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We're all hooked on something. Here's the way out, according to an MD who became a beloved nun. Sister Dang Nghiem, MD, ("Sister D") was born in 1968 in Vietnam during the Tet Offensive, the daughter of a Vietnamese mother and an American soldier. She lost her mother at the age of twelve and immigrated to the United States at the age of seventeen with her brother. Living in various foster homes, she learned English and went on to earn a medical degree from the University of California – San Francisco. After suffering further tragedy and loss, she quit her practice as a doctor to travel to Plum Village monastery in France founded by Zen Master Thich Nhat Hanh, where she was ordained a nun in 2000, and given the name Dang Nghiem, which means adornment with nondiscrimination. She is the author of a memoir, Healing: A Woman's Journey from Doctor to Nun (2010), and Mindfulness as Medicine: A Story of Healing and Spirit (2015). This episode is part of our monthlong Do Life Better series.  We talk about: Sister D's Buddhist version of the 12 step program, which is a combination of two canonical buddhist lists: the 4 Noble Truths and the Eightfold Path How willpower doesn't fit into the Buddhist path of understanding and working with addiction  How to change addiction at its root Practical applications of mindfulness Self-compassion The importance of social support Her thoughts on our relationships to our phones  And more Related Episodes:  This Episode Will Make You Stronger | Sister Dang Nghiem The Science Of Manifestation | James Doty Sign up for Dan's newsletter here Follow Dan on social: Instagram, TikTok Ten Percent Happier online bookstore Subscribe to our YouTube Channel Our favorite playlists on: Anxiety, Sleep, Relationships, Most Popular Episodes Full Shownotes: https://www.meditatehappier.com/podcast/tph/sister-d-899 Additional Resources: Plum Village Deer Park Monastery  Deer Park Monastery YouTube channel For an exclusive offering related to this episode, go to www.DanHarris.com

Most people think strength training is just about building muscle or losing weight. But new research is revealing something far more important.After 40, the right kind of exercise may actually help protect your brain, improve memory, and slow cognitive decline.In this episode of the Functional Longevity Podcast, Chris Borda breaks down the latest research on exercise and brain health, including findings from the University of California San Francisco on how movement impacts brain function at the cellular level, and research from Yale School of Public Health showing that many adults can continue improving physically and mentally as they age.You will learn:• How strength training supports brain health after 40• Why coordination and balance training matter more than most people realize• What many people get wrong about exercise and aging• How to structure workouts for long term cognitive and physical performanceThis episode is not about training harder. It is about training smarter so you can stay strong, sharp, and independent for years to come.#FunctionalLongevity #BrainHealth #StrengthTraining #HealthyAging #Over40Fitness #Longevity #CognitiveHealth #ExerciseForLife #FitnessAfter40 #AgingWell #MuscleAndMind #BrainFunction #StrengthForLife #ActiveAging #WorkoutSmart #HealthyLifestyle #BalanceTraining #MobilityTraining #ChrisBorda #YESFitness

Andrew Clugston, PhD, a postdoctoral fellow in the Sweet-Cordero Lab at UCSF joins us on OsteoBites to discuss his OutSmarting Osteosarcoma funded work, in partnership with the RISE Foundation, on defining tumor-specific vulnerabilities by mapping oncogenic structural variation in osteosarcoma.The genomes of osteosarcoma (OS) cancer cells are among the most complex cancer genomes ever observed. Initially formed by hundreds to thousands of incorrectly repaired DNA breaks (structural variants; SVs), OS genomes contain DNA structures that are unique to that patient and tumor cell, combining genes and regulatory features from across the genome in ways that effectively re-wire that cell's gene expression mechanisms. OS cells are also susceptible to further SVs over time and in response to treatment, potentially allowing OS tumors to evolve rapidly. But these complex and tumor-specific genomic structures may also harbor tumor-specific vulnerabilities. By mapping the many unique DNA structures among patient-derived OS tumor cells, Dr. Clugston has attempted to demonstrate that it is possible both to describe the essential structures within these cells and to search them for novel target genes vulnerable to existing drugs and treatment protocols. Using chromatin conformation capture sequencing (HiC) to observe the shape of the genome and optical genome mapping (OGM) to identify tumor-specific DNA structures, Dr. Clugston has produced tumor-specific maps for multiple patient-derived OS tumor cell lines and has begun development of a search process based on long-read mapping techniques that he hopes will inform future patient-specific treatment protocols.Andrew Clugston grew up in the small town of Lake Luzerne, New York. He received a BS in Biochemistry and an MS in Chemistry at the Rochester Institute of Technology, and he received his PhD in Integrative Systems Biology at the University of Pittsburgh. During his PhD he learned to use and develop bioinformatics tools and techniques to study the role of the genome in kidney as well as eye development, and in the process became fascinated with the importance of 3-dimensional organization in regulating cell behavior. Andrew has since joined the Sweet-Cordero laboratory in the Pediatric Oncology Division at the University of California San Francisco as a Postdoctoral Fellow. There, he applies his knowledge and skillset to study how disruptions in these organizational principles allow osteosarcoma cells to develop and proliferate, and how these changes reveal tumor-specific vulnerabilities that can be exploited for fast and effective treatment options that improve the lives of patients.

Artificial intelligence is being positioned as the next major transformation in healthcare, but the industry has seen similar waves of technological change before. In Part 1 of a three-part series, host J. Carlisle Larsen speaks with Robert Wachter, M.D., Chair of the Department of Medicine at University of California-San Francisco and author of A Giant Leap: How AI Is Transforming Healthcare and What That Means for Our Future, about how to understand this moment in AI. Drawing on lessons from the rollout of electronic health records, Wachter explains why previous efforts to digitize healthcare often fell short of expectations and what may be different this time. Hosted on Acast. See acast.com/privacy for more information.

Transcript Paper: Gearhardt AN, Brownell KD, Brandt AM. From Tobacco to Ultraprocessed Food: How Industry Engineering Fuels the Epidemic of Preventable Disease. Milbank Q. 2026;104(1):0202.https://doi.org/10.1111/1468-0009.70066 https://www.milbank.org/quarterly/articles/from-tobacco-to-ultraprocessed-food-how-industry-engineering-fuels-the-epidemic-of-preventable-disease/ Ashley, let's talk a little bit about, just set the stage for what this paper was all about, and since it was your brainchild, you approached Allan and me about being involved. Tell us what you set out to do and why you thought these issues were worth digging into. Ashley - You know, I've just been so struck that when we think of cigarettes, they were something that's so common, so normal that we kind of think, oh, they've always just sort of been there. But truly, they're just taking a natural plant from the ground and through advancements and corporate engineering and technology and knowhow, they took a poisonous plant and made it into the most deadly and addictive drug in human history. And yet that was, you know, just accompanied by tons of debate. It didn't look like other addictive substances. And I just really felt like, man, we're reliving this history right now when it comes to how we've altered our food supply. I wanted to really bring you all together and see if we could really lay that story out of the, the parallels of these two public health crises. We'll get in a minute into the issue of what you discovered, but tell us what you covered, what the paper was meant to do. Ashley - The paper really goes back from how you take the tobacco plant in the field, or the corn in the field, and walks essentially through all the kind of levers that are being pulled to transform it in very specific ways. And through specific technologies and corporate practices that are being shared by modern cigarettes and ultra processed foods. These products maybe look harmless on their face initially, or don't look like they're just maybe pleasurable or craveable. But truly, I would argue that they've crossed thresholds into things that are addictive and clearly damaging many people's lives. Okay, so several decades ago, I don't know who came up with a term, but there was a lot of discussion about similarities between tobacco industry behavior and food industry behavior. And the press started publishing cover pieces that would say food is the next tobacco. And it was a term that the food industry really didn't like, and they don't want that comparison at all. It'll be interesting to see whether they deserve it. You clearly made that connection in this paper. Allan, let's turn to you. Oh my God. I mean, we could do a 15-hour podcast and not cover the history of the tobacco industry. There's so much to say, enough that you wrote a massive book about it. But give an overall sense, if you will, of the kind of tactics and morality of that industry. Allan - Well, as Ashley already mentioned, early in the 20th Century we wouldn't really be thinking much of cigarettes, and they were just a very peripheral sales consumer item. And over the course of the 20th Century, we came to a point in the middle of the century of the 1970s, and '80s where about half of all American adults were smoking cigarettes regularly. I wanted to understand that. How do you take something that's at the very margin of the economy and culture and make it a dominant consumer force? And I think in that way, we have certain parallels to ultra processed foods. But then there were the questions, how do you make it so popular? Is it dangerous to use? Is it addictive? Does it cause disease? And how do you resist regulation and other public health approaches to try to keep people smoking? And I found a lot of evidence in each of those areas, both of how the industry acted. And when you say, you know, it's ultra processed food like cigarettes, we're learning a lot about ultra processed foods. But we know a ton about what the industry did to make the 20th Century what I call the Cigarette Century. And we have seen really important declines in smoking in the last 30-40 years. It's a remarkable public health effort. But at the same time, the industry worked incredibly hard and, in some ways brilliantly, to maintain the popularity of their product. And underlying all this is the idea that nicotine is highly addictive. And the industry came to understand that certainly before consumers did. And as a result, they could engineer, manage, manipulate the addictive character of a product that kills. I think looking for parallels, both in terms of how the industry did it and how perhaps public health law regulation can undo it, is the critical aspect of what we've been working on together. Okay. So, the tobacco industry did more than just take a plant, dry it out, chop it up, and roll it up in some paper. Then people might be driving whatever natural pleasure there would be from that product. But they did more, didn't they? Allan - Yes. And you talked about nicotine in particular. So how manipulated was this industrial process and was it designed to create such high levels of addiction? Allan - Well, for a long time we couldn't be sure about that. And we have learned that the industry had learned sophisticated techniques of industrial production of cigarettes. So, it wasn't like just chopping up tobacco and putting it in paper. You know, they added many additives. They added liquids. They dried it out, they put it in long strips of tobacco for cutting and packaging. And they had innovated the technologies, instead of human beings rolling cigarettes, they were able through machinery and technology to produce hundreds of thousands of cigarettes a day. And then they had to figure out how do we sell this tremendous volume of cigarettes in order to make our industry truly lucrative. So, there were those aspects. And certainly by the middle of the 20th Century, many people realize that - I smoke regularly and I crave my next cigarette and I'm smoking a pack a day, sometimes two packs a day. And people would ask, well, is it a habit? Is it habituating? Is it addictive? And as the science of addiction really grew in the middle of the 20th Century, we began to realize it had all the characteristics of addiction. But we really didn't know exactly what the companies were doing. And what we did learn in the '80s and '90s is that the companies had a precise ability to manage the nicotine in their product. And they did, so that even as they put filters on and they claimed they had safer cigarettes, they were also producing increasingly addictive cigarettes where we have craving, we have withdrawal, we have tolerance. The basic categories, that structure, how we understand addiction. Okay. We'll dive into some of those in a little more detail, but thanks for that background. Ashley, people kind of get it that drugs can be addictive and they know that alcohol can be addictive. They know that cigarettes can. But what about food? Ashley - Yes, so I think one of the things that when I take a step back, is that the reward and motivation system that alcoholic beverages, cigarettes can start to hijack and drive towards compulsive problematic use, that was laid down in the brain to make sure we were getting enough food. It's really sensitive to food reward, energy density. But the thing is you actually consume nicotine probably most days. Nicotine is actually in a lot of plants like tomato and eggplant, but nobody's getting addicted to the chemical in that delivery vehicle. I would argue the same thing's happening. When we look at our research nobody's getting addicted to minimally processed foods like bananas and broccoli, and salmon filets. It's when you're able to process and titrate and hedonically engineer food reward in a way that mimics the intensity and the sensory appeal and the spikes and crashes and the craveability of something like cigarettes, that you start to see people losing control. And when I read Allan's book, my husband was watching over my shoulder. And he's like, you know, if you highlight every single sentence, it's not gonna help you because you've highlighted the whole book. And reading what Allan laid out about how each wave of cigarette addiction, it wasn't because we suddenly discovered what nicotine was, it's because the industry got better at manipulating engineering, designing, flooding the market with it. And then health washing it, so people didn't really understand what they were getting into. And to me, that is what we've done to our food supply. And the result of that has been the astronomical increases in diet related disease and health concerns. Tell us about the concept of ultra processed food and how that fits in. Ashley - Yes. Yeah, that's a great question. So, ultra processed food is a concept that actually came out at about the same time as the Yale Food Addiction Scale, that Kelly and I published together, about how to operationalize who might be showing signs of addiction and certain foods. Carlos Monteiro from Brazil was noticing that his grocery store was starting to be flooded by foods that you could not make in your home kitchen. I have exactly no idea how to make a double stuffed Oreo or a flaming hot Cheeto, or a Cherry Coca-Cola. And as these products that were industrially created with additives and flavor enhancers that are kind of biologically novel, that's when the disease risk started to go up. And so, these foods are so fundamentally changed in they're kind of most archetypal forms of things, like sodas and, you know, your sweet, savory sort of snacks, that a whole new category had to be created for them. To really distinguish them from, you know, grandma's homemade cookies or, you know, an apple or an orange. Ashley, you're brilliant at framing things. And one of the things that I learned from you a long time ago, and I've used a thousand times in discussions with people, is thinking about food, like turning the coca plant into cocaine and into crack cocaine. That if you take the coca plant into its natural form, people can live in harmony with it. You don't really have addiction. But when you process it and it becomes cocaine, then things change dramatically. And when you hyper process it, like the hyper palatable foods and the ultra processed foods, then the crack cocaine becomes incredibly addictive. So that same sort of phenomenon I think applies here. And it's a very compelling way to think about this. Allan, let's get back to the addiction thing and tobacco. One of the most stunning things I remember about the tobacco history. Is the videotape of the seven tobacco company executives testifying before Congress that nicotine wasn't addictive. Swearing, you know, sworn statements about nicotine. Tell us about that and what that kind of meant in history. Allan - It's a great story and it has a kind of visual linkage to many of us who actually saw those congressional hearings. And it was a brilliant sort of performative politics, if you will. And there had been more and more knowledge that the industry was manipulating nicotine to make cigarettes that they were claiming were safer and not addictive, even more highly addictive. And David Kessler, the head of the FDA under Clinton, had really been a major player in this. And one thing I should say is we were learning more and more about the industry because people were suing them. And they would typically lose the suits, but they would get hundreds, hundreds of thousands of documents. And the industry also had whistleblowers who were coming forward and saying, of course we know it's addictive. So, Henry Waxman, a really fantastic congressman who represented consumers invited all seven of the major tobacco CEOs to a hearing on nicotine. And he went one by one - do you believe nicotine is addictive? And they would say, Congressman, I do not believe that nicotine is addictive. And it's like any great prosecutor, he had figured out how to get them essentially to perjure themselves in front of a congressional, and video news audience. And in fact, the Department of Justice considered for some time whether they should be put on trial and indicted for perjury before Congress. But it was so in congress, with what we had come to know, especially experts, but even, you know, parents and the public and citizens had come to know that it was incredibly difficult to get off of nicotine. It just didn't comport with our existing knowledge. And we're not quite to that point with ultra processed foods yet, but I think we have a good chance to get there because as we understand what they're doing better and we have a sophisticated understanding of the characteristics of addiction, that same question will be put ultimately to CEOs of the food industry. Especially those who are producing these highly addictive products. And there are many people who are involved in this. So, they will tell a story of how we understood we could make our product sell better and be used at a much higher level if we could make it addictive. And regrettably, as we learn more about addictive addiction, we not only learn perhaps how to help people who are addicted. But we often learn how to make certain products even more highly addictive. Ashley, let's take what Allan said and apply it into the food arena. So, if you think about the criteria for addiction, like Allan had mentioned: cravings, withdrawal, and tolerance, and, tolerance being the need to have more of the substance over time in, in order to produce the same pharmacologic effect. How do those things apply to foods? Ashley - Yes. There there's very strong parallels there. And I actually have a paper I wrote with Dr. Alex DiFeliceantonio, where we took the 1988 Surgeon General's report on the addictiveness of tobacco and nicotine in particular. And we took what they identified as the necessary and sufficient criteria to prove that it was addictive. It was a watershed moment for tobacco. And the major one is that people consume it compulsively. Meaning, you know, they want to cut down and they can't. They know it's harming them and they can't. Clearly we see that with ultra processed food. That it shifts mood. It increases pleasure. It reduces negative affect through its mechanism on the brain. And I think if you look at any marketing, you know, they're always saying you're craving meet your maker, get your bliss point. You're not you unless you're eating a Snickers. They show that it was highly reinforced. And that is, you know, animals and humans will work really hard to get access to it. With nicotine one of the major points of that is that animals, about 20% of the time, would work to get nicotine over cocaine. And that was quite striking because cocaine is so powerfully addictive. Well in those same models, animals will work for processed sweet taste and choose it 80% of the time over cocaine. It just shows that when we start altering, processing food reward into these unnaturally intensely stimulating packages, our brains were not evolved to protect itself against that. And then the final pieces that's been kind of added over time has been the cravings. I mean, if you think about what is the core of addiction, it's the craveability of it. That they maximize that. So, you can't stop thinking about anything else. And when I read, and we even quote in our paper, spots where, you know, industries, the big food is having webinars and how to turn cravings into corporate wins. And how to take snackers who are consuming, because their cravings feel unmanageable, but here's how you can keep them snacking even though they want to quit. And so, the craving really seems to me, based on my read of what I've seen from the industry, is the core engine of driving and selling ultra processed food. So, these foods, and I've heard you say this, Ashley, you know, they have less to do with the farm and, you know, these sort of romantic ideas of the farmer growing crops and the crops being harvested and coming to a farmer's market. These are really industrial lab-based, you know, heavy duty factory related products. And there's a real question, isn't there, about what you even should call them food. Ashley - Yes, absolutely. I actually grew up on a farm and I never ate anything that we grew on the farm because it was all due to Ag policy. Just, corn to go into high fructose corn syrup, soy to go into soybean oil. And I was surrounded by what looked like lots of food, but in reality, it was not. And some of the things that I learned in writing this paper with you all is just to what degree ultra processing allows them to even control the molecular structure and size of the different starch chemicals. That carby kind of access point in food. Allan talks in his book about how you can treat tobacco. So, you break it down and make it molecularly more bioavailable so nicotine gets more rapidly into the body. That's a huge driver of addictive potential. I found in ours that they were actually using enzymes that mimic what's in the saliva in your mouth. And hitting starches with it. Essentially you were predigesting, pre salivating, essentially the starch creating what's called a starch slurry. And that's a base of so many common ultra processed foods like cereals and savory snacks. Many of these products really have far more in common with that cigarette and have almost nothing in common, you know, with the apple or the can of beans anymore. You know, that image that you said about pre salivating food. I mean, it's in some ways as if the industry is spitting in your food to bypass your own biological mechanisms that occur when the food gets in the mouth and. People get a kind of a yuck response to that, but it deserves that kind of a response. Let's dive into the paper and talk about what you reported, Ashley. You talk a lot about the kind of processes. You just mentioned one of them, but there are a lot more. What are some of the specific techniques to food processing that surprised you when you started digging in. How did you get this information? Ashley - Yes, so one of the functions that actually didn't surprise me, but it made me look at it in new light, is the work on how we really changed the way we saw cigarettes when we realized they weren't just taking a plant and drying it and rolling it up. But that they were actually curating and titrating these just right doses of nicotine. So, you get stimulated, but not too satisfied and you don't feel overwhelmed by the amount of nicotine. When we realized that was very intentional and designed and titrated, that really changed this from a natural kind of product, it's just a plant to, oh, this is an in industry engineered product. They're controlling so much of this. We all know that they are altering the amount of sweetened refined carbohydrates and fats in our food. I mean, that's just plain knowledge. And at levels that go way beyond what exists in nature. But I think I've become very obsessed with extrusion technology. Extrusion is something where they take really high pressure, high shear mechanical impact, high pH, high temperature. And they can break the corn or the potatoes and things into this slurry that is broken down again into this kind of predigested molecular base that on its own is nasty. No one is like, oh, starch, slurry, yes! They need all the sensory and flavor additives to blitz that and texturize it so it can trick your brain into thinking it's appealing. I realized that actually has such a strong parallel to modern cigarette where, as Allan talks about in his book, one of the major technological advances was creating reconstituted tobacco where they take the tobacco scraps and they do the same sort of process to create what they call a tobacco slurry. That was then very easy to manipulate by putting flavor and preservative additives in it, and that's what makes up a large component of modern cigarette. And so, when we look at these processes and those sensory additives, the flavors, that are put in it, cigarettes have more sugar and flavor additives in them by weight than they do nicotine. And so many of those flavor additives are actually in our ultra processed food supply. Why? Because the flavor and sensory profiles are what you start to become really emotionally attached to. And that starts to drive brand loyalty from a very young age. I could go on and on and on. Oh man, we could be here for a day, so I'm really inhibiting myself. I'll be exhausted. I'll have to go get an ultra processed food from this. But it was stunning to me to see how the goals of the engineering were so shared. And I guess it shouldn't surprise us because, you know, we know that the tobacco companies like Philip Morris and RJ Reynolds actually created, manufactured and sold many of our favorite ultra processed foods that are now in our modern food supply, like Fig Newton's and you know, Hawaiian Punch and things. It really came from the same industrial practices. So Allan, I want to bring this back to the tobacco industry in a minute, but Ashley, I wanted to ask you first. I'm going to make a characterization. Tell me if I'm off on this. The industry is kind of manipulating every possible characteristic of a product. Its fragrance, its color, its texture, everything in the ways you mentioned. It becomes this industrialized product much more than a food. People consume it. They get immense reward from it because it's delivering a drug, basically, to the brain very quickly in a very efficient way. People then, of course, want more of that sensation. If tolerance exists, then it means they need more of the food over time in order to get the same reward. And then you've got a public health nightmare on your hand because people aren't just eating a little bit of these foods, they're eating a lot of these foods. And they're designed in order to produce that very impact. Does that seem fair? Ashley - Absolutely. That sums it up quite nicely. Okay, Allan, back to the tobacco experience. This kind of information that Ashley is talking about in the context of food, and you talked about in the context of tobacco. Manipulation of the product. As this kind of damning information became public knowledge, how did that happen in the tobacco arena? And then what was the consequence? Was it, you mentioned whistleblowers; was it investigative journalism? The hearings you mentioned were important. Scientific research, discovery. It sounds like a whole lot of things happened that made this information available to the public, which in turn changed public opinion against the industry. Allan - Yes, I think that's exactly right. It changed public opinion and it changed public policy and it took a long time. So, these are aspects that I think we have to, you know, acknowledge in thinking about public health and especially these powerful commercial interests that spend a lot of money on lobbying. They spend a lot of money on advertising. They know how to get to kids. These are very challenging. I do think, you know, early in the anti-tobacco campaigns, there were a few lawyers who said, well, we're going to sue them because they have misled, deceived, and in some instances probably acted criminally to build their addictive and extremely harmful life-threatening product. And people said, well, you know, it's everybody's decision whether they want to smoke and people quit all the time, so you're not going to do very well. And I think as a young academic type, I was very skeptical of the suits against the companies. But one thing that happened that I think was unanticipated, the lawyers asked for the company's records and their research reports and what people were doing. And they took depositions and the lawyers often lost the case, but they won an incredible archive that was incredibly self-incriminating of what the industry knew. When they knew it and how they continued to act to sell a harmful product. And I think that began to change things. So once you have documents, you know you're going to be more successful in court. Once you have some documents, you can call the CEOs in and say is it addictive? When they say no, you have documentation to challenge them about their own industry. Obviously, education is important. Investigative journalism. A lot of the documents not only came from the court suits, but from whistleblowers who snuck them out of law firms. Some of the whistleblowers came directly from the industry where they said, here's what my bosses told me. They need to know can you make this cigarette even more addictive? And they knew, for example, that taking nicotine out of cigarettes, which is not that difficult to do given the extent of manipulation, had to be something that was resisted. We could end the tobacco pandemic by just removing nicotine. Even if we did, you know, 10% a year. Many people would be able to stop smoking who cannot. But we had to array a kind of knowledge and practice and advocacy that really hadn't existed till the second half of the 20th Century. Ashley, when Allan mentioned these archives that exist on tobacco industry behavior, there's some food things in there, aren't there? Tell us about that connection between tobacco and food companies. Ashley - Yes, so you know, actually, Dr. Laura Schmidt at University of California - San Francisco, has done this just stunning work by using those same tobacco archives. Because they owned alcoholic beverage and ultra processed food and beverage companies she's been able to show really how much these industries kind of spoke back and forth. The different sectors of Philip Morris and RJ Reynolds, you know, they're big conglomerates. They were pulling scientists working on the cigarettes, or the marketers working on marketing cigarettes to kids, and putting them on and intentionally using that playbook to sell their ultra processed foods and beverages. That's very clear and very intentional. They might not say as blatantly. I feel like they learned their lesson a little bit. Oh, we're going to make this more addictive. They use synonyms even out in the public. Some of it that we report in this paper is not hidden. It's industry trade newsletters. It's interviews on 60 minutes with labor scientists where they're saying, yeah, we design these products, so you get a big flavor burst. And then it fades really rapidly because that makes you want to keep coming back for more and more and more. And yeah, addictive is a good word for that. And so there is this moment where it just becomes so implausible that they don't know that they have crossed the Rubicon into something that is hooking people. That plausible deniability that we're just, you know, giving consumers what they want, not actually engineering their desires to override what they know they should have to nourish themselves. It just feels beyond the pale to me to believe that's the case. Allan, look, you mentioned delay. And I'd like to talk about that a little bit more. There's a point in time when the science on something becomes robust. And you're very certain say that tobacco is causing lung cancer and heart disease.  And then you can't change things the next day or the next week. So, a little bit of delay is probably acceptable and to be understood. But the delay in this case between that knowledge and significant public health action policy action wasn't measured in days, weeks, months, or even years. It was decades. And you can count the number of attributable deaths to that delay in the millions. What did the industry do to make that delay as long as possible in terms of planting doubt, conflicts of interest with science and things like that? Allan - This is highly relevant to our moment because I make a few claims in the book. One is that the industry invented disinformation and misinformation. And there's always this way that says, well, I know that study appeared, but we need more information. And this was very clever on the part of the tobacco companies because they said, well, you know, that science shows this, but that science is unreliable. And we need to use different methods. And lung cancer is not a result of cigarette smoking, it's actually genetic. And maybe there are a few people that shouldn't be smoking cigarettes. We should be able to identify what's different about them. They kept finding strategies of delay, manipulation, building uncertainty. There's one of the tobacco documents in this phase that says, from now on, our product is doubt. And what they really needed to do to sell the product was to create doubt about a science that was highly robust and really important to consumers. On the other hand, I think consumers are sensitive to being manipulated. They don't like that. They don't like being tricked. They know these industries, especially tobacco industry, you know, is disreputable. And as that became the case, what did they know and what are they selling. We began to see some slow shifts in public awareness. And, you know, it's so interesting presenting the cigarette problem to a jury in 1970 became radically different than presenting the case against the tobacco companies in the 1990s. And a lot had changed, A lot had been documented and, you know, we never even thought of the idea that a company would scientifically mislead us probably until in any consequential way till the middle of the 20th Century. And now we're incredibly skeptical and I think taking advantage of the public skepticism, both politically and culturally is going to be one of the important issues of pushing back against what I've called rogue industries. They're operating unethically; in many cases, unlawfully. They're misrepresenting what they produce. And they have the idea that having addicted customers is the best customer. And Warren Buffet once said, you know the tobacco industry, that's crazy. It cost a dime to make it. You sell it for a dollar and its addictive. He said, what industry could be more, you know, lucrative than tobacco? Ashley, how do those things apply into the food area now? Ashley - Oh, my brain is just exploding with all the things I want to say. But I think I have an answer to Warren Buffett, which is if you've pulled all those same levers and pretend to people that it's food, and it's because we all have to eat, you know? And I walk around a grocery store and I, in my head, I'm like, if I waved a magic wand, and all the products in here that are masquerading as food but are actually ultra processed, chemically adulterated starch, slurries essentially disappeared. There is so little food in my grocery store. Real food. And it's also expensive. We would be rioting in the streets if we really saw the degree that we're not being adequately nourished or supported in our current environment. And it's the mirage of abundance that is totally hooking us. You know, taking us hook, line, and sinker. And so, you know, I'll have people often say to me, you know, it's food. Like can't really be addictive. We all need to eat. And to me that is absolutely true. Just like we all need pain management. And there used to be a belief, a myth, that if you were in pain, you couldn't get addicted to painkillers like opiates which we now know is incredibly wrong. That just because we need calories to survive doesn't mean that if you manipulate and hedonically engineer those products, that it won't impact the brain in a way that can drive it in compulsive problematic ways. It's so essential for us to carve out, yes, you need real nourishing food. This is real nourishing food and these other things. I'd love it if the grocery store, it's like you're walking around this spot, you know you're getting real food. Sure, you want to go get those Cheetos, go for it. But it's in a very clear designated area that you're not being tricked into thinking that you're eating something that's nourishing you when it's really addicting you. So, people have very strong affective attachments to foods. Particular foods that they like. Some of it is kind of what you grew up with, what your parents gave you, but a lot of it's marketing as well. And you mentioned a Cheeto or Coca-Cola, or a Dorito or a Twinkie or whatever it is. People don't want that taken away from them. Tell me if this is correct, the problem isn't so much that people eat Cheetos. It's that they overeat Cheetos, and then you add to that all the other thing, not just that food. But then you've got a real problem. Could it be a matter of just removing some of the especially troublesome ingredients from that. If you look at the list of ingredients on these foods, there could be 25 or 30 different ingredients. Well, what if, what if 12 of them got taken out or 13 or 15 of them got taken out? You'd still have the food; it would still have its taste. People could enjoy it, but it's not hijacking your biology. Ashley - Yes, I'm very skeptical of that as the response, because as Allan lays out in his book, we were like, okay, if we just get the tar out of the cigarette. You know, it's all fine, Vapes, right? Oh, you're vaping. It's fine. It will be harmless because our reward system is so porous to different levers that signal food reward. We see it with the non-sugar sweeteners. Look, we took all the sugar out, we gave you Diet Coke, we gave you non-sugar sweeteners. It's a get out of jail free card. And now we're realizing how much that messes up our gut microbiome, could potentially lead to earlier brain aging and so, you know, abstinence, clearly making this stuff illegal, that's never the goal. But I think that sense of saying, oh, we can just engineer our way out of this is unlikely. And we have the alternative. You know, for what should be the majority of what we're eating. I love a Reese's Cup, right? I will have an ultra processed food, but it shouldn't be 60% of the food supply, or 70% of what my kids are getting for their calories. And so again, that clear understanding that this is something that's fundamentally different from the food that nourishes us. We have the answer which is real food. If we poured even a tiny amount of the investment, even closing the tax loopholes on things like ultra processed food marketing to kids that they get tax breaks on and invested that into technology to make real food in its original food matrix affordable, accessible, convenient. That stuff is tasty. Have a fresh apple. It's just everything's been wired for that to be the minority of our food supply. That's often unaffordable and we all feel really time poor. These are solvable problems. We've just been shoving all our money towards how we make new flavor additives to sell high fructose corn syrup, starch, slurries. So, we just need to have the right in incentives in mind. Your point is very well taken that government trying to say, okay, let take out this ingredient or that ingredient is stepping into a trap. It makes all the sense to me in the world that that is a trap because. Using that philosophy requires a trust in the industry that if you ask them to take out these 12 things, they're not going to put in 12 new things that might even make things worse. And both of these industries, tobacco and the food industry have done everything but earn our trust so that's a very good cautionary note that you raised. I would say in the tobacco area, the idea of that we think that, you know, vaping will be harm reduction. And there's been a strong political notion that we should be, you know, doing harm reduction. And of course, in many instances, harm reduction can be helpful. But I found in tobacco, that I can't trust the industry to make a harm reduction product that's not going to get kids addicted. That's going to, you know, make sure that we're not using both tobacco and nicotine in the form of vape or other products. And so while many people who I admire in the public health world have said, yes, harm reduction is the way to go. I don't think that's true with tobacco. We have a lot of children and adolescents today who are profoundly addicted to nicotine. So, this discussion has led to lots of, oh my God, kind of observations from both of you. Paints a pretty scary picture of the food supply. How much manipulation there is. And how much harm gets caused by it. I'm hoping we might end on a bit of a positive note if there is one here. I'd like to ask each of you, is there a reason to be hopeful about the future? Allan, let me start with you. You're looking in on this with a unique perspective because of your years and years of working on tobacco. As you look in on the food space and see what's happening, what do you think? Allan - Well, I tend to be an optimist. I believe public policies can make a difference. I believe the courts can be used to serve consumers who have been harmed in the market. So, I have seen those things work to a really significant degree around the cigarette. Especially in countries where we have resources for education, where we can make policies that sometimes work or mostly work. I don't think I ever would've thought when I started this work in like the 1980s that we would've gotten so far. I once said to my son when he was seven, he was taking a flight with me. And I said, you know, people used to smoke on airplanes. And he said, no, that's impossible. And he just couldn't believe the idea that we had let people smoke on airplanes. And I've been collecting cigarette packages that were given out by the big airlines. Of course, you and I, Kelly, remember probably, when they start to put smokers in the back of the plane. But the smoke was wafting throughout it. And a lot of things that seem almost impossible now, were actually reduced through regulation and politics and public health. I'm very hopeful that we can use what we've learned about how to get smoking from 50% of the population down to 15 or 12, as bad as that is. And apply it to other gigantic risks like ultra processed foods. All right, thanks for that positive note. Ashley, what do you think are there grounds for being positive? Ashley - Yes, I'm also a huge optimist. I feel wildly optimistic. I just, from listening to consumer sentiment right now, the degree to which corporations are able to hack our limbic systems, I mean, you see it right now with social media and sports betting. I think in our bones as a society, we're starting to just get fed up. And to me there is nothing that is more clear cut of how industries can manipulate us than taking food, the thing we most evolved to care about and to find rewarding and nourishing, and somehow jacking it up into an addictive, harmful substance. And I have two little kids. I have a five and 7-year-old and I am just as a mom full of rage every time I go grocery shopping because they've just shoved protein in a Pop-Tart, now they're trying to tell me it's a health food. I think we're catching onto them, and I think that there is no way to go but up. And again, we already have the solution. In opiates, we are still struggling to find non-addictive pain management. We have non-addictive food and it's called, you know, minimally processed real foods. So, it's just about putting the incentives in the right place. BIOS Ashley Gearhardt, Ph.D., is a Professor of Psychology in the Clinical Science area at the University of Michigan. She also earned her B.A. in psychology from The University of Michigan as an undergraduate. While working on her doctorate in clinical psychology at Yale University, Dr. Gearhardt became interested in the possibility that certain foods may be capable of triggering an addictive process. To explore this further, she developed the Yale Food Addiction Scale (YFAS) to operationalize addictive eating behaviors, which has been linked with more frequent binge eating episodes, an increased prevalence of obesity and patterns of neural activation implicated in other addictive behaviors. It has been cited over 800 times and translated into over ten foreign languages. Her areas of research also include investigating how food advertising activates reward systems to drive eating behavior and the development of food preferences and eating patterns in infants. She has published over 100 academic publications and her research has been featured on media outlets, such as ABC News, Good Morning America, the Today Show, the Wall Street Journal, and NPR. Allan M. Brandt is the Amalie Moses Kass Professor of the History of Medicine and Professor of the History of Science at Harvard University, where he holds a joint appointment between the Faculty of Arts and Sciences and Harvard Medical School.  Brandt served as Dean of the Graduate School of Arts and Sciences from 2008 to 2012.  He earned his undergraduate degree at Brandeis University and a Ph.D. in American History from Columbia University.  His work focuses on social and ethical aspects of health, disease, medical practices, and global health in the twentieth century.  Brandt is the author of No Magic Bullet:  A Social History of Venereal Disease in the United States since 1880 (paperback, 1987; 35th Anniversary Edition, 2020); and co-editor of Morality and Health (1997).  He has written on the social history of epidemic disease, the history of public health and health policy, and the history of human experimentation, among other topics.  His book on the social and cultural history of cigarette smoking in the U.S., The Cigarette Century: The Rise, Fall, and Deadly Persistence of the Product that Defined America, was published by Basic Books in 2007 (paperback, 2009).  It received the Bancroft Prize from Columbia University in 2008 and the Welch Medal from the American Association for the History of Medicine in 2011, among other awards.   Brandt has been elected to the National Academy of Medicine and the American Academy of Arts and Sciences.  In 2015, he was awarded the Everett Mendelsohn Excellence in Mentoring Award by the Harvard Graduate School of Arts and Sciences.  In 2019-20, Brandt was a recipient of fellowships from the American Council of Learned Societies and the Radcliffe Institute for Advanced Study.  He recently served as the interim chair of the Department of Global Health and Social Medicine at Harvard Medical School.  Brandt is currently writing about the history and ethics of stigma and its impact on patients and health outcomes.  

Jamie Hartmann-Boyce and Nicola Lindson discuss emerging evidence in e-cigarette research and interview Dr Pamela Ling, University of California San Francisco. Associate Professor Jamie Hartmann-Boyce and Associate Professor Nicola Lindson discuss the new evidence in e-cigarette research and interview Dr Pamela Ling, Professor of Medicine and Director of the Center for Tobacco Control Research and Education at the University of California San Francisco. In the March 2026 podcast Pamela Ling talks to Nicola Lindson about her newly published study that recruited approximately 500 13 to 21 year olds to test whether Instagram support groups can help people to quit vaping compared to referral to a quitline. This randomized clinical study was funded by the UCSF Helen Diller Comprehensive Cancer Center and the Tobacco-Related Diseases Research Program and is published in the American Journal of Preventive Medicine. The intervention, Instagram direct message support groups, was delivered over 5 weeks and involved motivational interviewing, social support, skill building, and group quit attempts. The control group was referral to Quitline in California, the resources for this included telephone, online, texting or mobile app. Pam Ling's study found that social media support groups were acceptable to adolescents and young adults and improved abstinence rates on average over 6 months compared to quitline referral. Pam Ling discusses the finding that social media platforms may be a useful way to deliver social supports for nicotine vaping cessation that is accessible and utilised by young people. This podcast is a companion to the electronic cigarettes Cochrane living systematic review and Interventions for quitting vaping review and shares the evidence from the monthly searches. Our searches for the EC for smoking cessation review carried out on 1st March 2026 found: 1 new (Papadosifaki et al, Archives Hellenic Medicine 2026;43(2):205-211) and 3 linked reports (10.1093/ntr/ntag038; 10.1093/sleep/zsag028; 10.1017/S1463423626100942). Our search for our interventions for quitting vaping review carried out on 1st March 2026 found: 1 new (discussed in this podcast 10.1016/j.amepre.2026.108314), 5 linked reports (10.1016/j.acap.2025.103181, 10.1038/s41386-024-02012-z, 10.1186/s40814-026-01782-1, 10.1016/S2468-2667(26)00021-6, 10.1016/S2468-2667(26)00020-4) and 2 new ongoing (ACTRN12626000031369 2026, NCT07392125 2026). For further details see our webpage under 'Monthly search findings': https://www.cebm.ox.ac.uk/research/electronic-cigarettes-for-smoking-cessation-cochrane-living-systematic-review-1 For more information on the full Cochrane review of E-cigarettes for smoking cessation updated in November 2025 see: https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD010216.pub10/full For more information on the full Cochrane review of Interventions for quitting vaping published in November 2025 see: https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD016058.pub3/full This podcast is supported by Cancer Research UK.

In episode 71 of Going anti-Viral, Dr Peter Hunt joins host Dr Michael Saag to provide a review of the science presented at the 2026 Conference on Retroviruses and Opportunistic Infections (CROI). Dr Hunt is a Professor of Medicine at the University of California San Francisco and is the Associate Chief for Research in the Zuckerberg San Francisco General Hospital Department of Medicine, and Co-Director of the UCSF-Bay Area Center for AIDS Research for Basic and Translational Science. He was also a Vice Chair of the Scientific Program Committee for CROI 2026. Dr Hunt provides an in-depth overview of the key scientific presentations at CROI, highlighting breakthroughs in HIV research, pediatric HIV treatment, biology of the HIV capsid, vaccine research, and innovative therapies. Dr Hunt and Dr Saag also discussed new antiretroviral formulations and highlights of the state of HIV cure research.0:00 – Introduction 1:13 – Valganciclovir in infants with HIV and CMV pneumonia4:25 – Differences between pediatric and adult CMV infection7:34 – Plenary by Dr Wesley Sundquist on structural biology and the HIV capsid12:00 – Other plenary presentations at CROI 202614:27 – Powerful Martin Delaney presentation by Peter Staley15:50 – Plenary by Dr Jeanne Marrazzo on Doxy PEP and resistance concerns16:30 – Vaccine development and neutralizing antibodies by Dr Kevin Saunders17:25 – New symposium: Hot Takes on the Clinical Highlights of CROI 202619:38 – New antiretroviral formulations and long-acting agents25:10 – HIV cure research, overview of TACK agents, and a poster on an efavirenz intensification study28:39 – A look ahead to CROI 2027 and closing remarks Resources:Watch Peter Staley's presentation at CROI 2026 YouTubeGoing-anti-Viral: Episode 70 - Peter Staley Apple PodcastsGoing-anti-Viral: Episode 69 - Dr Kevin Saunders Apple PodcastsCROI 2026: https://www.croiconference.org/__________________________________________________Produced by IAS-USA, Going anti–Viral is a podcast for clinicians involved in research and care in HIV, its complications, and other viral infections. This podcast is intended as a technical source of information for specialists in this field, but anyone listening will enjoy learning more about the state of modern medicine around viral infections. Going anti-Viral's host is Dr Michael Saag, a physician, prominent HIV researcher at the University of Alabama at Birmingham, and volunteer IAS–USA board member. In most episodes, Dr Saag interviews an expert in infectious diseases or emerging pandemics about their area of specialty and current developments in the field. Other episodes are drawn from the IAS–USA vast catalogue of panel discussions, Dialogues, and other audio from various meetings and conferences. Email podcast@iasusa.org to send feedback, show suggestions, or questions to be answered on a later episode.Follow Going anti-Viral on: Apple Podcasts YouTubeXFacebookInstagram...

Welcome to The Mental Breakdown and Psychreg Podcast! Today, Dr. Berney and Dr. Marshall discuss the differences between Adult ADHD, normal aging, and mild cognitive impairment. Read the articles from the National Library of Medicine here, from the Alzheimer's Association here, and from the University of California San Francisco 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 differences between Adult ADHD, normal aging, and mild cognitive impairment. Read the articles from the National Library of Medicine here, from the Alzheimer's Association here, and from the University of California San Francisco 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!

Host: Stephanie Christenson, MD Guest: Diego Maselli, MD, FCCP COPD is increasingly recognized as a heterogeneous disease, and for a subset of patients, type 2 inflammation plays a meaningful role in exacerbation risk and treatment response. Given that, Drs. Stephanie Christenson and Diego Maselli come together to examine how insights into the pathobiology of type 2 inflammation can directly inform clinical decision making in COPD. Specifically, they discuss the practical use of blood eosinophil counts to phenotype patients, assess risk, and guide therapy selection within the context of GOLD 2025 and 2026 guidance. Dr. Christenson is an Associate Professor at the University of California San Francisco in the Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, and Dr. Maselli is a Professor of Medicine at the Long School of Medicine at UT Health in San Antonio. This episode of Deep Breaths: Updates from CHEST was supported by a non-promotional, non-CME educational program brought to you by CHEST in collaboration with and sponsored by GSK.

Developed by the AUA Residents and Fellows Committee, each episode of the Training Transformed podcast series features an interview with a urology faculty member and resident physician surrounding an innovative facet of resident education at their institution. Tune in for our fifth episode as moderator, Dr. Kayla Graham, chats with Dr. Max Bowman and medical student, Lynn Leng, about their revamped Morbidity & Mortality conference model at the University of California San Francisco.

Dr. Patel is the Chief of Cardiology at Vitruvian Health and a board-certified interventional and structural cardiologist. He attended medical school at the Emory University School of Medicine in Atlanta, Georgia, and completed his residency training in internal medicine at the University of California San Francisco in San Francisco, California. He earned his Master in Business Administration degree at Northwestern University-Kellogg School of Management in Evanston, Illinois.He also completed his fellowships in cardiology at the Northwestern University Feinberg School of Medicine in Chicago, Illinois, and then further trained in structural and interventional cardiology at the Emory University School of Medicine in Atlanta, Georgia.https://vitruvianhealth.com/services/heart-vascular

Dr. Patel is the Chief of Cardiology at Vitruvian Health and a board-certified interventional and structural cardiologist. He attended medical school at the Emory University School of Medicine in Atlanta, Georgia, and completed his residency training in internal medicine at the University of California San Francisco in San Francisco, California. He earned his Master in Business Administration degree at Northwestern University-Kellogg School of Management in Evanston, Illinois.He also completed his fellowships in cardiology at the Northwestern University Feinberg School of Medicine in Chicago, Illinois, and then further trained in structural and interventional cardiology at the Emory University School of Medicine in Atlanta, Georgia.https://vitruvianhealth.com/services/heart-vascular

Presented by Karly Hampshire, MD; Natasha Sood, MD, MPH; and Bhargavi Chekuri, MD (Moderator)STFM Conference on Medical Student Education Closing Session | Sunday, February 1, 2026Climate change is the greatest health threat of the 21st century, yet medical education has been slow to prepare future physicians for its wide-ranging impacts on health systems and patient care. In this session, we spotlight the power of student-led innovation in advancing climate and health education through two globally recognized initiatives: the Planetary Health Report Card (PHRC) and Climate Resources for Health Education (CRHE). Both began as grassroots projects by medical students who identified gaps in their training and took action to fill them. PHRC now benchmarks health professional schools internationally on planetary health curriculum, research, and operations, while CRHE has developed a growing library of open-access teaching materials to equip faculty with ready-to-use climate and health resources.Through a panel discussion with the co-founders of PHRC and CRHE, participants will hear first-hand stories of how these initiatives were built, scaled, and sustained as international collaborations. Panelists will reflect on their “aha” moments, early challenges, and lessons learned in fostering inter-institutional collaboration, leveraging mentorship, and bridging the gap between education and clinical practice. As both panelists now train as residents, they will also share how their perspectives on climate and health education have evolved with greater exposure to patient care and health systems.This session will equip educators, learners, and leaders with practical insights on cultivating an entrepreneurial mindset, leveraging collaboration, and supporting the next generation of change agents in climate and health education.Learning ObjectivesUpon completion of this session, participants should be able to:Describe how trainee-led initiatives have advanced climate and health integration in medical education worldwide.Identify strategies for fostering collaboration, mentorship, and sustainability in grassroots educational innovations.Apply lessons from student innovators to support the development of new climate and health education efforts at their own institutions. Copyright © Society of Teachers of Family Medicine, 2026Karly Hampshire, MDKarly Hampshire is an internal medicine resident at Columbia University pursuing a career at the intersection of medical education, climate change, and health. As a medical student at University of California San Francisco, Karly founded the Planetary Health Report Card Initiative, a student-led, metric-based initiative to evaluate and inspire planetary health engagement at health professional schools worldwide, now active in over 180 health professional schools in 10 disciplines in 21 countries. She was also awarded the Emerging Physician Leader Award from Health Care without Harm for her Interview without Harm Initiative, an advocacy, research, and educational campaign urging decisionmakers to prioritize sustainability and equity in evolving decisions about the future of medical training interviews post-COVID. She currently is in the inaugural cohort of the GME Certificate of Distinction in Climate Change, Sustainability and Health at Columbia University.Natasha Sood, MD, MPHNatasha Sood is a resident at the Brigham and Women's Hospital Department of Anesthesiology. She received her Bachelor of Science from the University of Michigan and her Master of Public Health from Columbia University in Environmental Health Science with a specialization in Climate Change and Health. While in medical school at Penn State College of Medicine, Natasha co-founded the national organization, Medical Students for a Sustainable Future (MS4SF), and w

Dr. Patel is the Chief of Cardiology at Vitruvian Health and a board-certified interventional and structural cardiologist. He attended medical school at the Emory University School of Medicine in Atlanta, Georgia, and completed his residency training in internal medicine at the University of California San Francisco in San Francisco, California. He earned his Master in Business Administration degree at Northwestern University-Kellogg School of Management in Evanston, Illinois.He also completed his fellowships in cardiology at the Northwestern University Feinberg School of Medicine in Chicago, Illinois, and then further trained in structural and interventional cardiology at the Emory University School of Medicine in Atlanta, Georgia.https://vitruvianhealth.com/services/heart-vascular

The House of Lord's amendments to England and Wales assisted dying bill might be causing a constitutional crisis. Lords have tabled 1,277 amendments—which is a record for any equivalent bill in history - and over half of those came from just seven peers. This has led to accusations of "delaying tactics" or "filibustering" to run down the clock deliberately and run this bill off the road. Although some of these amendments have been described as unworkable, repetitious and unnecessary; others reflect serious, legitimate concerns, around the prevention of coercion, how to identify victims of domestic abuse and the broader impact on the disabled community, and whether it's wise to introduce assisted dying while palliative and social care services are so stretched. 300 territories around the world, allow physician assisted death - so we asked experts from Canada and California to reflect on those objections, and if there is any evidence of this issues arising where they live. James Downer is Professor and Head of the Division of Palliative Care at the University of Ottawa, and Catherine Forest is clinical associate professor of family medicine at the University of California San Francisco.   Reading list: Scrutiny of the assisted dying bill is vital but obstruction in the House of Lords could mean it never becomes law

Is transecting urethroplasty still the default, or is reconstructive urology moving beyond it? In this episode of BackTable Urology, Dr. Ben Breyer (University of California San Francisco) joins host Dr. George Koch (Ohio State University) to discuss evolving approaches in reconstructive urology with an emphasis on complex stricture cases. --- SYNPOSIS Throughout the conversation, Dr. Breyer reflects on his path into the subspecialty and breaks down the evolution of reconstructive practice, particularly the shift from anastomotic urethroplasty to non-transecting techniques. Dr. Breyer and Dr. Koch also discuss managing complex urethral strictures, including cases involving prior radiation and inflammatory conditions, while emphasizing thoughtful patient selection and surgical planning. Finally, they explore the current training landscape, challenges in patient access to subspecialty reconstructive care, and why patient-reported outcomes will play a central role in shaping future innovation in urethral reconstruction. --- TIMESTAMPS 00:00 - Introduction05:40 - Evolution of Surgical Techniques10:01 - Managing Complex Cases14:19 - Education and Training in Reconstructive Urology23:45 - The Future of Reconstructive Urology28:45 - The Journey of a Reconstructive Urologist30:45 - Challenges in Urology Training and Practice35:35 - Addressing Urologist Shortages in Rural Areas48:34 - Innovations and Research in Reconstructive Urology57:25 - Final Thoughts

Scientific research grants were abruptly terminated for hundreds of researchers including those in the ATS community in 2025. Many of these resulted in research that had already been done and was in final stages being discarded. Important studies done with community collaboration are at risk. Neeta Thakur, MD, of the University of California San Francisco, was one such researcher. Her EPA grant to study the effects of wildfire smoke on vulnerable communities was abruptly terminated. Dr. Thakur discusses her experience receiving the cuts, collaborating with other researchers on a lawsuit to restore the funding and finish the research, and how these cuts will affect the future of health and patient outcomes with Air Health Our Health host Erika Moseson, MD, MA. For more on funding cuts, listen to prior ATS Breathe Easy podcast episodes: - ATS Breathe Easy - The Real Cost of Federal Budget Cuts: https://www.youtube.com/watch?v=49g5RBSqMkE - ATS Breathe Easy - The Human Cost of the NIH Cuts: https://www.youtube.com/watch?v=9dIlg_L7qqI 

Happy Black History Month! We're kicking off the month with a story that was suggested by Janice on Instagram. Nowadays, when you call for emergency services, you expect the speedy arrival of an ambulance staffed by personnel who have the skills to save your life en route if necessary. But, believe it or not, that's actually a new concept. Before the 1960s, your call would have been answered (quite slowly) by a police paddy wagon or even a hearse and there would be virtually no pre-hospital care other than basic first aid. It took until 1967 for folks in Pittsburgh, Pennsylvania to realize that there had to be better way and the Freedom House Ambulance Service was born. If you've never heard of it, there's a reason for that. The Freedom House Ambulance Service was staffed by all Black paramedics, taken off the streets of Pittsburgh's impoverished Hill District. They were trained up and put to work and they absolutely killed it, revolutionizing emergency medical services country-wide. But history has a way of erasing these types of stories. So, let's fix that! Support the show! Join the Patreon (patreon.com/historyfixpodcast)Buy some merchBuy Me a CoffeeVenmo @Shea-LaFountaineSources: EMS1 "How Pittsburgh's 'Freedom House' Shaped Modern EMS Systems"University of Pittsburgh "Freedom House Ambulance Service of Pittsburgh - Making Medical History"University of California San Francisco "America's First Paramedics Were Black. Their Achievements Were Overlooked for DecadesWikipedia "Freedom House Ambulance Service"Shoot me a message! Support the show

Clinical trial results unveiled today at ACTRIMS Forum 2026 suggest that fenebrutinib may be a novel and effective treatment option for people living with primary progressive multiple sclerosis.  In this exclusive episode providing the first expert discussion of the complete dataset, FENtrepid trial leads Prof. Amit Bar-Or (University of Pennsylvania) and Dr. Stephen Hauser (University of California San Francisco) break down what the fenebrutinib results really show. Together, they explore: Why BTK inhibition is uniquely positioned to address progressive MS biology How fenebrutinib compared to ocrelizumab in the Phase 3 FENtrepid PPMS trial What the data suggest for patients with non-relapsing, chronic disease Listen for a deep dive into the science and the clinical implications. Editorial Note: At 21:49, the discussion refers to Müller cells. The correct term is Kupffer cells. 

Patients with Parkinson disease and other movement disorders have significant palliative care needs that are poorly met under traditional models of care. Clinical trials demonstrate that specialist palliative care can improve many patient and family outcomes. In this episode, Aaron Berkowitz, MD, PhD, FAAN, speaks with Benzi M. Kluger, MD, MS, FAAN, author of the article "Neuropalliative Care in Movement Disorders" in the Continuum® December 2025 Neuropalliative Care issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology at the University of California San Francisco in the Department of Neurology in San Francisco, California. Dr. Kluger is the Julius, Helen, and Robert Fine Distinguished Professor of Neurology in the Departments of Neurology and Medicine (Palliative Care) at the University of Rochester in Rochester, New York. Additional Resources Read the article: Neuropalliative Care in Movement Disorders Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Guest: @BenziKluger Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Benzi Kluger about his article on neuropalliative care in Parkinson disease and related movement disorders, which is found in the December 2025 Continuum issue on neuropalliative care. Welcome to the podcast, Dr Kluger, and could you please introduce yourself to our audience? Dr Kluger: I'm Benzi Kluger. I'm a professor of neurology and palliative medicine at the University of Rochester. I'm the chief of our neuropalliative care service, I'm the director of our Palliative Care Research Center, and I'm also the founding president of the International Neuropalliative Care Society. Dr Berkowitz: Wow, that is a large number of hats that you wear in a very important area of palliative care. So, your article is a fantastic article that covers a lot of concepts in palliative care that I myself was not familiar with and really applies them in a very nuanced way to patients with Parkinson's disease and related disorders. So, I'm looking forward to learning from you today to discuss some of the concepts you talk about in the article and how you apply them in your daily practice of palliative care in this particular patient population. So, one of the key points in your article is that we're often so focused on treating the motor symptoms of Parkinson's disease and other degenerative movement disorders that we are often at risk of underdiagnosing and undertreating the nonmotor symptoms, which in some cases, as you mentioned in the article, are more disabling to the patient than the motor symptoms that we tend to focus on. So, from a palliative care perspective, what are some of the nonmotor symptoms that you find tend to be underdiagnosed and undertreated in this patient population? Dr Kluger: The literature suggests---and we've replicated it, actually, Lisa Schulman published a paper twenty-five years ago and the data is almost exactly the same when it comes to things like depression, pain, fatigue, constipation, sleep---that you miss it about 50% of the time. And there's a number of reasons for that. One is that these are subjects that people don't always like to talk about. People don't like talking about depression. People don't like talking about poop and constipation. And I think there are things that neither the patient or the caregiver nor the physician are necessarily comfortable with. And they're also sometimes confusing of, which doctor should I talk to this about? Should I talk to my primary care doctor, should I talk to my neurologist? And so I think the key here is really having a checklist and being proactive about it. In the article, I suggest a template or previsit questionnaire that you can use, but I think it's just about being automatic about it. And it just takes the burden off of the patient and the family to bring them up and letting them know that this is a safe space and this is the right space to talk about these symptoms. Dr Berkowitz: That's very helpful to know. So, having some type of checklist or template just so we go all through them and, as you said, it sort of destigmatizes, just, this is the list of things, and I'm going to just ask about all of them. So we check in on those particular symptoms, whether they're present or not. Are there any particular symptoms that jump out to you as ones that tend to be missed---either because we don't ask about them or patients are less comfortable mentioning them---that in your practice, when you've elicited them, have allowed for particular intervention that's really improved the quality of life for patients in this group? Dr Kluger: Yeah, I'll mention a few that I think come up and are very pertinent. One is mood. And, to use depression---but we could also use anxiety as an example---again, these are topics that people don't always want to talk about. And I think it's important---we may get to this a little bit more later---is being careful to distinguish between depression and grief, sadness, normal worry, frustration. A lot of times the way I'll ask that when I'm talking to a patient is, you know, I hear you're using the word depressed. I want to make sure. does this feel to you like normal sadness given that you have an illness that sucks, or does this really feel like it's above and beyond that and you feel like you'd need a little extra help to get your emotions under control? The second one, which is kind of related, is other behavioral symptoms, including PD psychosis and hallucinations. And there, I think, the thing is that people are quite frankly afraid that they're losing their mind or going insane. So, I think that's another critical one. And then one that, you know, it's kind of a low-hanging fruit but people don't want to talk about, is constipation. And when we did our large randomized control trial of palliative care, our single biggest effect size was actually that we did a better job of treating constipation than usual care. And I think the only trick there is that we asked about it. Dr Berkowitz: I see. So, do you then as part of your routine practice and seeing these patients with Parkinson's disease in particular, you have a particular checklist you go through during the appointment or, as you mentioned, you- one could do it before the appointment. But you tend to go through this in the visit, and is there any palliative care wisdom you have for us, those who are not trained in palliative care, to making sure we really elicit these symptoms in an effective way and how much they're bothering the patient? Dr Kluger: Two things that I've seen work---and we've done a lot of implementation studies. One is that, if it works for your practice, having patients fill out a questionnaire or survey in advance. And I think one of the highest-yield things there too is for blank lines to allow patients to write in what their top three problems are. And I've found when we've used it, and I think other people have found, that it's a huge time saver. People hand them the form, they look to see what's at checked a yes or what's checked as high, and then that becomes the agenda for the visit. The other thing that I think works equally well is just having a template, and at this point its just kind of, like, hard-wired into my neurons that, you know, no matter what we talked about in the HPI, I'll always ask about sleep and mood and bowel and bladder and pain to make sure that I don't miss those things. Dr Berkowitz: You mentioned in your article that palliative care needs in patients with Parkinson's disease really differ over the course of the illness and may be different at the time the initial diagnosis is given versus as the disease progresses versus the latest, most advanced stages of the disease. Can you talk a little bit more about how your approach to these patients changes over time from a palliative care perspective? Dr Kluger: Yes. And I'll also add, I think some of this is going to be more relevant to our listeners than to me. I'm now almost entirely in a neuropalliative care clinic, but for early-stage illness, it's really primary palliative care. And just to reinforce, this is palliative care that's provided by neurologists and primary care doctors, not specialist palliative care. I think that mindset's particularly important around the time of diagnosis. One of the things that, for me, was most eye-opening when we were doing qualitative interviews and studies was how devastating the diagnosis of Parkinson's disease was for patients and their families. And that was not something that I really anticipated. I think, like a lot of people and a lot of movement disorder doctors, I kind of thought of Parkinson's disease as a relatively good-news diagnosis. And that was often the way I pitched it, and we talked about Sinemet and DBS and exercise and all these things, but I have a relativity bias. And that bias is, I know that Parkinson's is better than PSP or MSA or brain cancer. But for the individual getting that diagnosis, that's it's not good news because their relativity bias is, I didn't have Parkinson's before and now I do. And for the rest of my life I'm going to have Parkinson's. And for the rest of my life, there may be things that I can do today that I won't be able to do tomorrow or next week. And so that was… yeah. And I think it really changed my practice and was pretty eye-opening for me. In the article, I mentioned the SPIKES (S-P-I-K-E-S) protocol for talking about serious conversations or talking about bad news. But I think one of the keys there for the time of diagnosis is asking people about their perceptions of Parkinson's. And part of that's also asking them what they know and what they're worried about. And you may be surprised that when you ask somebody about Parkinson's, you know, sometimes they may say it was good news. It's been three years, I've been trying to find an answer, and I feel like I've been being blown off. And sometimes you might say, this is the thing I feared the most. My uncle died of Parkinson's in a nursing home. And I also find that more often than not, even in end-of-life, that a lot of times the serious illness conversations I have, the facts that I have to present people, are better than their fears. And that's true at the time of diagnosis. But I think if we don't go into it and we don't ask people what they're feeling and what their perceptions are, then we miss this opportunity to support them. So that's the early stage. And in midstage, I think the, you know, the real keys there are to catch nonmotor symptoms early, to catch things like pain and depression and constipation before they become really bad or even lead to a hospital stay. And also starting to plant the seed and maybe doing some advanced care planning so that we are- people feel more prepared for the end stages of Parkinson's. And I think there, too, people ask about the future; when we tell them everyone's different or you don't have to worry about that now, that doesn't help an individual very much. So, oftentimes in the middle stages of the illness, people do want to know, am I going to go to a nursing home? How much longer is this going to be? You don't need a crystal ball, but if you can give people the best case, the worst case, the most likely case, that can be very helpful for life planning. And then as we're getting to more advanced and endstage, the lens that I'm looking at people with really is, should we begin talking about hospice? And we know again, from data that as a system---not just neurologists, but as a system---we're missing this all the time. And that if you have Parkinson's disease, you're about 50% chance of dying in a hospital, which is not where people want to die. And so, when I see people with more advanced disease, I'm asking questions about weight loss, and are they sleeping more during the day, and is there an acceleration in their decline of function? So, not just asking about where they are, but what's the rate of decline so that I can give people months of hospice as opposed to either them dying in a hospital or just scrambling for hospice in the last few days of their life. Dr Berkowitz: Another important palliative care concept you discussed in this article that was new to me is the concept of total pain, where you talk about aspects of pain beyond the physical and emotional pain we often think of when we hear the word pain. Can you talk a little bit about this concept of total pain, and then in particular how you apply it specifically when caring for patients with Parkinson's disease and related disorders? Dr Kluger: Yeah, absolutely. In the article there's a figure, and this is a- one of the foundational concepts of palliative care is this idea of total pain. Which is that the pain of a serious illness, whether that be cancer or Parkinson's, is not simply physical. There's also emotional components. And that also goes beyond the psychiatric. So, that includes grief and worry and frustration, and it also includes loneliness. And I think with Parkinson's disease, actually, one of one of the quotes that really sticks with me from some of our qualitative interviews was a woman who talked about her Parkinson's as a "flamboyant illness" because her tremor and her dyskinesias were always coming out at inopportune times. And it wasn't something I thought about, but there's this cosmetic aspect of having a movement disorder. There's also a cosmetic aspect of drooling or of using a walker. And so, there is a social stigma associated with Parkinson's, and people also lose a lot of social capital. Part of that is that often times neighbors and friends and family don't feel comfortable being around that person anymore. They don't know what to say. And so, sometimes coaching or connecting them with a chaplain or a counselor can be helpful in maintaining those social networks. There's a social pain. There's a spiritual and existential pain. And when I ask people a question, I ask almost everybody, is, what's the toughest part of this for you? A lot of times things fall into that bucket. And it's my loss of independence. I'm no longer able to do the things that bring me joy. I feel guilty that I'm going to be a burden to my family. My relationships are changing. So those are things that are essentially spiritual and existential. And then the last bucket, there are logistical things. And this can be lost driving and how do I get around, the cost of doctor visits, spending time with doctors, co-pays for medications; in the case of Parkinson's disease, the logistics of taking medication every two to three hours. So those all contribute to the total pain or the multiple dimensions of suffering. And that is something that I think about---in fact, in our assessment and plan, one of the things I like to mark out is sources of suffering. And that could be from any of those parts of the pie chart. Dr Berkowitz: And how do you approach this at the bedside? So, there are different concepts here. Obviously, physical pain, everyone is familiar with probably the concept of emotional pain. But as you get out in these concentric circles into sort of spiritual, existential pain, how do you sort of start these discussions with patients to elicit some of these aspects of their suffering? Dr Kluger: You know, the most common question I ask is, what's the toughest part of this for you? And very often that's going to lead into these existential and spiritual issues. I'll also ask people at the start of visits is, just tell me overall, big picture, how's your quality of life? Sometimes the answer is pretty good. Sometimes it sucks. Sometimes it's I have none. I know we're going to talk a little bit about joy later. But I'll also often times follow that up with, what do you enjoy or look forward to? And sometimes I get a response to that, and sometimes I get there's nothing in my life right now. But foundationally, I feel like those are all, you know, definitely spiritual and existential issues. And I'll ask people, too, where do you find meaning? What are your sources of support? I know for different physicians, people have different comfort with this, but I do find it helpful also to ask people, are you spiritual or religious? Because that can sometimes open up a window to other means of coping. An example of that---I mean, not everybody is going to have access to a chaplain. Some people will. But oftentimes one of the things that I do is encourage people to reconnect with their spiritual community. And so, I've had some very heartwarming winds where somebody would say, you know what, I haven't been to church for a while. And people at churches or synagogues or mosques are often looking for opportunities to help. And so that I think is another, I think, really important message. But I think one of the- my favorite parts of my job is kind of opening up these bridges and opening up these connections. And helping people to recognize, I would kind of put it under a larger practice of grace, is that asking for help can be a gift to another person. And if you're strong enough to ask for help, you're giving, you know, sometimes a really tremendous gift to another individual. If somebody has a strong community that they're connected with, doesn't have to be religious. it could be that they were a high school sports coach, it could be that they were involved in a book club, it could be that they were DJ or ran a restaurant or who knows what. Those all can provide opportunities for bringing people together and bringing together community. And again, thinking about the total pain of having a neurologic illness like Parkinson's, that loss of community, that loss of connection, is one of the things that's most painful. Dr Berkowitz: So, when people think about palliative care, they tend to think about pain and suffering and a lot of the topics we've been talking about. But you also talk about joy in your article, and you alluded to it a moment ago, working with your patients to find what brings them joy, opportunities for joy. As I was reading this, I was trying to imagine sitting across from a patient who has maybe just received the diagnosis of Parkinson's or is in a stage of the disease where, as you mentioned, they might be quite depressed, whether that's capital-D depression or sadness related to their loss of independence and other aspect. Sitting across from a patient who is suffering so much and has come maybe to a palliative care doctor such as yourself to alleviate suffering and have pain and other symptoms addressed, how do you begin a conversation about joy in that context and have the patient feel comfortable to open up? And how do you then use that conversation to help them improve their quality of life? Dr Kluger: Yeah, that's a great question. And it's one that actually comes up every time I talk about joy because it can be daunting. And there certainly are situations where I don't bring it up. You know, if we are deep into a session about grief or we're talking about kind of an unexpected bad turn of events, there's times where it would be insensitive to try to push, you know, an agenda of joy or something like that. And yet I would say that particularly residents and students who work with me, you know, may be surprised at how often I do bring it up. And I would say it's probably 95% of the time or more where I am able to talk about joy. And as an example, you know, we might be talking about grief and loss and changes in independence. And then I would say, you know, I want to make sure that we have time to talk about this, and we'll connect you to our chaplain or counselors so that you can talk about and process your grief. And at the same time, I want to make sure that we don't lose sight that there are still opportunities for joy and love and meaning in your life. And I want to make sure that we make space and time to talk about those things too. So, it's creating that balance. That's a transition that, even when you're on a very heavy subject---in fact, I would say maybe even particularly when you're getting into a heavy subject---that you can talk about joy and love and meaning. I gave a talk at the American Academy of Neurology a few years ago where I referred to them as weapons that you can use against some curable illnesses. One example is, my approach to chronic pain often centers around joy. So, I'll have somebody who comes in with back pain. My goal with that person is not for them to take Percocet four times a day to eliminate their back pain. When I talk to that person, I may find out that their grandson's soccer games and boxing class are the two most important things in their life. So maybe we take Percocet three or four times a week a half-hour before those activities so that you can get that joy back in your life. And so, we kind of use joy as a way and as a goal to reclaim those parts of your life that are most important to you. So, that's a pretty concrete example. Even for people nearing end of life, it could be giving people permission to eat more of their favorite food, often times ice creams, milkshakes---which is great, because we want people to gain weight at that point. Getting out into nature, even if they can't hike or do things the way they used to, that they might be able to go out with their family. Having simple touch, spending time together, really trying to prioritize what's most important. In the article, we talk about the total joy of life or the total enjoyment of living. But I like to be systematic about thinking about opportunities for living and make sure that we're just as systematic about thinking about what are the opportunities for joy as we are about thinking about the sources of suffering. Dr Berkowitz: I'm sure I only sort of scratched the surface of palliative care in general, let alone specifically related to Parkinson's disease and other related disorders. For our listeners who may be interested in learning more about neuropalliative care specifically or getting a little more training in this, any recommendations? Dr Kluger: Yeah, absolutely. Thanks for asking me that. There is a growing community of people interested in neuropalliative care, and so I would really encourage people who are passionate about this and want to get connected to this community to consider joining the International Neuropalliative Care Society. We're a young and growing community. I think you'll find a lot of like-minded individuals. And whether you're thinking about going into neuropalliative care as a specialty or doing a fellowship or just making it more a part of your practice, you'll find a lot of like-minded individuals. And then at the end of the article, there are some websites, but there are opportunities: for example, Vital Talk, the education palliative and end-of-life care neurology curriculum out of Northwestern, where people can dig deeper and kind of do their own mini-fellowship to try to bolster these skills. Dr Berkowitz: Gives, certainly, me a lot to think about. I'm sure it gives our listeners a lot to think about as well in implementing some of the palliative care concepts you tell us about today and discuss in much more detail in your article as we see these patients and, hopefully, can refer them to talented expert colleagues like yourself in palliative care, but don't always have that opportunity. And as you said, there's always opportunities to be practicing palliative care, even though we're not palliative care specialists. So, I encourage all the listeners to read your article, which goes through these concepts and many more as well some sort of key points and strategies for implementing them as you gave us many examples today. So again, today I've been interviewing Dr Benzi Kluger about his article on neuropalliative care in Parkinson disease and related movement disorders, which is found in the December 2025 Continuum issue on neuropalliative care. Be sure to check out Continuum Audio episodes from this and other issues, and thank you again to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Dementia is often a highly burdensome disease process for patients, their caregivers and families, and the community at large. Palliating symptoms and providing guidance surrounding advance care planning and prognostication are integral components of the management plan. In this episode, Katie Grouse, MD, FAAN, speaks with Neal Weisbrod, MD, an author of the article "Neuropalliative Care in Dementia" in the Continuum® December 2025 Neuropalliative Care issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California San Francisco in San Francisco, California. Dr. Weisbrod is a neurologist at Hartford Healthcare with the Ayer Neuroscience Institute in Mystic, Conneticut. Additional Resources Read the article: Neuropalliative Care in Dementia Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Neal Weisbrod about his article on neuropalliative care in dementia, which appears in the December 2025 Continuum issue on neuropalliative care. Welcome to the podcast, and please introduce yourself to our audience.  Dr Weisbrod: Thank you. I'm really excited to be here. I'm Neal Weisbrod. I'm a neurologist and palliative care physician currently working at Hartford Healthcare in Mystic, Connecticut. Dr Grouse: To start, I'd like to ask why you think it's important that neurologists read your article? Dr Weisbrod: The primary reason I think it's really important to read the article is because these are just really common problems that neurologists run into in clinical practice. So, Alzheimer disease and many other dementias are extremely common, and managing the burdensome symptoms and the complex discussions that we have to have with the patients and their families as they go through the course of dementia is something that is very common in clinical practice. And so my hope is that by reading this article, clinicians will pick up a few tools, a few new ideas for how to make these conversations easier and for how to help these patients get through the disease with a little bit less suffering. Dr Grouse: I learned a lot from reading your article, and I really encourage our listeners to check it out. But I was curious what you feel that you discussing your article would come as the biggest surprise to our listeners? Dr Weisbrod: So, I think that the most surprising thing a lot of people will see reading this article is the section on prognosis. A lot of times it seems families are counseled, when they're talking about the prognosis of Alzheimer disease, that it could be ten years or longer. But really, the data show that for many patients, the median prognosis is closer to three to eight years. And that is a little bit longer for Alzheimer disease than many other types of dementia, but also gets significantly shorter as patients get older. So, we're looking at a closer to three-year median prognosis for patients who are over eighty-five, whereas patients in their sixties are probably closer to the eight or nine-year median prognosis. And so I think that piece will hopefully help people give a little bit more accurate counseling about prognosis.  Dr Grouse: I'm glad you brought that up because I was wondering, why is it so important that we are careful to make sure that we're giving prognostic information for our patients and maybe even updating it as their clinical status changes? Dr Weisbrod: I think first of all, it's a really common thing that patients and families are thinking about and worried about. They don't necessarily always seem to ask as much as they want to know. I think there's a lot of fear around that conversation, even though it's really important. And then there's also often tension between the family and caregivers tend to want to know more than patients do. I think that it really helps people plan for the future as well as possible to know what their future might be. And we have a lot of limitations in predicting the future, but using the best information we can, laying out what we think the likely range is, allows people to make a lot more clear plans for their future. Dr Grouse: I'd imagine it's also pretty helpful for hospice referrals, too, having that data.  Dr Weisbrod: Yeah, definitely. And there's a lot of angst about when to refer patients who have dementia to hospice. The most important thing I think about when I'm making a hospice referral is that I don't have to be right. And I think it takes a lot of that concern off to just say, all I'm doing is making a connection, getting someone who's potentially interested in the hospice, who has a really advanced serious illness connected to a hospice agency. And then they can go through the full evaluation with the hospice and the hospice medical director and determine whether they're eligible. So, I think there are really helpful thresholds to think about that would be a good trigger. Like a patient who we think has advanced dementia, who has a hospitalization for pneumonia or a fracture of the hip or some other really serious acute medical condition, I think is a really good trigger to start to think about hospice. But most importantly, it's just the connection, and I tell the patients that upfront. I tell them that you're going to have a conversation and we'll decide whether you're a good fit, and if not, the hospice will usually just check in with you over time and decide when is the right time in the future. Dr Grouse: That's really helpful. And I think just a really great reminder to our listeners about thinking about hospice sooner or at certain critical points in their patient care rather than waiting, maybe, before it's gone on too long and may be of less use later on. I was wondering, in your own clinical practice, what do you think is the most challenging aspect of providing care to patients with dementia?  Dr Weisbrod: I think this one's easy. I would say managing the time has to be the most difficult part. I think that taking care of patients who have dementia is time-consuming. There's a lot of different priorities that we have to manage the time around. How much time are we going to spend doing cognitive testing? How much time are we going to spend doing counseling? How much time are we going to spend making up a treatment plan and discussing medications? How much time are we going to spend on advanced care planning? And the way I try to combat that is really just trying to think about what I'm going to prioritize in a certain visit and not try to accomplish everything. I'll tell patients and their families, the next time you come in, we're going to have a conversation focusing on advanced care planning. Or, the next time you come in, we're going to sit down and try to talk through all the questions you have about what the future might hold. That way I in that visit, I don't feel like, oh, I have to do updated cognitive testing and I have to review all the next steps in medication, and that allows me to take it in more bite-sized chunks. Dr Grouse: You made some of the great points, and specifically you mentioned advanced care planning. Your article makes a really strong case for the importance of advanced care planning, yet you definitely acknowledge the many barriers to initiating discussions that clinicians face. In your patients with dementia, can you walk us through how you integrate discussions about advanced care planning with your patients and their families?  Dr Weisbrod: Yeah, I think this is still something that is evolving in my practice, and I don't think there's any perfect way of doing it. I think there's a lot of right ways of doing it, and as long as we're thinking about it a lot and bringing it up periodically, that's probably the best. What I try to do, though, is after I discuss what I think is the most likely diagnosis with patients and their families, I try to have a fairly close follow-up visit after that. Allow them to digest that information, to often do a little bit of their own research, to talk about it as a family. And then when they come in for that next appointment, I try to at least lay some groundwork about advanced care planning, asking them what they've completed already, and then based on what they've already done to that point, talking to them about what I think the next step would be. If they have done nothing, usually it's just, hey, I really think you should start to think about who would be making decisions for you if you lose the ability to make your own decisions and counsel them about power of attorney paperwork and establishing a healthcare surrogate. When it's patients who have already done some of that initial prep, I think that it's really important to keep in mind it's a longitudinal discussion and you can take it in small pieces over time. Often that helps because you can really establish that rapport and that trust. And then I like to just keep checking in whenever there's major changes in the patient's health or condition, like admission to the hospital or transfer to an assisted living facility or memory care clinic. Those are good times to remember, hey, I really need to revisit this conversation.  Dr Grouse: It's probably good to also mention another really important point from your article, which was that impairment of decision-making in patients with dementia can actually start significantly even in the phase of mild cognitive impairment. Yet these patients will need to make many medical decisions with their neurologist as they go through this journey. How can we make sure our patients have capacity and make decisions appropriately regarding their care? Dr Weisbrod: Yeah, I think that's a definite challenge of taking care of patients with cognitive disorders of any type, including those with stroke and multiple sclerosis, that have some cognitive impairment. In my opinion, the most important way to help manage that is to make sure when we are making important decisions about the future that we're having a deep exploration of the values and the reasoning behind that. And definitely teach back is the most helpful way that I use to explore those values and the logic behind patients' decisions. So, I think we have to have a really low threshold to move on to a formal evaluation of capacity; if there's any inconsistency between what the patient's saying now and what their families say they've said in the past, or if they're having struggled to come up with a really clear logic behind their decision, then I think we have to have a low threshold to move on to a formal evaluation of capacity. So, I think having the family involved, having other people who know the patient really well, usually helps identify some of those periods where it seems like the patient's not making the decision that really reflects their true wishes. Dr Grouse: Now I wanted to switch gears a little bit and get into the management of neuropsychiatric symptoms, which you spend a lot of time on and I think a lot of neurologists find very challenging. What are some nonpharmacologic approaches that can help patients with significant neuropsychiatric symptoms?  Dr Weisbrod: I really like the DICE paradigm for coming up with nonpharmacologic approaches. The DICE paradigm is an acronym. The D is Describe, I is Investigate, C is Create, and E is Evaluate. The idea is that we're exploring what's happening behind the symptoms, we're creating a plan to intervene, and then we're evaluating the outcome of that plan and creating a sort of feedback loop there. But ultimately, I think, when we're creating a solution, thinking about how we can change the environment is the most important thing. We have very limited ability to change the way that someone who has severe cognitive dysfunction reacts to their environment, but we can often change the environment to not produce that reaction in the first place. One example is with wandering behaviors. Trying to change the environment where you put locks that don't have deadbolts that you can use on the inside of the house, you have to have a key on the inside of the house, and then the family can put that key somewhere safe where the patient is not likely to find it and be able to unlock the door and wander out unsafely. I also think it's really important to acknowledge that as doctors, we are maybe not the best people to always have the answer when it comes to changing a patient's environment. And so, I think we really need to rely on the wisdom of support groups and other people who are going through the challenge of dementia. Our interdisciplinary care teams like social workers and nurses who have experience in managing dementia, and really try to plug the caregivers into as many of these avenues as possible so that they can learn from all of that community of wealth and not always rely on the doctor to have the answer. Dr Grouse: Switching gears to pharmacologic management, which is a lot of what we do for patients as neurologists. Thinking about agitation, pharmacologic management of agitation can be very challenging. And reading your article, it reminds me how disheartening it is to reflect and how modest the effect of the available options are, along with the many potential risks of their use, When nonpharmacologic interventions fail, what should neurologists recommend for their patients with agitation? Dr Weisbrod: Yeah, I definitely agree. It's every time I go back and look at this literature and look at what's new, it is a bit disheartening. But even in the face of all that, I really feel like SSRIs are my first-line therapy for most of these patients. I always try to ask myself what might be causing the patient discomfort that they are then manifesting as agitation because they don't have a better way of expressing themselves. Often, I feel like that's anxiety or depression or some other psychological symptom that we might be able to address with an SSRI. So, I tend to use sertraline and escitalopram, start those early and as long as patients are tolerating it, give it a really good trial. Outside of that, escalating to other pharmacologic approaches, even though there's such controversy in the data about antipsychotics and even though there are very real risks, sometimes I think we essentially do need a chemical sedative. And I think that it's important to have a very frank conversation upfront with the caregivers and the medical decision maker for that patient. Make sure we are counseling them on the risk, the increased risk of mortality, and also to make it a time-limited trial. So, I think that saying we're going to try this medication (if the patient's decision maker agrees, obviously) for a month or two months or three months. But I definitely wouldn't want them to just have an open-ended plan where they're going to stay on it indefinitely. It should have some end point where we say, hey, is this working or not? And if it's working, then we'd make a decision, is the improvement in quality of life worth the risks? And if we're not seeing that improvement, then we definitely need to stop it. Dr Grouse: That seems very reasonable. And then thinking more towards some of the other types of symptoms that can be really challenging, I was really surprised to see how often uncontrolled pain is a significant contributor in patients with dementia. And certainly, both uncontrolled pain and poor sleep can worsen cognitive function and neuropsychiatric symptoms in general. But of course, there's ongoing concerns about side effects of these therapies and how they can also potentially worsen things. How should we be approaching management of pain and insomnia or poor sleep in these patients?  Dr Weisbrod: I think the key is just to start with really low burden treatments and escalate carefully and start with low doses of higher risk medications. So, when I think the low burden treatments for pain, scheduling acetaminophen, 1000 milligrams every eight hours, seems like a trivial thing to do, maybe? But it's actually surprising how much scheduled acetaminophen can take the edge off of pain and might be able to avoid some of these flare-ups of neuropsychiatric symptoms, may be able to really improve that pain a little bit. I do think it really has to be scheduled, though. Trying to rely on patients who have significant cognitive dysfunction to use a PRN medication is going to lead to a lot of problems and undertreatment. And then on the sleep disorder side, I think starting with low-dose Trazodone and gradually increasing the dose of Trazodone as a really safe way of initially approaching the insomnia. And then only when it's a more refractory case do I reach for the high-risk medications. Like for pain, we're talking about opiates. I think there's a lot of very reasonable concern about using opioids in patients who have cognitive dysfunction. But if there is a really good reason to think that they have severe pain, like they have a past pain disorder, I think that just like with antipsychotics, there are definitely real risks to these medications. But at the end of the day, if we are improving someone's quality of life dramatically and the patient's medical decision maker is willing to take on those risks, then we're really doing the patients a favor. Dr Grouse: Now, another issue that you mentioned in your article, which I see a lot and often struggle with myself, is how and when to deprescribe certain types of medications such as cholinesterase inhibitors and memantine. Any tips or tricks to how to approach this?  Dr Weisbrod: My approach to this has also evolved a bit over the years. The new data that cholinesterase inhibitors may have a mortality benefit in patients with Alzheimer disease has changed my thinking a little bit. But there are still lots of situations where it's just too burdensome or patients seem to be having side effects. And so, I think about deprescribing. The most important thing in my mind is really thorough counseling before deprescribing with the patient's family and medical decision maker. I think that letting them know that we might actually be holding things more stable with the medication than we realize, there could be a flare-up, that we can resume the medication if that flare-up happens but we don't always guarantee getting back to the same point. I think having that conversation ahead of time will ward off some of the worst issues that you have afterwards. And then I think doing a taper of cholinesterase inhibitors over two weeks to a month is probably the most prudent because of some of the data about withdrawal and exacerbation of neuropsychiatric symptoms or cognitive worsening. Memantine, I think the data is a lot more shaky on withdrawal. And so, I think it's less important to gradually taper memantine. But I think that once again, just having the conversation upfront and letting the family know these are the things we have to look out for and these are the risks is going to be the most important. Dr Grouse: That's really helpful and a great strategy to take advantage of. Another, I think, really difficult topic that I wanted to ask you about was the discussion around nutrition and whether or not to consider putting in some type of a permanent tube for tube feeds. How do you approach that conversation? Certainly a difficult one.  Dr Weisbrod: Yeah, I think it's easily one of the most difficult conversations to have in the care of patients who have dementia. And there's so much emotion in the families when they're having this discussion. And I think really acknowledging there's a huge emotional piece of the conversation is one key piece. For families and caregivers, they're thinking, I don't want my loved one to starve to death. That's usually the most important thing in their mind. We have to address that concern in the conversation, or they're never going to get to a point of satisfaction with the decision that's being made. So, I think while there is still some controversy in the literature about artificial nutrition for patients who have dementia, the bulk of data indicates that it is not helpful for patients. It may exacerbate dementia, it leads to more restraint. And so, I think unless there's some reversible medical condition that we're just trying to do artificial nutrition to get them through, like, they have a stroke and we're expecting that their dysphasia is going to improve because of the stroke is going to heal. Those situations might be a good reason, but if we really think that the driving factor behind their dysphasia is their dementia, I think we should be guiding the families away from that. And I think that explaining that as dementia gets really advanced, the body is slowly shutting down. The body is not needing as much nutrition, and forcing more nutrition in has not been shown to help people who have dementia. Really putting it in that sort of language is going to help the families understand and be comfortable with that decision. I also think that it's really helpful to consider talking to families about what they can do and not have the entire conversation be about what we're not doing or not putting in a feeding tube for artificial nutrition. So, I think really good counseling about, we can do comfort feeding, we can expand what food we're giving the person who has dementia and really focus on foods that they really enjoy and not worry so much about the health and nutrition anymore. I think that focus on what they can take control of can also help make the decision easier for families.  Dr Grouse: I really like that approach. And I agree, it does seem that it being such an emotional decision with just so much a concern about this underlying feeling of not caring for their family member. I think that is a really great way to look at it  and to kind of start off that conversation. Now, I'd love to hear more about what drew you to this field when you first got into your career as a neurologist. Dr Weisbrod: I had an interesting journey to doing neuropalliative care. Definitely didn't know that's what I was going to do when I started neurology residency. At University of Rochester, we had amazing palliative care physicians that were involved in medical school, and so I got a little bit of exposure to it early on. Then when I was in neurology residency, I first of all realized that I really enjoyed making sure that what we were doing respected a patient's wishes. And so, as other people seemed to run away from those conversations, I was really drawn to them. And so that definitely made me realize that that might be more of the right field for me. But also, as I went through neurology residency, I really discovered that I love so many different things in neurology, and that made me not want to subspecialize and focus on a narrower set of conditions in neurology. So, doing palliative care fellowship was a really good way of getting a specialist tool set and expanding my knowledge in one area, but staying a neurologist, generalist. And I think it also really enhances a lot of the other things I do in neurology. It gives me a lot of additional skills on how to counsel patients and how to prepare for the future in general. I think there's a lot about just good bedside manner in palliative care education. I feel like it helped me become a better neurologist, and I decided that I really loved the palliative care piece as well.  Dr Grouse: Well, we're certainly all grateful that you found this aspect of your career and have been able to share the skills you've honed with us as well. And we really appreciate you taking the time to talk with us about your excellent article today, which I encourage everybody to read.  Dr Weisbrod: Yeah, thank you. It's been wonderful to be on, and I hope that people can take away a few small points from the article. Dr Grouse: Again, today I've been interviewing Dr Neal Weisbrod about his article on neuropalliative care in dementia, which appears in the December 2025 Continuum issue on neuropalliative care. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

From March 6, 2024: Executive branch constraints and the posture of the media have shifted in significant ways over the past two decades. Lyrissa Lidsky and Christina Koningisor, law professors at the University of Florida and the University of California San Francisco, respectively, argue in a forthcoming law review article that these changes—including the erosion of certain post-Watergate reforms and the decline of local news—have created a First Amendment disequilibrium. They contend that the twin assumptions of the press's power to extract information and check government authority on the one hand, and the limitations on executive branch power on the other, that undergird First Amendment jurisprudence no longer hold, leaving the press at a significant First Amendment disadvantage. Lawfare Research Fellow Matt Gluck spoke with Lidsky and Koningisor about the current state of First Amendment jurisprudence, the ways in which the press used to be stronger, executive branch power on the federal and state levels, how the authors think our current First Amendment architecture should change, and more.To receive ad-free podcasts, become a Lawfare Material Supporter at www.patreon.com/lawfare. You can also support Lawfare by making a one-time donation at https://givebutter.com/lawfare-institute.Support this show http://supporter.acast.com/lawfare. Hosted on Acast. See acast.com/privacy for more information.

Medication mismanagement is one of the most costly and preventable problems in healthcare as it impacts patient safety, outcomes, and billions in annual spending. In this episode, we're joined by Yoona Kim, who cofounded Arine to use AI-driven medication intelligence for improving patient outcomes. Join us in a conversation about the key factors that contribute to medication errors, why culturally sensitive care is central to Arine's approach, and how smarter use of data can shape future healthcare policy.Yoona Kim is the co-founder and CEO of the healthcare technology company Arine. After studying human biology at Stanford, she was trained as both a pharmacist (PharmD from the University of California San Francisco) and health economist (PhD from the University of Texas at Austin). She previously served as Vice President at Proteus Digital Health and held leadership positions in research and consulting at global pharmaceutical companies.

The National Institutes of Health have historically funded scientists to find cures for diseases and protect public health. NIH funding has led to the discovery of immune therapies for cancer, antiviral treatments and prevention of HIV, and ground-breaking research into memory loss and Alzheimer's disease. After a year of funding cuts and freezes that have rocked the medical research field to its core, we catch up with leading researchers at the University of California to talk about the impact this has had on their work and our ability to fight humanity's most puzzling illnesses. Guests: Monica Gandhi, infectious disease expert and professor of medicine at University of California San Francisco - she is the director of the UCSF Gladstone Center for AIDS Research and the medical director of the San Francisco General Hospital HIV Clinic, Ward 86 Pamela Munster, professor of medicine at the University of California San Francisco; co-director, Center for BRCA Research, Medical Oncology; distinguished professor in Hereditary Cancer Research Megan Molteni, science writer, STAT News Joel Spencer, associate professor of Bioengineering, University of California Merced - his lab uses funding from NIH to study the thymus, with implications for cancer treatment and healthy aging Learn more about your ad choices. Visit megaphone.fm/adchoices

In this episode of Health Gig, Doro and Tricia welcome Dr. Tracey Woodruff, the director of the Reproductive Health and the Environment program at the University of California-San Francisco. From her background in public health and work at the EPA, Dr. Woodruff presents critical findings about how environmental policies impact individuals mortality and morbidity. She addresses challenges and breakthroughs, as well as provides listeners with useful tips to reduce their exposure to toxic chemicals.

Send us a textSchedule an Rx AssessmentSubscribe to Master The MarginWhat does it really take to start and sustain a successful compounding pharmacy in 2026? In this episode, Scotty Sykes, CPA, CFP®, and Austin Murray sit down with Amy Summers, PharmD, BCSCP and of Restore Health Consulting, to discuss how pharmacy owners can move from idea to implementation when entering the compounding space.We cover:Designing a purpose-built facility for USP standards and your product mixThe mindset shift from dispensing to creating and how to balance quality with patient careMarket analysis, relationships, and niche focus in building a sustainable businessKey trends driving growth, consolidation, and private investment in the compounding industryMore About Our Guest:Amy Summers, PharmD, BCSCP is an independent consultant, specializing in business, operations, quality assurance, and regulatory compliance matters for the pharmaceutical compounding industry. She earned her PharmD degree from the University of California San Francisco and was among the first pharmacists in the nation to earn a Board Certified Sterile Compounding Pharmacist (BCSCP) credential. Dr. Summers has spent her entire career as a pharmacist in various settings centered around non-sterile and sterile compounding. She has formerly served as Director of Operations and Pharmacist in Charge at organizations engaged in compounding and also as Managing Director of a FDA-registered 503B outsourcing facility. With extensive experience in USP standards, accreditation, cGMP, and regulatory compliance, Dr. Summers has also served as an expert witness for matters related to compounding.Stay connected with Amy and Restore Health Consulting: Amy Summers LinkedInRestore Health Consulting WebsiteRestore Health Consulting LinkedInStay connected with us on social media:Facebook: https://www.facebook.com/sykesandcoTwitter: https://twitter.com/OllinSykesLinkedIn: https://www.linkedin.com/company/sykes-&-company-p-a-?trk=tyahScotty Sykes – CPA, CFP® LinkedIn: https://www.linkedin.com/in/scottysykes/More on this topic:Podcast: The Trusted Pharmacist: Advocacy and Building a Resilient PharmacyPodcast: From Counter to Capitol

Pulsatile tinnitus — the perception of a rhythmic sound in sync with the heartbeat — can be a key indicator of underlying vascular or structural pathology. In this episode, JNIS new Editor-in-Chief Dr. Michael Chen speaks with Dr. Madhavi Duvvuri and Dr. Matthew Robert Amans, authors of Non-invasive imaging modalities for diagnosing pulsatile tinnitus: a comprehensive review and recommended imaging algorithm. They are both from the University of California San Francisco, USA. They discuss the current evidence base, highlight the strengths and limitations of non-invasive imaging techniques such as MRI, MRA, CT, and CTA, and outline a practical algorithm for streamlining diagnosis.    Please subscribe to the JNIS podcast on your favourite platform to get the latest podcast every month. If you enjoy our podcast, you can leave us a review or a comment on Apple Podcasts (https://apple.co/4aZmlpT) or Spotify (https://spoti.fi/3UKhGT5). We'd love to hear your feedback on social media - @JNIS_BMJ.

In this episode of Inside GRAPPA, host Dr. Mio Nakamura (University of Michigan) speaks with Dr. Tina Bhutani-Jacques, MD, MAS, FAAD (Synergy Dermatology / University of California San Francisco) about her groundbreaking study on the role of sleep in psoriasis disease severity. Funded by the GRAPPA Pilot Research Grant, Dr. Bhutani-Jacques's work is the first prospective cohort study to objectively examine sleep patterns in psoriasis patients.

In episode 60 of Going anti-Viral, Dr Donald Abrams joins host Dr Michael Saag to discuss medical cannabis. Dr Abrams is a professor emeritus at the University of California San Francisco and a specialist in integrative oncology at the Osher Center for Integrative Health. Dr Abrams has studied complementary and alternative therapies, including mind-body treatments, botanical therapies, medical use of cannabis and herbal therapies used in traditional Chinese medicine. He continues to research the health effects of medical cannabis. Dr Abrams was previously at the forefront in HIV/AIDS research and treatment at San Francisco General Hospital and served as chief of the medical oncology service from 2003 to 2017. Dr Saag and Dr Abrams discuss the history of medical cannabis and the challenges Dr Abrams experienced in researching its use for medical therapy. They discuss the medical benefits of cannabis and the recommendations that clinicians may make as well as addressing the differences in products available including THC and CBD. They also discuss research in whether use of cannabis in young adults is related to schizophrenia. Finally, Dr Saag and Dr Abrams discuss the future of medical cannabis and whether physicians should continue to provide a role in its use, whether the scheduling of cannabis as a controlled substance will change, and the type of research that is needed to continue to explore where its use is beneficial. 0:00 – Introduction1:20 – Overview of the history of medical cannabis 4:10 – The fight for medical cannabis research and its use in people with AIDS 10:59 – Understanding the medical benefits of cannabis particularly for pain, insomnia, nausea, vomiting, anxiety, and depression 13:15 – How physicians navigate recommendations for the use of cannabis and the differences with the types of cannabis whether inhaled, digested, or tinctures 18:13 – CBD vs. THC: understanding the differences and other possible cannabinoid therapeutics23:25 – The role of physicians in the future of medical cannabis, the need for more research, and the overall availability for people who want it 25:57 – Overview of research if there a relationship between the use of cannabis and schizophrenia in young adults __________________________________________________Produced by IAS-USA, Going anti–Viral is a podcast for clinicians involved in research and care in HIV, its complications, and other viral infections. This podcast is intended as a technical source of information for specialists in this field, but anyone listening will enjoy learning more about the state of modern medicine around viral infections. Going anti-Viral's host is Dr Michael Saag, a physician, prominent HIV researcher at the University of Alabama at Birmingham, and volunteer IAS–USA board member. In most episodes, Dr Saag interviews an expert in infectious diseases or emerging pandemics about their area of specialty and current developments in the field. Other episodes are drawn from the IAS–USA vast catalogue of panel discussions, Dialogues, and other audio from various meetings and conferences. Email podcast@iasusa.org to send feedback, show suggestions, or questions to be answered on a later episode.Follow Going anti-Viral on: Apple Podcasts YouTubeXFacebookInstagram...

A few years ago, vaping was at the top of every parent's list of worries — including Sanjay's. But in just a few short years, the landscape has shifted again. Teen vaping rates have dropped, but new nicotine products have quickly taken their place. Dr. Pamela Ling, a professor at University of California San Francisco who has spent her career studying the tobacco industry's tactics, joins Dr. Sanjay Gupta to talk about why nicotine remains such a moving target — and how parents can help their kids stay ahead of it. Producer: Jesse Remedios Senior Producer: Dan Bloom Showrunner: Amanda Sealy Technical Director: Dan Dzula Executive Producer: Steve Lickteig Learn more about your ad choices. Visit podcastchoices.com/adchoices

Facioscapulohumeral muscular dystrophy (FSHD) is one of the most common forms of muscular dystrophy, affecting individuals across the lifespan with variable severity. Advances in genetic understanding and therapeutic development have led to an era of promising disease-modifying strategies. In this episode, Katie Grouse, MD FAAN, speaks with Renatta N. Knox, MD, PhD, author of the article “Facioscapulohumeral Muscular Dystrophy” in the Continuum® October 2025 Muscle and Neuromuscular Junction Disorders issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California San Francisco in San Francisco, California. Dr. Knox is an assistant professor of neurology in the Division of Pediatric Neurology and Neuromuscular Section at Washington University School of Medicine in St. Louis, Missouri. Additional Resources Read the article: Facioscapulohumeral Muscular Dystrophy Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN  Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Renatta Knox about her article on fascioscapulohumeral muscular dystrophy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Welcome to the podcast, and please introduce yourself to our audience. Dr Knox: Hi Katie, thank you so much for the invitation for the audio interview. I'm looking forward to our conversation. As she mentioned, my name is Renata Knox. It's a pleasure to be here today. Dr Grouse: I'd like to start by asking, what is the key message that you hope your readers will take from your article? Dr Knox: I would say two things. The first is an appreciation and understanding of the unique genetic mechanism that leads to FSHD. And the second is the really exciting therapy landscape that we find ourselves in. So, we're hopeful that there will actually be disease-modifying therapies for FSHD soon. Dr Grouse: We're really looking forward to learning more about that. Now, before we get to that piece, could you just remind us of the clinical manifestations and features that are specific to FSHD? Dr Knox: So, one of the most unique things about FSHD that we see clinically is the pattern of weakness. So, one of the first features is that it's asymmetric. And then there are certain muscle groups that typically are affected, and that's partly where the name comes from. So, we see effects in the face, the limbs, the trunk; and so, those are some of the unique features that we see clinically. Dr Grouse: I'd love it if you could walk us through how you approach diagnosing a patient who presents with proximal weakness where FSHD is in your differential. Dr Knox: Yeah, it's a really great question. So, I would say it depends. So, I actually focus on FSHD in my clinical practice. So, many times patients are referred to me because there's a very high suspicion or there's a known family history of FSHD. So, that's one category of cases. I would say the other category of case is where it's, as you said, maybe more proximal weakness more broadly. Someone that's before me who has a known family history, they really have some of the characteristic physical features---which I'm pretty attuned to, as this is, you know, part of my subspecialty---I'll actually go directly to FSHD genetic testing. And that is one of the unique features of this disease, that the next-generation sequencing panels that are typically used for some of our other muscle diseases, FSHD is not captured on those. So, we actually have to send targeted testing for FSHD to diagnose it. So, that is one category where, again, I have a very high suspicion either based on their clinical presentation and/or a known family history, then I will actually go directly to FSHD-targeted genetic testing. In the second case, where it is one of the conditions that I'm considering among others, I will do more broad testing. So, I will get a CK level to see if there's evidence of muscle breakdown. I'll likely also do one of the next-generation sequencing panels that we have access to, which will allow us to identify, potentially, one to two hundred potential muscle diseases. And then again, if FSHD is higher on my differential in that second group of patients, then I will also send targeted FSHD-specific testing. Dr Grouse: That's really helpful. And I'm wondering if you have any thoughts about common pitfalls that you've seen when providers are trying to work this up? Dr Knox: I don't know if I would say pitfalls. I think I would acknowledge that it's challenging. My subspecialty training in neuromuscular medicine and also gene therapy. And so FSHD is pretty high on my radar. But I would say in neurology in general---and then, you know, the general medical population---,it really isn't something that many people are seeing. So, I would say what patients will communicate to us sometimes is some frustration that maybe it took time to make the diagnosis, but I just have a deep understanding that it's not something that is on many people's radars. And I think, again, it's tricky because it's not picked up on these next-generation sequencing panels, which many of us can send pretty easily. It will be missed. And I will say the biggest pitfall is, again, if you're not thinking about it and you don't send that testing, you actually- it's very difficult to diagnose it. Dr Grouse: Thank you so much for highlighting that. I think there are many people who are not aware that those different panels really aren't picking that up and that they have to test specifically. So, I think that's a great thing for all of us to keep in mind. Are there any tips or tricks to the diagnosis, other than the genetic issues that you mentioned, that sometimes can really bring this diagnosis to the forefront? Dr Knox: I think things that really tip me off to having a higher suspicion for FSHD is facial weakness that we can detect on our exam. Scapular winging---again, there's a small subset of disorders which can impact that. Someone who's presenting with foot drop, you know, with facial weakness, I think definitely about FSHD more. Also, clinically, kind of the presentation or things that they're beginning to have difficulty with is a tip-off. So, if someone is an athlete, like, they're a volleyball player or basketball player and they say, oh, I'm having difficulties, you know, with movements that require them to elevate their arm, which can be a sign of the shoulder weakness that we classically see. Or someone who says, oh, I'm having a harder time shampooing my hair or combing my hair. So those can be tip-offs again, which are basically referencing the type of weakness that they have. Another feature of FSHD which isn't necessarily as broadly appreciated is that pain and fatigue are very common. So, if someone is coming in and saying, actually, I also have a significant amount of fatigue as well or a lot of pain, that's something that can tip me off to it. Hearing loss is something that we can also see in up to 20% of patients with FSHD. So, if they are having those symptoms or saying they're ringing in their ears, these are some things that will make me begin to think about it more. Dr Grouse: Oh, really helpful. I also found it really fascinating reading some of the very FSHD-specific clinical signs, some interesting- some diagrams and pictures as well, that are very specific to the pattern of weakness that develops in FSHD. So, I encourage our listeners to check that out. But are there any highlights from those little clinical pearls that you'd like to point out? Dr Knox: I think the poly-hill sign---so, these are these literal hills that we can see in the shoulders of patients with FSHD---is pretty classic. Popeye arms, which is this older term that we still use that has to do with which muscle groups are preserved versus those that have atrophy. So that's a common feature. And then I would say, really, the asymmetry is something that is a unique feature in FSHD. And again, we did our best to provide good representative images. So again, as you mentioned, Katie, I would really encourage people to look at those images and then think about cases that they may have seen and how similar they are so they can begin to recognize those signs as well. Dr Grouse: Now going back to the genetic topic, the complex genetic underpinnings of FSHD are really well-explained in your article; and again, worth taking a look at to remind ourselves of everything that's of that pathology. Now, I was wondering though, if you could give us a brief overview of how we should approach genetic testing in a suspected case of FSHD? You mentioned some specific panels, but it does sound like there's some more complexity to it as well. Dr Knox: Yes, and I'll just kind of briefly explain that complexity. Part of the thing that we're detecting in the genetic testing is the repeat number. And so, we're actually looking for a contraction in a repeat number. So, not an expansion, which were typical for some of the diseases that we think about, the trinucleotide repeat disorders. And this is why it's not captured in the next-generation sequencing panels, because they do not currently have the ability to do that. And so, again, what the type of testing that I do really depends on my suspicion. So again, if my suspicion is very high for FSHD---they have a family history, they have the classic features---then I will actually go directly to an FSHD-specific testing, which is available from various sources. If, again, it's among different things that I'm thinking about, I will get a CK lab. I typically will also send a next-generation sequencing panel specific for muscle diseases, perhaps muscular dystrophy; again, depending on what I'm thinking about. And then I will also send in a specific FSHD genetic test as well. People are beginning to use whole-genome sequencing, which is capturing some of our true nucleotide repeat disorders and becoming more comprehensive. So, my hope is that as that becomes more standard of care---like, whole-exome sequencing can be gotten pretty routinely now---that it may be easier for us to make some of these diagnoses. Dr Grouse: Well, that's really helpful, and thanks for that overview. Now another thing that you mentioned that I thought was really interesting in your article was that patients with, you know, history of FSHD, perhaps in the family, who are pregnant and want to screen for this disease would not be able to use sort of the more common screening tests like cell-free DNA testing and may have to go to other means to do that. What is generally their route to this type of testing? Dr Knox: Yeah, great question, and really important question for family planning purposes, and it definitely comes up in clinical practice. And so again, because of the unique genetics of FSHD, you actually have to do invasive genetic testing currently to be able to test it. And so that's, you know, amnio or chorio, and then send it to a lab that can perform, again, FSHD-specific testing on the samples that are presented. And there are obviously labs that are capable of doing that and centers that are capable of doing that, but it is not picked up on the cell-free DNA panels that are being very routinely used. You or your provider has to be thinking about it to send that specific testing, similar to our patients that come into clinic and have not yet been diagnosed. Dr Grouse: Once you have the diagnosis, what are our options for therapy? I think it sounds like at this current time, it looks to be mostly supportive. What are some of the supportive care options we should keep in mind? Dr Knox: Yes, so that is definitely accurate. Care today is supportive, but again, we're very excited about the clinical trial and therapy landscape for FSHD. So, I work very closely with my physical therapy colleagues that are in clinic with me. So, we work very closely with physical and occupational therapists to help with supportive measures, adaptive measures, doing assessments, helping our patients to be able to move and exercise safely and effectively. As I mentioned, pain is very common in FSHD and so we can treat that with medications. The most common medication that we use to treat for pain in FSHD are NSAIDs. And then other than that it's really, you know, supportive measures. Do they need to see other subspecialists? There are some surgical options. Those are used very rarely to help with some of the scapular weakness, but typically it's physical therapy, occupational therapy, supportive devices. We treat the pain as we're able to, and then we work with other subspecialists to screen, monitor and support our patients to the best of our ability. Dr Grouse: Well, without further ado, I'd love to hear more about what's coming down the pipeline in clinical trials. What can we look forward to seeing, hopefully, in future years to treat these patients? Dr Knox: Yes. And so, this is actually what got me interested in the neuromuscle space in general is that, because we now for many years have known the genetic cause of many of these disorders as well as some of the underlying mechanisms, we can actually use advances in therapeutics to do what we call targeted therapies. So, rather than treating symptoms or indirect methods or doing kind of broad drug screens---which, again, still do take place and still do have their place---we actually can target mechanisms directly. And so, we know that the underlying biology of FSHD is due to this protein called DUX4 being expressed when it should not be. So, it's what we call a toxic gain of function. And so, the targeted way to address this is to suppress DUX4 expression. And so, kind of broadly speaking, what we're really excited about are a couple of products that are currently in clinical trials right now that actually caused DUX4 suppression to be suppressed. And again, these are targeted pathways. And so, again, the hope is that by doing that, we can hopefully slow the progression of the disease, potentially stop progression of the disease, and potentially reverse. Again, we don't know if that might be possible, but that is one of the hopes. Dr Grouse: Well, that's really exciting, and I know we're all looking forward to more coming down the pipeline soon, and hopefully more things that can really offer some exciting treatments for our patients with this condition. Now, a little more deep-dive into our patients who are diagnosed. You've reviewed some of the treatments currently available and hopefully may someday soon be available. Are there other things that we should be keeping in mind in this population? For instance, screenings that we should be doing for other extramuscular manifestations that we need to be thinking about? Dr Knox: I will answer that question two ways. I think something that's very important to acknowledge is the impact that these diagnoses and these conditions have on our patient practically, psychologically. One of the other unique features of FSHD is, it's autosomal-dominant. So, if it is in a family, you can have many family members who are affected, but the variability is very high. And so, you can have in the same family someone who is wheelchair-dependent, and someone else in the family with the same underlying genetics who has no signs or symptoms or is very mildly affected. And that is something that is definitely challenging for our families and patients to navigate if they're very different than their family members with the same condition. And just navigating the world with a condition that, you know, can be physically debilitating and cause changes to what they're able to do or not able to do, progression is something that's very difficult to handle. So, I think that's one set of things. And we try our best, you know, with my team and my other colleagues in the space, to support our families and patients in the best way that we can. Secondly, there is very important screening that needs to be done for this condition. So, one of the things- and the current guidelines which are actually being updated, the last update was in 2015 is all patients that undergo pulmonary function testing or PFTs. And so that's something we do at baseline and we do at least annually in my practice. Young kids who are presenting very early or patients with certain genetics that we know are more predisposed to extra muscular manifestations, we recommend screening for hearing, which is one of the manifestations, and ophthalmologic exam to look for retinovascular changes, which is one of the manifestations as well. Those are the more common ones that are typically done. There's also some evidence in pediatric patients with very severe manifestations that there may be some cognitive impacts, learning impacts. And so, that is something we're also thinking about screening and supporting our patients in that way. And again, we typically work with these patients in a multidisciplinary team depending on what manifestations and the degrees to which they're impacted by the disorder. Dr Grouse: Thank you so much for that answer. I think a lot of us forget sometimes when we get really focused on what can we do now, that we forget to kind of stop and reflect on sort of the more holistic approach. How is this affecting the patient? How is this affecting the patient's family dynamic, and what other ways are they going through life with this condition that we need to be thinking about? So, I appreciate you bringing that up. I wanted to ask, sort of based on what you're talking about and what you mentioned already, you happened to mention that what initially drew you that to this work was your interest in some of the really exciting breakthroughs in the field. Well, was there anything else that drew you to, specifically, congenital neuromuscular diseases, and FSHD in particular? Dr Knox: I'm a physician scientist by training, and so I would describe myself also as a molecular biologist. So, I love getting into the nitty gritties of disease mechanisms, what genes are doing in bodies, how they function. And so, as I mentioned earlier, in the neuromuscle space, we've known for many years the genetic cause of many of these disorders and have done great, you know, mechanistic work to kind of define why we see the disease. And then now we're at this intersection of that knowledge marrying with these really novel therapeutic approaches, gene therapy approaches, being able to intersect and then in very creative ways actually target diseases very directly. And so, I would say it really is the combination of those two things. FSHD has a really fascinating unique biology, which again, we encourage everyone to read about more in the article. That really drew me to it. I'm very interested in gene regulation, transcription. This is one of the underlying mechanisms that is gone awry in the disorder, and then that being married to advances in therapeutics. So, you could wed those two pieces of information and actually meaningfully impact patient 's lives. And again, that's the real privilege and honor to witness is how these therapies can transform lives. And I saw it happened with this one case for this one disorder when I was a resident where there was no treatment. Young children, unfortunately, would not survive the disease. And then I saw the therapy come be in development and literally change the trajectory. And this is what we're very hopeful for in the FSHD space, that wedding, this wonderful basic science research, translational research, companies working together to develop these therapies that can transform lives. It is just so beautiful to witness and see, and it's something that I get to do. You know, it's a part of my job, so it's a real privilege. Dr Grouse: Well, I have to say, it's really inspiring hearing you talk about it. And I imagine that many neurologists-in-training who are listening to this may be inspired as well and may be convinced to go into this field for that very reason. So, thank you so much for sharing all of this information with us today. I learned a lot, and I think all of our listeners have too. Dr Knox: Thank you. It's really been a pleasure. Dr Grouse: Again, today I've been interviewing Dr Renatta Knox about her article on fascioscapulohumeral muscular dystrophy, which appears in the October 2025 Continuum issue on muscle and neuromuscular junction disorders. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Abortion later in pregnancy is often misunderstood and heavily targeted through both policy and stigma. Erika Christensen, co-founder of Patient Forward and later abortion patient and advocate, Jenn Chalifoux, later abortion patient and advocate, and Dr. Diana Greene Foster, demographer and Professor at the University of California San Francisco and lead of the Turnaway Study, sits down to share their personal stories and talk with us about why access to later abortion will always be needed.Some people—including young people, people with chronic health conditions, and people who have been recently pregnant—are late to discover they are pregnant. That means those who make this discovery later in pregnancy in states with six-week abortion bans do not have access to abortion. Further into pregnancy, costs rise, available providers decrease, and barriers to care mount. Since Dobbs, ten states have enshrined viability measures into their constitutions, and 41 states still ban abortion at some point in pregnancy. The good news? Culture is shifting—more Americans agree that legislators should not be involved in pregnancy decisions, including in the third trimester. There are also more clinics and providers for abortion later in pregnancy than there were previously, and states are continuing to repeal viability limits. Support the showFollow Us on Social: Twitter: @rePROsFightBack Instagram: @reprosfbFacebook: rePROs Fight Back Bluesky: @reprosfightback.bsky.social Buy rePROs Merch: Bonfire store Email us: jennie@reprosfightback.comRate and Review on Apple PodcastThanks for listening & keep fighting back!

Ataxia is a neurologic symptom that refers to incoordination of voluntary movement, typically causing gait dysfunction and imbalance. Genetic testing and counseling can be used to identify the type of ataxia and to assess the risk for unaffected family members. In this episode, Katie Grouse, MD, FAAN, speaks with Theresa A. Zesiewicz, MD, FAAN, author of the article “Ataxia” in the Continuum® August 2025 Movement Disorders issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California San Francisco in San Francisco, California. Dr. Zesiewicz is a professor of neurology and director at the University of South Florida Ataxia Research Center, and the medical director at the University of South Florida Movement Disorders Neuromodulation Center at the University of South Florida and at the James A. Haley Veteran's Hospital in Tampa, Florida. Additional Resources Read the article: Ataxia Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Theresa Zesiewicz about her article on ataxia, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, and please introduce yourself to our audience.  Dr Zesiewicz: Well, thank you, Dr Grouse. I'm Dr Theresa Zesiewicz, otherwise known as Dr Z, and I'm happy to be here. Dr Grouse: I have to say, I really enjoyed reading your article. It was a really great refresher for myself as a general neurologist on the topic of ataxia and a really great reminder on a great framework to approach diagnosis and management. But I wanted to start off by asking what you feel is the key message that you hope our listeners will take away from reading your article. Dr Zesiewicz: Yes, so, thanks. I think one of the key messages is that there has been an explosion and renaissance of genetic testing in the past 10 years that has really revolutionized the field of ataxia and has made diagnosis easier for us, more manageable, and hopefully will lead to treatments in the future. So, I think that's a major step forward for our field in terms of genetic techniques over the last 10 years, and even over the last 30 years. There's just been so many diseases that have been identified genetically. So, I think that's a really important take-home message. The other take-home message is that the first drug to treat Friedreich's ataxia, called omaveloxolone, came about about two years ago. This was also a really landmark discovery. As you know, a lot of these ataxias are very difficult to treat. Dr Grouse: Now pivoting back to thinking about the approach to diagnosis of ataxia, how does the timeline of the onset of ataxia symptoms inform your approach? Dr Zesiewicz: The timeline is important because ataxia can be acute, subacute or chronic in nature. And the timeline is important because, if it's acute, it may mean that the ataxia took place over seconds to hours. This may mean a toxic problem or a hypoxic problem. Whereas a chronic ataxia can occur over many years, and that can inform more of a neurodegenerative or more of a genetic etiology. So, taking a very detailed history on the patient is very important. Sometimes I ask them, what is the last time you remember that you walked normal? And that can be a wedding, that can be a graduation. Just some timeline, some point, that the patient actually walked correctly before they remember having to hold onto a railing or taking extra steps to make sure that they didn't fall down, that they didn't have imbalance. That sometimes that's a good way to ask the patient when is the last time they had a problem. And they can help you to try to figure out how long these symptoms have been going on. Dr Grouse: I really appreciate that advice. I will say that I agree, it can sometimes be really hard to get patients to really think back to when they really started to notice something was different. So, I like the idea of referencing back to a big event that may be more memorable to them. Now, given that framework of, you know, thinking through the timeline, could you walk us through your approach to the evaluation of a patient who presents to your clinic with that balance difficulties once you've established that? Dr Zesiewicz: Sure. So, the first thing is to determine whether the patient truly has ataxia. So, do they have imbalance? Do they have a wide base gait? That's very important because patients come in frequently to your clinic and they'll have balance problems, but they can have knee issues or hip issues, neuropathy, something like that. And sometimes what we say to the residents and the students is, usually ataxia or cerebellar symptoms go together with other problems, like ocular problems are really common in cerebellar syndromes. Or dysmetria, pass pointing, speech disorder like dysarthria. So, not only do you need to look at the gait, but you should look at the other symptoms surrounding the gait to see if you think that the patient actually has a cerebellar syndrome. Or do they have something like a vestibular ataxia which would have more vertigo? Or do they have a sensory ataxia, which would occur if a person closes his eyes or has more ataxia when he or she is in the dark? So, you have to think about what you're looking at is the cerebellar syndrome. And then once we look to see if the patient truly has a cerebellar syndrome, then we look at the age, we look at---as you said before, the timeline. Is this acute, subacute, or chronic? And usually I think of ataxia as falling into three categories. It's either acquired, it's either hereditary, or it's neurodegenerative. It can be hereditary. And if it's not hereditary, is it acquired, or is it something like a multiple system atrophy or a parkinsonism or something like that? So, we try to put that together and start to narrow down on the diagnosis, thinking about those parameters. Dr Grouse: That's really a helpful way to think through it. And it is true, it can get very complex when patients come in with balance difficulties. There's so many things you need to think about, but that is a great way to think about it. Of course, we know that most people who come in to the Movements Disorders clinic are getting MRI scans of their brains. But I'm curious, in which cases of patients with cerebellar ataxia do you find the MRI to be particularly helpful in the diagnosis? Dr Zesiewicz: So, an MRI can be very important. Not always, but- so, something like multiple system atrophy type C where you may see a hot cross bun sign or a pontine hyperintensity on the T2-weighted image, that would be helpful. But of course, that doesn't make the diagnosis. It's something that may help you with the diagnosis. In FXTAS, which is fragile X tremor/ataxia syndrome, the patient may have the middle cerebellar peduncle sign or the symmetric hyperintensity in the middle cerebellar peduncles, which is often visible but not always. Something like Wernicke's, where you see an abnormality of the mammillary bodies. Wilson's disease, which is quite rare, T2-weighted image may show hyperintensities in the putamen in something like Wilson's disease. Those are the main MRI abnormalities, I think, with ataxia. And then we look at the cerebellum itself. I mean, that seems self-evident, but if you look at a sagittal section of the MRI and you see just a really significant atrophy of the cerebellum, that's going to help you determine whether you really have a cerebellar syndrome. Dr Grouse: That's really encouraging to hear a good message for all of us who sometimes feel like maybe we're missing something. It's good to know that information can always come up down the line to make things more clear. Your article does a great review of spinal cerebellar ataxia, but I found it interesting learning about the more recently described syndrome of SCA 27B. Would you mind telling us more about that and other really common forms of SCA that's good to keep in mind? Dr Zesiewicz: Sure. So, there are now 49 types of spinal cerebellar ataxia that have been identified. The most common are the polyglutamine repeat diseases: so, spinocerebellar ataxia type 3 or type 2, type 6, are probably the most common. One of the most recent spinocerebellar ataxias to be genetically identified and clinically identified is spinocerebellar ataxia 27B. This is caused by a GAA expansion repeat in the first intron of the fibroblast growth factor on chromosome 13. And the symptoms do include ataxia, eye problems, downbeat nystagmus, other nystagmus, vertical, and diplopia. It appears to be a more common form of adult-onset ataxia, and probably more common than was originally thought. It may account for a substantial number of ataxias, like, a substantial percentage of ataxias that we didn't know about. So, this was really a amazing discovery on SCA 27B. Dr Grouse: Now a lot of us I think feel a little anxious when we think about genetic testing for ataxia simply because there's so many forms, things are changing quickly. Do you have a rule of thumb or a kind of a framework that we can think of as we approach how we should be thinking about getting genetic testing for the subset of patients? Dr Zesiewicz: Sure. And I think that this is where age comes into play a lot. So, if you have a child who's 10, 11, or 12 who's having balance problems in the schoolyard, does not have a history of ataxia in the family, the teachers are telling you that the child is not running correctly, they're having problems with physical education, that is someone who you would think about testing for Friedreich's ataxia. A preteen or a child, that would be one thing that would be important to test. When you talk to your patient, it's important to really take a detailed family history. Not just mom or dad, but ethnicity, grandparents, etc. And sometimes, once in a while, you come up with a known spinal cerebellar ataxia. Then you can just test for that. So, if a person is from Portugal or has Portugal background and they have ataxia and the parents had ataxia, you would think of spinal cerebellar ataxia type 3. Or if they're Brazilian, or if the person is from a certain area of Cuba and mom and dad had ataxia and that person has ataxia, you would think of spinal cerebellar ataxia type 2. Or if a person has ataxia and their parent had blindness or visual problems, you may be more likely to think of spinal cerebellar ataxia type 7, for example. If they have that---either they have a known genetic cause in in the family, first degree family, or they come from an area of the world in which we can pinpoint what type we think it is---you can go ahead and get those tests. If not, you can take an ataxia comprehensive panel. Many times now, if you take the panel and the panel is negative, it will reflex to the whole exome gene sequencing, where we're finding really unusual and more rare types of ataxia, which are very interesting. Spinal cerebellar ataxia type 32, spinal cerebellar ataxia type 36, I had a spinal cerebellar ataxia type 15. So, I think you should start with the age, then the family history, then where the person is from. And then, if none of those work out, you can get a comprehensive panel, and then go on to whole exome gene sequencing. Dr Grouse: That's really, really useful. Thank you so much for breaking that down in a really simple way that a lot of us can take with us. Pivoting a little bit now back towards different types of acquired ataxias, what are some typical lab tests that you recommend for that type of workup? Dr Zesiewicz: Again, if there's no genetic history and the person does not appear to have a neurodegenerative disease, we do test for acquired ataxias. Acquired ataxias can be complex. Many times, they are in the autoimmune family. So, what we start with are just basic labs like a CBC or a CMP, but then we tried to look at some of the other abnormalities that could cause ataxia. So, celiac disease, stiff person syndrome. So, you would look at anti-glutamic acid decarboxylase antibodies, Hashimoto's---so, antithyroglobulin antibodies or antithyroperoxidase antibodies would be helpful. You know, in a case of where the patients may have an underlying neoplasm, maybe even a paraneoplastic workup, such as an anti-Hu, anti-Yo, anti-Ri. A person has breast cancer, for example, you may want to take a paraneoplastic panel. I've been getting more of the anti-autoimmune encephalitis panels in some cases, that were- that are very interesting. And then, you know, things that sometimes we forget now like the syphilis test, thyroid-stimulating test, take a B12 and folate, for example. That would be important. Those are some of the labs. We just have on our electronic chart a group of acquired labs for ataxia. If we can't find any other reason, we just go ahead and try to get those. Dr Grouse: Now, I'm curious what you think is the most challenging aspect of diagnosing a patient with cerebellar ataxia? Dr Zesiewicz: So, for those of us who see many of these patients a day, some of the hardest patients are the ones that---regardless of the workup that we do, we've narrowed it down, it's not hereditary. You know, they've been through the whole exome gene sequencing and we've done the acquired ataxia workup. It doesn't appear to be that. And then we've looked for parkinsonism and neurodegenerative diseases, and it doesn't appear to be that either; like, the alpha-synuclein will be negative. Those are the toughest patients, where we think we've done everything and we still don't have the answer. So, I've had patients in whom I've taken care of family members years and years ago, they had a presumed diagnosis, and later on I've seen their children or other family members. And with the advent of the genetic tests that we have, like whole exome gene sequencing, we have now been able to give the patient and the family a definitive diagnosis that they didn't have 25 years ago. So, I would say don't give up hope. Retesting is important, and as science continues and we get more information and we make more landmark discoveries in genetics, you may be better able to diagnose the patient. Dr Grouse: I was wondering if you had any recommendations regarding either some tips and tricks, some pearls of wisdom you can impart to us regarding the work of ataxia, or conversely, any big pitfalls that you can help us avoid? I would love to hear about it. Dr Zesiewicz: Yeah, there's no easy way to treat or diagnose ataxia patients. I've always felt that the more patients you see- and sounds easy, but the more patients you see, the better you're going to become at it, and eventually things are going to fall into place. You'll begin to see similarities in patients, etc. I think it's important not only to make sure that a person has ataxia, but again, look at the other signs and symptoms that may point to ataxia that you'll see in a cerebellar syndrome. I think it's important to do a full neuroexam. If a person has spasticity, that may point you more towards a certain type of ataxia than if a person has no reflexes, for example, that we see in Friedreich's ataxia. Some of the ocular findings are very interesting as well. It's important to know if a person has a tremor. I've seen several Wilson's disease cases in my life with ataxia. They're very important. I think a full neuroexam and also a very detailed history would be very helpful. Dr Grouse: Tell us about some promising developments in the diagnosis and management of ataxia that we should be on the lookout for. Dr Zesiewicz: The first drug for Friedreich's ataxia was FDA-approved two years ago, which was an NRF2 activator, which was extremely exciting and promising. There are also several medications that are now in front of the FDA that may also be very promising and have gone through long clinical trials. There's a medication that's related to riluzole, which is a medication used for amyotrophic lateral sclerosis, that has been through about seven years of testing. That is before the FDA as well for spinal cerebellar ataxia. Friedreich's ataxia has now completed the first cardiac gene therapy program with AAV vectors, which- we're waiting for full results, but that's a cardiac test. But I would assume that in the future, neurological gene therapy is not far behind if we've already done cardiac gene therapy and Friedreich's ataxia. So, you know, some of these AAV vector-based genetic therapies may be very helpful, as well as ASO, antisense oligonucleotides, for example. And I think in the future, other things to think about are the CRISPR/Cas9 technology for potential treatment of ataxia. It is a very exciting time, and some major promising therapies have been realized in the past 2 to 3 years. Dr Grouse: Well, that's really exciting, and we'll all look forward to seeing these becoming more clinically applicable in the future. So, thank you so much for coming to talk with us today. Dr Zesiewicz: Thank you. Dr Grouse: Again, today I've been interviewing Dr Theresa Zesiewicz about her article on ataxia, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

When it comes to your demons, your baggage, you have a choice: transform or transmit. Sister Dang Nghiem, MD, (“Sister D”) was born in 1968 in Vietnam during the Tet Offensive, the daughter of a Vietnamese mother and an American soldier. She lost her mother at the age of twelve and immigrated to the United States at the age of seventeen with her brother. Living in various foster homes, she learned English and went on to earn a medical degree from the University of California – San Francisco. After suffering further tragedy and loss, she quit her practice as a doctor to travel to Plum Village monastery in France founded by Zen Master Thich Nhat Hanh, where she was ordained a nun in 2000, and given the name Dang Nghiem, which means adornment with nondiscrimination. She is the author of a memoir, Healing: A Woman's Journey from Doctor to Nun (2010), and Mindfulness as Medicine: A Story of Healing and Spirit (2015). In this episode we talk about: The “beginning anew” practice:  what it is, plus why and how it helps.  Is focusing on yourself self-indulgent? The four kinds of people, according to the buddha The concept of “soulmate” in a Buddhist context Related Episodes: Buddhist Strategies For Reducing Everyday Addictions (To Your Phone, Food, Booze, And More) | Sister Dang Nghiem This Episode Will Make You Stronger | Sister Dang Nghiem “I am enough” (guided meditation by Sister D)   Join Dan's online community here Follow Dan on social: Instagram, TikTok Subscribe to our YouTube Channel On Sunday, September 21st from 1-5pm ET, join Dan and Leslie Booker at the New York Insight Meditation Center in NYC as they lead a workshop titled, "Heavily Meditated – The Dharma of Depression + Anxiety." This event is both in-person and online. Sign up here!    Get ready for another Meditation Party at Omega Institute! This in-person workshop brings together Dan with his friends and meditation teachers, Sebene Selassie, Jeff Warren, and for the first time, Ofosu Jones-Quartey. The event runs October 24th-26th. Sign up and learn more here! To advertise on the show, contact sales@advertisecast.com or visit https://advertising.libsyn.com/10HappierwithDanHarris  

Welcome to the Mediumship Sister's Podcast! Season 6, episode 12!Today on the podcast, Paige and Ciarra, welcome guests, Wendie Coulter, Dr. Llyod Costello and Cay Randal- May PHD from the National Organization for Medical Intuition, known as NOMI. We share about medical intuition, ongoing research and the mission to advance this skill into mainstream healthcare. Come join the evolution to advance professional Medical Intuition , become a supporter and learn more about NOMI*NOMI members day coming up September 28, 2025 https://www.nomimedicalintuition.org/missionAs a medical intuitive and professional member with NOMI, Paige wanted to share these amazing trail blazers who are advancing awareness and research of Medical Intuition into main stream healthcare. Medical intuition can be the missing piece in traditional healthcare, where intuitive's can access the whole person , seeing beyond into the body, mind, spirit and emotions and work hand and hand with physicians to treat the whole person and can be recognized as a stand alone treatment.Get to know our guests~*Wendie Colter, MCWC, CMIP, the president of NOMI, Wendie is the founder/CEO of The Practical Path®, Inc., presenting accredited certification programs in Medical Intuition for wellness professionals and the public. She is a Certified Medical Intuitive Practitioner, Master Certified Wellness Coach, and President of the National Organization for Medical Intuition (NOMI). She is an invited speaker at prominent integrative health and educational organizations. Her trailblazing research on Medical Intuition is published in the peer-reviewed Journal of Integrative and Complementary Medicine. Wendie is the author of the multiple award-winning book, Essentials of Medical Intuition: A Visionary Path to Wellness (Watkins Publishing), endorsed by Dr. Bernie Siegel, Dr. Kenneth Pelletier, Dr. Larry Dossey, Dr. Shamini Jain, and others. In private practice for more than twenty years.https://www.thepracticalpath.com*Cay Randall-May PHD, Certified Medical Intuitive Certified Energy Healing Practitioner. Cay has served clients throughout the world as a medical intuitive and general intuitive consultant for many decades. A founding member of NOMI, I was certified as a medical intuitive by the American Board of Scientific Medical Intuition and noted for my accuracy by C. Norman Shealy, M.D., Ph.D. From early childhood I was mentored by my grandmother, an accomplished psychic. Over the years I added many additional courses of study in extended sensory perception, and have taught extensively. My academic background in comparative anatomy/physiology as well as energy medicine/spirituality adds scientific and metaphysical depth to my work.https://cayrandallmay.comLlyod Costello, MD, vice president of NOMI. Dr. Lloyd Costello is a Board Certified Family Practitioner in private practice in San Bernardino California. He received his medical degree at the University of California Davis and completed a residency program in Family and Community Medicine at the University of California San Francisco and San Francisco General Hospital. He also served as Director of Ambulatory Care at the White Memorial Family Practice Residency program in East Los Angeles. In addition, he earned a Master's Degree in Spiritual Psychology at the University of Santa Monica. He has worked with traditional as well as non-traditional and indigenous healers and is in the process of becoming a Certified Medical Intuitive. He foresees the use of medical intuitives as an integral part of the health care team.https://www.youtube.com/@MediumshipSistersPodcast@themediumshipsisters Follow us on InstagramCiarra Saylor Douglas @ciarrasaylor_mediumship here https://www.ciarralovesart.com/shop-1 Mariana Lucker @star.aligned.alchemy www.staralignedalchemy.com Paige Sturgeon @thewildspiritpaige www.thewildspiritpaige.com www.redhillphotography.com recorded 9/3/25

Chorea describes involuntary movements that are random, abrupt, and unpredictable, flowing from one body part to another. The most common cause of genetic chorea in adults is Huntington disease, which requires comprehensive, multidisciplinary care as well as support for care partners, who may themselves be diagnosed with the disease. In this episode, Aaron Berkowitz, MD, PhD FAAN speaks with Kathryn P. L. Moore, MD, MSc, author of the article “Huntington Disease and Chorea” in the Continuum® August 2025 Movement Disorders issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology at the University of California San Francisco in the Department of Neurology in San Francisco, California. Dr. Moore is an assistant professor and director of the Parkinson's Disease and Movement Disorders Fellowship in the department of neurology at Duke University in Durham, North Carolina. Additional Resources Read the article: Huntington Disease and Chorea Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Guest: @KatiePMooreMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Berkowitz: This is Dr Aaron Berkowitz with Continuum Audio, and today I'm interviewing Dr Kathryn Moore about her article on diagnosis and management of Huntington disease and chorea, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, Dr Moore. Could you please introduce yourself to our audience? Dr Moore: Yeah, thank you so much. I'm so excited to be here. I'm Dr Moore. I'm an assistant professor of neurology at Duke University, where I work as a movement disorder specialist. I run our fellowship there and help with our residency program as well. So, I'm excited to speak with our listeners about chorea today. Dr Berkowitz: Fantastic. And we're excited to talk to you about chorea. So, as a general neurologist myself, I only see chorea pretty rarely compared to other movement disorders like tremor, myoclonus, maybe the occasional tic disorder. And like anything I don't see very often, I always have to look up the differential diagnosis and how to evaluate a patient with chorea. So, I was so glad to read your article. And next time I see a patient with chorea, I know I'll be referring to your article as a great reference to have a framework for how to approach it. I hope our readers will look at all these helpful tables on differential diagnosis based on distribution of chorea in the body, potential etiologies, time course of onset and evolution, associated drug-induced causes, what tests to send. So, I highly recommend our listeners read the article. Keep those tables handy for when a patient comes in with chorea. I'm excited to pick your brain about some of these topics today. First, how do you go about distinguishing chorea from other hyperkinetic movement disorders when you see a patient that you think might have chorea? Dr Moore: One of the wonderful things about being a movement disorder specialist is we spend a lot of time looking at movements and training our brain to make these distinctions. The things that I would be looking out for chorea is involuntary, uncontrolled movements that appear to be brief and flowing from one part of the body to another. So, if you can watch a patient and predict what movements they're going to do, this probably isn't chorea. And it should be flowing from one part of the body to another. So, not staying just in one part of the body or having sustained movements. It can be difficult to distinguish between a tic or dystonia or myoclonus. Those things tend to be more predictable and repetitive than the chorea, which tends to be really random and can look like dancing. Dr Berkowitz: That's very helpful. So, once you've decided the patient has chorea, what's your framework for thinking about the differential diagnosis of the cause of the patient's chorea? Dr Moore: Well, that could be really challenging. The differential for chorea is very broad, and so the two things that I tend to use are age of the patient and acuity of onset. And so, if you're thinking about acute onset of chorea, you're really looking at a structural lesion like a stroke or a systemic issue like infection, hyperglycemia, etc. Where a gradually progressive chorea tends to be genetic in nature. When you're thinking about the difference between a child and an adult, the most common cause of chorea in a child is Sydenham's chorea. And actually, the most common cause of chorea that I tend to see is Parkinson's disease medication. So, if anybody's seen dyskinesia in Parkinson's disease, you've seen chorea. But it's those two things that I'm using, the age of the patient and the acuity. Somewhere in the middle, though---so, if you have subacute onset of chorea---it's important to remember to think about autoimmune conditions or paraneoplastic conditions because these are treatable. Dr Berkowitz: That's very helpful. So, like in any chief concern in neurology, we're using the context like the age and then the time course. And then a number of other helpful points in your article about the distribution of chorea in the body. Any comments you'd like to make about- we have this very helpful table that I thought was very interesting. So, you really get deep into the nuances of chorea and the movement disorder specialist expert level. Are there any aspects of parts of the body affected by chorea or distribution of chorea across the body that help you hone your differential diagnosis? Dr Moore: Certainly. I think where the chorea is located in the body can be helpful, but not as helpful as other conditions where you're localizing a lesion or that sort of thing. Because you can have a systemic cause of chorea that causes a hemichorea; that you can have hyperglycemia causing a hemichorea, or even Sydenham's chorea being a hemichorea. But things that we think about, if the forehead is involved, I would think about Huntington's disease, although this is not pathognomonic. And if it's involving the face or the mouth, you can think about neuroacanthocytosis or, more commonly, tardive dyskinesia. Hemichorea would make me think about some of those systemic issues like hyperglycemia, Sydenham's chorea, those sorts of things, but I would rely more on the historical context and the acuity of presentation than the distribution itself. Dr Berkowitz: Got it. That's very helpful. So those can be helpful features, but not sort of specific for any particular condition. Dr Moore: Exactly. Dr Berkowitz: Yeah, I often see forehead chorea mentioned as sort of specific to Huntington's disease. Since I don't see much Huntington's disease myself, what does forehead chorea look like? What is the forehead doing? How do you recognize that there is chorea of the forehead? It's just sort of hard for me to imagine what it would look like. Dr Moore: It's really tricky. I think seeing the eyebrows go up and down or the brows furrow in an unpredictable way is really what we're looking for. And that can be hard if you're having a conversation. My forehead is certainly animated as we're talking about one of my favorite topics here. One of the tricks that I use with the fellows is to observe the forehead from the side, and there you can see the undulation of the forehead muscles. And that can be helpful as you're looking for these things. I think where it's most helpful to use the forehead is if you're trying to determine if someone with a psychiatric history has tardive dyskinesia or Huntington's disease, because there can be quite a lot of overlap there. And unfortunately, patients can have both conditions. And so, using the forehead movement can be helpful to maybe direct further testing for Huntington's disease. Dr Berkowitz: Oh, wow, that's a very helpful pearl. So, if you see, sort of, diffuse chorea throughout the body and the forehead is involved, to my understanding it may be less specific. But in the context of wondering, is the neuropsychiatric condition and movement disorder related by an underlying cause in the case of seeing orofacial dyskinesias, is the relationship a drug having caused a tardive dyskinesia or is the whole underlying process Huntington's, the absence of forehead might push you a little more towards tardive dyskinesia, presuming there is an appropriate implicated drug and the presence of forehead chorea would really clue you in more to Huntington's. Did I understand that pearl? Dr Moore: That's exactly right, and I'm glad you brought up the point about making sure, if you're considering tardive dyskinesia, that there has been an appropriate drug exposure. Because without that you can't make that diagnosis. Dr Berkowitz: That's a very helpful and interesting pearl, looking at the forehead from the side. That is a movement disorders pearl for sure. Sort of not just looking at the forehead from one angle and trying to figure out what it's doing, but going to look at the patient in profile and trying to sort it out. I love that. Okay. So, based on the differential diagnosis you would have crafted based on whether this is sort of acute, subacute, chronic, the age of the patient, whether it's unilateral, bilateral, which parts of the body. How do you go about the initial evaluation in terms of laboratory testing, imaging, etc.? Dr Moore: Well, certainly in an acute-onset patient, you're going to get a number of labs---and that's listed out for you in the paper---and consider imaging as well, looking for an infarct. One thing our learners will know is that sort of the typical answer to what's the infarct causing hemichorea would be the subthalamic nucleus. But really, those infarcts can be almost anywhere. There are case reports for infarcts in a wide variety of places in the brain leading to hemichorea. So, I think some general blood work and an MRI of the brain is a good place to start. For someone who has a more chronic course of the development of chorea, there are certain labs that I would get---and an MRI, because if you get an MRI and there's heavy metal deposition or other disease, structurally, that indicates a certain condition, that can help you pretty considerably. But otherwise, I'm looking for inflammatory markers, heavy metals, HIV, some general other things that are outlined, to help make sure that I'm not missing something that's treatable before I go down the route of genetic testing. And we may talk about this in a little bit, but if you start out with genetic testing and then you sort of have to back up and do more systemic testing, that can be very disjointed when it comes to good patient care. Dr Berkowitz: That's very helpful. So yeah, if it's acute, obviously this is the most straightforward scenario, acute and unilateral. We're imagining something lesional, as you said, either a stroke or---not sort of sudden, but fast, but not sudden---you might think of another structural lesion. Toxoplasmosis, right, has an affinity for the basal ganglia if you were seeing this in a patient who is immunocompromised. But in a case that, probably as you alluded to, sort of what we would see most commonly in practice, those still relatively rare, sort of subacute to chronic symmetric chorea. There's a long list of tests that are recommended. In your article and in other texts, I've read lupus testing, anti-phospholipid antibodies… but the list is long. I'll refer readers to your article. Out of curiosity as a specialist, how often do you see any of these labs come back revealing any underlying diagnosis in a patient who's otherwise healthy and just has developed chorea and comes to you with that chief concern? I feel like I've sent that mega-workup a few times; I'm obviously a general neurologist, but not nearly as many times as you have been. It's- I can't remember a time where something has come up, maybe an ANA one to forty or something like this that we don't think is relevant. But in your practice, how often do you end up finding a reversible cause in the laboratory testing versus ending up starting to go down the genetic testing route, which we'll talk about in a moment? Dr Moore: It's not common, but it is important that we capture these things. Because for a lot of those laboratory tests, there are treatments that are available, or other health implications if those come back positive. So, the case I think of is a polycythemia vera patient who had diffused subacute onset chorea and was able to be treated, was temporarily managed with medication for her chorea, and as her PV improved, she was able to come off those medications. As I was alluding to before---and I'm sure we'll talk about genetic testing---if you test for HD and it's negative, do you go down the route of additional expensive genetic testing, or do you then circle back and go, oops, I missed this treatable condition? As we talk about genetic testing as well, getting HD testing is a pretty involved process. And so, we want to make sure we are checking all those boxes before we move forward. So, it's not common, but we do catch some treatable conditions, and that's really important not to miss. Dr Berkowitz: That's very interesting. So, you diagnosed that polycythemia vera by blood smear, is that how you make the diagnosis? Dr Moore: Yes. Dr Berkowitz: And is that a once-in-a-career-so-far type of thing, or does that happen time to time? Dr Moore: For me, that's a once-so-far, but I don't doubt that I'll see it again. Dr Berkowitz: Great. And how about lupus and some of these other things we look for in the absence of other systemic features? Have you picked up any of these or heard of colleagues picking up something on laboratory testing? They said, oh, this patient came in for a referral for genetic testing, negative Huntington's disease. And good news, we found polycythemia vera; good news, we found undiagnosed lupus and we reversed it. I'm just curious, epidemiologically, seeing these long lists and not having the subspecialty practice that you do, how often you find a reversible cause like we do for neuropathy all the time, right? Oh, it's diabetes, it's B12---maybe not reversible, but preventing progression---or reversible dementia work up. You get so excited when you find low B12 and you replete the patient's B12, and they get better when they had been concerned they were developing an irreversible condition. How often does one in your subspecialty find a reversible cause on that initial mega-lab screen? Dr Moore: I think it's really uncommon, and maybe the folks that do are caught by someone else that never make it to Huntington's clinic, but I don't tend to see those cases. There are, of course, case reports and well-described in the literature about lupus and movement disorders and things of that nature, but that doesn't come to our clinic on a regular basis for sure. Dr Berkowitz: Got it. That's helpful to hear. Well, we've alluded to genetic testing a number of times now, so let's go ahead and talk about it. A lot of your article focuses on Huntington disease, and I was thinking about---in the course of our medical training in medical school, and then neurology residency, for those of us who don't become movement disorder experts like yourself---we learn a lot about Huntington disease. That's sort of the disease that causes chorea, until we later learned there are a whole number of diseases, not just the reversible causes we've been talking about, but a number of genetic diseases which you expertly reviewing your article. So, what are some of the red flags that suggest to you that a patient with chronically progressive chorea---and whom you're concerned for Huntington's or another genetic cause---what are some things you notice about the history, about the exam, the symptoms, the signs, the syndrome, that suggest to you that, actually, this one looks like it might not turn out to be HD. I think this patient might have something else. And as you have alluded to, how do you approach this? Do you send HD testing, wait for it to come back, and then go forward? Are there genetic panels for certain genetic causes of chorea? Do you skip just a whole exome sequencing, or will you miss some of the trinucleotide repeat conditions? How do you approach this in practice? Dr Moore: I'll try to tackle all that. One thing I will say is that a lot of patients with chorea, regardless of the cause, can look very similar to one another. So, if you're looking at chronic onset chorea, perhaps with some neuropsychiatric features, I'm going to most often think about HD because that's the most common cause. Certainly, as we mentioned before, if there's a lot of tongue protrusion, I would think about the acanthocytic conditions, neurocanthocytosis and McCloud syndrome. But generally in those conditions, we're looking at HD as the most likely cause. Certainly, if there is epilepsy or some other syndromic types of things going on, I may think more broadly. But it's important to know that while HD, as you mentioned, is the cause of chorea, many of our patients will have parkinsonism, tics, dystonia, a whole host of other movement phenomenologies. So, that wouldn't dissuade me from thinking about HD. When we think about the kind of patients that you're describing, upwards of 95% of those people will have Huntington's disease. And the process for genetic testing is fairly involved. The Huntington's Disease Society of America has organized a set of recommendations for providers to go about the process of genetic testing in a safe and supportive way for patients and their families. And so that's referred to in the article because it really is important and was devised by patients and families that are affected by this disease. And so, when we're thinking about genetic testing for HD, if I reveal that you have HD, this potentially affects your children and your parents and your siblings. You can have a lot of implications for the lives and health and finances of your family members. We also know that there is high suicidality in patients with HD, in patients who are at risk for HD; and there's even a higher risk of suicidality in patients who are at risk but test negative for HD. So, we do recommend a supportive environment for these patients and their families. And so, for presymptomatic patients or patients who are at risk and don't have chorea, this involves making sure we have, sort of, our ducks in a row, as it were, when we think about life insurance, and, do you have somebody supportive to be with you through this journey of genetic testing, no matter what the results are? So, oftentimes I'll say to folks, you know, there's this 20-page policy that I encourage you to look at, but there are Huntington's Disease Centers of Excellence across the country that are happy to help you with that process, to make sure that the patients are well supported. This is an individual genetic test because, as you mentioned, it is a CAG repeat disorder. And unfortunately, there is no chorea panel. So, if an HD test comes back negative, what we'll do then is think about what's called the HD phenocopies. As I mentioned before, some of these patients who look like they have HD will have a negative HD test. And so, what do you do then? Well, there's a handful of phenocopies---so, other genetic mutations that cause a very similar presentation. And so, we try to be smart, since there's not a panel, we try to be smart about how we choose which test to do next. So, for instance, there's a condition called DRPLA that is present in an African-American family here in my area, in North Carolina, as well as in Japan. And so, if someone comes from those backgrounds, we may decide that that's the next test that we're going to do. If they are white European descent, we may consider a different genetic test; or if they're sub-Saharan African, we may choose a different one from that. However, even if you do a really thorough job, all those blood tests, all those genetic tests, you will occasionally get patients that you can't find a diagnosis for. And so, it's important to know even when you do a good job, you may still not find the answer. And so, I think trying to do things with this complex of the presentation in a systematic way for yourself so you're not missing something. So, going back to our answer about, how do I look at lupus and polycythemia vera and all of that, to think about it in a systematic way. That when you get to the end and you say, well, I don't have an answer, you know you've tried. Dr Berkowitz: That's very helpful to hear your approach to these challenging scenarios, and also how to approach the potential challenging diagnosis for patients and their families getting this diagnosis, particularly in the presymptomatic phase. And your article touches on this with a lot of nuance and thoughtfulness. So, I encourage our listeners to have a read of that section as well. So, last here, just briefly in our final moments, you discuss in your article the various symptomatic treatments for chorea. We won't have time to go into all the details of all the many treatments you discussed, but just briefly, how do you decide which medication to start in an individual patient with chorea for symptomatic management? What are some of the considerations related to the underlying condition, potential side effect profiles of the particular medications, or any other considerations just broadly, generally, as you think about choosing one of the many medications that can be used to treat chorea? Dr Moore: Certainly. So, there is a group of FDA-approved medications, VMAT2 inhibitors, that we can choose from, or the off-label use of neuroleptics. And so, there's a lot of things that go into that. Some of that is insurance and cost and that sort of thing, and that can play a role. Others are side effects. So, for the VMAT2 inhibitors, they all do have a black box warning from the FDA about suicidality. And so, if a patient does struggle with mental health, has a history of suicidality, psychiatric admissions for that sort of thing, then I would be more cautious about using that medication. All patients are counseled about that, as are their families, to help us give them good support. So, the neuroleptics do not tend to have that side effect and can help with mood as well as the chorea and can be helpful in that way. And some of them, of course, will have beneficial side effects. So, olanzapine may help with appetite, which can be important in this disease. So, the big considerations would be the black box warning and suicidality, as well as, are we trying to just treat chorea or are we treating chorea and neuropsychiatric issues? Dr Berkowitz: Fantastic. Thank you for that overview. And again, for our listeners, there's a lot more detail about all of these medications, how they work, how they're used in different patient populations, their side effects, etc, to be reviewed in your excellent article. Again, today, I've been interviewing Dr Kathryn Moore about her article on diagnosis and management of Huntington's disease in chorea, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues. And thank you so much to our listeners for joining today. And thank you again, Dr Moore. Dr Moore: Thanks for having me. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

On this week's episode of Joint Action discover how ultra-processed foods may be silently contributing to osteoarthritis. Dr Gabby Joseph joins us to discuss her research research linking poor diet quality to greater knee pain, poorer physical function and thinner knee cartilage. Dr Gabby Joseph is a scientist and statistician with over 20 years of experience leading research funded by the US government at the University of California San Francisco, Her work focuses on musculoskeletal imaging, predictive modelling, and clinical study design, with a focus on applying advanced statistical and machine learning methods to improve patient outcomes She is the co-Director of The University of California's Clinical & Translational Musculoskeletal Imaging group and passionate about making sense of complex data so that it can be used to improve real-world care. RESOURCESUltra-processed food consumption is associated with knee osteoarthritis: Data from the Osteoarthritis InitiativeCONNECT WITH USTwitter: @ProfDavidHunter @jointactionorgInstagram: @osteoarthritisresearchgroupEmail: osteoarthritis.research@sydney.edu.auWebsite: www.jointaction.info/podcast Hosted on Acast. See acast.com/privacy for more information.

BUFFALO, NY – August 29, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on August 29, 2025, titled “In vivo manipulation of the protein homeostasis network in rhabdomyosarcoma.” In this study led by first author Kristen Kwong and corresponding author Amit J. Sabnis from the Department of Pediatrics, Division of Oncology, University of California San Francisco, researchers discovered that disrupting the protein quality control system in cancer cells slows tumor growth in rhabdomyosarcoma (RMS), the most common pediatric soft tissue cancer. This finding points to a new strategy for treating high-risk childhood cancers that often resist current therapies. Rhabdomyosarcoma is a rare and aggressive cancer that primarily affects children and adolescents. Standard treatments like chemotherapy and radiation often have limited long-term success in high-risk cases. This study explored a different approach: targeting the cellular machinery that maintains protein quality, known as the proteostasis network. Cancer cells rely heavily on this system to survive stress caused by rapid growth and genetic instability. “To examine whether MAL3-101 or more drug-like proteostasis inhibitors represent a new therapeutic strategy for RMS, we screened proteostasis components that might recapitulate the effects of MAL3-101 in vivo.” The researchers first used a compound called MAL3-101 to disrupt protein control in RMS cells. They then identified which parts of the protein quality system were affected. Based on those findings, they searched for more drug-like compounds that could target the same pathways. They focused on a protein called p97, which plays a critical role in removing damaged or misfolded proteins. When they blocked p97 using a drug called CB-5083, the cancer cells could no longer manage internal stress and began to self-destruct. In both laboratory models and mice implanted with human RMS tumors, the treatment significantly slowed or stopped tumor growth. The drug triggered a stress response in the cells known as the unfolded protein response, which can lead to either recovery or programmed cell death. However, not all tumors responded the same way. Some resisted the treatment by activating a backup system called autophagy, which allows cells to recycle parts of themselves under stress. By comparing tumors that responded well to those that did not, the researchers found that higher autophagy activity could serve as a warning sign for resistance. This insight may help identify which patients are more likely to benefit from therapies that target protein quality control. While the results are promising, the drug's effectiveness depended on the tumor's genetic profile and how it handled stress. Combining p97 inhibition with other treatments or blocking alternative survival pathways like autophagy may improve outcomes. The researchers also noted the importance of developing safer and more targeted drugs to reduce side effects. This study opens new possibilities for personalized cancer treatment, particularly for children with aggressive or relapsed RMS. By weakening the systems that cancer cells depend on to survive, rather than only using toxic treatments to kill them, scientists aim to develop more effective and less harmful therapies for young patients. DOI - https://doi.org/10.18632/oncotarget.28764 Correspondence to - Amit J. Sabnis - amit.sabnis@ucsf.edu Video short - https://www.youtube.com/watch?v=YsdffTkXNRQ To learn more about Oncotarget, visit https://www.oncotarget.com. Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

“You have to love what you do, especially in healthcare, and the earlier you find that, the better. So that's why I love to see HOSA helping young people find what it is that they want to do,” says Dr. David Kelly, a fellow in oculofacial surgery at University of California San Francisco and HOSA's board chair. You can still hear the excitement in Dr. Kelly's voice describing his earliest experiences with HOSA -- a student led organization with 300,000 plus members that prepares future health professionals to become leaders in international health – even though they happened sixteen years ago when he was a sophomore in highschool. Through hundreds of competitive events and hands-on projects, HOSA creates a framework for developing skills in communication, professionalism and leadership starting in middle school. Programs are offered throughout highschool and college as well, which Dr. Kelly took advantage of before becoming an active alumnus and joining the HOSA board as a way of giving back to an organization that has given so much to him. Since taking the reins as board chair last year, one key focus has been preparing to mark HOSA's 50th anniversary in 2026. Dr. Kelly sees the occasion as not only an opportunity to celebrate what HOSA has accomplished, but to ensure it is positioned to continue helping the healthcare industry tackle important challenges in the future. Examples include chronic workforce shortages and improving how clinicians communicate with patients and team members.  Join host Lindsey Smith on this uplifting Raise the Line episode for an optimistic look at the next generation of healthcare leaders.Mentioned in this episode:HOSAHOSA Alumni Registration If you like this podcast, please share it on your social channels. You can also subscribe to the series and check out all of our episodes at www.osmosis.org/raisethelinepodcast

Originally broadcast August 7, 2025 Experts who believe in the “food is medicine” concept say recent decisions made in Washington could have a devastating effect. Dr. Hilary Seligman, a nationally recognized expert on food insecurity and health outcomes at the University of California San Francisco, spoke to “Conversations on Health Care.” The interview highlighted that […] The post Food is Medicine Advocate Urges Evidence-Based Solutions Amid SNAP Cutbacks appeared first on Healthy Communities Online.

Originally broadcast August 7, 2025 Experts who believe in the “food is medicine” concept say recent decisions made in Washington could have a devastating effect. Dr. Hilary Seligman, a nationally recognized expert on food insecurity and health outcomes at the University of California San Francisco, spoke to “Conversations on Health Care.” The interview highlighted that cutbacks to the Supplemental Nutrition Assistance Program (SNAP) are projected to reduce federal spending by $186 billion over the next decade. She believes this could... Read More Read More The post Food is Medicine Advocate Urges Evidence-Based Solutions Amid SNAP Cutbacks appeared first on Healthy Communities Online.

More than half of states — from deep blue California to solidly red Louisiana — want to bring Medicaid behind bars in hopes of saving the lives of people as they leave jail and prison.Guests:Lee ReedShira Shavit, MD, Professor of Family and Community Medicine, University of California San Francisco; Executive Director, Transitions Clinic NetworkJacey Cooper, Director, California Medicaid ProgramCindy Beane, MSW, LCSW, Commissioner, West Virginia Bureau of Medical ServicesAmy Katzen, JD, MPP, Director of Policy and Strategy, Rhode Island Executive Office of Health and Human ServicesMike Levine, Medicaid Director, MassHealthDana Flannery, Former Senior Policy Advisor, Arizona Health Care Cost Containment SystemKhalil Cumberbatch, MSW, Director of Strategic Partnerships, Council on Criminal JusticeLearn more and read a full transcript on our website.Support this type of journalism today, with a gift.Follow us on Twitter. Hosted on Acast. See acast.com/privacy for more information.

In episode 53 of Going anti-Viral, Dr George Rutherford joins host Dr Michael Saag to provide an update on emerging infectious diseases. Dr Rutherford is a Professor Emeritus of Epidemiology, Preventive Medicine, Pediatrics and History at the University of California San Francisco and of the Center for Global Strategic Information and Public Health Practice at the UCSF Institute for Global Health Sciences. Dr Rutherford discusses his experience during the early onset of the COVID-19 pandemic and shares lessons learned. Dr Saag and Dr Rutherford also discuss the success of Operation Warp Speed in accelerating the development, manufacture, and distribution of COVID-19 vaccines. They also review new emerging infections like influenza A (H5N1) and arthropod viruses like West Nile, dengue, and chikungunya. Dr Saag and Dr Rutherford review efforts by the federal government to dismantle public health programs and discuss the potential impact of these cuts on future pandemics. 0:00 – Introduction1:05 – Dr Rutherford's experience during the early onset of COVID-19 5:36 – Lessons learned from the COVID-19 pandemic8:30 – The success of Operation Warp Speed10:14 – Review of new emerging infections: H5N1 influenza A and arthropod viruses like West Nile, dengue, and chikungunya17:40 – The impact on public health of misinformation on social media and the recent dismantling of public health programs22:12 – Steps needed to respond to future pandemics and how can public health continue to provide services in the face of budget cuts __________________________________________________Produced by IAS-USA, Going anti–Viral is a podcast for clinicians involved in research and care in HIV, its complications, and other viral infections. This podcast is intended as a technical source of information for specialists in this field, but anyone listening will enjoy learning more about the state of modern medicine around viral infections. Going anti-Viral's host is Dr Michael Saag, a physician, prominent HIV researcher at the University of Alabama at Birmingham, and volunteer IAS–USA board member. In most episodes, Dr Saag interviews an expert in infectious diseases or emerging pandemics about their area of specialty and current developments in the field. Other episodes are drawn from the IAS–USA vast catalogue of panel discussions, Dialogues, and other audio from various meetings and conferences. Email podcast@iasusa.org to send feedback, show suggestions, or questions to be answered on a later episode.Follow Going anti-Viral on: Apple Podcasts YouTubeXFacebookInstagram...

Normal pressure hydrocephalus (NPH) is a pathologic condition whereby excess CSF is retained in and around the brain despite normal intracranial pressure. MRI-safe programmable shunt valves allow for fluid drainage adjustment based on patients' symptoms and radiographic images. Approximately 75% of patients with NPH improve after shunt surgery regardless of shunt type or location. In this episode, Aaron Berkowitz, MD, PhD, FAAN, speaks with Kaisorn L. Chaichana, MD, author of the article “Management of Normal Pressure Hydrocephalus” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology at the University of California San Francisco in the Department of Neurology in San Francisco, California. Dr. Chaichana is a professor of neurology in the department of neurological surgery at the Mayo Clinic in Jacksonville, Florida. Additional Resources Read the article: Management of Normal Pressure Hydrocephalus Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Guest: @kchaichanamd Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Kaisorn Chaichana about his article on management of normal pressure hydrocephalus, which he wrote with Dr Jeremy Cutsforth-Gregory. The article appears in the June 2025 Continuum issue on disorders of CSF dynamics. Welcome to the podcast, and please introduce yourself to our audience. Dr Chaichana: Yeah, thank you for having me. I'm Kaisorn Chaichana. I'm a neurosurgeon at Mayo Clinic in Jacksonville, Florida. Part of my practice is doing hydrocephalus care, which includes shunts for patients with normal pressure hydrocephalus. Dr Berkowitz: Fantastic. Well, before we get into shunt considerations and NPH specifically, which I know is the focus of your article, I thought it would be a great opportunity for a neurologist to pick a neurosurgeon's brain a bit about shunts. So, to start, can you lay out for us the different types of shunts and shunt procedures, the advantages, disadvantages of each type of shunt, how you think about which shunt procedure should be used for which patient, that type of thing? Dr Chaichana: Yeah. So, there are different types of shunts, and the most common one that is used is called a ventricular peritoneal shunt. So, it has a ventricular catheter, it has a catheter that tunnels underneath the skin and it goes into the peritoneum where the fluid goes from the ventricular system into the peritoneum. Typically, the shunts are in the ventricle because that is the largest fluid-filled space in the brain. Other terminal areas include the atrium, which is really the jugular vein, and those are called ventricular atrial shunts. You can also have ventricular pleural shunts, which end in the pleural space and drain flui into the pleural space. Those are pretty much the most common ventricular shunts. There's also a lumboperitoneal shunt that drains from the lumbar spine, similar to a lumbar drain into the peritoneum. For the lumbar shunts, we don't typically have a lumbar pleural or lumbar atrial shunt just because of the pressure dynamics, because the lumbar spine is below the lung and as well as the atrium. And so, the drainage pattern is very different than ventricular peritoneal which is top to bottom. The most common shunt, why we use the ventricular peritoneal shunt the most, is because it has the most control. So, the peritoneum is set at a standard pressure in the intraabdominal pressure, whereas the ventricular atrial shunt depends on your venous return or venous pressure and your ventricular pleural shunt varies with inspiration and expiration. So, the easiest way for us to control the fluid, the ventricular system is through the ventricular peritoneal shunt. And that's why that's our most common shunt that we use. Dr Berkowitz: Fantastic. So, as you mention in the article, neurologists may be reluctant to offer a shunt to patients with NPH because many patients may not improve, or they improve only transiently; and out of fear of shunt complications. So, of course, as neurologists, we often only hear about a patient's shunt when there is a problem. So, we have this sort of biased view of seeing a lot of shunt malfunction and shunt infection. Of course, we might not see the patient if their shunt is working just fine. How common are these complications in practice, and how do you as a neurosurgeon weigh the risks against the often uncertain or transient benefits of a shunt in a patient with NPH who may be older and multiple medical comorbidities? How do you think about that and talk about it with patients? Dr Chaichana: When you hear about shunt complications, most of the shunt complications you hear about are typically in patients with congenital hydrocephalus. Those patients often require several shunt revisions just from either growing or the shunt stays in for a long time or the ventricular caliber is a lot less than some with normal pressure hydrocephalus. So, we don't really see a lot of complications with normal pressure hydrocephalus. So that shunt placement in these patients is typically pretty safe. The procedure's a relatively short procedure, around 30 minutes to 45 minutes to place a shunt, and we can control the pressure within the shunt setting so that we don't overdrain---which means too much fluid drains from the ventricular system---which can cause things like a subdural, which is probably the most common complication associated with normal pressure hydrocephalus. So, to obviate those risks, what we do is typically insert the shunt and then keep the shunt setting at a high setting. The higher the setting, the less it drains, and then we bring it slowly down based on the patient's symptoms to try to minimize the risk of this over drainage in the subdural hematoma while at the same time benefiting the patient. So, there's a concern for shunt in patients with normal pressure hydrocephalus. The concern or the complication risks are very low. The problem with normal pressure hydrocephalus, though, is that over time these patients benefit less and less from drainage or their disease process takes over. So, I do recommend placing this shunt as soon as possible just so that we can maximize their quality of life for that period of time. Dr Berkowitz: So, if I'm understanding you, then the risk of complication is more sort of due to the mechanical factors in patients with congenital hydrocephalus or sort of outgrowing the shunt, their pressure dynamics may be changing over time. And in your experience, an older patient with NPH, although they may have more medical comorbidities, the procedure itself is relatively quick and low-risk. And the actual complications due to mechanical factors, my understanding, are just much less common because the patient is obviously fully grown and they're getting one sort of procedure at one point in time and tend to need less revision, have less complication. Is that right? Dr Chaichana: Yeah, that's correct. The complication risk for normal hydrocephalus is a lot less than other types of hydrocephalus. Dr Berkowitz: That's helpful to know. While we're talking about some of these complications, let's say we're following a patient in neurology with NPH who has a shunt. What are some of the symptoms and signs of shunt malfunction or shunt infection? And what are the best studies to order to evaluate for these if we're concerned about them? Dr Chaichana: Yeah. So basically, for shunt malfunction, it's basically broken down into two categories. It's either overdrainage or underdrainage. So, underdrainage is where the shunt doesn't function enough. And so basically, they return to their state before the shunt was placed. So that could be worsening gait function, memory function, urinary incontinence are the typical symptoms we look for in patients with normal pressure hydrocephalus and underdrainage, or the shunt is not working. For patients that are having overdrainage, which is draining too much, the classic sign is typically headaches when they stand up. And the reason behind that is when there's overdrainage, there's less cerebrospinal fluid in their ventricular system, which means less intracranial pressure. So that when they stand up, the pressure differential between their head and the ground is more than when they're lying down. And because of that pressure differential, they usually have worsening headaches when standing up or sitting up. The other thing are severe headaches, which would be a sign of a subdural hematoma or focality in their neurological symptoms that could point to a subdural hematoma, such as weakness, numbness, speaking problems, depending on the hemisphere. How we work this up is, regardless if you're concerned about overdrainage or underdrainage, we usually start with a CAT scan or an MRI scan. Typically, we prefer a CAT scan because it's quicker, but the CAT scan will show us if the ventricular caliber is the same and/or the placement of the proximal catheter. So, what we look for when we see that CAT scan or that MRI to see the location of the proximal catheter to make sure it hasn't changed from any previous settings. And then we see the caliber of the ventricles. If the caliber of the ventricles is smaller, that could be a sign of overdrainage. If the caliber of the ventricles are larger, it could be a sign of underdrainage. The other thing we look for are subdural fluid collections or hydromas or subdural hematomas, which would be another sign of lower endocranial pressure, which would be a sign of overdrainage. So those are the biggest signs we look for, for underdrainage and overdrainage. Other things we can look for if we're concerned of the shunt is fractured, we do a shunt X-ray and what a shunt x-ray is is x-rays of the skull, the neck and the abdomen to see the catheter to make sure it's not kinked or fractured. If you're really concerned, you can't tell from the x-ray, another scan to order is a CT of the chest and abdomen and pelvis to look at the location of the catheter to make sure there's no brakes in the catheter, there's no fluid collections on the distal portion of the catheter, which would be a sign of shunt malfunction as well. Other tests that you can do to really exclude shunt malfunction is a shunt patency test, and what that is a nuclear medicine test where radionucleotide is injected into the valve and then the radionucleotide is traced over time or imaged through time to make sure that it's draining appropriately from the valve into the distal catheter into the peritoneum or the distal site. If there's a shunt malfunction that's not drainage, that radioisotope would remain stagnant either in the valve or in the catheter. There's overdrainage, we can't really tell, but there will be a quick drainage of the radioisotope. For shunt infection, we start with an imaging just to make sure there's not a shunt malfunction, and that usually requires cerebrospinal fluid to test. The cerebrospinal fluid can come from the valve itself, or it can come from other areas like the lumbar spine. If the lumbar spine is showing signs of shunt infection, then that usually means the shunt is infected. If the valve is aspirated with- at the bedside with a butterfly needle into the valve and that shows signs of shunt infection, that also could be a sign of infection. Dr Berkowitz: That's very helpful. You mentioned CT and shunt series. One question that often comes up when obtaining neuroimaging in patients with a shunt, who have NPH or otherwise, is whether we need to call you when we're doing an MRI to reprogram the shunt before or after. Is there a way we can know as a neurologists at the bedside or as patients carry a card, like with some devices where we know whether we have to call and bother our neurosurgery colleagues to get this MRI? Or if the radiology techs ask us, is this safe? And is the patient's shunt going to get turned off? How do we go about determining this? Dr Chaichana: Yeah, so unfortunately, a lot of patients don't carry a card. We typically offer a card when we do the shunt, but that card, there's two problems with it. One is it tells the model, but the second thing is it has to be updated any time the shunt is changed to a different setting. Oftentimes patients don't know that shunt setting, and often times they don't know that company brand that they use. There are different types of shunts with different types of settings. If there's ever concern as to what type of shunt they have, an x-ray is usually the best bet to see with a shunt series, or a skull x-ray. A lateral skull x-ray usually looks at the valve, and the valve has certain radio-dense markers that indicate what type of shunt it is. And that way you can call neurosurgery and we can always tell you what the shunt setting is before the MRI is done. Problem with an MRI scan if you do it without a shunt x-ray before is that you don't know the setting before unless the patient really knows or it's in the patient chart, and the MRI can need to change the setting. It doesn't usually turn it off, but it would change the setting, which would change the fluid dynamics within their ventricular system, which could lead to overdrainage or underdrainage. So, any time a patient needs MRI imaging, whether it's even the brain MRI, a spine MRI, or even abdominal MRI, really a shunt x-ray should be done just to see the shunt setting so that it could be returned to that setting after the MRI is done. Dr Berkowitz: So, the only way to know sort of what type of shunt it would be short of the patient knowing or the patient getting care at the same hospital where the shunt was placed and looking it up in the operative reports would be a skull film. That would then tell us what type of shunt is there and then the marking of the setting. And then we would be able to call our colleagues in neurosurgery and say, this patient is getting an MRI this is the setting, this is the type of shunt. And do we need to call you afterwards to come by and reprogram it? Is that right? Dr Chaichana: That's correct, yeah. Dr Berkowitz: Is there anything we would be able to see on there, or it's best we just- best we just call you and clarify? Dr Chaichana: The easiest thing to do is, when you get the skull x-ray, you can Google different types of shunts or search for different shunts, and they'll have markers that show the type of shunt it is as well as the setting that it's at. And just match it up with the picture. Dr Berkowitz: And as long as it's not a programmable shunt, there's no concern about doing the MRI. Is that right? Dr Chaichana: Correct. So, if it's a programmable shunt, even if it's MRI-compatible, we still like to get the setting before and make sure the setting after the MRI is the same. Nonprogrammable shunts can't be changed with MRI scans, and those don't need neurosurgery after the MRI scan, but it should be confirmed before the scan is done. Dr Berkowitz: Very helpful. Okay, so let's turn to NPH specifically. As you know, there's a lot of debate in the literature, some arguing, even, NPH might not even exist, some saying it's underdiagnosed. I think. I don't know if it was last year at our American Academy of Neurology conference or certainly in recent years, there was a pro and con debate of “we are underdiagnosing NPH” versus “we are overdiagnosing NPH.” What's your perspective as a neurosurgeon? What's the perspective in neurosurgery? Is this something we're underdiagnosing, and the times you shunt these patients you see miraculous results? Is this something that we're overdiagnosing, you get a lot of patients sent to that you think maybe won't benefit from a shunt? Or is it just really hard to say and some patients have shunt-responsive noncommunicating hydrocephalus of unclear etiology and either concurrent Parkinson's disease, Alzheimer's, cervical lumbar stenosis, neuropathy, vestibular problems, and all these other issues that play into multifactorial gait to sort of display a certain amount of the percentage of problem in a given patient or take overtime? What's your perspective if you're open to sharing it, or what's the perspective of neurosurgery? Is this debated as it is in neurology or this is just a standard thing you see and patients respond to shunt to some degree in some proportion of the time? And what are the sort of predictors you see in your experience? Dr Chaichana: Yeah, so, for me, I'd say it's too complicated for a neurosurgeon to evaluate. We rely on neurology to tell us whether or not they need a shunt. But I think the problem is, obviously, a part of the workout for at least the ones that I like to do, is that I want them to have a high-volume lumbar puncture with pre- and postgait analysis to see if there's really an objective measure of them improving. If they have an objective measure of improvement---and what's even better is that they have a subjective measure of improvement on top of the objective measure of improvement---then they benefit from a shunt. The problem is, some patients do benefit even though they don't have objective performance increases after a high-volume shunt. And those are the ones that make me the most worrisome to do the shunt, just because I don't like to do a procedure where there's no benefit for the patient. I do see, according to the literature as well, that there's around a 30 to 40%, even 50%, increase in gait function, even in patients that don't have large improvements following the high-volume lumbar puncture. And those are the most challenging patients for us as neurosurgeons because we'll put the shunt in, they say we're no better in terms of their gait, no better in terms of their urinary incontinence. We try to lower their shunt down to a certain setting and we're kind of stuck after that point. The good thing about NPH, though, is that, from the neurosurgery side, the shunt, like I said, is a pretty benign, low-risk procedure. So, we're not putting the patient through a very severe procedure to see if there's any benefit. So, in cases where we try to improve their quality of life in patients that don't have a benefit from high-volume lumbar puncture, we give them the odds of whether or not it's improving and say it might not improve. But because the procedure's minimally invasive, I think it's a good way to see if we can benefit their quality of life. Dr Berkowitz: Yeah, it's a very helpful perspective. Yeah, those are the most challenging cases on our side as well, right. If the patient- we think they may have NPH, or their gait and/or urinary and/or cognitive problems are- at least have a component of NPH that could be reversible, we certainly want to do the large volume lumbar puncture and/or consider a lumbar drain trial, all discussed in other articles and interviews for this issue of Continuum, But the really tough ones, as you said, there is this literature on patients who don't respond to the large-volume lumbar puncture for some reason but still may be shunt responsive. And despite all the imaging predictors and all the other ways we try to think about this, it's hard to know who's going to benefit. I think that's really a helpful perspective from your end that, as you say in the very beginning of your article, right, maybe there's a little bit too much fear of shunting on the neurology side because when we hear about shunts, it's often in the setting of complication. And so, we're not sort of getting the full spectrum of all the patients you shunt and you see who are doing just fine. They might not improve---the question is related to NPH---but at least they're not harmed by the shunt, and we're maybe overbiased and/or seeing a overly representative sample of negative shunt outcomes when they're actually not that common in practice. Is that a fair summary of your perspective? Dr Chaichana: Yeah, that's correct. So, I mean, complications can occur---and anytime you do a surgery, there are risks of complications---but I think they're relatively low for the benefit that we can help their quality of life. And the procedure's pretty short. So, the risk, it mostly outweighs the benefits in cases with normal pressure hydrocephalus. Dr Berkowitz: Very helpful perspective. So, well, thanks so much again. Today I've been interviewing Dr Kaisorn Chaichana about his article on management of normal pressure hydrocephalus, which he wrote with Dr Jeremy Cutsforth-Gregory. This article appears in the most recent issue of Continuum on disorders of CSF dynamics. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Our health and the health of our soil are deeply intertwined. Modern agriculture has become heavily dependent on synthetic inputs and industrial practices that strip the land of vitality, and the farmers of agency. Many farmers no longer eat what they grow, suffer from poor health, and experience alarming rates of depression and suicide. But there's a path forward: regenerative farming not only restores soil health and increases nutrient density in food, it also revitalizes rural communities and offers economic resilience. By reconnecting with natural systems and rebuilding diversity in our soil, food, and microbiomes, we reclaim both ecological balance and human well-being. In this episode, I discuss, along with Allen Williams, Dr. Daphne Miller, and Ian Somerhalder the many facets of modern-day farming, including what we need to pay attention to and why we need to reclaim our soil. Allen Williams is a founding partner of Understanding Ag, LLC and the Soil Health Academy, and is a partner in Joyce Farms, Inc. He has consulted with more than 4,000 farmers and ranchers in the US and other countries, on operations ranging from a few acres to over 1 million acres. Allen and his partners pioneered many of the early regenerative agriculture principles and practices and now teach those to farmers globally. He is a “recovering academic,” having served 15 years on the faculty at Louisiana Tech University and Mississippi State University teaching genetics and physiology. Allen has been featured in the Carbon Nation film series, Soil Carbon Cowboys, on the Dr. Oz show, ABC Food Forecast News, and in Kiss The Ground, A Regenerative Secret, The Farmer's Footprint film series, and the Sacred Cow film series.  Dr. Daphne Miller is a practicing family physician, Clinical Professor at the University of California San Francisco, and Founder of the Health from the Soil Up Initiative. She is the author of two books: The Jungle Effect: Healthiest Diets from Around the World and Farmacology: Total Health from the Soil Up. A pioneer in the “Healthy Parks, Healthy People” initiative, Miller helped build linkages between our medical system and our park system and writes her patients “park prescriptions” to get outdoors. She also developed a soil learning lab for health professionals at Paicines Ranch in Hollister California. Ian Somerhalder is an American actor, philanthropist, and entrepreneur. Best known for his iconic roles on "Lost" and "The Vampire Diaries," he is co-founder of The Absorption Company (a revolutionary supplement company formulated for increased absorption) and co-owner of Brother's Bond Bourbon. His recent work includes executive producing the documentary "Common Ground" (2023), which highlights regenerative agriculture's innovative solutions to combat climate change. This episode is brought to you by BIOptimizers. Head to bioptimizers.com/hyman and use code HYMAN10 to save 10%. Full-length episodes can be found here: Can Regenerative Agriculture Reverse Climate Change And Chronic Disease? Why Your Health Depends on the Soil Why Our Farms Hold the Key to a Healthier Future

Mifepristone is the first (and extremely safe) in two medications that people will take during a medication abortion—and access to it is under blatant attack in the courts. Dr. Ushma Upadhyay, Public Health Scientist based at University of California San Francisco, and Julia Kaye, Senior Staff Attorney with the ACLU's Reproductive Freedom Project, sit down to talk with us about recent anti-abortion propaganda and how it could be used to shape the FDA's regulations of medication abortion.A past case, Alliance for Hippocratic Medicine v. FDA, was brought by anti-abortion groups to a federal judge in Texas known to have a hostile record against abortion with the goal of challenging the FDA's mifepristone regulations. The Supreme Court ruled that these groups could not challenge the regulations in June 2024. Anti-abortion Attorneys General of Missouri, Kansas, and Idaho are now attempting to revive this litigation, called Missouri v. FDA. Meanwhile, a new report from a Project 2025-backed organization falsely states that 11% of people who have a medication abortion have a serious adverse event. Sec. Kennedy has cited this report as a basis for conducting a “complete review” of the FDA's mifepristone regulations. For more information, check out Boom! Lawyered: https://rewirenewsgroup.com/boom-lawyered/ Support the showFollow Us on Social: Twitter: @rePROsFightBack Instagram: @reprosfbFacebook: rePROs Fight Back Bluesky: @reprosfightback.bsky.social Email us: jennie@reprosfightback.comRate and Review on Apple PodcastThanks for listening & keep fighting back!

Tensions between Robert F. Kennedy Jr. and his employees at the Department of Health and Human Services are mounting, as he made a series of claims about autism this week — contradicting his agency's findings. Plus, President Donald Trump unveiled an executive order to lower drug prices as his administration explores tariffs that could raise them.Shefali Luthra of The 19th, Jessie Hellmann of CQ Roll Call, and Anna Edney of Bloomberg News join KFF Health News' Emmarie Huetteman to discuss these stories and more.Plus, KFF Health News' Julie Rovner interviews two University of California-San Francisco researchers about an upcoming Supreme Court case that could have major ramifications for preventive care. Plus, for “extra credit” the panelists suggest health policy stories they read this week that they think you should read, too: Emmarie Huetteman: KFF Health News' “States Push Medicaid Work Rules, but Few Programs Help Enrollees Find Jobs,” by Sam Whitehead, Phil Galewitz, and Katheryn Houghton. Anna Edney: ProPublica's “Unsanitary Practices Persist at Baby Formula Factory Whose Shutdown Led to Mass Shortages, Workers Say,” by Heather Vogell. Jessie Hellmann: The Hill's “Military's Use of Toxic ‘Forever Chemicals' Leaves Lasting Scars,” by Sharon Udasin and Rachel Frazin. Shefali Luthra: The 19th's “Trump's Push for ‘Beautiful Clean Coal' Could Lead to More Premature Births,” by Jessica Kutz. Visit our website to read a transcript of this episode. Hosted on Acast. See acast.com/privacy for more information.

A Buddhist doctor/nun on how we're all addicted to something—and how to reduce craving.Sister Dang Nghiem, MD, (“Sister D”) was born in 1968 in Vietnam during the Tet Offensive, the daughter of a Vietnamese mother and an American soldier. She lost her mother at the age of twelve and immigrated to the United States at the age of seventeen with her brother. Living in various foster homes, she learned English and went on to earn a medical degree from the University of California – San Francisco. After suffering further tragedy and loss, she quit her practice as a doctor to travel to Plum Village monastery in France founded by Zen Master Thich Nhat Hanh, where she was ordained a nun in 2000, and given the name Dang Nghiem, which means adornment with nondiscrimination. She is the author of a memoir, Healing: A Woman's Journey from Doctor to Nun (2010), and Mindfulness as Medicine: A Story of Healing and Spirit (2015).This episode is part of our monthlong Do Life Better series. We talk about:Sister D's Buddhist version of the 12 step program, which is a combination of two canonical buddhist lists: the 4 Noble Truths and the Eightfold PathHow willpower doesn't fit into the Buddhist path of understanding and working with addiction How to change addiction at its rootPractical applications of mindfulnessSelf-compassionThe importance of social supportHer thoughts on our relationships to our phones And moreRelated Episodes:Do Life BetterThis Episode Will Make You Stronger | Sister Dang NghiemThe Science Of Manifestation | James DotySign up for Dan's newsletter hereFollow Dan on social: Instagram, TikTokTen Percent Happier online bookstoreSubscribe to our YouTube ChannelOur favorite playlists on: Anxiety, Sleep, Relationships, Most Popular EpisodesFull Shownotes: https://www.meditatehappier.com/podcast/tph/sister-d-899See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

It's been five years since the first laboratory-confirmed case of COVID-19 in the U.S., a bleak milestone in the early days of a pandemic that touched the lives of everyone. For the lucky ones, the virus mainly meant more precautions: mask-wearing, the occasional COVID test. But for others, a COVID-19 infection turned into long COVID. This is a chronic condition that lingers long after a COVID infection, and can reduce one's ability to live their day-to-day life.It's been estimated that about 400 million people worldwide have had long COVID. Some researchers say that number is much higher. But there's a lack of research on successful treatments for long COVID.Some patients living with the condition have taken things into their own hands. A recent investigation documented the experiences of 13 long COVID patients who tried taking Paxlovid for longer than the typical 5-day course. The patients had mixed results, adding to a growing body of evidence that there will not be one silver bullet for treating the condition.Joining Ira to talk about the results are two authors of the study, who have both had long COVID for years: Dr. Alison Cohen, assistant professor of epidemiology and biostatistics at the University of California San Francisco, and Dr. Julia Moore Vogel, senior program director at Scripps Research in La Jolla, California.Transcripts for each segment will be available after the show airs on sciencefriday.com. Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.