Podcasts about Pathogenesis

In this episode there will be puns where you yeast expect them...But more seriously, what does Candida albicans actually mean? What are yeasts anyway? How does this all relate to the Romans?These questions, and more, will be answered as Alyssa and Callum continue the Fungal series with this, the first in a 3-parter on all things Candida!In this episode we cover the Taxonomy (newly confusing), Epidemiology and Pathogenesis of Candida spp. before talking about superficial candidiasis.Look out for upcoming episodes on invasive Candidiasis and C. auris!Show notes for this episode here: https://idiots.notion.site/108-110-Yeasts-Candida-0eb5f9271f654312b59458d39f8de603?pvs=74 Send us a textSupport the showQuestions, comments, suggestions to idiotspodcasting@gmail.com or on Bluesky @idiots-pod.bsky.socialPrep notes for completed episodes can be found here (Not all episodes have prep notes).If you are enjoying the podcast please leave a review on your preferred podcast app!Feel like giving back? Donations of caffeine gratefully received!https://www.buymeacoffee.com/idiotspod

Guest: Hans Katzberg, MD Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a complex immune-mediated condition affecting the peripheral nervous system. Join Dr. Hans Katzberg, Professor of Medicine at the University of Toronto, as he explains the pathophysiology behind CIDP, risk factors in disease development, and diagnostic strategies.

For a captioned version or to access the transcript, please visit https://www.pharmaron.com/knowledge-center/dmpk-podcast-11-gut-microbiome/.In this podcast, Chris Bode (Pharmaron US Labs) interviews Peter Turnbaugh, a microbiologist and Professor of Microbiology and Immunology at the University of California San Francisco. Over the past 15-20 years, Peter has produced so much groundbreaking research in the endlessly fascinating field of the gut microbiome. His work is not limited to DMPK by any means, but in this episode, we discuss drug metabolism by gut bacteria and its impact on pharmacokinetics. Clinically, reduced efficacy and/or increased side effects observed in some patients can be attributed to the gut microbiome, including narrow therapeutic index drugs such as digoxin. You will come away with an appreciation for scientific creativity and the sometimes unexpected benefits of doing an experiment that everyone thinks is going to fail. We speculate on how much there is to learn about the possible interactions between the gut microbiome and drugs for obesity, including GLP1 agonists. Finally, we talk about some practical considerations in terms of studying bacterial drug metabolism in vitro.   The episode explores the following: How important is the gut microbiome in terms of drug metabolism? What do we know about the balance between control of the microbiome by the host and control of the host by the microbiome? What are some of the challenges of studying gut bacterial drug metabolism in vitro? Could gut bacteria play a role in the efficacy and/or side effects of GLP1 agonists such as semaglutide, used to treat obesity and diabetes? Speaker:Peter J. Turnbaugh – Professor, Department of Microbiology & Immunology at the University of CaliforniaPeter J. Turnbaugh, Ph.D., is a Professor in the Department of Microbiology & Immunology, the G.W. Hooper Research Foundation, and the Benioff Center for Microbiome Medicine at the University of California, San Francisco. He is also a CZ Biohub-San Francisco Investigator. For the past two decades, his research has focused on the metabolic activities of the trillions of microbes that colonize our adult bodies. Dr. Turnbaugh and his research group use interdisciplinary approaches in preclinical models and human cohorts to study how the gut microbiome influences nutrition and pharmacology. He received a B.A. in Biochemistry, Biophysics, and Molecular Biology from Whitman College and a Ph.D. in Microbial Genetics and Genomics from Washington University in Saint Louis. From 2010-2014 he was a Bauer Fellow in the FAS Center for Systems Biology at Harvard University, where he established an independent research group before starting his faculty position at the University of California, San Francisco. Notable honors include the Kipnis Award in Biomedical Sciences, the Needleman Pharmacology Prize, the Damon Runyon-Rachleff Innovation Award, the Searle Scholars Award, the Burroughs Wellcome Fund Investigators in the Pathogenesis of Disease Award, and fellowship in the American Academy of Microbiology.Stay tuned for more podcasts in our Pharmaron DMPK Insights Series!

La deshidratación crónica leve es una epidemia, se calcula que hasta el 55% de la población joven puede padecerla. Es una condición con frecuencia pasada por alto y que tiene serios efectos negativos sobre la cognición, la salud cardiovascular, gastrointestinal, articular, entre otros. En este episodio explicamos de qué se trata la deshidratación crónica leve, los efectos que produce, cómo detectarla y cómo prevenirla.Enlaces a nuestras redes sociales:Instagram⁠⁠⁠@brainfulnesspod⁠⁠⁠⁠⁠⁠@ladoctoraneuro⁠⁠Youtube⁠⁠@brainfulness⁠⁠Twitter/X⁠⁠⁠@brainfulness⁠pod⁠⁠Página web⁠⁠www.brainfulnes.life⁠⁠Blog⁠⁠https://brainfulness.life/blogReferencias bibliográficasMitchell, H. H., Hamilton, T. S., Steggerda, F. R., & Bean, H. W. (1945). The chemical composition of the adult human body and its bearing on the biochemistry of growth. Journal of Biological Chemistry, 158(3), 625-637.Maroudas A. Fluid transport in cartilage. Ann Rheum Dis. 1975 Dec;34 Suppl 2:Suppl 77-81. PMID: 25330584.Kenney, E. L., Long, M. W., Cradock, A. L., & Gortmaker, S. L. (2015). Prevalence of inadequate hydration among US children and adolescents: A population-based analysis. Journal of the Academy of Nutrition and Dietetics, 115(6), 943-951.Valtin H. "Drink at least eight glasses of water a day." Really? Is there scientific evidence for "8 x 8"? Am J Physiol Regul Integr Comp Physiol. 2002 Nov;283(5):R993-1004. doi: 10.1152/ajpregu.00365.2002. PMID: 12376390.Sawka MN, Burke LM, Eichner ER, Maughan RJ, Montain SJ, Stachenfeld NS. Hydration and Performance. Sports Science Exchange. 2007;20(2):1-5.Benton D, Burgess N. The effect of the consumption of water on the memory and attention of children. Appetite. 2009;53(1):143-6.Benton D, Young HA. Reducing calorie intake may not help you lose body weight. Perspect Psychol Sci. 2017;12(5):703-714. (Nota: Este es un ejemplo más reciente; el estudio de 2016 mencionado en la respuesta no es accesible, así que se proporciona esta alternativa.)Palma L, Tavares L, Santos O, et al. Dietary water affects human skin hydration and biomechanics. Clin Cosmet Investig Dermatol. 2015;8:413-21.Dennis EA, Dengo AL, Comber DL, et al. Water consumption increases weight loss during a hypocaloric diet intervention in middle-aged and older adults. Obesity (Silver Spring). 2010;18(2):300-7.Manz F, Wentz A. The importance of good hydration for the prevention of chronic diseases. Nutr Rev. 2005;63(6 Pt 2):S2-S5.Dennis EA, Dengo AL, Comber DL, et al. Water consumption increases weight loss during a hypocaloric diet intervention in middle-aged and older adults. Obesity (Silver Spring). 2010;18(2):300-7.Boschmann M, Steiniger J, Hille U, et al. Water-induced thermogenesis. J Clin Endocrinol Metab. 2003;88(12):6015-9.Shirreffs SM, Maughan RJ. The effect of alcohol on athletic performance. Curr Sports Med Rep. 2006;5(4):192-6.Sawka MN, Burke LM, Eichner ER, et al. American College of Sports Medicine position stand. Exercise and fluid replacement. Med Sci Sports Exerc. 2007;39(2):377-90.Jeukendrup AE, Currell K. Should energy drinks be banned from sport? Int J Sport Nutr Exerc Metab. 2008;18(5):519-29.Rehrer NJ, Brouns F, Beckers EJ, et al. Physiological changes and gastro-intestinal symptoms as a result of ultra-endurance running. Eur J Appl Physiol Occup Physiol. 1992;64(1):1-8.Rosner MH, Kirven J. Exercise-associated hyponatremia. Clin J Am Soc Nephrol. 2007;2(1):151-61.Hew-Butler T, Ayus JC, Kipps C, et al. Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, 2007. Clin J Sport Med. 2008;18(2):111-21.Ayus JC, Arieff A. Pathogenesis and prevention of hyponatremia. Endocrinol Metab Clin North Am. 1993;22(2):437-49.

Dr. Moshe Mittelman is hosting the world-leading expert Dr. Michael Savona and they have an attractive conversation on several mechanisms involved in the pathogenesis of MDS, including the interaction between genetics, inflammation and aging.   

Complement 3 glomerulopathy (C3G) is an ultra-rare kidney disease characterized by overactivation of the alternative complement pathway. This program provides insights into the pathogenesis of the disease. FA-11319389 12/24

In 2023, measles claimed an estimated 107,000 lives, yet vaccination has prevented a staggering 60 million deaths since 2000. Despite this, measles remains a pressing issue in many developing countries, particularly in parts of Africa and Asia. On this episode of Transmissible: A Public Health Podcast, we dive deep into the science behind this highly contagious disease. From its pathogenesis and epidemiology to the life-saving MMR vaccine and the fascinating history of measles—including its 10th-century description as being "more dreaded than smallpox"—host Jessica unpacks it all. Drawing on her career as a contractor with CDC, her experience with rare pathogens, and her passion for public health, Jessica sheds light on why measles remains a global challenge. Whether you're a public health enthusiast or just curious about infectious diseases, this episode promises to be both informative and engaging. Tune in to learn something new about a virus that's been plaguing humanity for 5,000 years. Citations: https://asm.org/articles/2019/may/measles-and-immune-amnesia#:~:text=During%20the%20acute%20phase%20of,new%2C%20MV%2Dspecific%20lymphocytes. https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-13-measles.html (vaccine safety info) https://archive.cdc.gov/www_cdc_gov/csels/dsepd/ss1978/lesson3/section2.html https://www.sciencedirect.com/science/article/abs/pii/S1045187001000589 https://www.fda.gov/vaccines-blood-biologics/vaccines/measles-mumps-and-rubella-virus-vaccine-live https://www.fda.gov/vaccines-blood-biologics/priorix https://www.cdc.gov/vaccines/vpd/mmr/hcp/about.html#vaccine-safety https://jamanetwork.com/journals/jama/article-abstract/308400#google_vignette https://www.sciencedirect.com/science/article/pii/S0755498222000422 https://scielo.org.za/scielo.php?script=sci_arttext&pid=S0256-95742010000400013 https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=1358&context=thebridge Measles, Mumps, Rubella Vaccination and Autism: A Nationwide Cohort Study: Annals of Internal Medicine: Vol 170, No 8 A Population-Based Study of Measles, Mumps, and Rubella Vaccination and Autism | New England Journal of Medicine Measles cases surge worldwide, infecting 10.3 million people in 2023 Legal: The information provided in this podcast is for informational purposes only and should not be considered medical, legal, or professional advice. Always consult with a qualified healthcare provider, public health expert, or relevant professional for guidance specific to your individual circumstances. The views expressed in this podcast are those of the host and do not necessarily reflect the opinions, policies, or positions of any current or former employers, educational institutions, or affiliations. While every effort is made to ensure the accuracy and reliability of the information presented, the host and podcast assume no responsibility for errors, omissions, or any consequences arising from the use of this information.

Listener discretion is advised. References: Gutierrez, E. (2023). The Vasopressor & Inotrope Handbook: A Practical Guide for Healthcare Professionals. Hu W, Wang X, Su G. Infective endocarditis complicated by embolic events: Pathogenesis and predictors. Clin Cardiol. 2021 Mar;44(3):307-315. doi: 10.1002/clc.23554. Epub 2021 Feb 1. PMID: 33527443; PMCID: PMC7943911. Marik PE, Farkas JD. The Changing Paradigm of Sepsis: Early Diagnosis, Early Antibiotics, Early Pressors, and Early Adjuvant Treatment. Crit Care Med. 2018 Oct;46(10):1690-1692. doi: 10.1097/CCM.0000000000003310. PMID: 30216303.

A new year brings new questions and more insights to the topic of Highly Pathogenic Avian Influenza. Dr. Mike Brasher is joined by leading experts in the field of avian influenza, Dr. Dave Stallknecht, Dr. Richard Webby, and Dr. Jennifer Ballard to discuss the current status of avian influenza, what we've learned since 2022, and what we still don't understand. Recent changes have been noted in the genetic code of the circulating virus, but what does this mean for the risk it poses to birds, mammals, and humans? How do we study these changes? What waterfowl species are most affected, and do we understand why these effects differ among species? Also discussed is recent science about risks to hunting dogs, what hunters need to do if they observe sick or dead birds, why hunters should be vigilant about being tested for avian flu if they feel ill, and how we can all work to reduce the likelihood of the virus becoming more severe. Tune in for an information-packed episode that is of growing relevance to everyone.Listen now: www.ducks.org/DUPodcastSend feedback: DUPodcast@ducks.org

In this Better Edge podcast episode, Margrit Urbanek, PhD, associate professor of Endocrinology, and doctoral student Rosie Bauer discuss key insights from their recent research on the potential role of a rare genetic variation in the LMNA gene in the development of PCOS.

Welcome to another insightful episode of PICU on Call, a podcast dedicated to current and aspiring intensivists. In this episode, our hosts, Dr. Pradip Kamat, Dr. Rahul Damania, and their colleague, Dr. Jordan Dent, delve into the complexities of managing pneumonia in pediatric patients. The discussion is anchored around a clinical case involving a 10-year-old girl presenting with difficulty breathing and a fever, suggestive of pneumonia. We will break down the key themes and insights from the case, providing a comprehensive guide to understanding and managing pediatric pneumonia.Case PresentationThe episode begins with a detailed case presentation:Patient: 10-year-old girl, 28-week preemie with chronic lung disease.Symptoms: Progressive respiratory distress over eight days, worsening cough, increased work of breathing, hypoxemia (oxygen saturation in the low 80s despite supplemental oxygen).Findings: Chest X-ray reveals bilateral lower lobe infiltrates and a left-sided pleural effusion. Lab results show elevated CRP and a positive respiratory PCR for a bacterial pathogen.This case sets the stage for an in-depth discussion on the various aspects of pediatric pneumoRisk Factors for PneumoniaUnderstanding the risk factors for pneumonia is crucial for early identification and prevention. These risk factors can be categorized into three main groups:Host FactorsIncomplete Immunization Status: Children who are not fully vaccinated are at higher risk.Young Age: Infants and young children have immature immune systems, making them more susceptible.Lower Socioeconomic Status: Limited access to healthcare and poor living conditions can increase risk.Environmental FactorsExposure to Tobacco Smoke: Secondhand smoke can damage the respiratory tract and impair immune function.Seasonal Variations: Pneumonia cases peak during fall and winter due to increased circulation of respiratory viruses.Contact with Other Children: Daycare settings and schools can facilitate the spread of infections.Healthcare-Associated FactorsProlonged Mechanical Ventilation: Increases the risk of ventilator-associated pneumonia (VAP).Nasogastric Tube Placement: Can introduce pathogens into the respiratory tract.Neuromuscular Blockade: Impairs the ability to clear secretions.Inadequate Humidification: Dry air can damage the respiratory mucosa.Pathogenesis of PneumoniaPneumonia occurs when pathogens invade the lower respiratory tract, triggering an inflammatory response. This leads to fluid...

A nearby house fire has brought several patients to your hospital via ambulance, where you are the sole provider on duty. These patients require urgent triage and stabilization before transfer to the regional burn center. You are very concerned about inhalation injury and are tasked with making complex clinical decisions in a high-pressure situation. What are the next steps? Join Drs. Kevin Foster, Tina Palmeri, Ryan Rihani, Tommy Tran, and Kiran Dyamenahalli as they explore the intricacies of managing smoke inhalation injury and more! Hosts: Tommy Tran, Tristar Skyline Medical Center Kiran Dyamenahalli, MGH Sumner Redstone Burn Center Kevin Foster, Arizona Burn Center Tina Palmeri, UC Davis Firefighters Burn Institute Regional Burn Center Ryan Rihani, UT Health Dunn Burn Center Tam Pham, Harborview Medical Center (Editor) Learning Objectives: Understand the etiology and common scenarios associated with inhalation injury  Understand the effect of inhalation injury on morbidity and mortality Describe indications for invasive airway management (intubation, bronchoscopy, and mechanical ventilation). Describe complications of inhalation injury and their management. References: Fournier, M., Turgeon, A. F., Doucette, S., Morrisette, M., Archambault, P., & Bouchard, N. (2016). Nebulized heparin for inhalation injury in burn patients: A systematic review and meta-analysis. Critical Care, 20(1), 1-10. https://doi.org/10.1186/s13054-016-1285-8 Norris, C., LaLonde, C., Slater, H., & Purser, D. (2005). Survival from inhalation injury. Burns, 31(7), 803-815. https://doi.org/10.1016/j.burns.2005.04.003 Li, W., Tang, X., Chen, Y., & Zhao, Z. (2021). Update on smoke inhalation injury: Pathogenesis, diagnosis, and treatment. Journal of Thoracic Disease, 13(4), 1797-1808. https://doi.org/10.21037/jtd-20-3328 Hahn, S. M., Kim, Y. H., Kim, K. H., & Lee, S. U. (2020). Advances in the diagnosis and treatment of smoke inhalation injury in burn patients. Acute and Critical Care, 35(1), 1-10. https://doi.org/10.4266/acc.2020.00175 Bittner, E. A., Shank, E., Woodson, L., & Martyn, J. A. (2015). Acute and long-term outcomes of burn injuries: A focus on inhalation injury. Clinics in Chest Medicine, 36(4), 549-560. https://doi.org/10.1016/j.ccm.2015.08.007 Romanowski, K. S., & Palmieri, T. L. (2019). Inhalation injury in burns: Pathophysiology, diagnosis, and treatment. Journal of Burn Care & Research, 40(5), 517-523. https://doi.org/10.1093/jbcr/irz123 Dyamenahalli, K., Garg, G., Shupp, J. W., Kuprys, P. V., Choudhry, M. A., & Kovacs, E. J. (2019). Inhalation injury: Unmet clinical needs and future research. Journal of Burn Care & Research, 40(5), 570-584. https://doi.org/10.1093/jbcr/irz055 Please visit https://behindtheknife.org to access other high-yield surgical education podcasts, videos and more.   If you liked this episode, check out our recent episodes here: https://app.behindtheknife.org/listen

Understanding Myasthenia Gravis, including pathophysiology and causes. Also features Myasthenia Gravis symptoms (and crisis!), as well as diagnosis and treatment. Consider subscribing on YouTube (if you found any of the info useful!): https://www.youtube.com/channel/UCRks8wB6vgz0E7buP0L_5RQ?sub_confirmation=1Patreon: https://www.patreon.com/rhesusmedicineBuy Us A Coffee!: https://www.buymeacoffee.com/rhesusmedicineTimestamps:0:00 What is Myasthenia Gravis?0:19 Myasthenia Gravis Pathophysiology1:38 Myasthenia Gravis Symptoms3:44 Myasthenia Gravis Causes4:30 Myasthenia Gravis Diagnosis 6:15 Myasthenia Gravis TreatmentReferencesBMJ Best Practice (2024) - “Myasthenia Gravis”. Available at https://bestpractice.bmj.com/topics/en-gb/238National Institute of Neurological Disorder and Stroke - “Myasthenia Gravis”. Available at https://www.ninds.nih.gov/health-information/disorders/myasthenia-gravisRubin, M - MSD Manual Pro (2024) - “Myasthenia Gravis”. Available at https://www.msdmanuals.com/professional/neurologic-disorders/peripheral-nervous-system-and-motor-unit-disorders/myasthenia-gravisMyasthenia Gravis Foundation Of America - “Cautionary Drugs”. Available at https://myasthenia.org/living-with-mg/mg-emergency-preparedness/cautionary-drugs/Phillips, D. W (2016) - “Pathogenesis of myasthenia gravis: update on disease types, models, and mechanisms**”.** Available at https://pmc.ncbi.nlm.nih.gov/articles/PMC4926737/MyastheniaGravis.Com - Available at https://myasthenia-gravis.com/Please remember this podcast and all content from Rhesus Medicine is meant for educational purposes only and should not be used as a guide to diagnose or to treat. Please consult a healthcare professional for medical advice. 

Dr. John Fleetham chats with Dr. Ludovico Messineo and Dr. Simon Joosten about their articles "Hypnotics on Obstructive Sleep Apnea Severity and Endotypes: A Systematic Review and Meta-Analysis" and "The Arousal Threshold: The ‘Weakest Link' in OSA Pathogenesis." 

A leader for conducting rigorous randomized trials of humans along with animal models for understanding nutrition and metabolism, Dr. Kevin Hall is a Senior Investigator at the National Institutes of Health, and Section Chief of the Integrative Physiology Section, NIDDK. In this podcast, we reviewed his prolific body of research a recent publications. The timing of optimizing our diet and nutrition seems apropos, now that we're in in the midst of the holiday season!Below is a video snippet of our conversation on his ultra-processed food randomized trial.Full videos of all Ground Truths podcasts can be seen on YouTube here. The current one is here. If you like the YouTube format, please subscribe! The audios are also available on Apple and Spotify.Note: I'll be doing a Ground Truths Live Chat on December 11th at 12 N EST, 9 AM PST, so please mark your calendar and join!Transcript with links to publications and audioEric Topol (00:05):Well, hello. This is Eric Topol with Ground Truths, and I'm really delighted to have with me today, Dr. Kevin Hall from the NIH. I think everybody knows that nutrition is so important and Kevin is a leader in doing rigorous randomized trials, which is not like what we usually see with large epidemiologic studies of nutrition that rely on food diaries and the memory of participants. So Kevin, it's really terrific to have you here.Kevin Hall (00:34):Thanks so much for the invitation.Ultra-Processed FoodsEric Topol (00:36):Yeah. Well, you've been prolific and certainly one of the leaders in nutrition science who I look to. And what I thought we could do is go through some of your seminal papers. There are many, but I picked a few and I thought we'd first go back to the one that you published in Cell Metabolism. This is ultra-processed diets cause excessive caloric intake and weight gain. (Main results in graph below.) So maybe you can take us through the principle findings from that trial.Kevin Hall (01:10):Yeah, sure. So that was a really interesting study because it's the first randomized control trial that's investigated the role of ultra-processed foods in potentially causing obesity. So we've got, as you mentioned, lots and lots of epidemiological data that have made these associations between people who consume diets that are very high in ultra-processed foods as having greater risk for obesity. But those trials are not demonstrating causation. I mean, they suggest a strong link. And in fact, the idea of ultra-processed foods is kind of a new idea. It's really sort of appeared on the nutrition science stage probably most prominently in the past 10 years or so. And I first learned about this idea of ultra-processed foods, which is really kind of antithetical to the way most nutrition scientists think about foods. We often think about foods as nutrient delivery vehicles, and we kind of view foods as being the fraction of carbohydrates versus fats in them or how much sodium or fiber is in the foods.Kevin Hall (02:17):And along came this group in Brazil who introduced this new way of classifying foods that completely ignores the nutrient composition and says what we should be doing is classifying foods based on the extent and purpose of processing of foods. And so, they categorize these four different categories. And in the fourth category of this so-called NOVA classification scheme (see graphic below) , they identified something called ultra-processed foods. There's a long formal definition and it's evolved a little bit over the years and continues to evolve. But the basic ideas that these are foods that are manufactured by industries that contain a lot of purified ingredients made from relatively cheap agricultural commodity products that basically undergo a variety of processes and include additives and ingredients that are not typically found in home kitchens, but are typically exclusively in manufactured products to create the wide variety of mostly packaged goods that we see in our supermarkets.Kevin Hall (03:22):And so, I was really skeptical that there was much more about the effects of these foods. Other than that they typically have high amounts of sugar and saturated fat and salt, and they're pretty low in fiber. And so, the purpose of this study was to say, okay, well if there's something more about the foods themselves that is causing people to overconsume calories and gain weight and eventually get obesity, then we should do a study that's trying to test for two diets that are matched for these various nutrients of concern. So they should be matched for the macronutrients, they should be matched for the sugar content, the fat, the sodium, the fiber, and people should just be allowed to eat whatever they want and they shouldn't be trying to change their weight in any way. And so, the way that we did this was, as you mentioned, we can't just ask people to report what they're eating.Kevin Hall (04:19):So what we did was we admitted these folks to the NIH Clinical Center and to our metabolic ward, and it's a very artificial environment, but it's an environment that we can control very carefully. And so, what we basically did is take control over their food environment and we gave them three meals a day and snacks, and basically for a two-week period, they had access to meals that were more than 80% of calories coming from ultra-processed foods. And then in random order, they either received that diet first and give them simple instructions, eat as much as little as you want. We're going to measure lots of stuff. You shouldn't be trying to change your weight or weight that gave them a diet that had no calories from ultra-processed foods. In fact, 80% from minimally processed foods. But again, both of these two sort of food environments were matched for these nutrients that we typically think of as playing a major role in how many calories people choose to eat.Kevin Hall (05:13):And so, the basic idea was, okay, well let's measure what these folks eat. We gave them more than double the calories that they would require to maintain their weight, and what they didn't know was that in the basement of the clinical center where the metabolic kitchen is, we had all of our really talented nutrition staff measuring the leftovers to see what it was that they didn't eat. So we knew exactly what we provided to them and all the foods had to be in our nutrition database and when we compute what they actually ate by difference, so we have a very precise estimate about not only what foods they chose to ate, but also how many calories they chose to eat, as well as the nutrient composition.And the main upshot of all that was that when these folks were exposed to this highly ultra-processed food environment, they spontaneously chose to eat about 500 calories per day more over the two-week period they were in that environment then when the same folks were in the environment that had no ultra-processed foods, but just minimally processed foods. They not surprisingly gained weight during the ultra-processed food environment and lost weight and lost body fat during the minimally processed food environment. And because those diets were overall matched for these different nutrients, it didn't seem to be that those were the things that were driving this big effect. So I think there's a couple of big take homes here. One is that the food environment really does have a profound effect on just the biology of how our food intake is controlled at least over relatively short periods of time, like the two-week periods that we were looking at. And secondly, that there's something about ultra-processed foods that seem to be driving this excess calorie intake that we now know has been linked with increased risk of obesity, and now we're starting to put some of the causal pieces together that really there might be something in this ultra-processed food environment that's driving the increased rates of obesity that we've seen over the past many decades.Eric Topol (07:18):Yeah, I mean I think the epidemiologic studies that make the link between ultra-processed foods and higher risk of cancer, cardiovascular disease, type 2 diabetes, neurodegenerative disease. They're pretty darn strong and they're backed up by this very rigorous study. Now you mentioned it short term, do you have any reason to think that adding 500 calories a day by eating these bad foods, which by the way in the American diet is about 60% or more of the average American diet, do you have any inkling that it would change after a few weeks?Kevin Hall (07:54):Well, I don't know about after a few weeks, but I think that one of the things that we do know about body weight regulation and how it changes in body weight impact both metabolism, how many calories were burning as well as our appetite. We would expect some degree of moderation of that effect eventually settling in at a new steady state, that's probably going to take months and years to achieve. And so the question is, I certainly don't believe that it would be a 500 calorie a day difference indefinitely. The question is when would that difference converge and how much weight would've been gained or lost when people eventually reached that new plateau? And so, that's I think a really interesting question. Some folks have suggested that maybe if you extrapolated the lines a little bit, you could predict when those two curves might eventually converge. That's an interesting thought experiment, but I think we do need some longer studies to investigate how persistent are these effects. Can that fully explain the rise in average body weight and obesity rates that have occurred over the past several decades? Those are open questions.Eric Topol (09:03):Yeah. Well, I mean, I had the chance to interview Chris van Tulleken who wrote the book, Ultra-Processed People and I think you might remember in the book he talked about how he went on an ultra-processed diet and gained some 20, 30 pounds in a short time in a month. And his brother, his identical twin brother gained 50, 60 pounds, and so it doesn't look good. Do you look at all the labels and avoid all this junk and ultra-processed food now or are you still thinking that maybe it's not as bad as it looks?Kevin Hall (09:38):Well, I mean I think that I certainly learned a lot from our studies, and we are continuing to follow this up to try to figure out what are the mechanisms by which this happen. But at the same time, I don't think we can throw out everything else we know about nutrition science. So just because we match these various nutrients in this particular study, I think one of the dangers here is that as you mentioned, there's 60% of the food environment in the US and Great Britain and other places consist of these foods, and so they're unavoidable to some extent, right? Unless you're one of these privileged folks who have your backyard garden and your personal chef who can make all of your foods, I'm certainly not one of those people, but for the vast majority of us, we're going to have to incorporate some degree of ultra-processed foods in our day-to-day diet.Kevin Hall (10:24):The way I sort of view it is, we really need to understand the mechanisms and before we understand the mechanisms, we have to make good choices based on what we already know about nutrition science, that we should avoid the foods that have a lot of sugar in them. We should avoid foods that have a lot of saturated fat and sodium. We should try to choose products that contain lots of whole grains and legumes and fruits and vegetables and things like that. And there's some of those, even in the ultra-processed food category. I pretty regularly consume a microwavable ready meal for lunch. It tends to be pretty high in whole grains and legumes and low in saturated fat and sugar and things like that. But to engineer a food that can heat up properly in a microwave in four minutes has some ultra-processing technology involved there. I would be pretty skeptical that that's going to cause me to have really poor health consequences as compared to if I had the means to eat homemade French fries every day in tallow. But that's the kind of comparison that we have to think about.Eric Topol (11:36):But I think what you're touching on and maybe inadvertently is in that NOVA class four, the bad ultra-processed foods, there's a long, long list of course, and some of those may be worse than others, and we haven't seen an individual ranking of these constituents. So as you're alluding to what's in that microwave lunch probably could be much less concerning than what's in these packaged snacks that are eaten widely. But I would certainly agree that we don't know everything about this, but your study is one of the most quoted studies ever in the ultra-processed food world. Now, let me move on to another trial that was really important. This was published in Nature Medicine and it's about a plant-based diet, which is of course a very interesting diet, low-fat versus an animal-based ketogenic diet. Also looking at energy intake. Can you take us through that trial?Plant-Based, Low Fat Diet vs Animal-Based, Low Carbohydrate Ketogenic DietKevin Hall (12:33):Sure. So it's actually interesting to consider that trial in the context of the trial we just talked about because both of these diets that we tested in this trial were relatively low in ultra-processed foods, and so both of them contained more than a kilogram of non-starchy vegetables as a base for designing these, again, two different food environments. Very similar overall study design where people again were exposed to either diets that were vegan plant-based diet that was really high in starches and was designed to kind of cause big insulin increases in the blood after eating the meals. And the other diet had very, very few carbohydrates of less than 10% in total, and we built on that kind of non-starchy vegetable base, a lot of animal-based products to kind of get a pretty high amount of fat and having very low carbohydrates. Both diets in this case, like I mentioned, were pretty low in ultra-processed foods, but what we were really interested in here was testing this idea that has come to prominence recently, that high carbohydrate diets that lead to really large glucose excursions after meals that cause very high insulin levels after meals are particularly obesogenic and should cause you to be hungrier than compared to a diet that doesn't lead to those large swings in glucose and insulin and the prototypical case being one that's very low in carbohydrate and might increase the level of ketones that are floating around in your blood, which are hypothesized to be an appetite suppressant. Same sort of design, these minimally processed diets that one was very high in carbs and causes large swings in insulin and the other that's very low in carbs and causes increases in ketones.Kevin Hall (14:22):We ask people, again, while you're in one food environment or the other, don't be trying to gain weight or lose weight, eat as much or as little as you'd like, and we're going to basically measure a lot of things. They again, don't know what the primary outcome of the study is. We're measuring their leftovers afterwards. And so, the surprise in this particular case was that the diet that caused the big swings in glucose and insulin did not lead to more calorie consumption. In fact, it led to about 700 calories per day less than when the same people were exposed to the ketogenic diet. Interestingly, both food environments caused people to lose weight, so it wasn't that we didn't see the effect of people over consuming calories on either diet, so they were reading fewer calories in general than they were when they came in, right. They're probably eating a pretty ultra-processed food diet when they came in. We put them on these two diets that varied very much in terms of the macronutrients that they were eating, but both were pretty minimally processed. They lost weight. They ended up losing more body fat on the very low-fat high carb diet than the ketogenic diet, but actually more weight on the ketogenic diet than the low-fat diet. So there's a little bit of a dissociation between body fat loss and weight loss in this study, which was kind of interesting.Eric Topol (15:49):Interesting. Yeah, I thought that was a fascinating trial because plant-based diet, they both have their kind of camps, you know.Kevin Hall (15:57):Right. No, exactly.Immune System Signatures for Vegan vs Ketogenic DietsEric Topol (15:58):There are people who aren't giving up on ketogenic diet. Of course, there's some risks and some benefits and there's a lot of interest of course with the plant-based diet. So it was really interesting and potentially the additive effects of plant-based with avoidance or lowering of ultra-processed food. Now, the more recent trial that you did also was very interesting, and of course I'm only selecting ones that I think are particularly, there are a lot of trials you've done, but this one is more recent in this year where you looked at vegan versus ketogenic diets for the immune signature, immune response, which is really important. It's underplayed as its effect, and so maybe you can take us through that one.[Link to a recent Nature feature on this topic, citing Dr. Hall's work]Kevin Hall (16:43):Yeah, so just to be clear, it's actually the same study, the one that we just talked about. This is a secondary sort of analysis from a collaboration we had with some folks at NIAID here at the NIH to try to evaluate immune systems signatures in these same folks who wonder what these two changes in their food environment. One is vegan, high carbohydrate low-fat diet and the other, the animal-based ketogenic diet. And again, it was pretty interesting to me that we were able to see really substantial changes in how the immune system was responding. First of all, both diets again seem to have improved immune function, both adaptive and innate immune function as compared to their baseline measurements when they came into the study. So when they're reading their habitual diet, whatever that is typically high in ultra-processed foods, they switched to both of these diets.Kevin Hall (17:39):We saw market changes in their immune system even compared to baseline. But when we then went and compared the two diets, they were actually divergent also, in other words, the vegan diet seemed to stimulate the innate immune system and the ketogenic diet seemed to stimulate the adaptive immune system. So these are the innate immune system can be thought of. Again, I'm not an immunologist. My understanding is that this is the first line defense against pathogens. It happens very quickly and then obviously the adaptive immune system then adapts to a specific pathogen over time. And so, this ability of our diet to change the immune system is intriguing and how much of that has to do with influencing the gut microbiota, which obviously the gut plays a huge role in steering our immune system in one direction versus another. I think those are some really intriguing mechanistic questions that are really good fodder for future research.Eric Topol (18:42):Yeah, I think it may have implications for treatment of autoimmune diseases. You may want to comment about that.Kevin Hall (18:51):Yeah, it's fascinating to think about that the idea that you could change your diet and manipulate your microbiota and manipulate your gut function in a way to influence your immune system to steer you away from a response that may actually be causing your body damage in your typical diet. It's a fascinating area of science and we're really interested to follow that up. I mean, it kind of supports these more anecdotal reports of people with lupus, for example, who've reported that when they try to clean up their diet for a period of time and eliminate certain foods and eliminate perhaps even ultra-processed food products, that they feel so much better that their symptoms alleviate at least for some period of time. Obviously, it doesn't take the place of the therapeutics that they need to take, but yeah, we're really interested in following this up to see what this interaction might be.Eric Topol (19:46):Yeah, it's fascinating. It also gets to the fact that certain people have interesting responses. For example, those with epilepsy can respond very well to a ketogenic diet. There's also been diet proposed for cancer. In fact, I think there's some even ongoing trials for cancer of specific diets. Any comments about that?Kevin Hall (20:10):Yeah, again, it's a really fascinating area. I mean, I think we kind of underappreciate and view diet in this lens of weight loss, which is not surprising because that's kind of where it's been popularized. But I think the role of nutrition and how you can manipulate your diet and still you can have a very healthy version of a ketogenic diet. You can have a very healthy version of a low-fat, high carb diet and how they can be used in individual cases to kind of manipulate factors that might be of concern. So for example, if you're concerned about blood glucose levels, clearly a ketogenic diet is moderating those glucose levels over time, reducing insulin levels, and that might have some positive downstream consequences and there's some potential downsides. Your apoB levels might go up. So, you have to kind of tune these things to the problems and the situations that individuals may face. And similarly, if you have issues with blood glucose control, maybe a high carbohydrate diet might not be for you, but if that's not an issue and you want to reduce apoB levels, it seems like that is a relatively effective way to do that, although it does tend to increase fasting triglyceride levels.Kevin Hall (21:27):So again, there's all of these things to consider, and then when you open the door beyond traditional metabolic health markers to things like inflammation and autoimmune disease as well as some of these other things like moderating how cancer therapeutics might work inside the body. I think it's a really fascinating and interesting area to pursue.Eric Topol (21:55):No question about it. And that also brings in the dimension of the gut microbiome, which obviously your diet has a big influence, and it has an influence on your brain, brain-gut axis, and the immune system. It's all very intricate, a lot of feedback loops and interactions that are not so easy to dissect, right?Kevin Hall (22:16):Absolutely. Yeah, especially in humans. That's why we rely on our basic science colleagues to kind of figure out these individual steps in these chains. And of course, we do need human experiments and carefully controlled experiments to see how much of that really translates to humans, so we need this close sort of translational partnership.On the Pathogenesis of Obesity, Calories In and Calories OutEric Topol (22:35):Yeah. Now, you've also written with colleagues, other experts in the field about understanding the mechanisms of pathogenesis of obesity and papers that we'll link to. We're going to link to everything for what we've been discussing about calories in, calories out, and that's been the longstanding adage about this. Can you enlighten us, what is really driving obesity and calories story?Kevin Hall (23:05):Well, I co-organized a meeting for the Royal Society, I guess about a year and a half ago, and we got together all these experts from around the world, and the basic message is that we have lots of competing theories about what is driving obesity. There's a few things that we all agree on. One is that there is a genetic component. That adiposity in a given environment is somewhere between 40% to 70% heritable, so our genes play a huge role. It seems like there's certain genes that can play a major role. Like if you have a mutation in leptin, for example, or the leptin receptor, then this can have a monogenic cause of obesity, but that's very, very rare. What seems to be the case is that it's a highly polygenic disease with individual gene variants contributing a very, very small amount to increased adiposity. But our genes have not changed that much as obesity prevalence has increased over the past 50 years. And so, something in the environment has been driving that, and that's where the real debates sort of starts, right?Kevin Hall (24:14):I happen to be in the camp that thinks that the food environment is probably one of the major drivers and our food have changed substantially, and we're trying to better understand, for example, how ultra-processed foods which have risen kind of in parallel with the increased prevalence of obesity. What is it about ultra-processed foods that tend to drive us to overconsume calories? Other folks focus maybe more on what signals from the body have been altered by the foods that we're eating. They might say that the adipose tissue because of excess insulin secretion for example, is basically driven into a storage mode and that sends downstream signals that are eventually sensed by the brain to change our appetite and things like that. There's a lot of debate about that, but again, I think that these are complementary hypotheses that are important to sort out for sure and important to design experiments to try to figure out what is more likely. But there is a lot of agreement on the idea that there's something in our environment has changed.Kevin Hall (25:17):I think there's even maybe a little bit less agreement of exactly what that is. I think that there's probably a little bit more emphasis on the food environment as opposed to there are other folks who think increased pollution might be driving some of this, especially endocrine disrupting chemicals that have increased in prevalence. I think that's a viable hypothesis. I think we have to try to rank order what we think are the most likely and largest contributors. They could all be contributing to some extent and maybe more so in some people rather than others, but our goal is to try to, maybe that's a little simple minded, but let's take the what I think is the most important thing and let's figure out the mechanisms of that most important thing and we'll, number one, determine if it is the most important thing. In my case, I think something about ultra-processed foods that are driving much of what we're seeing. If we could better understand that, then we could both advise consumers to avoid certain kinds of foods because of certain mechanisms and still be able to consume some degree of ultra-processed foods. They are convenient and tasty and relatively inexpensive and don't require a lot of skill and equipment to prepare. But then if we focus on the true bad guys in that category because we really understand the mechanisms, then I think that would be a major step forward. But that's just my hypothesis.Eric Topol (26:43):Well, I'm with you actually. Everything I've read, everything I've reviewed on ultra-processed food is highly incriminating, and I also get frustrated that nothing is getting done about it, at least in this country. But on the other hand, it doesn't have to be either or, right? It could be both these, the glycemic index story also playing a role. Now, when you think about this and you're trying to sort out calories in and calories out, and let's say it's one of your classic experiments where you have isocaloric proteins and fat and carbohydrate exactly nailed in the different diets you're examining. Is it really about calories or is it really about what is comprising the calorie?Kevin Hall (27:29):Yeah, so I think this is the amazing thing, even in our ultra-processed food study, if we asked the question across those people, did the people who ate more calories even in the ultra-processed diet, did they gain more weight? The answer is yes.Kevin Hall (27:44):There's a very strong linear correlation between calorie intake and weight change. I tend to think that I started my career in this space focusing more on the metabolism side of the equation, how the body's using the calories and how much does energy expenditure change when you vary the proportion of carbs versus fat, for example. The effect size is there, they might be there, but they're really tiny of the order of a hundred calories per day. What really struck me is that when we just kind of changed people's food environments, the magnitude of the effects are like we mentioned, 500 to 700 calories per day differences. So I think that the real trick is to figure out how is it that the brain is regulating our body weight in some way that we are beginning to understand from a molecular perspective? What I think is less well understood is, how is that food intake control system altered by the food environment that we find ourselves in?The Brain and GLP-1 DrugsKevin Hall (28:42):There are a few studies now in mice that are beginning to look at how pathways in the brain that have been believed to be related to reward and not necessarily homeostatic control of food intake. They talk to the regions of the brain that are related to homeostatic control of food intake, and it's a reciprocal sort of feedback loop there, and we're beginning to understand that. And I think if we get more details about what it is in our foods that are modulating that system, then we'll have a better understanding of what's really driving obesity and is it different in different people? Are there subcategories of obesity where certain aspects of the food environment are more important than others, and that might be completely flipped in another person. I don't know the answer to that question yet, but it seems like there are certain common factors that might be driving overall changes in obesity prevalence and how they impact this reward versus homeostatic control systems in the brain, I think are really fascinating questions.Eric Topol (29:43):And I think we're getting much more insight about this circuit of the reward in the brain with the food intake, things like optogenetics, many ways that we're getting at this. And so, it's fascinating. Now, that gets me to the miracle drug class GLP-1, which obviously has a big interaction with obesity, but of course much more than that. And you've written about this as well regarding this topic of sarcopenic obesity whereby you lose a lot of weight, but do you lose muscle mass or as you referred to earlier, you lose body fat and maybe not so much muscle mass. Can you comment about your views about the GLP-1 family of drugs and also about this concern of muscle mass loss?Kevin Hall (30:34):Yeah, so I think it's a really fascinating question, and we've been trying to develop mathematical models about how our body composition changes with weight gain and weight loss for decades now. And this has been a long topic, one of the things that many people may not realize is that people with obesity don't just have elevated adiposity, they also have elevated muscle mass and lean tissue mass overall. So when folks with obesity lose weight, and this was initially a pretty big concern with bariatric surgery, which has been the grandfather of ways that people have lost a lot of weight. The question has been is there a real concern about people losing too much weight and thereby becoming what you call sarcopenic? They have too little muscle mass and then they have difficulties moving around. And of course, there are probably some people like that, but I think what people need to realize is that folks with obesity tend to start with much higher amounts of lean tissue mass as well as adiposity, and they start off with about 50% of your fat-free mass, and the non-fat component of your body is skeletal muscle.Kevin Hall (31:45):So you're already starting off with quite a lot. And so, the question then is when you lose a lot of weight with the GLP-1 receptor agonist or with bariatric surgery, how much of that weight loss is coming from fat-free mass and skeletal muscle versus fat mass? And so, we've been trying to simulate that using what we've known about bariatric surgery and what we've known about just intentional weight loss or weight gain over the years. And one of the things that we found was that our sort of expectations for what's expected for the loss of fat-free mass with these different drugs as well as bariatric surgery, for the most part, they match our expectations. In other words, the expected amount of fat loss and fat free mass loss. The one outlier interestingly, was the semaglutide study, and in that case, they lost more fat-free mass than would be expected.Kevin Hall (32:44):Now, again, that's just raising a little bit of a flag that for whatever reason, from a body composition perspective, it's about a hundred people underwent these repeated DEXA scans in that study sponsored by Novo Nordisk. So it's not a huge number of people, but it's enough to really get a good estimate about the proportion of weight loss. Whether or not that has functional consequences, I think is the open question. There's not a lot of reports of people losing weight with semaglutide saying, you know what? I'm really having trouble actually physically moving around. I feel like I've lost a lot of strength. In fact, it seems to be the opposite, right, that the quality of the muscle there seems to be improved. They seem to have more physical mobility because they've lost so much more weight, that weight had been inhibiting their physical movement in the past.Kevin Hall (33:38):So it's something to keep an eye on. It's an open question whether or not we need additional therapies in certain categories of patients, whether that be pharmacological, there are drugs that are interesting that tend to increase muscle mass. There's also other things that we know increase muscle mass, right? Resistance exercise training, increase this muscle mass. And so, if you're really concerned about this, I certainly, I'm not a physician, but I think it's something to consider that if you go on one of these drugs, you might want to think about increasing your resistance exercise training, maybe increasing the protein content of your diet, which then can support that muscle building. But I think it's a really interesting open question about what the consequences of this might be in certain patient populations, especially over longer periods of time.Dietary Protein, Resistance Exercise, DEXA ScansEric Topol (34:30):Yeah, you've just emphasized some really key points here. Firstly, that resistance exercise is good for you anyway. And get on one of these drugs, why don't you amp it up or get it going? The second is about the protein diet, which it'd be interesting to get your thoughts on that, but we generally have too low of a protein diet, but then there are some who are advocating very high protein diets like one gram per pound, not just one gram per kilogram. And there have been studies to suggest that that very high protein diet could be harmful, but amping up the protein diet, that would be a countering thing. But the other thing you mentioned is a DEXA scan, which can be obtained very inexpensively, and because there's a variability in this muscle mass loss if it's occurring, I wonder if that's a prudent thing or if you just empirically would just do the things that you mentioned. Do you have any thoughts about that?Kevin Hall (35:32):Yeah, that's really a clinical question that I don't deal with on a day-to-day basis. And yeah, I think there's probably better people suited to that. DEXA scans, they're relatively inexpensive, but they're not readily accessible to everyone. I certainly wouldn't want to scare people away from using drugs that are now known to be very effective for weight loss and pretty darn safe as far as we can tell, just because they don't have access to a DEXA scanner or something like that.Eric Topol (36:00):Sure. No, that makes a lot of sense. I mean, the only reason I thought it might be useful is if you're concerned about this and you want to track, for example, how much is that resistant training doing?Kevin Hall (36:13):But I think for people who have the means to do that, sure. I can't see any harm in it for sure.Continuous Glucose Sensors?Eric Topol (36:19):Yeah. That gets me to another metric that you've written about, which is continuous glucose tracking. As you know, this is getting used, I think much more routinely in type one insulin diabetics and people with type 2 that are taking insulin or difficult to manage. And now in recent months there have been consumer approved that is no prescription needed, just go to the drugstore and pick up your continuous glucose sensor. And you've written about that as well. Can you summarize your thoughts on it?Kevin Hall (36:57):Yeah, sure. I mean, yeah, first of all, these tools have been amazing for people with diabetes and who obviously are diagnosed as having a relative inability to regulate their glucose levels. And so, these are critical tools for people in that population. I think the question is are they useful for people who don't have diabetes and is having this one metric and where you target all this energy into this one thing that you can now measure, is that really a viable way to kind of modulate your lifestyle and your diet? And how reliable are these CGM measurements anyway? In other words, do they give the same response to the same meal on repeated occasions? Does one monitor give the same response as another monitor? And those are the kinds of experiments that we've done. Again, secondary analysis, these trials that we talked about before, we have people wearing continuous glucose monitors all the time and we know exactly what they ate.Kevin Hall (37:59):And so, in a previous publication several years ago, we basically had two different monitors. One basically is on the arm, which is the manufacturer's recommendation, the other is on the abdomen, which is the manufacturer's recommendation. They're wearing them simultaneously. And we decided just to compare what were the responses to the same meals in simultaneous measurements. And they were correlated with each other thankfully, but they weren't as well predictive as you might expect. In other words, one device might give a very high glucose reading to consuming one meal and the other might barely budge, whereas the reverse might happen for a different meal. And so, we asked the question, if we were to rank the glucose spikes by one meal, so we have all these meals, let's rank them according to the glucose spikes of one device. Let's do the simultaneous measurements with the other device.Kevin Hall (38:53):Do we get a different set of rankings? And again, they're related to each other, but they're not overlapping. They're somewhat discordant. And so, then the question becomes, okay, well if I was basically using this one metric to kind of make my food decisions by one device, I actually start making different decisions compared to if I happen to have been wearing a different device. So what does this really mean? And I think this sort of foundational research on how much of a difference you would need to make a meaningful assessment about, yeah, this is actionable from a lifestyle perspective, even if that is the one metric that you're interested in. That sort of foundational research I don't think has really been done yet. More recently, we asked the question, okay, let's ignore the two different devices. Let's stick to the one where we put it on our arm, and let's ask the question.Kevin Hall (39:43):We've got repeated meals and we've got them in this very highly regimented and controlled environment, so we know exactly what people ate previously. We know the timing of the meals, we know when they did their exercise, we know how much they were moving around, how well they slept the night before. All of these factors we could kind of control. And the question that we asked in that study was, do people respond similarly to the same meal on repeated occasions? Is that better than when you actually give them very different meals? But they match overall for macronutrient content, for example. And the answer to that was surprisingly no. We had as much variability in the glucose response to the same person consuming the same meal on two occasions as a whole bunch of different meals. Which suggests again, that there's enough variability that it makes it difficult to then recommend on for just two repeats of a meal that this is going to be a meal that's going to cause your blood glucose to be moderate or blood glucose to be very high. You're going to have to potentially do this on many, many different occasions to kind of figure out what's the reliable response of these measurements. And again, that foundational research is typically not done. And I think if we're really going to use this metric as something that is going to change our lifestyles and make us choose some meals other than others, then I think we need that foundational research. And all we know now is that two repeats of the same meal is not going to do it.Eric Topol (41:21):Well, were you using the current biosensors of 2024 or were you using ones from years ago on that?Kevin Hall (41:27):No, we were using ones from several years ago when these studies were completed. But interestingly, the variability in the venous measurements to meal tests is also very, very different. So it's probably not the devices per se that are highly variable. It's that we don't really know on average how to predict these glucose responses unless there's huge differences in the glycemic load. So glycemic load is a very old concept that when you have very big differences in glycemic load, yeah, you can on average predict that one kind of meal is going to give rise to a much larger glucose excursion than another. But typically these kind of comparisons are now being made within a particular person. And we're comparing meals that might have quite similar glycemic loads with the claim that there's something specific about that person that causes them to have a much bigger glucose spike than another person. And that we can assess that with a couple different meals.Eric Topol (42:31):But also, we know that the spikes or the glucose regulation, it's very much affected by so many things like stress, like sleep, like exercise. And so, it wouldn't be at all surprising that if you had the exact same food, but all these other factors were modulated that it might not have the same response. But the other thing, just to get your comment on. Multiple groups, particularly starting in Israel, the Weizmann Institute, Eran Segal and his colleagues, and many subsequent have shown that if you give the exact same amount of that food, the exact same time to a person, they eat the exact same amount. Their glucose response is highly heterogeneous and variable between people. Do you think that that's true? That in fact that our metabolism varies considerably and that the glucose in some will spike with certain food and some won't.Kevin Hall (43:29):Well, of course that's been known for a long time that there's varying degrees of glucose tolerance. Just oral glucose tolerance tests that we've been doing for decades and decades we know is actually diagnostic, that we use variability in that response as diagnostic of type 2 diabetes.Eric Topol (43:49):I'm talking about within healthy people.Kevin Hall (43:53):But again, it's not too surprising that varying people. I mean, first of all, we have a huge increase in pre-diabetes, right? So there's various degrees of glucose tolerance that are being observed. But yeah, that is important physiology. I think the question then is within a given person, what kind of advice do we give to somebody about their lifestyle that is going to modulate those glucose responses? And if that's the only thing that you look at, then it seems like what ends up happening, even in the trials that use continuous glucose monitors, well big surprise, they end up recommending low carbohydrate diets, right? So that's the precision sort of nutrition advice because if that's the main metric that's being used, then of course we've all known for a very long time that lower carbohydrate diets lead to a moderated glucose response compared to higher carbohydrate diets. I think the real question is when you kind of ask the issue of if you normalize for glycemic load of these different diets, and there are some people that respond very differently to the same glycemic load meal compared to another person, is that consistent number one within that person?Kevin Hall (45:05):And our data suggests that you're going to have to repeat that same test multiple times to kind of get a consistent response and be able to make a sensible recommendation about that person should eat that meal in the future or not eat that meal in the future. And then second, what are you missing when that becomes your only metric, right? If you're very narrowly focused on that, then you're going to drive everybody to consume a very low carbohydrate diet. And as we know, that might be great for a huge number of people, but there are those that actually have some deleterious effects of that kind of diet. And if you're not measuring those other things or not considering those other things and put so much emphasis on the glucose side of the equation, I worry that there could be people that are being negatively impacted. Not to mention what if that one occasion, they ate their favorite food and they happen to get this huge glucose spike and they never eat it again, their life is worse. It might've been a complete aberration.Eric Topol (46:05):I think your practical impact point, it's excellent. And I think one of the, I don't know if you agree, Kevin, but one of the missing links here is we see these glucose spikes in healthy people, not just pre-diabetic, but people with no evidence of glucose dysregulation. And we don't know, they could be up to 180, 200, they could be prolonged. We don't know if the health significance of that, and I guess someday we'll learn about it. Right?Kevin Hall (46:36):Well, I mean that's the one nice thing is that now that we have these devices to measure these things, we can start to make these correlations. We can start to do real science to say, what a lot of people now presume is the case that these spikes can't be good for you. They must lead to increased risk of diabetes. It's certainly a plausible hypothesis, but that's what it is. We actually need good data to actually analyze that. And at least that's now on the table.Eric Topol (47:04):I think you're absolutely right on that. Well, Kevin, this has been a fun discussion. You've been just a great leader in nutrition science. I hope you'll keep up your momentum because it's pretty profound and I think we touched on a lot of the uncertainties. Is there anything that I didn't ask you that you wish I did?Kevin Hall (47:23):I mean, we could go on for hours, I'm sure, Eric, but this has been a fascinating conversation. I really appreciate your interest. Thank you.Eric Topol (47:30):Alright, well keep up the great stuff. We'll be following all your work in the years ahead, and thanks for joining us on Ground Truths today.**************************************Footnote, Stay Tuned: Julia Belluz and Kevin Hall have a book coming out next September titled “WHY WE EAT? Thank you for reading, listening and subscribing to Ground Truths.If you found this fun and informative please share it!All content on Ground Truths—its newsletters, analyses, and podcasts, are free, open-access.Paid subscriptions are voluntary. All proceeds from them go to support Scripps Research. Many thanks to those who have contributed—they have greatly helped fund our summer internship programs for the past two years. I welcome all comments from paid subscribers and will do my best to respond to them and any questions.Thanks to my producer Jessica Nguyen and to Sinjun Balabanoff for audio and video support at Scripps Research.Note on Mass Exodus from X/twitter:Many of you have abandoned the X platform for reasons that I fully understand. While I intend to continue to post there because of its reach to the biomedical community, I will post anything material here in the Notes section of Ground Truths on a daily basis and cover important topics in the newsletter/analyses. You can also find my posts at Bluesky: @erictopol.bsky.social, which is emerging as an outstanding platform for sharing life science. Get full access to Ground Truths at erictopol.substack.com/subscribe

The Filtrate:Joel TopfSwapnil HiremathWith Special Guest:Michelle Hladunewich, Nephrologist at the University of TorontoMir Melamed, Maternal-Fetal Medicine at the University of TorontoEditor Simon TopfShow NotesPriscilla Smith's letter:Dear Joel and the Freely Filtered team,I am a long-time fan of your podcast and was looking forward to hearing your recently aired discussion of the Praecis study of sflt1:PlGF use in preeclampsia. Preeclampsia and renal disease in pregnancy are areas that many nephrologists report a lack of knowledge or confidence in discussing and managing. I am a nephrologist who has been co-leading a renal pregnancy clinic in London while writing a PhD on progression of renal disease in pregnancy. I have had the immense privilege of working with experts and key opinion leaders in preeclampsia research both in the UK and internationally. As you know, preeclampsia is a serious and significant condition contributing to global maternal mortality and is also associated with future CKD and CVD risk so is both relevant and important within our professional group.Sadly, I found myself disappointed by the episode and felt it was a missed opportunity. I appreciate that you had difficulties obtaining appropriate experts to join the discussion, but perhaps it would have been better to delay production. While you all valiantly proceeded to discuss this important study, the topic is complex and there appeared to be a lack of understanding of the surrounding literature and pathogenesis of preeclampsia. Sadly, the maternal medicine expert's comments at the end of the podcast added little as she seemed determine to negate any benefit from the results despite declaring she had no experience or expertise in the use of these biomarkers.There are many people who understand the clinical aspects of preeclampsia as well as having direct experience of the use and utility of these biomarkers who would have been able to contribute much to your conversation. I look forward to future discussions of renal disease in pregnancy on your podcast and would be happy to suggest some expert panellists if you ever find yourself stuck.Kind regards,Priscilla Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia (JCI 2003)sFlt background: Pathogenesis of Preeclampsia and Therapeutic Approaches Targeting the Placenta (PubMed)PlGF background: Perspectives on the Use of Placental Growth Factor (PlGF) in the Prediction and Diagnosis of Pre-Eclampsia: Recent Insights and Future Steps (PubMed)The PRAECIS trial (NephJC | NEJM Evidence)

In another installment in the ongoing Arthritis & Rheumatology immunology series, guest David S. Pisetsky, MD, PhD, author of Unique Interplay Between Antinuclear Antibodies and Nuclear Molecules in the Pathogenesis of Systemic Lupus Erythematosus, takes us on a deep dive into research in SLE on how the combination of ANAs and immunologically active DNA can create new structures that can promote inflammation throughout the body as well as drive organ inflammation and damage.

Enterococci are commensal microbes, part of the healthy microflora populating the human gut. But they are also opportunistic pathogens and notorious nosocomial agents with intrinsic traits that promote their pathogenesis and make them difficult to kill. In the third instalment of the Nightmare Series, hosts Angela Huttner and Thomas Tängdén are joined by enterococcal experts Kimberly Kline (University of Geneva) and Louis Rice (Brown University) to discuss what make vancomycin-resistant enterococci, or VRE, such a clinical nightmare. Enterococcus faecalis and Enterococcus faecium are the focus. This episode was edited by Kathryn Hostettler and peer-reviewed by Dr. Nunzia Esposito of the University of Naples Federico II, Naples, Italy. Literature  Stellfox ME et al. J Antimicrob Chemother 14 Feb 2024. doi: 10.1128/mbio.03396-23  Rogers R & Rice LB. Clin Infect Dis 15 Jan 2024. doi: 10.1093/cid/ciad613 Lebreton F et al. Cell 18 May 2017. doi: 10.1016/j.cell.2017.04.027 Donskey CJ et al. N Engl J Med 28 Dec 2000. doi: 10.1056/NEJM200012283432604

The Filtrate:Jennie LinJoel TopfJosh WaitzmanSwapnil HiremathWith Special GuestsPedro TeixeiraJay KoynerEditor Sophia AmbrusoShow NotesThe article: A Randomized Trial of Intravenous Amino Acids for Kidney ProtectionNephJC SummaryKDIGO Clinical Practice Guideline for Acute Kidney Injury (PDF)Steve Coca study Evaluation of Short-Term Changes in Serum Creatinine Level as a Meaningful End Point in Randomized Clinical Trials (PubMed)Using Nephrocheck to prevent AKI: Prevention of cardiac surgery-associated AKI by implementing the KDIGO guidelines in high risk patients identified by biomarkers: the PrevAKI randomized controlled trial (PubMed)Brenner's Review of protein intake and renal hemodynamics: Dietary Protein Intake and the Progressive Nature of Kidney Disease: — The Role of Hemodynamically Mediated Glomerular Injury in the Pathogenesis of Progressive Glomerular Sclerosis in Aging, Renal Ablation, and Intrinsic Renal Disease (NEJM)Husain-Syed a look at preoperative renal functional reserve and risk of AKI: Preoperative Renal Functional Reserve Predicts Risk of Acute Kidney Injury After Cardiac Operation (PubMed)Dana Fuhrman review of renal functional reserve: The Role of Renal Functional Reserve in Predicting Acute Kidney Injury (PubMed)Use of SGLT2i prevented AKI in the placebo controlled trials. Clinical Adverse Events Associated with Sodium-Glucose Cotransporter 2 Inhibitors: A Meta-Analysis Involving 10 Randomized Clinical Trials and 71 553 Individuals (PubMed)Assessment of P values for demographic data in randomized controlled trials (PubMed)Tubular SecretionsSwapnil The Lord of the Rings: Rings of Power Season 2 on Amazon Prime (Wikipedia)Josh Fortnite (Website)Pedro CRRT Academy at University of Alabama Birmingham (Website)Jay Koyner Slow Horses on AppleTV (Wikipedia)Jennie Linn #KidneyWk Run Club Friday 10/25 at 6:15 am PST Meet in front of Sally's Fish House ~2 miles. Easy pace (10-12 min/mile) (Strava)Joel Topf Your Honor on Netflix (Wikipedia)

Summary From the 2024 Annual SF Dermatology Society sessions, Dr. Amit Pandya discusses the complexities of vitiligo, a common skin disorder affecting millions worldwide. He explores the importance of understanding patient perspectives, the pathogenesis of vitiligo, and the latest treatment approaches. This talk emphasizes the need for personalized patient care and the significance of early intervention for better outcomes. The session concludes with a call for increased awareness and education in dermatology.   Takeaways Vitiligo affects about 1% of Americans and 70 million people worldwide. Patients with vitiligo often feel abandoned due to a lack of specialized care. The peak age of onset for vitiligo is during young adulthood, which can be particularly stressful. Understanding the pathogenesis of vitiligo is crucial for effective treatment. The treatment of vitiligo requires patience and realistic expectations from patients. Photographs are essential for monitoring treatment progress in vitiligo patients. Public education is needed to encourage early treatment for vitiligo. Dermascopy can help assess the prognosis of vitiligo patients. Shared decision-making is vital in managing treatment options for patients. Every patient's experience with vitiligo is unique and should be approached individually.   Chapters 00:00 - Introduction to the Future of Dermatology Podcast 00:58 - The Importance of Vitiligo Awareness 02:53 - Understanding Vitiligo: Patient Perspectives 06:07 - Pathogenesis of Vitiligo 08:55 - Treatment Approaches for Vitiligo 11:50 - Prognosis and Patient Management 15:10 - Conclusion and Future Directions

Beyond the Digest are bonus episodes to the DermSurgery Digest that include reviews of interesting and relevant articles in dermatologic surgery literature. This episode features articles from the Journal of the National Comprehensive Cancer Network(JNCCN), the Journal of the American Academy of Dermatology (JAAD) and JAMA Dermatology. Articles include:Mohs Micrographic Surgery in the Surgical Treatment Paradigm of Melanoma In Situ and Invasive Melanoma: A Clinical Review of Treatment Efficacy and Ongoing Controversies. JAADEstablishing Consensus for Mohs Micrographic Surgery Techniques in the Treatment of Melanoma in Situ for Future Clinical Trials: A Modified Delphi Study. JNCCNRecurrence Rate of Small Melanoma In Situ on Low-Risk Sites Excised With a 5-mm Excisional Margin. JAMA DermatologyRecurrence Rate of Melanoma In Situ Excised With a 5-mm Excisional Margin. JAMA DermatologySubcutaneous Injection of Tranexamic Acid Reduces Postoperative Bleeding Following Mohs Micrographic Surgery: A Single Institution Cohort Study. JAADHistopathological Discrepancy of Biopsy Specimens Compared to Subsequent Mohs Surgery or Wide Local Excision Specimens. JAADExtramammary Paget Disease. Part I. Epidemiology, Pathogenesis, Clinical Features, and Diagnosis. JAADExtramammary Paget Disease. Part II. Evidence-based Approach to Management. JAADBeyond the Digest contributors to this episode include: Dermatologic Surgery Digital Content Editor Naomi Lawrence, MD; Beyond the Digest Co-host Yesul Kim, MD; Tara Jennings, MD; Sydney Proffer, MD; and Katie Shawan, MD. Your feedback is encouraged. Please contact communicationstaff@asds.net.

On episode #62 of the Infectious Disease Puscast, Daniel and Sara review the infectious disease literature for the weeks of 8/15/24 – 8/28/24. Host: Daniel Griffin and Sara Dong Subscribe (free): Apple Podcasts, RSS, email Become a patron of Puscast! Links for this episode Viral Clinician Specialty and HIV PrEP Prescription Reversals and abandonments (JAMA Network: JAMA Internal Medicine) The association between adherence to antiretroviral therapy and viral suppression under dolutegravir-based regimens (JIAS Journal of the International AIDS Society) Dexamethasone in adults with viral meningitis (CMI Clinical Microbiology and Infection) Oropouche Virus Disease Among U.S. Travelers — United States, 2024 (MMWR) Oropouche fever, the mysterious threat (LANCET: Infectious Diseases) Bacterial High rates of Non-susceptibility to common oral antibiotics in Streptococcus pneumoniae clinical isolates (OFID) New York State Department of Health Directs Providers to Discontinue Use of Ciprofloxacin to Prevent Meningococcal Disease Due to Increasing Antimicrobial Resistance (NY State: Department of Health) Tularemia Associated with Harbor Seal Necropsy — Kitsap County, Washington, October 2023 (MMWR) FDA Marketing Authorization Enables Increased Access to First Step of Syphilis Diagnosis (FDA) Clinical impact of pleural fluid Streptococcus pneumoniae PCR testing in children with complicated pneumonia (CID) The Role of the Gut, Urine and Vaginal Microbiome on the Pathogenesis of Urinary Tract Infection (OFID) Fungal The Last of US Season 2 (YouTube) Two dose levels of once-weekly fosravuconazole versus daily itraconazole in combination with surgery in patients with eumycetoma in Sudan (LANCET Infectious disease) Parasitic Usefulness of real-time PCR for urogenital schistosomiasis in preschool children in Angola (PLoS Neglected Tropical Diseases) Helminth infection driven gastrointestinal hypermotility alterations in smooth muscle instead of enteric neurons (PLoS Pathogens) Die-off reaction of Demodex mites after treating demodicosis with oral ivermectin (JAAD case reports) Miscellaneous Prevalence of carbapenem-resistant gram negative bacteria among neonates suspected for sepsis in Africa (BMC Infectious Diseases) New era of targeted clinical guidelines: IDSA (CID) Defining the landscape of educational experiences in transplant infectious diseases (OFID) Music is by Ronald Jenkees Information on this podcast should not be considered as medical advice.

Facing pre-diabetes or are your blood sugar markers are climbing up? Or maybe you just get hangry and feel like you have a lot of energy ups and downs. We've got a powerful two-pronged approach that might be right for you!   LET'S TALK THE WALK! ***NEW*** Facebook Group for Our Community! Join here for support, motivation and fun! Wellness While Walking Facebook page Wellness While Walking on Instagram Wellness While Walking on Twitter Wellness While Walking website for show notes and other information wellnesswhilewalking@gmail.com RESOURCES AND SOURCES (some links may be affiliate links) Good Energy, Dr. Casey Means The Blood Sugar Solution, Dr. Mark Hyman Eat to Beat Your Diet, Dr. William Li Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized (Supplemental Information -- Shows What the Processed vs Unprocessed Diets Consisted Of), cell.com WWW Ep. 213: Cheetos Are the Perfect Food WWW Ep. 142: Hormesis, The Good Stressors Benjamin Bikman on Instagram (Shorter article) Pre-Diabetes: Your Chance to Prevent Type 2 Diabetes, cdc.gov (Longer and more comprehensive – don't be put off, you can do it!) Metabolic Syndrome: Risk Factors, Diagnosis, Pathogenesis, and Management with Natural Approaches, sciencedirect.com DIABETES "Delay in Glucose Peak Time…in Type 2 Diabetes Patients," ncbi.nlm.nih.gov "Type 1 Diabetes," mayoclinic.org "Insulin Resistance," webmd.com (**Good article to start with**) "Diabetes," who.int "Type 1 Diabetes Linked to Lower Life Expectancy in Study," webmd.com "Diabetes Report," cdc.gov "Diabetes: Facts, Statistics, and You," healthline.com "Insulin Resistance Syndrome," webmd.com "Type 2 Diabetes, Symptoms and Causes," mayoclinic.org "Insulin Resistance and Pre-Diabetes," niddk.nih.gov   HOW TO RATE AND REVIEW WELLNESS WHILE WALKING How to Leave a Review on Apple Podcasts on Your iOS Device 1.   Open Apple Podcast App (purple app icon that says Podcasts). 2.   Go to the icons at the bottom of the screen and choose “search” 3.   Search for “Wellness While Walking” 4.   Click on the SHOW, not the episode. 5.   Scroll all the way down to “Ratings and Reviews” section 6.   Click on “Write a Review” (if you don't see that option, click on “See All” first) 7.   Then you will be able to rate the show on a five-star scale (5 is highest rating) and write a review! 8.   Thank you! I so appreciate this!   How to Leave a Review on Apple Podcasts on a Computer  1.   Visit Wellness While Walking page on Apple Podcasts in your web browser (search for Apple Podcasts or click here)  https://www.apple.com/apple-podcasts/ 2.   Click on “Listen on Apple Podcasts” or “Open the App” 3.   This will open Apple Podcasts and put in search bar at top left “Wellness While Walking” 4.   This should bring you to the show, not a particular episode – click on the show's artwork 5.   Scroll down until you see “Rating and Reviews” 6.   Click on “See All” all the way to the right, near the Ratings and Review Section and its bar chart 7.   To leave a written review, please click on “Write a Review” 8.   You'll be able to leave a review, along with a title for it, plus you'll be able to rate the show on the 5-star scale (with 5 being the highest rating) 9.   Thank you so very much!! OTHER APPS WHERE REVIEWS ARE POSSIBLE Spotify Castbox Podcast Addict Podchaser Podbean Overcast (if you star certain episodes, or every one, that will help others find the show)  Goodpods   HOW TO SHARE WELLNESS WHILE WALKING Tell a friend or family member about Wellness While Walking, maybe while you're walking together or lamenting not feeling 100% Follow up with a quick text with more info, as noted below! (My favorite is pod.link/walking because it works with all the apps!) Screenshot a favorite episode playing on your phone and share to social media or to a friend via text or email! Wellness While Walking on Apple – click the up arrow to share with a friend via text or email, or share to social media Wellness While Walking on Spotify -- click the up arrow to share with a friend via text or email, or share to social media Use this universal link for any podcast app: pod.link/walking – give it to friends or share on social media Tell your pal about the Wellness While Walking website Thanks for listening and now for sharing! : )       DISCLAIMER Neither I nor many of my podcast guests are doctors or healthcare professionals of any kind, and nothing on this podcast or associated content should be considered medical advice. The information provided by Wellness While Walking Podcast and associated material, by Whole Life Workshop and by Bermuda Road Wellness LLC is for informational and entertainment purposes only. It is not intended to be a substitute for professional medical advice, diagnosis or treatment. Always seek the advice of your physician or other qualified health care provider with any questions you may have regarding a medical condition or treatment, and before undertaking a new health care regimen, including walking.     Thanks for listening to Wellness While Walking, a walking podcast and a "best podcast for walking"!          

I was lucky. A doctor tested me for diabetes, for seemingly no reason. Too many of us are walking around with pre-diabetes or Type 2 diabetes without a diagnosis, because our medical system doesn't…. well, tune in for what it doesn't do and what we need to do to make up for it. We can do it!   LET'S TALK THE WALK! ***NEW*** Facebook Group for Our Community! Join here for support, motivation and fun! Wellness While Walking Facebook page Wellness While Walking on Instagram Wellness While Walking on Twitter Wellness While Walking website for show notes and other information wellnesswhilewalking@gmail.com     RESOURCES AND SOURCES (some links may be affiliate links) DON'T SIT AND WAIT FOR DIABETES! Benjamin Bikman on Instagram Good Energy, Dr. Casey Means (Shorter article) Pre-Diabetes: Your Chance to Prevent Type 2 Diabetes, cdc.gov (Longer and more comprehensive – don't be put off, you can do it!) Metabolic Syndrome: Risk Factors, Diagnosis, Pathogenesis, and Management with Natural Approaches, sciencedirect.com DIABETES "Delay in Glucose Peak Time…in Type 2 Diabetes Patients," ncbi.nlm.nih.gov "Type 1 Diabetes," mayoclinic.org "Insulin Resistance," webmd.com (**Good article to start with**) "Diabetes," who.int "Type 1 Diabetes Linked to Lower Life Expectancy in Study," webmd.com "Diabetes Report," cdc.gov "Diabetes: Facts, Statistics, and You," healthline.com "Insulin Resistance Syndrome," webmd.com "Type 2 Diabetes, Symptoms and Causes," mayoclinic.org "Insulin Resistance and Pre-Diabetes," niddk.nih.gov SLEEP HEADPHONES (I strongly recommend you use a corded, and not a wireless product) CozyPhones AcousticSheep Sleep Phones GRATITUDE "Gratitude Influences Sleep Through the Mechanism of PreSleep Cognitions," greatergood.berkeley.edu   HOW TO RATE AND REVIEW WELLNESS WHILE WALKING How to Leave a Review on Apple Podcasts on Your iOS Device 1.   Open Apple Podcast App (purple app icon that says Podcasts). 2.   Go to the icons at the bottom of the screen and choose “search” 3.   Search for “Wellness While Walking” 4.   Click on the SHOW, not the episode. 5.   Scroll all the way down to “Ratings and Reviews” section 6.   Click on “Write a Review” (if you don't see that option, click on “See All” first) 7.   Then you will be able to rate the show on a five-star scale (5 is highest rating) and write a review! 8.   Thank you! I so appreciate this!   How to Leave a Review on Apple Podcasts on a Computer  1.   Visit Wellness While Walking page on Apple Podcasts in your web browser (search for Apple Podcasts or click here)  https://www.apple.com/apple-podcasts/ 2.   Click on “Listen on Apple Podcasts” or “Open the App” 3.   This will open Apple Podcasts and put in search bar at top left “Wellness While Walking” 4.   This should bring you to the show, not a particular episode – click on the show's artwork 5.   Scroll down until you see “Rating and Reviews” 6.   Click on “See All” all the way to the right, near the Ratings and Review Section and its bar chart 7.   To leave a written review, please click on “Write a Review” 8.   You'll be able to leave a review, along with a title for it, plus you'll be able to rate the show on the 5-star scale (with 5 being the highest rating) 9.   Thank you so very much!! OTHER APPS WHERE REVIEWS ARE POSSIBLE Spotify Castbox Podcast Addict Podchaser Podbean Overcast (if you star certain episodes, or every one, that will help others find the show)  Goodpods   HOW TO SHARE WELLNESS WHILE WALKING Tell a friend or family member about Wellness While Walking, maybe while you're walking together or lamenting not feeling 100% Follow up with a quick text with more info, as noted below! (My favorite is pod.link/walking because it works with all the apps!) Screenshot a favorite episode playing on your phone and share to social media or to a friend via text or email! Wellness While Walking on Apple – click the up arrow to share with a friend via text or email, or share to social media Wellness While Walking on Spotify -- click the up arrow to share with a friend via text or email, or share to social media Use this universal link for any podcast app: pod.link/walking – give it to friends or share on social media Tell your pal about the Wellness While Walking website Thanks for listening and now for sharing! : )       DISCLAIMER Neither I nor many of my podcast guests are doctors or healthcare professionals of any kind, and nothing on this podcast or associated content should be considered medical advice. The information provided by Wellness While Walking Podcast and associated material, by Whole Life Workshop and by Bermuda Road Wellness LLC is for informational and entertainment purposes only. It is not intended to be a substitute for professional medical advice, diagnosis or treatment. Always seek the advice of your physician or other qualified health care provider with any questions you may have regarding a medical condition or treatment, and before undertaking a new health care regimen, including walking.     Thanks for listening to Wellness While Walking, a walking podcast and a "best podcast for walking"!        

In this episode, we dive into the complexities of Bartonella, a genus of gram-negative, facultative intracellular bacteria known for its ability to evade the immune system and persist in host cells such as endothelial cells and erythrocytes. We explore the specific pathogenesis mechanisms of Bartonella henselae, including its interaction with cell adhesion molecules which facilitate its intracellular entry and survival. Additionally, we discuss the clinical manifestations and epidemiological significance of Bartonella as a common co-infection in Lyme disease patients, emphasizing its role in chronic symptoms such as swollen lymph nodes and vascular-related skin lesions. Topics: 1. Introduction - Overview of Chronic Inflammatory Response Syndrome and biotoxin illness. 2. Overview of Bartonella - Definition and general characteristics of Bartonella as a genus of gram-negative bacteria. - Explanation of facultative intracellular pathogens and their survival mechanisms. 3. Transmission Modes - Common vectors: fleas, lice, ticks, and the role of arthropod vectors in Bartonella transmission. - Other transmission routes: animal scratches/bites (particularly from cats), contaminated needles / blood transfusions. 4. Pathogenesis of Bartonella - Initial entry and dissemination through the circulatory system. - Predilection for endothelial cells and specific mechanisms of endothelial cell invasion. - Role of Bartonella adhesin A and its interaction with fibronectin and integrins. - Signaling pathways and cytoskeletal changes leading to endocytosis. 5. Immune Evasion and Infection Persistence - Intracellular residency in endothelial cells to evade neutrophils. - Ability to infect and persist in red blood cells and macrophages. - Impact on lymph nodes and immune response leading to swollen lymph nodes. 6. Clinical Manifestations - Specific diseases caused by different Bartonella species: - Bartonella henselae: Cat scratch fever - Bartonella quintana: Trench fever - Bartonella bacilliformis: Carrion's disease - Symptoms of Bartonella infections, including swollen lymph nodes, bone pain, and skin markings. - Severe cases leading to Bacillary Angiomatosis and vascular-related skin lesions. 7. Summary and Implications - Recap of Bartonella's impact as a Lyme co-infection. - Reminder of the diversity of Bartonella species and their varied clinical presentations. - Importance of tailored medical guidance due to the complexity of co-infections. Thank you to our episode sponsor: ⁠⁠⁠⁠Liver Medic⁠⁠⁠⁠⁠ Use code Chloe20 to save 20% on ⁠⁠⁠⁠⁠⁠"Leaky Gut Repair"⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠Brendan's YouTube Channel⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠https://x.com/livermedic⁠⁠⁠⁠⁠⁠ Thanks for tuning in! Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Follow Chloe on TikTok @chloe_c_porter Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to purchase products, subscribe to our mailing list, and more! --- Support this podcast: https://podcasters.spotify.com/pod/show/chloe-porter6/support

Uncover the unexpected link between chronic inflammation, PCOS, and endometriosis. Learn actionable tips to manage it effectively and improve these hormonal disorders. You may be surprised how simple lifestyle changes can lead to improved symptom management and an overall better quality of life. We uncover how adopting an anti-inflammatory diet, exercise, stress coping strategies, and professional support can make a real difference in your hormonal health. There's a path forward, and you can start making a positive change today. In this episode, we: Discuss the two different types of inflammation and how they impact your body Explore inflammation's role in worsening PCOS and endometriosis features Discover effective strategies for managing chronic inflammation to better your health Episode links: PCOS Recovery Program Waitlist (available wordlwide) 1-on-1 Dietitian Nutrition Coaching Programs (available for Ontario and British Columbia residents) References: Aboeldalyl, S., James, C., Seyam, E., Ibrahim, E. M., Shawki, H. E.-D., & Amer, S. (2021). The Role of Chronic Inflammation in Polycystic Ovarian Syndrome-A Systematic Review and Meta-Analysis. International Journal of Molecular Sciences, 22(5), 2734-. https://doi.org/10.3390/ijms22052734 Grassi, A. (2023). PCOS Nutrition Center. The Best Ways to Lower Inflammation for PCOS. https://www.pcosnutrition.com/lower-inflammation-for-pcos/ Helena Teede et al. International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome 2023. Monash University. https://doi.org/10.26180/24003834.v1  Hussain, Y., Khan, H., Alotaibi, G., Khan, F., Alam, W., Aschner, M., Jeandet, P., & Saso, L. (2022). How Curcumin Targets Inflammatory Mediators in Diabetes: Therapeutic Insights and Possible Solutions. Molecules (Basel, Switzerland), 27(13), 4058-. https://doi.org/10.3390/molecules27134058 Pahwa R, Goyal A, Jialal I. Chronic Inflammation. [Updated 2023 Aug 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK493173/ Rudnicka, E., Suchta, K., Grymowicz, M., Calik-Ksepka, A., Smolarczyk, K., Duszewska, A. M., Smolarczyk, R., & Meczekalski, B. (2021). Chronic Low Grade Inflammation in Pathogenesis of PCOS. International Journal of Molecular Sciences, 22(7), 3789-. https://doi.org/10.3390/ijms22073789 Rudnicka, E., Kunicki, M., Suchta, K., Machura, P., Grymowicz, M., & Smolarczyk, R. (2020). Inflammatory Markers in Women with Polycystic Ovary Syndrome. BioMed Research International, 2020, 4092470–10. https://doi.org/10.1155/2020/4092470 Shorakae, S., Ranasinha, S., Abell, S., Lambert, G., Lambert, E., de Courten, B., & Teede, H. (2018). Inter‐related effects of insulin resistance, hyperandrogenism, sympathetic dysfunction and chronic inflammation in PCOS. Clinical Endocrinology (Oxford), 89(5), 628–633. https://doi.org/10.1111/cen.13808 Helena Teede et al. International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome 2023. Monash University. https://doi.org/10.26180/24003834.v1 

Episode 171: Postpartum Blues, Depression, and PsychosisFuture Dr. Nguyen defines and explains the difference between baby blues, depression, and psychosis. Dr. Arreaza added comments about screening and management of these conditions. Written by Vy Nguyen, OMSIII, Western University of Health Sciences, College of Osteopathic Medicine of the Pacific. Comments by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Introduction.Pregnancy is one of the most well-celebrated milestones in one's life. However, once the baby is born, the focus of the family and society quickly shifts to the new member. It is important to continue to care for our mothers and offer them support physically and mentally as they begin their transition into their role. Peripartum mood disorders affect both new and experienced mothers as they navigate through the challenges of motherhood. The challenges of motherhood are not easy to spot, and they include sleep deprivation, physical exhaustion, dealing with pain, social isolation, and financial pressures, among other challenges. Let's focus on 3 aspects of the postpartum period: Postpartum Blues (PPB), Post-partum Depression (PPD) and Post-partum Psychosis (PPP). By the way, we briefly touched on this topic in episode 20, a long time ago. Postpartum blues (PPB) present as transient and self-limiting low mood and mild depressive symptoms that affect more than 50% of women within two or three days of childbirth and resolve within two weeks of onset. Symptoms vary from crying, exhaustion, irritability, anxiety, appetite changes, and decreased sleep or concentration to mood lability. Women are at risk for PPB.Several factors are thought to contribute to the increased risk of postpartum blues including a history of menstrual cycle-related mood changes, mood changes associated with pregnancy, history of major depression, number of lifetime pregnancies, or family history of postpartum depression. Pathogenesis of PPB: While pathogenesis remains unknown, hormonal changes such as a dramatic decrease in estradiol, progesterone, and prolactin have been associated with the development of postpartum blues. In summary, PPB is equivalent to a brief, transient “sad feeling” after the delivery. Peripartum depression (PPD) occurs in 20% of women and is classified as depressive symptoms that appear within six weeks to 1 year after childbirth. Those with baby blues have an increased risk of developing postpartum depression. About 50% of “postpartum” major depressive episodes begin before delivery, thus the term has been updated from “postpartum” to “peripartum” depressive episodes. Some risk factors include adolescent patients, mothers who deliver premature infants, and women living in urban areas. Interestingly, African American and Hispanic mothers are reported to have onset of symptoms within two weeks of delivery instead of six like their Caucasian counterparts. Additional risks include psychological risks such as a personal history of depression, anxiety, premenstrual syndrome, and sexual abuse; obstetric risks such as emergency c-sections and hospitalizations, preterm or low birth infant, and low hemoglobin; social risks such as lack of social support, domestic violence in form of spousal physical/sexual/verbal abuse; lifestyle risks such as smoking, eating sleep patterns and physical activities. Peripartum depression can present with or without psychotic features, which may appear between 1 in 500 or 1 in 1,000 deliveries, more common in primiparous women. Pathogenesis of PPD: Much like postpartum blues, the pathogenesis of postpartum depression is unknown. However, it is known that hormones can interfere with the hypothalamic-pituitary-adrenal axis (HPA) and lactogenic hormones. HPA-releasing hormones increase during pregnancy and remain elevated up to 12 weeks postpartum. The body receptors in postpartum depression are susceptible to the drastic hormonal changes following childbirth which can trigger depressive symptoms. Low levels of oxytocin and prolactin also play a role in postpartum depression causing moms to have trouble with lactation around the onset of symptoms. The USPSTF recommends screening for depression in the adult population, including pregnant and postpartum persons, as well as older adults. Edinburgh Postnatal Depression Scale (EPDS) can be used in postpartum and pregnant persons (Grade B recommendation).Postpartum psychosis (PPP) is a psychiatric emergency that often presents with confusion, paranoia, delusions, disorganized thoughts, and hallucinations. Around 1-2 out of 1,000 new moms experience postpartum psychosis with the onset of symptoms as quickly as several days and as late as six weeks after childbirth. Given the high risk of suicide and harm, individuals with postpartum psychosis require immediate evaluation and treatment. Postpartum psychosis is considered multifactorial, and the single most important risk factor is first pregnancy with family or personal history of bipolar 1 disorder. Other risk factors include a prior history of postpartum psychosis, family history of psychosis, history of schizoaffective disorder or schizophrenia, or discontinuation of psychiatric medications. Studies show that patients with a history of decreased sleep due to manic episodes are twice as likely to have postpartum psychosis at some point in their lives. However, approximately 50% of mothers who experience psychosis for the first time do not have a history of psychiatric disorder or hospitalization. Evaluation.Symptoms of postpartum blues should not meet the criteria for a major depressive episode and should resolve in 2 weeks. The Edinburg Postpartum Depression Scale which is a useful tool for assessing new moms with depressive symptoms. Postpartum depression is diagnosed when the patient presents with at least five depressive symptoms for at least 2 weeks. According to the DSM5, postpartum depression is defined as a major depressive episode with peripartum onset of mood symptoms during pregnancy or in the 4 weeks following delivery. Symptoms for diagnosis include changes in sleep, interest, energy, concentration, appetite, psychomotor retardation or agitation, feeling of guilt or worthlessness, and suicidal ideation or attempt. These symptoms are not associated with a manic or hypomanic episode and can often lead to significant impediments in daily activities. Peripartum-onset mood episodes can present with or without psychotic features. The depression can be so severe that the mother commits infanticide. Infanticide can happen, for example, with command hallucinations or delusions that the infant is possessed.While there are no standard screening criteria in place of postpartum psychosis, questionnaires mentioned earlier such as the Edinburg Postpartum Depression Scale can assess a patient's mood and identify signs of depression and mania. It is important after a thorough history and physical examination to order labs to rule out other medical conditions that can cause depressive and psychotic symptoms. Disorders like electrolyte imbalance, hepatic encephalopathy, thyroid storm, uremia, substance use, infections, and even stroke can mimic a psychiatric disorder. So, How can we treat patients who are diagnosed with a peripartum mood disorder?Management.On the spectrum of peripartum mood disorders, postpartum blues are the least severe and should be self-limiting by week 2. However, patients should be screened for suicidal ideation, paranoia, and homicidal ideation towards the newborn. Physicians should provide validation, education, and resources especially support with sleep and cognitive therapy and/or pharmacotherapy can be recommended if insomnia persists. Regarding postpartum depression, the first-line treatment includes psychotherapy and antidepressants. For those with mild to moderate depression or hesitant to start on medications, psychosocial and psychotherapy alone should be sufficient. However, for those with moderate to severe symptoms, a combination of therapy and antidepressants, such as selective serotonin reuptake inhibitors, is recommended. Once an effective dose is reached, patients should be treated for an additional 6 to 12 months to prevent relapse. In severe cases, patients may need to be hospitalized to treat their symptoms and prevent complications such as self-harm or infanticide.Most SSRIs can be detected in breast milk, but only 10 percent of the maternal level. Thus, they are considered safe during breastfeeding of healthy, full-term infants. So, you mentioned SSRIs, but also SNRIs, bupropion, and mirtazapine are reasonable options for treatment. In patients who have never been treated with antidepressants, zuranolone (a neuroactive steroid) is recommended. Zuranolone is easy to take, works fast, and is well tolerated. Treatment with zuranolone is consistent with practice guidelines from the American College of Obstetricians and Gynecologists.While there are no current guidelines to manage postpartum psychosis, immediate hospitalization is necessary in severe cases. Patients can be started on mood stabilizers such as lithium, valproate, and lamotrigine, and atypical antipsychotics such as quetiapine, and olanzapine, to name a few. Medications like lithium can be eliminated through breast milk and can expose infants to toxicity.The use of medications such as SSRIs, carbamazepine, valproate, and short-acting benzodiazepines are relatively safe and can be considered in those with plans to breastfeed. Ultimately, it is a decision that the patient can make after carefully discussing and weighing the pros and cons of the available medical management. While the prognosis of peripartum mood disorders is relatively good with many patients responding well to treatments, these disorders can have various negative consequences. Individuals with a history of postpartum blues are at increased risk of developing postpartum depression. Similarly, those with a history of postpartum psychosis are at risk of experiencing another episode of psychosis in future pregnancies. Additionally, postpartum depression can have a detrimental effect on mother-infant bonding and affect the growth and development of the infant. These children may have difficulties with social interactions, cognitive development, and depression. In summary, following the birth of a baby can pose new challenges and often is a stressful time for not only the mother but also other family members. Validation and reassurance from primary care physicians in an empathetic and understanding manner may offer support that many mothers may not have in their close social circle. As the first contact, primary care physicians can identify cues and offer support promptly that will not only improve the mental well-being of mothers but also that of the growing children.___________________________Conclusion: Now we conclude episode number 171, “Postpartum blues, depression, and psychosis.” These conditions may be more common than you think. So, be alert during your prenatal and postpartum visits and start management as needed. Psychotherapy and psychosocial therapy alone may be effective but do not hesitate to start antidepressants or antipsychotics when necessary. Make sure you involve the family and the patient in the decision-making process to implement an effective treatment.This week we thank Hector Arreaza and Vy Nguyen. Audio editing by Adrianne Silva.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Raza, Sehar K. and Raza, Syed. Postpartum Psychosis. National Library of Medicine. Last updated Jun 26, 2023. https://www.ncbi.nlm.nih.gov/books/NBK544304/Balaram, Kripa and Marwaha, Raman. Postpartum Blues. National Library of Medicine. Last updated Mar 6, 2023. https://www.ncbi.nlm.nih.gov/books/NBK554546/Mughal, Saba, Azhar, Yusra, Siddiqui, Waquar. Postpartum Depression. National Library of Medicine. Last updated Oct 7, 2022. https://www.ncbi.nlm.nih.gov/books/NBK519070/Royalty-free music used for this episode: Good Vibes by Simon Pettersson, downloaded on July 20, 2023, from https://www.videvo.net/royalty-free-music/.

Parkinson's disease is a neurodegenerative disorder characterized by uncontrollable movements, stiffness, and cognitive decline. Curious? Come learn more! Please rate, review, and subscribe and if you have any questions, comments, concerns, queries, or complaints, please email me at neuroscienceamateurhour@gmail.com or DM me at NeuroscienceAmateurHour on Instagram.Also if you have the means/desire to financially support this podcast - please go to https://www.buymeacoffee.com/neuroscienceI really appreciate it!!!Citations and relevant papers are below. National Institute on Aging. Parkinson's Disease: Causes, Symptoms, and Treatments. National Institute on Aging. Hogg E, Frank S, Oft J, Benway B, Rashid MH, Lahiri S. Urinary Tract Infection in Parkinson's Disease. Journal of Parkinson's Disease. 2022;12(3):743-757. ‌Yu J. Stages of Parkinson's | Parkinson's Foundation. www.parkinson.org. Published 2022. ‌Zhang ZX, Dong ZH, Román GC. Early Descriptions of Parkinson Disease in Ancient China. Archives of Neurology. 2006;63(5):782. ‌2-Minute Neuroscience: Direct Pathway of the Basal Ganglia. www.youtube.com. 2-Minute Neuroscience: Indirect Pathway of the Basal Ganglia. www.youtube.com. ‌Thanvi B, Lo N, Robinson T. Levodopa-induced dyskinesia in Parkinson's disease: clinical features, pathogenesis, prevention and treatment. Postgraduate Medical Journal. 2007;83(980):384-388. Zhang JF, Wang XX, Feng Y, Fekete R, Jankovic J, Wu YC. Impulse Control Disorders in Parkinson's Disease: Epidemiology, Pathogenesis and Therapeutic Strategies. Frontiers in Psychiatry. 2021;12. Hisahara S, Shimohama S. Dopamine Receptors and Parkinson's Disease. International Journal of Medicinal Chemistry. 2011;2011:1-16. Houston. Tmc.edu. Published October 20, 2020. https://nba.uth.tmc.edu/neuroscience/m/s3/chapter04.html‌Ovallath S, Sulthana B. Levodopa: History and Therapeutic Applications. Annals of Indian Academy of Neurology. 2017;20(3):185-189. ‌Levodopa | Parkinson's Foundation. www.parkinson.org. https://www.parkinson.org/living-with-parkinsons/treatment/prescription-medications/levodopa‌Kelly MJ, Baig F, Hu MTM, Okai D. Spectrum of impulse control behaviours in Parkinson's disease: pathophysiology and management. Journal of Neurology, Neurosurgery & Psychiatry. 2020;91(7):703-711. ‌Gerfen CR, Surmeier DJ. Modulation of Striatal Projection Systems by Dopamine. Annual Review of Neuroscience. 2011;34(1):441-466. ‌Sayare S. The Woman Who Could Smell Parkinson's. The New York Times. https://www.nytimes.com/2024/06/14/magazine/parkinsons-smell-disease-detection.html. Published June 14, 2024. ‌Blandini F, Nappi G, Tassorelli C, Martignoni E. Functional changes of the basal ganglia circuitry in Parkinson's disease. Progress in Neurobiology. 2000;62(1):63-88. ‌Lanciego JL, Luquin N, Obeso JA. Functional Neuroanatomy of the Basal Ganglia. Cold Spring Harbor Perspectives in Medicine. 2012;2(12):a009621-a009621. Climate ConfidentWith a new episode every Wed morning, the Climate Confident podcast is weekly podcast...Listen on: Apple Podcasts SpotifySupport the Show.

In this episode, Charmaine, a seasoned dietitian, and Ghalia, an expert coach in the Reversing Diabetes Program, unravel the complexities of managing diabetes in the digital age. Navigating through the overwhelming and often conflicting information online, they shed light on scientifically backed blood glucose lowering hacks that actually work!Join the journey as they share two commonly overlooked factors that can help you progress further in your journey towards reversing diabetes!If you are looking to know more about what you can do starting from today to improve your insulin sensitivity and metabolic health so that you can reverse diabetes, then this podcast episode is a must-listen!ReferencesSpiegel, K., Leproult, R., & Van Cauter, E. (1999). Impact of sleep debt on metabolic and endocrine function. The Lancet, 354(9188), 1435-1439.Buxton, O. M., Pavlova, M., Reid, E. W., Wang, W., Simonson, D. C., & Adler, G. K. (2010). Sleep restriction for 1 week reduces insulin sensitivity in healthy men. Diabetes, 59(9), 2126-2133.Spiegel, K., Tasali, E., Penev, P., & Van Cauter, E. (2004). Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Annals of Internal Medicine, 141(11), 846-850.Chaput, J. P., Després, J. P., Bouchard, C., & Tremblay, A. (2007). Short sleep duration is associated with reduced leptin levels, elevated ghrelin levels, and increased body mass index. Sleep, 30(11), 1429-1437.Donga, E., Van Dijk, M., Van Dijk, J. G., Biermasz, N. R., Lammers, G. J., van Kralingen, K. W., ... & Romijn, J. A. (2010). A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects. Journal of Clinical Endocrinology & Metabolism, 95(6), 2963-2968.Leproult, R., Copinschi, G., Buxton, O., & Van Cauter, E. (1997). Sleep loss results in an elevation of cortisol levels the next evening. Sleep, 20(10), 865-870.Rizza, R. A. (2010). Pathogenesis of fasting and postprandial hyperglycemia in type 2 diabetes: Implications for therapy. Diabetes, 59(11), 2697-2707.Rosmond, R., Dallman, M. F., & Björntorp, P. (1998). Stress-related cortisol secretion in men: Relationships with abdominal obesity and endocrine, metabolic and hemodynamic abnormalities. Journal of Clinical Endocrinology & Metabolism, 83(6), 1853-1859.Black, P. H. (2003). The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X. Brain, Behavior, and Immunity, 17(5), 350-364.Purnell, J. Q., Kahn, S. E., Samuels, M. H., Brandon, D., Loriaux, D. L., & Schwartz, R. S. (2009). Enhanced cortisol production rates, free cortisol, and 11β-HSD-1 expression correlate with visceral fat and insulin resistance in men: Effect of weight loss. American Journal of Physiology-Endocrinology and Metabolism, 296(2), E351-E357.Adam, T. C., & Epel, E. S. (2007). Stress, eating and the reward system. Physiology & Behavior, 91(4), 449-458.   12. Choi, J. H., Joseph, L., & Pilote, L. (2013). Obesity and C-reactive protein in various populations: A systematic review and meta-analysis. Obesity Reviews, 14(3), 232-244.⇰FREE WEBINAR TRAINING & OTHER LINKS: https://stan.store/reversingdiabetesrevolutionMy name is Charmaine and I'm the registered dietitian who helps people reverse Typ

Don't worry, Helen is OK. She's missing from this episode, but will be back next week. In her absence, Lynne brings you the lost episode, finally. She will tell you about an alleged Powerade poisoner and how this specific poison (antifreeze) affects your innards. In the end you'll also hear about the founding of the modern FDA.  National Suicide Prevention Lifeline: 1-800-273-8255 National toll-free Poison Help Hotline: 1-800-222-1222. Special note: Dr. Helen Shui is truly a doctor, but is working under a pseudonym for privacy reasons. Dr. Lynne Kramer is using her real name.  Music by Helen Shui and Caplixo. Cover art by Lynne Kramer.  Sources: Mass. Woman Charged With Murder in Boyfriend's Poisoning With Antifreeze by Kaitlin McKinley Becker and Lara Salahi Salisbury woman held without bail in poisoning case - press release from Essex District Attorney's Office Woman suspected of fatally poisoning boyfriend with antifreeze in Powerade and recording him ‘thrashing about' is ordered to stay behind bars by Matt Naham The Tragic Case of Poisoning That Finally Got Us Safe Drugs by Mikkael A. Sekeres The Accidental Poison That Founded the Modern FDA by Julian G. West Sulfanilamide Disaster by Carol Ballentine Ethylene Glycol Toxicity by Aruba Iqbal; Jason J. Glagola; and Thomas M. Nappe Ethylene Glycol Toxicity: Chemistry, Pathogenesis, and Imaging by Michael M. Moore, M.D., Sangam G. Kanekar, M.D., and Rajiv Dhamija, M.D. Survival and complete recovery after severe acute ethylene glycol poisoning - a case report by Andreja Sinkovic and Rok Stopar Ethylene glycol poisoning reviewed and updated by Jesse Borke, MD, and David C Dugdale MD What Are the Toxicological Effects of Ethylene Glycol Poisoning? By ATSDR Testing for Ethyl Alcohol (Alcohol) and Other Volatiles by Amitava Dasgupta and Amer Wahed Clinical Features of Reported Ethylene Glycol Exposures in the United States by Meghan A Jobson, Susan L Hogan, Colin S Maxwell, Yichun Hu, Gerald A Hladik, Ronald J Falk, Michael C Beuhler, and William F Pendergraft 3rd Please contact us with questions/concerns/comments at defunctdoctorspodcast@gmail.com. @defunctdoctorspodcast on Instagram, Facebook, X (Twitter), Threads, YouTube, and TikTok.  Follow Lynne on Instagram @lynnedoodles555

Featuring perspectives from Ms Courtney Arn, Dr Floor J Backes, Dr Kathleen N Moore and Ms Jaclyn Shaver, including the following topics: Introduction: The Incidence, Pathogenesis and Prognosis of Ovarian Cancer (0:00) Genetic Testing for Newly Diagnosed Advanced Ovarian Cancer (11:01) The Role of PARP Inhibitor Maintenance for Newly Diagnosed Advanced Ovarian Cancer (19:02) Side Effects Associated with PARP Inhibitors (29:58) Dosing, Adherence and Other Issues with PARP Inhibitors for Ovarian Cancer (48:29) The Potential Role of PARP Inhibitors in Combination with Anti-PD-1/PD-L1 Antibodies for Advanced Ovarian Cancer Management (54:11) PARP Inhibitors for Relapsed/Refractory Ovarian Cancer (1:00:36) The Current Role of Mirvetuximab Soravtansine for Ovarian Cancer Treatment (1:07:14) Toxicities with Mirvetuximab Soravtansine (1:11:53) The Incidence and Management of HER2-Positive Ovarian Cancer (1:18:18) NCPD information and select publications

The Filtrate:Joel TopfSwapnil HiremathAC GomezNayan AroraWith Special Guest:Anuja Java, complement god and pre-eclampsia research (Twitter)Shannon M. Clark, MD, FACOG, an honest to god, true, maternal-fetal medicine specialist. (Website | Instagram)Editor Nayan AroraShow NotesCHIP Study from 2015 (NEJM | NephMadness 2015) CHAP study from 2022 (NEJM | NephJC)NephMadness 2024 coverage of the diagnosis of preeclampsia sFlt background: Pathogenesis of Preeclampsia and Therapeutic Approaches Targeting the Placenta (PubMed)PlGF background: Perspectives on the Use of Placental Growth Factor (PlGF) in the Prediction and Diagnosis of Pre-Eclampsia: Recent Insights and Future Steps (PubMed)The PRAECIS trial (NephJC | NEJM Evidence)You may just want to listen to Anna Burgner discuss preeclampsia with Kenar Jhaveri and Koyal Jain (GN in Ten) for the NephMadness PodCrawlBene Gesserit (Wikipedia)Pathogenesis of preeclampsia: the genetic component (PubMed)Tubular SecretionsSwap Slow Horses on Apple TV (Wikipedia)AC Hidden Figures (Amazon)Nayan Baseball, little leagueAnuja Young Sheldon (Wikipedia)Joel Dune audiobook (Amazon)

Our March pick for The Morbidly Curious Book Club -- "Pathogenesis" with author Jonathan Kennedy Join the Morbidly Curious Book Club Today: themorbidlycuriousbookclub.com “In medicine, pathogenesis refers to the origins and development (genesis) of a disease (pathos), with a particular focus on the way that pathogens infect our cells and the effect this has on our bodies. In the pages that follow, we will explore how viruses, bacteria, and other microbes impact aggregations of bodies–that is, the body politic, body economic, and body social … Over the last couple of years, COVID-19 has affected all our lives to such an extent that it has become a cliche to say that the pandemic is unprecedented and extraordinary. But when we place coronavirus in its historical and scientific context, it becomes very clear that there is little about it that is new or remarkable. Recurring outbreaks of infectious diseases have been a feature of human existence for millennia. Epidemics have played a critical role in, among other things, the transformation from a planet inhabited by multiple species of humans to one in which jomo sapiens reigned supreme; the replacement of nomadic foraging with sedentary agriculture; the decline of the great empires of antiquity; the rise of new world religions; the transition from feudalism to capitalism; European colonialism; and the Agricultural and Industrial revolutions. In other words, bacteria and viruses have been instrumental in the emergence of the modern world … We don't make history in circumstances of our own choosing … It's a bacterial world, and we're just squatting here.” Welcome to the Morbidly Curious Book Club's Podcast! In this episode, we are discussing our March 2024 book pick, “PATHOGENESIS: A History of the World in Eight Plagues” by Jonathan Kennedy. About: This humbling and revelatory book shows how infectious disease has shaped humanity at every stage, from the first success of Homo sapiens over the equally intelligent Neanderthals to the fall of Rome and the rise of Islam. How did the Black Death lead to the birth of capitalism? And how did the Industrial Revolution lead to the birth of the welfare state? In this revelatory book, Dr Jonathan Kennedy argues that the myth of human exceptionalism overstates the role that we play in social and political change. Instead, it is the humble microbe that wins wars and topples empires. Infectious diseases are not just something that happens to us, but a part of who we are. The only reason humans don't lay eggs is that a virus long ago inserted itself into our DNA. In fact, 8% of the human genome was put there by viruses. We have been thinking about the survival of the fittest all wrong: human evolution is not simply about our strength and intelligence, but about what viruses can and can't use for their benefit. Drawing on the latest research in fields ranging from genetics and anthropology to archaeology and economics, Pathogenesis takes us through 60,000 years of history, exploring eight major outbreaks of infectious disease that have made the modern world. Bacteria and viruses were protagonists in the demise of the Neanderthals, the growth of Islam, the transition from feudalism to capitalism, the devastation wrought by European colonialism, and the evolution of the United States from an imperial backwater to a global superpower. Even Christianity rose to prominence in the wake of a series of deadly pandemics that swept through the Roman Empire in the second and third centuries: Caring for the sick turned what was a tiny sect into one of the world's major religions. By placing disease at the center of his wide-ranging history of humankind, Kennedy challenges some of the most fundamental assumptions about our collective past—and urges us to view this moment as another disease-driven inflection point that will change the course of history. Provocative and brimming with insight, Pathogenesis transforms our understanding of the human story by confronting our ongoing battle with infectious diseases globally. Kennedy shows how germs have been responsible for some of the seismic revolutions in human history, and how the crises they precipitate offer vital opportunities to change course. Join the Patreon page here to donate: https://patreon.com/TheMorbidlyCuriousBookClub?utm_medium=clipboard_copy&utm_source=copyLink&utm_campaign=creatorshare_creator&utm_content=join_link Inquiries: themorbidlycuriousbookclub@gmail.com

In this bonus episode of Blood Podcast, Associate Editor, Dr. Freda Stevenson is joined by Drs. Karin Tarte, Andrea Ratke, and Leandro Cerchietti to discuss the Review Series on the influence of the tumor microenvironment on the pathogenesis of B-cell lymphomas. Find the full review series in Blood Journal volume 143 issue 12. 

Today, Ali and Asif discuss the controversial topic of whether you can separate the art from the artist (3:05). They discuss various opinion articles on this subject and the 'cancelling' of historical figures such as Oscar Wilde and various politicians. They discuss how different types of art may allow this separation to be made easier or harder. They compare authors to actors/directors to stand up comedians and singers. They also discuss how weak versus strong apologies can change someone's viewpoint on an artist. The guys conclude by discussing the case of Michael Jackson and the sexual abuse allegations against him. Because Jackson suffered from vitiligo, in the second half the guys discuss this skin disease (38:36). Asif talks about the presumed cause as well as how it is diagnosed. Ali then asks Asif about the psychological toll the disease can take as well as the treatment and prognosis.    The opinions expressed are those of the hosts, and do not reflect those of any other organizations. This podcast and website represents the opinions of the hosts. The content here should not be taken as medical advice. The content here is for entertainment and informational purposes only, and because each person is so unique, please consult your healthcare professional for any medical questions.    Music courtesy of Wataboi and 8er41 from Pixabay   Contact us at doctorvcomedian@gmail.com   Follow us on Social media: Twitter: @doctorvcomedian Instagram:  doctorvcomedian   Show Notes: It's Okay to Like Good Art by Bad People: https://www.theatlantic.com/magazine/archive/2023/05/separate-art-from-artist-cancel-culture-monsters-book/673497/ Can You Love the Art and Hate the Monster https://www.newyorker.com/books/under-review/can-you-love-the-art-and-hate-the-artist This New Book Asks: Can You Separate the Art From the Artist? https://www.anothermag.com/design-living/14867/monsters-a-fans-dilemma-claire-dederer-cancel-culturehttps://www.nytimes.com/2021/11/03/opinion/music-pop-culture-justice.html Can We Separate Art from the Artist? Should We? https://observer.com/2023/01/can-we-separate-art-from-the-artist-should-we/ What do we do when the art we love was created by a monster? https://www.vox.com/culture/2018/10/11/17933686/me-too-separating-artist-art-johnny-depp-woody-allen-michael-jackson-louis-ck What Do We Do with the Art of Monstrous Men? https://www.theparisreview.org/blog/2017/11/20/art-monstrous-men/ Rihanna: I have forgiven Chris Brown, I truly love him: https://uk.news.yahoo.com/rihanna-chris-brown-112742317.html?guccounter=1&guce_referrer=aHR0cHM6Ly93d3cuZ29vZ2xlLmNvbS8&guce_referrer_sig=AQAAAHQ_aSIGLrcQ0yotID_BwInwuH3Ebaz4Y2W_eqc6tfSey2PpDBXElC2YbC0tfdGCchWPoKs90wjV2aRkrvzLQKftF-gs-YXUQJmnuV0dTuQRUWG9g6EWkLmj5z-IjL-1QDDz4qrVz7rxLOXIR8C1jCG08XJ5Vhq8rsxUPT2yp4xj Jian Ghomeshi found not guilty on choking and all sex assault charges: https://www.cbc.ca/news/canada/toronto/jian-ghomeshi-sexual-assault-trial-ruling-1.3505446 Rob Ford on drug use: 'You name it, I pretty well covered it': https://www.cbc.ca/news/canada/toronto/rob-ford-on-drug-use-you-name-it-i-pretty-well-covered-it-1.2693774 Why are celebrities accused of sexual harassment so bad at apologies? https://www.salon.com/2018/01/06/why-are-celebrities-accused-of-sexual-harassment-so-bad-at-apologies/ I Made the Pizza Cinnamon Rolls from Mario Batali's Sexual Misconduct Apology Letter https://www.everywhereist.com/2018/01/i-made-the-pizza-cinnamon-rolls-from-mario-batalis-sexual-misconduct-apology-letter/  Aziz Ansari Is Guilty. Of Not Being a Mind Reader https://www.nytimes.com/2018/01/15/opinion/aziz-ansari-babe-sexual-harassment.html Shane Gillis was fired from ‘SNL' for racist and homophobic jokes. Now he's going to host: https://www.nbcnews.com/news/shane-gillis-saturday-night-live-fired-now-hosting-rcna137161 Winnie Harlow: Her Emotional Story With Vitiligo: https://www.healthinsight.ca/advocacy/winnie-harlow-her-emotional-story-with-vitiligo/ Bullies made Winnie Harlow suicidal but now Lewis Hamilton's stunning girlfriend loves the skin she's in: https://www.thesun.co.uk/tvandshowbiz/1752326/bullies-made-winnie-harlow-suicidal-but-now-lewis-hamiltons-stunning-girlfriend-loves-the-skin-shes-in/ Vitiligo: A Narrative Review: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9586189/ Vitiligo: https://www.ncbi.nlm.nih.gov/books/NBK559149/ Beyond skin white spots: Vitiligo and associated comorbidities: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9995999/ Vitiligo, from Pathogenesis to Therapeutic Advances: State of the Art: https://www.mdpi.com/1422-0067/24/5/4910 Understanding the symptoms of vitiligo: https://www.medicalnewstoday.com/articles/245081#treatment

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/SVX865. CME/MOC/AAPA credit will be available until March 7, 2025.Evolving Concepts in the Pathogenesis of Inflammatory Dermatologic Disorders and the Rationale for Targeted Biologic Therapy: Focus on Moderate to Severe Atopic Dermatitis, Prurigo Nodularis, Chronic Urticaria, and Bullous Pemphigoid In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Sanofi and Regeneron Pharmaceuticals.Disclosure PolicyAll relevant conflicts of interest have been mitigated prior to the commencement of the activity.Faculty/Planner DisclosuresCo-Chair/PlannerAdam Friedman, MD, FAAD, has a financial interest/relationship or affiliation in the form of:Consultant and/or Advisor for Arcutis Biotherapeutics, Inc.; Incyte; Janssen Pharmaceuticals, Inc.; and Regeneron Pharmaceuticals Inc./Sanofi.Grant/Research Support from Incyte and Janssen Pharmaceuticals, Inc.Speaker for Bristol Myers Squibb; Incyte; Janssen Pharmaceuticals, Inc.; and Regeneron Pharmaceuticals Inc./Sanofi.Co-Chair/PlannerShawn Kwatra, MD, has a financial interest/relationship or affiliation in the form of:Consultant and/or Advisor for AbbVie Inc.; Amgen Inc.; Arcutis Biotherapeutics, Inc.; Asian Pharmaceuticals Pvt. Ltd.; Bristol Myers Squibb; Cara Therapeutics; Castle Biosciences, Inc.; Celldex Therapeutics; Dermavant Sciences, Inc.; Galderma; Genzada Pharmaceuticals USA, Inc.; Incyte; Johnson & Johnson Services, Inc.; LEO Pharma A/S; Novartis Pharmaceuticals Corporation; Pfizer; Regeneron Pharmaceuticals Inc.; and Sanofi.Grant/Research Support from Galderma; Incyte; Pfizer; and Sanofi.Co-Chair/PlannerPeter A. Lio, MD, has a financial interest/relationship or affiliation in the form of:Consultant and/or Advisor for AbbVie Inc.; Almirall, S.A.; Amyris, Inc.; AOBiome; ASLAN Pharmaceuticals Pte Ltd; Bristol Myers Squibb; Burt's Bees Products Company; Concerto Biosciences; Dermavant Sciences, Inc.; Galderma S.A.; Leo Pharma Inc.; Lilly; L'Oréal USA, Inc.; Merck & Co., Inc.; Micreos B.V.; MyOR; Pfizer; Pierre Fabre group; Regeneron Pharmaceuticals Inc./Sanofi Genzyme; Theraplex; UCB, Inc.; and Verrica Pharmaceuticals.Grant/Research Support from AbbVie Inc. and Regeneron Pharmaceuticals Inc./Sanofi Genzyme.Speakers Bureau participant with AbbVie Inc.; Galderma S.A.; Incyte; Leo Pharma Inc.; Lilly; L'Oréal USA, Inc.; Pfizer; and Regeneron Pharmaceuticals Inc./Sanofi Genzyme.Co-Chair/PlannerProfessor Dedee Murrell has a financial interest/relationship or affiliation in the form of:Consultant and/or Advisor for Amryt Pharma plc; Castle Creek Biosciences, Inc.; Krystal Biotech; and RHEACELL GmbH & Co. KG.Planning Committee and Reviewer DisclosuresPlanners, independent reviewers, and staff of PVI, PeerView Institute for Medical Education, do not have any relevant financial relationships related to this CE activity unless listed below.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/SVX865. CME/MOC/AAPA credit will be available until March 7, 2025.Evolving Concepts in the Pathogenesis of Inflammatory Dermatologic Disorders and the Rationale for Targeted Biologic Therapy: Focus on Moderate to Severe Atopic Dermatitis, Prurigo Nodularis, Chronic Urticaria, and Bullous Pemphigoid In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Sanofi and Regeneron Pharmaceuticals.Disclosure PolicyAll relevant conflicts of interest have been mitigated prior to the commencement of the activity.Faculty/Planner DisclosuresCo-Chair/PlannerAdam Friedman, MD, FAAD, has a financial interest/relationship or affiliation in the form of:Consultant and/or Advisor for Arcutis Biotherapeutics, Inc.; Incyte; Janssen Pharmaceuticals, Inc.; and Regeneron Pharmaceuticals Inc./Sanofi.Grant/Research Support from Incyte and Janssen Pharmaceuticals, Inc.Speaker for Bristol Myers Squibb; Incyte; Janssen Pharmaceuticals, Inc.; and Regeneron Pharmaceuticals Inc./Sanofi.Co-Chair/PlannerShawn Kwatra, MD, has a financial interest/relationship or affiliation in the form of:Consultant and/or Advisor for AbbVie Inc.; Amgen Inc.; Arcutis Biotherapeutics, Inc.; Asian Pharmaceuticals Pvt. Ltd.; Bristol Myers Squibb; Cara Therapeutics; Castle Biosciences, Inc.; Celldex Therapeutics; Dermavant Sciences, Inc.; Galderma; Genzada Pharmaceuticals USA, Inc.; Incyte; Johnson & Johnson Services, Inc.; LEO Pharma A/S; Novartis Pharmaceuticals Corporation; Pfizer; Regeneron Pharmaceuticals Inc.; and Sanofi.Grant/Research Support from Galderma; Incyte; Pfizer; and Sanofi.Co-Chair/PlannerPeter A. Lio, MD, has a financial interest/relationship or affiliation in the form of:Consultant and/or Advisor for AbbVie Inc.; Almirall, S.A.; Amyris, Inc.; AOBiome; ASLAN Pharmaceuticals Pte Ltd; Bristol Myers Squibb; Burt's Bees Products Company; Concerto Biosciences; Dermavant Sciences, Inc.; Galderma S.A.; Leo Pharma Inc.; Lilly; L'Oréal USA, Inc.; Merck & Co., Inc.; Micreos B.V.; MyOR; Pfizer; Pierre Fabre group; Regeneron Pharmaceuticals Inc./Sanofi Genzyme; Theraplex; UCB, Inc.; and Verrica Pharmaceuticals.Grant/Research Support from AbbVie Inc. and Regeneron Pharmaceuticals Inc./Sanofi Genzyme.Speakers Bureau participant with AbbVie Inc.; Galderma S.A.; Incyte; Leo Pharma Inc.; Lilly; L'Oréal USA, Inc.; Pfizer; and Regeneron Pharmaceuticals Inc./Sanofi Genzyme.Co-Chair/PlannerProfessor Dedee Murrell has a financial interest/relationship or affiliation in the form of:Consultant and/or Advisor for Amryt Pharma plc; Castle Creek Biosciences, Inc.; Krystal Biotech; and RHEACELL GmbH & Co. KG.Planning Committee and Reviewer DisclosuresPlanners, independent reviewers, and staff of PVI, PeerView Institute for Medical Education, do not have any relevant financial relationships related to this CE activity unless listed below.

Dr. Neelika Malavige is the Head of Dengue Global Programme and Scientific Affairs at the Drugs for Neglected Diseases Initiative and a Professor in the Department of Immunology and Molecular Medicine at the University of Sri Jayewardenepura. Her research focuses on dengue: its pathogenesis, vascular leak, immune correlates of protection, and biomarkers. She talks about the disease burden of dengue and her investigations into risk factors for severe disease. She also discusses her research on COVID-19 vaccines and the role of the microbiome in colon cancer, as well as how she's working to grow research capabilities in Sri Lanka.

Dr. Eric Skaar is Director of the Institute for Infection, Immunology and Inflammation, Director of the Division of Molecular Pathogenesis, the Ernest W. Goodpasture Chair in Pathology, and Vice Chair for Research and a University Distinguished Professor in the Department of Pathology, Microbiology, and Immunology at Vanderbilt University. Eric is a bacteriologist who studies the impact of nutrition on infectious disease. His research examines how the food we eat affects our susceptibility to bacterial infection and how the bacteria that infect us get food once they are inside our bodies. He earned his B.S. in Bacteriology from the University of Wisconsin-Madison, his Ph.D. in Immunology and Microbial Pathogenesis from Northwestern University, and his M.P.H. in Epidemiology and Biostatistics from Northwestern University. Afterwards, he completed a postdoctoral fellowship in microbiology at the University of Chicago before joining the faculty at Vanderbilt in 2005. Eric has received numerous awards and honors for his research including being named an American Asthma Foundation Scholar, receipt of Vanderbilt University's Stanley Cohen Award for Excellence in Research Bridging Disciplines, the Pfizer ASPIRE Young Investigator Award, the Vanderbilt Chancellor's Award for Research, and more. He has also won a variety of awards for exceptional mentorship and teaching, including the Vanderbilt Molecular Pathology and Immunology Graduate Program Teacher of the Year Award, the F. Peter Guengerich, Ph.D., Award, the Vanderbilt University Medical Center Postdoc Mentor of the Year Award, and others. In addition, he is an elected Fellow of the American Association for the Advancement of Science and the American Academy of Microbiology. In our interview, Eric shares more about his life and science.

Attention Deficit Hyperactivity Disorder (ADHD) is: A neurobiological disorder that presents in childhood with the core symptoms of inattention, hyperactivity, and/or impulse control problems. The symptoms are present across multiple domains: social, domestic, academic, as well as cognitive and behavioral functioning. Pathogenesis: not very well understood. Deficits are in area of: - Frontal-subcortical areas dealing with executive function - May also involve working memory impairments and information processing speed deficits Neuroimaging shows structural brain abnormalities in ADHD: - smaller volumes of frontal cortex, cerebellum, and subcortical structures. - Abnormalities in the prefrontal and parietal circuits. Early studies suggest that the subcortical abnormalities noted in childhood normalize in adulthood but that cortical abnormalities may last. Studies suggest hypoactivity of dopamine and norepinephrine in the frontal-subcortical circuits contributes to presentation. Genetically, risk of ADHD in parents or siblings is increased 2-8x and twin studies show heritability of 76%. ADHD is a syndrome with two core symptom categories: hyperactivity/impulsivity and inattention. One potential intervention for attention problems is to get rid of digital distractions. I use Zenze - a robust app-blocking app which allows you to block any apps or content you'd like according to whatever schedule you'd like. You can block social media apps during work hours or video streaming at night - whatever you need. Personally, I use it to block all social media/video/entertainment apps at nighttime to prevent bedtime binging. Link: https://apps.apple.com/us/app/zenze-phone-time-limit/id6447419790https://play.google.com/store/apps/details?id=org.atmana.zenze&pcampaignid=web_share Brain Health with Dr. Nissen brings you advancements in medicine, #neuroscience, psychiatry, and #nutrition to help you live a better life. Dr. Nissen's expert interviews reveal new, evidence-based approaches to enhancing mental health, sharpening cognition, and optimizing performance. With topics such as #Alzheimer's disease, #neuromodulation, #depression, the Mediterranean #Diet, and #psychedelics, this show is sure to expose listeners to new topics on the frontiers of medicine and neuroscience. Join our community at DrNissen.com Subscribe to the podcast at https://podcasts.apple.com/us/podcast... Dr. Nissen is a medical doctor (M.D.) and therapist. This show is intended for entertainment and educational purposes only and does not substitute personalized medical advice. By listening to this podcast, no doctor-patient relationship is established. Please speak with your doctor before attempting any medical or major diet and lifestyle changes. Check out Dr. Nissen's children's book on empathy and emotional intelligence, Emily Empathy! http://bit.ly/emilyempathy #depression #mentalhealth #wellness #health #healthylifestyle #medicine #treatment #medical #healthcare #psychotherapy #adhd #adhdmom #executivefunction

El papel de la microbiota en la salud y en las enfermedades está siendo destacado por numerosos estudios desde su descubrimiento hace unas décadas. Dependiendo de las regiones localizadas, la microbiota se puede clasificar en microbiota intestinal, oral, respiratoria y cutánea.  Las comunidades microbianas están en simbiosis con nosotros, el huésped, contribuyendo a la homeostasis y regulando la función inmunitaria. Sin embargo, la disbiosis de la microbiota puede provocar una desregulación de las funciones corporales y un sinnúmero de enfermedades como las enfermedades cardiovasculares, enfermedades inflamatorias y autoimmunes, los cánceres, y las enfermedades respiratorias, entre otros.  Nuestro invitado es el Dr. Jaime Belkind-Gerson quien por segunda vez, se une a esta conversación en Pediatras en Línea.  El Dr. Belkind-Gerson es Profesor Asociado de Pediatría, Director del Programa de Neurogastroenterología, Director del Laboratorio de Investigación Nervioso Entérico del Instituto de Salud Digestivo de la Escuela de Medicina de la Universidad de Colorado, Children´s Hospital Colorado. Instagram: @jaimebelkindgerson    Lectura sugerida en este episodio:  ​​Microbiota in health and diseases | Signal Transduction and Targeted Therapy (nature.com) ​​The human microbiome in disease and pathology - PubMed (nih.gov) ​​​​IJMS | Free Full-Text | The Role of the Human Microbiome in the Pathogenesis of Pain (mdpi.com)   ¿Tienes algún comentario sobre este episodio o sugerencias de temas para un futuro podcast? Escríbenos a pediatrasenlinea@childrenscolorado.org.  

An Interview with Kevin Winthrop_ Three Questions About COVID 19 Does GnRHa Reduce Premature Ovarian Insufficiency in SLE Patients on Cyclophosphamide_ Identifying New Biomarkers in the Pathogenesis of SLE-PAH Less (Glucocorticoids) is More in Lupus Nephritis Lupus and the Patient Perspective Lupus Nephritis Therapy Paradigm Shift PR3+ in Lupus Nephritis Racial and Ethnic Differences in Efficacy of Beliumumab in SLE Reproductive History, HPV Vaccination Among Women with SLE and  RA The Lupus APOL1 Story

Identifying New Biomarkers in the Pathogenesis of SLE-PAH No Increased Mortality in Patients with RA Receiving Checkpoint Inhibitors Simulated JAK Trials to Counter ORAL Survelliance The FOREMOST Study_ Apremilast in PsA The SMART Study_ Split Dose Oral Methotrexate Upadacitinib for Pain_ Is That Real_

View the Show Notes Page for This Episode Become a Member to Receive Exclusive Content Sign Up to Receive Peter's Weekly Newsletter Ted Schaeffer is an internationally recognized urologist who specializes in prostate cancer. In this episode, Ted delves deep into the realm of prostate health, starting with strategies for vigilance and effective management of the issues that can arise with aging, including urinary symptoms, prostatitis, pelvic pain, and prostate inflammation. Ted sheds light on the popular drug finasteride, renowned for its dual purpose in prostate shrinkage and hair loss prevention, as well as the contentious topic of post-finasteride syndrome. Ted then shifts to the topic of cancer, explaining how androgens, genetics, and non-genetic factors contribute to the pathogenesis of prostate cancer. He provides valuable insights into cancer screening, examining blood-based screening tools like PSA and the use of MRI in facilitating biopsies and their interpretation. Finally, he explores the various treatment options for prostate cancer, including surgical interventions, androgen deprivation therapy, and more. We discuss: Changes to the prostate with age and problems that can develop [3:45]; Behavioral modifications to help manage nocturnal urinary frequency and other lower urinary tract symptoms [8:30]; Pharmacologic tools for treating nocturnal urinary frequency and lower urinary tract symptoms [16:30]; Surgical tools for treating symptoms of the lower urinary tract [26:15]; HoLEP surgery for reducing prostate size [32:30]; Prostate size: correlation with cancer and considerations for small prostates with persistent symptoms [40:30]; Prostatitis due to infection: symptoms, pathogenesis, and treatment [46:45]; Prostatitis caused by factors besides infection [58:45]; How to minimize risk of urosepsis in patients with Alzheimer's disease [1:05:00]; Prostate cancer: 5-alpha reductase inhibitors, how androgens factor into pathogenesis, and more [1:10:00]; Post-finasteride syndrome [1:18:15]; The relationship between testosterone and DHT and the development of prostate cancer over a man's lifetime [1:26:30]; How genetic analysis of a tumor can indicate the aggressiveness of cancer [1:35:15]; Pathogenesis and genetic risk factors of prostate cancer and the use of PSA to screen for cancer [1:37:45]; Non-genetic risk factors for prostate cancer [1:45:45]; Deep dive into PSA as a screening tool: what is PSA, definition of terms, and how to interpret results [1:56:30]; MRI as a secondary screening tool and the prostate biopsy options [2:13:15]; Ted's ongoing randomized trial comparing different methods of prostate biopsy [2:24:00]; Determining when a biopsy is necessary, interpreting results, explaining Gleason score, and more [2:27:00]; Implications of a Gleason score of 7 or higher [2:46:45]; Metastasis of prostate cancer to different body locations, treatment options, staging, and considerations for patients' quality of life and survival [2:53:30]; How prostate cancer surgery has improved [3:09:30];; Questions to ask your neurologist if you are considering prostatectomy for cancer [3:21:45]; and More. Connect With Peter on Twitter, Instagram, Facebook and YouTube

Today, you'll learn about how researchers are using stem cells to cure infertility in mice, the health benefits of honey made by ants, and the potential emotional toll of using AI at work. Ovarian Failure Cure “Stem Cell Therapy Restores Fertility in Mouse Model.” by Katie Brighton. 2023. https://www.technologynetworks.com/tn/news/stem-cell-therapy-restores-fertility-in-mouse-model-376618“Fertility restoration in mice with chemotherapy induced ovarian failure using differentiated iPSCs.” by Kevin M. Elias, et al. 2023. https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(23)00280-3/fulltext“Pathogenesis and Causes of Premature ovarian Failure: An Update.” by Mahbod Ebrahimi, M.D. & Firoozeh Akbari Asbagh, M.D. 2011. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4059950/“Mechanisms of epigenetic memory.” by Agustina D'Urso & Jason H. Brickner. 2014. https://www.sciencedirect.com/science/article/abs/pii/S0168952514000584Honeypot Ants “Western science catches up with First Nations' medicinal use of ant honey.” The University of Sydney. 2023. https://www.scimex.org/newsfeed/western-science-catches-up-with-first-nations-medicinal-use-of-ant-honey“Honeypot Ant Facts.” Fact Animal. N.d. https://factanimal.com/honeypot-ant/“Honeypot Ant: Good At Sharing.” San Diego Zoo Wildlife Explorers. 2023. https://sdzwildlifeexplorers.org/animals/honeypot-antAI Insomnia“Loneliness, insomnia linked to work with AI systems.” American Psychological Association. 2023. https://www.sciencedaily.com/releases/2023/06/230612114659.htm“Loneliness, insomnia linked to work with AI systems.” American Psychological Association. 2023. https://www.apa.org/news/press/releases/2023/06/loneliness-insomnia-ai-systems Hosted on Acast. See acast.com/privacy for more information.

Pathogenesis: A History of the World in Eight Plagues author Jonathan Kennedy joins us to discuss how microscopic pathogens have shaped our world. What We Discuss with Jonathan Kennedy: If we were to weigh all the bacteria on Earth, their mass would be about 1,000 times more than all humans. If all of the viruses on the planet were laid end to end, they would stretch for 100 million light years. About eight percent of the human genome's DNA comes from retroviral infections we've endured over our evolution. From them, we've inherited memory and the ability to give birth to live young. Our gut microbiota communicates with our brains and can directly affect our mood and influence our behavior. We modern humans have our ancestors' romantic soirees with Neanderthals to thank for genetic defenses against countless viral diseases. How the transition from hunting and gathering to agriculture was a double-edged sword that brought us innovative progress and population-decimating pandemics. And much more... Full show notes and resources can be found here: jordanharbinger.com/875 This Episode Is Brought To You By Our Fine Sponsors: jordanharbinger.com/deals Sign up for Six-Minute Networking — our free networking and relationship development mini course — at jordanharbinger.com/course! Like this show? Please leave us a review here — even one sentence helps! Consider including your Twitter handle so we can thank you personally!

In this two-part series, we come to you LIVE! from the 2023 Annual meeting of the American Association of Endocrine Surgeons in Birmingham, Alabama. If you think evaluating and managing patients with primary hyperparathyroidism is difficult, patients with secondary and tertiary hyperparathyroidism can be even more difficult to evaluate and manage. Join Drs. Barb Miller, Sophie Dream, Jessica Liu McMullin, and Herb Chen as they break down the controversies and complexities associated with evaluation and management of these patients and discuss the recently published AAES guidelines on the definitive surgical management of patients with secondary and tertiary renal hyperparathyroidism. Part 1 focuses on the impetus for creation of these guidelines, the differences in evaluation and indication for surgery when seeing patients with renally mediated hyperparathyroidism, and preoperative planning. Part 2 focuses on intraoperative and postoperative management, parathyroid autotransplantation, and renal transplant recipients. Hosts:  - Barbra S. Miller, MD (Moderator), Clinical Professor of Surgery, The Ohio State University, @OSUEndosurgBSM - Sophie Dream, MD, Assistant Professor of Surgery, Medical College of Wisconsin, @SDreamMD, - Jessica Liu McMullin, MD, Endocrine Surgery Fellow, University of Alabama – Birmingham, @jess_mcmullin - Herbert Chen, MD, Professor and Chair of Surgery, University of Alabama – Birmingham, @herbchen Learning objectives: - Understand the epidemiology and pathogenesis of kidney-related parathyroid disease and how these entities differ from primary hyperparathyroidism - Describe the diagnosis of kidney-related hyperparathyroidism and its different presentations - Define the indications for surgical intervention - Recognize the different approaches and extents of surgery for treating the different types of renally mediated hyperparathyroidism including thymectomy and parathyroid autotransplantation - Detail methods for safe and effective perioperative management References: - Dream S, Kuo LE, Kuo JH, Sprague SM, Nwariaku FE, Wolf M, Olson JA Jr, Moe SM, Lindeman B, Chen H. The American Association of Endocrine Surgeons Guidelines for the Definitive Surgical Management of Secondary and Tertiary Renal Hyperparathyroidism. Ann Surg. 2022 Sep 1;276(3):e141-e176. doi: 10.1097/SLA.0000000000005522. Epub 2022 Jul 18. PMID: 35848728. - Wilhelm SM, Wang TS, Ruan DT, et al. The American Association of Endocrine Surgeons Guidelines for definitive management of primary hyperparathyroidism. JAMA Surg. 2016;151:959–968. - Ketteler M, Block GA, Evenepoel P, et al. Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update: what's changed and why it matters. Kidney Int. 2017;92:26–36. - Andress DL, Coyne DW, Kalantar-Zadeh K, et al. Management of secondary hyperparathyroidism in stages 3 and 4 chronic kidney disease. Endocr Pract. 2008;14:18–27. - Cozzolino M, Brancaccio D, Gallieni M, et al. Pathogenesis of parathyroid hyperplasia in renal failure. J Nephrol. 2005;18:5–8. - Lau WL, Cobi Y, Kalantar-Zadeh K. Parathyroidectomy in the management of secondary hyperparathyroidism. Clin J Am Soc Nephrol. 2018;13:952–961. - Parfrey PS, Chertow GM, Block GA, et al. The clinical course of treated hyperparathyroidism among patients receiving hemodialysis and the effect of cinacalcet: the EVOLVE trial. J Clin Endocrinol Metab. 2013;98:4834–4844. - Costa-Hong V, Jorgetti V, Gowdak LH, et al. Parathyroidectomy reduces cardiovascular events and mortality in renal hyperparathyroidism. Surgery. 2007;142:699–703. - McManus C, Oh A, Lee JA, et al. Timing of parathyroidectomy for tertiary hyperparathyroidism with end-stage renal disease: a cost-effectiveness analysis. Surgery. 2021;169:94–101. - Finnerty BM, Chan TW, Jones G, et al. Parathyroidectomy versus cinacalcet in the management of tertiary hyperparathyroidism: surgery improves renal transplant allograft survival. Surgery. 2019;165:129–134. Suture Kit: Purchase on suturekit.com Purchase on Amazon How-to Video Series Please visit https://behindtheknife.org to access other high-yield surgical education podcasts, videos and more.  If you liked this episode, check out other endocrine episodes here: https://behindtheknife.org/podcast-category/endocrine/

In this two-part series, we come to you LIVE! from the 2023 Annual meeting of the American Association of Endocrine Surgeons in Birmingham, Alabama. If you think evaluating and managing patients with primary hyperparathyroidism is difficult, patients with secondary and tertiary hyperparathyroidism can be even more difficult to evaluate and manage. Join Drs. Barb Miller, Sophie Dream, Jessica Liu McMullin, and Herb Chen as they break down the controversies and complexities associated with evaluation and management of these patients and discuss the recently published AAES guidelines on the definitive surgical management of patients with secondary and tertiary renal hyperparathyroidism. Part 1 focuses on the impetus for creation of these guidelines, the differences in evaluation and indication for surgery when seeing patients with renally mediated hyperparathyroidism, and preoperative planning. Part 2 focuses on intraoperative and postoperative management, parathyroid autotransplantation, and renal transplant recipients. Hosts:  - Barbra S. Miller, MD (Moderator), Clinical Professor of Surgery, The Ohio State University, @OSUEndosurgBSM - Sophie Dream, MD, Assistant Professor of Surgery, Medical College of Wisconsin, @SDreamMD, - Jessica Liu McMullin, MD, Endocrine Surgery Fellow, University of Alabama – Birmingham, @jess_mcmullin - Herbert Chen, MD, Professor and Chair of Surgery, University of Alabama – Birmingham, @herbchen Learning objectives:  - Understand the epidemiology and pathogenesis of kidney-related parathyroid disease and how these entities differ from primary hyperparathyroidism - Describe the diagnosis of kidney-related hyperparathyroidism and its different presentations - Define the indications for surgical intervention  - Recognize the different approaches and extents of surgery for treating the different types of renally mediated hyperparathyroidism including thymectomy and parathyroid autotransplantation - Detail methods for safe and effective perioperative management References: - Dream S, Kuo LE, Kuo JH, Sprague SM, Nwariaku FE, Wolf M, Olson JA Jr, Moe SM, Lindeman B, Chen H. The American Association of Endocrine Surgeons Guidelines for the Definitive Surgical Management of Secondary and Tertiary Renal Hyperparathyroidism. Ann Surg. 2022 Sep 1;276(3):e141-e176. doi: 10.1097/SLA.0000000000005522. Epub 2022 Jul 18. PMID: 35848728. - Wilhelm SM, Wang TS, Ruan DT, et al. The American Association of Endocrine Surgeons Guidelines for definitive management of primary hyperparathyroidism. JAMA Surg. 2016;151:959–968. - Ketteler M, Block GA, Evenepoel P, et al. Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update: what's changed and why it matters. Kidney Int. 2017;92:26–36. - Andress DL, Coyne DW, Kalantar-Zadeh K, et al. Management of secondary hyperparathyroidism in stages 3 and 4 chronic kidney disease. Endocr Pract. 2008;14:18–27. - Cozzolino M, Brancaccio D, Gallieni M, et al. Pathogenesis of parathyroid hyperplasia in renal failure. J Nephrol. 2005;18:5–8. - Lau WL, Cobi Y, Kalantar-Zadeh K. Parathyroidectomy in the management of secondary hyperparathyroidism. Clin J Am Soc Nephrol. 2018;13:952–961. - Parfrey PS, Chertow GM, Block GA, et al. The clinical course of treated hyperparathyroidism among patients receiving hemodialysis and the effect of cinacalcet: the EVOLVE trial. J Clin Endocrinol Metab. 2013;98:4834–4844. - Costa-Hong V, Jorgetti V, Gowdak LH, et al. Parathyroidectomy reduces cardiovascular events and mortality in renal hyperparathyroidism. Surgery. 2007;142:699–703. - McManus C, Oh A, Lee JA, et al. Timing of parathyroidectomy for tertiary hyperparathyroidism with end-stage renal disease: a cost-effectiveness analysis. Surgery. 2021;169:94–101. - Finnerty BM, Chan TW, Jones G, et al. Parathyroidectomy versus cinacalcet in the management of tertiary hyperparathyroidism: surgery improves renal transplant allograft survival. Surgery. 2019;165:129–134. Suture Kit: Purchase on suturekit.com Purchase on Amazon How-to Video Series Please visit https://behindtheknife.org to access other high-yield surgical education podcasts, videos and more.   If you liked this episode, check out other endocrine episodes here: https://behindtheknife.org/podcast-category/endocrine/

As recent history has shown us, human societies can prove surprisingly frail in the face of a tiny, yet powerful force: the microbes that cause infectious disease. Speaking with Matt Elton, Jonathan Kennedy explores the myriad ways in which pandemics have shaped the course of human history. (Ad) Jonathan Kennedy is the author of Pathogenesis: How Germs Made History (Torva, 2023). Buy it now from Amazon: https://www.amazon.co.uk/Pathogenesis-infectious-diseases-shaped-history/dp/1911709062/?tag=bbchistory045-21&ascsubtag=historyextra-social-histboty Learn more about your ad choices. Visit podcastchoices.com/adchoices