’s a risk of bleeding as well. Most patients, if you do it just that way, tend to get a gradual decline in their vision because you’re always allowing a certain amount of damage to occur before you start treating again.

The other problem with that is that you’re constantly having the patient coming in and doing tests. We use primarily optical coherence tomography, or OCT, to do high resolution imaging of the retina to see if there is fluid there—and we also use fluorescein angiography, but the OCT is really the most powerful and least invasive method—but that test then needs to be done over and over and over again. If you’re trying to balance things out, as I said, doctors are trying to find other ways that are a little bit better than PRN—just doing it as needed—because you lose over time. My biggest thing is making sure that I do it at a regular intervals if they do need injections and not letting those injection times get drawn out too long so that they have damage that re-accumulates, and to try to preserve as much vision as possible.

The ones that I see that get into trouble are people and their doctors that get tired of the whole thing and they go, “Well do you mind if I come back in 6 weeks instead of 4 weeks?” or “Listen I was really busy, I missed my appointment, how do things look now?” and you start falling behind and damage occurs. I would urge the people listening that are getting this treatment—I know it’s unpleasant, I know you dread every time you have to go in and I know that it messes you up for at least a day or so as you’re trying to cope with the effects of the injection—not so much pain, but it does distort vision and things of that sort—but I really urge you to try to keep up on the schedule and try to get the best results you can. It’s really dramatic. I’ve had patients who have retained, 20/20, 20/25, 20/30 vision now for years with carefully titrating when we do these injections. So PRN is an approach, but it’s one that one has to be very cautious about using.

GUY EAKIN: Thank you for clarifying that. You know, you talk about retaining vision, there’s always questions. And we have a question from Robert from Maryland about how many injections does a patient typically need if they are going to notice an improvement? So, for the patients who are going to see an improvement, what’s the timeline, how do we manage our expectations, when should they start thinking if “I’m going to see an improving, now’s about the time”?

MICHAEL GORIN: Well, that’s a very good question, and it’s very individual. There are some patients who literally from a single injection will notice an improvement in their vision, increased peripheral vision, or even quality of central vision. So some people respond very dramatically just from one or two injections. For other people, the process is much slower and the expectations have to be more adjusted. If a person already had longstanding evidence of wet macular degeneration in their eye and they’ve had damage already occur, their recovery of vision may not be great—in fact, it may be lousy. They may have lousy vision even under the best of circumstances, with these drugs, but it may in fact preserve more of the vision they have lost, like peripheral vision. So, I’ve had patients who’ve been legally blind in an eye, whom we’ve treated, who after the course of five or six injections say you know, “my peripheral vision is better, the vision in this eye is not interfering with my other eye, I feel I can drive more effectively because I can use that peripheral vision in that eye without it causing me confusion with the vision in my better eye.”

And in some cases, I’ve had patients who have been able to stay and live independently who otherwise would not have been able to. So it’s different for each person, it often depends on the general health of the person and their motivation. If you think your doctor is giving up on you prematurely, get another doctor, and if you think your doctor is being overly aggressive, talk to the doctor and see maybe if it isn’t worth pushing so hard, if this is so disruptive to your life. In general, you have to know where you are in the disease process in terms of what you can reasonably expect. 

GUY EAKIN: Absolutely, and I think that segues nicely into a question from Margie from Wisconsin, who was told that she no longer needed to go to her retina specialist’s office and was wondering if she might have to start going again in the future. If your eye care provider has given up on you, what are the clues to know whether the decision to discontinue a treatment has been a rational one that makes sense, or might stimulate us to go find another doctor? Is that a fair question?

MICHAEL GORIN: I think it’s a fair question. It’s a challenging one. It’s complicated. In part, it has to do with if you have an eye, for example, that is really severely damaged, you have a lot of scarring and damage to the retina as a result of the macular degeneration, the vision is extremely poor—maybe at best count fingers or hand motions, or you can just see movements but you can’t make out anything—and the other eye is substantially better. If one eye is much, much worse off, you might reach a point where you might say to the doctor—or the doctor might say—it’s not worth giving you more injections because we know that we can’t restore enough vision to help that eye.

On the other hand, that may change if you’re on a blood thinner—for example, for atrial fibrillation, which many of our patients are—you may want the doctor to continue injections even in that terrible eye, because bleeding in that eye in someone who’s on an anticoagulant could be really terrible complication and make their lives really miserable with a painful blind eye. So, there’s a situation where you might continue treatment in an eye that has no hope of good vision in order to prevent a possible complication because of other medical factors. On the other hand, if you’re in that situation and you decide not to treat that really poor eye, your surveillance of the good eye should be perhaps be a little more frequent, and I would definitely not just let that person be forgotten.

Now in other cases, the other situation is where the person says, “Look, yeah, my vision is really crappy, but this is the eye I have to live with, this is the best I’ve got.” In those situations, again, I think the doctor is obligated to be fairly aggressive in trying to maintain the vision and stabilize it so that you don’t lose more. Again, I want to remind people, we don’t want to do more injections than we have to, because there are concerns that—this VEGF molecule that I’ve talked about is not a bad molecule, it’s not something you should be fearful of, it’s actually essential for the health of the eye as well, so when we suppress it with these drugs on a long term basis, we worry that we might be jeopardizing the health of some of the other cells in the eye. So, again, we use it because the benefit greatly outweighs the risk, but once you reach a point where the person is stable, it would be nice not to keep injecting when there’s no evidence of it causing any further benefit, because sustained loss suppression of the VEGF may not be good as well. I hope this helps, I mean it is confusing, it’s a tough decision actually for every patient, what to do.

GUY EAKIN: Well it sounds like it’s no less tough of a decision for the doctor who has to care for them. I do want to leave a reminder that you can briefly leave the call to ask your question just by pressing *3 to submit your question to an operator who will pass that along to me and Dr. Gorin. And if for some reason you’re disconnected from the call, the number to call back in is 877-229-8493 and there’s an ID code associated with that, that’s 112435. So, Dr. Gorin, I have a question. I watch probably too much TV and see a lot of drug advertisements, and there is often a comment in there that you shouldn’t take a drug if you have a particular condition. And we’re spending a lot of time talking about these wonderful anti-VEGF drugs for macular degeneration. I’m wondering if there are any drugs that AMD patients should be avoiding, and maybe not just drugs, maybe it’s behaviors, too. What do you counsel patients with AMD not to do?

MICHAEL GORIN: Well, we do counsel them not to smoke, because smoking is the only well-established risk factor. And so it may be too late for some of you who are older and smoked in your younger days, but certainly if you’re worried for your children. And, as you know, it is a genetic condition to a large extent, but not an absolute—it’s called complex, because it’s not simply passed down from parent to child. So, one piece of advice is, if you have macular degeneration and you have concerns about the increased risk for your children, certainly encourage them to avoid smoking and to eat a healthy diet, etc., that’s all that’s pretty much out there in literature.

In terms of drugs to avoid, certainly we prefer that patients who have active wet macular degeneration not be on anticoagulant, but the reality is, many of our older citizens do have atrial fibrillation or have a history of blood clotting and are on either Warfarin or Pradaxa. These drugs are meant to reduce the chance of getting clots, and so we can certainly handle that, it does not affect the safety of the injections. I know you would worry that…will that injection trigger bleeding in the eye, but that actually almost never happens, even with patients who are on these medications, and that’s because when we inject the medicine in the eye for a brief period of time, the pressure of the eye goes up quite high and it acts like a finger holding down on a bleeding blood vessel; it prevents bleeding from occurring, and by the time that pressure comes down, very rarely do people have a bleeding problem. So, those drugs are not reason not to have an injection done, but it may be a reason why you would want to keep having injections if you still have active wet macular degeneration, because as long as those vessels are leaking and potentially bleeding, a person on an anticoagulant could have a much worse outcome.

I actually don’t know of any other drugs that we would tell people they can’t take. As I said, there are complications for some people with these injections, like glaucoma can occur where the pressure stays elevated in the eye. Again, it’s a matter of trade-off: we can treat glaucoma if we have to, if pressure gets elevated, with surgery. We will take care of it, but losing your central vision is really a very unfortunate situation and one that it’s worth our efforts even if there are potential problems to try to treat.

GUY EAKIN: Well let’s turn to questions about the future for a second. Henry from Pennsylvania has asked a question about new potential therapies that involve growth factors, and of course in the VEGF molecule, and Henry is asking how we are coming along with FGF as a new potential treatment. So, where do we stand with the future of using growth factors as therapies for macular degeneration?

MICHAEL GORIN: I think there is real promise. The drug companies are very interested in this, because it’s a great source of revenue and they can be even more in the future. There are trials going on with Fovista, which is a drug that goes in after another growth factor. It’s very promising, but, you know—interestingly, because of the enormous success of anti-VEGF drugs, it’s raised the bar very high. You can’t simply prove that it works better than nothing, you have to prove that the combination or the use of this new agent is better than what we currently have. That’s a good thing, but it is more challenging, so there are clinical trials going on now with a combination of Fovista and Lucentis to see if the combination is more effective than Lucentis alone. I think that this will be helpful for a sub-group of patients, but it is probably unlikely that we will need to use it on everybody.

The real challenge is going to be two things: one is how can we deliver the drug on a more sustained basis so you don’t need so many injections, because of the risk and discomfort and cost; and secondly, we need to get at medications that get to the underlying cause of the macular degeneration itself. No combination of drugs that block wet macular degeneration are going to be fully effective if we don’t actually stop the underlying process that’s leading to the situation in the first place. So, really, that’s where I think ultimately we will have to be investing more in the research and drug development.

GUY EAKIN: Well, thank you. I’d be remiss as an employee of the BrightFocus Foundation if I didn’t mention that helping to spark the research that looks at underlying mechanisms of age-related macular degeneration is the bread and butter of the Foundation, and certainly a parallel interest to the educational programs, which this is a part of. But following up on the future of therapies, we have the provocative question coming from William from New York, that says, “Cut to the chase. If you’re able to transplant parts, why can’t you transplant eyes?” So, I know in the news we’ve seen ambitions toward whole eye transplants. What complicates that and how far off is that into the future?
MICHAEL GORIN: Well actually the question should not be transplanting parts. The back of the eye, the retina, is really part of one’s brain. It is the same tissue; it comes out as the brain develops, you have the development of the optic nerves and the tissue that goes out to form the retina, the neuroectoderm. So really, when you talk about transplanting an eye—I mean, we can already transplant corneas, for example, but that’s just the front of the eye. When you talk about trying to restore the function and integrity of the retina, you are actually talking about essentially brain transplantation.

Now, you’ve heard recently of somebody who’s talked about transplanting a whole head of somebody on a body, and it’s raised some interesting hackles. The problem really comes in, not so much putting the tissue into someone’s body, but getting it to connect. Essentially, if you were to transplant the back of the eye, you would have to have all those neurons that are in the retina not only stay connected to each other but then form connections all the way back into the brain again through axons that are very, very long and difficult. Now you’re right, we might eventually reach a point where we could treat it like a spinal cord transection, we might be able to do that. But that’s what’s holding us back now. With a heart, the nervous connections for a heart, are really very minimal. You can use a pacemaker, essentially, to trigger the contractions of the heart, and hooking up the plumbing is not as hard as the wiring. So that’s what is holding us back.

Many people are very excited about stem cell. But, you know, stem cells are a real challenge—you’re reading about people who are offering stem cell therapies at the moment, but what they are really proposing is to inject cells into parts of the body where those cells don’t replace lost cells but simply provide a kind of biological factor that makes everybody a little bit healthier to maintain or restore function—not restore but maintain function. Where people really hope that stem cells will have a future is being able to replace cells that have been lost, but just keep in mind that’s a major challenge because when the retina gets damaged, the cells that remain are not the same anymore. They rewire to stay alive, they change their connections with each other, and there is scar tissue that forms in those areas, so you have cells that normally wouldn’t be present forming tissue—bands of tissue in the retina as well. So, putting stem cells in, they have to navigate through this landscape that’s been horribly damaged and sort of make repairs and make connections in order to restore function. I often use the analogy to trying to rebuild a bombed out neighborhood. You can’t do it until you clear away the wreckage and you reestablish electrical and plumbing and sewage lines into the area before you can start building homes again. You’re asking a lot of these stem cells, and people are working toward doing it, but it’s certainly not there yet.

GUY EAKIN: Well thank you. So we have another interesting question, returning more toward the basics of wet macular degeneration. Melanie from Colorado has heard from her clients who have told her that their wet macular degeneration has reverted back to dry—and we’ve already talked about how those terms are not as descriptive as terms a professional doctor might use—but in general, is that possible? Do we see dynamics like that? That the wet form might subside or might resolve completely and someone might be left with the dry form?

MICHAEL GORIN: Well I personally hate those terms, because they are so confusing. Dry macular degeneration essentially refers to that which is not wet. So, when the person has wet macular degeneration, they are treated sufficiently and successfully so that the blood vessel that was there is no longer active, no longer leaking or bleeding, and it can go into a quiescent state from anywhere from a short period of time to years, as I’ve pointed out. You can refer to that retina as “dry” because they have no fluid there, but in the sense that the blood vessel is not completely eliminated. Even the newest technology shows that even in those cases where it’s fully controlled, with really careful imaging we can find evidence of that original vessel partially being there. So you can have a person who has been wet, who I refer to as goes into sort of remission, and that remission can be long lasting.

I’ve tried all through this discussion to carefully avoid any allusion of wet macular degeneration and this abnormal blood vessel to cancer, because these blood vessels are growing in response to an injury and they are not a tumor. But I would argue that the term wet macular degeneration is like making almost a diagnosis of somebody who had cancer who you treated and has no evidence of cancer. Are they truly now with no cancer, or do we consider them in remission? As you know, most of us would sort of view that as a remission state, they will still always have to be under surveillance, they will still always have to be watched. One has a higher chance of recurrence of the disease, or even new disease, in these patients, and so I think that’s a better way to think of it than just saying they’ve gone back to some earlier stage of the disease 

GUY EAKIN: Thank you for clarifying that, that certainly makes a tremendous amount of sense. I think we have time for one final question. We will leave the last one on the hopeful future on therapy. So Mary from Michigan has asked if Dr. Gorin could talk a little bit about physical therapy, such as the implantable miniature telescopes. So, rather than a drug, what do we know about that and who is using those types of technology?

MICHAEL GORIN: Well there are a number of centers, it is an FDA approved device to put in a miniature telescope in an eye, in order to essentially magnify an image for somebody. I’m not a big proponent for it, but I will tell you why. When you magnify the image in one eye, that makes you reliant on the other eye for a normal view of the world with normal depth perception and normal perception of objects around you. Because just imagine if you were holding up a monocular telescope to one eye and you were trying to walk around, you would have to use the other eye to not walk into things because your perception of depth and everything is off with the telescope. I’m not a big fan of that. I think it’s great to be able to use both of your eyes and your peripheral vision to help orient yourself in the world.

Also, because the disease is in both eyes in most patients, it may be worse in one eye than the other but it may not always stay the same degree of severity in both eyes and so you can have a situation where you chose your better eye for the telescope and then gradually over time that eye gets worse and now you really need to rely on the other eye but you can’t do surgery in that eye with the telescope because you need that eye to see your peripheral vision as well, so you’ve limited your options. Personally, I understand people’s desire to not have something that’s in front of their face or handheld, but, you know the point is, if you have something that you’re holding in front of your face, you can take it away when you don’t want it and you can make it stronger when you want to and you can use it in situations when you need it and put it aside when you don’t. When you have something that is implanted in the eye, your options are less, to be honest with you. So, I apologize for those who may be out there who have it and are really happy with it, I think that’s great. But I have a hard time recommending that as an option for most of my patients. It’s just too limiting.

For people with really, really advanced macular degeneration, there are technologies developed to create an artificial electronic retina that’s implantable. Right now, the acuity that’s achievable with those is really very low, still, and so those are not yet really great options for the macular degeneration patient who still has good peripheral vision but has lost central vision. Those devices do not yet give good enough restoration of central vision to be totally worthwhile. There are some other technologies that are being developed, such as where they insert genes into the remaining cells in the retina that did not detect light and make them light detecting. That may be another way of restoring vision in those patients. So, there are lots of strategies going on that are not there yet. I would say to those who have macular degeneration out there, having lived with so many patients over the years, I understand it’s a real hardship and a real difficult adjustment for many of you. It’s robbed you of much of the joy you expected to have in your older years. But truly the real thing that defines how well you will live with this disease is your attitude. That’s not to put the burden on you, it’s to say that if you become depressed from this and feel defeated, you will be defeated, and I have seen patients with terrible vision particularly from the early days, when we didn’t have these injections, who managed to still remain active and engaged and found ways to enjoy their lives even with very poor vision. And, of course, I take care of children and young adults who go blind, as well, and I see what they are capable of doing. No question, it’s much harder when you’re older.

I would say having a good attitude and if you are feeling depressed or if your loved one has this condition is showing evidence of depression, please don’t ignore that, please get them help, they become clinically depressed at a very high rate. Medication does help to some extent, but that may make the difference between them continuing to lead a full and contributing life to those around them and for themselves and becoming isolated and withdrawn, and while we all hope there will be treatments that offer better vision for those who have already lost vision or that will preserve the vision that you have, maintaining the right attitude is so important, and getting low vision help to let you do the things you want to do. It’s amazing what’s available now and the technologies to allow you to do things with poor vision that are in the general commercial world now: watches that talk to you, Siri on your iPhone, various other adaptive tools, and if you can allow yourself to explore new ways of doing the things that are important to you without the constantly grieving for the loss that you’ve experienced, you’ll do well. Are you still there?

GUY EAKIN: Absolutely, and you’re reminding me of all the reasons we enjoy talking to you, with your tremendous technical expertise combined with an absolutely tremendous empathy for your patients. This is all the time that we’ve had to talk today. I want to thank you, Dr. Gorin, for speaking, and everyone on the call who joined in either to listen or to ask questions.

Within about a week we will be posting the recording and the transcript of the call on our website. You can also listen to and download past chats that we’ve had through iTunes, but you can call in at 1-800-437-2423 and request a print transcript. As Dr. Gorin just mentioned, our next chat will actually be what he was referring to, “Tips for Living with Low Vision,” and we encourage you to register and submit questions in advance. We will be sending anyone who is registered for this chat today, we will be sending you a reminder email so that you can register for the July 10th chat right now, and request free informational materials from the BrightFocus foundation, such as a an essential facts brochure on macular degeneration, or those previous chat transcripts that I mentioned. You can do so just by staying on the line right after the call concludes, by leaving a message, or by calling us at BrightFocus at 1-800-437-2423. Again, that’s 1-800-437-2423. And you can always get these resources if you or someone you love can go to brightfocus.org on our website.

Again, Dr. Gorin, thank you so much for sharing your expertise today. You’ve covered a tremendous amount of material, I know there are many people out there who are listening and walking away with answers they have been looking for. For those who are still on the line with us, we did have a poll, so as we conclude the conversation today, join everyone in thanking Dr. Gorin and as we sign off, I’d like to ask a simple question of our listeners. So, overall, how would you have rated this phone call chat? If you found the chat very helpful, please press 1 on your telephone; if you only found this chat only somewhat helpful, please let us know that by pressing 2; and if you didn’t find it helpful at all and we have more work to do, please press 3. Again, thank you, Dr. Gorin, and thank you to everybody who joined us today.

The information provided here 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 only be taken under medical supervision. BrightFocus Foundation does not endorse any medical products or therapies.

• BrightFocus Foundation, 1-800-437-2423, or visit us at www.brightfocus.org
• Common Treatments for Macular Degeneration
• Macular Degeneration: Essential Facts
• Macular Degeneration Treatments Fact Sheet
• Macular Degeneration: Frequently Asked Questions
• VEGF inhibitors currently available: Beovu, Avastin, Lucentis, Eylea, and Macugen
• Self-tests such as trying to read by covering one eye, then the other
• Healthy diet
  • Leafy greens, such as spinach, kale, and collard greens
  • Eat fish twice a week