Podcasts about th17

Guest: Dr. Shabaana Khader is a Professor and Chair of the Department of Microbiology at the University of Chicago. She discusses how the immune system responds to Mycobacterium tuberculosis, why tuberculosis remains one of the world's deadliest infectious diseases, and the challenges of developing more effective vaccines. She highlights the role of lung-resident immunity, including Th17 responses and lymphoid structures, in controlling infection, and explains how advances in our understanding of host–pathogen interactions are guiding the design of next-generation TB vaccines. Featured Products and Resources: Learn about STEMCELL’s optimized protocols and reagents for immunotherapy research. Download a free Nature Reviews Immunology T cell nomenclature wallpaper. The Immunology Science Round Up Personalized HPV Cancer Vaccine – A multifunctional nanovaccine combining HPV antigens, tumor membranes, and bacterial adjuvants generates durable anti-tumor immunity against HPV-associated cervical cancer. HIV Rewires T Cell Identity – HIV can reprogram infected CD4+ T cells into CD8+ T cells, revealing a previously unrecognized component of the viral reservoir. Decoding Acute Pancreatitis – A single-cell atlas of severe acute pancreatitis identifies a TNF-α–driven immune-endothelial circuit that causes microvascular failure and disease progression. Discovery of Ruptoblasts – A newly discovered cell type, the ruptoblast, protects planarians through an explosive cytotoxic mechanism termed ruptosis. Image courtesy of Dr. Shabaana Khader Subscribe to our newsletter! Never miss updates about new episodes. Subscribe

What really separates roflumilast (Zoryve) from other PDE4 inhibitors — and why does it matter for your patients with atopic dermatitis, psoriasis, or seborrheic dermatitis? In this episode, Dr. Ted Lane sits down with Dr. Chris Bunick, Associate Professor of Dermatology at Yale School of Medicine and Editor-in-Chief of Dermatology Times, for a deep dive into the biochemistry, formulation science, and clinical implications behind this breakthrough topical treatment. In this episode, you'll learn: Why roflumilast binds PDE4 with 200x more potency than apremilast — and 1,000x more than crisaborole How cyclic AMP inhibition controls upstream cytokine pathways (TH1, TH2, TH17) across multiple inflammatory skin diseases The science behind the Crotofos emulsifier — and why the right emulsifier protects the skin barrier instead of stripping ceramides Why formulating at pH 5.5 matters for filaggrin, keratin, and barrier integrity How the roflumilast foam is specifically engineered for scalp conditions and hair-bearing areas What's next in topical formulation innovation — from targeted dermal delivery to longevity skincare Whether you're a dermatologist, resident, PA, NP, or skincare enthusiast who wants to understand the why behind cutting-edge topicals, this episode is packed with clinical and scientific insight you won't find anywhere else.

Today, we're diving into autoimmunity—what it actually is, why it happens, and how ultra-processed foods may be contributing to the problem. Autoimmune disease is often misunderstood. Some will tell you diet has nothing to do with it. Others claim diet is the cure. The truth is more nuanced—and that's exactly what we explore in this episode. You'll learn: What autoimmunity really is (and why it's a case of mistaken identity) How inflammation and the immune system interact The critical role of gut health and the microbiome How ultra-processed foods disrupt intestinal integrity and immune signaling Why stress and hyper-palatable foods create a harmful cycle A practical experiment you can try to see how diet impacts your own biomarkers This isn't about selling supplements or pushing extremes. It's about understanding the science so you can make informed decisions about your health. As always, this episode is backed by scientific literature. Full citations are included below, with abbreviated versions available on shorter clips. If you're dealing with autoimmune symptoms—or just want to better understand how food impacts your immune system—this episode is for you.   Full citation list: Hall KD, et al. “Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake.” Cell Metabolism, 2019.     Supports the formulation argument: UPF intake increased spontaneous calorie intake and weight gain even with diets matched for presented calories, sugar, fiber, sodium, and macronutrients. This is your anchor for “hyper-palatability and formulation change physiology, not just psychology.”   Narula N, et al. “Association of Ultra-Processed Food Intake With Risk of Inflammatory Bowel Disease: Prospective Cohort Study.” BMJ, 2021.     Best human disease-level citation for the episode. Supports the claim that higher UPF intake is associated with greater IBD risk, making the gut-immune link clinically meaningful rather than purely theoretical.   Chassaing B, et al. “Randomized Controlled-Feeding Study of Dietary Emulsifier Carboxymethylcellulose Reveals Detrimental Impacts on the Gut Microbiota and Metabolome.” Gastroenterology, 2022.     Best emulsifier paper for human translation. Supports the claim that CMC can perturb the microbiota and metabolome and may contribute to barrier-hostile gut ecology in susceptible individuals.   Daniel N, et al. “Human Intestinal Microbiome Determines Individualized Responses to Dietary Emulsifier Carboxymethylcellulose.” Cellular and Molecular Gastroenterology and Hepatology, 2024.     Useful nuance paper. Supports the point that emulsifier sensitivity is not identical across all people and that host-microbiome context matters.   Shil A, et al. “Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium Through Activation of the Sweet Taste Receptor T1R3.” Nutrients, 2020.     Best citation for the “sugar-free does not mean barrier-neutral” point. Supports direct epithelial barrier effects of common artificial sweeteners in experimental models.   Peng L, et al. “Butyrate Enhances the Intestinal Barrier by Facilitating Tight Junction Assembly via Activation of AMP-Activated Protein Kinase in Caco-2 Cell Monolayers.” Journal of Nutrition, 2009.     Classic mechanistic citation for butyrate. Supports the claim that loss of fermentable fiber and reduced butyrate production can weaken barrier function.   Kumar KP, et al. “The Interplay Between the Microbiota, Diet and T Regulatory Cells in Maintaining Intestinal Homeostasis.” Frontiers in Microbiology, 2023.     Useful for the tolerance language. Supports the argument that diet and microbial metabolites shape Treg biology and mucosal tolerance.   Haase S, et al. “Sodium Chloride Triggers Th17 Mediated Autoimmunity.” Frontiers in Immunology, 2019.     Key citation for high salt and autoimmune-prone immune skewing. Supports the claim that excess salt can promote pathogenic Th17 biology relevant to autoimmune disease.   Wilck N, et al. “Salt-Responsive Gut Commensal Modulates TH17 Axis and Disease.” Nature, 2017.     Strong bridge between salt, microbiome, and Th17 signaling. Supports the point that salt is not just a blood pressure story; it is also an immune-story.   Vitales-Noyola M, et al. “Analysis of Sodium Chloride Intake and Treg/Th17 Lymphocytes in Patients With Rheumatoid Arthritis and Systemic Lupus Erythematosus.” Journal of Immunology Research, 2018.     Helpful human-facing citation for salt and immune skewing in autoimmune populations. Use cautiously, but it strengthens translation from theory to autoimmune terrain.   Phuong-Nguyen K, et al. “Advanced Glycation End-Products and Their Effects on Gut Health.” Nutrients, 2023.     Good review for the AGE section. Supports the argument that AGE-rich processed foods may worsen oxidative stress, microbiota balance, and barrier function.   Chen Y, et al. “Dietary Advanced Glycation End-Products Elicit Toxicological Effects by Disrupting Gut Microbiota and Increasing Colon Permeability in Rats.” Journal of Toxicology and Environmental Health, 2021.     Useful mechanistic support for the processing-chemistry section. Reinforces the claim that dietary AGEs can alter microbial ecology and increase permeability.   Monteiro CA, et al. “Ultra-Processed Foods: What They Are and How to Identify Them.” Public Health Nutrition, 2019.   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.  

Guest: Dr. Amanda Lund is an Associate Professor at the NYU Grossman School of Medicine. She discusses how the lymphatic vasculature serves as a critical and dynamic interface between tissues and the immune system, challenging the traditional view of lymphatics as passive conduits. She highlights how lymphatic vessels actively regulate immune responses by controlling fluid flow, antigen transport, and cell migration during infection and cancer, and explores their emerging roles in shaping immunity and tissue biology. Featured Products and Resources: Download the free cell separation e-book from STEMCELL Technologies. Learn how to isolate highly pure immune cells and efficiently process human samples. The Immunology Science Round Up MHC I Shapes CD4 Immunity– MHC class I unexpectedly regulates CD4+ T cell cytotoxicity by protecting target cells from ferroptosis. Re-Emergence of Oropouche Virus – Scientists have mapped the resurgence and long-term burden of Oropouche virus, revealing widespread infection across Latin America. Scalable In Vivo T Cell Engineering – A new in vivo CRISPR-based system enables precise, stable generation of CAR T cells. Gut–Brain Axis in Autoimmunity – Intestinal epithelial cells initiate autoimmune neuroinflammation via TH17 cell responses that migrate to the central nervous system. Image courtesy of Dr. Amanda Lund. Subscribe to our newsletter! Never miss updates about new episodes. Subscribe

In this episode of Tea with Dr D, host James Q. Del Rosso, DO, is joined by Christopher Bunick, MD, PhD, and later Lisa Swanson, MD, for a deep look at phosphodiesterase-4 (PDE4) inhibition in dermatology, with a special focus on topical roflumilast.  Dr Bunick opens with a primer on the science of PDE4, an enzyme that degrades cyclic AMP (cAMP), an intracellular messenger that regulates anti-inflammatory pathways. In conditions such as atopic dermatitis (AD) and psoriasis, overactive PDE4 leads to reduced cAMP and amplified inflammation. By “gumming up” PDE4, roflumilast restores a more balanced, anti-inflammatory state.  He explains why PDE4 inhibition is relevant across multiple inflammatory pathways, including Th1, Th2, and Th17, and why roflumilast has demonstrated stronger efficacy than earlier inhibitors like crisaborole. Molecularly, roflumilast mimics cyclic AMP's binding to PDE4 across 3 key sites, producing far tighter binding than apremilast and crisaborole, which translates to superior clinical potency.  Dr Bunick illustrates this with a case of palmoplantar pustular psoriasis that cleared dramatically within 8 weeks on topical roflumilast after multiple biologic and corticosteroid failures, highlighting its durability and barrier-restoring properties. He and Dr Del Rosso contrast this with the limitations of chronic steroid use, noting that roflumilast supports long-term control without barrier compromise.  The discussion also touches on vitiligo, where Dr Bunick shares an early case of repigmentation following roflumilast treatment, suggesting possible cAMP-mediated stimulation of melanogenesis. They highlight the molecule's innovative aqueous-based formulation, optimized for skin-compatible pH and excellent tolerability.  In Part 2, Dr Swanson joins to discuss pediatric use. She reviews the 0.15% cream for AD in patients ≥6 years and the 0.05% cream for ages 2–5, both once-daily, steroid-free options that minimize burning and stinging compared with earlier PDE4 inhibitors. They review clinical data that demonstrate rapid itch relief, strong efficacy across IGA and EASI end points, and sustained control with twice-weekly maintenance.  Tune in to hear how PDE4 inhibition, and particularly topical roflumilast, is redefining nonsteroidal therapy across age groups and disease states in dermatology. 

Łuszczyca wydaje się chorobą skóry, ale to tylko wierzchołek góry lodowej. Dr Tomasz Kantyka odkryje przed nami molekularną burzę, która rozgrywa się między komórkami skóry a układem odpornościowym – od keratynocytów i fibroblastów po neutrofile i limfocyty Th17.Zaczniemy od porównania zdrowej i chorej skóry pod mikroskopem – co się zmienia i jakie ma to konsekwencje dla funkcji skóry? Zagłębimy się w podłoże choroby. Co dzieje się na poziomie molekularnym w łuszczycy, i które komórki ze sobą współdziałają? Poznamy rolę cytokin prozapalnych, dysfunkcji układu odpornościowego i wiele innych. Gościem dr. Mariusza Gogóla jest dr Tomasz Kantyka - lider grupy Proteoliza i Modyfikacja Potranslacyjna Białek w Małopolskim Centrum Biotechnologii UJ.Dr Mariusz Gogól jest biochemikiem i popularyzatorem nauki. Można go także oglądać m.in. na kanale    / @zlewkatotalna   Dofinansowano ze środków Ministerstwa Edukacji i Nauki z programu Społeczna Odpowiedzialność Nauki w ramach projektu „Nauka na żywo: Człowiek".

We are not talking about gluten, dairy, sugar, or even leaky gut. We're talking about the silent saboteurs—the things that are messing with your gut health every single day... and no one's warning you about them.Join the 60 Day gut reset and transform your health! $200OFF with code 'SECRETOFFER! https://checkout.teachable.com/secure/1716725/checkout/order_q9s5bzn3?coupon_code=SECRETOFFERINSTA: @wholistichomeopath

Coffee is most likely one of your IBS triggers but you just might not know it! I dive into the science of how coffee interacts with our body and gut in this episode.Join the 60 Day gut reset and transform your health! $200OFF with code 'SECRETOFFER! https://checkout.teachable.com/secure/1716725/checkout/order_q9s5bzn3?coupon_code=SECRETOFFERINSTA: @wholistichomeopath

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.

#56. Ting som nevnes i denne episoden: aktivering av T- og B-celler. Effektorceller versus hukommelsesceller. Th1 vs Th2 vs Th17 vs. follikulære T-hjelpeceller. CD40 og CD40 ligand (CD40L). Antistoffproduserende celler (plasmablaster og plasmaceller). Opsonisering. Antistoffavhengig cellemediert cytotoksisitet (ADCC). Komplementmediert cytotoksisitet (CDC).Tredje sesong er muliggjort gjennom et stipend fra Norsk revmatologisk forening. Hosted on Acast. See acast.com/privacy for more information.

Trample Damage joins us once again in the present to follow up on our initial review and take an in depth look at all the pieces of TH17, and how they add up to the current endgame experience. You can find all Trample's Content through this link, and you can support him in game with code "trample" for all Supercell game purchases. You can also support this podcast by using either code "coolrick" or code "spencer" or just by sharing our episodes with your clan and friends. Here's a fun random YT Channel link as thanks to a friendTimestamps:(00:00) Intro(02:20) Firespitters(10:47) Giga Bomb and Inferno Artillery(15:58) 3rd Merges(23:54) Throwers(27:56) Minion Prince(33:55) Yeti Bombs(41:44) MGT, Furnace, Sneezy(44:56) QoL Changes(52:05) Final Grades(1:00:54) Listener Questions and Shoutouts

6 months ago Trample Damage and Cool Rick got a peek at TH17 in Helsinki during the World Finals week. This is our initial reactions to what we saw. Next episode Trample will return for a mid lifecycle TH17 review to discuss what we got right, what we got wrong, and what we want for the rest of this year. Timestamps:(00:00) Intro and Initial Reactions(04:53) Defense(21:39) Overall Difficulty and Offense(44:42) Give me a Grade for Th17

A proteína STING atua como moduladora da atividade das células do grupo TH17, que são essenciais na defesa do organismo contra bactérias e fungos, mas quando trabalham em excesso provocam inflamações descontroladas

Send us a textShort Summary: How diet shapes the gut microbiome and impacts health, with microbiologist Dr. Peter Turnbaugh breaking down the complex science.About the guest: Peter Turnbaugh, PhD is a professor of microbiology and immunology at the University of California, San Francisco, where he leads a lab studying the gut microbiome's role in nutrition and drug response.Note: Podcast episodes are fully available to paid subscribers on the M&M Substack and everyone on YouTube. Partial versions are available elsewhere. Full transcript and other information on Substack.Episode Summary: Nick talks to Peter Turnbaugh discuss the pitfalls of oversimplified diet labels in research, Turnbaugh's studies comparing plant-based and animal-based diets in humans, and how these shifts rapidly alter gut microbes and short-chain fatty acid profiles. Key Takeaways:The term “high-fat diet” in research is often misleading, as it can include high carbs and vary widely, complicating study comparisons.In a 2014 study, switching humans to a plant-based (high-fiber) or animal-based (ketogenic, no-fiber) diet changed their gut microbiome within one day, showing its remarkable adaptability.Ketogenic diets reduce Bifidobacterium in the gut, which may lower inflammation-linked immune cells (Th17), potentially aiding conditions like multiple sclerosis.Short-chain fatty acids (e.g., butyrate) don't just come from fiber; they persist even on zero-fiber ketogenic diets, hinting at alternative microbial pathways.Gut microbes can activate or deactivate drugs, like antibiotics or digoxin, suggesting microbiomes may explain why drugs work differently across individuals.Ketone bodies like BHB alone can mimic some ketogenic diet effects on the microbiome and immunity, simplifying research and hinting at therapeutic potential.Related episode:M&M #203: Metagenomics, Microbiome Transmission, Gut Microbiome in Health & Disease | Nicola Segata*Not medical advice.Support the showAll episodes, show notes, transcripts, etc. at the M&M Substack Affiliates: Lumen device to optimize your metabolism for weight loss or athletic performance. Use code MIND for 10% off. Readwise: Organize and share what you read. Athletic Greens: Comprehensive & convenient daily nutrition. Free 1-year supply of vitamin D with purchase. KetoCitra—Ketone body BHB + potassium, calcium & magnesium, formulated with kidney health in mind. Use code MIND20 for 20% off any subscription. MASA Chips—delicious tortilla chips made from organic corn and grass-fed beef tallow. No seed oils or artificial ingredients. Use code MIND for 20% off. For all the ways you can support my efforts

Grab a beverage and join Kat, Darth Yoda and CallMeTee as we review TH17 and the February update and discuss the ore economy in Clash of Clans!

The first TH17 update brings us the Multi Gear Tower, Troop Launcher, Minion Prince Metal Pants, and loads of QoL changes.Use code "corrupt" to support our guest with any in game purchases and⁠ check out his content on youtube.Timestamps:(00:00) Intro(01:43) Multi Gear Tower(07:49) Troop Launcher(16:49) New Troop and Spell Levels(24:40) Defense Levels and Supercharging(31:13) Metal Pants(36:03) Snake Bracelet and Rethinking Equipment(42:03) The Alchemist(46:37) Quality of Life and Misc(1:02:13) Listener Questions

RedThorn's own swashbuckling coleader - King Redbeard - joins Kat to talk about TH17, the Blood & Legends tournament and what is going on with Clash of Clans these days!?

www.twitch.tv/crystal2joinhttp://discord.gg/buG3ETtZZr

Kat, $C-Note$ and Ace sat down to celebrate the ClashMas Season and give their thoughts on TH17 so far.

Controllable Heroes event, Clashmas cosmetics, and what we want from the future of TH17. Links: ⁠Minion Prince fanart contest⁠ ⁠Into the Clash-iverse Spotify episode 1⁠ (its also on Apple) Timestamps: (00:00) Intro (01:53) Controllable Heroes (07:10) Treasure Chests (12:21) Clashmas Cosmetics (21:31) Talkin TH17 (28:57) Hero Hall and Future of Heroes (36:03) Next Update Requests (43:20) Listener Questions (54:14) Shoutouts and Goodbye

Introducing the Teagle! CallMeTee and Darth Yoda from Sons of Guns join Kat to review TH16, the TH17 update. Plus a discussion about Hard Mode and Yoda tells us how he really feels about Legends League.

An autoimmune disease is a condition in which the immune system attacks its own tissues. It is typically characterized by low regulatory T-cells and high Th17 and Th2 cells. T-reg cells prevent autoimmune diseases by supporting an appropriate immune response. There are natural ways to support your immune system so that it operates at an optimal level. Poor gut health and gut inflammation can block the function of vitamin D3. Without enough vitamin D, T-reg cells do not work properly. The majority of the population is vitamin D-resistant. To support the immune system, you need 8,000 to 10,000 IU of vitamin D daily, but even more to overcome resistance. Poor gut health, inflammation, and low vitamin D are a perfect storm for developing an autoimmune condition. B. infantis and L. reuteri are vital for your immune system, but many people don't have them because these probiotics are very sensitive to antibiotics. These two important microbes help prevent autoimmune diseases, greatly affect T-reg cells, and suppress inflammatory immune cells. L. reuteri helps increase oxytocin, one of the most potent anti-stress hormones. High cortisol levels mean high stress, which suppresses the immune system. The best way to consume l. reuteri is to cultivate it in a dairy product. If you're low in selenium, you will have higher amounts of inflammatory immune cells. Selenium helps lower Th17, Th2 cells, and auto-antibodies involved in autoimmune disorders. Prolonged fasting can improve your immune system by increasing T-reg cells and creating new stem cells. L. reuteri strain https://www.amazon.com/BioGaia-Osfort... Super Gut book link: https://amzn.to/4dIxTy2 Yogurt Recipe: https://www.culturedfoodlife.com/reci... **I am finding that using only ONE TBS of prebiotic fiber in the recipe makes a better-quality product. How to Make It: https://drdavisinfinitehealth.com/201...https://www.culturedfoodlife.com/l-re... MICROBIOME MASTER CLASS WEBSITE: https://innercircle.drdavisinfinitehe... Yogurt Maker—https://lvnta.com/lv_lrJY1A8ZLtxmwUpYdX Yogurt Jars—https://lvnta.com/lv_qB2B90JNh0hQjaMoXk Yogurt Containers—https://lvnta.com/lv_SFt3wnanoNkBHrf0Rs

Kat sat down with Duck from the Good Guys to discuss the aftermath of th16 and what he hopes to see from TH17. Plus... the great Mutant Possum reveal!!

Today, we're going to take a look at the underlying cause of autoimmune disease. Your immune system has two parts: the innate immune system that you're born with and the acquired immune system that's created through a series of infections. Over time, the acquired immune system becomes stronger and offers protection against infection. The innate immune system is not the problem when it comes to autoimmune diseases. Autoimmune disorders typically involve problems with the T-regulatory cells or T-cells. Also called suppressor T-cells, these cells are the peacemakers of the immune system and stop the immune reaction when the job is done. Prednisone, the synthetic version of cortisol, is commonly used as a treatment for autoimmune diseases. Both prednisone and vitamin D have reduce inflammation, but Vitamin D empowers and enhances the immune system. Prednisone suppresses the innate and the acquired immune systems. Vitamin D shifts the immune system to increase the T-cells. Inflammatory TH1 and TH17 cells are usually too high when someone has an autoimmune disease. Vitamin D suppresses both of these cells, reducing inflammation. Prednisone raises your blood glucose levels while vitamin D does not. Vitamin D enhances the cells that makes insulin and helps to regulate your blood sugars. Prednisone can break down your bone, leading to osteoporosis. Vitamin D helps you absorb calcium and supports bone remineralization. The thymus gland makes T-cells. As we age, the thymus gland deteriorates and our immune systems decline. Vitamin D slows down this process, but you need larger, therapeutic doses. Vitamin D does not work without the cofactors magnesium, vitamin K2, and zinc. Dr. Coimbra of Brazil created a protocol that involves increasing vitamin D to penetrate any resistance. This lowers the parathyroid hormone which means that vitamin D levels have significantly increased. DATA: https://www.coimbraprotocol.com/gener... https://ajcn.nutrition.org/article/S0... http://www.vitamindprotocol.com/vitam...

Discussing the big pieces from Stuart's AMA, TH17 speculation, and going over our wishlists for Clash of Clans in 2025. Links: Stuart's Full AMA Hit Rates for TH12-TH16 through the years Index of all Clash of Clans Podcasts Timestamps: (00:00) Intro (03:57) AMA TH17 Features (Hero, Merging, Army Changes) (16:03) AMA Equipment Future (New Levels? Torch) (22:14) AMA General Game Stuff (Legends, Hard Mode, Live Service (37:11) Our Top 5 Wishlists for Clash of Clans (50:01) Listener Questions (59:15) Superfluous Nonsense

Community Manager Frame is in the hot seat, answering questions about the state of the game, the future, bugs, the gold pass fiasco and loads more in this special extra long episode. Timestamps: (00:00) - All about Frame (06:07) - Future of cosmetics and pricing (10:47) - Will treasure chests be monetized? (13:43) - What will 2025 bring? (17:29) - How hard will TH17 be? (19:26) - Engaging (or not) with Reddit (23:42) - Gold Pass switcheroo (29:43) - Has there been a shift to focus more on revenue? (35:30) - Tencent influence (39:03) - Increase in bugs & glitches (43:06) - Customer support issues (46:05) - Future of eSports (51:22) - BB and/or CC content coming? (54:07) - Unlimited Heroes Event (57:15) - Return of merch (59:14) - Supercell Make (1:00:35) - Mashup Madness (1:02:50) - Haaland (1:04:19) - Building & troop cosmetics (1:06:51) - Clan notices (1:09:01) - Legendary equipment coming? (1:10:26) - Planning for more decorations (1:13:46) - Expanding Hard Mode to legends or CWL (1:14:34) - Win Trading in Legends League (1:16:28) - Monthly discord chats with the CMs (1:20:24) - Frame being awesome

Your immune system is so much more than just fighting off the occasional cold. It is deeply connected to EVERYTHING in your body and can be a primary root cause of many common (but not normal) health issues! From chronic fatigue, IBS, and painful periods to stubborn weight loss resistance, skin issues, and more the immune system plays a role! In this episode, we're diving deep into how your immune system works, what happens when TH1, TH2, and TH17 cells go into overdrive, and the signs that your immune system might be out of balance. If you're dealing with autoimmune conditions, chronic inflammation, or mysterious symptoms that just won't go away, this episode is for you. I'll be breaking down how to spot the signs, understand your body's signals, and most importantly, what you can do to support and rebalance your system based on your unique symptoms and health history. If you need help getting to the root cause of your health issues or symptoms click here to apply for coaching!

BUFFALO, NY- August 16, 2024 – A new #review was #published as the #cover paper of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 15, entitled, “Types of cell death and their relations to host immunological pathways”. Various immune pathways in the host, such as TH1, TH2, TH3, TH9, TH17, TH22, TH1-like, and THαβ, have been identified. While TH2 and TH9 responses primarily target multicellular parasites, host immune pathways against viruses, intracellular microorganisms (like bacteria, protozoa, and fungi), and extracellular microorganisms utilize programmed cell death mechanisms to initiate immune responses and effectively eliminate pathogens. In their review, researchers Kuo-Cheng Lu, Kuo-Wang Tsai, Yu-Kuen Wang, and Wan-Chung Hu from Taipei Tzu Chi Hospital, Fu Jen Catholic University, Taoyuan Armed Forces General Hospital, Tri-Service General Hospital and Ming Chuan University, reviewed these cell death pathways associated with the host immunological pathways. "These relationships can help us understand the host defense mechanisms against invading pathogens and provide new insights for developing better therapeutic strategies against infections or autoimmune disorders.” DOI - https://doi.org/10.18632/aging.206035 Corresponding authors - Wan-Chung Hu - Wanchung.Hu09@tzuchi.com.tw Video short - https://www.youtube.com/watch?v=oPaevm0vpR8 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206035 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, apoptosis, autophagy, ferroptosis, necroptosis, NETosis, pyroptosis About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

John Alcorn, PhD is a scientist at UPMC Children's Hospital of Pittsburgh and an associate professor in the University of Pittsburgh School of Medicine. The Alcorn lab is focused on T cell immunity, host defense, epithelial cell biology, and lung physiology. A primary lab focus is on Influenza infection and the host defense mechanisms of T helper 17 cells. His lab has recently shown that the TH17 effector cytokines IL-17 and IL-22 are required for host defense against a variety of extracellular pathogens.

What we think TH17 might bring us, as well as talking about the future of Heroes. Links: Frame's AMA Godly's Defense Concepts Timestamps: (00:00) Intro and last thoughts on Haaland event (05:55) MORE event (11:43) Frame's AMA (14:35) TH17 Predictions (38:03) Future of Heroes (47:08) Listener Questions and Outro, stick around --- Send in a voice message: https://podcasters.spotify.com/pod/show/reddit-talks-clash/message

Kat welcomes Itzu for a frank discussion on hero equipment, TH16 and what he wants to see at TH17.

In this episode of Derms and Conditions, our host, James Q. Del Rosso, DO, interviews April Armstrong, MD, MPH, a professor and Chief of Dermatology at UCLA, about the development of tapinarof, a novel nonsteroidal topical treatment for psoriasis.  They begin by discussing Dr Armstrong's history of professional interest in psoriasis. The conversation then moves to focus solely on tapinarof, a topical cream that works by modulating the aryl hydrocarbon receptor (AhR).  Dr Armstrong explains the unique mechanism of action of tapinarof and its effects on Th17 cytokines, antioxidant activity, and skin barrier function. She also discusses the efficacy demonstrated in clinical trials, with nearly 40% of patients achieving PASI 75 after 12 weeks, as well as the remittive effect in maintaining clear or almost clear skin.  They address the safety profile of tapinarof, including the occurrence of folliculitis and contact irritation, and provide tips for its use in clinical practice. Dr Armstrong also emphasizes its versatility and potential as a combination therapy with systemic medications. All in all, the episode provides listeners with an expansive understanding of tapinarof as an effective and well-tolerated nonsteroidal treatment for plaque psoriasis.

Autoimmune progesterone dermatitis - Sirolimus for KP rubra - Spironolactone does not cause cancer - Dupi -> Th17/23 issues - Berdazimer for molluscum - Want to donate to the cause? Do so here! http://www.uofuhealth.org/dermasphere Check out our video content on YouTube: https://www.youtube.com/@dermaspherepodcast and VuMedi!: https://www.vumedi.com/channel/dermasphere/ The University of Utah's Dermatology ECHO: ⁠https://physicians.utah.edu/echo/dermatology-primarycare - ⁠ Connect with us! - Web: ⁠https://dermaspherepodcast.com/⁠ - Twitter: @DermaspherePC - Instagram: dermaspherepodcast - Facebook: https://www.facebook.com/DermaspherePodcast/ - Check out Luke and Michelle's other podcast, SkinCast! ⁠https://healthcare.utah.edu/dermatology/skincast/⁠ Luke and Michelle report no significant conflicts of interest… BUT check out our friends at: - ⁠Kikoxp.com ⁠(a social platform for doctors to share knowledge) - ⁠https://www.levelex.com/games/top-derm⁠ (A free dermatology game to learn more dermatology!)

BUFFALO, NY- February 13, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 2, entitled, “IL-17 promotes IL-18 production via the MEK/ERK/miR-4492 axis in osteoarthritis synovial fibroblasts.” The concept of osteoarthritis (OA) as a low-grade inflammatory joint disorder has been widely accepted. Many inflammatory mediators are implicated in the pathogenesis of OA. Interleukin (IL)-18 is a pleiotropic cytokine with versatile cellular functions that are pathogenetically important in immune responses, as well as autoimmune, inflammatory, and infectious diseases. IL-17, a proinflammatory cytokine mainly secreted by Th17 cells, is upregulated in OA patients. However, the role of IL-17 in OA progression is unclear. In this new study, researchers Kun-Tsan Lee, Chih-Yang Lin, Shan-Chi Liu, Xiu-Yuan He, Chun-Hao Tsai, Chih-Yuan Ko, Yuan-Hsin Tsai, Chia-Chia Chao, Po-Chun Chen, and Chih-Hsin Tang from National Chung-Hsing University, Taichung Veterans General Hospital, Shin-Kong Wu Ho-Su Memorial Hospital, Mackay Medical College, China Medical University, Show-Chwan Memorial Hospital, Fu-Jen Catholic University, National Taiwan Normal University, Asia University, and China Medical University Hsinchu Hospital used synovial tissues collected from healthy donors and OA patients to detect the expression level of IL-18 by immunohistochemistry stain. “Elucidation of the molecular mechanisms and main factors involved in OA pathogenesis may help with the development of novel therapeutic targets that relieve OA pain or prevent the disease from progressing.” The OA synovial fibroblasts (OASFs) were incubated with recombinant IL-17 and subjected to Western blot, qPCR, and ELISA to examine IL-18 expression level. The chemical inhibitors and siRNAs which targeted signal pathways were used to investigate signal pathways involved in IL-17-induced IL-18 expression. The microRNAs which participated IL-18 expression were surveyed with online databases miRWalk and miRDB, followed by validation with qPCR. This study revealed significantly higher levels of IL-18 expression in synovial tissue from OA patients compared with healthy controls, as well as increased IL-18 expression in OASFs from rats with severe OA. In vitro findings indicated that IL-17 dose-dependently promoted IL-18 production in OASFs. Molecular investigations revealed that the MEK/ERK/miR-4492 axis stimulated IL-18 production when OASFs were treated with IL-17. “This study provides novel insights into the role of IL-17 in the pathogenesis of OA, which may help to inform OA treatment in the future.” DOI - https://doi.org/10.18632/aging.205462 Corresponding authors - Po-Chun Chen - pcchen@ntnu.edu.tw, and Chih-Hsin Tang - chtang@mail.cmu.edu.tw Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Question: How to Find the Root Cause of Autoimmunity? Short Answer: Autoimmune conditions are likely driven by deficiencies of vitamins A and D, which contribute to post-infectious autoimmunity by compromising the rhythmic rise and fall of myeloid-derived suppressor cells (MDSCs), and to autoimmunity regardless of infections through impaired suppression of Th17 helper T cells. More broadly, infections and tissue damage are the most likely drivers of autoimmunity onset. However, energy metabolism governs everything through the second law of thermodynamics, which holds that energy must be used to prevent everything from randomly mixing, and this includes randomly mixing the immune defense against pathogens with immune attacks on the host. In this example, we discuss how a respiratory chain disorder would compromise absorption and distribution of zinc and compromise the oxidation of NADH to NAD+, and how both of these would interact with a genetic impairment in acetaldehyde dehydrogenase to prevent the activation of vitamin A to retinoic acid. Autoimmunity thus results as one of many symptoms of vitamin A deficiency driven not by lack of vitamin A, but rather by impaired activation of vitamin A, secondary to impaired energy metabolism.  This is a clip from a live Q&A session open to CMJ Masterpass members. In addition to this episode, you can access two other free samples using this link: https://chrismasterjohnphd.substack.com/p/questions-on-nac-biofilms-vitamin In that batch of free episodes you will also find the answer to this question: Can NAC hurt your gut health? Why Would Vitamin C Cause Joint Pain, Muscle Pain, and Brain Fog? If you want to become a Masterpass member so you can participate in the next live Q&A, or so you can have access to the complete recording and transcript of each Q&A session, you can save 10% off the subscription price for as long as you remain a member by using this link to sign up: https://chrismasterjohnphd.substack.com/qanda Learn more about the Masterpass here: https://chrismasterjohnphd.substack.com/about This snippet is from the May 13, 2023 AMA. The full recording and transcript is reserved for Masterpass members. Here is a preview of what's included: GLA to lower hydroxyhaemopyrrolin-2-one? When would I use the StrateGene and Genova Methylation Panel for nutritional testing? Energy metabolism as a root cause of gut issues? Nutrition for skin healing? Nutrition for hypnic jerks? Suggestions for snoring or sleep apnea? Nutrition to protect against restaurant meals? What is the cause of crusty eyes in the morning? What causes brain fog? How much oxalate should one eat each day? Should I be concerned about low alkaline phosphatase? What nutrients give tall children to short parents? Energy metabolism impairment mimicking Wilson's disease. Can taking digestive enzymes reduce our own production? Rapid-fire response to non-winners from the question contest. Here's a link to the full AMA: https://chrismasterjohnphd.substack.com/p/recording-and-transcript-of-the-may  Access the show notes, transcript, and comments here.  

What's the deal with Armra and why is every health influencer talking about it? Is there solid research to back up its extraordinary claims? How does colostrum compare to serum bovine immunoglobulins in terms of sourcing, tolerance and efficacy? Tune in to hear us unpack this buzzworthy new product and whether it is worth the hefty price tag.    In this episode, we discuss the benefits of colostrum and immunoglobulins and whether Armra is all it's cracked up to be. Whenever we look at a buzzworthy new product, we want to understand the active compound and its mechanism of action, and whether the actual proprietary compound has been tested in clinical trials. Learn how Armra stacks up and why we ultimately prefer serum immunoglobulins (such as our GI Immune Builder) over dairy based colostrum.     Also in this episode: What is colostrum?Breast Milk: Nature's Perfect Food  Addressing Leaky GutGI Lining Support What's up with Armra?Technical Paper on Armra Clinical Trial on Armra (Results Pending) Serum Bovine Immuglobulins vs. ColostrumGI Immune Builder Serum-derived bovine immunoglobulin/protein isolate: postulated mechanism of action for management of enteropathy Bovine immunoglobulin/protein isolate binds pro-inflammatory bacterial compounds and prevents immune activation in an intestinal co-culture model Bovine immunoglobulin protein isolates for the nutritional management of enteropathy Dietary requirement for serum-derived bovine immunoglobulins in the clinical management of patients with enteropathy Serum-derived bovine immunoglobulin/protein isolate in the alleviation of chemotherapy-induced mucositis Attenuation of colitis by serum-derived bovine immunoglobulin/protein isolate in a defined microbiota mouse model Oral serum-derived bovine immunoglobulin/protein isolate has immunomodulatory effects on the colon of mice that spontaneously develop colitis Evaluation of serum-derived bovine immunoglobulin protein isolate in subjects with diarrhea-predominant irritable bowel syndrome Potential mechanisms of effects of serum-derived bovine immunoglobulin/ protein isolate therapy in patients with diarrhea-predominant irritable bowel syndrome Impact of serum-derived bovine immunoglobulin/ protein isolate therapy on irritable bowel syndrome and inflammatory bowel disease: a survey of patient perspective Management of inflammatory bowel disease with oral serum-derived bovine immunoglobulin Evaluation of oral serum-derived bovine immunoglobulins in HIV-infected patients with chronic idiopathic diarrhea N-acetyl glucosamine Collagen-induced arthritis: severity and immune response attenuation using multivalent N-acetyl glucosamine N-acetylglucosamine inhibits T-helper 1 (Th1)/ T-helper 17 (Th17) cell responses and treats experimental autoimmune encephalomyelitis N-acetylglucosamine: production and applications.  A pilot study of N-acetyl glucosamine, a nutritional substrate for glycosaminoglycan synthesis, in paediatric chronic inflammatory bowel disease N-acetylglucosamine for treatment of inflammatory bowel disease Naturally Nourished Episode 347 Functional Approaches to Lyme Disease Ultimate Medicine Cabinet Bundle   This episode is sponsored by: Noble Origins, an animal-based organs focused company serving up Nose-To-Tail Protein With Organs, Collagen, & Colostrum. Our Noble Organs Complex is a powdered blend of high-quality beef organs from New Zealand-sourced grass-fed Beef liver, heart, kidney, pancreas, and spleen. Bring Nose-to-tail nutrition to the masses that need it most: Americans. We do this through a delicious once-a-day shake that the whole family can love. Check it out here and use code ALIMILLERRD to get a free bag of Noble Organs Complex at checkout.

Today we speak with an expert on sugar and things meant to replace it. The stakes are high. Very high. Sugar consumption in the population is astronomical and so is the use of sugar replacements. Knowing the impacts of both could help experts provide dietary guidance and help consumers make decisions. Dr. Robert Lustig is Professor Emeritus of Pediatrics in the Division of Endocrinology at the University of California, San Francisco. He specializes on the regulation of energy balance by the central nervous system; body weight regulation, appetite, metabolism, and is very well known for his work on sugar and their substitutes and on policies aimed at improving the diet of the population. A YouTube video on the effects of consuming sugar called “Sugar: The Bitter Truth,” has now been viewed 24 million times. Interview Summary   URL for “The Bitter Truth video (https://youtu.be/dBnniua6-oM)   Let's start out with this - so the big hope is that sugar replacements, artificial sweeteners, non-nutritive sweeteners, all known as different things, replace sugar and that people can enjoy sweet taste without the calories. But, of course, the picture is way more complicated. Being an endocrinologist, you are in a good position to explain what happens when the sweeteners enter the body. I'd like to get to that in just a moment, but let's lead off with another question. Why is it so important for people to consume less sugar?   First, let's talk about what sugar is. The food industry tells you that sugar is just empty calories. I wish that were true. If that were true, then you could basically spend your discretionary calories on sugar with no problem. But it's not true. There are two molecules in dietary sugar: the sucrose or the high fructose corn syrup or honey maple syrup agave. They are all basically the same. One molecule of something called glucose, one molecule of something called fructose. Glucose is the energy of life. Glucose is metabolizable by every cell on the planet. Glucose is so important that if you don't consume it, your body makes it. The liver will take fats and turn it into glucose. It will take amino acids and turn it into glucose process called gluconeogenesis. Glucose actually makes your cells work better. It makes your mitochondria function better, the mitochondria being the little energy burning factories inside each of your cells. Glucose, for lack of a better word, we can call good. Fructose, on the other hand, it is completely different, is metabolized completely differently inside the body and inside the liver. What fructose does is it inhibits mitochondrial function. It actually inhibits three separate enzymes necessary for mitochondria to do their job. So, fructose inhibits energy generation. Now, the food industry will tell you fructose is four calories per gram. Fructose is ready energy. That is why they put high fructose corn syrup in the sports drinks, for example. Well, turns out, that fructose may be ready energy for a bomb calorimeter, but it is not ready energy for your mitochondria. You don't burn in a bomb calorimeter (a laboratory instrument), you burn via your mitochondria. It turns out, mitochondria are actually poisoned by fructose. So in fact, fructose is a chronic, dose-dependent mitochondrial toxin and this is why we have to eat less of it. But the problem is the food industry keeps putting it in anyway despite the fact that it is killing us.   How much more of it are people consuming than what you might suggest?   The American Heart Association years ago came up with a upper limit per day of about 25 grams, which would be about six teaspoons per day. I was actually part of that group that came up with that and I stick to it because that's what the data show. We are currently consuming 94 grams. We are consuming almost quadruple the amount that is the upper limit. Now, the notion that something could have empty calories but still be bad for you is not a crazy one. We have two things in our diet that we know are calories but are clearly toxic to us. One is alcohol. Alcohol, seven calories per gram, but alcohol is a poison. And then also trans fats. Trans fats are nine calories per gram, but trans fats are a poison. So just because something has calories doesn't have anything to do with its metabolic impact.   Where are people getting all the sugar from? I'm assuming it's not from their sugar bowl.   Exactly. It is not the sugar they add. It is the sugar the food industry adds. Now, where is it? Well, the obvious source is soft drinks. That's number one by far and away. I mean soft drinks are basically, you know, the devil incarnate. Several municipalities have actually figured that out, and it's one of the reasons we have soda taxes because it's actually directed at the problem. A lot of it is in other things that we identify as sweet: candy, cakes, ice cream. A lot of it is in other things like breakfast, cereal, yogurt, even cured meats. It is in a whole host of other things. When you add it all up, 65% of the sugar you consume is in ultra-processed foods. It is not in regular food. It is not in sugar you added to your own food. It is in ultra-processed foods. An ultra-processed food is the vehicle by which the payload, that is that fructose, is doing its damage.   Thanks for that background. We're really here to talk about the artificial sweeteners but it is irresistible talking to you about sugar in general because you described the whole picture in such a compelling way. So thank you for that. So, onto the artificial sweeteners. What are the main ones in the food supply?   Well, there are a whole bunch. The most common ones that the food industry uses the most, obviously aspartame, which is Equal. And also sucralose, which is Splenda. But there are others now out on the market: Neotame, there's Acesulfame-K, there's monk fruit, there's Stevia, and all the Steviol glycoside derivatives. There's now Allulose, and there's Tagatose. There's a whole host of different sweeteners that are considered "non-nutritive” meaning they don't have calories.   These things show up in ways that people don't necessarily recognize. I mean Diet Coke, Diet Pepsi, those sort of things, it's obvious they're artificially sweetened. But these things are showing up in a lot of places, aren't they?   Indeed. The food industry now understands that sugar is a problem and people have been calling for less sugar but what they're not calling for is less sweet. And so the industry has a job. It has to deal with that dichotomy.   I know understanding their impacts is complicated by the fact that there are a lot of these things and they're all chemically different from one another. I'm imagining they have different metabolic effects. What happens when these things get into the body?   Right, and that is the issue. It has nothing to do with calories. People think calories are the issue. This has nothing to do with calories. That's one of the reasons, Kelly, that I'm committed to one concept: kill the calorie. Kill the calorie as a unit of measure. It was never appropriate. It was actually subterfuge, and it was actually promoted and promulgated by the food industry because if it is about calories, they can assuage their culpability for what they've done to our food supply. This has nothing to do with calories. This has to do with metabolic health.   Now, the World Economic Forum just published a white paper called the, "True Purpose of Nutrition," and it comes down to two words: metabolic health. That is what is going on inside the cell and that's where the artificial sweeteners do their damage, inside the cell. That's what we have to talk about. There are several places in the body where artificial sweeteners can do damage that have absolutely nothing to do with calories. The first, you put something sweet on your tongue. Message goes tongue to brain, "Sugar's coming." Brain sends a message to the pancreas, "Sugar's coming, release the insulin." Then the sugar never comes because it was a diet sweetener. What does the pancreas do? It turns out it releases the insulin anyway even though it had no calories, even though it wasn't sugar, just because of the sweet taste. So this is known as the cephalic phase of insulin secretion. That insulin is driving energy storage into fat, number one, and it's also driving cell proliferation in your coronary arteries, cell proliferation in your breast tissue, in other words, cardiovascular disease and cancer and ultimately leading to burnout of your pancreas, and now you've got diabetes too. Even though these artificial sweeteners have no calories, they still generate an insulin response, which is still problematic from a metabolic standpoint.   So because of the sweet taste and the body's response to that, I'm assuming what you're saying would be true to all of sweeteners?   Exactly. All of them do that. The next step is the artificial sweetener goes down your gullet, goes into your intestine, and the intestine has these bacteria in it called the microbiome. Most people have now heard of that. Different bacteria lead to different effects in the intestine. But think of your intestine - I mean it's a sewer. It has a whole lot of S-H-you-know-what in there. The goal of the intestine is to keep the S-H-you-know-what IN the lumen of the intestine and not allow it into the bloodstream. It uses three barriers. It has a physical barrier called the mucin layer. It has a biochemical barrier known as tight junctions or zonulins. It also has an immunological barrier called Th17 cells. Those three barriers have to work right to keep the junk out of your bloodstream because if the junk gets into your bloodstream, you now have systemic inflammation, which drives insulin resistance and drives chronic metabolic disease as well. So keeping your intestine in tiptop shape is really important. Well, it turns out those diet sweeteners alter the microbiome. Some of those bacteria like those sweeteners and utilize them to make toxic byproducts, which damage the mucin layer, damage that biochemical tight junction barrier and allow for things to seep through. This is a process called leaky gut. For reasons that are still unclear, sugar tends to deplete those Th17 cells, rendering the immunologic barrier devoid of function. The sum total of which means all the you-know-what in your intestine ends up in your bloodstream, goes to your liver, generates insulin resistance, and you are off to the chronic metabolic disease races as well, from diet sweeteners having nothing to do with calories.   What an amazing picture your painting of these things.   We've got one more mechanism. At the fat cell, now this I really don't understand and it's early data but seems to be consistent. Turns out adipocytes, fat cells, have receptors for diet sweeteners. Don't ask me why. I don't know why. But it turns out, diet sweeteners can act like insulin right at the fat cell to increase energy deposition into the fat cell. Growing those fat cells all by themselves, due to the diet sweetener rather than due to insulin. Now how dumb is that? As a result, there are a lot of different ways diet sweeteners might end up causing problems as well, having nothing to do with calories, having nothing to do with fructose. There was a paper that came out in the European Journal of Clinical Nutrition. It was a meta-analysis of sugar and also of diet sweeteners in terms of diabetes and heart disease. What I can say in one sentence to sum up what this paper showed is that the toxicity of one Coca-Cola equals the toxicity of two diet Coca-Colas. Half as bad. That doesn't mean good. It means half as bad.   Boy, I mean, any one of the three major pathways to harm would be of concern. If you add them all together, it is a pretty striking picture, isn't it? I imagine, even if somebody knew about this, they might say, well, you know, I'm willing to accept those risks. I mean, even though you are making them sound substantial, but I'm willing to accept those risks if these products help me control my weight. Do they?   Well, they don't. That's part of the problem. There is not one study, not one study in the entire world's literature, that shows that switching from sugared beverages to diet beverages actually controls weight. The reason is because even though the diet sweeteners don't release as much insulin now, when you drink the diet sweetener, the pancreas releases it later. That's actually been shown in several studies now. You get a delayed insulin response, so that the 24-hour insulin burden is the same whether you consume the sugar or the diet sweetener.   Let's talk about safety for a minute. What about sort of the typical toxicology concerns that people have had for years about these substances, irrespective of what they're doing to the pancreas and to the other, the microbiome, et cetera? What about the just kind of pure safety of them?   Right, so the one that has generated the most heat, not too much light, unfortunately, is aspartame, NutraSweet. It turns out that aspartame has a very long and checkered history. Did you know that aspartame was made by Searle, G.D. Searle? And, do you know who the CEO of G.D. Searle was at the time that aspartame was approved by the FDA?   I do not.   His name was Donald Rumsfeld.   An interesting character in history.   Indeed, wouldn't you think? It turns out that G.D. Searle actually buried most of the toxicology of aspartame in order to get it approved. It is a long complicated and involved story, which we don't have time for. I'm not even privy to most of the details on that. The bottom line was it ultimately did get approved despite the fact that there was a significant amount of concern about toxicology of this compound. Those questions still remain today. That is one. Another one that is a big issue is sucralose. Sucralose is also called Splenda. Sucralose is a chlorinated poly-fructose and it's extremely sweet, no question about that. It seems to have some GI side effects that a lot of people don't like. It also has now been associated with cancer. And most recently, the one that's gotten the most attention and almost assuredly, Kelly, the reason you called me is the paper that came out about three weeks ago in science about erythritol. So erythritol is a sugar alcohol, and now the meta-analysis of erythritol consumption suggests that it may in fact contribute to heart disease. Now, is that true? Meta-analysis are complicated. People think meta-analysis are the piece de resistance, the highest bar of medical information and analysis. I have four words for meta-analysis: garbage in, garbage out. Meta-analyses are only as good as the studies that they base the data on. If those studies were done by the food industry, which almost all of these are, because that's who stands to benefit from them. These are almost never NIH studies. These are almost always food industry studies, as you know, the odds are 7.61 times more likely to find in favor of the compound of interest. So all of these are, shall we say, biased. All of these are tainted, and meta-analyses are basically a conglomeration of tainted studies. So what do you expect the result to be?   Thanks for that background. I'm imagining also regarding toxicology and safety, that some of the newer sweeteners like Splenda for example, sucralose, there hasn't been enough years of use to pick up long-term chronic effects.   Well certainly, if you're using cardiovascular or cancer events, you're absolutely right. A lot of these events, you know, take a long time to manifest themselves. Sometimes, a generation or even two generations for that matter, especially for heart disease and cancer. The 15-year-old is drinking 10 diet sodas. When do you expect the heart attack to show up? You know, it's complicated.   So we use biomarkers to try to answer these questions, but then the biomarker has to actually be a good proxy for those events and often they're not. Let me give you an example, LDL. Everybody thought LDL was the bad guy. Turns out triglycerides are the way worse guy. LDL has a hazard risk ratio for heart disease of 1.3. Triglycerides have a hazard risk ratio of 1.8. Triglycerides are 50% more important in determining heart disease than LDL is, but we use LDL as the biomarker because it's more stable. So you have to use the right biomarker and you have to interpret it properly and it actually has to mean something and it has to change relatively acutely. All of which are problematic for all of these biomarkers. It's hard. It's hard to do these kinds of analyses. Having said that, my group, a scientific advisory team that I convened to help an offshore ultra-processed food company improve the health of their products. We've published this just last month in Frontiers in Nutrition. The company is called Kuwaiti Danish Dairy Company, or KDD. The title of the paper is, "The Metabolic Matrix: Re-Engineering Ultra-processed Foods to Protect the Liver, Feed the Gut, and Support the Brain." We did a deep dive on diet sweeteners. We looked at all of these diet sweeteners and their proxies, all the biomarkers. The one that actually popped out that looked to be the most beneficial, at least acutely, is a new one that we're actually kind of interested in and is picking up speed and it's called allulose. Allulose currently is 12 times the cost of sugar, but that's coming down. It turns out allulose lowers LDL and raises HDL. So it may have a better cardiovascular profile, but again, all the caveats that we mentioned before.   That's very interesting. So given your interest in pediatrics, what about children using these sweeteners?   I am totally against children using sugar because they get fatty liver disease and Type 2 diabetes, and I am totally against them using diet sweeteners because, number one, we don't know what they're going to do. Number two, they don't actually lead to weight loss. That data we do have. So as far as I'm concerned, we really only have one option and that is de-sweeten our lives. We have to de-sweeten the food.   Perfect lead in to the next question I was going to ask. So do you think it is possible for people to become accustomed to less sweetness? I mean, let's say the food industry is required to gradually reduce sugar and sweetness from the sweeteners. What do you think would happen?   Absolutely. It is not only possible, it is eminently doable. And I know why and we have the data for why that is. So there is a very smart lady, neuroscientist at the University of Michigan by the name of Monica Dus, who has done all this work in fruit flies of all places. She has shown the desensitization of the tongue to sugar has to do with changes in receptors and changes in specific substrates in the taste buds of the tongue. When you stop the sugar availability, it takes three weeks for those receptors to increase and repopulate, and for those problematic substrates to go away. You can actually retrain your tongue in three weeks to be much more sensitive to the sugar that is in the food naturally. After a three-week abstinence period or a reduction or a weaning period, a blueberry will taste like a sugar bomb in your mouth. So we know this can happen and we actually have proven this for salt previously. The UK, as you know Kelly, back in 2003, the Blair government convened all the food industry concerns in Great Britain. So Marks & Spencer, and Weight Rose, and Tesco, et cetera, all around the big table, didn't let media in, and basically said to every single food industry concerned in Great Britain, "Look, we have a hypertension and stroke problem and it's because of the salt content of the food and we are going to play referee here in the government. And each of you is going to reduce the salt content of your food by 10% per year over a three-year period so that you'll reduce your salt by 30% at the end of this and everyone's going to play together, so that there's no competitive disadvantage and most importantly, we're not going to tell anybody." That's what they did. Sure enough, in 2011, a paper appeared in Burge Medical Journal, demonstrating a 40% reduction in hypertension and stroke because of the public health effort that the Blair government made in terms of reducing the amount of salt in processed food. We can do the same with sugar today.   The salt example is a good one because I think many people have sort of experienced this in their day-to-day lives, even in the United States, where industry hasn't done exactly what's happening in Britain. People have tried to reduce salt in their diet, add less salt, and buy products with less salt. And then sometimes they'll go back and consume something that they had before and find it extremely salty, even unpleasantly salty. It's interesting to hear on the sugar front that that same experience might be possible and that there's a biological reason for it. It is not just that you psychologically get accustomed to different levels of sugar, in this case, but there's a biological change occurring that might help keep that going.   Absolutely. You can change people's behavior by changing their biochemistry. This is how I got into this field by using a drug that suppressed insulin and getting kids who were 400 pounds due to their brain tumor to actually lose weight and start exercising because we got their insulin down. You can fix the biochemistry and the behavior will follow suit. The food industry could do that and we wouldn't even notice.   So I'm guessing I know the answer to this question before I even ask it, but let's go ahead. Would you suggest the food industry be mandated to make gradual reductions in sugar, just like you mentioned with salt in the UK?   Absolutely, I'm working toward that. The only thing that I say is we should not tell anybody.   So it would be sort of a stealth move then. You would not necessarily have to make a big deal of it to the public, because they might assume there's going to be a change in the desirability and the pleasure of the products when that's not necessarily the case.   As soon as you do something to their food, someone's going to scream, "Nanny state!" This is not nanny state. Ultimately, this is a public health problem. We have to deal with it with a public health solution. You know, that means changing things. If the amount of sugar in our food supply went down, say by 3% every six months down, so that we were able to cut our sugar consumption by 25%, which would be the same basically as what a tax would do. We would save so many billions of dollars in healthcare costs, and we would increase productivity so much. We actually published a paper, a microsimulation analysis in BMJ years ago where we quantified the savings to government, to insurers, to the public. If we actually got sugar down and, you know, actually listened to what the USDA told us, it would be amazing. There is data, there's a pathway forward, there's precedent for doing it. I absolutely think that is where we need to go.   Rob, you're making me feel very smart at the moment, because I figured this was going to be a podcast filled with information and helpful bits of knowledge and it sure was. I'm really grateful that you were able to join us and the topic couldn't be more important. Thank you again for being with us.     Bio   Robert H. Lustig, M.D., M.S.L. is Emeritus Professor of Pediatrics in the Division of Endocrinology, and Member of the Institute for Health Policy Studies at UCSF. Dr. Lustig is a neuroendocrinologist, with expertise in metabolism, obesity, and nutrition. He is one of the leaders of the current “anti-sugar” movement that is changing the food industry. He has dedicated his retirement from clinical medicine to help to fix the food supply any way he can, to reduce human suffering and to salvage the environment. Dr. Lustig graduated from MIT in 1976, and received his M.D. from Cornell University Medical College in 1980. He also received his Masters of Studies in Law (MSL) degree at University of California, Hastings College of the Law in 2013. He is the author of the popular books Fat Chance (2012), The Hacking of the American Mind (2017), and Metabolical: The Lure and the Lies of Processed Food, Nutrition, and Modern Medicine (2021). He is the Chief Science Officer of the non-profit Eat REAL, he is on the Advisory Boards of the UC Davis Innovation Institute for Food and Health, the Center for Humane Technology, Simplex Health, Levels Health, and ReadOut Health, and he is the Chief Medical Officer of BioLumen Technologies, Foogal, Perfact, and Kalin Health.  

In pursuit of mechanisms and evidence-based approaches, gut health has been revealed as a critical cornerstone of neurological health. In this episode, we're going into detail on what the gut layers are. I hope this video will help someone else who's trying to understand how the gut works for purposes of biohacking with functional medicine, nutrition, supplements, etc. For any intervention, is there evidence of a relationship, and is there data that it worked in other humans? We talk about: what the gut mucus is made out of elements of the gut barrier - the many ways the body keeps microbes and partially digested food away kinds of intestinal epithelial cells (Goblet cells, Paneth cells, M cells, etc.) and their functions types of gut associated lymphoid tissue (GALT) and their distinctions - lamina propria, Peyer's patches, lymph nodes the enteric nervous system and enteroendocrine cells different types of CD4+ T cells: Th1, Th2, Th17, and Treg, what they respond to, and their major outputs the mechanism of nutrient absorption the mechanism of leaky gut (paracellular transport through tight junctions) Here's the video: https://youtu.be/sIn_VxH6zDA Transcript of the video, for those who are pressed for time: https://www.brainforest.org/post/leaky-gut-anatomy I hope this helps someone understand their gut a little better on the path to health. Stay tuned for our next podcast on the relationship between leaky gut and aging. Share this resource with others who are studying gut anatomy on the path to health!

Vijay Kuchroo is the Samuel L. Wasserstrom Professor of Neurology at Harvard Medical School, Senior Scientist at Brigham and Women's Hospital, and Co-Director of the Center for Infection and Immunity, at the Brigham Research Institutes, Boston. He is also an associate member of the Broad Institute, and a participant in a Klarman Cell Observatory project that focuses on T cell differentiation. He is the founding Director of the Evergrande Center for Immunologic Diseases at Harvard Medical School and Brigham and Women's Hospital. His major research interests include autoimmune diseases—particularly the role of co-stimulation—the genetic basis of experimental autoimmune encephalomyelitis and multiple sclerosis, as well as cell surface molecules and regulatory factors that regulate the induction of T cell tolerance and dysfunction. His laboratory bred several transgenic mice that serve as animal models for human multiple sclerosis. The Kuchroo laboratory was also the first to describe the TIM family of genes, and identified Tim-3 as an inhibitory receptor expressed on T cells, which is now being exploited for cancer immunotherapy. He was first to describe the development of highly pathogenic Th17 cells, which have been shown to induce multiple different autoimmune diseases in humans. Kuchroo is the lead author on a paper describing the development of Th17, which is one of the most cited papers in the field of Immunology.Kuchroo came to the United States in 1985, as a Fogarty International Fellow at The National Institutes of Health, Bethesda, MD for one year, before joining the department of pathology at Harvard Medical School, as a research fellow. Later, he joined the Center for Neurologic Diseases at Brigham and Women's Hospital as a junior faculty member in 1992.He obtained his degree in Veterinary Medicine from the College of Veterinary Medicine, Hisar, India. Subsequently, he specialized in pathology at the University of Queensland, Brisbane Australia, where he obtained a Ph.D. in 1985. He received the Fred Z. Eager Research Prize and medal for his Ph.D. research work at the University of Queensland. Based on his contributions, he was awarded the Javits Neuroscience Award by the National Institutes of Health in 2002 and the Ranbaxy prize in Medical Research from the Ranbaxy Science Foundation in 2011. He was named Distinguished Eberly Lecturer in 2014, and obtained a Nobel Laureate Peter Doherty Lecture/Prize in 2014.Kuchroo has 25 patents and has founded 5 different biotech companies including CoStim Pharmaceuticals and Tempero Pharmaceuticals. He also serves on the scientific advisory boards and works in advisory capacity to a number of internationally recognized pharmaceutical companies including: Biocon, Syngene, Pfizer, Novartis and Glaxo-Smith-Klein (GSK).Alix Ventures, by way of BIOS Community, is providing this content for general information purposes only. Reference to any specific product or entity does not constitute an endorsement nor recommendation by Alix Ventures, BIOS Community, or its affiliates. The views & opinions expressed by guests are their own & their appearance on the program does not imply an endorsement of them nor any entity they represent. Views & opinions expressed by Alix Ventures employees are those of the employees & do not necessarily reflect the view of Alix Ventures, BIOS Community, affiliates, nor its content sponsors.Thank you for listening!BIOS (@BIOS_Community) unites a community of Life Science innovators dedicated to driving patient impact. Alix Ventures (@AlixVentures) is a San Francisco based venture capital firm supporting early stage Life Science startups engineering biology to create radical advances in human health.Music: Danger Storm by Kevin MacLeod (link & license)

Sinus problems are rampant. Americans spend over $1 Billion annually to treat sinus problems with over-the-counter medications, which is crazy. It's not just common in the chronic illness world and in the autoimmune world, and ESPECIALLY in the mold world, it's common in everyone. Sinus inflammation is interesting. I have had really great success healing my own sinuses. I'm not recommending that everyone (or anyone) do what I did, but what I REALLY DID was I spent several years intensely studying deep immunology and the Ear, Nose, and Throat and Allergy literature, read 100s of studies, and used things like high dose supplements and essential oils to have really good success with nasal polyps and chronic sinusitis. I haven't had sinus issues for over 3 years. Here is a video of what I did to get rid of nasal polyps, it's crazy.  When I talk about sinuses, I'm also talking about ENT areas - ear infections, tonsils, sore throats, pharyngitis, which includes things like Strep and PANDAS, but most of my success was with the nose. The whole ENT region is a hotbed of infections and pathogens, and is right across the wall from the brain, and things like antibodies, histamine, chemical toxins, inflammatory cytokines, and mycotoxins from mold can ride the "olfactory elevator" (as Dr. Jill Crista calls it) right up to the brain - right to deep, midline areas like the frontal cortex (brain fog, etc), pituitary (hormones), amygdala (anxiety, fear, etc), hypothalamus (temp, dysautonomia, etc), neurological dysfunctions and more.  Sinus inflammation drives many immune mechanisms, including Th2 and eosinophilic inflammation, mast cell activation and histamine, and Th17 inflammation, which is tissue-damaging autoimmune inflammation and will drive autoimmune progression. THAT IS THE MOST IMPORTANT PIECE OF THE PUZZLE!  One thing that can drive this immune activation are chronic biofilms including Strep, Staph (MARCoNS), and Mold/Yeast that are incredibly persistent and antibiotic resistant. Biofilm colonies, like in the gut, grow on sinuses, adenoids, tonsils (that's why they remove them!) and ENT surfaces - and when they adhere to a surface they are over 1000x harder to kill, and they are highly persistent and antibiotic resistant. THIS IS THE OTHER MOST IMPORTANT PIECE! In this episode I talk about 4 levels of supporting sinus inflammation naturally:1 - Breathe Clean Air!!!! Allergies are obviously an issue....You can't be living in mold....I talk about air purifiers, mold candles, HVAC filters, and more.2 - Fix your Gut and Balance your Immune System - I talk about using things like probiotics, herbal killers, SCFA, vitamins D and A, glutathione, perilla, quercetin, luteolin, etc to support barrier integrity, mast cell activation, Th2 dominance.3 - Break Biofilms and Kill Infections - Nasal Spray, Neti Pot, Nebulizer, Gargle - I talk about using essential oils, iodine, hydrogen peroxide, silver, propolis, aqualaurin, biocidin, etc to break up biofilms and help kill pathogens. 4 - Maintain - I talk about the importance of breathing clean air, doing regular nasal rinses, and more to maintain. This is not medical advice, but many people have seen their ENT with very little answer besides antihistamines, antibiotics, or steroids, so these are just some of the things that people are doing out there, and hopefully it can help you solve YOUR puzzle!I also mention this, my favorite newsletter and started by an amazing ENT surgeon:www.sinusitiswellness.com

Welcome to Season 5 of Living Well with MS, where we are pleased to welcome holistic health practitioner and expert Magic Barclay as our guest!  Keep reading for the key episode takeaways and Magic's bio. Make sure you sign up to our newsletter to hear our latest tips and news about living a full and happy life with MS. And if you're new to Overcoming MS, visit our introductory page to find out more about how we support people with MS. Bio: Magic Barclay is the lead practitioner and founder of ‘Wholistic Natural Health Australia', a holistic health practice. She also is a host of the podcast “A Magical Life: Health, Wealth and Weight Loss”. Magic's life changed when she faced multiple life-threatening conditions and at the same time, found herself divorced and raising her two children alone. She decided to find the root cause of her health issues and that set her on a path of life-changing learning that affected her whole family. Magic is a Master Practitioner in immune health, mould toxicity recovery and Psycho-Neuro-Endocrine-Immunology (the study of the interaction between psychological processes and the nervous and immune systems of the human body) of trauma. She tells us that she is a “mum of two amazing humans and two gorgeous furbabies, a grower of organic food for her family and a passionate native gardener”. Magic's mission is to help people heal naturally, reconnect to the environment and reach their own potential. She mainly works with women aged 45-65 who feel unheard or misled by mainstream medicine and anyone who wants to bring their health back to basics. Selected Key Takeaways: The purpose of functional medicine Functional medicine involves looking at the systems of the body. It looks at what each system does and how it works with the other systems. We often say, "no system works alone." We particularly look at the root cause because if you don't look at that, then other issues keep arising. Belief in yourself is a powerful part of healing If people don't believe in themselves, they're not going to get well. We see a lot of people just given diagnosis after diagnosis, label after label, and they start believing that's who they are. Magic believes that this is a really awful way to live because you're a person, you are not the label that was given to you by your doctor. You are still a person. So, what they do in functional medicine is uncover: Who is that person? And who do [they] want to be? Reduce stress by acknowledging the stressor isn't forever If you find yourself around people that increase your stress, don't be around them or decide to be around them for five or 10 minutes. Give yourself a time cap and tell yourself after 10 minutes “I'm out of this situation and I'll be okay”. If you find you are stressed by work, a doctor's appointment or driving, either take yourself out of the situation, find an alternative, or give yourself a time limit so that you know internally it's not forever. And don't sit there thinking, “I'm so stressed,” as your body hears that and guess what? It replies, "Really? This is a low level of stress, you want to be stressed? I'll raise the bar." Related Links: Magic's Wholistic Natural Health Find out more about PNEI and Dr. Gabor Maté https://drgabormate.com/ Make natural laundry detergent from horse chestnuts/ conkers/ buckeyes https://wastelandrebel.com/make-laundry-detergent-out-of-chestnuts/ Parkinson's protein from gut to brain https://www.nih.gov/news-events/nih-research-matters/tracking-spread-parkinsons-proteins-gut-brain The Blood Brain Barrier in MS https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8395058/ Th1 and Th17 response in MS https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5491887/ Don't miss out: Subscribe to this podcast and never miss an episode. You can catch any episode of Living Well with MS here or on your favourite podcast listening app. If you like Living Well with MS, please leave a 5-star review on Apple Podcasts or wherever you tune into the show. Feel free to share your comments and suggestions for future guests and episode topics by emailing podcast@overcomingms.org. Make sure you also sign up to our newsletter to hear our latest tips and news about living a full and happy life with MS. If you enjoy this podcast and want to support the ongoing work of Overcoming MS, you can leave a donation here.

Dr. Vijay Kuchroo is the Samuel L. Wasserstrom Professor of Neurology at Harvard Medical School. His major research interests include the role of co-stimulation in autoimmune diseases, as well as cell surface molecules and regulatory factors that regulate the induction of T cell tolerance and dysfunction. He talks about the conditions necessary to differentiate Th17 cells and their role in autoimmunity. He also discusses his group's discovery of Tim-3, an inhibitor receptor on T cells which is now being exploited for cancer immunotherapy.

Recently a review article from 2020 caught my eye; Reconsidering the Role of Melatonin in Rheumatoid Arthritis. Sleep is a major issue for RA, and many patients and clinicians are turning to melatonin to aid with sleep issues, are we causing more harm than good? Melatonin has been known:  as a powerful antioxidant and anti-inflammatory properties to help with regulating T cell responses, T helper (Th)1, Th17, and regulatory T cells (Tregs). to help modulate the circadian rhythm and enhance sleep On the flip side, there is evidence from animal studies showing there are receptors for melatonin on synovial macrophages which promote the release of some Th-1-type proinflammatory cytokines. It has also been pointed out that the higher blood concentrations of melatonin in arthritic patients, especially in the early morning, might explain the morning stiffness and joint swelling experienced by patients - but does that mean that melatonin should be completely avoided? So far most of that evidence is coming from animal studies but are they translating with similar outcomes in human RCT? Let's dive into 2  human trials to see how melatonin impacts your RA clients. Save the Date! Dr. Alison Danby, ND will be running a 1-day Autoimmune 101 Workshop for clinicians on Friday, October 21, 2022. Registration opens September 21st. Join our mailing list to make sure you are in the know to grab those Early Bird Savings.  References: https://confident-clinician-club.s3.ca-central-1.amazonaws.com/The+Expert+Clinician/Autoimmune+101/TCC+Podcast/RA+%26+Melatonin+2007++(1).pdf https://confident-clinician-club.s3.ca-central-1.amazonaws.com/The+Expert+Clinician/Autoimmune+101/TCC+Podcast/RA+and+melatonin+-+2020+RCT+(1).pdf

At Cornell University in Ithaca, NY, Mandy joins Immune to discuss her career and her research on understanding how Th17 cells develop and are influenced to be ‘good' or ‘bad' in their function. Hosts: Vincent Racaniello, Cynthia Leifer, Steph Langel, and Brianne Barker Guest: Mandy McGeachy Subscribe (free): Apple Podcasts, Google Podcasts. RSS, email Become a patron of Immune! Links for this episode Th17 cytokines in health and disease (Immunity) Time stamps by Jolene. Thanks! Music by Steve Neal. Immune logo image by Blausen Medical Send your immunology questions and comments to immune@microbe.tv

There are many health benefits associated with good quality sea salt, and it's something I recommend to my patients and personally add to my food regularly.At the same time, we know that too much salt can be problematic. Research shows that excessive salt consumption can increase Th17 cells and inhibit Tregs (the opposite of what we want to happen - check out last week's bonus episode for a quick summary).So, should everyone with Graves' disease and Hashimoto's avoid salt?Today I'm sharing the research around salt intake and autoimmunity and how you can safely consume salt as a part of your diet.In this episode, you'll learn:Why I regularly use and recommend sea saltWhat studies show about the correlation between a high-salt diet and autoimmunityMy recommendations for daily salt consumptionAs always, I hope you found this episode valuable, and I look forward to catching you in the next episode!To learn more, visit the show notes at https://savemythyroid.com/podcast/can-salt-trigger-thyroid-autoimmunity/.

Ok so let's talk about gut health. Gut health and detox are pretty much the two most important topics, and toxins affect gut health....but good gut health is necessary for proper detoxification.....I think gut health wins. At least for this next podcast series :) Gut health is foundational to health, inflammation, and aging. It's so crucial, but so few people seem to have it mastered IF they are still experiencing symptoms, and I mean ANY symptoms - joint pain, fatigue, anxiety, depression, bipolar, metabolic, certainly autoimmune flares, not just digestive symptoms. I'm going to go deeper into some specific topics in the next few episodes, but this one is an overview, and I made a list of the 10 most important things for gut health. The first 3 are symptoms, the next 4 are mechanisms, and the last 3 are infections, and understanding these 10 things will give you a pretty good grasp on understanding gut health and digestion overall!Diarrhea - I talk about IBS, IBD, low microbiome and good bacteria/probiotics, glutamine, mast cells, and hydrogen SIBO....Constipation - I talk dysbiosis/methane, and a LOT about vagal motor outflow and vagus nerve activity that controls motility as well as HCL, bile, enzymes....Bloating - When I hear bloating I think small intestine and fermentation. Dysbiosis is often at the root, which includes proper digestion (HCL and bile), and I touch on SIBO/SIFO, avoiding FODMAPs foods....Digestion - This is critical!! Chewing your food, being in parasympathetic mode, then proper stomach acid - it can be too high (mast cells) or too low (more common), pancreatic digestive enzymes, bile from the gallbladder (steatocrit), and of course VAGUS BABY!Dysbiosis - The 10 lbs of bacteria in your gut can become imbalanced. Low good bacteria, general microbiome imbalances…..and LPS!!!!!Leaky Gut - Everyone can have some intestinal permeability, is yours pathological, and if so what kind is it - paracellular or transcellular? Food Sensitivities - IgG testing, and how food sensitivities can drive autoimmune reactivity, general inflammatory tone, and initiate T cell mediated tissue damageSIBO - Bloating! Fermentation of fibers, starches, sugars, FODMAPs ...why you need HCL, bile, vagus outflow……Why I think SIBO testing is dumb….Candida - OMG….the single biggest thing I see. Antibiotics, sugar, stress, birth control, mold exposure, can drive a Th17 inflammatory response (autoimmune), can also drive Th2 (and both will decrease Th1)......and why I love urinary organic acids testing for fungal issues.Parasites - this I am going to do a whole episode on because it's crazy, it's quite frankly pretty controversial in the autoimmune world, is it better to have or to not have them??? The answer is IT DEPENDS. But I do talk about someone who was diagnosed with Ulcerative Colitis and it actually seemed to be a parasitic infection, pretty interesting story :)Share this with someone, subscribe, leave a rating and review, and follow me elsewhere!

T-helper 17 (Th17) cells and regulatory T cells (Tregs) play a role in developing autoimmune conditions like Graves' disease and Hashimoto's.Today I'm sharing everything you need to know about these cells since you'll hear me refer to them a lot in future podcast episodes.In this episode, you'll learn:Where Th17 and Treg cells originateThe role of Th17 and Treg cellsHow Th17 and Treg cells are connected to autoimmune conditionsNutrients, supplements, and natural agents that have been shown to increase regulatory T cells and decrease Th17 cellsTune in for next week's Q&A episode, where I'll discuss something many people commonly use in their homes that can increase Th17 cells.I hope you found this episode valuable, and I look forward to catching you in the next episode!To learn more, visit the show notes at https://savemythyroid.com/podcast/what-are-th17-and-treg-cells/.

Oleic acid, a key to activating the brain's ‘fountain of youth'   Baylor College of Medicine, March 22, 2022   Many people dread experiencing the cognitive and mood declines that often accompany reaching an advanced age, including memory disorders such as Alzheimer's disease and mood conditions like depression. While searching for new ways to prevent or treat these and other related conditions, a team at Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute (Duncan NRI) at Texas Children's Hospital identified a missing piece of the puzzle of how memory and mood are sustained and regulated in the brain. Their study, published in the Proceedings of the National Academy of Sciences, reveals that oleic acid produced in the brain is an essential regulator of the process that enables learning and memory and supports proper mood regulation. The finding has paved the path to discovering potential new therapeutic strategies to counteract cognitive and mood decline in patients with neurological disorders.   (NEXT)   Chemical found in leafy greens shown to slow growth of COVID-19 and common cold viruses   Johns Hopkins University School of Medicine, March 23, 2022   Researchers at Johns Hopkins Children's Center report evidence from lab experiments that a chemical derived from a compound found abundantly in broccoli and other cruciferous plants may offer a potentially new and potent weapon against the viruses that cause COVID-19 and the common cold. In a study described March 18 in the journal Communications Biology, the scientists showed that sulforaphane, a plant-derived chemical, known as a phytochemical, already found to have anti-cancer effects, can inhibit the replication of SARS-CoV-2, the coronavirus that causes COVID-19, and another human coronavirus in cells and mice. Sulforaphane's natural precursor is particularly abundant in broccoli, cabbage, kale and Brussels sprouts. First identified as a "chemopreventive" compound by a team of Johns Hopkins scientists decades ago, natural sulforaphane is derived from common food sources, such as broccoli seeds, sprouts and mature plants, as well as infusions of sprouts or seeds for drinking. Previous studies, including those at Johns Hopkins Medicine, have shown sulforaphane to have cancer and infection-prevention properties by way of interfering with certain cellular processes.   (NEXT)   New clues about how a high-salt diet contributes to cardiometabolic diseases found deep in the brain   Medical College of Georgia and Georgia State University, March 22, 2022    Deep in the brain a group of large neurons produce a hormone which prompts our bodies to hold onto more fluid and increase blood pressure. Scientists say these neurons play a critical role in enabling our bodies to maintain healthy homeostasis by using this skill set to efficiently eliminate the excessive salt we consume in an unhealthy meal. But scientists at the Medical College of Georgia and Georgia State University also say that the chronic high-salt diet most Americans consume can turn this system against us, resulting in hyperactivity of these neurons, continuing production of this hormone vasopressin, constriction of blood vessels and increasing our risk for common cardiometabolic diseases like high blood pressure and heart disease. They are finding that salt loading increases the firing of vasopressin-producing neurons, increases constriction of blood vessels and decreases local blood flow. More typically when neurons become active, blood flow to them increases, in a process called neurovascular coupling. This helps ensure working neurons have the adequate oxygen and nutrients needed to sustain increased activity.   (NEXT)   Vitamin D may keep low-grade prostate cancer from becoming aggressive   University of South Carolina, March 22, 2022   In cases of low-grade prostate cancer, many urologists do not treat the disease, but instead do what's called "active surveillance. The cure—meaning surgery or radiation—is probably worse than the disease, so they wait a year and then do another biopsy to see where the patient stands. However, knowing that they have even low-grade prostate cancer can cause patients and their families excessive anxiety, which prompts some of the men to undergo an elective prostatectomy, despite the risk of complications such as infection, urinary incontinence and erectile dysfunction.   (NEXT)   How sugar promotes inflammation   University of Wurzburg (Germany), March 22, 2022   People who consume sugar and other carbohydrates in excess over a long period of time have an increased risk of developing an autoimmune disease. In affected patients, the immune system attacks the body's own tissue and the consequences are, for example, chronic inflammatory bowel diseases such as Crohn's disease and ulcerative colitis, type 1 diabetes and chronic inflammation of the thyroid gland. The underlying molecular mechanisms that promote autoimmune diseases are multilayered and complex. Now, scientists at the Julius Maximilians University of Würzburg (JMU) have succeeded in deciphering new details of these processes. Their work support the notion that excessive consumption of glucose directly promotes the pathogenic functions of certain cells of the immune system and that, conversely, that a calorie-reduced diet can have a beneficial effect on immune diseases. In their study, the scientists focused on a group of cells of the immune system that have not been known for very long: T helper cells of type 17, also called Th17 lymphocytes, which play an important role in regulating (auto-) inflammatory processes.

In Episode #65, Dr. Jill Interviews Dr. Lauren Tessier on Mold and Mycotoxins and how to test and treat for this common cause of autoimmunity. Learn more about immune dysfunction including TH17 dominance and it's link to autoimmunity.