Podcasts about rcts

Lots of talk these days about ultra-processed foods (UPFs). Along with confusion about what in the heck they are or what they're not, how bad they are for us, and what ought to be done about them. A landmark in the discussion of ultra-processed foods has been the publication of a book entitled Ultra-processed People, Why We Can't Stop Eating Food That Isn't Food. The author of that book, Dr. Chris van Tulleken, joins us today. Dr. van Tulleken is a physician and is professor of Infection and Global Health at University College London. He also has a PhD in molecular virology and is an award-winning broadcaster on the BBC. His book on Ultra-processed People is a bestseller. Interview Summary Chris, sometimes somebody comes along that takes a complicated topic and makes it accessible and understandable and brings it to lots of people. You're a very fine scientist and scholar and academic, but you also have that ability to communicate effectively with lots of people, which I very much admire. So, thanks for doing that, and thank you for joining us. Oh, Kelly, it's such a pleasure. You know, I begin some of my talks now with a clipping from the New York Times. And it's a picture of you and an interview you gave in 1995. So exactly three decades ago. And in this article, you just beautifully communicate everything that 30 years later I'm still saying. So, yeah. I wonder if communication, it's necessary, but insufficient. I think we are needing to think of other means to bring about change. I totally agree. Well, thank you by the way. And I hope I've learned something over those 30 years. Tell us, please, what are ultra-processed foods? People hear the term a lot, but I don't think a lot of people know exactly what it means. The most important thing to know, I think, is that it's not a casual term. It's not like 'junk food' or 'fast food.' It is a formal scientific definition. It's been used in hundreds of research studies. The definition is very long. It's 11 paragraphs long. And I would urge anyone who's really interested in this topic, go to the United Nations Food and Agricultural Organization website. You can type in NFAO Ultra and you'll get the full 11 paragraph definition. It's an incredibly sophisticated piece of science. But it boils down to if you as a consumer, someone listening to this podcast, want to know if the thing you are eating right now is ultra-processed, look at the ingredients list. If there are ingredients on that list that you do not normally find in a domestic kitchen like an emulsifier, a coloring, a flavoring, a non-nutritive sweetener, then that product will be ultra-processed. And it's a way of describing this huge range of foods that kind of has taken over the American and the British and in fact diets all over the world. How come the food companies put this stuff in the foods? And the reason I ask is in talks I give I'll show an ingredient list from a food that most people would recognize. And ask people if they can guess what the food is from the ingredient list. And almost nobody can. There are 35 things on the ingredient list. Sugar is in there, four different forms. And then there are all kinds of things that are hard to pronounce. There are lots of strange things in there. They get in there through loopholes and government regulation. Why are they there in the first place? So, when I started looking at this I also noticed this long list of fancy sounding ingredients. And even things like peanut butter will have palm oil and emulsifiers. Cream cheese will have xanthum gum and emulsifiers. And you think, well, wouldn't it just be cheaper to make your peanut butter out of peanuts. In fact, every ingredient is in there to make money in one of two ways. Either it drives down the cost of production or storage. If you imagine using a real strawberry in your strawberry ice cream. Strawberries are expensive. They're not always in season. They rot. You've got to have a whole supply chain. Why would you use a strawberry if you could use ethyl methylphenylglycidate and pink dye and it'll taste the same. It'll look great. You could then put in a little chunky bit of modified corn starch that'll be chewy if you get it in the right gel mix. And there you go. You've got strawberries and you haven't had to deal with strawberry farmers or any supply chain. It's just you just buy bags and bottles of white powder and liquids. The other way is to extend the shelf life. Strawberries as I say, or fresh food, real food - food we might call it rots on shelves. It decays very quickly. If you can store something at room temperature in a warehouse for months and months, that saves enormous amounts of money. So, one thing is production, but the other thing is the additives allow us to consume to excess or encourage us to consume ultra-processed food to excess. So, I interviewed a scientist who was a food industry development scientist. And they said, you know, most ultra-processed food would be gray if it wasn't dyed, for example. So, if you want to make cheap food using these pastes and powders, unless you dye it and you flavor it, it will be inedible. But if you dye it and flavor it and add just the right amount of salt, sugar, flavor enhancers, then you can make these very addictive products. So that's the logic of UPF. Its purpose is to make money. And that's part of the definition. Right. So, a consumer might decide that there's, you know, beneficial trade-off for them at the end of the day. That they get things that have long shelf life. The price goes down because of the companies don't have to deal with the strawberry farmers and things like that. But if there's harm coming in waves from these things, then it changes the equation. And you found out some of that on your own. So as an experiment you did with a single person - you, you ate ultra-processed foods for a month. What did you eat and how did it affect your body, your mood, your sleep? What happened when you did this? So, what's really exciting, actually Kelly, is while it was an n=1, you know, one participant experiment, I was actually the pilot participant in a much larger study that we have published in Nature Medicine. One of the most reputable and high impact scientific journals there is. So, I was the first participant in a randomized control trial. I allowed us to gather the data about what we would then measure in a much larger number. Now we'll come back and talk about that study, which I think was really important. It was great to see it published. So, I was a bit skeptical. Partly it was with my research team at UCL, but we were also filming it for a BBC documentary. And I went into this going I'm going to eat a diet of 80% of my calories will come from ultra-processed food for four weeks. And this is a normal diet. A lifelong diet for a British teenager. We know around 20% of people in the UK and the US eat this as their normal food. They get 80% of their calories from ultra-processed products. I thought, well, nothing is going to happen to me, a middle-aged man, doing this for four weeks. But anyway, we did it kind of as a bit of fun. And we thought, well, if nothing happens, we don't have to do a bigger study. We can just publish this as a case report, and we'll leave it out of the documentary. Three big things happened. I gained a massive amount of weight, so six kilos. And I wasn't force feeding myself. I was just eating when I wanted. In American terms, that's about 15 pounds in four weeks. And that's very consistent with the other published trials that have been done on ultra-processed food. There have been two other RCTs (randomized control trials); ours is the third. There is one in Japan, one done at the NIH. So, people gain a lot of weight. I ate massively more calories. So much so that if I'd continued on the diet, I would've almost doubled my body weight in a year. And that may sound absurd, but I have an identical twin brother who did this natural experiment. He went to Harvard for a year. He did his masters there. During his year at Harvard he gained, let's see, 26 kilos, so almost 60 pounds just living in Cambridge, Massachusetts. But how did you decide how much of it to eat? Did you eat until you just kind of felt naturally full? I did what most people do most of the time, which is I just ate what I wanted when I felt like it. Which actually for me as a physician, I probably took the breaks off a bit because I don't normally have cocoa pops for breakfast. But I ate cocoa pops and if I felt like two bowls, I'd have two bowls. It turned out what I felt like a lot of mornings was four bowls and that was fine. I was barely full. So, I wasn't force feeding myself. It wasn't 'supersize' me. I was eating to appetite, which is how these experiments run. And then what we've done in the trials. So, I gained weight, then we measured my hormone response to a meal. When you eat, I mean, it's absurd to explain this to YOU. But when you eat, you have fullness hormones that go up and hunger hormones that go down, so you feel full and less hungry. And we measured my response to a standard meal at the beginning and at the end of this four-week diet. What we found is that I had a normal response to eating a big meal at the beginning of the diet. At the end of eating ultra-processed foods, the same meal caused a very blunted rise in the satiety hormones. In the 'fullness' hormones. So, I didn't feel as full. And my hunger hormones remained high. And so, the food is altering our response to all meals, not merely within the meal that we're eating. Then we did some MRI scans and again, I thought this would be a huge waste of time. But we saw at four weeks, and then again eight weeks later, very robust changes in the communication between the habit-forming bits at the back of the brain. So, the automatic behavior bits, the cerebellum. Very conscious I'm talking to YOU about this, Kelly. And the kind of addiction reward bits in the middle. Now these changes were physiological, not structural. They're about the two bits of the brain talking to each other. There's not really a new wire going between them. But we think if this kind of communication is happening a lot, that maybe a new pathway would form. And I think no one, I mean we did this with very expert neuroscientists at our National Center for Neuroscience and Neurosurgery, no one really knows what it means. But the general feeling was these are the kind of changes we might expect if we'd given someone, or a person or an animal, an addictive substance for four weeks. They're consistent with, you know, habit formation and addiction. And the fact that they happened so quickly, and they were so robust - they remained the same eight weeks after I stopped the diet, I think is really worrying from a kid's perspective. So, in a period of four weeks, it re-altered the way your brain works. It affected the way your hunger and satiety were working. And then you ended up with this massive weight. And heaven knows what sort of cardiovascular effects or other things like that might have been going on or had the early signs of that over time could have been really pretty severe, I imagine. I think one of the main effects was that I became very empathetic with my patients. Because we did actually a lot of, sort of, psychological testing as well. And there's an experience where, obviously in clinic, I mainly treat patients with infections. But many of my patients are living with other, sort of, disorders of modern life. They live with excess weight and cardiovascular disease and type two diabetes and metabolic problems and so on. And I felt in four weeks like I'd gone from being in my early 30, early 40s at the time, I felt like I'd just gone to my early 50s or 60s. I ached. I felt terrible. My sleep was bad. And it was like, oh! So many of the problems of modern life: waking up to pee in the middle of the night is because you've eaten so much sodium with your dinner. You've drunk all this water, and then you're trying to get rid of it all night. Then you're constipated. It's a low fiber diet, so you develop piles. Pain in your bum. The sleep deprivation then makes you eat more. And so, you get in this vicious cycle where the problem didn't feel like the food until I stopped and I went cold turkey. I virtually have not touched it since. It cured me of wanting UPF. That was the other amazing bit of the experience that I write about in the book is it eating it and understanding it made me not want it. It was like being told to smoke. You know, you get caught smoking as a kid and your parents are like, hey, now you finish the pack. It was that. It was an aversion experience. So, it gave me a lot of empathy with my patients that many of those kinds of things we regard as being normal aging, those symptoms are often to do with the way we are living our lives. Chris, I've talked to a lot of people about ultra-processed foods. You're the first one who's mentioned pain in the bum as one of the problems, so thank you. When I first became a physician, I trained as a surgeon, and I did a year doing colorectal surgery. So, I have a wealth of experience of where a low fiber diet leaves you. And many people listening to this podcast, I mean, look, we're all going to get piles. Everyone gets these, you know, anal fishes and so on. And bum pain it's funny to talk about it. No, not the... it destroys people's lives, so, you know, anyway. Right. I didn't want to make light of it. No, no. Okay. So, your own experiment would suggest that these foods are really bad actors and having this broad range of highly negative effects. But what does research say about these things beyond your own personal experience, including your own research? So, the food industry has been very skillful at portraying this as a kind of fad issue. As ultra-processed food is this sort of niche thing. Or it's a snobby thing. It's not a real classification. I want to be absolutely clear. UPF, the definition is used by the World Health Organization and the United Nations Food and Agricultural Organization to monitor global diet quality, okay? It's a legitimate way of thinking about food. The last time I looked, there are more than 30 meta-analyses - that is reviews of big studies. And the kind of high-quality studies that we use to say cigarettes cause lung cancer. So, we've got this what we call epidemiological evidence, population data. We now have probably more than a hundred of these prospective cohort studies. And they're really powerful tools. They need to be used in conjunction with other evidence, but they now link ultra-processed food to this very wide range of what we euphemistically call negative health outcomes. You know, problems that cause human suffering, mental health problems, anxiety, depression, multiple forms of cancer, inflammatory diseases like Crohn's disease and ulcerative colitis, metabolic disease, cardiovascular disease, Alzheimer's and dementia. Of course, weight gain and obesity. And all cause mortality so you die earlier of all causes. And there are others too. So, the epidemiological evidence is strong and that's very plausible. So, we take that epidemiological evidence, as you well know, and we go, well look, association and causation are different things. You know, do matches cause cancer or does cigarettes cause cancer? Because people who buy lots of matches are also getting the lung cancer. And obviously epidemiologists are very sophisticated at teasing all this out. But we look at it in the context then of other evidence. My group published the third randomized control trial where we put a group of people, in a very controlled way, on a diet of either minimally processed food or ultra-processed food and looked at health outcomes. And we found what the other two trials did. We looked at weight gain as a primary outcome. It was a short trial, eight weeks. And we saw people just eat more calories on the ultra-processed food. This is food that is engineered to be consumed to excess. That's its purpose. So maybe to really understand the effect of it, you have to imagine if you are a food development engineer working in product design at a big food company - if you develop a food that's cheap to make and people will just eat loads of it and enjoy it, and then come back for it again and again and again, and eat it every day and almost become addicted to it, you are going to get promoted. That product is going to do well on the shelves. If you invent a food that's not addictive, it's very healthy, it's very satisfying, people eat it and then they're done for the day. And they don't consume it to excess. You are not going to keep your job. So that's a really important way of understanding the development process of the foods. So let me ask a question about industry and intent. Because one could say that the industry engineers these things to have long shelf life and nice physical properties and the right colors and things like this. And these effects on metabolism and appetite and stuff are unpleasant and difficult side effects, but the foods weren't made to produce those things. They weren't made to produce over consumption and then in turn produce those negative consequences. You're saying something different. That you think that they're intentionally designed to promote over consumption. And in some ways, how could the industry do otherwise? I mean, every industry in the world wants people to over consume or consume as much of their product as they can. The food industry is no different. That is exactly right. The food industry behaves like every other corporation. In my view, they commit evil acts sometimes, but they're not institutionally evil. And I have dear friends who work in big food, who work in big pharma. I have friends who work in tobacco. These are not evil people. They're constrained by commercial incentives, right? So, when I say I think the food is engineered, I don't think it. I know it because I've gone and interviewed loads of people in product development at big food companies. I put some of these interviewees in a BBC documentary called Irresistible. So rather than me in the documentary going, oh, ultra-processed food is bad. And everyone going, well, you are, you're a public health bore. I just got industry insiders to say, yes, this is how we make the food. And going back to Howard Moskovitz, in the 1970s, I think he was working for the Campbell Soup Company. And Howard, who was a psychologist by training, outlined the development process. And what he said was then underlined by many other people I've spoken to. You develop two different products. This one's a little bit saltier than the next, and you test them on a bunch of people. People like the saltier ones. So now you keep the saltier one and you develop a third product and this one's got a bit more sugar in it. And if this one does better, well you keep this one and you keep AB testing until you get people buying and eating lots. And one of the crucial things that food companies measure in product development is how fast do people eat and how quickly do they eat. And these kind of development tools were pioneered by the tobacco industry. I mean, Laura Schmidt has done a huge amount of the work on this. She's at University of California, San Francisco (UCSF), in California. And we know the tobacco industry bought the food industry and for a while in the '80s and '90s, the biggest food companies in the world were also the biggest tobacco companies in the world. And they used their flavor molecules and their marketing techniques and their distribution systems. You know, they've got a set of convenience tools selling cigarettes all over the country. Well, why don't we sell long shelf-life food marketed in the same way? And one thing that the tobacco industry was extremely good at was figuring out how to get the most rapid delivery of the drug possible into the human body when people smoke. Do you think that some of that same thing is true for food, rapid delivery of sugar, let's say? How close does the drug parallel fit, do you think? So, that's part of the reason the speed of consumption is important. Now, I think Ashley Gearhardt has done some of the most incredible work on this. And what Ashley says is we think of addictive drugs as like it's the molecule that's addictive. It's nicotine, it's caffeine, cocaine, diamorphine, heroin, the amphetamines. What we get addicted to is the molecule. And that Ashley says no. The processing of that molecule is crucially important. If you have slow-release nicotine in a chewing gum, that can actually treat your nicotine addiction. It's not very addictive. Slow-release amphetamine we use to treat children with attention and behavioral problems. Slow-release cocaine is an anesthetic. You use it for dentistry. No one ever gets addicted to dental anesthetics. And the food is the same. The rewarding molecules in the food we think are mainly the fat and the sugar. And food that requires a lot of chewing and is slow eaten slowly, you don't deliver the reward as quickly. And it tends not to be very addictive. Very soft foods or liquid foods with particular fat sugar ratios, if you deliver the nutrients into the gut fast, that seems to be really important for driving excessive consumption. And I think the growing evidence around addiction is very persuasive. I mean, my patients report feeling addicted to the food. And I don't feel it's legitimate to question their experience. Chris, a little interesting story about that concept of food and addiction. So going back several decades I was a professor at Yale, and I was teaching a graduate course. Ashley Gerhardt was a student in that course. And, she was there to study addiction, not in the context of food, but I brought up the issue of, you know, could food be addictive? There's some interesting research on this. It's consistent with what we're hearing from people, and that seems a really interesting topic. And Ashley, I give her credit, took this on as her life's work and now she's like the leading expert in the world on this very important topic. And what's nice for me to recall that story is that how fast the science on this is developed. And now something's coming out on this almost every day. It's some new research on the neuroscience of food and addiction and how the food is hijacking in the brain. And that whole concept of addiction seems really important in this context. And I know you've talked a lot about that yourself. She has reframed, I think, this idea about the way that addictive substances and behaviors really work. I mean it turns everything on its head to go the processing is important. The thing the food companies have always been able to say is, look, you can't say food is addictive. It doesn't contain any addictive molecules. And with Ashley's work you go, no, but the thing is it contains rewarding molecules and actually the spectrum of molecules that we can find rewarding and we can deliver fast is much, much broader than the traditionally addictive substances. For policy, it's vital because part of regulating the tobacco industry was about showing they know they are making addictive products. And I think this is where Ashley's work and Laura Schmidt's work are coming together. With Laura's digging in the tobacco archive, Ashley's doing the science on addiction, and I think these two things are going to come together. And I think it's just going to be a really exciting space to watch. I completely agree. You know when most people think about the word addiction, they basically kind of default to thinking about how much you want something. How much, you know, you desire something. But there are other parts of it that are really relevant here too. I mean one is how do you feel if you don't have it and sort of classic withdrawal. And people talk about, for example, being on high sugar drinks and stopping them and having withdrawal symptoms and things like that. And the other part of it that I think is really interesting here is tolerance. You know whether you need more of the substance over time in order to get the same reward benefit. And that hasn't been studied as much as the other part of addiction. But there's a lot to the picture other than just kind of craving things. And I would say that the thing I like about this is it chimes with my. Personal experience, which is, I have tried alcohol and cigarettes and I should probably end that list there. But I've never had any real desire for more of them. They aren't the things that tickle my brain. Whereas the food is a thing that I continue to struggle with. I would say in some senses, although I no longer like ultra-processed food at some level, I still want it. And I think of myself to some degree, without trivializing anyone's experience, to some degree I think I'm in sort of recovery from it. And it remains that tussle. I mean I don't know what you think about the difference between the kind of wanting and liking of different substances. Some scientists think those two things are quite, quite different. That you can like things you don't want, and you can want things you don't like. Well, that's exactly right. In the context of food and traditional substances of abuse, for many of them, people start consuming because they produce some sort of desired effect. But that pretty quickly goes away, and people then need the substance because if they don't have it, they feel terrible. So, you know, morphine or heroin or something like that always produces positive effects. But that initial part of the equation where you just take it because you like it turns into this needing it and having to have it. And whether that same thing exists with food is an interesting topic. I think the other really important part of the addiction argument in policy terms is that one counterargument by industrial scientists and advocates is by raising awareness around ultra-processed food we are at risk of driving, eating disorders. You know? The phenomenon of orthorexia, food avoidance, anorexia. Because all food is good food. There should be no moral value attached to food and we mustn't drive any food anxiety. And I think there are some really strong voices in the United Kingdom Eating Disorder scientists. People like Agnes Ayton, who are starting to say, look, when food is engineered, using brain scanners and using scientific development techniques to be consumed to excess, is it any wonder that people develop a disordered relationship with the food? And there may be a way of thinking about the rise of eating disorders, which is parallel to the rise of our consumption of ultra-processed food, that eating disorders are a reasonable response to a disordered food environment. And I think that's where I say all that somewhat tentatively. I feel like this is a safe space where you will correct me if I go off piste. But I think it's important to at least explore that question and go, you know, this is food with which it is very hard, I would say, to have a healthy relationship. That's my experience. And I think the early research is bearing that out. Tell us how these foods affect your hunger, how full you feel, your microbiome. That whole sort of interactive set of signals that might put people in harmony with food in a normal environment but gets thrown off when the foods get processed like this. Oh, I love that question. At some level as I'm understanding that question, one way of trying to answer that question is to go, well, what is the normal physiological response to food? Or maybe how do wild animals find, consume, and then interpret metabolically the food that they eat. And it is staggering how little we know about how we learn what food is safe and what food nourishes us. What's very clear is that wild mammals, and in fact all wild animals, are able to maintain near perfect energy balance. Obesity is basically unheard of in the wild. And, perfect nutritional intake, I mean, obviously there are famines in wild animals, but broadly, animals can do this without being literate, without being given packaging, without any nutritional advice at all. So, if you imagine an ungulate, an herbivore on the plains of the Serengeti, it has a huge difficulty. The carnivore turning herbivore into carnivore is fairly easy. They're made of the same stuff. Turning plant material into mammal is really complicated. And somehow the herbivore can do this without gaining weight, whilst maintaining total precision over its selenium intake, its manganese, its cobalt, its iron, all of which are terrible if you have too little and also terrible if you have too much. We understand there's some work done in a few wild animals, goats, and rats about how this works. Clearly, we have an ability to sense the nutrition we want. What we understand much more about is the sort of quantities needed. And so, we've ended up with a system of nutritional advice that says, well, just eat these numbers. And if you can stick to the numbers, 2,500 calories a day, 2300 milligrams of sodium, no more than 5% of your calories from free sugar or 10%, whatever it is, you know, you stick to these numbers, you'll be okay. And also, these many milligrams of cobalt, manganese, selenium, iron, zinc, all the rest of it. And obviously people can't really do that even with the packaging. This is a very long-winded answer. So, there's this system that is exquisitely sensitive at regulating micronutrient and energy intake. And what we understand, what the Academy understands about how ultra-processed food subverts this is, I would say there are sort of three or four big things that ultra-processed does that real food doesn't. It's generally very soft. And it's generally very energy dense. And that is true of even the foods that we think of as being healthy. That's like your supermarket whole grain bread. It's incredibly energy dense. It's incredibly soft. You eat calories very fast, and this research was done in the '90s, you know we've known that that kind of food promotes excessive intake. I guess in simple terms, and you would finesse this, you consume calories before your body has time to go, well, you've eaten enough. You can consume an excess. Then there's the ratios of fat, salt, and sugar and the way you can balance them, and any good cook knows if you can get the acid, fat, salt, sugar ratios right, you can make incredibly delicious food. That's kind of what I would call hyper palatability. And a lot of that work's being done in the states (US) by some incredible people. Then the food may be that because it's low in fiber and low in protein, quite often it's not satiating. And there may be, because it's also low in micronutrients and general nutrition, it may be that, and this is a little bit theoretical, but there's some evidence for this. Part of what drives the excess consumption is you're kind of searching for the nutrients. The nutrients are so dilute that you have to eat loads of it in order to get enough. Do you think, does that, is that how you understand it? It does, it makes perfect sense. In fact, I'm glad you brought up one particular issue because part of the ultra-processing that makes foods difficult for the body to deal with involves what gets put in, but also what gets taken out. And there was a study that got published recently that I think you and I might have discussed earlier on American breakfast cereals. And this study looked at how the formulation of them had changed over a period of about 20 years. And what they found is that the industry had systematically removed the protein and the fiber and then put in more things like sugar. So there, there's both what goes in and what gets taken out of foods that affects the body in this way. You know, what I hear you saying, and what I, you know, believe myself from the science, is the body's pretty capable of handling the food environment if food comes from the natural environment. You know, if you sit down to a meal of baked chicken and some beans and some leafy greens and maybe a little fruit or something, you're not going to overdo it. Over time you'd end up with the right mix of nutrients and things like that and you'd be pretty healthy. But all bets are off when these foods get processed and engineered, so you over consume them. You found that out in the experiment that you did on yourself. And then that's what science shows too. So, it's not like these things are sort of benign. People overeat them and they ought to just push away from the table. There's a lot more going on here in terms of hijacking the brain chemistry. Overriding the body signals. Really thwarting normal biology. Do you think it's important to add that we think of obesity as being the kind of dominant public health problem? That's the thing we all worry about. But the obesity is going hand in hand with stunting, for example. So, height as you reach adulthood in the US, at 19 US adults are something like eight or nine centimeters shorter than their counterparts in Northern Europe, Scandinavia, where people still eat more whole food. And we should come back to that evidence around harms, because I think the really important thing to say around the evidence is it has now reached the threshold for causality. So, we can say a dietary pattern high in ultra-processed food causes all of these negative health outcomes. That doesn't mean that any one product is going to kill you. It just means if this is the way you get your food, it's going to be harmful. And if all the evidence says, I mean, we've known this for decades. If you can cook the kind of meal, you just described at home, which is more or less the way that high income people eat, you are likely to have way better health outcomes across the board. Let me ask you about the title of your book. So, the subtitle of your book is Why We Can't Stop Eating Food That Isn't Food. So, what is it? The ultra-processed definition is something I want to pay credit for. It's really important to pay a bit of credit here. Carlos Montero was the scientist in Brazil who led a team who together came up with this definition. And, I was speaking to Fernanda Rauber who was on that team, and we were trying to discuss some research we were doing. And every time I said food, she'd correct me and go, it is not, it's not food, Chris. It's an industrially produced edible substance. And that was a really helpful thing for me personally, it's something it went into my brain, and I sat down that night. I was actually on the UPF diet, and I sat down to eat some fried chicken wings from a popular chain that many people will know. And was unable to finish them. I think our shared understanding of the purpose of food is surely that its purpose is to nourish us. Whether it's, you know, sold by someone for this purpose, or whether it's made by someone at home. You know it should nourish us spiritually, socially, culturally, and of course physically and mentally. And ultra-processed food nourishes us in no dimension whatsoever. It destroys traditional knowledge, traditional land, food culture. You don't sit down with your family and break, you know, ultra-processed, you know, crisps together. You know, you break bread. To me that's a kind of very obvious distortion of what it's become. So, I don't think it is food. You know, I think it's not too hard of a stretch to see a time when people might consider these things non-food. Because if you think of food, what's edible and whether it's food or not is completely socially constructed. I mean, some parts of the world, people eat cockroaches or ants or other insects. And in other parts of the world that's considered non-food. So just because something's edible doesn't mean that it's food. And I wonder if at some point we might start to think of these things as, oh my God, these are awful. They're really bad for us. The companies are preying on us, and it's just not food. And yeah, totally your book helps push us in that direction. I love your optimism. The consumer facing marketing budget of a big food company is often in excess of $10 billion a year. And depends how you calculate it. I'll give you a quick quiz on this. So, for a while, the Robert Wood Johnson Foundation was by far the biggest funder of research in the world on childhood obesity. And they were spending $500 million a year to address this problem. Just by which day of the year the food industry has already spent $500 million just advertising just junk food just to children. Okay, so the Robert V. Wood Foundation is spending it and they were spending that annually. Annually, right. So, what's, by what day of the year is the food industry already spent that amount? Just junk food advertising just to kids. I'm going to say by somewhere in early spring. No. January 4th. I mean, it's hysterical, but it's also horrifying. So, this is the genius of ultra-processed food, of the definition and the science, is that it creates this category which is discretionary. And so at least in theory, of course, for many people in the US it's not discretionary at all. It's the only stuff they can afford. But this is why the food industry hate it so much is because it offers the possibility of going, we can redefine food. And there is all this real food over there. And there is this UPF stuff that isn't food over here. But industry's very sophisticated, you know. I mean, they push back very hard against me in many different ways and forms. And they're very good at going, well, you're a snob. How dare you say that families with low incomes, that they're not eating food. Are you calling them dupes? Are you calling them stupid? You know, they're very, very sophisticated at positioning. Isn't it nice how concerned they are about the wellbeing of people without means? I mean they have created a pricing structure and a food subsidy environment and a tax environment where essentially people with low incomes in your country, in my country, are forced to eat food that harms them. So, one of the tells I think is if you're hearing someone criticize ultra-processed food, and you'll read them in the New York Times. And often their conflicts of interest won't be reported. They may be quite hidden. The clue is, are they demanding to seriously improve the food environment in a very clear way, or are they only criticizing the evidence around ultra-processed food? And if they're only criticizing that evidence? I'll bet you a pound to a pinch of salt they'll be food-industry funded. Let's talk about that. Let's talk about that a little more. So, there's a clear pattern of scientists who take money from industry finding things that favor industry. Otherwise, industry wouldn't pay that money. They're not stupid in the way they invest. And, you and I have talked about this before, but we did a study some years ago where we looked at industry and non-industry funded study on the health effects of consuming sugar sweetened beverages. And it's like the ocean parted. It's one of my favorites. And it was something like 98 or 99% of the independently funded studies found that sugar sweetened beverages do cause harm. And 98 or 99% of the industry funded studies funded by Snapple and Coke and a whole bunch of other companies found that they did not cause harm. It was that stark, was it? It was. And so you and I pay attention to the little print in these scientific studies about who's funded them and who might have conflicts of interest. And maybe you and I and other people who follow science closely might be able to dismiss those conflicted studies. But they have a big impact out there in the world, don't they? I had a meeting in London with someone recently, that they themselves were conflicted and they said, look, if a health study's funded by a big sugary drink company, if it's good science, that's fine. We should publish it and we should take it at face value. And in the discussion with them, I kind of accepted that, we were talking about other things. And afterwards I was like, no. If a study on human health is funded by a sugary drink corporation, in my opinion, we could just tear that up. None of that should be published. No journals should publish those studies and scientists should not really call themselves scientists who are doing it. It is better thought of as marketing and food industry-funded scientists who study human health, in my opinion, are better thought of as really an extension of the marketing division of the companies. You know, it's interesting when you talk to scientists, and you ask them do people who take money from industry is their work influenced by that money? They'll say yes. Yeah, but if you say, but if you take money from industry, will your work be influenced? They'll always say no. Oh yeah. There's this tremendous arrogance, blind spot, whatever it is that. I can remain untarnished. I can remain objective, and I can help change the industry from within. In the meantime, I'm having enough money to buy a house in the mountains, you know, from what they're paying me, and it's really pretty striking. Well, the money is a huge issue. You know, science, modern science it's not a very lucrative career compared to if someone like you went and worked in industry, you would add a zero to the end of your salary, possibly more. And the same is true of me. I think one of the things that adds real heft to the independent science is that the scientists are taking a pay cut to do it. So how do children figure in? Do you think children are being groomed by the industry to eat these foods? A senator, I think in Chile, got in hot water for comparing big food companies to kind of sex offenders. He made, in my view, a fairly legitimate comparison. I mean, the companies are knowingly selling harmful products that have addictive properties using the language of addiction to children who even if they could read warning labels, the warning labels aren't on the packs. So, I mean, we have breakfast cereals called Crave. We have slogans like, once you stop, once you pop, you can't stop. Bet you can't just eat one. Yeah, I think it is predatory and children are the most vulnerable group in our society. And you can't just blame the parents. Once kids get to 10, they have a little bit of money. They get their pocket money, they're walking to school, they walk past stores. You know, you have to rely on them making decisions. And at the moment, they're in a very poor environment to make good decisions. Perhaps the most important question of all what can be done. So, I'm speaking to you at a kind of funny moment because I've been feeling that a lot of my research and advocacy, broadcasting... you know, I've made documentaries, podcasts, I've written a book, I've published these papers. I've been in most of the major newspapers and during the time I've been doing this, you know, a little under 10 years I've been really focused on food. Much less time than you. Everything has got worse. Everything I've done has really failed totally. And I think this is a discussion about power, about unregulated corporate power. And the one glimmer of hope is this complaint that's been filed in Pennsylvania by a big US law firm. It's a very detailed complaint and some lawyers on behalf of a young person called Bryce Martinez are suing the food industry for causing kidney problems and type two diabetes. And I think that in the end is what's going to be needed. Strategic litigation. That's the only thing that worked with tobacco. All of the science, it eventually was useful, but the science on its own and the advocacy and the campaigning and all of it did no good until the lawyers said we would like billions and billions of dollars in compensation please. You know, this is an exciting moment, but there were a great many failed lawsuits for tobacco before the master settlement agreement in the '90s really sort of changed the game. You know, I agree with you. Are you, are you optimistic? I mean, what do you think? I am, and for exactly the same reason you are. You know, the poor people that worked on public health and tobacco labored for decades without anything happening long, long after the health consequences of cigarette smoking were well known. And we've done the same thing. I mean, those us who have been working in the field for all these years have seen precious little in the ways of policy advances. Now tobacco has undergone a complete transformation with high taxes on cigarettes, and marketing restrictions, and non-smoking in public places, laws, and things like that, that really have completely driven down the consumption of cigarettes, which has been a great public health victory. But what made those policies possible was the litigation that occurred by the state attorneys general, less so the private litigating attorneys. But the state attorneys general in the US that had discovery documents released. People began to understand more fully the duplicity of the tobacco companies. That gave cover for the politicians to start passing the policies that ultimately made the big difference. I think that same history is playing out here. The state attorneys general, as we both know, are starting to get interested in this. I say hurray to that. There is the private lawsuit that you mentioned, and there's some others in the mix as well. I think those things will bring a lot of propel the release of internal documents that will show people what the industry has been doing and how much of this they've known all along. And then all of a sudden some of these policy things like taxes, for example, on sugared beverages, might come in and really make a difference. That's my hope. But it makes me optimistic. Well, I'm really pleased to hear that because I think in your position it would be possible. You know, I'm still, two decades behind where I might be in my pessimism. One of the kind of engines of this problem to me is these conflicts of interest where people who say, I'm a physician, I'm a scientist, I believe all this. And they're quietly paid by the food industry. This was the major way the tobacco industry had a kind of social license. They were respectable. And I do hope the lawsuits, one of their functions is it becomes a little bit embarrassing to say my research institute is funded [by a company that keeps making headlines every day because more documents are coming out in court, and they're being sued by more and more people. So, I hope that this will diminish the conflict, particularly between scientists and physicians in the food industry. Because that to me, those are my biggest opponents. The food industry is really nice. They throw money at me. But it's the conflicted scientists that are really hard to argue with because they appear so respectable. Bio Dr. Chris van Tulleken is a physician and a professor of Infection and Global Health at University College London. He trained at Oxford and earned his PhD in molecular virology from University College London. His research focuses on how corporations affect human health especially in the context of child nutrition and he works with UNICEF and The World Health Organization on this area. He is the author of a book entitled Ultraprocessed People: Why We Can't Stop Eating Food That Isn't Food. As one of the BBC's leading broadcasters for children and adults his work has won two BAFTAs. He lives in London with his wife and two children.

Dr. Chad Kollas has spent more than two decades challenging myths and misinformation about opioids in pain care. In this episode, he joins us to break down the FDA's latest opioid label changes, explain why they matter for patients, and share his perspective as a palliative care physician who has been on the frontlines of this debate since the early 2000s.We talk about:The significance of the FDA's new opioid labelThe ethical failures of randomized controlled trials (RCTs) in pain patientsHow propaganda has shaped the narrative around opioidsWhat patients and providers need to know moving forwardIf you've ever wondered how we got here and what hope there is for change you won't want to miss this conversation.Dr. Chad Kollas' study: https://pmc.ncbi.nlm.nih.gov/articles/PMC10790545/

Reflections on Fatherhood – April 17, 2025I wrote this on the day Brady was born, but I didn't feel comfortable releasing it until now. I'm embarrassed to admit how often I write a post but I'm too much of a coward to release it because of fear. Anyway, here it is…On Parenting, Policy, and TrustI'm running into this again and again. I'm being told how to raise my kid by people who speak with total confidence but don't have the evidence to back it up. First it was postpartum exercise. Then co-sleeping. Then newborn sleep, feeding, meds, positions. All of it.Take the postpartum workout restriction. Laken was told not to exercise for six weeks after birth. No nuance. Just a flat-out rule. But when I dug into it, I couldn't find any randomized controlled trials (RCTs) proving that intense exercise before six weeks postpartum causes harm. Most studies actually show that light to moderate activity within 2–4 weeks is not only safe but also beneficial, especially for mental health. The PAMELA trial, for example, found improved mood and no complications from early activity. Another study in Frontiers in Psychology showed reduced anxiety with postpartum aquatic exercise starting around 4–6 weeks. No RCTs showed harm from earlier or more intense activity. None.The six-week rule is based on tradition and expert opinion, not hard data. It reminds me of old hip replacement protocols, when doctors used to keep patients immobile for weeks. That delayed healing. Now, patients get up within hours. What if postpartum care is stuck in the same outdated thinking?Then there's co-sleeping. We were told that if we sleep with Brady, he could die. Period. Again, it sounded final. But when I dug deeper, I found that most of the data comes from unsafe environments, sofas, intoxicated parents, loose bedding, or premature babies. I couldn't find a single documented case where a full-term baby died while sleeping in a safe bed with a healthy, sober, non-smoking, alert parent in a safe setup. Not one. Yet we're treated like we're reckless just for asking the question.The deeper I look, the more I realize these aren't solid, research-backed facts. They're guidelines written by committees, made for the lowest common denominator, passed off as “science.” They're based on risk reduction for a system that assumes most people won't take care of themselves, won't ask questions, won't think for themselves. So they make rules to cover the masses and act like they apply to everyone.They treat me like I'm stupid, reckless, or drunk. I'm not. I'm a fully capable, sober, alert father. And I want real information, not patronizing lectures and oversimplified warnings. I want the truth. Not broad strokes built for fear and liability.It feels like collectivism disguised as care. A nanny state in a lab coat. Disconnected from tradition, from cultural wisdom, from what parents have done for thousands of years. And it leaves no space for personal responsibility, nuance, or trust.I don't want rules made for people who aren't paying attention.I'm paying attention. I'm asking questions. I'm choosing to be fully present.That should count for something.Year Of The Opposite - Travis Stoliker's Substack is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. Get full access to Year Of The Opposite - Travis Stoliker's Substack at www.yearoftheopposite.com/subscribe

A recent network meta-analysis published in the journal Nutrients systematically compared the effectiveness of seven common nutritional supplements for treating knee osteoarthritis (KOA). The analysis included 39 randomized controlled trials (RCTs) with a total of 4,599 patients. Researchers evaluated the impact of eggshell membrane, vitamin D, Boswellia, curcumin, ginger, krill oil, and collagen against a placebo for improving pain, stiffness, and function. The results showed that compared to a placebo, Boswellia provided statistically significant improvements across all measures, including WOMAC pain (mean difference [MD] = -10.58), stiffness (MD = -9.47), function (MD = -14.00), and VAS pain (MD = -17.26). Bayesian analysis consistently ranked Boswellia as the most likely to be the best option for pain and stiffness relief. Other supplements also showed benefits; krill oil, curcumin, and collagen significantly improved function, while collagen, curcumin, and ginger significantly reduced VAS pain scores. Importantly, no supplement was associated with an increase in adverse events compared to the placebo. The authors conclude that certain supplements, particularly Boswellia, appear to be effective and well-tolerated for managing KOA symptoms.Disclaimers:• "This information is for educational purposes only and should not be interpreted as medical advice." • "The study discussed is a network meta-analysis of randomized controlled trials conducted on humans. Further research may be needed to confirm these findings." • "Always consult with a qualified healthcare professional before making any changes to your diet, supplement regimen, or treatment plan, especially if you have a medical condition or are taking medications." #Boswellia #Curcumin #Collagen #KrillOil #GingerZhang Y, Gui Y, Adams R, Farragher J, Itsiopoulos C, Bow K, Cai M, Han J. Comparative Effectiveness of Nutritional Supplements in the Treatment of Knee Osteoarthritis: A Network Meta-Analysis. Nutrients. 2025; 17(15):2547. https://doi.org/10.3390/nu17152547Alchepharma,Ralph Turchiano,citation,research,study,Knee osteoarthritis,nutritional supplements,Boswellia,curcumin,collagen,ginger,krill oil,eggshell membrane,vitamin D,network meta-analysis,randomized controlled trials,WOMAC pain,WOMAC stiffness,WOMAC function,VAS pain,joint pain relief,osteoarthritis treatment,supplement efficacy,anti-inflammatory supplements

เวลานั่งฟังการวิเคราะห์งานวิจัยเรื่องเดียวกัน ระหว่าง Health Influencer 2 คน น้องๆจะได้เห็นความสามารถที่ต่างกันอย่างชัดเจน จนทำให้น้องๆรู้ได้ด้วยตัวเองว่าควรจะเชื่อใคร เมื่อวานพี่ปุ๋มเสร็จภารกิจงาน เข้ามานั่งในรถเตรียมขับกลับบ้าน เปิด YT เจอ vdo ล่าสุด Dr.Gil Carvalho MD., PhD เจ้าของช่อง Nutrition Made Simple วิเคราะห์ Systematic review and meta-analysis ล่าสุดปี 2025 ชื่อ Saturated Fat Restriction for Cardiovascular Disease Prevention: A Systematic Review and Meta-Analysis of Randomized Controlled Trials โดย Satoru Yamada et al. (จริงๆพี่สรุปคร่าวๆ meta-analysis ฉบับนี้ไปแล้วในไลฟ์#98 ล่าสุด กลับไปดูย้อนหลังกันได้ค่ะ) แต่ Gil สรุปได้เฉียบมากค่ะพี่ Yamada เค้าสรุป meta-analysis ฉบับนี้ของเค้าแบบ bold statement มากค่ะว่า “The evidence available from RCTs does not support saturated fat restriction for the prevention of cardiovascular disease”“หลักฐานจาก randomized controlled trials ที่มีอยู่ ณ ขณะนี้ ไม่ได้สนับสนุนการจำกัดการบริโภคไขมันอิ่มตัวว่าจะช่วยป้องกันโรคหลอดเลือดหัวใจได้” แล้วพี่ก็จำได้ว่า Nick Norwitz ซึ่งถือว่าเป็นตัว Top เรื่องความรู้วิชาการของกลุ่มที่ปฏิเสธอันตรายของกรดไขมันอิ่มตัวกับการเพิ่มความเสี่ยงโรคหลอดเลือดหัวใจ ด้วยทึ่เขากำลังศึกษาปี 4 คณะแพทยศาสตร์อยู่ที่ Harvard Medical School และจบ PhD. Biochemistry หรือ Physioligy พี่จำไม่ได้ชัดเจนจาก Oxford University ทำ vdo สรุป meta-analysis ฉบับนี้แบบอวยยศสุดๆ พี่ก็เลยตัดสินใจฟัง Nick วิเคราะห์ meta-analysis ฉบับเดียวกันนี้อย่างตั้งใจเพื่อเปรียบเทียบกับ Gil แล้วพี่ก็นั่งหัวเราะอยู่คนเดียวในรถ #อะไรของมึง ขับรถกลับบ้านมาแวะกินข้าวนั่งเขียนโพสต์นี้ที่จุดพักรถ พี่ต้องรีบเขียน เดี๋ยวลืม 5555 ขอเขียนเบื้องต้นก่อนว่า ถ้าใครก็ตามที่มี critical thinking จะเห็นความแตกต่างในความสามารถวิเคราะห์งานวิจัยฉบับเดียวกัน แต่คุณภาพการวิเคราะห์ต่างกันแบบเกรด A (Gil) กับ เกรด C (Nick) ชัดเจน พี่วาง vdo ของทั้ง 2 คนไว้ในคอมเมนท์นะคะ ซึ่ง Gil ให้ความกระจ่างสุดๆว่า meta-analysis ของ Yamada 2025 ฉบับนี้ ซึ่ง include RCTs ทั้งหมด 9 trials ทำไมถึง Garbage in-Garbage out ในขณะที่ Nick Norwitz ไม่วิเคราะห์อะไรเกี่ยวกับคุณภาพของ RCT ทั้ง 9 ฉบับที่เข้า inclusion criteria ซึ่ง Yamada นำมาใส่ใน meta-analysis ฉบับนี้เลย มีแต่อวยยศ สรรเสริญ meta-analysis ฉบับนี้โดยไม่อธิบายว่าทำไมสรรเสริญ ดียังไงเหรอ นอกจากแค่เป็น meta-analysis ของ RCTs ส่วนการวิเคราะห์ของ Nick ที่เหลือมีแต่ “เรื่องเล่า” 4 เหตุผลหลักที่ทำให้กรดไขมันอิ่มตัวถูกทำให้เป็นผู้ร้าย ซึ่งก็หนีไม่พ้น Conspiracy theory บริษัทยาหลอกลวงประชาชน จะได้ขายยาลดไขมันต่อไป ไม่มีใครกล้าหาญจะขัดแย้งความเชื่อกระแสหลัก (นอกจากเค้า ) ที่พี่ไม่ได้ให้เกรด D เพราะพูดมีเหตุผลอยู่ 2 เรื่องเกี่ยวกับกรดไขมันอิ่มตัว เดี๋ยวไปอธิบายใน streamyard ค่ะ ขอสรุปอีกครั้งว่า ด้วย totality of evidences การแทนที่กรดไขมันอิ่มตัวด้วยกรดไขมันไม่อิ่มตัวเชิงซ้อน ลดระดับ LDL-C —> ลดความเสี่ยงโรคหลอดเลือดหัวใจค่ะ #หาคำตอบสุขภาพจากงานวิจัยไม่ใช่จากเรื่องเล่า #FatOutHealthspans

In this episode, Drs Trexler and Helms discuss various topics including updates on Eric's surgery, the valuable (but very modest) effects of protein intake on muscle gains, incontinence after contest prep,  the relationship between sleep quality and nutrient timing, the recent ban on smelling salts in the NFL, and more. Time stamps: 00:00 Introduction 01:11  Preview of next week's episode (non-responders, hyper-responders, etc) 07:01 Trex's surgery update 12:11 Discussion on Protein Meta-Analyses and Research Updates (how much does protein intake actually matter for gains?) 33:10 Why meta-analyses differ from RCTs in terms of "expiration dates" 44:15 The Impact of Training vs. Nutrition (for muscle growth) 51:41 Q&A: Supplementation for Lifters (and Specifically Vegans Who Lift) 55:49 Incontinence, Increased Urine Output, and Contest Prep 59:16 Chrono Nutrition and Sleep Quality 01:11:28 The Role of Smelling Salts in Sports Performance (and Football)

Nesse episódio, Leandro Lima, médico clínico e gastroenterologista e editor do Portal Afya, fala sobre sobre a vitamina E e seu impacto na doença hepática esteatótica associada à disfunção metabólica (MASLD). O especialista ainda analisa uma revisão publicada na Cochrane que avaliou os efeitos da vitamina E em mais de 3.500 pacientes com MASLD provenientes de 16 RCTs.Confira esse e outros posts no ⁠Portal Afya⁠ e siga nossas redes sociais!⁠Facebook⁠⁠Instagram⁠⁠Linkedin⁠⁠Twitter

In the second of our two podcasts with Francis Annan of UC Berkeley on his research on mobile money first in Ghana, then beyond, Tim Phillips discusses how he worked with commercial providers, not just to set up the RCTs designed to investigate the extent and reduce financial fraud, but to ensure that the insights could be scaled up.  While contacting sceptical commercial providers can often meet with little or no response, he says, the ability to frame research in a way that makes them realise the commercial value as well as the social value can get, and keep, their attention – and lead to a long-run partnership that achieves more than working independently or through regulators. 

ไลฟ์ #97: ประวัติศาสตร์ของ ไขมัน คอเลสเตอรอล กับ โรคหลอดเลือดหัวใจวันอาทิตย์ 20 ก.ค. 2568เวลา 18.00 น.เมื่อเร็วๆนี้ มี A Systematic Review and Meta-analysis of Randomized Controlled Trials ตีพิมพ์เมื่อวันที่ 28 เม.ย. 2568 ใน Japan Medical Association and the Japanese Association of Medical Sciences ซึ่งสรุปอย่างที่เรียกว่า “Bold statement” มากว่า “ข้อมูลจาก paper ฉบับนี้บ่งชี้ว่า ไม่ควรแนะนำให้ลดการลดการบริโภคไขมันอิ่มตัวเพื่อการป้องกันโรคหลอดเลือดหัวใจและการเสียชีวิต”

ไลฟ์ #98: ประวัติศาสตร์ของ ไขมัน คอเลสเตอรอล กับ โรคหลอดเลือดหัวใจ (ตอนจบ)วันเสาร์ 26 ก.ค. 2568เวลา 18.00 น.เมื่อเร็วๆนี้ มี A Systematic Review and Meta-analysis of Randomized Controlled Trials ตีพิมพ์เมื่อวันที่ 28 เม.ย. 2568 ใน Japan Medical Association and the Japanese Association of Medical Sciences ซึ่งสรุปอย่างที่เรียกว่า “Bold statement” มากว่า “ข้อมูลจาก paper ฉบับนี้บ่งชี้ว่า ไม่ควรแนะนำให้ลดการลดการบริโภคไขมันอิ่มตัวเพื่อการป้องกันโรคหลอดเลือดหัวใจและการเสียชีวิต”พี่ได้ข้อมูลหักล้าง meta-analysis ฉบับนี้มาซึ่งดีมากว่าถ้าข้อมูลที่ใส่เข้า garbage in - ผลลัพธ์มันก็คือ garbage out ค่ะในขณะเดียวกัน พี่จะอธิบาย Systematic reviews and Meta-analysis of cohort studies หรือ RCTs ที่มีออกมาตั้งแต่ปี 2010-2022 ให้ข้อมูลตรงกันข้ามว่า การจำกัด saturated fat เพิ่มการบริโภค polyunsaturated fat ไม่ชัดเจนในการลดความเสี่ยงโรคหลอดเลือดหัวใจ เช่น1. Patty W Siri-Tarino และคณะ ในปี 20102. E.Ramsden และคณะ ในปี 20133. Rajiv Chowdhury และคณะ ในปี 20144. Reimara ในปี 20225. Yamada และคณะ ในปี 2025ว่ามีข้อบกพร่องอะไรในการศึกษาแบบ systematic reviews and meta-analysis เหล่านี้ เวลาเจอกูรู้สุขภาพเอาการศึกษาเหล่านี้มาชวนเชื่อ (เห็นบ่อยค่ะ โดยเฉพาะของ Siri-Tarino และ E.Ramsden) จะได้มีภูมิคุ้มกันต่อข้อมูลผิดๆเหล่านี้ค่ะพบกันวันเสาร์ทึ่ 26 ก.ค. เวลา 18.00 น.ค่ะ#หาคำตอบสุขภาพจากงานวิจัยไม่ใช่จากเรื่องเล่า#FatOutHealthspans

Send us a textDr. Bobby unpacks the surge of health hype—from red light therapy to NAD⁺ boosters—and empowers listeners to stay curious yet skeptical using science-backed tools and critical thinking.Are claims like “boost your mitochondria” or “natural detox” real breakthroughs—or today's version of snake oil? Dr. Bobby explores why health hype is everywhere, why we're vulnerable to it, and how to sift compelling theories from proven treatments. He outlines examples of widely accepted beliefs that ultimately didn't hold up to rigorous scrutiny. Inserting stents to open clogged arteries seemed sensible, but studies like the COURAGE and ORBITA trials found no added benefit over medical management (NEJM). Dr. Bobby then turns to newer fads. Claims around NAD⁺ boosters (like NMN or NR), red light therapy, PRP for knee pain, and hydrogen water often rely on plausible-sounding mechanisms or mouse studies—but currently lack human RCTs to back them up. While these ideas may sound promising, human trials are either missing or preliminary.Why does this hype persist? Financial incentives are everywhere: the U.S. spends over $5 trillion annually on health, and the supplement market alone is worth $150 billion. Influencers, professionals, and even well-meaning providers may promote approaches they financially benefit from. As patients, we're often eager for solutions to symptoms like fatigue or anxiety—especially when conventional medicine doesn't have a satisfying answer. This opens the door for pseudoscience, placebo effects, and the viral spread of misinformation.To navigate this environment, Dr. Bobby outlines seven action steps. First, demand human evidence: ask if a treatment has been tested in RCTs, replicated, and proven in diverse populations. He recommends Examine.com for non-biased supplement research and revisiting his episode on evaluating health headlines (#22). Second, follow the money—financial conflicts should raise your skepticism. Third, be alert to hypey language like “miracle cure” or “doctor secrets”—phrases designed to manipulate, not inform. Fourth, understand the placebo effect, especially with vague symptoms. Fifth, ask  questions: “Compared to what?” “In whom?” “For how long?” “With what risks?” These shift the focus from excitement to real evaluation. Sixth, adopt what Dr. Bobby calls the mindset of a curious skeptic—open to ideas, but insistent on evidence. Finally, he urges listeners to consult evidence-literate doctors who will explore with you, both mainstream and emerging treatments with a critical eye—see episode #20 for more on choosing the right provider.Takeaways: Ask, “Has this been tested in people?” before jumping on a health trend. Beware buzzwords and financial conflicts—science, not sales, should guide your decisions. Embrace curiosity, but anchor it in real-world evidence to truly live long and well.

Is everyone really low in vitamin D? Or have we been sold a narrative that doesn't hold up under scrutiny? In this mind-blowing episode, Tara sits down with Regina and Kristin, the investigative duo behind the Normal Curves podcast, to explore the truth behind the so-called "vitamin D deficiency epidemic." Spoiler: it may have been manufactured by outdated, flawed science—and driven by people with major conflicts of interest. This is a must-listen for anyone taking vitamin D or worried about their levels. If you've been told your D is “low,” this episode might change everything. In this episode we cover: How the original vitamin D reference ranges were set (and how they were quietly reversed in 2024) Why testing vitamin D routinely may be doing more harm than good The role of conflicts of interest in shaping clinical guidelines What the latest randomized controlled trials (RCTs) actually show about supplementing vitamin D for disease prevention Why observational data can mislead us, and how low D might be the consequence—not the cause—of illness How much sun you actually need to make enough vitamin D (hint: it's a lot less than you think) Why the “low D” narrative stuck around even after the science was overturned If you're thinking about taking D, already taking D, or have been told your vitamin D is "low" (it likely isn't) then this one is for you.   WATCH THIS EPISODE ON YOUTUBE -https://www.youtube.com/@TaraThorne   Regina Nuzzo is a Gallaudet professor, award-winning science journalist, and co-host of the Normal Curves podcast. She brings statistics to life for students and audiences worldwide, often using sex-science examples to keep things lively. Her writing has appeared in Nature, The New York Times, Scientific American, and the Los Angeles Times, where she wrote a column on the science of sex and relationships. Alongside co-host Kristin Sainani, she penned a long-running statistics column for Physical Medicine & Rehabilitation and now teaches a Stanford summer course on statistics for clinical informatics. Regina's work earned the American Statistical Association's Excellence in Statistical Reporting Award.   Kristin Cobb Sainani is a Stanford professor, science journalist, and co-host of the Normal Curves podcast. She brings statistics and scientific writing to students and audiences around the world. She also works as a statistician on sports medicine projects. Kristin has written widely about health, science, and statistics for both academic and popular audiences. She was a health columnist for Allure magazine for ten years and, alongside co-host Regina Nuzzo, penned a long-running statistics column for the journal Physical Medicine & Rehabilitation. In 2018, she received Stanford's Biosciences Award for Excellence in Graduate Teaching. Known for her statistical sleuthing and ability to cut through academic jargon, Kristin champions clear language and rigorous methods in science.   Mentioned in this episode: Normal Curves Podcast https://www.normalcurves.com/vitamin-d-part-1-is-the-deficiency-epidemic-real/   https://www.normalcurves.com/vitamin-d-part-2-good-for-more-than-just-your-bones/   Normal Curves Website: https://www.normalcurves.com/     EQUIP PRIME PROTEIN – Click HERE to grab yours and use my code: TARA to get 15% off. When you sign up for a subscription via my link, you'll save 30% on the first month & 15% on any subsequent months! 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Dr. Hoffman continues his conversation with Jonathan Rubin, CEO of the Seed Oil Free Alliance.

The Seed Oil Controversy: Unpacking Health Risks and Alternatives with Jonathan Rubin, CEO of the Seed Oil Free Alliance. The discussion focuses on the potential health hazards posed by seed oils, which have become ubiquitous in the American diet. They explore how these oils may be linked to chronic disease and obesity and compare this with the mainstream view that considers them harmless. Jonathan shares insights from his personal health journey and explains the mission and methodology of the Seed Oil Free Alliance, which aims to provide consumers with reliable information and certification for seed oil-free products. The episode also covers the historical context of seed oil consumption, the science behind omega-6 fatty acids, and practical alternatives for a healthier diet.

Sit to Stand Test & Surgical Vitality PodcastFIVE PRIMARY POINTS of this week's PODCAST* Tame the “Brain-on-Fire” ProblemRunaway neuro-inflammation accelerates multiple sclerosis, stroke, Alzheimer's and Parkinson's. Prioritize lifestyle tactics that cross the blood–brain barrier—sleep, anti-inflammatory diet, and stress control—while watching developments in next-gen brain-penetrant drugs.* Ice Is Medicine: Use Cold Exposure to Re-Route Energy Away from InflammationBrief, controlled cold stress (a 90-second cold shower in the morning, progressing to 3–5 min ice baths or cold plunges 2–3×/week) forces the body to burn calories for heat, starving inflammatory pathways and even improving auto-immune outcomes in animal models. Always clear major cold work with your physician first.* Move Before You Medicate for Depression & AnxietyA meta-analysis of 26 RCTs (>2,500 participants) shows exercise rivals—or beats—pharmacotherapy for mood disorders. Aim for a baseline of 30 min brisk walking or resistance work most days; any movement is better than none, and mixed aerobic + strength routines offer the strongest mental-health bump.* Inflammation in Your 20s Predicts Brainpower in Your 40sAn 18-year cohort study linked consistently high—or even slowly rising—CRP levels with poorer mid-life cognition. Action: get a baseline CRP, track it yearly, and deploy weight control, resistance training, and nutrient-dense, time-restricted eating (“eat less, eat less often”) to keep levels low.* Double-Down on Purpose & Gratitude—They're Biological Anti-InflammatoriesA strong life purpose lowers IL-6 and CRP, while daily gratitude practice calms the amygdala and drops TNF-α. Practical micro-habit: each week thank five people (voice or face-to-face), and block 15 minutes on Sunday to revisit your “why.” Pair with twice-weekly strength training to release anti-inflammatory myokines and boost BDNF for memory.Listen to the full podcast to learn more and please leave your comments below. This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit vitalityexplorers.substack.com/subscribe

In this episode of Iron Culture, Dr. Eric Helms talks about his forthcoming article in the MASS Research Review covering the purported harms of high-protein diets. This isn't your typical oversimplified dunk-fest that readily dismisses concerns about high-protein diets. Instead, Helms reviews a thorough paper that reviews common concerns in detail and assessed their plausibility in an objective manner. The claims include:  Claim 1 – protein reduces lifespan Claim 2 – protein makes bones weaker Claim 3 – protein harms kidneys Claim 4 – protein causes diabetes After that, Dr. Eric Trexler discusses a recent Instagram thread that pulled him into arguments against his will. The post was about his recent article on ketogenic diets and seed oils – two topics that are always bound to attract some controversy and heated debate. This conversation discusses the strengths and limitations of different types of scientific research and also touches on bias, objectivity, and the process of seeking the truth with an open mind. Time stamps: 0:00 Intro 3:00 Helms' new article about the purported harms of high-protein diets 19:25 Claim 1 – protein reduces lifespan 27:48 Claim 2 – protein makes bones weaker 43:38 Claim 3 – protein harms kidneys 50:53 Claim 4 – protein causes diabetes 57:22 Trex's social media beefs – keto and seed oils 1:03:40 Types of observational studies 1:08:35 Seeking truth versus defending biases 1:17:32 Limitations versus fatal flaws 1:24:19 Limitations of RCTs (randomized controlled trials) 1:32:23 Wrapping up

Longevity Supplements: Do NMN and NR Actually Work? Read on to find out what the research says. Overview:In this week's episode, we dive into the popular supplements NMN and NR that are touted to increase longevity and healthspan. We break down what these supplements actually are, what the research says about their effects on muscle and physical function, and whether you should spend your money on them. Key Takeaways: 0:45 - What are NMN and NR? Precursors to NAD+, which declines with age 2:30 - Animal studies show benefits, but what about humans?3:45 - Results of a systematic review of RCTs in older adults on muscle strength and physical function 5:00 - Studies sponsored by industry show benefits, but lower quality evidence6:30 - Are they worth spending your money on? CTA: Dive into the research and decide for yourself - listen to the full episode now!See omnystudio.com/listener for privacy information.

In this special keynote episode, I'm excited to share the recording of Professor Tim Friede's thought-provoking presentation from The Effective Statistician Conference 2024. Tim, a leading expert in biostatistics and clinical trial design, dives deep into the combination of randomized controlled trials (RCTs) and real-world data (RWD)—especially in the context of rare diseases. Drawing from his work at the University Medical Center Göttingen and numerous European research initiatives, Tim presents a compelling case for integrating RWD to support small or underpowered RCTs using advanced statistical models. He shares real-world examples (including CJD and Alport syndrome), simulation insights, and practical recommendations that can change how we approach evidence generation in low-prevalence populations. What You'll Learn:

Send us a textWelcome back Rounds Table Listeners! Today we have another special episode— Trial Files turns two years old this June, and we're celebrating with an episode summarizing the Top 5 RCTs in the Trial Files catalogue to date. Dr. Mike Fralick takes us through five trials in 15 minutes. Here we go!1. Effects of Semaglutide on Chronic Kidney Disease in Patients with Type 2 Diabetes (0:00 - 3:08)2. Restrictive or Liberal Transfusion Strategy in Myocardial Infarction and Anemia (3:09 - 5:37)3. Once-Weekly Semaglutide in Persons with Obesity and Knee Osteoarthritis (5:38 - 8:33)4. Antibiotic Treatment for 7 versus 14 Days in Patients with Bloodstream Infections (8:34 - 11:22)5. Finerenone in Heart Failure with Mildly Reduced or Preserved Ejection Fraction (11:23 - 13:23)Happy 2nd Birthday, Trial Files!A free monthly newsletter on practice-changing trials, delivered straight to your inbox-- sign up at https://trialfiles.substack.com/ (13:24 - 14:19)Questions? Comments? Feedback? We'd love to hear from you! @roundstable @InternAtWork @MedicinePods

In this keynote episode, Professor Sebastian Schneeweiss from Harvard Medical School shares groundbreaking insights from his extensive research into emulating randomized controlled trials (RCTs) using real-world data (RWD). Recorded live at The Effective Statistician Conference 2024, this talk explores whether non-randomized studies based on electronic health records and claims data can reach conclusions as reliable as those from traditional RCTs. Prof. Schneeweiss, also Chief of the Division of Pharmacoepidemiology and Pharmacoeconomics at Brigham and Women's Hospital, walks us through the RCT DUPLICATE project, a major FDA-funded initiative that evaluated whether regulatory decisions could be replicated through high-quality real-world evidence (RWE). From the successes to the limitations—and everything in between—this episode is packed with lessons for statisticians, regulators, and pharmaceutical leaders interested in the future of data-driven healthcare decisions.

In this explosive episode, Jonathan Howard and Wendy Orent confront the accelerating dismantling of America's public health infrastructure. They begin with the NIH staff revolt—documented in the newly published Bethesda Declaration—and Jay Bhattacharya's astonishing lack of awareness during Senate testimony. From there, they shift to RFK Jr.'s controversial appointments to the CDC's Advisory Committee on Immunization Practices (ACIP), many of whom are tied to disinformation campaigns and anti-vaccine advocacy. The hosts expose the hypocrisy in the medical rhetoric of figures like Vinay Prasad, who once championed randomized controlled trials (RCTs) as the gold standard—until now. With the CDC gutted, the FDA undermined, and common sense replacing real science, they ask: how do we preserve truth in an age of weaponized misinformation? Connect with us further on https://sciencebasedmedicine.org/author/jonathanhoward/  The Fine Print The content presented in the "We Want Them Infected" Podcast and associated book is intended for informational and educational purposes only.    The views and opinions expressed by the speakers, hosts, and guests on the podcast do not necessarily reflect the views of the creators, producers, or distributors. The information provided in this podcast should not be considered as a substitute for professional medical, scientific, or legal advice. Listeners and readers are encouraged to consult with relevant experts and authorities for specific guidance and information.   The creators of the podcast and book have made reasonable efforts to ensure that the information provided is accurate and up to date. However, as the field of medical science and the understanding of the COVID-19 pandemic continue to evolve, there may be new developments and insights that are not covered in this content.   The creators are not responsible for any errors or omissions in the content or for any actions taken based on the information provided. They disclaim any liability for any loss, injury, or damage incurred by individuals who rely on the content.   Listeners and readers are urged to use their judgment and conduct their own research when interpreting the information presented in the "We Want Them Infected" podcast and book. It is essential to stay informed about the latest updates, guidelines, and recommendations related to COVID-19 and vaccination from reputable sources, such as government health agencies and medical professionals. By accessing and using the content, you acknowledge and accept the terms of this disclaimer.   Please consult with appropriate experts and authorities for specific guidance on matters related to health, science, and the COVID-19 pandemic.  

Send us a textAre seed oils really driving chronic disease (and sunburns), or is it hype?Episode Summary: Dr. Brian Kerley talks about the health impacts of seed oils, their high omega-6 fatty acid content, and their role in chronic diseases through mechanisms like lipid peroxidation and oxidative stress. They explore how these industrially processed oils may contribute to conditions like heart disease and obesity, discuss the challenges of studying their long-term effects, and highlight the cultural and political dimensions of dietary trends.About the guest: Brian Kerley, MD is a family medicine-trained hospitalist physician who gained online prominence as the "Seed Oil Disrespecter" through his meme account, raising awareness about the health risks of seed oils.Discussion Points:Seed Oils & Health Risks: Seed oils (e.g., soybean, corn, etc.) are high in omega-6 polyunsaturated fatty acids (PUFAs), linked to oxidative stress and lipid peroxidation, producing toxic compounds like 4-HNE and acrolein that damage cells.Evolutionary Perspective: The high omega-6 levels in modern diets are evolutionarily novel, deviating from natural omega-6 to omega-3 ratios found in traditional diets, potentially exacerbating health issues across diverse populations.Challenges with RCTs: Randomized controlled trials (RCTs) often fail to capture the long-term effects of seed oils due to the need for extended washout periods (up to 8 years) and the pervasive presence of omega-6 in modern food environments.Cultural & Political Coding: Dietary trends like seed oil avoidance have become politically charged, with Kerley noting the polarization between institutional health narratives and alternative health communities, complicating public health discussions.Personal Impact: Dr. Kerley's focus on seed oils stems from personal experiences, including managing his daughter's mitochondrial disorder, highlighting the personal stakes in dietary choices.Related episode:M&M 192: Seed Oils, Chronic Disease, Diet & Religious Cults, Mainstream Medicine vs. Independent Research | Tucker Goodrich*Not medical advice.Support the showAll episodes, show notes, transcripts, and more at the M&M Substack Affiliates: KetoCitra—Ketone body BHB + potassium, calcium & magnesium, formulated with kidney health in mind. Use code MIND20 for 20% off any subscription (cancel anytime) Lumen device to optimize your metabolism for weight loss or athletic performance. Code MIND for 10% off Readwise: Organize and share what you read. 60 days FREE through link SiPhox Health—Affordable at-home blood testing. Key health markers, visualized & explained. Code TRIKOMES for a 20% discount. MASA Chips—delicious tortilla chips made from organic corn & grass-fed beef tallow. No seed oils or artificial ingredients. Code MIND for 20% off For all the ways you can support my efforts

Send us a textA critique of SSRIs and pharma's influence on medicine, including SSRI-induced sexual dysfunction, suicidality, and violence. Long Summary: Dr. David Healy critiques modern medicine, focusing on SSRIs and psychiatric medicine, including: how pharmaceutical companies manipulate clinical trial data, ghostwrite studies, and influence medical practice, often ignoring patient experiences; highlighting issues like post-SSRI sexual dysfunction (PSSD), the immediate sensory effects of SSRIs, and their potential to induce suicidal or violent behavior; challenging the reliance on randomized controlled trials (RCTs) over individual patient reports; and more.About the guest: David Healy, MD, PhD, a psychiatrist and pharmacologist, has decades of experience researching the serotonin system and SSRIs, working across Ireland, the UK, Canada, and the US. He is a professor at McMaster University and a vocal critic of pharmaceutical industry practices.Discussion Points:SSRIs cause near-immediate sensory effects, like genital numbing, in most people.Post-SSRI sexual dysfunction (PSSD) can persist for years or decades after stopping the drug, affecting many long-term users.Healy argues RCTs prioritize averages over individual experiences, often missing serious side effects like suicidality.Pharmaceutical companies ghostwrite studies and manipulate data, with journals like the New England Journal of Medicine publishing misleading articles.Serotonin theory of depression lacks evidence.Industry tactics include dismissing patient reports as anecdotes and using high doses in trials to mask weak efficacy.SSRIs can increase suicide risk, not just during initiation but also when adjusting doses or withdrawing, as seen in cases like the Aurora movie theater shooting.Regulatory bodies like the FDA often fail to investigate adverse effects due to bureaucratic processes and lack of follow-up.Healy emphasizes doctors' failure to prioritize patient observations, driven by industry-influenced standards of care.Related episode:M&M 88: Depression, Serotonin, SSRIs, Psychiatry & Social Media | Joanna Moncrieff*Not medical advice.Support the showAll episodes, show notes, transcripts, and more at the M&M Substack Affiliates: KetoCitra—Ketone body BHB + potassium, calcium & magnesium, formulated with kidney health in mind. Use code MIND20 for 20% off any subscription (cancel anytime) Lumen device to optimize your metabolism for weight loss or athletic performance. Code MIND for 10% off Readwise: Organize and share what you read. 60 days FREE through link SiPhox Health—Affordable at-home blood testing. Key health markers, visualized & explained. Code TRIKOMES for a 20% discount. MASA Chips—delicious tortilla chips made from organic corn & grass-fed beef tallow. No seed oils or artificial ingredients. Code MIND for 20% off For all the ways you can support my efforts

Send us a textWhat really helps prevent injuries—and what should you do when one inevitably strikes? In this episode, I use my friend Tim's pickleball injury as a jumping-off point to explore what the evidence actually says about ice, rest, NSAIDs, stretching, and more.When Tim skipped his warm-up and pulled a calf muscle, it raised a question many of us face: was it avoidable? While ancient wisdom and modern influencers often shout conflicting advice, this episode sorts through the noise to uncover what's evidence-backed, what's outdated, and what might actually delay healing. For pain, yes, ice works—cooling slows nerve conduction and can help with comfort, as seen in this study of ankle injuries. But does it reduce inflammation in a helpful way? Possibly not. Some research suggests that vasoconstriction may hinder the delivery of reparative cells and removal of waste, as noted in this trial.The evolution from RICE to PEACE to MEAT and even PEACE & LOVE reflects our shifting understanding. A meta-analysis of 22 randomized trials found no conclusive benefit of ice when added to compression or elevation. As for NSAIDs like ibuprofen, the Cochrane Review revealed no significant advantage over acetaminophen in pain relief or swelling reduction—and no clear evidence they speed up recovery.What about rest? Surprisingly, prolonged rest may do more harm than good. The Deyo study and later NEJM data show that continued normal activity (within pain tolerance) results in faster recovery than either bed rest or structured exercises, at least for acute low back pain—offering insights that might extend to other strains or sprains.Can you prevent injuries altogether? Static stretching (think toe touches) doesn't show strong support in RCT reviews, and while a recent meta-analysis found a small reduction in muscle injuries, the impact was modest. Dynamic stretching remains inconclusive according to current evidence.The takeaway? When treatments or prevention strategies are studied over and over yet results remain ambiguous, it likely means any real benefit is small—a principle I call “Dr. Bobby's Law of Many Studies.” Compare that with fall prevention in older adults: 66 RCTs involving 47,000 people showed strength and balance training significantly reduces falls by 20–30%. When something works, it tends to show up clearly and consistently.Takeaways: If you're injured, ice and NSAIDs can ease discomfort—but don't count on them to speed up healing. Resting too much may slow recovery; try gentle movement instead. Stretching might help a bit with prevention, but don't expect miracles. Evidence

JACC's June 10 issue, focusing on the ACS guideline, features a series of videos with unique perspectives. In this video, JACC: Executive Associate Editor Karthik Murugiah, MBBS, MHS, FACC, introduces his paper discussing the guideline's reliance on four landmark RCTs in AMI-CS. Several sweeping changes in recommendations for MCS use have been codified that should influence practice and improve care for these high-risk patients. While IABP use is expected to decrease, use of mAFP is likely to increase but should be judicious, with caution against overgeneralizing given the narrow selection criteria of DanGer Shock. Evaluating real-world practice patterns and outcomes of patients with AMI-CS based on these recommendations will be paramount.

PRP in the Epidural Space for Radiculopathy Brooklyn Based Pain Physician, David Rosenblum, MD known for his work publishing and teaching Regenerative Pain Medicine and Ultrasound Guided Pain Procedures hosts this podcast covering the latest and most advanced concepts in Pain Medicine. Summary Dr. David Rosenblum delivered a comprehensive lecture covering several key topics in pain management. He discussed his upcoming speaking engagements at PainWeek, ASPN and great upcoming meetings like the Latin American Pain Society, and other conferences. Dr. Rosenblum shared his extensive experience with PRP (Platelet-Rich Plasma) epidural injections, reviewing multiple research studies that support their efficacy. He highlighted three significant studies: a randomized control trial comparing PRP epidural injections to traditional treatments, a CT-guided epidural PRP study, and a 2025 meta-analysis comparing PRP to steroids. Dr. Rosenblum emphasized that PRP treatments are showing comparable or better results than traditional steroid injections, with potentially fewer required treatments and longer-lasting relief. He noted that while PRP is currently not covered by insurance, it represents a growing trend in 'natural' treatment approaches that patients increasingly prefer. Chapters Introduction and Upcoming Events Dr. Rosenblum announced his upcoming lectures at Pain Week focusing on ultrasound and regenerative medicine, followed by presentations at the Latin American Pain Society in Chile and the New York, New Jersey Pain Conference. He mentioned the SoMeDocs online pain conference accessible through nrappain.org, and upcoming ultrasound training sessions in New York City. PRP Epidural Research Review Dr. Rosenblum discussed a randomized control trial involving 30 patients receiving transforaminal epidural injections. The study showed that PRP patients demonstrated significant improvements in leg pain scores at 6, 12, and 24 weeks. He noted that while the study didn't use contrast, he personally prefers using contrast diluted with saline for better visualization. CT-Guided Epidural Study Analysis Dr. Rosenblum reviewed a study comparing CT-guided epidural PRP versus steroid injections, questioning the necessity of CT guidance. The study included 60 patients and showed similar results between PRP and steroid groups at six weeks, though he criticized the short follow-up period, noting that PRP typically takes months to show full effects. Meta-Analysis Discussion Dr. Rosenblum presented a 2025 meta-analysis comparing PRP to steroids in epidural injections. The analysis included 310 patients across five RCTs, demonstrating comparable efficacy between PRP and steroid injections without increased adverse events. He emphasized that his clinical experience shows patients typically require fewer PRP injections compared to steroid treatments.         Register for Next Weeks SoMeDocs Pain Conference References Wongjarupong, Asarn, et al. "“Platelet-Rich Plasma” epidural injection an emerging strategy in lumbar disc herniation: a Randomized Controlled Trial." BMC Musculoskeletal Disorders 24.1 (2023): 335. Bise, Sylvain, et al. "Comparison of interlaminar CT-guided epidural platelet-rich plasma versus steroid injection in patients with lumbar radicular pain." European radiology 30 (2020): 3152-3160. Muthu S, Viswanathan VK, Gangadaran P. Is platelet-rich plasma better than steroids as epidural drug of choice in lumbar disc disease with radiculopathy? Meta-analysis of randomized controlled trials. Exp Biol Med (Maywood). 2025 Feb 4;250:10390. doi: 10.3389/ebm.2025.10390. PMID: 39968415; PMCID: PMC11832311.

PRP in the Epidural Space for Radiculopathy Brooklyn Based Pain Physician, David Rosenblum, MD known for his work publishing and teaching Regenerative Pain Medicine and Ultrasound Guided Pain Procedures hosts this podcast covering the latest and most advanced concepts in Pain Medicine. Summary Dr. David Rosenblum delivered a comprehensive lecture covering several key topics in pain management. He discussed his upcoming speaking engagements at PainWeek, ASPN and great upcoming meetings like the Latin American Pain Society, and other conferences. Dr. Rosenblum shared his extensive experience with PRP (Platelet-Rich Plasma) epidural injections, reviewing multiple research studies that support their efficacy. He highlighted three significant studies: a randomized control trial comparing PRP epidural injections to traditional treatments, a CT-guided epidural PRP study, and a 2025 meta-analysis comparing PRP to steroids. Dr. Rosenblum emphasized that PRP treatments are showing comparable or better results than traditional steroid injections, with potentially fewer required treatments and longer-lasting relief. He noted that while PRP is currently not covered by insurance, it represents a growing trend in 'natural' treatment approaches that patients increasingly prefer. Chapters Introduction and Upcoming Events Dr. Rosenblum announced his upcoming lectures at Pain Week focusing on ultrasound and regenerative medicine, followed by presentations at the Latin American Pain Society in Chile and the New York, New Jersey Pain Conference. He mentioned the SoMeDocs online pain conference accessible through nrappain.org, and upcoming ultrasound training sessions in New York City. PRP Epidural Research Review Dr. Rosenblum discussed a randomized control trial involving 30 patients receiving transforaminal epidural injections. The study showed that PRP patients demonstrated significant improvements in leg pain scores at 6, 12, and 24 weeks. He noted that while the study didn't use contrast, he personally prefers using contrast diluted with saline for better visualization. CT-Guided Epidural Study Analysis Dr. Rosenblum reviewed a study comparing CT-guided epidural PRP versus steroid injections, questioning the necessity of CT guidance. The study included 60 patients and showed similar results between PRP and steroid groups at six weeks, though he criticized the short follow-up period, noting that PRP typically takes months to show full effects. Meta-Analysis Discussion Dr. Rosenblum presented a 2025 meta-analysis comparing PRP to steroids in epidural injections. The analysis included 310 patients across five RCTs, demonstrating comparable efficacy between PRP and steroid injections without increased adverse events. He emphasized that his clinical experience shows patients typically require fewer PRP injections compared to steroid treatments.         Register for Next Weeks SoMeDocs Pain Conference References Wongjarupong, Asarn, et al. "“Platelet-Rich Plasma” epidural injection an emerging strategy in lumbar disc herniation: a Randomized Controlled Trial." BMC Musculoskeletal Disorders 24.1 (2023): 335. Bise, Sylvain, et al. "Comparison of interlaminar CT-guided epidural platelet-rich plasma versus steroid injection in patients with lumbar radicular pain." European radiology 30 (2020): 3152-3160. Muthu S, Viswanathan VK, Gangadaran P. Is platelet-rich plasma better than steroids as epidural drug of choice in lumbar disc disease with radiculopathy? Meta-analysis of randomized controlled trials. Exp Biol Med (Maywood). 2025 Feb 4;250:10390. doi: 10.3389/ebm.2025.10390. PMID: 39968415; PMCID: PMC11832311.

PRP in the Epidural Space for Radiculopathy Brooklyn Based Pain Physician, David Rosenblum, MD known for his work publishing and teaching Regenerative Pain Medicine and Ultrasound Guided Pain Procedures hosts this podcast covering the latest and most advanced concepts in Pain Medicine. Summary Dr. David Rosenblum delivered a comprehensive lecture covering several key topics in pain management. He discussed his upcoming speaking engagements at PainWeek, ASPN and great upcoming meetings like the Latin American Pain Society, and other conferences. Dr. Rosenblum shared his extensive experience with PRP (Platelet-Rich Plasma) epidural injections, reviewing multiple research studies that support their efficacy. He highlighted three significant studies: a randomized control trial comparing PRP epidural injections to traditional treatments, a CT-guided epidural PRP study, and a 2025 meta-analysis comparing PRP to steroids. Dr. Rosenblum emphasized that PRP treatments are showing comparable or better results than traditional steroid injections, with potentially fewer required treatments and longer-lasting relief. He noted that while PRP is currently not covered by insurance, it represents a growing trend in 'natural' treatment approaches that patients increasingly prefer. Chapters Introduction and Upcoming Events Dr. Rosenblum announced his upcoming lectures at Pain Week focusing on ultrasound and regenerative medicine, followed by presentations at the Latin American Pain Society in Chile and the New York, New Jersey Pain Conference. He mentioned the SoMeDocs online pain conference accessible through nrappain.org, and upcoming ultrasound training sessions in New York City. PRP Epidural Research Review Dr. Rosenblum discussed a randomized control trial involving 30 patients receiving transforaminal epidural injections. The study showed that PRP patients demonstrated significant improvements in leg pain scores at 6, 12, and 24 weeks. He noted that while the study didn't use contrast, he personally prefers using contrast diluted with saline for better visualization. CT-Guided Epidural Study Analysis Dr. Rosenblum reviewed a study comparing CT-guided epidural PRP versus steroid injections, questioning the necessity of CT guidance. The study included 60 patients and showed similar results between PRP and steroid groups at six weeks, though he criticized the short follow-up period, noting that PRP typically takes months to show full effects. Meta-Analysis Discussion Dr. Rosenblum presented a 2025 meta-analysis comparing PRP to steroids in epidural injections. The analysis included 310 patients across five RCTs, demonstrating comparable efficacy between PRP and steroid injections without increased adverse events. He emphasized that his clinical experience shows patients typically require fewer PRP injections compared to steroid treatments.         Register for Next Weeks SoMeDocs Pain Conference References Wongjarupong, Asarn, et al. "“Platelet-Rich Plasma” epidural injection an emerging strategy in lumbar disc herniation: a Randomized Controlled Trial." BMC Musculoskeletal Disorders 24.1 (2023): 335. Bise, Sylvain, et al. "Comparison of interlaminar CT-guided epidural platelet-rich plasma versus steroid injection in patients with lumbar radicular pain." European radiology 30 (2020): 3152-3160. Muthu S, Viswanathan VK, Gangadaran P. Is platelet-rich plasma better than steroids as epidural drug of choice in lumbar disc disease with radiculopathy? Meta-analysis of randomized controlled trials. Exp Biol Med (Maywood). 2025 Feb 4;250:10390. doi: 10.3389/ebm.2025.10390. PMID: 39968415; PMCID: PMC11832311.

JCO PO author Dr. Dean A. Regier at the Academy of Translational Medicine, University of British Columbia (UBC), and the School of Population and Public Health, BC Cancer Research Institute shares insights into his JCO PO article, “Clinical Effectiveness and Cost-Effectiveness of Multigene Panel Sequencing in Advanced Melanoma: A Population-Level Real-World Target Trial Emulation.” Host Dr. Rafeh Naqash and Dr. Regier discuss the real-world clinical effectiveness and cost-effectiveness of multigene panels compared with single-gene BRAF testing to guide therapeutic decisions in advanced melanoma. Transcript Dr. Rafeh Naqash:Hello and welcome to JCO Precision Oncology Conversations, where we bring you engaging conversations with authors of clinically relevant and highly significant JCO PO articles. I'm your host, Dr. Rafeh Naqash, Podcast Editor for JCO Precision Oncology and Assistant Professor at the OU Health Stephenson Cancer Center in the University of Oklahoma. Today, we are excited to be joined by Dr. Dean A. Regier, Director at the Academy of Translational Medicine, Associate Professor at the School of Population and Public Health, UBC Senior Scientist at the British Columbia Cancer Research Institute, and also the senior author of the JCO Precision Oncology article entitled "Clinical Effectiveness and Cost-Effectiveness of Multigene Panel Sequencing in Advanced Melanoma: A Population-Level Real-World Target Trial Emulation." At the time of this recording, our guest's disclosures will be linked in the transcript. Dean, welcome to our podcast and thank you for joining us today. Dr. Dean Regier:Thank you. I'm delighted to be here. Dr. Rafeh Naqash:So, obviously, you are from Canada, and medicine, or approvals of drugs to some extent, and in fact approvals of gene testing to some extent is slightly different, which we'll come to learn about more today, compared to what we do in the US—and in fact, similarly, Europe versus North America to a large extent as well. Most of the time, we end up talking about gene testing in lung cancer. There is a lot of data, a lot of papers around single-gene panel testing in non-small cell lung cancer versus multigene testing. In fact, a couple of those papers have been published in JCO PO, and it has shown significant cost-effectiveness and benefit and outcomes benefit in terms of multigene testing. So this is slightly, you know, on a similar approach, but in a different tumor type. So, could you tell us first why you wanted to investigate this question? What was the background to investigating this question? And given your expertise in health economics and policy, what are some of the aspects that one tends or should tend to understand in terms of cost-effectiveness before we go into the results for this very interesting manuscript? Dr. Dean Regier:Yeah, of course, delighted to. So, one of the reasons why we're deeply interested in looking at comparative outcomes with respect to single- versus multigene testing— whether that's in a public payer system like Canada or an insurer system, a private system in the United States— is that the question around does multigene versus single-gene testing work, has not typically tested in randomized controlled trials. You don't have people randomized to multigene versus single-gene testing. And what that does, it makes the resulting evidence base, whether it's efficacy, safety, or comparative cost-effectiveness, highly uncertain. So, the consequence of that has been uneven uptake around the world of next-generation sequencing panels. And so if we believe that next-gen sequencing panels are indeed effective for our patients, we really need to generate that comparative evidence around effectiveness and cost-effectiveness. So we can go to payers, whether it be single payer or a private insurer, to say, "Here are the comparative outcomes." And when I say that uptake has been uneven, uptake there's been actually plenty, as you know, publications around that uneven uptake, whether it be in Europe, in the United States, in Canada. And so we're really interested in trying to produce that evidence to create the type of deliberations that are needed to have these types of technologies accessible to patients. And part of those deliberations, of course, is the clinical, but also in some contexts, cost-effectiveness. And so, we really start from the perspective of, can we use our healthcare system data, our learning healthcare system, to generate that evidence in a way that emulates a randomized controlled trial? We won't be able to do these randomized controlled trials for various, like really important and and reasons that make sense, quite frankly. So how can we mimic or emulate randomized controlled trials in a way that allows us to make inference around those outcomes? And for my research lab, we usually think through how do we do causal inference to address some of those biases that are inherent in observational data. So in terms of advanced melanoma, we were really interested in this question because first of all, there have been no randomized controlled trials around next-gen sequencing versus single-gene testing. And secondly, these products, these ICIs, immune checkpoint inhibitors, and BRAF and MEK inhibitors, they are quite expensive. And so the question really becomes: are they effective? And if so, to what extent are they cost-effective? Do they provide a good reason to have information around value for money? Dr. Rafeh Naqash:So now going to the biology of melanoma, so we know that BRAF is one of the tumor-agnostic therapies, it has approvals for melanoma as well as several other tumor types. And in fact, I do trials with different RAF-RAS kinase inhibitors. Now, one of the things that I do know is, and I'm sure some of the listeners know, is the DREAMseq trial, which was a melanoma study that was an NCI Cooperative Group trial that was led by Dr. Mike Atkins from Georgetown a couple of years back, that did show survival benefit of first-line immunotherapy sequencing. It was a sequencing study of whether to do first-line BRAF in BRAF-mutant melanoma followed by checkpoint inhibitors, or vice versa. And the immune checkpoint inhibitors followed by BRAF was actually the one that showed benefit, and the trial had to stop early, was stopped early because of the significant benefit seen. So in that context, before we approach the question of single-gene versus multigene testing in melanoma, one would imagine that it's already established that upfront nivolumab plus ipilimumab, for that matter, doublet checkpoint inhibitor therapy is better for BRAF-mutant melanoma. And then there's no significant other approvals for melanoma for NRAS or KIT, you know, mucosal melanomas tend to have KIT mutations, for example, or uveal melanomas, for that matter, have GNAQ, and there's no targeted therapies. So, what is the actual need of doing a broader testing versus just testing for BRAF? So just trying to understand when you started looking into this question, I'm sure you kind of thought about some of these concepts before you delved into that. Dr. Dean Regier:I think that is an excellent question, and it is a question that we asked ourselves: did we really expect any differences in outcomes between the testing strategies? And what did the real-world implementation, physician-guided, physician-led implementation look like? And so, that was kind of one of the other reasons that we really were interested is, why would we go to expanded multigene panel sequencing at all? We didn't really expect or I didn't expect an overall survival a priori. But what we saw in our healthcare system, what happened in our healthcare system was the implementation in 2016 of this multigene panel. And this panel covered advanced melanoma, and this panel cost quite a bit more than what they were doing in terms of the single-gene BRAF testing. And so when you're a healthcare system, you have to ask yourself those questions of what is the additional value associated with that? And indeed, I think in a healthcare system, we have to be really aware that we do not actually follow to the ideal extent randomized controlled trials or trial settings. And so that's the other thing that we have to keep in mind is when these, whether it's an ICI or a BRAF MEK inhibitor, when these are implemented, they do not look like randomized controlled trials. And so, we really wanted to emulate not just a randomized controlled trial, but a pragmatic randomized controlled trial to really answer those real-world questions around implementation that are so important to decision making. Dr. Rafeh Naqash:Sure. And just to understand this a little better: for us in the United States, when we talk about multigene testing, we generally refer to, these days, whole-exome sequencing with whole-transcriptome sequencing, which is like the nuclear option of of the testings, which is not necessarily cheap. So, when you talk about multigene testing in your healthcare system, what does that look like? Is it a 16-gene panel? Is it a 52-gene panel? What is the actual makeup of that platform? Dr. Dean Regier:Excellent question. Yeah, so at the time that this study is looking at, it was 2016, when we, as BC Cancer—so British Columbia is a population right now of 5.7 million people, and we have data on all those individuals. We are one healthcare system providing health care to 5.7 million people. In 2016, we had what I call our "home-brew" multigene panel, which was a 53-gene panel that was reimbursed as standard of care across advanced cancers, one of them being advanced melanoma. We have evolved since then. I believe in 2022, we are using one of the Illumina panels, the Focus panel. And so things have changed; it's an evolving landscape. But we're specifically focused on the 53-gene panel. It was called OncoPanel. And that was produced in British Columbia through the Genome Sciences Centre, and it was validated in a single-arm trial mostly around validity, etc. Dr. Rafeh Naqash:Thank you for explaining that. So now, onto the actual meat and the science of this project. So, what are some of the metrics from a health economy standpoint that you did look at? And then, methodology-wise, I understand, in the United States, we have a fragmented healthcare system. I have data only from my institution, for that matter. So we have to reach out to outside collaborators and email them to get the data. And that is different for you where you have access to all the data under one umbrella. So could you speak to that a little bit and how that's an advantage for this kind of research especially? Dr. Dean Regier:Yeah. In health economics, we look at the comparative incremental costs against the incremental effectiveness. And when we think about incremental costs, we think not just about systemic therapy or whether you see a physician, but also about hospitalizations, about all the healthcare interactions related to oncology or not that a patient might experience during their time or interactions with the healthcare system. You can imagine with oncology, there are multiple interactions over a prolonged time period depending on survival. And so what we try to do is we try to—and the benefit of the single-payer healthcare system is what we do is we link all those resource utilization patterns that each patient encounters, and we know the price of that encounter. And we compare those incremental costs of, in this case, it's the multigene panel versus the single-gene panel. So it's not just the cost of the panel, not just the cost of systemic therapy, but hospitalizations, physician encounters, etc. And then similarly, we look at, in this case, we looked at overall survival - we can also look at progression-free survival - and ask the simple question, you know, what is the incremental cost per life-year gained? And in that way, we get a metric or an understanding of value for money. And how we evaluate that within a deliberative priority setting context is we look at safety and efficacy first. So a regulatory package that you might get from, in our case, Health Canada or the FDA, so we look at that package, and we deliberate on, okay, is it safe and is it effective? How many patients are affected, etc. And then separately, what is the cost-effectiveness? And at what price, if it's not cost-effective, at what price would it be cost-effective? Okay, so for example, we have this metric called the incremental cost-effectiveness ratio, which is incremental cost in the numerator, and in this case, life-years gained in the denominator. And if it is around $50,000 or $100,000 per life-year gained—so if it's in that range, this ratio—then we might say it's cost-effective. If it's above this range, which is common in oncology, especially when we talk about ICIs, etc., then you might want to negotiate a price. And indeed, when we negotiate that price, we use the economic evaluation, that incremental cost-effectiveness ratio, as a way to understand at what price should we negotiate to in order to get value for money for the healthcare system. Dr. Rafeh Naqash:Thank you for explaining those very interesting terminologies. Now, one question I have in the context of what you just mentioned is, you know, like the drug development space, you talked about efficacy and safety, but then on the safety side, we talk about all-grade adverse events or treatment-related adverse events—two different terminologies. From a healthcare utilization perspective, how do you untangle if a patient on a BRAF therapy got admitted for a hypoxic respiratory failure due to COPD, resulting in a hospitalization from the cost, overall cost utilization, or does it not matter? Dr. Dean Regier:We try to do as much digging into those questions as possible. And so, this is real-world data, right? Real-world data is not exactly as clean as you'd get from a well-conducted clinical trial. And so what we do is we look at potential adverse event, whether it's hospitalization, and the types of therapies around that hospitalization to try- and then engage with clinicians to try to understand or tease out the different grades of the adverse event. Whether it's successful or not, I think that is a real question that we grapple with in terms of are we accurate in delineating different levels of adverse events? But we try to take the data around the event to try to understand the context in which it happens. Dr. Rafeh Naqash:Thank you for explaining that, Dean. So, again to the results of this manuscript, could you go into the methodology briefly? Believe you had 147 patients, 147 patients in one arm, 147 in the other. How did you split that cohort, and what were some of the characteristics of this cohort? Dr. Dean Regier:So, the idea, of course, is that we have selection criteria, study inclusion criteria, which included in our case 364 patients. And these were patients who had advanced melanoma within our study time period. So that was 2016 to 2018. And we had one additional year follow. So we had three total years. And what we did is that we linked our data, our healthcare system data. During this time, because the policy change was in 2016, we had patients both go on the multigene panel and on the single-gene BRAF testing. So, the idea was to emulate a pragmatic randomized controlled trial where we looked at contemporaneous patients who had multigene panel testing versus single-gene BRAF testing. And then we did a matching procedure—we call it genetic matching. And that is a type of matching that allows us to balance covariates across the patient groups, across the multigene versus BRAF testing cohorts. The idea again is, as you get in a randomized controlled trial, you have these baseline characteristics that look the same. And then the hope is that you address any source selection or confounding biases that prohibit you to have a clean answer to the question: Is it effective or cost-effective? So you address all those biases that may prohibit you to find a signal if indeed a signal is there. And so, what we did is we created—we did this genetic matching to balance covariates across the two cohorts, and we matched them one-to-one. And so what we were able to do is we were able to find, of those 364 patients in our pool, 147 in the multigene versus 147 in the single-gene BRAF testing that were very, very similar. In fact, we created what's called a directed acyclic graph or a DAG, together with clinicians to say, “Hey, what biases would you expect to have in these two cohorts that might limit our ability to find a signal of effectiveness?” And so we worked with clinicians, with health economists, with epidemiologists to really understand those different biases at play. And the genetic matching was able to match the cohorts on the covariates of interest. Dr. Rafeh Naqash:And then could you speak on some of the highlights from the results? I know you did survival analysis, cost-effectiveness, could you explain that in terms of what you found? Dr. Dean Regier:We did two analyses. The intention-to-treat analysis is meant to emulate the pragmatic randomized controlled trial. And what that does is it answers the question, for all those eligible for multigene or single-gene testing: What is the cost-effectiveness in terms of incremental life-years gained and incremental cost per life-years gained? And the second one was around a protocol analysis, which really answered the question of: For those patients who were actually treated, what was the incremental effectiveness and cost-effectiveness? Now, they're different in two very important ways. For the intention-to-treat, it's around population questions. If we gave single-gene or multigene to the entire population of advanced melanoma patients, what is the cost-effectiveness? The per-protocol is really around that clinical question of those who actually received treatment, what was the incremental cost and effectiveness? So very different questions in terms of population versus clinical cost and effectiveness. So, for the intention-to-treat, what we found is that in terms of life-years gained is around 0.22, which is around 2.5 months of additional life that is afforded to patients who went through the multigene panel testing versus the single-gene testing. That was non-statistically significant from zero at the 5% level. But on average, you would expect this additional 2.5 months of life. The incremental costs were again non-statistically significant, but they're around $20,000. And so when we look at incremental cost-effectiveness, we can also look at the uncertainty around that question, meaning what percentage of incremental cost-effectiveness estimates are likely to be cost-effective at different willingness-to-pay thresholds? Okay? So if you are willing to pay $100,000 to get one gain of life-years, around 52.8% of our estimates, in terms of when we looked at the entire uncertainty, would be cost-effective. So actually that meets the threshold of implementation in our healthcare system. So it's quite uncertain, just over 50%. But what we see is that decision-makers actually have a high tolerance for uncertainty around cost-effectiveness. And so, while it is uncertain, we would say that, well, the cost-effectiveness is finely balanced. Now, when we looked at the population, the per-protocol population, those folks who just got treatment, we actually have a different story. We have all of a sudden around 4.5 or just under 5 months of life gained that is statistically significantly different from zero, meaning that this is a strong signal of benefit in terms of life-years gained. In terms of the changes in costs or the incremental costs, they are larger again, but statistically insignificant. So the question now is, to what extent is it cost-effective? What is the probability of it being cost-effective? And at the $100,000 per life-year gained willingness-to-pay, there was a 73% chance that multigene panel testing versus single-gene testing is cost-effective. Dr. Rafeh Naqash:So one of the questions I have here, this is a clarification both for myself and maybe the listeners also. So protocol treatment is basically if you had gene testing and you have a BRAF in the multigene panel, then the patient went on a BRAF treatment. Is that correct? Dr. Dean Regier:It's still physician choice. And I think that's important to say that. So typically what we saw in both in our pre- and post-matching data is that we saw around 50% of patients, irrespective of BRAF status, get an ICI, which is appropriate, right? And so the idea here is that you get physician-guided care, but if the patient no longer performs on the ICI, then it gives them a little bit more information on what to do next. Even during that time when we thought it wasn't going to be common to do an ICI, but it was actually quite common. Dr. Rafeh Naqash:Now, did you have any patients in this study who had the multigene testing done and had an NRAS or a KIT mutation and then went on to those therapies, which were not captured obviously in the single-gene testing, which would have just tried to look at BRAF? Dr. Dean Regier:So I did look at the data this morning because I thought that might come up in terms of my own questions that I had. I couldn't find it, but what we did see is that some patients went on to clinical trials. So, meaning that this multigene panel testing allowed, as you would hope in a learning healthcare system, patients to move on to clinical trials to have a better chance at more appropriate care if a target therapy was available. Dr. Rafeh Naqash:And the other question in that context, which is not necessarily related to the gene platform, but more on the variant allele frequency, so if you had a multigene panel that captured something that was present at a high VAF, with suspicion that this could be germline, did you have any of those patients? I'm guessing if you did, probably very low number, but I'm just thinking from a cost-effective standpoint, if you identify somebody with germline, their, you know, first-degree relative gets tested, that ends up, you know, prevention, etc. rather than somebody actually developing cancer subsequently. That's a lot of financial gains to the system if you capture something early. So did you look at that or maybe you're planning to look at that? Dr. Dean Regier:We did not look at that, but that is a really important question that typically goes unanswered in economic evaluations. And so, the short answer is yes, that result, if there was a germline finding, would be returned to the patient, and then the family would be able to be eligible for screening in the appropriate context. What we have found in economic evaluations, and we've recently published this research, is that that scope of analysis is rarely incorporated into the economic evaluation. So those downstream costs and those downstream benefits are ignored. And when you- especially also when you think about things like secondary or incidental findings, right? So it could be a germline finding for cancer, but what about all those other findings that we might have if you go with an exome or if you go with a genome, which by the way, we do have in British Columbia—we do whole-genome and transcriptome sequencing through something called the Personalized OncoGenomics program. That scope of evaluation, because it's very hard to get the right types of data, because it requires a decision model over the lifetime of both the patients and potentially their family, it becomes very complicated or complex to model over patients' and families' lifetime. That doesn't mean that we should not do it, however. Dr. Rafeh Naqash:So, in summary Dean, could you summarize some of the known and unknowns of what you learned and what you're planning in subsequent steps to this project? Dr. Dean Regier:Our North Star, if you will, is to really understand the entire system effect of next-generation sequencing panels, exome sequencing, whole genomes, or whole genomes and transcriptome analysis, which we think should be the future of precision oncology. The next steps in our research is to provide a nice base around multigene panels in terms of multigene versus single-gene testing, whether that be colorectal cancer, lung cancer, melanoma, etc., and to map out the entire system implications of implementing next-generation sequencing panels. And then we want to answer the questions around, “Well, what if we do exomes for all patients? What if we do whole genomes and transcriptomes for all patients? What are the comparative outcomes for a true tumor-agnostic precision oncology approach, accounting for, as you say, things like return of results with respect to hereditary cancers?” I think the challenge that's going to be encountered is really around the persistent high costs of something like a whole-genome and transcriptome sequencing approach. Although we do see the technology prices going down—the "$1,000 genome" or “$6,000 genome" on whatever Illumina machine you might have—that bioinformatics is continuing to be expensive. And so, there are pipelines that are automated, of course, and you can create a targeted gene report really rapidly within a reasonable turnaround time. But of course, for secondary or what I call level two analysis, that bioinformatics is going to continue to be expensive. And so, we're just continually asking that question is: In our healthcare system and in other healthcare systems, if you want to take a precision oncology approach, how do you create the pipelines? And what types of technologies really lend themselves to benefits over and above next-generation sequencing or multigene panels, allowing for access to off-label therapies? What does that look like? Does that actually improve patients? I think some of the challenges, of course, is because of heterogeneity, small benefiting populations, finding a signal if a signal is indeed there is really challenging. And so, what we are thinking through is, with respect to real-world evidence methods and emulating randomized controlled trials, what types of evidence methods actually allow us to find those signals if indeed those signals are there in the context of small benefiting populations? Dr. Rafeh Naqash:Thank you so much, Dean. Sounds like a very exciting field, especially in the current day and age where cost-effectiveness, financial toxicity is an important aspect of how we improve upon what is existing in oncology. And then lots more to be explored, as you mentioned. The last minute and a half I want to ask about you as an individual, as a researcher. There's very few people who have expertise in oncology, biomarkers, and health economics. So could you tell us for the sake of our trainees and early career physicians who might be listening, what was your trajectory briefly? How did you end up doing what you're doing? And maybe some advice for people who are interested in the cost of care, the cost of oncology drugs - what would your advice be for them very briefly? Dr. Dean Regier:Sure. So I'm an economist by training, and indeed I knew very little about the healthcare system and how it works. But I was recruited at one point to BC Cancer, to British Columbia, to really try to understand some of those questions around costs, and then I learned also around cost-effectiveness. And so, I did training in Scotland to understand patient preferences and patient values around quality of care, not just quantity of life, but also their quality of life and how that care was provided to them. And then after that, I was at Oxford University at the Nuffield Department of Population Health to understand how that can be incorporated into randomized control trials in children. And so, I did a little bit of learning about RCTs. Of course, during the way I picked up some epidemiology with deep understanding of what I call econometrics, what others might call biostatistics or just statistics. And from there, it was about working with clinicians, working with epidemiologists, working with clinical trialists, working with economists to understand the different approaches or ways of thinking of how to estimate efficacy, effectiveness, safety, and cost-effectiveness. I think this is really important to think through is that we have clinical trialists, we have people with deep understanding of biostatistics, we have genome scientists, we have clinicians, and then you add economists into the mix. What I've really benefited from is that interdisciplinary experience, meaning that when I talk to some of the world's leading genome scientists, I understand where they're coming from, what their hope and vision is. And they start to understand where I'm coming from and some of the tools that I use to understand comparative effectiveness and cost-effectiveness. And then we work together to actually change our methods in order to answer those questions that we're passionate about and curious about better for the benefit of patients. So, the short answer is it's been actually quite a trajectory between Canada, the UK. I spent some time at the University of Washington looking at the Fred Hutch Cancer Research Center, looking at precision oncology. And along the way, it's been an experience about interdisciplinary research approaches to evaluating comparative outcomes. And also really thinking through not just at one point in time on-off decisions—is this effective? Is it safe? Is it cost-effective?—not those on-off decisions, but those decisions across the lifecycle of a health product. What do those look like at each point in time? Because we gain new evidence, new information at each point in time as patients have more and more experience around it. And so what really is kind of driving our research is really thinking about interdisciplinary approaches to lifecycle evaluation of promising new drugs with the goal of having these promising technologies to patients sooner in a way that is sustainable for the healthcare system. Dr. Rafeh Naqash:Awesome. Thank you so much for those insights and also giving us a sneak peek of your very successful career. Thank you for listening to JCO Precision Oncology Conversations. Don't forget to give us a rating or review, and be sure to subscribe so you never miss an episode. You can find all ASCO shows at asco.org/podcast. Thank you. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.      

Dr. Jonathan Howard and Wendy Orent examine the alarming elevation of wellness influencer Casey Means as Surgeon General nominee, despite lacking a medical license or conventional medical credibility. They delve into Vinay Prasad's appointment as head of vaccine regulation, scrutinizing his past critiques of RCT deficiencies—and the impossible standards he now sets for himself. The episode also investigates the troubling rise of an autism registry, likened to authoritarian categorization, and NIH's internal collapse under Jay Bhattacharya, whose leadership is marked by mass layoffs and denial of responsibility. With science policy veering into cronyism, dismantling, and performative governance, the episode argues that we're witnessing a historic erosion of public health leadership—led not by scientists, but social media provocateurs. Connect with us further on https://sciencebasedmedicine.org/author/jonathanhoward/  The Fine Print The content presented in the "We Want Them Infected" Podcast and associated book is intended for informational and educational purposes only.  The views and opinions expressed by the speakers, hosts, and guests on the podcast do not necessarily reflect the views of the creators, producers, or distributors. The information provided in this podcast should not be considered as a substitute for professional medical, scientific, or legal advice. Listeners and readers are encouraged to consult with relevant experts and authorities for specific guidance and information. The creators of the podcast and book have made reasonable efforts to ensure that the information provided is accurate and up to date. However, as the field of medical science and the understanding of the COVID-19 pandemic continue to evolve, there may be new developments and insights that are not covered in this content. The creators are not responsible for any errors or omissions in the content or for any actions taken based on the information provided. They disclaim any liability for any loss, injury, or damage incurred by individuals who rely on the content. Listeners and readers are urged to use their judgment and conduct their own research when interpreting the information presented in the "We Want Them Infected" podcast and book. It is essential to stay informed about the latest updates, guidelines, and recommendations related to COVID-19 and vaccination from reputable sources, such as government health agencies and medical professionals. By accessing and using the content, you acknowledge and accept the terms of this disclaimer. Please consult with appropriate experts and authorities for specific guidance on matters related to health, science, and the COVID-19 pandemic.

New treatment alert! The FDA recently approved Tapinarof, applied as a cream, for kids 2 years and up. We ask Dr. Leon Kircik from Icahn School of Medicine, NY, who led the clinical trials about the safety, efficacy and side effects of Tapinarof. And because we are parents too, we ask: How quickly does it work? Can you start/stop it as needed? How easy will it be to access? And more. If you like our podcast, please consider supporting it with a tax deductible donation. Research discussedTapinarof Improved Outcomes and Sleep for Patients and Families in Two Phase 3 Atopic Dermatitis Trials in Adults and ChildrenMaximal usage trial of tapinarof cream 1% once daily in pediatric patients down to 2 years of age with extensive atopic dermatitisTapinarof cream 1% once daily: Significant efficacy in the treatment of moderate to severe atopic dermatitis in adults and children down to 2 years of age in the pivotal phase 3 ADORING trialsTapinarof cream in the treatment of atopic dermatitis in children and adults a systematic review and meta-analysisEfficacy and safety of Ruxolitinib, Crisaborole, and Tapinarof for mild-to-moderate atopic dermatitis: a Bayesian network analysis of RCTs

This podcast was created using NotebookLM. This podcast underscores the significant underrepresentation of older adults in clinical trials, particularly randomized controlled trials (RCTs), despite their increasing population and the high prevalence of chronic diseases within this demographic. 

Today, we have a fascinating discussion focusing on therapy after lumbar disc herniation surgery. We delve into a massive study that brings together findings from 55 randomized controlled trials, shedding new light on the best approaches to post-surgical rehab and the role of physical therapy. With significant implications for your chiropractic practice, we'll explore key insights on how physical therapy post-surgery can reduce pain, improve function, boost return-to-work rates, and even lower anxiety.Episode Notes: Physical therapies after surgery for lumbar disc herniation- evidence synthesis from 55 randomized controlled trials (RCTs) and a total of 4,311 patientsThe Best Objective Assessment of the Cervical Spine- Provide reliable assessments and exercises for Neuromuscular Control, Proprioception, Range of Motion, and Sensorimotor-Integration. Learn more at NeckCare.comTurncloud EHR- Minimalist design, without being sparse. Practical, yet elegant. Turncloud's design was to find the most efficient path in a day in the life of a chiropractic office. Connect with their team at www.turncloud.com Patient Pilot by The Smart Chiropractor is the fastest, easiest to generate weekly patient reactivations on autopilot…without spending any money on advertising. Click here to schedule a call with our team.Our members use research to GROW their practice. Are you interested in increasing your referrals? Discover the best chiropractic marketing you aren't currently using right here!

Not all salts are created equal!

Join JACC Associate Editor Khurram Nasir, MBBS, FACC, and author Rohan Khera, MD, FACC, as they discuss the latest study on tirzepatide presented at ACC.25 and published in JACC. Tirzepatide, a dual GIP/GLP-1 receptor agonist, exerts pleiotropic effects on cardiometabolic health. This study evaluated its efficacy in improving cardiometabolic outcomes in individuals with T2D. An individual participant data meta-analysis was conducted, pooling data from seven Phase 3 RCTs comparing tirzepatide with placebo or standard antihyperglycemic agents. The study outcomes included cardiometabolic components of metabolic syndrome (MetS), elevated BMI, and MetS. Tirzepatide significantly reduced the odds of these abnormalities and effectively resolved MetS, with superior efficacy observed in younger individuals and those not on baseline SGLT2is. These findings support the potential of tirzepatide to improve cardiometabolic health in T2D.

Send us a textIn this episode, I had the pleasure of speaking with Dr Ilana Levene, who is now a Neonatology subspeciality trainee at Oxford, England. Ilana has done some fantastic work on exploring the important topic of human milk expression. She described her randomized control trial in using relaxing techniques to facilitate human milk expression in the NICU. She shared the challenges that she had in conducting her RCT. We also talked about RCTs with negative results and how negative results are also important in conducting research. Ilana has now created a website with printables for parents and staff in the NICU on human milk expression. This can be assessed for free here : http://www.hifn.org/printable . Ilana also shared her interest in perinatal equity and shared details on her project Spectrum which involves gathering photos of the lactating breast conditions/chest from people with a wide spectrum of skincolours. These will be provided as a free educational image library. Currently she is chairing a priority setting partnership for LGBTQIA+ perinatal care. As always, feel free to send us questions, comments, or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through Instagram or Twitter, @nicupodcast. Or contact Ben and Daphna directly via their Twitter profiles: @drnicu and @doctordaphnamd. The papers discussed in today's episode are listed and timestamped on the webpage linked below. Enjoy!

Welcome to Mad In America Radio. My name is Bob Whitaker, and today my guest is Italian psychiatrist, Giovanni Fava. From 1992 to 2022, Dr. Fava edited the journal Psychotherapy and Psychosomatics. We will be talking about the importance of that journal and what may be lost now that the publisher, Karger, may be taking it in a new direction. Here's why this journal, under Dr. Fava's leadership, was so important to us all. When psychiatry talks about how its drug treatments are evidence-based, it points to RCTs and meta-analyses of those RCTs as proof that its drugs are more effective than placebo. However, Psychotherapy and Psychosomatics under Dr. Fava's guidance presented a very different evidence base to its readers. First, his journal told of how clinical experiences should govern our understanding of the impact of psychiatric treatments, particularly over longer periods of time. Second, his journal told of how RCTs and meta-analyses when used to direct clinical practices can lead to harm. Third, his journal told of the corrupting influence of pharmaceutical money on the creation of psychiatric diagnoses and drug trials. When Dr. Fava became editor of Psychotherapy and Psychosomatics in 1992, it had a low impact factor. When he resigned as editor in 2022, it had an impact factor that made it one of the most influential journals in psychiatry and psychology. He left the journal in good hands in 2022 and he remained involved as an honorary editor. However, in December, Karger fired one of the two editors in chief, Dr. Fava then resigned as honorary editor, and most of the editorial board resigned as well. The future of this journal, which had been so essential to our understanding of the impact of psychiatric treatments is now unclear. *** Thank you for being with us to listen to the podcast and read our articles this year. MIA is funded entirely by reader donations. If you value MIA, please help us continue to survive and grow. https://www.madinamerica.com/donate/ To find the Mad in America podcast on your preferred podcast player, click here: https://pod.link/1212789850 © Mad in America 2025. Produced by James Moore https://www.jmaudio.org

Dr. Ebony Hoskins and Dr. Andreas Obermair discuss the surgical management of gynecologic cancers, including the role of minimally invasive surgery, approaches in fertility preservation, and the nuances of surgical debulking. TRANSCRIPT Dr. Ebony Hoskins: Hello and welcome to the ASCO Daily News Podcast, I'm Dr. Ebony Hoskins. I'm a gynecologic oncologist at MedStar Washington Hospital Center in Washington, DC, and your guest host of the ASCO Daily News Podcast. Today we'll be discussing the surgical management of gynecologic cancer, including the role of minimally invasive surgery (MIS), approaches in fertility preservation, and the nuances of surgical debulking, timing, and its impact on outcomes. I am delighted to welcome Dr. Andreas Obermair for today's discussion. Dr. Obermair is an internationally renowned gynecologic oncologist, a professor of gynecologic oncology at the University of Queensland, and the head of the Queensland Center for Gynecologic Cancer Research. Our full disclosures are available in the transcript of this episode. Dr. Obermair, it's great speaking with you today. Dr. Andreas Obermair: Thank you so much for inviting me to this podcast. Dr. Ebony Hoskins: I am very excited.  I looked at your paper and I thought, gosh, is everything surgical? This is everything that I deal with daily in terms of cancer in counseling patients. What prompted this review regarding GYN cancer management? Dr. Andreas Obermair: Yes, our article was published in the ASCO Educational Book; it is volume 44 in 2024. And this article covers some key aspects of targeted precision surgical management principles in endometrial cancer, cervical cancer, and ovarian cancer. While surgery is considered the cornerstone of gynecologic cancer treatment, sometimes research doesn't necessarily reflect that. And so I think ASCO asked us to; so it was not just me, there was a team of colleagues from different parts of the United States and Australia to reflect on surgical aspects of gynecologic cancer care and I feel super passionate about that because I do believe that surgery has a lot to offer. Surgical interventions need to be defined and overall, I see the research that I'm doing as part of my daily job to go towards precision surgery. And I think that is, well, that is something that I'm increasingly passionate for. Dr. Ebony Hoskins: Well, I think we should get into it. One thing that comes to mind is the innovation of minimally invasive surgery in endometrial cancer. I always reflect on when I started my fellowship, I guess it's been about 15 years ago, all of our endometrial cancer patients had a midline vertical incision, increased risk of abscess, infections and a long hospital stay. Do you mind commenting on how you see management of endometrial cancer today? Dr. Andreas Obermair: Thank you very much for giving the historical perspective because the generation of gynecologic oncologists today, they may not even know what we dealt with, what problems we had to solve. So like you, when I was a fellow in gynecologic oncology, we did midline or lower crosswise incisions, the length of stay was, five days, seven days, but we had patients in hospital because of complications for 28 days. We took them back to the operating theaters because those are patients with a BMI of 40 plus, 45, 50 and so forth. So we really needed to solve problems. And then I was exposed to a mentor who taught minimal invasive surgery. And in Australia he was one of the first ones who embarked on that. And I can remember, I was mesmerized by this operation, like not only how logical this procedure was, but also we did rounds afterwards. And I saw these women after surgery and I saw them sitting upright, lipstick on, having had a full meal at the end of the day. And I thought, wow, this is the most rewarding experience that I have to round these patients after surgery. And so I was thinking, how could I help to establish this operation as standard? Like a standard that other people would accept this is better. And so I thought we needed to do a trial on this. And then it took a long time. It took a long time to get the support for the [LACE - Laparoscopic Approach to Cancer of the Endometrium] trial. And in this context, I just also wanted to remind us all that there were concerns about minimal invasive surgery in endometrial cancer at the time. So for example, one of the concerns was when I submitted my grant funding applications, people said, “Well, even if we fund you, wouldn't be able to do this trial because there are actually no surgeons who actually do minimally invasive surgery.” And at the time, for example, in Australia, there were maybe five people, a handful of people who were able to do this operation, right? This was about 20 years ago. The other concern people had was they were saying, could minimally invasive surgery for endometrial cancer, could that cause port side metastasis because there were case reports. So there were a lot of things that we didn't know anyway. We did this trial and I'm super happy we did this trial. We started in 2005, and it took five years to enroll. At the same time, GOG LAP2 was ramping up and the LACE trial and GOG LAP2 then got published and provided the foundations for minimally invasive surgery in endometrial cancer. I'm super happy that we have randomized data about that because now when we go back and now when people have concerns about this, should we do minimally invasive surgery in P53 mutant tumors, I'm saying, well, we actually have data on that. We could go back, we could actually do more research on that if we wanted to, but our treatment recommendations are standing on solid feet. Dr. Ebony Hoskins: Well, my patients are thankful. I see patients all the time and they have high risk and morbidly obese, lots of medical issues and actually I send them home most the same day. And I think, you know, I'm very appreciative of that research, because we obviously practice evidence-based and it's certainly a game changer. Let's go along the lines of MIS and cervical cancer. And this is going back to the LACC [Laparoscopic Approach to Cervical Cancer] trial.  I remember, again, one of these early adopters of use of robotic surgery and laparoscopic surgery for radical hysterectomy and thought it was so cool. You know, we can see all the anatomy well and then have the data to show that we actually had a decreased survival. And I even see that most recent updated data just showing it still continued. Can you talk a little bit about why you think there is a difference? I know there's ongoing trials, but still interested in kind of why do you think there's a survival difference? Dr. Andreas Obermair:  So Ebony, I hope you don't mind me going back a step. So the LACC study was developed from the LACE trial. So we thought we wanted to reproduce the LACE data/LAP2 data. We wanted to reproduce that in cervix cancer. And people were saying, why do you do that? Like, why would that be different in any way? We recognize that minimally invasive radical hysterectomy is not a standard. We're not going to enroll patients in a randomized trial where we open and do a laparotomy on half the patients. So I think the lesson that really needs to be learned here is that any surgical intervention that we do, we should put on good evidence footing because otherwise we're really running the risk of jeopardizing patients' outcomes. So, that was number one and LACC started two years after LACE started. So LACC started in 2007, and I just wanted to acknowledge the LACC principal investigator, Dr. Pedro Ramirez, who at the time worked at MD Anderson. And we incidentally realized that we had a common interest. The findings came totally unexpected and came as an utter shock to both of us. We did not expect this. We expected to see very similar disease-free and overall survival data as we saw in the endometrial cancer cohort. Now LACC was not designed to check why there was a difference in disease-free survival. So this is very important to understand. We did not expect it. Like, so there was no point checking why that is the case. My personal idea, and I think it is fair enough if we share personal ideas, and this is not even a hypothesis I want to say, this is just a personal idea is that in endometrial cancer, we're dealing with a tumor where most of the time the cancer is surrounded by a myometrial shell. And most of the time the cancer would not get into outside contact with the peritoneal cavity. Whereas in cervix cancer, this is very different because in cervix cancer, we need to manipulate the cervix and the tumor is right at the outside there. So I personally don't use a uterine manipulator. I believe in the United States, uterine manipulators are used all the time. My experience is not in this area, so I can't comment on that. But I would think that the manipulation of the cervix and the contact of the cervix to the free peritoneal cavity could be one of the reasons. But again, this is simply a personal opinion. Dr. Ebony Hoskins: Well, I appreciate it. Dr. Andreas Obermair: Ebony at the end of the day, right, medicine is empirical science, and empirical science means that we just make observations, we make observations, we measure them, and we pass them on. And we made an observation. And, and while we're saying that, and yes, you're absolutely right, the final [LACC] reports were published in JCO recently. And I'm very grateful to the JCO editorial team that they accepted the paper, and they communicated the results because this is obviously very important. At the same time, I would like to say that there are now three or four RCTs that challenge the LACC data. These RCTs are ongoing, and a lot of people will be looking forward to having these results available. Dr. Ebony Hoskins: Very good. In early-stage cervical cancer, the SHAPE trial looked at simple versus radical hysterectomy in low-risk cervical cancer patients. And as well all know, simple hysterectomy was not inferior to radical hysterectomy with respect to the pelvic recurrence rate and any complications related to surgery such as urinary incontinence and retention. My question for you is have you changed your practice in early-stage cervical cancer, say a patient with stage 1B1 adenocarcinoma with a positive margin on conization, would you still offer this patient a radical hysterectomy or would you consider a simple hysterectomy? Dr. Andreas Obermair:  I think this is a very important topic, right? Because I think the challenge of SHAPE is to understand the inclusion criteria. That's the main challenge. And most people simplify it to 2 cm, which is one of the inclusion criteria but there are two others and that includes the depth of invasion. Dr. Marie Plante has been very clear. Marie Plante is the first author of the SHAPE trial that's been published in the New England Journal of Medicine only recently and Marie has been very clear upfront that we need to consider all three inclusion criteria and only then the inclusion criteria of SHAPE apply. So at the end of the day, I think what the SHAPE trial is telling us that small tumors that would strictly fulfill the criteria of a 1B or 1B1 cancer of the cervix can be considered for a standard type 1 or PIVA type 1 or whatever classification we're trying to use will be eligible. And that makes a lot of sense. I personally not only look at the size, I also look at the location of the tumor. I would be very keen that I avoid going through tumor tissue because for example, if you have a tumor that is, you know, located very much in one corner of the cervix and then you do a standard hysterectomy and then you have a positive tumor margin that would be obviously, most people would agree it would be an unwanted outcome. So I'd be very keen checking the location, the size of the tumor, the depths of invasion and maybe then if the tumor for example is on one side of the cervix you can do a standard approach on the contralateral side but maybe do a little bit more of a margin, a parametrial margin on the other side. Or if a tumor is maybe on the posterior cervical lip, then you don't need to worry so much about the anterior cervical margin, maybe take the rectum down and maybe try to get a little bit of a vaginal margin and the margin on the uterus saccals. Just really to make sure that you do have margins because typically if we get it right, survival outcomes of clinical stage 1 early cervix cancer 1B1 1B 2 are actually really good. It is a very important thing that we get the treatment right. In my practice, I use a software to record my treatment outcomes and my margins. And I would encourage all colleagues to be cognizant and to be responsible and accountable to introduce accountable clinical practice, to check on the margins and check on the number on the percentage of patients who require postoperative radiation treatment or chemo radiation. Dr. Ebony Hoskins: Very good. I have so many questions for you. I don't know the statistics in Australia, but here, there's increased rising of endometrial cancer and certainly we're seeing it in younger women. And fertility always comes up in terms of kind of what to do. And I look at the guidelines and, see if I can help some of the women if they have early-stage endometrial cancer. Your thoughts on what your practice is on use of someone who may meet criteria, if you will. The criteria I use is grade 1 endometrioid adenocarcinoma. No myometria invasion. I try to get MRI'd and make sure that there's no disease outside the endometrium. And then if they make criteria, I typically would do an IUD. Can you tell me what your practice is and where you've had success? Dr. Andreas Obermair: So, we initiated the feMMe clinical trial that was published in 2021 and it was presented in a Plenary at one of the SGO meetings. I think it was in 2021, and we've shown complete pathological response rates after levonorgestrel intrauterine device treatment. And so in brief, we enrolled patients with endometrial hyperplasia with atypia, but also patients with grade 1 endometrial adenocarcinoma. Patients with endometrial hyperplasia with atypia had, in our series, had an 85 % chance of developing a complete pathological response. And that was defined as the complete absence of any atypia or cancer. So endometrial hyperplasia with atypia responded in about 85%. In endometrial cancer, it was about half, it was about 45, 50%. In my clinical practice, like as you, I see patients, you know, five days a week. So I'm looking after many patients who are now five years down from conservative treatment of endometrial cancer. There are a lot of young women who want to get pregnant, and we had babies, and we celebrate the babies obviously because as gynecologist obstetricians it couldn't get better than that, right, if our cancer patients have babies afterwards. But we're also treating women who are really unfit for surgery and who are frail and where a laparoscopic hysterectomy would be unsafe. So this phase is concluded, and I think that was very successful. At least we're looking to validate our data. So we're having collaborations, we're having collaborations in the United States and outside the United States to validate these data. And the next phase is obviously to identify predictive factors, to identify predictors of response. Because as you can imagine, there is no point treating patients with a levonorgestrel intrauterine joint device where we know in advance that she's not going to respond. So this is a very, very fascinating story and we got our first set of data already, but now we just really need to validate this data. And then once the validation is done, my unit is keen to do a prospective validation trial. And that also needs to involve international collaborators. Dr. Ebony Hoskins: Very good. Moving on to ovarian cancer, we see patients with ovarian cancer with, say, at least stage 3C or higher who started neoadjuvant chemotherapy. Now, some of these patients are hearing different things from their medical oncologist versus their gynecologic oncologist regarding the number of cycles of neoadjuvant chemotherapy after getting diagnosed with ovarian cancer. I know that this can be confusing for our patients coming from a medical oncologist versus a gynecologic oncologist. What do you say to a patient who is asking about the ideal number of chemotherapy cycles prior to surgery? Dr. Andreas Obermair: So this is obviously a very, very important topic to talk about. We won't be able to provide a simple off the shelf answer for that, but I think data are emerging.  The ASCO guidelines should also be worthwhile considering because there are actually new ASCO Guidelines [on neoadjuvant chemotherapy for newly diagnosed, advanced ovarian cancer] that just came out a few weeks ago and they would suggest that we should be aiming for R0 in surgery. If we can maybe take that as the pivot point and then go back and say, okay, so what do need to do to get the patient to zero?  I'm not an ovarian cancer researcher; I'm obviously a practicing gynecologic oncologist. I think about things a lot and things like that. In my practice, I would want a patient to develop a response after neoadjuvant chemotherapy. So, if a patient doesn't have a response after two or three cycles, then I don't see the point for me to offer her an operation. In my circle with the medical oncologists that I work with, I have a very, very good understanding. So, they send the patient to me, I take them to the theater. I take a good chunk of tissue from the peritoneum. We have a histopathologic diagnosis, we have a genomic diagnosis, they go home the same day. So obviously there is no hospital stay involved with that. They can start the chemotherapy after a few days. There is no hold up because the chances of surgical complication in a setting like this is very, very low. So I use laparoscopy to determine whether the patient responds or not. And for many of my patients, it seems to work. It's obviously a bit of an effort and it takes operating time. But I think I'm increasing my chances to make the right decision. So, coming back to your question about whether we should give three or six cycles, I think the current recommendations are three cycles pending the patient's response to neoadjuvant chemotherapy because my aim is to get a patient to R0 or at least minimal residual disease. Surgery is really, in this case, I think surgery is the adjunct to systemic treatment. Dr. Ebony Hoskins: Definitely. I think you make a great point, and I think the guideline just came out, like you mentioned, regarding neoadjuvant. And I think the biggest thing that we need to come across is the involvement of a gynecologic oncologist in patients with ovarian cancer. And we know that that survival increases with that involvement. And I think the involvement is the surgery, right? So, maybe we've gotten away from the primary tumor debulking and now using more neoadjuvant, but surgery is still needed. And so, I definitely want to have a take home that GYN oncology is involved in the care of these patients upfront. Dr. Andreas Obermair: I totally support that. This is a very important statement. So when I'm saying surgery is the adjunct to medical treatment, I don't mean that surgery is not important. Surgery is very important. And the timing is important. And that means that the surgeons and the med oncs need to be pulling on the same string. The med oncs just want to get the cytotoxic into the patients, but that's not the point, right? We want to get the cytotoxic into the patients at the right time because if we are working under this precision surgery, precision treatment mantra, it's not only important what we do, but also doing it at the right time. And ideally, I I would like to give surgery after three cycles of neoadjuvant chemotherapy, if that makes sense. But sometimes for me as a surgeon, I talk to my med onc colleagues and I say, “Look, she doesn't have a good enough response to her treatment and I want her to receive six cycles and then we re-evaluate or change medical treatment,” because that's an alternative that we can swap out drugs and treat upfront with a different drug and then sometimes they do respond. Dr. Ebony Hoskins:  I have maybe one more topic. In the area I'm in, in the Washington D.C. area, we see lots of endometrial cancer and they're not grade 1, right? They're high-risk endometrial cancer and advanced. So a number of patients with stage 3 disease, some just kind of based off staging and then some who come in with disease based off of the CT scan, sometimes omental caking, ascites. And the real question is we have extrapolated the use of neoadjuvant chemotherapy to endometrial cancer. It's similar, but not the same. So my question is in an advanced endometrial cancer, do you think there's still a role, when I say advanced, I mean, maybe stage 4, a role for surgery? Dr. Andreas Obermair: Most definitely. But the question is when do you want to give this surgery? Similar to ovarian cancer, in my experience, I want to get to R0. What am I trying to achieve here? So, I reckon we should do a trial on this. And I reckon we have, as you say, the number of patients in this setting is increasing, we could do a trial. I think if we collaborate, we would have enough patients to do a proper trial. Obviously, we would start maybe with a feasibility trial and things like that. But I reckon a trial would be needed in this setting because I find that the incidence that you described, that other people would come across, they're becoming more and more common. I totally agree with you, and we have very little data on that. Dr. Ebony Hoskins: Very little and we're doing what we can. Dr. Obermair, thank you for sharing your fantastic insights with us today on the ASCO Daily News Podcast and for all the work you do to advance care for patients with gynecologic cancer. Dr. Andreas Obermair: Thank you, Dr. Hoskins, for hosting this and it's been an absolute pleasure speaking with you today. Dr. Ebony Hoskins: Definitely a pleasure and thank you to our listeners for your time today. Again, Dr. Obermair's article is titled, “Controversies in the Surgical Management of Gynecologic Cancer: Balancing the Decision to Operate or Hesitate,” and was published in the 2024 ASCO Educational Book. And you'll find a link to the article in the transcript of this episode. Finally, if you value the insights that you hear on the ASCO Daily News Podcast, please take a moment to rate, review and subscribe wherever you get your podcasts. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity or therapy should not be construed as an ASCO endorsement. Find out more about today's speakers: Dr. Ebony Hoskins @drebonyhoskins Dr. Andreas Obermair @andreasobermair Follow ASCO on social media:       @ASCO on Twitter       ASCO on Bluesky   ASCO on Facebook       ASCO on LinkedIn       Disclosures:   Dr. Ebony Hoskins: No relationships to disclose. Dr. Andreas Obermair: Leadership: SurgicalPerformance Pty Ltd. Stock and Ownership Interests: SurgicalPerformance Pty Ltd. Honoraria: Baxter Healthcare Consulting or Advisory Role: Stryker/Novadaq Patents, Royalties, and Other Intellectual Property: Shares in SurgicalPerformance Pty Ltd. Travel, Accommodation, Expenses: Stryker    

Vanessa Spina is a Sport Nutrition Specialist (SNS) and the Best Selling author of Keto Essentials. She is a researcher who studied biomedical science at the University of Toronto, an international speaker and host of the wildly popular Optimal Protein Podcast, ranked in the Top 20 podcasts in the Nutrition category in the USA and globally #1-20. It has been nominated twice as a top 3 Best Podcast at the Metabolic Health Summit.  Vanessa founded Ketogenic Girl in 2015 with online audience of over half a million. Vanessa has created three innovative wellness products. The Tone device, a breath ketone analyzer which measures acetone, the ketone detected on the breath. The second is a new red light therapy line called the Tone LUX Collection. The third is a supplement line called Tone that includes Tone Protein, a protein powder that is scientifically formulated to initiate Muscle Protein Synthesis in every serving with the addition of leucine, and the new Tone Collagen which has clinical studies (RCTs) proving its effectiveness.  She has been featured as a nutrition expert in articles published in the Orlando Sentinel, Eat This, Parade, Reader's Digest and more. Instagram: @ketogenicgirl @optimalproteinpodcast @tonedevice @thetonelux Twitter: @ketogenicgirl Website: Www.ketogenicgirl.com Timestamps: 00:00 Trailer 01:12 Introduction 04:09 Children's innate eating wisdom 07:44 Rising awareness of food quality 10:29 European dietary habits and trends 15:02 Carnivore diet ended my food obsession 17:49 Revamped keto focus on ketones 19:03 Asymptomatic progress and protein satiety 22:26 MCT and ketone supplements for focus 27:36 Ketones: alternative brain fuel 31:53 High-fat foods and nutrition 33:23 Balanced diet preference over carnivore 38:02 Drunken attempt to avoid onions 41:05 New book on high-protein diets 44:28 Whey protein and insulin response 46:23 Whey protein isolate benefits 51:02 Red meat misconceptions persist 52:55 Where to find Vanessa Join Revero now to regain your health: https://revero.com/YT Revero.com is an online medical clinic for treating chronic diseases with this root-cause approach of nutrition therapy. You can get access to medical providers, personalized nutrition therapy, biomarker tracking, lab testing, ongoing clinical care, and daily coaching. You will also learn everything you need with educational videos, hundreds of recipes, and articles to make this easy for you. Join the Revero team (medical providers, etc): https://revero.com/jobs ‪#Revero #ReveroHealth #shawnbaker  #Carnivorediet #MeatHeals #AnimalBased #ZeroCarb #DietCoach  #FatAdapted #Carnivore #sugarfree Disclaimer: The content on this channel is not medical advice. Please consult your healthcare provider.

Dr. Jonathan Howard and Wendy Orent discuss the growing public health disasters under RFK Jr.'s leadership at HHS. They cover the first measles death of a child in over 30 years, the cancellation of a crucial flu vaccine advisory meeting, and the termination of funding for a promising oral COVID vaccine trial.    Meanwhile, RFK Jr. moves to eliminate public commentary on HHS decisions, and scientific institutions continue to suffer massive cuts. They highlight the Orwellian doublespeak of Vinay Prasad and others who once demanded more RCTs—only to stay silent as Kennedy cancels them.    Finally, they introduce the Bill Cassidy Profile in Cowardice Award, recognizing the senator who had the power to stop this but chose not to. Connect with us further on https://sciencebasedmedicine.org/author/jonathanhoward/  The Fine Print The content presented in the "We Want Them Infected" Podcast and associated book is intended for informational and educational purposes only.    The views and opinions expressed by the speakers, hosts, and guests on the podcast do not necessarily reflect the views of the creators, producers, or distributors. The information provided in this podcast should not be considered as a substitute for professional medical, scientific, or legal advice. Listeners and readers are encouraged to consult with relevant experts and authorities for specific guidance and information.   The creators of the podcast and book have made reasonable efforts to ensure that the information provided is accurate and up to date. However, as the field of medical science and the understanding of the COVID-19 pandemic continue to evolve, there may be new developments and insights that are not covered in this content.   The creators are not responsible for any errors or omissions in the content or for any actions taken based on the information provided. They disclaim any liability for any loss, injury, or damage incurred by individuals who rely on the content.   Listeners and readers are urged to use their judgment and conduct their own research when interpreting the information presented in the "We Want Them Infected" podcast and book. It is essential to stay informed about the latest updates, guidelines, and recommendations related to COVID-19 and vaccination from reputable sources, such as government health agencies and medical professionals. By accessing and using the content, you acknowledge and accept the terms of this disclaimer.   Please consult with appropriate experts and authorities for specific guidance on matters related to health, science, and the COVID-19 pandemic.  

The treatment of asymptomatic aortic stenosis, the move to composite endpoints in trials, IFR vs FFR and high-frequency low tidal volume ventilation for AF ablation are the topics John Mandrola, MD, discusses in today's podcast. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I Aortic valve intervention for Asymptomatic AS Lindman editorial https://jamanetwork.com/journals/jamacardiology/fullarticle/2829881 Trends https://pmc.ncbi.nlm.nih.gov/articles/PMC11308430/ Podcast EARLY TAVR Nov 8, 2024 This Week in Cardiology Podcast https://www.medscape.com/viewarticle/1001865 Faith Healing and Subtraction Anxiety https://www.ahajournals.org/doi/10.1161/circoutcomes.118.004665 Early TAVR trial https://www.nejm.org/doi/10.1056/NEJMoa2405880 EVOLVED https://jamanetwork.com/journals/jama/fullarticle/2825540 AVATAR https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.121.057639 II Trial Endpoints Shepshelovich https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2830023 Brown meta-analysis https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2785560 III IFR vs FFR—a debate b/w RCTs and observational data 5-year DEFINE https://jamanetwork.com/journals/jamacardiology/fullarticle/2824470 5-year SwedeHeart IFR https://doi.org/10.1016/j.jacc.2021.12.030 Eftekhari meta-analysis https://doi.org/10.1093/eurheartj/ehad582 Gotberg SWEDEHEART Registry https://doi.org/10.1016/j.jcin.2024.12.003 Editorial of SWEDEHEART-Registry https://doi.org/10.1016/j.jcin.2024.12.014 IV High-frequency low-tidal-volume ventilation for AF ablation Osorio et al https://doi.org/10.1016/j.hrthm.2024.07.094 You may also like: The Bob Harrington Show with the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net

Another negative AF ablation trial, predicting AF after stroke, the value of RCTs, troponin testing in the ED and surgical aortic valve choice are the topics John Mandrola, MD, discusses this week. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I AF ablation Coronary Sinus Isolation for High-Burden Atrial Fibrillation: A Randomized Clinical Trial https://doi.org/10.1016/j.jacep.2024.09.017 Approaches to Catheter Ablation for Persistent Atrial Fibrillation (STAR AFII) https://www.nejm.org/doi/full/10.1056/NEJMoa1408288 Effect of Catheter Ablation With Vein of Marshall Ethanol Infusion vs Catheter Ablation Alone on Persistent Atrial Fibrillation: The VENUS Randomized Clinical Trial https://doi.org/10.1001/jama.2020.16195 Hybrid Convergent Procedure for the Treatment of Persistent and Long-Standing Persistent Atrial Fibrillation: Results of CONVERGE Clinical Trial https://www.ahajournals.org/doi/10.1161/CIRCEP.120.009288 II Post-Stroke AF monitoring Prediction of atrial fibrillation after a stroke event: a systematic review with meta-analysisMeta-analysis 10.1016/j.hrthm.2025.01.026 Dabigatran for Prevention of Stroke after Embolic Stroke of Undetermined Source https://www.nejm.org/doi/full/10.1056/NEJMoa1813959 Rivaroxaban for Stroke Prevention after Embolic Stroke of Undetermined Source (Navigate ESUS https://www.nejm.org/doi/full/10.1056/NEJMoa1802686 Apixaban to Prevent Recurrence After Cryptogenic Stroke in Patients With Atrial Cardiopathy (ARCADIA) https://jamanetwork.com/journals/jama/fullarticle/2814933 III RCTs Large simple randomized controlled trials—from drugs to medical devices: lessons from recent experience https://trialsjournal.biomedcentral.com/articles/10.1186/s13063-025-08724-x Outcomes 1 Year after Thrombus Aspiration for Myocardial Infarction (TASTE) https://www.nejm.org/doi/full/10.1056/NEJMoa1405707 IV Troponin Testing in the ED Cardiac Biomarker Testing in US Emergency Departments https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2829344 Updating Our Thinking on Troponin Use and Interpretation https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2777967 V Choice of AVR Bioprosthetic vs Mechanical Aortic Valve Replacement in Patients 40-75 Years https://doi.org/10.1016/j.jacc.2025.01.013 You may also like: The Bob Harrington Show with the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net

US doc's pay, the ticagrelor controversy and new RCTs, clopidogrel beats ASA, holding antiplatelets for non-cardiac surgery, and Prof Cleland and ASA dogma are the topics John Mandrola, MD, covers this week. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I. US Healthcare Mandrola's Top 10 Stories in 2024 https://www.medscape.com/viewarticle/mandrolas-top-10-stories-2024-2024a1000mxe?_gl=1*dcvmkh*_gcl_au*MTgzOTY2ODQ0Ni4xNzI5MjU4NjUz CMS Proposal II. Ticagrelor Controversy New Investigation Casts Doubt on Landmark Ticagrelor Trial https://www.medscape.com/viewarticle/new-investigation-casts-doubt-landmark-ticagrelor-trial-2024a1000n1d Doshi Review https://www.bmj.com/content/387/bmj.q2550 PLATO https://www.nejm.org/doi/full/10.1056/NEJMoa0904327 ISAR REACT 5 https://www.nejm.org/doi/full/10.1056/NEJMoa1908973 Bates Review https://www.ahajournals.org/doi/epub/10.1161/JAHA.123.031606 Victor Serebuany and Dan Atar Editorial https://doi.org/10.1093/eurheartj/ehp545 III. New Ticagrelor vs Clopdiogrel trial Preprint: https://www.medrxiv.org/content/10.1101/2024.11.06.24316875v1.full-text IV. Clopidogrel Better Than ASA Even in HBR Substudy Long-Term Aspirin vs Clopidogrel After Coronary Stenting by Bleeding Risk and Procedural Complexity HOST-EXAM 10.1016/S0140-6736(21)01063-1 HOST-EXAM-Extended https://doi.org/10.1161/CIRCULATIONAHA.122.062770 V. ASA During Non-Cardiac Surgery ASSURE DES https://doi.org/10.1016/j.jacc.2024.08.024 VII. Professor Cleland on ASA for Secondary Prevention Cleland Editorial https//jamanetwork.com/journals/jamacardiology/article-abstract/2827201 ASA Meta-analysis 10.1016/S0140-6736(09)60503-1 AMIS https://jamanetwork.com/journals/jama/fullarticle/368745 SAPAT 10.1016/0140-6736(92)92619-Q You may also like: The Bob Harrington Show with the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net