Challenging Medical Dogma to Save Her Child - Dr. Tracy Dixon-Salazar, Executive Director of the LGS Foundation
Michael Carrese: Hi, everybody, I'm Michael Carrese, and today on Raise the Line, we continue our focus on rare diseases with a look at Lennox-Gastaut syndrome, a severe form of childhood-onset epilepsy. We could not have a better guide on hand because my guest, Dr. Tracy Dixon-Salazar, is not only executive director of the LGS Foundation, but she's been helping her own daughter deal with the condition for the past thirty years; she uncovered the genetic driver of LGS; and she identified a novel precision therapy that improved her child's life.
Dr. Dixon-Salazar earned her PhD in neurobiology and neurosciences from UC San Diego and has nearly thirty years of nonprofit leadership and advocacy experience. It's a great pleasure to have you on the program today.
Dr. Dixon-Salazar: Thank you for having me.
Michael: So let's start, as we always do with our guests, by learning more about their backgrounds. In your case, I would love to know what you were all about before you encountered LGS.
Dr. Dixon-Salazar: Wow. You're going to make me go back, back in time. You know, I was a very young mother. I had my daughter when I was twenty-two years old, and I had two children at the time, so I had my son even younger. I hadn't really done well in high school and I really had no ambitions on life. You know, I grew up not really having a lot of guidance or structure, not really having parents around, and so I was just existing and then I met and fell in love with my now husband, we've been together thirty plus years. He was in the Marine Corps, and I was following him around. I joined the Navy after high school. I had done my four years and now I was being a mom.
And then one day out of the blue, Savannah had a seizure and both of us were so uneducated and unschooled that we thought she was choking. We heard her in the middle of the night hacking and gagging and we ran into her room and she was stiff as a board and blue in the face and she had drool and blood sort of coming out of her mouth, and her eyes were rolled up in her head and we thought, “Oh my gosh, she's choking,” because neither of us had ever heard about or seen a seizure.
Dr. Dixon-Salazar: That was our harsh introduction into the world of seizures and Lennox-Gastaut syndrome, and it's been equally harsh, I think, every day since then.
Michael: Yes. I can't imagine the fright and bewilderment that a parent must face at a time like that. How were you able to move forward?
Dr. Dixon-Salazar: I mean, going back to that night of the first seizure, that was really the turning point when you think about before and after. So, the Tracy before was a mom taking care of her kids, just letting life live me and going through the motions. It's not that I wasn't intelligent or engaged, I just didn't really know how to be. I remember the paramedics came that night -- the seizure was over by the time they got there -- and they said, “Her airway is clear. But what you described sounds just like a seizure.” Both my husband and I were like, “What's a seizure?”
Over the next six months, we took her to the doctor. She had a couple more of these episodes. They wouldn't even call them seizures back then because they didin't want to label her with epilepsy. Our first introduction to the stigma of epilepsy was actually from the doctors themselves who didn't want to call it epilepsy, which in hindsight is somewhat ridiculous. You know, if you have a ravenous mountain lion standing behind you and someone tells you it's a kitty cat, you still have a ravenous mountain lion behind you.
Dr. Dixon-Salazar: But, all of her tests came back normal. She was just a healthy two-year-old and then six months later, by the time of three, the seizures really just came back. They came back with a vengeance. She started having them every day, hundreds a day, too many to count. She finally got the epilepsy diagnosis around three and it wasn't until she was five years old, she got the Lennox-Gastaut Syndrome diagnosis and it was at that moment that I realized that the medical system didn't really know what to do with her. The prevailing dogma that we were hearing out of doctors' mouths was not matching our home life scenario, and I'll just explain that really quick.
So the doctors were saying, thankfully, we don't need to know what causes seizures in order to treat it and yet by the time she was five, she had tried and failed six or seven different treatments. They would say, seizures don't damage the brain and here, my two-year-old, once she started having seizures, stopped developing. Now, remember, this was thirty years ago. The dogma is still around, but it's not as prevalent as it was back then. I'm like, my gosh of course seizures damage the brain because I'm watching my child not develop at all anymore. And then they would say that you can't die from epilepsy, and yet there were multiple times during that period when we had to resuscitate her or that she got aspiration pneumonia and almost died.
So, I'm like, not only do they not know what to do with her, but there seems to be this prevailing dogma that's totally antithetical to what I'm actually seeing in my real life. I realized I had to fight. I had to become her advocate - that mother and father love, you'll do anything for your babies -- and so I had to become educated. I had to become an advocate for her. I had to try to keep this kid alive because no one really knew what to do with her.
It wasn't anything, you know, nefarious or deliberate, but nobody really knew what to do with this kid who was having...you know, a good day was five to ten seizures and a bad day was hundreds, too many to count. That was our life from the time she was five with the LGS diagnosis until the age of eighteen. She had more than 40,000 seizures and was seizing all the time and I just, I had to figure it out. You figure it out because you love your kid.
Michael: Yeah. But holy cow. What a daunting challenge. And for the clinical folks in the audience, what causes LGS? What's going wrong here?
Dr. Dixon-Salazar: Yeah. So, nobody is born with LGS. We often think of it as a metastasizing or spreading, and it's not a good word for the scientists out there. It's not the same as mechanisms of cancer metastasis. But what happens is, the children start seizing usually in the first five years of life and then there's something about the seizures that they become uncontrolled and then you start to see an abnormal EEG between seizures - not just during seizures, but between -- and it's because the brain is developing so rapidly in the first five years of life that the seizures then start to change the way the brain develops. What happens is the brain wires itself wrong and that is LGS.
So, to get the LGS diagnosis, you have to have pediatric-onset seizures that are almost always uncontrolled. I mean, you never see people with controlled seizures evolving to LGS. You have to have more than one type of seizure. So, this is really unique. Children, as the brain develops, their seizures will change types and you often don't see this in adults. Adults with epilepsy, they have kind of one set seizure type, or it might start one place and spread. But they don't evolve and change and move around in the brain. You have very specific features on the EEG test, which is a test to measure your brain waves, and these features are called slow spike and wave (SSW) and generalized paroxysmal fast activity or GPFA.
Everyone with LGS has SSW and GPFA and so it's this moving target, but it's pretty much established by age six in the major majority of patients with LGS. It's a wiring defect, no matter what caused your early life seizures -- and there's tons of causes of that -- but no matter what caused your early life seizures, they all have the same EEG features. The brain has sort of wired itself to have seizures and because they're having so many seizures daily in most patients, they stop learning.
Then I'll just add one thing to that. If you go back to what started the seizures that then evolved into LGS? We have no idea what causes LGS. But what started the seizures? And it's pretty much everything in the kitchen sink. About half of LGS cases are genetic and there's more than a thousand genes now. We have Down syndrome kids that start having seizures and evolve into LGS syndrome, tuberous sclerosis complex, various sodium channel mutations like SCN1A, SCN2A, SCN8A. There are all these genes. Anything that predisposes early life seizures that's a gene is an at-risk for developing LGS, and then the other half are acquired. So, early life birth injury, a cord around the neck, lack of oxygen...we've got a group of families that their kids developed cancer in very, very young age and then post-chemo developed seizures that then evolved into Lennox-Gastaut.
So, it starts out this very heterogeneous, mixed cause disorder with a smorgasbord of different causes that converge all onto the same exact EEG pattern and the same exact wiring defect. It's very complicated.
Dr. Dixon-Salazar: And I get people who say, “Can you describe LGS in like two minutes?” I'm like, “No. No.”
Michael: That was very helpful to everybody to have that context. So, you know, we've talked to lots of parents on the program who have kids with rare diseases, and they all tell a similar sort of story about encountering a medical community that really didn't know much at all, so they had to educate themselves. But boy, in your case, you reallyeducated yourself, and as I mentioned at the beginning, went on to do this really important research. So, talk about that experience and how the research evolved and the results.
Dr. Dixon-Salazar: Yeah. You know, it really started out with two ideas. The first one was what could make a healthy two-year-old all of a sudden out of the blue start having seizures and then six months later, their life is completely derailed? Like forever. So, that was the first thing...like, what's the switch? I was very curious about that. The second thing was no one really looking for the cause. I mean, again, when you go back to this dogmatic way of thinking, I'm like, “Well, what if we knew the cause? Maybe we could have helped her in the beginning.” I very literally was this this naive. I thought no one in the world was studying epilepsy. So, I thought I'm going to be like the first person in the world that's studying this and looking for answers and I'm happy to report that during my education, I have met many thousands and thousands of people -- tens of thousands that are studying epilepsy -- but not a lot that study LGS.
I originally enrolled in college because I used to go to the library and check out books that were like ten years old -- there was internet at the time -- but you could only check out internet at the library for an hour.
Michael: Oh, my God.
Dr. Dixon-Salazar: This is how long ago this was. The Internet was very, very young. It was less than five years old, so there wasn't much on it anyway. You could get inter-library loans from Library of Congress and stuff. So, I’d get ten-year-old books and things and I would read about just generally what could cause epilepsy? I realized that I didn't understand the paper. I had to enroll in college to take some English classes and so I did. I enrolled in college, took some English classes and got an A in English. Apparently, I must have learned something in high school. I must have retained something. All those C's and D's and F's all of a sudden became A's now that I had motivation.
I also realized that the papers I was reading weren't in English at all...they were in science and medicine, which are two different languages in and of themselves. The fourth class I took was an ecology and evolution class and we learned about genetics. We learned about Gregor Mendel. I was at a junior college because I had years of remediating to do before I could get in any real classes and I remember learning about Gregor Mendel and thinking, “This is it. This is it. This is the switch. It's genetics. It's genetics.” I meet parents today and they're like, “I need to raise $10 million. I am going to cure my child who’s four.” I'm like, “Oh, wow. I wish I had that level of self-confidence.” I didn't. I just wanted to maybe one day know what caused Savannah seizures.
So, I spent seven years getting my bachelor's and then realized that I could go to grad school because grad school -- if you are competitive enough to get in -- you could offset your cost of tuition and get a stipend and stuff because we were very, very poor. Both my husband and I grew up pretty poor and didn't have a lot of money as we were raising our young family and then, of course, get a rare disease and then you'll have no money ever.
Michael: Yeah. Yeah.
Dr. Dixon-Salazar: Then ultimately, I got my PhD and did a postdoc in neurogenetics. My PhD was all in how the brain puts itself together. Postdoc was finding genes that cause these early life epilepsies and then giving a lot of mice and flies and stem cells and organoids these diseases and trying to fix them. I never really thought I was going to be able to help Savannah. It was never the goal, but ended up sort of heading that direction.
Michael: And what was that discovery that put you on that path?
Dr. Dixon-Salazar: So, my first year as an undergrad, I had volunteered in a genetics lab and we were using single capillary sequencers to sequence a couple of exons at a time. Then, I took four and a half years to do my PhD and I come back and we're sequencing whole exomes. I started my postdoc the first year that the exome capture kits were released so you could capture just the part of the DNA where the exons were. Looking back, I thought, “Oh, my gosh, this is incredible.” We were finding all these genes, and one day my postdoctoral advisor asked me how my daughter was doing. I broke down into tears -- which is every postdoctoral advisor's dream to have their postdoc cry uncontrollably -- and he said, “Why don't we sequence Savannah?” I was like, “OK.” It was kind of an ugly cry. It was kind of a novel thought back then, because our lab really focused on studying inherited forms of these neurological diseases and we didn't sequence sporadic, really. We didn't have a family history. Savannah was really one of the first sporadic that we went after trying to find the gene.
So, we sequence dad and me and my job was to do the sequencing and analyze. We had a million-line spreadsheets where we were analyzing variants because we were building a pipeline for analysis and variation and it took me over a year. I just kept looking. First pass analysis didn't find anything. Second pass...but then as tools would get created and you would get more information or more genes would be discovered that were linked to disease, you could look at them and ultimately, there were these tools that came out that allowed you to group genetic variants into the pathways that they listed they lived in.
All of us are walking around with several hundred unique rare variants. They're just ours and they're not in the general population. Usually they might be de novo -- meaning mom and dad didn't give them to us -- they kind of arose either in the sperm or the egg or after the sperm and egg came together and they could be advantageous, they could be deleterious. We know that rare diseases are a lot of these de novo deleterious mutations. We grouped all of Savannah’s 300 in pathways and the calcium signaling pathway really stood out for that.
To make a long story short, that led us to discover that she's got seven mutations in L-type calcium channel genes. A very, very high mutation load. L-type calcium channels are really special in the brain for how they help neurons talk to each other and they let calcium in the cell. She's basically got too much calcium going in when these things open and there was a drug on the market that blocks L-type calcium channels. It's called Verapamil. It's been around forever. It's not used in epilepsy at all. It's used in high blood pressure and in arrhythmias but it's FDA approved.
We had nothing left. I mean, by the time Savannah was eighteen, she had tried and failed twenty-six different treatments -- drugs, diets, devices and surgeries and alternative therapies. She was having about 300 seizures a month on average. She was functioning still at that two- to three-year-old age level. She was sleeping about eighteen hours a day. She was on seven medications at the time, plus a vagus nerve stimulating device, which stimulates your vagus nerve. Every week, at least two to four times, she would go into nonstop seizures, and you have to stop these with rescue drugs like Valium and other benzos. She was getting aspiration pneumonia a lot and was just very near death. We were losing her. So, we talked to her doctor and put her on this drug, Verapamil and within two weeks, she had just a miraculous response. It was a ninety-five percent reduction in seizures and a 100 percent reduction in her status epilepticus and nobody is more surprised than me.
Michael: Unbelievable. I mean, was this the first case that you know of where that medication had been used and had that effect?
Dr. Dixon-Salazar: Yes. Yes. If you look back at the literature, it looked like there's a valley of time where no epilepsy drugs were approved by the FDA and then one got approved and that's right around the time Verapamil started getting studied. And then a negative interaction between that new drug and Verapamil was shown. Then, you just never see Verapamil in the literature again for epilepsy, which is interesting.
Michael: Yeah. So what impact did the medication have on her day-to-day life?
Dr. Dixon-Salazar: Oh, man. So, it's been eleven years. Savannah just turned thirty a couple of weeks ago and it’s night and day. She is only on four medicines and her vagus nerve machine is off. She started to learn again. This was the biggest thing for me. If you had told me that drug number twenty-seven was going to change her quality of life and her ability to learn, I'd be like, no, the brain's too damaged. She had 40,000 seizures across a sixteen-year period until she was eighteen. So no way. Too much brain damage. She defied us all. She can walk now. She's very ataxic, but she can walk on her own. She can talk. She doesn't sleep eighteen hours a day anymore. She probably sleeps about twelve, so she does sleep a lot. She probably has about two to four seizures a week, which is bad -- two to four seizures in a lifetime is bad -- but if you're talking about seventy-five to one hundred a week down to three or four, I mean, that's huge.
Dr. Dixon-Salazar: She doesn't go into status anymore, so she's not getting constant rectal delivery of these benzodiazepine drugs...these are emergency rescue meds to stop the seizures. They have the lovely benefit of being rectal, which is so fun. She's just thriving. She's very social. You know, we used to count how many words that she used in a sentence. Like, “Oh, she spoke a three-word sentence today!” We stopped after like forty. She's sassy. I feel like I met her for the first time. She's very strong and opinionated, very sassy. She's got a great sense of humor. Sometimes I think that's like typical for her age. It's allowed us to have some of these normal experiences. Like a few years ago, I was going to some event and I had to wear a dress, which is not my favorite thing to do in life. She sat on the bed and she's like, “Mom, what you doing?” And I'm like, “I'm picking out a dress.” And she went, “I help?” I'm like, “Yeah.” And so she helped me pick out a dress and some shoes. It just dawned on me that this is a thing that mothers and daughters do that we never could do. She's just very social and she can remember stuff. She actually remembers like who the people in our lives are and she misses them and she can use FaceTime and work the DVD and the iPad like there's no tomorrow.
So, it's been incredible. It's just been night and day and it probably took us about four years to stop living the secluded, self-imprisoned life that we had set up for ourselves. Now we go out to dinner sometimes. We never did that. You can't when your kid is seizing all the time. Why bother?
Michael: Yeah. Right. Can't do that. And what about the impact on the wider LGS community of this drug and anything else that's come from it?
Dr. Dixon-Salazar: Yeah. I ended up presenting at the American Epilepsy Society meeting when I was still a postdoc in front of five to six thousand people -- that's the professional society for epilepsy doctors, mostly -- and it was the first time anybody had heard of this concept of precision medicine or genomic medicine or repurposed medicine for this. I remember it was very humbling because I had to tell the story as an outsider, as if I was a postdoc studying the patient because I couldn't get through it without crying. I could cry a little bit right now, just thinking back on it. But at the end of the of the presentation, I revealed with a lot of tears that it was my daughter and that it had an impact on.
You know, if you time this back, I think that this really launched the precision medicine movement in the epilepsy space as a whole. People weren't really thinking about sporadics. We didn't know about de novo mutations back then at all. And I remember it was just very humbling to give that lecture and then to see the field rush to this concept of, “We're finding all these genes and we can start to change these dogmatic ways of thinking. We do need to know what causes it in order to treat it.” If you look at epilepsy as a whole, they say seventy percent of people with epilepsy is more the adult-onset epilepsy and they have intractability. But that's very different than twenty to thirty percent of these really severe childhood onsets. So, first you got that separation and then second, you got this movement.
My first fifteen years of being an advocate was me saying, “Why aren't we developing drugs in children? Why aren't we developing and doing any studies in pediatrics, who are the people who need it most in my mind?” I would hear things like, “Oh, there's no appetite from pharma. There's no path through the FDA.” But that pivoted. It wasn't it wasn't, obviously, just my story alone. The Orphan Drug Act came in. The thing they would always say was, “We're not going to develop a drug against LGS because it's too rare. You're too rare to care about.” That's what I heard for fifteen years, and it was depressing. But this completely changed me from a feeling of, “Oh, my gosh, I'm never going to make a difference in this field. No one wants to hear from patients and LGS is never going to get studied because it's too rare and it's pediatric.” It was kind of that feeling.
It's like, “We don't want to study developmental epilepsy because developmental is so complicated. It's sort of like not wanting to study women in populations because menses messes everything up, right? It's like it was that same dogmatic way of thinking and so for me, it was that turning point where all of a sudden, the genomic revolution plus the orphan drug revolution that was going on...plus there was an imaging revolution. If you look at the history of brain imaging across time and functional imaging, that was happening. All of a sudden, my despair turned to, “I was this teeny tiny one domino in a one million domino puzzle that's going to change the world for the future LGSers.”
That's really what kind of moved me to advocacy. I mean, if I wanted an easier life, I should have stayed in academia, to be honest. In advocacy, there's no money, there's no prestige, nobody's done it so there's like no path. At least I knew I had to get papers and grants to be successful in academia. But now I'm like...oh, man.
Michael: So, you're out of the academic realm altogether?
Dr. Dixon-Salazar: I'm out of the academic realm now, and 100% in advocacy.
Michael: OK. Wow. What's the state of things now? Are other drugs coming along? Is there promise? I mean, we hear so much about advances such as CRISPR and all these other things going on. What's the story with LGS?
Dr. Dixon-Salazar: It's night and day. Actually, I'm giving a talk next week on this. What did it look like thirty years ago and what does it look like now in the rare disease and the rare epilepsy space? It's night and day. All of those dogmas that I mentioned about not knowing what causes it and you can't die and brain damage...they're gone. They're gone. They're proven. And, yeah, there's some old timers that still sort of hold to that, but for the most part, those are gone.
We now talk about LGS secondary to calcium channel mutations, or LGS secondary to your trisomy 21 mutations. You now have two ways to treat the disease. You could treat the Lennox-Gastaut Syndrome -- which is the EEGs and the network -- and you hear the doctors say, “They look like they're going Lennox-Gastaut.” So, the EEG becomes very erratic and we're looking at doing prevent trials five to ten years from now. Can you stop it? They say, looks like they're going LGS...oh, my goodness, stop it. But also you can get your etiological treatment just like Savannah, and so there's a ton of research that's going on with repurposed drugs for the etiologies early on.
We know from cases like Savannah -- and many, many reports now, too -- that even if they don't find a medicine until they're thirty, it can change their lives and the family's lives. Then, of course, gene therapy is rapid and on the rise. We work really closely with a lot of the foundations. Many, many families have started gene specific foundations -- you know this -- and many of them have a predisposition for Lennox-Gastaut syndrome. I'm always so happy when these gene groups start up. I mean, we now probably work with over 200 gene-specific groups where their gene is predisposed. A subset will develop LGS, and they're focused on that early stage. I can't fund research for a thousand genes.
Dr. Dixon-Salazar: Right? But I can focus on research to stop that evolution to LGS while they're focusing early. Like, our friends at TESS Research Foundation are going into gene therapy trials next year on SCN2A and really working on N of 1 trials. Then there's tons of repurposing work going on. Can we repurpose this drug over here, you know, to target the pathway? It gives me so much hope. I had no hope for the first fifteen years in this space. I'm not going to lie. It just felt like I was this tiny little rock hitting my head against a bigger rock wall and not making any dent. Now, it feels like all of us are thousands and tens of thousands of rocks that are throwing ourselves up against this wall and with the orphan drug change and with the changes that we've seen in our ability for patients to have a voice in the whole process...like no one wanted to hear from me fifteen years ago, but now patients have a platform. The system is slowly changing. I hope one day I get a chance to write this down or that somebody sees it, because to see something so dysfunctional change even a little bit for the better in your lifetime is actually a really beautiful, beautiful thing.
Michael: Oh, my goodness. What an incredible story. Absolutely incredible. I'm just so admiring of your persistence and advocacy for your daughter and all these other people as well. How can people get involved and help out if they want to?
Dr. Dixon-Salazar: Oh, that's a great question. I'm at the Lennox-Gastaut Syndrome Foundation. We are constantly looking for people that want to be a part of our mission. The biggest thing that I would ask everybody to do is please go online and get training in seizure first aid. Everyone can do this. The Epilepsy Alliance of America offers free first aid training. You can do it online. You can do it in your own time, but get seizure first aid training. You need to know what to do in case of a seizure. Lennox-Gastaut Syndrome is rare, but one in ten people will have a seizure in their lifetime.
Dr. Dixon-Salazar: One in twenty-six will develop epilepsy. So epilepsy itself is not rare. That's the first thing I would suggest.
The second thing is, if you directly want to support the LGS Foundation, we have a group of families that are just devastated and exhausted by this disease. There's hope for the future, but for the most part, families are still living with daily seizures. Savannah's a miracle story in a lot of ways, and I'm fighting for that. So, if you can donate, if you can share our social media posts and raise awareness of this disease -- or if you want to go even further and volunteer in some way --please don't hesitate to reach out to LGSfoundation.org. I'm Tracy. You can find my email on the website too and we're really just trying to help a group of people that can barely get out of bed in the morning because they're living in crisis mode all the time. I know this because this was us sixteen years. Empower them to take one step today to fight back against this disease. It's a population that's hard to self-mobilize, so we're going to need everybody to help us. We're not afraid to ask for help. We need help. So please, go to LGSfoundation.org. We will take any help we can get.
Michael: I hope people respond. So, as we wrap up, we always like to ask our guests to give advice to the med students, nursing students, and early career professionals in the audience about approaching a career in healthcare. But given your story, I think they're probably quite inspired by how you managed to go from being not such a great high school student to becoming a PhD So, what advice do you have for pushing on and I guess building the confidence that you were talking about along the way?
Dr. Dixon-Salazar: You know, I think the thing I've learned -- I've learned many things -- but one of them is that this is a game of persistence. There are so many people that quit, you know, and there's all these quotes out there that say, “You only fail if you don't try,” and there's obviously some truth to that. But if it's something you really want to do, then you'll do it and it's really about being persistent. You're going to get kicked and knocked down. Believe me, I know that. We all know that. But just keep going at it, and find the thing that you care about. You're not always going to love your job, but if you generally care about what you're working on and what you're doing, I think that's important.
I also have a few sort of self-serving pieces of advice for the medical community. The first one would be that patients and families can have more than one diagnosis, right? We have a lot of people that are now coming in and saying, “I don't have LGS. I have calcium channel overactivation disorder.” I'm like, “That's great. You can't get any services based on calcium channel overactivation disorder -- like occupational therapy or speech therapy for your kid -- but knock yourself out.” The reality is my daughter has epilepsy. She also has Lennox-Gastaut syndrome. She also has calcium channel overactivation disorder. She also has intellectual disability.
When you're interacting with patients and families, all of those diagnoses are needed. Let's not get so stuck in our ivory towers about what's working at the medical system, but involve patients. Talk to them. We want to help solve our own problems. We can't do it without doctors. We can't do it without researchers. We can't do it without the whole system, but we want to help. So, just ask us and we'll help you and we can make, I think, better things together and save time and money.
The other thing I would just say is challenge the dogmas. Aways challenge the dogmas. One of my favorite lectures was by Dr. Ramachandran, who was talking about phantom limb. He did a lot of phantom limb research. He teaches at UC San Diego, and he asked us to talk about the dogmas that have been overcome in our lifetimes. One of the first ones that was mentioned was actually that DNA always goes to RNA which always makes a protein. Now we know in 2023, that's not always true. Every piece of DNA does not make an RNA, does not make a protein, right? There's all these sort of crossed pieces of it.
I'm always shocked at how often I hear in the community, “we were surprised to learn,” or “we didn't expect this,” or “I don't believe that is true.” The whole point of science and medicine and progress is to overthrow dogma, right? To overthrow these ways of thinking that are stale and old and to change our way of thinking with new data. We get sort of stuck in our ways. I get that, but don't hesitate to take those things and really analyze them and challenge them if they need to be challenged.
Michael: A fantastic inspirational message to end on. I just want to thank you so much, Dr. Dixon-Salazar, for taking the time to be with us today. We just wish you all the best and continued success in your incredibly important work.
Dr. Dixon-Salazar: Thank you.
Michael: I'm Michael Carrese. Thanks for checking out today's show and remember to do your part to raise the line and strengthen the healthcare system. We're all in this together.