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Dr. John Sweetenham and Dr. Marc Braunstein highlight top research on hematologic malignancies from the 2025 ASCO Annual Meeting, including abstracts on newly diagnosed chronic phase CML, relapsed B-cell lymphoma, and multiple myeloma. Transcript Dr. John Sweetenham: Hello, and welcome to the ASCO Daily News Podcast. I'm your host, Dr. John Sweetenham. On today's episode, we'll be discussing promising advances in newly diagnosed chronic phase CML, relapsed B-cell lymphoma, multiple myeloma, and other hematologic malignancies that were presented at the 2025 ASCO Annual Meeting. Joining me for this discussion is Dr. Marc Braunstein, a hematologist and oncologist at the NYU Perlmutter Cancer Center. Our full disclosures are available in the transcript of this episode.  Marc, there were some great studies in the heme space at this year's Annual Meeting, and it's great to have you back on the podcast to highlight some of these advances. Dr. Marc Braunstein: Yes, I agree, John, and thank you so much for inviting me again. It's great to be here.  Dr. John Sweetenham: Let's start out with Abstract 6501. This was a study that reported on the primary endpoint results of the phase 3B ASC4START trial, which assessed asciminib versus nilotinib in newly diagnosed chronic phase CML. And the primary endpoint of this, as you know, was time to treatment discontinuation because of adverse events. Can you give us your insights into this study? Dr. Marc Braunstein: Absolutely. So, like you mentioned, you know, asciminib is an allosteric inhibitor of the BCR-ABL kinase that has activity in CML, and that includes patients with the T315I mutation that confers resistance to first- and second-generation TKIs. So, the ASC4FIRST study, which was published last year in the New England Journal of Medicine, showed superior efficacy of asciminib compared to investigator-selected first- or second-generation TKIs, actually leading to the FDA approval of asciminib in first-line CML. So, the authors of that study presented data at this year's ASCO meeting from the phase 3 ASC4START comparing safety and time to discontinuation due to adverse events of asciminib versus nilotinib, a second-generation TKI. So, 568 patients with newly diagnosed CML were randomized one-to-one to once-daily asciminib or twice-daily nilotinib. So, at a median follow-up of 9.7 months, about 11% in the asciminib group and 17% in the nilotinib group discontinued treatment, with significantly fewer discontinuations with asciminib due to adverse events. There was also a secondary endpoint of major molecular response, which was also better with asciminib. For example, the MR 4.5, which is a deep response, was 2.5% versus 0.4% favoring asciminib by week 12. So, I think in conclusion, these results build on the ASC4FIRST study, making the case for the superior safety and efficacy of asciminib versus other first- or second-generation TKIs in newly diagnosed CML. Dr. John Sweetenham: Thanks, Marc. Do you think this is going to change practice? Dr. Marc Braunstein: I think so. I think there are still some questions to be answered, such as what resistance mutations occur after first-line treatment with asciminib. But I think the sum of these studies really make the case for using asciminib upfront in CML. Dr. John Sweetenham: Okay, great. Thank you. And let's move on to our second abstract. This was Abstract 7015 and was reported from Mass General Hospital. And this was a study in patients with relapsed and refractory diffuse large B-cell lymphoma and reported the 2-year results of the so-called STARGLO study. This is a comparison of glofitamab, a T-cell engaging bispecific antibody, with gemcitabine and oxaliplatin in this group of patients. Can you tell us a little bit about your impressions of this study? Dr. Marc Braunstein: Absolutely. So just for background, the treatment landscape for relapsed/refractory large B-cell lymphoma is expanding, now with two bispecific antibodies targeting CD20 that are approved after two or more lines of therapy. Among these, glofitamab was approved in 2023 based on phase 2 data showing an objective response rate of 52%, with 39% complete responses in relapsed/refractory large B-cell lymphoma patients after a median of three prior lines of therapy. Distinguishing glofitamab from epcoritamab, the other approved bispecific, glofitamab was given for 12 cycles and then stopped. Additionally, when combined with gemcitabine and oxaliplatin in the phase 3 STARGLO study, there was significantly improved overall survival compared to rituximab plus gemcitabine and oxaliplatin in transplant-ineligible relapsed/refractory large B-cell lymphoma patients at a median follow-up of 11 months.  The authors of that study published last year in Lancet now present at ASCO this year the 2-year follow-up of the STARGLO study. Two hundred and seventy-four patients with a median of one prior line of therapy were randomized two-to-one to glofitamab plus GemOx versus rituximab plus GemOx, with the primary endpoint of overall survival. Here, the median overall survival was not reached versus 13.5 months, with a median PFS also significantly improved at about 14 months versus 4 months in the control. CRS of note in the glofitamab arm was mostly grade 1 or 2, with only about 2.3% grade 3 events. And three of the four patients had grade 1 or 2 neurotoxicity. So, John, putting this into context, I think it's encouraging that we now have randomized data showing the superiority of a bispecific plus chemotherapy over rituximab plus chemotherapy in transplant-ineligible patients. And while only 8% of the patients in the STARGLO study had prior anti-CD19 CAR T-cell therapy, I think this regimen could be considered in those patients who are ineligible for transplant or CAR T-cell therapy. Dr. John Sweetenham: Yeah, I agree. I think a couple of other compelling numbers to me were the fact that around 55% of these patients were alive at 2 years in the group who'd received glofitamab, and that almost 90% of those having that arm of the study who had a CR at the end of treatment were alive at 12 months. So, clearly, it's an active agent and also a kind of great off-the-shelf fixed-duration alternative in these relapsed and refractory patients. Dr. Marc Braunstein: I agree, and I would also note that the phase 3 SKYGLO study is looking at glofitamab plus Pola-R-CHP versus Pola-R-CHP alone. So, we may even be using these eventually in the first-line setting. Dr. John Sweetenham: Absolutely. Let's stay on the theme of diffuse large B-cell lymphoma and look at one other abstract in that space, which was Abstract 7000. This was a study from the HOVON group in the Netherlands, which looked at the prospective validation of end-of-treatment circulating tumor DNA in the context of a national randomized trial. What are your thoughts on this? Dr. Marc Braunstein: So, non-invasive liquid biopsies to detect and monitor cancers via circulating tumor-derived DNA or ctDNA, you know, is really emerging as a valuable tool in both solid and liquid tumors to understand disease biology, and also for drug development. So, to date, the most established application of ctDNA in lymphoma, I would say, is really for monitoring of minimal residual disease. So, in this correlative study by Steven Wang and colleagues in the HOVON group, they evaluated the prognostic significance of MRD status as assessed by ctDNA following first-line treatment with curative intent with either R-CHOP or dose-adjusted R-EPOCH. At the end of treatment, encouragingly, 76% of patients were MRD-negative, and 24% were MRD-positive. Now, of note, MRD-positive status at the end of treatment predicted inferior progression-free survival at 2 years, with only 28% of patients who are MRD-positive being progression-free versus 88% who are MRD-negative. And in fact, all the patients who failed to achieve a complete response after first-line treatment and were MRD-positive ultimately relapsed. So, circulating tumor cells are rarely found in large B-cell lymphomas, and so this study really builds on accumulating data that ctDNA has clinical value to detect residual disease with a non-invasive approach. So, there are many implications of how we could potentially use this to detect early signs of relapse, to potentially escalate treatment for consolidation if patients remain MRD-positive. So, I think this will eventually become utilized in clinical practice. Dr. John Sweetenham: Yeah, I agree. I think it's interesting that it provided an independent assessment of response, which was independent, in fact, of the results of PET-CT scanning and so on, which I think was very interesting to me. And the authors of the abstract actually commented in their presentation that they think this should be integrated as part of the standard response assessment now for patients with large B-cell lymphoma. Would you agree with that? Dr. Marc Braunstein: I would. For one thing, it allows repeated sampling. It's a non-invasive approach; it doesn't necessarily require a bone marrow biopsy, and it may have more sensitivity than conventional response measures. So, I think having a standardized system to assess ctDNA will be helpful, and definitely, I think this will be a valuable biomarker of disease response. Dr. John Sweetenham: Okay, great. Thanks. We're going to change gear again now, and we're going to highlight two abstracts in the multiple myeloma space. The first one of these is Abstract 7507. And this abstract reported on the long-term results of the CARTITUDE study for patients with relapsed and refractory multiple myeloma. What are your comments on this presentation? Dr. Marc Braunstein: So, this study actually got a lot of press, and I've already had multiple patients asking me about CAR T-cells as a result. Just as some background, CAR T-cells targeting BCMA, which is pretty much universally expressed on malignant plasma cells in myeloma, have really shown remarkable responses, especially in heavily pretreated patients, showing superior progression-free survival in both later and earlier phases of the disease, including in randomized studies in patients with second-line or beyond. So, the CARTITUDE-1 was really the original Phase 1/2 study of ciltacabtagene autoleucel, one of the two approved anti-BCMA CAR T-cell products, which was investigated in patients with a median of six to seven prior lines of therapy. So, these were patients who were pretty heavily pretreated. So, in the study presented by Voorhees at this year's ASCO meeting, this was the long-term follow-up at a median of 5 years from the one-time CAR infusion in these patients with a median of five prior lines of therapy. And remarkably, of the 97 patients, 33% remained progression-free at 5 years plus, without needing any further myeloma treatment during that time. And among those 33% of patients, 23% had high-risk cytogenetics, which we know are notoriously difficult to achieve responses in. What was interesting that they presented as correlative studies was there were some biomarkers that were distinguishing the patients who had the long PFS, including enrichment of more naive T-cells in the product, lower neutrophil-to-T-cell ratio, higher hemoglobin and platelets at baseline, and higher CAR T-cell levels relative to soluble BCMA levels. And the fact that they reported a median overall survival of 61 months in these really heavily pretreated patients, I think these data are impressive. I think we're going to continue to be using CAR T even earlier in the disease status than fifth or sixth line, as it was studied in CARTITUDE-1. There are even ongoing studies looking at first-line treatment with CAR T-cells. Dr. John Sweetenham: So, do you think that those 33% of patients who are disease-free at 5 years, do you think any of those are cured?  Dr. Marc Braunstein: That was one of the headlines in the press. I think if we're going to discuss things like "operational cures," where we're transforming myeloma into really a chronic disease, where patients can live practically a normal life expectancy, I think the measure of 5 years, especially in this population that was explored in CARTITUDE-1, I think we can call that close to a cure. Dr. John Sweetenham: Okay. Well, thank you. Exciting data, for sure. We're going to conclude today with another abstract in the multiple myeloma space. And this was Abstract 7500, which looked at an MRD, minimal residual disease-driven strategy following induction and transplant-eligible newly diagnosed multiple myeloma patients and reported on the primary endpoints of the phase 3 MIDAS trial. Can you walk us through this one, Marc? Dr. Marc Braunstein: Absolutely. It is a bit more complicated than the prior one we discussed because this is a randomized study with four arms. So, I'll start by saying that anti-CD38-based quadruplet regimens continue to show superior outcomes in both transplant-eligible and -ineligible newly diagnosed multiple myeloma patients. The MIDAS study mentioned is an open-label phase 3 trial with four arms in transplant-eligible newly diagnosed myeloma patients.  And initially, these patients were all treated with quadruplet therapy with the anti-CD38 antibody isatuximab combined with carfilzomib, lenalidomide, and dexamethasone in 718 newly diagnosed myeloma patients. So, they received the quadruplet regimen for six cycles and then were randomized based on their MRD status at 10 to the negative fifth following six cycles of induction. And that first randomization, if they were MRD-negative, was to either consolidation with six more cycles of the quadruplet regimen or transplant, autologous transplant, plus two cycles additionally of the quadruplet regimen. And both arms were followed by lenalidomide maintenance. The primary endpoint was MRD negativity at 10 to the negative sixth prior to entering the lenalidomide maintenance component. And in addition, the patients who were MRD-positive after induction were randomized to transplant plus two cycles of consolidation or a tandem autologous transplant. So, the median follow-up of the study was about 16 months, and the pre-maintenance rate of MRD negativity was high, between 84 to 86% between the two arms who were MRD-negative, which was not significantly different. And as far as the 233 patients who were MRD-positive, the pre-maintenance MRD negativity was also not significantly different at 40% for those who received autologous transplant, and 32% who received a tandem transplant. So, there's a lot of debate in the myeloma field about the evolving role of autologous transplant and whether transplant still plays a significant role in patients who are either MRD-negative after induction or who have deep remissions and are of standard risk. So, I think these data suggest that patients who are MRD-negative after induction with a quadruplet regimen studied here, which was Isa-KRd, plus consolidation, may possibly be able to forego consolidation with autologous transplant. And likewise, for those patients who are MRD-positive after induction, tandem transplant didn't seem to provide much of a benefit compared to single transplant, which is consistent with prior studies such as the StaMINA study. Dr. John Sweetenham: So, where do you think this leaves us, Marc? Are we going to need more studies before we have any definitive guidance on whether an autologous transplant is still appropriate for those patients who are MRD-negative? Dr. Marc Braunstein: Well, as clinicians, we want to do what's best for our patient. And in myeloma, the best we can do is to get as deep remissions as possible, meaning MRD negativity. And so, I think it's clear from the MIDAS study and others that quadruplet regimens provide the deepest remissions when given upfront. We can debate the role of autologous transplant. I think certainly the role of tandem autologous transplant is fading. But as far as a single autologous transplant as consolidation, I think it's reasonable as a goal to try to achieve MRD negativity after the transplant, especially for patients who remain MRD-positive after induction. Dr. John Sweetenham: Okay, great. Marc, thanks as always for sharing your insights on the heme malignancies studies from the ASCO meeting this year and for joining us on the ASCO Daily News Podcast. Always appreciate hearing your thoughtful and balanced input on these. Dr. Marc Braunstein: My pleasure. Thank you, John. Dr. John Sweetenham: And thank you to our listeners for joining us today. You'll find links to the abstracts discussed today in the transcript of this episode. Finally, if you value the insights that you hear on the ASCO Daily News Podcast, please take a moment to rate, review, and subscribe wherever you get your podcasts.   Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions.  Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.   Find out more about today's guest:  Dr. John Sweetenham Dr. Marc Braunstein   @docbraunstein     Follow ASCO on social media:   @ASCO on Twitter  ASCO on Bluesky  ASCO on Facebook   ASCO on LinkedIn     Disclosures:  Dr. John Sweetenham:  Consulting or Advisory Role: EMA Wellness  Dr. Marc Braunstein:  Consulting or Advisory Role: Pfizer, Bristol-Myers Squibb/Celgene, Adaptive Biotechnologies, GlaxoSmithKline, ADC Therapeutics, Janssen Oncology, Abbvie, Guidepoint Global, Epizyme, Sanofi, CTI BioPharma Corp  Speakers' Bureau: Janssen Oncology  Research Funding (Institution): Janssen, Celgene/BMS

Jerome was diagnosed with muscle invasive bladder cancer on January 29, 1997. The diagnosis was based on a transurethral resection surgery. Having done his research, he contacted a doctor at Harvard and Mass General Hospital about a clinical trial for a bladder sparing protocol. To Jermoe's surprise, Dr.Shipley called back and shared the protocol with Jerome's medical team and the treatment began a couple of weeks later. The treatment involved chemotherapy in conjunction with radiation therapy.  Jerome experienced several recurrences over the years, each time treating them with surgery and infusions. In 2018 a recurrence involved hospitalization and tubes were placed in each kidney. This time Jerome was faced with a decision to have a radical cystectomy or given the choice to do immunotherapy. By 2019 there was little evidence of bladder cancer and infusions continued, with no side effects. He still has a tube in one kidney and is otherwise thriving! email: Jerome@mountainsangha.org phone: 415-299-0428 website: www.mountainsangha.org Book: Healing with the 7 Principles of Mindfulness, by Jerome FreedmanHere is what Dr. Kelly Turner, PhD has to say about Healing with the 7 Principles of Mindfulness: “Dr. Freedman speaks from experience, both as a cancer survivor himself, and the father of a Radical Remission cancer survivor. His book, “Healing with the 7 Principles of Mindfulness” gives readers a nurturing, helping hand throughout the entire cancer journey, especially with regard to developing a meditation practice. –Kelly Turner, PhD, Author of the NYTimes Bestseller “Radical Remission: Surviving Cancer Against All Odds” Stop Cancer in Its Tracks: How to Embrace Mindfulness In Healing by Jerome Freedman ___________________________ To learn more about the 10 Radical Remission Healing Factors, connect with a certified RR coach or join a virtual or in-person workshop visit www.radicalremission.com. To watch Episode 1 of the Radical Remission Docuseries for free, visit our YouTube channel here.  To purchase the full 10-episode Radical Remission Docuseries visit Hay House Online Learning. To learn more about Radical Remission health coaching with Liz or Karla, Click Here Follow us on Social Media: Facebook  Instagram YouTube __________________________ Thank you to our friends from The Healing Oasis for sponsoring this episode of the podcast.  The Healing Oasis is a first of its kind in beautiful British Columbia, Canada where we encourage the body to heal from cancer using alternative therapies & cancer fighting meals at a wellness retreat center in nature. Our top naturopathic cancer doctor will prescribe a protocol tailored specifically for you. There's no place quite like it. Start your healing journey today! Learn More about The Healing Oasis by visiting these links: Website   Testimonials Video Overview

Episode OverviewIn this episode, Kristen interviews Erin Schultz, founder of Her Personal Finance, about building a successful niche business serving women in medicine, tech, and law. Erin shares her journey from Harvard Business School graduate to personal finance educator and financial planner, discussing how she built an audience on social media and the power of niching down.Guest BioErin Schultz is the founder of Her Personal Finance (founded in 2015). She's a Harvard Business School graduate who specializes in helping physicians and research scientists balance student loan payments with retirement savings. Her online classes are offered in partnership with Mass General Hospital, and she has helped hundreds of clients navigate hospital benefits and financial planning.Timestamps[00:00] Introduction to Erin Schultz[01:15] Erin's Journey from Harvard to Personal Finance[03:54] Building a Social Media Presence[04:58] Engaging with Content and Community[08:19] The Importance of Niching Down[10:33] Personal Stories and Professional Connections[19:31] Adapting Content for Different Platforms[22:34] Resources and Final ThoughtsKey Takeaways1. Niche down ruthlessly - Erin's focus on women in specific high-earning professions allows her to become a true expert2. Personal stories drive engagement - Educational content performs worse than personal narratives3. Be approachable, not traditional - Standing out from "dusty old guys from Fidelity"4. Repurpose content strategically - Same story, different formats for different platforms5. Address real pain points - Fertility costs, childcare planning, student loansConnect with Erin- Instagram: [@herpersonalfinance](https://instagram.com/herpersonalfinance)- LinkedIn: [Erin Schultz](https://linkedin.com/in/erinschultz)- Website: [herpersonalfinance.com](http://herpersonalfinance.com)- Bimonthly newsletter covering topics like car payments, 401(k)s, and student loans

A shooting outside Mass General Hospital shuts down roads for a time in Boston, the White House takes another shot at Harvard, and public defenders gather at the State House. Stay in "The Loop" with #iHeartRadio.

As artificial intelligence (AI) tools become increasingly mainstream, they can potentially transform neurology clinical practice by improving patient care and reducing clinician workload. Critically evaluating these AI tools for clinical practice is important for successful implementation. In this episode, Katie Grouse, MD, FAAN speaks with Peter Hadar, MD, MS, coauthor of the article “Clinical Applications of Artificial Intelligence in Neurology Practice” in the Continuum® April 2025 Neuro-ophthalmology issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California San Francisco in San Francisco, California. Dr. Hadar is an instructor of neurology at Harvard Medical School and an attending physician at the Massachusetts General Hospital in Boston, Massachusetts. Additional Resources Read the article: Clinical Applications of Artificial Intelligence in Neurology Practice Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Guest: @PeterNHadar Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast. Dr Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Peter Hadar about his article on clinical applications of artificial intelligence in neurology practice, which he wrote with Dr Lydia Moura. This article appears in the April 2025 Continuum issue on neuro-ophthalmology. Welcome to the podcast, and please introduce yourself to our audience. Dr Hadar: Hi, thanks for having me on, Katie. My name is Dr Peter Hadar. I'm currently an instructor over at Mass General Hospital, Harvard Medical School, and I'm excited to talk more about AI and how it's going to change our world, hopefully for the better. Dr Grouse: We're so excited to have you. The application of AI in clinical practice is such an exciting and rapidly developing topic, and I'm so pleased to have you here to talk about your article, which I found to be absolutely fascinating. To start, I'd like to hear what you hope will be the key takeaway from your article with our listeners. Dr Hadar: Yeah, thank you. The main point of the article is that AI in medicine is a tool. It's a wonderful tool that we should be cautiously optimistic about. But the important thing is for doctors, providers to be advocates on their behalf and on behalf of their patients for the appropriate use of this tool, because there are promises and pitfalls just with any tool. And I think in the article we detail a couple ways that it can be used in diagnostics, in clinical documentation, in the workflow, all ways that can really help providers. But sometimes the devil is in the details. So, we get into that as well. Dr Grouse: How did you become interested in AI and its application, specifically in the practice of neurology? Dr Hadar: When I was a kid, as most neurologists are, I was- I nerded out on a lot of sci-fi books, and I was really into Isaac Asimov and some of his robotics, which kind of talks about the philosophy of AI and how AI will be integrated in the future. As I got into neurology, I started doing research neurology and a lot of folks, if you're familiar with AI and machine learning, statistics can overlap a lot with machine learning. So slowly but surely, I started using statistical methods, machine learning methods, in some of my neurology research and kind of what brought me to where I am today. Dr Grouse: And thinking about and talking about AI, could you briefly summarize a few important terms that we might be talking about, such as artificial intelligence, generative AI, machine learning, etcetera? Dr Hadar: It's a little difficult, because some of these terms are nebulous and some of these terms are used in the lay public differently than other folks would use it. But in general, artificial intelligence is kind of the ability of machines or computers to communicate independently. It's similar to as humans would do so. And there are kind of different levels of AI. There's this very hard AI where people are worried about with kind of terminator-full ability to replicate a human, effectively. And there are other forms of narrow AI, which are actually more of what we're talking about today, and where it's very kind of specific, task-based applications of machine learning in which even if it's very complex, the AI tools, the machine learning tools are able to give you a result. And just some other terms, I guess out there. You hear a lot about generative AI. There's a lot of these companies and different algorithms that incorporate generative AI, and that usually kind of creates something, kind of from scratch, based on a lot of data. So, it can create pictures, it can create new text if you just ask it. Other terms that can be used are natural language processing, which is a big part of some of the hospital records. When AI tools read hospital records and can summarize something, if it can translate things. So, it turns human speech into these results that you look for. And I guess other terms like large language models are something that also have come into prominence and they rely a lot on natural language processing, being able to understand human speech, interpret it and come up with the results that you want. Dr Grouse: Thank you, that's really helpful. Building on that, what are some of the current clinical applications of AI that we may already be using in our neurologic practice and may not even be aware that that's what that is? Dr Hadar: It depends on which medical record system you use, but a very common one are some of the clinical alerts that people might get, although some of them are pretty basic and they can say, you know, if the sodium is this level, you get an alert. But sometimes they do incorporate fancier machine learning tools to say, here's a red flag. You really should think about contacting the patient about this. And we can talk about it as well. It might encourage burnout with all the different flags. So, it's not a perfect tool. But these sorts of things, typically in the setting of alerts, are the most common use. Sorry, and another one is in folks who do stroke, there are a lot of stroke algorithms with imaging that can help detect where the strokes occur. And that's a heavy machine learning field of image processing, image analysis for rapid detection of stroke. Dr Grouse: That's really interesting. I think my understanding is that AI has been used specifically for radiology interpretation applications for some time now. Is that right? Dr Hadar: In some ways. Actually, my background is in neuroimaging analysis, and we've been doing a lot of it. I've been doing it for years. There's still a lot of room to go, but it's really getting there in some ways. My suspicion is that in the coming years, it's going to be similar to how anesthesiologists at one point were actively bagging people in the fifties, and then you develop machines that can kind of do it for you. At some point there's going to be a prelim radiology read that is not just done by the resident or fellow, but is done by the machine. And then another radiologist would double check it and make sure. And I think that's going to happen in our lifetime. Dr Grouse: Wow, that's absolutely fascinating. What are some potential applications of AI in neurologic practice that may be most high-yield to improve patient care, patient access, and even reduce physician burnout? Dr Hadar: These are separate sort of questions, but they're all sort of interlinked. I think one of the big aspects of patient care in the last few years, especially with the electronic medical record, is patients have become much more their own advocates and we focus a lot more on patient autonomy. So, they are reaching out to providers outside of appointments. This can kind of lead to physician burnout. You have to answer all these messages through the electronic medical record. And so having, effectively, digital twins of yourself, AI version of yourself, that can answer the questions for the patient on your off times is one of the things that can definitely help with patient care. In terms of access, I think another aspect is having integrated workflows. So, being able to schedule patients efficiently, effectively, where more difficult patients automatically get one-hour appointments, patients who have fewer medical difficulties might get shorter appointments. That's another big improvement. Then finally, in terms of physician burnout, having ambient intelligence where notes can be written on your behalf and you just need to double-check them after allows you to really have a much better relationship with the patients. You can actually talk with them one on one and just focus on kind of the holistic care of the patient. And I think that's- being less of a cog in the machine and focusing on your role as a healer would be actually very helpful with the implementation of some of these AI tools. Dr Grouse: You mentioned ambient technology and specifically ambient documentation. And certainly, this is an area that I feel a lot of excitement about from many physicians, a lot of anticipation to be able to have access to this technology. And you mentioned already some of the potential benefits. What are some of the potential… the big wins, but then also potential drawbacks of ambient documentation? Dr Hadar: Just to kind of summarize, the ambient intelligence idea is using kind of an environmental AI system that, without being very obtrusive, just is able to record, able to detect language and process it, usually into notes. So, effectively like an AI scribe that is not actually in the appointment. So, the clear one is that---and I've seen this as well in my practice---it's very difficult to really engage with the patient and truly listen to what they're saying and form that relationship when you're behind a computer and behind a desk. And having that one-on-one interaction where you just focus on the patient, learn everything, and basically someone else takes notes for you is a very helpful component of it. Some of the drawbacks, though, some of it has to do with the existing technology. It's still not at the stage where it can do everything. It can have errors in writing down the medication, writing down the exact doses. It can't really, at this point, detect some of the apprehensions and some of the nonverbal cues that patients and providers may kind of state. Then there's also the big one where a lot of these are still done by startups and other companies where privacy may be an issue, and a lot of patients may feel very uncomfortable with having ambient intelligence tools introduced into their clinical visit, having a machine basically come between the doctor and the patient. But I think that over time these apprehensions will lessen. A lot of the security will improve and be strengthened, and I think that it's going to be incorporated a lot more into clinical practice. Dr Grouse: Yeah, well, we'll all be really excited to see how that technology develops. It certainly seems like it has a lot of promise. You mentioned in your article a lot about how AI can be used to improve screening for patients for certain types of conditions, and that certainly seems like an obvious win. But as I was reading the article, I couldn't help but worry that, at least in the short term, these tools could translate into more work for busy neurologists and more demand for access, which is, you know, already, you know, big problems in our field. How can tools like these, such as, like, for instance, the AI fundoscopic screening for vascular cognitive risk factors help without adding to these existing burdens? Dr Hadar: It's a very good point. And I think it's one of the central points of why we wanted to write the article is that these AI in medicine, it's, it's a tool like any other. And just like when the electronic medical record came into being, a lot of folks thought that this was going to save a lot of time. And you know, some people would say that it actually worsened things in a way. And when you use these diagnostic screening tools, there is an improvement in efficiency, there is an improvement in patient care. But it's important that doctors, patients advocate for this to be value-based and not revenue-based, necessarily. And it doesn't mean that suddenly the appointments are shorter, that now physicians have to see twice as many patients and then patients just have less of a relationship with their provider. So, it's important to just be able to integrate these tools in an appropriate way in which the provider and the patient both benefit. Dr Grouse: You mentioned earlier about the digital twin. Certainly, in your article you mentioned, you know, that idea along with the idea of the potential of development of virtual chatbot visits or in-person visits with a robot neurologist. And I read all this with equal parts, I think excitement, but horror and and fear. Can you tell us more about what these concepts are, and how far are we from seeing technology like this in our clinics, and maybe even, what are the risks we need to be thinking about with these? Dr Hadar: Yeah. So, I mean, I definitely think that we will see implementation of some of these tools in our lifetime. I'm not sure if we're going to have a full walking, talking robot doing some of the clinical visits. But I do think that, especially as we start doing a lot more virtual visits, it is very easy to imagine that there will be some sort of video AI doctor that can serve as, effectively, a digital twin of me or someone else, that can see patients and diagnose them. The idea behind the digital twin is that it's kind of like an AI version of yourself. So, while you only see one patient, an AI twin can go and see two or three other patients. They could also, if the patients send you messages, can respond to those messages in a way that you would, based on your training and that sort of thing. So, it allows for the ability to be in multiple places at once. One of the risks of this is, I guess, overreliance on the technology, where if you just say, we're just going to have a chatbot do everything for us and then not look at the results, you really run the risk of the chatbot just recommending really bad things. And there is training to be had. Maybe in fifty years the chatbot will be at the same level as a physician, but there's still a lot of room for improvement. I personally, I think that my suspicion as to where things will go are for very simple visits in the future and in our lifetime. If someone is having a cold or something like that and it goes to their primary care physician, a chatbot or something like that may be of really beneficial use. And it'll help segment out the different groups of simple diagnosis, simple treatments can be seen by these robots, these AI, these machine learning tools; and some of the more complex ones, at least for the early implementation of this will be seen by more specialized providers like neurologists and subspecialist neurologists too. Dr Grouse: That certainly seems reasonable, and it does seem that the more simple algorithmic things are always where these technologies will start, but it'll be interesting to see where things can go with more complex areas. Now I wanted to switch gears a little bit in the article- and I thought this was really important because I see it as being certainly one of the bigger drawbacks of AI, is that despite the many benefits of artificial intelligence, AI can unfortunately perpetuate systemic bias. And I'm wondering if you could tell us a little bit more about how this happened? Dr Hadar: I know I'm beating a dead horse on this, but AI is a tool like any other. And the problem with it is that what you put in is very similar to what you get out. And there's this idea in computer science of “garbage in, garbage out”. If you include a lot of data that has a lot of systemic biases already in the data, you're going to get results that perpetuate these things. So, for instance, if in dermatologic practices, if you just had a data set that included people of one skin color or one race and you attempted to train a model that would be able to detect skin cancer lesions, that model may not be easily applicable to people of other races, other ethnicities, other skin colors. And that can be very damaging for care. And it can actually really, really hurt the treatments for a lot of the patients. So that is one of the, kind of, main components of the systemic biases in AI. The way we mitigate them is by being aware of it and actually implementing, I guess, really hard stops on a lot of these tools before they get into practice. Being sure, did your data set include this breakdown of sex and gender, of race and ethnicity? So that the stuff you have in the AI tool is not just a very narrow, focused application, but can be generalized to a large population, not just of one community, one ethnic group, racial group, one country, but can really be generalized throughout the world for many patients. Dr Grouse: The first step is being aware of it, and hopefully these models will be built thoughtfully to help mitigate this as much as possible. I wanted to ask as well, another concern about AI is the safety of private data. And I'm wondering, as we're starting to do things like use ambient documentation, AI scribe, and other types of technologies like this, what can we tell our patients who are concerned about the safety of their personal data collected via these programs, particularly when they're being stored or used with outside companies that aren't even in our own electronic medical records system? Dr Hadar: Yeah, it's a very good question, and I think it's one of the major limitations of the current implementation of AI into clinical practice, because we still don't really have great standards---medical standards, at least---for storing this data, how to analyze this data. And my suspicion is that at some point in the future, we're going to need to have a HIPAA compliance that's going to be updated for the 21st century, that will incorporate the appropriate use of these tools, the appropriate use of these data storage, of data storage beyond just PHI. Because there's a lot more that goes into it. I would say that the important thing for how to implement this, and for patients to be aware of, is being very clear and very open with informed consent. If you're using a company that isn't really transparent about their data security and their data sharing practices, that needs to be clearly stated to the patient. If their data is going to be shared with other people, reanalyzed in a different way, many patients will potentially consider not participating in an AI implementation in clinic. And I think the other key thing is that this should be, at least initially, an opt-in approach as opposed to an opt-out approach. So patients really have- can really decide and have an informed opinion about whether or not they want to participate in the AI implementation in medicine. Dr Grouse: Well, thank you so much for explaining that. And it does certainly sound like there's a lot of development that's going to happen in that space as we are learning more about this and the use of it becomes more prevalent. Now, I also wanted to ask, another good point that you made in your article---and I don't think comes up enough in this area, but likely will as we're using it more---AI has a cost, and some of that cost is just the high amount of data and computational processing needed to use it, as well as the effects on the environment from all this energy usage. Given this drawback of AI, how can we think about potential costs versus the benefits, the more widespread use of this technology? Or how should we be thinking about it? Dr Hadar: It's part of a balance of the costs and benefits, effectively, is that AI---and just to kind of name some of them, when you have these larger data centers that are storing all this data, it requires a lot of energy consumption. It requires actually a lot of water to cool these things because they get really hot. So, these are some of the key environmental factors. And at this point, it's not as extreme as it could be, but you can imagine, as the world transitions towards an AI future, these data centers will become huge, massive, require a lot of energy. And as long as we still use a lot of nonrenewable resources to power our world, our civilization, I think this is going to be very difficult. It's going to allow for more carbon in the atmosphere, potentially more climate change. So, being very clear about using sustainable practices for AI usage, whether it be having data centers specifically use renewable resources, have clear water management guidelines, that sort of thing will allow for AI to grow, but in a sustainable way that doesn't damage our planet. In terms of the financial costs… so, AI is not free. However, on a given computer, if you want to run some basic AI analysis, you can definitely do it on any laptop you have and sometimes even on your phone. But for some of these larger models, kind of the ones that we're talking about in the medical field, it really requires a lot of computational power. And this stuff can be very expensive and can get very expensive very quickly, as anyone who's used any of these web service providers can attest to. So, it's very important to be clear-eyed about problems with implementation because some of these costs can be very prohibitive. You can run thousands and you can quickly rack up a lot of money for some very basic analysis if you want to do it in a very rapid way, in a very effective way. Dr Grouse: That's a great overview. You know, something that I think we're all going to be having to think about a lot more as we're incorporating these technologies. So, important conversations I hope we're all having, and in our institutions as we're making these decisions. I wanted to ask, certainly, as some of our listeners who may be still in the training process are hearing you talk about this and are really excited about AI and implementation of technology in medicine, what would you recommend to people who want to pursue a career in this area as you have done? Dr Hadar: So, I think one of the important things for trainees to understand are, there are different ways that they can incorporate AI into their lives going forward as they become more seasoned doctors. There are clinical ways, there are research ways, there are educational ways. A lot of the research ways, I'm one of the researchers, you can definitely incorporate AI. You can learn online. You can learn through books about how to use machine learning tools to do your analysis, and it can be very helpful. But I think one of the things that is lacking is a clinician who can traverse both the AI and patient care fields and be able to introduce AI in a very effective way that really provides value to the patients and improves the care of patients. So that means if a hospital system that a trainee is eventually part of wants to implement ambient technology, it's important for physicians to understand the risks, the benefits, how they may need to adapt to this. And to really advocate and say, just because we have this ambient technology doesn't mean now we see fifty different patients, and then you're stuck with the same issue of a worse patient-provider relationship. One of the reasons I got into medicine was to have that patient-provider interaction to not only be kind of a cog in the hospital machine, but to really take on a role as a healer and a physician. And one of the benefits of these AI tools is that in putting the machine in medicine, you can also put the humanity back in medicine at times. And I think that's a key component that trainees need to take to heart. Dr Grouse: I really appreciate you going into that, and sounds like there's certainly need. Hoping some of our listeners today will consider careers in pursuing AI and other types of technologies in medicine. I really appreciate you coming to talk with us today. I think this is just such a fascinating topic and an area that everybody's really excited about, and hoping that we'll be seeing more of this in our lives and hopefully improving our clinical practice. Thank you so much for talking to us about your article on AI in clinical neurology. It was a fascinating topic and I learned a lot. Dr Hadar: Thank you very much. I really appreciate the conversation, and I hope that trainees, physicians, and others will gain a lot and really help our patients through this. Dr Grouse: So again, today I've been interviewing Dr Peter Hadar about his article on clinical applications of artificial intelligence in neurology practice, which he wrote with Dr Lydia Moura. This article appears in the most recent issue of Continuum on neuro-ophthalmology. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. Thank you for listening to Continuum Audio.

You can text us here with any comments, questions, or thoughts!In this episode, Kemi welcomes Dr. Allison Wu. Dr. Wu is Principal Investigator of the Wunderfull Lab. She is a clinician-researcher board certified in pediatric gastroenterology and nutrition as well as obesity medicine. Her research focuses on epidemiology and health services research in pediatric nutrition and obesity. She completed her fellowship in Pediatric Gastroenterology, Hepatology & Nutrition at Boston Children's Hospital and the Harvard-wide Pediatric Health Services Research Fellowship at Mass General Hospital for Children. She is also an alumnus of our Get That Grant® coaching program! Together, they explore Dr. Wu's unique journey that intertwines her love for science, nutrition, and working with children, shaped by her family's background in academia and the restaurant business. Join the conversation as Dr. Wu shares her experiences with coaching, her insights on how supportive environments can foster growth, confidence, and collaboration and the importance of grant writing in creating meaningful change. Conversation Highlights: Navigating maternity leave and career transitions The role of coaching in professional growth Building community and collaboration in academia The importance of intentionality in career development  Loved this convo? Please go find Dr. Wu on LinkedIn to show her some love!  

The first two episodes in this Healthcare is Hard podcast series on “Opportunities in Oncology” explored the relationship between academic medical centers and community care, with guests Dr. Stephen Schleicher from Tennessee Oncology, and Dr. Harlan Levine from City of Hope. For the third and final episode in the series, Dr. Daphne Haas-Kogan joined Keith Figlioli for a conversation that dives more deeply into patient care, innovations in care delivery and the opportunities for entrepreneurs.Dr. Haas-Kogan is Chair of the Department of Radiation Oncology at Mass General Hospital, Brigham and Women's Hospital, and Boston Children's Hospital. She is also the Willem and Corrie Hees Family Professor of Radiation Oncology at Harvard Medical School.Dr. Haas-Kogan received her undergraduate degree in biochemistry and molecular biology from Harvard University and her medical degree at UCSF. She completed her residency in radiation oncology at UCSF in 1997 and became vice-chair for research at UCSF in 2003, and educational program director in 2008. Dr. Haas-Kogan's laboratory research focuses on molecular underpinnings of brain tumors and pediatric cancers. She leads large multi-institutional initiatives funded by NIH/NCI, philanthropic organizations, and industry collaborators.For this episode of Healthcare is Hard, some of the topics Dr. Haas-Kogan discussed with Keith include:The collaborative approach to care. Dr. Haas-Kogan talked about how most people with cancer struggle with many other medical issues – some predating cancer diagnosis, some precipitated by the treatment itself – and how several care teams are required to treat the patient wholistically. She also discussed how important it is for academic medical centers and community hospitals to work together, the responsibilities each holds to the patient, and the goal of making sure patients receive the same exact care regardless of location.The precision of radiation oncology. There are generally three pillars of cancer treatment. The first is surgery to remove tumors, the second is medication to kill cancer cells with drugs, and the third is radiation therapy to destroy cancer cells. Dr. Haas-Kogan described how radiation oncology is, in many ways, a combination of surgical oncology and medical oncology. It requires the precision of surgery – especially when treating a tumor close to critical structures like the brain stem or spinal cord – but can also be applied in a single day or over the course of weeks, similar to medication. She discussed how this allows for unique collaboration between academic researchers and community physicians, along with opportunities for creative workforce solutions.AI in oncology. The impact artificial intelligence has already had on oncology would have been unimaginable five or 10 years ago, and Dr. Haas-Kogan says the opportunities for entrepreneurs in the space are huge. As an example of the impact AI has already made, she talked about how radiation oncologists traditionally spend hours defining exactly what they want treated and the dose of radiation required. But now, AI is doing most of that, saving physicians precious time. She talked about how medicine is an art and how treatment like this is very nuanced, so she very often makes changes after reviewing AI-generated recommendations. But she says advancements are coming quickly.To hear Dr. Haas-Kogan and Keith discuss these topics and more, listen to this episode of Healthcare is Hard: A Podcast for Insiders.

Kat Koppett is the Eponymous Founder of Koppett, a consultancy specializing in the use of improv and storytelling techniques to enhance individual and group performance. She has worked with diverse clients including Meta, Apple, Prezi, PwC, NASA, Havas Health, Mass General Hospital, the United Nations and the Clinton Global Initiative.Her book Training to Imagine: Practical Improvisational Theatre Techniques to Enhance Creativity, Teamwork, Leadership, and Learning , is considered a seminal work in the field of Applied Improv and is used by professionals around the world. She has given two TEDx talks on the use of improv to enhance non-theatrical performance.In 2019, Kat was the winner of the North American Simulation and Gaming Association (NASAGA)'s Ifill-Reynold's Lifetime Achievement Award. She is the co-director and a performing member of the Mopco Improv Theatre, a founding member and the current vice-president of the Applied Improvisation Network, and the co-host of the podcast, Performance Shift: The Art of Successfully Navigating Change.Give this a listen! Hosted on Acast. See acast.com/privacy for more information.

Dr. Ben Kleinstiver, whose lab is located at the Center for Genomic Medicine at Mass General Hospital, joins us to talk about programmable nucleases, genome editing, and the applications of this technology in the future of healthcare.

(00:00) The guys discuss the Four Nation’s Faceoff Tournament and Team USA’s and Bruins’ defenseman Charlie McAvoy being hospitalized at Mass General Hospital and will miss the championship game against Team Canada back in the United States on Thursday night. (11:31) Zo and Beetle address the news from yesterday about the Cincinnati Bengals putting the franchise tag on wide receiver Tee Higgins and what this means for the Patriots going forward with potentially pursuing a deal for the all-pro route-runner. (26:01) The guys discuss Mike Breer saying teams with cap space and draft picks should call the Cowboys about acquiring Micah Parsons and if the Patriots should be all-in on Parsons. (33:48) The guys finish out the hour by circling back to the Four Nation’s Faceoff and which nations should be represented in next year's rendition of the tournament.

In this episode, we visit the Bulfinch Building at the Massachusetts General Hospital to examine one of the most, if not the most, significant discoveries in modern medicine. Sarah Alger, the Director of the Paul S. Russell, MD Museum of Medical History and Innovation, shows us the hospital's Ether Dome where the first public surgery using an anesthetic was performed. Back at the MHS, we sit down with Chief Historian Peter Drummey and Curator of Art and Artifacts Emerita Anne Bentley to learn more about the contentious history of this innovation. Learn more about episode objects here: https://www.masshist.org/podcast/season-4-episode-3-painless-revolution Email us at podcast@masshist.org. Episode Special Guest: Sarah Alger is the George and Nancy Putnam Director of Mass General Hospital's Paul S. Russell, MD Museum of Medical History and Innovation. She was a founding editor of Proto, a thought leadership publication that was sponsored by MGH for 17 years. This episode uses materials from: The Bond (Instrumental) by Chad Crouch (Attribution-NonCommercial 4.0 International)        Psychic by Dominic Giam of Ketsa Music (licensed under a commercial non-exclusive license by the Massachusetts Historical Society through Ketsa.uk)        Curious Nature by Dominic Giam of Ketsa Music (licensed under a commercial non-exclusive license by the Massachusetts Historical Society through Ketsa.uk)

In this episode of BrainStorm host Meryl Comer continues her compelling interview with "Rockstar of Science" Dr. Rudy Tanzi, the pioneering Director of the Genetics and Aging Research Unit and Director of the McCance Center for Brain Health at Mass General Hospital. Dr. Tanzi unveils the secrets of brain health and Alzheimer's research. Exploring his innovative SHIELD framework, Dr. Tanzi offers practical strategies for cognitive wellness, from sleep and stress management to diet and lifelong learning.The episode takes an innovative turn with AI-generated questions that probe the challenges of Alzheimer's research. Dr. Tanzi provides candid insights into prevention, early intervention, and the future of medical science, sharing an unexpectedly optimistic view of combating cognitive decline. Blending scientific expertise with actionable advice, this episode is a must-listen for anyone interested in brain health, aging, and medical innovation.Support the show

Join BrainStorm host Meryl Comer as she kicks off 2025 with "Rockstar of Science" Dr. Rudy Tanzi, the pioneering Director of Genetics and Aging Research and Director of the McCance Center for Brain Health at Mass General Hospital. Dr. Tanzi delves into the new FDA-approved drugs, early cognitive blood tests, and why treating Alzheimer's should mirror our approach to heart disease by focusing on prevention long before symptoms appear. Drawing from his decades of research, Dr. Tanzi shares his vision for the future: a simple daily pill that could prevent Alzheimer's just like statins prevent heart disease. Whether you are concerned about brain health or fascinated by cutting-edge medical science, this episode offers hope and practical wisdom from one of the field's most influential voices. You don't want to miss it!Support the show

Like tens of millions of people, Stephen Dubner thought he had a penicillin allergy. Like the vast majority, he didn't. This misdiagnosis costs billions of dollars and causes serious health problems, so why hasn't it been fixed? And how about all the other things we think we're allergic to? SOURCES:Kimberly Blumenthal, allergist-immunologist and researcher at Mass General Hospital and Harvard Medical School.Theresa MacPhail, associate professor of science and technology studies at Stevens Institute of Technology.Thomas Platts-Mills, professor of medicine at the University of Virginia.Elena Resnick, allergist and immunologist at Mount Sinai Hospital. RESOURCES:Allergic: Our Irritated Bodies in a Changing World, by Theresa MacPhail (2023)."Evaluation and Management of Penicillin Allergy: A Review," by Erica S. Shenoy, Eric Macy, and Theresa Rowe (JAMA, 2019)."The Allergy Epidemics: 1870–2010," by Thomas Platts-Mills (The Journal of Allergy and Clinical Immunology, 2016)."Randomized Trial of Peanut Consumption in Infants at Risk for Peanut Allergy," by George Du Toit, Graham Roberts, et al. (The New England Journal of Medicine, 2015). EXTRAS:Freakonomics, M.D.

Chime In, Send Us a Text Message!In this episode, we explore the critical role of social determinants of health (SDOH) in stroke prevention and recovery with an incredible panel of experts from the Bugher Collaborative. Our guests include:Dr. Nirupama Yechoor, Principal Investigator at Mass General Hospital and leader of the Bugher Collaborative.Dr. Devanshi Choksi, neurologist and colleague of Dr. Yechoor at Mass General.Rachel Kitagawa and Sofia Constantinescu, neurology postgraduates from Yale University.We dive into:The Bugher Collaborative: Its mission, the partnership between Mass General, Yale, and UCSF, and how it addresses equity in stroke care.Research Highlights: Insights into how socioeconomic status, access to care, and community support affect stroke outcomes.Yale's Findings: Key demographic differences uncovered through their research and what they reveal about health equity.The Road Ahead: Next steps for the collaborative and their vision for improving stroke care.Magic Wand Wishes: What each guest would change to improve stroke prevention and recovery if they had unlimited resources.This conversation builds on our discussion of the 2024 ASA Stroke Prevention Guidelines, offering a deeper dive into the intersection of health equity and stroke care.Resources and Links:Learn more about the Bugher CollaborativeDr. Nirupama Yechoor's BioDr. Devanshi Choksi's BioRachel Kitagawa's BioSofia Constantinescu's BioSupport Our Show! Thank you for helping us to continue to make great content. We appreciate your generosity! Support the showShow credits:Music intro credit to Jake Dansereau. Our intro welcome is the voice of Caroline Goggin, a stroke survivor and our first podcast guest! Please listen to her inspiring story on Episode 2 of the podcast.Connect with Us and Share our Show on Social:Website | Linkedin | Twitter | YouTube | FacebookKnow Stroke Podcast Disclaimer: Our podcast and media advertising services are for informational purposes only and do not constitute the practice of medical advice, diagnosis or treatment.

Dr. Sandra Hassink is joined by Dr. Lauren Fiechtner, the Director of Nutrition at MassGeneral Hospital for Children in the Division of Gastroenterology and Nutrition. She is also the Associate Professor of Pediatrics at Harvard Medical School. Together they discuss early feeding and food introduction.   Related Resources: • Building a Foundation for Healthy Active Living Modules (tinyurl.com/bdd5tsu6) • Healthy Active Living From Birth to Age 2, Resource Portal (tinyurl.com/4e7zvfnd) • The Role of the Pediatrician in the Promotion of Healthy, Active Living (tinyurl.com/5n8xv2du)

We must all be compassionate. You never know what someone else is going through. - Keely Krantz Keely Krantz got her start in PR, eventually leading the launch of high-profile, global brands. A proud Boston College graduate, she was fortunate to have a mentor who had broken through glass ceilings and believed in passing it on. Says Keely “Janet Diederichs at Edelman Public Relations in Chicago challenged me to be someone I would never have aspired to if it hadn't been for her guidance. I learned to be bold and aggressive.” At the height of Keely's career, she became a mom and decided to stay at home with her kids, choosing parenthood and volunteerism over a career. It was this devotion to community and the greater good that inspired Keely and her husband Jason to make the largest gift in the history of Mass General Hospital cancer research history last year. Says Keely: “We don't want to see small, incremental changes. We want to see fundamental, monumental, landscape-changing breakthroughs in the treatment of cancer, and we are willing to take big risks at the Krantz Family Research Center on physician-scientists who have big, aggressive ideas. We want to swing for the fences.” A few months later, Keely launched her next big chapter as the founder of the O'Dell Women's Center www.odellwomenscenter.com in Springfield, Massachusetts. Named after her 98-year-old grandmother, who was a maternity nurse in the community for 40 years, the O'Dell Center is a first-of-its-kind in Springfield with 10,000 square feet of collaborative space that houses Dress for Success/Western Mass and other non-profits that advance educational and career opportunities for low-income women. In just one year, $250,000 in grants have been awarded. For Keely, this new chapter is the culmination of a story rooted in faith and the lessons of her parents. “Anything is possible” are three words I heard all the time when I was growing up. Says Keely. “I want to be a connector, surrounded by the mantra that respect and kindness go hand in hand. I want to do good.” For 23 minutes of inspiration, just hit that download button. #women #community #cancer @massgeneralcancercenter

This is a conversation with Dr. David Amaral, a distinguished professor at the MIND Institute and scientific director of Autism BrainNet, and Dorothy Frisch, an activist and supporter of the program. Autism BrainNet is funded by the Simons Foundation to collect and study postmortem brain samples from individuals with autism to understand the neurological basis of the disorder better. Currently, there are no biomarkers for autism, so studying the brains and accomplishments of those who had autism can lead to a better understanding of the abilities and challenges seen on the autism spectrum. David explains, "We went to the Simons Foundation and, with their support, have established a network in the United States. We have three collection sites: one at the UC Davis Mind Institute in Sacramento, one at UT Southwestern in Dallas, Texas, and one at the Mass General Hospital in Boston, where a postmortem brain donation can be sent. Those brains are then prepared in ways that will facilitate all kinds of research both now and in the future. We have developed this resource to foster autism research throughout the world. What we are seeing now that we've just celebrated our 10th anniversary is that we've collected nearly 400 brain donations so far, and we're seeing an increasing demand from researchers worldwide to get access to that resource." Dorothy elaborates, "I was the main support person for my older cousin, Gregory Blackstock, for a couple of decades. He needed a lot of executive function help. He lived on his own but couldn't make critical decisions very well. As long as everything went along without any hitch, he was generally fine. But as he got older and experienced more physical infirmities, then I needed to step up more. So then he was very obviously autistic, so it was kind of peripherally interesting to me." "One of his savant traits was that he was an incredible artist. He also spoke many languages that he picked up by ear. He had a perfect pitch and learned the accordion, but he could easily transfer that information to playing the organ and the piano. He had almost total recall of anything that crossed his path that interested him. And so, just being around him and being involved with furthering his artistic career gave me further insights about the people I met who were interested in autism."   #AutismBrainNet #BrainDonation #AutismResearch #Autism #BrainResearch autismbrainnet.org Download the transcript here  

David explains, "We went to the Simons Foundation and, with their support, have established a network in the United States. We have three collection sites: one at the UC Davis Mind Institute in Sacramento, one at UT Southwestern in Dallas, Texas, and one at the Mass General Hospital in Boston, where a postmortem brain donation can be sent. Those brains are then prepared in ways that will facilitate all kinds of research both now and in the future. We have developed this resource to foster autism research throughout the world. What we are seeing now that we've just celebrated our 10th anniversary is that we've collected nearly 400 brain donations so far, and we're seeing an increasing demand from researchers worldwide to get access to that resource." Dorothy elaborates, "I was the main support person for my older cousin, Gregory Blackstock, for a couple of decades. He needed a lot of executive function help. He lived on his own but couldn't make critical decisions very well. As long as everything went along without any hitch, he was generally fine. But as he got older and experienced more physical infirmities, then I needed to step up more. So then he was very obviously autistic, so it was kind of peripherally interesting to me." "One of his savant traits was that he was an incredible artist. He also spoke many languages that he picked up by ear. He had a perfect pitch and learned the accordion, but he could easily transfer that information to playing the organ and the piano. He had almost total recall of anything that crossed his path that interested him. And so, just being around him and being involved with furthering his artistic career gave me further insights about the people I met who were interested in autism."   #AutismBrainNet #BrainDonation #AutismResearch #Autism #BrainResearch autismbrainnet.org Listen to the podcast here

Nishi Vootukuru (@Nishi_Vootukuru) and Dr. Ezra Schwartz (@ezraschwartz10) interview Dr. William Shutze and Dr. Anahita Dua (@AnahitaDua) to discuss the Get a Pulse on PAD Campaign.   The Get a Pulse on PAD initiative (#PulseonPAD), launched in February, 2024, is a patient education and advocacy campaign designed to increase the understanding of peripheral artery disease's risk factors and potential symptoms.     Dr. Shutze is a vascular surgeon with Texas Vascular Associates in Dallas, Texas and the Secretary of the SVS. Dr. Shutze completed his medical studies at Baylor University after completing general surgery residency at University of Alabama in Birmingham. Dr. Shutze returned to Baylor to complete his vascular fellowship. Dr. Shutze is one of the Get a Pulse on PAD initiative's chairs and a leading expert in PAD. He has actively published in the field with over 100 abstracts and articles, with his most recent work focusing on prosthetics, and advocating for successful prosthetic referral after amputation.    Dr. Dua is a vascular surgeon at Mass General Hospital and associate professor at Harvard Medical School. At Mass General, she is the director of the Vascular Lab, co-director of the Peripheral Artery Disease Center and Limb Evaluation and Amputation Program (LEAPP), associate director of the Wound Care Center, director of the Lymphedema Center and director of clinical research for the division of vascular surgery. She serves as the Editor-in-Chief of Journal of Vascular Surgery-Vascular Insights. Dr. Dua completed her undergraduate medical studies at the Aberdeen University School of Medicine in Aberdeen, Scotland. She then completed her general surgery residency at the Medical College of Wisconsin and vascular fellowship at Stanford University Hospital. She holds multiple master's degrees including degrees in trauma sciences and business administration in healthcare management. She also completed certificate programs at the Massachusetts Institute of Technology in health economics and outcomes research as well as in drug and device development. Dr. Dua is a prolific researcher, researcher, and advocate, with much of her work centered on PAD. She furthers patient care not only through research but through her political work as Founder of the Healthcare for Action political action committee (PAC) and member of the SVS PAC Steering Committee.    Special thank you to Jacob Soucey (@JacobWSoucy)   Resources: https://www.secondscount.org/get-a-pulse-pad https://evtoday.com/news/pad-pulse-alliance-survey-highlights-disconnect-in-public-knowledge-of-pad-risks Association of Black Cardiologists (ABC) Society for Cardiovascular Angiography & Interventions (SCAI) Society of Interventional Radiology (SIR) CardioVascular Coalition (CVC) Outpatient Endovascular and Interventional Society (OEIS) https://vascular.org/advocacy/political-action-committee https://evtoday.com/articles/2021-may/the-arc-act-fighting-amputation-via-legislation https://evtoday.com/articles/2006-may/EVT0506_10.html#:~:text=The%20Screening%20Abdominal%20Aortic%20Aneurysm,screening%20as%20a%20Medicare%20benefit CLariTI Study: Natural Progression of High-Risk Chronic Limb-Threatening Ischemia Socioeconomic and hospital-related predictors of amputation for critical limb ischemia  ARC Act of Congress Painkiller: TV Series  Congressman Payne  SAAAVE Act   Follow us @audiblebleeding Learn more about us at https://www.audiblebleeding.com/about-1/ and provide us with your feedback with our listener survey.  

WBZ NewsRadio's Chaiel Schaffel reports.

This episode will explore hospitals, health care, and sustainability. Today, my guest is Dr. Jonathan Slutzman. Dr. Slutzman is the Director of the Center for the Environment and Health and Medical Director for Environmental Sustainability at Massachusetts General Hospital. We discuss this critical topic and the significant sustainability initiatives that the Mass General Hospital is leading toward a greener future for the good of patients, society, and the planet.

This episode will explore hospitals, health care, and sustainability. Today, my guest is Dr. Jonathan Slutzman. Dr. Slutzman is the Director of the Center for the Environment and Health and Medical Director for Environmental Sustainability at Massachusetts General Hospital. We discuss this critical topic and the significant sustainability initiatives that the Mass General Hospital is leading toward a greener future for the good of patients, society, and the planet.

In this Leveling Up Episode of the PRS Global Open Deep Cuts Podcast, Dr. John Semple discusses his unusual pathway into medicine, three dimensional thinking, prepectoral breast reconstruction, the use of allograft and synthetic meshes, fat grafting in radiated breasts, some tips to make fat harvest easier, how to be a good mentor and a good leader, and how he got involved in climate science. Read a recent classic PRS Global Open article by Dr. Semple and co-authors, “Patient Outcomes after Fat Grafting to the Radiated Chest Wall before Delayed Two-stage Alloplastic Breast Reconstruction”: https://bit.ly/SempleFatGrafting  Dr. John Semple is a Professor in the Department of Surgery at the University of Toronto, and the head of the division of plastic surgery at Women's College Hospital. He is also an adjunct faculty member at the wilderness Medicine Program at Mass General Hospital in Boston, and an adjunct professor at the Ontario College of Art and Design, where was a former chair of the Board of Governors. He trained in art at OCAD and became a fully trained medical illustrator, then went into medicine, training in plastic surgery at the University of Toronto and then completing a microsurgery fellowship at the Toronto General Hospital. He is a past president of the Canadian Society of Plastic Surgeons, and received the Lavina Lickley Lifetime achievement award form the department of surgery at the University of Toronto. He also has a keen interest in mountaineering - and has been to Everest North Col 4 times, and has published numerous papers on the effects of climate change in the Himalayas.  Your host, Dr. Puru Nagarkar, is a board-certified plastic and hand surgeon, and Assistant Professor of Surgery at the University of Texas Southwestern Medical Center in Dallas. #PRSGlobalOpen #DeepCutsPodcast #PlasticSurgery #LevelingUp

In this episode, Chris Koddermann interviews two members of the Center for the Neuroscience of Psychedelics at Mass General Hospital: founding director, author, and co-founder of three drug development companies, Dr. Jerry Rosenbaum; and psychiatrist and associate director and director of cognitive neuroscience, Sharmin Ghaznavi, MD, Ph.D. Rosenbaum and Ghaznavi bonded over an interest in rumination, and wondered: How could the plasticity-inducing effects of psychedelics change these negative loops people find themselves in? How important is the ability to break out of those loops – and learn new patterns – when our concept of self is so central to who we are? Ghaznavi is studying the effects of psilocybin on rumination and scanning patients at multiple times throughout the process to track data we still don't really have: how psychedelic-induced neuroplasticity changes over time, and why. They discuss: How much of a role the default mode network takes in the therapeutic benefits of psychedelics: Is it overblown? Hyperscanning, which involves scanning two individuals at the same time, looking for potential concordance in signal and/or an increased alliance between the therapist and patient The Schultes Legacy Project and the work of Stephen Haggarty to explore the potential of largely unstudied psychoactive plants Critiques of the recent ruling on Lykos and MDMA-assisted therapy and the clash between the FDA and the advisory committee: Were they really on the same page? The false dichotomy of neuroscience vs. patient experience: Does the subjective experience actually increase plasticity and other measurable benefits? and more! For links, head to the show notes page.

In this episode of Research Renaissance, host Deborah Westphal dives into a fascinating conversation with Dr. Sudeshna Das, Associate Professor of Neurology at Mass General Hospital and Harvard Medical School. Dr. Das is a pioneer in the field of biomedical informatics and a 2022 Toffler Scholar. Her work focuses on developing tools for multi-scale data integration from molecular to clinical data and applying data science approaches to study neurodegenerative diseases, particularly Alzheimer's disease.Guest Introduction: Dr. Sudeshna DasDr. Sudeshna Das is an Associate Professor of Neurology at Mass General Hospital and Harvard Medical School. She specializes in biomedical informatics and has a keen interest in developing tools for integrating diverse data sets, from molecular to clinical, to understand complex diseases like Alzheimer's. Dr. Das has a rich background in engineering and computational biology, making significant contributions to the field of drug discovery and neurodegenerative disease research.Key Discussion PointsCareer Motivation and Journey:Dr. Das shares her early inspiration to cure cancer, driven by personal experiences with family members who had the disease.Her transition from engineering to biomedical informatics and the unique challenges and opportunities she faced as a female engineer in India.Biomedical Informatics and Data Integration:Explanation of biomedical informatics, bioinformatics, and computational biology.The importance of integrating large, high-dimensional data sets and real-world data for research.Challenges in managing and analyzing big data and high-velocity data.Alzheimer's Disease Research:The focus on understanding the roles of different cell types in Alzheimer's disease, particularly astrocytes, and their progression from protective to exhausted states.The significance of recent findings on the role of T cells in Alzheimer's disease and their potential as therapeutic targets.Future of Alzheimer's Research:The promise of new technologies like spatial transcriptomics and artificial intelligence in advancing Alzheimer's research.The potential of AI tools, such as graph neural nets, to model disease pathways and predict effective treatments for individual patients.The long-term goal of developing personalized treatments for Alzheimer's disease.Mentoring and Funding:Dr. Das's commitment to mentoring young researchers and her approach to guiding students through complex research landscapes.The role of foundations like the Karen Toffler Charitable Trust in providing crucial funding for preliminary research.Stay tuned for more episodes of Research Renaissance by subscribing to our podcast. For further information and updates, visit our website at TofflerTrust.org. We welcome your thoughts and suggestions, so feel free to reach out! Until then, onward and upward.To learn more about the breakthroughs discussed in this episode and to support ongoing research, visit our website at tofflertrust.org. Technical Podcast Support by Jon Keur at Wayfare Recording Co.

Pradeep is a brilliant geneticist and Director of Preventive Cardiology, holds the Paul & Phyllis Fireman Endowed Chair in Vascular Medicine at Mass General Hospital and on faculty at Harvard Medical School and the Broad Institute. His prolific research has been illuminating for the field of improving our approach to reduce the risk of heart disease. That's especially important because heart disease is the global (and US) #1 killer and is on the increase. We didn't get into lifestyle factors here since there was so much ground to cover on new tests. drugs, and strategies.A video snippet of our conversation on ApoB. Full videos of all Ground Truths podcasts can be seen on YouTube here. The audios are also available on Apple and Spotify.Transcript with links to key publications and audioEric Topol (00:06):Well, welcome to Ground Truths. I'm Eric Topol and with me is Pradeep Natarajan from Harvard. He's Director of Preventative Cardiology at the Mass General Brigham Health System and he has been lighting it up on the field of cardiovascular. We're going to get to lots of different parts of that story and so, Pradeep welcome.Pradeep Natarajan (00:31):Thanks Eric, really delighted and honored to be with you and have this discussion.Eric Topol (00:36):Well, for years I've been admiring your work and it's just accelerating and so there's so many things to get to. I thought maybe what we'd start off with is you recently wrote a New England Journal piece about two trials, two different drugs that could change the landscape of cardiovascular prevention in the future. I mean, that's one of the themes we're going to get to today is all these different markers and drugs that will change cardiology as we know it now. So maybe you could just give us a skinny on that New England Journal piece.Two New Lipid Targets With RNA DrugsPradeep Natarajan (01:16):Yeah, yeah, so these two agents, the trials were published at the same time. These phase two clinical trials for plozasiran, which is an siRNA against APOC3 and zodasiran, which is an siRNA against ANGPTL3. The reason why we have medicines against those targets are based on human genetics observations, that individuals with loss of function mutations and either of those genes have reduced lipids. For APOC3, it's reduced triglycerides for ANGPTL3 reduced LDL cholesterol and reduced triglycerides and also individuals that have those loss of function mutations also have lower risk for coronary artery disease. Now that's a very similar parallel to PCSK9. We have successful medicines that treat that target because people have found that carriers of loss of function mutations in PCSK9 lead to lower LDL cholesterol and lower coronary artery disease.(02:11):Now that suggests that therapeutic manipulation without significant side effects from the agents themselves for APOC3 and ANGPTL3 would be anticipated to also lower coronary artery disease risk potentially in complementary pathways to PCSK9. The interesting thing with those observations is that they all came from rare loss of function mutations that are enriched in populations of individuals. However, at least for PCSK9, has been demonstrated to have efficacy in large groups of individuals across different communities. So the theme of that piece was really just the need to study diverse populations because those insights are not always predictable about which communities are going to have those loss of function mutations and when you find them, they often have profound insights across much larger groups of individuals.Eric Topol (03:02):Well, there's a lot there that we can unpack a bit of it. One of them is the use of small interfering RNAs (siRNA) as drugs. We saw in the field of PCSK9, as you mentioned. First there were monoclonal antibodies directed against this target and then more recently, there's inclisiran which isn't an RNA play if you will, where you only have to take it twice a year and supposedly it's less expensive and I'm still having trouble in my practice getting patients covered on their insurance even though it's cheaper and much more convenient. But nonetheless, now we're seeing these RNA drugs and maybe you could comment about that part and then also the surprise that perhaps is unexplained is the glucose elevation.Pradeep Natarajan (03:53):Yeah, so for medicines and targets that have been discovered through human genetics, those I think are attractive for genetic-based therapies and longer interval dosing for the therapies, which is what siRNAs allow you to do because the individuals that have these perturbations, basically the naturally occurring loss of function mutations, they have these lifelong, so basically have had a one-time therapy and have lived, and so far, at least for these targets, have not had untoward side effects or untoward phenotypic consequences and only reduce lipids and reduce coronary artery disease. And so, instead of taking a pill daily, if we have conviction that that long amount of suppression may be beneficial, then longer interval dosing and not worrying about the pill burden is very attractive specifically for those specific therapeutics. And as you know, people continue to innovate on further prolonging as it relates to PCSK9.(04:57):Separately, some folks are also developing pills because many people do feel that there's still a market and comfort for daily pills. Now interestingly for the siRNA for zodasiran at the highest dose, actually for both of them at the highest doses, but particularly for zodasiran, there was an increase in insulin resistance parameters actually as it relates to hyperglycemia and less so as it relates to insulin resistance, that is not predicted based on the human genetics. Individuals with loss of function mutations do not have increased risks in hyperglycemia or type 2 diabetes, so that isolates it related to that specific platform or that specific technology. Now inclisiran, as you'd mentioned, Eric is out there. That's an siRNA against PCSK9 that's made by a different manufacturer. So far, the clinical trials have not shown hyperglycemia or type 2 diabetes as it relates inclisiran, so it may be related to the specific siRNAs that are used for those targets. That does merit further consideration. Now, the doses that the manufacturers do plan to use in the phase three clinical trials are at lower doses where there was not an increase in hyperglycemia, but that does merit further investigation to really understand why that's the case. Is that an expected generalized effect for siRNAs? Is it related to siRNAs for this specific target or is it just related to the platform used for these two agents which are made by the same manufacturer?Eric Topol (06:27):Right, and I think the fact that it's a mystery is intriguing at the least, and it may not come up at the doses that are used in the trials, but the fact that it did crop up at high doses is unexpected. Now that is part of a much bigger story is that up until now our armamentarium has been statins and ezetimibe to treat lipids, but it's rapidly expanding Lp(a), which for decades as a cardiologist we had nothing to offer. There may even be drugs to be able to lower people who are at high risk with high Lp(a). Maybe you could discuss that.What About Lp(a)?Pradeep Natarajan (07:13):Yeah, I mean, Eric, as you know, Lp(a) has been described as a cardiovascular disease risk factors for quite so many years and there are assays to detect lipoprotein(a) elevation and have been in widespread clinical practice increasing widespread clinical practice, but we don't yet have approved therapies. However, there is an abundance of literature preclinical data that suggests that it likely is a causal factor, meaning that if you lower lipoprotein(a) when elevated, you would reduce the risk related to lipoprotein(a). And a lot of this comes from similar human genetic studies. The major challenge of just relating a biomarker to an outcome is there are many different reasons why a biomarker might be elevated, and so if you detect a signal that correlates a biomarker, a concentration to a clinical outcome, it could be related to that biomarker, but it could be to the other reasons that the biomarker is elevated and sometimes it relates to the outcome itself.(08:10):Now human genetics is very attractive because if you find alleles that strongly relate to that exposure, you can test those alleles themselves with the clinical outcome. Now the allele assignment is established at birth. No other factor is going to change that assignment after conception, and so that provides a robust, strong causal test for that potential exposure in clinical outcome. Now, lipoprotein(a) is unique in that it is highly heritable and so there are lots of different alleles that relate to lipoprotein(a) and so in a well powered analysis can actually test the lipoprotein(a) SNPs with the clinical outcomes and similar to how there is a biomarker association with incident myocardial infarction and incident stroke, the SNPs related to lipoprotein(a) show the same. That is among the evidence that strongly supports that this might be causal. Now, fast forward to many years later, we have at least three phase three randomized clinical trials testing agents that have been shown to be very potent at lowering lipoprotein(a) that in the coming years we will know if that hypothesis is true. Importantly, we will have to understand what are the potential side effects of these medicines. There are antisense oligonucleotides and siRNAs that are primarily in investigation. Again, this is an example where there's a strong genetic observation, and so these genetic based longer interval dosing therapies may be attractive, but side effects will be a key thing as well too. Those things hard to anticipate really can anticipate based on the human genetics for off target effects, for example.(09:52):It's clearly a risk signal and hopefully in the near future we're going to have specific therapies.Eric Topol (09:57):Yeah, you did a great job of explaining Mendelian randomization and the fact the power of genetics, which we're going to get into deeper shortly, but the other point is that do you expect now that there's these multiple drugs that lower Lp(a) efficiently, would that be enough to get approval or will it have to be trials to demonstrate improved cardiovascular outcomes?Pradeep Natarajan (10:24):There is a great regulatory path at FDA for approval just for LDL cholesterol lowering and inclisiran is on the market and the phase three outcomes data has not yet been reported because there is a wide appreciation that LDL cholesterol lowering is a pretty good surrogate for cardiovascular disease risk lowering. The label will be restricted to LDL cholesterol lowering and then if demonstrated to have clinical outcomes, the label could be expanded. For other biomarkers including lipoprotein(a), even though we have strong conviction that it is likely a causal factor there hasn't met the bar yet to get approval just based on lipoprotein(a) lowering, and so we would need to see the outcomes effects and then we would also need to understand side effects. There is a body of literature of side effects for other therapies that have targeted using antisense oligonucleotides. We talked about potential side effects from some siRNA platforms and sometimes those effects could overtake potential benefits, so that really needs to be assessed and there is a literature and other examples.(11:31):The other thing I do want to note related to lipoprotein(a) is that the human genetics are modeled based on lifelong perturbations, really hard to understand what the effects are, how great of an effect there might be in different contexts, particularly when introduced in middle age. There's a lot of discussion about how high lipoprotein(a) should be to deliver these therapies because the conventional teaching is that one in five individuals has high lipoprotein(a), and that's basically greater than 75 nanomoles per liter. However, some studies some human genetic studies to say if you want to get an effect that is similar to the LDL cholesterol lowering medicines on the market, you need to start with actually higher lipoprotein(a) because you need larger amounts of lipoprotein(a) lowering. Those are studies and approaches that haven't been well validated. We don't know if that's a valid approach because that's modeling based on this sort of lifelong effect. So I'm very curious to see what the overall effect will be because to get approval, I think you need to demonstrate safety and efficacy, but most importantly, these manufacturers and we as clinicians are trying to find viable therapies in the market that it won't be hard for us to get approval because hopefully the clinical trial will have said this is the context where it works. It works really well and it works really well on top of the existing therapies, so there are multiple hurdles to actually getting it directly to our patients.How Low Do You Go with LDL Cholesterol?Eric Topol (13:02):Yeah, no question about that. I'm glad you've emphasized that. Just as you've emphasized the incredible lessons from the genetics of people that have helped guide this renaissance to better drugs to prevent cardiovascular disease. LDL, which is perhaps the most impressive surrogate in medicine, a lab test that you already touched on, one of the biggest questions is how low do you go? That is Eugene Braunwald, who we all know and love. They're in Boston. The last time I got together with him, he was getting his LDL down to close to zero with various tactics that might be extreme. But before we leave these markers, you're running preventive cardiology at man's greatest hospital. Could you tell us what is your recipe for how aggressive do you go with LDL?Pradeep Natarajan (14:04):Yeah, so when I talk to patients where we're newly getting lipid lowering therapies on, especially because many people don't have a readout of abnormal LDL cholesterol when we're prescribing these medicines, it's just giving them a sense of what we think an optimal LDL cholesterol might be. And a lot of this is based on just empirical observations. So one, the average LDL cholesterol in the modern human is about 100 to 110 mg/dL. However, if you look at contemporary hunter gatherers and non-human primates, their average LDL is about 40 to 50 and newborn babies have an LDL cholesterol of about 30. And the reason why people keep making LDL cholesterol lowering medicines because as you stack on therapies, cardiovascular disease events continue to reduce including down to these very low LDL cholesterol values. So the population mean for LDL cholesterol is high and everybody likely has hypercholesterolemia, and that's because over the last 10,000 years how we live our lives is so dramatically different and there has not been substantial evolution over that time to change many of these features related to metabolism.(15:16):And so, to achieve those really low LDL cholesterol values in today's society is almost impossible without pharmacotherapies. You could say, okay, maybe everybody should be on pharmacotherapies, and I think if you did that, you probably would reduce a lot of events. You'll also be treating a lot of individuals who likely would not get events. Cardiovascular disease is the leading killer, but there are many things that people suffer from and most of the times it still is not cardiovascular disease. So our practice is still rooted in better identifying the individuals who are at risk for cardiovascular disease. And so, far we target our therapies primarily in those who have already developed cardiovascular disease. Maybe we'll talk about better identifying those at risk, but for those individuals it makes lots of sense to get it as low as possible. And the field has continued to move to lower targets.(16:07):One, because we've all recognized, at least based on these empirical observations that lower is better. But now increasingly we have a lot of therapies to actually get there, and my hope is that with more and more options and the market forces that influence that the cost perspective will make sense as we continue to develop more. As an aside, related aside is if you look at the last cholesterol guidelines, this is 2018 in the US this is the first time PCSK9 inhibitors were introduced in the guidelines and all throughout that there was discussions of cost. There are a lot of concerns from the field that PCSK9 inhibitors would bankrupt the system because so many people were on statins. And you look at the prior one that was in 2013 and cost was mentioned once it's just the cost effectiveness of statins. So I think the field has that overall concern.(17:01):However, over time we've gotten comfortable with lower targets, there are more medicines and I think some of this competition hopefully will drive down some of the costs, but also the overall appreciation of the science related to LDL. So long-winded way of saying this is kind of the things that we discussed just to give reassurance that we can go to low LDL cholesterol values and that it's safe and then we think also very effective. Nobody knows what the lower limit is, whether zero is appropriate or not. We know that glucose can get too low. We know that blood pressure can be too low. We don't know yet that limit for LDL cholesterol. I mean increasingly with these trials we'll see it going down really low and then we'll better appreciate and understand, so we'll see 40 is probably the right range.Eric Topol (17:49):40, you said? Yeah, okay, I'll buy that. Of course, the other thing that we do know is that if you push to the highest dose statins to get there, you might in some people start to see the hyperglycemia issue, which is still not fully understood and whether that is, I mean it's not desirable, but whether or not it is an issue, I guess it's still out there dangling. Now the other thing that since we're on LDL, we covered Lp(a), PCSK9, the siRNA, is ApoB. Do you measure ApoB in all your patients? Should that be the norm?Measuring ApoBPradeep Natarajan (18:32):Yeah, so ApoB is another blood test. In the standard lipid panel, you get four things. What's measured is cholesterol and triglycerides, they're the lipids insoluble in blood to get to the different tissues that get packaged in lipoprotein molecules which will have the cholesterol, triglycerides and some other lipids and proteins. And so, they all have different names as you know, right? Low density lipoprotein, high density lipoprotein and some others. But also in the lipid panel you get the HDL cholesterol, the amount of cholesterol in an HDL particle, and then most labs will calculate LDL cholesterol and LDL cholesterol has a nice relationship with cardiovascular disease. You lower it with statins and others. Lower risk for cardiovascular disease, turns out a unifying feature of all of these atherogenic lipoproteins, all these lipoproteins that are measured and unmeasured that relate to cardiovascular disease, including lipoprotein(a), they all have an additional protein called ApoB. And ApoB, at least as it relates to LDL is a pretty good surrogate of the number of LDL particles.(19:37):Turns out that that is a bit better at the population level at predicting cardiovascular disease beyond LDL cholesterol itself. And where it can be particularly helpful is that there are some patients out there that have an unexpected ratio between ApoB and LDL. In general, the ratio between LDL cholesterol and ApoB is about 1.1 and most people will have that rough ratio. I verify that that is the expected, and then if that is the expected, then really there is no role to follow ApoB. However, primarily the patients that have features related to insulin resistance have obesity. They may often have adequate looking LDL cholesterols, but their ApoB is higher. They have more circulating LDL particles relative to the total amount of LDL cholesterol, so smaller particles themselves. However, the total number of particles may actually be too high for them.(20:34):And so, even if the LDL cholesterol is at target, if the ApoB is higher, then you need to reduce. So usually the times that I just kind of verify that I'm at appropriate target is I check the LDL cholesterol, if that looks good, verify with the ApoB because of this ratio, the ApoB target should be about 10% lower. So if we're aiming for about 40, that's like 36, so relatively similar, and if it's there, I'm good. If it's not and it's higher, then obviously increase the LDL cholesterol lowering medicines because lower the ApoB and then follow the ApoB with the lipids going forward. The European Society of Cardiology has more emphasis on measuring ApoB, that is not as strong in the US guidelines, but there are many folks in the field, preventive cardiologists and others that are advocating for the increasing use of ApoB because I think there are many folks that are not getting to the appropriate targets because we are not measuring ApoB.Why Aren't We Measuring and Treating Inflammation?Eric Topol (21:37):Yeah, I think you reviewed it so well. The problem here is it could be part of the standard lipid panel, it would make this easy, but what you've done is a prudent way of selecting out people who it becomes more important to measure and moderate subsequently. Now this gets us to the fact that we're lipid centric and we don't pay homage to inflammation. So I wrote a recent Substack on the big miss on inflammation, and here you get into things like the monoclonal antibody to interleukin-6, the trial that CANTOS that showed significant reduction in cardiovascular events and fatal cancers by the way. And then you get into these colchicine trials two pretty good size randomized trials, and here the entry was coronary disease with a high C-reactive protein. Now somehow or other we abandon measuring CRP or other inflammatory markers, and both of us have had patients who have low LDLs but have heart attacks or significant coronary disease. So why don't we embrace inflammation? Why don't we measure it? Why don't we have better markers? Why is this just sitting there where we could do so much better? Even agents that are basically cost pennies like colchicine at low doses, not having to use a proprietary version could be helpful. What are your thoughts about us upgrading our prevention with inflammation markers?Pradeep Natarajan (23:22):Yeah, I mean, Eric, there is an urgent need to address these other pathways. I say urgent need because heart disease has the dubious distinction of being the leading killer in the US and then over the last 20 years, the leading killer in the world as it takes over non-communicable diseases. And really since the early 1900s, there has been a focus on developing pharmacotherapies and approaches to address the traditional modifiable cardiovascular disease risk factors. That has done tremendous good, but still the curves are largely flattening out. But in the US and in many parts of the world, the deaths attributable to cardiovascular disease are starting to tick up, and that means there are many additional pathways, many of them that we have well recognized including inflammation. More recently, Lp(a) that are likely important for cardiovascular disease, for inflammation, as you have highlighted, has been validated in randomized controlled trials.(24:18):Really the key trial that has been more most specific is one on Canakinumab in the CANTOS trial IL-1β monoclonal antibody secondary prevention, so cardiovascular disease plus high C-reactive protein, about a 15% reduction in cardiovascular disease and also improvement in cancer related outcomes. Major issues, a couple of issues. One was increased risk for severe infections, and the other one is almost pragmatic or practical is that that medicine was on the market at a very high price point for rare autoinflammatory conditions. It still is. And so, to have for a broader indication like cardiovascular disease prevention would not make sense at that price point. And the manufacturer tried to go to the FDA and focus on the group that only had C-reactive protein lowering, but that's obviously like a backwards endpoint. How would you know that before you release the medicine? So that never made it to a broader indication.(25:14):However, that stuck a flag in the broader validation of that specific pathway in cardiovascular disease. That pathway has direct relevance to C-reactive protein. C-reactive protein is kind of a readout of that pathway that starts from the NLRP3 inflammasome, which then activates IL-1β and IL-6. C-reactive protein we think is just a non causal readout, but is a reliable test of many of these features and that's debatable. There may be other things like measuring IL-6, for example. So given that there is actually substantial ongoing drug development in that pathway, there are a handful of companies with NLRP3 inflammasome inhibitors, but small molecules that you can take as pills. There is a monoclonal antibody against IL-6 that's in development ziltivekimab that's directed at patients with chronic kidney disease who have lots of cardiovascular disease events despite addressing modifiable risk factors where inflammatory markers are through the roof.(26:16):But then you would also highlighted one anti-inflammatory that's out there that's pennies on the dollar, that's colchicine. Colchicine is believed to influence cardiovascular disease by inhibiting NLRP3, I say believed to. It does a lot of things. It is an old medicine, but empirically has been shown in at least two randomized controlled trials patients with coronary artery disease, actually they didn't measure C-reactive protein in the inclusion for these, but in those populations we did reduce major adverse cardiovascular disease events. The one thing that does give me pause with colchicine is that there is this odd signal for increased non-cardiovascular death. Nobody understands if that's real, if that's a fluke. The FDA just approved last year low dose colchicine, colchicine at 0.5 milligrams for secondary prevention given the overwhelming efficacy. Hasn't yet made it into prevention guidelines, but I think that's one part that does give me a little bit pause. I do really think about it particularly for patients who have had recurrent events. The people who market the medicine and do research do remind us that C-reactive protein was not required in the inclusion, but nobody has done that secondary assessment to see if measuring C-reactive protein would be helpful in identifying the beneficial patients. But I think there still could be more work done on better identifying who would benefit from colchicine because it's an available and cheap medicine. But I'm excited that there is a lot of development in this inflammation area.Eric Topol (27:48):Yeah, well, the development sounds great. It's probably some years away. Do you use colchicine in your practice?Pradeep Natarajan (27:56):I do. Again, for those folks who have had recurrent events, even though C-reactive protein isn't there, it does make me feel like I'm treating inflammation. If C-reactive protein is elevated and then I use it for those patients, if it's not elevated, it's a much harder sell from my standpoint, from the patient standpoint. At the lower dose for colchicine, people generally are okay as far as side effects. The manufacturer has it at 0.5 milligrams, which is technically not pennies on the dollar. That's not generic. The 0.6 milligrams is generic and they claim that there is less side effects at the 0.5 milligrams. So technically 0.6 milligrams is off label. So it is what it is.CHIP and Defining High Risk People for CV DiseaseEric Topol (28:40):It's a lot more practical, that's for sure. Now, before I leave that, I just want to mention when I reviewed the IL-1β trial, you mentioned the CANTOS trial and also the colchicine data. The numbers of absolute increases for infection with the antibody or the cancers with the colchicine are really small. So I mean the benefit was overriding, but I certainly agree with your concern that there's some things we don't understand there that need to be probed more. Now, one of the other themes, well before one other marker that before we get to polygenic risk scores, which is center stage here, defining high risk people. We've talked a lot about the conventional things and some of the newer ways, but you've been one of the leaders of study of clonal hematopoiesis of indeterminate potential known as CHIP. CHIP, not the chips set in your computer, but CHIP. And basically this is stem cell mutations that increase in people as we age and become exceptionally common with different mutations that account in these clones. So maybe you can tell us about CHIP and what I don't understand is that it has tremendous correlation association with cardiovascular outcomes adverse as well as other system outcomes, and we don't measure it and we could measure it. So please take us through what the hell is wrong there.Pradeep Natarajan (30:14):Yeah, I mean this is really exciting. I mean I'm a little bit biased, but this is observations that have been made only really over the last decade, but accelerating research. And this has been enabled by advances in genomic technologies. So about 10 years or plus ago, really getting into the early days of population-based next generation sequencing, primarily whole exome sequencing. And most of the DNA that we collect to do these population-based analyses come from the blood, red blood cells are anucleate, so they're coming from white blood cells. And so, at that time, primarily interrogating what is the germline genetic basis for coronary artery disease and early onset myocardial infarction. At the same time, colleagues at the Broad Institute were noticing that there are many additional features that you can get from the blood-based DNA that was being processed by the whole exome data. And there were actually three different groups that converged on that all in Boston that converged on the same observation that many well-established cancer causing mutations.(31:19):So mutations that are observed in cancers that have been described to drive the cancers themselves were being observed in these large population-based data sets that we were all generating to understand the relationship between loss of function mutations in cardiovascular disease. That's basically the intention of those data sets for being generated for other things. Strong correlation with age, but it was very common among individuals greater than 70; 10% of them would have these mutations and is very common because blood cancer is extremely, it's still pretty rare in the population. So to say 10% of people had cancer causing driver mutations but didn't have cancer, was much higher than anyone would've otherwise expected. In 2014, there were basically three main papers that described that, and they also observed that there is a greater risk of death. You'd say, okay, this is a precancerous lesion, so they're probably dying of cancer.(32:17):But as I said, the absolute incidence rate for blood cancer is really low and there's a relative increase for about tenfold, but pretty small as it relates to what could be related to death. And in one of the studies we did some exploratory analysis that suggested maybe it's actually the most common cause of death and that was cardiovascular disease. And so, a few years later we published a study that really in depth really looked at a bunch of different data sets that were ascertained to really understand the relationship between these mutations, these cancer causing mutations in cardiovascular disease, so observed it in enrichment and older individuals that had these mutations, CHIP mutations, younger individuals who had early onset MI as well too, and then also look prospectively and showed that it related to incident coronary artery disease. Now the major challenge for this kind of analysis as it relates to the germline genetic analysis is prevalence changes over time.(33:15):There are many things that could influence the presence of clonal hematopoiesis. Age is a key enriching factor and age is the best predictor for cardiovascular disease. So really important. So then we modeled it in mice. It was actually a parallel effort at Boston University (BU) that was doing the same thing really based on the 2014 studies. And so, at the same time we also observed when you modeled this in mice, you basically perturb introduce loss of function mutations in the bone marrow for these mice to recapitulate these driver mutations and those mice also have a greater burden of atherosclerosis. And Eric, you highlighted inflammation because basically the phenotype of these cells are hyper inflamed cells. Interestingly, C-reactive protein is only modestly elevated. So C-reactive protein is not fully capturing this, but many of the cytokines IL-1β, IL-6, they're all upregulated in mice and in humans when measured as well.(34:11):Now there've been a few key studies that have been really exciting about using anti-inflammatories in this pathway to address CHIP associated cardiovascular disease. So one that effort that I said in BU because they saw these cytokines increased, we already know that these cytokines have relationship with atherosclerosis. So they gave an NLRP3 inflammasome inhibitor to the mice and they showed that the mice with or without CHIP had a reduction in atherosclerosis, but there was a substantial delta among the mice that are modeled as having CHIP. Now, the investigators in CANTOS, the manufacturers, they actually went back and they survey where they had DNA in the CANTOS trial. They measured CHIP and particularly TET2 CHIP, which is the one that has the strongest signal for atherosclerosis. As I said, overall about 15% reduction in the primary outcome in CANTOS. Among the individuals who had TET2 CHIP, it was a 64% reduction in event.(35:08):I mean you don't see those in atherosclerosis related trials. Now this has the caveat of it being secondary post hoc exploratory, the two levels of evidence. And so, then we took a Mendelian randomization approach. Serendipitously, just so happens there is a coding mutation in the IL-6 receptor, a missense mutation that in 2012 was described that if you had this mutation, about 40% of people have it, you have a 5%, but statistically significant reduction in coronary artery disease. So we very simply said, if the pathway of this NLRP3 inflammasome, which includes IL-6, if you have decreased signaling in that pathway, might you have an even greater benefit from having that mutation if you had CHIP versus those who didn't have CHIP. So we looked in the UK Biobank, those who didn't have CHIP 5% reduction, who had that IL-6 receptor mutation, and then those who did have CHIP, if they had that mutation, it was about a 60% reduction in cardiovascular disease.(36:12):Again, three different lines of evidence that really show that this pathway has relevance in the general population, but the people who actually might benefit the most are those with CHIP. And I think as we get more and more data sets, we find that not all of the CHIP mutations are the same as it relates to cardiovascular disease risk. It does hone in on these key subsets like TET2 and JAK2, but this is pretty cool as a preventive cardiologist, new potential modifiable risk factor, but now it's almost like an oncologic paradigm that is being applied to coronary artery disease where we have specific driver mutations and then we're tailoring our therapies to those specific biological drivers for coronary artery disease. Hopefully, I did that justice. There's a lot there.Why Don't We Measure CHIP?Eric Topol (36:57):Well, actually, it's phenomenal how you've explained that, but I do want to review for our listeners or readers that prior to this point in our conversation, we were talking about germline mutations, the ones you're born with. With CHIP, we're talking about acquired somatic mutations, and these are our blood stem cells. And what is befuddling to me is that with all the data that you and others, you especially have been publishing and how easy it would be to measure this. I mean, we've seen that you can get it from sequencing no less other means. Why we don't measure this? I mean, why are we turning a blind eye to CHIP? I just don't get it. And we keep calling it of indeterminate potential, not indeterminate. It's definite potential.Pradeep Natarajan (37:51):Yeah, no, I think these are just overly cautious terms from the scientists. Lots of people have CHIP, a lot of people don't have clinical outcomes. And so, I think from the lens of a practicing hematologists that provide some reassurance on the spectrum for acquired mutation all the way over to leukemia, that is where it comes from. I don't love the acronym as well because every subfield in biomedicine has its own CHIP, so there's obviously lots of confusion there. CH or clinical hematopoiesis is often what I go, but I think continuing to be specific on these mutations. Now the question is why measure? Why aren't we measuring it? So there are some clinical assays out there. Now when patients get evaluated for cytopenias [low cell counts], there are next generation sequencing tests that look for these mutations in the process for evaluation. Now, technically by definition, CHIP means the presence of these driver mutations that have expanded because it's detectable by these assays, not a one-off cell because it can only be detected if it's in a number of cells.(38:55):So there has been some expansion, but there are no CBC abnormalities. Now, if there's a CBC abnormality and you see a CHIP mutation that's technically considered CCUS or clonal cytopenia of unknown significance, sometimes what is detected is myelodysplastic syndrome. In those scenarios still there is a cardiovascular disease signal, and so many of our patients who are seen in the cancer center who are being evaluated for these CBC abnormalities will be detected to have these mutations. They will have undergone some risk stratification to see what the malignancy potential is. Still pretty low for many of those individuals. And so, the major driver of health outcomes for this finding may be cardiovascular. So those patients then get referred to our program. Dana-Farber also has a similar program, and then my colleague Peter Libby at the Brigham often sees those patients as well. Now for prospective screening, so far, an insurance basically is who's going to pay for it.(39:51):So an insurance provider is not deemed that appropriate yet. You do need the prospective clinical trials because the medicines that we're talking about may have side effects as well too. And what is the yield? What is the diagnostic yield? Will there actually be a large effect estimate? But there has been more and more innovation, at least on the assay and the cost part of the assay because these initial studies, we've been using whole exome sequencing, which is continuing to come down, but is not a widely routine clinical test yet. And also because as you highlighted, these are acquired mutations. A single test is not necessarily one and done. This may be something that does require surveillance for particular high risk individuals. And we've described some risk factors for the prevalence of CHIP. So surveillance may be required, but because there are about 10 genes that are primarily implicated in CHIP, that can substantially decrease the cost of it. The cost for DNA extraction is going down, and so there are research tests that are kind of in the $10 to $20 range right now for CHIP. And if flipped over to the clinical side will also be reasonably low cost. And so, for the paradigm for clinical implementation, that cost part is necessary.Eric Topol (41:10):I don't know the $10 or $20 ones. Are there any I could order on patients that I'm worried about?Pradeep Natarajan (41:17):Not yet clinical. However, there is a company that makes the reagents for at least the cores that are developing this. They are commercializing that test so that many other cores, research cores can develop it. I think it's in short order that clinical labs will adopt it as well too.Eric Topol (41:36):That's great.Pradeep Natarajan (41:37):I will keep you apprised.What About Polygenic Risk Scores?Eric Topol (41:39):I think that's really good news because like I said, we're so darn lipid centric and we have to start to respect the body of data, the knowledge that you and others have built about CHIP. Now speaking of another one that drives me nuts is polygenic risk score (PRS) for about a decade, I've been saying we have coronary disease for most people is a polygenic trait. It's not just a familial hypercholesterolemia. And we progressively have gotten better and better of the hundreds of single variants that collectively without a parental history will be and independently predict who is at double, triple or whatever risk of getting heart disease, whereby you could then guide your statins at higher aggressive or pick a statin, use one or even go beyond that as we've been talking about. But we don't use that in practice, which is just incredible because it's can be done cheap.(42:45):You can get it through whether it's 23andMe or now many other entities. We have an app, MyGeneRank where we can process that Scripss does for free. And only recently, Mass General was the first to implement that in your patient population, and I'm sure you were a driver of that. What is the reluctance about using this as an orthogonal, if you will, separate way to assess a person's risk for heart disease? And we know validated very solidly about being aggressive about lipid lowering when you know this person's in the highest 5% polygenic risk score. Are we just deadheads in this field or what?Pradeep Natarajan (43:30):Yeah, I mean Eric, as you know, lots of inertia in medicine, but this one I think has a potential to make a large impact. Like CHIP mutations, I said news is about 10% in individuals greater than 70. The prospect here is to identify the risk much earlier in life because I think there is a very good argument that we're undertreating high risk individuals early on because we don't know how to identify them. As you highlighted, Dr. Braunwald about LDL cholesterol. The other part of that paradigm is LDL cholesterol lowering and the duration. And as we said, everybody would benefit from really low LDL cholesterol, but again, you might overtreat that if you just give that to everybody. But if you can better identify the folks very early in life, there is a low cost, low risk therapy, at least related to statins that you could have a profound benefit from the ones who have a greater conviction will have future risk for cardiovascular disease.(44:21):You highlighted the family history, and the family history has given the field of clues that genetics play a role. But as the genome-wide association studies have gotten larger, the polygenic risk scores have gotten better. We know that family history is imperfect. There are many reasons why a family member who is at risk may or may not have developed cardiovascular disease. A polygenic risk score will give a single number that will estimate the contribution of genetics to cardiovascular disease. And the thing that is really fascinating to me, which is I think some of a clinical implementation challenge is that the alleles for an individual are fixed. The genotyping is very cheap. That continues to be extremely cheap to do this test. But the weights and the interpretation of what the effects should be for each of the SNPs are continually being refined over time.(45:18):And so, given the exact same SNPs in the population, the ability to better predict cardiovascular diseases getting better. And so, you have things that get reported in the literature, but literally three years later that gets outdated and those hypotheses need to be reassessed. Today, I'll say we have a great relative to other things, but we have a great polygenic risk score was just reported last year that if you compare it to familial hypercholesterolemia, which has a diagnostic yield of about 1 in 300 individuals, but readily detectable by severe hypercholesterolemia that has about threefold risk for cardiovascular disease. By polygenic risk score, you can find 1 in 5 individuals with that same risk. Obviously you go higher than that, it'll be even higher risk related to that. And that is noble information very early in life. And most people develop risk factors later in life. It is happening earlier, but generally not in the 30s, 40s where there's an opportunity to make a substantial impact on the curve related to cardiovascular disease.(46:25):But there is a lot of momentum there. Lots of interest from NIH and others. The major challenge is though the US healthcare system is really not well set up to prevention, as you know, we practice healthcare after patient's developed disease and prevent the complications related to progression. The stakeholder incentives beyond the patient themselves are less well aligned. We've talked a lot here today about payers, but we don't have a single payer healthcare system. And patients at different times of their lives will have different insurers. They'll start early in life with their parents, their first employer, they'll move on to the next job and then ultimately Medicare. There's no entity beyond yourself that really cares about your longevity basically from the beginning and your overall wellness. That tension has been a major challenge in just driving the incentives and the push towards polygenic risk scores. But there are some innovative approaches like MassMutual Life Insurance actually did a pilot on polygenic risk scoring.(47:33):They're in the business of better understanding longevity. They get that this is important data. Major challenges, there are federal protections against non-discrimination in the workplace, health insurance, not necessarily life insurance. So I think that there are lots of things that have to be worked out. Everybody recognizes that this is important, but we really have to have all the incentives aligned for this to happen at a system-wide level in the US. So there's actually lots of investment in countries that have more nationalized healthcare systems, lots of development in clinical trials in the UK, for example. So it's possible that we in the US will not be the lead in that kind of evidence generation, but maybe we'll get there.The GLP-1 DrugsEric Topol (48:16):Yeah, it's frustrating though, Pradeep, because this has been incubating for some time and now we have multi ancestry, polygenic risk scores, particularly for heart disease and we're not using it, and it's not in my view, in the patient's best interest just because of these obstacles that you're mentioning, particularly here in the US. Well, the other thing I want to just get at with you today is the drugs that we were using for diabetes now blossoming for lots of other indications, particularly the glucagon-like peptide 1 (GLP-1) drugs. This has come onto the scene in recent years, not just obviously for obesity, but it's anti-inflammatory effects as we're learning, mediated not just through the brain but also T cells and having extraordinary impact in heart disease for people with obesity and also with those who have heart failure, about half of heart failure for preserved ejection fraction. So recently you and your colleagues recently published a paper with this signal of optic neuropathy. It was almost seven eightfold increase in a population. First, I wanted to get your sense about GLP-1. We're also going to get into the SGLT2 for a moment as well, but how do you use GLP-1? What's your prognosis for this drug class going forward?Pradeep Natarajan (49:55):As it relates to the paper, I can't claim credit as one of my former students who is now Mass Eye and Ear resident who participated, but we can talk about that. There's obviously some challenges for mining real world data, but this was related to anecdotes that they were observing at Mass Eye and Ear and then studied and observed an enrichment. In general though, I feel like every week I'm reading a new clinical trial about a new clinical outcome benefit as it relates to GLP-1 receptor agonists. This is kind of one thing that stands out that could be interrogated in these other clinical trials. So I would have that caveat before being cautious about ocular complications. But the data has been overwhelmingly beneficial, I think, because at minimum, obesity and inflammation are relayed to myriad of consequences, and I'm really excited that we have therapies that can address obesity that are safe.(50:52):There's a legacy of unsafe medicines for obesity, especially related to cardiovascular disease. So the fact that we have medicines that are safe and effective for lowering weight that also have real strong effects on clinical outcomes is tremendous. We in cardiology are increasingly using a range of diabetes medicines, including GLP-1 receptor agonists and SGLT2 inhibitors. I think that is also the secular changes of what influences cardiovascular disease over time. I talked about over the last 10 years or so with this increase in deaths attributable to cardiovascular disease. If you look at the influences of traditional clinical risk factors today, many of them have decreased in importance because when abnormal, we recognize them, in general we modify them when recognized. And so, many of the things that are unaddressed, especially the features related to insulin resistance, obesity, they start rising in importance. And so, there is a dramatic potential for these kinds of therapies in reducing the residual risks that we see related to cardiovascular disease. So I'm enthusiastic and excited. I think a lot more biology that needs to be understood of how much of this is being influenced specifically through this pathway versus a very effective weight loss medicine. But also interesting to see the insights on how the effect centrally on appetite suppression has profound influences on weight loss as well too. And hopefully that will lead to more innovations in weight management.The SGLT-2 DrugsEric Topol (52:25):And likewise, perhaps not getting near as much play, but when it came on the cardiovascular scene that an anti-diabetic drug SGLT2 was improving survival, that was big, and we still don't know why. I mean, there's some ideas that it might be a senolytic drug unknowingly, but this has become a big part of practice of cardiology in patients with diabetes or with preserved ejection fraction heart failure. Is that a fair summary for that drug?Pradeep Natarajan (53:00):Yeah, I totally agree. I mean, as there has been increased recognition for heart failure preserved ejection fraction, it has been almost disheartening over the last several years that we have not had very specific effective therapies to treat that condition. Now, it is a tremendous boon that we do have medicines interestingly focused on metabolism that are very helpful in that condition for heart failure with preserved ejection fraction. But there is still much more to be understood as far as that condition. I mean, the major challenge with heart failure, as you know, especially with heart failure preserved ejection fraction, it likely is a mix of a wide variety of different etiologies. So in parallel with developing effective therapies that get at some aspect is really understanding what are the individual drivers and then targeting those specific individual drivers. That requires a lot of unbiased discovery work and further profiling to be done. So lot more innovation, but relative to heart failure itself, it is not had widespread recognition as heart failure reduced ejection fraction. So much more to innovate on, for sure.Eric Topol (54:07):Right, right. Yeah, I am stunned by the recent progress in cardiovascular medicine. You have been center stage with a lot of it, and we've had a chance to review so much. And speaking of genetics, I wanted to just get a little insight because I recently came across the fact that your mother here at the City of Hope in Southern California is another famous researcher. And is that, I don't know what chromosome that is on regarding parental transmission of leading research. Maybe you can tell me about that.Pradeep Natarajan (54:41):Yeah, I mean, I guess it is a heritable trait when a parent has one profession that there is a higher likelihood that the offspring will have something similar. So both of my parents are PhDs, nonphysicians. There is a diabetes department at the City of Hope, so she's the chair of that department. So very active. We do overlap in some circles because she does investigate both vascular complications and renal complications. And then sometimes will ask my advice on some visualization. But she herself has just had a science translational medicine paper, for example, just a couple of months ago. So it's fun to talk about these things. To be honest, because my parents are researchers, I was not totally sure that I would be a researcher and kind of wanted to do something different in medicine. But many of my early observations and just how common cardiovascular disease is around me and in my community and wanting to do something useful is what got me specifically into cardiology.(55:45):But obviously there are numerous outstanding, important questions. And as I went through my career, really focused on more basic investigations of atherosclerosis and lipids. What got me excited sort of after my clinical training was the ability to ask many of these questions now in human populations with many new biological data sets, at least first centered on genetics. And the capabilities continue to expand, so now I teach first year Harvard medical students in their genetics curriculum. And when I talk to them just about my career arc, I do remind them they're all doing millions of things and they're exploring lots of things, but when they get to my shoes, the capabilities will be tremendously different. And so, I really advise them to take the different experiences, mainly in an exercise for asking questions, thoughtfully addressing questions, connecting it back to important clinical problems. And then once they start to understand that with a few different approaches, then they'll totally take off with what the opportunities are down the road.Eric Topol (56:51):No, it's great. I mean, how lucky somebody could be in the first year of med school with you as their teacher and model. Wow. Pradeep, we've really gone deep on this and it's been fun. I mean, if there's one person I'm going to talk to you about cardiovascular risk factors and the things that we've been into today, you would be the one. So thank you for taking the time and running through a lot of material here today, and all your work with great interest.Pradeep Natarajan (57:24):Thanks, Eric. I really appreciate it. It's tremendous honor. I'm a big fan, so I would be glad to talk about any of these things and more anytime.***************Thanks for listening, reading or watching!The Ground Truths newsletters and podcasts are all free, open-access, without ads.Please share this post/podcast with your friends and network if you found it informative!Voluntary paid subscriptions all go to support Scripps Research. 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We kicked off the program with four news stories and different guests on the stories we think you need to know about!World Lung Cancer Day is coming up (8/1), and only 6% of Americans eligible for screenings actually get them. Dr. Efren Flores - thoracic radiologist at Mass General Hospital joined Dan to discuss.Boneless Chicken Wings Can Have Bones After All, Ohio Supreme Court Rules! John Rizvi – The Patent Professor and Dan review this ruling.Survey: 70% of parents say back-to-school shopping is too expensive! Bill Dendy – Financial Strategist looked at the expenses. New England athletes as they go for gold in the Paris Olympics! More than 40 athletes with local roots or college ties will vie for glory in this year's Games. Amin Touri Boston Globe Multiplatform Editor and Web Producer checked in! Ask Alexa to play WBZ NewsRadio on #iHeartRadio!

On this episode of Ropes & Gray's podcast series, Decoding Digital Health, Christine Moundas, a health care partner and co-chair of the firm's digital health initiative, is joined by Dr. Bernardo Bizzo, a senior director at Mass General Brigham AI and assistant professor of radiology in the Department of Radiology at Mass General Hospital. Dr. Bizzo discusses his work in the field of digital health and AI, including the development and clearance of AI products by the FDA. They also explore the promising aspects of AI in health care and the challenges involved in developing and deploying AI tools. 

Food insecurity has been a growing problem in Massachusetts for years, especially since the start of the COVID pandemic. Inflation hasn't helped, with food prices skyrocketing at the grocery store and at local restaurants. A new report from the Greater Boston Food Bank in collaboration with Mass General Brigham takes a closer look at the factors driving this concerning trend. Catherine D'Amato, President and CEO of the Food Bank, and Dr. Lauren Fiechtner, Director of Nutrition at the Mass General Hospital for Children, break down the highlights of the report with Nichole and share resources for those who are in need.

Anna Handorf, MD, sheds light on the innovative concept of Tiny Talks in the latest episode of the Faculty Factory Podcast. Tiny Talks serve as a novel medical education tool, designed to deliver concise, impactful virtual chalk talks. Dr. Handorf spearheaded Tiny Talks to help residents overcome scheduling conflicts that often lead to missed educational opportunities. The core objective of Tiny Talks is to distill lengthy lectures into brief, engaging presentations lasting seven minutes or less. Dr. Handorf is an instructor at Harvard Medical School and a pediatric hospitalist at Newton Wellesley Hospital in Newton, Massachusetts. As a former medical education research fellow at Mass General Hospital and Harvard Medical School, she penned an insightful article titled “Let's Chalk About It: Introducing the TinyTalks Curriculum, a Paradigm for Short, Virtual Chalk Talks,” published in Academic Medicine in March 2024. In this week's Faculty Factory Podcast interview, Dr. Handorf elaborates on the structured approach, encompassing a hook, frame, and delivery, essential for crafting an effective Tiny Talk. Learn More Follow Dr. Handorf: https://x.com/AnnaHandorf Email: ahandorf@mgb.org Read the article from Academic Medicine: https://journals.lww.com/academicmedicine/abstract/9900/let_s_chalk_about_it__introducing_the_tinytalks.816.aspx?utm_source=sfmc&utm_medium=email&utm_campaign=amexpress&utm_content=newsletter

This week, Dr. Scott Sigman sits down with Dr. Kevin Raskin, Associate Professor and Chief of Oncology at Mass General Hospital. Here, they discuss his training in musculoskeletal oncology, the passion and team approach he shares with his patients, and more.

Curious about the forces driving healthcare pricing and access? Join us for an enlightening conversation with Sarah Emond, President and CEO of the Institute for Clinical and Economic Review (ICER). Sarah's upbringing in a family passionate about policy and social justice laid the foundation for her impactful career in health policy. We explore her educational journey from Smith College to Brandeis University's Heller School, and how her professional experiences in clinical research and biopharmaceutical consulting shaped her path to ICER.Unravel the complex world of health technology assessment (HTA) in the US as Sarah breaks down the challenges and opportunities within a fragmented healthcare system. ICER's pivotal role in evaluating new medical technologies is discussed in depth, including its interactions with international agencies like the UK's NICE. Sarah sheds light on ICER's evolution from a small initiative within Mass General Hospital to a powerful voice in global HTA practices, emphasizing the importance of fair pricing, patient access, and sustainable innovation funding.Equity in healthcare takes center stage as Sarah introduces ICER's updated value assessment framework. Learn about new tools like the clinical trial diversity rating and the Health Improvement Distribution Index (HIDI) designed to promote representation of diverse populations in clinical trials. We also tackle the high costs and value-based pricing of innovative treatments, including gene and cell therapies, and the necessity of evolving payment systems to ensure continuous innovation. Tune in to gain a comprehensive understanding of the pressing challenges and future directions in healthcare pricing, equity, and access.Host David E. Williams is president of healthcare strategy consulting firm Health Business Group. Produced by Dafna Williams.

Dr. Alessio Fasano, who is considered the world's leading expert in celiac disease and gluten-related disorders, returns for his second appearance on STEM-Talk. Although just 2 million Americans have celiac disease, an estimated 20 million Americans suffer from gluten sensitivity. Alessio is a professor and director of the Mucosal Immunology and Biology Research Center at Massachusetts General Hospital. In addition to celiac disease and gluten-related disorders, Alessio's research is also focused on the microbiome, intestinal permeability and autoimmune disorders, which he discussed in his first interview on STEM-Talk, episode 20. Since Alessio's first appearance on STEM-Talk in 2016, he has published two books, “Gluten Freedom” and “Gut Feelings: The Microbiome and Our Health,” which we discuss in today's interview. We also talk to Alessio about an exciting new project that's bringing together an international consortium of researchers and scientists for a long-term study that will follow infants who are genetically at risk of developing celiac. Alessio is a researcher and physician who wears many hats. He is the director of the Center for Celiac Research and Treatment and chief of the Division of Pediatric Gastroenterology and Nutrition at Mass General Hospital. He also is a professor of pediatrics at Harvard Medical School and a professor of nutrition at Harvard's T.H. Chan School of Public Health. Show notes: [00:03:58] Marcas opens the interview welcoming Alessio back to STEM-Talk, mentioning that since his last appearance he has written two books: Gluten Freedom and Gut Feelings: The Microbiome and Our Health. Marcas asks Alessio how he became interested in pediatrics and gastroenterology. [00:05:42] Ken mentions that Alessio moved to the U.S. in the 1990s and spent 20 years in Maryland at the Center for Vaccine Development in Baltimore. Ken goes on to mention that while Alessio was there, he founded The Center for Celiac Research in 1996, and in 2003, Alessio accepted an offer to join Massachusetts General Hospital. Ken asks how that move came about. [00:08:53] Marcas asks about Alessio's early career working on cholera, where he discovered the zonula occuldens toxin, the bacteria that causes cholera. Marcas asks Alessio to talk about this finding and the insights he gleaned from it. [00:16:03] Ken asks about Alessio's discovery of zonulin, which is the molecule that modulates gut permeability in humans. Ken asks Alessio to share how this discovery led him to investigate celiac disease, which is triggered by gluten. [00:20:25] Ken asks Alessio what his thoughts are on why the medical community, historically, has not taken celiac disease seriously. [00:24:08] Marcas mentions that as we age, there is evidence that the gut becomes leakier, which is highly related to chronic inflammation. Marcas asks Alessio whether this happens to the gut over time due to diet and lifestyle rather than the typical aging process. [00:28:45] Ken mentions that there has been an increase in the diagnosis of celiac disease. Ken asks Alessio if that is due to an actual increase in the prevalence of the disease, or is it tied to a growing appreciation that clinicians have now for the disease? [00:29:32] Marcas mentions that Alessio's book, Gluten Freedom, which he co-authored with his colleague Susie Flaherty, was referred to by the Celiac Disease Foundation as “a must have,” and “an excellent reference for those with gluten related disorders.” Marcas asks Alessio about this reception to his book. [00:31:24] Marcas mentions that the only viable treatment for individuals with celiac disease has been a gluten-free diet, with pharmaceutical companies having had little interest until recently in investigating the disease. Now there are more than 20 drug therapies in development for celiac. Marcas asks Alessio about the progress being made to develop pharmacological interventions for celiac.

DIPG: Eternal Hope versus Terminal Corruption Guests: Dean Fachon, author with wife Wendy Fachon Neil Fachon was a 19-year-old engineering-student at Northeastern University when he was diagnosed with Diffuse Intrinsic Pontine Glioma (DIPG), an inoperable brain stem cancer. His family was with him at Mass General Hospital when the neuro-oncologist said he had three months to live. “Six, if you start radiation.” With no time to lose, the family searched out every conceivable treatment, as quickly as possible. Neil chose to enroll in a clinical trial at the Burzynski Clinic in Houston. Though dogged by controversy throughout his career, Dr. Stanislaw Burzynski has achieved miraculous results treating many patients with “incurable” cancers, including some with DIPG. The medical system designed to protect patients like Neil instead proved as intractable as the disease in his brain. DIPG: Eternal Hope versus Terminal Corruption is the first book of a trilogy, covering the time from misdiagnoses to diagnosis, and from choosing and commencing treatment to being denied treatment. Through a long series of moves and counter moves, Neil was caught in the middle of a life and death chess game, against an opponent that was less than above board. This book is dedicated to everyone who feels abandoned by the very institutions we believed were established to safe guard our rights. Dean Fachon is publishing his son's story to commemorate Brain Tumor Awareness Month (May) and DIPG Awareness Day, which is May 17. Dean Fachon has a Bachelors Degree in English Literature from Colgate University and a Masters Degree in Technical Communication from Rensselaer Polytechnic Institute. He wrote technical publications for IBM and DEC, and is the author of Grand Illusion a treatise on fiat money. Dean's wife, Wendy,, is a writer for Natural Awakenings magazine, a contributing author of Shining a Light on Grief, Volume 2, author of The Difference Maker, and host of the Story Walking Radio Hour here on D7RN. DIPG: Eternal Hope versus Terminal Corruption DIPG, by author Dean Fachon is the 1st book of a trilogy, covering the time from misdiagnoses to diagnosis, and from choosing and commencing treatment to being denied treatment. Through a long series of moves and counter moves Neil, Dean's son was caught in the middle of a life and death chess game…https://dipgbook.com/ Call In and Chat with Deborah during Live Show: 833-220-1200 or 319-527-2638 Learn more about Deborah here:  www.lovebyintuition.com

“The first casualty of war is truth—the second is empathy. Empathy has to call for backup. The backup is in the form of radical empathy.” -Lou Agosta, Assistant Professor of Medical Education at Ross Medical University at Saint Anthony Hospital We have a difficult six months ahead of us. A contentious presidential election looms in the U.S., the world continues to be war-torn, and companies find themselves mired in social topics that threaten to win over one half of consumers or stakeholders while alienating the other half. Could consciously practiced empathy make the difference between community success and fragmented failure? Perhaps. Dr. Helen Riess is the Associate Clinical Professor of Psychiatry at Harvard Medical School and the Director of Empathy Research and Training in Psychotherapy Research group in the Department of Psychiatry at Mass General Hospital. She is also the author of a book called The Empathy Effect. She has studied not just the power of empathy, but also the ability to monitor it neuroscientifically. Dr Riess may have found proof of something that many leaders believe… empathy is not a soft skill after all. In this episode of the Art of Supply podcast, Kelly Barner focuses on empathy as a business strategy: A review of Dr. Riess' findings and what they teach us about the physical experience of empathy How empathy can not only be learned and improved over time, it can also be lost or diminished How an expanded understanding of empathy can affect our performance at work - and in life, too Links: Kelly Barner on LinkedIn Art of Supply LinkedIn newsletter Art of Supply on AOP Subscribe to This Week in Procurement

Do We Trust Jesus?Luke 5:4-5 “And when he had ceased speaking, he said to Simon, “Put out into the deep and let down your nets for a catch.” And Simon answered, “Master, we toiled all night and took nothing! But at your word, I will let down the nets.”I like this verse because it reminds me that I am not the only one who argues with the Lord. I am not the only one with a reply other than “Yes” when Jesus asks me to do something.  Simon had been out fishing all night and had not caught any fish. He was tired and, I am sure, very discouraged. Then Jesus asked him to push his boat back into the sea a bit so that Jesus could stand on it and talk to all those on the shore. Simon did so.Then, after Jesus had finished teaching those on the shore, He told Simon to go out into the deep and let down his nets for a catch. Can you imagine how frustrated Simon felt and how tired he probably was? He was washing his nets out to call it a day when Jesus climbed on His boat, and who knows how long Jesus preached before telling Simon to go out into the deep. Then He tells Simon to put his net out into the water again. Jesus is a carpenter, and Simon is a fisherman. I am sure He didn't understand why He should do what this man said, and yet He did it anyway and yielded more fish than their nets could hold, and the nets began to break. There were so many fish that they filled both boats so full that the boats began to sink.Have you ever been in a situation like this before? Have you ever felt like God or Jesus was asking you to do something you really didn't want to? There could be many reasons why we don't want to do what He asks us to do. Simon was tired and frustrated. He might have also felt that his efforts were in vain. But despite all these, he obeyed. This story reminds us that even when we are tired, frustrated, or feel like our efforts are in vain, we should still obey God's word, for He has a plan that we might not understand.In this verse, the Lord knew that if Peter obeyed him, he would catch more fish than He could have imagined. God knows the same thing about you and me. He knows that if we obey Him, he will provide more than we need, whether in our jobs, families, or friends. Where is God calling you?  What has He been asking you to do, and yet you have been ignoring Him because you have tried it before many times, and so you figure it won't work this time either? What areas of your life are you desperate to see change?In this verse, Peter is desperate to catch some fish and has tried all night with no luck. When he listened to the Lord and then saw how many fish they caught, he finally recognized Jesus for who he really was. Peter recognized Jesus as Lord. It says in verse 8, “But when Simon Peter saw it, he fell down at Jesus' knees, saying, “Depart from me, for I am a sinful man, O Lord.” Has Jesus ever helped you come face to face with your sinfulness? Has He ever answered one of your prayers in a way that there was no question it was God who answered that prayer?I have had this happen many times. I am grateful to my parents because they told us about times in their lives when this happened to them, and so I began to be aware of when it was happening in my life, too. We miss so much when we are not looking for it. When you intentionally try to see God working in your life, you will see God working in your life. Notice I didn't say you might see God. I am 100% confident that you will see it if you intentionally look for where God is working in your life. This is the main reason why I do Witness Wednesdays on this podcast. If you hear how God works in other people's lives, you will become more aware of how He works in your life, too!I can see how God worked his miracles in my son Noah's surgery and recovery. Actually, how we even discovered he needed surgery. Noah was having headaches, and they were treating them with medicine, and that wasn't really working. The neurologist ordered an MRI to ensure it wasn't too serious. If she hadn't ordered the MRI, she would have never found out that he had a Chiari malformation. You can only see them on an MRI. Then we were supposed to have surgery at a hospital that was an hour and 40 minutes away from our house. The surgeon could not get Noah on his surgical calendar until July. Noah wants to go to college in Europe at the end of the summer.We asked if they could put in a referral for Mass General Hospital, as it is less than an hour's drive. They put in the referral, and after we got the records transferred, they set up a pairing with a surgeon who does both pediatric and adult surgeries. They were able to get him scheduled within a few weeks. Also, they scheduled him for after spring break, so I was able to take Noah to England to look at some colleges. It was amazing timing that only God could have arranged.Then, on the day of the surgery, Noah had an awesome nurse who happened to be his birthday twin. She was so kind and distracted him from thinking about the surgery. The surgeon said it was an excellent surgery, and he thinks Noah will be very pleased with it. Noah was in the hospital for four days and was not really in much pain at all. He could walk the halls, get up and use the restroom, talk to the nurses. He thought he would be in bed for the first week or two when he came home. But he has felt great. He has had to sleep more than he wanted also, yet he was happy he was able to sit up in his computer chair for long periods of time without pain. He said he felt much better than he thought he would and that he is glad they did the surgery as he can feel that there is more room in the back of his head now.Praise God—He is so good. He not only helped arrange the surgery, the timing, and the doctor, but He also ensured a successful surgery and a painless and speedy recovery—just what we prayed for! I don't know what you are praying for or what you are waiting for. Whatever it is, I want you to know that God knows what it is, and He is working on it for you. He is figuring out how to get that for you in His perfect timing and also in accordance with your plans as well.God knew that Peter needed fish that day. He knew he was discouraged, tired, and probably angry. God cared about Peter's needs and Peter's wants. This miracle happened for two reasons. First, God cared about Peter and his needs and wants. Second, Peter let down the nets. Peter said yes. He didn't understand why he was doing it. He didn't know what Jesus knew. He did it because Jesus asked Him to, and because of that obedience, Jesus made it fruitful.What is Jesus calling you to do? Has He given you the answer to your problem, and yet you are afraid to let down your net? What if the answer to your prayers is on the other side of your obedience to do what Jesus is telling you to do? What if the thing getting in the way of you catching all the fish is your reluctance to obey Jesus? What if you took that step today and did what He has asked you to do? What could you catch in your net?Dear Heavenly Father, I ask you to bless everyone listening to this episode today. Lord, please show us what things you are calling us to do and then give us the grace to accomplish them. Help give us the courage to take that step of faith, trusting that you will fill our nets. We love you, Lord, and we are sorry for not doing as you ask. You are Lord of Lords and King of Kings, and we ask all of this in accordance with your will and in Jesus's holy name, Amen!Thank you so much for joining me on this journey to walk boldly with Jesus. Week 2 of our “Come as You Are” mentoring series is tomorrow. Last week, we looked at several scriptures showing that Jesus does not want perfection before He wants us to come to Him. He wants us to come to him just as we are. If you join mentoring today or tomorrow, you can join us for Week 2 of this series, and you will also get a link to watch previous mentoring sessions as well. I hope you will join us today! We had a great discussion after the mentoring session last week. I look forward to meeting you here again tomorrow. Remember Jesus loves you, just as you are, and so do I! Have a blessed day!Today's Word from the Lord was received in June 2023 by a member of my Catholic Charismatic Prayer Group. If you have any questions about the prayer group, these words, or how to join us for a meeting please email CatholicCharismaticPrayerGroup@gmail.com. Today's Word from the Lord is, “My children, when you are full of worry and fear, come to me. Give me your hand in trust, and I will help you. All your cares that you give to me I take care of in my time, not your time.” www.findingtruenorthcoaching.comCLICK HERE TO DONATECLICK HERE to sign up for Mentoring CLICK HERE to sign up for Daily "Word from the Lord" emailsCLICK HERE to sign up for free audio training about inviting Jesus into your daily lifeCLICK HERE to buy my book Total Trust in God's Safe Embrace

Dr. Lisa Wong joins us for Episodes 8...and 9! Marlon sits down with Dr. Lisa Wong, pediatrician, musician, arts advocate, and author. She is the Co-Founder of the Arts and Humanities Initiative at Harvard Medical School, pediatrician at Milton Pediatric Associates, and an assistant clinical professor of pediatrics at Harvard Medical School. Dr. Wong also co-founded and serves as associate co-director of the Arts and Humanities Initiative, and the former president and a current violinist in the Longwood Symphony Orchestra, Boston's medical community ensemble. 

America's military must return our service members back to society ready to lead. Special operators are given the best tools in the military to do their jobs. They're also completely immersed into the special forces lifestyle with almost no distractions. Yet when they leave service, they're often left to themselves to find the right tools and to figure out what training they need to be successful in the next chapter. Two of America's most important organizations have partnered to bring our Veterans the best tools and training all wrapped up into an immersive, life changing program. For the third episode of our 2023 Army Navy Game tailgate series Fran Racioppi sat down with retired Brigadier General Jack Hammond, CEO of Home Base. Home Base is founded and supported by the Boston Red Sox and Mass General Hospital; a formidable team dedicated to winning and solving the most complex challenges in medicine and athletic performance.Home Base provides leading edge clinical care to the medical challenges faced by our veterans; including the effects of prolonged blast exposure, mental trauma, diabetes and even cancer. Veterans train directly with the best medical and athletic performance professionals in the industry with one goal in mind; return our military personnel back to society ready to perform at the highest level and continue to lead others. Take a listen, watch or read our conversation…and whether you're from Beantown or not, this is a Red Sox game you want to be a part of. The Jedburgh Podcast and the Jedburgh Media Channel are an official program of The Green Beret Foundation. Learn more on The Jedburgh Podcast Website. Subscribe to us and follow @jedburghpodcast on all social media. Watch the full video version on YouTube. Highlights:0:00 Welcome to the Army Navy Game Tailgate3:50 Home Base is built by the Boston Red Sox & Mass General7:06 Two months of therapy in two weeks11:18 How Home Base is treating Operator Syndrome16:38 How to support Home Base17:50 Proven results of the programQuotes: “When you look at the opportunity with those two powerhouse organizations and what the potential is to actually bend the curve and make a difference; they had me at hello.” (5:30) “We have access to the best clinical resources in the world. Bar none.” (6:12) “We created this 14-day intensive clinical program…that compresses two years of therapy into two weeks.” (8:55)“We're gonna be able to figure out what are the downstream chronic illnesses associated with concussive injury.” (13:49) “If you don't have the tools to do a job, it's like a monkey trying to change a tire with a screwdriver.” (19:50)

What is silent reflux? Find out in this episode of the MindBodySpace podcast, hosted by Dr. Juna. Every last Friday of the month, she is joined by her guest Dr. April Hirschberg to discuss evidence backed ways to decrease stress and increase resilience. Dr. April is a board certified psychiatrist specializing in lifestyle and mind-body medicine at Mass General Hospital, Harvard Medical School. They delve into how stress management and healthy lifestyle choices play a critical role in combating mental and physical health issues. This episode particularly focuses on gastroesophageal reflux disease (GERD), its symptoms, consequences, and misdiagnosis. They share personal experiences and insights into how stress exacerbates digestive issues, the significance of the gut-brain axis, and the role of the enteric nervous system. Practical advice is offered on managing stress through breathing exercises, mindfulness, proper diet, hydration, and the importance of not eating late to prevent reflux. Additionally, they emphasize the critical nature of seeking medical advice for persistent symptoms and the benefits of incorporating movement and enjoyable activities into daily routines for overall well-being. 00:00 Unveiling the Mystery: Why Stop Eating Early? 00:16 Welcome to the MindBodySpace Podcast 00:21 Stress Management with Dr. Hirschberg 01:31 The Gut-Brain Connection and Stress Impact 01:47 Misdiagnosed Reflux 07:40 Lifestyle Changes and Managing Reflux 15:15 Mindful Eating and Stress Reduction Techniques 22:15 Embracing Movement and Self-Care for Digestive Health 27:32 Closing Thoughts and Encouragement --- Support this podcast: https://podcasters.spotify.com/pod/show/mindbodyspace/support

In this episode of Oncology Brothers, join hosts Drs. Rahul and Rohit as they dive into the management of colon cancer with special guest Dr. Aparna Parikh, a medical oncologist from Mass General Hospital. Dr. Parikh shares insights on the treatment algorithm for colon cancer, including the use of circulating tumor DNA and the latest advancements in treatment options. From localized disease to metastatic space, the discussion covers key aspects of managing colon cancer. Tune in to learn about the evolving landscape of colon cancer treatment and the importance of personalized patient-centered care. Don't miss out on this informative episode with the Oncology Brothers and Dr. Aparna Parikh!

Regardless of the underlying cause of spinal cord disease, we have many tools at our disposal to improve symptoms and function in these patients. Even better, technology in this area is advancing rapidly. In this episode, Lyell Jones, MD, FAAN, speaks with Kathy Chuang, MD, author of the article “Symptomatic Treatment of Myelopathy,” in the Continuum February 2024 Spinal Cord Disorders issue. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Chuang is an instructor in neurology at Harvard Medical School and assistant in neurology co-director at Paralysis Center, Massachusetts General Hospital and Spaulding Rehabilitation Hospital in Boston, Massachusetts. Additional Resources Read the article: Symptomatic Treatment of Myelopathy Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Transcript  Full transcript available on Libsyn   Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, a companion podcast to the journal. Continuum Audio features conversations with the guest editors and authors of Continuum, who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article by visiting the link in the show notes. Subscribers also have access exclusive audio content not featured on the podcast. As an ad-free journal entirely supported by subscriptions, if you're not already a subscriber, we encourage you to become one. For more information on subscribing, please visit the link in the show notes. AAN members, stay tuned after the episode to hear how you can get CME for listening. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum Lifelong Learning in Neurology. Today, I'm interviewing Dr Kathy Chuang, who has recently authored an article on symptomatic management of myelopathy in the latest issue of Continuum, on spinal cord disorders. Dr. Chuang is a neurologist and physical medicine and rehabilitation specialist at Mass General, where she serves as Co-Director of the MGH Paralysis Program and Chief of the Neuromuscular Rehabilitation Program. Dr Chuang, welcome, and thank you for joining us today. Would you introduce yourself to our listeners? Dr Chuang: Hi, my name is Kathy Chuang. As you said, I'm a neurologist at Mass General Hospital specializing in neuromuscular medicine, also physiatry, physical medicine, and rehab. And I'm glad to be here. Dr Jones: Thank you for joining us. Basically, if we want to know more about managing spinal cord disorders, we have come to the right person, right? Dr Chuang: I try to do my best with all patients - yep. Dr Jones: For our listeners who are new to Continuum, Continuum is a journal dedicated to helping clinicians deliver the highest quality neurologic care to their patients, and we do this with high-quality and current clinical reviews. For our long-time Continuum Audio listeners, you'll notice a few different things with our latest issue and series of author interviews. For many years, Continuum Audio has been a great way to learn about our Continuum articles. Starting with our issue on spinal cord disorders (this issue), I'm happy to announce that our Continuum Audio interviews will now be available to all on your favorite open podcast platform, with some exciting new content in our interviews. Dr. Chuang, your article is absolutely full of extremely helpful and clinically relevant recommendations for the treatment of myelopathy, regardless of the cause. If there were one single most important practice-changing recommendation that you'd like our listeners to take away, what would that be? Dr Chuang: I think the most important thing to take away is that spinal cord injury of any type spans so many organ systems, it is good to get people - or multidisciplinary care - involved early on. There's eighteen model systems for spinal cord injuries scattered across the US. Those can be great avenues of resources for patients and for practitioners, for people around. Physical medicine and rehab specialists (our physiatrists or spinal cord injury specialists) can be very useful. And then, also for each individual organ system, there are specialists involved. And so, having that multidisciplinary care is probably the most important thing for a patient that's suffering from myelopathy because every patient is different and coordinating that care is so important to them. Dr Jones: So, teamwork is probably the most important thing, and I think most of our listeners who have taken care of patients with spinal cord disorders realize that that's really key. Your article - it leads off with such a great review of one of the big problems with myelopathy, which is spasticity management. From a medication perspective, I think many of us struggle with the balance between controlling the spasticity and some of the side effects of those medications, like sedation. How do you walk that fine line, Dr. Chuang? Dr Chuang: Spasticity management, like everything else, is patient directed. It depends on what the patient is most complaining of. If a patient has spasticity but they're not actually having any complaints from it, we don't need to treat, because of fear of side effects. I tend to try to use focal procedures (like botulinum toxin injections) earlier on, in order to try and spare side effects of antispasticity medications. Use of other conservative therapies, like bracing, stretching, is very essential. Another thing to consider is that dantrolene doesn't usually have side effects - cognitive side effects, at least - and actually can be monitored pretty closely for hepatotoxicity, which is its major side effect. Other possibilities are the baclofen pumps, which can be very useful in patients with spinal cord injury because their spasticity is often more in their lower limbs than in their upper limbs. By using multimodality approaches, we can definitely limit the amount of cognitive side effects of medications. Dr Jones: That's fantastic. Do you start with that multimodal at the beginning, or do you step into it with one, then the other, then the other? Dr Chuang: I usually start off with a low-dose baclofen because they usually have generalized tone - first, in order to see if they have cognitive side effects with it and if so, at what dose. Also, so that insurers have a trial of some medication before we proceed to something as expensive as botulinum toxin injection. But yes, if there's significant focal spasticity, especially, I try to bring in botulinum toxin injections as early as possible, just because of the possibility of minimizing the effect. Dr Jones: That's a great point - that you can start these from multiple angles and start them early. And great point about dantrolene - I think the hepatotoxicity makes many of us nervous. But it's a key point there - that it can spare some of the cognitive side effects. Dr Chuang: Yes, and actually, it can be monitored pretty closely. As long as a patient has access to labs, we can check liver function tests weekly or every two weeks until you're on a stable dose, and after that, only at intervals. And it can be weaned off just as quickly. Dr Jones: Fantastic. Another issue that you cover really nicely in the article, that I think is an underrecognized complication of spinal cord diseases - neuropathic pain. What's your approach to that problem, Dr. Chuang? Dr Chuang: Neuropathic pain is very, very tough to treat a lot of times. I usually give the chance of gabapentin, pregabalin, and duloxetine early, just to see if we can start managing their pain early and to try to prevent potentiation of pain. But I also tend to try to get pain management specialists on early, and also keep in mind that there can be other causes of pain other than just the actual spinal cord injury itself. Because of deafferentation and reafferentation, patients may think of neuropathic pain, and it could be something as simple as appendicitis. If there's a change in pain, there always needs to be a workup for acute causes. Again, multidisciplinary treatment, especially with pain specialists, can be really helpful. Dr Jones: Great point about thinking of other causes, including appendicitis or the musculoskeletal things that I'm sure can be pain generators in this pain population, right? Dr Chuang: Yeah, it's very common. Patients can often fracture themselves just with a simple transfer and that can cause a huge flare-up of pain. So, not all pain should be just dismissed as being neuropathic or just from the spinal cord injury itself. Dr Jones: Great point - thank you. Another topic that you cover - that I think is mystifying to many of us - is the neurogenic bladder problems that occur in patients with myelopathy. You talk about the different types - how do you tell them apart? Dr Chuang: It's hard to tell them apart from a patient perspective because a patient will just say that they have difficulty with urination. With a spastic bladder or detrusor sphincter dyssynergia, oftentimes, patients will complain of a short stream and having to force things out. And with an atonic bladder or flaccid bladder, they have difficulty initiating a stream. What can be useful are postvoid residuals - where, if a patient is in the hospital, or if you have access to an ultrasound, or if they see a urologist - after they void, you measure the amount of urine left in their bladder. You can see whether it's a smaller amount, which is suggestive of a spastic bladder, versus a large amount, or an atonic or flaccid bladder. The standard procedure that's done to measure these are also urodynamic studies that are done, oftentimes, by urologists, where they can actually measure pressure volumes and oftentimes get EMG recordings of the actual bladder - the sphincters. Dr Jones: Perfect. When you do those postvoid residuals (easiest done with ultrasound), what's the general cutoff you use to say - that's a small amount that might be suggestive of a spastic bladder? Dr Chuang: I would say, probably less than a hundred. And then, if it was flaccid, more than five hundred. If there's in between, it may fall into either category. Dr Jones: Got it. When you think about neurogenic bladder, what are the treatment options? How do they vary between the different types that patients may have? Dr Chuang: If you have an atonic or flaccid bladder, the main possibilities for patients just are, oftentimes, Credé maneuvers (or pressure on the bladder) in order to try and help with the bladder to squeeze urine out. But a lot of times they need clean intermittent catheterization or maybe placement of a suprapubic catheter long term. For patients who have a spastic bladder or detrusor sphincter dyssynergia, we can use anticholinergic medications, like bethanechol, tolterodine - those medications - in order to try to relax the sphincter a little bit and then allow the urine to pass through. You can also have BOTOX injections to these sphincters of the bladder as well, which can be useful to relax them so that they can allow the urine to pass through. But a lot of times, a mainstay of treatment is intermittent catheterization, also for patients with severe detrusor sphincter dyssynergia, so that we can maintain small bladder volumes and not develop hydronephrosis, urinary tract infections, and complications of holding urine in the bladder. Dr Jones: Thanks for that, Dr. Chuang. Another part of your article that I thought was really fascinating, and probably will cover some new ground for our readers and listeners, is the use of nerve transfers or surgical treatment of weakness, basically. Tell us about that and how it's used in patients with myelopathy. Dr Chuang: For patients with myelopathy, it's used often in the upper extremities. If a patient has voluntary control of either elbow flexion or elbow extension (usually, elbow flexion), you can oftentimes have the ability to transfer nerves into the finger flexors and allow voluntary hand closure. If there's supination or wrist extension, you can oftentimes allow transfers of branches of the nerve - for example, from the supinator, or from the branch to the extensor carpi radialis brevis, into the finger extensor - so that, over a period of nine to twelve months, we'll be able to slowly regrow the nerve back in and allow the denervated muscle to become reinnervated with a voluntary controlled muscle and then restore voluntary finger extension, which can be extremely beneficial - just being able to voluntarily open and close their hands. Dr Jones: Right. And it sounds like the goal is really that functional use of grip and use of the upper limb. Not really so much for transfers, I imagine - is that not so much the goal? Dr Chuang: If there's less than antigravity strength of elbow extension and reasonable external rotation strength, you may be able to get elbow extension strong enough antigravity, and at that point a patient may be able to transfer independently - with a lot of training. Dr Jones: Wow, that's fantastic - thank you. There's lots of therapeutic options, really, for many of these complications, which I think is an important point for our readers and our listeners to take home. When you look into the future, Dr. Chuang, what do you see on the horizon as the next generation of care for patients with spinal cord disorders? Dr Chuang: I see a huge, expanding field, both of therapeutics - there are stem cell trials all over the world; there are neurorestorative hormones that are being tried. I'm very excited about the advent of robotics, with motors being basically shrunk down to the size of millimeters, and exoskeletons becoming lighter and lighter. I suspect that, long term, we'll be able to have robotic exoskeletons to be able to help patients walk and move their limbs normally. I know there are clinical trials right now involving orthoses that are controlled with brain interfaces that will hopefully help restore function in patients who need it. Dr Jones: It sounds like science fiction, but a lot of that technology exists now, right? Dr Chuang: Yes, it does. We definitely have prototypes of multigear hands with multiple directions. Now, the problem is trying to find the way to control these motors and to control these robotic hands and legs. Dr Jones: Caring for patients with myelopathy I imagine can be challenging, but I imagine it can also be quite rewarding. Tell us, Dr. Chuang, what drew you to this work specifically, and what do you find most exciting about it? Dr Chuang: I want to help people move better. I'm a physiatrist by training, and our job as physiatrist is to try to get people back to their activities of daily living as soon as possible; to try to remove any barriers to becoming active, independent people in their society. And so, I think that spinal patients that suffer from myelopathies or other spinal cord injuries have a lot of potential in the amount of activities that they can do and the way that they can contribute. I've seen patients who have been paralyzed and unable to move their hands at all develop tenodesis scripts, initially in order to just pick up things and then later obtain voluntary control of opening and closing their fingers. And it's huge in terms of what they can do in their everyday lives. Just being able to see that is just really rewarding. And even being able to help patients navigate society around them is just a hugely rewarding experience. Dr Jones: I imagine that must be really fantastic to see folks regain those milestones. Dr Chuang: Yes. Dr Jones: It's pretty unusual for someone to have done a neurology and a physiatry residency. So, between me and you and all of our listeners, which residency was better? Dr Chuang: Wouldn't trade one without the other. Probably wouldn't have done the one without the other, either! Dr Jones: What a great, diplomatic answer. Okay, good. Dr Chuang: It's true. Dr Jones: Yeah. You avoided offending all the neurologists and physiatrists out there. And really fascinating discussion, Dr. Chuang. It's an outstanding article. I think it's a must-read for anyone who takes care of patients with spinal cord disorders. I want to thank you Dr. Wang for joining us and for such a thoughtful, fascinating discussion on symptomatic management of spinal cord disorders. Dr Chuang: Thank you, Dr. Jones for having me today. Dr Jones: Again, we've been speaking with Dr. Kathy Chuang, author of an article on symptomatic treatment of myelopathy in Continuum's most recent issue on spinal cord disease - please check it out. And thank you to our listeners for joining today. Dr. Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, please consider subscribing to the journal. There's a link in the episode notes. We'd also appreciate you following the podcast and rating or reviewing it. AAN members, go to the link in the episode notes and complete the evaluation to get CME for this episode. Thank you for listening to Continuum Audio.

He has a miraculous health-related story. On the sports side, he played football in high school and college, including in the Glenwood Football League and training camp with the New York Jets' farm team. During his first two years he became the best table tennis player in college. As a Pulmonary Fellow at Mass General Hospital, he worked with some of the world-class runners competing from the Boston Marathon. He is the author of a novel called, "A Man Like You and Me: A Supernatural Adventure Story," whose purpose, he says, is to increase faith in God in the reader, and is about supernatural events that started in his life in 1982.

Welcome to Episode 27 of the 2DocsToc Podcast, where we learn the vast effects of stress on the mind and body, along with how to help manage that stress with, Dr, Sheila Bee. Here's what you'll discover in this episode! Introduction: we sit down with Dr. Sheila Bee, an internist from Colorado Springs, who has taken a new step by incorporating lifestyle medicine and stress management into her practice. Main Themes: Pivot to Lifestyle Medicine: Dr. Sheila Bee shares her journey from traditional healthcare to a practice focused on preventive measures. She expresses concern about the conventional system's neglect of prevention and the impact this has on patient health. Understanding Stress: The discussion breaks down the concept of stress, differentiating between the positive aspects of stress and the damaging effects of toxic stress. Listeners will gain insights into how stress can transition from being helpful to harmful. Holistic Stress Management: Dr. B highlights her stress management program, which includes meditation techniques. The conversation covers the necessity of a holistic approach to health, touching upon critical components such as sleep, social connections, diet, exercise, and mindful substance use. The Evolution of Stress: Stress is explored from an evolutionary standpoint, originally serving as a survival mechanism, and its evolution to address modern triggers like overcommitment and uncertainty. Mindset Matters: The power of mindset is a key theme, with Dr. B explaining how one's perception of situations can determine whether they are seen as opportunities for growth or as threats. Additional Resources: The episode highlights the SMART course (Stress Management and Resiliency Training) from the Benson Henry Institute at Harvard Medical School and Mass General Hospital. This eight-week program aims to elicit the relaxation response with proven strategies. Personalization in Stress Management: Emphasizing adaptability, the program caters to individual needs and can be undertaken alone or in a group setting, featuring stress awareness activities and coping logs. Mindset's Role in Stress Response: Dr. Bee and the hosts discuss the significance of mindset in shaping our physiological stress response, reinforcing the theme of perception's power over our well-being. Conclusion: In summary, this episode sheds light on the vital role of stress management and lifestyle medicine in modern healthcare. Dr. Sheila Bee's insights offer a paradigm shift towards a more proactive, preventive, and personalized approach to health. Subscribe to Two Docs Talk for more insightful discussions on health, wellness, and the future of medicine. Our Website: ⁠2docstoc.com⁠ ⁠rob@2docstocpodcast.com⁠ This podcast is provided for informational purposes only, it is not medical advice. --- Send in a voice message: https://podcasters.spotify.com/pod/show/2docstoc/message

Tune in for a deep chat about psychedelic research, psychedelic assisted therapies, trauma healing, and more! Our guest Elowyn Samadhi, PhD (she/they) is a licensed clinical psychologist who specializes in the treatment of PTSD and other trauma-related disorders. She works in private practice and at Sage Integrative Health, a holistic psychedelic clinic in the Bay Area. Elowyn served as an independent rater for the Phase II and III MAPS MDMA trials for 4 years and began providing post-IV ketamine integration in 2015 at Mass General Hospital. She completed ketamine-assisted psychotherapy training with Polaris Insight Center and the MAPS MDMA-Assisted Therapy training. She also completed the UC-Berkeley Psilocybin Advanced Facilitator Training under the mentorship of Dr. Susana Bustos and is qualified to provide legal psilocybin services in Oregon. Dr. Samadhi serves as lead psilocybin therapist for the UCSD phantom limb pain clinical trial and has trained several of the co-therapists. She has guest lectured for Alchemy Community Therapy Center in Oakland and Beckley Academy, and supervises and mentors several psychedelic therapists-in-training. Elowyn is in her final year of the 3-year Somatic Experiencing training. Dr. Samadhi has a passion for teaching somatic therapy, safe and reparative touch work, as well as the ritual and spiritual praxis of guiding. Elowyn is biracial and bisexual and the bedrock of her spiritual path is non-dual, tantric, animistic, and pagan. We talk about psychedelic assisted healing modalities, the current research on psychedelics, MAPs, neuroplasticity, trauma healing,   Elowyn: https://www.elowynsamadhiphd.com/ https://tetheredhealing.com/   Past episode mentioned: https://slutsscholars.libsyn.com/198-the-war-on-drugs-with-ifetayo-harvey-of-thepoc-psychedelic-collective     FOLLOW US  Twitter Instagram Facebook Send questions, comments, stories, rants to: SlutsAndScholars@gmail.com Sluts And Scholars is a production of sluts and scholars media.   Loving disclaimer:  Sluts and Scholars is a podcast produced by Sluts & Scholars Media, LLC. It is a shame free educational podcast made for your entertainment and informational desires only. The podcast, any opinions we share, and any resources including social media and emails from us are not therapy, medical care or professional advice and do not create a patient-client relationship. None of the information, opinions, suggestions, resources or exercises mentioned in this podcast should be used without clearance from your health care provider. All opinions, information and ideas expressed by the guests are solely their own. If you need emergency mental health or medical help, please call 911 or 988 or go to your nearest emergency center. We hope you enjoy the show. 

Prebiotics! Probiotics! Symbiotics! Postbiotics! WHAT DOES IT ALL MEAN? Where are all of these "biotics" all living?? Well, the short answer is- they're living inside YOU! Talk about the human gut microbiome is everywhere. We thought it would be helpful to have our expert in gut health, Alessio Fasano, MD to give us insights on the microbiome, and how important it is to our health. You may remember Dr. Fasano from Episode 40- "Is Gluten Bad For Me?"! Dr. Alessio Fasano is a pediatric gastroenterologist, research scientist, and entrepreneur. He is the Chief of Pediatric Gastroenterology and Nutrition at Mass General Hospital for Children. Learn more about Dr. Fasano and his research about celiac disease, gluten sensitivity, and the microbiome here. Link to information on Dr. Fasano's book (with co-author Susie Flaherty) "Gut Feelings: The Microbiome and Our Health". Topics covered in this episode include: What is the gut microbiome? Why is it important? How does the gut microbiome work? What factors influence the composition of the gut microbiome? How can I improve my gut microbiome? What is the connection between the gut microbiome and digestion? Can the gut microbiome affect my mental health? Are there links between the gut microbiome and certain diseases? How can I measure or analyze my gut microbiome? Can I restore my gut microbiome after taking antibiotics? Is the gut microbiome different in individuals of different ages? Can I customize my diet for a healthier gut microbiome? What is the difference between prebiotics/probiotics/symbiotics and postbiotics? Thanks for tuning in, folks! and please sign up for our "PULSE CHECK" monthly newsletter! Signup is easy, right on our website page, and we PROMISE we will not spam you! We just want to send you cool articles, videos and thoughts :) For more episodes, limited edition merch, or to become a Friend of Your Doctor Friends (and more), follow this link! This includes the famous "Advice from the last generation of doctors that inhaled lead" shirt :) Also, CHECK OUT AMAZING HEALTH PODCASTS on The Health Podcast Network   Find us at: Website: yourdoctorfriendspodcast.com  Email: yourdoctorfriendspodcast@gmail.com  Connect with us: @your_doctor_friends (IG) Send/DM us a voice memo/question and we might play it on the show! @yourdoctorfriendspodcast1013 (YouTube) @JeremyAllandMD (IG, FB, Twitter) @JuliaBrueneMD (IG) @HealthPodNet (IG)

When Jesse Janelle was in elementary school, she experienced a lot of anxiety. When feeling panicked, she went to the nurses' office, visiting there regularly. Jesse didn't know it then, but this is where her personal and professional development journey began. One day, 11-year-old Jesse was in the nurse's office having a particularly bad panic attack. The nurse called in the guidance counselor, who was asked to help sometimes. Jesse must have been extra anxious this time because the guidance counselor shook her by the shoulders and yelled, “Stop it right now,” in her face. At that moment, Jesse became disassociated from her body. Her thoughts separated from her ‘felt sense': her ability to know what was happening in her body. Jesse later understood this to be her sense of self-trust. Going into high school and then college, Jesse was high-performing. Attending Boston College, she got straight A's. Because she wasn't feeling connected to her body, she intellectualized many of her struggles. Jesse studied psychology and meditation, attaching deep academic and intellectual perspectives to those arenas. Around her graduation from college, Jesse began to connect with those areas in a felt way, enabling her to be more in touch with who she really was. Jesse's professional career began as an intern at Harvard Medical School's Institute of Coaching in its founding years, where she got immersed in evidence-based coaching research. As her experience and expertise grew, she consulted and coached leaders in top organizations such as McKinsey, Mass General Hospital, The Walt Disney Company, and Amazon.  Today, Jesse is the founder and CEO of . She is an ICF-certified transformational coach and speaker. Jesse has distilled her learnings from her work in leadership development, psychology, ontology, somatics, and spirituality into a coaching method she calls Soul Sessions. This method is grounded in metaphor coaching and intuitive inquiry. This method can be learned and applied independently of a professional coaching session. Using a surprising tool, tarot cards, Jesse helps professionals access and unlock the power of their intuition to make better decisions faster. In this week's learn more about Jesse's journey: Jesse was selected in 2022 for the inaugural cohort of Forefront, powered by Marshall Goldsmith and the 100 coaches, for her impact on the field of leadership development. In 2023, she delivered her TEDx talk, .   Learn more and connect with Jesse here:  Save 7 hours a week with a 7-minute daily tarot self-coaching practice:

Dr. Elizabeth Mort, Primary Care MD and Associate at Mass General Hospital discusses patient safety in the US, challenges faced during the pandemic, the roles C-suite executives in enhancing patient safety, AI in healthcare, and the role of organizational culture.

Elizabeth is thrilled to welcome back Dr. Uma Naidoo, a true triple threat bridging the realms of food and medicine. As a Harvard-trained psychiatrist, professional chef, and nutrition specialist, Dr. Uma is a pioneering force in the field. Her groundbreaking work includes founding and directing the first hospital-based nutritional psychiatry service in the United States and holding the position of Director of Nutritional and Lifestyle Psychiatry at Mass General Hospital, coupled with a faculty role at Harvard Medical School. Dr. Uma, celebrated as Harvard's Food Mood expert, is also the best-selling author of "This is Your Brain on Food."In this episode, Dr. Uma talks about the profound connection between food and mental health, offering an approachable and science-backed method to alleviate anxiety. Ahead of the launch of her latest book, "Calm Your Mind with Food," she shares some of the latest research unraveling the intricate relationship between anxiety, the brain, gut, immune system, and metabolism. Dr. Uma also talks about some easy swaps we can make to feel better using the C.A.L.M approach and a few of her favorite healing foods that she always keeps in her personal kitchen. Episodes Here Say Hi To Elizabeth and Purely Elizabeth: Website | InstagramDr. Uma: Website | IG | Calm Your Mind with Food | This is Your Brain On Food Mentioned: 2021 Episode with Dr. Uma American Psychological Association  Midsomer Murders The 7 Spiritual Laws of Success 

Often podcasts meet clinical reality.  That's why we do this podcast- to address real world issues in palliative care, geriatrics, and bioethics.  But rarely does the podcast and clinical reality meet in the same day. Within hours of recording this podcast, I joined a family meeting of an older patient who had multiple medical problems including cancer, and a slow but inexorable decline in function, weight, and cognition.  Physical therapy had walked with him that day and noted improvement compared to previous walks, suggesting that he should be discharged to a skilled nursing facility for rehabilitation on discharge.  The patient's capacity to make decisions was marginal, and his sons were shouldering much of the responsibility. The sons were very focused on rehabilitation, and the patient gave his assent. In the meeting, I used the language suggested by Sarguni Singh, “I worry that going to SNF for rehab may not result in your being independent.”  We additionally discussed hospice care as an option for care that might follow the trial of rehabilitation. Today we talk with Sarguni Singh, hospitalist-researcher at the University of Colorado, Ann Henshaw, Occupational Therapist who teaches at George Washington and works clinically at Georgetown, and Tamra Keeney, Physical Therapist-researcher at Mass General Hospital and Harvard Medical School.  Lynn Flint, author of the NEJM perspective titled, “Rehabbed to Death,” joins Eric and I as co-host. We cover a lot of ground in this podcast, including an evidence based toolkit to promote collaboration between therapy fields and palliative care, outcomes of rehabilitation for people with advanced cancer (hint: not much hospice, lots of re-hospitalization), and a JAGS study on use of post-acute care among patients with heart failure.  We also heard from Tamra about her opinion piece in which she laments, “The role of rehabilitation is often myopically constrained to facilitation of efficient discharge planning.”  Therapists are so much more. At the end of the day, I lamented that physical, occupational, and speech therapists aren't more tightly integrated with palliative care teams.  As Lynn says at the end of the podcast, to paraphrase, “Physical therapy, occupational therapy, speech therapy - all this therapy for older frail patients is a core part of good palliative care.” And our guests sing along with “Sweet Caroline” - so good, so good, so good! -@AlexSmithMD   This episode of the GeriPal Podcast is sponsored by UCSF's Division of Palliative Medicine, an amazing group doing world class palliative care.  They are looking for physician faculty to join them in the inpatient and outpatient setting.  To learn more about job opportunities, please click here: https://palliativemedicine.ucsf.edu/job-openings