Podcasts about adipose tissue

***JOIN THE NEXT MASTER YOUR FASTING CHALLENGE THAT STARTS May 7th, 2025!*** We'll GUIDE you on how to FAST to LOSE FAT for good, and use 'fast cycling' to achieve uncommon results! ⁠REGISTER HERE!⁠ Click the Link for DATES, DETAILS, and FAQs! In this science-packed episode, Dr. Scott Watier and Tommy Welling reveal how significant weight loss transforms fat tissue at a cellular level, creating metabolic changes that make results more sustainable. They explain how losing 16-20% of body weight through fasting remodels adipose tissue—reducing inflammatory leptin levels by 40% while increasing beneficial adiponectin—which improves insulin sensitivity and reduces hunger even during extended periods without food. The hosts share why many people struggle to maintain their new eating patterns long-term despite initial success, and provide practical strategies for optimizing your lifestyle beyond the honeymoon phase. They emphasize how success comes from transitioning from seeing time-restricted eating as a temporary weight loss tool to adopting it as part of your identity, developing consistent schedules that become automatic rather than requiring constant willpower. This episode offers a comprehensive roadmap for optimizing both biological and psychological aspects of your weight loss journey, helping listeners move from short-term results to sustainable lifestyle change. Take the NEW FASTING PERSONA QUIZ! - The Key to Unlocking Sustainable Weight Loss With Fasting! Resources and Downloads: SIGN UP FOR THE DROP OF THE ULTIMATE GUIDE TO BLOOD SUGAR CONTROL GRAB THE OPTIMAL RANGES FOR LAB WORK HERE! - NEW RESOURCE! - December 2024 FREE RESOURCE - DOWNLOAD THE NEW BLUEPRINT TO FASTING FOR FAT LOSS! SLEEP GUIDE DIRECT DOWNLOAD DOWNLOAD THE FASTING TRANSFORMATION JOURNAL HERE! Partner Links: Get your FREE BOX OF LMNT hydration support for the perfect electrolyte balance for your fasting lifestyle with your first purchase here! Get 30% off a Keto-Mojo blood glucose and ketone monitor (discount shown at checkout)! Click here! Our Community: Let's continue the conversation. Click the link below to JOIN the Fasting For Life Community, a group of like-minded, new, and experienced fasters! The first two rules of fasting need not apply! If you enjoy the podcast, please tap the stars below and consider leaving a short review on Apple Podcasts/iTunes. It takes less than 60 seconds, and it helps bring you the best original content each week. We also enjoy reading them! Article Links: https://diabetesjournals.org/care/article-abstract/doi/10.2337/dc24-2739/158098/Effect-of-Marked-Weight-Loss-on-Adipose-Tissue?redirectedFrom=fulltext https://pmc.ncbi.nlm.nih.gov/articles/PMC4975085/

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on “Weekend Warrior” Physical Activity and Adipose Tissue Deposition

Commentary by Dr. Jian'an Wang.

JACC Associate Editor Neha J. Pagidipati, MD, FACC, speaks with author Christopher M. Kramer, MD, FACC about this substudy of the SUMMIT trial published in JACC and presented at AHA, demonstrating that tirzepatide therapy in obesity-related HFpEF led to reduced LV mass and paracardiac adipose tissue as compared to placebo and the change in LV mass paralleled weight loss. These physiologic changes may contribute to the reduction in heart failure events seen in the main SUMMIT trial.

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances discusses a recently published original research paper on AI prediction of cardiovascular events using opportunistic epicardial adipose tissue assessments from computed tomography calcium score.

During fasting, fatty acids are mobilized from stored triacylglycerol in adipose tissue through the activation of Hormone-Sensitive Lipase by epinephrine which results in the release of 3 fatty acids to the bloodstream.

Send us a textAbout the guest: Sean Hartig, PhD is an associate professor at the Baylor College of Medicine, where is lab studies adipose (fat) tissue, metabolic regulation, and obesity & energy balance disorders.Episode summary: Nick and Dr. Hartig discuss: visceral vs. subcutaneous fat; white, brown, and beige adipose tissue; physiology of fat cells; obesity, insulin resistance, and leptin resistance; hormones & fertility; GLP-1 drugs for weight loss; and more.Related episodes:Obesogens, Oxidative Stress, Dietary Sugars & Fats, Statins, Diabetes & the True Causes of Metabolic Dysfunction & Chronic Disease | Robert Lustig | #140GLP-1, Weight Loss Drugs, Ozempic, Obesity, NMDA Receptors, Metabolism & Brain Health | Christoffer Clemmensen | #161*This content is never meant to serve as medical advice.Support the Show.All episodes (audio & video), show notes, transcripts, and more at the M&M Substack Try Athletic Greens: Comprehensive & convenient daily nutrition. Free 1-year supply of vitamin D with purchase.Try SiPhox Health—Affordable, at-home bloodwork w/ a comprehensive set of key health marker. Use code TRIKOMES for a 10% discount.Try the Lumen device to optimize your metabolism for weight loss or athletic performance. Use code MIND for 10% off.Learn all the ways you can support my efforts

Muscles & Mindset Podcast Episode: Finding Your "Enough": Exploring Abundance vs. Scarcity Introduction Welcome to the Muscles & Mindset Podcast with Dr. Ali Novitsky. In this episode, your favorite obesity medicine doc/fitness guru/physician coach delves into the concept of "enough" and how understanding it can lead to a more abundant life, both physically and mentally. This episode is inspired by Dr. Ali's recent six-week slow travel experience in Greece, which provided her with numerous "a-ha moments" that she is excited to share with you. Key Themes What is "Enough"? We explore the idea of "enough" in various aspects of life: Tangible Aspects: Money, weight loss, muscle mass, clothes, shoes, and purses. Intangible Aspects: Emotional and mental fulfillment, showing up as a parent or partner. Abundance vs. Scarcity Dr. Ali discusses how feelings of scarcity often manifest in tangible ways when we feel disconnected in our lives. For example, feeling a lack of money when there is emotional disconnection. Our brains tend to make abstract concepts tangible, which can lead to a scarcity mindset. Personal Experience in Greece The Packing Fiasco Dr. Ali shares a humorous yet enlightening story about arriving in Greece with eight full suitcases, only to realize that she had packed WAY more than necessary. This experience highlighted the concept of "enough" and how we often overestimate our needs. Living Simply Living in a three-bedroom apartment in Syros, Greece, with her family taught her the value of simplicity. They had fewer clothes, shopped daily for groceries, and wasted less. This minimalist lifestyle made her feel more abundant and less stressed. Practical Applications of "Enough" Financial "Enough" Dr. Ali Novitsky discusses setting a tangible "enough" for yearly income and focusing on meeting that without feeling scarcity. If individuals feel scarcity despite meeting their financial goals, it may be rooted in past experiences. Weight Loss "Enough" In her weight loss programs, Dr. Novitsky emphasizes "optimal weight loss," which focuses on maintaining muscle mass while losing body fat. She encourages setting realistic weight loss goals based on muscle mass and body fat ratio rather than arbitrary numbers. Reflections and Changes Personal Growth Dr. Novitsky's time in Greece prompted significant personal growth. She realized that she is enough as a partner, mother, daughter, and friend. This newfound self-acceptance has led to changes in her goals, lifestyle, and what she is willing to tolerate. Professional Offerings Dr. Novitsky introduces several programs designed to help individuals achieve optimal health: Muscles and Mindset: Beginner and advanced strength training programs. Transform for Physicians: A CME program extending from six months to a year. Optimal GLP-1 Weight Loss: Support for those on GLP-1 agonists. Nutrition Training for Healthcare Providers: A six-week live training program starting October 7th. Conclusion Dr. Novitsky encourages everyone to reflect on what "enough" means in their lives and how they can shift from a scarcity mindset to one of abundance. She thanks the audience for joining her on this journey and looks forward to helping them find their abundance. Until next time, stay healthy and abundant! Timestamps 00:00:00 - Introduction to Muscles and Mindset Podcast 00:00:30 - Return from Greece and Aha Moments 00:01:02 - Exploring the Concept of "Enough" 00:01:33 - Abundance vs. Scarcity Mindset 00:02:07 - Tangible vs. Intangible "Enough" 00:02:28 - Personal Insights from Greece 00:03:10 - Setting Tangible Goals 00:04:04 - Addressing Scarcity Mentality 00:05:08 - Travel Story: Overpacking for Greece 00:06:16 - Challenges with Excess Baggage 00:07:06 - Arrival in Syros and Realizations 00:08:20 - Living with Less: Apartment Experience 00:09:14 - Daily Life in Greece: Simplicity and Abundance 00:10:09 - Grocery Shopping and Waste Reduction 00:11:03 - Reflecting on Personal Priorities 00:11:23 - Weight Loss: What is Enough? 00:12:06 - Optimal Weight Loss vs. Traditional Dieting 00:13:00 - Setting Realistic Weight Loss Goals 00:14:04 - Personal Weight Loss Journey 00:15:08 - Embracing Abundance in Life 00:16:01 - Self-Acceptance and Personal Growth 00:17:07 - Daily Routine in Greece: Yoga and Community 00:18:04 - Redefining Productivity and Worth 00:19:09 - Changes in Goals and Lifestyle 00:20:03 - Upcoming Programs and Offerings 00:21:08 - Transform for Physicians Program 00:21:30 - Optimal GLP-1 Weight Loss Program 00:21:51 - Nutrition Training for Healthcare Providers 00:22:34 - Conclusion and Finding Abundance Resources The Muscles & Mindset Program - 12 months for only $199! Enroll TODAY. Nutrition Training Program for Healthcare Providers is enrolling now! You can learn more HERE. Dr. Ali's Advanced Strength Training program is now available for exercises at a higher level. See the details HERE. Optimal GLP-1 Weight Loss Program - next program starts November, 2024. Learn more and join the waitlist HERE. 31 Days of FIT. Learn more HERE. Follow Dr. Ali Novitsky on TikTok | Facebook | Instagram | YouTube Subscribe to The Muscles and Mindset Podcast on Spotify | Apple Podcasts *Ali Novitsky MD, this podcast, and podcast write-up are NOT providing medical advice. We do not recommend you start any exercise program without first consulting with your doctor!*

Save 20% on all Nuzest Products WORLDWIDE with the code MIKKIPEDIA at www.nuzest.co.nz, www.nuzest.com.au or www.nuzest.comThis week on the podcast Mikki speaks to Prof Vicki Vieira-Potter about sex differences in adipose tissue. They explore some of the surprising challenges and breakthroughs in research on adipose tissue and oestrogen, particularly post-menopause. They delve into the role of exercise in mitigating the metabolic risks associated with menopause and how certain compounds like ERb ligands and beta 3 adrenergic receptor agonists might mimic the effects of exercise at a molecular level. Finally, they discuss the impact of dietary choices, like a soy phytoestrogen-rich diet and almonds, on obesity, and how sleep restriction can influence our metabolism and glucose response.Can be found here https://insidescientific.com/profile/victoria-vieira-potter/Paper can be found here: https://www.ncbi.nlm.nih.gov/myncbi/victoria.vieira-potter.1/bibliography/public/Dr. Vicki Vieira-Potter is an Associate Professor in the Department of Nutrition and Exercise Physiology at the University of Missouri, Columbia (MU). Her laboratory studies how estrogen loss affects energy metabolism and focuses on brain and adipose tissue-specific mechanisms. She and her team have demonstrated that aerobic fitness and exercise are protective against metabolic complications associated menopause; they use a variety of animal models and biomolecular techniques to address these research questions. She directs the Rodent Metabolic Phenotyping Core at MU. Dr. Vieira-Potter holds an undergraduate degree from Wheaton College (Norton, MA), and graduate degrees from the University of New Hampshire and the University of Illinois at Urbana Champaign, respectively. She completed postdoctoral training at the at Tufts (HNRCA) where she focused on obesity and metabolism. She has 70+ peer-reviewed publications in the area of adipose tissue/cardiometabolic disease. Contact Mikki:https://mikkiwilliden.com/https://www.facebook.com/mikkiwillidennutritionhttps://www.instagram.com/mikkiwilliden/https://linktr.ee/mikkiwillidenCurranz supplement: MIKKI saves you 25% at www.curranz.co.nz or www.curranz.co.uk off your first order

Today, I'd like to discuss a study conducted by researchers in Germany.Dr. Manuel Cornely, a prolific author on lipedema, spearheaded this investigation.The paper, titled Assessing the Healthiness of Subcutaneous Adipose Tissue Expansion in Lipedema through Circulating Parameters, debuted in October 2022 within the pages of Frontiers in Endocrinology.

This podcast covers the insulin-dependent uptake of glucose by GLUT-4 in muscle and adipose tissue. This insulin-dependent uptake by these tissues contributes to the reduction of plasma glucose after a meal. Check out the link below for the video podcast: https://youtu.be/_vyijJKL4oY --- Send in a voice message: https://podcasters.spotify.com/pod/show/a-j-ghalayini/message

In this episode of the metabolic classroom, Dr. Ben Bikman takes the helm to explore the multifaceted role of fat tissue as an endocrine organ. He begins by challenging the conventional view of fat tissue as merely a storage depot for energy, emphasizing its crucial role in hormone production and regulation.Dr. Bikman introduces the concept of endocrine organs and highlights the often overlooked status of fat tissue as one such organ. He discusses how fat tissue releases hormones into the bloodstream, exerting significant metabolic effects throughout the body.The lecture delves into sex-specific differences in fat distribution and hormone production, with a focus on the influence of estrogen on fat storage and hormone levels in women. Dr. Bikman further explores the impact of menopause on fat tissue and hormonal changes, shedding light on how shifts in hormone production affect metabolism and fertility.Leptin, the first discovered fat-derived hormone, is dissected in detail by Dr. Bikman, who elucidates its role in appetite regulation, metabolic processes, and fertility. He discusses how excess fat can lead to leptin resistance, compromising its effectiveness in metabolic regulation.Other hormones such as adiponectin, estrogen, TNF alpha, plasminogen activator inhibitor 1 (PAI-1), and T3 are also explored for their metabolic effects and their association with fat cell size.The lecture concludes with a focus on brown adipose tissue and its production of T3, highlighting its role in regulating metabolic rate, particularly in response to stimuli like cold exposure.In summary, Dr. Bikman provides a comprehensive overview of the endocrine functions of adipose tissue, emphasizing the intricate relationship between fat cells and hormone regulation, with implications for metabolism, inflammation, and overall health.00:01 - Introduction to Adipose Tissue as an Endocrine Organ01:07 - Sex-Specific Differences in Fat Distribution03:21 - Impact of Menopause on Fat Tissue and Hormone Production05:45 - Endocrine Effects of Fat Distribution07:58 - Role of Fat Tissue in Aromatization and Estrogen Production10:13 - Impact of Fat Cell Size on Hormone Production12:24 - Detailed Exploration of Leptin14:45 - Examination of Adiponectin and its Metabolic Effects18:17 - TNF Alpha and its Impact on Inflammation and Insulin Resistance21:05 - Plasminogen Activator Inhibitor 1 (PAI-1) and its Implications for Clotting22:16 - Brown Adipose Tissue and its Production of T324:30 - Conclusion and Summary#insulinresistance #metabolicsyndrome #metabolichealth #type2diabetes #type1diabetes #weightloss #intermittentfasting #intermittantfasting #fasting #lowcarb Learn more at: https://www.insuliniq.com Hosted on Acast. See acast.com/privacy for more information.

Commentary by Dr. Candice Silversides and Dr. Valentin Fuster

Today's excerpt is from a complimentary webinar featuring Siobhan Huggins, made available by Lipedema Simplified as part of Lipedema Awareness Month in June 2021.In this segment, Siobhan delves into a comparison between obesity-related fat and lipedema fat, highlighting the distinctions and similarities.Furthermore, she explores the notion that lipedema may be linked to a connective tissue disorder.

In this flash briefing episode, Dr. Ken Sikaris explores the role of adipose tissue in humans as well as the various categories of fat tissue.

Many of us think of adipose tissue as just a place to store excess fat to be used for energy. However, adipose tissue is very biologically active and secretes some important hormones and mediators called adipokines. These messengers help regulate glucose and lipid metabolism, control hunger, and affect insulin levels. That being said, ALL of our hormones work together like a symphony – cortisol, thyroid hormones, sex hormones, and don't forget the adipokines. In today's episode, we discuss important bioactive messengers created by our fat tissue (leptin and adiponectin), how they affect us systemically, and strategies to optimize them. Today on The Lab Report: 3:40 Adipose tissue, adipokines, and types of fat 7:40 What are adipokines? 10:25 Adiponectin does great things 13:00 How to increase adiponectin 14:20 Better Know a Biomarker – Leptin! 17:40 Obesity and leptin resistance 19:25 Treating leptin resistance 21:35 Leptin vs. ghrelin 23:15 Adiponectin/leptin ratio Subscribe, Rate, & Review The Lab Report Thanks for tuning in to this week's episode of The Lab Report, presented by Genova Diagnostics, with your hosts Michael Chapman and Patti Devers. If you enjoyed this episode, please hit the subscribe button and give us a rating or leave a review. Don't forget to visit our website, like us on Facebook, follow us on Twitter, Instagram, and LinkedIn. Email Patti and Michael with your most interesting and pressing questions on functional medicine: podcast@gdx.net. And, be sure to share your favorite Lab Report episodes with your friends and colleagues on social media to help others learn more about Genova and all things related to functional medicine and specialty lab testing. To find a qualified healthcare provider to connect you with Genova testing, or to access select products directly yourself, visit Genova Connect. Disclaimer: The content and information shared in The Lab Report is for educational purposes only and should not be taken as medical advice. The views and opinions expressed in The Lab Report represent the opinions and views of Michael Chapman and Patti Devers and their guests.See omnystudio.com/listener for privacy information.

References Luigi Boccherini: Symphony Op. 12 No. 4 in D Minor JCI Insight. 2016 Nov 17; 1(19): e87748 Front Immunol. 2023; 14: 1149366 Adv Biol Regul.2019 Jan;71:41-54. Int. J. Mol. Sci. 2019, 20(6), 1505 --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support

Full article: https://www.ajronline.org/doi/10.2214/ajr.23.29570  Childhood obesity is a growing epidemic globally. Precisely quantifying abdominal fat distribution on MRI could be valuable for research and clinical care, but manual segmentation is extremely tedious. Farzaneh Ghazi Sherbaf, MD discusses a recent study in which the authors developed and validated an AI method to automatically segment subcutaneous and visceral abdominal fat on MRI in adolescents. The work has implications for making obesity research and care more effective through automated, personalized abdominal fat mapping.

Dr Glenn McConell chats with Professor David Wright from the University of British Columbia, Canada. He has undertaken a lot of important work on the effect of exercise on muscle glucose uptake and mitochondria and then has branched out to examine the effect of exercise training on mitochondria in adipose tissue (fat). We discussed his work around that and then talked about an interesting new focus of his work around the metabolic effects of antipsychotics. He is finding that exercise can prevent the acute blood glucose raising effects of antipsychotics. A very interesting chat.0:00. Introduction and how David got into research6:10. His transition from muscle to fat research10:05. Exercise activates AMPK in muscle and fat10:57. Adipose tissue breakdown during exercise13:58. Adrenaline/epinephrine15:28. Exercise training effects on fat mitochondria21:00. Why so much fat turnover during exercise24:00. Fat use during ex in lean vs obese26:25. Adrenaline regulation of fat adaptations to ex training29:50. AMPK regulation of fat32:05. Cross talk between organs during exercise34:55. White, beige, brown adipose tissue39:00. Human vs rodents brown adipose tissue44:25. Adipokines and exercise training48:40. Ectopic fat49:40. Antipsychotics, obesity and diabetes51:15. Each dose of an antipsychotic increases blood glucose53:00. Exercise prevents these glucose effects of antipsychotics59:00. GLP-1, glucagon and antipsychotics1:03:20. Poor exercise adherence, do fasting instead?1:05:15. Ketogenic diets and antipsychotics1:08:50. Ketogenic diets and mental health1:11:03. Clinicians awareness etc.1:12:45. Sex and age differences1:15:00. Acute vs chronic effects1:15:40. Takeaway messages1:19:27. Outro (9 seconds)Inside Exercise brings to you the who's who of research in exercise metabolism, exercise physiology and exercise's effects on health. With scientific rigor, these researchers discuss popular exercise topics while providing practical strategies for all.The interviewer, Emeritus Professor Glenn McConell, has an international research profile following 30 years of Exercise Metabolism research experience while at The University of Melbourne, Ball State University, Monash University, the University of Copenhagen and Victoria University.He has published over 120 peer reviewed journal articles and recently edited an Exercise Metabolism eBook written by world experts on 17 different topics (https://link.springer.com/book/10.1007/978-3-030-94305-9).Connect with Inside Exercise and Glenn McConell at:Twitter: @Inside_exercise and @GlennMcConell1Instagram: insideexerciseFacebook: Glenn McConellLinkedIn: Glenn McConell https://www.linkedin.com/in/glenn-mcconell-83475460ResearchGate: Glenn McConellEmail: glenn.mcconell@gmail.comSubscribe to Inside exercise:Spotify: shorturl.at/tyGHLApple Podcasts: shorturl.at/oFQRUYouTube: https://www.youtube.com/@insideexerciseAnchor: https://anchor.fm/insideexerciseGoogle Podcasts: shorturl.at/bfhHIAnchor: https://anchor.fm/insideexercisePodcast Addict: https://podcastaddict.com/podcast/4025218Not medical advice

In this flash briefing, Dr. Paul Mason explains the impact of heightened Lipoprotein Lipase (LPL) levels on individuals dealing with lipedema.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.28.550986v1?rss=1 Authors: Henry, R. J., Barrett, J. P., Vaida, M., Khan, N. Z., Makarevich, O., Ritzel, R. M., Faden, A. I., Stoica, B. A. Abstract: Obesity increases the morbidity and mortality of traumatic brain injury (TBI). We performed a detailed analysis of transcriptomic changes in the brain and adipose tissue to examine the interactive effects between high-fat diet-induced obesity (DIO) and TBI in relation to central and peripheral inflammatory pathways, as well as neurological function. Adult male mice were fed a high-fat diet (HFD) for 12 weeks prior to experimental TBI and continuing after injury. Combined TBI and HFD resulted in additive dysfunction in the Y-Maze, novel object recognition (NOR), and Morris water maze (MWM) cognitive function tests. We also performed high-throughput transcriptomic analysis using Nanostring panels of cellular compartments in the brain and total visceral adipose tissue (VAT), followed by unsupervised clustering, principal component analysis, and IPA pathway analysis to determine shifts in gene expression programs and molecular pathway activity. Analysis of cellular populations in the cortex and hippocampus as well as in visceral adipose tissue during the chronic phase after combined TBI-HFD showed amplification of central and peripheral microglia/macrophage responses, including superadditive changes in select gene expression signatures and pathways. These data suggest that HFD-induced obesity and TBI can independently prime and support the development of altered states in brain microglia and visceral adipose tissue macrophages, including the disease-associated microglia/macrophage (DAM) phenotype observed in neurodegenerative disorders. The interaction between HFD and TBI promotes a shift toward chronic reactive microglia/macrophage transcriptomic signatures and associated pro-inflammatory disease-altered states that may, in part, underlie the exacerbation of cognitive deficits. Targeting of HFD-induced reactive cellular phenotypes, including in peripheral adipose tissue macrophages, may serve to reduce microglial maladaptive states after TBI, attenuating post-traumatic neurodegeneration and neurological dysfunction. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Commentary by Dr. Valentin Fuster

References JCI Insight. 2016 Nov 17; 1(19): e87748. Graduate Biochemistry lecture archives-Guerra Nutrition. 2020 Oct;78:110935. --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message

Boosting Brown Fat: Metabolic Functions, Variations, and Strategies for Increasing Metabolic Rate Introduction: In recent years, there has been growing interest in brown adipose tissue (BAT) due to its unique metabolic properties and potential implications for combating obesity and related metabolic disorders. Brown fat is distinct from white adipose tissue (WAT) in terms of its color, cell composition, and metabolic functions. This essay aims to explore the complexities of the brown fat system, discussing the variations between brown and white fat, the mechanisms for increasing brown fat activity, the dangers of excessive white fat accumulation, and effective strategies to boost metabolic rate. I. Variations between Brown Fat and White Fat: Brown adipose tissue and white adipose tissue are two types of adipose (fat) tissues found in the human body, differing in their composition and functions. Brown fat is characterized by its high mitochondrial content, which gives it a brownish color, and the presence of a unique protein called uncoupling protein 1 (UCP1). In contrast, white fat stores energy in the form of triglycerides and primarily serves as a reservoir for energy storage. Listen to learn more! --- Support this podcast: https://podcasters.spotify.com/pod/show/healthfacts/support

Some Natural Ways To Lower Fatty Toxins In Adipose Tissue Dr. Joshua Helman, M.D.• https://www.healthpromoting.com/clinic-services/staff/joshua-helman-md #JoshuaHelman #WholeFood#PlantBased #Vegan #integrativemedicine  Dr. Joshua Helman, M.D., is a Harvard-trained physician licensed in fourteen states. He has two degrees in Biochemistry, (bachelor's from Harvard magna cum laude and master's from the University of Cambridge, UK). He is Board Certified by the American Board of Emergency Medicine and the American Board of Lifestyle Medicine. His medical degree (M.D.) is from Harvard Medical School and MIT. He has worked on the front lines in Emergency Rooms throughout this country over the past 20 years, where he has been shocked by the death and pain resulting from the increased incidence of chronic diseases. He is also the former Medical Director of Hippocrates Health Institute. His areas of interest include toxins, exosomes, mold, biofilm, Lyme disease, chronic neurologic diseases, trauma and fasting. As a plant-based physician, he embraces an integrative approach including the importance of diet and lifestyle for optimal health. Dr. Helman is inspired by patients' ability to change their bad habits and adopt a better lifestyle, in order to improve and sometimes reverse chronic diseases. His own journey to better health took roughly 10 years, so he is sympathetic with patients who face setbacks, struggles and challenges with their own changes. In his free time, he likes to exercise, travel and hike. To Contact Dr. Joshua Helman, M.D.https://www.healthpromoting.com/clinic-services/staff/joshua-helman-md Disclaimer:Medical and Health information changes constantly. Therefore, the information provided in this podcast should not be considered current, complete, or exhaustive. Reliance on any information provided in this podcast is solely at your own risk. The Real Truth About Health does not recommend or endorse any specific tests, products, procedures, or opinions referenced in the following podcasts, nor does it exercise any authority or editorial control over that material. The Real Truth About Health provides a forum for discussion of public health issues. The views and opinions of our panelists do not necessarily reflect those of The Real Truth About Health and are provided by those panelists in their individual capacities. The Real Truth About Health has not reviewed or evaluated those statements or claims. 

You step on to your bathroom scale, the room gets dim, and as you see the higher than expected number, a blood curdling scream comes out…YOU ARE FAT is written on the mirror in chocolate. (A little dramatic but did I get the tone right?)Look, YOU are not fat; you just have fat. And there is absolutely no human trait directly related to extra adipose tissue. But it is normal to have a weight range (an amount of fat) you are comfortable with, and when that number has creeped up, it's also normal to feel uncomfy.So, like, what do you do?First, DONT FREAK THE FUCK OUT. It is what it is; don't let it take over your personality, don't jump to extremes, don't hop aboard the yo yo diet train...  Just calmly and collectively make your way to step two.CURIOSITY AND CALM COURSE COLLECTION. Hmmmm, this fat didn't get here all on its own; something happened. But what? Reflect on your habits, make a hypothesis, and then test that hypothesis in a calm, simple way.Lastly, all the while…DO IT FAT. (By IT, I mean life, sex, self love, shopping, beach trips, you name it.) Don't put your life on hold for a thinner self; ultimately, the confidence and self love you need to become thin happens when you're fat.But for real, letting your habits slip is not evil, consuming more calories than you're expending does not make you a bad person.  It's all just information.Listen all the way to the end of the episode for an update on the pod. Chat soon!What's Inside:Why do you feel so strongly about extra adipose tissue?3 steps for when the scale is creeping up and you're uncomfy.Embodying confidence, self love, and the do anything attitude—even when you're fat.This episode we talked about being fat, but I've talked about a lot of goals and grit and well you know the name of the show…what was your favorite? What do you want to see more of?Let me know on Insta!Mentioned In This Episode:Fit Feels Goodinfo@fitfeelsgood.comOonagh on Insta

What is brown fat?Brown fat, also called brown adipose tissue, is a type of body fat that keeps you warm when you get cold. Brown fat also stores energy and helps your body burn calories. Brown fat starts working (activates) in cold temperatures.What are the types of fat in my body?There are different types of fat in your body. Healthcare providers identify each type of fat by its color and function, including:White fat: Most of the fat in your body is white fat. White fat stores energy in various places around your body. White fat insulates your organs. Too much white fat leads to obesity.Brown fat: Brown fat is smaller than white fat. It stores energy and burns that energy to regulate your body temperature. Brown fat helps you burn calories by creating heat right before your body starts to shiver (thermogenesis). It also helps regulate sugar (glucose) and fat metabolism.Beige fat: Beige fat is a combination of white and brown fat cells. These cells burn calories to regulate body temperature by converting white fat cells to brown.

Saturday Rant: Do not make this dieting mistake  Sign up here to do the 5 for 50 challenge with us! If you enjoyed this episode, make sure and give us a five star rating  and leave us a review on iTunes, Podcast Addict, Podchaser and Castbox. Sign up for the next Follow-Through Challenge Follow me on Social Media:Amy on IGAmy on FacebookCheck out the Amy Ledin WebsiteJoin the Follow-Through Challenge offered every 6 weeksAmy Ledin's 16-week Fat Loss Academy Resources:Lean Bodies Consulting (LBC)Follow LBC on IGCheck out the LBC Community on FBLBC University#5for50 #5for50FamilyEdition #AmyLedin #AmyLedin.com #ErikLedin #LeanBodiesConsulting #LBC #Kamele #KamelePerez  

Commentary by Dr. Valentin Fuster

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.09.527726v1?rss=1 Authors: Inoue, O., Goten, C., Hashimuko, D., Yamaguchi, K., Takeda, Y., Nomura, A., Ootsuji, H., Takashima, S., Iino, K., Takemura, H., Halurkar, M., Lim, H.-W., Hwa, V., Sanchez-Gurmaches, J., Usui, S., Takamura, M. Abstract: Therapeutic angiogenesis using mesenchymal stem/stromal cell grafts have shown modest and controversial effects in preventing amputation for patients with critical limb ischemia. Through single-cell transcriptomic analysis of human tissues, we identified CD271+ progenitors specifically from subcutaneous adipose tissue (AT) as having the most prominent pro-angiogenic gene profile distinct from other stem cell populations. AT-CD271+ progenitors demonstrated robust in vivo angiogenic capacity, over conventional adipose stromal cell grafts, characterized by long-term engraftment, augmented tissue regeneration, and significant recovery of blood flow in a xenograft model of limb ischemia. Mechanistically, the angiogenic capacity of CD271+ progenitors is dependent on functional CD271 and mTOR signaling. Notably, the number and angiogenic capacity of CD271+ progenitors was strikingly reduced in insulin resistant donors. Our study highlights the identification of AT- CD271+ progenitors with in vivo superior efficacy for limb ischemia. Furthermore, we showcase comprehensive single-cell transcriptomics strategies for identification of suitable grafts for cell therapy. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.02.526843v1?rss=1 Authors: Tsai, P.-Y., Shui, B., Lee, S., Liu, Y., Qu, Y., Cheng, C., Edwards, K., Wong, C., Meng-Killeen, R., Soloway, P., Barrow, J. J. Abstract: Non-shivering thermogenesis (NST) has strong potential to combat obesity, however, a safe molecular approach to activate this process has not yet been identified. The sulfur amino acid taurine has the ability to safely activate NST and confer protection against obesity and metabolic disease in both mice and humans, but the mechanism of action is unknown. In this study, we discover that a suite of taurine biosynthetic enzymes, especially that of cysteamine dioxygenase (ADO), significantly increases in response to beta-3 adrenergic signaling in inguinal tissues (IWAT) in order increase intracellular concentrations of taurine. We further show that ADO is critical for thermogenic mitochondrial function as its ablation in thermogenic adipocytes significantly reduces taurine levels which lead to declines in mitochondrial oxygen consumption rates. Finally, we demonstrate via assay for transposase-accessible chromatin with sequencing (ATAC-Seq) that taurine supplementation has the ability to remodel the chromatin landscape to increase the chromatin accessibility and transcription of genes, such as glucose-6-phosphate isomerase 1 (Gpi1), that are critical for NST. Taken together, our studies highlight a potential mechanism for taurine in the activation of NST that can be leveraged toward the treatment of obesity and metabolic disease Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

This week we welcome Dr. Ryan Banting back to the podcast! Listen in as we discuss the "tripledemic," flu shots, weightloss, improving health vs. treating illness, the Liver King being full of more than just liver, and more. Host: Cale Matthews Audio Engineer: Art Pipok Visit us at solid7podcast.com to rate the show, buy us a Jocko Go, see upcoming events, follow us on social media, support worthy causes, and become a Patreon supporter.

Brown fat can help you lose weight!

This podcast describes the specific metabolic effects of insulin on liver, muscle and adipose tissue. Similar content is available at: MEDBIOCHEM.ORG --- Send in a voice message: https://anchor.fm/a-j-ghalayini/message

Back to school means back to structure! It's time to reset, renew and rebuild your routine so you can get back on track to crushing your body transformation goals and getting the most out of your training plan. In this one-on-one chat with coach Jenny, she shares with us the most common mistakes she sees regularly that can hinder your weight loss results or have a negative impact on your progress and performance.  JOIN The YOUR BEST BODY PRIVATE COMMUNITY and for the Password say "Jenny invited me"JOIN The YOUR BEST BODY PROGRAM If you enjoyed this episode, make sure and give us a five star rating  and leave us a review on iTunes, Podcast Addict, Podchaser and Castbox. STRONG Fitness Magazine Subscription Use discount code STRONGGIRLResourcesSTRONG Fitness MagazineSTRONG Fitness Magazine on IGTeam Strong GirlsCoach JVBFollow Jenny on social mediaInstagramFacebookYouTube  

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.08.25.505298v1?rss=1 Authors: Willows, J. W., Gunsch, G., Paradi, E., Blaszkiewicz, M., Tonniges, J. R., Pino, M. F., Smith, S. R., Sparks, L. M., Townsend, K. L. Abstract: Peripheral neuropathy is a pathophysiological state of nerve degeneration and loss of tissue innervation. The most prominent cause of small fiber neuropathy is diabetes which can be demyelinating in nature, but this has not yet been explored in adipose tissue. Both demyelinating neuropathies and axonopathies implicate Schwann cells (SCs), the peripheral glial required for nerve myelination and regeneration after injury. Here, we perform a comprehensive assessment of SCs and myelination patterns of subcutaneous white adipose tissue (scWAT) nerves, including changes that occur with obesity and other imbalanced energy states in mice and humans. We found that mouse scWAT is densely innervated by both myelinated and unmyelinated sensory and sympathetic nerves. Accordingly, scWAT is home to both myelinating and non-myelinating SCs; the greater proportion of which are myelinating. Furthermore, SCs were found closely associated with synaptic vesicle-containing nerve terminals in scWAT. Obese BTBR ob/ob mice exhibit diabetic peripheral neuropathy in scWAT, and display concordant demyelination specific to small fibers, which was also associated with a decrease in the pan-SC marker Sox10 and compensatory increase in Krox20 gene expression. Together this suggests that adipose SCs may be involved in regulating the plasticity or the neuropathy of adipose tissue nerves. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

Welcome back to Hunger Hunt Feast! Listen in as Zane Griggs and guest J. Gulinello, M.S.discuss the Effect Of Seed Oils On Mitochondria, Animal Food Benefits & The War On Meat and much more.  QUICK NOTES FROM ZANE: The effect of processed vegetable oils aka seed oils on metabolic health Increased concentrations of linoleic acid in human fat tissue Linoleic acid has a half-life of 680 days in the human body Benefits of animal protein and micronutrients in animal foods The agenda to move people away from eating meat by international organizations   Links For This Episode:  Ancestral Wellness Retreat: October 6, 2022 in Martha's Vineyard https://www.perpetualhealth.co   Selected Psychological Aspects of Meat Consumption https://pubmed.ncbi.nlm.nih.gov/30223443   Linoleic Concentrations in Adipose Tissue https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4642429/   Type 2 Diabetes Blamed On Egg Consumption https://pubmed.ncbi.nlm.nih.gov/19017774/   Re-evaluation of the Minnesota Coronary Experiment  https://www.bmj.com/content/353/bmj.i1246   Re-evaluation of the Sydney Diet Heart Study https://pubmed.ncbi.nlm.nih.gov/23386268/   www.perpetualhealth.co IG: @perpetualhealthco   Connect with Zane: ReLyte Electrolytes by Redmond Real Salt: https://shop.redmond.life?afmc=Zane Follow me on Instagram: https://www.instagram.com/zanegriggsfitness Follow me on YouTube: https://www.youtube.com/c/ZaneGriggs QUICK EPISODE SUMMARY Welcome back J. Gulinello, M.S. The impact of highly concentrated Linoleic acid on the body The chronic effects of seed oils What happens when toxins enter the mitochondria J's two favorite studies on seed oils  The Bitcoin and Beef paradigm  The real health benefit of animal foods  Are all kinds of bacteria bad for humans? The truth we have known for 1935 and longer What The WHO says about meat consumption  A look into J's upcoming events   

Jenny sits down with Team STRONG Girls franchisee owner and recent cover athlete Jaclyn Phillips, who returns for her second podcast sesh to talk about the coveted “X-frame” - the antidote to aging and ultimate form goal that our STRONG coaching business focuses on. Jac draws on her many years of fitness training to reveal the top 5 mistakes women make when growing their glutes and how to avoid and correct common practices that simply don't help us build the muscle and frame we aspire to have.  Important Links:Get Jac's STRONG Fitness Magazine May/June 2022 issue here: STRONG - Jaclyn Phillips (simplecirc.com)Jac's first episode -  Breaking the Shame of Mental Illness with Jaclyn Phillips FREE GLUTE GUIDE: https://getjacd.lpages.co/glute-activationFollow Jac on IG: @jaqioh  JOIN The YOUR BEST BODY PRIVATE COMMUNITY and for the Password say "Jenny invited me"JOIN The YOUR BEST BODY PROGRAM   If you enjoyed this episode, make sure and give us a five star rating  and leave us a review on iTunes, Podcast Addict, Podchaser and Castbox. STRONG Fitness Magazine Subscription Use discount code STRONGGIRLResourcesSTRONG Fitness MagazineSTRONG Fitness Magazine on IGTeam Strong GirlsCoach JVBFollow Jenny on social mediaInstagramFacebookYouTube   

When going on vacation or attending a special occasion, it can be stressful when you've been on plan. Amy discusses how to not stress over it, make a decision, and follow through.    If you enjoyed this episode, make sure and give us a five star rating  and leave us a review on iTunes, Podcast Addict, Podchaser and Castbox. Sign up for the next Follow-Through Challenge Follow me on Social Media:Amy on IGAmy on Facebook Resources:AmyLedin.comLean Bodies Consulting (LBC)LBC University  

Hi friends!! This episode is about Activating Fat to Make it Metabolically Active! Brown & Beige Adipose Tissue (BAT) & "Browning" White Adipose Tissue; Wasting Energy with Mitochondrial Uncoupling and UCP1 Introducing the brand new TONE Device! Struggling to lose weight or reach your fitness goals? The TONE is a new breath acetone meter which lets you know if your body is burning fat and  how much! All TONE devices are NOW SHIPPING Worldwide!! Order the Black & Gold TONE HERE Order the Black & Rose Gold TONE HERE Get Your FREE ebook on keto: https://www.ketogenicgirl.com/pages/free-ebook Try the Higher Protein Keto Meal Plans & Coaching: https://www.ketogenicgirl.com Special thank you to Fast Keto sponsors: Try Athletic Greens! ONE tasty scoop of Athletic Greens contains 75 vitamins, minerals and whole food-sourced ingredients, including a multivitamin, multimineral, probiotic, greens superfood blend and more, that all work together to fill the nutritional gaps in your diet, increase energy and focus, aid with digestion and supports a healthy immune system, all without the need to take multiple products or pills. Visit www.athleticgreens.com/ketogenicgirl and join health experts, athletes and health conscious go-getters around the world who make a daily commitment to their health every day. Again, simply visit www.athleticgreens.com/ketogenicgirl and get your FREE year supply of Vitamin D and 5 free travel packs today. Pregnant or nursing women should seek professional medical advice before taking this or any other dietary supplement. - ButcherBox is offering new members a free Grilling Bundle in their first order. This is a deal you don't want to miss! Sign up at butcherbox.com/FASTKETO  and get two, 10 oz ribeyes, 5 pounds of chicken drumsticks, and a pack of burgers for FREE. That's butcherbox.com/FASTKETO to claim this deal! - Prior to beginning a new diet you should undergo a health screening with your physician to confirm that a new diet is suitable for you and to rule out any conditions and contraindications that may pose risks or are incompatible with a new diet, including by way of example: conditions affecting the kidneys, liver or pancreas; muscular dystrophy; pregnancy; breast-feeding; being underweight; eating disorders; any health condition that requires a special diet [other conditions or contraindications]; hypoglycemia; or type 1 diabetes. A new diet may or may not be appropriate if you have type 2 diabetes, so you must consult with your physician if you have this condition. Anyone under the age of 18 should consult with their physician and their parents or legal guardian before beginning such a diet. Use of Ketogenic Girl videos are subject to the Ketogenicgirl.com Terms of Use and Medical Disclaimer. All rights reserved. If you do not agree with these terms, do not listen to, or view any Ketogenic Girl podcasts or videos.  

***JOIN THE FASTING LIFESTYLE CHALLENGE THAT STARTS JULY 20, 2022! -New to fasting or want to get back on track? -Struggling to break through a plateau? -Ready to finally stop obsessing about your diet? We'll teach you how to finally LOSE weight for good and use 'fast cycling' to achieve uncommon results! Join us JUNE 1st for the Fasting Lifestyle Challenge!  REGISTER HERE! Click the Link for DATES, DETAILS, and FAQ's! https://www.thefastingforlife.com/live   In this episode, Dr. Scott and Tommy discuss some of the additional benefits of fasting when compared to a low-calorie type diet or caloric restriction, intermittent energy restriction ameliorates adipose tissue-associated inflammation in adults with obesity.   Show Transcript: www.thefastingforlife.com/blog   Let's continue the conversation. Click the link below to JOIN the Fasting For Life Community, a group of likeminded, new and experienced fasters! The first two rules of fasting need not apply!   Fasting For Life Community - Join HERE   This week in the community…   New to the podcast and wondering where to start? Head to the website and download our FREE Fast Start Guide, 6 simple steps to put One Meal a Day Fasting (OMAD) into practice!   Maybe you are an experienced faster and wondering about your results and IF they could be linked to INSULIN resistance? Head over to the website and download our FREE Insulin Resistance Assessment!   Or get both here at our website:  www.thefastingforlife.com/resources   If you enjoy the podcast, would you please tap on the stars below and consider leaving a short review on Apple Podcasts/iTunes? It takes less than 60 seconds, and it makes a difference in helping bring you the best original content each week. We also really enjoy reading them!   Sign up for the Fasting For Life newsletter at www.thefastingforlife.com   Follow Fasting For Life: www.facebook.com/thefastingforlife www.instagram.com/thefastingforlife   Join the Community on Facebook!   Reference Links: Intermittent energy restriction ameliorates adipose tissue-associated inflammation in adults with obesity: A randomised controlled trial https://pubmed.ncbi.nlm.nih.gov/28446382/

Hi friends!! This episode is all about Ice Baths for Fat Loss: What is Cold Induced Thermogenesis, Brown Adipose Tissue & More on This Biohack! We define what Cold Induced Thermogenesis (CIT) and  Brown Adipose Tissue (BAT) is, all the research behind it and  fat loss, and also how they are implemented. This podcast is for informational purposes only and is not a recommendation, cold exposure has risks including shock and hypothermia and anyone listening must check with their doctor that this is a safe practice for them before attempting it. Supervision is also a good idea for anyone doing ice baths due to the aforementioned risks. Introducing the brand new TONE Device! Struggling to lose weight or reach your fitness goals? The TONE is a new breath acetone meter which lets you know if your body is burning fat!  All TONE devices are NOW SHIPPING Worldwide!! Order the Black & Gold TONE HERE Order the Black & Rose Gold TONE HERE Follow @optimalproteinpodcast on Instagram to see visuals and posts mentioned on this podcast. Link to join the facebook group for the podcast: https://www.facebook.com/groups/2017506024952802/ Follow Vanessa on instagram to see her meals, recipes, informative posts and much more! Click here @ketogenicgirl Try the Higher Protein Keto Meal Plans & Coaching: https://www.ketogenicgirl.com- Prior to beginning a ketogenic diet you should undergo a health screening with your physician to confirm that a ketogenic diet is suitable for you and to rule out any conditions and contraindications that may pose risks or are incompatible with a ketogenic diet, including by way of example: conditions affecting the kidneys, liver or pancreas; muscular dystrophy; pregnancy; breast-feeding; being underweight; eating disorders; any health condition that requires a special diet [other conditions or contraindications]; hypoglycemia; or type 1 diabetes. A ketogenic diet may or may not be appropriate if you have type 2 diabetes, so you must consult with your physician if you have this condition. Anyone under the age of 18 should consult with their physician and their parents or legal guardian before beginning such a diet. Use of Ketogenic Girl videos are subject to the Ketogenicgirl.com Terms of Use and Medical Disclaimer. All rights reserved. If you do not agree with these terms, do not listen to, or view any Ketogenic Girl podcasts or videos.  

Today's guest is returning for round 2 on Jenny's podcast, and this time we're diving deep into intermittent fasting! Rita Catolino, who is now a regular contributor to STRONG Fitness Magazine, shares with us her insight on the benefits of fasting and how to approach and structure your fasting based on your lifestyle and goals. Her perspective helps us understand the purpose and formula of intermittent fasting, and the importance of giving our bodies what we need for optimum wellness and digestion. BIO:Rita Catolino B.A. Certified Trainer Health and Wellness Expert Best Selling Author Health Revolution 12-week Program (Sweden) Over 13 years' experience helping people transform their lives through proper nutrition, training and other methods.  Programs include 4 Weeks To Fab, 12 Week Transformation ProgramCover model, fitness columnist, retired bikini competitor, mom of 2.  JOIN The YOUR BEST BODY PRIVATE COMMUNITY and for the Password say "Jenny invited me"JOIN The YOUR BEST BODY PROGRAM If you enjoyed this episode, make sure and give us a five star rating  and leave us a review on iTunes, Podcast Addict, Podchaser and Castbox. STRONG Fitness Magazine Subscription Use discount code STRONGGIRLResourcesSTRONG Fitness MagazineSTRONG Fitness Magazine on IGTeam Strong GirlsCoach JVBFollow Jenny on social mediaInstagramFacebookYouTube    

Create a character specifically in the area, like dieting, that we're trying to level up so we have clarity on how we should behave. Sometimes when we're dieting, when we're on plan, we're on plan and when we're off plan, I don't even know who we're trying to represent!  We need to create a character who embodies how we should behave. If you enjoyed this episode, make sure and give us a five star rating  and leave us a review on iTunes, Podcast Addict, Podchaser and Castbox. Sign up for the next Follow-Through Challenge Follow me on Social Media:Amy on IGAmy on Facebook Resources:AmyLedin.comLean Bodies Consulting (LBC)LBC University 

I dagens episode snakker jeg om myten rundt Detox. Jeg leste her om dagen en artikkel som startet med å si MYTE at detox renser kroppen, og som fortsatte å si at detox var helt unødvendig fordi kroppen renser seg selv helt naturlig… Så her er mine tanker rundt det hele, hva tenker jeg er typiske signaler eller symptomer for oss å se etter når leveren er overarbeidet og noen tips du kan fokusere på! Hvis du trenger hjelp til å knekke din energikode, så tilbyr jeg alle som er klar til å prioritere helsa si en gratis kartleggingssamtale: du kan booke den HER Referanser til forskning rundt leveren: Genuis SJ, Kyrillos E. The chemical disruption of human metabolism. Toxicol Mech Methods. 2017 Sep;27(7):477-500. doi: 10.1080/15376516.2017.1323986. Epub 2017 Jun 7. PMID: 28446067. Hodges RE, Minich DM. Modulation of Metabolic Detoxification Pathways Using Foods and Food-Derived Components: A Scientific Review with Clinical Application. J Nutr Metab. 2015;2015:760689. doi:10.1155/2015/760689 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4488002/ Jackson, E., Shoemaker, R., Larian, N., & Cassis, L. (2017). Adipose Tissue as a Site of Toxin Accumulation. Comprehensive Physiology, Volume 7, Issue 4, P. 1085–1135. Ziem G, McTamney J (1997). Profile of Patients with Chemical Injury and Sensitivity. Environmental Health Perspectives. Volume 105, (Suppl 2), pp 417–436. Valussi, M., (2011). Functional foods with digestion-enhancing properties. International Journal of Food Sciences and Nutrition, Volume 63 (sup1), pp.82-89. Hodges, R. and Minich, D., 2015. Modulation of Metabolic Detoxification Pathways Using Foods and Food-Derived Components: A Scientific Review with Clinical Application. Journal of Nutrition and Metabolism, Volume 2015, pp.1-23. Les mer om Energikode HER og du kan følge Mari på instagram for å få lære enda mer. Book en gratis kartleggingssamtale med Mari HER

We spend so much time talking about fat loss and dieting, that most people just expect the other side of getting to their goal as the easy part, which is not true. Stats show that 95% of people gain their weight back within 3-5 years. This would confirm that where people struggle the most- keeping off the weight thus never needing to diet again. This is not talked about enough. And something I plan to talk about more and more as I see less and less women have lasting change in that they keep it off forever.  References: Creating Food RulesFollow-Through Challenge If you enjoyed this episode, make sure and give us a five star rating  and leave us a review on iTunes, Podcast Addict, Podchaser and Castbox. Sign up for the next DAC Bootcamp Follow me on Social Media:Amy on IGAmy on Facebook Resources:AmyLedin.comLean Bodies Consulting (LBC)LBC University 

He's back! My guess is that you have come from the same era as me in that you have had this idea that cardio is necessary for fat loss. Maybe you have even taken it as far as me where at my peak, I was doing an hour + of cardio just to maintain. When I hired Lean Bodies Consulting 13 years ago, this was an area that Erik really changed the amount I did on a weekly basis. He also taught me that doing more of the popular intense cardio (or crossfit, orange theory, metabolic circuits) actually works against you as you get older. I knew that YOU all need to get an earful like I once did, and jump off the crazy train of doing tons of cardio. Erik dives in with the science behind it all.  References: Escalade vs Honda CivicTo Become an LBC ClientWebsite/ArticlesLean Bodies Consulting on FaceBook If you enjoyed this episode, make sure and give us a five star rating  and leave us a review on iTunes, Podcast Addict, Podchaser and Castbox. Sign up for the next DAC Bootcamp Follow me on Social Media:Amy on IGAmy on Facebook Resources:AmyLedin.comLean Bodies Consulting (LBC)LBC University  

There is a proven link between obesity and more severe cases of COVID-19 and that link is inflammatory hormones and visceral belly fat. Dr. Ashley Lucas, founder of PHD Weight Loss, shares how to drop visceral belly fat FOR GOOD. She shares why it's important to fully collapse this organ so that weight maintenance is easier. We also discuss personal carb thresholds, or your personal carb tolerance as it relates to your ability to lose weight. This was a fascinating interview and we covered a lot! Here are the highlights:Things Dr. Lucas learned in registered dietician school that she has flipped upside down for type 2 diabetes. Why getting rid of excess visceral fat is critical to maintain your weight loss and prevent regain. PHD Weight Loss Protocol including nutrition, behavioral, and emotional aspects. Why obesity is linked to a more severe COVID-19 response due to the link between interleukin-6, cytokines, visceral fat, and COVID. How adipose tissue (fat) is an actual endocrine organ and how to get rid of it.How to determine your own personal carbohydrate threshold - why some people can eat more carbs and maintain their weight than others. Why exercise is great for wellness, but not that helpful for weight loss. Why visceral fat leads to more food cravings.Why losing the mental weight is VITAL to losing and keeping off physical weight.  CoachingIf you're ready to lose the weight for good, you've come to the right place!Join our online course and coaching program Zivli, to learn the science behind weight loss and habit change so you can lose weight, get healthy, and prevent disease.To learn more, go to https://www.zivli.com/join. Free Weight Loss ResourcesWeight Loss Masterclass to Lower Insulin Resistance & InflammationHow to Actually Reach Your Goals | Free Weight Loss Mindset TrainingThe Ultimate Food Guide | What to Eat to Burn Fat Connect on Social>> Subscribe to My YouTube Channel>> Like My Facebook Page>> Follow Me on Instagram>> Connect on LinkedIn>> View My Website Connect with Dr. Ashley Lucas>> Follow on Instagram>> View Her Website Subscribe & Review in Apple PodcastsAre you subscribed to my podcast? If you're not, I want to encourage you to do that today. I don't want you to miss an episode. Click here to subscribe in Apple Podcasts.Now if you're feeling extra loving, I would be really grateful if you left me a review over on Apple Podcasts, too. Those reviews help other people find my podcast and they're also fun for me to go in and read. Just click here to review, select “Ratings and Reviews” and “Write a Review” and let me know what your favorite part of the podcast is. Thank you!

If you enjoyed this episode, make sure and give us a five star rating  and leave us a review on iTunes, Podcast Addict, Podchaser and Castbox.  Sign up for the next DAC Bootcamp  Follow me on Social Media:Amy on IGAmy on Facebook  Resources:AmyLedin.comLean Bodies Consulting (LBC)LBC University  Amy Ledin Bio: The Co-Owner and Operator at Lean Bodies Consulting. Amy Ledin has been in the online wellness space for over a decade. Her coaching in this space has led to her passion in helping women build strong personal integrity. Fighting cancer for now close to 7 years, Amy loves sharing her mindset hacks and strategies that helped her through her fight to not just be a survivor, but an overcomer. 

Steve clearly lets us know what caused the stands to collapse in Washington. The crew also talk about the cognitive function of Antonio Brown. Learn more about your ad-choices at https://www.iheartpodcastnetwork.com

If you want to improve your metabolic health, you might turn to common methods like eating enough protein or getting a good night's rest. I'm a big proponent of both of those strategies, but there's another key player in this equation that doesn't get enough attention—brown adipose tissue.  Brown adipose tissue, or brown fat, is a distinct type of body fat that plays multiple roles in the body, including maintaining body temperature, improving insulin sensitivity and metabolic function, and more. Specifically, when it comes to metabolic health the function and responsibility of brown fat is often overlooked, but the science is fascinating.  On today's show, we're taking you behind the scenes of brown adipose tissue to gain a better understanding of what it is and how it works. You're also going to learn specific action steps you can take to influence your body's brown fat ratios and functionality for better metabolic health. I hope this episode gives you the knowledge and tools you need to improve your health and reach your goals. Enjoy!  In this episode you'll discover: A distinction between brown fat and white fat. The main function of brown fat (and why infants have high levels of this fat). What gives brown fat its brown color.  The link between brown fat levels and metabolic function. What beige fat is and how it works. Where brown fat is located in the body.  What themogenin is and how it works. The surprising role that brown fat plays in an obese body. How brown fat impacts the endocrine, cardiovascular, and immune system. The effects cold exposure has on brown adipose tissue activation. How long-term mild cold exposure can stimulate brown fat growth. Which foods are helpful in influencing the activity of brown adipose tissue.  The connection between dietary cholesterol and body fat. How (and why) to incorporate sea vegetables into your diet. The importance of consuming essential fatty acids.  How exercise can increase the production of brown fat. Items mentioned in this episode include: Foursigmatic.com/model -- Get an exclusive discount on your daily health elixirs! Beekeepersnaturals.com/model -- Get a special 25% discount on natural remedies! Do These Things to Have More Energy with Dr. Andrew Huberman – Episode 523 The 3 Dominant Fats of the Brain – Episode 496 Join TMHS Facebook community - Model Nation  Be sure you are subscribed to this podcast to automatically receive your episodes:  Apple Podcasts Stitcher Spotify Soundcloud *Download Transcript

If you enjoyed this episode, make sure and give us a five star rating  and leave us a review on iTunes, Podcast Addict, Podchaser and Castbox.  Sign up for the next DAC Bootcamp  Follow me on Social Media:Amy on IGAmy on Facebook  Resources:AmyLedin.comLean Bodies Consulting (LBC)LBC University  Amy Ledin Bio: The Co-Owner and Operator at Lean Bodies Consulting. Amy Ledin has been in the online wellness space for over a decade. Her coaching in this space has led to her passion in helping women build strong personal integrity. Fighting cancer for now close to 7 years, Amy loves sharing her mindset hacks and strategies that helped her through her fight to not just be a survivor, but an overcomer.   

Commentary by Dr. Valentin Fuster

How nutritional ketosis affects immunity. We discuss Covid-19 and metabolic function and the relationship between inflammation and immune function. As well as, the role of insulin dysfunction and excess adipose tissue and immune function.  Thank you to our sponsors: Athletic Greens - athleticgreens.com/stephanieOrion Red Light Therapy - Use promo code STEPHANIE10 for 10% off - https://www.orionrlt.ca/?ref=StephanieLumen - Use promo code DRSTEPHANIE25 for $25 Dollars off - https://www.lumen.me/LMNT Electrolytes - FREE 7 flavor sample pack at http://drinklmnt.com/DrEstimaPRIMADINE - Code DRSTEPHANIE10 for 10% off -https://oxfordhealthspan.com/discount/DRSTEPHANIE10Ancestral Supplements - Use Promo code ASA10 takes 10% off any purchase- https://ancestral-supplements.myshopify.com/?rfsn=5900205.652074&utm_source=refersion&utm_medium=affiliate&utm_campaign=5900205.652074Some of the links above are affiliate links. Making a purchase through these links won't cost you anything (and in many cases give you a discount), but we will receive a small commission. This is an easy, free way of supporting the podcast. Thank you! Social: https://www.instagram.com/dr.stephanie.estimahttps://www.facebook.com/groups/betterwithdrstephanie Membership Site:https://hellobetty.club/  Episode Overview: 5:53 Introduction7:43 Inflammation and Immune Function9:20 Covid-1913:20 Therapeutic Ketosis18:08 Ketosis and Metabolic Function24:02 Insulin26:20 Adipose Tissue34:46 Fiber and Carb Timing38:26 Estima Diet42:49 Conclusion Episodes Referenced: David Sinclair EpisodeDom D'agostino Episode  Studies Referenced: https://academic.oup.com/ajcn/advance-article/doi/10.1093/ajcn/nqab270/6369073https://www.medrxiv.org/content/10.1101/2021.07.08.21260210v1.full.pdf  More information about the book at The Betty Body Book Join the Betty Booty ChallengeJoin the Hello Betty Community here! 

Here Windy Cole, DPM, CWSP shares information on adipose tissue grafting and new innovations surrounding this treatment modality.

A 2016 study found that more than 50% of the population said they'd prefer public spaces like offices, hotels, airplanes and healthcare facilities be fragrance-free. Despite this, fragrance use is ubiquitous: it's found in everything from perfumes, beauty products, and cleaning supplies to plastics, paints, and disinfectants. The problem with these synthetic and artificial fragrances is the health effects they can have on our bodies. Chemicals used to create or prolong these “fresh” scents often have deleterious effects on our health like neurological, metabolic, respiratory, and hormonal imbalances. Today's episode continues the summer series, answering your questions about hormones. Listen in as Erin gets into the nitty gritty answering your questions about fragrance effects on hormone health, and lays out what to be aware of in products we often use on our bodies or in our home. This is a topic everyone can benefit from because most people don't even know how toxic synthetic fragrances are, nor how pervasive they are in products many of us use daily. In this episode: -Small steps we can take to get closer to non toxic living [4:38] -Starting with the basics [6:56] -Fragrance and endocrine disruptors [8:11] -“Overly sensitive” or canaries in the coalmine? [11:30] -A non exhaustive list of product types that contain artificial or synthetic fragrances [13:02] -The real problem with fragranced products [17:16] -How these fragrances can affect our health [19:28] -Why and how synthetic fragrances linger [22:17] -VOCs: what they are and common sources [23:36] -Best way to protect yourself from outdoor pollution [25:27] -Let's talk about phthalates [26:08] -Xenoestrogens and estrogen dominance [27:58] -How these chemicals impact our metabolism [29:55] -Mitochondrial dysfunction symptoms [32:11] Resources mentioned: Your Hormone Revival™ (get on the waitlist - next round starts Sept 19th!) https://www.erinholthealth.com/hormones Forrester Cabinets: https://forrestercabinets.com/ Research articles about fragrance: FRAGRANCE IN THE WORKPLACE IS THE NEW SECOND-HAND SMOKE http://www.national-toxic-encephalopathy-foundation.org/fragsmoke.pdf Scientific American's Scent of Danger: Are There Toxic Ingredients in Perfumes and Colognes https://www.scientificamerican.com/article/toxic-perfumes-and-colognes/ The Danger of Toxic Consumer Products, Fragrances https://www.huffpost.com/entry/toxic-chemicals_b_625648 Fragranced consumer products: exposures and effects from emissions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5093181/ Investigation of relationships between urinary biomarkers of phytoestrogens, phthalates, and phenols and pubertal stages in girls https://pubmed.ncbi.nlm.nih.gov/20308033/ Phthalates induce proliferation and invasiveness of estrogen receptor-negative breast cancer through the AhR/HDAC6/c-Myc signaling pathway https://pubmed.ncbi.nlm.nih.gov/22049059/ Exposure to Environmental Endocrine Disruptors and Child Development https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3572204/ Baby Care Products: Possible Sources of Infant Phthalate Exposure https://pediatrics.aappublications.org/content/121/2/e260?sso=1&sso_redirect_count=1&nfstatus=401&nftoken=00000000-0000-0000-0000-000000000000&nfstatusdescription=ERROR%3a+No+local+token Adipose Tissue as a Site of Toxin Accumulation https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6101675/ The Impact of Bisphenol A and Phthalates on Allergy, Asthma, and Immune Function: a Review of Latest Findings https://link.springer.com/article/10.1007/s40572-015-0066-8 Concentrations of Urinary Phthalate Metabolites Are Associated with Increased Waist Circumference and Insulin Resistance in Adult U.S. Males https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1892109/ Phthalates and Metabolism: Exposure Correlates with Obesity and Diabetes in Men https://ehp.niehs.nih.gov/doi/full/10.1289/ehp.115-a312b Fragranced consumer products: exposures and effects from emissions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5093181/ Organifi supplement powder (save 20% on your order with code FUNK) https://organifi.com/FUNK Coyote River Hemp Co CBD products (save 10% & free shipping on your order with code FUNK10) https://coyoteriverhempco.com/ Bio-Kult Boosted probiotic supplement (save 15% on your order with code FUNK15) https://www.bio-kult.com/bio-kult-boosted/p9 Follow Erin on Insta https://www.instagram.com/the.funktional.nutritionist/ Related pods: Ep 48: Exploring Female Hormones & Birth Control with Dr. Jolene Brighten https://www.erinholthealth.com/funktional-nutrition-podcast/2019/2/14/48-exploring-female-hormones-amp-birth-control-with-dr-jolene-brighten Ep 55: How to Tell if Your Blood Sugar is a Problem https://www.erinholthealth.com/funktional-nutrition-podcast/2019/4/3/episode-55? Ep 65: Everything You Ever Wanted to Know About Weight Loss erinholthealth.com/funktional-nutrition-podcast/2019/6/20/episode-65-everything-you-ever-wanted-to-know-about-weight-loss

Dr. Sarah Gray is an Associate Professor in the Northern Medical Program at the University of Northern British Columbia and an Affiliate Associate Professor in the Department of Cellular & Physiological Sciences at UBC. Dr. Gray’s work examines the biological mechanisms of metabolism as it relates to obesity and type 2 diabetes.

Dr. Kelsey Collins, a postdoctoral researcher at Washington University in St. Louis, USA, discusses the findings of her recent publication in PNAS, titled 'Adipose tissue is a critical regulator of osteoarthritis', including the unique mouse model used and what this tells us about the role of fat tissue in OA. https://www.pnas.org/content/118/1/e2021096118/tab-article-info

Welcome all to IS PHARMACOLOGY DIFFICULT Podcast! I am Dr Radhika Vijay.In today's episode I will be opening the verbal documentary about various drug reservoirs found in our body apart from plasma proteins! One thing you need to get real clear in your mind is that Drug Binding is not equal to drug action! Hope that gets real well understood!I will start my talk with tissue binding of drug, to nucleoproteins, etc. Then I will lay emphasis on the importance of sites/tissues/places like aqueous humor, peritoneal cavity, cerebrospinal fluid, etc.Fat/Adipose tissue serves as a very good site of collection of lipid soluble drugs, then what state of body affects this accumulation is all that matters! Then I will be telling you about drug dwelling in connective tissues like bone, nails, etc. Keratin precursor cells assimilating certain drugs will be a worth mention here! Sharing with you all my quick cappucino moments from Grasswood Cafe in city of lakes, India and with a promise to spill the leftover coffee in upcoming episodes, I will call it for the Majestic Monday, hope it becomes mannered and manageable for you all by all means! For all the updates and latest episodes of my podcast, please visit www.ispharmacologydifficult.com where you can also sign up for a free monthly newsletter of mine. It actually contains lot of updates about the medical sciences, drug information and my podcast updates also. You can follow me on different social media handles like twitter, insta, facebook and linkedin. They all are with same name "IS PHARMACOLOGY DIFFICULT". If you are listening for the first time, do follow me here, whatever platform you are consuming this episode, stay tuned, do rate and review on ITunes, Apple podcasts, stay safe, stay happy, stay enlightened, Thank you!!

This month on Episode 23 of Discover CircRes, host Cindy St. Hilaire highlights the topics covered in the April 2nd Compendium on Hypertension issue, as well as discussing two articles from the April 16 issue of Circulation Research. This episode also features an in-depth conversation with Dr Kathryn Moore from the New York University School of Medicine, discussing her study, miR-33 Silencing Reprograms the Immune Cell Landscape in Atherosclerotic Plaques.   Article highlights:   Compendium on Hypertension   Mustroph, et al. CASK Regulates Excitation-Contraction Coupling   Ward, et al. NAA15 Haploinsufficiency and CHD   Cindy St. Hilaire:         Hi, and welcome to Discover CircRes, the podcast of the American Heart Association's journal, Circulation Research. I'm your host, Dr Cindy St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh. Cindy St. Hilaire:         Today, I'm going to be highlighting the topics presented in our April 2nd Compendium on Hypertension, as well as two articles from the April 16th issue of Circ Res. I also will speak with Dr Kathryn Moore from New York University School of Medicine about her study, miR-33 Silencing Reprograms the Immune Cell Landscape in Atherosclerotic Plaques. So the April 16th issue of Circulation Research is a compendium on hypertension. As introduced by Rhian Touyz and Ernesto Schiffrin, there are over 10,000 articles in PubMed related to hypertension. Hypertension is a major cause of morbidity and mortality worldwide, and data trends suggest that fewer and fewer patients are able to control their blood pressure medically. Further, the recent Sprint trial showed us that lowering blood pressure to levels below previously recommended values strongly correlated with significantly reduced rates of cardiovascular events and risk of death. Cindy St. Hilaire:         As such, the April 2nd issue of Circ Res provides an extensive and expansive review on the current knowledge in the field. The series starts with an article on hypertension in low and middle-income countries by Aletta Schutte and colleagues. There they present the stark differences in the trajectory, healthcare, inequality, and established and emerging risks that are specific to low and middle-income countries. Cindy St. Hilaire:         Robert Carey and colleagues present an evidence-based update in their article titled Guideline-Driven Management of Hypertension. In Pathophysiology of Hypertension, David Harrison and colleagues present the concept of the mosaic theory of hypertension originally proposed by Dr Irvine Page in the 1940s, which proposes that hypertension is the result of multiple factors that in some, raise blood pressure and induce end-organ damage. This article further refines this theory by incorporating what is known regarding the role of things like oxidative stress, inflammation, genetics, sodium homeostasis, and the microbiome in hypertension pathogenesis. Cindy St. Hilaire:         Phil Chowienczyk and Jay Humphrey and colleagues cover the contribution of Arterial Stiffness and Cardiovascular Risk in Hypertension and identify steps required for making arterial stiffness measurements a keystone in hypertension management, and cardiovascular disease prevention as a whole. In Renin Cells, The Kidney, And Hypertension, Maria Luisa Sequeira Lopez and Ariel Gomez cover the major mechanisms that control the differentiation and fate of renin cells, the chromatin events that control the memory of the renin phenotype, and the major pathways that determine the cells’ plasticity. Cindy St. Hilaire:         Meena Madhur and Annet Kirabo and colleagues penned the article, Hypertension: Do Inflammation and Immunity Hold the Key to Solving this Epidemic? In this Teview, they covered the emerging concepts of how environmental, genetic, and microbial-associated mechanisms promote both innate and adaptive immune cell activation and help lead to hypertension. Cindy St. Hilaire:         In the article, The Gut Microbiome in Hypertension. Dominik N. Müller and colleagues present insights into the host-microbiome interaction and summarize the evidence of its importance in the regulation of blood pressure and provide recommendations for ongoing and future research. Cindy St. Hilaire:         Paul Cohen, James Sowers, and colleagues cover Obesity, Adipose Tissue, and Vascular Dysfunction in which they discuss the abnormal remodeling of specific adipose tissue depots during obesity and how this contributes to the development of hypertension, endothelial dysfunction, and vascular stiffness. Cindy St. Hilaire:         Clinton Webb, Satoru Eguchi, Rita Tostes, and colleagues cover Vascular Stress Signaling in Hypertension. In this Review, they discuss common adaptive signaling mechanisms against stresses, including the unfolded protein response, antioxidant response element signaling, autophagy, mitophagy, mitochondrial fission and fusion, STING-mediated responses, and activation of pattern recognized receptors. And how all of these responses contribute to vascular stress and ultimately hypertension. Cindy St. Hilaire:         Rhian Touyz and colleagues then specifically dig into the topic of Oxidative Stress and Hypertension, focusing in on recent advances in delineating the primary and secondary sources of reactive oxygen species, the posttranslational oxidative stress modification ROS induces on protein targets important for redox signaling, their interplay between ROS and endogenous antioxidant systems, and the role of inflammation activation and endoplasmic reticular stress in the development of hypertension. Cindy St. Hilaire:         Curt Sigmund and then colleagues cover the Role of the Peroxisome Proliferator Activated Receptors in Hypertension. In this Review, they discuss the tissue- and cell-specific molecular mechanisms by which PPARs in different organ systems modulate blood pressure and related phenotypes, such as endothelial cell dysfunction. Importantly, they also discuss the role of placental PPARs in preeclampsia which is a life-threatening form of hypertension that accompanies pregnancy. Cindy St. Hilaire:         Daan van Dorst, Stephen Dobbin, and colleagues provide the Review, Hypertension and Prohypertensive Antineoplastic Therapies in Cancer Patients. Many cancer therapies have prohypertensive effects. And this Review covers some of the mechanisms by which these antineoplastic agents lead to hypertension and details the current gaps in knowledge that future clinical studies must investigate, to identify the exact pathophysiology and the optimal management of hypertension associated with anticancer therapy. Cindy St. Hilaire:         In Hypertension, a Moving Target in COVID-19, Massimo Volpe, Reinhold Kreutz, and Carmine Savoia, review available data on the role of hypertension and its management in COVID-19. Cindy St. Hilaire:         Melvin Lobo and colleagues review Device Therapy of Hypertension. In this Review, they discussed the newer technologies, which are predominantly aimed at neuromodulation of peripheral nervous system targets, and discuss the preclinical data that underpin their rationale and the human evidence that supports their use. Cindy St. Hilaire:         Last but not least, in Artificial Intelligence in Hypertension: Seeing Through a Glass Darkly, Anna Dominiczak and colleagues cover a clinician-centric perspective on artificial intelligence and machine learning as applied to medicine and hypertension. In this Review, they focus on the main roadblocks impeding implementation of this technology in clinical care and describe efforts driving potential solutions. Cindy St. Hilaire:         This is an expansive set of Reviews written by the leading experts in the field and provides an up-to-date assessment of all aspects of hypertension. The graphics, and the articles are absolutely beautiful. And I'm sure we will be seeing a lot of them in upcoming presentations. Hopefully at AHA and the other sub-meetings when we're all back in person. Cindy St. Hilaire:         In the April 16th issue, I want to highlight the article, Loss of CASK Accelerates Heart Failure Development. The first author is Julian Mustroph, and the corresponding authors are Lars Maier and Stefan Wagner from the University Medical Center in Regensburg, Germany. Despite advances in cardiovascular medicine, heart failure takes the lives of tens of thousands of Americans each year. To develop novel treatments, a better understanding of the conditions of molecular pathology is needed. One contributing factor in heart failure is increased activity of the Ca/calmodulin-dependent kinase II (CaMKII). Cindy St. Hilaire:         In this paper, the authors suggest a way to get CaMKII levels under control. Ca/CaM-dependent serine protein kinase or CASK, suppresses CaMKII neurons and the team showed that CASK is also expressed in human heart cells, where it associates with CaMKII. Next, they engineered mice to CASK specifically in cardiomyocytes, finding that when these animals are subjected to beta-adrenergic stimulation, cardiomyocyte like CaMKII activity was significantly greater than that seen in control animals. Calcium spark frequency and the propensity for arrhythmia were also increased. Furthermore, in a mouse model of heart failure, mice lacking CASK fared worse and had reduced survival compared to the wild type control animals while boosting CASK expression in wild type animals reduced the elevated CaMKII activity and calcium sparks associated with heart failure. The author suggests that increasing CASK activity might be a heart failure treatment strategy worthy of further study. Cindy St. Hilaire:         The last article I want to share from the April 16th issue is titled, Mechanisms of Congenital Heart Disease Caused by NAA15 Haploinsufficiency. The first author is Tarsha Ward, and the co-senior authors are Kris Gevaert, Christine Seidman, and JG Seidman from Harvard University in Boston, Massachusetts. A number of genetic variants are associated with congenital heart disease, including loss of function variants of the gene encoding NAA15,  a sub N-terminal acetyltransferase complex called NatA, which acetylates a large portion of newly forming proteins. To find out how these variants contribute to defective heart development, the authors performed genome editing on human pluripotent stem cells to convert one or both copies of NAA15 gene into congenital heart disease linked to variants. The team then examined cardiomyocyte differentiation, protein acetylation, and protein expression in the edited and unedited cells. Cindy St. Hilaire:         They found that while NAA15 haploinsufficiency cells were able to develop into cardiomyocytes seemingly normally, the cell's contractile ability was significantly impaired. Cells homozygous for NAA15 variants failed to differentiate and had poor viability. The team also found that while only a small number of proteins had reduced end terminal acetylation in NAA15 haploinsufficiency cells, over 500 proteins had altered expression levels, four of which were encoded by congenital heart disease-linked genes. This work provides the first insights into the effects of NAA15 variants in human cells and sets the stage for analyzing other congenital heart disease-linked variants in this manner. Cindy St. Hilaire:         Today, Dr Kathryn Moore from NYU School of Medicine is with me to discuss her study, miR-33 Silencing Reprograms the Immune Cell Landscape in Atherosclerotic Plaques, which is in our April 16th issue of circulation research. So thank you so much for joining me today, Kathryn. Kathryn Moore:          My pleasure. Cindy St. Hilaire:         Atherosclerosis is the result of lipid-induced chronic inflammation, and while lipids are kind of thought to be an initial driver, therapies that target lipids alone, such as statins, they're not sufficient. They can obviously bring things down and improve things a lot, but a lot of research now is focused on uncovering the nuances of the inflammatory component of atherosclerosis to help identify new targets for therapies. One specific arm of this research has focused on resolving atherosclerotic inflammation. And my first question to you is, what exactly does resolving inflammation mean in the context of an atherosclerotic plaque? And maybe could you give us a little primer on some of those key cell types or processes involved in that. Kathryn Moore:          I'm really fascinated by the resolution of inflammation and in particular, in the atherosclerotic plaques. So inflammation used to be thought of as an active process, almost a one-way process, which in order to resolve had to stop. But actually, the pro-inflammatory and anti-inflammatory responses are a continuum. And so inflammation resolution, we now recognize is an active process, and it's not just a matter stopping the influx of immune cells but these cells take on new phenotypes and different functions. And the immune cells themselves are required for resolution of inflammation and tissue repair. And so we're really interested in looking at what those pathways are, that tip the balance between pro-inflammatory responses and pro-resolving responses and how to incite them in the plaque so that you can start to remodel the plaque to be more stable or have a more favorable phenotype, or even to regress the plaque, to shrink the plaque in size. Cindy St. Hilaire          This study specifically focused on microRNA-33, and I believe your lab was one of the very first to look at this specific, but also other micro RNAs in atherosclerosis. And the prior research that you and others have shown is that this microRNA modulates a variety of genes that control lipid metabolism. You found this in mice, but also in monkeys. And really by using anti-miRs against this microRNA, you can induce cholesterol efflux and that cholesterol will leave the liver and the macrophage cells, and it's incorporated into the protective HDL particles and excreted. Cindy St. Hilaire:       And so it has this really nice protective effect. However, the effects seen in these animal studies were suggested that microRNA-33 had HDL independent action, which I think is where your story starts. So could you tell us some of the premises or the gaps in knowledge between those first initial findings of miR-33 that led you to conduct this study and then kind of what the design of the study was? Kathryn Moore:          So, as you mentioned, we discovered miR-33 as an inhibitor of cholesterol efflux and the pathways that lead to the generation of HDL, the so-called good cholesterol. And when you inhibit miR-33 in mice and monkeys, you can raise plasma levels of HDL. But we also saw that in mice that had been fed a Western diet continuously, we saw favorable changes in the atherosclerotic plaque under conditions where we didn't see the increase in HDL. So if the mice are on a Western diet, the levels of miR-33 in the liver are very low, and inhibiting it doesn't cause the increase in HDL cholesterol. But we still saw this 25% regression in atherosclerotic plaques. And that got us thinking about the other things that miR-33 could be doing and around the same time, I was also very interested in immunometabolism and how the metabolic state of macrophages influences their function. Kathryn Moore:          And Mihail Memet, who is a former postdoc in my lab made the discovery that miR-33 could inhibit fatty acid oxidation in macrophages and that this polarized the cells to a more inflammatory phenotype. So when we give the miR-33 inhibitors, we're raising a level of fatty acid oxidation in the macrophages and they become more tissue reparative. And so we suspected that could be the mechanism going on in the plaque but those studies, those initial studies were done over five years ago. And that was before the advent of single-cell technologies, which have really revolutionized how we're studying the atherosclerotic plaque. So in this study, we were able to apply some of these more high dimensional analyses of all of the immune cells in the plaque. And really look at how inhibiting miR-33 was altering their transcriptome and their phenotype. Cindy St. Hilaire:         Yeah, so that is a perfect segue to my next question, which is you're doing this single-cell RNA-sequencing on tissue, but it's not just any tissue. It's not like a nice spleen that you can kind of pop open and all the cells fall out nicely and you can fax them or whatever. This is from an aorta, which itself is fibrous and tough on top of the atherosclerotic plaque, which is also difficult. So can you discuss maybe some of the challenges regarding doing this exact kind of analysis with this tissue and maybe some of the limitations or controls that you used to help really refine your result? Kathryn Moore:           It is a little bit challenging to learn how to digest the aorta to release the immune cells, so to isolate the CD45+ immune cellsthat then go on to the sequence that takes some trial and error to get the right conditions. But actually, once you've done that a couple of times, it's not as difficult as it seems but I think that one of the challenges of doing these types of studies is integrating the results that we get from the single-cell RNA-sequencing with the other technologies that we've used in the past to analyze atherosclerosis. Kathryn Moore:          So, previously when we were analyzing atherosclerotic plaque size or immune cell content, we are doing this through histology and immunostaining. And single-cell RNA-sequencing has identified all these new immune cell subsets based on transcriptomic signatures. And they don't really match up nicely with the protein signatures that we've used in the past. Cindy St. Hilaire:         Yeah. Kathryn Moore:          I saw this as a great opportunity to try to integrate all these techniques. And see if we could come to some middle ground. To understand how maybe the new subsets that we're identifying with single-cell RNA-seq from the aortic immune cells matched some of the things that we were able to do by looking at histology and tracing monocytes and macrophage entry and retention in the plaque. Cindy St. Hilaire:         How did it line up? What's the nice Venn diagram of this study and what we've all been doing previously? Kathryn Moore:          Well, it's a challenge, but what I thought was really really fascinating was we did monocyte-macrophage tracing experiments. Because one of the things we find when we inhibit miR-33 is we have a 50% decrease in the macrophage content of the plaque, but how is that happening? And what we found was there was an increase in the recruitment of monocytes into the plaque which may sound surprising if the plaque is shrinking, but they are the cells that are needed. They're the cleanup crew that are being introduced. But we saw a decrease in retention of macrophages and a decrease in proliferation and an increase in macrophage death and clearance of the apoptosis cells. And then through the single-cell RNA-sequencing, we were able to look at the different macrophage subsets. We had resident macrophages, Trem2hi metabolic macrophages, and MHCIIhi inflammatory macrophages. Kathryn Moore:          We were able to look at their transcriptomes and say, "Which of these subsets are most likely to be performing those functions that we saw before?" And that was fun because that was like piecing together a puzzle. And what we saw, what it leads us to believe is that the Trem2hi metabolic macrophages are the ones that are undergoing aptosis. They have an increase in aptosis genes and eat-me signals and the MHCIIhi, having an increase in athoscoertic genes like mirTK that will help them clear the dying cells and the MHCIIhi macrophages also have decreased markers of proliferation. So although we used to think about macrophages as this one big pool, now we're able to say that these different subsets are performing different functions. And to me that's really exciting. Cindy St. Hilaire:        Oh, that is exciting. And it's also extremely complicated because I was having enough trouble with just the two types of macrophages of a couple of years ago. The study showed that inhibiting this miR-33 using these anti-miR-33 oligos, and you're just kind of injecting oligos against it. And you're doing this in mice with established atherosclerosis. This helped to alter these monocyte and macrophage populations in the plaque itself. Cindy St. Hilaire:        Do you think a function of the success of this study and essentially this therapy in the mouse is really dependent on the fact that it's targeting these circulating cells that are then going to the plaque? And I guess part of that question is, do you think part of this is because it's a circulating cell that can take it up, and then change and be delivered to the location it's going to, as opposed to that oligo targeting the plaque itself and the cells that are already residing there. Do you have any sense of that? Kathryn Moore:          So it's interesting because one of the things that we did with our single-cell RNA-seq was to look at all immune cells in the plaque and say, "How many miR-33 target genes are changing in the ones from the treated mice?" And in the monocytes, you see very little change in miR-33 target genes. And that's consistent with what we know from Regulus Therapeutics who designed the anti-miR-33 antisense oligonucleotides. So we don't think that the ASO are being taken up in the circulation. I think they're actually being taken up by the macrophages in the plaque. And one of the great things about trying to target macrophages is they're very phagocytic. So they're going to be the ones that take up these ASOs, and the single-cell really allowed us to see whether it was just macrophages that were being affected or whether there were other immune cell populations that also seemed to have miR-33 induce changes. And of course it's hard from the single-cell to infer whether this is direct or indirect. Cindy St. Hilaire:         Yeah. Kathryn Moore:          But it seemed as if T-cells also were targeted by the anti-miR-33, definitely macrophages. We saw some changes in dendritic cells, very little changes in K cells, for example. And no changes in monocytes. And so it also begins to tell us how many different cell types are being affected and who's driving the bus when it comes to these changes. But by far the most miR-33 target genes change were the macrophage populations. And I think that's really due to their phagocytic ability. Cindy St. Hilaire:         So I know there's a great divergence generally in microRNAs between mice and humans or really any species, but there are homologs to this in humans. What is the same and what is different between, I guess, this particular targeting micro RNA or what we know about it in mice and humans? Kathryn Moore:          So mice have only one copy of miR-33, whereas humans and monkeys have two copies but those two copies are very similar in sequence. They differ only by two nucleotides. So you can use the same antisense oligonucleotides to target in mice and in non-human primates, for example. It's never been tried in humans. Cindy St. Hilaire:         Yeah, of course. Not yet. Kathryn Moore:          But it has been tried in monkeys, and we were able to effectively inhibit both miR-33a and miR-33b in the non-human primates. But the different variants of miR-33 have different transcriptional regulation. So they're induced under different conditions. And I think that's one way that mice and humans will really differ-the conditions where you'd have high levels of miR-33 will be different. Cindy St. Hilaire:         Got it. Yeah. And the mice has that in the SREBP gene and humans. Kathryn Moore:          And miR-33a is an SREBP-2 gene, which is SREBF2. And in humans there's an additional copy, which is SREBF. So it's in both of the SREBP genes in humans. Cindy St. Hilaire:         Interesting. So I wonder, we need to ask the evolutionary biologist. Did they segregate together? I mean, I guess they must have. That's really interesting. That's cool. Kathryn Moore:          One of the things that I love about miR-33 is that the SREBP-2 gene is turned on when cholesterol levels are low and it acts to increase the pathways involved in cholesterol synthesis and uptake. And miR-33 is transcribed at the same time. And what it does is it blocks the exits for cholesterol from the cell and from the body. And so it's just this hidden gem in the locus that sort of boosts SREBP-2 function. Cindy St. Hilaire:         Its amazing stuff works out like that. I love it. So if we were going to leverage this inflammation resolution as atherosclerotic therapy, wherein the continuum of the disease, should we target? You know, we have obviously atherosclerotic plaque does not happen overnight. Teenagers can even have evidence of a fatty streak. If we were going to leverage antisense oligos as therapy, especially specifically against miR-33, where do you think would be a good place to target? And do we know, or have the kind of imaging capabilities to maybe identify that window right now in patients? Kathryn Moore:          That's an interesting question. So lipid-lowering therapies will remain the first line of treatment for atherosclerosis, but lipid-lowering alone is insufficient to regress the plaque. It can stabilize plaques, but it doesn't really cause them to shrink. And when you think about the patient population that presents with cardiovascular disease, it's adults, for the most part. These are people in their fifties and sixties, and we've missed the chance to stop the early events. And so those are the majority of the people that are being treated. And I think there is room there to treat inflammation at the same time in the hopes of tipping that balance between pro-inflammatory events and then inflammation resolution. So we know surprisingly little about that tipping point. And now I think when miR-33 inhibition is fascinating in that it can affect both lipid metabolism and inflammation. And so I think that as an add-on therapy with lipid-lowering, it would be interesting, but of course, I'm not ready. Cindy St. Hilaire:         We're not there yet. Cindy St. Hilaire:         So I guess what's next for this line of research? What are kind of the next questions that the single-cell RNA-seq discovered for you? Was there anything kind of surprising or really exciting that you want to pursue next? Kathryn Moore:          One of the things that I thought was really interesting was that the different macrophage subpopulations had different miR-33 target genes being de repressed. And that's probably not surprising, but I didn't initially think that would happen, but of course, the subpopulations are identified based on their unique transcriptomes. So they're not all the same, which means that they'll have different levels of miR-33, and they'll have different levels of the miR-33 target genes. And so Abca1, which we think about all the time as a miR-33 target gene that's involved in cholesterol efflux, it went up in Trem2hi macrophages and the resident macrophage population, but not in the MHCIIhi. The target genes and the MHCIIhi were different than the other two populations. And I think this now gives us a chance to sort that out. Kathryn Moore:          And some of the targets in the MHCIIhi macrophages were ones that are involved in chromatin reorganization- Cindy St. Hilaire:         Oh, interesting. Kathryn Moore:          ... and inscriptional regulation. And when I looked across the other subsets, I could see that common pattern in T-cells and B-cells that were changing. And I think that's one way that miR-33 could have a broad impact. MiR-33 is a little bit of a unique microRNA. It has a very potent impact on these pathways. Other microRNAs often can change gene expression by 10 to 20%, but miR-33, when we inhibit it, we see really powerful effects. And I think that if it is involved in targeting genes that mediate chromogenic reorganization or transcriptional complex formation, that gives us a hint of how it could be having additional impact. Cindy St. Hilaire:         That's really cool. And this was an absolutely beautiful story, not only in kind of dissecting out the mechanisms at play, but you know, those beautiful tisney plots and the nice graphics of the single-cell stuff. Kathryn Moore:          The first author of the paper, Milessa Afonso, is a postdoc that just left the lab, and she worked so hard on this and did such a beautiful job. Cindy St. Hilaire:         Well, it's a wonderful story and I'm really happy we were able to publish it. So, Dr Moore, thank you so much for joining me today. Kathryn Moore:                      My pleasure. Thank you. Cindy St. Hilaire:        That's it for the highlights from the April 2nd and 16th issues of Circulation Research. Thank you so much for listening. Please check out the CircRes Facebook page and follow us on Twitter and Instagram with the handle @circres and hashtag DiscoverCircRes. Thank you to our guest, Dr Kathryn Moore. This podcast is produced by Ashara Ratnayaka, edited by Melissa Stoner, and supported by the Editorial Team of Circulation Research. Copy text for the highlighted articles was provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire and this is Discover CircRes, your on-the-go source for the most exciting discoveries in basic cardiovascular research.    

Good morning and welcome to the ride! Did Sister O'dell just channel her inner Billy Ray Valentine? The Chief Love Officer has some words to say about a jezebel. Our family from The Talk Sheryl Underwood kept it cool! President Biden's $1.9 trillion COVID-19 relief bill has passed. Does having curves extend your life? The hidden Black of the palace (Duke of Ottingham) hits the radio to give his opinion about Pierce Morgan and Sharon Osborne. Married To Medicine is the focal point of Reality Update. Steve gives his answer to a question from Carla's Reality Update about prenuptial agreements. Today the show wraps up with Tommy asking Steve a question. Learn more about your ad-choices at https://www.iheartpodcastnetwork.com

This week we welcome Benjamin Bikman. Ben earned his Ph.D. in Bioenergetics and was a postdoctoral fellow with the Duke-National University of Singapore in metabolic disorders. Currently, his professional focus as a scientist and professor to better understand chronic modern-day diseases, with special emphasis on the origins and consequences of obesity and diabetes. With a particular emphasis on the role of insulin. He frequently publishes his research in peer-reviewed journals and presents at international science meetings. In this episode, We discuss all things Insulin Resistance and Insulin Sensitivity. Such as Linoleic Acid Effects on Insulin, PCOS, Erectile Dysfunction, and Migraines. Ben also gives us his dietary recommendations for managing insulin resistance. Join The Better! Community On Facebook. Get the show notes here.

Dr Philip Smith, Digital and Education Editor of Gut and Consultant Gastroenterologist at the Royal Liverpool Hospital interviews Dr Rima Chakaroun who is a Clinician Scientist, Resident physician at the University Hospital in Leipzig, Germany, specialising in Endocrinology and Metabolic disease and a postdoctoral researcher and clinical investigator working on microbiome signatures in obesity in gut and beyond. The podcast is focused on "Adipose tissue derived bacteria are associated with inflammation in obesity and type 2 diabetes" published in paper copy in Gut in October 2020. https://gut.bmj.com/content/69/10/1796

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.04.283226v1?rss=1 Authors: Held, N. M., Buijink, R., Elfrink, H. L., Kooijman, S., Janssens, G. E., Vaz, F. M., Michel, S., Houtkooper, R. H., Weeghel van, M. Abstract: Lipid metabolism is under the control of the circadian system and circadian dysregulation has been linked to obesity and dyslipidemia. These factors and outcomes have also been associated to, or affected by, the process of aging. Here, we investigated whether murine white (WAT) and brown (BAT) adipose tissue lipids exhibit rhythmicity and if this is affected by aging. To this end, we have measured the 24 hour lipid profiles of WAT and BAT using a global lipidomics analysis of >1100 lipids. We observed rhythmicity in nearly all lipid classes including glycerolipids, glycerophospholipids, sterol lipids and sphingolipids. Overall, ~22% of the analyzed lipids were considered rhythmic in WAT and BAT. Despite a general accumulation of lipids upon aging the fraction of oscillating lipids decreased in both tissues to 14% and 18%, respectively. Diurnal profiles of lipids in BAT appeared to depend on the lipid acyl chain length and this specific regulation was lost in aged mice. Our study revealed how aging affects the rhythmicity of lipid metabolism and could contribute to the quest for targets that improve diurnal lipid homeostasis to maintain cardiometabolic health during aging. Copy rights belong to original authors. Visit the link for more info

Commentary by Dr. Valentin Fuster

In this episode, Dr. Scott and Tommy shine a light on a new interpretation of old data. They examine a study that reveals there is a fat free component of adipose (fat) tissue, which could actually mean that many previous studies examining diet and fat loss effects on lean skeletal muscle tissue may have incorrectly interpreted their findings. This is very encouraging news for anyone who has exercised with resistance while attempting to lose fat. Listen, take action, and share with a friend who needs less cardio and more resistance while burning fat!   https://onlinelibrary.wiley.com/doi/full/10.1002/oby.22393   Show Transcript: www.thefastingforlife.com/blog   If you enjoy the podcast, would you please tap on the stars below and consider leaving a short review on Apple Podcasts/iTunes? It takes less than 60 seconds, and it really makes a difference in helping to bring you the best original content each week. We also just enjoy reading them!   Sign up for the Fasting For Life newsletter at www.thefastingforlife.com   Follow Fasting For Life: www.facebook.com/thefastingforlife www.instagram.com/thefastingforlife

The US department of Health and Human Services says the most common way to determine, if a person is overweight or obese is to calculate body mass index (BMI), which is an estimate of body fat, based on comparing a person’s weight to his or her height. However, BMI can be flawed with more lean muscle weight, such as the case with a fit person or athlete.The Centers for Disease Control and Prevention (CDC) comments that, “BMI does not measure body fat directly, but research has shown that BMI is moderately correlated with more direct measures of body fat obtained from skinfold thickness measurements, bioelectrical impedance, underwater weighing, dual energy x-ray absorptiometry (DXA) and other methods.” When BMI is added to a person’s potential health comorbidities (high blood pressure, cardiovascular, liver, or kidney disease), there can be a higher risk to complications associated with viral-associated diseases, such as Covid-19. “BMI appears to be strongly correlated with various adverse health outcomes consistent with these more direct measures of body fatness,” notes the CDC.For adults, a BMI of 18.5 to 24.9 is considered normal weight; 25.0 to 29.9 is considered overweight; 30.0 to 39.9 is considered obese, and 40.0 and higher is considered extremely obese.The World Health Organization (WHO) states that the number of obese people has tripled worldwide in the last twenty years – reaching the status of a global epidemic – mainly associated with improper dietary habits and a sedentary lifestyle.According to April 2020 research – Obesity, Bioactive Lipids, and Adipose Tissue in Insulin Resistance – published in the online, peer reviewed journal Nutrients, “obesity is a state of pathological increase in the amount of adipose tissue, which boosts the risk of numerous diseases, such as cardiovascular disease, some types of cancer, and type 2 diabetes.” The study authors from the Department of Hygiene, Epidemiology and Metabolic Disorders, Medical University of Bialystok, Poland, stress that “there are a number of causes leading to the development of obesity, including genetic and environmental factors. The contribution of genetic factors to obesity is very important and is thought to be responsible for 40–70% of obesity cases.”However, note the Polish researchers, “it appears that non-genetic factors, especially environmental factors such as unhealthy eating habits and lack of physical activity, also play a substantial role in generating obesity.” Let’s add sleep duration and daytime sleepiness to the list of complications that may affect being overweight and obese.When insulin resistant – a precursor to type 2 diabetes and obesity – insulin stimulates fat storage and inhibits fat breakdown for energy. Under normal conditions, insulin is an anabolic (building) hormone that increases the uptake of amino acids by muscle tissue and enhances protein synthesis (making muscle).The American Diabetes Association (ADA) defines insulin resistance as, “a condition in which the response of cells to insulin is impaired with respect to carbohydrates, lipids, and proteins, resulting in elevated blood glucose levels.”The ADA further states that, “insulin has a wide spectrum of effects on metabolic processes in adipocytes (fat cells); therefore, it is considered the most important hormone regulating anti-lipolytic processes, and deterioration of cell sensitivity to this hormone or impairment of the insulin pathway may affect the metabolism of adipose (fat) tissue.” The central accumulation of fat tissue – known as an android visceral fat - is consistent with a male fat pattern. Female fat accumulation – known as a gynoid fat pattern – is the increase of subcutaneous (under the skin) fat in the hip and thigh regions. Read the rest at MackieShilstone.com

In today’s episode, Greg and Eric share a little bit of good news, followed by a Feats of Strength segment. That’s followed by a Research Roundup segment discussing brand new research on the influence of genes on caffeine responses, recovery postures during high-intensity exercise, time-restricted feeding (intermittent fasting), and concurrent training (cardio + lifting). After that, Greg and Eric field some listener questions in a Q&A segment covering topics including cold exposure, the effects of race and ethnicity on body composition estimation, nutrition during deloads, and hangover prevention tips. Finally, Evan Peikon is featured in this week’s On The Rise segment, and a few off-topic questions are answered to play us out.If you’d like to submit a question for a future Q&A segment, please go to tiny.cc/sbsqa. If you’d like to recommend someone for a future “On the Rise” segment, please go to tiny.cc/creators. If you’d like to receive Research Roundup emails, please sign up for our email list at https://www.strongerbyscience.com/newsletter/.  TIME STAMPSAnnouncements (0:01:00). Good news (0:02:47). Breakthrough For Kenyan Scientists Who Discover Natural Microbe That Completely Stops Malaria in Mosquitoes: https://www.goodnewsnetwork.org/microbe-completely-stops-malaria-in-mosquitoes-discovered/. Specially-Trained Dogs Have Saved 45 Rhinos From Poachers in South Africa: https://www.goodnewsnetwork.org/dogs-have-saved-45-rhinos-from-poachers/. Feats of Strength (0:06:38). Research Roundup (0:16:38). To receive research roundup emails, you can sign up at: https://www.strongerbyscience.com/newsletter/. Caffeine and genetics (0:17:40). Grgic et al. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7161272/. https://pubmed.ncbi.nlm.nih.gov/32168870/. Effects of Two Different Recovery Postures during High-Intensity Interval Training (0:33:52). Michaelson et al. https://journals.lww.com/acsm-tj/fulltext/2019/02150/effects_of_two_different_recovery_postures_during.1.aspx. Four Weeks of Time-Restricted Feeding Combined With Resistance Training Does Not Differentially Influence Measures of Body Composition, Muscle Performance, Resting Energy Expenditure, and Blood Biomarkers (0:45:37).  Stratton et al. https://pubmed.ncbi.nlm.nih.gov/32316561/. Adaptations to strength training differ between endurance-trained and untrained women (0:58:14). Vikmoen et al. https://link.springer.com/article/10.1007/s00421-020-04381-x. Q&A (1:09:48). Can cold exposure be used as a fat loss strategy? (1:10:01). Do you buy the idea that certain ethnicities have a genetic tendency to store fat in different places? (1:24:04). Should nutrition be altered during a deload? (1:31:51). Best hangover cure/prevention tips? (1:37:41). On the Rise (1:49:39). Evan Peikon: https://www.instagram.com/evan_peikon/. https://www.trainingthinktank.com/To play us out (1:53:32): Pancakes vs. waffles? Cool Ranch Doritos vs. Nacho Cheese? R or SPSS or Excel? 

Cold showers and cold plunges are widely spoken about in the world of wellness, but are they really worth the pain and discomfort theyput you through? In this episode of the Align podcast, I dive into cold- exposure therapy–why it’s essential for optimizing your life, and how to do it properly to ensure you are reaping the full benefits. I also give you a deep explanation on brown adipose tissue, what it is and where it comes from, and the science-backed benefits of Wim Hof-style breathing techniques.   What you’ll learn:  Wim Hof breathing techniques  The science behind holding your exhales The benefits of cold-exposure therapy  Why you want more brown adipose tissue  Why you need to place good stress on your body regularly How to easily set up a cold plunge at home How to perform a cold plunge for the greatest results    Links discussed in this episode:  Wim Hof: Inner Fire, Reversing Disease, Breathing  7-Minute Guided Breath-Work and Meditation

In this podcast we talk to Dr Corinna Storz and Dr Sophia Rado, winners of this year’s BJR/Jusha Early Career Investigator Award.

Interview with Alexia Mattei, MD, author of Feasibility of First Injection of Autologous Adipose Tissue–Derived Stromal Vascular Fraction in Human Scarred Vocal Folds: A Nonrandomized Controlled Trial

Interview with Alexia Mattei, MD, author of Feasibility of First Injection of Autologous Adipose Tissue–Derived Stromal Vascular Fraction in Human Scarred Vocal Folds: A Nonrandomized Controlled Trial

In this episode of the Heart podcast, Digital Media Editor, Dr James Rudd, is joined by Professor Charalambos Antoniades from Oxford, UK. They discuss his novel method of measuring coronary plaque inflammation using CT imaging, and how this method might be important for predicting heart attacks. If you enjoy the show, please leave us a podcast review at https://itunes.apple.com/gb/podcast/heart-podcast/id445358212?mt=2 Link to published paper: https://heart.bmj.com/content/early/2018/07/24/heartjnl-2017-312324

Commentary by Dr. Valentin Fuster

Commentary by Dr. Valentin Fuster

Sheila Collins explains that natriuretic peptides protect mice from the metabolic consequences of a high-fat diet by acting on adipose tissue.

In general, Lipoedema is a poorly understood disease in the United States; statistics show it is markedly under-diagnosed in this country. Lipedema is a painful fat disorder that, if untreated, can cause multiple health problems leading to mobility issues.   The quality of life, emotionally and physically, for a Lipedema patient often suffers because the disease is typically dismissed as simple obesity. How often have you seen a woman who appears to be a size 8 or 10 from the waist up and a size 18 or more from the waist down with unusually large, column-like legs?  Women who have this body profile more often than not are exhibiting classic early stage Lipoedema. As Lipoedema progresses, fat will increase in the lower body.  Unfortunately, Lipedema patients tend to gain weight in the lipedemic areas, and can only lose it in the non-lipedemic areas. Even bariatric surgery will only result in fat loss primarily from the waist up. Lipedemic fat cannot be exercised or even starved away. Information used from www.CureLipedema.org. There are estimates that put the incidence of lipedema as high as 11% of the adult female population. We are talking millions of women here. Join Sharry as she demonstrates how to use her software Lipoedema Factors. Often mistaken for Obesity, Lipedema is an entirely different issue brought on by the body's inability to move and appropriately metabolis fatty materials within the body. Often identified with a small upper torso and large hips and legs; this unrecognized disease if often misdiagnosed. Not intended to diagnose, prescribe for, treat, mitigate or cure any medical condition.

Jon Giles, MD, MPH at Columbia University

Brian Feldman explains how a secreted protease inhibits diet- and glucocorticoid-induced differentiation of adipocytes.

Michael Symonds, Karolinska Institutet, gives a talk for the UBVO Instrument and Institutions Interviews series.

CREB-regulated transcription coactivator 3 (CRTC3) is found in adipocytes, where it may promote obesity through disruption of catecholamine signaling. We wished to assess whether CRTC3 is a soluble protein secreted by adipose tissue, explore whether CRTC3 is detectable and quantifiable in the circulation, and ascertain whether CRTC3 serum concentrations are related to metabolic markers in children.

Dr. Naima Moustaid-Moussa discusses her review on n-3 fatty acids and how they may alleviate adipose tissue inflammation and insulin resistance.

Major advances in understanding and treating breast cancer have been made in the last two decades, yet it remains a significant problem with breast cancer being the most commonly identified cancer and the leading cause of cancer death among women worldwide. For many years breast cancer research has mainly focused on genetically changed cancer cells. However, recently the importance of the stromal compartment surrounding cancer cells in facilitating tumor growth, invasion and metastasis has been widely recognized. Cumulating evidence suggests that in particular carcinoma-associated myofibroblasts play a key role within the tumor stroma and influence many aspects of carcinogenesis. Nevertheless, the cell type of origin as well as the precise mechanisms by which these cells develop has not been conclusively established and remains controversial. The role of human adipose tissue derived stem cells (hASCs) in this context has not been studied so far. hASCs are locally adjacent to epithelial breast cancer cells and might represent early response cells within the tumor stroma. Hence, the aim of this study was to investigate whether carcinoma-associated myofibroblasts may originate from hASCs. The present study revealed that a significant percentage of hASCs differentiate into myofibroblast-like cells expressing alpha smooth muscle actin (α-SMA) and tenascin-C when exposed to conditioned medium from the human epithelial breast cancer cell lines MDMAB231 and MCF7. This process is induced by transforming growth factor beta 1 (TGFβ1) secreted from breast cancer cells. It was shown that conditioned medium from MDMAB231 and MCF7 contains significant amounts of TGFβ1. It could further be demonstrated that the differentiation of hASCs towards myofibroblasts is dependent on TGFβ1 signaling via phosphorylation of Smad2 and Smad3 in hASCs. The induction of myofibroblasts can be abolished using a neutralizing antibody to TGFβ1 as well as by pretreatment of hASCs with SB431542, a selective inhibitor of the TGFβ1 activin receptor-like kinases 4, 5 and 7. Additionally, hASC-derived myofibroblasts exhibit functional properties of carcinoma-associated myofibroblasts such as the increased secretion of the tumor-promoting soluble factors SDF-1α and CCL5. Furthermore hASC-derived myofibroblasts as well as conditioned medium from these cells promote the in vitro invasion of MDAMB231 breast cancer cells. Moreover inhibition of the TGFβ1 signaling pathway in hASCs reduces the potential of these cells to enhance the invasion of breast cancer cells. Overall, the data of the present study suggest that human adipose tissue derived stem cells can differentiate into carcinoma-associated myofibroblast under the influence of TGFβ1 secreted from breast cancer cells in vitro. The differentiation of hASCs towards these tumor-promoting cells can be abolished by targeting the TGFβ1 signaling pathway. Hence, inhibition of the TGFβ1 signaling pathway may prove to be an interesting target for breast cancer therapies. In vivo studies on the cancer microenvironment under special consideration of the interactions between hASCs and cancer cells should be of interest for breast cancer research in the future.

Numerous epidemiological studies have consistently demonstrated the strong association between type 2 diabetes mellitus (T2DM) and an increased risk to develop cardiovascular disease. The pathogenesis of T2DM and its complications are characterized by pancreatic, adipose tissue and vascular inflammation. CD40 and CD40L, members of the tumour necrosis factor (receptor) TNF(R) family, are well known for their role in immunity and inflammation. Here we give an overview on the role of CD40-CD40L interactions in the pathogenesis of T2DM with a special focus on pancreatic, adipose tissue and vascular inflammation. In addition, we explore the role of soluble CD40L (sCD40L) as a potential biomarker for the development of cardiovascular disease in T2DM subjects. Finally, the therapeutic potential of CD40-CD40L inhibition in T2DM is highlighted.

Low-carbohydrate, high-fat (LC-HF) diets are popular for inducing weight loss in overweighed adults. Adaptive thermogenesis increased by specific effects of macronutrients on energy expenditure has been postulated to induce this weight loss. We studied brown adipose tissue (BAT) morphology and function following exposure to different LC-HF diets. Methods: Male Wistar rats were fed a standard control diet ad libitum or pair-fed isoenergetic amounts of three experimental diets for 4 weeks. The diets had the following macronutrient composition (% metabolizable energy: carbohydrates, fat, protein): control (64.3/16.7/19), LC-HF-low protein (LC-HF-LP, 1.7/92.8/5.5), LC-HF-normal-protein (LC-HF-NP, 2.2/78.7/19.1), and a high fat diet with carbohydrates (“high fat”, 19.4/61.9/18.7). Results: Body weight gain was reduced in all pair-fed experimental groups as compared to rats fed the control diet, with more pronounced effect in rats on LC-HF diets than on the high fat diet with carbohydrates. High fat diets increased expression of PGC1α and ADRB3 in BAT indicating higher SNS outflow. However, UCP1 mRNA expression and expression of UCP1 assessed by immunohistochemistry was not different between diet groups. In accordance, analysis of mitochondrial function in-vitro by extracellular flux analyser (Seahorse Bioscience) and measurement of inducible thermogenesis in vivo (primary endpoint), explored by indirect calorimetry following norepinephrine injection, did not show significant differences between groups. Histology of BAT revealed increased lipid droplet size in rats fed the high-fat diet and both LC-HF diets. Conclusion: All experimental diets upregulated expression of genes which are indicative for increased BAT activity. However, the functional measurements in vivo revealed no increase of inducible BAT thermogenesis. This indicates that lower body weight gain with LC-HF diets and a high fat diet in a pair-feeding setting is not caused by increased adaptive thermogenesis in BAT.

Objectives: Pericardial adipose tissue (PAT) is associated with coronary artery plaque accumulation and the incidence of coronary heart disease. We evaluated the possible incremental prognostic value of PAT for future cardiovascular events. Methods: 145 patients (94 males, age 60 10 years) with stable coronary artery disease underwent coronary artery calcification (CAC) scanning in a multislice CT scanner, and the volume of pericardial fat was measured. Mean observation time was 5.4 years. Results: 34 patients experienced a severe cardiac event. They had a significantly higher CAC score (1,708 +/- 2,269 vs. 538 +/- 1,150, p < 0.01), and the CAC score was highly correlated with the relative risk of a future cardiac event: 2.4 (1.8-3.7; p = 0.01) for scores > 400, 3.5 (1.9-5.4; p = 0.007) for scores > 800 and 5.9 (3.7-7.8; p = 0.005) for scores > 1,600. When additionally a PAT volume > 200 cm(3) was determined, there was a significant increase in the event rate and relative risk. We calculated a relative risk of 2.9 (1.9-4.2; p = 0.01) for scores > 400, 4.0 (2.1-5.0; p = 0.006) for scores > 800 and 7.1 (4.1-10.2; p = 0.005) for scores > 1,600. Conclusions:The additional determination of PAT increases the predictive power of CAC for future cardiovascular events. PAT might therefore be used as a further parameter for risk stratification. Copyright (C) 2012 S. Karger AG, Basel

Hibernation is an ingenious adaptation that some animals employ to survive difficult conditions in winter. This unit examines the differences between hibernation and torpor, and discusses the characteristic signs of hibernation behaviour. It explores the triggers that bring on hibernation, and whether internal signals or external season cues are predominant. It also examines the physiological adaptations that occur in hibernating animals. This unit builds on and develops ideas introduced in the openlearn unit on Animals at the extreme: the desert environment (S324_1). This study unit is just one of many that can be found on LearningSpace, part of OpenLearn, a collection of open educational resources from The Open University. Published in ePub 2.0.1 format, some feature such as audio, video and linked PDF are not supported by all ePub readers.

The extreme challenges of life in the polar regions require the animals who make their habitat there to make many adaptations. This unit explores the polar climate and how animals like reindeer, polar bears, penguins, sea life and even humans manage to survive there. It looks at the adaptations to physiological proceses, the environmental effects on diet, activity and fecundity, and contrasts the strategies of aquatic and land-based animals in surviving in this extreme habitat. This unit builds on and develops ideas from two other 'Animals at the extreme' units: The desert environment (S324_1) and Hibernation and torpor (S324_2). This study unit is just one of many that can be found on LearningSpace, part of OpenLearn, a collection of open educational resources from The Open University. Published in ePub 2.0.1 format, some feature such as audio, video and linked PDF are not supported by all ePub readers.

Protein kinase G is required for the differentiation and fat-burning function of brown adipose tissue.