Podcasts about Interleukin

Dr. Deb Muth 00:00:09 Hi there, how are you? Bob Miller 00:00:10 Excellent! Pedaling as fast as humanly possible, but doing okay. Dr. Deb Muth 00:00:14 Good, good. Well, I’m looking forward to our conversation today. This should be amazing. Bob Miller 00:00:20 Yeah, it should be a lot of fun. Dr. Deb Muth 00:00:22 Yeah, anything that’s off-limits for you in, our conversation? Bob Miller 00:00:28 No. Dr. Deb Muth 00:00:29 Okay, anything you want me to make sure we cover for you? Bob Miller 00:00:33 Well, I mean, is it okay if we put a little plug-in for our software? Dr. Deb Muth 00:00:35 Absolutely. Bob Miller 00:00:36 Yeah. Dr. Deb Muth 00:00:37 Absolutely. Bob Miller 00:00:36 Yeah. Dr. Deb Muth 00:00:37 Absolutely. Bob Miller 00:00:38 Hey, can we… can we do a screen share? Yes, we can. Yeah, because I want to show you some maps, and… Dr. Deb Muth 00:00:43 Okay. Things like that, yeah, so… Perfect. So just let me know when you want to do screen share. Bob Miller 00:00:48 Okay. Dr. Deb Muth 00:00:49 And yeah, feel free to plug your software wherever you want to. Bob Miller 00:00:53 Okay, well, good. Let me pull up a, a slide for that, and give me one second, I just want to shut the door to my office to get the noise down. Dr. Deb Muth 00:01:01 No worries. Bob Miller 00:01:16 And, how should I refer to you? Dr. Debb? Dr. Muth, what do you like? Dr. Deb Muth 00:01:18 Dr. Deb is great, or Deb, either way, I’m pretty informal, so… Bob Miller 00:01:22 Yeah, and… Bob is fine for me. Okay. Yeah. Yeah, there you go. Why people feel like they need this, son. Special name, it’s like, seriously. Dr. Deb Muth 00:01:33 Right? I agree. Bob Miller 00:01:35 When I work with my clients, it’s like, Dr. Millison, just, just bop, just, just bop. Dr. Deb Muth 00:01:41 Yep, that’s how I am, too. Just call me Deb, it’s good. Dr. Deb Muth 00:01:44 They feel a little awkward with that, you know? They’re not used to that, but… Bob Miller 00:01:48 Alright. And you’re a naturopath, medical doctor. Dr. Deb Muth 00:01:52 A nastropathic doctor and a nurse practitioner. Oh, nice. Yeah, so I got the best of both worlds, right? Bob Miller 00:01:58 Yeah, damn. Okay. Alright, so here we go… There we go. Alright, so I got that ready, and then I will do a, I will do a screen share. I think you’re gonna really, appreciate what we’ve come up with. We’ve come up with the concept of, Cellular CPR. Dr. Deb Muth 00:02:23 Oh, nice! Bob Miller 00:02:24 And that is, construct the cell membrane, Protect the cell membrane. And restore it if it’s damaged. Dr. Deb Muth 00:02:32 Love that. Bob Miller 00:02:34 I love that. Yeah, so that’s what we’re focusing on, and then how, You know, we want to get to the point that, you know, most people think of genetics, they think of, like, 23andMe or Ancestry. Dr. Deb Muth 00:02:44 Yeah. Bob Miller 00:02:45 And then you have the professional geneticists who are looking at, you know, odd things that could create a disease. We’re looking at functional genomics. Dr. Deb Muth 00:02:54 Which is so much better. Bob Miller 00:02:56 Yeah. Are you familiar with what we do here, or… Dr. Deb Muth 00:02:58 A little bit, a little bit. So, it’ll be new to me, too, so I’m excited. Bob Miller 00:03:03 And how much time do we have? Dr. Deb Muth 00:03:04 We have an hour, give or take a little bit on either side. Do you have a hard stop anywhere? Bob Miller 00:03:10 No, no, I put a, I moved my clients around, and I don’t have anybody till, 3.30, so we’re good. Okay. Dr. Deb Muth 00:03:16 Perfect. Alright. Bob Miller 00:03:18 It’s like we’re getting started early as well, so… Dr. Deb Muth 00:03:19 Yeah, we’re getting started a little bit early, so that’s good. Bob Miller 00:03:22 Yeah, I just got my office cleaned up, so… Dr. Deb Muth 00:03:23 Okay, good. All right, are you all set to get started? Bob Miller 00:03:28 I’m good to go, my friend. Dr. Deb Muth 00:03:29 I’m gonna just record a little intro and a little bit of a, hook for people, and then we’ll get started. I’ll ask you to kind of tell us a little bit about yourself, and then we’ll just take this conversation wherever it’s supposed to go. Bob Miller 00:03:39 Okay, you got it. Dr. Deb Muth 00:03:40 Alright, sounds good. So what if the reason you’re not healing isn’t your diet, your supplements, or your labs, but it’s actually your genes? Dr. Bob Miller is uncovering how genetic variants, when combined with modern toxins, explain why some of us stay sick no matter what we try. Today, we’re talking genetic pathways, detox blocks, and the new science every wellness warrior needs to know. Welcome back to Let’s Talk Wellness Now, the show where we uncover the root causes of chronic illness, exploring cutting-edge regenerative medicine, and empower you to heal from the inside out. I’m Dr. Deb, your medical detective, and today, our guest, Dr. Bob Miller, is a true pioneer in functional genomics. He’s a board-certified traditional naturopath and the founder of Neutrogenetic Research Institute. And he’s the leading groundbreaking research on how genetic variants influence chronic illness, inflammation, and detoxification. His work has been recognized on international stages, uncovering links between genetic expression and conditions like Lyme disease, mast cell activation, or MCAS, and mitochondrial dysfunction. I’m so excited to talk to Dr. Bob today. He is gonna reveal some things that even I don’t know about, so I’m excited to learn alongside of you guys. So… Dr. Bob, let’s get started. Tell us a little bit about yourself, and kind of how you got on this journey. Bob Miller 00:05:04 Well, that’s, that’s interesting. I was sort of like a mid-career coming to the natural health field, because in my early 30s, I found myself with a severe case of ulcerative colitis. Bob Miller 00:05:15 And I was in the hospital for 21 days. probably within hours of death, pleading to death. And they told me I’ve got one option, and that is cut out the colon and wear a bag. Didn’t sound like a lot of fun. Dr. Deb Muth 00:05:27 Not an option I would want. Bob Miller 00:05:29 So, you know, the medical folks wasn’t real happy with me, but I said, yeah, I’d like to explore some alternative things.Never thinking that I’d get into this field, and then I just, you know, worked with some herbalists and things that I found absolutely fascinating. So, that’s how I got into this around 30 years ago. And, haven’t looked back since, and just having a… having a blast as we now move into how our genetics impacts things. So, that’s what we’re gonna… that’s what we’re gonna talk about today. Dr. Deb Muth 00:05:58 I’m excited to talk about this genetic thing. When you started over 30 years ago, what kind of patience and problems first inspired you to dig deeper into that root cause healing and kind of get into the genetic piece of it? Bob Miller 00:06:10 Sure. Well, you know, as a… now, I’m in a part of the country called Lancaster County, Pennsylvania, where there’s a lot of Amish and Mennonite, and they gravitate towards these things.So, this is their first thing to do, and that doesn’t work, then they’ll go other routes. So, you know, back then, we just saw typical, you know, a little tired, constipation. You know, a little bit of fatigue, arthritis, those kind of things. But things have changed dramatically over the years, as people are now getting more chronically sick. You know, it’s worse than it’s ever been. And what we’re finding is the, the culprits Primarily is mold exposure and Lyme disease. When people get those two together, they’re just… it’s an inflammatory cascade that nobody can seem to unravel. So that’s where we spend a lot of our time. And we’re also spending a lot of time looking at mental health, like ADD, ADHD. And, we give… this year I’ll be speaking at three autism conferences. And we can dig into that a little bit as to why we think we’re seeing such a dramatic increase. And aside from autism, that used to be 1 out of 1,000, now it’s 1 out of 33, or 23. You know, we’re also seeing dramatic increases in ADD, ADHD. People are stressed out. And today, I think we’ll have the time to actually go through and show how environmental factors combine with genetics to cause that to happen. So we’ll… we should have a fun visit here today. And today, I think we’ll have the time to actually go through and show how environmental factors combine with genetics to cause that to happen. So we’ll… we should have a fun visit here today. Dr. Deb Muth 00:07:37 This should be a fun visit. We can cover lots of topics. I am so excited. So, you founded Nutri Genetic Research Institute in 2015. What did you hope to accomplish, and what kind of surprised you in your findings so far about that? Bob Miller 00:07:51 Well, you know, let’s back up at what, you know, genetics is used for. Everybody’s familiar with 23andMe and Ancestry that, you know, tells you where your ancestors came from. Then you have your professional geneticists. I mean, these are people with a degree in genetics. And they’ll look for, you know, very odd sort of things that are prone to relate to a disease. So there are disease-related genetics. Well, in functional, we don’t look at either of those. We look at For example, how you’re breaking down your fats and utilizing them. How you’re recycling your glutathione. How you might be handling your iron. And none of those are disease-causing on their own.And none of those are disease-causing on their own. But when they pile up on you, and then combine that with environmental factors, that’s when things start to go south on us. So, that’s what we’re doing, we’re looking at patterns. And our first foray into this was, we did studies on Lyme disease. And our first foray into this was, we did studies on Lyme disease. So, we looked at, like, I think 50 people with Lyme disease. We looked at their genome. So, we looked at, like, I think 50 people with Lyme disease. We looked at their genome. And we found patterns that were more evident in those with Lyme. Now, this doesn’t… these genetics don’t mean you get Lyme, it just means if you get Lyme, you react worse to it. And we found patterns that were more evident in those with Lyme. Now, this doesn’t… these genetics don’t mean you get Lyme, it just means if you get Lyme, you react worse to it. So, as you know, some people get Lyme, they go on a round of antibiotics, and they’re done. So, as you know, some people get Lyme, they go on a round of antibiotics, and they’re done. Others have a little more struggle, and then others are struggling terribly for years. So there’s an old adage of genetics loads the gun, environment pulls the trigger. Dr. Deb Muth 00:09:14 Yeah, that is so true, and I think when we’re talking about Lyme and mold and things like that, we forget sometimes that our genetics can predispose us to be more sensitive to those things, and if we have genetic pathways where we don’t clear things properly, it’s harder for us to get them out of the body. And then you add on that whole rain barrel effect that we’ve always used as a functional medicine term, right? If the barrel’s half full, you’re okay. If it’s full, and now it’s spilling over, it’s a bigger problem. Have you guys found, too, that some of these environmental things actually are changing the genetics of people, or how they’re processing their own genetics? Bob Miller 00:09:53 Well, let’s go back to, Genetics 101. But we’ll go back a little bit further. So, what an interesting mechanism, what a miracle the body is. Bob Miller 00:10:03 Fats, carbohydrates, proteins, drink water, breathe air, expose the sunlight, and somehow everything gets made. I mean, when you just step back and think about that, it’s like, It’s pretty darn amazing. Dr. Deb Muth 00:10:15 I always tell women, you know, the fact that we get pregnant and we have healthy pregnancies and births is a miracle, because if we had to try to control that, that wouldn’t work so well. Bob Miller 00:10:25 Right. Well, that’s another miracle. These microscopic sperm and egg, human being, 9 months later, it’s like. But even inside of us. We are making our hair, our skin, our nails, our blood vessels, our ATP, our energy, it’s all being created. Well, that gets created by enzymes. So, enzymes take one substance, combine it with something else, and make something new. Then another enzyme comes along and does the same thing. Your DNA is the instructions on how to make the enzymes. So, when we are conceived. If it’s a, if it’s a female, of course, it’s the XX, the two chromosomes. You know, we’ve… everybody’s seen those… the genetics that… Listed pair. So, if it’s a female, the father donated the X enzyme. And the mother has no choice but to give the eggs, so that’s female. If the father donates the Y, you have a male that’s in chromosome number 1. Then 2 through 23 is the rest of the instructions on how to make enzymes. So, what can happen? We can get what are called SNPs, single nucleotide polymorphisms. And SNPs just mean that the instructions to make the enzyme’s not quite as good. So, if one parent gives a SNP on the making of an enzyme, The enzyme’s fine. It works. But, general rule of thumb, It may only work at 70-80% of efficiency. Now, a good analogy is think of an 8-cylinder and a 6-cylinder car. If parents give you good information, that’s like having an 8-cylinder car. If one parent gives you that snip, it’s like having a 6-cylinder car. Now, is a 6-cylinder car a fine car? Sure. It’ll get you from point A to point B, but it’s just going to have the power of an 8-cylinder. Then if both parents give you a SNP on the same enzyme, it may be 30-40%, and that’s like having a 4-cylinder car. Sits in the driveway, looks the same, puts gas in it, everything. But if you’ve got a 4-cylinder car. Probably not a good idea to go cross-country pulling a trailer behind you up and down mountains. Dr. Deb Muth 00:12:29 This is true. Bob Miller 00:12:32 So… We can get an 8-cylinder, 6-cylinder, or 4-cylinder enzyme. Now, if it’s not under a lot of stress, if that 4-cylinder car is just taking you to the bank and the grocery store. It’s just as good as an 8-cylinder car. But if you gotta pull that trailer, and there’s a lot of stress on it, being mountains, it’s gonna struggle. Now, there’s one other little caveat to this, and that is some genetic mutations are gain-of-function. They actually work faster. Now, we have enzymes that do all kinds of things. We have enzymes that make and recycle our antioxidants, but we also have enzymes that make inflammation. No, that’s a good thing, because if we get a virus or bacteria, if you didn’t make inflammation to kill it, well, we’d all die of infection. So, you know, we tend to think of free radicals as bad, antioxidants as good. They both play an important role. But interestingly, some of the major enzymes that make inflammation, they can be overactive. They can be turbocharged. And when they’re stimulated by environmental toxins, they overreact. Bob Miller 00:13:40 And therein lies the problem. When they overreact, we have a problem. Bob Miller 00:13:46 So, if we have genes that overreact when stimulated. And then the enzymes that take care of inflammation are underactive. Then you’re gonna be more inflamed. You know, the majority of people that, you know, come for functional medicine Or naturopathic help, or… Inflammation that they can’t seem to get under control. Dr. Deb Muth 00:14:06 Right. Bob Miller 00:14:07 And we will be, you know, during this hour, we’re going to look at some of the pathways that make that happen. So, what we can do then, we can’t change our genetics. When you’re conceived, that’s the hand you’re dealt. When your life would be over, if someone would take some tissue and measure, it’d be exactly the same as conception. Does it change. Bob Miller 00:14:28 The enzyme’s ability to do its job may be compromised. Because remember I said there’s a, the enzyme takes a cofactor. So an enzyme takes substance A, cofactor, make substance B. Well, if that cofactor’s not there, the enzyme’s not going to work either. So, you could have an 8-cylinder car, and if there’s no gas in it, it’s not going anywhere. So… It’s the strength of the enzyme, it’s the cofactor to do the A to B conversion. And that’s what we’re going to get into. So, many people say, well, where did these SNPs come from? Nobody knows for sure. Sometimes they’re what’s just called de novo, when the sperm and egg go together, the instructions get mixed up a little bit. We do believe a lot of it came from a long time ago, when we were almost wiped out by sexually transmitted diseases. And those STDs were altering the genes when the conception, in other words, when the sperm went into the egg, the STDs were interfering. And causing the problem, so… I often joke, if you want to blame somebody. Blame your great-great-great-great-great-great-great-grandparents for, being a bit promiscuous, so… Dr. Deb Muth 00:15:31 Yeah, for being… having a little too much fun, right? Bob Miller 00:15:35 So, we don’t know for sure, but, you know, there are some that, But most of the SNPs that we get inherit from our parents. So, if you look at a child. And you look at the SNPs. 99.9% of the time, it came from one of the parents. Dr. Deb Muth 00:15:50 In identical twins, do they have the exact same identical makeup? Bob Miller 00:15:54 Yep, Dr. Deb Muth 00:15:56 But not in fraternal twins, correct? Bob Miller 00:15:59 No, no, those could be different, Jeff. Dr. Deb Muth 00:16:00 It could be different because they have different sacs, they’re not sharing that same genetic makeup. Bob Miller 00:16:04 Yeah, so keep in mind, both your mother and your father have, you know, the two And so you get one from one parent, one from another. Dr. Deb Muth 00:16:13 So… Bob Miller 00:16:14 Interesting situation. I had, 3, 3 boys. And, we were looking at an enzyme related to breaking down oxalates. Now, the mother and father each had one SNP, and that’s called heterozygous. Three boys, and they all come together, they’re Amish boys, they’re a lot of fun. And I looked at their genomes, and the one boy didn’t have any SNPs at all. And one had won. And the other one had two. Dr. Deb Muth 00:16:41 Interesting. Bob Miller 00:16:42 So, we don’t quite know how these things get handed off, but with the parents each having one, you could have a child with none, one, or two. So, the one, his ability to break down oxalates, which is fine. The other one was slightly impaired, and the other one was dramatically impaired. So, you can have 3 children, and it all depends what the parents have. Now, if a parent has a homozygous, or 2 copies. And the other parent has nothing. Every child will have one. Okay. If both parents are homozygous, that they both have two, Every child will have two. Dr. Deb Muth 00:17:19 too. Bob Miller 00:17:20 Yes, so that’s the way it works, but, you know, but it’s somewhat rare that both parents are homozygous on an enzyme, but it can happen. Dr. Deb Muth 00:17:27 Do we think that infections today, like Lyme disease or mold exposure, things like that, if the parent, the woman, primarily, I’m thinking, is pregnant, and she actively has these infections. Can those infections affect the genetics, kind of like a past sexual transmission did where we thought back in the day? Bob Miller 00:17:47 Yeah, I… I mean, I’m not that much of a geneticist to answer that for sure, but my thought would be no, that at conception, the pattern’s made. Dr. Deb Muth 00:17:55 Okay. And then that’s… that’s the hand you’re dealt. Bob Miller 00:17:58 Yeah. So, I tell people we have good news and bad news. The good news is we can compensate for the weakness. The bad news is we can compensate for the weakness. Dr. Deb Muth 00:18:09 That is so very true. Bob Miller 00:18:11 Yeah, we can’t, because I often get asked, so we’ll do some things now, and we’ll check my genes again, and they’ll be better. It’s like, nope. Dr. Deb Muth 00:18:18 Oh, – – Bob Miller 00:18:19 You gotta play the hands you’re dealt, so… Dr. Deb Muth 00:18:21 That’s right. Bob Miller 00:18:22 You can test your genetics… if you’re looking at the same enzyme, you can test it every year. It’s not gonna change. It’s like the blueprint. Dr. Deb Muth 00:18:30 It’s good and bad, right? It’s the one test you only have to do once in your lifetime. Bob Miller 00:18:34 No, unless, you know, like, our. Dr. Deb Muth 00:18:36 All the time. Bob Miller 00:18:37 Yeah, now our test looks at, called the Functional Genomic Analysis Test of your genomic Resource. We look at 220,000 steps. Dr. Deb Muth 00:18:46 Wow, that’s a lot. Bob Miller 00:18:47 That’s not all of them. Dr. Deb Muth 00:18:49 Right. Bob Miller 00:18:50 So, maybe in the next year, we’re gonna come out with our third version of the chip. And then, if someone wants to get those new things that weren’t on it, they’d have to repeat. But whatever we measured is gonna stay the same. Dr. Deb Muth 00:19:03 That’s a lot of SNPs to look at. Bob Miller 00:19:05 Keeps us busy. Dr. Deb Muth 00:19:06 But there’s still, but there’s still SNPs that we. Bob Miller 00:19:09 That we’d like to have that we don’t have, so… Bob Miller 00:19:11 We started out with version 1 on our genetic test, then we worked with version 2, and we’re already compiling a list of what version 3 would look like. So if somebody has our version 2, And we’re saying, you know what, it’d be nice if we could see these, well, then you’d repeat, but it won’t change what you already know, so… Dr. Deb Muth 00:19:29 Got it, got it. So, when you started out, and you started looking at the research of Lyme disease and chronic infections, which detox pathways are most important for people who struggle with those conditions? Bob Miller 00:19:43 Okay. You know what might make sense as we do a screen share, and I’ll actually show you the pathway. Does that make sense? Bob Miller 00:19:48 Alright, so… let’s see if I… let me just press the share… Dr. Deb Muth 00:19:52 Yep, you should just be able to press share. Bob Miller 00:19:54 And… number 2. Okay. Are we seeing the screen there? Bob Miller 00:20:01 Okay. Dr. Deb Muth 00:20:02 So, this is a map that we made. Bob Miller 00:20:05 And by the way, this is not… All-inclusive of all the things we look at, but we believe this is a core issue. So, where we’re going to start here, there’s something called the microglia. And the microglia are glial cells. They’re in the brain and the central nervous system. And they’re very interesting little creatures, because most of the time, and this is just a drawing of what they sort of look like. Most of the time, they’re in what’s called the M2 anti-inflammatory mood. What that means, these little guys pick up dirt, debris, Recycle them. Turns on an enzyme called interleukin-10 that’s anti-inflammatory. And just kind of does general housekeeping. And just kind of does general housekeeping. However, when a trigger comes along. However, when a trigger comes along. They… it’s the same glial cell, but it moves over to a very pro-inflammatory enzyme. A pro-inflammatory glial cell. And it triggers these 3 enzymes, Actually, these four. That are pro-inflammatory. Tumor necrosis vector alpha, Interleukin-6. NF Kappa B, Inos. Now, these create inflammation. So you might think, well, why is that good? Well, if you have some foreign invader, virus, bacteria coming in, parasite. If you didn’t have these guys coming to the rescue, you would just die of infection. So, these guys are your friend unless they’re your worst enemy. Because TNFA, and we’ll show you when we actually do a demo account, TNFA can be overactive. So, in other words, it over-responds. Interleukin-6 can be overactive. And if Kappa-B can be overactive. The INOS, and I’ll explain each of these as we go through a demo, can be overactive. Now, what that means is, you’re very good at killing virus and bacteria. But this is where autoimmune disease comes in, and just inflammatory conditions. Now, this is just speculation, but we think what happened is, as you know. Thousands of years ago, we didn’t have refrigeration, we didn’t have sewer, we didn’t have pure water, and we didn’t have antibiotics. So, if you made it to 40, you were an old-timer, because everybody was dying of infection. So, what we believe happened is, by what’s called natural selection, Having these overactive. A thousand years ago was to your advantage. Dr. Deb Muth 00:22:31 Hmm. Bob Miller 00:22:32 But now… We have pure water, we have refrigeration, we have sewers, we have antibiotics. But now we have environmental factors that are stimulating them. Now it’s to our disadvantage. And we’ll talk about that a little bit as it relates to the hemochromatosis genes and maybe the G6PD. Dr. Deb Muth 00:22:48 Yep. Bob Miller 00:22:49 Now, why are we becoming so inflamed? Let’s look at the triggers. Now, one of my, favorite expressions is. I was born all the way back in 1954. Dr. Deb Muth 00:23:01 And it was a different world back then. Bob Miller 00:23:05 These are some of the triggers. And we’ll get into these, but right now, high fructose corn syrup, And the high-fat diet. High fructose corn syrup only came about in 1968. So now we’re being exposed to high fructose corn syrup. Then… we didn’t have these, these viruses like COVID. Dr. Deb Muth 00:23:26 Yeah. Bob Miller 00:23:27 Now, there’s now pretty strong evidence that COVID Was actually, you know, made as a gain of function. It’s debated, and I’m not taking an opinion on it, but there’s some people who believe Lyme disease was also a part of experimentation. Dr. Deb Muth 00:23:40 Go. Bob Miller 00:23:41 Then we have molds, and it appears as though mold is getting stronger. you know, 20 years ago, when I was seeing folks, mold wasn’t on the radar. I would say 7 out of the 10 folks we speak to today have mold problems. Yeah, 20 years ago, we talked more about mold allergy being an issue versus mold toxicity being an issue. Right. So… I know some folks are, you know, speculating what’s happening, but one of the theories out there is that EMF is strengthening mold. I don’t know if you ever heard that theory, and I don’t… Dr. Deb Muth 00:24:13 I have. Bob Miller 00:24:14 I’m not claiming it’s true, but it’s an interesting theory. Then even, you know, your black mold from water-damaged buildings. Then our air pollution is getting worse. We’re getting more toxic metals. Dr. Deb Muth 00:24:26 You know, if we have a… Bob Miller 00:24:27 You know, we’re gonna look back someday and say, what were we thinking, smearing aluminum into our armpits? The, what were we doing putting mercury in our teeth? Then, you know, glyphosate. When I was a kid, there was no glyphosate. So, all of these herbicides and pesticides. Polychlorinated biphenols, And then EMF. So, we love our cell phones, you know, and I think unless you, or in the middle of the desert, or down in a cave, you’re being exposed to EMF somewhere. So, you know, we have our cell phones with us, we have, We have Wi-Fi, the towers are everywhere. And we don’t know long-term, but we may find that this can… this creates some inflammation. And I don’t know if you get any folks, but do you have any folks that have… are they EMF sensitive? Dr. Deb Muth 00:25:16 Oh yeah, we have a whole bunch of them. Bob Miller 00:25:18 Yeah, and then if you have any TBIs, So, plenty of things here. that will stimulate into the microglia, M1. Now, you could say, well. We’re all pretty much exposed to the same thing. Why do some people get hit harder than others? So here’s where we’re gonna start. There’s an enzyme called Nrf2 and RF2. And Nrf2 is the enzyme that senses when there’s inflammation. And turns on hundreds of anti-inflammatory enzymes. We’ll show when we do the demo, you can have genetic weakness on NERF2. And NERF2 inhibits and slows down microglia M1. supports M2. Now, if it’s not complicated enough, there’s an enzyme called KEEP1. And KEEP1 inhibits NRF2. And you can actually have gain of function on keep 1, that makes Keap 1 stronger. So… A lot of the people who land on my doorstep So… A lot of the people who land on my doorstep Both parents gave a mutation on KEEP1, making it overactive. Both parents gave a mutation on KEEP1, making it overactive. Dr. Deb Muth 00:26:31 Hmm. Dr. Deb Muth 00:26:31 Hmm. Bob Miller 00:26:32 Suppressing Nrf2, nerve 2 might be weak. So, nobody’s putting the brakes on, M1. And by the same token, Nerve 2 supports M2. Then there’s a process called mTOR and autophagy. mTOR stands for mammalian tard of rapamycin, the growth of new cells. And then autophagy, taking our dead cells and recycling them. We need a balance between the two of them. If we didn’t have mTOR, the sperm and the egg would never become the baby, the baby would never become the adult, we wouldn’t make new cells. But our cells are constantly, you know, the old cells dying off. Autophagy is where we take that debris from the cell and recycle it, just like a farmer Plows the crop under at the end of the year. The dead plant then becomes the fuel for the spring, your dead cell becomes the fuel for the spring, and that’s autophagy. So we’re gonna look back someday and say, what were we thinking? We give our animals growth hormones so they get fatter faster. Oh my. So, we consume those animals, and inventory runs faster. Now, for anybody who’s, You know, maybe above 40, 45 years old. Think back when you were 12, and what did girls look like? They were primarily flat-chested little girls. Now they look like 16-year-olds. Because environmentally, we’re jacking up mTOR. So, mTOR stimulates microglia M1, suppresses microglia M2. Probably 80% of the folks we visit with. This is the part of the problem. NRF2 is weak. mTOR is strong. Environmental factors come along. And this guy gets carried away. He doesn’t do that burst and move back. Stays here. We’re calling that How environmental factors create a locked-in, pro-inflammatory. and neurotoxic phenotype. In other words, once it starts, it just keeps… Feeding upon itself. Alright, so what happens now when microglia is overactive. it triggers these 3 enzymes, TNFA, N of kappa B, And interleukin-6. Each one of these can have genetics that make them run stronger. Then it stimulates an enzyme called NLRP3, Which makes what are called inflammasomes. Now, guess what inflammasomes can be? Your best friend or your worst enemy? Because they will, if you’ve got, again, a virus or bacteria, or possibly even some bad cells in the body. They will zap them. Well, that’s good. Unless it’s overactive. Unless it’s overactive. And then what it does, through interleukin-1 beta, makes excess glutamate. And then what it does, through interleukin-1 beta, makes excess glutamate. Anxiety, gut inflammation, OCD, ADD, autism. And, you know, glutamate, we’ll talk about that a little bit, but glutamate makes you intelligent, highly motivated go-getter. but can also be excitatory. And then, look what it does. Let’s see, do I have the drawing tool here? Yes, I do. Okay. So, it comes down through here, Makes the glutamate. Comes back up through here. through the ADORA 2A enzyme, Then we’ve got a feedback loop that feeds upon itself. Then, through interleukin-18, we make histamine. and mast cells. And then through histamine receptor site number 1, we come back and spin it. And now you’ve just got this spinning feedback loop. So, the glutamate will make you anxious, the histamine will give you allergies and make you anxious. And you’re allergic to everything, and you’re feeling horrible. Now, it doesn’t end there, Dr. Dad. It then goes on to make something called gast dermins that creates pyroptosis, where it actually starts punching a hole in the cell membrane. And you’re only going to be as healthy as your cells are. Just a little background. You know, we’re made up of trillions of cells, and each one of them has what’s called a lipid bilayer, made from lipids, which comes from fats. And you’re only going to be as healthy as those membranes are. So that’s why we coined an interesting phrase. Cellular CPR. Construct the cell. Protect the cell. And restore the cell membrane. And we believe that’s going to be revolutionary in the functional medicine world. So… It’s not hard to figure out that if you start punching holes in the cell membrane, that’s not a good thing, okay? Bob Miller 00:31:22 Now… There’s an interesting molecule called NAD. Thicotide adenoside dinucleotide. And anybody who’s in the, you know, listening to the health podcasts and things, they’re… They’re, they’re learning about NAD. And I’m going to show you a chart later, all the good things that NAD does, but For the most part, it helps what’s called sirtuins. And sirtuins are quite interesting. If anybody’s looking at longevity. The sirtuins is where they’re looking at.Because sirtuins turn on good things. Turn off bad things. And I’ll show some charts on that later. So for right here, this sirtuin uses NAD, to slow down NF-kappa-B. CERT 2 uses NAD to slow down an ORP3. So, if we’ve got genetic weakness on these, or we don’t have enough NAD, We don’t hold this pathway back. Make sense? Dr. Deb Muth 00:32:24 Yeah, makes perfect sense. Bob Miller 00:32:25 Now, I’ll show this a little bit later. So, people are like, oh, well, I’m gonna start taking some NAD. Dr. Deb Muth 00:32:31 Right. Bob Miller 00:32:32 And there’s functional doctors who give NAD intravenous. It was just this morning, I was talking to a woman who said, Oh my gosh. I went and got intravenous NAD, and it took me a month to recover from that. Dr. Deb Muth 00:32:45 Hmm. Bob Miller 00:32:46 what happens is, and I’ll show this in a little more detail, there’s an enzyme called CD38, that’s stimulated by NF-kappa-B. And it takes NAD, To make intracellular calcium. that stimulates NLRP3 and actually makes things worse. So, if we have this guy upregulated, and I’ll show a chart what does that. taking NAD will make you worse. Again, when I go into the software, I’ll show you that whole pathway, so… I would encourage people, you know, just don’t go out and start taking massive amounts of NAD, you know, stick your toe in the water, see how you do. Because everything you’ve heard about, how good it is, is true, unless this guy says, oh, thank you very much, let me make more inflammation. Now, this might be part of our innate immune system, that if we have some pathogen that’s gonna kill us. By golly, we want that to happen. But if this is happening by environmental factors, Then it’s detrimental. So the immune system that protected us a thousand years ago now might be turning on us because of the environmental factors that we showed earlier. All right. Then there’s an enzyme called PARP that’s NAD-dependent, and that actually repairs strain breaks in your DNA. Now, the next thing that happens… is there’s an enzyme called NADPH oxidase that gets stimulated. and something called INOS. Now, I’m sure most people know about nitric oxide. It’s a gas that dilates your blood vessels. That’s why sometimes they’ll even give people drugs, nitroglycerin, to boost their nitric oxide. That’s why people are doing beetroots and other things to boost their nitric oxide. But there’s an OS3 enzyme that makes the nitric oxide that’s good for blood flow. But there’s an INOS That makes nitric oxide to kill pathogens. probably might be the third or fourth time I’ve said this. That’s a good thing, unless it isn’t. So, if it’s killing some pathogen, great. It was just misfiring. it combines… With superoxide that’s made by this enzyme, and makes something called peroxynitrite, which is one nasty free radical that chews you up and spits you out. So, the NOx enzyme, NADPH oxidase, uses NADPH, To make this free radical called superoxide. If we have time, we’ll get into it. NADPH is what your body needs to recycle your antioxidants.So, I coined the phrase, the NADPH steel. Where the NOX enzyme takes this very important NADPH, And rather than being useful, makes superoxide. Now, again, is that fine if you’ve got some bacteria to kill? Of course. But if it’s just chronically running, it’s just making all this chronic inflammation. Then it makes something called hydrogen peroxide. And we need to clear hydrogen peroxide by 3 enzymes, catalase, thyroid reduction. And glutathione peroxidase. If we have genetic issues on here, or we don’t have the cofactors. There’s something called the Fenton reaction, discovered in 1895 by Dr. Fenton. Where hydrogen peroxide combines with iron to make what are called hydroxyl radicals. And guess what they do? They create lipid peroxides, That damages your cell membranes. Now, again, the body’s pretty darn amazing. We have glutathione, And here’s where your body’s taking glutathione and recycling it. But look who’s needed to recycle it. NADPH. So, if this guy up here is chewing it up, We don’t recycle our glutathione. And then an enzyme called glufon peroxidase 4, Takes this damaged lipid and repairs it. So, here we’ve got this protecting, we want to protect it by not having this happen. But then we also need this guy to do the restoration. So, there’s a lot that can go wrong in here, Dr. Deb. Dr. Deb Muth 00:37:07 There’s a lot that could go wrong. And I can imagine some of my listeners are thinking that lipid peroxidase, is that the same thing as what they’re thinking of when we talk about lipids and cholesterol? Is that the same process that’s happening there? Bob Miller 00:37:22 Well, no, no, the lipids can be used to make cholesterol, but here we’re talking about where they’re going to build the cell membrane. And they’re being… and they’re being, destroyed. If anybody would like to see a visual representation of this, just go on YouTube. And type in, ferrooptosis Animation. cool little video, it’s about 3 minutes long, and it shows the lipids coming over, being oxidized, and now GPX4 fixes them, so… YouTube, Pharaoptosis Animation, cute little video. It’s just that really… Shows vividly what we’re… what we’re talking about here. Now, this is… Dr. Deb Muth 00:37:59 And so this is very common, too. Like, a lot of people do hydrogen peroxide IVs. Dr. Deb Muth 00:38:04 And so, if somebody doesn’t know their genetics, they could have a problem with doing those, just like they could doing the NADHIVs, correct? Bob Miller 00:38:13 Sure, yeah, yeah, yeah. So, I’ve talked to so many, you know, of course, the hydrogen peroxide kills pathogens. I mean, that’s what it does. So… but I’ve spoken to so many people that said. I had one client that said they’ve never been the same after having one hydrogen peroxide infusion. Dr. Deb Muth 00:38:30 Interesting. Bob Miller 00:38:31 Yeah. So… it can be… I see why people use it, because it. Bob Miller 00:38:36 pathogens, But on the other hand. And now’s a good time to speak about… I don’t have it on here, but there’s a, there’s an enzyme called the HFE gene. And that is what causes you to absorb iron. And there’s mutations in it that cause something called hemochromatosis. Were you overabsorb iron? Now, true hemochromatosis is when both parents give you a mutation. But there’s now growing evidence even a heterozygous can cause a little bit more iron absorption, not to the human chromatosis point, but overabsorption. So, if you overabsorb iron, And you have too much hydrogen peroxide that’s not cleared, All kinds of inflammation. Now, what’s happened is sometimes this inflammation Will damage the red blood cells. And some well-meaning doctor says, oh, you need some iron. And they take iron and it makes it worse. So, can’t tell you how many people I’ve said, you’ve got the overabsorption of iron, and they say, well, that can’t be right, because I’m low in iron. Well, that could be because it’s being chewed up here. Dr. Deb Muth 00:39:40 Sure. GPX1 and TXN turn it into, to water. The, catalase turns it into water and oxygen. Dr. Deb Muth 00:39:58 Now, I see a lot of my clients who have mutations or SNPs on that GPX gene, on that glutathione gene. And they really struggle to clear a lot of their toxins. Bob Miller 00:40:12 Sure. Dr. Deb Muth 00:40:14 Yeah, absolutely. Well, GPX4. Bob Miller 00:40:18 is what, repairs, but you can see GPX1 Is what uses glutathione. To turn hydrogen peroxide. So, but it all depends upon having enough glutathione. Dr. Deb Muth 00:40:30 Yeah. Bob Miller 00:40:31 Well, guess who controls making a glutathione? Dr. Deb Muth 00:40:34 Nerf 2. Bob Miller 00:40:37 So, if you have a keep one weakness, or strength to two… I’m sorry, keep one is too strong. Nrf2 is too weak. You don’t make glutathione. So, when a lot of people do that, it’s like, well, I’m gonna take glutathione. Dr. Deb Muth 00:40:51 Right. Bob Miller 00:40:52 And some do great, and some do poorly. You know, because… and I’ll show this on one of the other charts. You can see here that the, The glutathione has to be recycled. And if we don’t recycle it, it actually turns into superoxide free radical. So… NADPH are the cofactors, For taking the oxidi… here’s oxidized glutathione, here’s reduced. So, this is a good glutathione. After it does its job, you can see it becomes oxidized.We need to recycle it. Well, if we have weakness on the enzyme that does that, or a weakness in Nrf2, or not enough NADPH. The oxidized glutathione never gets recycled. So, I’ve talked to a lot of people who said, oh, glutathione made me so sick, and say, well. Dr. Deb Muth 00:41:43 Yeah. Bob Miller 00:41:44 You need it, but you need to recycle it. Dr. Deb Muth 00:41:46 Can you speak for just a brief moment, too, about MTHFR? That is a very popular gene, it’s all over social media as the major gene, but can you speak to a little bit about that, and how that fits into this whole process of things? Because it is just such a small piece. Dr. Deb Muth 00:42:04 understanding genetics. Bob Miller 00:42:06 Yeah, to be honest, it drives me nuts. Dr. Deb Muth 00:42:08 Me too. Bob Miller 00:42:11 Alright, so… You know, there are people on social media I won’t say what I think, I’ll be kind. But… But the, And, you know, they might mean well. But they talk about, if you have MTHFR and COMT and PEMT, that’s… oh my goodness, that’s horrible, and we’ll fix that for you, and you’ll be fine. Bob Miller 00:42:36 it just irritates me to no end. And it really could get anybody who’s doing this legitimately in trouble. I mean, I’m afraid someday, you know, there might be some cracking down on this kind of nonsense. Now, to answer your question about MTHFR. Dr. Deb Muth 00:42:51 I mean, it really is, but I’ll tell you what, why don’t we hold that thought until I go to another map and I can actually… Okay. Bob Miller 00:42:56 But the real… the cliff notes is the MTHFR puts a methyl group on your folate, which is needed, but it has gotten way, way, way too much attention. And people learn they have MTHFR, and they start taking a multivitamin with methylfolate, then they take a B vitamin with methylfolate. Dr. Deb Muth 00:43:13 And they’re pushing it too hard. Bob Miller 00:43:15 Yeah. So I can’t tell you how many people I’ve helped by saying, stop it. Dr. Deb Muth 00:43:20 Yeah, take less of it. Bob Miller 00:43:21 Take less of it, yeah. So, yeah. Yeah, there’s a… If somebody, say, ranked the enzymes at their level of importance, MTHFR might be 40 or 50 on a scale of 100, you know. Keep one Nerf two. big deals. Dr. Deb Muth 00:43:40 deals. Bob Miller 00:43:41 NQO1 that I didn’t even talk about yet, NQO1, takes your, NA… your NAD goes into NADH, To make electrons for the electron transport chain. you need NQ01 to bring that back. If that’s not working, and I’ll show you on the NAD map how disastrous that can be. Now, the next piece is here, and I think You know, if you talk to any school teachers and say, if you’ve taught for more than 10 years, how are the kids today? Every one of them says, more ADD, ADHD, more autism. Just look at human beings, we’ve never been so agitated. You know, everybody, and it might be a social media thing, but people take a position on something, and if anybody doesn’t share that position, they view them as the enemy. Dr. Deb Muth 00:44:29 And it’s kind of scary what’s happening to us. Bob Miller 00:44:33 So, we can’t agree to disagree anymore. We see anybody who has a differing opinion as the enemy. And, you know, there was… there’s people that didn’t have Christmas dinners together, because they had political differences, like… Dr. Deb Muth 00:44:44 Excuse me. Bob Miller 00:44:45 can’t you put your political differences aside to have Christmas together, you know? Dr. Deb Muth 00:44:49 Right? Bob Miller 00:44:50 become that, you know, no matter what your position is, and I’m not saying anyone’s right or wrong, I’m just saying. You know, in the old days, they used to say that the Republicans and Democrats in Congress would argue policy and then go have dinner together. And now everybody’s all up in arms, angry. Dr. Deb Muth 00:45:05 Yeah. Bob Miller 00:45:06 So… There’s likely multiple reasons for that. But let me show you one of them. That, you know, to what degree this is… very important, we don’t know, but I think We’re beginning to believe this is very important. So, there’s something… there’s a neurotransmitter called GABA. And God buys the don’t worry, relax, be happy. Chill. Okay. Dr. Deb Muth 00:45:31 Nobody has enough of that anymore. Bob Miller 00:45:33 Well, yeah, you’ll be surprised what I’m gonna show you. So, let me see if I can find a, Let me see if I can find the right slide here. Let me look for it here. So, there’s something called a GABA receptor site. And here you can see… This is a neuron, and this is where you, The neuron normally is excitatory. However, there’s normally low chloride in the neuron. Dr. Deb Muth 00:46:09 Hmm. Bob Miller 00:46:10 So, GABA itself is neither relaxing. For excitatory, all GABA does, it opens up what’s called a chloride channel. And then chloride, which has a negative charge, will flow into the neuron. Follow me there? Dr. Deb Muth 00:46:26 Yep. Bob Miller 00:46:27 And as it does, it changes this from a positive charge to a negative charge, And it’s relaxing. and inhibitory. Dr. Deb Muth 00:46:34 Hmm. Bob Miller 00:46:36 Now, on the other hand, there’s enzymes called NKCC1, That will push chloride in. and KCC2 that will bring chlor… oops and bring chloride out. And then there’s a sodium channel. And, sodium has a positive charge. And glutamate will push that in. So, as long as this is happening. And GABA says, receptor sites, open, chloride goes in, Chill. However, If NKCC1 Pushes extra chloride in. KCC2 doesn’t pull it out. and GABA hits the receptor site, the GABA comes flowing out, Sodium comes in, And now it’s excitatory. So Gabba didn’t change. GABA just opened the receptor site, that’s all it does. Dr. Deb Muth 00:47:33 Yeah. Bob Miller 00:47:34 But it’s the chloride balance that’s going to determine whether this is relaxing or not. Now, these are the things that go along with when they lose that KCC2 or gain NKCC1. Pain and sensitivity, burning electrical, neuropathic pain. Normal touch hurts. Sound and light sensitivity. Tinnitus can flare. Headaches and migraines. Seizure tendency. Body jolts. Spasticity, cramps, stiffness, startle reflex. Trouble falling asleep, non-restorative sleep. Anxiety, stress, reactivity, that’s what we have now. Hyperarousal, panic-like surges, irritability, racing thoughts. Brain fog, slowed processing, working memory slip-ups. Mental fatigue. Episodes of racing hearts, sweaty palms, guts on edge. Those are all the things that happen when this GABA switch occurs. Now, here’s what happens, and this is what I’m going to be presenting at an autism conference. When you have a newborn, they need that NKCC dominant to develop. By early childhood, it should… or, sorry, early adulthood. we should move over to the KCC dominant, that’s the taking the chloride out. Nice-looking 25-year-old boys, functioning very well. However, when we get microglia M1 upregulated. Because of environmental toxins, processed foods, Tylenol, aluminum. they stay in NKCC1 dominant, and there’s ADD, ADHD, Autism, the whole spectrum. because… They’ve not moved over to the… They’ve not moved over to the KCC2. And again, this is caused by… Environmental factors. Stimulating the microglia. And then, interleukin-1, interleukin-18 weakens KCC2, interleukin-1 beta, Strengthens NKCC1. high chloride. We open up the chloride channel, In Rebell Excitatory. So, I think when, When the pediatricians get ahold of this, they’re going to be very excited to know that This could be why we’re seeing such a rise, and not just autism, but ADD, ADHD, anxiety, the whole shit mess. Dr. Deb Muth 00:49:58 thing. Bob Miller 00:49:59 Yeah, so… and you can see NF-kappa-B stimulates that. These stimulate it, and I think that’s why everyone’s getting so anxious. Now, there’s a little bit more to it, and we’ll get into this when we look at some of the maps, but… The, the glutamate, Which is excitatory. will stimulate the NMDA receptor, make more glutamate, And glutamate will inhibit KCC2. And then we also need an astrocyte To, take both ammonia And glutamate, and… Turn them back into glutamine. And I’m going to talk to you a little bit about arachidenic acid, and if we have too much arachidenic acid. or TNFA is upregulated, that doesn’t happen. Ammonia goes up, and there may be multiple reasons for this, but this is a reason why some of the autistic kids do flapping. Dr. Deb Muth 00:50:49 Hmm. Bob Miller 00:50:50 Because they’re not clearing their ammonia. And you can tell if somebody has high ammonia by… they get that old person smell, you know. Dr. Deb Muth 00:51:00 Yup. Bob Miller 00:51:01 your vehicle cycle’s not taking out the, the ammonia. Now, last pathway here. There’s growing interest in mast cell activation. So, back here, we talked about peroxynitride. And that will stimulate mast cells, and those are white blood cells that are your best friend, unless they’re your worst enemy. Then it’ll make histamine. And there’s enzymes called histidine decarboxylase that’ll make more. Dr. Deb Muth 00:51:28 I’m sure everybody’s heard of DAO, the enzyme that degrades histamine. Yep. Bob Miller 00:51:31 We can have genetic weakness, we don’t make that. There’s an enzyme called histamine and methyltransferase, That, That breaks down the histamine. Then if we don’t do that, it’ll get stuck in the histamine receptor site. And then it’ll make something called, renin. Which will cause angiotensinogen to turn into angiotensin. One, that turns into angiotensin II,And that’s where people make aldosterone, where they’ll get the, The swollen ankles and high blood pressure. But interestingly, there’s an enzyme called ACE2, that takes this guy and turns it into angiotensin 1-7, Which is anti-inflammatory and also inhibits… TNFA. Now, you can have weakness on ACE2, But… and anybody’s saying, that sounds familiar? Dr. Deb Muth 00:52:25 That’s where COVID comes in, using ACE2. Bob Miller 00:52:28 And now we just found there’s literature that if you get COVID long enough, it can actually make ACE2 not be able to work as well. So look what it does. It comes down here, stimulates the NADPH oxidase, More superoxide. More peroxynitrite. And we’re on a cycle here. We’ve actually named this the Home Cycle Hypothesis, the proposed feed-forward loop. That just keeps feeding on itself. All being caused by… Primarily, The environmental factors. But hitting those who have genetic weakness the hardest. That’s why. Dr. Deb Muth 00:53:08 To the people. Bob Miller 00:53:09 Don’t live in a moldy house. One person is sick as can be, and the other person says, well, you must be imagining things, because I don’t feel anything. Dr. Deb Muth Yeah. Same thing with long haul, right? Two people can both get sick, one gets sick and never seems to recover, and somebody else gets sick, and they have absolutely no problems with it at all. Bob Miller 00:53:30 Sure. Well, think about it, if you get COVID, and ACE2 is weak, and some of this other stuff is going on. This thing just starts feeding upon itself. Dr. Deb Muth 00:53:38 Keep creating more inflammation, more complications, nothing’s calming down. Bob Miller 00:53:43 Yeah. Now, you, you ask about, MTHFR. So, this is the, this is the, the software called Functional Genomic Analysis. There’s a demo report we have. So, let’s talk a little bit about, MTHFR. So, we actually have a map called a methylation map. Now, what happens is, when you do your saliva test, you, you know, you spit, you put some saliva. in a collection kit, goes to a lab, takes out the DNA data, sends it to the computer, and now you can actually see it visually. Okay. So, it’s gonna take a second for this, data to load up, it’s, and each of these Circles, each of these ovals, is an enzyme. And the data gets loaded up to see where it is. So, until it gets loaded up here, I didn’t preload this. There it goes. So… The primary thing about methylation is There’s a nasty substance called homocysteine that, if it’s too high, can really be detrimental. The body takes methylfolate, and combines with methyl B12, To bring this back up to methionine. And then through the MAT genes, we make SAMI, S-adml methionine. Which is involved in so many processes. Then after it does its thing, it turns back into homocysteine. And this thing needs to keep spinning around. That’s why, you know, it’s a good idea to keep homocysteine at, do you have a number that you’d like? 7, 8? What do you like for a number? Dr. Deb Muth 00:55:24 Yeah, I like mine below 7. Bob Miller 00:55:26 Yeah. So if the homocysteine goes too high. It, caused all kinds of problems. So, here’s where you ask about the MTHFR. So, here you can see on this individual. I click on MTHFR, and you can see it comes up here, here’s the C677. And you can see here where it says, variants. I’ll… I’ll draw in case somebody’s having a hard time seeing that. So, you can see there’s nothing in there. That means there’s no genetic mutations. If one parent would have given a mutation, there’d be a 1. If both parents did, there’d be a 2. Now, here’s why Yes, methylation is important, I’m not saying it isn’t important, but look at this MTHFRC677. In my software. Only 42.5% of the population does not have a mutation. 44.7% have won. 12.9 have 2. So, this isn’t some rare, oh my god, I’m gonna die… Kind of thing, yeah. Dr. Deb Muth 00:56:27 Right. Bob Miller 00:56:28 So, And then what happens is that, and again, I’m not dismissing methylation, I… we could do a whole show on methylation. Bob Miller 00:56:36 get it. But I think that what people are doing is they’re, they’re learning about MTHFR, they get it measured, they panic. They start taking massive amounts of methylfolate, which many times is to their detriment. Dr. Deb Muth 00:56:50 Well, it’s… and isn’t it true, too, with MTHFR, like, you have to also look at MTR, MTRR, and the more we stack up of those, the more complicated than MTHFR can be. It’s not… it’s not as simple as just saying MTHFR 677 versus 1298. It’s more complex than that, kind of like what you’ve already shown with some of the other things. There’s more to it than just that one little sliver. Bob Miller 00:57:17 Oh, sure, well, let’s take a look. So, remember I said there’s a cofactor? One of the cofactors is called FAD. Just a Bob Miller observation, that’s all. But when people have trouble with their riboflavin and they don’t have enough FAD, They’re doing much worse than people who have just a C677. So, right here, you could have perfect C677th. And if you don’t have the cofactor, it’s not gonna work, okay? Dr. Deb Muth 00:57:48 And as you said, there’s an MTR enzyme. Bob Miller 00:57:51 that takes methylfolate and methyl B12, to spin it around. So, here on this individual. here’s your… here’s your B vitamins, or I’m sorry, your B12s. There’s an enzyme called TCN1 that takes it from the stomach into the blood. Then there’s other enzymes that take it from the blood into the tissue. And if you’re having trouble here. Well, then you’re not going to have this working, so… Even if you don’t have MTHFR, And you have MTR, like this, no, I’m sorry, this person doesn’t. But they have the MTRR, and then they don’t have enough B12, this isn’t gonna work, aside from that. And then there’s a middle pathway. And then there’s enzymes called the MAT1. they take the methionine to the salmon. If that’s not working, we stick… we get stuck in methionine. So, it’s, it’s not just an MTHFR. And then, one of the things that people forget about. is through these CBS enzymes and CTH, We make cysteine, which is needed to make glutathione. The master antioxidant. So, it really is that… I call it the, The 3D chess game played underwater. Dr. Deb Muth 00:59:07 It really is. I mean, I see people who have CVS, COMT, glutathione, MGHFR genes. And some of them function just fine. Like, they have Like, I look at this person and I’m like, oh my gosh, I don’t know how they’re functioning because they’re double mutated on so many pathways, but yet they don’t have a lot of symptoms, they don’t have a lot of complications. Somehow their body has figured out a way to adapt to what it has so it can stay alive and it can function at a high functioning level. Bob Miller 00:59:36 Yeah, and they may be, you know, eating right? Yeah. Staying out of a moldy house. reducing stress. So, it’s diet, it’s stress, it’s genetics, environmental factors. So, yeah, we can’t just say somebody’s gonna be good or somebody’s gonna be bad. You know, some people get scared, oh, I got all these, it’s like, well… Bob Miller 00:59:56 Are you living in a moldy house? You know, and if you live in a moldy house and your glucuronidation pathway doesn’t do well, or if you’re, you know, a smoker, or you’re constantly eating junk food, I mean, all. Bob Miller 01:00:07 things come together. Although, you know, when we focus on genetics, we’re well aware that this is just a piece of it. You know, you could have identical twins, Genetically, and if one… Is exposed to mold and smokes and drinks and stressed out. They’re gonna be a whole lot sicker than their sibling. Bob Miller 01:00:28 Yep. Dr. Deb Muth 01:00:29 Yeah, it’s that concept of taking twins, and one gets raced with one family, and one gets raced with another family, and they don’t have the same… problems that… that each other have, you know? It’s a very unique situation, we don’t think about that enough. Bob Miller 01:00:44 Alright, so again, genetics loads the gun, environment pulls the trigger. So, if you’ve got a loaded gun, but you don’t have the triggers, you’re okay. Dr. Deb Muth 01:00:53 Yeah. Bob Miller 01:00:54 Yeah. So, remember I said I was going to talk about NAD? So, here’s NAD, and what it does, it turns into NADH. And what NADH does, it, Comes down this pathway, what’s called the electron transport chain. And that makes your ATP, that’s your energy. So, if this wasn’t working, we wouldn’t be alive, because we wouldn’t have energy. So it donates an electron, that’s why it’s called electron transport chain. So, we need NAD, To make this, to make the energy. But remember I said that NQ01, this would probably be, like, on my top 10 list of… Bob Miller 01:01:36 Much more important than MTHFR. This one takes NADH back to NAD. If we’re stuck over here, We’re low in this NAD+, But what happens is, NQO1 also provides CoQ10. And CoQ10 Is what’s needed for the electron transport chain to flow. So if we get too many electrons up here. And they don’t turn them into energy. They make a nasty free radical called superoxide. Okay. Now, NAD plus also makes NADPH, And that is needed. Remember I said we need to recycle our antioxidants. So, if we have a problem with FAD from riboflavin. Yeah, we don’t have enough NADPH, Glutathione’s not getting recycled, and you’re gonna be inflamed. And you take glutathione, you’ll feel worse. There’s another enzyme called thimoredoxin. Same thing, needs NADPH and FAD. And same way with your nitric oxide, there’s an enzyme called NOS3, That makes the nitric oxide that dilates your blood vessels. And if we don’t have enough NADPH or fat, You’re gonna make superoxide. Rather than nitric oxide. Now, remember

LBCT: Interleukin-6 Inhibition in Acute Myocardial Infarction at Risk of Cardiogenic Shock: A Randomized Controlled Trial

Nutrition Nugget! Bite-sized bonus episodes offer tips, tricks and approachable science. This week, Jenn is talking about Art Galleries and a study that claims visiting them can measurably improve your physical and mental well-being. Could standing in front of a famous painting actually lower your stress hormones and calm your body's inflammatory responses? The research points to some surprising numbers, but is the benefit really about the art itself, the gallery environment, or simply doing something that brings you joy? Jenn has some thoughts on the science and the study's limitations, but you might be surprised by her final take. Tune in to find out whether your next museum visit could actually be a prescription for better health. Like what you're hearing? Be sure to check out the full-length episodes of new releases every Wednesday. Have an idea for a nutrition nugget? Submit it here: https://asaladwithasideoffries.com/index.php/contact/ RESOURCES:Become a Happy Healthy Hub MemberJenn's Free Menu PlanA Salad With a Side of FriesA Salad With A Side Of Fries MerchA Salad With a Side of Fries InstagramUse Your Heart Rate Monitor to Improve Your Health (feat. Torkil Færø)KEYWORDS: Jenn Trepeck, Nutrition Nugget, Salad With A Side Of Fries, Health Tips, Wellness Tips, Art Therapy and Wellbeing, Art Gallery Benefits, Cortisol Reduction, Stress Relief Activities, Inflammatory Markers, Interleukin 6, TNF Alpha, Heart Rate Variability, Cultural Experiences And Health, Viewing Original Art, Art And Mental Health, Chronic Disease Prevention, Mind Body Connection, Physiological Responses To Art, Skin Temperature Monitoring, Wellness Podcast, Nutrition Nugget, Salad With A Side Of Fries, Jenn Trepeck, Health And Wellness Tips, Stress And Inflammation, Art And Cortisol, Wellbeing Research, King's College London Study, Art Fund Research, Courtauld Gallery, Original Art Vs Reproductions, Immune System And Stress, Inflammatory Response, Metabolic Disease Prevention, Heart Disease Risk Reduction, Emotional Arousal, Cultural Wellness, Novel Experiences And Health, Joy And Wellbeing, Art Fair Experience, Museum Benefits, Mind Body Wellness, Stress Management Strategies, Holistic Health, Lifestyle And Inflammation, The Mental and Physical Health Benefits of Visiting Art Galleries, Does Visiting Art Galleries Reduce Stress And Inflammation, Can Viewing Original Artwork Lower Cortisol Levels

Are we meant to fight aging… or embrace it?In today's culture, aging is often seen as something to resist, reverse, or hide. But what if aging is not the problem? What if it's a natural, meaningful process that reflects a life fully lived?In this episode, we explore a new perspective on aging—one that honors the beauty of wrinkles, gray hair, and the wisdom that comes with time. We also share how Bio-Touch Healing supports healthy aging by helping the body reduce stress and maintain balance.Research has shown that Bio-Touch may help increase Interleukin-12 (IL-12), a key component of immune function—offering a simple, natural way to support the body as it ages.Join us as we shift the conversation from “anti-aging” to healthy aging, connection, and self-awareness.✨ Aging is not something to fight—it's something to support and celebrate.Learn more about Bio-Touch:www.justtouch.com❤️ A Simple TruthYou may not be able to control what's happening around you…but you can support how your body responds.

Discover the five scientifically-backed root causes driving autoimmune disorders that traditional medicine overlooks. From vitamin D deficiency and gut damage to hidden infections, antioxidant depletion, and chronic stress—learn the framework for understanding what's really happening in your body and where to start your healing journey. (494 characters) SEO Keyword: root causes of autoimmune disorders FEATURED PRODUCT Zen – Bovine Adrenal Support When your body is battling an autoimmune disorder, your adrenal glands are working overtime to produce cortisol and combat inflammation. Zen features bovine adrenal gland extracts designed to support adrenal function, helping your body manage stress responses and maintain energy levels—critical factors when addressing the chronic stress patterns that contribute to autoimmune development and flare-ups discussed in this episode.

Chronic inflammation is quietly fueling the biggest diseases of our generation, and most people have no idea it's happening. The real causes aren't just aging or injuries, but hidden stressors that keep your immune system stuck in emergency mode. By the end of this episode, you'll understand what's actually triggering inflammation and how to turn off the alarm so your body can heal. Watch The Dr. Josh Axe Show every Monday & Thursday on YouTube: https://www.youtube.com/@drjoshaxe?sub_confirmation=1 

A Gluten Free Podcast Episode 216 Today's highlight is from my episode with Olivia Moscatelli, a PhD student and scientist researching coeliac disease at the Walter and Eliza Hall Institute (WEHI) in Melbourne. Olivia works alongside Associate Professor Jason Tye-Din, one of the world leading experts in coeliac disease research worldwide. Not only is Olivia making pivotal contributions in the field, but she also brings a unique and deeply personal perspective as she lives with coeliac disease herself. In the full episode we dive into Olivia's coeliac diagnosis, what led her into the world of coeliac disease research and the groundbreaking studies she's currently working on that could transform the way coeliac disease is diagnosed and treated in the future. Links Listen to the full episode here Join A Gluten Free Podcast Facebook group here 

Visit ⁠⁠⁠⁠https://longevitybuilders.com/⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠to discover book and The Longevity Builder Health Lab.Discover Your Longevity Score in 3 Minuteshttps://longevitybuildersscore.com/Take our science-backed assessment to uncover your physical health age, identify risks, and get a personalized roadmap to add healthy years to your life.Episode SummaryIn this episode of The Longevity Lab, we explore the fascinating convergence of billion-dollar medical breakthroughs and the raw power of human sweat. We dive into the world of Natural Killer (NK) cells—the "special forces" of your immune system—and how they serve as the ultimate bouncers of your biological city.We start with the revolutionary work of Dr. Patrick Soon-Shiong, the billionaire surgeon behind the "Cancer BioShield." Learn how his "Triangle Offense" uses low-dose chemotherapy and the FDA-approved drug Anktiva to wake up dormant NK cells and hunt down "invisible" tumors.Then, we pivot to the track. Discover how chasing an elite VO2 Max isn't just about athletic performance—it's about biological de-aging. We break down the science of how high-intensity exercise mimics cutting-edge immunotherapy by flooding your system with adrenaline and IL-6, mobilizing a "search party" of NK cells that can increase by up to 500% in a single workout.Whether you are interested in the future of cancer treatment or looking to build a "BioShield" through your own fitness, this episode reveals how to empower your body's natural assassins.The "Missing-Self" Mystery: Why NK cells can see the cancer cells that hide from the rest of your immune system.The Soon-Shiong Protocol: A deep dive into Anktiva (IL-15) and the future of "off-the-shelf" immune reinforcements.The VO2 Max Advantage: Why moving from average fitness to the top 25% provides the biggest "longevity bang for your buck."Exercise as Medicine: The specific role of Epinephrine and Interleukin-6 in guiding your immune cells to the front lines.The 1% Goal: What happens to the immune system of a 60-year-old with the fitness of a 20-year-old.[00:00] Introduction: The primitive warriors living inside you.[05:30] Dr. Patrick Soon-Shiong and the "Cancer BioShield."[12:45] Natural Killer Cells 101: Perforins, Granzymes, and the "Kiss of Death."[22:15] The Proof: From the "Missing-Self" hypothesis to real-time imaging of cell lysis.[30:00] VO2 Max: The gold standard for more than just your heart.[38:20] Building your own BioShield: Incremental gains and elite protection.Dr. Patrick Soon-Shiong: Inventor of Abraxane and architect of the "Triangle Offense" against cancer.The Pioneers: The story of Rolf Kiessling, Ronald Herberman, and Klas Kärre.Anktiva (N-803): The IL-15 superagonist currently changing the landscape of immunotherapy."Your pursuit of an elite VO2 Max is a natural biological mimic of the most advanced cancer protocols on earth."What You'll LearnKey TimestampsFeatured in this Episode

The Secret Sauce for Shedding Pounds isn't just about diet or workouts—it's your liver. In this episode, Nurse Doza breaks down how your liver impacts fat loss through detox, blood sugar regulation, hormone balance, inflammation reduction, and mindset. If you're stuck in your weight loss journey, your liver may be the key. 5 KEY TAKEAWAYS The liver produces antioxidants like glutathione that directly reduce inflammation and support fat metabolism. Hormone balance—especially estrogen and cortisol regulation—depends on liver health. Blood sugar regulation starts with the liver, which stores and processes glucose after meals. Fat cells become inflamed without proper liver function, leading to leptin resistance and weight gain. Sustainable fat loss requires mindset shifts—and liver support helps you regain control. FEATURED PRODUCT

A Gluten Free Podcast Episode 197I've had many coeliac disease researchers on this show to share their latest research and findings. Today I want to collate all the exciting coeliac disease research around the world I'm watching right now. I hope you enjoy listening and please get in touch if you learn more developments in the research I talk about during this episode or you know of others that are worth talking about. What we'll chat about: * Reflecting on last my episode with the new Director for the Center for Celiac Disease Research and Treatment, Dr Maureen Leonard * Dr Jason Tye Din & Olivia Moscatelli from WEHI with their Interleukin 2 diagnostic breakthrough allowing patients to avoid the need to consume gluten while testing for coeliac disease accurately * Dr Maureen Leonard's work on the Celiac Disease Genomic Environmental and Metabolomic Study * How the CDGEMM study with help us understand how and why coeliac disease is activating in children * Italy passing a law to screen their population for coeliac disease and Type 1 diabetes in ages 1-17 * The importance of researching the mental health impacts of coeliac disease * Potential therapeutic for Coeliac Disease from Topas Therapeutics (TPM502) * Gluten Threshold study at Wesley Research Institute  * Hookworms and parasite study for coeliac disease treatmentLinks Interleukin Diagnostic tool blog postEpisode with Dr Maureen Leonard Celiac Disease Genomic Environmental, Microbiome and Metabolomic Study Italy's paediatric population screening for coeliac disease and Type 1 diabetes Coeliac Disease research in the UK TPM 502 Gluten Threshold Study Are you looking for a low cost business, that is easy to run and has a high return on investment? OMG! Decadent Donuts wants you! Join this creative, inclusive and rapidly expanding business today. Apply here: https://omgdecadentdonuts.com/opportunity/ Thanks to our sponsor Happy Tummies! Happy Tummies is a one-stop-shop for allergen-friendly and gluten free products and also stocking their very own brand - Free From Family Co. Click here to have our discount code GFFAMILY automatically applied & save 10% off Free From Family Co products! Celiac Cruise - a 100% gluten free vacation cruise is setting sail on two Australian cruises in 2026: one to the South Pacific and the other to New Zealand. There'll of course be awesome 100% gluten free food onboard, heaps of fun stuff to do, educational talks and a community of people who understand each other. Buy your tickets here & see ya onboard gluten free fam!

Hosts Roz and Dr. Sanchez-Fueyo discuss the key articles of the September issue of the American Journal of Transplantation. [03:30] Blunted cardiac reserve as a marker of cirrhotic cardiomyopathy—Cardiac outcomes following liver transplantation and comparison to the existing guidelines [14:18] Back-table intra-arterial administration of C1 esterase inhibitor to deceased donor kidney allografts improves posttransplant allograft function: Results of a randomized double-blind placebo-controlled clinical trial [25:55] Donor-derived cell-free DNA is associated with the degree of immunosuppression in lung transplantation [36:24] A two-threshold algorithm using donor-derived cell-free DNA fraction and quantity to detect acute rejection after heart transplantation [45:00] Cell therapy with human Interleukin 10–producing ILC2s enhances islet function and inhibits allograft rejection

View the Show Notes Page for This Episode Become a Member to Receive Exclusive Content Sign Up to Receive Peter's Weekly Newsletter Eric Verdin is a physician-scientist and the CEO of the Buck Institute for Research on Aging whose career has centered on understanding how epigenetics, metabolism, and the immune system influence the aging process. In this episode, Eric traces his scientific journey from studying viruses and histone deacetylases (HDACs) to leading aging research at the Buck Institute, offering insights into how aging impairs immune and nervous system function—including thymic shrinkage, chronic inflammation, and reduced vaccine response—and how these changes impact lifespan. He explores the metabolic underpinnings of aging, such as oxidative stress and insulin and IGF-1 signaling, and he discusses practical tools like zone 2 cardio, ketogenic diets, and GLP-1 drugs. The conversation also covers declining NAD levels with age, the roles of NAD-consuming enzymes such as sirtuins and CD38, and what current NAD-boosting strategies (like NMN, NR, and IV NAD) can and can't accomplish. Eric weighs in on promising longevity interventions including rapamycin, growth hormone for thymic regeneration, and anti-inflammatory therapies, while also examining the promise and limitations of current biological age tests and the potential of combining epigenetic, proteomic, and organ-specific metrics with wearables to guide personalized longevity care. We discuss: Eric's scientific journey from virology to the field of geroscience [2:45]; How dysfunction in the immune system and central nervous system can drive aging throughout the body [5:00]; The role of metabolism and oxidative stress in aging, and why antioxidant strategies have failed to deliver clear benefits [8:45]; Other aspects of metabolism linked to aging: mitochondrial efficiency, fuel utilization, and glucose-modulating drugs [16:30]; How inefficient glucose metabolism drives insulin, IGF-1 signaling, and accelerates aging [21:45]; The metabolic effects of GLP-1 agonists, and the need to move beyond crude metrics like BMI in favor of more precise assessments of metabolic health [27:00]; The case for immune health as a “fifth horseman” [36:00]; How the innate and adaptive immune systems work together to build immune memory [39:45]; Why vaccines lose effectiveness with age: shrinking of the thymus gland and diminished T-cell diversity [44:15]; Exploring growth hormone, thymic regeneration, and the role of exercise in slowing immune aging [48:45]; The challenges of identifying reliable biomarkers for immune function, and the potential of rapamycin analogs to enhance vaccine response in older adults [57:45]; How rapamycin's effects on the immune system vary dramatically by dosage and frequency [1:03:30]; The limitations of mouse models in aging research and the need for cautious interpretation of rapamycin's benefits in humans [1:08:15]; NAD, sirtuins, and aging: scientific promise amid commercial hype [1:15:45]; How CD38 drives age-related NAD decline, influences immune function, and may impact longevity [1:23:45]; How NMN and NR supplementation interact with CD38 and NAD metabolism, and potential risks like homocysteine elevation and one-carbon cycle depletion [1:31:00]; Intravenous NAD: limited evidence and serious risks [1:37:00]; Interleukin-11 (IL-11) as a new target in immune aging, the dual role of chronic inflammation in aging, and the need for better biomarkers to guide interventions [1:43:00]; Biological aging clocks: types of clocks, promise, major limitations, and future outlook [1:48:30]; The potential of proteomics-based aging clocks for detecting organ-specific decline and frailty [2:00:45]; and More. Connect With Peter on Twitter, Instagram, Facebook and YouTube

The Secret Sauce for Shedding Pounds isn't just about diet or workouts—it's your liver. In this episode, Nurse Doza breaks down how your liver impacts fat loss through detox, blood sugar regulation, hormone balance, inflammation reduction, and mindset. If you're stuck in your weight loss journey, your liver may be the key. 5 KEY TAKEAWAYS The liver produces antioxidants like glutathione that directly reduce inflammation and support fat metabolism. Hormone balance—especially estrogen and cortisol regulation—depends on liver health. Blood sugar regulation starts with the liver, which stores and processes glucose after meals. Fat cells become inflamed without proper liver function, leading to leptin resistance and weight gain. Sustainable fat loss requires mindset shifts—and liver support helps you regain control. FEATURED PRODUCT

In this episode, we dive into a two-part story of intrigue starting from a paradigm shift in understanding of T cell biology because of a mouse model of post-measles encephalopathy, to the eventual recognition of the IL-23/17 immune axis. •    Intro 0:01 •    In this episode 0:12  •    Interleukin-17 (IL-17) is a relatively recent discovery 1:34 •    The beginning of TH-17 2:20 •    Looking at autoimmune encephalopathy: A story of measles 03:30 •    1790's woman with post measles inflammatory process in the brain 10:26 •    What is causing post-infection encephalitis? 12:00 •    Acute disseminated encephalomyelitis 12:30 •    How did we find out the immune system was behind this - The rabies vaccine 13:09 •    Similarity between the rabies vaccine and infections like measles 16:04 •    T-cell lymphocytes 17:12 •    The forgotten thymus 18:00 •    What's the function of T-cells? 19:35 •    How do you tell T-cells apart? 21:14 •    The Human Leukocyte Differentiation Antigens Party 24:05 •    The godfather of T-cells 24:45 •    The TH-1 and TH-2 axis 27:30 •    Experimental Autoimmune Encephalomyelitis model screwed everything up 29:16 •    Interferon gamma 32:32 •    What's missing? IL-23 surprise 33:40 •    IL-17 in the 1990's 36:44 •    The world is introduced to TH-17 39:12 •    Let's recap what we learned 40:30 •    That is the end! 42:30 •    Thanks for listening 42:39 We'd love to hear from you! Send your comments/questions to Dr. Brown at rheuminationspodcast@healio.com. Follow us on Twitter @HRheuminations @AdamJBrownMD @HealioRheum. References: Bashyam H. J Exp Med. 2007;doi:10.1084/jem.2042fta Bennetto L, et al. J Neurol Neurosurg Psychiatry. 2004;doi:10.1136/jnnp.2003.034256 Berche P. Presse Med. 2022;doi:10.1016/j.lpm.2022.104149 El-behi M, et al. J Neuroimmune Pharmacol. 2010;doi:10.1007/s11481-009-9188-9 Gooderham MJ, et al. J Eur Acad Dermatol Venereol. 2018;doi:10.1111/jdv.14868 Hawkes JE, et al. J Immunol. 2018;doi:10.4049/jimmunol.1800013 Rogozynski N, et al. Immunol Lett. 2024;doi:10.1016/j.imlet.2024.106870 Sospedra M, et al. Annu Rev Immunol. 2005;doi:10.1146/annurev.immunol.23.021704.115707 Steinman L. Nat Med. 2007;doi:10.1038/nm1551 Disclosures: Brown reports no relevant financial disclosures.

Broadcast from KSQD, Santa Cruz on 6-19, 2025: Dr. Dawn presents the VITAL study evidence showing 2,000 IU daily vitamin D prevents telomere shortening in immune cells, effectively slowing biological aging by three years. Groundbreaking mouse research reveals maternal iron deficiency can alter fetal sex development. When iron levels dropped 60%, the SYR gene controlling male development switched off, causing 6 of 39 XY offspring to develop ovaries instead of testes. Thus, mammalian sex can be influenced by environmental factors just like in amphibians and fish. Dr. Dawn connects this to gender identity questions, advocating supporting puberty blockers based on their 30-year safety record. Dr. Dawn advocates widespread CPR and AED training after describing a successful Buffalo airport rescue. With 350,000 annual out-of-hospital cardiac arrests and 90% fatality rates, immediate AED intervention can triple survival odds. She promotes the Pulsepoint app registering 185,000 AEDs and praises countries like Norway achieving 90% population CPR training through driver's license requirements. Post-Roe v. Wade data shows vasectomies doubled in men aged 19-26 while tubal ligations rose 70%, mostly in abortion-ban states. Dr. Dawn notes the irony that policies intended to increase births prompted widespread voluntary sterilization. Environmental concerns from January 2025 Moss Landing battery fire and LA wildfires highlight toxic contamination from burning lithium, plastics, and building materials. She advocates fire-resistant landscaping and home hardening, noting some fire-resistant homes survived while surroundings burned. British research shows pet ownership provides life satisfaction equivalent to $90,000 annual income boost. Dr. Dawn experiences this firsthand, noting pets provide family-like benefits without complex interpersonal dynamics. Sleep study reveals 15 minutes additional nightly sleep improves cognitive performance in tweens. Children sleeping 7.25 versus 7.10 hours showed better academics and larger brain volumes, though Dr. Dawn questions causation versus correlation. Mayo Clinic identified Interleukin-23 as a reliable cellular senescence biomarker across multiple tissues. Natural compounds like quercetin, fisetin, and luteolin can reduce these aging markers, supporting her dietary supplementation philosophy.

Broadcast from KSQD, Santa Cruz on 6-19, 2025: Dr. Dawn presents the VITAL study evidence showing 2,000 IU daily vitamin D prevents telomere shortening in immune cells, effectively slowing biological aging by three years. Groundbreaking mouse research reveals maternal iron deficiency can alter fetal sex development. When iron levels dropped 60%, the SYR gene controlling male development switched off, causing 6 of 39 XY offspring to develop ovaries instead of testes. Thus, mammalian sex can be influenced by environmental factors just like in amphibians and fish. Dr. Dawn connects this to gender identity questions, advocating supporting puberty blockers based on their 30-year safety record. Dr. Dawn advocates widespread CPR and AED training after describing a successful Buffalo airport rescue. With 350,000 annual out-of-hospital cardiac arrests and 90% fatality rates, immediate AED intervention can triple survival odds. She promotes the Pulsepoint app registering 185,000 AEDs and praises countries like Norway achieving 90% population CPR training through driver's license requirements. Post-Roe v. Wade data shows vasectomies doubled in men aged 19-26 while tubal ligations rose 70%, mostly in abortion-ban states. Dr. Dawn notes the irony that policies intended to increase births prompted widespread voluntary sterilization. Environmental concerns from January 2025 Moss Landing battery fire and LA wildfires highlight toxic contamination from burning lithium, plastics, and building materials. She advocates fire-resistant landscaping and home hardening, noting some fire-resistant homes survived while surroundings burned. British research shows pet ownership provides life satisfaction equivalent to $90,000 annual income boost. Dr. Dawn experiences this firsthand, noting pets provide family-like benefits without complex interpersonal dynamics. Sleep study reveals 15 minutes additional nightly sleep improves cognitive performance in tweens. Children sleeping 7.25 versus 7.10 hours showed better academics and larger brain volumes, though Dr. Dawn questions causation versus correlation. Mayo Clinic identified Interleukin-23 as a reliable cellular senescence biomarker across multiple tissues. Natural compounds like quercetin, fisetin, and luteolin can reduce these aging markers, supporting her dietary supplementation philosophy.

One big reason Celiac Disease is underdiagnosed is that it requires gluten ingestion for testing accuracy. Many people cut out gluten and feel better and There are so many who don't want to go back to eating gluten free a diagnosis. That's why this new research is so exciting: New blood test for celiac disease can diagnose autoimmune condition without need to eat glutenResearch, published in the journal Gastroenterology, on Interleukin-2 has helped to create a new testing method that would allow people who are already on a gluten free diet to be accurately tested for Celiac Disease, without the need for gluten ingestion.“By stimulating T cells after a blood draw, patients can avoid the need to return to gluten and the suffering that often comes with that – for the sole purpose of diagnosis. That is a major step towards improving outcomes for patients.”Read more here: https://www.theguardian.com/society/2025/jun/10/new-blood-test-for-coeliac-disease-can-diagnose-autoimmune-condition-without-need-to-eat-glutenI would love to hear from you! Leave your messages for Andrea at contact@baltimoreglutenfree.com and check out www.baltimoreglutenfree.comInstagramFacebookGluten Free College 101Website: www.glutenfreecollege.comFacebook: http://www.Facebook.com/Glutenfreecollege Hosted on Acast. See acast.com/privacy for more information.

In dieser Hörgang-Episode spricht Prof. Dr. Georg Stary von der Universitätsklinik für Dermatologie der MedUni Wien über aktuelle Entwicklungen in der Behandlung von Psoriasis. Im Fokus steht das neue Christian-Doppler-Labor für chronisch-entzündliche Hautkrankheiten, das Stary leitet – ein Projekt, das akademische Forschung mit industrieller Expertise verbindet. Ein zentrales Thema des Gesprächs ist die Rolle der T-Zellen im Immunsystem und deren Fehlsteuerung bei der Schuppenflechte. Prof. Stary erklärt anschaulich, wie bestimmte Botenstoffe wie Interleukin-17 und -23 die Entzündungsreaktion vorantreiben – und wie neue Therapien gezielt in diesen Prozess eingreifen können. Besonders vielversprechend: Ansätze, die nicht nur die Symptome lindern, sondern das Gleichgewicht des Immunsystems nachhaltig wiederherstellen. Ein neu entdecktes Enzym könnte dabei eine Schlüsselrolle spielen. Darüber hinaus gibt Stary Einblicke in aktuelle Studien, den Einfluss von Umweltfaktoren wie Fettleibigkeit und das Potenzial, diese Erkenntnisse auch auf andere chronisch-entzündliche Erkrankungen zu übertragen. Eine informative Episode für alle, die moderne Dermatologie und translationalen Fortschritt hautnah erleben wollen.

A Gluten Free PodcastEpisode 176On today's episode I chat with Associate Professor Dr Bob Anderson — a world-renowned gastroenterologist, immunologist and trailblazer in coeliac disease research. From his foundational work at the Walter and Eliza Hall Institute (WEHI) to creating Nexvax2, leading Novoviah Pharmaceuticals, and becoming President of the International Society for the Study of Coeliac Disease (ISSCD), Bob has shaped the coeliac research landscape as we know it.We discuss how his career began, what he's most excited about in current research, and what's ahead for coeliac disease globally — including a look at ICDS 2026 in Melbourne.What We Cover

In this week's episode we'll learn about the role of interleukin-1 signaling in the bone marrow microenvironment in the development of myelodysplastic syndromes, the immune checkpoint regulator VISTA as a potential target for preventing graft-vs-host disease, and epcoritamab plus gemcitabine and oxaliplatin in transplant-ineligible relapsed/refractory diffuse large B-cell lymphoma.Featured Articles:IL-1R1 and IL-18 signals regulate mesenchymal stromal cells in an aged murine model of myelodysplastic syndromesTargeting cell-surface VISTA expression on allospecific naïve T cells promotes toleranceEpcoritamab plus GemOx in transplant-ineligible relapsed/refractory DLBCL: results from the EPCORE NHL-2 trial

A Gluten Free Podcast Episode 174In today's episode I'm joined by Olivia Moscatelli, a PhD student and scientist researching coeliac disease at the Walter and Eliza Hall Institute (WEHI) in Melbourne. Olivia works alongside Associate Professor Jason Tye-Din, one of the world leading experts in coeliac disease research. Not only is she making pivotal contributions to the field, but she also brings a unique and deeply personal perspective—because she lives with coeliac disease herself.We'll dive into Olivia's diagnosis story, what led her into the world of scientific research, and the groundbreaking studies she's currently working on that could transform the way coeliac disease is diagnosed and treated in the future.What we'll cover: 

In today's episode, we are happy to hear from our clinic's Dr. Scott and one of his patients, Keith about his successful experience tackling gut health issues. Keith's case posed a very common conundrum that we've seen in many with gut health issues - are we dealing with bacterial overgrowth (SIBO), fungal overgrowth (candida) or potentially both? We'll walk through some of the key indications that Keith's initial SIBO diagnosis was actually a candida case, and we'll cover the best testing and treatments that led to Keith's recovery.  Need help navigating your digestive or other health conditions? Learn more about our virtual clinic: https://drruscio.com/virtual-clinic/

How to lower chronic inflammation naturally. Here are 17 things that either have been shown to work or don't work. Chronic inflammation, that low-grade inflammation that occurs, even though you are not sick, is implicated in diseases ranging from arthritis, diabetes, cancer and heart disease. The term “Inflamm-aging” is a reference to how inflammation is linked to the aging process.   ·      What is chronic inflammation ·      Diseases associated with chronic inflammation, including Inflammaging ·      How to test for inflammation: C-reactive protein (CRP) and Interleukin 6 (IL-6) ·      Effects of Weight loss on inflammation markers CRP, IL-6 and TNF alpha (TNF alpha) ·      Cholesterol, LDL and chronic inflammation ·      How exercise affects inflammation ·      what foods raise systemic inflammation? ·      Health conditions associated with pro-inflammatory eating. ·      Chronic inflammation telomere effects ·      Foods that reduce inflammation & Advanced glycation end products ·      Fiber and the microbiome. Short-chain fatty acids (Butyrate) ·      Skin moisturizing ·      Curcumin and turmeric ·      Ginger ·      Garlic and garlic powder &  Aged Garlic Extract ·      Vitamin B12, B6, Folic Acid & Homocysteine ·      Nattokinase ·      Homotaurine ·      Fish oil ·      Resveratrol & NF-kB (Nuclear Factor-kB) ·      Vitamin D ·      Vitamin C and Orange juice ·      What is the best way to reduce chronic inflammation (most return on investment)   Supplement Facts Coffee Mug: https://joecannon.creator-spring.com/listing/supplement-facts-mug   Consultations  https://supplementclarity.com/private-consultations/     Get My Rhabdo Book   Education is the best defense against getting rhabdomyolysis. I've been teaching about rhabdo for over 10 years. If you are in the US, you can order my book directly from me. Purchase My Rhabdo Book Order on Amazon       Connect With Me Joe-Cannon.com SupplementClarity.com YouTube    About Me   For over 30 years I've been sorting nutrition facts from fiction, busting myths and helping people understand dietary supplements using clinical research as my litmus test.    I have an MS in exercise science and a BS in biology & chemistry. I've written several books, including Rhabdo, the first book about exercise-induced rhabdomyolysis.   Disclaimer   Episodes are for information only. I'm NOT a medical doctor. NO medical advice is given or implied. ALWAYS consult your physician for the best health advice for you. I participate in the Amazon Associates program which means if you click on a link to amazon and make a purchase, I may make a small commission at no extra cost to you.    

Description: Co-hosts Ryan Piansky, a graduate student and patient advocate living with eosinophilic esophagitis (EoE) and eosinophilic asthma, and Holly Knotowicz, a speech-language pathologist living with EoE who serves on APFED's Health Sciences Advisory Council, interview Jason Ingraham, an adult living with eosinophilic fasciitis (EF), and Dr. Catherine Sims, a rheumatologist at Duke University and a Health Services Research Fellow at the Durham Veterans' Affairs Hospital. They discuss Jason's experiences living with EF and Dr. Sims's experience treating EF. They share Jason's journey to diagnosis and the importance of working with a group of specialists. They share tips on medication and physical therapy, how to communicate with your medical team, and manage your activity and mindset. Disclaimer: The information provided in this podcast is designed to support, not replace the relationship that exists between listeners and their healthcare providers. Opinions, information, and recommendations shared in this podcast are not a substitute for medical advice. Decisions related to medical care should be made with your healthcare provider. Opinions and views of guests and co-hosts are their own.   Key Takeaways: [:50] Ryan Piansky introduces the episode, brought to you thanks to the support of Education Partners Bristol Myers Squibb, GSK, Sanofi, and Regeneron, and co-host, Holly Knotowicz.   [1:14] Holly introduces today's topic, eosinophilic fasciitis, with guests, Jason Ingraham and Dr. Catherine Sims.   [1:25] Jason is an adult living with eosinophilic fasciitis (EF). Dr. Sims is a rheumatologist at Duke University and a Health Services Research Fellow at the Durham Veterans' Affairs Hospital.   [1:52] Dr. Sims explains what EF is. Patients may present with symptoms of large plaques on their skin, edema of arms and legs, Raynaud's Phenomenon, contractures of arms or legs, limited mobility, or loss of the ability to do tasks they used to do.   [2:42] EF, as with most eosinophilic disorders, doesn't follow the textbook. Some people will present with one symptom and some with multiple symptoms. There is a disconnect between how we diagnose conditions like EF and how patients present.   [3:01] There are major and minor criteria for the diagnosis. As in Jason's case, it takes time for the symptoms to present. Things develop over time. It took multiple specialists to diagnose Jason.   [3:38] Eosinophilic conditions are incredibly different from each other. When Dr. Sims sees a patient with high eosinophils, she thinks of three major buckets: infection, autoimmune diseases, and cancer.   [4:12] Patients will often see many different specialists. In Jason's case, they had done a skin biopsy that wasn't as helpful as they hoped. That led him to get a deep muscle biopsy to collect the lining of the muscle.   [4:47] Fasciitis is the inflammation of the muscle lining or fascia. A sample of the fascia can demonstrate under the microscope if there is a thickening, swelling, or inflammation of the lining of the muscle.   [5:24] Dr. Sims as a rheumatologist treats a number of rare diseases. Eosinophilic fasciitis is an ultra-rare disease.    [5:43] Jason had a local primary care doctor and a rheumatologist who both did a really good job and referred him to Dr. Sims. She had the benefit of their hard work to guide her next steps. Because EF is so rare, she has pitched Jason's case twice in rheumatology grand rounds sessions.   [6:18] During one of these sessions, Dr. Sims was advised to get the fascial biopsy that ultimately led to the diagnosis. She benefited from the intelligence and input of dozens of doctors.   [6:59] In the Fall of 2022, while hiking on vacation with his wife, Jason was extremely fatigued, and his forearms and lower legs swelled. His socks left deep impressions. It was difficult to reach his feet to put socks on. He spent a lot of time uncharacteristically resting.   [8:09] Jason's primary care doctor ran lots of blood tests. He thought it might be a tick bite. Jason started seeing specialists, having tests and hospital visits.   [8:57] Jason worked with a rheumatologist in Wilmington, an infectious disease doctor, and a hematologist/oncologist who reached out to a Duke expert. He also saw a pulmonologist and a dermatologist. He got the referral to Dr. Sims for March of 2023.   [9:57] The first diagnosis Jason received was after his first hospital stay in January of 2023, when he had bone marrow biopsies, CT scans, ultrasound, and other tests. He was deemed to have idiopathic hypereosinophilic syndrome (IHES).   [10:30] It was only a few weeks before his local rheumatologist said his panels were back and one tipped it from an IHES diagnosis to eosinophilic granulomatosis with polyangiitis (EGPA). He joined the Vasculitis Foundation and researched EGPA.   [11:03] Dr. Sims told Jason that EGPA was a working diagnosis but he didn't check all the boxes. There was the underlying thought that maybe it was something else. He had a second flare when he came off of prednisone in June of 2023.   [11:48] Dr. Sims scheduled Jason for a muscle biopsy while he was off steroids. That's how he got the diagnosis of eosinophilic fasciitis (EF). Jason says the disorder is hard for him to pronounce and he can barely spell the words.   [12:52] Jason's wife Michelle encouraged Jason to track his symptoms and medications and keep track of data. Going from specialist to specialist, the first thing he did was give the history.   [13:31] Jason found it helpful to create a spreadsheet of data with blood test results, meds, how he was feeling each day, his weight, and even notes about when he had difficulty putting his socks on. Jason is an advocate of owning your continuity of care as you see different doctors.   [14:42] Jason says the doctors at Duke talk very well between themselves.   [14:49] Jason likes to look back at that spreadsheet and see how far he's come, looking at the dosage he was on during and after flares and the dosage he's on now, or zero, on some of the medications. That's a little bit of a victory.   [15:16] Holly works at a private hospital without Epic or CareEverywhere so she gives physical notes to her patients to give to their doctors. She comments that a great PCP, like the one Jason had, can make all the difference in the world.   [16:18] Jason's PCP, Dr. Cosgrove, referred Jason to Duke for a second opinion. That was where he met Dr. Sims. He's glad to have both Dr. Sims and his PCP accessible.   [17:35] Jason says the number of questions you have with this type of thing is immense. When you look up EF, you find very little and the literature isn't easily digestible by patients. Being able to reach out to your doctors for a quick question is super helpful. [17:56] Jason has been able to do telehealth follow-ups and not always have to travel or take off work, which has been extremely helpful. He has been at Duke a good handful of times for various things but remote follow-ups are helpful.   [18:52] Dr. Sims says people just don't know about EF as it is an ultra-rare diagnosis. Even physicians don't understand what causes it. It's lumped in with all other eosinophilic conditions but these disorders don't all present the same way.   [19:19] EoE doesn't look like EF, even though they're both driven by the same immune cells. Dr. Sims says the first need is educating providers and patients on what the diagnosis is; awareness in general when a patient is having this swelling of extremities.   [19:44] Dr. Sims says at his baseline, Jason is very active with multi-mile hikes. When Dr. Sims met him, he was off from the baseline of what he was able to do. Being aware of your baseline and changes from that is very informative for doctors.   [20:07] Dr. Sims talks about the patient being a liaison between multiple specialists. Bringing data to your subspecialist always helps facilitate care and come up with a bigger picture of what's happening.   [20:23] Jason first went to Dr. Sims with the diagnosis of EGPA. She said, let's treat the EGPA and see what happens but they kept an open mind. With ultra-rare diseases, sometimes it's difficult for patients not to have a label for their condition.   [20:45] Dr. Sims explains to her patients that sometimes we live in the discomfort of not having a label. She keeps an open mind and doesn't limit herself to just one diagnosis. She seeks feedback from providers who have seen this before and know what works.   [21:07] Just as Jason described, you will go through multiple diagnoses. Is this cancer? Is it a parasitic infection? Where did you travel? You will see many subspecialists. It's extremely anxiety-provoking.   [21:31] When Dr. Sims did her grand rounds, she gave a third of the presentation, and the other two thirds were presented by an infectious disease doctor and a hematologist. In these cases, you need more than one subspecialist to complete the workup.   [22:10] Dr. Sims says there are a lot of misconceptions that the patient will get the diagnosis right away and the right therapy and get better. There are multiple therapies, not just medications. There are lifestyle and work modifications; it's a gradual process.   [22:22] One of Dr. Sims's goals for Jason and Michelle is to get back to doing the things that they enjoy, tennis and hiking. That's a measurement of the quality of life that a patient has.   [22:34] Talking to your doctors about how you're feeling and how you're functioning is huge. It may be that this is your new normal, but it may also be that we can make adjustments to maximize your quality of life.   [23:00] There are misconceptions about the journey of diagnosis and treatment. Have a close relationship with your subspecialist. PCPs have a high burden of expectations. As a rheumatologist who treats rare diseases, it's helpful to take on a part of that burden.   [22:31] If you don't have good communication with your providers and they aren't listening to you, you can always go get another opinion. The provider relationship is life-long.   [23:43] It's important for your provider to take what's important to you into consideration when they make treatment decisions.   [25:00] As a rheumatologist, steroids are a first-line therapy for Dr. Sims. Their role is the quick control of inflammation. The goal is always to get you off of the steroids as soon as possible, in the safest way possible.   [25:17] When Jason came to Dr. Sims, he was on mepolizumab for the working diagnosis of EGPA. Mepolizumab is one of the primary therapies for EGPA. They talked about not making treatment changes as they were navigating what was happening.   [25:40] They didn't want to make a change of medication and then have that be mistaken for disease activity. They didn't want too many variables moving at once.   [25:47] Typically, the first-line therapy is steroids, meant to help with the swelling, pain, and tightness that patients will get lining their muscles and give them a bit more functionality and decreased pain.   [26:00] Long-term, Dr. Sims gives immunosuppressant medication. She prescribed methotrexate for Jason. In EF, the immune system is overly activated, attacking the lining of the muscles and causing the symptoms.   [26:51] If you suppress the immune system activity, that leads to decreased inflammation and symptoms in the patient. Steroid use, over a few months, is detrimental, with low bone density, weight gain, high blood pressure, and diabetes.   [27:14] Dr. Sims starts with prednisone and folds in medications like mycophenolate or methotrexate.   [27:19] Mepolizumab is an interleukin 5 blocker. Interleukin 5 is part of the immune system and is necessary for eosinophils to grow, function, and multiply. The goal of using mepolizumab is to lower the eosinophils that are contributing to the disease symptoms.   [27:48] Methotrexate, prednisone, and mepolizumab can work synergistically or independently. Most rheumatologists start with methotrexate or mycophenolate which have fewer side effects and have been around longer. We know how to manage those.   [28:08] If there is no response, we may add something like mepolizumab. As Jason was already on mepolizumab, Dr. Sims added methotrexate.   [28:20] IVIG, an infusion of immunoglobulin, has also been used as a quick way to control inflammation. It is used in other autoimmune diseases like myositis, which is inflammation of the muscle itself.   [29:08] With untreated eosinophilic fasciitis, the lining of the muscle may continue to be inflamed and can lead to fibrosis, damage that cannot be reversed. The patient can become very disabled. Contracture is one result of this.   [30:16] Jason says when he tried a new medication, he monitored if it was a good fit and if the side effects were less impactful than the underlying disease. Dr. Sims adjusted his dosages or tried to get off certain medicines as needed.   [30:59] After his muscle biopsy from his left calf, it took about a month to get back to walking easily. He was already in physical therapy, going many times for a variety of things. He had back pain, potentially related to his EF. His physical therapist was great.   [31:56] The stretches alternated between upper and lower body. Jason bought tools to do the stretches at home. When he's not feeling as well, he goes back to some of those same stretches. When he was on steroids, he took long walks to strengthen his bones.   [32:39] Jason started making phone calls to supportive family and friends on his walks and started listening to podcasts related to his condition or medications. Getting back to tennis and hiking is important to Jason. He's happy to be out there.   [33:20] Jason was open with his employer about his condition. Some of the weekly meds can make him not feel well. His employer gives him some flexibility. He has good days that far outnumber the bad days. He doesn't have to think about EF too much now.   [34:33] It's nothing like when he was in a flare, especially when he was in a flare before being diagnosed. What gets him through a bad day is giving himself some grace and understanding while he waits for his meds to catch up. He rests more than he wants to.   [35:33] Low-impact exercises like walking help Jason. He's trying to find a support network that gets EF. That led him to APFED, to find anyone experiencing something like what he was. He saw a conference that included a session on EF.   [36:09] Jason signed up for the conference and there he met Ryan's mother who has EF. They were each the first person the other had met with EF. They decided to connect after the conference. They talked on the phone for about an hour.   [36:39] She told Jason how she got into APFED and talked a lot about her son who had eosinophilic diseases. Soon after, Jason talked to Ryan as a primer for this podcast.    [38:15] Having a community to relate to, even if it's one person, is massive. It can make you feel less isolated.   [38:42] Holly says it's hard having a chronic illness. She thanks both Jason and Dr. Sims for sharing so much information and their journey and she asks for last words.   [38:58] Dr. Sims believes finding a community is critical. She interviews a lot of patients for research and isolation is a frequent theme. Even the doctor doesn't know what it's like to live with the condition you live with daily. As Jason said, give yourself grace.   [39:33] Dr. Sims tells her patients that they're different from the general population because they have to spend so much time and energy managing their condition that they can't do x, y, or z today, and that is OK. She says to stay motivated and positive.   [40:12] Find what works for you. Walking is good for your physical and mental health. Have the goal of getting back to what makes you happy. Take initiative and find non-medication ways to recuperate. You have control over ways you can feel better.   [40:43] Connect with others and share your story, like Jason did today. It may make someone's journey a little easier and make them feel less alone. Utilize your condition for good, for a bigger purpose.   [41:04] Jason had wished he could meet someone who could tell him what EF would be like over the years. He says to stay positive and find out what you have control over. Jason believes the future is bright for being able to do many things for a long time.   [42:26] For our listeners who would like to learn more about eosinophilic fasciitis, please visit APFED.org and check out the links in the shownotes.   [42:33] If you're looking to find a specialist who treats eosinophilic disorders, like Dr. Sims, you can use APFED's Specialist Finder at APFED.org/specialist.   [42:43] If you'd like to connect with others impacted by eosinophilic diseases, please join APFED's online community on the Inspire Network at APFED.org/connections/.   [42:55] Ryan thanks Jason and Dr. Sims for joining us for this excellent conversation. Holly also thanks APFED's Education Partners Bristol Myers Squibb, GSK, Sanofi, and Regeneron for supporting this episode.   Mentioned in This Episode: Dr. Catherine Sims, rheumatologist Duke University Hospital Durham VA Medical Center   APFED on YouTube, Twitter, Facebook, Pinterest, Instagram Real Talk: Eosinophilic Diseases Podcast apfed.org/specialist apfed.org/connections   Education Partners: This episode of APFED's podcast is brought to you thanks to the support of Bristol Myers Squibb, GSK, Sanofi, and Regeneron.   Tweetables:   “EF patients may present with large plaques on their skin, edema of arms and legs, Raynaud's Phenomenon, contractures of arms or legs, limited mobility, or loss of the ability to do tasks they used to do.” — Dr. Catherine Sims   “Steroids are … first-line therapy. Their role is the quick control of inflammation. The goal is always to get you off steroids as soon as possible, in the safest way possible.” — Dr. Catherine Sims   “Methotrexate, prednisone, and mepolizumab can work synergistically or independently. Most rheumatologists start with methotrexate or mycophenolate which have fewer side effects and have been around longer.” — Dr. Catherine Sims   “Stay positive and find out what you have control over. The future is bright for being able to do many things for a long time.” — Jason Ingraham

Literature Review Week Why do some people react to mosquitoes so vigorously? There is fascinating data for me in the Nature article, as I see lots of kids that react strongly to mosquitoes while others do not at all. A hyper primed immune reaction makes a lot of sense as the immune system is extra sensitive to the insult in individuals that have chronic allergic phenotypes. They are in effect polarized to see the outside world through an irritant lens and thus react in a more robust way. The cell called GD3 releases Interleukin 3 or IL-3 which is a cytokine signaling molecule that tells skin based sensory neurons to become more sensitive to allergens like house dust mites, environmental molds, and in this case mosquito saliva. Thus, the mosquito saliva induces more of the itch scratch cycle. The effect is to increase the gain sensitivity on the skin to 10. This is likely a main reason why having an allergic child take immunotherapy against allergens that they react to lowers the rheostat for all irritants. It is like a global check on the sensory system. This is another reason to consider SLIT and or SCIT immunotherapy in allergic children... Plus a discussion on the Joe Rogan podcast with Callie and Casey Means. Enjoy, Dr. M  

Over 20 years ago biologics were introduced for psoriasis and PsA. Since then even more targeted treatments have been introduced. Listen as dermatologist Dr. Steven Feldman from Wake Forest University School of Medicine, shares his perspectives on the latest treatments, resident memory T-cells, and what's to come (such as an oral IL-23 agent) with moderator Max Blitstein. This episode is provided with support from Bristol Myers Squibb. 

Immunotherapies continue to redefine treatment for many types of cancer and one of the first immunotherapies approved and used clinically as a therapeutic is Interleukin-2, or IL-2. Aulos Bioscience is an immuno-oncology company that has developed AU-007, a potential best-in-class IL-2, that improves on many of the other IL-2 products in development. In this episode, we discuss the promise of AU-007 with President and CEO, Aron Knickerbocker. Link to Interleukin-2 review article can be found here: https://www.nature.com/articles/s41587-022-01390-3

Subscribe to our channel: https://www.youtube.com/@optispan Check out paper #1 on IL-11 signaling: https://www.nature.com/articles/s41586-024-07701-9.pdf Check out paper #2 on combination trametinib/rapamycin treatment: https://www.biorxiv.org/content/biorxiv/early/2024/07/25/2024.07.25.605097.full.pdf Related episodes: An introduction to the study of RAPAMYCIN: https://www.youtube.com/watch?v=czx_-DqnnrQ&t=1s In this episode, Matt discusses two recent mouse lifespan studies: one focused on inhibiting IL-11 signaling, and one focused on combined trametinib and rapamycin treatment. IL-11, or Interleukin-11, is a protein that plays an important role in modulating inflammation and healing, while trametinib is an FDA-approved drug that targets certain cancers, particularly melanoma. You can find extensive discussion of rapamycin in our R-Files series linked above. Matt explains the "900-day rule" for evaluating mouse lifespan studies such as these two, and provides his take on whether these results are game-changers for the geroscience field as well as whether we should consider these interventions for human use at this time. Producers: Tara Mei, Nicholas Arapis Video Editor: Jacob Keliikoa DISCLAIMER: The information provided on the Optispan podcast is intended solely for general educational purposes and is not meant to be, nor should it be construed as, personalized medical advice. No doctor-patient relationship is established by your use of this channel. The information and materials presented are for informational purposes only and are not a substitute for professional medical advice, diagnosis, or treatment. We strongly advise that you consult with a licensed healthcare professional for all matters concerning your health, especially before undertaking any changes based on content provided by this channel. The hosts and guests on this channel are not liable for any direct, indirect, or other damages or adverse effects that may arise from the application of the information discussed. Medical knowledge is constantly evolving; therefore, the information provided should be verified against current medical standards and practices. More places to find us: Twitter: https://twitter.com/optispanpodcast Twitter: https://twitter.com/optispan Twitter: https://twitter.com/mkaeberlein Linkedin: https://www.linkedin.com/company/optispan https://www.optispan.life/ Hi, I'm Matt Kaeberlein. I spent the first few decades of my career doing scientific research into the biology of aging, trying to understand the finer details of how humans age in order to facilitate translational interventions that promote healthspan and improve quality of life. Now I want to take some of that knowledge out of the lab and into the hands of people who can really use it. On this podcast I talk about all things aging and healthspan, from supplements and nutrition to the latest discoveries in longevity research. My goal is to lift the veil on the geroscience and longevity world and help you apply what we know to your own personal health trajectory. I care about quality science and will always be honest about what I don't know. I hope you'll find these episodes helpful!

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances discusses a recently published original research paper on Interleukin-6 and Cardiovascular Events in Healthy Adults in the Multi-Ethnic Study of Atherosclerosis

Bei Menschen wird mit zunehmendem Alter ein bestimmtes Protein produziert, das für verschiedene Alterserkrankungen verantwortlich ist. Interleukin 11. Auch Mäuse besitzen dieses Protein. Forschende des Medical Research Council Laboratory of Medical Science und des Imperial College London konnten das Protein in Mäusen jetzt erfolgreich abschalten. Ihre Ergebnisse haben sie in der Fachzeitschrift Nature veröffentlicht. So konnten die Forschenden zeigen, dass durch das Ausschalten des Gens die Lebenserwartung der Mäuse um bis zu 25 Prozent verlängert werden kann. | Diese Podcast-Episode steht unter der Creative Commons Lizenz CC BY-NC-ND 4.0.

In this week's episode we'll discuss new insights on the role of GM-CSF in establishing immune memory. The authors propose that the coordination of opposing immune memory programs, driven by GM-CSF, may be essential to efficient, yet controlled, innate immune responses. After that: Interleukin-1 inhibition in TTP. Researchers explore the potential of recombinant IL-1 receptor antagonist, anakinra, in a murine model of thrombotic thrombocytopenic purpura—an uncommon but potentially fatal disorder with limited therapeutic options. Finally, we'll learn about CAR T-cell therapy outcomes by race and ethnicity in large B-cell lymphoma. Non-Hispanic Black patients had lower rates of response and progression-free survival in axi-cel clinical trials and real-world data, raising awareness and giving further insights into potential inequitable access to care.Featured Articles:GM-CSF receptor expression determines opposing innate memory phenotypes at different stages of myelopoiesis Mortality, cardiac and cerebral damage reduction by IL-1 inhibition in a murine model of TTP Real-World and Clinical Trial Outcomes in Large B-cell Lymphoma with Axicabtagene Ciloleucel Across Race and Ethnicity 

Send us a Text Message.In this FRIDAY 5 episode of "The Autoimmune RESET," VJ Hamilton explores key markers of inflammation from a functional medicine perspective. VJ dives into the roles of C-Reactive Protein (CRP), Erythrocyte Sedimentation Rate (ESR), Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-6 (IL-6), and Homocysteine in indicating both acute and chronic inflammation. VJ explains how genetic variations in IL-6 and TNF-alpha can predispose individuals to higher inflammation levels and discusses the importance of tracking symptoms even when these markers are normal. VJ also cover how localized inflammation, such as in the gut, can be detected using calprotectin. Learn how understanding these markers can provide a comprehensive view of your health and guide effective holistic management strategies. Tune in for valuable insights into maintaining a balanced lifestyle and reducing inflammation naturally.If you would like to book a free initial consultation with VJ Hamilton, The Autoimmunity Nutritionist, to find out about allergy testing and how nutritional therapy and functional testing could improve your health, you can book an appointment here.Learn more about the functional medicine services at The Autoimmunity Nutritionist Clinic here.Thanks for listening! You can join The Autoimmune Forum on Facebook or find me on Instagram @theautoimmunitynutritionist.

Send us a Text Message.A Gluten Free Podcast Episode 127 My guest on today's episode is Associate Professor, gastroenterologist & coeliac disease researcher, Jason Tye-Din. We'll talk about his own allergy journey & personal connection to coeliac disease, developing simple diagnoses, gluten exposure testing, possible preventions for this condition & the mental health research around coeliac disease.   What we'll cover: * Jason's personal journey of living with a peanut allergy * Jason's wife's coeliac disease diagnosis * Developing simple & effective diagnoses: Interleukin 2 (possibility of avoiding gluten challenge & gastroscopy in future) * Stool & urine gluten exposure testing  * The current research into brain fog & other various mental health associations with coeliac disease * Disorder of the gut/brain axis (DGBI), gut hypnotherapy & the gut microbiome * Australia first ENDIA study (Environmental Determinants of Islet Autoimmunity) in relation to Type 1 Diabetes & coeliac disease research * How to get involved & find out more about the research & trials Links WEHI website Current coeliac disease clinical trials Buy tickets to A Gluten Free Evening

Although immunotherapies for patients with solid tumors such as melanoma can be dramatically successful, the majority of patients are resistant and require alternative treatments. While the cytokine interleukin-12 is well known for potentiating the effect of immunotherapies, such as checkpoint blockade, it couldn’t be used because of toxicity. At the 2023 AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics, Jun Ishihara, PhD, a lecturer at London’s Imperial College reported on a protein bioengineering approach in which IL/12 is bound to collagen from the extracellular matrix of the tumor. This targets the cytokine’s action to operate specifically on cancer while hopefully avoiding most of the off-target toxicities previously observed with unbound IL/12. After the conference, OncTimesTalk’s Peter Goodwin called to see him at his London laboratory.

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: Update on Chinese IQ-related gene panels, published by Lao Mein on December 14, 2023 on LessWrong. It turns out that Chinese 23-and-me-esque gene panel already include intelligence markers! For example, 23mofang uses Interleukin 3 as a proxy for brain volume, citing this paper. It's... only significant in women. Not a good sign. But the cited study notes a Danish gene-correlation study that included brain scans, from which they obtained brain volume. Apparently, the correlation is true across races. In any case, I've been reaching out to past coworkers, and they agree with my assessment that a polygenic database for the purpose of embryo selection would be easy and mostly cheap to do. Being Chinese, we of course have no issues with including factors like eye color, height, intelligence, ect. However, I have several questions before I proceed further. What is the overall demand? How many customers would be interested? What specific traits are parents most interested in? Funding is the single biggest obstacle I face, and I will be applying for AstralCodexTen funding. If enough interest is displayed or if I get charitable funding, my gut feeling is that I can offer analysis for

In today's episode, we're exploring 3 different topics. First, we'll unravel the intriguing world of beta-glucans and their dual role in regulating the immune system. Then, we'll venture into the ancient practice of Agni Sara, a yoga exercise renowned for strengthening digestive organs. Finally, we'll unveil two unique methods to trigger the acute relaxation response, encouraging parasympathetic activity. Stay tuned for this 3-topic episode! Topics: 1. Agni Sara Exercise - Definition and Purpose - Origin and Traditional Yoga Practice - Physical and Energetic Benefits - Research Study on Agni Sara - Study Involving 12 Volunteers - Ultrasound Examination of Superior Mesenteric Artery - Increase in Blood Flow and Digestive Function Improvement - Traditional Agni Sara Exercise Instructions 2. Beta-Glucans - Definition and Classification - Interaction with the Immune System - Immune System Review - Role of Dectin-1 Receptors - Immune-Boosting Effects - Stimulation of Immune Cells, Phagocytosis, & Antibody Production - Modulation of Inflammation - Stimulation of Interleukin 10 - Balancing Immune Response - Food Sources of Beta-Glucans - Mushrooms Rich in Beta-Glucans - Mushroom Extract Supplements 3. Tibetan Singing Bowls and the Acute Stress Response - Introduction to Tibetan Singing Bowls - Composition and Original Use - Sound Characteristics - Benefits of Tibetan Singing Bowls (TSB) - Impact on Distress, Anxiety, Depression, and More - Physiological Effects on Heart Rate, Respiration, and More - Research Study on Acute Relaxation Response - Comparison of TSB and Progressive Muscle Relaxation (PMR) - Evaluation of HRV, Alpha Power Band (EEG), and Anxiety - Study Findings - Promotion of Acute Relaxation Response by TSB and PMR - TSB's Pronounced Effect on HRV Parameters and Alpha Band Activity - Acknowledgment of Individual Preferences for Relaxation Techniques - Emphasis on Research-Backed Tools for Stress Reduction Thanks for tuning in! Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" If you liked this episode, please leave a rating and review or share it to your stories over on Instagram. If you tag @synthesisofwellness, Chloe would love to personally thank you for listening! Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Follow Chloe on TikTok @chloe_c_porter Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to purchase products, subscribe to our mailing list, and more! Or visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠linktr.ee/synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to see all of Chloe's links, schedule a BioPhotonic Scanner consult with Chloe, or support the show! Thanks again for tuning in! --- Support this podcast: https://podcasters.spotify.com/pod/show/chloe-porter6/support

This amazing study demonstrates the influence of plant-based (high-fiber) and/or fermented food diets on our immune system. Researchers found that fermented foods like yogurt, kimchi, and kombucha caused a reduction of 19 cytokines including IL-6, IL-12b, and IL-10. This reduction may potentially lead to reduction in chronic inflammation. Let's review this study. DrBeen: Medical Education Online https://www.drbeen.com/ FLCCC | Front Line COVID-19 Critical Care Alliance https://covid19criticalcare.com/ References (August 18, 2023) Gut Microbiota-Targeted Diets Modulate Human Immune Status - PMC https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9020749/ Figure - PMC https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9020749/figure/F6/ Interleukin-6 as a Multifunctional Regulator: Inflammation, Immune Response, and Fibrosis - Ernest Choy, Stefan Rose-John, 2017 https://journals.sagepub.com/doi/10.5301/jsrd.5000265#:~:text=IL%2D6%20is%20produced%20by,cells%2C%20fibroblasts%2C%20and%20hepatocytes . Role of Interleukin 10 Transcriptional Regulation in Inflammation and Autoimmune Disease - PMC https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410706/#:~:text=In%20vivo%2C%20major%20sources%20of,granulocytes%20like%20neutrophils%20and%20eosinophils . Regulation of IL-10 and IL-12 production and function in macrophages and dendritic cells - PMC https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4754024/#:~:text=Interleukin%2D12%20signaling,dendritic%20cells%20(DCs)%202 . Interleukin-10 production by effector T cells: Th1 cells show self control - PMC https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118719/ Disclaimer: This video is not intended to provide assessment, diagnosis, treatment, or medical advice; it also does not constitute provision of healthcare services. The content provided in this video is for informational and educational purposes only. Please consult with a physician or healthcare professional regarding any medical or mental health related diagnosis or treatment. No information in this video should ever be considered as a substitute for advice from a healthcare professional.

This weeks guest is Professor Marcel Nold, MD. Dr. Nold is a clinician scientist in the research environment of neonatal immunology and microbiomes at Monash University in the city of Monash in Melbourne, Australia. Professor Nold received his Doctor of Medicine degree at the JW Goethe-University at Frankfurt am Main, Germany, including final year rotations in Zürich (Switzerland), Montréal (Canada) and Capetown (South Africa). For his biomedical research training he spent six years at the Pharmazentrum at Frankfurt am Main and three years as a research Fellow at the laboratory of Professor Dinarello, at the University of Colorado Denver. In 2009 he was recruited to The Ritchie Centre in Melbourne and finished his specialist training at Monash Newborn. Professor Nold is a leading researcher worldwide in the field of immune cytokine signaling and was the key contributor to identifying Interleukin 37 or IL37. His research has been published in the journals Nature Immunology, Science Immunology and many others. His academic Inflammation in Neonatal Diseases Research Group and his industry programs aim to characterise underlying pathways of inflammation in early life diseases, with a focus on interventional immunology in cardiopulmonary and intestinal diseases of the preterm. For the purposes of this interview, Dr. Nold is a researcher with a view of the maternal child dyad that is prevention focused and health span conscious. His research has led to many critical discoveries in the neonatal health space that I find deeply intriguing. We get into some deep immunology at times which is critical for total understanding. Enjoy, Dr. M

Welcome to Olink Proteomics in Proximity Podcast! Below are some useful resources from this episode: Highlighted publication: Diaz-Canestro C, Chen J, Liu Y, Han H, Wang Y, Honoré E, Lee CH, Lam KSL, Tse MA, Xu A. A machine-learning algorithm integrating baseline serum proteomic signatures predicts exercise responsiveness in overweight males with prediabetes. Cell Rep Med. 2023 Feb 21;4(2):100944. doi: 10.1016/j.xcrm.2023.100944. Epub 2023 Feb 13: https://www.cell.com/cell-reports-medicine/pdf/S2666-3791(23)00036-8.pdf PMID: 36787735; PMCID: PMC9975321: https://pubmed.ncbi.nlm.nih.gov/36787735/ Highlighted platform that was used to measure proteins in this study with a next-generation sequencing (NGS) readout (Olink® Explore): https://olink.com/products-services/explore/ Here is general information from Wikipedia about IL-6, one of the protein biomarkers identified in this study: https://en.wikipedia.org/wiki/Interleukin_6 Here is general information from Wikipedia about TFF-2, one of the protein biomarkers identified in this study: https://en.wikipedia.org/wiki/Trefoil_factor_2 Would you like to subscribe to the podcast on your favorite player or app? You can do so here: Apple Podcasts: https://apple.co/3T0YbSm Spotify Podcasts: https://open.spotify.com/show/2sZ2wxO... Google Podcasts: https://podcasts.google.com/feed/aHR0... Amazon Music: https://music.amazon.com/podcasts/d97... Podcast Addict: https://podcastaddict.com/podcast/409... Deezer: https://www.deezer.com/show/5178787 Player FM: https://player.fm/series/series-3396598 In case you were wondering, Proteomics in Proximity refers to the principle underlying Olink Proteomics assay technology called the Proximity Extension Assay (PEA), and more information about the assay and how it works can be found here: https://bit.ly/3Rt7YiY For any questions regarding information Olink Proteomics, please email us at info@olink.com or visit our website: https://www.olink.com/WHAT IS PROTEOMICS IN PROXIMITY?Proteomics in Proximity discusses the intersection of proteomics with genomics for drug target discovery, the application of proteomics to reveal disease biomarkers, and current trends in using proteomics to unlock biological mechanisms. Co-hosted by Olink's Dale Yuzuki, Cindy Lawley and Sarantis Chlamydas.

What's new in treatments for spondyloarthritis? Learn more about the rationale for novel therapies and the latest data. Credit available for this activity expires: 03/09/24 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/988291?ecd=bdc_podcast_libsyn_mscpedu

The IdeaSpace Philippines Accelerator Program Cohort 10 is having its Demo Day this March 2, 2023, which is also in celebration for IdeaSpace Philippines 10th anniversary! Ano nga ba ang IdeaSpace? What will happen in the Demo Day? Let's know with Shor Macalbe, Program Manager for Startup Development at IdeaSpace Philippines! IN THIS EPISODE | 00:00  Introduction | 00:49 Ano ang IdeaSpace Philippines Accelerator Program? | 03:03 How is Cohort 10 special/different compared with the previous cohorts? | 05:52 Can we know some of the programs, trainings, mentorships, and opportunities the startups have received? | 07:06 Who are these startups in Cohort 10 and how were they chosen? | 09:46 When is the Demo Day? What will happen? | 15:59 Happy 10th year anniversary IdeaSpace! Will there be Cohort 11? | 17:30 How can listeners know more about IdeaSpace Philippines? IDEASPACE PHILIPPINES | Website: ideaspacefoundation.org | Facebook: facebook.com/ideaspaceph QBO INNOVATION HUB | Website: qbo.com.ph | Facebook: facebook.com/QBOPhilippines OFFICIAL E-LEARNING PARTNER | Ask Lex PH Academy: asklexph.com | Get 5% discount by using the code: ALPHAXSUP CHECK OUT OUR PARTNERS | TechShake: techshake.asia | OneCFO: onecfoph.co (mention Start Up Podcast PH as referral!) | Pinoy IP Works: pinoyipworks.com | Packetworx: packetworx.com | LookingFour Buy & Sell Online: lookingfour.com | NutriCoach: nutricoach.com | Benjoys Food Products: benjoysfoodproducts.com | 8CHAIN: 8chain.io | AltSwitch, Twala, Eplayment, InterLeukin, Hive Energy PH START UP PODCAST PH | YouTube: youtube.com/StartUpPodcastPH | Spotify: open.spotify.com/show/6BObuPvMfoZzdlJeb1XXVa | Apple Podcasts: podcasts.apple.com/us/podcast/start-up-podcast/id1576462394 | Facebook: facebook.com/startuppodcastph | Instagram: instagram.com/startuppodcastph | LinkedIn: linkedin.com/company/startuppodcastph SUPPORT THE PODCAST | Patreon: patreon.com/StartUpPodcastPH | Unionbank: 109426505649 | GCash: 09623871744 This episode is edited by: Krislyn Nepomuceno

Howard Brown is an author, Silicon Valley entrepreneur, interfaith peacemaker, two-time stage IV cancer survivor, and healthcare advocate. For over three decades, Howard's business innovations, leadership principles, mentoring, and resilience in beating cancer against long odds have made him a sought-after speaker and consultant for businesses, nonprofits, congregations, and community groups. His hard-earned wisdom about resilience after beating cancer twice has led him to become a nationally known patient advocate and “cancer whisperer” to many families. Howard, his wife Lisa, and his daughter Emily currently reside in Michigan. ✨A few highlights from the show: 1. Medical technologies that played a role in Howard's recovery and expanding his family: bone marrow transplant, In vitro fertilization (IVF)/Intracytoplasmic sperm injection (ICSI), Cytoreductive Surgery (CRS) and Hyperthermic Intraperitoneal Chemotherapy (HIPEC), scans to video, liquid biopsy, tumor burden, clinical trials, immunotherapy, and Interleukin-2 2. It is important that you, your loved ones or family, or a patient advocate ask about what medical technologies are available to treat the type of cancer that you have. As you can see from Howard's experience, there are many options that may help save your life and improve your quality of life. 3. Don't isolate yourself. Isolation brings darkness. 4. Call for help and hold on to hope. 5. Find your happy place and go there!

Please join author Subodh Verma and Guest Editor Christopher Granger as they discuss the article "Empagliflozin and Left Ventricular Remodeling in People Without Diabetes: Primary Results of the EMPA-HEART 2 CardioLink-7 Randomized Clinical Trial." Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. We're your co-host. I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr. Peder Myhre: And I'm Dr. Peder Myhre, social media editor and doctor at Akershus University Hospital at University of Oslo in Norway. Dr. Carolyn Lam: Peder, I am so excited to be discussing this issue. So many great articles and a feature discussion coming up on the SGLT2 inhibitor, empagliflozin. And do you think it's got effects on left ventricular remodeling in people without diabetes? Very interesting question. Dr. Peder Myhre: That is so interesting, Carolyn. I can't wait to hear this discussion. Dr. Carolyn Lam: Yep, I agree, but we got to wait till we discuss the other papers in today's issue. I want to go first. So we know that non-vitamin K oral anticoagulants, or NOACs, they've become the standard therapy for preventing stroke and ischemic thromboembolism in most patients with atrial fibrillation. But, what is the effectiveness and safety of NOACs in patients on dialysis? That is hemodialysis. The AXADIA-AFNET 8 study sought to test the hypothesis that apixaban would be non-inferior to vitamin K antagonists in these very patients undergoing hemodialysis. Dr. Peder Myhre: Oh wow. This is really a gap of knowledge that we've been waiting to hear more about. NOACs in patients with hemodialysis. Tell us about this trial, Carolyn. Dr. Carolyn Lam: Sure. So this is from corresponding author, Dr. Reinecke, and colleagues, from University of Munster in Germany. And it's an investigator initiated prospective randomized open-blinded outcome assessment of 97 patients with atrial fibrillation on chronic hemodialysis randomized to either apixaban 2.5 mg BID, or a vitamin K antagonist, aiming for an INR between 2 and 3. Over a median follow-up time of 429 days for apixaban, and 506 days for the vitamin K antagonist, the composite primary safety outcome of first, major bleeding, clinically relevant, non-major bleeding, or all cause death, occurred in 46% of patients on apixaban, and 51% of patients on the vitamin K antagonist. That would be a hazard ratio of 0.91, with a p for non-inferiority being 0.157. How about the primary efficacy outcome? While this was a composite of ischemic stroke, all cause death, myocardial infarction, or deep vein thrombosis, and/or pulmonary embolism, and that occurred in 21% of patients on apixaban and 31% of patients on the vitamin K antagonists. Again, no difference when there was testing. So, in summary, Peder, there were no differences in the safety or efficacy observed between apixaban and vitamin K antagonists in patients with atrial fibrillation on chronic hemodialysis. Of note, however, even receiving oral anticoagulations, these patients remain at very high risk of cardiovascular events. So these data really support the consideration of apixaban for prevention of cardiovascular complications in patients with atrial fibrillation on chronic hemodialysis, but larger studies are definitely needed. Dr. Peder Myhre: Oh wow, Carolyn, that is so clinically relevant. And the next paper is also a clinically relevant paper. And it comes to us from the SPRINT authors. And to remind you, the SPRINT study was a study of intensive systolic blood pressure lowering compared to standard blood pressure lowering. And the results demonstrated that there was a robust reduction in both heart failure endpoints and all cause mortality. And in this sub-study that comes to us from corresponding author Jarett Berry from University of Texas Tyler School of Medicine, these authors look at the mechanisms through which intensive blood pressure lowering reduces the risk of these endpoints. And given the important role of cardiac injury and neurohormonal activation in the pathways leading from hypertension to heart failure, and strong association that has been observed between hypertension and levels of cardiac troponin and NT-proBNP, the authors hypothesized that intensive systolic blood pressure lowering would decrease levels of high sensitivity cardiac troponin T and NT-proBNP. Dr. Carolyn Lam: Cool. That's interesting. So how did they do this, and what did they find? Dr. Peder Myhre: So, as expected, Carolyn, the authors found that increases in troponin and NT-proBNP from baseline to 1 year were associated with a higher risk of heart failure and death. And there were really no significant interaction by treatment assignment. But let's look at the changes in troponin. And these results showed that randomization to intensive blood pressure lowering versus standard blood pressure lowering resulted in a significant 3% increase in cardiac troponin T level over 1 year follow up, and a higher proportion of participants with more than 50% increase, and that's with an odds ratio of 1.47. And Carolyn, in contrast, NT-proBNP decreased by 10% in intensive blood pressure arm. And these patients had substantially lower probability of increasing more than 50% in NT-proBNP, with an odds ratio of 0.57 compared to the standard arm. And now, to the most interesting part of this analysis, Carolyn, the association of randomized treatment assignment on changes in troponin was completely attenuated after accounting for changes in eGFR during the follow up, whereas the association of treatment with NT-proBNP changes were completely attenuated after adjusting for changes in systolic blood pressure. So Carolyn, the authors highlight in their discussion the importance of non-cardiac factors influencing variation in cardiac biomarkers, and raise questions about the potential role of cardiac troponin T as a surrogate marker for heart failure or death in blood pressure lowering studies. Dr. Carolyn Lam: Wow, very interesting. Thanks, Peder. Can I tell you now about a preclinical study? Very interesting, because it shows that cardiac inflammation and hypertrophy are regulated by a heart-brain interaction. Dr. Peder Myhre: Wow, Carolyn, a heart-brain interaction. I'm excited to hear more about this. Please explain. Dr. Carolyn Lam: I'd love to, but first some background. Interleukin-1 beta, now that is a pro-inflammatory cytokine that causes cardiac hypertrophy and heart failure. I need to familiarize you with this, the nucleotide-binding domain leucine-rich containing family, pyrin domain-containing-3, NLRP3 for short, which is an inflammasome, which is a cytosolic multiprotein complex that mediates active interleukin-1 beta production. Okay? So you know these terms, and now I want to tell you about the study. This is an elegant series of experiments performed by co-corresponding authors, Dr. Higashikuni, from University of Tokyo, and Dr. Sata, from Tokushima University Graduate School of Medicine, and their colleagues. They first showed that genetic disruption of the NLRP3 inflammasome resulted in significant loss of interleukin-1 beta production, cardiac hypertrophy, and contractile function during pressure overload. Next, a bone marrow transplantation experiment revealed an essential role of NLRP3 inflammasome in cardiac non-immune cells in myocardial interleukin-1 beta production and the cardiac phenotype. It was extracellular ATP released from sympathetic nerve terminals that induced the hypertrophic changes of cardiac cells in an NLRP3 and interleukin-1 beta dependent manner in vitro. And finally, depletion of ATP release from sympathetic efferent nerves, or ablation of cardiac afferent nerves, or a lipophilic beta-blocker, all reduced cardiac extracellular ATP, and inhibited the NLRP3 inflammasome activation, the interleukin-1 beta production, and the adaptive cardiac hypertrophy during pressure overload. So all of this suggests that controlling the neuronal brain signals might have therapeutic potential for the treatment of hypertensive heart disease. Neat, huh? Dr. Peder Myhre: Oh, that is so interesting. The heart and brain interaction. And, Carolyn, we're going to stay in the field of preclinical science. And now we're going to talk about another field that is really interesting, and that is regeneration of cardiomyocytes. Because, Carolyn, developmental cardiac tissue holds remarkable capacity to regenerate after injury, and consists of regenerative mononuclear and deployed cardiomyocytes. Whether reprogramming metabolism promotes persistence of these regenerative mononuclear and deployed cardiomyocytes that enhance cardiac function in repair after injury is unknown. Therefore, these researcher, led by corresponding author, Mohsin Khan, from Temple University School of Medicine, investigated whether the RNA binding protein, LIN28a, which is a master regulator of cellular metabolism, plays a role in cardiac repair following injury. Dr. Carolyn Lam: Wow. That is always, always interesting, regeneration and repair following injury. So what did the authors find? Dr. Peder Myhre: Well, Carolyn, through a number of elegant experiments, the authors made the following key findings. For the first time, they documented a role for RNA binding protein LIN28A in regulating cardiomyocyte turnover in the postnatal and adult heart. And LIN28a overexpression promotes cardiomyocyte cell cycle activity during postnatal development and extends cardiac regenerative ability of the mammalian heart to postnatal day 7. And in the adult heart, the authors could demonstrate that LIN28a drives new myocyte formation, augmenting cardiac structure and function after myocardial injury. And Carolyn, I'm sure you're going to ask the clinical implications of this study. Dr. Carolyn Lam: Indeed. Dr. Peder Myhre: And that is that these results may suggest a novel translational role for LIN28a based strategy to replenish cardiomyocytes in the adult heart after injury. Dr. Carolyn Lam: Very nice, Peder. Thank you. Also in the issue is a Research Letter by Dr. Bick on interleukin-6 receptor polymorphism attenuates clonal hematopoiesis mediated coronary artery disease risk among many individuals in the UK Biobank. There's also Cardiology News by Tracy Hampton, where she highlights few really interesting things, like aging cardiomyocytes accumulate new genetic mutations that was published in Nature Aging, cytokines promote tissue repair after a heart attack in mice, and that was published in Science, and scientists identifying molecular alterations in a failing heart at a single cell resolution, which was published in Nature. Dr. Peder Myhre: And there are a couple of other papers also in this issue, Carolyn. And there's first, an exchange of letters by Drs. Halushka, Lu, and Mayr, regarding the article "Circulating MicroRNA-122-5p is Associated with a Lack of Improvement in Left Ventricular Function after TAVR and Regulates Viability of Cardiomyocytes Through Extracellular Vesicles." And finally, we have an "On My Mind" piece by doctors Monda and Limongelli entitled "An Integrated Sudden Cardiac Risk Prediction Model for Patients with Hypertrophic Cardiomyopathy." Dr. Carolyn Lam: Oh, nice. Nice full issue. Thank you, Peder. Let's go to our feature discussion now. Shall we? Dr. Peder Myhre: Let's go. Dr. Greg Hundley: Welcome listeners to this feature discussion on January 24th. And we have with us Dr. Subodh Verma, from St. Michael's University in Toronto, Canada. And a guest editor, Dr. Christopher Granger, from Duke University in Durham, North Carolina. Welcome gentlemen. Well, Subodh, we will start with you. Can you describe for us some of the background information that went into the preparation of your study, and what was the hypothesis that you wanted to address? Dr. Subodh Verma: First, my great pleasure to be here, and thank you very much for the opportunity to discuss this paper with your viewers. As you know, SGLT2 inhibitors have been truly transformative therapies. From a heart failure perspective, we know that they prevent incident heart failure in people with diabetes who have vascular disease or risk factors. They also have been shown to treat prevalent heart failure in people with heart failure and either a reduced, mildly reduced, or preserved ejection fraction independent of glycemic status. And really, these have been the basis of very strong recommendations to use these agents in the prevention of heart failure in people with diabetes, and also in the treatment of prevalent heart failure in people with and without diabetes. Now, the fact that these drugs have such broad effects in people with heart failure has led to a theory that maybe these drugs could be introduced earlier on in the natural history of heart failure in people who neither have diabetes nor have significant heart failure, the so-called sort of stage A or stage B patient. But there really have been no clinical trials evaluating this question. There've been a lot of translational randomized trials that have provided some mechanistic insights about LV remodeling in people with diabetes or in people with prevalent heart failure. And we hypothesized that maybe the first step to evaluate whether SGLT2 inhibitors may have favorable effects on cardiac remodeling in people without diabetes or without heart failure would be to conduct a randomized double-blind control trial looking at indices of left ventricular remodeling in a population that I've just described. Dr. Greg Hundley: Very nice, Subodh. So you've started us into your study design. Maybe describe that a little more fully, and then who was included in your study population? Dr. Subodh Verma: So EMPA-HEART 2 CardioLink was a multi-center double-blind placebo control randomized trial in which we studied the effects of empagliflozin, an SGLT2 inhibitor, at a dose of 10 mg per day versus placebo in people who did not have type 2 diabetes or significant heart failure. We included people who were adults between the age of 40 and 80 who met 1 of 2 entry criteria. Either they had to have one major criteria, which was an increase in left ventricular mass index by specific echo criteria or MRI criteria, or they could have increased LVH as identified by ECG or by intraventricular septal or posterior wall thickness. They could also get in if they had resistant hypertension, hypertension despite being on 3 antihypertensive agents, or the second strata was entry through 2 minor criteria, which included a history of myocardial infarction, a GFR between 30 or 60, or evidence of overweight or obesity. Dr. Greg Hundley: And how many subjects did you randomize? Dr. Subodh Verma: So we randomized, of the 318 that we screened, 169 were randomized to receive empagliflozin 10 mg or a placebo. Patients had a baseline cardiac MRI done, and then the exposure was 6 months. They had a follow-up MRI at the end of 6 months. And the primary outcome measure was a 6-month change in left ventricular mass index from baseline to 6 months between the two groups. Dr. Greg Hundley: Very nice. And so , Subodh, can you describe for us now, what did you find? What were your study results? Dr. Subodh Verma: So, first and foremost, what we found in terms of baseline characteristics was that we enrolled a population of people with a mean age of around 60 with a BMI of around 30 kg/m2, predominantly men, about 80% or so were men. These were patients who did not have significant heart failure. The NT-proBNP at baseline was around 50 pg/mL. The eGFR was around 80 mL/minute, and the vast majority of these patients actually had a history of hypertension. Of course, none of them had diabetes by definition. The hemoglobin A1C was around 5.8%. Now what we found was, despite the fact that we went after patients who we thought would be enriched for a baseline increase in LV mass indices, the baseline LV mass index was mildly elevated, was around 63 g/m2. And over the course of 6 months, we did not find any significant difference in terms of LV mass regression between the placebo and empagliflozin groups. In fact, the adjusted treatment effect was minus 0.30 g/m2, which was not statistically significant. No other differences were found in terms of other indices of a remodeling, including left ventricular and diastolic or end systolic volume indices or in terms of left ventricular ejection fraction. There was a 2% increase in ejection fraction, and the p-value for that was 0.07, but really was not statistically significant. Dr. Greg Hundley: And very nice. And realizing that women may have smaller LV masses, any stratified analysis that evaluated effects on men versus women? And then what about, perhaps in the higher quartile versus lower quartile, of age? Dr. Subodh Verma: Right. So, Greg, we actually did look at various subgroups and covariates, including gender, including age. And age or gender did not really influence the overall result that we obtained. There was really a neutral result in empagliflozin, irrespective of these 2 covariates. We also looked at baseline blood pressure, baseline NT-proBNP, LV mass indices, the presence or absence of heart failure, chronic kidney disease. So for the covariates that we have evaluated over a short term of 6 months in this relatively low risk population, we did not find any heterogeneity the result, per se. Dr. Greg Hundley: Very good. Well, Subodh, thank you so much for that beautiful presentation. And listeners, now we're going to turn to our guest editor, Dr. Chris Granger. And Chris is an expert in the field of heart failure. Also, a lot of familiarity with HFpEF, which sounds a little bit, we're looking at precursors. We don't have HFpEF yet, but maybe trying to inhibit this from happening using empagliflozin. How do you put these results in the context with other studies that have emphasized utilizing SGLT2 inhibitors in patients with sort of a preserved ejection fraction and absence of diabetes? Dr. Christopher Granger: Yeah. Well thanks, Greg. And again, congratulations, Subodh, to your study. And I think you framed some of the context here as these drugs, the SGLT2 inhibitors, as being transformative, which I think is exactly right. And it's such a fascinating story. Right? These drugs, which we thought originally, with their cause of glucose spilling in the urine, and a modest decrease in blood glucose, might have a role for modestly improving glucose control in diabetes. And low and behold, they've turned out to be one of the great stories I think in recent, across all of medicine, in terms of their consistent and substantial improving clinical outcomes for patients with heart failure, with diabetes and cardiovascular disease, and now even kidney protection, and much broader implications. And their well tolerated, and they don't have dose titration. So there's some practical appeal to this class of drugs in terms of their benefits, in terms of clinical outcomes. But we're left with having this amazing evidence-based generated without really understanding why are these drugs so effective? And what are they doing? And you've provided, I think, an important piece to the puzzle. We did have the data from patients with diabetes and heart failure, with diabetes and left ventricular hypertrophy, that there is a modest reduce in LV mass with SGLT2 inhibitors. And what you've shown is that for patients that with mild LVH, with risk for LVH, that we simply don't see a substantial reduction in LV mass with the use of these drugs. So I think that provides this evidence that that's not a major cause of benefit, at least in this earlier phase of development of heart failure. And I think it really underscores the fact that there's a lot of work to do still to understand. We know that the renal effects are obvious place that these drugs have such an important benefit. And then the linkage of renal disease and cardiac performance is one of the areas, I think, that's a very exciting aspect of a probable contribution of the mechanism of these drugs. But I think in the end, we're left with still not really understanding why these drugs are so beneficial. But understanding that, I think, will be important, both for opening new avenues of targeting pathways, as well as being able to tell the clinical community, okay, you have these important benefits, but people do want to also know why are we seeing these benefits. Dr. Greg Hundley: Very nice. Well, listeners, we're going to turn back to Dr. Verma here. Subodh, what do you see is the next study to be performed in this sphere of research? Dr. Subodh Verma: Well, first, my thanks to Professor Granger, Chris, for handling this paper and for his very thoughtful comments. And he's absolutely right. We have such wonderful clinical data, and these results, of course, should not in any way take away from the importance of using empagliflozin or other SGLT2 inhibitors in the prevention of heart failure in people with diabetes, or in the treatment of HFpEF or HFrEF. But we're struggling with trying to understand what is the dominant mechanism of action here. And, in the previous precursor to EMPA-HEART 2, we did EMPA-HEART 1 in people with diabetes, and we saw a modest effect that was statistically significant of reduction in LV mass index. And we did not see this, of course, in a lower risk population without diabetes. And that tells me that remodeling may be occurring to a modest effect, it may require a longer time to actually show its benefits, but that this is unlikely a dominant sort of mechanism through which these drugs are working. And I do share Chris's thoughts that one of the key mechanisms of benefit that needs to be further explored is looking at the renal cardiac axes. We know that these drugs are profoundly renal protective, and that the benefits may actually be secondary to improvements in renal hemodynamics, improvements in renal function. And I think that is a population that needs to be, that's a mechanism that needs to be studied further. So I think the next generation of translational mechanistic studies need to really tease out the renal cardiac axes, maybe tease out populations that are at risk but have more significant left ventricular hypertrophy, maybe evaluate patients for a longer duration of treatment, or select people who truly have significant hypertension at baseline. I think those are groups and questions that need further exploration. And, of course, the translational science needs to be also studied in the context of larger completed clinical trials, where biomarkers are currently available and they can be linked, of course, to the outcomes in those trials. So those are some of my thoughts as to where the field could move towards. Dr. Greg Hundley: Very nice. And Chris, do you have anything to add? Dr. Christopher Granger: Subodh, I think that was a great summary. And I might just make a comment on the other end of the spectrum. That is, we have these drugs and the evidence of their benefit, and yet they're grossly underused in the populations that have proven to have benefit. Now it takes some time to educate, to get people familiar with, and get them to integrate these treatments into practice, but there's an enormous opportunity, and I think there is a linkage here. I think when people understand the mechanism, and when they're thoughtful about how these drugs may be working, that that really helps to make the case that the drug should be used, and that people are on board with using them. So I think there's this linkage here, there's the need to both better understand mechanism, and there's the need to have systems of care where these treatments are integrated to provide the benefit that's been so clearly shown in the randomized trials. Dr. Greg Hundley: Very nice. Well, listeners, we want to thank Dr. Subodh Verma, from St. Michael's University in Toronto, and our guest editor, Dr. Chris Granger, from Duke University in Durham, North Carolina, for bringing this paper highlighting that among people with neither diabetes nor significant heart failure but with risk factors for adverse cardiac remodeling, that SGLT2 inhibition with empagliflozin did not, did not, result in a meaningful reduction in LV mass index after 6 months. Well, on behalf of Carolyn, Peder, and myself, we want to wish you a great week, and we will catch you next week on the run. This program is copyright of the American Heart Association 2023. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, please visit ahajournals.org.

Louisa Nicola is a neurophysiologist and brain coach for many professional athletes and Wall Street execs. She discusses science-based tools and strategies to boost brain health and mental performance. Support your Workout Sessions and Healthy Hydration with this Creatine Electrolyte Combo by MYOXCIENCE Save 15% with code podcast at checkout Link to the Video Interview: https://bit.ly/3R7noel Connect with Louisa: https://www.neuroathletics.com.au Show Notes: 03:10 Louisa was elite triathlete when she realized the impact the brain had on all aspects of performance. She and her fellow athletes were not taught about sleep or nutrition. 04:20 The nervous system must be optimized to optimize performance throughout the body and as a person. 05:35 We used to sleep about 12 hours a day in prehistoric times. Sleep regenerates our brains. 06:20 There are 4 stages of sleep. Stage one is as you are falling asleep. Stage 2 is light sleep. Stage 3 is deep sleep/slow wave sleep/non-REM sleep. Stage 4 is REM sleep. Stages 3 and 4 are the most important stages for our brains. 06:52 During deep sleep, hormones are secreted: testosterone, estrogen, growth hormone. The glymphatic system is your brains sewage system. It cleans toxins, including amyloid beta. A buildup of these toxins can lead to neurodegenerative diseases. 07:50 Your brain is comprised of neurons and others. Glial cells bind neurons together. During deep sleep, glial cells shrink, making way for the cerebral spinal fluid in your brain to wash out the trash. 08:55 A groggy wakeup may be an indication that you are not getting into deep sleep. 30% of your total sleep time should be deep sleep. 20% of total sleep time should be REM sleep. 09:30 REM sleep is where memory consolidation and learning take place. 10:30 The biggest disruptor of sleep is anxiety and stress. This activation of the sympathetic nervous system may prevent you from falling asleep or wake you in the night. 10:55 Alcohol is the biggest inhibitor of REM sleep. Blue light blocking glasses are helpful, but do not block out all light. 12:00 Eating less than 2 hours before bed keeps us awake through digestion and the increase in our core body temperature. Core body temperature must drop at least 2 degrees for us to go to sleep and stay asleep. 15:00 Alcohol inhibits the action of GABA, our calming neurotransmitter. Cortisol peaks with alcohol. Alcohol and marijuana sedate you. It does not elicit sleep stages. 16:15 You are preparing for sleep the minute you wake up. Consistency is key. 17:20 Try to get as much sleep as possible before you get on a plane. It is called Sleep Banking. 18:10 Your prefrontal cortex is the ruler of your brain. It is where cognition happens: attention, reaction time, processing speed. 6 hours of sleep is a sleep deprived state, in the scientific literature. 10:20 As we age, we have a lower efficacy of our frontal lobe. There is a thinning of our cerebral cortex. Thinning in the prefrontal cortex causes a lower decision rate and worsening of our processing speed, inhibition and impulse control. 21:20 We can slow brain ageing through lifestyle interventions, such as sleep, good nutrition and exercise. 21:40 There is an atrophy of our brain white matter, where our myelinated neurons live, as we get older. Our processing speed declines. This can be seen using an EEG. 25:50 Mild cognitive impairment is a predementia state. 27:30 You should be working on your brain. It is the control center of your entire body. 27:50 You can stave off predementia states and the slowing of cognition through exercise. 29:45 Head trauma can cause an accumulation of talc proteins tolC proteins and amyloid beta, which is somewhat comparable to Alzheimer's disease. 30:30 A hard hit may require a month's recovery. Within 24 hours post trauma, decreasing the temperature of the brain, eating a high fat diet, or having exogenous ketones can help heal the brain. 33:40 Ingesting exogenous ketones can help prevent trauma from happening to the brain. 36:00 EPA/DHA are anti-inflammatory. If you have a high omega 3 index of 8% or more, you can increase your life expectancy by 5 years. 37:10 A risk factor for all-cause mortality is a low omega 3 index. 37:40 Quality supplements reduce risk of oxidation and toxicity. EPA/DHA feeds your brain what it is made of. It is made of water and fat. A high omega 3 index helps with cell membrane fluidity. 39:25 A standard omega 3 blood panel does not test the red blood cell. Red blood cell cycle lasts about 120 days. You need to ingest EPA/DHA daily for cardiac, brain and overall health. 41:20 Farm raised seafood does not contain the same amount of nutrients. 41:30 Omega 3 is made of EPA, DHA and ALA. ALA is the plant form found in flax and chia seeds. To get the recommended dose of omega 3 through ALA is a lot of food. ALA gets converted into DHA. 42:20 Your eyes are the only neurologic tissue outside your brain. Vision changes may be a way to indirectly assess brain health. 45:05 Most 2019 deaths were attributable to heart disease and brain diseases. 45:40 A healthy performing brain can make sound decisions, be rational and practice impulse control. 47:00 Your brain fatigues faster if you are not eating well, sleeping well, and exercising. You need brain energy. Stress and an inflamed brain disrupts pathways in the brain. 48:50 People who have type 2 diabetes and obesity have a higher rate of neural inflammation. 49:50 When we exercise there is a release of myokines, muscle-based proteins (peptide hormones). They act on different organs in positive ways. They are water soluble, and some can pass the blood-brain barrier. Binding receptors to myokines are on heart muscle, spleen, liver and more. Once bound, they create a chemical reaction. 51:10 Interleukin 6 myokine, is secreted with the contraction of a muscle. It is pro-inflammatory cytokine… unless it is released from a muscle – where it is released as anti-inflammatory. It affects immunity and different areas of the brain. 52:00 Irisin myokine is a messenger molecule. It crosses the blood-brain barrier to the prefrontal cortex, where it affects cognition, and hippocampus, where it induces BDNF, that induces neurogenesis. 53:56 When you learn something and immediately exercise, you can have greater capacity to remember. If you sleep for 20 minutes after learning something, you will embed everything you learned. 54:30 Irisin release is increased 1 hour after exercise. 54:50 Workouts of 70 to 80% of you one rep max for a robust release of irisin. More of a release is given during resistance training, than aerobic. The more resistance, the more the release. 58:10 You can stave of neurodegenerative diseases and states by 20 years by inducing exercise protocols that impact myokine release. 58:50 50 million people worldwide are affected by Alzheimer's disease. That rate is set to triple by 2050. 59:30 EPA/DHA can clear accumulated proteins in your brain. 00:01:00 Demyelinating diseases, MS, are becoming more prevalent. Chronic stress and chronic cortisol may be the cause.  

*READ THE TOPICS COVERED BEFORE LISTENING*** Case study of a 92 year old with delirium Causes of delirium Geriatric toxicology Geriatric STI's and sexual health REFERENCES: Alex Yartsev. Pharmacology and toxicology in old age. June 30, 2016. Deranged Physiology. Available from https://derangedphysiology.com/main/required-reading/pharmacology-and-toxicology/Chapter%201.3.4/pharmacology-and-toxicology-old-age Frankowski AC, Clark LJ. Sexuality and Intimacy in Assisted Living: Residents' Perspectives and Experiences. Sex Res Social Policy. 2009 Dec 1;6(4):25-37. doi: 10.1525/srsp.2009.6.4.25. PMID: 25568640; PMCID: PMC4283937. Kristen Fontes MD, Alex Koyfman MD, Brit Long MD. Common ED Medication Errors: Polypharmacy. EmDocs. July 3, 2017. Available from http://www.emdocs.net/common-ed-medication-errors-polypharmacy/ Nat. Research Council (US) Cute on Chemical Toxicology and Aging. Aging in Today's Environment. Washington (DC): National Academies Press (US); 1987. 4, Principles of Toxicology in the Context of Aging. Available from: https://www.ncbi.nlm.nih.gov/books/nbk218724/ Rashid, M.H., Sparrow, N.A., Anwar, F. et al. Interleukin-6 mediates delirium-like phenotypes in a murine model of urinary tract infection. J Neuroinflammation 18, 247 (2021). https://doi.org/10.1186/s12974-021-02304-x Stanford Medicine 25. Website: Fundoscopic/Opthalomoscopic Exam. Available from https://stanfordmedicine25.stanford.edu/the25/fundoscopic.html https://www.theseniorlist.com/sti-older-americans/

On this week's podcast, John Mandrola, MD discusses fish oil, America's heart health, pharmacists and prescribing and statins This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I - Fish Oil - New Biomarker Data Add to Concerns Over REDUCE-IT Trial https://www.medscape.com/viewarticle/976490 - Effects of Randomized Treatment With Icosapent Ethyl and a Mineral Oil Comparator on Interleukin-1β, Interleukin-6, C-Reactive Protein, Oxidized Low-Density Lipoprotein Cholesterol, Homocysteine, Lipoprotein(a), and Lipoprotein-Associated Phospholipase A2: A REDUCE-IT Biomarker Substudy https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.122.059410 - Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia https://www.nejm.org/doi/full/10.1056/nejmoa1812792 - Effect of High-Dose Omega-3 Fatty Acids vs Corn Oil on Major Adverse Cardiovascular Events in Patients at High Cardiovascular RiskThe STRENGTH Randomized Clinical Trial https://jamanetwork.com/journals/jama/fullarticle/2773120 - Effect of icosapent ethyl on progression of coronary atherosclerosis in patients with elevated triglycerides on statin therapy: final results of the EVAPORATE trial https://academic.oup.com/eurheartj/article/41/40/3925/5898836 II - US Heart Health - New AHA Checklist: Only 1 in 5 Adults Have Optimal Heart Health https://www.medscape.com/viewarticle/976519 - Life's Essential 8: Updating and Enhancing the American Heart Association's Construct of Cardiovascular Health: A Presidential Advisory From the American Heart Association https://www.ahajournals.org/doi/10.1161/CIR.0000000000001078 - Status of Cardiovascular Health in US Adults and Children Using the American Heart Association's New "Life's Essential 8" Metrics: Prevalence Estimates from the National Health and Nutrition Examination Survey (NHANES), 2013-2018 https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.122.060911 III - Pharmacist Prescribing - Paxlovid Is Here: A Pharmacist's Prescribing Pearls https://www.medscape.com/viewarticle/973260 - Coronavirus (COVID-19) Update: FDA Authorizes Pharmacists to Prescribe Paxlovid with Certain Limitations https://www.fda.gov/news-events/press-announcements/coronavirus-covid-19-update-fda-authorizes-pharmacists-prescribe-paxlovid-certain-limitations IV - Statin Eligibility - New European Guidelines ‘Drastically' Reduce Statin Eligibility https://www.medscape.com/viewarticle/976715 - Statin Eligibility for Primary Prevention of Cardiovascular Disease According to 2021 European Prevention Guidelines Compared With Other International Guidelines https://jamanetwork.com/journals/jamacardiology/article-abstract/2793729 - Time to Revisit Using 10-Year Risk to Guide Statin Therapy https://jamanetwork.com/journals/jamacardiology/article-abstract/2793732 - Mendelian randomization studies: using naturally randomized genetic data to fill evidence gaps https://doi.org/10.1097/mol.0000000000000247 You May Also Like: Medscape editor-in-chief Eric Topol, MD, and master storyteller and clinician Abraham Verghese, MD, on Medicine and the Machine https://www.medscape.com/features/public/machine The Bob Harrington Show with Stanford University Chair of Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net

How to Stimulate Your Vagus Nerve with a TENS DeviceUPDATED Vagus Nerve Stimulation Video with new Ear ClipsResearch Studies on Vagus Nerve and Brain (video)Vagus Nerve Stimulation "has been life-changing!" (video)BUY a TENS and EAR CLIPS: www.autoimmunedocpodcast.comThe Vagus Nerve is the primary nerve of the parasympathetic nervous system, and it has gained wild popularity lately in the scientific and biohacking, alternative wellness, and autoimmune disease communities. As the primary nerve of the PNS, the vagus is largely responsible for "pushing the brakes" on the stress response, the sympathetic nervous system. The vagus innervates the heart, lungs, liver, spleen, gallbladder, diaphragm, entire digestive tract, and more. It's two way nerve 'superhighway system' acts as the modulator of the "gut-brain connection", sending sensory signals upward from all of your organs and sending signals downward regulating stomach acid, enzyme, and bile release, digestive motility, and more, and back up to your brain. Decreased vagal tone is associated with both inflammatory digestive diseases as well as psychiatric diseases like depression and PTSD. The vagus also sends nerves to the spleen, and its activation blocks the release of Tumor Necrosis Factor Alpha (TNFa), and in the liver blocks Interleukin 6 release from Kuppfer cells, all through something called the Cholinergic Anti-Inflammatory pathway. The only place on the outside of the body that the vagus nerve travels is part of the ear, oddly enough, but the vagus nerve can be stimulated by acupressure or my preferred method which I talk about in the podcast - using an inexpensive TENS Device with an ear clip. The vagus nerve can also be stimulated by yoga, mediation, acupuncture, chiropractic, deep breathing, contrast showers, humming, gargling, and gagging, and I speak on all of these things in this episode!

WHO在12月7日更新對於Omicron的了解 https://www.who.int/publications/m/item/weekly-epidemiological-update-on-covid-19—7-december-2021 流行病學 在南非從11月第二週開始確診就有上升，11月29日到12月5日通報了62021例，比前一週增加了111%。檢測陽性率也從1.2%增加到22.4%。 從11月中開始主要在豪登省開始的群聚主要是在大學學生之間。 而鄰近的非洲國家也有疫情上升的情形：包括史瓦帝尼 (1990%); 辛巴威 (1361%); 莫三比克 (1207%), 納米比亞 (681%)和賴索托 (219%). 這些國家的疫苗完整覆蓋率皆很低，從納米比亞的12.1%到賴索托的26.7%。南非自己則是25.2%。 目前不確定疫情上升的原因，這可能和變種病毒的散布，增加檢測量，放鬆公衛措施還有疫苗覆蓋率低都有關。非洲外，在某些其他國家也有報告到上百例的Omicron案例。目前已經在57個國家都有確認案例，但多半地域主要流行的還是Delta，目前還很難對於Omicron會不會影響全球的新冠流行病學做出確切結論。 傳染力 雖然似乎有證據表明Omicron可能比其他變種具有生長優勢，但尚不清楚這是否會轉化為傳染力增加。歐洲疾病預防控制中心以模型預測，如果目前1%的感染是由Omicron引起的，若他有Delta 2.2倍的傳染力，可能到2022年1月1日他會佔新增感染的50%以上。若有Delta 1.3倍的傳染力，則需要到2022年3月1日。 目前有許多正在或計劃進行的流行病學研究，包括詳細的群突發調查、接觸者追踪和家庭傳播研究，將有助於增加我們對其傳染力的理解。 疾病嚴重程度 目前僅有極有限的資料，這使得評估疾病嚴重程度的是否有變化非常有挑戰性。截至12月6日，在 18 個歐盟國家確認且有嚴重程度的所有212例確診病例皆是無症狀或輕症。而南非本週因新冠住院的人數增加了82%（從 502 人增加到 912 人），但目前不確定Omicron的比例。即使疾病嚴重程度相同或低於Delta，如果更多人被感染，預計住院人數會增加。並且在病例發生率增加和死亡人數增加之間是存在存在時間差的。 對於Omicron的臨床狀況還需要更多資訊，WHO鼓勵各國為住院患者數據的收集和共享做出貢獻。 再感染的風險 南非當地已經自然感染者大概佔60~80%，成人完整疫苗注射則僅有35%。初步發現自然感染針對Omicorn保護力降低可以再感染，因此在南非還是可以造成流行。接下來應該繼續研究打疫苗者突破感染的機率，還有雖然再次感染是否會比較不容易重症。 對疫苗的影響 需要更多資料。進行中的研究包括對先前接種過疫苗或感染過的人的中和抗體研究，以及疫苗有效性研究，將有助於增加我們對免疫逃逸的理解。 對診斷工具的影響 針對PCR，S-gene target failure (SGTF)可以做為疑似Omicron的指標。但還是需要定序確認，因為Alpha還有一部份的Gamma還有Delta也有可能有此現象。 針對抗原快篩，因為多半是偵測N蛋白的構造，初步評估不會受影響。 對治療的影響 Interleukin-6 Receptor Blockers 和類固醇應該是會有效的。其他還需要更多資料。 結論 對於Omicron很多還是未知的，接下來幾週應該更多資訊會出來。 Omicron變異或是好事？專家：像感冒可加速終結疫情 https://news.ltn.com.tw/news/world/breakingnews/3754307 Omicron變種病毒走向 李秉穎：一個症狀可以看出感冒化 https://udn.com/news/story/120940/5942736 南非當地於12月4日發布的臨床狀況初步觀察 Tshwane District Omicron Variant Patient Profile - Early Features https://www.samrc.ac.za/news/tshwane-district-omicron-variant-patient-profile-early-features Early data from South Africa hints Omicron variant may cause less severe Covid, but more research is needed https://www.statnews.com/2021/12/04/omicron-covid19-south-africa-data/ Omicron變種病毒懶人包 傳染力 重症 疫苗有效性 要打加強針嗎？ https://linshibi.com/?p=39815 小額贊助支持本節目： https://pay.firstory.me/user/linshibi Powered by Firstory Hosting