Podcasts about Colchicine

Colchicine

Do you use colchicine for acute gout flares?  Are you aware of the risk factors for toxicity?   Check out the Prescriber update for March 2025     www.rnzcuc.org.nz podcast@rnzcuc.org.nz https://www.facebook.com/rnzcuc https://twitter.com/rnzcuc   Music licensed from www.premiumbeat.com Full Grip by Score Squad   This podcast is intended to assist in ongoing medical education and peer discussion for qualified health professionals.  Please ensure you work within your scope of practice at all times.  For personal medical advice always consult your usual doctor 

Little Miss Innocent: Passion. Poison. Prison. Kimberly. Katie. Uneducated. Opinions. Judgmental. Chiropractor. Messy. Car. Messy. Case. Anonymous. Letter. Colchicine. Email. Framing. Affair. Screenshots. Receipts. Timeline. Sister. Opinions. Supplements. One. Question. Who killed Mary Yoder?! Official Description from Hulu: Kaitlyn Conley, a 31-year-old former receptionist, claims she has been wrongfully convicted of the 2015 killing of Mary Yoder, her former boss and the mother of her ex-boyfriend Adam. Get spicy without anyone getting murdered. Check out Dipsea sexy stories! Right now, listeners of this show can get an extended 30-day free trial! Just go to DipseaStories.com/ DATEDATELINE to start your free trial! Upgrade your sleep during Boll & Branch's Annual Spring Event! For a limited time get 20% off at BollAndBranch.com/datedateline. Exclusions apply. See site for details. To advertise on this podcast please email: ad-sales@libsyn.com   Or go to:  https://advertising.libsyn.com/ADatewithDateline Learn more about your ad choices. Visit podcastchoices.com/adchoices

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on Potential Impact of Colchicine on Atherosclerotic Cardiovascular Disease in the United States

Contributor: Aaron Lessen, MD Educational Pearls: Colchicine is most commonly used for the prevention and treatment of gout There is research investigating the anti-inflammatory and cardioprotective effects of colchicine  This drug has a narrow therapeutic index: a small margin between effective dose and toxic dose Colchicine overdoses can be unintentional or intentional and are associated with poor outcomes Phase 1: 10 - 24 hours after ingestion Patient looks well but may have mild symptoms mimicking gastroenteritis Phase 2: 24 hours - 7 days after ingestion Multiple organ dysfunction syndrome (MODS) Phase 3: recovery is usually within a few weeks of ingestion Treatment for colchicine overdose Treat early and aggressively Gastrointestinal decontamination with activated charcoal and orogastric lavage  Dialysis and ECMO for MODS treatment References Finkelstein Y, Aks SE, Hutson JR, Juurlink DN, Nguyen P, Dubnov-Raz G, Pollak U, Koren G, Bentur Y. Colchicine poisoning: the dark side of an ancient drug. Clin Toxicol (Phila). 2010 Jun;48(5):407-14. doi: 10.3109/15563650.2010.495348. PMID: 20586571. Gasparyan AY, Ayvazyan L, Yessirkepov M, Kitas GD. Colchicine as an anti-inflammatory and cardioprotective agent. Expert Opin Drug Metab Toxicol. 2015;11(11):1781-94. doi: 10.1517/17425255.2015.1076391. Epub 2015 Aug 4. PMID: 26239119. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

The CLEAR SYNERGY (OASIS 9) Trial: A 2x2 Factorial Randomized Controlled Trial of Colchicine versus placebo and Spironolactone versus placebo in Patients with Myocardial Infarction.

CLEAR SYNERGY (OASIS 9): A 2x2 Factorial Randomized Controlled Trial of Colchicine Versus Placebo and Spironolactone Versus Placebo in Patients with Myocardial Infarction

Tapinarof trials for AD - Minoxidil kills cats - Colchicine for aphthous stomatitis - Onychopapillomas and BAP1 - Physicians compensation models: Important and overlooked - To sign up for Luke's atopic dermatitis CME activity, go to: impactedu.gathered.com/invite/4QbYEVpbzq Want to donate to the cause? Do so here!
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1st AHA 2024: OASIS 9 Trial

Co-STAR: Colchicine in Patients with Aortic Stenosis Undergoing Transcatheter Aortic Valve Replacement: A Double-Blind Randomized Controlled Trial

Thank you for joining us for another episode of the Low Carb MD Podcast. Dr. Mohammed Alo is a cardiologist based out of northwest Ohio. Dr. Alo grew up in Toledo, Ohio, attended St. John's Jesuit High School and then went on to complete an Economics degree and graduated Magna Cum Laude from the University of Toledo. He worked in politics, business, computers, sales, and networking and then went to medical school in Chicago at Midwestern University's Chicago College of Osteopathic Medicine. He has a passion for teaching and travels the country giving talks on various topics. Most of his lectures focus on teaching other physicians on various cardiology topics that span a wide gamut of topics from cardiology, to health and fitness, to diet and weight loss. Dr. Alo has countless research publications and articles in scientific, peer-reviewed journals. He's had thousands of articles published in magazines in print and online. In this episode, Drs. Tro and Mohammed talk about… (01:29) Why Dr. Mohammed chose to go into medicine and become a doctor (05:10) What Drs. Tro and Mohammed agree about (11:32) The genetics of familial hypercholesterolemia patients, how these patients are treated, and the health complications they face (23:41) Lifelong lowering of lipids, atherosclerosis, preventing atherosclerosis, and when to consider using medication (33:04) CCT scans, LDL, and high LDL's association with atherosclerosis (42:05) The power of zero study and coronary artery calcium in cardiac risk assessment (45:12) Tro's LDL levels and atherosclerotic/cardiac event risk (59:09) The findings of the ACCORD trial which studied the effects of intensive glucose lowering in the management of patients with type 2 diabetes mellitus (01:08:22) Pros and cons of statins and other drugs (01:16:04) Smoking and endothelium destruction; diabetes and cardiovascular risk (01:20:50) Whether or not plaque can be reduced/reversed (01:24:20) Fish oil pills, Colchicine, and cardiac health (01:30:03) Summing up points of disagreement as well as common ground For more information, please see the links below. Thank you for listening!   Links:   Dr. Mohammed Alo: Website: https://mohammedalo.com/ YouTube: https://www.youtube.com/user/TheMohammedAlo Cholesterol TRUTHS (book): https://www.dralo.net/cholesterol   Dr. Brian Lenzkes:  Website: https://arizonametabolichealth.com/ Twitter: https://twitter.com/BrianLenzkes?ref_src=twsrc^google|twcamp^serp|twgr^author   Dr. Tro Kalayjian:  Website: https://www.doctortro.com/ Twitter: https://twitter.com/DoctorTro Instagram: https://www.instagram.com/doctortro/ SMHP Position Statement: https://journalofmetabolichealth.org/index.php/jmh/article/view/100#:~:text=The%20SMHP%20recommends%20open%20access,research%20on%20TCR%20for%20T1DM   Toward Health App Join a growing community of individuals who are improving their metabolic health; together.  Get started at your own pace with a self-guided curriculum developed by Dr. Tro and his care team, community chat, weekly meetings, courses, challenges, message boards and more.    Apple: https://apps.apple.com/us/app/doctor-tro/id1588693888  Google: https://play.google.com/store/apps/details?id=uk.co.disciplemedia.doctortro&hl=en_US&gl=US Learn more: https://doctortro.com/community/ 

In this episode, Dr. Paul Ridker, a pioneer in the field of cardiovascular inflammation, joins the CardioNerds (Dr. Gurleen Kaur, Dr. Richard Ferraro, and Dr. Nidhi Patel) to discuss the evolving landscape of inflammation as a key factor in cardiovascular risk reduction. The discussion dives into the importance of biomarkers like high-sensitivity C-reactive protein (hs-CRP) in guiding treatment strategies, the insights gleaned from landmark trials like the JUPITER and CANTOS studies, and the future of targeted anti-inflammatory therapies in cardiology. Show notes were drafted by Dr. Nidhi Patel. Audio editing by CardioNerds academy intern, Grace Qiu.  This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Targeting Inflammation for Cardiovascular Risk "If you don't measure it, you can't treat it”: Incorporate hs-CRP into routine practice for patients at risk of cardiovascular events, as it provides crucial information for risk stratification and management. Recognize the dual benefits of statins in lowering both LDL and inflammation, particularly in patients with elevated hs-CRP. Encourage patients to adopt heart-healthy habits, as lifestyle changes remain foundational in reducing both cholesterol and inflammatory risk. Reminder that most autoimmune or inflammatory diseases, from psoriasis to Addison's disease to lupus to scleroderma to inflammatory bowel disease, have been shown to have elevated cardiovascular risk Ongoing randomized trials including ZEUS, HERMES, and ARTEMIS will inform whether novel targeting of IL-6 can safely lower cardiovascular event rates or slow renal progression Show notes - Targeting Inflammation for Cardiovascular Risk Why is it important to measure both LDL and hs-CRP, and what factors increase hs-CRP? Inflammation and hyperlipidemia are synergistic in promoting atherosclerosis. They interact to exacerbate plaque formation and instability, increasing the risk of cardiovascular events. Just like we measure blood pressure and LDL to know what to treat, we should measure hs-CRP to guide targeted therapy. Clinical Example: in Ms. Flame's case, despite achieving target LDL levels with statins, her elevated hs-CRP indicates ongoing inflammation and residual cardiovascular risk that should be assessed. Residual inflammatory risk should be assessed in both primary and secondary prevention. Increased BMI1, smoking2, a sedentary lifestyle3, and genetics4 (such as a higher risk of metabolic disease in South Asians) all raise hs-CRP levels. SGLTi5 and GLP-1 agonists6 have also been shown to decrease hs-CRP levels. What data do we have to support measuring hs-CRP?  Women's Health Study7: an early study showing that hs-CRP predicted risk at least as well as LDL cholesterol and that models incorporating hs-CRP in addition to lipids were significantly better at predicting risk than models based on lipids alone. JUPITER Trial8 (Primary Prevention): Among patients with normal LDL but elevated hs-CRP there was a 44% reduction in major cardiovascular events (>50% in MI and stroke) and a 20% reduction in all-cause mortality in patients treated with statins. These results led to changes in guidelines in recognizing the need to measure and treat inflammation. CANTOS Trial9 (Secondary Prevention): Randomized >10K patients with previous MI and hs-CRP ≥ 2mg/L and found that canakinumab reduced hs-CRP level from baseline in a dose-dependent manner, without reduction in the LDL, ApoB, TG, or blood pressure. What are the guidelines and supportive data on using Colchicine? 

On this episode of the Real Life Pharmacology podcast, we cover 5 more medications in the top 200. Metronidazole is an antibiotic for infection. One of the most common complaints from patients involves reporting of a metallic taste in the mouth. Levetiracetam is an anti-seizure medication. Sedation, dizziness, and other adverse effects of the central nervous system are the most common complications. Colchicine is a gout medication. The most memorable side effect associated with this medication is diarrhea. Olanzapine is an antipsychotic. Olanzapine carries a higher risk for metabolic syndrome compared to other antipsychotics. Dutasteride is a 5 alpha-reductase inhibitor that is indicated for the treatment of BPH. If you are looking for all of our study materials and Amazon books, check them out at Meded101.com/store!

In this episode of Hart2Heart with Dr. Mike Hart is joined by Dr. Anish Koka to a cardiologist based in Pennsylvania. They dive deep into a range of topics related to cardiology, focusing on cardiac health, the impacts of the C19Vax on the heart, and the potential benefits of various blood markers in assessing heart disease risk. Dr. Koka shares his knowledge on the vaccine's long-term effects, the role of statins, aspirin use, and the relevance of markers like LDL, HDL, triglycerides, and Lp(a). Additionally, they discuss how these markers influence treatment decisions in practice and explore novel approaches to cardiovascular health. Guest Bio and Links: Dr. Anish Koka is a Philadelphia-based cardiologist with a passion for patient-centered care and personalized treatment plans. He runs a private practice and frequently writes and speaks on healthcare policy and cardiac health. Listeners can learn more about Dr. Anish Koka at his website and on substack @anishkokamd  Show Notes: (0:00) Welcome back to the Hart2Heart Podcast with Dr. Mike Hart    (0:15) Dr. Hart introduces Dr. Anish Koka to the listeners (0:50) Dr. Koka gives a brief introduction and background of himself  (4:00) Myocarditis and COVID-19 vaccines (6:00) No long-term rise in cardiac issues post-vaccine (9:00) Long-term cardiac complication (12:30) A closer look at triglyceride to HDL ratio (18:00) The history of LDL and its impact on heart health (22:30) The law of diminishing returns in cholesterol management (26:30) Role of CRP in cardiac risk assessment (31:00) Colchicine - a powerful anti-inflammatory drug (35:30) A possible new marker for cardiovascular risk - Lp(a) (44:00) Particle size testing - worth it? (47:30) High oxidized LDL (52:00) Aspirin - general approaches --- Dr. Mike Hart is a Cannabis Physician and Lifestyle Strategist. In April 2014, Dr. Hart became the first physician in London, Ontario to open a cannabis clinic. While Dr. Hart continues to treat patients at his clinic, his primary focus has shifted to correcting the medical cannabis educational gap that exists in the medical community.  Connect on social with Dr. Mike Hart: Social Links: Instagram: @drmikehart Twitter: @drmikehart Facebook: @drmikehart

In this CCO Nephrology podcast episode, hear from cardiologist Erin D. Michos, MD, MHS, FACC, FAHA, FASE, FASPC, and nephrologist Mark J. Sarnak, MD, MS, as they discuss new and emerging therapies designed to target residual inflammatory risk associated with ASCVD and CKD.    Episode outline:   Colchicine: inhibition of NLRP3 inflammasome assembly/activationCanakinumab (anti–IL-1β monoclonal antibody)Ziltivekimab (anti–IL-6 monoclonal antibody)Other emerging targets/therapies To learn more about targeting residual risk associated with systemic inflammation, find more educational activities and resources with the links below:   CME-certified text module with animated pathophysiology video and faculty voice audio clips ClinicalThought commentaries Podcast episode 1, discussing residual risk associated with systemic inflammation and the role of cardiologists and nephrologists in mitigating risk in ASCVD and CKD Podcast episode 2, discussing novel therapeutic approaches to address residual inflammatory risks in patients with ASCVD and CKD 

CardioNerds Cardio-Rheumatology Series Co-Chairs Dr. Rick Ferraro, Dr. Gurleen Kaur, and Episode Lead Dr. Ronaldo Correa discuss “The Role of Inflammation in Cardiovascular Disease” with Dr. Antonio Abbate. Join the CardioNerds as they kick off the Cardio-Rheumatology series with Dr. Antonio Abbate. In this episode, Dr. Abbate, a leading expert in cardio-immunology, discusses the role of inflammation in cardiovascular disease. We explore the molecular mechanisms linking inflammation to atherosclerosis, the impact of chronic low-grade systemic inflammation on heart disease, and potential therapeutic targets. Dr. Abbate shares insights on how genes and lifestyle factors contribute to inflammation, the use of inflammatory markers in clinical practice, and emerging anti-inflammatory therapies in atherosclerotic cardiovascular disease. Tune in for an enlightening conversation on the intersection of inflammation and cardiovascular health. Dr. Ronaldo Correa drafted the notes. Episode audio was engineered by Dr. Amit Goyal. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Cardio-Rheumatology: The Role of Inflammation in Cardiovascular Disease Inflammation is key in the pathogenesis and progression of atherosclerosis. Estimating systemic inflammation is part of a comprehensive preventive assessment (primary/secondary). Patients with autoimmune inflammatory diseases are at a higher risk for cardiovascular events. C-reactive protein (CRP) can estimate systemic inflammation and help assess residual inflammatory risk in patients with traditional intermediate/low cardiovascular disease, guiding management consideration with lipid-lowering therapy, aspirin, and colchicine. The pharmacological management of atherosclerosis is evolving beyond primarily lipid-lowering therapies to focus on targeting the underlying residual inflammatory process. Colchicine (inflammasome blocker as an anti-mitotic drug) is approved for use in chronic stable CVD in selected cases, and interleukin pathway blockers, especially IL-1 and IL-6, are under clinical trial investigation. First things first! Prioritize treating and optimizing traditional risk factors and comorbidities and emphasize lifestyle modifications to reduce cardiovascular disease (control diabetes and hypertension, reduce or cease smoking/alcohol, lose weight, and engage in regular physical activity). They all impact inflammation directly or indirectly Show notes - Cardio-Rheumatology: The Role of Inflammation in Cardiovascular Disease Notes: Notes drafted by Dr. Ronaldo Correa. What is the link between inflammation and cardiovascular atherosclerosis? Inflammation is involved both in the pathogenesis and progression of atherosclerosis.Histopathological coronary atherosclerosis studies have demonstrated the presence of inflammatory mediators as well as a central role of factors of innate immunity such as macrophages and T cells which can interact with vascular smooth muscle cells in the progression of atherosclerotic plaque.Patients with autoimmune inflammatory conditions have earlier and higher cardiovascular event rates (accelerated atherosclerosis due to residual inflammatory risk). Elevated inflammatory markers (for example, high CRP) predict cardiovascular events. How should inflammation be considered in the context of residual cardiovascular risk? Inflammation may be the inciting factor in atherosclerosis, or it may amplify the process driven primarily by other risk factors. Therefore, treating the comorbidities and traditional CVD contributors is key to reducing the vicious inflammatory cycle.Assessing residual risk using inflammatory markers can assist in management. C-reactive protein (CRP) can estimate systemic inflammation and help assess re...

Hello, Hello! This one is a bit longer than the usual episode, but I wanted to actually finish everything I had planned, Starting off with what was left out of last weeks episode, Colchicine. Then we dive into the wild world of anesthesia and paralytics that are known for their use during surgery/procedures but have also had a rough history recreationally and criminally. We discuss such famous cases as the deaths of Michael Jackson and Matthew Perry, as well as that of Elijah McClain, who died as a result of poisoning during an interaction with police and paramedics. I want to warn you guys that there is some talk of drug abuse, attempted suicide, and racism/racial profiling and excessive force involving police/EMS. Please feel free to let us know your thoughts as we process these cases together and learn about more poisons and their uses + effects! We are so grateful for our listeners and supporters! You guys are the best! Follow us on socials: The Poisoner's Almanac on IG- ⁠https://www.instagram.com/poisoners_almanac?utm_source=ig_web_button_share_sheet&igsh=ZDNlZDc0MzIxNw==⁠ Adam- ⁠https://www.tiktok.com/@studiesshow?is_from_webapp=1&sender_device=pc⁠ Becca- ⁠https://www.tiktok.com/@yobec0?is_from_webapp=1&sender_device=pc⁠ --- Support this podcast: https://podcasters.spotify.com/pod/show/goldstar002/support

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. Many thanks for that—they greatly helped fund our summer internship programs for 2023 and 2024.Thanks to my producer Jessica Nguyen and Sinjun Balabanoff for audio and video support at Scripps Research.Note: you can select preferences to receive emails about newsletters, podcasts, or all I don't want to bother you with an email for content that you're not interested in. Get full access to Ground Truths at erictopol.substack.com/subscribe

Buck shares his experience visiting a cardiologist and discusses his family history of heart disease. He explains the importance of coronary calcium CT scans and the significance of calcium scores. Buck also highlights the role of lipoprotein little a (Lp(a)) in cardiovascular disease and the potential for new medications to target and lower Lp(a) levels. He explores the use of low-dose colchicine as an anti-inflammatory treatment for coronary artery disease and atrial fibrillation.

Vulnerable plaque and scientific method; industry payments to trainees; tirzepatide or semaglutide; trial interpretation; and PFA are the topics John Mandrola, MD, covers in today's podcast. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I. Non-invasive Imaging for Vulnerable Plaque   PET Imaging Finds Vulnerable Plaques That Cause MI https://www.medscape.com/viewarticle/pet-imaging-finds-vulnerable-plaques-cause-mi-2024a1000cm2 JACC paper https://doi.org/10.1016/j.jacc.2024.03.419 Original JAMA-Card paper https://jamanetwork.com/journals/jamacardiology/fullarticle/2806690 II. Industry Payments to Fellows JAMA Network Letter https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2821267 III. GLP-1a Class Effect? Semaglutide Significantly Improves Chronic Kidney Disease https://www.medscape.com/viewarticle/semaglutide-significantly-improves-chronic-kidney-disease-2024a10009w9 Mounjaro Beats Ozempic, So Why Isn't It More Popular? https://www.medscape.com/viewarticle/mounjaro-beats-ozempic-so-why-isnt-it-more-popular-2024a1000ckd JAMA-Internal Medicine: Semaglutide vs Tirzepatide https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2821080  SELECT trial https://www.nejm.org/doi/full/10.1056/NEJMoa2307563 FLOW trial https://www.nejm.org/doi/full/10.1056/NEJMoa2403347 SURPASS-CVOT – Rationale https://doi.org/10.1016/j.ahj.2023.09.007 IV. Colchicine and Trial Interpretation in the Lancet CONVINCE https://doi.org/10.1016/S0140-6736(24)00968-1 V. PFA Pulsed Field Ablation for AF: Are US Electrophysiologists Too Easily Impressed? https://www.medscape.com/viewarticle/pulsed-field-ablation-af-are-us-electrophysiologists-too-2024a1000d2v You may also like: The Bob Harrington Show with the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net

In this week's GameChangers we explore the emerging role of colchicine in the secondary prevention of cardiovascular disease. Drs. Wall and Boyd discuss colchicine's anti-inflammatory benefits, the challenges posed by side effects and drug interactions, and the latest research shaping its future in clinical practice. The GameChangerColchicine shows potential for secondary prevention in cardiovascular disease due to its anti-inflammatory properties, but its clinical use is limited by gastrointestinal side effects and drug interactions.  HostGeoff Wall, PharmD, BCPS, FCCP, BCGPProfessor of Pharmacy Practice, Drake UniversityInternal Medicine/Critical Care, UnityPoint HealthMathew Boyd, PharmDClinical Pharmacist, Unity Point ReferenceMeta-AnalysisClear Synergy Study Pharmacist Members, REDEEM YOUR CPE HERE! Not a member? Get a Pharmacist Membership & earn CE for GameChangers Podcast episodes! (30 mins/episode)CPE Information Learning ObjectivesUpon successful completion of this knowledge-based activity, participants should be able to:1. Identify the potential benefits of colchicine in secondary prevention of cardiovascular disease based on its anti-inflammatory properties.2. Discuss the limitations of colchicine use in clinical practice, including gastrointestinal side effects and drug interactions.0.05 CEU/0.5 HrUAN: 0107-0000-24-190-H01-PInitial release date: 06/17/2024Expiration date: 06/17/2025Additional CPE details can be found here.Follow CEimpact on Social Media:LinkedInInstagram

N Engl J Med 2019;381:2497-2505Background: Inflammation increases the risk of atherosclerosis, and reducing inflammation with canakinumab, a monoclonal antibody that neutralizes interleukin-1β, reduced plasma markers of inflammation and the risk of future myocardial infarctions but was associated with small yet statistically significant increased risk of fatal infections. Methotrexate, in the CIRT trial, did not reduce plasma markers of inflammation or cardiovascular events.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.Colchicine, extracted from the plant autumn crocus, is a potent inexpressive anti-inflammatory medication that has been used for centuries, and is used for conditions like gout, familial Mediterranean fever and pericarditis.The Colchicine Cardiovascular Outcomes Trial (COLCOT) sought to test the hypothesis that colchicine is superior to placebo in reducing cardiovascular events in patients with recent myocardial infarction.Patients: Eligible patients were adults who had myocardial infarction within 30 days of enrollment, had any planned revascularization completed, and were on guidelines recommended treatment. Exclusion criteria included severe heart failure, left ventricular ejection fraction

In his weekly clinical update, Dr. Griffin delves into discussing drinking “raw” milk possessing H5N1 influenza virus, if the virus can reproduce in the human gut, and the meaning of finding viral RNA in wastewater samples before reviewing the recent statistics on SARS-CoV-2 infection, the guidelines for spring administration of COVID vaccines boosters, withdrawal of AstraZeneca's SARS-CoV-2 vaccine from the European market, discusses the emergency use application of a pre-exposure prophylactic, continues to dispel the myth of viral rebound, when to use steroids and the benefits of convalescent plasma, what do when healthcare workers succumb to SARS-CoV-2 infection, if administration of colchicine for the management of COVID-19, compares and provides information for the enrollment into the NIH clinical trials of long COVID and its effects on sleep, exercise intolerance and the cognitive profile in multiple sclerosis and post-COVID, exercise intolerance and post-exertional malaise. For more information about cow and milk infection by H5N1 listen to the discussion with Richard Webby on TWiV 1113 and for long COVID-19 listen to TWiV 1088. Dr. Griffin also provides a list of apps for monitoring one's health including brain health. Subscribe (free): Apple Podcasts, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode Who demands milk infected with H5N1? (Futurism) Uncowed by milk possessing H5N1  (LA Times) Cow flu flying around for 4 months (CNN) The unpasteurized raw milk institute (Raw Milk Institute) Infection and reproduction of H5N1 in the human gut (JID) Wastewater samples identified H5N1 in 9 cities (medrxiv) Richard Webby, is H5N1 a concern? (TWiV 1113) COVID-19 national trend (CDC) COVID-19 deaths (CDC) Spring vaccineadvice (CIDRAP) Older adult spring booster available (CDC) Advisory committee for immunization practices slides (CDC) Advisory committee for immunization practices spring 2024 COVID-19 boosters (CDC) Withdrawal of Astra-Zeneca SARS-CoV-2 vaccine in Europe (European Medicines Agency) Astra-Zeneca withdraws SARS-CoV-2 vaccine from market (AP news) Global vaccine data/adverse event network (Vaccine) EUA for pemgarda (FDA) CDC Quarantine guidelines (CDC) Early phase of SARs-CoV-2 infection (COVID.gov) NIH COVID-19 treatment guidelines (NIH) Infectious Disease Society guidelines for treatment and management (IDSociety) Overuse ofantibiotics for COVID-19: a viral disease (European Society of Clinical Microbiology and Infectious Diseases) Molnupiravir safety and efficacy (JMV) Convalescent plasma recommendation for immunocompromised (IDSociety) Outpatient treatment with concomitant vaccine-boosted convalescent plasma (mBio) Updated respiratory virus guidances (CDC) What do when your heathcare provider is infected with SARS-CoV-2 (CDC) Managing healthcare staffing shortages (CDC) Steroids,dexamethasone at the right time (OFID) Anticoagulation guidelines (hematology.org) Colchicine for managing COVID-19 (BMC Pulmonary Medicine) Colchicine guidelines (ID Society) Long COVID evidence based review TWiV shout out (TWiV 1088) NIH long COVID sleep disturbance, exercise intolerance and post exertional malaise clinical trials (NIH News) COVID-19 Yorkshire rehabilitation scale (BML Open Respiratory Research) Visible heart monitor (Makevisible) Bearable app (Bearable) Tracking your chronic illness using Flaredown (Flaredown) Improving your brain health (BrainHQ)Vanderbilt's long COVID resources: podcasts and books (Vanderbilt University) Contribute to our Floating Doctors fundraiser Letters read on TWiV 1114 Dr. Griffin's COVID treatment summary (pdf) Timestamps by Jolene. Thanks! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-379 Overview: Recent data has shown that colchicine can improve outcomes in patients with known coronary artery disease (CAD), with consideration of colchicine now recommended by the American Heart Association (AHA). Hear valuable insights into the potential benefits and limitations to refine your clinical approach to managing CAD. Episode resource links: Nidorf SM, Fiolet ATL, Mosterd A, et al. Colchicine in Patients with Chronic Coronary Disease. N Engl J Med. 2020;383(19):1838-1847.  Mohammadnia N, Los J, Opstal TSJ, et al. Colchicine and diabetes in patients with chronic coronary artery disease: insights from the LoDoCo2 randomized controlled trial. Front Cardiovasc Med. 2023;10:1244529. Published 2023 Oct 6.  Roubille F, Bouabdallaoui N, Kouz S, et al. Low-Dose Colchicine in Patients With Type 2 Diabetes and Recent Myocardial Infarction in the COLchicine Cardiovascular Outcomes Trial (COLCOT). Diabetes Care. Published online January 5, 2024.  Guest: Alan M. Ehrlich, MD, FAAFP   Music Credit: Richard Onorato

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-379 Overview: Recent data has shown that colchicine can improve outcomes in patients with known coronary artery disease (CAD), with consideration of colchicine now recommended by the American Heart Association (AHA). Hear valuable insights into the potential benefits and limitations to refine your clinical approach to managing CAD. Episode resource links: Nidorf SM, Fiolet ATL, Mosterd A, et al. Colchicine in Patients with Chronic Coronary Disease. N Engl J Med. 2020;383(19):1838-1847.  Mohammadnia N, Los J, Opstal TSJ, et al. Colchicine and diabetes in patients with chronic coronary artery disease: insights from the LoDoCo2 randomized controlled trial. Front Cardiovasc Med. 2023;10:1244529. Published 2023 Oct 6.  Roubille F, Bouabdallaoui N, Kouz S, et al. Low-Dose Colchicine in Patients With Type 2 Diabetes and Recent Myocardial Infarction in the COLchicine Cardiovascular Outcomes Trial (COLCOT). Diabetes Care. Published online January 5, 2024.  Guest: Alan M. Ehrlich, MD, FAAFP   Music Credit: Richard Onorato

The mysteries of inflammation: deciphering how the flames of inflammation can both heal wounds and incite a series of events leading to cardiovascular diseases. Prepare to be enlightened as we explore the dual nature of this biological response and the groundbreaking research aimed at harnessing its power for our well-being.In a conversation with Kevin Geddings and Dr. Michael Koren, we tackle the promising frontiers of treating vascular inflammation and how repurposed medications, like Colchicine, are showing surprising benefits for heart health. Delving into the interconnected world of immune system diseases such as lupus and rheumatoid arthritis, we uncover the strategic approaches in clinical trials that could revolutionize the management of these conditions. For anyone touched by cardiovascular concerns or simply fascinated by medical innovation, this episode offers a glimpse into the evolving battle against pervasive health challenges.Recording Date: April 15, 2024Be a part of advancing science by participating in clinical researchShare with a friend. Rate, Review, and Subscribe to the MedEvidence! podcast to be notified when new episodes are released.Follow us on Social Media:FacebookInstagramTwitterLinkedInWant to learn more checkout our entire library of podcasts, videos, articles and presentations at www.MedEvidence.com Powered by ENCORE Research GroupMusic: Storyblocks - Corporate InspiredThank you for listening!

If you learned that radiologists looking at CT scans for the traditional signs of coronary artery disease catch only 20 percent of the people who actually have a high risk of a heart attack, and if you learned that there's a new AI-based test that can catch subtle signs of inflammation in the other 80 percent of patients—well, you'd probably want to get that test yourself, right? Harry's guests this week, Frank Cheng and Keith Channon, are from a UK-based company that has developed just such a test. Cheng is the company's CEO, and Channon is co-founder and chief medical officer. And under their leadership, Caristo has introduced a test called CariHeart that applies machine learning to the data in a three-dimensional CT scan of the heart. It looks for otherwise invisible signs of inflammation in the fat tissue around the major coronary arteries, and then it predicts the chances that the patient will suffer a heart attack in the next eight years. Doctors can use that information to decide whether a patient needs to take a cholesterol-lowering drug like a statin or an anti-inflammatory drug like colchicine. Caristo's test is being used on an experimental basis in the UK, and it hasn't yet been approved for use in the US. But it's a leading example of the way AI, put together with fundamental advances in our understanding of human biology, is really beginning to change the practice of medicine. Cheng and Channon say Caristo's test isn't intended to put cardiologists or radiologists out of work—it's designed to help them be more effective. And given that cardiovascular disease is the number one cause of death around the world, any technology that can help catch signs of coronary artery disease earlier could save a lot of lives.For a full transcript of this episode, please visit our episode page at http://www.glorikian.com/podcast Please rate and review The Harry Glorikian Show on Apple Podcasts or Spotify! Here's how to do that on Apple Podcasts:1. Open the Podcasts app on your iPhone, iPad, or Mac. 2. Navigate to The Harry Glorikian Show podcast. You can find it by searching for it or selecting it from your library. Just note that you'll have to go to the series page which shows all the episodes, not just the page for a single episode.3. Scroll down to find the subhead titled "Ratings & Reviews."4. Under one of the highlighted reviews, select "Write a Review."5. Next, select a star rating at the top — you have the option of choosing between one and five stars. 6. Using the text box at the top, write a title for your review. Then, in the lower text box, write your review. Your review can be up to 300 words long.7. Once you've finished, select "Send" or "Save" in the top-right corner. 8. If you've never left a podcast review before, enter a nickname. Your nickname will be displayed next to any reviews you leave from here on out. 9. After selecting a nickname, tap OK. Your review may not be immediately visible.On Spotify, the process is similar. Open the Spotify app, navigate to The Harry Glorikian Show, tap the three dots, then tap "Rate Show." Thanks!

Bienvenue sur RARE à l'écoute, la chaine de Podcast dédiée aux maladies rares. Pour ce quatrième épisode consacré à la Fièvre Méditerranéenne Familiale, nous recevons le Dr Véronique Hentgen, pédiatre au centre hospitalier de Versailles et coordinatrice du CeréMAIA, le centre de référence des maladies auto inflammatoires et de l'amylose, de la filière FAI2R. Nous abordons aujourd'hui la prise en charge de la fièvre méditerranéenne familiale, les enjeux du traitement, le parcours de prise en charge, la coordination des soins, le suivi des patients et les conseils à apporter aux familles. Si vous désirez vous informer et aller plus loin dans la connaissance de cette pathologie, nous vous donnons rendez-vous sur notre site internet www.rarealecoute.com. L'orateur n'a reçu aucune rémunération pour la réalisation de cet épisode.   Invitée : Dr Hentgen, pédiatre et coordinatrice du CéRéMAIA au centre hospitalier de Versailles https://www.fai2r.org/les-centres-fai2r/centres-de-reference-fai2r/crmr-versailles/  L'équipe : Virginie Druenne - Programmation Cyril Cassard - Animation Hervé Guillot - Production Crédits : Sonacom

This episode is sponsored by Farewell Coffee Roasters. Add BSFREEMD15 to your cart for 15% off your first order. Your first cup awaits! May and Tim start the episode with Tim sharing his skiing adventures in Utah while May paints at home. They discuss Tim's purchase of retro goggles and hats and humorously reference bringing back more wives as a business expense. They introduce the topic of wacky cold weather in Florida and its effects on people and animals. Tim presents a disturbing news story about a former Mayo Clinic doctor accused of fatally poisoning his wife with Colchicine. They discuss the suspicious circumstances surrounding the case and highlight the doctor's background in pharmacology and poison control. May teases their cocktail of the week and mentions upcoming shows. They delve into the effects of cold weather on Floridians, including myths and unusual animal behavior. Tim shares a fascinating story about alligators in brumation and how they adapt to freezing temperatures, while May talks about iguanas falling from trees due to the cold. Looking for something specific? Here you go! 00:00:00 - Introduction and Theme Discussion 00:03:15 - Cold Snap in Florida 00:05:30 - Unusual Weather Events in Florida History 00:08:00 - How Floridians React to Cold Weather 00:09:45 - List of Common Winter Gear in Florida 00:11:00 - Listener Mail and Comments 00:12:30 - Cocktail of the Week 00:14:00 - Cold Weather Myths and Survival Tips 00:15:30 - Animal Behavior in Cold Weather 00:17:00 - Tim's Personal Encounter with a Frozen Alligator 00:18:30 - May's Iguana Rescue Mission 00:20:00 - Wildlife Conservation and Cold Weather Research 00:21:30 - Tim and May's Favorite Winter Activities 00:23:00 - Listener Suggestions and Episode Teasers Our Advice! Everything in this podcast is for educational purposes only. It does not constitute the practice of medicine and we are not providing medical advice. No Physician-patient relationship is formed and anything discussed in this podcast does not represent the views of our employers.  The Fine Print! All opinions expressed by the hosts or  guests in this episode are solely their opinion and are not to be used as specific medical advice.  The hosts,  May and Tim Hindmarsh MD, BS Free MD LLC, or any affiliates thereof are not under any obligation to update or correct any information provided in this episode. The guest's statements and opinions are subject to change without notice. Thanks for joining us! You are the reason we are here.  If you have questions, reach out to us at doc@bsfreemd.com or find Tim and I on Facebook and IG. Please check out our every growing website as well at  bsfreemd.com (no www) GET SOCIAL WITH US! www.withkoji.com/@bsfreemd

Betty and Conner Bowman have a lot in common when they marry.  Betty Bowman  graduates from the University of Kansas School of Pharmacy with a Pharmaceutical Doctorate. Her works as a hospital pharmacist while Connor Bowman gets his Internal Medicine Residency. Betty Bowman takes a position at the Mayo Clinic, so when she falls ill suddenly, the Mayo Clinic is the logical place for treatment.  It seems Betty Bowman is suffering from food poisoning, having gastrointestinal distress and dehydration. Her condition doesn't get any better.  She takes a turn for the worse, with heart problems, fluid buildup in her lungs and then part of her colon was removed, after doctors discover necrotic tissue. Bowman dies from organ failure. Then the Southeast Minnesota Medical Examiner's Office alerts the Rochester Police Department to the suspicious nature of Betty Bowman's death. The Medical Examiner's office had to halt a cremation order.   According to court records, the Medical Examiner's Office received a call from CGK- a female friend of the Bowman's who said Betty and Connor Bowman were having marital issues and were talking about divorce following infidelity and a deteriorating relationship. In the Criminal Complaint it is stated that Conner Bowman told the Medical Examiner's Office that his wife should be cremated immediately, arguing that Betty Bowman did not want to be a cadaver.  Connor Bowman also begin asking one of the medical examiner investigators if the toxicology analysis being completed would be more thorough than the analysis typically done at the hospital. Bowman wanted a list of what was specifically going to be tested for. Friends of Betty Bowman began reaching out to investigators. An adult female friend of Betty Bowman told  the Rochester Police Department that she had texted with Betty Bowman  and that Bowman told her she was sick.   The friend told the detective that Betty Bowman was normally a healthy person. Another friend said a text from Betty Bowman said she thought a smoothie she had the night before might have caused her illness. Detectives began looking at all options and found husband Connor Bowman had  accessed Betty Bowman's patient account using his hospital credentials. From there he was able to locate internet searches conducted by Connor Bowman, a  Poison Specialist.    Connor Bowman was researching COLCHICINE,  a drug used to treat gout.  What's more he was  searches for information in determining what a lethal dose would be,  by entering his wife's weight.  Joining Nancy Grace Today: Dale Carson - High Profile Criminal Defense Attorney (Jacksonville), Former FBI Agent, Former Police Officer (Miami-Dade County), Author: "Arrest-Proof Yourself”, DaleCarsonLaw.com, Twitter: @DaleCarsonLaw  Caryn L. Stark - Psychologist, renowned TV and Radio trauma expert and consultant, www.carynstark.com, Instagram: carynpsych, FB: Caryn Stark Private Practice   Robin Dreeke - Behavior Expert & former FBI Special Agent / Chief of the FBI Counterintelligence Behavioral Analysis Program, Author: "Sizing People Up: A Veteran FBI Agents Manual for Behavior Prediction", peopleformula.com, Twitter: @rdreeke   Dr. Lyle D. Burgoon, Ph.D - Toxicology expert, President and CEO of Raptor Pharm & Tox, Ltd., Fellow of the Academy of Toxicological Sciences, Critical Science Podcast: https://critscipod.com, https://toxictruthblog.com, Twitter/X: @DataSciBurgoon   Charles Kelley - Reporter & Weekend Anchor for KTTC News, kttc.com, IG & TikTok: @charliemkelley, FB: Charles Kelley KTTC   See omnystudio.com/listener for privacy information.

Show Notes for Episode 29 of “The 2 View” – Toxoplasmosis, the OPAL trial, medical marijuana, appendicitis, and colchicine. CDC - Toxoplasmosis CDC – Parasites – Toxoplasmosis (Toxoplasma infection). Cdc.gov. Published June 9, 2023. Accessed September 26, 2023. https://www.cdc.gov/parasites/toxoplasmosis/index.html OPAL RCT for Opioids in Back Pain Jones C, O'Day R, Koes B, et. al. Opioid analgesia for acute low back pain and neck pain (the OPAL trial): a randomised placebo-controlled trial. The Lancet. Thelancet.com. Published July 22, 2023. Accessed September 26, 2023. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(23)00404-X/fulltext Sikina M, Kiel J. Re-evaluating Red Flags for Back Pain. Acep.org. Sports Med. Published August 17, 2022. Accessed September 26, 2023. https://www.acep.org/sportsmedicine/newsroom/newsroom-articles/august2022/re-evaluating-red-flags-for-back-pain Medical Marijuana Brooks M. Is Medical Cannabis the Answer to the Opioid Crisis? Medscape Emergency Medicine. Published October 3, 2022. Accessed September 26, 2023. https://www.medscape.com/viewarticle/981767?ecd=wnlinfocu4broadbroadpersoexpansion-editorial_20230603&uac=106964SV&impID=5490911 Novak S. Physicians Aren't Asking Enough Questions About Cannabis Use. Medscape Emergency Medicine. Published August 29, 2023. Accessed September 26, 2023. https://www.medscape.com/viewarticle/995954?ecd=WNLtrdalrtpos1230904etid5820671&uac=106964SV&impID=5820671 Appendicitis Appendicitis. Acep.org. Accessed September 26, 2023. https://www.acep.org/patient-care/clinical-policies/appendicitis Dora-Laskey A. Acute pain control. EM. Accessed September 26, 2023. https://www.saem.org/about-saem/academies-interest-groups-affiliates2/cdem/for-students/online-education/m3-curriculum/group-acute-pain-control/acute-pain-control Hidayat AI, Purnawan I, Mulyaningrat W, et al. Effect of Combining Dhikr and Prayer Therapy on Pain and Vital Signs in Appendectomy Patients: A Quasi-Experimental Study. NIH: National Library of Medicine. J Holist Nurs. Accessed September 26, 2023. https://pubmed.ncbi.nlm.nih.gov/37277995/ Smink D, Soybel D. Management of acute appendicitis in adults. UpToDate. Uptodate.com. Updated February 15, 2023. Accessed September 26, 2023. https://www.uptodate.com/contents/management-of-acute-appendicitis-in-adults Colchicine Chiabrando JG, Bonaventura A, Vecchié A, et al. Management of Acute and Recurrent Pericarditis: JACC State-of-the-Art Review. J Am Coll Cardiol. ScienceDirect. Published January 2020. Accessed September 26, 2023. https://www.sciencedirect.com/science/article/pii/S0735109719384840?via%3Dihub Gout clinical practice guidelines. American College of Rheumatology. Rheumatology.org. Accessed September 26, 2023. https://rheumatology.org/gout-guideline Telmesani A, Moss E, Chetrit M. The Use of Colchicine in Pericardial Diseases. American College of Cardiology. Published December 5, 2019. Accessed September 26, 2023. https://www.acc.org/Latest-in-Cardiology/Articles/2019/12/04/08/22/The-Use-of-Colchicine-in-Pericardial-Diseases Recurring Sources Center for Medical Education. Ccme.org. http://ccme.org The Proceduralist. Theproceduralist.org. http://www.theproceduralist.org The Procedural Pause. Emergency Medicine News. Lww.com. https://journals.lww.com/em-news/blog/theproceduralpause/pages/default.aspx The Skeptics Guide to Emergency Medicine. Thesgem.com. http://www.thesgem.com Trivia Question: Send answers to 2viewcast@gmail.com Be sure to keep tuning in for more great prizes and fun trivia questions! Once you hear the question, please email us your guesses at 2viewcast@gmail.com and tell us who you want to give a shout-out to. Be sure to listen in and see what we have to share!

Dr. Centor discusses the incidence of knee and hip replacements in patients receiving low-dose colchicine with Dr. Tuhina Neogi.

In this episode of The Common Sense MD, Dr. Rogers talks with Dr. Daniel O'Roark and Nolan Hensley, PA-C of Trinity Heart and Vascular Group about how to prevent heart disease. This conversation covers Statins, Colchicine, CT Angiograms, and more. Hope this helps some of you! What did you think of this episode of the podcast? Let us know by leaving a review! Connect with Performance Medicine! Sign up for our weekly newsletter: https://performancemedicine.net/doctors-note-sign-up/ Facebook: @PMedicine Instagram: @PerformancemedicineTN YouTube: Performance Medicine

Commentary by Dr. Valentin Fuster

Starting HF meds during hospitalization for HF, Impella, testosterone, and colchicine are the topics John Mandrola, MD, discusses in this week's podcast. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I. Starting HF Meds During Hospitalization for HF Starting Indicated Heart Failure Meds In-Hospital: Progress, Opportunities https://www.medscape.com/viewarticle/993539 - Opportunities and Achievement of Medication Initiation Among Inpatients With Heart Failure With Reduced Ejection Fraction https://www.jacc.org/doi/full/10.1016/j.jchf.2023.04.015 II. Impella - Comparative Effectiveness of Percutaneous Microaxial Left Ventricular Assist Device vs Intra-Aortic Balloon Pump or No Mechanical Circulatory Support in Patients With Cardiogenic Shock https://jamanetwork.com/journals/jamacardiology/fullarticle/2806562 - Evidence Generation for Novel Cardiovascular Devices—Putting the Horse Back in Front of the Cart https://jamanetwork.com/journals/jamacardiology/fullarticle/2806565 III. Testosterone Big Trial Reassures on Heart Safety of Testosterone in Men https://www.medscape.com/viewarticle/993322 - Cardiovascular Safety of Testosterone-Replacement Therapy https://www.nejm.org/doi/full/10.1056/NEJMoa2215025 IV. Colchicine for CV Disease Low-Dose Colchicine Approved for CVD: Now What? https://www.medscape.com/viewarticle/993578 - Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction https://www.nejm.org/doi/full/10.1056/nejmoa1912388 - Colchicine in Patients with Chronic Coronary Disease https://www.nejm.org/doi/full/10.1056/nejmoa2021372 You may also like: Medscape editor-in-chief Eric Topol, MD, and master storyteller and clinician Abraham Verghese, MD, on Medicine and the Machine https://www.medscape.com/features/public/machine The Bob Harrington Show with Stanford University Chair of Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net

Dr. Jack Cush reviews the news and reports from the past week on RheumNow.com. This week a new colchicine FDA approval, rising rate of IgG4 related disease and what's the safest biologic?

It is an honour to have the world famous cardiologist Dr Peter McCullough join us on Hearts of Oak again. We are getting a taster of the political shockwaves that are coming down the line with presidential candidate Vivek Ramaswamy recently saying that the public were duped on the COVID Jab and of course we have RFK Jr actively red-pilling the left. And just in the last week we have seen another slew of data on vaccine harms and excess deaths. The truth will be told and Dr McCullough is leading the vanguard as one of the main catalysts of getting this information out to the public. Dr. Peter McCullough is an internist, cardiologist, epidemiologist, managing the cardiovascular complications of both the viral infection and the injuries developing after the COVID-19 vaccine in Dallas, TX, USA. Since the outset of the pandemic, Dr. McCullough has been a leader in the medical response to the COVID-19 disaster and has published “Pathophysiological Basis and Rationale for Early Outpatient Treatment of SARS-CoV-2 (COVID-19) Infection,” the first synthesis of sequenced multidrug treatment of ambulatory patients infected with SARS-CoV-2 in the American Journal of Medicine and subsequently updated in Reviews in Cardiovascular Medicine. McCullough has 51 peer-reviewed publications on the infection and has commented extensively on the medical response to the COVID-19 crisis in The Hill, America Out Loud, and on FOX NEWS Channel. On November 19, 2020, Dr. McCullough testified in the US Senate Committee on Homeland Security and Governmental Affairs and throughout 2021 in the Texas Senate Committee on Health and Human Services, Colorado General Assembly, New Hampshire Senate, and South Carolina Senate concerning many aspects of the pandemic response. Dr. McCullough has two years of dedicated academic and clinical efforts in combating the SARS-CoV-2 virus. In doing so, he has reviewed thousands of reports, participated in scientific congresses, group discussions, press releases, and been considered among the world's experts on COVID-19. Dr. McCullough is also known for his iconic views on the state of medical truth in America and around the globe. He pierces through the thin veil of mainstream media stories that skirt the major issues and provide no tractable basis for durable insight. McCullough aims to bring critical information and insights to the viewers and listeners in a concise and understandable format. Sit back, take notes if you are so inclined, and you will always come away better informed and more settled in your direction forward regarding personal and family medical navigation, home and health products, diagnostic tests, pharmaceuticals, medical devices, and the path forward for you and your loved ones. 'The Courage to Face Covid 19' in hardback or paperback.... https://couragetofacecovid.com/products/the-courage-to-face-covid-19?variant=41888573685916 Follow and support Dr. McCullough at the links below Website: https://www.petermcculloughmd.com/ Substack: https://petermcculloughmd.substack.com/?utm_source=substack&utm_medium=email GETTR: https://gettr.com/user/p_mcculloughmd Twitter: https://twitter.com/P_McCulloughMD Truth: https://truthsocial.com/@petermcculloughmd Telegram: https://t.me/C19ExpertChannel America Out Loud: https://www.americaoutloud.com/the-mccullough-report/ Concerned Doctors: https://concerneddoctors.org/dr-peter-mccullough-videos/ Interview recorded 11.5.23 *Special thanks to Bosch Fawstin for recording our intro/outro on this podcast. Check out his art https://theboschfawstinstore.blogspot.com/ and follow him on GETTR https://gettr.com/user/BoschFawstin and Twitter https://twitter.com/TheBoschFawstin?s=20  To sign up for our weekly email, find our social media, podcasts, video, livestreaming platforms and more... https://heartsofoak.org/connect/ Please subscribe, like and share! Transcript (Hearts of Oak) Hello, Hearts of Oak, and welcome to another interview coming up in a moment with Dr. Peter McCullough. He re-joined us, having been with us last year, and we start on the political side. I saw him at CPAC, and Vivek Ramaswamy, who is a US presidential candidate for the Republicans, said on a talk show he was duped, and the American people were duped, on COVID vaccines. He said if he was doing it again, he would do it differently. Wow. So I asked Dr. McCullough his thoughts on that, And then on his thoughts on Robert Kennedy Jr. standing for the Democrats and how that will blow up in the conversation on the left. Then we're going to just a number of reports and studies that have come out. Trida vaccine injury syndromes converges on victims and Dr. McCullough said this is what he's seen more and more regularly. This is the usual syndrome that he is seeing. And long COVID, being vaxxed. So it seems as though there's a correlation with that, talking about mRNA in breast milk and the impact this has on pregnant women and their unborn children. Then the reactivation of funding, federal funding for the Eco Health Alliance, unbelievable, but it is true. Even though they've been discredited, they've now been handed half a million dollars for funding. And then myocarditis, not recovering 80% of six months after vaccination, only 20% of young people are recovering within six months from myocarditis. And Dr. McCullough writes this in his sub stack that you need to go to and delve into this and understand this more deeply. And then we end up with excess deaths. Huge range of topics. And as always, Dr. McCullough brings his expert analysis to all of them. And hello, Hearts of Oak. It is wonderful to have back with us once again, the world-renowned cardiologist and chief scientific officer of The Wellness Company. That's Dr. Peter McCullough. Dr. McCullough, thank you for your time today. (Dr Peter McCullough) Thanks for having me. Not at all. And I understand that you are one of the most published cardiologists ever in America. I think it was a thousand publications and 660 citations. So you bring a wealth of understanding and knowledge and background to this. So I appreciate your time today. Thank you. You know, people have always asked, what do all those citations mean? You know, as a general rule in the National Library of Medicine, about 25 citations would qualify somebody to be a professor of medicine. And those who really race up in terms of their academic contributions, it just means they've looked at more data. There's been more scholarship. I focused on heart and kidney disease at interaction, made key discoveries, led key innovative groups, you know, in many areas of medicine. I've led data safety monitoring boards for important drugs, devices, strategies, presented at the European Medicine Agencies, the National Institutes of Health, New York Academy of Sciences. So I was well known in medicine before COVID-19. Now, since the pandemic, I've directed my scholarship entirely to the, pandemic response, have over 60 peer-reviewed publications in this area, including the seminal papers describing the methods of treating COVID-19 to reduce hospitalization and death. Wow, well I want to delve into the medical side but as I saw you at, as I said before, saw you whenever I was over at CPAC and you were always in many interviews being mobbed, but, if I could ask you some, two political thoughts I had. I saw that Vivek Ramaswamy, who's a candidate for presidential candidate, standing for the Republican side. I think a few days ago, he had said, I think it was the Steve Deace show, that he well, he had had two doses of the jab, but he said that he was duped. And I thought that was quite key. And then he went on to say if he was if he were to do it again, he wouldn't have done it the same way. But that for him to say he was duped, what were your thoughts whenever you heard a presidential candidate saying something like that. You know, we've been looking for some signals from the presidential candidates regarding the vaccines. The COVID-19 vaccine debacle is one of the biggest issues on the minds of Americans, and many of the candidates have been skirting around it. They just haven't addressed where they stood. And congratulations to Steve Deace, a friend of mine who, you know, Ramaswamy is a young man. He doesn't have considerable experience. You know, many think that young candidates, they're largely angling from some experience and maybe a cabinet position. But it was nice when Deace asked him directly about it, where he said he took the two shots, he regretted it. He felt America was duped. That means to be fooled or deceived by the government narrative. Said he would have done things differently. And so he left it open. I think that's journalists like yourself and others will have to ask him, well, what would he have done differently there? A young man like him who's thin and fit, there's no theoretical benefit of the vaccines, just the real harms, the real hard data on fatal and non-fatal vaccine injury syndrome. So he probably felt like he, later on, realized he took a personal risk with his health and regrets it. Now, that's on the Republican side and I'm curious and intrigued to see how that's brought into the debate. But on the Democrat side, you have Robert Kennedy Jr. And whenever he announced he was running, I was fascinated because he would be on the opposite political side as me. But actually, during the last three years, you rub shoulders with people you wouldn't normally. And he has been extremely vocal throughout his whole life on vaccines. And what were your thoughts on that? Because I think that could just blow the whole discussion, because again, you're thinking to the Democrat side, this conversation maybe hasn't been had as fully as maybe on the right. And him stepping into that, to me that changes the whole conversation. It certainly does. Robert F. Kennedy Jr., who's the son of the late Bobby Kennedy, our former attorney general, and the nephew of John F. Kennedy, certainly comes from a storied, family history of politics. He's a lifelong Democrat. He's not anti-vaccine. I know him very well. He's simply pushing for safe and effective vaccines. He doesn't want to see any more Americans harmed by vaccine side effects. The benefits of any vaccine are not, compelling enough to have harm done to the population. And we know since 1986, all the vaccine manufacturers have liability protection. So that isn't fair when someone is paralyzed or has a terrible side effect from a vaccine. And I think pretty clearly he believes no one should, receive any pressure, coercion, or threat of reprisal for vaccines. It shouldn't be mandated for school or for employment or military service. And we should have, all the states in the country should have full tripartite vaccine exemptions, meaning philosophical exemption, don't feel like you don't need to take it on philosophical grounds, religious and medical. So there should be freedom. He's pushing for freedom. This is very important. Medical freedom is related to social and economic freedoms. They're all related. And that's what I told America when I gave my Lincoln Memorial address. You know, that was a few minutes before Kennedy was up on the steps of the Lincoln Memorial with me. So I think we're very well aligned on this. You know, what I find interesting is that the COVID Community States Program weighed in from North-eastern University and Harvard, and a huge sample. So they actually figured out who took the vaccine. And the answer is in America, 25% of adult Americans, like me, did not take the vaccine. I didn't take the COVID vaccine. Best decision I ever made. I feel great. I don't have to worry about blood clots or heart damage or any of these lingering effects that we're seeing now. So many people who skipped the vaccine are so grateful they made the right choice. So that 25%, many of them actually suffered reprisal for doing this. They lost their jobs, family strife. There was a lot of unnecessary consequences that happened to people who made the right decision. Now, We only have 60% of the adult Americans who vote, only 60% vote. The 25% who didn't take the vaccine like me are likely to vote. So now we have nearly half of the voting block for the presidency where the vaccine is the issue. And everybody wants to know where do the candidates stand on the failed COVID-19 vaccines. That uptick really intrigued me and it's something that's come out in the UK that we now have a database you can put in your zip code for you over there or postcode and you can find out supposedly the uptake and one of the striking things on that is the booster uptick is around 1 to 2% in many areas and I probably didn't necessarily believe a lot of the data that were getting. But that 25% that didn't, I thought, wow, there's at last some honesty with the figures. And I guess you looking at these figures of the last three years, there's been massive scepticism of the information we're being told. Well, I'm glad you mentioned that because as the COVID Community States Program, which was an academic epidemiologic program, as they were reporting 25% unvaccinated, the CDC at that time was reporting 8% unvaccinated. Well, what's the difference? And the answer is the CDC was over counting. If patients forgot their vaccine card, they went to a different pharmacy, they could have had a new card started at the booster stage and been counted again. So we now know that the CDC does not have accurate vaccination data. There tended to be overestimating vaccination. Our CDC is currently reporting 16% booster uptake, and that's almost certainly an overestimate. We need to know booster uptake by time. Because the boosters only last theoretically six months. Clinically, it's about half of that. So no matter who took a booster more than six months ago, they're effectively unvaccinated. Yeah. If I can just discuss some of the things you've posted, even just the last week on Twitter, and of course, if people go to your Twitter handle, they can get the link to your Substack, the website, everything is there and encourage people to to sign up. Certainly your Substack, which has been a fantastic source of information for many of us. And one of the actually it was America Outloud.com, which I know you write for, had the headline you put up a few days ago was try to vaccine injury syndromes converges on victims. It said amongst the most common and frustrating COVID-19 vaccine injury syndromes are small fibre neuropathy, pleurodynia and POTS, which I can't even pronounce what's there, and you had a lady who came on and acted as if she was going to see her doctor and discussed what, but tell us about some, because we hear all different side effects and we'll maybe touch on myocarditis a little bit, but it was those three coming together and it seems to be every week, every two weeks, there's another issue that comes up. It's true, but this triad that I pointed out far and away is the most common constellation. I've been seeing patients now with vaccine injuries now for two years, you know, steady flow in the clinic, so I really have a good handle on this. And so the triage is the following. One is pleurodynia, just some nonspecific chest pain. Sometimes it hurts to cough or take a deep breath or laugh. Sometimes when they put pressure on the chest, one can feel pain, which is called pleurodynia. The next one is a small fibre neuropathy, that is feeling numbness and tingling, prickling in the hands and the feet, usually sometimes the back of the legs. And then the third is POTS or Posterior Orthostatic Tachycardia Syndrome. And patients will recognize this because their heart rate unexpectedly will shoot up when they're doing nothing, then go down. Blood pressure up and down. When they exercise, things seem to be out of proportion to what they need in terms of exercise, and they feel generally unwell. And so I was lucky enough to have a patient reach out to me. She's very sophisticated, and she gave consent, and she told us her story and she had that triad. And I went through the questions I would ask her, the tests I would order to rule out serious problems like myocarditis, like major problems in the central nervous system, et cetera. And then what medicinal empiric approach would I take? And for the pleurodynia, the drug I prescribed the most is called Colchicine. This is a form of an anti-inflammatory. There's about two dozen trials in acute COVID-19 showing that it plays a role. So we know it's helpful there. The largest one of note's called the CO-Corona trial done out of the Montreal Heart Institute, over 4,000 subjects, probably the best and largest outpatient COVID study. So colchicine is also used to treat gout and forms of inflammation. So it seems to be very important for the pleurodinium. For the POTS, the posterior orthostatic tachycardia syndrome. That's actually too much adrenaline being released from the sympathetic chain of ganglia in the neck as well as the adrenal glands. And I found that it was a relatively underutilized beta blocker called Natalo, which has what's called intrinsic sympathomimetic activity. It seems to modulate the alpha and beta receptors just the way we need in order for that nervous system feedback loop to the brain to be corrected. And then the final triage in this entire problem is actually dissolving the spike protein itself, which is loaded up with COVID-19, the illness and serial vaccines. Remember, we get spike protein in our body, we can't get it out for months, if not a year or more, after the infection, as well as the vaccines. Each shot of the vaccine installs large amounts of spike protein. There we're utilizing nattokinase. Nattokinase is a natural enzyme that's derived from the fermentation of soy is discovered by the Japanese. A bacteria that breaks it down is Bacillus subtilis natto. And it creates this fermented product as an enzyme. The Japanese have been using it for over a thousand years. That is eat consuming natto. But we now have a supplement they've used for about two decades. They use it for cardiovascular applications. a form of a blood thinner, so it's a serious supplement to take. The current recommended dose is 2,000 fibrinolytic units or 100 milligrams twice a day, it's well within the range of safety. It's been safety tested up to 80,000 units at a single time, so it's well within the safety limit. The caveats are bleeding, mucosal bleeding from the nose or mouth, and then a soy allergies. Otherwise, it is a safe supplement. It's not immediate that this three-component therapeutic program works, but most patients after two months, they start to come back and they start to feel like they're on the way back. So I wanted to share that. Many of the doctors that are sought out nowadays are with The Wellness Company. I advise that company as a chief scientific officer so they're well aware of that approach. But I have to tell you, that's my most common approach I use in clinic and I'm glad we finally found something that can help people through this. I've tried hydroxychloroquine, ivermectin, fluvoxamine, prednisone, a whole variety of different drugs and I've really settled on these three. Two prescription drugs and then one over-the-counter supplement. That's really helpful. And I think many people are concerned that if they did have any of these and they went to see their normal doctor, that actually in the doctor's mind would not be thinking that actually these could be related and therefore their concerns could be dismissed. I agree. The first question a patient should ask a doctor is, did they take the COVID vaccine and did they push it on their patients? And if they did, the patient ought to have a serious conversation with it because that doctor made some grave mistakes with his or her own healthcare and obviously pushed a dangerous vaccine on their patients. And we now know large numbers of people have died after the vaccine, have suffered injuries or disabilities, and those doctors really owe their patients an apology. There was another tweet, you said, most people with long COVID are vaxxed, so multiple spike protein exposures are making Americans sick. And I know I've talked to UK friends and US friends, they seem to think the solution to long COVID is getting a booster and another booster. And tell me, tell us about that, because people are ill and with long COVID and some people it's quite a dark journey. It's true. Long COVID, remember this occurred before the vaccine, so the respiratory illness clearly causes it. It almost exclusively occurs in people who are sick enough to be hospitalized, about 50% will have it. They feel generally unwell, weight loss of skeletal muscle, hair loss, skin and nail changes, headache, ear ringing, fatigue, brain fog. It really bothers people. Now, with lesser degrees of severity of COVID, there's less and less long COVID. The best way to prevent it is actually early treatment. If we can snuff out the virus very early and get relatively little exposure to the virus in the body, that's the best way to do it. We again believe what's driving this is the pathogenic spike protein, the SARS-CoV-2 spike protein. Now, the vaccines install more spike protein. So there's no way the vaccine can make it better. It's going to clearly make it worse. But what we have in many countries, a good example is Australia, I was just there a few months ago. Virtually all of Australia was pre-vaccinated. They were all pre-vaccinated. Because the vaccines don't work, they get COVID anyway. So those who are having long COVID, it's far more severe in Australia because they've been pre-vaccinated and they've been loaded with the spike protein. So then we have to work our way out of it. But I wouldn't want anybody to think we should take a vaccine to reduce the chances of long COVID because the vaccines don't work, people get COVID anyway, and it just makes the long COVID syndromes worse. And so as we sit here today, a paper by Claussen and colleagues from Harvard suggests that 94% of Americans have already had COVID. I've already told you 75% took vaccines. So anybody with long COVID likely has had both exposures. Yeah, absolutely. There was another study or news piece from Trialsite News and that was on maternal mortality skyrocketing, gestational thrombotic complications up and MRA in the breast milk. And I think the MRA in the breast milk, that should fill a lot of people with big concern. I know that's been talked about before, but I mean, tell us about this because you end that tweet by saying COVID vaccine should never have been allowed in pregnant women. Early in 2021, Dr. Raphael Stricker in San Francisco, who runs, by the way, the largest fetal loss centre in the United States, he's an expert. He's an allergist, immunologist, but he's an expert on pregnant women and losing their babies. And Dr. Stricker and I published in trial site news that the COVID-19s were vaccine category X, and that's a regulatory category saying that they have a dangerous mechanism of action. They install the lethal spike protein in the body, and we have no experience in pregnant women. They were excluded from randomized trials and no assurances would be safe to the woman or the baby, none whatsoever. So it's pregnancy category X. It's very important. Pregnant women should have never taken the vaccine. Never, never. It doesn't matter what the doctors say. Pregnant women are responsible for themselves, their bodies, and their babies. Now, pregnant women have a lower risk of severe COVID outcomes as shown by Pinellas and colleagues in a paper in Annals of Internal Medicine. So, we weren't worried about pregnant women. If they got severe COVID, they're treatable, you know, and we can treat them with an array of drugs. By the way, hydroxychloroquine, very safe in pregnancy. We've, you know, it's been actually dedicated pregnancy studies with hydroxy. So, so we know for sure it's safe, as is aspirin, prednisone, and the other drugs that we normally use. Now, what's coming out is very, very disturbing. First, last summer in JAMA, a paper by Hannah and colleagues showed that breastfeeding women who take the vaccine, they actually are transmitting the messenger RNA through milk to the babies. And this is a terrible, very worrisome finding. Now genetic material getting into the bodies of recently arrived babies in the world. No idea what this is gonna do to the children. It can't be good. It's definitely not natural. The next piece of information came, first author is Hoyert, a single author paper, analysing data from the National Centre for Health Statistics. And there, it's published on the CDC website, March of 2023, showing record maternal mortality. That is, women dying during pregnancy or 42 days after the pregnancy. That was the definition according to their highest risk group, African Americans, but at all groups. They've erased progress in maternal mortality. Now, in the same sub-stack, I juxtapose the CDC report that indicates 65% of pregnant women have either taken the vaccine, ill-advised, before or during pregnancy. Despite our warnings that it's pregnancy category X, now we have the tragic case that unfolded last week of the death of U.S. Olympic sprinter Tori Bowie. And what we know there is this is just absolutely terrible. She's found dead at home, and she's seven months pregnant. The U.S. Track and Field Association has mandated COVID-19 vaccination, so they've been silent now. USTAF and family have been silent on whether or not she took the vaccine. But the concern is that she took it, and she had a fatal complication, either blood clot, heart damage, or some type of intracranial catastrophe. Wow, wow. And of course, we have learned, I think just could have been yesterday, about the reactivation of federal funding for Eco Health Alliance. To touch on that, because obviously, your government, our government, they haven't learned anything over these last three years. I think it's very intentional. Peter Daszak, who's the president of the Eco Health Alliance, they're basically an NIH contractor. They work with academic groups. They take the blueprint for viruses that are basically engineered in the lab by computer modelling by US researchers, and then they shuttle the plans over to the Chinese or other Asian countries where the the work is done in order to create new viruses. Daszak was involved in shuttling over the plans from Ralph Baric to create the chimeric SARS-CoV-2 virus. And Baric published this in 2015 in Nature Communications and proceedings of the National Academy of Sciences. They created SARS-CoV-2 and published the methods and how they did it, chimeric parts, of a virus from a bat, parts of a virus from a known coronavirus in order to get it to invade a human respiratory epithelial tract. Peter Daszak, early in 2021, led a group of doctors. After they had met on a conference call with Anthony Fauci and Francis Collins and Jeremy Farrar from the Wellcome Trust in the UK, Daszak led a group of authors to publish one of a series of papers. It was a dozen academic papers that were intentionally fraudulent. They were deceiving the public, describing the virus came out of nature when Daszak himself knew it came out of basically his plans that he drew up with Ralph Baric at the University of North Carolina Chapel Hill. This was an intentional cover-up campaign. This came out in the U.S. House Select Committee for the Coronavirus Origins, led by House Representative Comer, and it's shocking that the NIH, and actually the branch that Fauci used to lead, the National Immunology Infectious Disease and Allergy Branch, that they actually released his former R01 grant. His R01 grant was distilled to look among different bats to try to find viral strains that could jump into humans. I mean, it's just simply asking for trouble. Daszak is off, and you know, these are small grants, it was only about $500,000. It's not the size of the grant that matters, it's the fact that he's going to be able to now shuttle academic capital to Asia. Daszak says that now he's going to take this to the Duke University branch in Singapore, but the grant describes the bat caves in China going right back to the same work. So you're right. It appears as if the NIH is wilfully blind to this active cover-up. They don't care. They're pursuing this biological threat research. They must have been given orders high up to continue to do this. We have the National Security Administration, the FBI, Department of Energy and NIH, the House and the Senate all agreeing that the origin of SARS-CoV-2 was the lab. It was a US innovation contracted to the Chinese, and it leaked out of the lab in Wuhan, China. But to continue to pursue this, many are saying, and I agree, that it's reckless, it's irresponsible, and it really shows deep complicity that the biopharmaceutical complex is at work creating more biological threats for the world. And Peter Daszak is leading the way. Well, let's certainly watch what happens on that. On the, back to the specific medical side. You had written a piece on your website, and I think the headline was, myocarditis not recovering 80% at six months after vaccination. Tell us about it, because again, people are expecting that the body can recover quickly, but this says that only 20% of people with that had recovered over six months. Another disturbing report, this comes from Yale School of Medicine. They had 17 young teenagers in the hospital with myocarditis. Remember, teenagers should be going to high school. They shouldn't be hospitalized with myocarditis. They ill-advised took one of the COVID-19 vaccines and they got in deep trouble. Sky-high troponin levels showing heart damage, probably had chest pain, shortness of breath, arrhythmias, other manifestations, and they undergo serial MRIs. Now, they did rule out any exposure to COVID, so that was very clean. This is purely due to the vaccine. And they found that in 80%, the MRI at 200 days was not getting better. 20% it got better. You know, these small areas of late gadolinium enhancement that we see on MRI, they should resolve. Previous work done years ago by Bruckman and colleagues from Germany showed that the heart can remodel a small area of inflammation. I'm concerned that the genetic material, Pfizer and Moderna, is sufficiently long-lasting, the spike protein long-lasting, the body keeps producing more of it, that the children have ongoing cardiac injury and it's not clearing up on MRI. This could leave some to have a scar, and when they have a scar they could be at increased risk for two things, heart failure later on in life or cardiac arrest, particularly with sports. Wow, and on sports, we've seen a number of sports stars. The papers seem to be regularly full of another sports star having retired early or having complications. I mean, tell us about, because the stories are there, but maybe the dots are not necessarily being joined up. Well, let's take the issue of death in young people. There's a paper on my substack that I quote from about 15 years ago, and you can find it on the Courageous Discourse sub-stack, but it was basically describing death among college students. It does happen rarely. But the point of the paper was 87% of the time, we know the cause of death. Readily apparent, you know, cancer or suicide or homicide or a drug overdose, motor vehicle accident. What we're seeing now is scores of athletes, scores, sudden death and no explanation, no explanation at all. And it's called died suddenly, Edward Dowd has compiled an entire monograph on this in the life insurance roles of sudden unexplained death skyrocketing, mortality skyrocketing in every system. John Stockton, former Utah Jazz star, is keeping track of the athletes in the United States and there's hundreds now that have died, have died on the court or in practice. It seems to be the adrenaline that precipitates the sudden death with vaccine-induced myocarditis. And we knew actually before the COVID vaccines that we can't let young people with myocarditis exercise because it will trigger a sudden death event. So we knew this ahead of time. And what's happened is the sports teams have mandated the vaccines, but they haven't provided any safety safeguards for the athletes. And so they suffer heart damage. And then during competition, we never know who's going to have a cardiac arrest. Polycritus and myself analysed this issue, using really just a blog, a public blog of European athletes went down. But it's pretty rigorous. There had to be four or more reports, and you could easily identify that the athlete went down. And the data showed this, that before COVID-19, in the stable period of about 10 or 15 years before COVID-19, the number of cardiac arrests in Europe in the professional leagues, mainly soccer and rugby, but you call football. Age 35 and below, pro and semi-pro, number of cardiac arrests 29 per year. Now, fast forward with vaccination and in 2021 forward, that number came out now, you know, comparing apples to apples, 283. So there's about a tenfold increased risk of sudden death with mass-mandated COVID-19 vaccination. We have clear fatal cases of the COVID-19 vaccines causing myocarditis and sudden death with autopsies, so we know it's happening. And now the great concern is so many athletes have taken it, and they want to know what to do. They have great regret. It's been an absolute horror for our athletes unnecessarily to be vaccinated. A story that came out just today, and again we're seeing headlines that we wouldn't have seen a year ago, I think you're probably the same there, but the headline was, I had to reread this four or five times, the headline in the Daily Mirror was, Brits are dying in their tens of thousands and we don't really have any idea why. And they talked about between May and December 2022, that 32,000 excess deaths. And to have a headline that honest, we really have no idea. That's telling. And I'm assuming, I don't know whether it's in the States, whether you are beginning to, the media are beginning to drop little headlines like that in to begin to have the conversation or not yet. No, it's starting to happen. I was on national TV this morning and the morning anchor mentioned death after vaccination, so it's starting to come up. What we know is that every mortality system is reporting skyrocketing mortality, primarily of younger individuals. A paper published by Skidmore in BMC Infectious Diseases estimated in 2021 that 278,000 Americans had died due to the vaccine. And that matches roughly what VAERS was reporting for that year with a multiplier of about 30. It's very consistent with a paper from Columbia, same year, Pentecost and Seligman. So we have multiple sources of data. We think we lost about a quarter million Americans in the first year of the campaign due to the vaccine, a similar number in the next year. We may be over 600,000. Now, that's going to exceed the amount of casualties we had in the civil war. So this is a very, very serious problem. The vaccines were considered a wartime countermeasure. So the government agencies didn't consider it a public health measure. It's not considered like a standard pharmaceutical. It's considered like basically a war initiative, where there's going to be casualties. And boy, have there been casualties with this vaccine. So, before COVID, the general mortality that we had in the United States, or in UK for that matter, is known. And then it's 40% known antecedent heart disease, 40% known cancer, or 20% other causes. But in the vast majority, it's known. Death is not a mystery in our countries. And what we're seeing now is just a large fraction where they've taken a vaccine and they've died, and the official cause of death is unknown. And when autopsies are done, two papers, one by Schwab, one by Chavez, and there's been probably about 100 necropsy studies that we're compiling at this stage, they show that when an autopsy is done, 70 to 80% of the time, they have a clear-cut cause of death that's, related to the vaccine. Fatal myocarditis, fatal intracranial haemorrhage or clotting, blood clots and pulmonary embolism, or one of the fatal immunologic syndromes. These are published in well-described vaccine-induced thrombotic thrombocytopenic peria, multi-system inflammatory disease. So we have a huge scientific base that's indicating the vaccines are essentially killing large numbers of people worldwide. And is it possible that we could get to the point where any of these companies are liable for it, or is it irrelevant who's in the White House because they've been given that protection? People have said that two conditions may ultimately drop liability shields. The broad liability is not only from the 1986 Vaccine Indemnification Act, but also from the 2005 Prep Act, which says, listen, if we have an invasion of SARS-CoV-2, it's like a war. And so the wartime countermeasures are all, you know, have immunity. But the, two conditions are fraud, that if the public was defrauded by the vaccine manufacturers or the government agencies that were advancing them, the employers that were forcing them. And then the other is actually malicious intent, that indeed, if it was intentionally designed to be harmful, maybe documents would, you know, identify intent. But fraud and malicious intent are the two things that lawyers are looking at most closely. Because, you know, some of these cases are very obvious. Some take the vaccine, they die right in the vaccine centre, or they die the next day. Now, in the UK, as well as the United States, our government, by the way, holds both datasets. They have the entire death database, and they have the vaccine administration database. And if they merge them, we can see how many people die in the first day, in the second day, and look at the temporal relationship. Any death within 30 days, according to regulatory practice, should be assigned to the new drug, in this case the COVID-19 vaccine. And what's the, I mean, I had Tom Fitton on a few days ago from Judicial Watch, and they use freedom of information requests, which we have the same system here. They use it at another level than I've seen before. But will that have to be used as a way to get the data? Because obviously some of the data that had been released from Pfizer, there's so much and it's still been gone through. Will it have to be other freedom of information requests to get more of this data to actually put the jigsaw together. It's true. Well, you point out that the pharmaceutical companies kept their own separate safety data by obligation to the U.S. FDA for 90 days after release. So anything that happens 90 days after they release the product, they have to record everything. Pfizer had recorded 1,223 deaths within a few hours or a few days of taking their vaccine. So it should have been off the market in January of 2021, and Pfizer did not want to release that to the American public. They got a lawyer. The lawyer for the FDA wanted to block it for 55 years. So that was evidence that the US government is colluding with Pfizer to basically hide safety data in the Pfizer vaccine. Moderna still has not released their 90-day data, neither has Janssen or Novavax. So immediately, there should be strong calls for release of the safety data. It should be done under the prosecutorial power of the U.S. Congress, Senate, Department of Justice, Freedom of Information Act, but that's pretty slow and that's citizen-driven. We need our government agencies to step up and have the companies release the data. I mean, I want to know, is Moderna the same or even worse than Pfizer? I suspect it is, because all the studies that directly compared Moderna and Pfizer show greater toxicity with Moderna. There's a paper by Busby and colleagues on myocarditis that showed that. So, you know, our regulatory agencies, FDA, CDC, NIH, MHRA in the UK, and TGA in Australia, they have grossly let us down. They're actually participating in a fraudulent cover-up of a worldwide COVID-19 vaccine safety debacle. Just my final thought about you as a medical professional, and I've talked to UK doctors and they find it extremely difficult. Those who have spoken up, they've been punished. They've been pulled in front of disciplinary committees. And I know you've suffered as well. What is what is that like? And can doctors be vocal about their concerns or really have many had to stay quiet and how has it affected you? Doctors all need to step up. People are dying. They've died with the virus, untreated, and they've died now with the vaccine. This is not a time for doctors to be silent. They need to be bold and relentless, bring the truth forward. I haven't had a single doctor of my medical standing, the chief of medicine or division chief in cardiology or other medical specialty, actually ever look me in the eyes or send me an email or give me a call on the phone. Not a single one. They're absolutely ashamed of themselves. And I've had attacks from anonymous fact checkers making false claims. I've had attacks through certified letter or email, essentially trying to strip me of all my credentials. And every one of these attempts, I just get stronger. I've got a very, very strong voice out there in the world right now, and everybody knows it. I've given more media analysis. I've done more publications, more stage presentations on this issue than all the public health officials combined. And you can't find an area where I've been wrong or where I've been inconsistent. My views have changed as the virus has mutated, but I've been accurate and you know, the world knows it. And because I have so much media exposure, I have more than the public health officials. The world is coming to me and doctors in my circles for the truth. I think these government agencies and the biopharmaceutical complex is in trouble, and they're looking for the exits right now. We've had Francis Collins, head of the NIH, retire prematurely. Anthony Fauci, head of NIAID. We've seen now Rochelle Lewinsky, just two and a half years in the CDC, and a young woman, very junior, now leave the CDC. People are heading for the exits because they know they've committed wrongdoing. Dr. Peter McCullough, thank you so much for your time today. It's an honour to speak with you. Thank you. Thanks for having me. Be sure to follow me on my website, petermcullochmd.com. Make sure you check in my podcast, McCulloch Report on America Out Loud Talk Radio, 2 p.m. Eastern, Saturday and Sunday on the Apple iHeart Podcast Network starting on Tuesday. My book, Courage to Face COVID-19, and I'm starting a new TV show, full investigative TV show in Dallas on AFN Network with bestselling author John Leake. It's called The Second Opinion. I'll see you there or start in June. Thanks so much for having me on the program.

Last year, at the age of 41, I faced the heart-wrenching loss of three close friends within a mere five-month span. They were all between the ages of 41 and 44. The overwhelming grief I experienced plunged me into a profound depression for the first time in my life.Many of you are my friends, while others have yet to make my acquaintance. So it's probably a good idea if I start with a brief introduction. I'm a tech and marketing professional who helped build a web hosting company, LiquidWeb, alongside my friends Matt, Chris, Jer, and Gregg. Together, we grew the company to employ 480 employees on two continents and achieve $70 million in Annual Recurring Revenue (ARR). In 2015, we successfully sold the company to a private equity firm for a staggering $224 million.I've seldom mentioned this, as it may come across as boastful, but I became a multi-millionaire before reaching the age of 35. The wealth I amassed at such a young age exceeded my wildest expectations. This early financial success led me to believe that I had achieved life's ultimate goal, which I dubbed my "fake retirement." I didn't have a boss, so I indulged in late-night routines, sleeping until 2 pm and staying awake until 4 am. I often wore black t-shirts and sweatpants, projecting a slovenly image and demeanor. I ate whatever I pleased, avoided exercising, and generally shied away from physical activities. I even sported a shirt that mockingly read "SPORTS!" as an ironic statement.Before long, my unhealthy lifestyle began to take its toll. I gained over 60 pounds and developed a myriad of health issues, including high blood pressure, elevated triglycerides, high cholesterol, rosacea, and poor cardiac fitness. Simple tasks like climbing stairs left me sweating profusely, as I found myself in abysmal physical condition.My well-intentioned and caring doctors were quick to prescribe medications to address the various health issues resulting from my lifestyle. They prescribed fish oil for cholesterol management, Prednisone and Colchicine to combat gout, Valsartan to lower high blood pressure, and Fenofibrate to reduce elevated triglycerides.In no time, I found myself taking four pills daily. They appeared to be effective, at least initially, as my levels decreased. However, as I failed to make any lifestyle changes, my levels gradually began to rise again. Consequently, my dosages increased, putting me on an unsustainable and potentially harmful trajectory.Despite my poor health, life had its bright spots. I married an incredible woman who, I felt, was truly out of my league. Together, we had a son. I fulfilled my dreams of owning a lake house and a boat, and even drove a Tesla, allowing me to feel somewhat environmentally conscious amid my luxurious lifestyle. Additionally, I invested in companies that piqued my interest and became an active member of local boards that aligned with my passions.But suddenly, everything changed in February of 2022. My close friend Joe died of a heart attack due in part to alcohol abuse. Remarkably, throughout my 41 years of life, I had been fortunate enough to avoid experiencing the sudden loss of anyone close to me. Joe's passing deeply affected me, and I struggled to cope with the intense grief I encountered for the first time in my life.In July 2022, just a short while later, I faced the devastating loss of my best friend since age 2, Matt Hill, the founder of Liquidweb, who passed away at 41. Tragedy struck again merely 10 days later when my wife's cousin, a friend, and the officiant at our wedding, was fatally injured by a door in a bizarre accident. Despite my life appearing perfect by most standards, the overwhelming grief and confluence of these events plunged me into clinical depression. I would awaken feeling despondent and retire to bed with the same heavy sadness, struggling to find a sense of purpose.Rationally, I understood that my experiences paled in comparison to the hardships faced by others. This realization brought about feelings of guilt, making me question my right to feel depressed when I seemingly had it all. Yet, I found myself unable to break free from the grip of this profound sadness, even though logic told me it was unwarranted.My attempts to cope with the sadness proved unhelpful as well. Discussing my feelings with friends only seemed to dampen their spirits. Similarly, I unfairly burdened my wife with the expectation that she could miraculously heal my emotional pain. My frustration with her inability to do so put a strain on our marriage, and my demeanor became increasingly difficult to tolerate. I was truly insufferable to be around.I knew something had to change…“If every instinct you have is wrong, the opposite would have to be right.” Is a line Jerry Seinfeld says to George Costanza in the Seinfeld episode The Opposite.  I kept thinking of that quote. It was then that I revisited Admiral William H. McRaven's commencement speech, titled "Just Make Your Bed." In his address, he emphasizes the significance of waking up early and making your bed, as it provides an initial sense of accomplishment to start your day, setting off a chain reaction of positive transformations.“If you want to change the world, start by making your bed”. I decided this is where I would start!  Everyday I would wake up before 8am and make my bed.  This might seem like a small task, but for someone that was never a morning person, it was a challenge. This seemingly minor change of waking up early and making my bed had an unexpectedly profound impact on my life. It instilled in me a newfound confidence, nudged me towards an earlier bedtime, allowed me to enjoy breakfast with my 3-year-old, made me think twice about drinking alcohol the night before, and enhanced my productivity at work.It was a small change, but with a massive influence. Waking up early and making the bed was the antithesis of my behavior during depression. This got me thinking, what if I made more changes? Could they have an even greater impact? And so, I decided to embrace a "year of the opposite."My plan was simple: I would do the opposite of what I had done before. It didn't have to be radical, like speaking Spanish instead of English or biking instead of driving. It just had to challenge me and push me out of my comfort zone. For instance, since I never liked mustaches, I decided to grow one. And since I had never played golf, I decided to become a golfer. At the start of my Year of the Opposite, I didn't overwhelm myself with a long list of changes to make. Instead, I took it one challenge at a time. As I conquered each challenge, I gained more confidence and momentum.As my friends and family became aware of my Year of the Opposite, they started to offer their own suggestions for what I should tackle next. Before I knew it, the list of changes had grown longer and longer throughout the year.But because I was making the changes gradually and incrementally, the list didn't intimidate me. Instead, the longer the list grew the more confidence I gained to keep going, to keep pushing myself, and to keep discovering new things about myself along the way.In the following months, I made several significant changes: I quit drinking alcohol, stopped smoking weed, completed a half marathon, ran 7 miles barefooted, held my breath for 2 minutes and 45 seconds, ran a mile backward, briefly piloted an airplane, learned archery, swam about a mile across my lake, practiced shooting a pistol, won the Blazin Wing Challenge, and took a 9-minute cold plunge in a 35-degree lake, among other things.The transformation didn't occur instantaneously, but it certainly felt swift! Within two weeks, I experienced a daily surge of energy, as if I were on Adderall. Within a month, my depression had vanished. And within six months, all of my lifestyle-induced ailments were "cured." My high blood pressure, elevated triglycerides, rosacea, and high cholesterol were all resolved.In this newsletter, "The Year of the Opposite," I'll share the insights I gained and the outcomes I achieved. I'll discuss both the highs and the lows, as well as my blood work, test results, and the research and science behind what worked and what didn't.I want to be absolutely clear from the outset: none of my accomplishments over the past year were extraordinary or record-breaking. But that's precisely what makes them so remarkable! The changes I made are ones that anyone could implement if they desired to transform their life. If you're grappling with weight issues, sadness, anxiety, or depression, perhaps you could also adopt this approach and find it beneficial.Thank you so much for subscribing.  Next week I plan to share the results from my blood work, the changes in my cardiac fitness (VO2 Max), my weight change, and my blood pressure measurements.Uplift Weekly - Humans Are Awesome! Several years ago, I began sharing hard to find uplifting and positive stories on my Facebook page, summarizing them to the best of my ability. People seemed to really enjoy it. It's no secret that news outlets and social media often prioritize negative stories, as outrage tends to generate more clicks than happiness. Consequently, we find ourselves inundated with sensational, distressing stories from around the globe. This phenomenon not only contributes to societal polarization but also takes a toll on our mental well-being, as numerous studies have shown.With this newsletter, I hope to include a portion that I call "Uplift Weekly," I aim to counterbalance negativity by highlighting the remarkable achievements of humanity. I'll be focusing on technological advancements, scientific breakthroughs, and any news that instills a sense of hope and pride in our world and its people. Here's to hoping that the steady stream of human ingenuity provides ample content for our weekly dose of positivity! :)Without further ado, here is your Uplift Weekly* Scientists have made a breakthrough in creating a superconductor that works at room temperature, according to a recent publication in the journal Nature.* About 10-15% of our electricity on the electrical grid is lost just in the transmission of getting the energy to your house. When it comes to batteries, about 10-30% of the energy is lost. What if there were a type of material that electricity could flow through without any resistance and you didn't lose any of the power? That's what a SuperConductor is! Typically, superconductors only work at extremely low temperatures, which limits their practical applications. However, if a superconductor could work at room temperature, it could transform almost any technology that uses electric energy, from smartphones to maglev trains and even fusion power plants. The latest research, which still faces skepticism due to previous controversy around the scientists involved, could represent the first step towards this goal.* The Lives of Girls Around The World Are Getting Better. This article from Unicef highlights 6 amazing changes. * From 2012 to 2020, more girls completed secondary school - lower secondary school completion rose from 69% to 77% and upper secondary school completion rose from 49% to 59%.* The global adolescent birth rate has decreased from 51 to 42 births per 1,000 girls aged 15-19 since 2012.* New HIV infections among adolescent girls is down by 33% in a decade, but girls still account for most new infections among adolescents. * There are fewer child marriages. In the last 10 years the proportion of young women marriages has fallen from 23% to 19%. However, millions of girls still at risk of marrying young. * Female genital mutilation declined in the last decade, in the 31 countries where it is practiced it has decreased from 41% to 34%. Sadly it still affects the lives of millions of girls. Thank you for reading the first issue of The Year Of the Opposite Newsletter. Your support and encouragement mean a lot to me. If you're a paying subscriber, I'd be delighted to hear from you. Feel free to send me an email at travisstoliker@gmail.com or leave a comment below.If you found this newsletter valuable, please consider sharing it with someone who might enjoy it. Your help in spreading the word would be greatly appreciated. Get full access to Year Of The Opposite - Travis Stoliker's Substack at www.yearoftheopposite.com/subscribe

PODCAST HIGHLIGHTS: Coming Soon https://youtu.be/ALgozSStiNw Timestamps: 00:00 Introduction 04:25 Uric Acid blood test 05:58 Uric acid and cardiovascular disease connection 10:01 Physiological effects of uric acid 11:23 Foods that increase uric acid 11:54 Alopurinol medication 14:28 Colchicine 16:42 4 Stages of high uric acid 20:29 Vitamin C 21:45 Quercetin 24:44 Luteolin 27:09 Tart Cherry 28:00...... Continue Reading →

On this week's episode, Avery and Dylan discuss the shocking case of Mary Yoder. Dr. Mary Yoder was a successful chiropractor who seemed to have it all: a loving husband, three children, and a thriving practice. But on July 20th, 2015, she suddenly fell ill and died within 48 hours. The cause of death was later revealed to be colchicine poisoning, a rare and deadly substance that is used to treat gout. Who would want to kill Mary Yoder? And how did they get their hands on such a lethal drug?   Business Inquiries: truetime.pod@gmail.com Website: https://truetimepod.com/   Links: Go to https://betterhelp.com/truetime for 10% off your first month of therapy with BetterHelp and get matched with a therapist who will listen and help #sponsored Get your BarkBox today at https://barkbox.snlv.net/truetime She's Birdie: https://www.shesbirdie.com/?rfsn=7109833.8867bc She's Birdie 15% Discount Code: AVERYHAMMEL15 Amazon Affiliate Link - Birdie: https://amzn.to/3DCpDRd   Follow Us: Instagram: truetimepodcast Tik Tok: truetimepodcast Facebook: True Time Podcast Avery's Instagram: averyehammel Avery's Tik Tok: averyehammel   Case Sources: https://ocgov.net/sites/default/files/distatty/EvidenceProsecution/AdamYoder/M.%20Yoder-Medical%20Examiner%20Certification%20of%20Records.pdf https://www.oxygen.com/killer-motive/crime-news/kaitlyn-conley-poisons-ex-boyfriends-mom-mary-yoder https://medium.com/close-to-home/she-poisoned-her-ex-boyfriends-mother-45b34cd7427d https://thecinemaholic.com/mary-yoder-murder-where-is-kaitlyn-conley-now/ https://truecrimedaily.com/2016/10/26/receptionist-accused-of-murdering-chiropractor-boss-with-poison/ https://www.foxnews.com/entertainment/killer-motive-new-york-woman-poisoning-sons-ex-girlfriend-vengeance https://www.eannacefuneralhome.com/obituaries/Mary-Yoder-5/#!/TributeWall https://romesentinel.com/stories/waitress-cant-recall-when-husband-deceaseds-sister-were-at-diner,20191 https://www.newyorkupstate.com/news/2017/07/judge_gives_murder_suspect_katie_conley_1_more_chance_after_she_ignores_house_ar.html https://eu.uticaod.com/story/news/crime/2022/09/06/kaitlyn-conley-seeks-to-overturn-conviction-in-mary-yoder-killing/65469691007/ https://www.freekaitlynconley.com/ https://bpac.org.nz/BPJ/2014/September/safer-prescribing.aspx#:~:text=4-,Colchicine%20can%20cause%20significant%20toxicity%20and%20death,in%20some%20cases%20they%20overlap.&text=Acute%20overdose%20exceeding%200.5%20mg/kg%20is%20usually%20fatal.&text=Fatalities%20have%20been%20associated%20with%20doses%20as%20low%20as%207%20mg. https://www.mayoclinic.org/drugs-supplements/colchicine-oral-route/description/drg-20067653#:~:text=Colchicine%20is%20used%20to%20prevent,and%20heat https://www.mayoclinic.org/drugs-supplements/colchicine-oral-route/proper-use/drg-20067653   Intro Song: Trick or Treat (instrumental) by RYYZN https://soundcloud.com/ryyzn Creative Commons — Attribution 3.0 Unported — CC BY 3.0 Free Download / Stream: https://bit.ly/l_trick-or-treat Music promoted by Audio Library https://youtu.be/uNPXJ9CDzbc

Drs Stanley Cohen and Atul Deodhar discuss cardiovascular risk in patients with psoriatic arthritis and the impact of effective treatment. Relevant disclosures can be found with the episode show notes on Medscape (https://www.medscape.com/viewarticle/970784). The topics and discussions are planned, produced, and reviewed independently of advertiser. This podcast is intended only for US healthcare professionals. Resources Prevalence of Metabolic Syndrome in Psoriatic Arthritis: Systematic Literature Review and Results From the CARMA Cohort https://journals.lww.com/jclinrheum/Abstract/2022/03000/Prevalence_of_Metabolic_Syndrome_in_Psoriatic.22.aspx Metabolic Syndrome https://emedicine.medscape.com/article/165124-overview What Is the Framingham Risk Score (FRS)? https://www.medscape.com/answers/2500032-166149/what-is-the-framingham-risk-score-frs 2013 ACC/AHA Guideline on the Assessment of Cardiovascular Risk: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines https://www.sciencedirect.com/science/article/pii/S0735109713060312?via%3Dihub What Is the Systematic Coronary Risk Evaluation (SCORE)? https://www.medscape.com/answers/2500032-166154/what-is-the-systematic-coronary-risk-evaluation-score Anti-inflammatory Therapy With Canakinumab for Atherosclerotic Disease https://www.nejm.org/doi/pdf/10.1056/nejmoa1707914 Colchicine in Patients With Chronic Coronary Disease https://www.nejm.org/doi/10.1056/NEJMoa2021372 The Effects of Tumour Necrosis Factor Inhibitors, Methotrexate, Non-steroidal Anti-inflammatory Drugs and Corticosteroids on Cardiovascular Events in Rheumatoid Arthritis, Psoriasis and Psoriatic Arthritis: A Systematic Review and Meta-analysis https://ard.bmj.com/content/74/3/480 Psoriatic Arthritis Medication https://emedicine.medscape.com/article/2196539-medication Efficacy and Safety of Selective TYK2 Inhibitor, Deucravacitinib, in a Phase II Trial in Psoriatic Arthritis https://ard.bmj.com/content/81/6/815 FDA Requires Warnings About Increased Risk of Serious Heart-Related Events, Cancer, Blood Clots, and Death for JAK Inhibitors That Treat Certain Chronic Inflammatory Conditions https://www.fda.gov/drugs/drug-safety-and-availability/fda-requires-warnings-about-increased-risk-serious-heart-related-events-cancer-blood-clots-and-death

KSQD 5-18-2022: Problems with eyewitness testimony depends on confidence only for the first time questioned; The old anti-inflammatory drug colchicine has a new use in treating heart diseases; Microbiome fingerprint reveals severity of melanoma and possibly other types of cancer; Fecal transplant from young mouse into older mice extended life; Do anti-inflammatory drugs or natural supplements inhibit wound healing? Conflicting information about supplements found on the internet -- moderation is key; Weight gain and other changes with age in women is caused by reduction in estrogen after menopause; Very high HDL cholesterol level may be a genetic defect; Revealing an electrical signaling language among mushroom mycelia

Part two of our two-part episode, the murder of Mary Yoder. Yoder was a chiropractor in Buffalo N.Y. who was poisoned by Colchicine, and our guest -- Tony Martino -- was the digital forensic investigator who worked through the case.   As a 20-year veteran of the Utica, N.Y., Police Department, Tony Martino is an expert in cybersecurity, computer crime investigation and digital forensics. He's a recipient of the Wallie Howard Jr. Award for Excellence in Law Enforcement from the U.S. Attorney's Office. In this episode, we pick up where Part One left off: the first prosecution of the case ended in a hung jury, and the second trial was about to begin. But between cases Tony and his team found crucial digital evidence: a backup of the prime suspect's phone made before she had wiped key evidence from the device.

Part one of a two-part episode, with a case that involved so many truckloads of evidence we couldn't pack it all into one podcast. It involved two trials, three main suspects, and hours of forensic analysis by our guest and his team. This case is about the murder of Mary Yoder, a chiropractor in Buffalo N.Y. who was poisoned by Colchicine, a deadly substance that has agricultural and medical uses. Our guest today is Tony Martino, the forensic investigator who worked through the case.   As a 20-year veteran of the Utica, N.Y., Police Department, Anthony Martino is an expert in cybersecurity, computer crime investigation and digital forensics. A nine-year member of the United States Secret Service electronic crime task force, and co- founder of the Central New York Internet Crimes Against Children Task Force, Martino received the Wallie Howard Jr. Award for Excellence in Law Enforcement from the U.S. Attorney's Office.

The findings of COLCOT trial about colchicine post-MI

Show notes at pharmacyjoe.com/episode660. In this episode, I’ll discuss colchicine in patients admitted to hospital with COVID-19. The post 660: Does colchicine work in patients admitted to hospital with COVID-19? appeared first on Pharmacy Joe.

With the kind permission of investigative author John Leake—who recently joined us on the programme—TMR presents his important interview with the brilliant and courageous Dr Peter A McCullough. In the words of John Leake: "Dr. Peter McCullough has been the world's most prominent and vocal advocate for early outpatient treatment of SARS-CoV-2 (COVID-19) infection in order to prevent hospitalization and death. On May 19, 2021, I interviewed him about his efforts as a treating physician and researcher. From his unique vantage point, he has observed and documented a profoundly disturbing policy response to the pandemic—a policy response that may prove to be the greatest malpractice and malfeasance in the history of medicine and public health." "Dr McCullough is an internist, cardiologist, epidemiologist, and Professor of Medicine at Texas A & M College of Medicine, Dallas, TX USA. Since the outset of the pandemic, Dr McCullough has been a leader in the medical response to the COVID-19 disaster and has published “Pathophysiological Basis and Rationale for Early Outpatient Treatment of SARS-CoV-2 (COVID-19) Infection” the first synthesis of sequenced multidrug treatment of ambulatory patients infected with SARS-CoV-2 in the American Journal of Medicine and subsequently updated in Reviews in Cardiovascular Medicine. He has 40 peer-reviewed publications on the infection and has commented extensively on the medical response to the COVID-19 crisis in TheHill and on FOX NEWS Channel. On November 19, 2020, Dr McCullough testified in the US Senate Committee on Homeland Security and Governmental Affairs and throughout 2021 in the Texas Senate Committee on Health and Human Services, Colorado General Assembly, and New Hampshire Senate concerning many aspects of the pandemic response." [The audio included in this podcast is Copyright © 2021 John Leake, all rights reserved, and used here with express permission.] For show notes please visit https://themindrenewed.com

In this episode, you will know the new application of the ancient drug in cardiology and covid-19, you can also download the slides via this link:http://ecardiocast.com/wp-content/uploads/2021/06/colchicine.pdf

The recently published (in a pre-print server) COLCORONA study, sponsored by the Montreal Heart institute and conducted in 6 countries aimed to show if using colchicine would decrease risk of hospitalization and death in outpatients with COVID-19. Will it work? How's the study design? Learn the facts. Reference: Tardif J, Bouabdallaoui N, L'Allier P, et al. Efficacy of Colchicine in Non-Hospitalized Patients with COVID-19. Pre-Print. https://www.medrxiv.org/content/10.1101/2021.01.26.21250494v1 CPE details for GameChangers Podcast March 2021 Learning Objective: Apply the results of the CORCORONA study to patients with COVID-19 disease. 0107-0000-21-097-H01-P 0.25 CEU/2.5 Hrs (Knowledge) Initial Release Date: 03/02/21 Expiration Date: 03/02/24 Additional CPE information is located at https://www.ceimpact.com/podcast  See omnystudio.com/listener for privacy information. Learn more about your ad choices. Visit megaphone.fm/adchoices