Podcasts about national heart lung

Sifting through the overwhelming amount of books, news articles, social media influencers, pop-up speaker events, and retreats for menopause is overwhelming, confusing, and expensive. How should midlife women navigate menopause feeling lost, alone, and confused by conflicting information that is supposed to make us healthier, stronger, and more resilient?There's a lot of trial and error and good money spent on products, providers, treatments, and at-home devices that don't live up to their promises. Today, you will walk away with golden nuggets of evidence-based and practical strategies to help you navigate midlife and beyond. This episode covers how to know if the information that you are hearing or reading is evidence-based, why research on women in menopause is complicated to decipher, the nuances of weight resistance training versus cardio exercise, what's most important for midlife women nutritionally, and how to properly eat around your workouts. We also cover how to read protein powder labels and what to look for in amino acids, why creatine is a game-changer for women beyond muscle health, and how to strategize getting restorative sleep. Dr. Rachele Pojednic is an international authority on nutrition, supplementation, and physical activity interventions for muscle physiology, performance, and recovery. She received her PhD from Tufts University Friedman School of Nutrition Science and Policy and completed her postdoctoral training at Harvard Medical School at the Joslin Diabetes Center and Spaulding Rehabilitation Hospital. She has a faculty appointment at Stanford University and holds research appointments at the Institute of Lifestyle Medicine at Harvard Medical School and Edith Cowan University's Nutrition and Health Innovation Research Institute. She has received NIH research funding from the National Heart Lung and Blood Institute (NHLBI) and the Vermont Biomedical Research Network (VBRN), an NIH IDeA Network of Biomedical Research Excellence (INBRE) program. She currently serves on the Board of Governors for the American College of Sports Medicine (ACSM) Exercise Is Medicine® initiative. Dr. Pojednic has been an active fitness professional for over 20 years as a nutrition educator and coach for Olympic, Division I sports, and tactical athletes. She has a passion for science communication and is regularly featured in outlets such as NPR, Sirius Doctor Radio, Time, the Wall Street Journal, STAT News, Popular Science, Self, Shape, Women's Health, Forbes, and Runners World.Medical Disclaimer:By listening to this podcast, you agree not to use this podcast as medical advice or to make any lifestyle changes to treat any medical condition in yourself or others. Consult your physician for any medical issues that you may be having. This entire disclaimer also applies to any of the guests on my podcast.Connect with Rachele:Website: https://www.rachelepojednic.com/IG: @rachelepojednic2004 YouTube: @RachelePojednic_PhDCourses: https://strongprocess.com/Stay connected with JFW:Watch on my YouTube channel: https://www.youtube.com/@jillfooswellness/videosFollow me on Instagram: https://www.instagram.com/jillfooswellness/Follow me on Facebook: https://www.facebook.com/jillfooswellnessGrab discounts on my favorite biohacking products: https://www.jillfooswellness.com/health-productsEnjoy 20% savings and free shipping at Fullscript for your favorite supplements by leading brands:https://us.fullscript.com/welcome/jillfooswellnessSubscribe to the JFW newsletter at www.jillfooswellness.com and receive your FREE Guide on How To Increase Your Protein in 5 Easy Steps and your free Protein Powder Recipe Ebook. Schedule your complimentary 30-minute Zoom consultation here:https://calendly.com/jillfooswellness/30-minute-zoom-consultations

On this MADM, Sean Coady with the National Heart, Lung, and Blood Institute is sharing about the importance of heart health & beyond in rural communities. Listen & share. Sponsor: The SIMRP

On tonight's show, I have Sean Coady with National Heart, Lung, and Blood Institute (NHLBI) & Chef Jamie Gwen!

This week on the Here's What We Know Podcast, join us in this enlightening episode as we dive deep into the world of chronic pain with our guest, Dr. Afton Hassett, an experienced pain psychologist and the author of “Chronic Pain Reset”.  She offers informative content about how stress and mental health are intertwined with physical discomfort and delves into various aspects of chronic pain—its effects, causes, and potential treatments. Listen in and discover valuable insights about how your emotions can affect your perception of discomfort, and learn practical strategies for dealing with persistent affliction. And together, let's unlock the power of positivity in healing!In this Episode:The Intersection of Mental and Physical Health Resilience in Managing Chronic PainThe Power of Social InteractionCustomizing Treatment PlansThe Neuroscience Behind Pain The Invisible Nature Of Pain The Role Of Physical Activity And Sleep In Managing Chronic Pain Negative Impact Of Modern Devices On Sleep Quality  Understanding Chronic PainThe Biopsychosocial Aspects of PainRewiring the Brain The Limitations Of Pharmaceuticals The Power Of Holistic Methods  Pain Relief Through Enjoyable Activities This episode is sponsored by:Reed Animal HospitalSterling Oak CabinetryAbout Afton:Dr. Afton Hassett is a licensed clinical psychologist and an Associate Professor in the Department of Anesthesiology at the University of Michigan. She received her BFA from Colorado State University and her doctorate from Alliant International University in San Diego, CA. As a principal investigator at the Chronic Pain & Fatigue Research Center, she conducts interdisciplinary research related to exploring the role of cognitive, affective, and behavioral factors in chronic pain populations. She has published over 100 peer-reviewed articles and is a leader in the field of resilience and pain research. Her work has focused on exploring positive emotions and affective balance in people with pain; health-related quality of life in adult and pediatric rheumatology patients; and novel interventions to promote resilience and self-management for individuals with chronic pain. She is committed to education for individuals at many levels including patients, undergraduate and graduate students, medical residents, post-docs, physicians, and other healthcare providers. Dr. Hassett is the Director of Clinical Pain Research at the Back & Pain Center and the Past President of the Association of Rheumatology Health Professionals – a division of the American College of Rheumatology. Current funding sources include National Institute of Nursing Research (NINR), National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institute of Child Health and Human Development (NICHD), National Heart Lung and Blood Institute (NHLBI), Centers for Disease Control (CDC) and the University of Michigan. With over $14M of research funding from the National Institutes of Health (NIH), Afton's mission is to bring evidence-based strategies from research and academic settings to the people themselves. Her life's work is dedicated to helping people with chronic pain live lives with less pain, greater happiness, and renewed purpose in life.Website: https://aftonhassett.comInstagram: https://www.instagram.com/aftonhassettLinkedin: https://www.linkedin.com/in/afton-hassett-1982b323www.GaryScottThomas.com

Episode 128: Food insecurity and obesity.  Nausheen defines food insecurity, presents some statistics about obesity, and how food insecurity is linked to obesity. She ends her presentation with possible solutions to this problem.Written by Nausheen Hussain, OMS3, Western University of Health Sciences, College of Osteopathic Medicine of the Pacific. Editing by Hector Arreaza, MD.Welcome: 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.Arreaza: Hello, my name is Hector Arreaza. I am a family physician, currently practicing and teaching in the Central Valley of California. Today we will talk about an important and growing problem: Food insecurity and its relationship to obesity. I would like to introduce my guest today, Nasheen Hussain.Arreaza: Can you tell me what defines food insecurity? Nausheen: As defined by the U. S. Department of Agriculture (USDA), food insecurity is the limited availability of nutritionally adequate food or the limited access to this food. So, I want you to imagine you are living in a community where the closest grocery store is not within walking distance, you have no reliable access to transportation, and you are surrounded by liquor stores, McDonald's, and Burger King. Now you can see the two parts of that definition: the grocery store with healthy food exists, but it is too far, and you can't get to it. Whereas within walking distance is nonnutritious food. I want to challenge our audience to pay attention to these two concepts in the communities around them.Arreaza: I have noticed a concentration of fast-food places lining certain streets. Now that we understand the concept, do we know if there is a way to quantify or measure food insecurity?  Nausheen: Yes, Dr. Arreaza. So, the term “food swamp” actually describes what you just stated. To answer your question, yes. Food insecurity is actually measured by the USDA by a 6-18 item questionnaire - asking questions such as: Were you worried if food would run out before you got money to buy more? It is conducted as an annual supplement to the Current Population Survey. Arreaza: The Current Population Survey (CPS) is the primary source of labor force statistics for the population of the United States. It is sponsored jointly by the U.S. Census Bureau (bee-uro) and the U.S. Bureau of Labor Statistics (BLS). The CPS is conducted monthly. Nausheen: The 2021 questionnaire identified 12.5% of households in the U. S. as being food insecure. However, this may underestimate the true number of individuals who may be suffering from food insecurity. Arreaza: Screening for food insecurity is not been routinely done in many clinics. Food Insecurity: Preventive Services. An Update for This Topic is In Progress. LAST UPDATED: Jul 24, 2022. So now, let's talk about the connection of this to obesity. What factors in general increase the likelihood of obesity?Nausheen: Sure! Obesity is classified based on a person's body mass index or BMI, which is your weight in kilograms (or pounds) divided by the square of height in meters (or feet). A BMI of 30 or greater is considered to be in the obesity category. Obesity is affected by several factors, such as a person's genetics, level of activity, and a high-calorie diet consisting of low-nutrition food.Arreaza: How does food insecurity play into this? Nausheen: Think back to the example we discussed earlier. If a person is experiencing food insecurity due to a lack of access, they will use what is around them (fast food, 24-hour mart without fresh foods) so they can put food on the table. If it is due to financial inaccessibility, they will choose to, say, go to Jack in the Box for their $5.00 deals. Both of these lead to a diet filled with non-nutritious food. This shouldn't come as a surprise: most people that experience food insecurity are likely to be living in low-income communities. The generalization here is that these communities tend to have fewer parks, and if they are present, there tends to be a lot of litter and a cloud of unsafe space hovering over it. Arreaza: I see what you mean.Nausheen: These people will probably be less likely to go out for walks and take their kids out…leading to a sedentary lifestyle. The last association I see is that of mental health. People who are struggling to find food are likely to have stress due to their circumstances and there is a relationship that has been found between depression and the increased likelihood of developing obesity. As a recap, there are three effects of food insecurity that contribute to obesity: lack of adequate nutrition, lack of physical activity, and poor mental health. Arreaza: So, there are several factors of food insecurity that seem to be making individuals more likely to develop obesity. Why does it matter? Nausheen: Well obesity is the gateway to several other diseases such as diabetes and hypertension, which are known to the medical profession as "silent killer diseases." In short, what we typically refer to as "that person is larger built" can have major adverse effects on health and can substantially reduce a person's longevity and quality of life. If we can understand and reduce risks of developing obesity, we can prevent the onset of the disease and/or prevent the progression to more severe outcomes. To bring this more into perspective, the CDC found that from 2017-2020, 1 in 5 children had obesity and about 2 in 5 adults had obesity, with an overall prevalence of 41.9% in the U.S. Arreaza: Let's talk about possible solutions.Nausheen: I think the best solution to this issue has to be two parts. 1. Increased access to healthy foods. 2. Nutrition education on how foods you put into your body impact your health both now and long term. I work with urban farmers in Pomona, CA as part of a grassroots effort to increase access to nutritious foods. Arreaza: Tell me more about it.Nausheen: The system consists of several small-scale community farms that produce chemical-free, pesticide-free, fresh vegetables and fruits that are sold to the community members at a low price or a “pay what you can, take what you need” basis. I believe replicating this system in other communities is effective because 1. It is important for the people to know and trust where their food is coming from, and 2. People can volunteer to help the community farms thrive which not only allows for the sustainability of efforts but gives them a reason to be outside and be active which helps combat obesity! Arreaza: I believe nutrition education is a key element to combat obesity, but the battle is unfair. I see there needs to be a better effort from our government to control such things as the false advertisement of so-called “healthy foods” and “miracle supplements” that promise the cure of obesity. I feel like there needs to be more control of these vendors and pay for false science. Nausheen: Nutrition education itself is also important so that people understand what nutrients their bodies need, what foods can give it to them, how to cook those foods, and lastly how it all affects their health. This should start from elementary school with short lessons embedded into the school curriculum. Arreaza: Thank you for sharing that. This brings our episode to a close. If you are or if you know someone who is struggling with food insecurity, find some resources in your community such as food banks, Special Supplemental Nutrition Program for Women, Infants, and Children (WIC), and other resources. Nausheen: Find community gardens where you live._______________Conclusion: Now we conclude episode number 128 “Food insecurity and obesity.” Nausheen explained that a lack of access to fresh and healthy foods is linked to increased risk of obesity. Dr. Arreaza called for improved controls for scammers and pseudoscientists that frequently commit fraud to patients who are struggling with obesity.This week we thank Hector Arreaza and Nausheen Hussain. 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!_____________________Sources:Hartline-Grafton, H. (2018, April 18). Understanding the connections: Food insecurity and obesity (October 2015). Food Research & Action Center. Retrieved February 5, 2023, from https://frac.org/research/resource-library/understanding-connections-food-insecurity-obesity.U.S. Department of Health and Human Services. (2022, March 24). What are overweight and obesity? National Heart Lung and Blood Institute. Retrieved February 5, 2023, from https://www.nhlbi.nih.gov/health/overweight-and-obesity.Food Security in the U. S. - Measurement. USDA ERS - Measurement. (2022, October 17). Retrieved February 5, 2023, from https://www.ers.usda.gov/topics/food-nutrition-assistance/food-security-in-the-u-s/measurement.Craven, K., Patil, S. (unknown). Understanding Food Security & Obesity Paradox: A Case Study. Department of Family Medicine, Brody School of Medicine.Blasco BV, García-Jiménez J, Bodoano I, Gutiérrez-Rojas L. Obesity and Depression: Its Prevalence and Influence as a Prognostic Factor: A Systematic Review. Psychiatry Investig. 2020 Aug;17(8):715-724. doi: 10.30773/pi.2020.0099. Epub 2020 Aug 12. PMID: 32777922; PMCID: PMC7449839.Centers for Disease Control and Prevention. (2022, May 17). Childhood obesity facts. Centers for Disease Control and Prevention. Retrieved February 6, 2023, from https://www.cdc.gov/obesity/data/childhood.html.Centers for Disease Control and Prevention. (2022, May 17). Adult obesity facts. Centers for Disease Control and Prevention. Retrieved February 6, 2023, from https://www.cdc.gov/obesity/data/adult.htmlRoyalty-free music used for this episode: “Gushito - Latin Pandora." Downloaded on October 13, 2022, from https://www.videvo.net/ 

Learn about Ryan Olson and Brad Wipfli's Oregon Healthy Workforce Center research. They discuss how their Total Worker Health interventions have helped decrease sedentary behavior (sitting time) and increase physical activity in the workplace. Dr. Olson shares insight into studying team truck drivers in the Tech4Rest study and Dr. Wipfli shares his research studying call center workers in the Active Workplace study. Dr. Ryan Olson is a behavioral and occupational health psychologist who specializes in safety and health interventions for isolated workers, such as truck drivers and home care workers. Ryan is the Co-Director of the Oregon Healthy Workforce Center, a NIOSH Center of Excellence in Total Worker Health®. He also leads an Internationally recognized research program, funded by the National Heart Lung and Blood Institute, that is focused on the safety, health and well-being of commercial drivers.   Dr. Brad Wipfli is an Associate Professor and Assistant Dean of Graduate Academic Affairs in the OHSU-PSU School of Public Health. Brad's research concentrates on health promotion and health behavior, particularly on  identifying strategies to increase physical activity and improve physical and mental health. Learn about Dr. Brad Wipfli: https://ohsu-psu-sph.org/faculty-directory/name/brad-wipfli Access the Active Workplace Toolkit: https://www.yourworkpath.com/activeworkplace Learn about Dr. Ryan Olson: https://www.ohsu.edu/people/ryan-b-olson-phd Learn about the Olson Lab: https://www.ohsu.edu/oregon-institute-occupational-health-sciences/ryan-olson-lab Learn about Tech4Rest: https://www.yourworkpath.com/tech4rest --- Episode information: What's Work Got to Do With The Great Resignation? Guests: Ryan Olson, PhD and Brad Wipfli, PhD Host: Helen Schuckers, MPH Edited by: Helen Schuckers, MPH Produced by: Helen Schuckers, MPH and Anjali Rameshbabu, PhD Music by: Sam Greenspan, MPH Connect with us Oregon Institute of Occupational Health Sciences and Oregon Healthy Workforce Center on social media: Twitter: twitter.com/OHSUOccHealth Facebook: www.facebook.com/occhealthsci.ohsu LinkedIn: www.linkedin.com/company/occhealthsci Blog: blogs.ohsu.edu/occupational-health-sciences Community feedback is important to us. If you love our podcast and want to further support our podcast, please consider leaving us a positive review. Thank you!

A new study suggests that older adults who don't drink enough fluids could age more quickly and face a higher risk of disease. In the study, published in the journal eBioMedicine, researchers from the National Heart Lung and Blood Institute collected data from over 11,000 adults who had their first medical visits between the ages […] The post 361. Adults who don't hydrate might age faster appeared first on Dr. David Geier - Feel and Perform Better Than Ever.

Melissa has another great guest on today's episode of the podcast.  Join her as she talks with Stephanie Davis, Chair of the Capital Region Women in Bio and Small Business Program Coordinator at the National Heart Lung and Blood Institute for NIH.Stephanie and Melissa discuss Women in Bio and how Stephanie's leadership and volunteer efforts have contributed to success in her career.  She is also sharing how you can leverage Women in Bio for your career whether you are entry level or C-Suite.  We are also talking about the unique challenges of women in the workplace and how to overcome them and get to your next level.In this episode learn:Stephanie's career path and philosophy on career developmentHow Women in Bio can help you get to your next level whether you're entry level, an Executive, or anywhere in betweenThe current obstacles facing women who work in the sciences and what both companies and individuals can do to overcome themOne piece of advice Stephanie wished she had earlier in her careerPlease note: Stephanie joins the podcast in her personal capacity and the views expressed on this podcast do not represent the views of the National Institutes of Health or the Department of Health and Human Services.Mentioned in this episode:Learn more about Women in BioConnect with Stephanie on LinkedInSupporting (Postdoctoral) Women in Bio (Stephanie's article)Work with Melissa 1-1 by scheduling a consultation.Connect with MelissaLinkedInInstagram

In This episode, Dr. Gary Sherman welcomes Dr. Anu Lala to our conversation. Dr. Lala's clinical interests encompass all aspects of management of heart failure, including the selection and care of patients with mechanical circulatory support devices and heart transplantation as well as genetic cardiomyopathies -and- perioperative management of high-risk cardiac surgical cases. She believes in a patient-centered approach, where each individual's unique needs and preferences are essential components of developing a personalized treatment plan. Dr. Lala seeks to implement -guideline-directed -medical and device-based therapies while integrating emotional and spiritual aspects of care. (This is right up my alley) In addition to caring for patients, she serves as the Director of Heart Failure Research and as Data Coordinating Center Leader for the National Heart Lung and Blood Institute's (NHLBI) Cardiothoracic Surgery Network. Dr. Lala also leads the fellowship program in Advanced Heart Failure and Transplant. She has authored over 75 peer-reviewed scientific publications and is the principal investigator for a number of clinical trials in heart failure. Dr. Lala serves on local and national committees in the American Heart Association, American College of Cardiology, Heart Failure Society of America among others, devoted to advanced heart disease. In 2016, Dr Lala was named the American Heart Association Young Professionals Society Honoree for her service and commitment to education - and promoting cardiovascular health awareness. In 2020, she was recognized with the Proctor H. Harvey Teaching Award by the American College of Cardiology which honors a promising young member of the College who has distinguished herself by dedication and skill in teaching, and to stimulate continued careers in education.References:Dr. Anuradha Lala Tridade:  : https://www.mountsinai.org/profiles/anuradha-lala-trindadeThere's more to life than being happy | Emily Esfahani Smith:  https://youtu.be/y9Trdafp83UStrategic Empathy approaches: Never Split the Difference: Negotiating As If Your Life Depended On It , Chris Voss, Tahl Raz

Dr. Erik Jensen is an attending neonatologist in the division of neonatology at the Children's hospital of Philadelphia. He is an assistant professor of pediatrics at the Perelman School of Medicine at the University of Pennsylvania.Dr. Jensen's research seeks to improve the long-term respiratory health of premature infants through: (1) clinical and translational studies that aim to develop evidence-based strategies to prevent and treat BPD; (2) novel characterization of disease severity and phenotypes in BPD; and (3) application of health services research techniques to investigate the association between hospital-level factors and neonatal morbidity and mortality.Dr. Jensen's research is supported by grant funding from the National Heart Lung and Blood Institute (NHLBI), the National Institute of Child Health and Human Development (NICHD), and the American Lung Association (ALA). He is a member of the International BPD Collaborative pharmacology working group and the International Neonatal Consortium (INC) BPD working group. He has received multiple clinical and research awards. _____________________________________________________________________________________________________As always, feel free to send us questions, comments or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through instagram or twitter, @nicupodcast. Or contact Ben and Daphna directly via their twitter profiles: @drnicu and @doctordaphnamd. enjoy!

Story Arc: "Let's Ruin An Economy!" (pt.4) This episode of Rocks Fall, Everyone Dies! Bambi, Greg, and Sanjana interrogate a member of Dinozzo's crew; and Bengt, Martelo, and Lefou make a deal! Special guest player: Juan! Also known as Heart Bypass Surgery Coronary artery bypass grafting (CABG) is a procedure to improve poor blood flow to the heart. It may be needed when the arteries supplying blood to heart tissue, called coronary arteries, are narrowed or blocked. This surgery may lower the risk of serious complications for people who have obstructive coronary artery disease, a type of ischemic heart disease. CABG may also be used in an emergency, such as a severe heart attack. CABG uses blood vessels from another part of the body and connects them to blood vessels above and below the narrowed artery, bypassing the narrowed or blocked coronary arteries. One or more blood vessels may be used, depending on the severity and number of blockages. The blood vessels are usually arteries from the arm or chest, or veins from the legs. Risks and possible complications may occur with this procedure. After CABG, your doctor may recommend medicines and heart-healthy lifestyle changes to further reduce your symptoms, treat your disease, and help prevent complications such as blood clots. “Coronary Artery Bypass Grafting.” National Heart Lung and Blood Institute, U.S. Department of Health and Human Services, www.nhlbi.nih.gov/health-topics/coronary-artery-bypass-grafting. Cast & Credits: Producer, Editor & DM: Scott Editor & Bambi: Jin (https://www.twitch.tv/phantomquill) Social Media Manager & Greg: DeSombre Bengt: Tommy Sanjana: Lena Theme Music: Taylor Calise Additonal Sound Effects: Zapsplat.com Art: Jon Bliss (https://twitter.com/jonblissart) Recorded on our Discord server by Craigbot! (https://craig.chat/home/) Want to find out more about us? https://rfedpod.com/ Want to Email us? RFEDPod@gmail.com Want to follow us on Social media? Instagram: https://www.instagram.com/RFED_podcast/ Facebook: https://www.facebook.com/RFEDpod Twitter: https://twitter.com/RFEDpod YouTube: https://www.youtube.com/channel/UCT3QkpOLLIBwvSKZUZPq7IQ (we'll get a custom url when you subscribe to the channel!)

In this episode of Meeting Mic, we bring you pearls and perspectives from the American Thoracic Society 2021 International Conference, as well as Healio's top headlines from the virtual meeting. Leonard Bacharier, MD, discusses results of the VOYAGE study of dupilumab in children with asthma :35 Dennis Hwang, MD, shares data from a study that looked at severe obstructive sleep apnea and COVID-19 risk 7:11 Alayna Tackett, PhD, discusses results of her analysis of e-cigarette use and the association with wheeze and shortness of breath, even in young adults who don't smoke 10:25 Michael Wechsler, MD, shares data from the LIBERTY ASTHMA TRAVERSE Extension Study, which assessed long-term maintenance of oral corticosteroid reduction and efficacy with dupilumab in patients with asthma 14:01 Ana Hernandez Cordero, PhD, discusses data from an integrative genomic analysis of potential genetic risk factors for COVID-19 23:15 Read the full coverage here: https://www.healio.com/news/pulmonology/20210519/tezepelumab-reduces-exacerbations-in-broad-population-of-patients-with-severe-asthma https://www.healio.com/news/pulmonology/20210518/multiple-disease-progression-events-less-likely-with-continued-inhaled-treprostinil https://www.healio.com/news/pulmonology/20210517/monoclonal-antibody-cocktail-cut-covid19-hospitalization-death-by-70-in-outpatient-setting https://www.healio.com/news/pulmonology/20210516/fauci-covid19-vaccines-the-bright-light-of-this-extraordinary-challenge Disclosures: Bacharier reports he received speaker fees from AstraZeneca, GlaxoSmithKline, Regeneron and Sanofi; was on the data safety monitoring board for Cystic Fibrosis Foundation and DBV Technologies; and received research support from NIH, Sanofi and Vectura. Hernandez Cortez reports funding from MITACS and Providence Health Center. Hwang reports that efforts for the study were supported by grants from the American Academy of Sleep Medicine Foundation and from internal Kaiser research support. Tackett reports no relevant financial disclosures. The research was supported by the National Heart Lung and Blood Institute from the NIH and the Oklahoma Tobacco Settlement Endowment Trust. Wechsler reports he received consultant fees from AstraZeneca, Amgen, Boehringer Ingelheim, Cohero Health, Equillium, Genentech, GlaxoSmithKline, Novartis, Regeneron, Sanofi, Sentien and Teva.

MaryAnn Guerra has a career-long passion for bringing technology to market, accelerating innovation from the lab into commercial businesses and providing an incomparable client experience. As co-founder of Aesthetics Biomedical®, she understands the importance of designing experiences that create results. As a client of her own company, she values the opportunity to feel her very best at any age using leading-edge, FDA-cleared technology and treatment serums and recovery agents that truly make a difference. It is her privilege to advance these innovations through a network of respected doctors and med spas to make an impact on the battle against aging for men and women. Guerra also serves as Chairman of the Board, CEO, and co-founder of BioAccel, a non-profit organization with the mission to turn medical device breakthroughs into successful commercial ventures. Guerra has spent much of her career operating successful and progressive health, science, technology and start-up businesses. Guerra served as President of TGen Accelerators, LLC and Chief Operating Officer at TGen. Guerra has also had an impressive career at the National Institutes of Health, having held senior level positions, including: Executive Officer, National Heart Lung and Blood Institute and Deputy Director of Management & Executive Officer at the National Cancer Institute. Her never-ending quest to challenge her team, question the status quo and pursue innovation with an eye for making a difference at the highest level of quality is what drives her every day. --- Send in a voice message: https://anchor.fm/skincareanarchy/message

This week, join author Chintan Dave and Associate Editor Naveed Sattar as they discuss the risk of cardiovascular outcomes in Type 2 Diabetes patients following the addition of SGLT2 inhibitors versus sulfonylureas to baseline GLP-IRA therapy. TRANSCRIPT BELOW: Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast, summary, and backstage pass to the journal and its editors. We're your co-hosts, I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: And I'm Dr. Greg Hundley, Associate Editor, director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: Greg, I love today's featured paper. It's a question everybody's asking. It's about cardiovascular outcomes, potential benefits, following the addition of SGLT2T2 inhibitors versus sulfonylureas to baseline GLP-1 receptor agonist therapy. Now, okay, I'm going to keep you waiting because that was just a hook. We got to get to us summaries first. And I'm going to start. The first original paper I want to describe is an analysis of myocardial infarction from the ischemia trial. And it looks at the impact of different definitions on the incidents, prognosis and treatment comparisons. Dr. Carolyn Lam: Because I know you're going to ask, I'm going to tell us a little bit about ischemia. So in an ischemia and initial invasive strategy did not significantly reduce rates of cardiovascular events or all-cause mortality compared with a conservative strategy in patients with stable ischemic, heart disease, and moderate to severe myocardial ischemia. The most frequent component of the composite cardiovascular end points was myocardial infarction. So in the current report from Dr. Chaitman and colleagues from St. Louis University school of medicine, the aim was to compare treatment effects on the primary and major secondary competent end points in the ischemia trial using the pre-specified primary and secondary MI definitions. Dr. Greg Hundley: So Carolyn, what were those two EBI definitions, the primary and secondary? Dr. Carolyn Lam: Right. Now, I'm going to try to simplify this. So, for procedural MI, the primary MI definition use CK-MB as the preferred biomarker, whereas the secondary definition used cardiac troponin. Dr. Greg Hundley: Great, Carolyn. So what did they find? Dr. Carolyn Lam: So procedural MI definition had an important impact on event frequency and subsequent prognosis. When the pre-specified secondary MI definition was applied, the conservative strategy had a significantly lower composite event rate for the primary and major secondary trial end points, due to an increased number of procedural MIs in the invasive strategy. Furthermore, spontaneous Type One MI events associated with increased risk of cardiovascular death were reduced with an invasive strategy, which is either PCI or CABG. Dr. Greg Hundley: Nice, Carolyn. Well, my first paper actually is a favorite topic of yours, HFpEF. And it really involves the central command and the regulation of exercise rate response. It comes to us from Dr. Ben Levine and colleagues at the University of Texas Southwestern Medical Center in Dallas. Dr. Carolyn Lam: Yay. Dr. Greg Hundley: All right, Carolyn. So chronotropic incompetence is common in HFpEF. And it's linked to impaired aerobic capacity. Whether upstream, autonomic signaling pathways are responsible for raising exercise heart rate are impaired in patients with HFpEF, That's really unknown. Dr. Carolyn Lam: Yep. It is something that we wonder. And so what did Dr. Levine find? Dr. Greg Hundley: Thanks Carolyn. So the central command, so vaguely mediated and the metabo-barrow receptor function, which is sympathetically mediated in patients with HFpEF, We're not different from healthy senior controls, despite significantly lower peak whole body exercise, heart rates. So these results, Carolyn, demonstrate key reflex autonomic pathways, regulating exercise, heart rate responsiveness are actually intact in patients with HFpEF. Great new work from Dr. Ben Levine. Dr. Carolyn Lam: And I love the way you summarized that. Thank you, Greg. Well, my next paper is the first report implicating the cross priming function of dendritic cells in immunopathology after Type Two MI. And that includes inflammation, fibrosis and functional decline. Dr. Greg Hundley: So tell us a little bit more Carolyn about these dendritic cells? Dr. Carolyn Lam: Ah-ha so I was ready for that question. So after ischemic injury to the myocardium, dendritic cells respond to cardiomyocyte necrosis present the cardiac antigen to T-cells and potentially initiate a persistent auto-immune response against the heart. So cross priming dendritic cells may have the ability to activate both CD4-positive helper and CD8-positive cytotoxic T-cells in response to necrotic cells. And may thus be crucial players in exacerbating auto-immunity targeting the heart. Dr. Carolyn Lam: So, in this study, authors led by Dr. Sattler from Imperial College, London, performed some elegant mouse experiments and showed that cross-priming dendritic cells were present in the heart and activate it after ischemic injury. Depletion of these dendritic cell cross priming function, inhibited accumulation, and activation of cytotoxic T-cells and stopped myocardial immunopathology and functional decline. So with cross-priming, these authors provided a targetable pathway to prevent activation of T-cells cyto-toxicity and persistent post Mia immunopathology exacerbating heart failure risk. Dr. Greg Hundley: Oh, beautiful. Carolyn, what a great description there. So my next paper comes to us from Dr. David Park from the New York University school of medicine. So Carolyn elevated intracardiac pressure due to heart failure, induces electrical and structural remodeling of the left atrium that begets atrial myopathy and arrhythmias. At present the underlying molecular pathways that drive atrial remodeling during cardiac pressure overload are poorly defined. So the purpose of this study for these investigators was to characterize the response of the ETV1 signaling axis in the left atrium during cardiac pressure overload in humans, as well as mouse models. And explore the role of ETV1 in atrial electrical and structural remodeling. Dr. Carolyn Lam: Ah, another study involving both animal and human models. Very important subject too. So what were the results? Dr. Greg Hundley: Well, Carolyn, evidence from both the Cleveland Clinic, Biobank Human Subjects Repository and the animal science experiments revealed that ETV1 is downregulated in the left atrium during cardiac pressure overload. Thereby contributing to both the electrical and the structural remodeling that we observe in the left atrium during cardiac pressure overload. Dr. Carolyn Lam: Nice. Well, let's quickly finish up with what's in the mailbag. We've got a research letter by Dr. Randi on the lack of evidence of AEs to expression and replicative infection by SARS-CoV-2 in human endothelial cells. There's another by Dr. Stokes on the association of cigarette and electronic cigarette use patterns with levels of inflammatory and oxidative stress biomarkers among US adults. And another research letter by Dr. Hemelsoet on screening for Fabry disease in male patients with arrhythmia requiring pacemaker or ICD. Dr. Greg Hundley: Thanks Carolyn. So I've got a paper it's a cardiovascular case series from Dr. Workman that involves a case of presyncope after transcatheter aortic valve replacement. Dr. Özeke has an ECG challenge reminding us that common things occur commonly. Dr. Zaha has a Perspective entitled, "Mending Broken Hearts, a New Treatment Paradigm for Immune Checkpoint Inhibitor Induced Myocarditis." And then finally, Dr. David Goff, the director of the NHLBI has a wonderful perspective piece (Special Report). And it really addresses some results from the Bethesda conference at the National Heart Lung and Blood Institute and the American Heart Association. And it was co-sponsored the bending curve of cardiovascular disease mortality, the Bethesda plus 40 years Symposium. Dr. Greg Hundley: The report, Carolyn, summarizes the relevant research, policy, and practice opportunities discussed at the symposium, including participant led discussion that explored the challenges and barriers in promoting cardiovascular health, across lifespan. And established a potential framework for observational research interventions that would begin in early childhood. Well, Carolyn, how about now we jump forward to that feature discussion. Dr. Carolyn Lam: All right, now we can go. Dr. Greg Hundley: Well, listeners, we are to the feature discussion today. And we have with us Dr. Chintan Dave from Rutgers University in New Jersey, and our own associate editor, Dr. Naveed Sattar from Glasgow, Scotland. Welcome gentlemen. Chintan, could you explain to us some of the background information that went into the construct of your study and then what hypothesis did you want to test? Dr. Chintan Dave: So just for background, so we know that artheriscraotic cardiovascular events in heart failure typically occur in higher prevalence in patients with type two diabetes. What's been really exciting in recent years is that certain second-line therapies, namely SGLT2 inhibitors and GLP-1 receptor agonist in these large cardiovascular outcome trials have shown to reduce the incidents of cardiovascular events. So from these trials, we can infer that SGLT2 inhibitors typically reduce heart failure hospitalizations, and also have an impact on 3P-MACE, which is just the composite of cardiovascular death, non-fatal MI and non-fatal stroke hospitalizations. While GLP-1 receptor agonist tend to reduce, also have an impact on 3P-MACE, but they also have some modest benefits in heart failure hospitalizations as well. Dr. Chintan Dave: So now that we know that these agents reduce cardiovascular risk, what's not known is, whether or not, if we can use these agents together to further maximize a reduction in cardiovascular events. So in the cardiovascular outcome trials the dual use of SGLT2 two inhibitors and GLP-1 receptor agonists was rare and ranged from between 0% to 5.3%. So as a starting point, we said, "Okay, let's look at observational data to see what happens when you add SGLT2 inhibitors to patients who are already using GLP-1 receptor agonist." And we hypothesized that, given the orthogonal pharmacodynamic effects on cardiovascular risk, adding SGLT2 inhibitors to existing GLP-1 receptor therapy should further reduce cardiovascular events. Dr. Greg Hundley: Very good. And can you describe for us your study population and study design? Dr. Chintan Dave: Sure. So we used three databases in the US. Two of these databases were commercial claims data, which is typically your employer based insurance plans, which have patients between the ages of 18 and 64. And we supplemented that data with Medicare fee for service claims, which have patients over the age of 65. So within these three databases, we identified patients who have a diagnosis of type two diabetes and are already a GLP-1 receptor therapy or GLP-1RAs and initiating either SGLT2 inhibitors or sulfonylureas. Dr. Chintan Dave: And after we identified this patient population, we controlled for several pertinent variables that could be considered confounders, including socio-demographic variables, diabetes complications, and cardiovascular conditions. And we had two primary endpoints. The first primary end point of interest was a composite cardiovascular endpoint, which is defined as the composite of non-fatal MI or nonfatal stroke hospitalizations in all cause mortality. The reason we used all cause mortality instead of cost specific mortality is basically because we didn't have information on cause of death. So we have to resort to a more generic definition of mortality in the composite cardiovascular endpoint. The second primary endpoint that we used was heart failure hospitalizations. So we then in this population, estimated hazard ratios using basically a time to event framework. Dr. Greg Hundley: Okay. And what were your results? Dr. Chintan Dave: So after applying the eligibility criteria in all three databases and after doing a one-to-one propensity score matching, we had 12,500 patients who initiated SGLT2 inhibitors and 12,500 patients in the sulfonylurea groups. For the true primary end points the addition of SGLT2 inhibitors to baseline GLP-1RA therapy was associated with a 22% decrease in the incidents of composite cardiovascular end point or an adjusted hazard ratio of 0.78. And the caught 95% confidence intervals were statistically significant. For the endpoint of heart failure hospitalizations, we noted a 36% decrease in the risk of heart failure hospitalizations with the adjusted hazard ratio being 0.64. And again, that was statistically significant as well. Dr. Chintan Dave: The CCE or the Composite Cardiovascular Endpoints was driven primarily by non-statistical decreases in the risk of MI by about 25%, in all cause mortality by about 32%. But we also found no effect on stroke, which is also in line with what others have reported. The other thing we looked at was also to look at any evidence for heterogeneity in treatment effects by presence of cardiovascular diseases. And we found no statistical significant difference in that aspect. The last thing we looked at also was to look at any evidence of heterogeneity by baseline cardiovascular disease in the patient groups. And we found no evidence to that effect. Dr. Greg Hundley: Very nice. Well, Naveed help us put this study in perspective with some of the other research that I know you're familiar with related to the use of SGLT2 inhibitors and GLP-1 receptor agonists. Dr. Naveed Sattar: Yeah. Thanks Greg. So as we all know, the biggest gains in diabetes in the last few years is these two costs of the trucks SGLT2 inhibitors and GLP-1. We believe and the evidence suggests that SGLT2s, are more cardiorenal in its benefits, and GLP-1 more atherothrombotic. So the hope is that if you combine these drugs, you get additional benefits, but there are no trials that have actually tested this. So this particular paper being kind of first observational, look at adding an SGLT2 versus another drug on top of a GLP-1, tries to get at that particular question. And it provides an early hint that yes, if you add an SGLT2 on top of the GLP-1, you get additional benefits. Giving us some insight that yes, you combine these two classes of drugs, you might get additional benefit in one drug on its own. Dr. Naveed Sattar: Of course, this is not trial. Some of our readers are going to be nihilist and will not believe the data because it's not a trial, but that's fine. But it's done as well as it possibly can. This observational propensity analysis is well matched. The data have some kind of external validity in the sense that the greatest benefits or risks reductions, but for heart failure post-acquisition, which is what we would believe ratio to inhibitors. So there is some sense of validity here, but clearly colleagues, they want to know, and I actually had a patient in the clinic on Tuesday who was on a GLP-1 and actually was an SGLT2. And I wanted to add the GLP-1. And this kind of evidence provides me some evidence of confidence that yes, by adding both drugs, I might get additional benefits in that one drug on its own. Dr. Naveed Sattar: So what you're going to ask next, Craig, and I'll give my answer first. What we really need to do now is actually do the trials. And I think the trials will predominantly work, adding GLP-1 on people who are on SGLT2, because I think more people will be initially an SGLT2 because it's a oral therapy. Then we'll add GLP-1. Although we do have a new oral GLP-1 in play as well. So, that's the kind of paradigm we're in. Some hints, the combination gives you more than the single drug and I think that's really quite promising for people. Dr. Greg Hundley: Very nice. So Naveed suggesting a clinical trial to confirm some of these results. Chintan, do you have anything to add? What study do you think or what area of investigation in this field do you feel is next in line? Dr. Chintan Dave: Yeah, I mean, I would just start by saying that I agree with everything that Naveed said in the sense that this is a starting point. And that I think the key take home from this study that sort of is going to be published is basically that not only do SGLT2 inhibitors reduce the cardiovascular events in patients using GLP-1 therapy, but the fact that the magnitude of this reduction is very similar. What was noted in cardiovascular outcome trials of SGLT2 inhibitors for GLP use was very minimal. In other words, you can super impose the cardiovascular benefit profile of the SGLT2 inhibitors, which were seen in trials two patients using GLP-1 therapy. Dr. Chintan Dave: Now the converse is what needs to be done next, basically, where we need to look at what happens when you add GLP-1 receptor agonist, to SGLT2 inhibitors, as Naveed just said. And he raised a really good point in that more patients are going to be on SGLT2 inhibitors, because they want to avoid GLP-1 receptor agonist because they don't want to use injectable therapies. Of course we have oral semaglatites maybe that may mitigate these issues. But the fact that that aspect is still unknown, could potentially be really good idea for future studies. So that potentially would be a nice, good step. Dr. Greg Hundley: Excellent. Dr. Naveed Sattar: Can I see one last thing, Greg? There is a trial coming this year called AMPLITUDE‐O, which is a GLP-1 trial, which does have a fair number of people on base than SGLT2s. We might be able to get a curly hint at that ongoing trial in the next six months to a year. Dr. Greg Hundley: Excellent. Well, we want to thank both Chintan Dave from Rutgers and our own associate editor, Dr. Naveed Sattar from Glasgow, Scotland. And really presenting information from US Claims databases highlighting the addition of SGLT2 inhibitors to GLP-1 receptor agonists and finding there was an association with a further reduction of cardiovascular risk relative to the use of GLP-1 agonists alone. On behalf of both Carolyn and myself, we want to wish you a great week. And catch you next week On the Run. This program is copyright of the American Heart Association, 2021.  

Ascorbic acid or vitamin C is a known antioxidant. Clinicians have conducted numerous studies to discover its role and effectiveness on life-threatening diseases such as sepsis, acute respiratory distress syndrome (ARDS), cancer and COVID-19. Dr Alpha 'Berry' Fowler joins us in this episode to share his work on vitamin C and its role in improving the survival of critically ill patients. He also talks about ongoing trials on vitamin C and its possible benefits on COVID patients. If you want to know more about the research backing up the success of vitamin C in disease treatment, then this episode is for you.   Here are three reasons why you should listen to the full episode: Learn the mechanism of sepsis in lung disease. Discover the role of vitamin C in treating patients with sepsis and ARDS. Find out more about past and ongoing trials on vitamin C.   Resources Learn about Dr Fowler's Phase 1 safety trial of IV vitamin C in patients with severe sepsis. Explanation lecture of the CITRIS-ALI study by Dr Fowler JAMA publication on CITRIS-ALI Article on the sequential organ failure assessment (SOFA) scores and mortality of patients involved in the CITRIS-ALI trials Dr Paul Marik's protocol for sepsis using vitamin C and steroids   Episode Highlights [04:02] How Dr Fowler's Research on Bacterial Sepsis Began Dr Fowler started working on mouse models to investigate sepsis. A solution made from mouse pellets was injected into ten mice, five of which received a treatment of vitamin C. The septic mice in the control group all died while those treated with vitamin C were crawling around, drinking water and eating. Dr Fowler then started using animal models to determine how vitamin C treats sepsis. [09:05] How Sepsis Damages the Lungs In sepsis, the lung barrier is injured. The progression of sepsis traps activated neutrophils in the capillary space of the lungs. Activated neutrophils release their DNA and enzymes, damaging the capillaries. Plasma then fills the air spaces, causing the patient to drown in their fluid. [09:34] The Role of Vitamin C in a Septic Lung In vitamin C-treated mice, the lung’s barrier function is preserved. Vitamin C stops neutrophils from disgorging their DNA into the extracellular space. Free DNA has become a marker to predict mortality. Blood reanalysis showed vitamin C lowered free DNA circulation as a result. Vitamin C completely inhibits the expression and appearance of inflammatory proteins. [16:15] Phase 1 Safety Trial Outcomes In a randomised, blinded trial, 24 patients were enrolled to determine the safety of vitamin C. Organ failure score was tracked in all patients. The higher the score, the higher the incidence of mortality. Patients treated with vitamin C saw a dramatic and significant reduction in their organ failure score. Vitamin C also improved their chance of survival. Intermittent infusion of vitamin C every 6 hours could get the plasma level up to 3000 times the normal level. [25:47] Phase 2 Proof-of-Concept Trial Outcomes Patients enrolled in the study had septic ARDS. The vitamin C treatment resulted in no adverse event. After 96 hours, 19 of 83 placebo patients died while only 4 of 84 patients with vitamin C died. Upon follow-up after 28 days, 46% of placebo patients died while only 30% of treatment patients died. This was the first blinded trial to show vitamin C’s impact on the mortality of patients with ARDS. [28:17] Explaining the Inconsistency of the SOFA Score Jean-Louis Vincent created the SOFA score. Jean-Louis Vincent sent a letter to the editors of Dr Fowler's work that the data was incorrectly analysed. Reanalysis showed the patients who died had the top SOFA score. Vitamin C significantly impacted organ failure scores. Vitamin C treatment resulted in a significant number of ICU-free days, improved mortality and more hospital-free days at day 60. [36:05] Is There Another Trial Underway? The NIH tasked the Prevention and Early Treatment of Acute Lung Injury (PETAL) Network to turn towards COVID treatment.  Dr Fowler started a trial on vitamin C as a treatment for patients with early COVID pneumonia, and the results are dramatic. There is another trial for sepsis and vitamin C planned by the PETAL Network involving 1000 patients across 69 medical centres. [39:48] Why Larger Doses of Vitamin C Are Not Administered The primary concern for higher doses of vitamin C is the formation of renal stones. A safety trial is first recommended before vitamin C treatment for COVID pneumonia can begin.    7 Powerful Quotes from This Episode ‘The cage that the mice got the sepsis and the vitamin C, they were all crawling around, drinking water and eating. And I knew at that point that we had stumbled on something pretty significant’. ‘One of the first things we found was that the lungs of the treated mice that were septic, they weren’t injured’. ‘Most people understand sepsis as being a bacterial infection, but they don't understand that it's actually taking all the organs and causing oxidative damage to multiple organs, not just the lungs’. ‘We had kind of a basic grasp on the immune system and how vitamin C could alter the septic immune response and how vitamin C could protect the lung’. ‘Vitamin C was actually improving the possibility of survival’. ‘The amount of vitamin C that you administer is critical. Dose matters’. ‘You’re going to save not only thousands and eventually more — hundreds and thousands of lives. You’re going to reduce hospital bills enormously’.   About Dr Fowler In his 35 years of service at VCU, Alpha A. ‘Berry’ Fowler, M.D., Professor of Medicine and Director, VCU Johnson Center for Critical Care and Pulmonary Research, has had a profound influence at VCU and beyond. Considering his robust grant support and over 300 publications and abstracts in clinical areas including adult respiratory distress syndrome (ARDS) and sepsis, he might well be lauded for that alone.  Likewise, with over 16 years as Pulmonary Disease and Critical Care Medicine (PDCCM) Division Chair, with numerous ‘Top Doc’ awards and other honours, his pursuit of excellence in clinical care, impacting thousands of patients and their families, might well be the highlight of most careers.  To learn more about Dr Fowler’s research on vitamin C, you may contact him at 804-828-9071 or send a message to alpha.fowler@vcuhealth.org.    Enjoyed This Podcast? If you did, be sure to subscribe and share it with your friends! Post a review and share it! If you enjoyed tuning in, then leave us a review. You can also share this with your friends so that they can learn more about vitamin C. Have any questions? You can contact me through email (support@lisatamati.com) or find me on Facebook, Twitter, Instagram and YouTube. For more episode updates, visit my website. You may also tune in on Apple Podcasts. If you would like to work with Lisa one to one on anything from your mindset, to head injuries,  to biohacking your health, to optimal performance or executive coaching, please book a consultation with Lisa here: https://shop.lisatamati.com/collections/consultations Lisa's latest book Relentless chronicles the inspiring journey about how a mother and daughter defied the odds after an aneurysm left Lisa’s mum Isobel with massive brain damage at age 74 and the medical professionals told her there was absolutely no hope of any quality of life again. Lisa used every mindset tool, years of research and incredible tenacity to prove them wrong and to bring her mother back to full health within 3 years. Get your copy here: http://relentlessbook.lisatamati.com/ For Lisa’s other two best-selling books Running Hot and Running to Extremes chronicling her ultrarunning adventures and expeditions all around the world, go to https://shop.lisatamati.com/collections/books. Go to www.runninghotcoaching.com for Lisa and Neil’s online run training coaching. For their epigenetics health program all about optimising your fitness, lifestyle, nutrition and mind performance to your particular genes, go to  https://www.lisatamati.com/page/epigenetics-and-health-coaching/. For Lisa’s gorgeous and inspiring sports jewellery collection ‘Fierce’, go to https://shop.lisatamati.com/collections/lisa-tamati-bespoke-jewellery-collection. To pushing the limits, Lisa   Welcome to Pushing the Limits, the show that helps you reach your full potential with your host Lisa Tamati, brought to you by lisatamati.com. Lisa Tamati: Hi everyone and welcome to Pushing the Limits. This week I have an exciting interview with intensive care medicine doctor, Dr Berry Fowler, who is an intensivist from the Virginia Commonwealth University. The director of the VCU unit via 35 years of service at the VCU Johnson Center for Critical Care and Pulmonary Research. And he's also the author of a number of studies around vitamin C. So today we're continuing that conversation that we've been having in the last few weeks around the importance of vitamin C. Last week, we had Professor Margreet Vissers on, from Otago University, talking about—who worked with vitamin C in cancer. She's been studying this for 20 years. And Dr Berry Fowler has been studying vitamin C in regards to sepsis and pneumonia and how to use it in COVID. And he's been researching in this area with vitamin C for over 15 years. So some really amazing insights into this incredible vitamin and how it can help with all of these things. So please don't miss this episode. If you enjoy the content, please share it with your family and friends. You know, there’s some important messages that we're wanting to get out in this vitamin C thing that I've been doing, because I lost my father recently and this would have been a major player and I was desperate to get him help with intravenous vitamin C, and I was unable to until way too late. And so I'm desperately wanting to get out the information about this research about the clinical studies that have been done, the research that's been done, to share this really important information.  As always, I really appreciate a rating or review for the show. If you can do that, that'd be so so appreciated. And if you've got any questions, please email me at support@lisa tamati.com, if you want to discuss anything that was brought up in these topics, in this podcast. I'm also doing some one on one consultations. I have a limited number of spaces available for people who are wanting to work with me one on one. If you are facing difficulties in areas from whether it be around some of your health aspects like head injuries, obviously I've spent five years researching head injuries. I have a lot of knowledge around vitamin C. I have a lot of knowledge around biohacking, around epigenetics trained as an epigenetics coach, gene testing, and so on. And I work with a very small number of people who are needing help with these areas. As well as of course run coaching and mindset in high performance. So if you're wanting to get some one on one support with me, please reach out to me it's lisa@lisatamati.com. And I can send you the information there. Right over to the show now with Dr Barry fellow who is sitting in Virginia in the USA. Well welcome everybody to Pushing the Limits. This week. I have a very special interview continuing our series around intravenous vitamin C or vitamin C in general. I have Dr Barry Fowler with me, who is sitting in Virginia and Dr Fowler has agreed to come and have a little chat today about his work in this area. Dr Fowler, I've done a wonderful extra introduction. So we won't go into all your amazing credentials and your achievements, of which there have been many. But Dr Fowler, can you just give us a little bit of background? You are the director of the VCU Virginia University over in the States. Can you tell us a little bit about your work and your background? Dr Berry Fowler: Okay, well, I am professor of medicine in the Division of Pulmonary Disease and Critical Care Medicine and I'm one of the ancient doctors in the division, just turning 71 last week. I trained at the Medical College of Georgia in the US, then went to the Medical College of Virginia in the US, then went to the University of Colorado for pulmonary and critical care disease training, and then came back and joined the faculty at Virginia Commonwealth University which used to be the Medical College of Virginia, it's now VCU, in 1982 and I've been here ever since. Lisa: Wow. Dr Berry: I rose slowly through the ranks. I led the pulmonary division for a number of years, for approximately 17 years, and then stepped aside in 2016. And all during this time, at least for 13 years now, we've had this interest in vitamin C. And it's interesting how our interest in vitamin C developed. It first started at a very molecular level where we were studying cardiac ischemia, but some of the heart attendings. And then slowly began to get back to what we have been doing for years which was bacterial sepsis. And we had some molecular reasons that drove us towards vitamin C. And so first thing we did was we created an animal model of sepsis. And let me explain that. It was pretty straightforward to create. We had 30 gram mice and we went to the mouse cage and collected mouse pellets. Then took them to the laboratory and sonicated them really hard until it became a solution. Lisa:  So this is the fecal matter. Yes. Dr Berry: And we would take that solution and centrifuge it really hard so that all the solid matter went to the bottom of the tube and we just took off the liquid from the top, which contained multiple different kinds of organisms. Lisa:  So all the bacteria. Yes. Dr Berry: Yes. And so we took that, put it in the refrigerator overnight and then came in the next morning. And we had 10 mice. We had 5 control mice and then 5 treatment mice. So all the mice first were injected into their peritoneal space, you mentioned that earlier, with a tenth of an mL of this solution containing all this bacteria. And so all 10 mice. And then in the mice that were going to receive the vitamin C, we injected a tenth of an mL, which was 200 micrograms per gram of bodyweight of the mice and then closed off the light. By that point, it was about 4:00 in the afternoon. And just let the mice sit in the laboratory where we had left them and I always get to work at 6:00 in the morning and I was thinking, ‘Holy cow, I got to see what's going on.’ And so I went into the lab where we had the mice and the cage that was the control mice that were septic. They were all dead. In the cage that the mice got the sepsis and the vitamin C, they were all crawling around drinking water and eating. Lisa:  Wow. Dr Berry: And I knew at that point that we had stumbled on something pretty significant. This take us back to around 2010. Maybe 2009. My laboratory has had this intense interest in sepsis ever since I finished my training at the University of Colorado. And so what we decided is that we would begin to use the treatment animals and some control animals to determine exactly how vitamin C was working. Lisa:  To look at the molecular, the mechanism of action. Why is this happening? Why are they surviving better? Dr Berry: So what we did was—in these studies, we were always comparing the control mice to the treated mice. And one of the first things we found was that the lungs of the treated mice that were septic, they weren't injured. Lisa:  Wow. Dr Berry: And we have a number of ways to determine the way a lung is injured. One of the things that happens in sepsis, and this might have been what you and I were talking about earlier, is the lungs barrier function, which is the ability to keep the blood in the blood and keep the air in the air. Lisa:  Yes. Dr Berry: It gets injured. And so the bloodstream floods into the airspaces of the lung. Lisa: And fills it. Dr Berry: Yes. And one of the things we discovered was lung barrier function was preserved and the vitamin C treated septic mice. Lisa: Wow. So you're perceiving that it’s stopping the plasma and the neutrophils getting into the alveolar space. Dr Berry: Exactly.  Lisa: And the NET— of one of your lectures, you talk about neutrophil extracellular traps (NET). Is that a part of the barrier function?  Dr: Berry: Very nice. When are you starting medical school? Lisa: Thank you, Dr Fowler. Dr Berry: So what happens as sepsis progresses is that there are a bunch of molecules that live in the capillaries of the lung that begin to get expressed. And what they do is they trap neutrophils that are activated in the capillary space of the lung. And one of the things that happens in a highly activated neutrophil is they disgorge their DNA and all of the enzyme systems inside a neutrophil begin to damage the capillaries. And then what happens as the capillaries get injured, the plasma from the lung, just a vein from the bloodstream, just flows into the lungs. Lisa: So you’re basically lost—it's like your skin barrier, if you like, between the ear and your insides is disintegrating. Dr Berry: Well, one injury from sepsis is like drowning. Lisa: Wow, so you fill it with your own fluid. Dr Berry: The airspaces of the lung fill up with your own plasma. Lisa: So when you have, cause sepsis—I don't think most people are not aware of the progression of sepsis to acute respiratory distress syndrome. That this is a sort of a linear progression that happens, isn't it? That you actually get lung—because most people understand sepsis as being a bacterial infection but they don't understand that it's actually taking all the organs and causing oxidative damage to multiple organs, not just the lungs, but particularly the lungs. And so this is a very important finding that what you've had here because this means that if you can stop the vitamin C, if the vitamin C can stop the neutrophils from disgorging their own DNA into the extracellular space, which is then, that's in a marker, isn't it? That cell-free DNA, when you take a plasma drawn and you see that cell-free DNA floating around at a certain level, that's a predictor of mortality, isn't it? Dr Berry: Listen, you've done some fabulous reading. But let me just tell you, it's been known for several years that in septic individuals, one of the unfortunate things that will predict mortality is how high the cell-free DNA arises in the circulation. And I don't want to jump too far here, but I will tell you and the vitamin C trial that we reported one year ago this month, that when we reanalyzed the blood from those individuals, we found that vitamin C dramatically lowered the cell-free DNA in the treated patients. Lisa: Wow. That was in the CITRIS-ALI study? Dr Berry: Exactly. Lisa: Oh, okay. That's a new finding from that study because, yes, we will go through that progression of how you got to do that study. So let's bookmark that for a moment and backtrack because that is a very important finding for that study. So let’s backtrack a little bit. So we are talking about vitamin C being able to protect the lungs if we put it very simply and protect the barrier function of the lungs, stop the neutrophils from disgorging the DNA and causing these traps, which is a predictor of mortality. What are other things is vitamin C doing? And why is a septic patient, without fail, going to be very low in vitamin C? So you’re using that for Vitamin C. Dr Berry: I'll get to that in a minute. But what we demonstrated in a huge number of murine mouse studies is that the septic lung in a control animal, the septic lung began to express many inflammatory proteins. And that's just your endogenous immune system trying to protect itself. But we showed in the next cage, in the septic mice that we had treated with Vitamin C, that the expression and the appearance of those inflammatory proteins was totally inhibited completely.  Lisa: Wow. Dr Berry: Yes. The idea of leaping from preclinical animal studies into humans was that we had kind of a basic grasp on the immune system and how Vitamin C could alter the septic immune response and how Vitamin C could protect the lung. Well, protecting the lung in terms of septic critical illness is very, very important. Lisa: Absolutely. And so then you went to a phase one safety trial, which was really to look at some basic markers. Is this going to be damaging for people if they get vitamin C and look at hypertension? And is it going to affect the kidneys and so on. I think some of those safety mechanisms. Can you tell us a little bit about that phase one safety trial and then the outcomes of that trial? Dr Berry: Well, I can tell you, I had this really close colleague. His office sat right next to mine. He's a molecular biologist, basic scientist. And after we'd done all these murine studies, one day he walked in, he looked at me, said, ‘Fowler, this needs to go into the hospital. We've developed all this data. You've got to make it happen to get it into the hospital’. We designed this little safety trial, enrolled 24 patients. The safety trial was randomized and it was blinded. And so half the trial was just controlled sepsis. The other half was septic patients treated with Vitamin C and we had no idea who the hell was giving vitamin C to people who were critically ill. Lisa: Yes. Dr Berry: And we found it had no impact. But one of the things we were shocked at, and we were just trying to define, was vitamin C safe?  Lisa: Yes. Dr Berry: One of the things we tracked was what is called an Organ Failure Score. And we found that all of the patients treated with Vitamin C, their Organ Failure Score reduced dramatically and significantly. Lisa: Wow. Dr Berry: And the way Organ Failure Scores, basically you're counting numbers. A higher number is a higher incidence of mortality. Lower numbers are improved and that vitamin C was actually improving the possibility of survival. Lisa: So this is like, in my father's case, is the sepsis progressed and I was unable to get him Vitamin C as we discussed earlier, Dr Fowler, early enough for him to get to survive. But as I watched his sepsis progress, more and more organs started to fail. So his liver started to fail. His kidneys started to fail. His heart started to fail. And so this is the Organ Failure Score. If this person's Organ Failure Score is going up, that is a very strong predictor of mortality. Dr Berry: Yes. Lisa: Okay, so this was reduced with the people who received the Vitamin C in the small trial. Dr Berry: So what we did, we took the data, we combined it with our preclinical data, and applied to the National Heart Lung and Blood Institute. They had just published an announcement where they were asking for anybody who could think of some clever trial. And we said, ‘Well’. And so we submitted an application. What the NIH wanted, they wanted the proposal for a phase two, proof of concept trial. Lisa: Right. Dr Berry: And so what we proposed was a trial that had seven medical centers. I have friends in seven medical centers around the US. And with this application in and that was I guess you guys don't remember Hurricane Sandy. Lisa: Yes, I do. Dr Berry: Hurricane Sandy was just—it killed the Atlantic Coast of the US. And the National Heart Lung and Blood Institute happens to sit on the Atlantic Coast in Washington, D.C. And it was a year and a half before we found out that we had received the highest priority score because of the application that we had submitted. And the NIH gave us 3.2 million dollars to do a multicenter, randomized, double blind, placebo-controlled trial, proposing to administer 50 milligrams per kilogram of intravenous Vitamin C every six hours for ninety six hours. Patients were continuously receiving vitamin C. Lisa: Can you explain why that continuous topping up that level is important every six hours? Dr Berry: That's a great question. So from the safety trial that we had performed, we analyzed the plasma Vitamin C levels that we had achieved by infusing. So basically someone your size, for example, would probably get maybe 3 1/2 grams intravenously every six hours for ninety six hours. And what we showed was, we could get the plasma level up to basically three thousand times the normal plasma level. So from a normal diet, human plasma levels of vitamin C are about 70 to 80 micromolar. When you give the protocol that we had settled with, we got the Vitamin C levels up to five millimolar. Lisa: Wow. Dr Berry: Yes. And so that's what we were shooting for in this NIH trial. And that's what we did. We charged into it, the trial. What we had proposed again, was the Organ Failure Score as well as the two biomarkers. We also proposed in the secondary outcomes, days on mechanical ventilation. Lisa: Yes, which is hugely important. Dr Berry: And what we were studying specifically, was patients who were septic, who had gone on to develop acute lung injury called Acute Respiratory Distress Syndrome, ARDS. And so when a patient was septic, like your father, we would become a fly on the wall and visit the patient every day until a lung injury developed. And that's when they would get randomized. Lisa: This was a critical—from my analysis of the data, that was a critical thing in the phase. So you had to wait until I basically had developed ARDS before you were able to put them. So this wasn't really a sepsis trial, but more of an ARDS trial. So the progression of the sickness comes into play here, doesn't it? If you’ve gone through day one, like in the phase... Dr Berry: In the safety trial... Lisa: Yes. Dr Berry: The second aseptic individual walked in the door, that's when they got random. Lisa: Which is a much better, more effective with the timing. Dr Berry: We had a couple of patients who got Vitamin C in the emergency room. Lisa: Yes, wow.  Dr Berry: You know you have to get informed consent. You have to get the pharmacy on board and get the patient enthused. Lisa: I wish I'd had you tending to my father. We could have had that from the moment he got to the emergency. That would have been, I think we would have had a different outcome. But so this was a key point that you had to wait until I had developed ARDS. So in this CITRIS-ALI trial, so here you have, I think it was 47 patients in the control and 47 in the intervention group, was it right? Dr Berry: 83. And 84 in the Vitamin C treatment. Lisa: Oh, 83. I'm sorry. Sorry. So 167. One of the big questions I had in my— why was mortality not one of the primary objectives of the study? Dr Berry: That has been the most frequent question. When we answered the NIH, they had put out a program called, UM1, and we applied to the UM1 program and they were not interested in mortality as a primary outcome. Part of it was this. There had been hundreds of sepsis trials and nobody had ever shown any impact on a treatment for sepsis. And so NIH didn't want to get burned again so they said that they wanted a physiological outcome. That was the Organ Failure Score. And they wanted a biochemical outcome. Those were the biomarkers. Lisa: It's the C-reactive protein, procalcitonin and thrombomodulin. And yes. So the reasoning was that we don't want to shoot for the stars here and automatically hope for a decrease in mortality and a decrease of days in hospital. We're going to go for something else just to see if this has legs, so to speak, if this treatment is possible, possibly going to work. And that's why they went for the safer scores, rather than the mortality. Looking back, do you think... Dr Berry: By the way, we haven't talked about this yet, but SOFA stand for Sequential Organ Failure Assessment Score. Lisa: Thank you. Yes, it's amazing the jargon that you pick up and then forget that you haven't explained yourself. So what actually was the outcome? This was a seven multicenter trial. You did a double blinded. This was incredibly important because I know Dr Paul Marik had also done a study with intravenous Vitamin C, thiamine, and hydrocortisone. And one of the criticisms that was thrown at him was that it wasn’t a double blind, randomized controlled trial, so it didn't have any meaning, which is absolutely tragic. So this was—what was the outcomes of this phase two trial? Dr Berry: So we enrolled 170 patients. One of the placebo patients we had to take out because that patient did not have septic ARDS. They had Acute Eosinophilic Pneumonia. That's something else to discuss later. And then in the Vitamin C arm, we had two patients with Acute Leukemia who had no coagulation in their bloodstream and they were hemorrhaging into their lung and that was not sepsis. So as I mentioned, we had 83 in the control placebo and 84 in the vitamin C-treated group. First of all, we saw no, and I emphasize capital N-O, adverse events. There was not a single adverse event.  Lisa: Exactly. Dr Berry: All right. And so what we showed was in 96 hours, placebo patients in the trial, 19 of 83 died within 96 hours. Lisa: Wow. Dr Berry: In the Vitamin C group, 4 of 84 patients died. And if you look at the statistics and the analysis of that, the difference is P=0.0007. We then followed the patients out because in sepsis trials, there's always this demand to see what is happening to a patient at 28 days. Lisa: Yes. Dr Berry: And what we showed was 46% of placebo patients died and only 30% of the Vitamin C treated septic patients with ARDS died. Lisa: Wow, that's a huge result in my mind. Dr Berry: And that was the first trial. I'm not slapping myself on the back, but I will just tell you, that was the first trial to ever show in a blinded fashion, an impact on ARDS.  Lisa: Yes. On mortality of ARDS. Dr Berry: Yes. Lisa: And this was extremely sick people. Now, unfortunately, the SOFA scores didn't show any difference and the C-reactive protein markers didn't show any difference. Dr Berry: So let me explain. Lisa: Is it because... Yes, is it because of the mortality. Dr Berry: So we thought publishing the results of the trial in probably one of the most important journals on the planet, JAMA, which as it turns out, is a very, very conservative journal. And they had their ideas about what we could and we couldn't say. So we published, and this is very important for you to listen to and all of your listeners, we published that there was no difference in the SOFA scores at 96 hours. And immediately, letters to the editor started coming in and one of the most important letters to the editor was the person who created the SOFA score. His name is Jean-Louis Vincent in Brussels, Belgium. He told us that we had analyzed the data incorrectly and that what we were reporting was a survivorship bias. Lisa: What does that mean? Dr Berry: And what he said we needed to do, and he provided five publications where he had important statisticians tell him that analyzing the data, like we reported, as a worst rank, best rank scenario, that we had to reanalyze it so that the patients who died, what we were reporting was the SOFA scores on the people who had survived. Lisa: Not the ones who died. Dr Berry: We had not considered the SOFA score on the patients who died. Lisa: And because they died so quickly. Dr Berry: So what we did was we went back and the people who died along the way, those 19 patients, they got the top SOFA score. The patients who survived and left the unit, they got a low SOFA score. And so when we reanalyzed the data, according to the way these letters that had come in from Dr Vincent and two or three other colleagues, it turns out that Vitamin C significantly impacted the Organ Failure Score. Lisa: Wow.  Dr Berry: And then we—here's the important thing, we reported that February 25th of 2020. So you can go to JAMA, you can look it up and you can see our response to the SOFA score reanalysis. Lisa: Because this was a key factor in my father's case. They threw the CITRIS-ALI trial at me and the original data from JAMA, which said negative result, which when I analyzed... Dr Berry: That lets you know that the doctors were not reading JAMA. Lisa: Exactly. And they weren't on the up to date and they did not look at secondary outcomes and they did not look at the parameters of the score and I was not able to present the case. They had just read it briefly. Dr Berry: Let me go on. We had a strong trend to ventilator-free days and the people who got the Vitamin C, but it just missed statistical significance. Lisa: Yes. Dr Berry: But we had a strong significance for the people who got Vitamin C in Intensive Care Unit-free days. Lisa: Which is huge. Dr Berry: So the people who got Vitamin C had a significantly higher number of ICU-free days. There was an improved mortality. The other thing is patients who got Vitamin C had significantly more hospital-free days at day 60. Lisa: Wow. So they were actually out of the system altogether. Do you think—now this is controversial, I'm playing devil's advocate here. But do you think the fact that it costs so much for someone to be in ICU when they have sepsis—I think in America it's something like, to the order of 60,000 dollars US a day—and the medications that they are typically on are costing around 20,000 dollars a day, do you think that if you come along with Vitamin C and you start dropping the mortality rate, you start dropping the days? Is that part of the resistance to accept and acknowledge these findings, that the pharmaceutical companies are going to lose out on profit? Dr Berry: Oh no no no. No, no, no. At VCU, Virginia Commonwealth University—that Anitra knows well—the average care cost per day is about 46,000 per day because that accounts for medical care, nursing care, radiology, all laboratory data, respiratory care, caring for the ventilator. All of that is somewhere in the neighborhood of about 45 to 50,000 dollars per day. And so, if you have a treatment, first of all, that gets people out of the ICU earlier and keeps them out of the hospital, think about the impact on the cost of care. Lisa: Yes, it’d be huge. Dr Berry: But here's the other thing. There's not going to be any drug company out there who would argue with that. They are all trying to do the best they can with their different antibiotics, but the common antibiotics that are administered in an ICU when patients are septic levofloxacin, meropenem, vancomycin. Just one day of meropenem is 1500 per day. Lisa: Exactly. It's a lot of money.  Dr Berry: Yes.  Lisa: So you don't think that... Dr Berry: And listen to this. That's the cost of the drug. That's not the cost of pharmacy preparing the drug, cost of nursing administering the drug and so on and so on and so on.  Lisa: Okay, so all right. So if you can work this problem out and if you can get this in all ICUs around the world, we're going to save not only thousands and eventually more hundreds of thousands of lives, you're going to reduce the hospital bills enormously. So this is incredibly important work. And you've proven—so the statisticians proved in that phase two trial that the way that you are measuring it was incorrect because a lot of people, as you said, 19 died in those first four days in the control group and only four, so that skewed—if you like—the statistics to initially look like we hadn't had a win here. Now, that's been rescinded and you've managed to get JAMA to publish it in a different light, that the SOFA score was impacted. What has been the effect now? Have you got another trial underway or have you got one in sight? Because this work’s too important, obviously, not to be taken further into a phase three. Dr Berry: All right, so you are in New Zealand where there's not much COVID.  Lisa: No. Dr Berry: We are in the United States, where it's a pandemic, where we are close to 220,000 people who have died from the virus. We are at 50,000 new cases per day. Lisa: Oh my God. It's so...  Dr Berry: And there are somewhere in the neighborhood of 1,800 to 2,000 patients dying per day of COVID. And so because of that, the network that I'm part of, that unfortunately—I'm going to have to jump off and listen to it, because it's been going on since 2:00, the annual meeting of the Prevention and Early Treatment of Acute Lung Injury Network, abbreviated P-E-T-A-L, the PETAL Network. The PETAL Network was tasked by the NIH to turn sharply towards COVID treatments. Lisa: Yes. That makes sense. Dr Berry: And so we were thinking, ‘Well, maybe vitamin C to treat patients with early COVID pneumonia’. And so what we did was we started a trial. We have studied 20 patients now and that trial is complete, where patients who develop COVID infection and develop early COVID pneumonia, so it's just at the start of an oxygen requirement, are treated with Vitamin C and the results have been pretty dramatic. We are in the midst of writing that up. But again, it's a—open label trial. It's not blinded. Everybody in the world knows that an open label trial does not have the power like we did with CITRIS-ALI. Lisa: Yes. Dr Berry: And so what is happening at a world level is that all of the health organizations around the world have come to bear to try to design treatments for COVID pneumonia. Lisa: Yes. Dr Berry: And that is ongoing right now. And there are like 9 or 10 major networks in, across the world. Probably, I'm not sure if New Zealand is included in that, but Europe, the US, possibly Australia. I don't know if they commit to participating in what is called the network of networks formation. Lisa: Yes. Dr Berry: So right now, the next trial for patients with sepsis that's not COVID is going to be conducted by the PETAL Network where we will be probably next April, starting a trial with a thousand patients. Lisa: Wow.  Dr Berry: Using vitamin C conducted by the PETAL Network. Lisa: Gotcha. Dr Berry: And the PETAL Network has 69 medical centers. So doing a trial that would get a thousand patients can be done within a year. Lisa: Wow. So this is exciting stuff because this is hopefully you'll be able to reproduce and show a strong correlation between intravenous vitamin C and I'd like to see the decrease in the mortality rate. That would be a key factor. Some centers are already using vitamin C because as you mentioned before, there were no adverse reactions. And this is like in all of the studies that I've seen there has never— this is a low risk intervention and my argument when fighting for my father was that, ‘He's dying. There is no other options. Why can't I throw the bus in? Why can't I put intravenous Vitamin C’? And they were like, ‘You still have to go through all the ethics committees’. I had to sign off from every single doctor and every single nurse in the ICU unit of which there are many. Dr Berry: Well, let me make another statement. So Paul Marik, who was using 1.5 grams of Vitamin C, 200 milligrams of thiamine and 50 milligrams of hydrocortisone, administered every six hours. That meant that the patients were only getting 7 grams. Lisa: Very small amount. Dr Berry: In the CITRIS-ALI, I mean, some patients got 16 to 18 or 20 grams. Lisa: Yes. Dr Berry: According to body weights, 50 milligrams per kilogram. In the aftermath of that article that you mentioned that Marik published, there have been efforts to repeat that trial. The vitamins trial came out in January, using that and it failed. Then another trial, the ACTS trial using the Marik protocol failed. And then a trial that I just participated in called the VICTAS trial completely failed. And so the Marik protocol is not an effective treatment for sepsis. And well, look. As I think Anitra Carr mentioned to me a couple of years back, the amount of vitamin C that you administer is critical. Lisa: Absolutely. Dr Berry: So dose matters. And the adult, again, of your size, you probably weigh 120 pounds or something would probably get somewhere in the neighborhood of about 12 and a half to 13 grams, spread out over a 24-hour period. And then you would get it for four days. Lisa: Yes. And that is still a relatively low dose. Dr Berry: It is. Lisa: When I'm doing intravenous vitamin C with my mum, I did it with my dad prior and unfortunately, months prior to his aneurysm. Too little, too late. We were getting 30 grams. We get 30 grams a week. When I take my mum and niece today for an intravenous Vitamin C is a prophylactic as I try to keep her, as a 79 year old healthy, 30 grams. So why—I had this question certainly with Dr Marik’s protocol. It seemed to me to be very low, although the six hourly is obviously a very important point as well. Why not do the bigger dosages? Like in Japan, I know they did a study with up to a hundred grams of Vitamin C in a burns case, a burns trial, where they had some markers of sepsis there. Why are you not trying higher levels? Dr Berry: Let me come in here quick? Because I'm going to have to jump off in about 8 minutes. But listen to this. The major concern for those high doses of vitamin C, and if you talk to the oncologists who have been using it for years, they will give, like you said, they will give massive doses. And I'm talking massive, like in somebody with pancreatic cancer, they will get 60 to 80 grams intravenously, Monday, Wednesday and Friday for seven weeks. Lisa: Yes. Dr Berry: But the major concern, in somebody who's septic, who's hypotensive, in shock, that you're giving vitamin C, one of the major concerns is that it causes a significant rise in oxalate crystals formatiion in the kidneys. Now, I will mention here in the CITRIS trial, we had no evidence of renal stone formation. Lisa: No. And I mean, that was one of the arguments that the doctors had at me, ‘You could have damaged his kidneys’. And I said, ‘Well, the last time I looked, being dead damages your kidneys too’. To me, that wasn't even a consideration. And he had—after the very first vitamin C, and for my dad, his kidney function went from 27 percent to 33 percent. He's actually improved his kidney function overnight. And I know that's just one anecdotal case, but kidney stones are not going to kill you either. So surely that's not the most important consideration here when you've got a septic patient who is on death's doorstep. Dr Berry: With vitamin C struggling in the United States after the CITRIS trial, the Federal Food and Drug Administration, they always have to be concerned about adverse events. And we have put together a trial randomized and double blind using Vitamin C in patients with COVID-pneumonia. That's about to start. Lisa: Wonderful. Dr Berry: And we had, I unfortunately let my IND, Investigational New Drug lapse after CITRIS. And so I've had to claw our way back into the good graces of the FDA. And one of their major, major, major complaints was, ‘You're going to be forming renal stones’. And we're using the same protocol that we used in CITRIS. So FDA got their nephrologists involved and finally gave us the IND. But for us to begin treatment of COVID pneumonia, they have demanded that we first do a small safety trial to show that we are not causing any renal stone formation. We can get that done. We currently have somewhere in the neighborhood of 60 to 70 COVID patients in the MCV hospitals right now. Lisa: Wow. Well, Dr Fowler, look, I know I'd love to spend another five hours with you discussing all this because I think it's incredibly important, both for COVID and for the sepsis and for pneumonia and for obviously, for cancer. I just want to thank you for your dedication to this. I mean, you could be in retirement and sunning yourself somewhere, relaxing, but, you know... Dr Berry: That's right. Lisa: You know that this work is critically important. And I heard one of your lectures is the equivalent of two 747 planes going down every day filled with people. Dr Berry: Every day in the United States. Lisa: In the United States alone. Dr Berry: That’s just in the U.S. Lisa: Yes. And these people, thousands of families being destroyed with losing loved ones. I'm one of those, unfortunately, sitting here all the way in New Zealand. And so this work is incredibly important. So please keep going. And I'm desperate to hear what comes from this COVID clinical trials and the other sepsis trials, obviously. So thank you so much for your work, Dr Fowler, and I really appreciate you. Dr Berry: It's been wonderful meeting you and speaking with you, and your and your audience. And when you have Anitra on a couple of weeks, give her my regards. Lisa: I will definitely do that, Dr Fowler. That's been awesome. Thank you, Dr Fowler. And all the very best there in Virginia. Dr Berry: Take care. Bye. That’s it this week for Pushing the Limits. Be sure to rate, review and share with your friends, and head over and visit Lisa and her team at lisatamati.com.  

In the second of our two-part series on race, racism, and health, we have a discussion with pediatrician and researcher Dr. Nia Heard-Garris on talking to kids and loved ones about racism: why it’s important, how to maintain momentum, and (if you haven't already) where on earth to start. You may recognize her from the recent CNN/Sesame Street Town Hall on racism, so we'll get her recommendations for anti-racist resources for kids and adults alike.Dr. Nia Heard-Garris, MD, MSc is a pediatrician and physician-investigator at the Ann & Robert H. Lurie Children’s Hospital of Chicago and in the Department of Pediatrics at Northwestern University Feinberg School of Medicine. She examines the influence of social adversities, including the impact of racism on subsequent child and adolescent health. Dr. Heard-Garris is also interested in the factors that contribute to a child’s ability to thrive despite these experiences. In August 2019, she received her career development award (K01), which is funded by the National Heart Lung and Blood Institute, and with this award she plans to investigate adolescent cardiometabolic health. She believes in using research to better inform clinical practice and policy that supports children, their families, and their communities. Dr. Heard-Garris is also an active member of the American Academy of Pediatrics (AAP) and serves as the Chair and founding member of the Provisional Section of Minority Health, Equity, and Inclusion. Dr. Heard-Garris completed a prestigious Robert Wood Johnson Foundation Clinical Scholars Fellowship at the University of Michigan. She earned her Master of Science in Health and Healthcare Research. She received her Doctor of Medicine (MD) from Howard University College of Medicine and helped to launch the student-run free clinic serving DC residents. Dr. Heard-Garris earned her Bachelor of Science in biology at Spelman College in Atlanta, Georgia. She lives with her husband and 6-year-old son in Chicago.

Dr Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr Greg Hundley: And I'm Dr Greg Hundley associated editor from the Pauly Heart Center at VCU health in Richmond, Virginia. Well Carolyn, this week's feature investigates the compass trial and is going to examine the role of combination antiplatelet and anticoagulation therapy in patients with diabetes and cardiovascular disease. But before we get to that feature discussion, how about we grab a cup of coffee and jump in and discuss some of the other papers in the issue? Dr Carolyn Lam: You bet, Greg. I've got my coffee right here, and I'd like to start by talking about paclitaxel containing devices. You may already know this, but it was nice to revise that these significantly reduce re intervention in patients with symptomatic femoral, popliteal, peripheral artery disease, as we may expect. However, a recent aggregate data meta-analysis reported increase late mortality in pad patients treat it with these paclitaxel containing devices. Thus today's authors, Dr Rocha-Singh from Prairie Heart Institute of Illinois at St. John's hospital and their colleagues performed an individual patient data meta-analysis to evaluate mortality using data from eight randomized controlled trials of FDA approved paclitaxel coated devices using de identified data that was provided by manufacturers. Dr Greg Hundley: Well, Carolyn, what did they find? Dr Carolyn Lam: So in 2,185 patients and 386 deaths from eight paclitaxel coated device trials with a four year median follow-up, there was a 4.6% absolute risk of increased mortality associated with paclitaxel coated device use compared to balloon angioplasty at a median of four years follow up, significant loss to follow up and withdrawal rates of 24% and 23% in balloon angioplasty and paclitaxel cohorts respectively through five years were observed. Recovery of lost vital status data reduced the observed paclitaxel device associated mortality rate. And there was no paclitaxel drug dose mortality relationship identified. Dr Greg Hundley: Oh, Carolyn, I think this is really an important finding, and we have a nice editorial, don't we? So what was the take home message? Dr Carolyn Lam: Yeah. In fact, this was discussed in an important editorial by doctors Royce, Chakraborty and Dao from the USFDA. Now listen up. So based on the prior aggregate data meta-analysis and subsequent FDA review, FDA had already communicated that clinicians should consider the increased rate of long-term mortality when making treatment recommendations. They had also implemented updated labeling for this device class to communicate the risk. So in this editorial, the FDA commended the authors of the current individual patient data meta-analysis for providing important information towards signal refinement, and also commend at their collaboration with device manufacturers to work together with a shared goal of patient safety. Now, there are still many unanswered questions, including the mechanism for the observed increase in late term mortality associated with these devices and how the benefit risk profile of these devices may shift across various patient populations. Dr Greg Hundley: Well Carolyn, my paper comes from Professor Antje Beling from Charité – Universitätsmedizin Berlin in Berlin. And it investigates heart specific immune responses in an animal model of auto immune related Meyer carditis mitigated by an immuno proteasome inhibitor and a genetic ablation. So Carolyn, this study used mouse models to understand mechanisms involved in immune checkpoint inhibitor related Maya carditis, a phenomenon that we can observe in 5% to 10% of patients that are receiving these checkpoint inhibitors for treatment of their cancer. Dr Carolyn Lam: So what did they find, Greg? Dr Greg Hundley: Several things, Carolyn. All immuno proteasome deficient strains of mice showed mitigated auto-immune related cardiac pathology with less inflammation, lower pro-inflammatory and chemo tactic cytokines, less interleukin 17 production and reduced fibrosis formation. The auto-immune signature during experimental proponent I auto immune carditis with high immuno proteasome expression, immunoglobulin G deposition, interleukin 17 production in heart tissue, and troponin I directed humeral auto immune responses was also present in two cases of immune mediated related my carditis. Thus demonstrating the activation of heart specific autoimmune reactions by this checkpoint inhibitor related myocarditis therapy. So Carolyn, perhaps by reversing heart specific auto immune responses, immuno proteasome inhibitors applied to these mouse models demonstrated their potential to, in the future, aid in the management of auto-immune bio carditis in humans, possibly including cases with immune mediated myocarditis heart-related specific auto-immunity. Dr Carolyn Lam: Oh, that's really nice, Greg. Thanks. How about a quiz? Remember what desmoplakin is Greg? Dr Greg Hundley: I think this is going to do something with right ventricular cardiomyopathy. Dr Carolyn Lam: Very nice. Desmoplakin is the primary force transducer between cardiac desmosomes and intermediate filaments. And mutations in Desmoplakin indeed cause an arrhythmogenic form of cardiomyopathy that has been variably associated with arrhythmogenic right ventricular cardiomyopathy. Clinical correlates of desmoplakin cardiomyopathy have been limited to small case series. Today's paper, by Dr Helms from University of Michigan and colleagues is the largest series of desmoplakin mutation carriers reported to date. Dr Greg Hundley: So Carolyn, what did they find here? Dr Carolyn Lam: Among 107 patients with pathogenic desmoplakin mutations and 81 patients with pathogenic Plakophilin-2 mutations as a comparison cohort, they found compelling evidence that desmoplakin cardiomyopathy is a distinct form of cardiomyopathy marked by a high proclivity for left ventricular hypertrophy and arrhythmias and associated with intermittent myocardial inflammatory episodes that appear clinically similar to myocarditis or sarcoidosis. Furthermore they found that diagnostic and risk stratification variables that performed well for Plakophilin-2 associated ARVC exhibited poor accuracy for the diagnosis and risk assessment of desmoplakin mutation carriers. So these results strongly indicate that a genotype specific management approach is essential for desmoplakin cardiomyopathy. Dr Greg Hundley: Wow, Carolyn. Lots of great science in this issue. Well, just like last week, we have got a lot of other papers in this issue. So let me tell you about a few that I've had a chance to preview. The first is a research letter by our own Dr Hesham Sadek from UT Southwestern Medical Center involving the homotypic fusion generates multi nucleated cardiomyocytes in the murine heart. Next is an ECG challenge. It's from Dr G. Neil Kay at the University of Alabama at Birmingham, and really reviews an ECG in a patient that presents with pulmonary embolism. Next, there's a case series from Dr Nil Uriel from Columbia University Medical Center regarding the variety of cardiovascular presentations of COVID-19. Next there's an on my mind piece that comes to us from Dr Ersilia DeFilippis from Columbia University College of and Physicians and Surgeons. And it involves cardiopulmonary resuscitation during this COVID-19 pandemic. And it presents a view from trainees on the front lines. Next, Carolyn, one of your faves, Dr Leslie Cooper from the Mayo Clinic provides an informative white paper on the description and proposed management of acute COVID-19 cardiovascular syndromes. Next is a paper from Dr Francine Marquez from Monash University, and it's a perspective piece on the impact, strategies and opportunities for early and mid-career cardiovascular researchers during the COVID-19 pandemic. So many studies have been stopped and this very nice article highlights the new opportunities in this pandemic. Next, Dr Anabel Volgman from Rush University Medical Center has a piece on the seniors on the sidelines, and it's a call to action. And then finally, Dr Andrew Chapman from University of Edinburgh and professor Christian Mueller from the University Hospital of Basel exchange letters to the editor regarding a prior article of high sensitivity cardiac troponin, and the universal definition of myocardial infarction. Dr Carolyn Lam: Nice. There's also a research letter by Dr Sandoval and colleagues who described the transition to using high sensitivity troponin T in a United States regional healthcare system, namely the Mayo Clinic enterprise. And they really showed that a small increase in MI diagnosis in part due to an increase in type two MI diagnosis occurred without an overall increase in hospital admissions or resource utilization using the high sensitivity cardiac troponin T implementation. And if I may mention, there is also a beautiful white paper by Dr Sana Al-Khatib, whom I was very lucky to coauthor with. And it's on the advancing research on the complex interrelations between atrial fibrillation and heart failure. This a report from the National Heart Lung and Blood Institute virtual workshop. Wow. A bonanza of an issue. Thanks so much, Greg. Let's move on to our feature discussion now. Dr Greg Hundley: Look forward to it. Dr Carolyn Lam: Today's feature discussion was in fact a late breaking clinical trial presentation at the American College of Cardiology meeting this year, 2020. And it's all about the compass trial, this time focusing on diabetes. I'm so, so pleased to have with us, the corresponding author Dr Deepak Bhatt from Brigham and Women's Hospital, as well as Dr Gregory Lip from University of Liverpool who was not only the guest editor, but also an editorialist for this paper. So welcome gentlemen. Deepak, could I start with you? This was an incredible presentation that was very well discussed. ACC not virtually, but I'm just so glad that we can have you on this podcast to tell us again, please, the rationale, the key findings and why this paper is just so important. Dr Deepak Bhatt: So the background really is that prior studies and particular registry studies, the reach registry, for example, have shown that patients with concomitant CAD and/or PAD, that is coronary artery disease and/or peripheral artery disease, plus diabetes, are folks that are extremely high risk of future ischemic events. This is true even if they are apparently stable outpatients. At any rate in the compass trial, these sorts of patients with CAD or PAD, stable patients, both with and without diabetes who are enrolled 27,000 plus patients randomized. And there were three arms in this study, aspirin alone, rivaroxaban alone and aspirin plus low dose rivaroxaban 2.5 milligrams twice a day. And that was the winner, that combination sometimes referred to as dual pathway inhibition significantly reduced the schemic events versus aspirin alone, a significant reduction in cardiovascular death MI stroke, as well a lower rate significantly so of cardiovascular death, and even all-cause mortality was lower. So the overall trial was positive, but what we wanted to examine in this analysis was specifically how to patients with diabetes fare, knowing that they're a higher risk group in general across multiple registries and studies? And indeed we found that they were higher risk, those with diabetes versus those without diabetes and compass, and indeed, though their relative risk reductions were similar, those patients with diabetes had numerically larger, absolute risk reductions than those without diabetes with this regimen of low dose rivaroxaban plus aspirin versus aspirin alone. Dr Carolyn Lam: Thanks Deepak. And I just have to refer the listeners to those beautiful figures in your paper. I mean, just one look at it really explains exactly what you were saying and really highlights that patients with diabetes are at higher risk of adverse events and also in one of the graphs of bleeding. Greg, could I bring you in here? You mentioned that in your editorial as well, that there has to be importantly acceptable bleeding risks. Could you expand on that? Dr Gregory Lip: The compass crowd was a game changer and in this high-risk subgroup, as Deepak elegantly has described. These are diabetic patients, and then we also have the subgroups we call with or without PCI. And those would be so of course, being the higher risk group of patients. Nonetheless, the comparison was basically a dual pathway inhibition, but a combination rivaroxaban plus aspirin compared to aspirin alone. But a high cardiovascular risk and high bleeding risk tend to track each other. So it was important that we certainly want to reduce the adverse outcomes of cardiovascular endpoints, we should certainly individualize our assessment of our patients and make sure that a patient is not an excessive high bleeding risk. I think overall, the study is very reassuring because there was no significant access in the overall population of the subgroup, at least in relation to fatal bleeding, critical organ bleeding or intracranial hemorrhage by dual path inhibition. But I think we, as physicians, just need to assess the patient in front of us just to make sure that particular patient is not at high risk particularly of bleeding, given that high risk of bleeding also generally is high cardiovascular risk as well. Dr Carolyn Lam: Thank you, Greg. And Deepak, perhaps maybe some words from you about this sort of risk benefit ratio? How do you see it? How do we apply these results? Dr Deepak Bhatt: I totally agree with everything Dr Lip said. Really, the key message when we're talking about antithrombotic numbers, something Dr Brunwald had said in this context, that is, there's no free lunch. When it comes to antithrombotics, there's always bleeding risks. There's just no way around that. In any trial that is adequately powered long enough, we'll find that, and that can include bad bleeding. Now, fortunately there was no significant excess and failure endocranial bleeding within the trial or within the subgroup of patients with diabetes. But nonetheless one needs to be cautious because these of course are carefully selected patients at low bleeding risk to get into the trial. There was a run in period. So when applying to real life, of course, there's the potential for bleeding. So we need to be really cautious about that. And it's also not a stat. So if we were talking about secondary prevention, either with or without diabetes, CAD, PAD, both of them together, of course, all those patients should be on Statin assuming they don't have a real type of contraindication. So that's kind of a no brainer. That's a matter of implementation science. A lot of patients that should be on Statin aren't, but that's not an issue of science. We already know the answer there. Here, it's not the case of everyone that is like this who has diabetes, or even who doesn't, who has CAD or PAD should be on this regimen. It needs to be carefully selected patients, patients that are a low bleeding risk. And sometimes doctors ask, "Well, how do you tell that?" Well, it's not always easy, but for sure there's some things that predict future bleeding risks such as prior bleeding. So prior bleeding, anemia, those are powerful predictors of future bleeding. And one would want to be really cautious in these largely stable outpatients that we're talking about in the compass trial in intensifying their antithrombotic regimen. But in the right patients, I think it's a really effective way of reducing important future vascular risk, whether that's cardiovascular risk consisting of MI related end points, stroke, peripheral ischemic end points, including amputation, which was significantly reduced in the trial, and within the subgroup of those with diabetes. So it's a matter of balancing those, but I do think with careful decision-making on the part of the physician, with discussion with the patient, with their understanding of the risks and benefits of intensifying the antithrombotic regimen beyond aspirin, there are a substantial number of patients who could benefit. Dr Gregory Lip: I whole fully agree with Deepak's comments. And we do have to bear in mind also that risk is also a fairly dynamic process and we may well be assessing the patient as the one off initially while we are initiating treatment. But of course risk, whether from cardiovascular risk or whether from bleeding risk particularly, also is influenced by increasing age and by incident comorbidities, which really means that risk reassessment should be performed in every patient we contact. With bleeding risks in particular, there are modifiable bleeding risk factors that we can mitigate. So proactive assessment or rather reassessment of risks, whether both from cardiovascular events and/or bleeding, is necessary as we follow up these patients. Dr Carolyn Lam: Thank you, both. Deepak, I'm just going to build a bit on your analogy of no free lunch. And maybe sort of a general question do you both, because it seems like we've got a bonanza of a buffet now when it comes to diabetes, especially with the new anti-diabetic drugs. So how do you think this fits in altogether? You talked about Statins. We now talk about low dose rivaroxaban in addition to aspirin, and you think diabetic patients should be treated with all? Maybe Deepak first, then Greg. Dr Deepak Bhatt: What a terrific question. In fact, that was asked of me by the late-breaking clinical-trial panel clinical trial panel. They said, "Well, how does it fit in? Because these data look terrific, but there's also other new diabetes drugs and approaches." So for sure, I would say again, barring a real contraindication, I would say everyone that we're talking about here should be on a statin and preferably if they can tolerate it, a high intensity statin. And if that doesn't do the trick in terms of LDL goal, I would say zetomyde. And potentially if they're in a region of the world where it's affordable a PCSK9 inhibitor. Then beyond that, I think we've got to pay attention to triglycerides these days, not just LDL cholesterol and if it's some patient that's sort of like REDUCE IT, well then, they should be on eicosapentaenoic. So we can modify LDL related and triglyceride related risks without too much effort or too much in the way of side effects. Then beyond that, I would say, we've got to think about blood pressure, inadequate control, especially in those with diabetes, but even those without that have cardiovascular disease. And then we have to think about glycemic control. And I don't mean the old-fashioned way, but I mean with some of the newer drugs. SGLT2 inhibitors in particular have been found to be useful for both. That's just the glycemia control part of things, more importantly, cardiovascular outcomes. In particular, heart failure and renal related outcomes. And then GLP 1 agonist as well have been shown to be very useful once more modifying cardiovascular outcomes, including atherosclerotic outcomes. So there is, as you say, quite the buffet. And assuming a patient can tolerate that polypharmacy and afford it, I do think the majority of patients with diabetes should be treated that well. And that's of course on top of lifestyle modification, weight loss is particularly important, plant-based diet, et cetera. But on top of that, then, with all those things that are being done and a patient is still at high ischemic risk but is at low bleeding risk, that's where I think, even in the deceptively stable appearing outpatient, it's worthwhile just running a mental checklist and saying, "Okay, are they on an SGLT2 inhibitor? Check. Did In someone measured their triglycerides? Check." And then on that checklist is, "Yeah, could they tolerate being on more than just aspirin alone in terms of bleeding risk? And if the answer to that is yes, might they benefit from adding this on?" And there are a lot of patients these results apply to, and I think a proportion of those patients who are otherwise optimally treated for their risk factors are the ones to target. Dr Carolyn Lam: Beautifully put. And Greg? Dr Gregory Lip: Deepak does raise an increasingly applied concept in how we approach our patients at high risk of cardiovascular events. That's the so called integrated or holistic approach to management. Because we have in the past tended to just focus on one strand of management. For example, we may well just be putting a lot of focus when on the analytic reduction and ignoring the rest. Well, we can't do that these days. We have to manage the whole patient and not just the bit of the patient. And this brings in this holistic approach, this integrated approach. And I think Deepak summarized that very nicely. It may require a number of medical approaches or medication-based approaches, but we have to practically look at the comorbidities like blood pressure reduction and also the lifestyle changes that Deepak's already summarized. So a holistic and integrated approach to our care of these patients. And in fact, some of the more recent studies showed nicely how this results in better outcomes in our patients at high cardiovascular risk. Dr Carolyn Lam: And in fact, those were exactly the last words of your editorial. A holistic and integrated care approach. Beautifully done, thank you both so much for this excellent discussion. Thank you, audience, for joining us today. You've been listening to Circulation on the Run. Don't forget to tune in again. Next week. Dr Greg Hundley: This program is copyright the American Heart Association 2020.  

The NIH agency's CIO discusses the importance of technology and big data to manage research. He brings to the agency a creative background in the animation industry and is now working on various health initiatives, including those researching sickle cell anemia.  

In this rapid-fire and powerful podcast, we talk about what constitutes as heart disease and the discussion around the risk factors that contribute towards heart disease. We touch basis on concerns with fats and even delve into processed foods, pharmaceutical industry and the challenges of our modern health care system. This one is LOADED! BIO: Dr. Ethan Weiss is a Principle Investigator in the Cardiovascular Research Institute (CVRI). Dr. Weiss received his M.D. from Johns Hopkins University School of Medicine where he also completed his internship and residency. He came to UCSF in 1998 to complete his cardiology fellowship and research training. Dr. Weiss' clinical interests include prevention, lipids, and the emerging intersection of endocrinology and cardiology with a specific focus on pre-diabetes and type 2 diabetes as risk factors for coronary disease. In addition, he has interests in the genetics of coronary disease, cardiovascular risk assessment, nutrition and lifestyle, and heart disease in the young. He works with his patients to use rational and evidence-based approaches - including lifestyle modifications and where necessary, drug therapy - to improve cardiovascular risk. His research interests are focused on understanding the mechanisms of metabolic disorders such as obesity, fatty liver disease, and diabetes including the role of growth hormone signaling and lipid metabolism. He also has an active program in clinical nutrition. He has severed as Principle Investigator on grants funded by the National Heart Lung and Blood Institute (NHLBI) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). He serves on the scientific advisory boards of multiple companies focused on using technology to favorably impact human health. Lastly, he is a recent co-founder of, Keyto Inc. (www.getkeyto.com), a new San Francisco based company aiming to facilitate the use of the ketogenic diet for weight loss. TIME STAMPS: 0:15 – Ketogeek Energy Pods, Affiliate Program Update & Miscellaneous 12:55 – Dr. Weiss’s journey into Cardiology and being a jack of all trades 17:59 – What exactly is “heart disease”? 21:10 – Risk factors and modeling of heart disease 23:12 – How can you map out heart disease from observational and controlled trials? 25:25 – A discussion about LDL cholesterol 31:35 – The role of triglycerides in the risk of heart disease 34:46 -  If you could take one diet with you, what would it be? 38:28 – What about concerns with seed oils? 40:50 – What about concerns with saturated fats? 43:57 – How to deal with sensationalist media scares about food? 49:03 – How would we deal with modern foods consumer demands such as vegan meats? 51:30 – Are we getting healthier? 54:03 – What about statins and the allegations against the drug industry? 59:33 – How do you find a health specialist nowadays? 1:02:17 – What does “Keyto” do? 1:0 3:55 – New studies you’re doing right now? 1:06:55 – Final Plugs GUEST LINKS: Twitter: https://twitter.com/ethanjweiss UCSF Link: https://profiles.ucsf.edu/ethan.weiss Get Keyto Website: https://shop.getkeyto.com/ Get Keyto Twitter: https://twitter.com/GetKeyto Keyto Instagram: https://www.instagram.com/keyto.health/ KETOGEEK LINKS: Shop Energy Pods Amazon: https://www.amazon.com/Ketogeek-Chocolate-Energy-Organic-Vanilla/dp/B07B88S36J Ketogeek Ghee on Amazon: https://www.amazon.com/dp/B07B29HM3D Ketogeek Merchandise, Ghee & Energy Pods: https://ketogeek.com/collections Ketogeek Newsletter: https://ketogeek.com/pages/sign-up Shop Energy Pods: https://ketogeek.com/collections/energy-pods Wholesale: https://ketogeek.com/pages/wholesale  

It is difficult enough for a brand to build trust among consumers these days. Having a consistent appearance and tone throughout a brand’s integrated marketing communications is critical to that mission, but it can be difficult to maintain. With large marketing departments and multiple sources producing content, it’s essential to have standards and oversight to ensure a brand speaks with one voice. In this podcast, we will learn how a governing set of brand guidelines can help to protect the brand, preserve uniformity, and ultimately build trust. ----more---- About Nathan's guest: David Hazelton has over 30 years of professional experience in design, branding, and marketing. As design director for ProShares, David is responsible for brand consistency across all channels of the company’s marketing, advertising, and corporate communications. Prior to joining ProShares, David spent over a decade in boutique agencies. During that time, he used his branding and marketing talents to enhance the brand image of clients like OSHA, the National Institute of Mental Health, the National Heart Lung and Blood Institute, and the U.S. Department of Agriculture.

It is difficult enough for a brand to build trust among consumers these days. Having a consistent appearance and tone throughout a brand’s integrated marketing communications is critical to that mission, but it can be difficult to maintain. With large marketing departments and multiple sources producing content, it’s essential to have standards and oversight to ensure a brand speaks with one voice. In this podcast, we will learn how a governing set of brand guidelines can help to protect the brand, preserve uniformity, and ultimately build trust. About Nathan's guest: David Hazelton has over 30 years of professional experience in design, branding, and marketing. As design director for ProShares, David is responsible for brand consistency across all channels of the company’s marketing, advertising, and corporate communications. Prior to joining ProShares, David spent over a decade in boutique agencies. During that time, he used his branding and marketing talents to enhance the brand image of clients like OSHA, the National Institute of Mental Health, the National Heart Lung and Blood Institute, and the U.S. Department of Agriculture.

This episode is the first in a series produced in collaboration with the Society for Vascular Surgery Young Surgeons Advisory Committee (SVS YSC). This episode will focus on establishing a research lab and setting the groundwork for a productive academic career. Our guests for this episode are two members of the Young Surgeons Advisory Committee, Dr. Mohamed Zayed and Dr. Nicholas Osborne. Dr. Mohamed Zayed (zayedm@wustl.edu) has been an assistant professor of surgery at Washington University in St. Louis since 2014.  He received his medical degree and Ph.D. in pharmacology from UNC and vascular surgery residency training from Stanford.  He has received many research awards for his translational research, including the Vascular Cures Wylie Scholar, American Surgical Association Foundation Fellow and in 2016 was awarded a K08 career development grant from the NIH, National Heart Lung and Blood Institute. Dr. Nicholas Osborne (nichosbo@umich.edu, @nichosbo) has been an assistant professor of vascular surgery at the University of Michigan in Ann Arbor, Michigan since 2014.  He received his medical degree from Dartmouth and general surgery residency and vascular surgery fellowship at the University of Michigan.  He has received multiple awards for his health services research from the American Heart Association, industry and has submitted a grant through the NIH Department for Health and Human Services. Resources discussed on the show: AAS: https://www.aasurg.org/awards/ AAS Fall Courses: Grant writing course: https://www.aasurg.org/aas-fall-courses/ ASC AAS Investigator's Course: https://academicsurgicalcongress.org/sic/ Wylie Scholars Grant: https://vascularcures.org/wylie-scholar-program-2/ VESS:  https://vesurgery.org/grants-awards/ AVF: https://www.veinforum.org/avf-foundation/bsn-jobst-research-grant/ AHA: https://professional.heart.org/professional/ResearchPrograms/ApplicationInformation/ScientistPrincipalinvestigators/UCM_316962_For-Scientists.jsp SVS: https://vascular.org/career-tools-training/awards-and-scholarships Association of VA Surgeons: https://www.vasurgeons.org/research-awards.html HHMI downloadable book: Making the Right Moves: A Practical Guide to Scientific Management for Postdocs and New Faculty Melina Kibbe's book: Success in Academic Surgery: Basic Science Three main categories of research funding: Institutional microgrants Internal funding mechanisms through research centers or foundations at your institution: university, VA, etc. SVS Other professional societies' awards: AHA, ADA, VESS, etc. Foundation award K award series: career development grants for early-stage investigators R01: highest level, most coveted NIH funding

Welcome, and Thank you for listening.  This week's nutrition discussion centers around choosing.  Is dairy worse than sugar?  Is it ok if it might be plant based? Do you really want to leave your comfort zone and join those of us who are focused on health?  We will discuss that topic and the topic of fueling for exercise.  What does the human body burn for exercise and what do we need to do to replace what is lost.  It is amazing that after all these years of being on the planet we are wired to worry about not getting enough.  The worry only seems to dim when we are stuffed to capacity with high calorie foods.  Picture the lion laying in the savannah after a feast, or the bear going to hibernate.  I get it for them.  They have to work to find food and it can be scarce for days.  Look around where you are right now.  I bet you can spot a source of food.  It might be in your hand.  We exercise to get our muscles stronger and to keep our bodies lean.  Yet the advertisers know just how to get you worried by warning to consume these fats and these branch chained amino acids.  They come along with very confident articles on just how your body burns fuel.   Spoiler alert: The National Heart Lung and Blood Institute says "much remains to be learned about free fatty acid metabolism during exercise"  We will talk about that and much more.   Don't forget to get your tickets to the 4th Annual Charlotte County Plant Based Nutrition Conference on March 30, 2019.  Go to doctordulaney.com to learn more and purchase your tickets.  You can also schedule a consultation with me or Addie Dulaney Majnaric RDN the day before the conference.  Email me at jami@doctordulaney.com with any questions.   Thank you for listening. 

Host: Harold Bays, MD, FNLA Dr. Harold Bays welcomes Dr, Alan Remaley, clinical pathologist and Section Chief of the Lipoprotein Metabolism Section in the Cardiopulmonary Branch of the National Heart Lung, and Blood Institute in Bethesda, MD. Their discussion centers on LDL cholesterol from a variety of little-known aspects: its history as a biomarker for disease status, the ways in which it gets specifically measured, and the rise of lipid-altering pharmacotherapies to combat excessive LDL levels.

Although virologists long assumed that lone viruses independently infect target cells, in the case of poliovirus and other enteroviruses, several viral particles can cluster within lipid vesicles—from which they collectively enter target cells, improving overall infectivity and yields, the NIH researchers report. Nihal Altan-Bonnet at the National Heart Lung and Blood Institute at the National Institutes of Health (NIH) in Bethesda, Md., and her collaborators focused on poliovirus, a particular type of enterovirus. This group also includes rhinovirus, Coxsackie viruses, and enterovirus 68, which is linked to a recent outbreak leading to paralysis among some infected children. In HeLa cells after replication and assembly, poliovirus congregates in clusters that are surrounded by double-membrane phosphatidylserine vesicles, ranging from 250 to 350 nm in diameter. Both rhinovirus and Coxsackie virus also form similar vesicles after infecting cells. The vesicles fuse with the plasma membrane of the host cell, and the viruses are released into the extracellular environment within this package, rather than as separate particles. Details appeared 12 February 2015 in Cell (doi:10.1016/j.cell.2015.01.032), and the research was featured in the May 2015 issue of Microbe.

In this audio interview, Dr. Nina Radford, Director of Clinical Research and a cardiologist at Cooper Clinic, discusses cholesterol in children. Earlier this year, the National Heart Lung and Blood Institute (NHLBI) and the major pediatric associations put some new guidelines out in terms of screening cholesterol in children. The panel discusses two cholesterol screening recommendations for children. 1) The Universal Screen - consider screening cholesterol in all children, regardless of risk, sometime between 9- and 11 years of age, the age range when atherosclerosis actually starts to begin. The panel believes this is a good time to identify kids who may be from families of high risk; and it's a good time to influence children to adopt healthier habits. 2) Targeted Screen - any time, from ages 2- to 21, cholesterol might be screened if the child has any other risks for heart disease - obesity; diabetes; or high blood pressure. The child should also be screened if either parent had a stroke early in life. Dr. Radford also talks about the treatment recommendations the NHLBI makes for children who have elevated cholesterol.

Three physiologists tell us why the prescription "drink when you are thirsty" is usually the best guideline for deciding when and how much to drink. We will talk to Heinz Valtin of Dartmouth Medical School (retired); Mark Knepper, the chief of the Laboratory of Kidney & Electrolyte Metabolism of the National Heart Lung and Blood Institute; and Samuel Cheuvront, of the Thermal and Mountain Medicine Division of the U.S. Army Research Institute of Environmental Medicine about water consumption. They will answer the question: "Must I drink 64 ounces of water each day?" (Begins at 3:47) To read the review of the eight-by-eight rule by Heinz Valtin, click here: In the Buzz in Physiology, we look at studies involving a prosthetic device known as the Cheetah Flex Foot and whether it gives a runner who is a bilateral amputee an unfair advantage over limb-intact runners. We also summarize a study in mice in which adult bone marrow stem cells were used as a non-invasive therapy to repair cardiac tissue. And finally, we'll look at a study that finds that electro-acupuncture successfully reduced sympathetic nerve activity, normalized menstrual cycles and reduced testosterone in women with polycystic ovarian syndrome. (Begins at 1:05)