Podcasts about pathological

Episode 212: Managing HFpEFHyo Mun and Jordan Redden (medical students) explain how to manage HFpEF with medications and touch some basics about nonpharmacologic treatments. Dr. Arreaza asks insightful questions to guide the discussion. Written by Hyo Mun, MSIV, American University of the Caribbean; and Jordan Redden, MSIV, Ross University School of Medicine. Comments by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Treatment of HFpEFArreaza: Mike, if you had to name the one therapy everyone with HFpEF should be on, what is it?Mike: That's easy! SGLT-2 inhibitors. This is the one slam-dunk we have in HFpEF. Empagliflozin (Jardiance) or dapagliflozin (Farxiga) should be started in essentially every patient with HFpEF, and it doesn't matter if they have diabetes or not.Jordan: And that's worth repeating, because people still think of these as “diabetes drugs.” They're not anymore. In HFpEF, SGLT-2 inhibitors reduce heart-failure hospitalizations, improve symptoms, improve quality of life, and even reduce cardiovascular death.Dr. Arreaza: They're also simple. Empagliflozin 10 mg daily or dapagliflozin 10 mg daily. No titration, no drama. The effectiveness of these meds was established around 2019 with DAPA-HF and later with DELIVER. These were trials thatdemonstrated that dapagliflozin reduces worsening heart failure and cardiovascular events across the full spectrum of heart failure, from reduced to preserved ejection fraction, independent of diabetes status.Mike: And the number needed to treat is about 28 to prevent one heart-failure hospitalization. That's excellent for a disease where we historically had almost nothing that worked.Jordan: They're also safe in chronic kidney disease down to an eGFR of about 25, which makes them even more useful in this population.Dr. Arreaza: Alright. We got SGLT-2 inhibitor, what's next?Mike: Volume management. Loop diuretics are still the backbone of symptom control in HFpEF. If the patient is volume overloaded, you diurese, and you diurese aggressively.Jordan: The goal is euvolemia. Dry weight, no edema, no orthopnea, no waking up gasping for air. A lot of these patients end up needing chronic oral loop diuretics to stay there.Dr. Arreaza: Something to remember: HFpEF patients don't tolerate congestion well, and being “a little wet” is not benign. Let's move into RAAS inhibition. Where do ARBs and ACE inhibitors fit in?Mike: Between ARBs and ACE inhibitors, ARBs are the winners in HFpEF. They actually reduce heart failure hospitalizations—drugs like candesartan, losartan, valsartan. ACE inhibitors? Not so much. They showed minimal benefit in older HFpEF patients, which is why we go with ARBs instead.Jordan: But a lot of clinicians get nervous about ACE inhibitors and ARBs because of kidney function, so it's worth talking through how these drugs actually work in the kidney.Dr. Arreaza: Yes, misunderstanding may lead to unnecessary drug discontinuation.Jordan: Under normal conditions, the afferent arteriole brings blood into the glomerulus, and the efferent arteriole is constricted by angiotensin II. That constriction keeps pressure high in the glomerulus and maintains filtration.Mike: Here's what happens with an ACE inhibitor: you block angiotensin II, the efferent arteriole relaxes, glomerular pressure drops, and GFR dips slightly. Creatinine bumps up a little, and that scares people, but that's actually the whole point—that's how you get kidney protection long-term.Jordan: High intraglomerular pressure causes hyperfiltration injury and scarring over time. Lowering that pressure protects the kidney long-term. The short-term GFR drop is the price you pay for long-term benefits.Dr. Arreaza: So let's talk about CKD, because this is where people panic.Mike: Right. ACE inhibitors and ARBs are not contraindicated in chronic kidney disease. In fact, they're recommended even in advanced stages. They reduce progression to kidney failure by about a third.Jordan: The key is how you use them. Start low. Check creatinine and potassium one to two weeks after starting, then periodically. A creatinine rise up to 30% from baseline is acceptable. That's not kidney injury, that's physiology.Dr. Arreaza: And what about potassium creeping up?Mike: You adjust the dose or add a potassium binder. You don't just automatically stop the drug.Dr. Arreaza: Now there is one absolute contraindication everyone needs to know about! (board exam test)Jordan: Bilateral renal artery stenosis. This is the big one. In these patients, the kidneys are completely dependent on angiotensin II–mediated efferent constriction to maintain GFR. Take that away, and GFR collapses.Mike: Creatinine can jump dramatically within days. If you see a creatinine rise of 20% or more shortly after starting an ACE inhibitor, you should be thinking about bilateral renal artery stenosis and stopping the drug immediately.Dr. Arreaza: After revascularization, though, many patients can tolerate ACE inhibitors again, so this isn't always permanent. What about cardiorenal syndrome? That's where things get uncomfortable.Mike: It is uncomfortable, but cardiorenal syndrome isn't a contraindication. These patients have severe heart failure and kidney disease, and their mortality is actually higher than patients with heart failure alone.Jordan: ACE inhibitors still reduce mortality and slow kidney disease progression in this group. Studies show that stopping ACE inhibitors during acute heart-failure admissions increases in-hospital mortality three- to four-fold.Dr. Arreaza: So we are cautious, but we don't avoid it.Mike: Exactly. Start low, titrate slowly, monitor labs closely, accept up to a 30% creatinine rise. You only stop if kidney function keeps worsening, or potassium gets dangerously high.Dr. Arreaza: Alright. Let's move on. What about mineralocorticoid receptor antagonists… MRA?Jordan: Spironolactone or eplerenone might reduce hospitalizations in HFpEF, but the data is mixed. This is more of a “select patients” situation.Mike: And you have to watch potassium and kidney function carefully, especially if they're already on an ACE inhibitor or ARB.Dr. Arreaza: What about sacubitril-valsartan, also known as Entresto®?Mike: Entresto may help patients with mildly reduced EF roughly in the 45 to 57% range. It's not first-line for HFpEF, but in select patients, it's reasonable.Dr. Arreaza: Now let's clarify one of the biggest sources of confusion: beta blockers.Jordan: Beta blockers are not a treatment for HFpEF itself. They're only indicated if the patient has another reason to be on them, like coronary disease or atrial fibrillation.Mike: And timing really matters here. You absolutely do not start beta blockers during acute decompensated heart failure. Their negative inotropic effects can make things worse when patients are volume overloaded.Jordan: But, and this is critical, you also don't stop them if the patient is already taking one. Abrupt withdrawal causes a sympathetic surge and dramatically increases mortality.Dr. Arreaza: If a patient is admitted on a beta blocker, what do we do?Mike: Continue it at the same dose or reduce it slightly if they're really unstable. Once they're euvolemic and stable, you can carefully titrate up.Jordan: And watch for chronotropic incompetence. HFpEF patients often rely on heart-rate response to exercise, and beta blockers can worsen exercise intolerance.Dr. Arreaza: Beyond medications, HFpEF is really about treating comorbidities. Aerobic activity can be an initial strategy to improve exercise intolerance and has evidence of improving aerobic function and quality of life. Sodium restriction: improves symptoms, does not decrease risk of death or hospitalizations.Mike: Hypertension control is huge. For diabetes, the SGLT-2 inhibitors will perform double duty. For obesity, weight loss improves symptoms, and GLP-1 agonists like semaglutide are absolute gamechangers.Jordan: Don't forget sleep apnea, atrial fibrillation, and lifestyle. Exercise improves the quality of life, even if it doesn't change hard outcomes. Lifestyle is the main treatment. Dr. Arreaza: And when should you refer to cardiology?Mike: You should refer when the diagnosis isn't clear; symptoms are not responding to treatment, difficult volume management, end-organ dysfunction, or if you are concerned about advanced heart failure.Dr. Arreaza: So, it has been a great discussion. What is the takeaway?Mike: HFpEF treatment isn't about one magic drug -- it's about volume control, SGLT2 inhibitors, smart use of RAAS blockade, and aggressive management of comorbidities.Jordan: And it's understanding the physiology, so you don't withhold life-saving therapies out of fear.Dr. Arreaza: Well said. If you found this helpful, share it with a friend or colleague and rate us wherever you listen. This is Dr. Arreaza, signing off.Jordan/Mike: Thanks! Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Barzin A, Barnhouse KK, Kane SF. Heart Failure With Preserved Ejection Fraction. Am Fam Physician. 2025;112(4):435-440.Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation. 2022;145(18):e895-e1032.Kittleson MM, Panjrath GS, Amancherla K, et al. 2023 ACC expert consensus decision pathway on management of heart failure with preserved ejection fraction. J Am Coll Cardiol. 2023;81(18):1835-1878.Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461.Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2022;387(12):1089-1098.Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med. 2014;370(15):1383-1392.Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction. Lancet. 2003;362(9386):777-781.Solomon SD, McMurray JJV, Anand IS, et al. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609-1620.Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069-1084.Xie Y, Xu E, Bowe B, Al-Aly Z. Long-term cardiovascular outcomes of COVID-19. Nat Med. 2022;28(3):583-590.Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from COVID-19. JAMA Cardiol. 2020;5(11):1265-1273.Basso C, Leone O, Rizzo S, et al. Pathological features of COVID-19-associated myocardial injury. Eur Heart J. 2020;41(39):3827-3835.Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med. 2021;27(4):601-615.Badve SV, Roberts MA, Hawley CM, et al. Effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in adults with estimated GFR less than 60 mL/min per 1.73 m². Ann Intern Med. 2024;177(8):953-963.Navis G, Faber HJ, de Zeeuw D, de Jong PE. ACE inhibitors and the kidney: a risk-benefit assessment. Drug Saf. 1996;15(3):200-211.Textor SC, Novick AC, Tarazi RC, et al. Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease. Ann Intern Med. 1985;102(3):308-314.Hackam DG, Spence JD, Garg AX, Textor SC. Role of renin-angiotensin system blockade in atherosclerotic renal artery stenosis and renovascular hypertension. Hypertension. 2007;50(6):998-1003.Ronco C, Haapio M, House AA, et al. Cardiorenal syndrome. J Am Coll Cardiol. 2008;52(19):1527-1539.Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure. JACC Heart Fail. 2015;3(8):647-653.Jondeau G, Neuder Y, Eicher JC, et al. B-CONVINCED: Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode. Eur Heart J. 2009;30(18):2186-2192.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Episode 211: Understanding HFpEF.  Hyo Mun and Jordan Redden (medical students) explain the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and how it differentiates from HFrEF. Dr. Arreaza asks insightful questions and summarizes some key elements of HFpEF. Written by Hyo Mun, MS4, American University of the Caribbean; and Jordan Redden, MS4, Ross University School of Medicine. Comments and edits by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.What is EF? Just imagine, the heart is a pump, blood gets into the heart through the veins, the ventricles fill up and then squeeze the blood out. So, the percent of blood that is pumped out is the EF. Let's start at the beginning. What is HFpEF?Mike: HFpEF stands for heart failure with preserved ejection fraction. Basically, these patients squeeze normally—their ejection fraction is 50% or higher—but here's the thing: the heart can't relax and fill the way it should. The muscle gets stiff, almost like a thick leather boot that just won't stretch. And because the ventricle can't fill properly, pressure starts backing up into the lungs and the rest of the body. That's when patients start experiencing shortness of breath, leg swelling, fatigue—all those classic symptoms.Dr. Arreaza: And this is where people get fooled by the ejection fraction.Mike: Exactly. The ejectionfraction tells you total left ventricular emptying, not just forward flow.Jordan: The classic example is severe mitral regurgitation. You can eject 60% of your blood volume and still be in cardiogenic shock because most of that blood is leaking backward into the left atrium instead of going into the aorta. So, you get pulmonary edema, hypotension, fatigue, all with a “normal” EF. Which is honestly terrifying if you're over-relying on echo reports without thinking clinically.Dr. Arreaza: And in HFpEF, functional mitral regurgitation often shows up later in the disease. It's not usually the primary cause; it's more of a marker of advanced disease. Moderate to severe MR in HFpEF independently predicts worse outcomes, including a higher risk of mortality or heart failure hospitalization. So, let's contrast this with HFrEF. How are these two different?Mike: HFrEF—heart failure with reduced ejection fraction—is a pumping problem. The heart muscle is weak and can't contracteffectively. Ejection fraction drops below 40%, and this is your classic systolic dysfunction.Jordan: HFpEF, on the other hand, is diastolic dysfunction. The heart muscle is thick, fibrotic, and noncompliant. It squeezes fine, but it just doesn't relax, even though the EF looks reassuring on paper.Mike: I like to explain it this way: HFrEF is a weak heart that can't squeeze. HFpEF is a stiff heart that can't relax. Totally different problems.Dr. Arreaza: And then there's the gray zone: heart failure with mildly reduced EF, or HFmrEF. That's an EF between 41 and 49% with evidence of elevated filling pressures. It really shares the features of both worlds. So, what actually causes HFpEF versus HFrEF?Jordan: HFpEF is basically what happens when all the problems of modern living catch up with you. You've got chronic hypertension, obesity, diabetes, metabolic syndrome, aging, systemic inflammation—all of these things slowly remodel the heart over years. The muscle gets thick and stiff, and eventually the ventricle just loses its ability to relax. So, HFpEF is really a disease of metabolic dysfunction and chronic stress in the heart. Mike: HFrEF is more about direct injury. Think about myocardial infarctions, ischemic cardiomyopathy, viral myocarditis, alcohol toxicity, chemotherapy like doxorubicin, genetic cardiomyopathies, or chronic uncontrolled tachycardia. These insults actually damage or kill heart muscle cells, leading to a dilated, weak ventricle that can't pump effectively.Dr. Arreaza: So the short version: HFpEF is caused by chronic metabolic and hypertensive stress, while HFrEF is caused mainly by myocardial damage. A question we get a lot: does HFpEF eventually turn into HFrEF? What do you guys think?Mike: In most cases, no. HFpEF patients usually stay HFpEF throughout their disease course. They don't just “burn out” and turn into HFrEF.Jordan: They're generally separate disease entities with different pathophysiology. A patient with HFpEF can develop HFrEF if they have a big myocardial infarction or ongoing ischemia that damages the muscle, but that's not the natural progression.Mike: Interestingly though, the opposite can happen. Some HFrEF patients actually improve their ejection fraction with good medical therapy—that's called HF with improved EF—and it's a great sign that treatment is working.Dr. Arreaza: Another question. How do HFpEF and HFrEF compare to restrictive cardiomyopathy and constrictive pericarditis?Jordan: Clinically, they can all look very similar: dyspnea, edema, fatigue, but the underlying mechanisms are completely different.Mike: In HFpEF, the myocardium itself is stiff from hypertrophy and fibrosis. The problem is intrinsic to the heart muscle, and EF stays preserved. Echoshows diastolic dysfunction with elevated filling pressures.Jordan: In HFrEF, the myocardium is weak. The ventricle is often dilated and contracts poorly, with a reduced EF.Mike: Restrictive cardiomyopathy is different. Here, the myocardium gets infiltrated by abnormal stuff—amyloid, iron, sarcoid—and that makes it extremely stiff. It can look like HFpEF on the surface, but it's usually more severe. On Echo You'll see biatrial enlargement, small ventricles, and preserved EF. And importantly, it's a pathologic diagnosis, so you need advanced imaging or biopsy to confirm it.Jordan: Constrictive pericarditis is another mimic, but here the myocardium is usually normal. The problem is that the pericardium is thickened, calcified, and rigid. This will physically prevent the heart from being filled. Imaging shows pericardial thickening, septal bounce, and respiratory variation in flow, and cath shows equalization of diastolic pressures, which is the hallmark of constrictive pericarditis.Dr. Arreaza: So the takeaway is: HFpEF is a clinical syndrome driven by common metabolic and hypertensive causes, while restrictive and constrictive diseases are specific pathologic entities. If “HFpEF” is unusually severe or not responding to treatment, you need to think beyond HFpEF. Which type of heart failure is more common right now?Mike: Good question, the answer is: HFpEF. It now accounts for up to 60% of all heart failure cases, and it's still rising.Dr. Arreaza: Why is that?Jordan: Because people are living longer, gaining weight, and developing more metabolic syndrome. HFpEF thrives in older, or people with obesity, hypertension, or diabetes: basically, the modern American population. At the same time, better treatment of acute MIs means fewer people are developing HFrEF from massive heart attacks.Mike: HFpEF is the heart failure epidemic of the 21st century. It's honestly the cardiology equivalent of type 2 diabetes.Dr. Arreaza: Let's talk aboutCOVID-19. (2025 and still talking about it) Does it actually increase heart failure risk?Mike: Yes, absolutely. COVID increases both acute and long-term heart failure risk.Jordan: During acute infection, COVID can cause myocarditis, trigger massive inflammation, and precipitate acute decompensated heart failure, especially in patients with pre-existing disease. It also causes microthrombi, which can injure the myocardium.Mike: And after infection, even mild cases are linked to a significantly higher risk of developing new heart failure within the following year. Both HFpEF and HFrEF rates go up.Dr. Arreaza: I remember seeing this in 2021, we had a patient with acute COVID and HFrEF, her EF was about 10%, I lost contact with the patient and at the end I don't know what happened to her. What's the pathophysiology of COVID and heart failure?Mike: COVID causes direct viral injury through ACE2 receptors, triggers massive inflammation that damages the endothelium and heart muscle, leads to microvascular clotting and fibrosis—all mechanisms that promote HFpEF.Jordan: Add autonomic dysfunction, persistent low-grade inflammation, and worsening metabolic syndrome, and you've got a perfect storm for heart failure.Dr. Arreaza: Bottom line: COVID is a cardiovascular disease as much as a respiratory one. If someone had COVID and now has unexplained dyspnea or fatigue, think about heart failure. Get an echo, get a BNP, start treatment. Last big question: why did we have so many therapies for HFrEF but essentially none for HFpEF for years?Mike: HFrEF is mechanistically straightforward. You've got a weak heart with excessive neurohormonal activation going on — so you block RAAS, block the sympathetic system, drop the afterload. The drugs make sense.Jordan: HFpEF is messy. It's not one disease. It's stiffness, fibrosis, inflammation, microvascular dysfunction, metabolic disease, atrial fibrillation, all overlapping. One drug can't fix all of that.Mike: And some drugs that worked beautifully in HFrEF actually made HFpEF worse. Take Beta blockers, for example.  They slow heart rate, which is a problem because HFpEF patients rely on heart rate to maintain their cardiac output.Jordan: The breakthrough came with SGLT-2 inhibitors: diabetes drugs that unexpectedly addressed multiple HFpEF mechanisms at once: volume, metabolism, inflammation, and myocardial energetics.Dr. Arreaza: The miracle drug for HFpEF! Alright, let's wrap up.Mike: Bottom line: HFpEF is common, complex, and dangerous: even if the EF looks “normal.”Jordan: And if you're relying on ejection fraction alone, HFpEF will humble you every time.Dr. Arreaza: If you liked this episode, share it with a friend or a colleague and rate us wherever you listen. This is Dr. Arreaza, signing off.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Barzin A, Barnhouse KK, Kane SF. Heart Failure With Preserved Ejection Fraction. Am Fam Physician. 2025;112(4):435-440.Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation. 2022;145(18):e895-e1032.Kittleson MM, Panjrath GS, Amancherla K, et al. 2023 ACC expert consensus decision pathway on management of heart failure with preserved ejection fraction. J Am Coll Cardiol. 2023;81(18):1835-1878.Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461.Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2022;387(12):1089-1098.Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med. 2014;370(15):1383-1392.Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction. Lancet. 2003;362(9386):777-781.Solomon SD, McMurray JJV, Anand IS, et al. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609-1620.Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069-1084.Xie Y, Xu E, Bowe B, Al-Aly Z. Long-term cardiovascular outcomes of COVID-19. Nat Med. 2022;28(3):583-590.Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from COVID-19. JAMA Cardiol. 2020;5(11):1265-1273.Basso C, Leone O, Rizzo S, et al. Pathological features of COVID-19-associated myocardial injury. Eur Heart J. 2020;41(39):3827-3835.Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med. 2021;27(4):601-615.Badve SV, Roberts MA, Hawley CM, et al. Effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in adults with estimated GFR less than 60 mL/min per 1.73 m². Ann Intern Med. 2024;177(8):953-963.Navis G, Faber HJ, de Zeeuw D, de Jong PE. ACE inhibitors and the kidney: a risk-benefit assessment. Drug Saf. 1996;15(3):200-211.Textor SC, Novick AC, Tarazi RC, et al. Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease. Ann Intern Med. 1985;102(3):308-314.Hackam DG, Spence JD, Garg AX, Textor SC. Role of renin-angiotensin system blockade in atherosclerotic renal artery stenosis and renovascular hypertension. Hypertension. 2007;50(6):998-1003.Ronco C, Haapio M, House AA, et al. Cardiorenal syndrome. J Am Coll Cardiol. 2008;52(19):1527-1539.Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure. JACC Heart Fail. 2015;3(8):647-653.Jondeau G, Neuder Y, Eicher JC, et al. B-CONVINCED: Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode. Eur Heart J. 2009;30(18):2186-2192.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/. 

On this episode of the CPC Podcast, Kevin, Brandon, and Rachel delve into the themes of complacency and self-deception within the context of faith and personal growth. Through humorous anecdotes and deep reflections, the hosts of CPC Together discuss practical ways to cultivate awareness, remembrance, and repentance.

Welcome to The Mental Breakdown and Psychreg Podcast! Today, Dr. Berney and Dr. Marshall discuss the signs of typical cognitive decline that happens as we age, and symptoms that suggest the need for an evaluation to rule out a potential dementia. Read the articles from The National Library of Medicine here, from Presbyterian Living here, and from the Alzheimer's Association here. You can now follow Dr. Marshall on twitter, as well! Dr. Berney and Dr. Marshall are happy to announce the release of their new parenting e-book, Handbook for Raising an Emotionally Healthy Child Part 2: Attention. You can get your copy from Amazon here. We hope that you will join us each morning so that we can help you make your day the best it can be! See you tomorrow. Become a patron and support our work at http://www.Patreon.com/thementalbreakdown. Visit Psychreg for blog posts covering a variety of topics within the fields of mental health and psychology. The Parenting Your ADHD Child course is now on YouTube! Check it out at the Paedeia YouTube Channel. The Handbook for Raising an Emotionally Health Child Part 1: Behavior Management is now available on kindle! Get your copy today! The Elimination Diet Manual is now available on kindle and nook! Get your copy today! Follow us on Twitter and Facebook and subscribe to our YouTube Channels, Paedeia and The Mental Breakdown. Please leave us a review on iTunes so that others might find our podcast and join in on the conversation!

Welcome to The Mental Breakdown and Psychreg Podcast! Today, Dr. Berney and Dr. Marshall discuss the signs of typical cognitive decline that happens as we age, and symptoms that suggest the need for an evaluation to rule out a potential dementia. Read the articles from The National Library of Medicine here, from Presbyterian Living here, and from the Alzheimer's Association here. You can now follow Dr. Marshall on twitter, as well! Dr. Berney and Dr. Marshall are happy to announce the release of their new parenting e-book, Handbook for Raising an Emotionally Healthy Child Part 2: Attention. You can get your copy from Amazon here. We hope that you will join us each morning so that we can help you make your day the best it can be! See you tomorrow. Become a patron and support our work at http://www.Patreon.com/thementalbreakdown. Visit Psychreg for blog posts covering a variety of topics within the fields of mental health and psychology. The Parenting Your ADHD Child course is now on YouTube! Check it out at the Paedeia YouTube Channel. The Handbook for Raising an Emotionally Health Child Part 1: Behavior Management is now available on kindle! Get your copy today! The Elimination Diet Manual is now available on kindle and nook! Get your copy today! Follow us on Twitter and Facebook and subscribe to our YouTube Channels, Paedeia and The Mental Breakdown. Please leave us a review on iTunes so that others might find our podcast and join in on the conversation!

Josh Slocum is back after almost 4 years of pushing back against this culture war. We talk about the madness becoming mainstream, cluster B psychology, the external locus of control, happiness in Canada, Alberta separation, media influence, reversal of reality, the climate thing, Trump and Carney and civil war.   In the second half we chat about American exceptionalism, the AWFUL's, these bitches, solutions, sex typical hard wire, sports, Tate on PBD, man hating, what they will say in the future, election fraud, hard realities, EU collapse, and cultural fatigue on this rise.   Mommy has been running the show, Dad hasn't come home for 60 years. Illuminating the abnormal psychology that's become the new normal.   We are in an abusive relationship with our government, our media, and increasingly, ourselves. Today's activists use the same tools as abusive families. They keep us in fear while we wonder if we've lost our minds. It's not a passing fashion and its not well-meaning misguided activism. It's abuse dynamics. Pathological narcissism, indiscriminate rage, and tactical emotional break-downs by bullies who claim that they are the victims. Domestic abuse has gone public, and feral. Join us to talk about it. https://www.youtube.com/@DisaffectedPodcast https://substack.com/@disaffectedpod?utm_source=account-card https://disaffected.com/   To gain access to the second half of show and our Plus feed for audio and podcast please clink the link http://www.grimericaoutlawed.ca/support.   For second half of video (when applicable and audio) go to our Substack and Subscribe. https://grimericaoutlawed.substack.com/ or to our Locals  https://grimericaoutlawed.locals.com/ or Rokfin www.Rokfin.com/Grimerica Patreon https://www.patreon.com/grimericaoutlawed   Support the show directly: https://grimericacbd.com/ CBD / THC Tinctures and Gummies https://grimerica.ca/support-2/ Our Adultbrain Audiobook Podcast and Website: www.adultbrain.ca Our Audiobook Youtube Channel:  https://www.youtube.com/@adultbrainaudiobookpublishing/videos Check out our next trip/conference/meetup - Contact at the Cabin www.contactatthecabin.com Other affiliated shows: www.grimerica.ca The OG Grimerica Show Join the chat / hangout with a bunch of fellow Grimericans  Https://t.me.grimerica grimerica.ca/chats   Discord Chats Darren's book www.acanadianshame.ca Eh-List Podcast and site: https://eh-list.ca/ Eh-List YouTube: https://www.youtube.com/@TheEh-List www.Rokfin.com/Grimerica Our channel on free speech Rokfin Leave a review on iTunes and/or Stitcher: https://itunes.apple.com/ca/podcast/grimerica-outlawed http://www.stitcher.com/podcast/grimerica-outlawed Sign up for our newsletter http://www.grimerica.ca/news SPAM Graham = and send him your synchronicities, feedback, strange experiences and psychedelic trip reports!! graham@grimerica.com InstaGRAM https://www.instagram.com/the_grimerica_show_podcast/  Purchase swag, with partial proceeds donated to the show www.grimerica.ca/swag Send us a postcard or letter http://www.grimerica.ca/contact/ ART - Napolean Duheme's site http://www.lostbreadcomic.com/  MUSIC Tru Northperception, Felix's Site sirfelix.bandcamp.com 

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Dr. Margarita Fedorova outlines how genetic, environmental, and pathological factors interact in Parkinson's disease and what this means for patient counseling.  Show citation:  Blauwendraat C, Morris HR, Van Keuren-Jensen K, Noyce AJ, Singleton AB. The temporal order of genetic, environmental, and pathological risk factors in Parkinson's disease: paving the way to prevention. Lancet Neurol. 2025;24(11):969-975. doi:10.1016/S1474-4422(25)00271-6  Show transcript:  Dr. Margarita Federova: Welcome to Neurology Minute. My name is Margarita Fedorova, and I'm a neurology resident at the Cleveland Clinic. Today we're exploring a framework for understanding how genetic, environmental, and pathological factors interact in Parkinson's disease and what this means for how we counsel our patients. A personal view paper by Blauwendraat and colleagues, published in The Lancet Neurology in September 2025, addresses a critical question. We've identified over 100 genetic loci for Parkinson's, but how do they act? The common saying is genetics loads the gun and environment pulls the trigger, but this paper suggests the relationship may be more complex. The key tool here is alpha-synuclein seeding amplification assays or SAAs. These detect misfolded alpha-synuclein protein in cerebrospinal fluid. Over 90% of Parkinson's patients test positive for misfolded alpha-synuclein using this assay. But here's what's notable. 2% to 16% of neurologically healthy older adults also test positive with prevalence increasing with age. This means there are more asymptomatic people with detectable alpha-synuclein pathology than people with actual Parkinson's disease. Most of these asymptomatic individuals will never develop symptoms. This raises an important question. What determines who converts to a disease and who doesn't? By integrating SAA results with genetic data, researchers can examine whether genetic factors drive initial protein misfolding or whether they modulate the response to pathology triggered by environmental or random events. Preliminary data suggests polygenic risk scores don't strongly associate with SAA positivity in healthy older adults. In other words, people with high genetic risk for Parkinson's aren't necessarily more likely to have misfolded alpha-synuclein if they're healthy. This suggests most Parkinson's genetic risk factors may not be causing initial misfolding. Instead, they may be determining what happens afterward, such as whether the pathology progresses to clinical disease. LRRK2 mutations support this model. About 33% of LRRK2 related Parkinson's patients are SAA-negative compared to only 7% in sporadic disease. This means many people with LRRK2 mutations develop Parkinson's without the typical alpha-synuclein pathology. LRRK2 mutations also show varied pathology. Sometimes alpha-synuclein, sometimes tau, sometimes neither. This suggests LRRK2 may modulate responses to different initiating events rather than directly causing protein misfolding. What does this mean for us as clinicians? Asymptomatic SAA-positive individuals could represent a window for intervention. If we can understand what protects them from converting to disease or what triggers that conversion, we could enable earlier identification of at risk individuals and potentially intervene before symptoms develop. The authors call for large scale studies using SAAs in older populations, combined with genetic analysis and longitudinal follow-up. By integrating pathological biomarkers with genetic and environmental data, we can better understand the temporal sequence of events in development of Parkinson's. This approach could fundamentally change how we think about disease prevention and early intervention, potentially allowing us to identify at risk individuals before symptoms appear and develop targeted prevention strategies. That's your neurology minute for today. Keep exploring, and we'll see you next time. If you want to read more, please find the paper by Cornelis Blauwendraat et al titled The Temporal Order of Genetic, Environmental and Pathological Risk Factors in Parkinson's Disease: Paving the Way to Prevention, published online in September 2025 in Lancet Neurology.

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Chelsey Cole is a psychotherapist focusing on narcissistic abuse and complex trauma. She is the best-selling author of If Only I'd Known, and has joined Dr. Rob to explore what narcissism really is and what it isn't. She offers clear signs and strategies of a grandiose narcissist, and offers hope for any partner who has been frustrated by assuming their narcissistic partner views relationships through the same lens they do. Unless you understand the views of a narcissist, you will never succeed in true communication and connection with them.    TAKEAWAYS: [2:10] Is he just selfish or is he a true narcissist?  [5:26] Characteristics of the grandiose narcissist.  [9:38] The danger of transactional views of relationships.  [10:31] Stages of the narcissist spectrum.  [14:45] Remorse motivation in a narcissist's mind.  [17:07] Steps in the cycle of narcissistic abuse.  [20:03] Characteristics of the moderate to severe narcissists.  [23:01] You're not crazy! Narcissists actually want the conflict you are avoiding.  [25:49] Pathological insecurity versus healthy insecurity.    RESOURCES: Sex and Relationship Healing @RobWeissMSW Sex Addiction 101  Seeking Integrity Free Sexual Addiction Screening Assessment Partner Sexuality Survey Chelsey Cole   Seeking Integrity Podcasts are produced in partnership with Podfly Productions.    QUOTES: “True narcissists don't have the stuff that it takes to create deep, committed relationships.”  “Narcissists believe they are always the exception to every rule.”  “For a true narcissist, their default is to not care about you, and to put their needs first.”  “Narcissists actually seek the conflict you are avoiding.” 

Welcome to episode 78 of Rapaport's Reality! Starring Kebe & Michael Rapaport. This is the reality television podcast that the whole reality world has been waiting for. The Rapaport's are here to discuss: The Golden Age of Reality TV Gia Guiadice Huge Shoutout New Years Resolution Jen Shaw coming out of jail Real Housewives Redemption Pathological In Potomac? Wendy & Eddie's jail situation 9th Year of Marriage Being in Israel Leak Gate & Grading Heather Gay Taking That Reality Ride This episode is not to be missed! An iHeartPodcasts Show Stand Up Comedy Tickets on sale at: MichaelRapaportComedy.com Produced by DBPodcasts.comFollow @dbpodcasts, @rapaportsreality, @michaelrapaport on Instagram & X Subscribe to Rapaport's Reality Feeds: iHeartRadio: https://www.iheart.com/podcast/867-rapaports-reality-with-keb-171162927/ Apple Podcasts: https://podcasts.apple.com/us/podcast/rapaports-reality-with-kebe-michael-rapaport/id1744160673 Spotify: https://open.spotify.com/show/3a9ArixCtWRhfpfo1Tz7MR Pandora: https://www.pandora.com/podcast/rapaports-reality-with-kebe-michael-rapaport/PC:1001087456 Amazon Music: https://music.amazon.com/podcasts/a776919e-ad8c-4b4b-90c6-f28e41fe1d40/rapaports-reality-with-kebe-michael-rapaportSee omnystudio.com/listener for privacy information.

BUFFALO, NY — November 18, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 3, 2025, titled “Growth hormone excess drives liver aging via increased glycation stress.” In this study, led by first author Parminder Singh alongside with corresponding authors Pankaj Kapahi from the Buck Institute for Research on Aging and Andrzej Bartke from Southern Illinois University School of Medicine, researchers investigated how elevated growth hormone (GH) levels contribute to liver aging and dysfunction. They found that excess GH disrupts liver metabolism in ways that resemble aging-related liver damage. The study suggests that managing glycation stress may help prevent or treat liver diseases linked to abnormal hormone levels. Excess GH is known to cause different disorders, but its long-term impact on internal organs like the liver has remained unclear. To address this, researchers used a mouse model engineered to overproduce bovine GH and examined how chronic hormone exposure affects liver function over time. “Pathological conditions such as acromegaly or pituitary tumors result in elevated circulating GH levels, which have been implicated in a spectrum of metabolic disorders, potentially by regulating liver metabolism.” The team found that young mice with GH overexpression showed molecular and cellular patterns similar to those in naturally aged livers. In both groups, genes involved in metabolism were suppressed, while those linked to immune and inflammatory responses were activated. On one hand, the metabolic changes were associated with the buildup of advanced glycation end products, harmful compounds formed when sugars attach to proteins or fats without proper regulation. On the other hand, the immune and inflammatory changes reflected a process known as “inflammaging,” a form of chronic, low-grade inflammation commonly associated with aging. By revealing the overlap between hormone-driven and age-related liver dysfunction, the study provides new insight into how GH may accelerate aging processes. Importantly, the team showed that reducing glycation stress can reverse many of these negative effects. Mice treated with a compound that lowers glycation levels demonstrated improved liver health, reduced insulin resistance, and enhanced physical function. This intervention also corrected several abnormal genetic patterns caused by excess GH. The findings point to a potential therapeutic strategy for liver diseases associated with aging and hormonal imbalances. Overall, this research identifies glycation and its byproducts as key contributors to liver damage caused by excess GH. It suggests that targeting glycation could offer broad therapeutic benefits, not only for hormone-related conditions but also for supporting liver health during aging. DOI - https://doi.org/10.18632/aging.206327 Corresponding authors - Andrzej Bartke - abartke@siumed.edu and Pankaj Kapahi - pkapahi@buckinstitute.org Abstract video - https://www.youtube.com/watch?v=6v8xi5muLwA Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206327 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, growth hormone, glycation stress, Gly-Low To learn more about the journal, visit https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

A cultural and clinical blind spot: the rise of female-coded Cluster B traits. Why do so many go undiagnosed? Why has misbehavior been rebranded as “trauma”?In this episode I break down how ideology, therapy culture, and social media have distorted our understanding of female pathology and why it matters more than ever.Join me for the Live Q&A this Saturday 1 PM ET—I'll take your questions. Upgrade to joing the Live and to watch the bonus video below! This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit hannahspier.substack.com/subscribe

This episode marks the beginning of a new educational series from Heal NPD, featuring Dr. Mark Ettensohn and his associates: Deanna Young, Psy.D. and Danté Spencer, MA. This series offers a rare window into clinical reasoning and supervision, bringing viewers inside real discussions about theory, diagnosis, and treatment of personality pathology. In this first seminar, the group examines an influential paper by Pincus & Lukowitsky (2010) and explores one of the central challenges in the field: how to define pathological narcissism. The conversation addresses the criterion problem surrounding narcissism. That is, the lack of a unified construct definition. It traces how this has led to conflicting models and measures of narcissism. Topics include the distinction between pathological narcissism and NPD, the interplay of grandiosity and vulnerability, the overlap with depression and trauma, and emerging dimensional approaches to understanding personality. This series is designed for clinicians, students, and anyone interested in a deeper and more integrative understanding of narcissism, personality, and self-regulation. To learn more about our work, visit www.HealNPD.org Citation for the article discussed: Pincus, A. L., & Lukowitsky, M. R. (2010). Pathological narcissism and narcissistic personality disorder. Annual Review of Clinical Psychology, 6, 421–446. https://doi.org/10.1146/annurev.clinpsy.121208.131215

In this episode, Jason Ferguson - former D1 football player, top sales leader, and now renowned author and speaker - shares GOLD about overcoming adversity, tapping into realistic but tenacious optimism, and building daily wins through high-performance routines.Check out Jason's book, "Nobody's Legend: Let Go of Who You Were, Rewrite Your Story, and Take Back Your Life": https://jfinspires.com/book/

During this session from the 2025 Neurodiverse Love Conference, Daniel Dashnaw discusses the concept of demand avoidance, challenging the conventional view that it is inherently pathological. Demand avoidance can sometimes serve as a healthy response to overwhelm, misaligned expectations, or autonomy needs.  He will also briefly touch on research from neurodiversity, social dynamics, and stress regulation. His goal is to expand demand avoidance as a spectrum behavior that can signal unmet needs or adaptive coping rather than wholesale dysfunction. He will also offer a few clinical insights into recognizing, understanding, and addressing demand avoidance in a compassionate and constructive way.Daniel Dashnaw MFT, is the co-founder of Couples Therapy Inc., the largest evidence-based couples therapy practice in the USA. Daniel specializes in working with the neurodiverse, in both his part time work in a public health agency, and his private practice. Known for his compassionate yet no-nonsense approach, he draws upon cutting-edge research and therapeutic techniques, including the Gottman Method and Emotionally Focused Therapy, to help couples rebuild trust, improve communication, and deepen their connection. You can reach Daniel at the link below:https://danieldashnawcouplestherapy.com/

Distinguishing Humane Nationalism from Pathological Ideologies Guest Name: Daniel Mahoney Summary:Nationalism must be distinguished from pathological forms like "blood and soil" ideology, which champions ethnic rooting and the subordination of others. Moderate, humane national loyalty is tied to self-government and common humanity, rejecting the path that leads to "zoological wars." Critics often unfairly conflate nationalism with isolationism or imperialism. 1916 SWITZERLAND

Distinguishing Humane Nationalism from Pathological Ideologies Guest Name: Daniel Mahoney Summary:Nationalism must be distinguished from pathological forms like "blood and soil" ideology, which champions ethnic rooting and the subordination of others. Moderate, humane national loyalty is tied to self-government and common humanity, rejecting the path that leads to "zoological wars." Critics often unfairly conflate nationalism with isolationism or imperialism. 1865 MONTENEGRO

We asked Dr. Im about the role of sleep in injury recovery, what is considered optimal sleep, and when someone should be referred for pathological sleep.Timestamps(8:50) What signs & symptoms may indicate less than optimal sleep(11:09) Sleep and recovery(17:16) Stages of sleep(18:23) Adapting stages of sleep(21:32) Recommendations to improve sleep quality(25:40) Special considerations for maintaining optimal sleep(27:21) Role of naps in improving sleep quality(30:39) Optimal timing of naps(31:49) Relationship of mental health and sleep(34:40) Pathological sleep(41:05) Changing the circadian rhythm (43:59) When to refer an athlete with pathological sleep(46:30) Monitoring sleepAction Item: What are some talking points you use with athletes to educate about their sleep and importance of sleep?--AT CORNER FACEBOOK GROUP: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://www.facebook.com/groups/atcornerpodcast⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Instagram, Website, YouTube, and other links: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠atcornerds.wixsite.com/home/links⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠EMAIL US: atcornerds@gmail.comSAVE on ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Medbridge⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠: Use code ATCORNER to get $101 off your subscriptionWant to host a podcast like ours? Use our link to sign up for Zencastr, the service we use to record our interviews: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://zencastr.com/?via=atcorner⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Music: Jahzzar (betterwithmusic.com) CC BY-SA---Sandy & Randy

Dr. Nadine Macaluso is a licensed marriage and family therapist, trauma expert, and author. Once married to Jordan Belfort, the "Wolf of Wall Street," she now uses her personal experiences and professional expertise to help others heal from trauma, build healthier relationships, and thrive. She is also the founder of the Surthriver™ community, where she empowers women to transform their pain into purpose.Connect with Dr. Nadine!https://www.instagram.com/therealdrnadinehttps://www.tiktok.com/@drnaelmftVisit Her Website To Learn More!drnae.comCHAPTERS:0:00 – Introduction1:45 – Meet Nadine Macaluso2:50 – Nadine talks about the relationship between her children and Jordan Belfort3:24 – Has Jordan changed over the years from being a pathological husband?4:02 – How Nadine raised her kids despite Jordan's traits5:02 – Nadine talks about her relationship with her father5:57 – Andy reflects on being raised by a single mom7:26 – Nadine's thoughts on Andrew Tate's view of “potent time with kids”8:36 – Should Andy avoid people with childhood trauma?9:49 – How Nadine was “used” in her past relationship with a pathological husband11:04 – Nadine shares when she decided to become a therapist12:02 – Nadine shares how therapy helped her survive chaos13:22 – Nadine talks about applying psychology to raising her children14:25 – Should parents cuddle babies every 3 hours or let them cry it out?15:28 – Nadine talks about the effects of using iPads with kids17:09 – Why families struggle to communicate feelings19:08 – Andy reflects on his experience with his dad only calling when he needed money21:01 – Are men becoming too emotional today?21:56 – Should men share financial struggles with their partners?23:10 – Did Andy's single mom influence his siblings' love lives?24:59 – Nadine shares how she met her husband after Jordan25:49 – Nadine talks about life inside a marriage26:59 – Nadine shares advice for finding a best-friend partner in life27:34 – Nadine shares the things she is giving the most of and needs the most in her life28:55 – How Nadine balances inbound requests vs. reaching out29:38 – Is Nadine introverted or extroverted?30:40 – Nadine talks about independence and individuality in relationships31:27 – Nadine talks about how she built her personal brand32:36 – Did Nadine finish her studies before or after the movie?33:26 – Meeting Margot Robbie before filming The Wolf of Wall Street33:43 – How actors play pathological characters in The Wolf of Wall Street34:09 – Nadine talks about the difference between narcissistic and pathological people35:43 – Nadine shares how to spot a pathological person39:11 – How Nadine's kids handled the Belfort name and the movie40:13 – How Nadine built a safe space for her kids40:55 – Nadine shares how to have proper communication about drugs with children42:19 – Did Nadine's kids openly share about their relationships?42:52 – Nadine shares how her kids always get along with each other44:01 – Nadine talks about how she built her $30/month Surthriver community for women46:16 – Does Nadine ever ask Jordan for business advice?46:41 – Who the Surthriver Community is for and how to join47:33 – Nadine talks about the meaning of a trauma bond48:06 – What are codependent relationships?48:59 – Nadine's recent life discoveries50:59 – Nadine's goals and focus for the next 6 months51:30 – Connect with Nadine52:11 – Outro

Your favorite psychologists, John Gartner and Harry Segal, review Trump's disastrous Alaska summit and marvel at how he has reverted to Putin's absurd Ukraine talking points. They also speak with Richard Wood, eminent clinical psychologist and expert on malignant narcissism, who shares his insights on Trump's pathology. Be sure to subscribe wherever you get your podcasts: Our site Subscribe on iTunes Subscribe on Spotify Subscribe on Amazon Music Subscribe on iHeartRadio We open with a “therapy session” framework—our way of inviting you into a collective examination of how Trump's behavior has infiltrated our daily lives. Too often, political coverage tip-toes around psychological insights. Not here. We argue that to understand Trump's volatility, his tantrums, and his rule-by-instinct style, you have to start with his inner life. Dr. Woods steps in to define malignant narcissism: a toxic cocktail of grandiosity, ruthlessness, and paranoia. He walks us through examples—obsessive self-aggrandizement, zero empathy for victims, and a ferocious need to dominate. When you hear Trump lob insults or bully subordinates, that's not business as usual. It's the playbook of someone for whom status and control override every other impulse. Too many pundits tiptoe around Trump's slurred speeches, jumbled tweets, and off-script rants. We don't. We break down the warning signs of cognitive fragility—memory lapses, word-salad tangents, even motor-skill stumbles. These aren't just gaffes; they're red flags that a leader who can't stay on message is a risk to national security. Why do millions still cheer him on? In a frank discussion, we and Dr. Woods explore how Trump transforms fear into solidarity. His promises of vengeance and identity-based appeals speak to grievances deeper than policy. When democracy feels abstract, demagoguery feels personal—and that's how authoritarian figures like Trump cement loyalty. We draw parallels to his moves in Washington itself: weaponizing local police, twisting museum exhibits to sanitize his image, and rewriting history to suit his narrative. It's not accidental. It's an orchestrated strategy to freeze dissent and manufacture consent. This episode doesn't leave you helpless. We outline concrete steps—peer education, fact-based conversations, and refusing to normalize destructive behavior cloaked in charismatic populism. Psychological insight isn't therapy; it's ammunition. It helps us name the tactics, defang the threats, and reclaim our public life. If you want to see past the tweets and the rallies and understand the man behind the façade, tune in to Shrinking Trump wherever you get your podcasts. Let's sharpen our collective lens—because democracy demands more than headline-chasing. It demands that we understand, confront, and ultimately shrink the power of rulers unfit to lead. Learn more about your ad choices. Visit megaphone.fm/adchoices

Join us (Dr. Henry Emmons and Dr. Aimee Prasek) as we dig into this phenomenon of 'pathological productivity.' We'll talk about how over-focusing on productivity can lead to mental and physical health issues, why us humans have a deep aversion to idleness, why rest can feel "bad," and most importantly, how we can get out of this kind of pathological productivity and embrace rest and play in ways that nourish us.   If you enjoyed this episode, please rate and review us wherever you listen to your favorite podcasts! Sources and Notes: Joy Lab Program: Take the next leap in your wellbeing journey with step-by-step practices to help you build and maintain the elements of joy in your life. Joy Lab episodes referenced: Where's Your Third Place? [ep. 171] Sometimes I Just Sits... (the power of solitude) [ep. 74] Four Thousand Weeks by Oliver Burkeman Series on authenticity from our Joy Lab podcast: Unmasking Your True Self: Exploring Authenticity and Awe [ep. 216] Embrace Your True Self: Accepted, Connected, & In The Game [ep. 217] The Road Most Travelled: Awakening Through Suffering [ep. 218]  Follow Your Bliss: Awakening to Joy [ep. 219] The Still Small Voice: Awakening with soulfulness [ep. 220] Chandola, T., Ling, W., & Rouxel, P. (2025). Are anxious Mondays associated with HPA-axis dysregulation? A longitudinal study of older adults in England. Journal of Affective Disorders, 389. Access here.   Full transcript here.   Please remember that this content is for informational and educational purposes only. It is not intended to provide medical advice and is not a replacement for advice and treatment from a medical professional. Please consult your doctor or other qualified health professional before beginning any diet change, supplement, or lifestyle program. Please see our terms for more information. If you or someone you know is struggling or in crisis, help is available. Call the NAMI HelpLine: 1-800-950-6264 available Monday through Friday, 10 a.m. – 10 p.m., ET. OR text "HelpLine" to 62640 or email NAMI at helpline@nami.org. Visit NAMI for more. You can also call or text SAMHSA at 988 or chat 988lifeline.org.  

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Will Karen Read's lying be centerstage in her civil trial? Here's one tale that Karen Read told that she has never had any questions about. Let's talk about it!Get access to exclusive content & support the podcast by becoming a Patron today! https://patreon.com/robertaglasstruecrimereportThrow a tip in the tip jar! https://buymeacoffee.com/robertaglassSupport Roberta by sending a donation via Venmo. https://venmo.com/robertaglassBecome a channnel member for custom Emojis, first looks and exclusive streams here: https://youtube.com/@robertaglass/joinShow Notes: Masshole Mafia "The Feds Are Coming! For Turtleboy & Karen Read?" - https://youtu.be/gWruNzMK1aE?si=P5K0oI366tUmsD-ZInnocence Fraud Watch "Cop Killer Karen Read, Her Alleged 5pm Appointment With Mansfield Plumber Called Richie & 6pm Call With Her Depraved Father William Read. Incl. Questions On Wrongful Death Civil Lawsuit" -https://theerrorsthatplaguethemiscarriageofjusticemovement.home.blog/2025/07/18/cop-killer-karen-read-her-5pm-appointment-with-alleged-mansfield-plumber-called-richie-6pm-call-with-her-depraved-father-william-read-incl-civil-suit/Choosing Therapy "17 Manipulation Tactics of Abusers" - https://www.choosingtherapy.com/manipulation-tactics/Thank you Patrons!Therese Tunks, JC, Lizzy D, Elizabeth Drake, Texas Mimi, Barb, Deborah Shults, Debra Ratliff, Stephanie Lamberson, Maryellen Sudol, Mona, Karen Pacini, Jen Buell, Marie Horton, ER, Rosie Grace, B. Rabbit, Sally Merrick, Amanda D, Mary B, Mrs Jones, Amy Gill, Eileen, Wesley Loves Octoberfest, Erin (Kitties1993), Anna Quint, Cici Guteriez, Sandra Loves GatsbyHannna, Christy, Jen Buell, Elle Solari, Carol Cardella, Jennifer Harmon, DoxieMama65, Carol Holderman, Joan Mahon, Marcie Denton, Rosanne Aponte, Johnny Jay, Jude Barnes, JenTheRN, Victoria Devenish, Jeri Falk, Kimberly Lovelace, Penni Miller, Jil, Janet Gardner, Jayne Wallace (JaynesWhirled), Pat Brooks, Jennifer Klearman, Judy Brown, Linda Lazzaro, Suzanne Kniffin, Susan Hicks, Jeff Meadors, D Samlam, Pat Brooks, Cythnia, Bonnie Schoeneman-Dilley, Diane Larsen, Mary, Kimberly Philipson, Cat Stewart, Cindy Pochesci, Kevin Crecy, Renee Chavez, Melba Pourteau, Julie K Thomas, Mia Wallace, Stark Stuff, Kayce Taylor, Alice, Dean, GiGi5, Jennifer Crum, Dana Natale, Bewildered Beauty, Pepper, Joan Chakonas, Blythe, Pat Dell, Lorraine Reid, T.B., Melissa, Victoria Gray Bross, Toni Woodland, Danbrit, Kenny Haines and Toni Natalie.

Episode 198: Fatigue.  Future doctors Redden and Ibrahim discuss with Dr. Arreaza the different causes of fatigue, including physical and mental illnesses. Dr. Arreaza describes the steps to evaluate fatigue. Some common misconceptions are explained, such as vitamin D deficiency and “chronic Lyme disease”. Written by Michael Ibrahim, MSIV, and Jordan Redden, MSIV, Ross University School of Medicine. Edits and comments by Hector Arreaza, MDYou are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Dr. Arreaza: Today is a great day to talk about fatigue. It is one of the most common and most complex complaints we see in primary care. It involves physical, mental, and emotional health. So today, we're walking through a case, breaking down causes, red flags, and how to work it up without ordering the entire lab catalog.Michael:Case: This is a 34-year-old female who comes in saying, "I've been feeling drained for the past 3 months." She says she's been sleeping 8 hours a night but still wakes up tired. No recent illnesses, no weight loss, fever, or night sweats. She denies depression or anxiety but does report a lot of work stress and taking care of her two little ones at home. She drinks 2 cups of coffee a day, doesn't drink alcohol, and doesn't use drugs. No medications, just a multivitamin. Regular menstrual cycles—but she's noticed they've been heavier recently.Jordan:Fatigue is a persistent sense of exhaustion that isn't relieved by rest. It's different from sleepiness or muscle weakness.Classification based on timeline:    •   Acute fatigue: less than 1 month    •   Subacute: 1 to 6 months    •   Chronic: more than 6 monthsThis patient's case is subacute—going on 3 months now.Dr. Arreaza:And we can think about fatigue in types:    •   Physical fatigue: like muscle tiredness after activity    •   Mental fatigue: trouble concentrating or thinking clearly (physical + mental when you are a medical student or resident)    •    Pathological fatigue: which isn't proportional to effort and doesn't get better with restAnd of course, there's chronic fatigue syndrome, also called myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is a diagnosis of exclusion after 6 months of disabling fatigue with other symptoms.Michael:The differential is massive. So, we can also group it by systems.Jordan:Let's run through the big ones.Endocrine / Metabolic Causes    • Hypothyroidism: A classic cause of fatigue. Often associated with cold intolerance, weight gain, dry skin, and constipation. May be subtle and underdiagnosed, especially in women.    • Diabetes Mellitus: Both hyperglycemia and hypoglycemia can cause fatigue. Look for polyuria, polydipsia, weight loss, or blurry vision in undiagnosed diabetes.    • Adrenal Insufficiency: Think of this when fatigue is paired with hypotension, weight loss, salt craving, or hyperpigmentation. Can be primary (Addison's) or secondary (e.g., due to long-term steroid use).Michael: Hematologic Causes    • Anemia (especially iron deficiency): Very common, especially in menstruating women. Look for fatigue with pallor, shortness of breath on exertion, and sometimes pica (craving non-food items).     • Vitamin B12 or Folate Deficiency: B12 deficiency may present with fatigue plus neurologic symptoms like numbness, tingling, or gait issues. Folate deficiency tends to present with megaloblastic anemia and fatigue.    • Anemia of Chronic Disease: Seen in patients with chronic inflammatory conditions like RA, infections, or CKD. Typically mild, normocytic, and improves when the underlying disease is treated.Michael: Psychiatric Causes    • Depression: A major driver of fatigue, often underreported. May include anhedonia, sleep disturbance, appetite changes, or guilt. Sometimes presents with only somatic complaints.    • Anxiety Disorders: Mental fatigue, poor sleep quality, and hypervigilance can leave patients feeling constantly drained.    • Burnout Syndrome: Especially common in caregivers, healthcare workers, and educators. Emotional exhaustion, depersonalization, and reduced personal accomplishment are key features.Jordan: Infectious Causes    • Epstein-Barr Virus (EBV):Mononucleosis is a well-known cause of fatigue, sometimes lasting weeks. May also have sore throat, lymphadenopathy, and splenomegaly.    • HIV:Consider it in high-risk individuals. Fatigue can be an early sign, along with weight loss, recurrent infections, or night sweats.    • Hepatitis (B or C):Can present with chronic fatigue, especially if liver enzymes are elevated. Screen at-risk individuals.    • Post-viral Syndromes / Long COVID:Fatigue that lingers for weeks or months after viral infection. Often, it includes brain fog, muscle aches, and post-exertional malaise.Important: Chronic Lyme disease is a controversial term without a consistent clinical definition and is often used to describe patients with persistent, nonspecific symptoms not supported by objective evidence of Lyme infection. Leading medical organizations reject the term and instead recognize "post-treatment Lyme disease syndrome" (PTLDS) for persistent symptoms following confirmed, treated Lyme disease, emphasizing that prolonged antibiotic therapy is not effective. Research shows no benefit—and potential harm—from extended antibiotic use, and patients with unexplained chronic symptoms should be thoroughly evaluated for other possible diagnoses.Michael: Cardiopulmonary Causes    •   Congestive Heart Failure (CHF): Fatigue from poor perfusion and low cardiac output. Often comes with dyspnea on exertion, edema, and orthopnea.    •   Chronic Obstructive Pulmonary Disease (COPD): Look for a smoking history, chronic cough, and fatigue from hypoxia or the work of breathing.    •   Obstructive Sleep Apnea (OSA): Daytime fatigue despite adequate hours of sleep. Patients may snore, gasp, or report morning headaches. High suspicion in obese or hypertensive patients.Jordan:Autoimmune / Inflammatory Causes    •   Systemic Lupus Erythematosus (SLE): Fatigue is often an early symptom. May also see rash, arthritis, photosensitivity, or renal involvement.    •   Rheumatoid Arthritis (RA): Fatigue from systemic inflammation. Morning stiffness, joint pain, and elevated inflammatory markers point to RA.    •   Fibromyalgia: A chronic pain syndrome with widespread tenderness, fatigue, nonrestorative sleep, and sometimes cognitive complaints ("fibro fog").Cancer / Malignancy    •   Leukemia, lymphoma, or solid tumors: Fatigue can be the first symptom, often accompanied by weight loss, night sweats, or unexplained fevers. Consider when no other cause is evident.Michael:Medications:Common culprits include:    ◦   Beta-blockers: Can slow heart rate too much.    ◦   Antihistamines: Sedating H1 blockers like diphenhydramine.    ◦   Sedatives or sleep aids: Can cause grogginess and daytime sedation.    •   Substance Withdrawal: Fatigue can be seen in withdrawal from alcohol, opioids, or stimulants. Caffeine withdrawal, though mild, can also contribute.Dr. Arreaza:Whenever we evaluate fatigue, we need to keep an eye out for red flags. These should raise suspicion for something more serious:    •   Unintentional weight loss    •   Night sweats    •   Persistent fever    •   Neurologic symptoms    •   Lymphadenopathy    •   Jaundice    •   Palpitations or chest painThis patient doesn't have these—but that doesn't mean we stop here.Dr. Arreaza:Those are a lot of causes, we can evaluate fatigue following 7 steps:Characterize the fatigue.Look for organic illness.Evaluate medications and substances.Perform psychiatric screening.Ask questions about quantity and quality of sleep.Physical examination.Undertake investigations.So, students, do we send the whole lab panel?Michael:Not necessarily. Labs should be guided by history and physical. But here's a good initial panel:    •   CBC: To check for anemia or infection    • TSH: Screen for hypothyroidism    • CMP: Look at electrolytes, kidney, and liver function    • Ferritin and iron studies    • B12, folate    • ESR/CRP for inflammation (not specific)    • HbA1c if diabetes is on the radarJordan:And if needed, consider:    • HIV, EBV, hepatitis panel    • ANA, RF    • Cortisol or ACTH stimulation testImaging? Now that's rare—unless there are specific signs. Like chest X-ray for possible cancer or TB, or sleep study if you suspect OSA.Dr. Arreaza:Unaddressed fatigue isn't just inconvenient. It can impact on quality of life, affect job performance, lead to mood disorders, delay diagnosis of serious illness, increase risk of accidents—especially driving. So, don't ignore your patients with fatigue!Jordan:And some people—like women, caregivers, or shift workers—are especially at risk.Michael:The cornerstone of treatment is addressing the underlying cause.Jordan:If it's iron-deficiency anemia—treat it. If it's depression—get mental health involved. But there's also: Lifestyle Support: Better sleep hygiene, light physical activity, mindfulness or CBT for stress, balanced nutrition—especially iron and protein, limit caffeine and alcoholDr. Arreaza:Sometimes medications help—but rarely. And for chronic fatigue syndrome, the current best strategies are graded exercise therapy and CBT, along with managing specific symptoms. Beta-alanine has potential to modestly improve muscular endurance and reduce fatigue in older adults, but more high-quality research is needed.SSRI: fluoxetine and sertraline. Iron supplements: Even without anemia, but low ferritin [Anecdote about low ferritin patient]Jordan:This case reminds us to take fatigue seriously. In her case, it may be multifactorial—work stress, caregiving burden, and possibly iron-deficiency anemia. So, how would we wrap up this conversation, Michael?Michael:We don't need to order everything under the sun. A focused history and exam, targeted labs, and being alert to red flags can guide us.Jordan:And don't forget the basics—sleep, stress, and nutrition. These are just as powerful as any prescription.Dr. Arreaza:We hope today's episode on fatigue has given you a clear framework and some practical tips. If you enjoyed this episode, share it and subscribe for more evidence-based medicine!Jordan:Take care—and get some rest~___________________________Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:DynaMed. (2023). Fatigue in adults. EBSCO Information Services. https://www.dynamed.com (Access requires subscription)Jason, L. A., Sunnquist, M., Brown, A., Newton, J. L., Strand, E. B., & Vernon, S. D. (2015). Chronic fatigue syndrome versus systemic exertion intolerance disease. Fatigue: Biomedicine, Health & Behavior, 3(3), 127–141. https://doi.org/10.1080/21641846.2015.1051291Kroenke, K., & Mangelsdorff, A. D. (1989). Common symptoms in ambulatory care: Incidence, evaluation, therapy, and outcome. The American Journal of Medicine, 86(3), 262–266. https://doi.org/10.1016/0002-9343(89)90293-3National Institute for Health and Care Excellence. (2021). Myalgic encephalomyelitis (or encephalopathy)/chronic fatigue syndrome: Diagnosis and management (NICE Guideline No. NG206). https://www.nice.org.uk/guidance/ng206UpToDate. (n.d.). Approach to the adult patient with fatigue. Wolters Kluwer. https://www.uptodate.com (Access requires subscription)Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

In this episode, we review the high-yield topic ⁠Pathological RBC Forms⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠from the Hematology section at ⁠⁠⁠⁠Medbullets.com⁠⁠⁠⁠⁠⁠Follow⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Medbullets⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ on social media:Facebook: www.facebook.com/medbulletsInstagram: www.instagram.com/medbulletsofficialTwitter: www.twitter.com/medbulletsLinkedin: https://www.linkedin.com/company/medbullets

Across centuries and continents, documented cases reveal supernatural forces that escalated beyond typical paranormal activity — resulting in physical harm, unexplained deaths, and encounters that defy conventional explanations.Join the DARKNESS SYNDICATE: https://weirddarkness.com/syndicateIN THIS EPISODE: Many ghost stories are frightening but leave the person encountering them shaken, but no more worse for wear. Perhaps a light touch on the shoulder, the moving of an object, a whisper in the ear, or a cold chill for the more intense cases. But then there are those hauntings that leave the person hysterical… or physically hurt… or even dead. We'll look at some of the most violent ghosts and hauntings of all time. (History's Most Violent Ghosts) *** Dixon, Illinois needed a bridge – Mr. L.E. Truesdell was an expert bridge builder. But people had doubts as to whether what he was being asked to do could be accomplished. The naysayers were ignored – and tragedy arrived, (The Truesdell Bridge Disaster) *** The witch trials in Salem, Massachusetts were horrid… the trials in Europe even more so. Now, imagine being a soldier tried as a witch because you returned with supernatural knowledge imparted to you after you were abducted by extraterrestrials. It sounds like the makings of a terrible novel and an even worse movie… but it's the true story of Major Thomas Weir. (The True Story of the Alien Abduction Witch Trial) *** He's believed to have killed over 50 women inside his soundproof torture trailer – which he called his “toy box.” We'll look at the case of serial killer David Parker Ray. (Evils of the Toybox Killer) *** Our criminal justice system tries to be the most fair in the world – considering the accused “innocent until proven guilty.” And while our system is not perfect, for the most part it does its job well. But because it is not perfect, once in a while a murderer walks… or even worse, an innocent defendant goes to prison. And in some cases, that innocent person is convicted and imprisoned based on one thing – they confessed to the crime that they didn't commit. Why would someone do that? (Why Do Innocent People Confess?) *** Port St. Lucie, Florida is full of disturbing urban legends – some true, many false – as urban legends go. But somehow, most all of these terrifying stories tie back to a single oak tree in a neighborhood park, and Florida's first serial killer. (The Devil Tree Hauntings)ABOUT WEIRD DARKNESS: Weird Darkness is a true crime and paranormal podcast narrated by professional award-winning voice actor, Darren Marlar. Seven days per week, Weird Darkness focuses on all thing strange and macabre such as haunted locations, unsolved mysteries, true ghost stories, supernatural manifestations, urban legends, unsolved or cold case murders, conspiracy theories, and more. On Thursdays, this scary stories podcast features horror fiction along with the occasional creepypasta. Weird Darkness has been named one of the “Best 20 Storytellers in Podcasting” by Podcast Business Journal. Listeners have described the show as a cross between “Coast to Coast” with Art Bell, “The Twilight Zone” with Rod Serling, “Unsolved Mysteries” with Robert Stack, and “In Search Of” with Leonard Nimoy.DISCLAIMER: Ads heard during the podcast that are not in my voice are placed by third party agencies outside of my control and should not imply an endorsement by Weird Darkness or myself. *** Stories and content in Weird Darkness can be disturbing for some listeners and intended for mature audiences only. Parental discretion is strongly advised.CHAPTERS & TIME STAMPS (All Times Approximate)…00:00:00.000 = Lead-In00:00:55.371 = Show Open00:04:12.885 = The Devil Tree Hauntings00:15:28.295 = History's Most Violent Ghosts00:36:32.777 = The True Story of the Alien Abduction Witch Trial00:45:55.817 = Evils of the Toybox Killer00:57:04.271 = The Truesdell Bridge Disaster01:07:45.917 = Why Do Innocent People Confess?01:15:48.277 = Show CloseSOURCES AND RESOURCES FROM THE EPISODE…“History's Most Violent Ghosts” by Robert F. Mason for Ranker: https://weirddarkness.tiny.us/3x42y575“The True Story of the Alien Abduction Witch Trial” by Marcus Lowth for UFO Insight: https://weirddarkness.tiny.us/bdhrv3hu“The Devil Tree Hauntings” posted at MiamiHaunts.com: https://weirddarkness.tiny.us/2sp2wakz“Evils of the Toybox Killer” by Jaclyn Anglis for All That's Interesting: https://weirddarkness.tiny.us/jep7tnxf“The Truesdell Bridge Disaster” by Kathi Kresol for HauntedRockford.com: https://weirddarkness.tiny.us/4c94hvjy“Why Do Innocent People Confess?” by Lea Rose Emery for Ranker: https://weirddarkness.tiny.us/bjtvenfv=====(Over time links may become invalid, disappear, or have different content. I always make sure to give authors credit for the material I use whenever possible. If I somehow overlooked doing so for a story, or if a credit is incorrect, please let me know and I will rectify it in these show notes immediately. Some links included above may benefit me financially through qualifying purchases.)= = = = ="I have come into the world as a light, so that no one who believes in me should stay in darkness." — John 12:46= = = = =WeirdDarkness® is a registered trademark. Copyright ©2025, Weird Darkness.=====Originally aired: July 24, 2023EPISODE PAGE at WeirdDarkness.com (includes list of sources): https://weirddarkness.com/ViolentHauntings

Some supplement companies make bold claims that can be a little misleading. One example is the idea that “protein turns to sugar, and sugar turns to fat,” which may sound simple but doesn't reflect how the body actually works. This kind of messaging can create confusion around how protein is processed and used for energy.In truth, the body has natural checks and balances. When blood sugar drops, it can convert protein into glucose for fuel but only as needed, and not in a way that directly leads to fat gain. Understanding how these processes work helps cut through the noise and make smarter choices about what to take.Highlights of the Podcast00:04 - False advertising concerns01:22 - How protein actually turns to sugar02:47 - Sugar storage hierarchy: glycogen before fat04:07 - Pathological scenario is unrealistic05:37 - Final stance and conditions for change

About this Episode When love turns toxic, it can be almost impossible to see clearly through the confusion, self-doubt, and emotional chaos that follow. If you've ever found yourself trapped in a cycle of hope, heartbreak, and uncertainty within a relationship, you're not alone—and there's a reason why breaking free can feel so overwhelming. The hidden dynamics of pathological partnerships and trauma bonds often keep people stuck, questioning their worth, and struggling to understand why things never seem to get better. In this episode, listeners are offered insight and validation as the conversation unpacks the complex nature of trauma bonds and toxic relationships. You'll discover how these destructive patterns form, what psychological traits might make someone more susceptible, and why distinguishing between harmful behaviors and truly pathological intentions is so important. With practical guidance and real-life examples, this episode shines a compassionate light on the path toward healing, empowerment, and, for those who need it most, a way out. Affectionately known as Dr. Nae, Dr. Nadine Macaluso is a therapist specializing in trauma healing and personal transformation. Her life inspired the character Naomi Belfort in The Wolf of Wall Street. After overcoming personal challenges, she earned a Master's degree in counseling and a Ph.D. in Somatic Psychotherapy. Dr. Macaluso helps individuals recover from trauma bonds, C-PTSD, and shame. She is also the author of Run Like Hell: A Therapist's Guide to Recognizing, Escaping, and Healing From Trauma Bonds. Check out the transcript of this episode on Dr. Jessica Higgin's website. Episode Highlights  06:28 Dr. Nadine Macaluso's personal journey and the roots of her work on trauma bonds. 09:49 Defining trauma bonds and the role of intermittent reinforcement in toxic relationships. 13:35 Intent, power imbalance, and the pathological partner in trauma bonds. 16:11 Pathological intent vs. reactive behaviors and repair. 19:20 Understanding Cluster B personality disorders and their impact on relationships. 21:23 Empowering the victim over diagnosing the pathological partner. 24:11 Who is most susceptible to trauma bonds? 28:16 Questioning labels: Codependency, attachment, and rethinking victim narratives. 32:34 Attachment styles, developmental trauma, and their role in toxic relationships. 34:31 Cultural myths about love, media influence, and the hope that keeps people stuck. 37:20 Reducing shame, cognitive dissonance, and reconnecting with self. 42:47 The process of leaving: Safety, planning, and overcoming guilt. 44:30 Post-traumatic growth: Finding strength, hope, and empowerment after leaving a toxic relationship. Mentioned Run Like Hell (*Amazon Affiliate link) (book) Women Who Love Psychopaths (*Amazon Affiliate link) (book) Big 5 Personality Quiz  Essentia's website (*Affiliate link) Stratami™ Organic Mattress (This is the mattress we purchased) (*Affiliate link) Classic REM5 Active Mattress – (The mattress we wish we could have gotten for the cooling feature) (*Affiliate link) Evolve in Love (program) Evolve in Love – Next level – Book Your Discovery Call Connect with Dr. Nadine Macaluso Websites: drnae.com Facebook: facebook.com/drnaelmft X: x.com/i/flow/login?redirect_after_login=%2Ftherealdrnadine YouTube: youtube.com/c/TheRealDrNadine Instagram: instagram.com/therealdrnadine LinkedIn: linkedin.com/in/therealdrnadine TikTok: tiktok.com/@drnaelmft Connect with Dr. Jessica Higgins Facebook: facebook.com/EmpoweredRelationship  Instagram: instagram.com/drjessicahiggins  Podcast: drjessicahiggins.com/podcasts/ Pinterest: pinterest.com/EmpowerRelation  LinkedIn: linkedin.com/in/drjessicahiggins  Twitter: @DrJessHiggins  Website: drjessicahiggins.com   Email: jessica@drjessicahiggins.com If you have a topic you would like it to be discussed, please contact us by clicking on the “Ask Dr. Jessica Higgins” button here.  Thank you so much for your interest in improving your relationship.  Also, I would so appreciate your honest rating and review. Please leave a review by clicking here.  Thank you!   *With Amazon Affiliate Links, I may earn a few cents from Amazon, if you purchase the book from this link.

Episode 175. Let's discuss what the normal grief process looks like, going through each of the 5 stages of grief with associated defense mechanisms. We'll also touch on the difference between the normal grief process and when it becomes pathological.This episode contains content about death and suicide.Visit First Line's website and blog: ⁠https://www.firstlinepodcast.comEditing Service for Pre-Med and Medical Students (CV, personal statement, applications): https://www.firstlinepodcast.com/servicesFor a discount on your TrueLearn subscription use ⁠https://truelearn.referralrock.com/l/firstline/⁠ and code firstlineContent on First Line is for educational and informational purposes only, not as medical advice. Views expressed are my own and do not represent any organizations I am associated with.

v tejto časti budeme hovoriť o elektronickom "tetovaní", o tom, kedy nám na Zemi dojde kyslík a o výskume, ktorý naznačuje, ako možno spomaliť kognitívne starnutie (zatiaľ u myší). Zdroje Electronic tattoo gauges mental strain An Extreme Drop in Oxygen Will Eventually Suffocate Most Life on Earth New Model Suggests We May Have Been Wrong About Earth's First Major Bursts of Oxygen How much longer will the oxygen-rich atmosphere be sustained on Earth? Astrocytic Hevin/SPARCL-1 Regulates Cognitive Decline in Pathological and Normal Brain Aging Barnes maze Image by Ulrich from Pixabay

Welcome, writers and book lovers. The Bleeders is a podcast about book writing and publishing. Make sure you subscribe to the companion Substack: https://thebleeders.substack.com/welcomeToday's guest is Sarah Fay, memoirist, writing coach, and Substack strategist. Her debut memoir, Pathological, chronicles her 25-year journey through the mental health system. In this episode, Sarah shares how she manifested her dream agent, her surprisingly fast path to publication (during the pandemic no less!), how she found the structure for Pathological, why she decided to serialize her second memoir, and more. Plus, she offers tips for thriving on Substack (and why it might be better than an MFA), along with practical advice on book PR. Follow Sarah on Substack @sarahfay.The Bleeders is hosted by Courtney Kocak. Follow her on Instagram @courtneykocak and Bluesky @courtneykocak.bsky.social. For more, check out her website courtneykocak.com.Courtney is teaching some upcoming workshops you might be interested in:How to Build a “Platform” for Writers Who Shudder at the Thought: https://writingworkshops.com/products/how-to-build-a-platform-for-writers-who-shudder-at-the-thought-zoom-seminarCreating Your Podcast: https://www.roadmapwriters.com/products/creating-your-podcast-0Podcasting for Writers: How to Start, Sustain & Grow Your Podcast: https://writingworkshops.com/products/podcasting-for-writers-how-to-start-sustain-grow-your-podcast-4-week-zoom-workshopStart a Newsletter to Supercharge Your Platform, Network and Business: https://writingworkshops.com/products/start-a-newsletter-to-supercharge-your-platform-network-business-zoom-seminarLand Big Bylines by Writing for Columns: https://writingworkshops.com/products/land-big-bylines-by-writing-for-columns-zoom-seminarThe Multi-Passionate Writer's Life: https://writingworkshops.com/products/the-multi-passionate-writers-life-zoom-seminar-with-courtney-kocak

Send us a textPathological jealousy, Sandbanks, Dorset murder.This case dates from 1972, it is an unknown case, I can find no information about it online. The information comes from files in the National Archives. The podcast is told in one take and there is no editing. I think there is some frog and sparrow noise in the background. I will attempt a change of subject matter for the next pod.

Many chronic conditions present with overlapping patterns of disharmony, making diagnosis and treatment complex. In this episode, we explore the Primary Pathological Triad (PPT)—a combination of Spleen yang qi deficiency, Liver qi stagnation, and Heat—and how these interconnected patterns contribute to modern health issues.Join us as we discuss why the PPT is so common, its impact on digestion, inflammation, and chronic disease, and how harmonizing formulas can effectively restore balance.Listen now to gain clinical insights into one of the most prevalent patterns in TCM!You can access the written article here: https://www.mayway.com/articles/the-primary-pathological-triadSee our Monthly Practitioner Discounts https://www.mayway.com/monthly-specialsSign up for the Mayway Newsletterhttps://www.mayway.com/newsletter-signupFollow ushttps://www.facebook.com/MaywayHerbs/https://www.instagram.com/maywayherbs/

Megyn Kelly is joined by Jordan Peterson, co-founder of Peterson Academy and author of "We Who Wrestle with God," to discuss the insane leftist policies that drove men and boys away from the Democratic party, how they're still missing the point even after Trump's landslide win, how it is "too little too late" for schools and universities to salvage their reputation, the decline of the Ivy League status, how young people are the more politically divided by gender than ever before, how Dems don't understand why there's this split and still think everything is about abortion, Andrew Tate's “pathological masculinity" and the wrong messenger to men and boys, why Dems are misguided about what makes Trump popular, what Olivia Wilde got wrong about him in the character based on him in “Don't Worry Darling,” what Peterson learned about Chris Pine after the movie came out, how Disney dropped the ball on Snow White, challenges young women face in the dating world, the issue with the mentality of “settling,” and more.More from Peterson: https://petersonacademy.com/Herald Group: Learn more at https://GuardYourCard.com  Done with Debt: https://www.DoneWithDebt.com  & tell them Megyn sent you!FYSI: https://FYSI.com/Megyn  or call 800-877-4000 Follow The Megyn Kelly Show on all social platforms:YouTube: https://www.youtube.com/MegynKellyTwitter: http://Twitter.com/MegynKellyShowInstagram: http://Instagram.com/MegynKellyShowFacebook: http://Facebook.com/MegynKellyShow Find out more information at: https://www.devilmaycaremedia.com/megynkellyshow

Have you ever asked your child to do a simple task, only to be met with an explosive reaction? In this episode, we interview Lydia Rex, Connected Families Certified Parent Coach, about Pathological Demand Avoidance (PDA), also known as Pervasive Drive for Autonomy. Lydia will help you step into your child's shoes and understand how […]

Sarah roped Susie into watching Love is Blind and now they have to talk about it (even though Susie is mad about it). We discuss the particular hellscape that is a reality tv reunion and the trauma it provides. We discuss why bangs are never the answer and you should never get a tattoo when you're in the throes of life's worst moments. Sarah talks about Belle Gibson who became a successful influencer, cookbook author, and lifestyle blogger based on a lie that she had terminal cancer she was treating homeopathically. We find out why young people aren't getting romantically involved and debate whether that's a bad or good thing. And we hear why reality tv causes insecurity in men and women in different ways. Plus, Susie explains what a "bed party" is and why people are spending lots of money for an instagram picture celebrating their kid going to college.Listen to more podcasts like this: https://wavepodcastnetwork.comJoin our Candy Club, shop our merch, sign-up for our free newsletter, & more by visiting The Brain Candy Podcast website: https://www.thebraincandypodcast.comConnect with us on social media:BCP Instagram: https://www.instagram.com/braincandypodcastSusie's Instagram: https://www.instagram.com/susiemeisterSarah's Instagram: https://www.instagram.com/imsarahriceBCP on X: https://www.x.com/braincandypodSponsors:Get 20% OFF by going to https://www.honeylove.com/braincandy! #honeylovepodGet up to 35% off PLUS 2 free gifts using code BRAINCANDY at https://shopbeam.com/BRAINCANDYSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Uncovers a powerful relationship between pathology and money: beginning in the nineteenth century, the severity of mental illness was measured against a patient's economic productivity. Madness and Enterprise: Psychiatry, Economic Reason, and the Emergence of Pathological Value (U Chicago Press, 2024) reveals the economic norms embedded within psychiatric thinking about mental illness in the North Atlantic world. Over the course of the nineteenth century, various forms of madness were subjected to a style of psychiatric reasoning that was preoccupied with money. Psychiatrists across Western Europe and the United States attributed financial and even moral value to an array of pathological conditions, such that some mental disorders were seen as financial assets and others as economic liabilities. By turning to economic conduct and asking whether potential patients appeared capable of managing their financial affairs or even generating wealth, psychiatrists could often bypass diagnostic uncertainties about a person's mental state. Through an exploration of the intertwined histories of psychiatry and economic thought, Nima Bassiri shows how this relationship transformed the very idea of value in the modern North Atlantic, as the most common forms of social valuation—moral value, medical value, and economic value—were rendered equivalent and interchangeable. If what was good and what was healthy were increasingly conflated with what was remunerative (and vice versa), then a conceptual space opened through which madness itself could be converted into an economic form and subsequently redeemed—and even revered. Nima Bassiri is assistant professor of literature at Duke University, where he is also the codirector of the Institute for Critical Theory. Morteza Hajizadeh is a Ph.D. graduate in English from the University of Auckland in New Zealand. His research interests are Cultural Studies; Critical Theory; Environmental History; Medieval (Intellectual) History; Gothic Studies; 18th and 19th Century British Literature. YouTube channel. Twitter. Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/intellectual-history

Uncovers a powerful relationship between pathology and money: beginning in the nineteenth century, the severity of mental illness was measured against a patient's economic productivity. Madness and Enterprise: Psychiatry, Economic Reason, and the Emergence of Pathological Value (U Chicago Press, 2024) reveals the economic norms embedded within psychiatric thinking about mental illness in the North Atlantic world. Over the course of the nineteenth century, various forms of madness were subjected to a style of psychiatric reasoning that was preoccupied with money. Psychiatrists across Western Europe and the United States attributed financial and even moral value to an array of pathological conditions, such that some mental disorders were seen as financial assets and others as economic liabilities. By turning to economic conduct and asking whether potential patients appeared capable of managing their financial affairs or even generating wealth, psychiatrists could often bypass diagnostic uncertainties about a person's mental state. Through an exploration of the intertwined histories of psychiatry and economic thought, Nima Bassiri shows how this relationship transformed the very idea of value in the modern North Atlantic, as the most common forms of social valuation—moral value, medical value, and economic value—were rendered equivalent and interchangeable. If what was good and what was healthy were increasingly conflated with what was remunerative (and vice versa), then a conceptual space opened through which madness itself could be converted into an economic form and subsequently redeemed—and even revered. Nima Bassiri is assistant professor of literature at Duke University, where he is also the codirector of the Institute for Critical Theory. Morteza Hajizadeh is a Ph.D. graduate in English from the University of Auckland in New Zealand. His research interests are Cultural Studies; Critical Theory; Environmental History; Medieval (Intellectual) History; Gothic Studies; 18th and 19th Century British Literature. YouTube channel. Twitter. Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/new-books-network

Uncovers a powerful relationship between pathology and money: beginning in the nineteenth century, the severity of mental illness was measured against a patient's economic productivity. Madness and Enterprise: Psychiatry, Economic Reason, and the Emergence of Pathological Value (U Chicago Press, 2024) reveals the economic norms embedded within psychiatric thinking about mental illness in the North Atlantic world. Over the course of the nineteenth century, various forms of madness were subjected to a style of psychiatric reasoning that was preoccupied with money. Psychiatrists across Western Europe and the United States attributed financial and even moral value to an array of pathological conditions, such that some mental disorders were seen as financial assets and others as economic liabilities. By turning to economic conduct and asking whether potential patients appeared capable of managing their financial affairs or even generating wealth, psychiatrists could often bypass diagnostic uncertainties about a person's mental state. Through an exploration of the intertwined histories of psychiatry and economic thought, Nima Bassiri shows how this relationship transformed the very idea of value in the modern North Atlantic, as the most common forms of social valuation—moral value, medical value, and economic value—were rendered equivalent and interchangeable. If what was good and what was healthy were increasingly conflated with what was remunerative (and vice versa), then a conceptual space opened through which madness itself could be converted into an economic form and subsequently redeemed—and even revered. Nima Bassiri is assistant professor of literature at Duke University, where he is also the codirector of the Institute for Critical Theory. Morteza Hajizadeh is a Ph.D. graduate in English from the University of Auckland in New Zealand. His research interests are Cultural Studies; Critical Theory; Environmental History; Medieval (Intellectual) History; Gothic Studies; 18th and 19th Century British Literature. YouTube channel. Twitter. Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/critical-theory

Uncovers a powerful relationship between pathology and money: beginning in the nineteenth century, the severity of mental illness was measured against a patient's economic productivity. Madness and Enterprise: Psychiatry, Economic Reason, and the Emergence of Pathological Value (U Chicago Press, 2024) reveals the economic norms embedded within psychiatric thinking about mental illness in the North Atlantic world. Over the course of the nineteenth century, various forms of madness were subjected to a style of psychiatric reasoning that was preoccupied with money. Psychiatrists across Western Europe and the United States attributed financial and even moral value to an array of pathological conditions, such that some mental disorders were seen as financial assets and others as economic liabilities. By turning to economic conduct and asking whether potential patients appeared capable of managing their financial affairs or even generating wealth, psychiatrists could often bypass diagnostic uncertainties about a person's mental state. Through an exploration of the intertwined histories of psychiatry and economic thought, Nima Bassiri shows how this relationship transformed the very idea of value in the modern North Atlantic, as the most common forms of social valuation—moral value, medical value, and economic value—were rendered equivalent and interchangeable. If what was good and what was healthy were increasingly conflated with what was remunerative (and vice versa), then a conceptual space opened through which madness itself could be converted into an economic form and subsequently redeemed—and even revered. Nima Bassiri is assistant professor of literature at Duke University, where he is also the codirector of the Institute for Critical Theory. Morteza Hajizadeh is a Ph.D. graduate in English from the University of Auckland in New Zealand. His research interests are Cultural Studies; Critical Theory; Environmental History; Medieval (Intellectual) History; Gothic Studies; 18th and 19th Century British Literature. YouTube channel. Twitter. Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/medicine

Chapters 00:00 Introduction and Current Work 02:51 Shockwave Therapy: Efficacy and Mechanisms 06:07 Understanding Tendon Pathologies 09:00 Calcification and Adaptation in Tendons 11:55 The Role of Shockwave in Clinical Practice 15:12 Platelet-Rich Plasma (PRP) Insights 18:06 Stem Cells and Tendon Healing 20:57 Adjuncts in Tendon Rehabilitation 23:48 Heel Wedges: Evidence and Application 27:06 Loading Strategies for Tendinopathy 30:04 Compression and Tendon Mechanics 32:56 The Importance of Loading in Rehabilitation 35:51 Tendon Stiffness: Heavy Loads vs. Plyometrics 42:01 Understanding Tendon Loading Mechanisms 45:25 Isometric vs. Eccentric Loading for Tendon Adaptation 48:23 Maximal Eccentrics: Techniques and Applications 51:45 Fluid Movement and Tendon Health 55:35 The Role of Metabolism in Tendon Adaptation 01:01:10 The Complexity of Tendon Pathology 01:06:29 The Dynamics of Fluid Movement in Tendons 01:11:11 Plyometrics vs. Isometrics: Strain and Adaptation 01:14:05 Blood Flow Restriction Training and Tendon Adaptation 01:18:21 Metabolic Factors in Tendon Healing   Takeaways Peter Malairis is a full-time professor at Monash University. Recent research shows shockwave therapy is ineffective for tendon pain. Calcification in tendons may be an adaptive response. PRP injections do not outperform placebo treatments. Stem cell therapy lacks sufficient evidence for tendon healing. Adjunct therapies should be accessible, cheap, and safe. Heel wedges have shown significant effects in treating Achilles tendinopathy. Loading strategies must be tailored to individual patient needs. Tendon stiffness is primarily improved through heavy loading. Fluid movement within tendons is essential for adaptation. Loading the tendon heavier leads to better fluid movement. Isometrics are crucial for early rehabilitation stages. Heavy maximal eccentrics are key for long-term adaptation. Fluid movement impacts stress relaxation in tendons. Tendon stiffness increases with appropriate loading. Metabolic health is essential for tendon adaptation. Pathological tendons may require different loading strategies. Fluid movement can help reduce pain and improve function. Plyometrics may not provide sufficient strain for adaptation. Blood flow restriction can be effective for tendon rehabilitation.     Notes: https://jackedathlete.com/podcast-131-tendons-with-peter-malliaras/

Dr. Neeraj Agarwal and Dr. Peter Hoskin discuss key abstracts in GU cancers from the 2025 ASCO Genitourinary Cancers Symposium, including novel therapies in prostate, bladder, and kidney cancer and the impact of combination therapies on patient outcomes. TRANSCSRIPT Dr. Neeraj Agarwal: Hello, and welcome to the ASCO Daily News Podcast. I'm Dr. Neeraj Agarwal, the director of the Genitourinary Oncology Program and professor of medicine at the Huntsman Cancer Institute at the University of Utah, and editor-in-chief of ASCO Daily News. Today, we'll be discussing practice-informing abstracts and other key advances in GU oncology featured at the 2025 ASCO Genitourinary Cancers Symposium. Joining me for this discussion is Dr. Peter Hoskin, the chair of this year's ASCO GU Symposium. Dr. Hoskin is a professor in clinical oncology in the University of Manchester and honorary consultant in clinical oncology at the Christie Hospital, Manchester, and University College Hospital London, in the United Kingdom. Our full disclosures are available in the transcript of this episode. Peter, thank you for joining us today. Dr. Peter Hoskin: Thank you so much, Neeraj. I am very pleased to be here. Dr. Neeraj Agarwal: The GU meeting highlighted remarkable advancements across the spectrum of GU malignancies. What stood out to you as the most exciting developments at the ASCO GU Symposium?  Dr. Peter Hoskin: The theme of this year's meeting was "Driving Innovation, Improving Patient Care," and this reflected ASCO GU's incredible milestone in GU cancer research over the years. We were thrilled to welcome almost 6,000 attendees on this occasion from over 70 countries, and most of them were attending in person and not online, although this was a hybrid meeting. Furthermore, we had more than 1,000 abstract submissions. You can imagine then that it fostered fantastic networking opportunities and facilitated valuable knowledge and idea exchanges among experts, trainees, and mentees. So, to start I'd like to come back to you for a second because the first day started with a focus on prostate cancer and some of the key clinical trials. And congratulations to you, Neeraj, on sharing the data from the TALAPRO-2 trial, which we were eagerly awaiting. I'd love to get your thoughts on the data that you presented. Could you tell us more about that trial, Abstract LBA18?  Dr. Neeraj Agarwal: Yes, Peter, I agree with you. It was such an exciting conference overall and thank you for your leadership of this conference. So, let's talk about the TALAPRO-2 trial. First of all, I would like to remind our audience that the combination of talazoparib plus enzalutamide was approved by the U.S. FDA in June 2023 in patients with metastatic castration-resistant prostate cancer harboring HRR gene alterations, after this combination improved the primary endpoint of radiographic progression-free survival compared to enzalutamide alone in the randomized, double-blind, placebo-controlled, multi-cohort phase 3 TALAPRO-2 trial. In the abstract I presented at ASCO GU 2025, we reported the final overall survival data, which was a key alpha-protected secondary endpoint in cohort 1, which enrolled an all-comer population of patients with mCRPC. So, at a median follow-up of around 53 months, in the intention-to-treat population, the combination of talazoparib plus enzalutamide significantly reduced the risk of death by 20% compared to enzalutamide alone, with a median OS of 45.8 months in the experimental arm versus 37 months in the control arm, which was an active control arm of enzalutamide. This improvement was consistent in patients with HRR alterations with a hazard ratio of 0.54 and in those with non-deficient or unknown HRR status, with a hazard ratio of 0.87. In a post hoc analysis, the hazard ratio for OS was 0.78 favoring the combination in those patients who did not have any HRR gene alteration in their tumors by both tissue and ctDNA testing. Consistent with the primary analysis, the updated rPFS data also favored the experimental arm with a median rPFS of 33.1 compared to 19.5 months in the control arm, and a hazard ratio of 0.667. No new safety signals were identified with extended follow-up. Thus, TALAPRO-2 is the first PARP inhibitor plus ARPI study to show a statistically significant and a clinically meaningful improvement in OS compared to standard-of-care enzalutamide as first-line treatment in patients with mCRPC unselected for HRR gene alterations. Dr. Peter Hoskin: Thank you, Neeraj. That's a great summary of the data presented and very important data indeed. There was another abstract also featured in the same session, Abstract 20, titled “Which patients with metastatic hormone-sensitive prostate cancer benefit more from androgen receptor pathway inhibitors? STOPCAP meta-analyses of individual participant data.” Neeraj, could you tell us more about this abstract? Dr. Neeraj Agarwal: Absolutely, I would be delighted to. So, in this meta-analysis, Dr. David Fischer and colleagues pooled individual participant data from different randomized phase 3 trials in the mHSPC setting to assess the potential ARPI effect modifiers and determine who benefits more from an ARPI plus ADT doublet. The primary outcome was OS for main effects and PFS for subgroup analyses. Prostate cancer specific survival was a sensitivity outcome. The investigators pooled data from 11 ARPI trials and more than 11,000 patients. Overall, there was a clear benefit of adding an ARPI on both OS and PFS, with hazard ratios of 0.66 and 0.51, respectively, representing a 13% and 21% absolute improvement at 5 years, respectively, with no clear difference by the class of agent. When stratifying the patients by age group, the effects of adding an ARPI on OS and PFS were slightly smaller in patients older than 75, than in those younger than 65, or aged between 65 and 75 years. Notably, in the trials assessing the use of abiraterone, we saw very little OS effects in the group of patients older than 75, however there was some benefit maintained in prostate-cancer specific survival, suggesting that other causes of death may be having an impact. The effects of the other ARPIs, or ‘lutamides' as I would call them, were similar across all three age subgroups on both OS and PFS. Therefore, the majority of patients with mHSPC benefit from the addition of ARPIs, and the benefits/risks of abiraterone and other ‘amides' must be considered in older patients.  Dr. Peter Hoskin: Thanks, Neeraj. Another great summary relevant to our day-to-day practice. Of course, there's ongoing collection of individual patient data from other key trials, which will allow robust comparison of ARPI doublet with triplet therapy (including docetaxel), guiding more personalized treatment.   Dr. Neeraj Agarwal: I agree with you, Peter, we need more data to help guide personalized treatment for patients with mHSPC and potentially guide de-escalation versus escalation strategies. Now, moving on to a different setting in prostate cancer, would you like to mention Abstract 17 titled, “Overall survival and quality of life with Lu-PSMA-617 plus enzalutamide versus enzalutamide alone in poor-risk, metastatic, castration-resistant prostate cancer in ENZA-p (ANZUP 1901),” presented by Dr. Louise Emmett? Dr. Peter Hoskin: Of course I will. So, ENZA-p was a multicenter, open-label, randomized, phase 2 trial conducted in Australia. It randomized 163 patients into adaptive doses (2 or 4 cycles) of Lu-PSMA-617 plus enzalutamide versus enzalutamide alone as first-line treatment in PSMA-PET-CT-positive, poor-risk, mCRPC. The interim analysis of ENZA-p with median follow-up 20 months showed improved PSA-progression-free survival with the addition of Lu-PSMA-617 to enzalutamide. Here, the investigators reported the secondary outcomes, overall survival, and health-related quality of life (HRQOL). After a median follow up of 34 months, overall survival was longer in the combination arm compared to the enzalutamide arm, with a median OS of 34 months compared to 26 months; with an HR of 0.55. Moreover, the combination improved both deterioration-free survival and health-related quality of life indicators for pain, fatigue, physical function, and overall health and quality of life compared to the control arm. Consistent with the primary analysis, the rPFS also favored the experimental arm with a median rPFS of 17 months compared to 14 months with a HR of 0.61. So, the addition of LuPSMA improved overall survival, and HRQOL in patients with high-risk mCRPC. Dr. Neeraj Agarwal: Thank you, Peter. Great summary, and promising results with Lu-177 and ARPI combination in first line treatment for mCRPC among patients who had two or more high risk features associated with early enzalutamide failure. Before we move on to bladder cancer, would you like to tell us about Abstract 15 titled, “World-wide oligometastatic prostate cancer (omPC) meta-analysis leveraging individual patient data (IPD) from randomized trials (WOLVERINE): An analysis from the X-MET collaboration,” presented by Dr. Chad Tang?  Dr. Peter Hoskin: Sure. So, with metastatic-directed therapy (MDT), we have a number of phase 2 studies making up the database, and the X-MET collaboration aimed to consolidate all randomized data on oligometastatic solid tumors. This abstract presented pooled individual patient data from all the published trials involving patients with oligometastatic prostate cancer who received MDT alongside standard of care (SOC) against SOC alone. The analysis included data from five trials, encompassing 472 patients with oligometastatic prostate cancer, and followed for a median of 41 months. Patients were randomly assigned in a 1:1 ratio to receive either MDT plus SOC or SOC alone. The addition of MDT significantly improved PFS. The median PFS was 32 months with MDT compared to 14.9 months with SOC alone, with an HR of 0.45. Subgroup analyses further confirmed the consistent benefits of MDT across different patient groups. Regardless of factors like castration status, receipt of prior primary treatment, stage, or number of metastases, MDT consistently improved PFS. In patients with mHSPC, MDT significantly delayed the time to castration resistance by nine months, extending it to a median of 72 months compared to 63 months in the SOC group with an HR of 0.58. In terms of OS, the addition of MDT improved the 48-month survival rate by 12%, with OS rates of 87% in the MDT+SOC group compared to 75% in the SOC alone group. Dr. Neeraj Agarwal: Thank you, Peter. These data demonstrate that adding MDT to systemic therapy significantly improves PFS, rPFS, and castration resistance-free survival, reinforcing its potential role in the treatment of oligometastatic prostate cancer. So, let's switch gears to bladder cancer and start with Abstract 658 reporting the OS analysis of the CheckMate-274 trial. Would you like to tell us about this abstract?  Dr. Peter Hoskin: Yes, sure, Neeraj. This was presented by Dr. Matt Milowsky, and it was additional efficacy outcomes, including overall survival, from the CheckMate-274 trial which evaluated adjuvant nivolumab versus placebo in patients with high-risk muscle-invasive bladder cancer after radical surgery. The phase 3 trial previously demonstrated a significant improvement in disease-free survival with nivolumab. With a median follow-up of 36.1 months, disease-free survival was longer with nivolumab compared to placebo across all patients with muscle-invasive bladder cancer, reducing the risk of disease recurrence or death by 37%. Among patients who had received prior neoadjuvant cisplatin-based chemotherapy, nivolumab reduced this risk by 42%, whilst in those who had not received chemotherapy, the risk was reduced by 31%. Overall survival also favored nivolumab over placebo, reducing the risk of death by 30% in all patients with muscle-invasive bladder cancer and by 52% in those with tumors expressing PD-L1 at 1% or higher. Among patients who had received prior neoadjuvant chemotherapy, nivolumab reduced the risk of death by 26%, whilst in those who had not received chemotherapy, the risk was reduced by 33%. Alongside this, the safety profile remained consistent with previous findings. Dr. Neeraj Agarwal: Thank you, Peter, for such a nice overview of this abstract. These results reinforce adjuvant nivolumab as a standard of care for high-risk muscle-invasive bladder cancer, offering the potential for a curative outcome for our patients. Dr. Peter Hoskin: I agree with you Neeraj. Perhaps you would like to mention Abstract 659 titled, “Additional efficacy and safety outcomes and an exploratory analysis of the impact of pathological complete response (pCR) on long-term outcomes from NIAGARA.” Dr. Neeraj Agarwal: Of course. Dr. Galsky presented additional outcomes from the phase 3 NIAGARA study, which evaluated perioperative durvalumab combined with neoadjuvant chemotherapy in patients with muscle-invasive bladder cancer. The study previously demonstrated a significant improvement in event-free survival and overall survival with durvalumab compared to chemotherapy alone, with a manageable safety profile and no negative impact on the ability to undergo radical cystectomy. Among the 1,063 randomized patients, those who received durvalumab had a 33% reduction in the risk of developing distant metastases or death and a 31% reduction in the risk of dying from bladder cancer compared to those who received chemotherapy alone. More patients who received durvalumab achieved a pathological complete response at the time of surgery with 37% compared to 28% in the chemotherapy-alone group. Patients who achieved a pathological complete response had better event-free survival and overall survival compared to those who did not. In both groups, durvalumab provided additional survival benefits, reducing the risk of disease progression or death by 42% and the risk of death by 28% in patients with a pathological complete response, while in those patients without a pathological complete response, the risk of disease progression or death was reduced by 23% and the risk of death by 16% when durvalumab was added to the chemotherapy. Immune-mediated adverse events occurred in 21% of patients in the durvalumab group compared to 3% in the chemotherapy-alone group, with grade 3 or higher events occurring in 3% compared to 0.2%. The most common immune-related adverse events included hypothyroidism in 10% of patients treated with durvalumab compared to 1% in the chemotherapy-alone group, and hyperthyroidism in 3% versus 0.8%. At the time of the data cutoff, these adverse events had resolved in 41% of affected patients in the durvalumab group and 44% in the chemotherapy-alone group. Dr. Peter Hoskin: Thank you, Neeraj, for the great summary. These findings further support the role of perioperative durvalumab as a potential standard of care for patients with muscle-invasive bladder cancer. Dr. Neeraj Agarwal: I concur with your thoughts, Peter. Before wrapping up the bladder cancer section, would you like to mention Abstract 664 reporting updated results from the EV-302 trial, which evaluated enfortumab vedotin in combination with pembrolizumab compared to chemotherapy as first-line treatment for patients with previously untreated locally advanced or metastatic urothelial carcinoma? Dr. Peter Hoskin: Yes, of course. Dr. Tom Powles presented updated findings from the EV-302 study, and in this abstract presented 12 months of additional follow-up for EV-302 (>2 y of median follow-up) and an exploratory analysis of patients with confirmed complete response (cCR). The study had a median follow-up of 29.1 months and previously demonstrated significant improvements in progression-free survival and overall survival with enfortumab vedotin and pembrolizumab. This is now the standard of care in global treatment guidelines. Among the 886 randomized patients, enfortumab vedotin and pembrolizumab reduced the risk of disease progression or death by 52% and the risk of death by 49% compared to chemotherapy. The survival benefit was consistent regardless of cisplatin eligibility or the presence of liver metastases. The confirmed objective response rate was higher with enfortumab vedotin and pembrolizumab at 67.5% compared to 44.2% with chemotherapy. The median duration of response was 23.3 months with enfortumab vedotin and pembrolizumab compared to 7.0 months with chemotherapy. A complete response was achieved in 30.4% of patients in the enfortumab vedotin and pembrolizumab group compared to 14.5% in the chemotherapy group, with the median duration of complete response not yet reached in the enfortumab vedotin and pembrolizumab group compared to 15.2 months in the chemotherapy group. Severe treatment-related adverse events occurred in 57.3% of patients treated with enfortumab vedotin and pembrolizumab compared to 69.5% in the chemotherapy group, while in patients who achieved a complete response, severe adverse events occurred in 61.7% of those treated with enfortumab vedotin and pembrolizumab compared to 71.9% with chemotherapy. Treatment-related deaths were reported in 1.1% of patients treated with enfortumab vedotin and pembrolizumab compared to 0.9% with chemotherapy, with no treatment-related deaths occurring in those who achieved a complete response. These findings clearly confirm the durable efficacy of enfortumab vedotin and pembrolizumab, reinforcing its role as the standard of care for the first-line treatment of patients with locally advanced or metastatic urothelial carcinoma, and no new safety concerns have been identified. Dr. Neeraj Agarwal: Thank you for this great summary. Moving on to kidney cancer, let's talk about Abstract 439 titled, “Nivolumab plus cabozantinib (N+C) vs sunitinib (S) for previously untreated advanced renal cell carcinoma (aRCC): Final follow-up results from the CheckMate-9ER trial.” Dr. Peter Hoskin: Sure. Dr. Motzer presented the final results from the phase 3 CheckMate-9ER trial, which compared the combination of cabozantinib and nivolumab against sunitinib in previously untreated advanced renal cell carcinoma. The data after more than five years follow-up show that the combination therapy provided sustained superior efficacy compared to sunitinib. In terms of overall survival, we see an 11-month improvement in median OS, 46.5 months for the cabo-nivo versus 35.5 months for sunitinib and a 42% reduction in the risk of disease progression or death, with median progression-free survival nearly doubling – that's 16.4 months in the combination group and 8.3 months with sunitinib. Importantly, the safety profile was consistent with the known safety profiles of the individual medicines, with no new safety concerns identified. Dr. Neeraj Agarwal: Great summary, Peter. These data further support the efficacy of cabo-nivo combination therapy in advanced renal cell carcinoma, which is showing a 11-month difference in overall survival. Dr. Peter Hoskin: Neeraj, before wrapping up this podcast, would you like to tell us about Abstract 618? This is titled “Prospective COTRIMS (Cologne trial of retroperitoneal lymphadenectomy in metastatic seminoma) trial: Final results.” Dr. Neeraj Agarwal: Sure, Peter. I would be delighted to. Dr Heidenrich from the University of Cologne in Germany presented the COTRIMS data evaluating retroperitoneal LN dissection in patients with clinical stage 2A/B seminomas. Seminomas are classified as 2A or B when the disease spreads to the retroperitoneal lymph nodes of up to 2 cm (CS IIA) or of more than 2 cm to up to 5 cm (CS 2B) in maximum diameter, respectively. They account for 10-15% of seminomas and they are usually treated with radiation and chemotherapy. However, radiation and chemo can be associated with long-term toxicities such as cardiovascular toxicities, diabetes, solid cancers, leukemia, particularly for younger patients. From this standpoint, Dr Heidenrich and colleagues evaluated unilateral, modified template, nerve-sparing retroperitoneal lymph node dissection as a less toxic alternative compared to chemo and radiation. They included 34 patients with negative AFP, beta-HCG, and clinical stage 2A/B seminomas. At a median follow-up of 43.2 months, the trial demonstrated great outcomes: a 99.3% treatment-free survival rate and 100% overall survival, with only four relapses. Antegrade ejaculation was preserved in 88% of patients, and severe complications such as grade 3 and 4 were observed in 12% of patients. Pathological analysis revealed metastatic seminoma in 85% of cases, with miR371 being true positive in 23 out of 24 cases and true negative in 100% of cases. It appears to be a valid biomarker for predicting the presence of lymph node metastases. These findings highlight retroperitoneal lymph node dissection is feasible; it has low morbidity, and excellent oncologic outcomes, avoiding overtreatment in 80% of patients and sparing unnecessary chemotherapy or radiotherapy in 10-15% of cases. Dr. Peter Hoskin: Great summary and important data on retroperitoneal lymphadenectomy in metastatic seminoma. These findings will help shape clinical practice. Any final remarks before we conclude today's podcast? Dr. Neeraj Agarwal: Before wrapping up this podcast, I would like to say that we have reviewed several abstracts addressing prostate, bladder, kidney cancers, and seminoma, which are impacting our medical practices now and in the near future. Peter, thank you for sharing your insights with us today. These updates are undoubtedly exciting for the entire GU oncology community, and we greatly appreciate your valuable contribution to the discussion and your leadership of the conference. Many thanks. Dr. Peter Hoskin: Thank you, Neeraj. Thank you for the opportunity to share this information more widely. I'm aware that whilst we have nearly 6,000 delegates, there are many other tens of thousands of colleagues around the world who need to have access to this information. And it was a great privilege to chair this ASCO GU25. So, thank you once again, Neeraj, for this opportunity to share more of this information that we discussed over those few days. Dr. Neeraj Agarwal: Thank you, Peter. And thank you to our listeners for joining us today. You will find links to the abstracts discussed today on the transcript of this episode. Finally, if you value the insights that you hear on the ASCO Daily News podcast, please take a moment to rate, review, and subscribe wherever you get your podcasts. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity or therapy should not be construed as an ASCO endorsement.  Find out more about today's speakers:   Dr. Neeraj Agarwal    @neerajaiims    Dr. Peter Hoskin Follow ASCO on social media:      @ASCO on Twitter      ASCO on Bluesky  ASCO on Facebook      ASCO on LinkedIn      Disclosures: Dr. Neeraj Agarwal: Consulting or Advisory Role: Pfizer, Bristol-Myers Squibb, AstraZeneca, Nektar, Lilly, Bayer, Pharmacyclics, Foundation Medicine, Astellas Pharma, Lilly, Exelixis, AstraZeneca, Pfizer, Merck, Novartis, Eisai, Seattle Genetics, EMD Serono, Janssen Oncology, AVEO, Calithera Biosciences, MEI Pharma, Genentech, Astellas Pharma, Foundation Medicine, and Gilead Sciences Research Funding (Institution): Bayer, Bristol-Myers Squibb, Takeda, Pfizer, Exelixis, Amgen, AstraZeneca, Calithera Biosciences, Celldex, Eisai, Genentech, Immunomedics, Janssen, Merck, Lilly, Nektar, ORIC Pharmaceuticals, Crispr Therapeutics, Arvinas Dr. Peter Hoskin: Research Funding (Institution): Varian Medical Systems, Astellas Pharma, Bayer, Roche, Pfizer, Elekta, Bristol Myers  

In this episode, Sarah and her former co-host, Jacob, discuss the possible hypothetical outcomes of Donald Trump learning the practice of mindfulness. Would he lie less? Would he treat women better? Would he still have run for president? How would a mindfulness practice change the thinking of someone like Donald Trump? Sarah also shares some revealing research about people with narcissistic traits practicing mindfulness. The results of these studies might surprise you. They certainly perplexed the researchers who conducted the trials.  Please share this episode if you like the content!Here is a link to an article outlining the various types of narcissism: https://tinyurl.com/ycks747n“Do bigger egos mean bigger presence? Facets of grandiose narcissism and mindfulness” Current Psychology; 2022 “Pathological narcissism and psychological distress: The mediating effects of vitality, initiative, and mindfulness” Personality and Individual Differences; 2022“Does mindfulness meditation increase empathy? An experiment” Self and Identity; 2017Important links:Sarah's Mindfulness Coaching website: http://www.sarahvallely.com The Aware Mind on Instagram https://www.instagram.com/aware_mind_podcast/TSD Mindfulness Virtual Meditation Center http://www.tsdmind.org Jacob's Personal Training website http://www.jacobderossett.com Jacob's YouTube Channel https://tinyurl.com/9yykwne9This episode is a meditation for beginners, and mindfulness for beginners resource. Intermediate and advanced meditators will also benefit. The Aware Mind produces content that supports stress reduction, anxiety relief, better concentration and focus, and trauma healing.The Aware Mind is produced by TSD Mindfulness, a virtual meditation center, offering mindfulness classes, certifications and private coaching. Sponsorded by RENVA Turmeric Shakes

An episode that defies the norms.Here's what's in store for today's episode: * Today, hosts Matt and Angela explore the intriguing and often debated world of Pathological Demand Avoidance with special guest Richard Woods.* Pathological Demand Avoidance, also known in more affirming circles as Persistent Drive for Autonomy, describes a strong need to question and resist demands, often co-occurring with autism. This trait can manifest as an intense drive for control, leading individuals to navigate the world in ways that prioritize autonomy and flexibility over compliance.* Most of what we know about PDA autism—and the stereotypes surrounding it—are heavily focused on children. In reality, PDA exists on a spectrum, and many adults also experience its traits, often in ways that go unrecognized or misunderstood.* Many neurotypicals see PDA as indistinguishable from Oppositional Defiant Disorder (ODD), when in reality, PDA is often the underlying factor in these cases, driven by a need for autonomy rather than intentional defiance.* We explore the validity of Theory of Mind in relation to PDA and the problems with pathologizing demand avoidance.* Our hosts and special guest discuss the misconception that PDA traits fade with age—when in reality, PDA individuals learn to accommodate themselves and establish clear boundaries as they grow into adulthood.* We explore the overlap between PDA and ODD, and why Richard believes that PDA isn't a form of autism, but rather a distinct profile of neurodivergence.* Additionally, we discuss how neurotypicals often struggle to differentiate CPTSD symptoms from autism, as many have never encountered a healthy, healed autistic person.* The discussion then shifts to how the world is not designed for autistic or disabled people in general, and how this lack of accessibility and understanding can exacerbate PDA traits, making self-advocacy and autonomy even more crucial.* We talk about labels, how they affect our ability to get our needs met, and what Richard's "post-autistic identity" entails in the broader conversation around neurodivergence and self-definition.* Finally, we reflect on the importance of self-advocacy, community, and embracing neurodivergence beyond medical labels, as well as the role of monotropic focus in the autistic experience.“May your stimming activities be many, and your flow states long.” About Richard Woods:Richard Woods is the leading Demand Avoidance Phenomena (Pathological Demand Avoidance) authority (by academic work and experience) and Author.He is attributed as autistic, but has a "post-autistic identity" as he is no longer basing his identity on psychiatric categories.“I tend to view PDA as literally about the management of stress. A lot of people express these features because they are distressed and or stressed by the demands being placed upon them. And often with autistic people, it seems to be more of a cognitive style. We're to be stressed when you put us in a very chaotic, very high-demanding world.” - Richard Woods“The modern life isn't built for autistics. It's so much noise, so much sound, so much that is visual and tactile. It's not built for disabled people in general.” - Richard Woods “That's the thing [about autistic kids] - when we have a safe person, when we have that anchor person, it frees us to be more objective, or to object rather, because it's safer to object. As opposed to a total stranger, you may not feel safe saying, ‘no, I don't want to do that. But with someone you trust, you say, ‘no, there's no way I'm going in there. You can't make me do that.' That's not going to happen, because you know you're not going to be met with that judgment and the criticism that comes along with that of a stranger.” - Matt In this episode, we take a deep dive into the world of Pathological Demand Avoidance (PDA) autism, a lesser-known but important part of the spectrum. From the intense need for autonomy to the challenges of navigating a demand-heavy world, we explore what PDA really is—and what it isn't. Join Matt and Angela as they break down common misconceptions, discuss how PDA presents in adults, and chat with expert Richard Woods about the affirming perspective of Persistent Drive for Autonomy. Have you experienced PDA traits in yourself or others? Share your thoughts with us using #AutisticCultureCatch on social media!Show Notes:There is substantial debate over what PDA is. Presently my view PDA is not an "autism profile"/ autism subgroup/ autism subtype, or anything of the kind. For a short 800 word overview of current debates on PDAby Richard Woods, please see below:https://www.researchgate.net/publication/354386742_Pathological_demand_avoidance_PDA_Its_four_schools_of_thoughthttps://tinyurl.com/4wynmydzRichard Woods ORCiD: https://orcid.org/0000-0002-8292-632Xhttps://www.pdasociety.org.uk/resources/identifying-features-ofpathological-demand-avoidance-using-the-diagnostic-interview-forsocial-andcommunication-disorders/https://monotropism.org/dinah/https://dlcincluded.github.io/MQ/Pathological Demand-Avoidance" (PDA) in Frontiers in Education, please see the call for papers below for more information:http://fron.tiers.in/rt/40032Related Shows:Reframing DSM Diagnosis Ready for a paradigm shift that empowers Autistics? Help spread the news!Follow us on InstagramFind us on Apple Podcasts and SpotifyLearn more about Matt at Matt Lowry, LPPJoin Matt's Autistic Connections Facebook GroupLearn more about Angela at AngelaKingdon.com Angela's social media: Twitter and TikTokOur Autism-affirming merch shop This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit www.autisticculturepodcast.com/subscribe

Dan Slepian is an Emmy-winning journalist, producer, and storyteller with nearly 30 years at NBC News. Known for his investigative work on Dateline, Dan has exposed injustices, solved cold cases, and helped exonerate the wrongfully convicted. His acclaimed podcast, Letters from Sing Sing, chronicles his 20-year fight to prove the innocence of John Adrian “JJ” Velazquez. A 2024 Pulitzer Prize finalist, Dan recently published The Sing Sing Files: One Journalist, Six Innocent Men, and a 20-Year Fight for Justice. Beyond journalism, he is a passionate advocate for criminal justice reform, focusing on the human cost of mass incarceration.In this episode, Dan discusses the systemic flaws in the justice system, including racial bias, prosecutorial misconduct, and the lack of accountability for wrongful convictions. He brings a deeply personal and professional lens to the conversation, emphasizing his commitment to truth over personal recognition. He shares insights into the realities of mass incarceration, describing how systemic failures—from flawed eyewitness procedures to prosecutorial pressure—lead to wrongful convictions. Dan also explores his relationship with JJ, which has evolved into a profound bond that underscores the human toll of these injustices. He speaks candidly about his investigative process, the importance of humanity and empathy, and his enduring advocacy for those wrongly imprisoned. His accounts of JJ's case and his Voices from Within program highlight the potential for transformation and healing within and beyond prison walls. Dan dives into his recent book, The Sing Sing Files, and the forthcoming documentary series The Sing Sing Chronicles, which humanizes those affected by the system. Dan's Reluctance Toward Self-Promotion: Dan discusses his discomfort with being in the spotlight + he reflects on the challenges of public advocacy while maintaining journalistic objectivity (3:26)Upbringing and Family Influence: Dan shares his childhood experiences + He credits his mother for instilling grit and resilience and his father for teaching empathy and the value of fighting for others (6:37)Navigating Advocacy and Family Dynamics: Dan recounts the depth of his 20-year connection with JJ + how Dan's work evolved from investigative reporting into a deeply personal mission for truth + how Dan's family became an integral supporter of JJ (9:52)Journey into Journalism: Dan recounts the early days of his career + He shares formative moments, like witnessing Michael Jordan before a game and the lessons they imparted about professionalism. (19:11)The Case of Robert Roberson: Robert Roberson's case, a man on death row convicted of killing his daughter + science have debunked much of the evidence used against Roberson + Dan emphasizes the racial and procedural inequities in death penalty cases and critiques the system's inefficiencies, high costs, and lack of deterrence (22:20)The Roots of Wrongful Convictions: Systemic issues leading to wrongful convictions + eyewitness misidentification, coerced confessions, and improper courtroom dynamics + JJ Velazquez's case exemplifies these failures + the need to humanize those impacted by wrongful convictions (34:53)Voices from Within and JJ Velazquez's Journey: Systemic bias in the justice system, , pointing out how former prosecutors often become judges in the same jurisdictions, fostering a “club-like” atmosphere + Dan's and JJ's collaboration on Voices from Within + challenging myths like “everyone in prison claims innocence + the long-lasting trauma caused by wrongful incarceration (45:00)The Emotional Catalyst for Justice: the emotional impact of his first encounter with JJ's children + Dan developed a familial bond with JJ's children + the lifelong impact of losing a parent to incarceration (51:56)The Pathology of Mass Incarceration: The Sing Sing Files, and the emotional impact of the documentary series The Sing Sing Chronicles + education and vocational training in prisons + need to treat prisoners with dignity and reintegrate them into society + mass incarceration as a moral failing of society (55:02)The Innocence Project and Personal Reflections: Dan credits the Innocence Project + Dan maintains his discomfort with being labeled as a trailblazer (1:111:07)Rapid Fast Round (1:12:46) Connect with Dan Slepian:InstagramLinkedInGet Dan's book - The Sing Sing Files!Listen to Dan's podcast - Letters from Sing Sing! Let's talk Connect:Instagram This podcast is produced by Ginni Media.

Dr. Rebecca Wattam is a Research Associate Professor in the Network Dynamics and Simulation Science Laboratory within the Biocomplexity Institute of Virginia Tech. Rebecca is the outreach and biology lead for a bioinformatics research center that scientists use to share and analyze their data on bacteria and bacterial genomes. This research center was originally funded to study bacteria that can make us sick in order to develop vaccines, identify drug targets, and predict outbreaks of illnesses. However, there are a lot of beneficial types of bacterial that are also now being studied based on their use for fermentation, alternate energy sources, probiotics, and other purposes. Rebecca is particularly interested in examining the similarities and differences between groups of bacteria. Living in Blacksburg, Virginia, Rebecca is close to the beautiful Appalachian Trail. She spends much of her free time hiking, canoeing, exploring the outdoors, and watching the wildlife. Rebecca received her B.S. and M.S. degrees from the University of New Mexico in Biology. Next, she attended the University of Wisconsin-Madison where she earned a joint Ph.D. degree in Entomology and Veterinary Science. Rebecca received a MacArthur Fellowship to conduct postdoctoral research at the University of Arizona in Tucson, and she completed a second postdoctoral fellowship there as well before accepting a position on the faculty at Virginia Tech. In our interview, Rebecca speaks more about her experiences in life and science.

In this episode, Dr. David Puder, alongside experts Anthony Bateman, Dr. Brandon Unruh, and Robert Drozek, delves into the complexities of treating pathological narcissism with Mentalization-Based Therapy (MBT). They explore practical strategies to help individuals with Narcissistic Personality Disorder develop self-awareness, emotional regulation, and healthier relationships. Learn how MBT can transform the therapeutic journey for those who often feel misunderstood or resistant to change. 

Do you find yourself constantly putting others' needs before your own? Have you ever wondered if being "too kind" could actually be harmful to your relationships and well-being? In today's crossover episode - Tony Overbay, a licensed marriage and family therapist, explores the complex concept of pathological kindness in relationships. Through a listener's letter from 'Cleo,' Tony delves into the challenges faced by those who prioritize others' needs to their detriment, often rooted in childhood experiences of being the family peacemaker. Cleo's story highlights issues with her emotionally inconsistent partner, Ray, unveiling the struggles of living with someone emotionally immature or narcissistic. Tony discusses recognizing these patterns, including the role of cognitive dissonance and trauma bonding in maintaining unhealthy relationships. He explores how highly sensitive people (HSPs) may be particularly vulnerable to these dynamics. The episode emphasizes the importance of developing a stable core identity, setting boundaries, and balancing kindness with self-care. Tony also touches on the challenges of breaking free from intermittent reinforcement in relationships and recognizing and trusting one's own perceptions. He stresses the role of therapy and self-awareness in breaking free from unhealthy cycles and fostering emotionally mature relationships while also offering hope to those who recognize themselves as the emotionally immature partner and want to change. 00:00 Introduction and Podcast Promotion 01:19 Introducing Cleo's Story 03:16 Cleo's Relationship Struggles 10:38 Understanding Pathological Kindness 16:28 The Impact of Pathological Kindness 21:36 Balancing Kindness and Self-Care 25:09 Exploring Self-Reliance and Its Pitfalls 25:24 The Dual Nature of Optimism 25:40 Understanding Humility and Self-Deprecation 26:26 The Complexities of Honesty 27:09 Patience vs. Passivity 27:24 Competence and Arrogance 28:00 Cleo's Relationship with Ray 29:04 The Struggle of Highly Sensitive People 29:48 The Challenge of Leaving Toxic Relationships 33:23 The Cognitive Dissonance and Trauma Bonding 45:04 The Importance of Self-Care and Boundaries 46:03 Encouragement for Personal Growth To learn more about Tony's upcoming re-release of the Magnetic Marriage course, his Pathback Recovery course, and more, sign up for his newsletter through the link at https://linktr.ee/virtualcouch Available NOW: Tony's "Magnetic Marriage Mini-Course" is only $25. https://magneticmarriage.mykajabi.com/magnetic-marriage-mini-course Subscribe to Tony's latest podcast, "Waking Up to Narcissism Q&A - Premium Podcast," on the Apple Podcast App. https://podcasts.apple.com/us/podcast/waking-up-to-narcissism-q-a/id1667287384 Go to http://tonyoverbay.com/workshop to sign up for Tony's "Magnetize Your Marriage" virtual workshop. The cost is only $19, and you'll learn the top 3 things you can do NOW to create a Magnetic Marriage. You can learn more about Tony's pornography recovery program, The Path Back, by visiting http://pathbackrecovery.com And visit Tony mentioned a product that he used to take out all of the "uh's" and "um's" that, in his words, "must be created by wizards and magic!" because it's that g

Do you find yourself constantly putting others' needs before your own? Have you ever wondered if being "too kind" could actually be harmful to your relationships and well-being? In today's crossover episode - Tony Overbay, a licensed marriage and family therapist, explores the complex concept of pathological kindness in relationships. Through a listener's letter from 'Cleo,' Tony delves into the challenges faced by those who prioritize others' needs to their detriment, often rooted in childhood experiences of being the family peacemaker. Cleo's story highlights issues with her emotionally inconsistent partner, Ray, unveiling the struggles of living with someone emotionally immature or narcissistic. Tony discusses recognizing these patterns, including the role of cognitive dissonance and trauma bonding in maintaining unhealthy relationships. He explores how highly sensitive people (HSPs) may be particularly vulnerable to these dynamics. The episode emphasizes the importance of developing a stable core identity, setting boundaries, and balancing kindness with self-care. Tony also touches on the challenges of breaking free from intermittent reinforcement in relationships and recognizing and trusting one's own perceptions. He stresses the role of therapy and self-awareness in breaking free from unhealthy cycles and fostering emotionally mature relationships while also offering hope to those who recognize themselves as the emotionally immature partner and want to change. 00:00 Introduction and Podcast Promotion 01:19 Introducing Cleo's Story 03:16 Cleo's Relationship Struggles 10:38 Understanding Pathological Kindness 16:28 The Impact of Pathological Kindness 21:36 Balancing Kindness and Self-Care 25:09 Exploring Self-Reliance and Its Pitfalls 25:24 The Dual Nature of Optimism 25:40 Understanding Humility and Self-Deprecation 26:26 The Complexities of Honesty 27:09 Patience vs. Passivity 27:24 Competence and Arrogance 28:00 Cleo's Relationship with Ray 29:04 The Struggle of Highly Sensitive People 29:48 The Challenge of Leaving Toxic Relationships 33:23 The Cognitive Dissonance and Trauma Bonding 45:04 The Importance of Self-Care and Boundaries 46:03 Encouragement for Personal Growth If you are interested in joining Tony's private Facebook group for women in narcissistic or emotionally immature relationships of any type, please reach out to him at contact@tonyoverbay.com or through the form on the website, https://www.tonyoverbay.com If you are a man interested in joining Tony's "Emotional Architects" group to learn how to better navigate your relationship with a narcissistic or emotionally immature partner or learn how to become more emotionally mature yourself, please reach out to Tony at contact@tonyoverbay.com or through the form on the website, https://www.tonyoverbay.com