4. Macular Degeneration: When the Center of Your World Goes Blurry

Imagine looking at your loved one's face and seeing a dark, blurry smudge right where their eyes should be. Or trying to read and watching the words in the center of the page disappear. That's what macular degeneration feels like — and it affects millions of Americans, many of whom had no idea it was coming.

I'm Dr. Parul Khator, a board-certified ophthalmologist and glaucoma specialist in Marietta, Georgia — and macular degeneration is one of the conditions I talk about with patients every single day. Because the more you understand it, the better equipped you are to protect your vision and catch it early.

In this episode, I'm breaking down everything you need to know about AMD — age-related macular degeneration — in plain English, with zero jargon.

In this episode, I'll cover:

• What the macula actually is and why it's so critical to the vision you rely on most
• The difference between dry and wet AMD — and why that distinction really matters
• The symptoms that should send you straight to your eye doctor
• Who is most at risk — and the lifestyle factors that can actually make a difference
• The treatment options available today and what the latest research means for patients

Macular degeneration doesn't have to mean the end of your independence or the life you love. But knowledge is your most powerful tool — and it starts right here. 👁️

📬 Have a question or topic you'd love me to cover? I'd love to hear from you! Email me at demystifytheeye1@gmail.com

📱 Follow along on social media: Find me everywhere @demystifytheeye

🌐 Learn more about Dr. Parul Khator, MD: https://www.gaeyepartners.com/metro-atlanta-eye-doctors/parul-khator-md/

⭐ Enjoying the podcast? Please take a moment to rate and review Demystify the Eye on Apple Podcasts — it helps more people find the show and means the world to me!

🎙️ Never miss an episode: Subscribe on Apple Podcasts, Spotify, Amazon Music, or wherever you listen!

Demystify the Eye is for educational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the guidance of your eye doctor or qualified healthcare provider with any questions you may have regarding your eye health.

Transcript

SPEAKER_01 0:00

Hello, my name is Parl Kator MD. I'm an ophthalmologist in Atlanta, Georgia, specializing in cataract and glaucoma surgeries. After practicing medicine for over a decade, I have learned that the more a patient knows about their disease, the better they do. Patient education is a passion of mine. But like most doctors, I have a lot of patients and not a lot of time to see them. So I created this podcast where I could spend the time I don't have during the day to give you insights into the eyeball and ocular disease. Let's empower you as a patient or a patient support system. Together, let's demystify the eye. Imagine in your head what five millimeters looks like. Think about a ruler on the centimeter scale. There are 10 little lines between the zero and one centimeter mark on that ruler. Count out five of those tiny little lines, and that is five millimeters. Now, imagine a circle that is five millimeters in diameter. I'll help you out here. A sharp pencil point is one millimeter across, a brand new crayon tip is two millimeters across, and a P is ten millimeters in diameter. So somewhere between a crayon tip and a P. Think about an eraser on the back of a number two pencil. That is five millimeters across. Pretty darn small. And yet, in humans, five millimeters of the retina in the back of our eyes is responsible for our most important vision. The vision that lets us watch TV, drive, read, see those itty bitty laugh lines in the corner of our mom's eyes, or the tiny nails on our baby's fingers. These five millimeters of tissue are some of our most important and are unfortunately the target of a very common eye disease known as age-related macular degeneration or ARMD for short. Statistics. The CDC, or Center for Disease Control, estimates that 12% of Americans 40 and older have macular degeneration. 200 million people worldwide are thought to be affected. Nearly 20 million people in the U.S. have some form. It is the number one cause of vision loss in people in the US over the age of 60. The name of this disease has age in it, age-related macular degeneration. This is because the risk of getting macular degeneration greatly increases with age. People in their 50s have a 2% risk, but by the time someone is over the age of 75, that risk goes from 2 to 30%. This is also a disease where race plays a major role. People who have white European ancestry, so what we would think of as Caucasians, are by far and away at highest risk. This is not to say that other races are not affected. Around 10% of Hispanics, 7% of Africans, and 7% of Asians are also affected. Pathophysiology. As you heard me say in the very first podcast, to understand a disease, you first need to understand the anatomy of the organ that is affected. So let's dive a bit into the anatomy of the macula. There is a layer of tissue that plasters the back wall of our eye, and this tissue is called the retina. Our eyes are globes, so imagine a globe where the back half is covered with this retinal tissue. Now imagine the back and centermost part of that globe. Take the eraser tip of a number two pencil, remember, this is five millimeters wide, and stamp it back there. And that is a portion of the retina known as the macula. Now imagine there is an even smaller circle in the center of that 80-bitty five millimeter circle. Imagine this circle is only one and a half millimeters wide. So between the tip of a sharpened pencil and the tip of a brand new crayon, this central circle is known as the fovea. Now imagine a dot in the center of this fovea that is only 0.15 millimeters wide. We are now in the range of micrometers, guys. This central dot is called the foveal pit or umbo, which I've always thought is a super fun word to say. To understand the importance of the fovea, just look at eagles. Wait, what? Let me explain. Many people believe that of all animals, the eagle has the best vision. An eagle can see eight times farther than a human. We think of perfect vision as 2020 vision. This means we can see clearly 20 feet away from us. Well, folks, an eagle is believed to have 25 vision. This means an eagle can see things clearly at 20 feet that we can only see five feet away from us. That is incredible vision. What is different about the eagle eye and the human eye? One of the biggest differences is the fovea. Humans have about 200,000 cells in the fovea, whereas an eagle has about one million. So the fovea is pretty darn important. Imagine if a human had 1 million cells in their fovea. What would you get? Well, Superman, of course. Now let's zoom out a bit to the retina itself. The retina is like the film in a camera. It takes all the photos you see and then sends them to your eye for processing. To be more specific, the retina converts light energy into electrical energy that the brain can understand. The human body, in my opinion, is a fascinating example of efficiency. We survive based on it. We need oxygen to enter our lungs efficiently, we need that oxygen to pump through our bodies efficiently, we need our liver to clear toxins efficiently, and the list goes on. One of the fascinating things about the retina is its inefficiency. Let me explain. The retina is made up of 11 different layers. The layer that actually captures the light we see is the tenth layer, the one almost farthest back from the front of the eye. So light has to go all the way through nine other layers to get to the ones that need to receive it. That light energy is then converted to electrical energy, and this energy has to travel all the way back up the nine layers to the topmost layer, where it then heads to the brain. How inefficient is that? There is a belief that we humans could see a lot better if our retinal anatomy was reversed. The tenth layer of the retina is made up of photoreceptors, which are the nerve cells that convert light into electrical signals. There are two types of photoreceptors, rods and cones. The rod photoreceptors become more active in low light situations. Rods cannot help us see color and they do not help us see very clearly. Think about when you get up in the middle of the night to go to the bathroom. The lights are dim and you have to find your way around because you can't see things too clearly. But you can usually make out the door frame or a wall, or at least your shins hope you can. The cells we talked about earlier and an eagle's eye that allows it to see eight times farther than us, those are cone cells. When we look directly at something, we see it super clearly in the center, and maybe it's a little harder to discern things in the periphery. This is because our maculas are filled with cones. That central fovea, the part of the back of our eye that is only 1.5 millimeters wide, the same size as the tip of a sharp pencil, is filled exclusively with cones. All of this makes sense. The central portion of the back of our eye, anatomically, is also responsible for our central, clearest, sharpest vision. The other nine layers of the retina help support the tissue, feed it, and clear waste from it. The other layer I'll tell you about in this podcast is the 11th layer, the one farthest back from the front of the eye. This is called the retinal pigment epithelial layer. We abbreviate it to RPE. If you look up a picture of the retina, you will see it has a beautiful sunset orange color. And this color comes from this layer of pigmented cells. The RPE does a lot of things, but its two most important functions are to absorb backscatter of light that comes through so the cones don't get overloaded. This gives us crisper images. The RPE also absorbs nutrients, aka food, and delivers that food to the rest of the retina. Behind the RPE layer is a lake of blood vessels called the choroid. Every single tissue in our body needs blood to give it oxygen and nutrients. Well, retinal tissue is the greediest tissue we have. Metabolically speaking, this tissue is the most high maintenance date you've ever seen. It consumes oxygen more rapidly than any other tissue in our body. So while everyone is else is ordering hamburgers, retinal tissue is ordering a filet mignon. To get that much oxygen, the retina needs a lot of blood supply. It actually has a dual blood supply. The top of the retina, that's the portion closest to the front of our eye, gets blood from blood vessels within the retina itself, and the back of the retina gets its blood supply from the choroid. Now, there has to be a demarcation line between the retinal pigment epithelium layer and the choroid layer. If there wasn't, there would be blood all over the back of our eye, and that would not give us crisp, clear vision. This demarcating line in humans is called the Brooks membrane, and it is the final piece of the macular degeneration puzzle. Think about this membrane like a sieve. If you blended oranges to make orange juice, you would want to take out the seeds and fiber before you drink it in order to give you the smoothest orange juice possible. Brooks membrane allows just the right amount of nutrients and molecules to get through to the retina pigment epithelium without the larger clumps. Now that you know the anatomy of the eye, you can really understand macular degeneration. Degeneration means a breakdown of tissue and a loss of its function. The tissue that breaks down in macular degeneration are the photoreceptors, so are cones, the retinal, pigment epithelium, and Brooks membrane. There can even be some changes in the choroid. Imagine you get older by a year, but all of these critical tissues in the back of your eye that are responsible for your crispest, clearest central vision get older by five years. You're going to have problems. Patients with macular degeneration lose their central vision. It becomes blurry or fuzzy. Straight lines can be distorted. Imagine a doorframe that is wavy in the middle. They can see dark spots or blind spots in the center of their vision. All of these changes really affect a patient functionally. People with macular degeneration have a hard time making out faces, driving, reading, watching TV. Color vision takes a hit, and they have a hard time telling black from navy or pink from red. These folks need a lot more light in order to see, but they also have a really hard time transitioning from low light to bright light, bright light situations, and vice versa. Macular degeneration is a bilateral disease, meaning it affects both eyes, but each eye can be affected differently. Meaning the disease can be asymmetric between the two eyes. People still have peripheral vision with macular degeneration, so they will never go totally blind. However, it can take away enough vision to make a person lose their independence. And this is the toughest thing about this disease. Two stages. The answer to these questions depends on the stage of macular degeneration. There are two major stages of AMD, dry and wet. And boy are they different. One takes vision slowly, the other very fast. One can be treated to actually improve vision, the other cannot. Let's start with dry macular degeneration. It's also called non-exudative AMD. In this stage, Brooke's membrane, the colander of the retina, gets thick. It fills up with protein and lipid, and these can actually form distinct clumps of debris in the back of the eye called drusen. Imagine a beautiful suburban neighborhood that has clean, lovely streets. Now, imagine the garbage collectors go on strike and stop coming to collect everyone's trash. Eventually, that neighborhood will get filled with piles of trash, little bags of it all over the streets and sidewalks. That's exactly what these drusen are like. The drusen sit right under the retinal pigment epithelium layer of the eye, and they can be tiny to quite large. You can have a few to lots and lots. When I look in the back of the eye, I can see these discrete yellowish clumps, and the quantity and size help me grade a patient as having early, intermediate, or advanced dry macular degeneration. When the Brooks membrane gets thick and stiff, it can no longer let as many nutrients through. And this causes the retinal pigment epithelium above to start to break down. It loses its color, resulting in patches of whitish tissue instead of deep orange. Finally, the cone cells on top lose their structure and ability to function as they begin to starve. The retina becomes thinner structurally and weaker functionally. The whole breakdown process of dry macular degeneration occurs pretty slowly. I'm talking 10 or 20 years. A person very gradually loses their vision, and this is a boon because it allows that person's brain time to adapt a little bit to the vision loss. The second stage of macular degeneration is wet macular degeneration, also known as exudative AMD. Here, the choroid starts to develop new blood vessels. Oh, more blood vessels. That's a great thing, right? That means more blood flow. Theoretically, new blood vessels should be a good thing, but in the eye, they usually are not. These clumps of new blood vessels are aggressive, not assertive like how you should be at work if your ideas are not being heard. I mean aggressive, like that friend who totally dominates all conversation when you're out to dinner with your friends. These blood vessels break through Brooke's membrane and into the retina. After doing this, they have the audacity to leak. They leak fluid and blood into the retina, and this can cause rapid and horrific vision loss. If the blood is not treated, it will form a nasty scar in the retina that will lead to central blindness. Thank goodness most people with macular degeneration have the dry kind. Someone in the dry stage may never progress to the wet stage. In fact, most do not. Only about 10 to 15% of people with dry AMD go on to develop wet AMD. But wet AMD is responsible for most cases of really blinding macular degeneration. Risk factors. If macular degeneration is such a horrible disease, of course we want to know what makes someone more at risk to develop it and more at risk to progress to the later stages. So let's talk about what the risk factors are for macular degeneration. Macular degeneration is a genetic disease, so family history is a big risk factor. This one you also cannot control. The second is age. I mean, of course, this is a risk factor. It's in the name of the disease after all. Smoking. Now, this is one you can control, and it's a really important one. There have been studies showing a person's disease can stop progressing if they quit smoking. High blood pressure. This makes sense as high blood pressure stresses every cell in our body and makes it harder for our bodies to get proper blood flow. So no wonder our greedy retinas can suffer the most. Weight. Not only do you have a higher risk of developing AMD the larger you get, but studies have found that obese people are much more likely to have AMD that progresses rapidly. Diet. This can go hand in hand with weight. Diets that are high in fat and low in omegas and vitamins are stressful for the macula. Sun exposure. The sun can age our skin and it can also age our maculas. So with all this information, what would you need to look like if you wanted to really decrease your risk of developing AMD? And I'm talking about things you can actually control. You would need to have on polarized sunglasses, be average weight, eat baked salmon with kale, say no to French fries, and absolutely say no to smoking. This really doesn't seem that bad. Diagnosis. One of the reasons I decided to go into ophthalmology is that it is such a visual field. If a patient comes in with a complaint, I can usually look right at the problem. If you have stomach pain, a primary care doctor can't look through your body into your stomach to see what's going on. We diagnose macular degeneration by looking right at the macula. This means to get a diagnosis, you need to go see an eye doctor. In the office, we will dilate your eyes and take a look at your macula to see if we see those drusin or any tissue degeneration. We will also do a macular OCT on your eyes. This is where a laser scans your macula and lets us view it in cross-section. We can see the jelly inside your eye, all the layers of your macula, and even the choroid. With a macular OCT, we can visualize those drusin, and importantly, we can see if there are any choroidal neovascular membranes forming. Remember, that is where abnormal and aggressive blood vessels from the choroid break through to the retina. Treatment. Macular degeneration gets treated differently depending on the stage. For the dry stage of macular degeneration, there really is no treatment. This stage is all about preventing disease progression. Here you will be asked to stop smoking, change your diet, and potentially take an I vitamin called Ocuvite Preservation. There were two huge clinical trials done on patients with macular degeneration to learn more about the disease. These studies, sponsored by the National Eye Institute, are called A-REDS and A-REDS 2. In these trials, researchers looked at whether nutritional supplements could help slow down the progression of the disease. These trials are remarkable to me because most of the time we are studying whether a pharmaceutical drug can help with a disease, not nutritional supplementation. I say bravo to the age. Reds researchers for taking a more holistic approach to this disease. What they found was encouraging. When they combined certain antioxidants with zinc and copper, they could keep high-risk AMD patients from progressing to more advanced stages of the disease. They could also reduce the risk of developing central vision loss by 19%. That is huge. The final combination of the antioxidants plus zinc plus copper was called the A-reds formula, A-R-E-D-S. Researchers then wanted to know if there would be even more benefit if they added omega-3 fatty acids or lutein and zeaxanthin, three things thought to be great for the eyes. They also wanted to know if they could take one of the ingredients out of the original A-reds formula, the beta-carotene. You see, some studies showed an increased risk of lung cancer if people were current or even former smokers and took high doses of beta-carotene. What they found was that adding omega-3 fatty acids to the formula did not decrease the risk of progression of AMD. However, they found they could substitute the old beta-carotene with lutein and zeaxanthin, since these are all in the same family of micronutrients. So the new formula was called AREDS2, and it is believed to be the best current formula at keeping macular degeneration from progressing, while at the same time not increasing the risk of lung cancer. That's good because we don't want to sacrifice one organ for another. You might be asking, how do I get a hold of this combination of nutrients? It is actually available in stores. It is tricky, however, because there are many macular degeneration I vitamins out there. But if you want the one that was proven in a clinical trial to be effective, you have to look for the box that says Ocuvite Preservision A Reds II formula. If you want to get an idea of how much nutrients we're talking about here, look at the nutrition label on the back of a box of Ocuvite Preservation A Reds II formula. There is 222% of the daily value of copper, 556% of the daily value of vitamin C, 727% of the daily value of zinc, and a staggering 1,200% of the daily value of vitamin E. This formula would make Popeye proud. Many patients ask me if they should be taking this vitamin even if they don't have macular degeneration, but someone in their family does. It's a great question. How preventative is this formula? The 8-reds trial actually showed no real benefit of taking the vitamin if you do not have macular degeneration or if you only have early macular degeneration. Basically, you don't need the big gun vitamin. Just take a regular multivitamin and you are doing plenty. The other very important thing I do for my patients with dry macular degeneration is make sure they do not go on to develop wet macular degeneration. I can do this by looking at a patient's macula and running the OCT scan in the office. But much more powerful than that is the at-home monitoring my patients do for themselves. Each macular degeneration patient gets something called an AMSLA grid. You can print one out off the internet. It's basically a grid with a small black dot in the center. You put it on your fridge and cover one eye while staring at the center dot. You're trying to see if the rest of the grid is intact. Are there any lines that are wavy, broken, or missing? Is there a gray cloud over a portion of the grid? All of those are signs you might be progressing to the wet stage of the disease, and that means an eye exam ASAP. The name of that grid, again, is AMSler grid, A-M-S-L-E-R. So what happens if you end up in the wet stage of the disease? What now? Ironically, this stage, which is considered the worst stage, actually has valid treatments. These treatments can actually reverse vision loss. The treatment is a medication which will tell the aggressive new blood vessels leaking behind the macula to stop leaking and even to regress. Wonderful. But how to get this medicine to the macula where it needs to work? You can't give it as a drop because drops don't penetrate to the back of the eye well. You can't give it as a pill because medicine from the bloodstream does not penetrate specifically enough to the back of the eye. So you have to inject the medicine into the back of the eye. Hold on. What? Yes, folks, it does sound like a horror movie, a clockwork orange on steroids. But it's really not a horror movie and it's not as painful as it sounds. The eye gets cleaned and anesthetized very well. A lid speculum or spring is placed in the eye so patient does not have to worry about blinking. Then a highly qualified doctor places a very small needle through the wall of the eye into the jelly in the back of the eye. The medicine is delivered and the needle is retracted. The entire injection only lasts for a few seconds. Does it hurt? Yes, it can be uncomfortable. Is it childbirth? No. Do patients feel it is worth it to restore their sight? Absolutely. The medicines that are injected do not last forever. So patients need to keep getting injections every 4 to 12 weeks, depending on their case. And yes, this does add up. I see patients with macular degeneration who are on their 33rd or 46th injection. Conclusion. Macular degeneration has no cure. But the good news is there are ways to prevent the progression of the disease if someone is in the slower dry phase. And there are treatments to stop or even reverse vision loss if someone is in the more aggressive wet phase. So, in other words, there is hope. I hope after listening to this podcast, you can appreciate the small but mighty macula. Until next time, see well and be well.

SPEAKER_00 29:10

Yes, and my mommy girl dump so they're pretty.

SPEAKER_01 29:14

Thank you.

SPEAKER_00 29:15

You're welcome.