Podcasts about Interleukin

This week, Dr. Joel Kahn explores important new research showing how elevated inflammation, measured by Interleukin-6 (IL-6), may dramatically increase cardiovascular risk in people with high Lipoprotein(a), or Lp(a). He explains why IL-6 is emerging as an important biomarker and reviews the other inflammation tests he routinely uses at the Kahn Center, including hs-CRP, MPO, Lp-PLA2, NT-proBNP, fibrinogen, ferritin, the sedimentation rate, and the white blood cell count. Dr. Kahn also discusses Lilly's newly approved oral weight loss medication, the ABCDEF framework for cardiovascular prevention, the growing evidence linking erectile dysfunction and sleep apnea to heart disease, new research on cannabis use and coronary artery plaque, and intriguing early findings on creatine's potential role in supporting the immune system and anti-tumor activity. Finally, thanks to this week's sponsor, the Fresh Pressed Olive Oil Club. Visit getfreshDrKahn.com to take advantage of their special introductory offer and experience the health benefits of fresh, polyphenol-rich olive oil.

Send us Fan MailA Gluten Free Podcast Episode 244 My guest on today's episode is Associate Professor, gastroenterologist and world-leading coeliac disease researcher, Jason Tye-Din. We'll talk about the latest updates on the Interleukin 2 blood test, updated advice around oats as part of a gluten free diet and all the other incredible research he and his team at WEHI are currently undertaking. What we'll cover: * Introducing Jason and our previous episode together * How coeliac disease is a systemic autoimmune disease that affects all parts and organs of the body * How the Interleukin 2 diagnostic tool works * Interleukin 2 blood test being used in various other coeliac disease research trials * Interleukin 2 blood test used in the Gluten Threshold Study to determine if T cells are being activated when participants are ingesting very low levels of gluten * Interleukin 2 (IL-2) blood test soon to be used in a trial involving children * Updates around this blood test and implementation plans * Non-biospy approach in diagnosing coeliac disease and how IL-2 could play a part in this * Working on a salivary coeliac disease test * How the IL-2 test might work in people with potential coeliac disease * Gluten Threshold Study and how IL-2 was used in the study * The response from the Gluten Threshold Study * World Health Organisation reference threshold for gluten and possibility to clear up confusion around ‘may contain gluten' statements * Defining an action level in a standard serve of food * Jason's advice on enzymes that claim to break down small amounts of gluten * Importance of not using symptoms as a measure of being glutened or not * Possible adjunct management drugs and other therapeutics other than a strict gluten free diet for people with coeliac disease* Advice for oats as part of a gluten free diet for Australian adults and children living with coeliac disease * ENDIA (Environmental Determinants of Islet Autoimmunity Study) updates * Eotaxin and brain fog coeliac disease study * Pros and cons around population screening of coeliac disease * NSW school children being tested for coeliac disease and Type 1 diabetes * International Celiac Disease Symposium 2026 in Melbourne Links Contact the nurses to be involved in WEHI studies - coeliac@wehi.edu.au Professor Jason Tye-Din's previous podcast appearanceSuitability of Oats as part of a gluten free diet for Australians living with coeliac disease ENDIA study https://www.icds2026.org/ Coeliac Disease Research LabJoin A Gluten Free Podcast Facebook Group 

Jim and Chris welcome back returning guest Dr. Phillip Snider for a Q&A episode that plays a little differently than usual. Listener emails open a broader discussion of healthspan and lifespan, (including how wealth, genetics, and lifestyle factors shape longevity), retirement planning for longevity, and Dr. Snider’s recommendation for additional tests to help assess your health risks. (5:15) — George cautions that median longevity statistics are heavily influenced by wealth, genetics, and individual behavior, and shares CDC data showing life expectancy rises significantly once someone reaches age 65. (29:45) — A listener asks Dr. Snider to discuss the value of the cardiac calcium score in assessing longevity. She also asks about the science behind statins, including their effect on plaque stability and a possible link to reduced dementia risk. Show Notes: Dr. Snider’s list of recommended tests: CAC test (coronary artery calcium,) or heart scan – a noninvasive, low-dose CT scan that measures calcified plaque in your arteries to predict future heart attack risk. hsCRP (high-sensitivity C-reactive protein) – measures inflammation in the body related to cardiovascular disease risk. IL-6 (Interleukin-6) – elevated levels are associated with multiple conditions including cardiovascular disease, diabetes (insulin resistance), cancer, and autoimmune disorders.  The sample has to be frozen before sending to the lab for processing, so it may need to be collected at a hospital lab or free-standing lab facility rather than at a doctor’s office. MPO (Myeloperoxidase) – measures an enzyme found in white blood cells (neutrophils and macrophages). It is a key biomarker of inflammation and oxidative stress. In the bloodstream, high MPO levels indicate that immune cells are actively attacking vessel walls, making it a powerful predictor of cardiovascular disease and plaque instability. Lp-PLA2 (lipoprotein-associated phospholipase A2) – measures a specialized inflammatory enzyme highly concentrated in unstable, rupture-prone fatty plaques within your arteries. Unlike general inflammatory markers (like hs-CRP), Lp-PLA2 is specifically localized to inflammation of blood vessels. The post Healthspan and Retirement Planning for Longevity with Dr. Snider: Q&A #2628 appeared first on The Retirement and IRA Show.

Send us Fan MailA Gluten Free Podcast Episode 242My guest on today's episode is Gastroenterologist and Director of the Coeliac Disease and Immune Health Research Program at Wesley Research Institute, Dr James Daveson. We'll talk about the Gluten Threshold Study results, how these results could inform international gluten free standards and the need for follow up larger scale studies. What we'll cover: * Aim of the study and what prompted it* Using Interleukin 2 to measure immune response in participants* How the Interleukin 2 test was used as a biomarker in this specific trial * Exploring the question of inadvertent gluten ingestion in causing damage to villi in people with coeliac disease * Carlo Cattassi's study in 2007 looking at the minimum amount of gluten causing an autoimmune response * James and his team looking at what is happening for people with coeliac disease consuming 10 mgs of gluten and under * The hawthorn effect * Specifics of the trial and how the study was run * Dropping the dose of gluten to see where the autoimmune response was occurring at lowering levels* Findings from the study* How the results could possibly change labelling and ‘gluten free' standards and guidelines not only in Australia but worldwide* Codex Alimentarius food labelling laws* Shortcomings from this trial * The potential heterogeneity of coeliac disease (various scales of severity of the disease) * Eliciting dose of gluten for people with coeliac disease * Varying symptoms of the participants throughout the Gluten Threshold study before and after the gluten challenge * Mistakes and surprises in the Gluten Threshold Study * Symptom scores * Anticipatory nausea and priming * The possibility of the immune system being primed before the ingestion of gluten for people with coeliac disease * The trauma of living with an autoimmune disease or other IBD conditions * Possible follow up studies from The Gluten Threshold Study * How this study could be used to a more universal approach to the ppm of gluten * Digestive Diseases Week in Chicago and how the response from the Gluten Threshold Study * The interest in novel therapeutics for people with coeliac disease to help people's guts alongside a gluten free diet * Enzymes that claim to break down inadvertent gluten ingestion for people with coeliac disease * Information on how to read the results of the Gluten Threshold Study, participate or help fund future studies and follow Wesley Research Institute on socialsLinksGluten Threshold Study ResultsWesley Research Institute: Coeliac Disease and Immune HealthFollow Wesley Research Institute on Instagram and Facebook Join A Gluten Free Podcast Facebook Group 

Many women are prescribed oral estrogen without ever being told what happens after it enters the body. In this episode, Dr. Brendan McCarthy takes a deeper look at estrone, the estrogen metabolite created when estradiol is taken orally, and explains why the delivery method of hormone therapy matters. You'll learn: The difference between estradiol and estrone Why oral estrogen creates significantly higher estrone levels How estrone may contribute to inflammation and insulin resistance The connection between estrogen metabolism and weight gain during perimenopause and menopause Why monitoring labs is essential when using hormone therapy The importance of understanding risks, benefits, and treatment options before starting hormones Dr. McCarthy also discusses the role of inflammation, body fat, metabolic health, and hormone delivery systems in creating long-term outcomes for women navigating menopause. This episode is about education, informed consent, and helping women better understand the science behind their care.   Citations: There is more than one estrogen; after menopause, estrone dominates Kuhl, Herbert. “Pharmacology of Estrogens and Progestogens: Influence of Different Routes of Administration.” Climacteric, vol. 8, no. S1, 2005, pp. 3–63. Body fat is an endocrine organ — aromatase converts androstenedione into estrone, and adipose becomes the dominant post-menopausal estrogen source Lee, Angel A., and Laura J. Den Hartigh. “Metabolic Impact of Endogenously Produced Estrogens by Adipose Tissue in Females and Males across the Lifespan.” Frontiers in Endocrinology, vol. 16, 2025, article 1682231. Inflamed fat raises IL-6; IL-6 tracks the insulin-resistant state Kern, Philip A., et al. “Adipose Tissue Tumor Necrosis Factor and Interleukin-6 Expression in Human Obesity and Insulin Resistance.” American Journal of Physiology-Endocrinology and Metabolism, vol. 280, no. 5, 2001, pp. E745–E751. IL-6 is part of the insulin-resistance machinery — it correlates with impaired insulin-stimulated glucose uptake Bastard, Jean-Philippe, et al. “Adipose Tissue IL-6 Content Correlates with Resistance to Insulin Activation of Glucose Uptake Both In Vivo and In Vitro.” The Journal of Clinical Endocrinology & Metabolism, vol. 87, no. 5, 2002, pp. 2084–2089. Inflammation amplifies aromatase — IL-6 raises aromatase via COX-2/PGE2 Bowers, Laura W., et al. “Obesity-Associated Systemic Interleukin-6 Promotes Pre-Adipocyte Aromatase Expression via Increased Breast Cancer Cell Prostaglandin E2 Production.” Breast Cancer Research and Treatment, vol. 149, no. 1, 2015, pp. 49–57. Human-tissue confirmation: HOMA-IR, IL-6, insulin, leptin, hsCRP track breast aromatase after menopause Brown, Kristy A., et al. “Menopause Is a Determinant of Breast Aromatase Expression and Its Associations with BMI, Inflammation, and Systemic Markers.” The Journal of Clinical Endocrinology & Metabolism, vol. 102, no. 5, 2017, pp. 1692–1701. Iyengar, Neil M., et al. “Effects of Obesity on Breast Aromatase Expression and Systemic Metabo-Inflammation in Women with BRCA1 or BRCA2 Mutations.” npj Breast Cancer, vol. 7, no. 1, 2021, article 18. The molecular crux: estrone drives ERα/NF-κB inflammatory signaling while estradiol opposes it Qureshi, Rehana, et al. “The Major Pre- and Postmenopausal Estrogens Play Opposing Roles in Obesity-Driven Mammary Inflammation and Breast Cancer Development.” Cell Metabolism, vol. 31, no. 6, 2020, pp. 1154–1172.e9. Estrone as a metabolic-risk signal — prospectively associated with diabetes (note: male cohort) Jasuja, Guneet Kaur, et al. “Circulating Estrone Levels Are Associated Prospectively with Diabetes Risk in Men of the Framingham Heart Study.” Diabetes Care, vol. 36, no. 9, 2013, pp. 2591–2596.   Dr. Brendan McCarthy is the founder and Chief Medical Officer of Protea Medical Center in Arizona. With over two decades of experience, he's helped thousands of patients navigate hormonal imbalances using bioidentical HRT, nutrition, and root-cause medicine. He's also taught and mentored other physicians on integrative approaches to hormone therapy, weight loss, fertility, and more. If you're ready to take your health seriously, this podcast is a great place to start.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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