Podcasts about Aspirin

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

The Daily Quiz - Science and Nature Today's Questions: Question 1: Aspirin was originally obtained from the bark of which tree? Question 2: Electrum is a natural alloy of gold and what other metal? Question 3: What Was The Colossus, Developed In Buckinghamshire In 1943? Question 4: What is Ecophysiology the study of? Question 5: Cocci, Spirilla, and Streptococci are types of what? Question 6: A Phon is a unit of what? Question 7: A 'Boomer" Is The Male Of Which Animal? Question 8: Which is an example of a sexually transmitted disease? This podcast is produced by Klassic Studios Learn more about your ad choices. Visit megaphone.fm/adchoices

In this episode, Ayesha and Andrew discuss the May 20, 2026 issue of JBJS, along with an added dose of entertainment and pop culture. Listen at the gym, on your commute, or whenever your case is on hold! Link: JBJS website: https://jbjs.org/issue.php Sponsor: This episode is brought to you by JBJS Clinical Classroom. Subspecialties: Knee, Hip, Shoulder, Basic Science, Foot & Ankle, Orthopaedic Essentials, Education & Training Chapters (00:00:02) - Case Is On Hold(00:01:48) - Clopidogrel Thromboprophylaxis in(00:11:33) - Clopidogrel vs Aspirin post-operative bleeding(00:15:26) - Custom 3-D acetabular implants for complex revision total lip(00:22:29) - Custom Implants(00:25:12) - Satisfied but Failed: Total Knee Arthroplasty(00:37:15) - CMS' new criteria for knee replacements(00:41:00) - medial unicompartmental knee arthroplasty, adverse outcomes(00:43:12) - medial unit compartmental knee arthroplasty

LBCT: Efficacy And Safety of Clopidogrel Versus Aspirin Monotherapy Beyond 12 Months After PCI In Patients at High Risk of Subsequent Cardiovascular Event

It was to be that little mouse's, and McAvoy's lucky Maui day…

In this episode, Ayesha and Andrew discuss the May 6, 2026 issue of JBJS, along with an added dose of entertainment and pop culture. Listen at the gym, on your commute, or whenever your case is on hold! Link: JBJS website: https://jbjs.org/issue.php Sponsor: This episode is brought to you by JBJS Clinical Classroom. Subspecialties: Trauma, Hand & Wrist, Knee, Infection, Shoulder, Orthopaedic Essentials, Basic Science, Hip Chapters (00:00:02) - JBJS: Your Case Is On Hold(00:03:03) - The January 2017 Issue(00:04:17) - Enoxaparin vs Aspirin for Thrombop(00:08:31) - Aspirin vs Enoxaparin: Cost and Quality of(00:13:51) - Thromboprophylaxis after trauma 1, cost effectiveness(00:18:37) - Highly Cross Linked Polyethylene vs Conventional Interventional K(00:25:18) - Fix It or No Fix(00:26:15) - Primary and Secondary Analysis of the Fix IT Study(00:33:10) - External fixation vs internal fixation: does it matter?(00:39:18) - Created: Dedicated Trauma Room for Hand Surgery(00:42:12) - Hand Surgery Wait Time in Canada

Ep. 209 features David and Kavin from Hydrastack, a startup using AI to transform how casino games are developed, converted, and distributed across channels.   Hear them discuss: The origin story of Hydrastack and how industry pain points around game distribution sparked the idea Why converting casino games from land-based to online can take 6–8 months and how Hydrastack cuts that down to weeks How their proprietary AI models ingest and transform existing game code instead of requiring full rewrites The massive inefficiencies in the current gaming supply chain and how they impact manufacturers, operators, and players Why “re-authoring” games from scratch is the industry's biggest bottleneck How Hydrastack's platform integrates directly into existing developer workflows (like Unity) The importance of combining deep industry experience with an outsider perspective to build better solutions Early traction, including pilot partnerships with major manufacturers and strong inbound interest Their business model: platform licensing + per-game conversion fees Insights from participating in programs like Zero Labs, Rice Business Plan Competition, and Booth's New Venture Challenge How AI is being adopted across gaming and why most companies still struggle to extract real value from it Their long-term vision to become the core platform for casino game development and distribution   The dedicated Startup Zone at SBC Summit Americas gives real-money gaming startups a platform to showcase to 10,000+ attendees — including investors, operators, suppliers, media, and key industry players.  Spaces are limited, secure yours now through https://www.bettingstartups.com/sbc-americas-2026   If you don't have a ticket for the event yet, use discount code BETTINGSTARTUPSVIP for 30% off your pass. Grab your ticket here: https://sbcevents.com/sbc-summit-americas/   Catch the video version of this episode here.   Learn more

Send us Fan MailHow dietary fatty acids regulate the initiation, propagation, and resolution of inflammation.TOPICS DISCUSSED:Parenteral nutrition history: IV nutrition evolved from soybean oil alone in the 1960s to complex blends including fish oil as the biology of ω-3s became understood.Three phases of inflammation: Initiation, propagation (driven by ω-6–derived prostaglandins and leukotrienes), and active resolution (driven by ω-3-derived resolvins and protectins).Pro-resolving mediators: Resolution is an active biological process, not passive; EPA and DHA generate resolvins and protectins that actively terminate inflammation.Aspirin's ω-3 mechanism: Aspirin inhibits arachidonic acid metabolism but allows EPA/DHA to access COX-2, upregulating pro-resolution mediators — a likely underappreciated mechanism of action.Cell membrane competition: EPA and DHA physically displace arachidonic acid in membranes, shifting the balance of mediators produced and improving resolution capacity.Linoleic acid & EPA synthesis: High linoleic acid intake saturates shared desaturase enzymes, inhibiting the body's conversion of ALA to EPA — meaning reducing ω-6 can raise ω-3 levels without supplementation.Dose & timing of ω-3 incorporation: ~2g/day of EPA+DHA shifts the arachidonic acid-to-EPA ratio enough to measurably reduce prostaglandin E2 production; white blood cells reflect changes within a month.ABOUT THE GUEST: Philip Calder, PhD is Professor of Nutritional Immunology in the Faculty of Medicine at the University of Southampton. His research focuses on how dietary fatty acids — particularly omega-3s — modulate immune responses and inflammatory processes across clinical and healthy populations.RELATED EPISODE:M&M 200: Dietary Fats & Seed Oils in Inflammation, Colon Cancer & Chronic Disease | Tim Yeatman & Ganesh HaladeSupport the showHealth Products by M&M Partners:AquaTru: Water filtration devices that remove microplastics, metals, bacteria, and more from your drinking water. Through link, $100 off AquaTru Carafe, Classic & Under Sink Units; $300 off Freestanding models.OmegaQuant: At-home blood testing to see fatty acid profiles, including omega-3 fatty acids. Use link to see options and support M&M.SiPhox Health: Comprehensive, cost-effective bloodwork from the comfort of home. Use code TRIKOMES for 20% off.KetoCitra—Ketone body BHB + electrolytes formulated for kidney health. Use code MIND20 for 20% off any subscription (cancel anytime)Seed Oil Scout: Find restaurants with seed oil-free options, scan food products to see what they're hiding, with this easy-to-use mobile app.SporesMD: Premium mushrooms products (gourmet mushrooms, nootropics, research). Use code 'nickjikomes' for 20% off.For all the ways you can support my efforts

John Maytham is joined by Prof Anna-Mart Engelbrecht, Professor in the Department of Physiological Sciences at Stellenbosch University, whose work explores complex cellular processes linked to disease – Can Aspirin reduce the risk of Cancer? Presenter John Maytham is an actor and author-turned-talk radio veteran and seasoned journalist. His show serves a round-up of local and international news coupled with the latest in business, sport, traffic and weather. The host’s eclectic interests mean the program often surprises the audience with intriguing book reviews and inspiring interviews profiling artists. A daily highlight is Rapid Fire, just after 5:30pm. CapeTalk fans call in, to stump the presenter with their general knowledge questions. Another firm favourite is the humorous Thursday crossing with award-winning journalist Rebecca Davis, called “Plan B”. Thank you for listening to a podcast from Afternoon Drive with John Maytham Listen live on Primedia+ weekdays from 15:00 and 18:00 (SA Time) to Afternoon Drive with John Maytham broadcast on CapeTalk https://buff.ly/NnFM3Nk For more from the show go to https://buff.ly/BSFy4Cn or find all the catch-up podcasts here https://buff.ly/n8nWt4x Subscribe to the CapeTalk Daily and Weekly Newsletters https://buff.ly/sbvVZD5 Follow us on social media: CapeTalk on Facebook: https://www.facebook.com/CapeTalk CapeTalk on TikTok: https://www.tiktok.com/@capetalk CapeTalk on Instagram: https://www.instagram.com/ CapeTalk on X: https://x.com/CapeTalk See omnystudio.com/listener for privacy information.

Broadcast from KSQD, Santa Cruz on 4-16-2026: Dr. Dawn opens with a follow-up from an email from Maryland about a friend in Switzerland, who has ongoing neurological and gastrointestinal symptoms. She reviews the earlier effort to connect him with functional-medicine resources in Switzerland, then focuses on a new observation that the patient may have had multiple parasitic infections during travel in Europe. Dawn agrees that this may have left a major gap in the workup and says that, in puzzling neurologic cases, a sleep-deprived EEG can sometimes reveal a “fingerprint” of brain-based dysfunction even if the patient is not actively having symptoms during the test. Dr. Dawn says that for people over 60 who have never had a heart attack or stroke, daily baby aspirin is no longer considered a good routine preventive measure because the bleeding risks, especially gastrointestinal bleeding, can outweigh the cardiovascular benefit. She makes the distinction that aspirin may still make sense for secondary prevention in people who already have established cardiovascular disease. She next reviews several medications that she thinks many older adults should reconsider. She explains that phenylephrine, which replaced easier access to pseudoephedrine in many cold remedies, has been found to work no better than placebo . She also says Colace is not very effective, and she strongly advises older adults to avoid Benadryl because it accumulates with age, increases fall risk, and may be associated with cognitive decline. She adds that beta blockers are no longer preferred first-line treatment for uncomplicated hypertension in many older patients, and that medications targeting the angiotensin pathway are generally favored instead. Dr. Dawn introduces Mira Achilles in the studio, describing her as her excellent administrative assistant. Mira explains that she gathered health questions from peers from her college world. Mira asks what best supports focus for someone with ADHD working at a desk job. Dr. Dawn says the two evidence-based pillars are cognitive behavioral therapy and exercise. She walks through practical strategies including using calendars, reminders, index cards, and to-do lists; sorting tasks by urgency and importance; breaking large projects into smaller steps; creating small reward loops by checking off progress; and deliberately reducing distractions in the work environment.. She emphasizes that movement and exercise improve attention and executive function, and that ADHD management often improves when sleep timing is stabilized. Another of Mira's peers asks whether women should avoid very cold showers or ice baths during the luteal phase or around menstruation. Dr. Dawn says the answer is not absolute, but she cautions that cold exposure can hit women differently depending on hormonal state. She notes that the luteal phase may make vasoconstriction and cold sensitivity more pronounced, and she raises concerns about the physiologic stress of cold immersion, including possible adverse effects on circulation and rewarming. Her overall tone is cautious rather than enthusiastic, especially for people who are already prone to feeling chilled or reactive. Another contributor asks why some people faint when seeing needles, blood, or medical procedures. Dr. Dawn explains the vasovagal response: a reflex in which blood pressure and heart rate suddenly drop, reducing blood flow to the brain. She offers simple countermeasures such as crossing the legs, tightening muscles, squatting, or using hand-grip tension to help push blood back toward the brain and prevent passing out. Dr. Dawn closes by asking whether cortisol is a “good” or a “bad” hormone. Dr. She answers that cortisol is essential: it helps regulate daily rhythms, energy balance, and the broader hormonal system, so it is not something to think of as inherently harmful. At the same time, she says problems arise when cortisol is chronically dysregulated or excessive, so the goal is to maintain a healthy rhythm and avoid overwhelming the adrenal system. Please go to KSQD.org and donate to support Ask Dr. Dawn on KSQD.

This week we review a recent Australian prospective assessment of aspirin resistance in children undergoing heart surgery. How common is this seen in this patient group and what are the reasons? What is the best test to perform to assess this and what tests may not be worthwile? Who deserves 'routine' testing for this possible problem? Cardiovascular surgeon Dr. Supreet Marathe of Queensland Children's Hospital in Brisbane, Australia shares the results of this recent publication. DOI: 10.1016/j.jtcvs.2025.09.013

A landmark 10-year follow-up of the HOST-EXAM trial published in The Lancet challenges a century-old assumption: aspirin may no longer be the default for lifelong secondary prevention after PCI.   Clopidogrel demonstrated a sustained reduction in ischemic and bleeding events (HR 0.86, p=0.005), with benefits that accumulated over time—yet without a mortality difference.   The implication is subtle but profound: we may be witnessing the quiet reshaping of antiplatelet strategy.   In cardiology, tradition often lingers—but data, eventually, prevails.

Nationally, the average price of gas hit $4 a gallon. In the Chicago Metro area, it's even higher – averaging $4.41 a gallon, according to AAA. Oil is a resource many of us might take for granted, but our daily lives depend on it. In the Loop learns about all the ways petroleum products show up in our day-to-day, from filling up at the gas pump to household plastics to items like toothpaste and shampoo. At the table to make it all make sense is Karen Weigert, In the Loop's sustainability contributor, and Cécile Shea, from the Chicago Council on Global Affairs. Plus, Brady Holst with the Illinois Soybean Association shares how rising oil prices are impacting farmers like him. For a full archive of In the Loop interviews, head over to wbez.org/intheloop.

Whatever happened to the Aspirin ads? These days they want us to get drugs for diseases nobody has. Laugh as I take you through the world of big money and bigger stupidity.

Welcome back to today's Friday Review where I'll be breaking down the best of the week!     I'll be sharing specifics on these topics:     Differences Between Yellow/Orange/Red BlueLight Blocking Glasses (product review) Your Body Adapts Before It Breaks (tip of the week) Aspirin & Colon Cancer (research) Joint Pain & Exercise (research)     For all the details tune in to today's Cabral Concept 3696 – Enjoy the show and let me know what you thought!   - - - For Everything Mentioned In Today's Show: StephenCabral.com/3696 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!  

Schmerzmittel gehören für viele zum Alltag – ob bei Kopfschmerzen, Rückenschmerzen oder nach einer Operation. In dieser Folge von „Aha! Zehn Minuten Alltagswissen“ erklären wir, wie Wirkstoffe wie Ibuprofen, Paracetamol oder Aspirin im Körper wirken, worin sie sich unterscheiden und ab wann ihre Einnahme problematisch werden kann. Zu Gast ist der Schmerzmediziner Dr. Andreas Böger vom Schmerzzentrum Kassel. Im zweiten Teil des Podcasts geht es um eine psychologische Frage: Warum merken wir uns Kritik oft stärker als Lob? REDAKTIONELLER HINWEIS: In einer früheren Version dieser Folge wurde fälschlicherweise gesagt, Paracetamol gehöre zur Gruppe der nichtsteroidalen Antirheumatika, also der NSAR. Das ist nicht korrekt. Wir bitten, das zu entschuldigen! "Aha! Zehn Minuten Alltags-Wissen" ist der Wissenschafts-Podcast von WELT. Wir freuen uns über Feedback an wissen@welt.de. Produktion: Sermet Agartan Redaktion: Fiona Wink Impressum: https://www.welt.de/services/article7893735/Impressum.html https://www.welt.de/services/article157550705/Datenschutzerklaerung-WELT-DIGITAL.html

All plants are toxic to varying degrees. I haven't changed my mind on that. But recently our oldest daughter came up with a business idea: – making salves from plantain leaves infused in beeswax and olive oil for their antibacterial properties — and it got me thinking about the role plants actually play in our household despite the fact that we're very much an animal-based, meat-centric family. The truth is, we do eat plants. We always have. The foundation hasn't changed — meat, organs, eggs, dairy and bone broth make up the vast majority of our calories, and comparing the nutrient content of beef liver to kale isn't a close fight. But adhering to an animal-based dietary framework doesn't mean plants are the enemy in every context. The oldest use case is medicinal. Aspirin comes from willow bark, metformin from the French lilac, morphine from poppies. I'm not eating willow bark for lunch, but if I have a headache, it makes perfect sense. Turmeric targets inflammatory pathways, ginger helps with nausea, and oregano oil has been one of our go-to remedies for respiratory and gut infections for years.  These aren't calories or micronutrients — we get those from animals. But for targeted medicinal use, plants have earned their place. Then there's flavor and the cultural connection that comes with food. Rosemary on a lamb roast, fresh basil on sourdough pizza, the smell of garlic roasting in a pan — those things make food better.  Food is family connection, tradition, and cultural identity. My wife is Costa Rican, I'm from Europe, and we grew up with certain meals that bring the family together. Some of those include plant-based ingredients, and the value of sharing that meal can override the marginal downsides. The real nuance is preparation. Fermenting, sprouting, soaking, peeling cooking — these methods can meaningfully reduce anti-nutrients like lectins and phytic acid.  We peel, slice, and ferment sweet potatoes in a saline solution for three days, which lowers the glycemic index and breaks down a lot of the problematic compounds.  We soak rice overnight and cook it in fresh water.  None of this turns plants into superfoods, but it makes them significantly more compatible with a species-appropriate diet – especially if you're sourcing organic or growing them yourself. The practical framework is straightforward: 80 to 90% quality animal foods, 10 to 20% well-chosen, well-prepared plants. If you're already eating nose to tail and building around nutrient density, you've won the big battle. The plant question is just fine-tuning. Learn More: My Animal-Based Food List (Free Download): https://michaelkummer.com/food-list/ MEAT vs. PLANTS (What's Better for Your Health?): https://www.youtube.com/watch?v=GqKzO_PkD-k&utm Plants vs. Meat: Why I Stopped Eating Veggies: https://michaelkummer.com/plants-vs-meat 99: Plants vs Animals: Why Meat Beats Plants for Nutrition: https://www.primalshiftpodcast.com/99-plants-vs-animals-why-meat-beats-plants-for-nutrition 49: From Almonds to Spinach: Dr. Schindler on Avoiding Common Dietary Traps: https://www.primalshiftpodcast.com/49-from-almonds-to-spinach-dr-schindler-on-avoiding-common-dietary-traps/  Thank you to this episode's sponsor, Apollo Neuro! Apollo is a wearable that delivers gentle vibrations to calm your nervous system and help your body stay in a restful state through the night. I've been wearing it for years and still notice a measurable difference — higher HRV and a lower resting heart rate on nights I use it. That's not placebo. That's my nervous system responding differently. If your sleep issues feel stress-related — and honestly, most of them are — Apollo is worth trying. To learn more, visit apolloneuro.com/michaelkummer and use code PRIMALSHIFT for $60 off. In this episode: 00:00 Intro  02:47 Animal-Based foundation 03:35 Plants as medicine 06:54 Flavor and food culture 10:34 Fermentation and prep 15:04 Plant tiers and avoids 16:42 Final thoughts Find me on social media for more health and wellness content: Website: https://michaelkummer.com/ YouTube: https://www.youtube.com/@MichaelKummer Instagram: https://www.instagram.com/primalshiftpodcast/ Pinterest: https://www.pinterest.com/michaelkummer/ Twitter/X: https://twitter.com/mkummer82 Facebook: https://www.facebook.com/realmichaelkummer/ [Medical Disclaimer] The information shared on this video is for educational purposes only, is not a substitute for the advice of medical doctors or registered dietitians (which I am not) and should not be used to prevent, diagnose, or treat any condition. Consult with a physician before starting a fitness regimen, adding supplements to your diet, or making other changes that may affect your medications, treatment plan, or overall health. [Affiliate Disclaimer] I earn affiliate commissions from some of the brands and products I review on this channel. While that doesn't change my editorial integrity, it helps make this channel happen. If you'd like to support me, please use my affiliate links or discount code.

Back on this day in 1899, Aspirin was patented. KTAR Timeline is brought to you by Beatitudes Campus.

National Oreo Cookie day. Entertainment from 2010. Battle of the Alamo ended, Dred Scott decision, Aspirin invented, Silly Putty went on sale. Todays birthdays - Michelangelo, Lou Costello, Ed McMahon, Mary Wilson, Kiki Dee, Rob Reiner, Tom Arnold, D.L. Hughley, Skip Ewing, Connie Britton. Nancy Reagan died.Intro - God did good - Dianna Corcoran   https://diannacorcoran.com/Oreo cookie TV commercialImma be - The Black Eyed PeasWhy don't we just dance - Josh TurnerBirthdays - In da club - 50 Cent     http://50cent.com/Who's on first - Abbott and CostelloPretty Baby - SupremesDon't go breaking my heart - Kiki Dee Elton JohnBurnin a hole in my heart - Skip EwingExit - Texy and I know it - Taylor Branch   Taylor on FacebookHistory & Factoids about today Playlist on SpotifyHistory & Factoids about today webpagecooolmedia.comcountryundergroundradio.com

Send a textThe Oncology Journal Club Podcast hosted by Professor Craig Underhill, Dr Kate Clarke and Professor Chris Jackson | Proudly Produced by The Oncology NetworkVisit oncologynetwork.com.au for Show Notes, to send us Voice Notes and more information. We explore practical wins and bold ideas across supportive care, colorectal cancer prevention, immunotherapy timing, digital triage and equity. From halving hot flushes with an NK1/NK3 blocker to biomarker-guided aspirin in colon cancer, we weigh value, risk and what truly improves lives.• Elinzanetant cutting severe hot flushes and improving treatment adherence• Current non-hormonal options and gaps in symptom control• Biomarker-selected aspirin reducing recurrences in colorectal cancer• Limits of DFS, toxicity trade-offs and subgroup signals• Rising early-onset colorectal cancer and system planning needs• Possible environmental and microbiome drivers under study• ASCO geriatric assessment guidance and G8 screening in clinics• PD-1 with short-course radiotherapy boosting rectal pCR rates• Large language models for safe, efficient symptom triage• Rare cancers report on access, cost, and rural inequities• Telehealth standards to link expertise closer to home• Healthy workplace culture to retain a resilient oncology workforceJoin the Oncology Network, registration is free, and leave us a voice note on the OJC page at oncologynetwork.com.au. Physicians, don't forget you can claim CME points for listening to the show!Thanks for listening

CardioNerds (Dr. Jenna Skowronski [Heart Failure Council Chair], Dr. Shazli Khan, and Dr. Josh Longinow) are joined by renowned leaders in the field of AHFTC (Advanced Heart Failure and Transplant Cardiology) and mechanical circulatory support, Dr. Jeff Teuteberg and Dr. Mani Daneshmand to continue the discussion of advanced heart failure therapies by taking a deep dive into the world of durable LVADs (Left Ventricular Assist Devices). In this episode, we will review the history of ventricular assist devices, the basics of LVAD function, selection criteria for LVAD therapy, and surgical nuances of LVAD implantation. Audio Editing by CardioNerds intern, Joshua Khorsandi. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls There have been significant advances in the field of MCS/LVAD therapy since the first implanted LVAD in the 1960s, to the first FDA approved device in the early 2000's, to now the HM3 LVAD, with the most important change being a centrifugal flow/magnetically levitated design that led to minimized hemocompatibility-related adverse events (HRAE's) (MOMENTUM 3 trial comparing HM2 and HM3).  The REMATCH trial in 2001 was a pivotal trial for LVAD therapy, demonstrating that in a population of patients with advanced HF (70% IV inotrope dependent), LVAD therapy significantly improved survival at both 1 and 2 years as compared to medical therapy alone.    MOMENTUM 3 trial was a landmark trial for the HM3 device, showing that in a population of end stage HF patients (86% inotrope dependent, 32% INTERMACS 1-2, and 60% DT strategy), 5-year survival with HM3 was 58% and HM3 had lower HRAE's compared with HM2.  There are both patient-specific factors and surgical considerations when it comes to candidacy for LVAD therapy.  RV function prior to LVAD is a key determinant for success post-LVAD  Many patients being considered for LVAD may not have robust RV function, however, predicting RV failure after LVAD is exceedingly difficult.   In general, it doesn’t matter how bad the RV may look on imaging; we care more about the pre-LVAD hemodynamics (look at the PAPi and RA/wedge ratio).   What happens in the OR may be the most important determinant of how the RV will do with the LVAD!  Notes Notes drafted by Dr. Josh Longinow.  1. Historical background of heart pumps and LVADs  LVAD Evolution   FDA approval year  2001  2008  2012  2017  Pump  HeartMate XVE   HeartMate II  Heartware HVAD  HeartMate III  Flow/Design Features  Pulsatile Technology   Continuous flow Axial design  Continuous flow  Centrifugal design  Continuous flow   Full MagLev + Centrifugal design  The 1960's ushered in the first ‘LVADs', when the first air-powered ‘LVAD' was implanted. It kept the patient alive for four days before the patient expired.   The first generation of LVADs were pulsatile pumps   The first nationally recognized, FDA approved LVAD was the HeartMate XVE (late 1990s to early 2000s, REMATCH trial). The XVE pump used compressed air (pneumatically driven) to power the pump.   Prior to the XVE, OHT was the standard of care for patients with advanced, end-stage heart failure.   The second and third generations of LVADs were non-pulsatile, continuous flow devices and included the HVAD, HM2, and HM3 devices.   MOMENTUM 3 was a landmark trial for the HM3 device, showing that in a population of sick patients with end stage HF (86% inotrope dependent, 32% INTERMACS 1-2, and 60% DT strategy), 5-year survival with HM3 was 58% and HM3 had lower HRAE's compared with HM2.   The only pump that is currently FDA approved for implant is the HM3, although other pumps are in clinical trials (BrioVAD system, INNOVATE Trial).  2. What are LVADs, and how do they work?   In simplest terms, the LVAD is a heart pump comprised of several key mechanistic components:   Inflow cannula  Mechanical pump   Outflow cannula  Driveline  Controller/Power source  The HM3 differs from its predecessors (HM2 and HVAD) in several key ways;   HM3 is placed intrapericardial whereas the HM2 was placed pre-peritoneal.   Perhaps most importantly, the HM3 is a fully magnetically levitated, centrifugal flow pump, whereas the HM2 is an axial flow device.  Axial flow pumps are not magnetically levitated, leading to more friction produced between the ruby bearing's contact with the pump rotors, and higher rates of hemocompatibility related adverse events (HRAEs, i.e. pump thrombosis) and the HM2 was ultimately discontinued in favor of the HM3 (MOMENTUM 3 trial).  3. What do the terms ‘Destination Therapy' (DT) or ‘Bridge to Transplant' (BTT) mean when it comes to LVADs?   When LVADs first came on the stage, EVERYONE was a BTT; these early pumps weren't designed for long term use (I.e. REMATCH Trial, Heartmate XVE)  Destination therapy means the LVAD was placed in leu of transplant because there are contraindications to transplant   REMATCH trial brought about the concept of “Destination therapy”, comparing outcomes in patients (with contraindications for transplant) who received an LVAD vs optimal medical therapy  Bridge to transplant means we are placing the LVAD in a patient who may not be a transplant candidate at this moment in time (is too sick, or conversely, not sick enough), but may be down the line   Bridge to recovery is another term used when the LVAD is being placed for a patient we think may have a recoverable cardiomyopathy  4. What are some factors we should consider when assessing a patient’s candidacy for LVAD, in general, and from a surgical perspective?   Patient factors   Older age might push us towards thinking LVAD rather than transplant  In general, age > 70 is the cutoff for transplant, but this is not a hard cut off and varies institution to institution    In general, think about things that help predict recovery after a major surgery; Frailty and Nutritional status are important, we try to optimize these prior to LVAD implant   Right ventricular function remains the Achilles heel of LV support  We know that needing temporary RV support post LVAD puts you on a different survival curve than patients who don’t need RVAD support  Studies have not been able to successfully predict who will develop RV failure after LVAD implantation  What happens in the time between when the patient goes to the OR and when they get back to the ICU is an important determinant who might develop RV failure post LVAD   Surgical techniques such as implanting the HM3 in the intra-thoracic cavity, rather than intra-pericardial may help maintain LV/RV geometry to help optimize the RV post LVAD   Surgical considerations for LVAD candidacy  Small, hypertrophied LV: HM3 inflow cannula is small, but small hypertrophied ventricles tend towards chamber collapse during systole causing suction, needing to run slower with lower flow rates  Chest size/diameter: pumps have gotten so small now, that for adults, these have become less of a consideration  BMI: low BMI used to be more of a concern with the older pumps due to where they were placed, and the relative size of the pump itself, not so much now with the smaller HM 3 pumps  Calcified LV apex: would increase risk of stroke, bleeding   Driveline tunneling becomes a concern in the super obese population, higher risk for driveline infections (might tunnel these driveline's shorter, and to a less fatty region of the abdomen, could even tunnel out the thoracic cavity in the super obese to limit skin motion)    5. Is there a role for MCS (i.e. temporary LVAD such as Impella) in pre-habilitation of patients prior to LVAD surgery?   The theory of being able to improve systemic perfusion, decongest the organs, and make the patient feel better prior to surgery makes sense, but becomes problematic due to the lack of a hard end point/time for prehabilitation which might risk delays in surgery   More likely that it can lead to delay in the surgery, with less-than-optimal benefit; you don't want to prolong the wait for surgery and increase the risk for complications prior to surgery    An Impella 5.5 is currently FDA approved for 2 weeks of support, not 2 months so timing is important to keep in mind  It’s unlikely that you will take a patient and convert them from a malnourished, cachectic person in 2 weeks’ time   6. Is there a role for LVAD therapy in the younger patient population? Should we be thinking of LVAD up front for these patients, with the goal of transplanting down the line?   Recovery may be more likely in certain populations, particularly younger females with smaller LV's; in those populations, perhaps bridge to recovery should be the focus, optimizing them on GDMT etc.   The replacement of transplant, with MCS (LVAD) in young patients has become a topic of discussion, because these pumps have become better and better, with the thinking that an LVAD could bridge a patient for 10 years or so, and they could get a transplant later   It is still a big unknown, but several concerns exist  Patients who get LVADs might end up with complications that become contraindication to transplant down the line (stroke, sensitization etc)   Patients and providers are more hesitant because of the more recent iteration for the UNOS criteria for OHT listing which no longer gives patients with an uncomplicated LVAD higher priority, and therefore they could end up waiting a longer time for a heart after undergoing LVAD  References Rose EA, Gelijns AC, Moskowitz AJ, et al. Long-term use of a left ventricular assist device for end-stage heart failure. N Engl J Med. 2001;345(20):1435-1443. doi:10.1056/NEJMoa012175  Mehra MR, Uriel N, Naka Y, et al. A Fully Magnetically Levitated Left Ventricular Assist Device – Final Report. N Engl J Med. 2019;380(17):1618-1627. doi:10.1056/NEJMoa1900486  Mancini D, Colombo PC. Left Ventricular Assist Devices: A Rapidly Evolving Alternative to Transplant. J Am Coll Cardiol. 2015;65(23):2542-2555. doi:10.1016/j.jacc.2015.04.039  Mehra MR, Goldstein DJ, Cleveland JC, et al. Five-Year Outcomes in Patients With Fully Magnetically Levitated vs Axial-Flow Left Ventricular Assist Devices in the MOMENTUM 3 Randomized Trial. JAMA. 2022;328(12):1233-1242. doi:10.1001/jama.2022.16197  Rose EA, Moskowitz AJ, Packer M, et al. The REMATCH trial: rationale, design, and end points. Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure. Ann Thorac Surg. 1999;67(3):723-730. doi:10.1016/s0003-4975(99)00042-9  Kittleson MM, Shah P, Lala A, et al. INTERMACS profiles and outcomes of ambulatory advanced heart failure patients: A report from the REVIVAL Registry. J Heart Lung Transplant. 2020;39(1):16-26. doi:10.1016/j.healun.2019.08.017  Mehra MR, Netuka I, Uriel N, et al. Aspirin and Hemocompatibility Events With a Left Ventricular Assist Device in Advanced Heart Failure: The ARIES-HM3 Randomized Clinical Trial. JAMA. 2023;330(22):2171-2181. doi:10.1001/jama.2023.23204  Mehra MR, Nayak A, Morris AA, et al. Prediction of Survival After Implantation of a Fully Magnetically Levitated Left Ventricular Assist Device. JACC Heart Fail. 2022;10(12):948-959. doi:10.1016/j.jchf.2022.08.002  Bhardwaj A, Salas de Armas IA, Bergeron A, et al. Prehabilitation Maximizing Functional Mobility in Patients With Cardiogenic Shock Supported on Axillary Impella. ASAIO J. 2024;70(8):661-666. doi:10.1097/MAT.0000000000002170 

We recently covered an SMFM abstract that was presented at the annual Pregnancy Meeting held in early February 2026. The authors were from my Alma Mater, UT Southwestern/Parkland Hospital. This was a well-done study comparing 162 milligrams aspirin to 81 milligrams of aspirin. The results were very encouraging! However, aspirin definitely has an awkward acumen. It would be wonderful if ALL the data just leaned in the same direction... but it doesn't! Enter our podcast family member, and my friend Alex. Alex sent me an incredible and insightful message which was a rebuttal to my Southwestern colleagues' findings. In this episode you'll hear Alex's rebuttal and clinical conundrum, and we will explain why these two seemingly paradoxical findings makes sense. Listen in for details.1. Khander, Amrin MD; Thomas, Charlene MS; Matthews, Kathy MD; Christos, Paul DrPH; Alcus, Claire BA; Alam, Tanvir BS; Bush, Leah BA; Deshmukh, Diksha BA; Chasen, Stephen T. MD; Riley, Laura E. MD; Skupski, Daniel W. MD; August, Phyllis MD, MPH; Malha, Line MD, MS. Comparison of 162 mg and 81 mg Aspirin for Prevention of Preeclampsia: A Randomized Controlled Trial. Obstetrics & Gynecology 147(1):p 87-96, January 2026. | DOI: 10.1097/AOG.0000000000006100

Send a textMajor bleeding remains the principal complication of oral anticoagulation. In patients with device-detected subclinical atrial fibrillation, the decision to anticoagulate requires careful balancing of stroke prevention against bleeding risk.In this episode of CLOT Conversations, Dr. Deborah Siegal discusses a prespecified subanalysis of the ARTESiA randomized clinical trial, recently published in JAMA Cardiology. ARTESiA demonstrated a 37% reduction in stroke and systemic embolism with apixaban compared to aspirin — but at the cost of increased major bleeding.This subanalysis goes deeper, examining the site, severity, and clinical course of bleeding events. Most bleeding was gastrointestinal and non-critical. Rates of intracranial and fatal bleeding were low and similar between treatment arms. The majority of events were not clinical emergencies, and many were defined by hemoglobin decline rather than catastrophic presentation.We explore what these findings mean for individualized risk assessment, the importance of modifiable bleeding risk factors such as NSAID use, and how physicians and patients can approach shared decision-making in subclinical AF.Abstract (subscription required for full paper): Siegal DM, Sticherling C, Healey JS, McIntyre WF, Christensen LS, Parkash R, Vanassche T, Conen D, Gold M, Granger CB, Nielsen JC. Major Bleeding With Apixaban vs Aspirin: A Subanalysis of the ARTESiA Randomized Clinical Trial. JAMA cardiology. 2025 Dec;10(12):1305-14.https://jamanetwork.com/journals/jamacardiology/fullarticle/2841075Support the showhttps://thrombosiscanada.caTake a look at our healthcare professional and patient resources, videos and publications on thrombosis from the expert members of Thrombosis Canada

Well, even though low dose aspirin has been recommended for the reduction of preeclampsia risk for many years, 2 controversies persist: 1. who should get it, and 2. the dose we should use. While the current US recommendation still focuses on 81 mg low dose aspirin, initiated after 12 weeks of gestation (based on risk factors), there's increased movement and growing data supporting both universal adoption and the higher dose of 162 mg. In this episode, we will briefly summarize brand new data out of UT Southwestern which was just published at the SMFM Annual Pregnancy meeting in Las Vegas. Listen in for details.1. https://www.smfm.org/news/new-studyroutine-aspirin-therapypreventsseverepreeclampsiainat-risk-populations2. ACOG CO 7433. The Effect of Aspirin on the Risk of Preeclampsia Based on the Fetal Medicine Foundation First Trimester Risk.4. Bujold E, Rolnik DL, Poon L, Syngelaki A, Wright D, Nicolaides KH. The effect of aspirin on the risk of preeclampsia based on the Fetal Medicine Foundation first-trimester risk. Am J Obstet Gynecol. 2025 Oct 31:S0002-9378(25)00808-7. doi: 10.1016/j.ajog.2025.10.032. Epub ahead of print. PMID: 41177290.

Commentary by Dr.  Jian'an Wang.

Contact us and share your opinionIn this episode we discuss the recent visit by BMA GPC Chair Katie Bramal-Stainer to a Derbyshire-Lincolnshire-Nottinghamshire LMC event. What were some of the questions in the room and what did we learn about contract timelines, content and the future of collective action for General Practice? We also discuss news stories covering some sudden and disruptive changes to GP Trainee assessment software, the shortage of yet another common drug (Aspirin!), and additional funding for cancer screening in areas of high deprivation.And… opportunities to join Gandhi and Andy at two upcoming eGPlearning events…GP5T11 Online GP Trainer Conference https://events.ringcentral.com/events/gp5t-11/registration PCNPlus26 Conference in Nottingham or online https://www.thcprimarycare.co.uk/pcnplus2026 Boost your triage skills with our dynamic 5-session live webinar course, tailored for primary care clinicians. Led by Dr. Gandalf and Dr. Ed Pooley, this comprehensive training covers all facets of remote patient triage—digital, on-call, and more. Gain practical knowledge, exclusive tips, and direct access to our experts through open Q&A sessions. Elevate your ability to manage primary care challenges effec Subscribe and hear the latest EPIC episode. Join Dr Mike as he shares how to get started and fly using EMIS to make your life easier with this clinical systembit.ly/EMIScourse

In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Aaron L. Berkowitz, MD, PhD, FAAN, who served as the guest editor of the February 2026 Neurology of Systemic Disease issue. They provide a preview of the issue, which publishes on February 2, 2026. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology in the Department of Neurology at the University of California, San Francisco, in San Francisco, California. Additional Resources Read the issue: continuum.aan.com Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Guest: @AaronLBerkowitz Full episode transcript available here Dr Jones: The human nervous system is so complex. You can spend your whole career studying it and still have plenty to learn. But the human brain does not exist in isolation. It's intricately connected with and reliant on other bodily systems. When those systems go awry, sometimes the first sign is in the nervous system. Today we will speak with Dr Aaron Berkowitz, an expert on the neurology of systemic disease, and learn a little about how these disorders can present and what we can do about it. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr Aaron Berkowitz, who is Continuum's guest editor for our latest issue of Continuum on the neurology of systemic disease. Dr Berkowitz is a professor of clinical neurology at the University of California, San Francisco, and he has an active practice as a neurohospitalist and in outpatient general neurology---and, importantly, as a clinician educator. In addition to numerous teaching awards, Dr Berkowitz has published several books and also serves on our editorial board for Continuum. Dr Berkowitz, welcome. Thank you for joining us. Why don't you introduce yourself to our listeners?  Dr Berkowitz: Thanks, Lyell. As you mentioned, I'm a general neurologist and neurohospitalist here in San Francisco, California at UCSF and very involved in resident education as well. And I was honored, flattered and a little bit frightened when I received the invitation to guest edit this massive issue on the neurology of systemic disease. But I've learned a ton, and it's been great to work with you and the incredible authors we recruited to write for us. And I'm excited to have the issue out in the world.  Dr Jones: Yeah, me too. And you and I have talked about it before: you're one of a very small group of people who have guest edited multiple issues on different topics, right?  Dr Berkowitz: That's right. I did the neuroinfectious disease issue in… was it 2020? 2021? Something like that.  Dr Jones: Yeah. So, congratulations, more people have walked on the moon than done what you've done. And I'm looking forward to chatting, Aaron, and really grateful for your work putting together a fantastic issue. I think our listeners will appreciate that the nervous system does not function in isolation. It's important to understand the neurologic manifestations of diseases that originate within the brain, spinal cord, nerves, muscles, etc., but also the manifestations of diseases that begin in other systems and, you know, may masquerade as a primary neurologic disorder. So, it's obviously an important topic for neurologists, since many of these patients are receiving care in another setting, perhaps from another specialist. I almost think of this issue of Continuum as a handbook for the consultant neurologist, inpatient or outpatient. I don't know. Do you think that's a fair characterization of the topic? Dr Berkowitz: Absolutely. I completely agree with you. I think, yeah, many of us go into neurology interested in our primary diseases, whether it's stroke or Parkinson's or neuropathy or particular interest in neurologic symptoms, whether they're cognitive, motor, sensory, visual. And we quickly learn in residency, right? As you said, a lot of what we see is neurologic manifestations of primary diseases. So, I don't know how similar this is to other training programs. But it seemed like, if I'm remembering correctly, my first year of residency was mostly on primary neurology services, general stroke, ICU. And we moved into the consultant role more in the PGY-3 year the next year. And I remember explaining to students rotating with us on the consult services, this is actually much more complex in a way, because the patient has some type of symptom in a much broader and much more complicated context of multiple things going on. And I call it "neurology in the wild." There's, like, neurology of, this patient's had a stroke and we know they have a stroke and we're trying to figure out why and treat it. That's all interesting. But our question here, is there a stroke needle buried in this haystack of all of these medical or surgical complications? And learning what I call neurology of X, which is really what this issue is; as you said, that there's a neurology of everything. There's a neurology of cardiac disease. There's a neurology of the peripartum. There's a neurology of rheumatologic disease. There's every new treatment that comes out in oncology has a neurology we learn, right? There's a neurology of everything.  Dr Jones: There's a lot of axes, right? There's the heart-brain axis and the kidney-brain axis. And… I think we cover everything except the spleen-brain axis, which maybe that's a thing, maybe not. I'll probably hear from all the spleen fans out there. So, I want to do a little bit of an experiment. We're going to do something new today on the podcast. Before we get into the questions, we're going to start with a Continuum Audio trivia question. So, this will be a first time ever. Dr Berkowitz, we all know that chronic hyperglycemia, or diabetes, can lead to many neurologic and systemic complications and that optimal glucose control is our goal. For our listeners, here's the question: what neurologic complication can occur from correcting hyperglycemia too quickly? What neurologic complication can occur from correcting hyperglycemia too quickly? Stick around to the end of our interview for the answer. So, Aaron, let's get right to it. You had a chance to review all the articles in this issue on the neurology of systemic disease. What do you think in all of those is the most exciting recent development for patients who fit into this category? Dr Berkowitz: Yeah, that's a great question. I think we talked about when we were putting this issue together, right, a lot of the Continuum subspecialty topics; there should have been updates on particular disease diagnostics, treatments, new phenotypes. Whereas here probably a lot less has changed in primary heart disease, primary cancer. As I'd like to say to our students trying to excite them about neurology, most specialties have new treatments, but I can name a large number of new diseases, right, that have been discovered since we've been out of training. So, a lot of the primary medicine stays the same, and the neurologic complications stay the same. But probably the thing that many readers will want to keep handy and will probably be much in need of update again in three years are the neurologic complications of all the new cancer treatments. So, if we think back to I finished training just over ten years ago when a lot of the fill-in-the-blank-umabs were coming out, CAR T therapy, and we were starting to see a lot of neurology, I remember, related to these and telling the oncologists and they said, oh, you just wait. We are seeing at the conferences that there's a lot of neurology to these. And I feel like that is always a moving target. And I think we are seeing a lot of those and it's hard to keep up with which treatments can cause which complications, which syndromes and which severities require holding the treatment when you can rechallenge longer-term complications of CAR T cell therapies now that we've learned more about the acute complications. So, Amy Pruitt from Penn has written us a fantastic article for this issue that covers a lot of the updates there. And I learned a lot from that. I feel like that's the one that just like every time the carnioplastic diseases are reviewed in Continuum, it seems like the table is another page longer from your colleagues there in Rochester teaching us about new antibodies. And I feel like, for this issue, that's one of the areas that felt like there was a lot of very new content to keep up with since last time.  Dr Jones: That's good news, right? It's good that we have new immunotherapies for cancer, but it does lead to neurologic catastrophes sometimes, and it is a moving target, really rapid. So, you mentioned that just over ten years ago you finished your training and now we see a lot more of these complex immunotherapy-related neurologic complications. What about in the other direction? Are there any things that you see less commonly now in your practice than you might have seen ten years ago right when you were finishing training?  Dr Berkowitz: I would say no, I think. I think we're seeing a lot of new stuff, and we're still seeing a high volume of the classic consults we tend to get, whether that's altered mental status in a patient who's systemically ill; weakness or difficulty reading from the ventilator in a patient who's critically ill; patient has endocarditis and has a stroke hemorrhage or mycotic aneurysm, what do we do? Yeah, one of the parts that was really fun and educational editing this issue is, I really wanted to ask the experts the questions I find that are really troubling and challenging and make sure we could understand their perspective on things like the endocarditis consult, which I always feel like each time there's some twist that even though the question is what do we do about this stroke and/or hemorrhage and/or aneurysm and is surgery safe? It seems like each time I always feel like I'm reinventing the wheel, trying to really sort out how to think about this. And we have a great article from Alvin Doss at Beth Israel and Steve Feskey from Boston Medical Center. It covers a lot of cardiology, as you know, in that article about a great section on endocarditis where every time it came back for review, I would say, but what about this? This comes up. What about this? Can you explain how you think about this for our readers? I don't know. I'd be curious to hear your perspective. It sounds like we agree on what has become more common. I don't think anything in neurology seems to become less… Dr Jones: Well, no, I guess we haven't really solved anything, I guess we haven't cured any problem. But that's okay, right? I mean, it's building on an established foundation of experience and history in our field. And you know, we mentioned earlier that in many ways this issue is kind of like a neurology consultant's handbook. We did something a little different with it in that sense. In addition to you serving as the guest editor, you have authored an article in the issue. It touches on something that we've talked about a couple of times, and I'd be interested to hear you talk through it with our listeners a little bit on how to approach the neurologic consultation. Tell us a little more about that and your article and how you approached it.  Dr Berkowitz: Oh, yeah, thanks. Well, thanks first of all for inviting me to think about a sort of introductory article to this issue. And I was trying to think about what to write about because, as you've said and we've been talking about, no one could know every neurologic complication of every medical disease, treatment, surgery, hospital context. Probably many of us don't even know all the muscle diseases, right, within neurology. So how could we know all this stuff? And we need some type of manual from our colleagues that can explain, okay, I know this patient has inflammatory bowel disease and they've had a stroke. Is that- are these related? Are these unrelated? And I thought the articles kind of answer all of these questions. What would I say beyond this patient has disease X and is on drug Y? Well, look up in this issue disease X and see what the neurology can be, common and rare and how often it's associated, how often it's the presenting feature, how often it means the treatment is failing, etc. I thought, I'm not sure there's much to say there. That's about a paragraph. And I thought, well, let's think even more broadly about neurologic consultation. And as you know, I like to think about diagnostic reasoning and clinical reasoning. And we talk a lot about framing bias right? And I think that is very common in consultative neurology because we'll be told in the consult or in the page or E-consult or whatever it is, this is a blank-year-old blank with a history of blank on treatment blank. And right away your mind is starting to say, oh, well, the patient just had heart disease, or, the patient is nine months pregnant, or, the patient is on an immune checkpoint inhibitor. And whether you want to do it or not, your mind is associating the patient's neurology with that. And it's- even if we know we're framing or anchoring, it's hard to kind of pull away from that. And most of the time, common things being common, a patient with cancer develops new neurology, It's probably the cancer, the treatment, or sometimes a paraneoplastic syndrome. But I've definitely found if you do a lot of inpatient neurology and a lot of consults that you're seeing so much and you have no choice but to apply these heuristics, because you're seeing a lot of volume quickly and the patients are in the hospital or they're being closely followed and outpatient setting by another specialist. You presume if you didn't get it quite right the first time, it's going to come back to you. And there's a little bit of difficulty figuring out, this is a case, actually, of all the altered mental status in acutely ill patients I got today, this is the one I should dig deeper in that I think this could turn out to be a stroke or encephalitis as opposed to delirium. I felt like that I really haven't approached that except knowing that it's easy to fall into traps. And so, I started to think about framing bias. You know, we talked about if we become aware of our biases, right, we're better at not falling prey to them. But it's subconscious. So, we might be applying it without even realizing, or even saying, I might be framing this case the wrong way, you can go right on framing it the wrong way. So, I want to kind of get a little more granular on what types of framing biases actually are relevant, specifically, to the console setting. And so, I tried to come up with a few more specific examples and try to think about ways that we could at least have a quick, if our knee-jerk is to associate primary disease X that the patient has or primary treatment X with neurologic symptom Y, what's at least a quick counter-knee jerk to say, what if it could be something else? So, for example, one of them I call "low signal-to-noise ratio bias." Altered mental status in the acutely ill hospitalized patient. What would you say, Lyell? 99 out of 100- 99.9 out of 100, it's not a primary neurologic disease. Is that fair to say? Dr Jones: Very high, yep. I agree. Dr Berkowitz: Yeah. But could it be a stroke? Could it be non-convulsive status epilepticus, meningitis encephalitis? So, how do we sort of counteract low signal-to-noise ratio bias, acknowledging it exists, acknowledging most of the time there is a low signal-to-noise, that it's not going to be neurology---to just for example, use the time course. This is pretty acute. Have I convinced myself this is not a stroke or a seizure or an acute neurologic infection? And if I'm not sure at the bedside, should I err on the side of more testing? Or the "curbside bias," as I call when your colleague just sends you a text message on your phone, No need to even open the chart, Dr Jones. Patient had a cerebellar stroke. Incidental. They're here for something else. Aspirin, right? Just like a super tentorial stroke. And you might reply thumbs up. And then imagine you open the CT scan and it's a huge cerebellar stroke with fourth ventricular compression- and patient can hide a lot of stroke back there, might just have a little ataxia. You were curbsided and that framed you to think, oh, they asked me, is aspirin okay for a cerebellar stroke and I said yes, without realizing actually the question should have been posed is, how do you manage a huge stroke with mass effect in the posterior fossa? So, these types of biases, I come up with five of them, I won't go through all of them. I'm in the article to sort of acknowledge for the reader, most of the time it's going to be what you look up in this issue, but how to think about the times where it might not be and how to be more precise about what framing is and different types of framing that occur specifically in the consultant arena. Dr Jones: And I think the longer we practice, the more of those low-frequency exceptions that you see. And, you know, and then it sticks in our mind and sometimes the bias swings the other way; people, you know, think primarily about the low frequency. And so, it's tricky. And what I really enjoyed about that article, we started talking about this probably more than a year ago, and more than a year ago, I would say relatively few clinicians were using a now widely popular large language model for clinical decision-making; we won't name the model. And now I think most clinicians are using it almost every day, right? And I think it puts a premium on how to think and how to engage with the patient, and less about the facts and the lists that a lot of conventional medical education really is derived from. So, I really appreciate that article. We can pat ourselves in the back. We had some foresight to put it in the issue, and I think it's a great addition to it. Dr Berkowitz: Thank you. Dr Jones: So, the list of potential topics when we think about the neurologic manifestations of systemic disease, we tend to break it down by organ systems, right? But the amount of things that could end up in the issue is almost infinite. Is there anything that, when you were putting this issue together---either in terms of the topics or editing the articles---is there anything that you wanted to include, but we just didn't have room? Dr Berkowitz: I certainly won't say we covered everything, but I will say we were able to recruit a fantastic team of authors. And as you and I also talked about at the beginning, although you could say, we're doing the movement disorders issue, let's find all the top movement disorders folks who are expert specialists in this field, there's not really a neurohematologist or a neurogastroenterologist out here. So, you and I put our heads together to think of phenomenal general neurologists in most cases, some subspecialists who know a lot about this but were also excited to read a lot more about it and assemble the existing knowledge by the practicing neurologist for the practicing neurologist. And I think with that approach and letting folks have kind of, you know, I asked some specific questions. These are topics I hope you'll cover. These are vexing questions in this area. I hope you'll find some answers to how often can this neurology be the primary feature of this rheumatologic disease with no systemic manifestations and when should we look or as we mentioned, the complicated endocarditis consult. I won't say we covered everything. This could be, and is, textbook-sized, and there are textbooks on this topic. But I think on the contrary, authors came back and had sections on things that I might not have thought to ask- to cover. Dr Sarah LaHue, my colleague here at UCSF, I asked for an article, as traditionally in this issue, on the neurology of pregnancy in the postpartum state and included, I think probably for the first time in Continuum, a fantastic review of neurologic considerations in patients in menopause, which I'm not sure has been covered before. So, things that I wouldn't have even thought to ask for. Our authors came back with some fantastic stuff. And the ICU article by Dr Shivani Ghoshal, instead of focusing just on altered mental status in the ICU, weakness in the ICU---those are all in there---I also asked her to discuss complications of procedures in the ICU. How often do procedures in the ICU cause local neuropathies or vascular injury, these types of things. Dr Jones: Yeah, me too. And I guess that's a great advertisement, that there probably are things that we didn't cover, but if there are, we can't think of them. We've done as best as we can. So now let's come back to our Continuum Audio trivia question for our listeners. And I'll repeat the question: what neurologic complication can occur from correcting hyperglycemia too quickly? And I actually think there might be two correct answers to this one. Dr Berkowitz, what do you think? Dr Berkowitz: Yeah, I was thinking of two things. I hope these are the things you're thinking of as well. One is what I think used to be referred to as insulin neuritis, sort of an acute painful small fiber neuropathy from after the initiation of insulin, I think also called treatment-induced diabetic neuropathy or something of that nature. And then the other one described, defined and classified by your colleagues there in Rochester, the diabetic lumbosacral radiculoplexis neuropathy or Bruns-Garland syndrome or a diabetic amyotropy, I think, can also---if I'm not mistaken---also occur in this context; you should have weight loss in association with diet treatment of diabetes. But how did I do? Dr Jones: Yeah, you win the prize, the first-ever prize. There's no monetary value to the prize, but pride, I think, is a good one. Yeah, those were the two I was thinking of. The treatment-induced neuropathy of diabetes is really nicely covered in Dr Rafid Mustafa's article on the neurologic complications of endocrine disorders. It's a rare condition characterized by the acute/subacute onset of diffuse neuropathic pain and some usually some autonomic dysfunction. And it occurs when you have rapid and substantial reductions in blood glucose levels. And you can almost map it out. There was a study from 2015 which is referenced in the article, which found that a drop in hemoglobin A1c of 2 to 3% over three months confers about a 20% absolute risk of developing this treatment-induced neuropathy of diabetes, and a drop of more than 4%, more than 80% risk. So, very substantial. And then in the other---we see this commonly in patients with diabetic lumbosacral radiculoplexis neuropathy---they have the subacute onset of usually asymmetric pain and weakness in the lower limbs that tends to occur more frequently in patients who have had recent better control of their sugar. We can also see it in the upper limbs too. So, you get a perfect score. Dr Berkowitz, well done. Again, I want to thank you. I want to thank you for such a great issue, a great article to kick off the issue, and a great discussion of the neurology of systemic disease. Today I learned a lot talking today, I learned a lot reading the issue. Really grateful for your leadership of putting it together, pulling together a really great author panel, and I think it will come in handy not just for our junior readers and listeners, but also our more experienced subscribers as well. Dr Berkowitz: Thank you so much. Like I said, it was a big honor to be invited to guest edit this issue. I've read it every three years since I started residency. It's always one of my favorite issues. As you said, a manual for consultative neurology, and I learned a ton from our authors and really appreciate the opportunity to work with you and the amazing Continuum team to bring this from an idea, as you said, probably over a year ago to a printed issue. So, thanks again, Lyell. Dr Jones: Thank you. And again, we've been speaking with Dr Aaron Berkowitz, guest editor of Continuum's most recent issue on the neurology of systemic disease. Please check it out, and thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. Thank you for listening to Continuum Audio.

Years ago, you might have heard that an aspirin a day keeps the cardiologist…

Dr. Rupsa Boelig, a 2025 March of Dimes Discovery Research Grant winner and an Associate Professor of Obstetrics and Gynecology in the Division of Maternal Fetal Medicine at Philadelphia's Thomas Jefferson University, discusses her new study on the metabolism of aspirin in pregnant women with diabetes or a higher BMI. She hopes the study findings will shed light on whether these women may benefit from a higher aspirin dose to help prevent preeclampsia and/or preterm birth.

Chief Medical Officer of Northwestern Medicine's Northwest region of hospitals Dr. Irfan Hafiz joins Bob Sirott to talk about myths concerning aspirin, the types of physical activities that could help prolong your lifespan, and technology that could help with the future of treating cancer. He also shares details about why it’s important to eat slower, […]

We unpack new studies that reshape how we counsel on VBAC after short intervals, update what we tell BRCA carriers about estrogen therapy, and explore how self-collected HPV tests can reduce screening gaps. We also question surgical marketing, workforce trends, and the shaky evidence behind aspirin dosing for preeclampsia.• Short interpregnancy interval as a VBAC risk factor, not a contraindication• Absolute uterine rupture rates in spontaneous vs induced labor• Estrogen therapy in BRCA carriers and treated gyn cancers• Cervical screening overuse and underscreening in insured populations• Self-collected HPV testing intervals and access benefits• OB-GYN workforce shortages and rural distribution gaps• Endometriosis surgery indications versus fertility claims• Robotics versus laparoscopy outcomes and training priorities• Aspirin dose trials, lack of placebo arms, and abruption signals• Reading statistics correctly and demanding better editorial standards0:00 Setting The Agenda: New Studies0:40 Short Interval Pregnancy And VBAC Risk3:10 Quantifying Uterine Rupture By Spacing8:10 Induction, Augmentation, And Rupture Math9:40 HRT In BRCA Carriers: New Evidence13:05 Estrogen After Gyn Cancers: Practice Gaps17:40 Cervical Screening: Overuse And Underscreening22:30 Self-Collected HPV Testing Guidance27:00 OB-GYN Shortages And Distribution33:20 Endometriosis Surgery And Fertility Claims41:20 Robotics Vs Laparoscopy: Outcomes And Training47:20 Aspirin Dosing For Preeclampsia: No Signal55:30 Interpreting Stats And Editorial Standards59:20 Closing Notes And Next StepsBe sure to check out thinking about obgyn.com for more information, and be sure to follow us on InstagramFollow us on Instagram @thinkingaboutobgyn.

For years, doctors have recommended taking Aspirin every day to help prevent heart attacks and stroke. Cardiologist Dr. Sonia Anand says that advice is still correct, but it only applies to certain patients. She cautions against taking too much Aspirin, because acetylsalicylic acid can increase the risk of bleeding in the stomach and brain.For transcripts of The Dose, please visit: lnk.to/dose-transcripts. Transcripts of each episode will be made available by the next workday. For more episodes of this podcast, click this link.

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-468 Overview: We first discussed aspirin use for primary prevention of cardiovascular disease in 2022 when the USPSTF recommended against it. In this follow-up episode, we review new trial data reinforcing that guidance and help you translate the evidence into safer prevention strategies. Build confidence in supporting patients with evidence-based approaches to reduce cardiovascular risk. Episode resource links: Aspirin, cardiovascular events, and major bleeding in older adults: extended follow-up of the ASPREE trial. Eur Heart J. 2025 Aug 12:ehaf514. doi: 10.1093/eurheartj/ehaf514. Epub ahead of print. PMID: 40796244. Guest: Robert A. Baldor MD, FAAFP   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com The views expressed in this podcast are those of Dr. Domino and his guests and do not necessarily reflect the views of Pri-Med.

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-468 Overview: We first discussed aspirin use for primary prevention of cardiovascular disease in 2022 when the USPSTF recommended against it. In this follow-up episode, we review new trial data reinforcing that guidance and help you translate the evidence into safer prevention strategies. Build confidence in supporting patients with evidence-based approaches to reduce cardiovascular risk. Episode resource links: Aspirin, cardiovascular events, and major bleeding in older adults: extended follow-up of the ASPREE trial. Eur Heart J. 2025 Aug 12:ehaf514. doi: 10.1093/eurheartj/ehaf514. Epub ahead of print. PMID: 40796244. Guest: Robert A. Baldor MD, FAAFP   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com The views expressed in this podcast are those of Dr. Domino and his guests and do not necessarily reflect the views of Pri-Med.

A Podcast from Obstetrics & Gynecology highlighting the latest research and practice updates in the field. This episode features interviews with Drs. Amrin Khander and Line Malha, authors of "Comparison of 162 mg and 81 mg Aspirin for Prevention of Preeclampsia: A Randomized Controlled Trial," and Erin Chang and Dr. Emily S. Miller, authors of "Smartphone Applications to Support Perinatal Mental Health."

Joyce talks about:The detailed account of what it took to capture Venezuelan President, Maduro. The media's agenda and cherry picking of information. Iran's antigovernment protests.Illegal immigration and the democratic machine. President Trump speaking on his health and Aspirin. Sid Rosenberg joins the 850 WFTL family Saturdays at 8am!See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

In episode 1984, Jack and Miles are joined by comedian and host of Rebrand, Mort Burke, to discuss… Trump: People Say I’m Jealous But My Kink Is Just Karma, Benny Johnson: Venezuela Rigged The 2020 Election! So Yeah! Trump Health? John Krasinski Laid The Groundwork For Venezuela Attack and more! U.S. plan to ‘run’ Venezuela clouded in confusion Benny Johnson: Venezuela Rigged The 2020 Election! So Yeah! Trump Health? John Krasinski Laid The Groundwork For Venezuela Attack Jack Ryan clip about Venezuela gets viral amid capture of Nicolàs Maduro. Did ‘Jack Ryan’ Predict U.S.’ Venezuela Intervention? Co-Creator Carlton Cuse Reacts To Season 2 Clip Going Viral, Shares Hopes For “Stability And Peace” Amazon's 'Jack Ryan' TV series lambasted for promoting Venezuela 'invasion' Jack Ryan is the Latest TV Show to Film at CIA Headquarters How Does Amazon's 'Jack Ryan' Compare to Real Life at the CIA? LISTEN: 4 Raws by EsDeeKidSee omnystudio.com/listener for privacy information.

Dr. Kahn kicks off 2026 by reviewing recent media reports on aspirin use and dosing for the prevention of cardiovascular events in the President of the United States. Much of the coverage overlooks an important factor: the relationship between aspirin dose and body weight. Dr. Kahn examines data from multiple studies suggesting that, in some cases, only higher-dose aspirin was effective in preventing cardiovascular events. As always, listeners are encouraged to discuss aspirin use and dosing with their own medical team. Additional topics this week include the health impact of carryout meals, kidney function and cystatin C, statin use in patients with diabetes, the risks associated with tramadol, cold drink–induced atrial fibrillation, and recent health reports involving Chevy Chase and Jelly Roll. Dr. Kahn also invites listeners to join an upcoming group 5-day PROLON Fasting Mimicking Diet, supported by dietitians and health educators. Order your PROLON kit now at prolonlife.com/drkahn to be ready to participate.

Most men think ED is just a performance issue. It's not. It's one of the earliest warning signs of cardiovascular decline and it often appears years before chest pain, shortness of breath, or heart attack symptoms.Thank you to our sponsors! -EMR-Tek | https://www.emr-tek.com/DAVE and use code DAVE for 40% off.-GOT MOLD? | Go to http://gotmold.com/shop and use DAVE10 to save 10% and see what's in your air.Chapters00:00 - The “Legal Blue Pill” Myth & Hidden Danger00:57 - What ED Actually Is (Not the Commercial Version)01:45 - Circulation, Arteries & the Real Root Cause03:27 - The Problem with Relying on ED Pills05:03 - Treat ED as a Cardiovascular Symptom05:55 - Patterns That Reveal Vascular Decline07:10 - The ED–Heart Attack Countdown Window08:14 - How To Fix This Problem10:10 - Microdosing Cialis for Vascular Support10:45 - Aspirin as Another Option11:15 - Lifestyle Drivers of Vascular Damage & Solutions13:15 - Movement, Walking & Circulation Basics13:40 - The Mitochondria–Erection Connection15:00 - Recharging Mitochondria16:02 - Chronic Inflammation: The Silent Culprit17:17 - Smoking, Vaping, Obesity & Diabetes18:30 - How To Reduce InflammationResources: • Dave Asprey's Latest News | Go to https://daveasprey.com/ to join Inside Track today. • Danger Coffee: https://dangercoffee.com/discount/dave15 • My Daily Supplements: SuppGrade Labs (15% Off) • Favorite Blue Light Blocking Glasses: TrueDark (15% Off) • Dave Asprey's BEYOND Conference: https://beyondconference.com • Dave Asprey's New Book – Heavily Meditated: https://daveasprey.com/heavily-meditated • Upgrade Collective: https://www.ourupgradecollective.com • Upgrade Labs: https://upgradelabs.com • 40 Years of Zen: https://40yearsofzen.com Connect with Dave Asprey!Website: https://daveasprey.comTikTok: https://www.tiktok.com/@daveaspreyofficialInstagram: https://www.instagram.com/dave.asprey/Facebook: https://www.facebook.com/Daveaspreyofficial/X: https://x.com/daveaspreyYouTube: https://www.youtube.com/c/daveaspreybprThe Human Upgrade Podcast: Instagram: https://www.instagram.com/TheHumanUpgradePodcast/ Facebook: https://m.facebook.com/Thehumanupgrade/See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-465 Overview: Many patients with coronary artery disease take aspirin, but how should clinicians navigate management when an anticoagulant is also needed? In this episode, we review indications for therapy, explore evidence on dual use, and discuss how to counsel patients on balancing cardiovascular benefits with the risks of combination therapy. Episode resource links: Lemesle G, Didier R, Steg PG, et al. Aspirin in Patients with Chronic Coronary Syndrome Receiving Oral Anticoagulation. N Engl J Med. Published online August 31, 2025. https://www.nejm.org/doi/full/10.1056/NEJMoa2507532 Guest: Alan M. Ehrlich, MD, FAAFP   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-465 Overview: Many patients with coronary artery disease take aspirin, but how should clinicians navigate management when an anticoagulant is also needed? In this episode, we review indications for therapy, explore evidence on dual use, and discuss how to counsel patients on balancing cardiovascular benefits with the risks of combination therapy. Episode resource links: Lemesle G, Didier R, Steg PG, et al. Aspirin in Patients with Chronic Coronary Syndrome Receiving Oral Anticoagulation. N Engl J Med. Published online August 31, 2025. https://www.nejm.org/doi/full/10.1056/NEJMoa2507532 Guest: Alan M. Ehrlich, MD, FAAFP   Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  

Nutritionist Leyla Muedin details key aspects of supplement use and addresses frequently asked questions. Topics include the importance of targeted supplementation, the rationale behind personalized dosages, best practices for starting new supplements, and managing common issues like nausea and bright yellow urine. Leyla also explains why some supplements may cause gastrointestinal discomfort and provides guidance on how to adjust dosages for optimal results. Emphasis is placed on the benefits of pharmaceutical-grade supplements available on Fullscript and the necessity of regular blood tests to fine-tune supplementation.

Low-dose aspirin, often called baby aspirin, is one of the most commonly recommended medications in pregnancy today. But despite how frequently it's prescribed, many patients still ask the same questions: Why do I need it? Is it safe? When should I start or stop? And who actually benefits? In this episode, we take a clear, evidence-based look at baby aspirin in pregnancy—cutting through myths, confusion, and mixed messaging. In this episode, we cover: What "baby aspirin" actually is (dose, formulation, and how it works) Why it's recommended in pregnancy, especially for preventing preeclampsia Who should take it—including high-risk and moderate-risk patients When to start and when to stop (timing matters) What the research says about safety for both parent and baby Common concerns and misconceptions, including bleeding risk What to do if you're unsure or were told conflicting advice Why baby aspirin matters: Preeclampsia remains one of the leading causes of pregnancy complications worldwide. Decades of high-quality research now show that low-dose aspirin, started early in pregnancy for the right patients, can significantly reduce risk—with an excellent safety profile. For many patients, this simple intervention can make a meaningful difference in pregnancy outcomes. Who this episode is for: Pregnant patients wondering "Do I really need this?" Anyone with a history of preeclampsia, hypertension, infertility, IVF, or pregnancy complications Clinicians counseling patients on aspirin use Anyone navigating pregnancy advice that feels unclear or contradictory The takeaway: Baby aspirin isn't about doing more—it's about doing the right thing at the right time, guided by evidence and individualized care. If you've been prescribed baby aspirin—or think you might benefit—this episode will help you understand why it's recommended and how to take it with confidence.   Got something you want to share or ask? Keep it coming.  We love hearing from you. Email us or send a voice memo, and you might just hear it on the next episode. Don't forget to like, comment, and subscribe—your questions could be featured in our next episode! For additional resources and information, be sure to visit our website at Maternal Resources: https://www.maternalresources.org/. You can also connect with us on our social channels to stay up-to-date with the latest news, episodes, and community engagement: YouTube: Dive deeper into pregnancy tips and stories atyoutube.com/maternalresources . Instagram: Follow us for daily inspiration and updates at @maternalresources . Facebook: Join our community at facebook.com/IntegrativeOB Tiktok: NatureBack Doc on TikTok Grab Our Book! Check out The NatureBack Method for Birth—your guide to a empowered pregnancy and delivery. Shop now at naturebackbook.myshopify.com .  

Join Kate, Gary and Mark (Henry has the day off) as we discuss 3 useful new studies: colorectal cancer screening reminders, aspirin or clopidogrel for secondary prevention of CV events, and lipid lowering drugs and dementia risk

Join us as we review recent articles and news featured in The DIGEST #70, including PSA screening, acetaminophen and autism, COVID19 vaccines and cancer, and aspirin and anticoagulation in coronary artery disease. Fill your brain hole with a delicious stack of hotcakes! Featuring Drs. Paul Williams (@PaulNWilliamz), Nora Taranto (@norataranto), Rahul Ganatra (@rbganatra), Laura Glick (@lauraglick) and Matt Watto (@doctorwatto). Claim free CME for this episode at curbsiders.vcuhealth.org! Episodes | Subscribe | Spotify | Swag! |Mailing List | Contact | CME! Credits Written and Hosted by: Nora Taranto MD; Rahul Ganatra MD MPH, Laura Glick MD, Paul Williams, MD, FACP, Adam Cifu MD, Matthew Watto MD, FACP Cover Art: Rahul Ganatra, MD MPH Reviewers: Rahul Ganatra MD MPH; Paul Williams, MD, FACP, Matthew Watto MD, FACP; Sai S Achi MD, MBA, FACP Technical Production: Pod Paste Showrunners: Matthew Watto MD, FACP; Paul Williams MD, FACP Show Segments Intro, disclaimer Prostate Cancer Screening Acetaminophen and Autism COVID19 vaccines and cancer risk Aspirin and anticoagulation in coronary artery disease Outro Sponsor: Aura Frames For a limited time, save on the perfect gift by visiting AuraFrames.com to get $35 off Aura's best-selling Carver Mat frames by using promo code CURB at checkout. Sponsor: DoxGPT by Doximity Visit doxgpt.com  and see how it can simplify your clinical workflow, from patient care to paperwork.  Sponsor: Continuing Education Company Use promo code Curb30 to get 30% off all online courses and webcasts—just for Curbsiders Listeners. Visit CMEmeeting.org/curbsiders to learn more. Sponsor: Freed Use code: CURB50 to get $50 off your first month when you subscribe!

1872 gelingt es dem Chemiker Wilhelm Haarmann erstmals Vanillin aus Rindensaft von Bäumen herzustellen. Das macht Vanillin zum ersten synthetischen Duftstoff der Welt und seine Herstellung läutete gleichzeitig den Beginn der modernen Duft- und Aromastoffindustrie ein. Wir sprechen in der Folge über Vanille, Vanillin und warum der Vanillerostbraten nach Knoblauch schmeckt. //Erwähnte Folgen * GAG263: Lavoisier und die Entdeckung des Sauerstoffs – https://gadg.fm/263 * GAG444: Die Erfindung von Heroin und Aspirin – https://gadg.fm/444 * GAG284: "There is death in the pot" - Friedrich Accum und die Lebensmittelfälscher – https://gadg.fm/284 * GAG279: Muskat und Manhattan – https://gadg.fm/279 * GAG527: Botanik, Baret und Bougainville – https://gadg.fm/527 * GAG483: Bounty, Brotfrucht und die Rum-Rebellion – https://gadg.fm/483 // Literatur * Björn Bernhard Kuhse, Wilhelm Haarmann auf den Spuren der Vanille: Forscher, Unternehmer und Pionier der Riechstoffe, 2012. * Klaus Stanzl, Die Geburtsstätten der Riechstoffindustrie. Wie die organische Chemie eine Industrie erblühen lässt, 2024. //Aus unserer Werbung Du möchtest mehr über unsere Werbepartner erfahren? Hier findest du alle Infos & Rabatte: https://linktr.ee/GeschichtenausderGeschichte //Geschichten aus der Geschichte jetzt auch als Brettspiel! Werkelt mit uns am Flickerlteppich! Gibt es dort, wo es auch Becher, T-Shirts oder Hoodies zu kaufen gibt: https://geschichte.shop // Wir sind jetzt auch bei CampfireFM! Wer direkt in Folgen kommentieren will, Zusatzmaterial und Blicke hinter die Kulissen sehen will: einfach die App installieren und unserer Community beitreten: https://www.joincampfire.fm/podcasts/22 //Wir haben auch ein Buch geschrieben: Wer es erwerben will, es ist überall im Handel, aber auch direkt über den Verlag zu erwerben: https://www.piper.de/buecher/geschichten-aus-der-geschichte-isbn-978-3-492-06363-0 Wer unsere Folgen lieber ohne Werbung anhören will, kann das über eine kleine Unterstützung auf Steady oder ein Abo des GeschichteFM-Plus Kanals auf Apple Podcasts tun. Wir freuen uns, wenn ihr den Podcast bei Apple Podcasts oder wo auch immer dies möglich ist rezensiert oder bewertet. Wir freuen uns auch immer, wenn ihr euren Freundinnen und Freunden, Kolleginnen und Kollegen oder sogar Nachbarinnen und Nachbarn von uns erzählt! Du möchtest Werbung in diesem Podcast schalten? Dann erfahre hier mehr über die Werbemöglichkeiten bei Seven.One Audio: https://www.seven.one/portfolio/sevenone-audio

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My guest is Dr. David Fajgenbaum, MD, professor of translational medicine and human genetics at the University of Pennsylvania. He explains how, unbeknownst to most doctors, many approved medications can successfully treat or even cure diseases other than the ones they are typically used to treat. He shares his story of escaping death from Castleman's disease by discovering a life-saving treatment using repurposed drugs that were approved for other purposes. Our conversation explores how researchers, physicians, and you—the general public—can explore novel treatments and cures to conditions the medical profession has deemed untreatable, including cancers. We also discuss the crucial role of mindset in battling diseases and the lesser-known use of compounds to promote health and longevity. Read the episode show notes at hubermanlab.com. Thank you to our sponsors AGZ by AG1: https://drinkagz.com/huberman Eight Sleep: https://eightsleep.com/huberman Rorra: https://rorra.com/huberman David: https://davidprotein.com/huberman Function: https://functionhealth.com/huberman Timestamps (0:00) David Fajgenbaum (4:06) Self-Agency in Healthcare; New Uses for Old Medicines (6:44) Other Uses of Aspirin & Viagra; Drug Development & Approved Use (8:53) Lidocaine & Breast Cancer; Pharmaceutical Companies & Incentives (11:36) Sponsors: Eight Sleep & Rorra (14:16) Pharmaceutical Companies, Patents & New Uses; Lithium (18:40) Tools: Finding Reliable Health Sources, Asking Questions & Disease Organizations; DADA2 Treatment (21:53) Medical Community & Connections; Integrated Medical Databases (24:36) Drug Repurposing, Thalidomide, Pembrolizumab (28:45) Medical Research Databases, Mapping Disease Connections (33:51) Every Cure Database & Programs, Bachmann-Bupp Syndrome; Colchicine & Heart Disease (37:57) Sponsors: AGZ by AG1 & David (40:41) David's Medical & Career Journey, Glioblastoma, Castleman Disease (49:10) Autoimmune Disease, Driven Personality, Stress & Immune System (52:52) Castleman Disease, Treatment, Chemotherapy (55:54) Physician Continuing Education, Santa Claus Theory of Civilization; Science Collaboration (1:03:32) Medical School, Relapse & “Overtime”, Finding a New Treatment, Rapamycin (1:12:46) Sport, Football & Resilience; Challenge & Personal Growth, Family (1:18:41) Sponsor: Function (1:20:29) Social Support; “Overtime”, Gratitude (1:23:19) Business School, Castleman Disease Treatment; Repurposing Drugs & AI (1:28:29) Drug Repurposing, POEMS Syndrome; Mitigating Risk (1:35:32) Nicotine, Compounds for Preventive Health; GLP-1 Agonists (1:40:51) Bioprospecting, Drug Development; AI, Prioritization & Novel Connections (1:46:18) Healthcare & Children; Hope, Action & Impact Circuit; Challenge & Super-Agers (1:52:50) Get Involved with Every Cure (1:56:20) Zero-Cost Support, YouTube, Spotify & Apple Follow, Reviews & Feedback, Sponsors, Protocols Book, Social Media, Neural Network Newsletter Disclaimer & Disclosures Learn more about your ad choices. Visit megaphone.fm/adchoices

View the Show Notes Page for This Episode Become a Member to Receive Exclusive Content Sign Up to Receive Peter's Weekly Newsletter In this “Ask Me Anything” (AMA) episode, Peter revisits the “proven, promising, fuzzy, noise, nonsense” scale and applies it to a variety of popular topics. He begins with a refresher on what each category represents before classifying a range of interventions based on the strength of their supporting evidence. The conversation spans three main areas: drugs for geroprotection (including GLP-1 receptor agonists, SGLT2 inhibitors, methylene blue, and telomere-lengthening supplements), the use of low-dose aspirin for cardiovascular disease prevention, and strategies to improve muscle mass through optimal protein intake and follistatin gene therapy. This episode provides a clear, evidence-based overview for listeners seeking to understand where these popular health and longevity interventions stand on the spectrum of scientific credibility. If you're not a subscriber and are listening on a podcast player, you'll only be able to hear a preview of the AMA. If you're a subscriber, you can now listen to this full episode on your private RSS feed or our website at the AMA #76 show notes page. If you are not a subscriber, you can learn more about the subscriber benefits here. We discuss: A scale for evaluating scientific claims: proven, promising, fuzzy, noise, or nonsense [1:30]; Strong convictions, loosely held: the mindset that separates great scientists from the rest [7:30]; GLP-1 receptor agonists: are there benefits beyond improving metabolic health and promoting weight loss? [12:45]; GLP-1 drugs and the brain: exploring the potential cognitive benefits [18:45]; GLP-1 drugs and lifespan: examining the evidence for potential geroprotective effects [23:00]; Rapamycin and geroprotection: why it remains in the “promising” category [25:45]; SGLT2 inhibitors and their potential geroprotective effect [27:30]; Methylene blue: examining the evidence of an anti-aging effect [34:45]; Methylene blue's potential neuroprotective effects: limited and inconsistent evidence in humans, and the challenges of dosing and safety [41:15]; Telomeres: what they are, how they relate to aging, and why telomere-lengthening supplements lack credible scientific evidence [43:45]; Does the idea of targeting telomere length to extend lifespan have scientific merit? [50:15]; Low-dose aspirin for cardiovascular disease prevention: weighing its clot-prevention benefits against bleeding risks across different populations [55:00]; Rethinking the protein RDA: why most people need twice the recommended amount for muscle health [1:00:45]; Debunking the protein–cancer myth: why higher protein intake doesn't promote tumor growth [1:06:15]; The biology of follistatin and myostatin, and why follistatin gene therapy has become an emerging topic of interest for muscle growth [1:13:15]; Follistatin gene therapy for muscle growth: state of the evidence in animals and humans, and the technical challenges and regulatory barriers [1:17:00]; Why injectable follistatin is theoretically possible but impractical for real-world use [1:23:15]; and More. Connect With Peter on Twitter, Instagram, Facebook and YouTube

On February 4, 1941, Bronx police officers were called to the home of John and Catherine Pappas for a report of a homicide. Based on the evidence, detectives theorized that someone had been invited into the Pappas apartment while Catherine was home alone and that same someone had strangled her to death, then ransacked the apartment looking for valuables. To investigators the scene resembled a fairly straightforward robbery-homicide; however, to detective Ed Burns, there were elements of the crime scene that bore a striking similarity to another assault and robbery case he'd been assigned to just two weeks earlier in another part of the Bronx. What followed was an investigation that exploded in size from a single robbery-gone-wrong that resulted in a murder to a sprawling serial sexual assault case that would eventually involve more than eighty victims in eight states, all victimized by the same man. The hunt for the Aspirin Bandit is among the more remarkable cases in New York criminal history, not only because of the number of victims, but also because of the tremendous effort and coordination put forth to catch the killer—effort and coordination that, in 1941, was virtually unheard of.Thank you to the Amazing Dave White (of BRING ME THE AXE PODCAST) for research and writing assistance!ReferencesBrooklyn Eagle. 1941. "Papas slayer, faced by victims, confesses." Brooklyn Eagle, March 4: 1.Connor, Christine, and Elise Greven. 2017. "Gentleman Killer." A Crime to Remember. Janaury 3.Dillon, Edward, and Howard Whitman. 1941. "Cigarets, aspirin clues to woman's strangler." Daily News (New York, NY), February 6: 4.New York Times. 1941. "Alarm for burglar sent in Pappas case." New York Times, February 8: 32.—. 1941. "Cvek found guilty of Pappas murder." New York Times, May 20: 46.—. 1941. "Cvek tells court he killed in anger." New York Times, May 16: 24.—. 1941. "Mystery cloaks woman's murder." New York Times, February 6: 15.—. 1941. "Pappas strangler admits 15 crimes." New York Times, March 5: 1.—. 1941. "Slayer of woman 'rebukes' press." New York Times, March 8: 34.—. 1941. "Sun lamp halts trial." New York Times, April 22: 23.Rice, William. 1941. "Cvek a killer? No surprise to his relatives." Daily News (New York, NY), March 5: 4. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.