Category: 8. Health

  • Experiencing pain? Sanjay Gupta explains why ‘It Doesn’t Have to Hurt’

    CNN Chief Medical Correspondent Sanjay Gupta vividly remembers the day he impaled himself on a wrought iron fence. He had just turned 12, and he was running through the neighborhood when he spontaneously decided to vault over a fence that he usually ran around. Except he didn’t quite make it.

    “One of the spikes caught me on my side and went in the back area of my side and out the front,” Gupta says. “It was the skin, thankfully, as opposed to going into the chest or into the abdomen, which would have been much worse, but it was sort of a classic in-out sort of injury.”

    Gupta says he was impaled for several minutes before his mother arrived to help hoist him off the fence. Looking back now, he remembers feeling a strange sense of euphoria when it happened, which he attributes to his body’s natural pain relief system.

    “For some people, it reacts really vigorously — like really, really churns out a bunch of endorphins,” he says. “And so you could have this really sort of ironic situation where you’ve got a terrible injury and you’re almost laughing. It’s a very protective sort of response from the body. And not everyone responds the same way.”

    In his new book, It Doesn’t Have to Hurt: Your Smart Guide to a Pain-Free Life, Gupta, a trained neurosurgeon, write about pain — what causes it, and the various medications that can be used to treat it. He also reflects on ways to train the mind to minimize certain kinds of pain, using distraction and meditation.

    “With pain, people are usually hyper-focused on a particular sensation. Being able to take them out of that hyper-focus can be really helpful,” he says. “The idea [is] that you could take someone’s pain score from really terrible pain to a zero out of 10 … for the 30 minutes that they are meditating. … I think the brain can be trained that way.”

    One of the best examples of how the brain can make a mistake is phantom limb pain … It was amputated, and yet it still hurts. I think that’s one of those sort of insights about the brain that I think led to a lot of learning about what exactly the brain’s role was with pain. If the brain’s the decider of pain, can it create pain as well? And the answer is yes.

    Referred pain is another sort of mistake. So some people may be having what should be chest pain from a heart attack, but instead of having chest pain, they may have jaw pain. They may have just left arm pain. … And then there’s sorts of things where whatever the reason may be, the brain continues to play the loop of pain over and over again. I guess that’s not so much a mistake as it is maybe some sort of glitch, where the pain loop doesn’t stop and it just gets recycled over and over again, and that’s chronic pain. So those are some of the ways that the brain can sort of either mistake or misinterpret the signals and the pain.

    What I think is really interesting is that we have this system within our body, the endogenous opioid system. … This is like our internal morphine system, endorphin system. We can activate this system in all sorts of different ways. And by activating, I mean exactly what it sounds like. You just basically release a lot of these endorphins, these basically personalized morphine molecules all throughout your body. And one of the ways that they have shown can really facilitate that is to not just practice gratitude, but to actively practice gratitude. Meaning, actually savor something. I’m not just grateful for this ice cream cone. I’m so enjoying this ice-cream cone. I’m just not grateful for being able to look at this sunset. I am gazing at every different color in the sky and just taking it all in. It’s a very active form of gratitude. And it seems to be very associated with basically activating the endogenous opioid system, which is really fascinating to me.

    So many techniques and medications that we use in real life take their inspiration from our human body, and that’s one of them. … With your own opioid system, it is very, very sensitive. So it can turn on and it can turn off really, really well. So instead of having the lingering sort of side effects of opioids and sedation and all these other things, the opioids that you make yourself can just be washed away very, very quickly. …

    I always say if the endogenous opioid system didn’t exist, women would probably never have more than one child. It can be a painful experience, but those [natural] opioids help with the pain. They help with the mood, and … [they] can actually inhibit your memory.

    I think for the most part, inflammation has sort of gotten a bad rap. … I think when you look at a sprained ankle, for example, and it looks swollen and red, the idea that I want to get rid of that. That’s associated with my pain makes intuitive sense. I think the idea that that inflammation serves a real purpose, that not only is it sort of helping protect the site of injury, but also sending all these various molecules to the site of injury to help with the healing. …

    The thing about pain is that everyone’s threshold is going to be a little bit different. … I think for a lot of people, they think they need to take anti-inflammatories. Oh, this is bad, I gotta treat that, that inflammation’s not good, that’s hurting my body. But if I flip the script on you and I say, “It’s not bad for your body, that is exactly how your body is supposed to work. This is your body doing its job.”

    The medication is called Suzetrigine. … It is a fascinating story of how it came about. There were these families of circus performers in Karachi, Pakistan. That got the attention of researchers, whatever, 25, 30 years ago. And they saw that these circus performers were able to do all these remarkable things, like they could put sharp things through their appendages and they could walk on hot coals and do all that sort of stuff. But what they found was that when they were doing this, they could feel the coals on their feet and they could feel that they were hot, they just didn’t have pain. … And that was pretty striking because it gave these researchers a clue as to which sodium channel blocker may be important when it came to just targeting pain and not sensation overall. They studied this family. They found that they had a gene in common. … And basically for 25 years, these researchers tried to replicate what that gene was doing in the body. … Now, one of the big challenges of creating a medicine like that is you didn’t want to take away pain forever. Pain has utility. It can keep you safe. It can teach you lessons. So they wanted to create a half-life for the drug. So they basically now have an oral formulation.

    I walked into it thinking that if I really examined all this literature, there was going to be a pretty compelling case made for using cannabis for all sorts of different pains … and I walked away not as impressed, to be quite honest, as I thought I would be. And this is just the data talking. I will say it’s hard to collect this data when you’re dealing with a substance that has been a level one substance in the United States for a long time. It’s just really hard to get good studies.  …

    But having said that, the best available data seem to suggest that for about a third of the people, it could be pretty effective, and maybe in some cases as effective as the best other options for that neuropathic pain. … For about two-thirds of people, it really did not seem to be that effective. And this is the case, I think, for about a third of people, they get significant benefit. And we don’t quite know who those third of the people are. We don’t know what makes them different than the other two-thirds that they’re getting that kind of relief.  

    Monique Nazareth and Susan Nyakundi produced and edited this interview for broadcast. Bridget Bentz and Molly Seavy-Nesper adapted it for the web.

    Audio transcript

    TERRY GROSS, HOST:

    This is FRESH AIR. I’m Terry Gross. When you’re in pain, it can be hard to think about anything else. My guest, neurosurgeon and CNN chief medical correspondent Sanjay Gupta, writes that over the past few decades, we’ve learned more than ever about the true nature of pain. We better understand what causes it, what may best relieve it and what we can do to minimize or even eliminate certain types of pain. Many of those life-changing insights have not yet been made easily available to the public. His new book is an attempt to change that. It’s called “It Doesn’t Have to Hurt.”

    Dr. Gupta is also the host of the podcast “Chasing Life.” He’s an associate professor of neurosurgery at the Emory University Hospital and is the author of four previous bestsellers. He’s won several Emmy Awards, as well as two duPont-Columbia Awards, the most recent one for his reporting on the medical use of marijuana – a subject we’ll talk about a little later in the interview. He also contributed to CNN’s Peabody Award-winning coverage of the devastation of Hurricane Katrina 20 years ago. Dr. Gupta, welcome back to FRESH AIR.

    SANJAY GUPTA: Thank you. What a pleasure. I always enjoy our conversations. Thank you for having me.

    GROSS: So I’ll start with something I’ve never said to a guest before, which is, tell us how you were impaled. This was just after your 12th birthday.

    GUPTA: I was a kid. I was just after 12 years old – just turned 12. And I was running through the neighborhood on a really beautiful day – I still remember – and there was a fence. And I think it was sort of a wrought iron fence, and it had some spikes on top. And I had – you know, obviously knew this fence. Typically, I didn’t try and jump over it. I went around it. But this day, I just – I think I felt kind of invincible. And I decided to sort of try and vault myself over, you know, put one hand on and then vault your legs over. And when I tried that, I didn’t quite make it. And one of the spikes caught me on my side and went in the back area of my side and out the front. So I was sort of stuck there on this fence. It was just high enough that I could not put my feet down to sort of, you know, hoist myself off the fence.

    GROSS: So it appears through your whole side?

    GUPTA: Yeah. It was the skin, thankfully, as opposed to going into the chest or into the abdomen, which would have been much worse. But it was sort of a classic in-out sort of injury. And the story is interesting because the – first of all, I was there for a couple of minutes before anyone saw me, which was really a very strange feeling. You know, I knew somebody was going to find me, but I think for a moment as a 12-year-old, I thought, what if they don’t? And – but eventually, a neighbor came out. And around the same time, my mom sort of – I don’t know how she became aware, but she kind of heard and she came over. And the neighbor went to go get this big sort of wire cutter thing, and he was going to basically cut it. But I couldn’t wait, actually. So with my mom’s help, she put her foot down. I mean, she put her hands down so I could put my foot on her hands, and I hoisted myself off the spike. So I actually came off the spike on my own before he cut it off.

    GROSS: Ouch (laughter). And you write that the tissues in the torso don’t have as many nerves and as much sensitivity as other parts of the body.

    GUPTA: Yeah. This was, I think, the first time I started sort of thinking about pain in a different way because, first of all, and I can tell you what it felt like, which was very different than what I would have imagined it to feel like before it happened. But yeah, one of the things is that the skin on the back, it has fewer of these nociceptors, these receptors that will actually transmit pain. And by fewer, it also means that they’re less dense over an area. When you have a higher density of nociceptors, that’s when they’re going to be more sensitive. And they’re transmitting signals very quickly ’cause they’re so close together, jam-packed together.

    When those nociceptors are further apart, you have less sensation. You have less what is called two-point discrimination, so your ability to tell the distance between two points is much greater on the back. The two points have to be much, much further apart before you can really tell that there’s two points. And it didn’t hurt as much as I think many other parts of the body would have.

    GROSS: OK. So now that we’ve established that you’ve experienced pain…

    GUPTA: (Laughter).

    GROSS: …What do you mean when you say that pain is created by the brain? In your case, pain was created by a very unnatural injury. But explain that the pain is created by the brain.

    GUPTA: Whenever we have some sort of thing that happens in the periphery of our body – in this case, it was my back – signals are then sent to the brain to basically be processed, to be translated and to be interpreted in some way. When those signals go up – it’s kind of like the brain is, you know, rapidly scrolling a social media feed and may say, OK, this is not that important. This is not that important. This is not that important. Oh, wait a second, this is incendiary, this particular post. Let’s pay a lot of attention to that.

    And it determines at that point, is this real, No. 1, or is it not? Is it noteworthy, meaning, how – you know, how significant is it? And what should I do about it? There are certain things that happen before you get to the brain, which is that you might have – like, if you touch a hot pan, your hand might jolt away from it. That’s happening reflexively. There are certain nerve fibers that do that. But when it comes to actually determining if something hurts and how much, that is the brain. The brain determines whether or not you have pain.

    GROSS: The brain sometimes makes mistakes in its interpretation…

    GUPTA: Yeah.

    GROSS: …Of pain too, and sometimes it sounds the alarm too loud and too long. How does the brain make mistakes, and what kind of pain does that lead to?

    GUPTA: One of the best examples of how the brain can make a mistake is phantom limb pain. In that case, a limb doesn’t even exist anymore…

    GROSS: It was amputated.

    GUPTA: …And yet it still hurts.

    GROSS: Yeah.

    GUPTA: It was amputated, and yet it still hurts. I think that’s one of those sort of insights about the brain that I think led to a lot of learning about what exactly the brain’s role was with pain. If the brain’s the decider of pain, can it create pain as well? And the answer is yes. Referred pain is another sort of mistake. So some people may be having what should be chest pain from a heart attack, but instead of having chest pain, they may have jaw pain. They may have just left arm pain. And some of those are common referrals. We know left arm pain, for example, is very associated with potential heart problem. Doctors are sort of trained – same thing with jaw pain.

    And then there’s sorts of things where, whatever the reason may be, the brain continues to play the loop of pain over and over again. I guess that’s not so much a mistake as it is some – maybe some sort of glitch, where the pain loop doesn’t stop and it just gets recycled over and over again. And that’s chronic pain. So those are some of the ways that the brain can sort of either mistake or misinterpret the signals and the pain.

    GROSS: So, you know, a lot of times someone will go to see a doctor, and they have chronic pain, but there’s no evidence of what’s causing it, and the injury has healed. So that’s a kind of brain misinterpretation?

    GUPTA: Some would argue that there is a reason, and it may have to do with everything from adverse childhood events to even more recent trauma to a history of depression or anxiety. As someone said to me – I think it was Mark Jensen at Mayo Clinic – that chronic pain never occurs in isolation. It always occurs with baggage attached, and that baggage could be depression, could be anxiety, could be adverse childhood experiences, could be poor sleep. It could be things that maybe seem more trivial. Could be you’re having a really bad day, and something that wouldn’t have hurt so much hurt a lot more because you’re having a bad day. Maybe you had a bad call with your parent. Whatever it may be, all these things – some more clear, some more arbitrary – seem to have some influence not just on your pain, but how much something’s going to hurt and how long it will hurt.

    GROSS: So one of the main themes of your book is, if the brain interprets pain, can we get the brain to interpret it differently, or at least turn down the volume of the alarm that it is sending? Do you believe the brain is really capable of being rewired like that?

    GUPTA: Yeah, I really do. And I’ve seen it firsthand. The idea that meditation could provide relief – maybe not super durable. It’s not something that lasts forever. But the idea that you could take someone’s pain score from really terrible pain to a 0 out of 10 – and I’m not exaggerating – but a 0 out of 10 for the 30 minutes that they are meditating, I think, is real proof of concept that there’s a lot that can happen within the brain that can be trained without drugs, without surgery. So, yeah, I think the brain can be trained that way.

    GROSS: Do you have a scientific medical explanation for why meditation can decrease pain for at least an interval of time?

    GUPTA: Dr. Eric Garland is probably the nation’s leading expert on this. He’s out of the University of California San Diego. And I spent a lot of time with him and asked that same question. And I think we don’t know is the most honest answer. I think where people sort of circle around is this idea that distraction could be one component of it. You know, with pain, people are usually hyperfocused on a particular sensation. Being able to take them out of that hyperfocus can be really helpful.

    There’s other people who believe that you’re actually decreasing the activity in certain areas of the brain. Specifically, an area known as the anterior cingulate cortex, which is an area where pain is processed. Pain is processed in many areas of the brain, but that’s one of the primary areas. But we don’t know for sure. It would require, I think, a lot more testing to really, you know, look at people’s brains while they meditate and understand what’s happening. And even then, the answers may not be clear.

    But what I think is clear, based on lots of data, is that people can get significant relief from meditation. And I even asked Dr. Garland to, like, give me context for what that means, significant relief. I mean, we can put numbers on it. But what he showed and what his most recent paper described was basically similar to 5 milligrams of oxycodone. That’s what meditation can do for you. Five milligrams of oxycodone is very effective. It also doesn’t last forever. It has a half-life. Meditation is sort of the same way. It doesn’t last forever, but you can reduce your pain scores to near zero for a period of time.

    GROSS: You actually meditated with the Dalai Lama. I assume you were reporting on him, which is how you got to get the invitation to meditate with him. And you were very self-conscious and distracted because you were not only meditating, you know, you were doing it with the Dalai Lama. You reluctantly admitted that to him after the session was over. And tell us what he said to you.

    GUPTA: (Laughter) He told me he also had a difficult time meditating, which really surprised me. I mean, you know, he’s the Dalai Lama. He’s been meditating, you know, basically his whole life. And he’s a master meditator. He gets up, I think, 3:30 in the morning, and he meditates for a couple of hours before he starts his regular day. And that was the time that I was meditating with him. But he sort of conceded that it can be challenging for people to meditate. You have to be very intentional about it.

    GROSS: Well, let’s take a pause here because I have to reintroduce you and take a break. My guest is neurosurgeon Sanjay Gupta, who is CNN’s chief medical correspondent. His new book is called “It Doesn’t Have To Hurt.” It’s about pain and pain management. We’ll talk more. After a break. This is FRESH AIR.

    (SOUNDBITE OF ROBBEN FORD AND BILL EVANS’ “CATCH A RIDE”)

    GROSS: This is FRESH AIR. Let’s get back to my interview with CNN chief medical correspondent Dr. Sanjay Gupta. He’s a neurosurgeon. His new book about pain and ways to control it is called “It Doesn’t Have To Hurt.”

    One of the points you make in the book is that researchers have found that pleasure and savoring, savoring food, savoring pleasure, making sure you make some space for pleasure or savoring in your life, that it isn’t a waste of time, that you’re actually rewiring your brain and countering pain in ways that strengthen with practice. Can you talk about that a little bit, about what that might mean?

    GUPTA: Sure. I think our default position, probably, as humans is to be creatures that have gratitude and savor and want to experience pleasure. That’s no surprise. But what I think is really interesting is that we have this system within our body. The endogenous opioid system, which is endorphins, which means endo, which means inside the body, and phins, which is morphine. This is like our internal morphine system, endorphin system. We can activate this system in all sorts of different ways. And by activating, I mean exactly what it sounds like. You just basically release a lot of these endorphins, these basically personalized morphine molecules all throughout your body.

    And one of the ways that they have shown can really facilitate that is to not just practice gratitude, but to actively practice gratitude, meaning actually savor something. I’m not just grateful for this ice cream cone. I’m like, just so enjoying this ice cream cone. I’m not just grateful for being able to look at this sunset. I am gazing at every different color in the sky and just taking it all in.

    It’s a very active form of gratitude, and it seems to be very associated with basically activating the endogenous opioid system, which is really fascinating to me. Some people would refer to this as sort of the mechanism behind placebo effect. Others say the placebo effect is going to be a lot more intricate than that. But when it comes to pain specifically, I think we know all these different things that we’re talking about, whether it be meditation, whether it be savoring – all these things mechanistically probably have some component of activating this really wonderful, intricate system in our bodies.

    GROSS: I guess it also teaches the person who is savoring or having pleasure to distract themselves from pain because just as pain distracts you from the things you need to do, having pleasure really distracts you from the pain.

    GUPTA: Yeah. I think what’s becoming increasingly clear – that these types of, you know, feel-good transmitters and endorphins are released in response to certain things that happen in our lives. You know, even going back to when I impaled myself on that fence, I think what was so interesting to me, and I was only 12 years old at the time, but when I reflected on it, it obviously hurt when I got impaled. But then I was basically pinned there on the fence for several minutes. And you know what, Terry? After a while, not only did it not hurt as much, I actually started to feel strangely a bit of euphoria…

    GROSS: Really?

    GUPTA: …Which is – yeah, which is really weird. But I think what happens for some people, and probably I fit into this, is that when you do have an injury or, you know, whatever might happen to you, if you activate your endogenous opioid system, for some people, it reacts really vigorously, like, really, really churns out a bunch of endorphins. And so you could have this really sort of ironic situation where you get a terrible injury, and you’re almost laughing. You’re like (laughter), oh, my God, you know? And it’s – I think it’s a very protective sort of response from the body. And not everyone responds the same way. Some people probably make fewer endorphins. And maybe if it had been raining on me and I hadn’t eaten well that day, maybe I would’ve made fewer endorphins. But for a period of time, I really had no pain. In fact, I remember I reached behind with my hand at one point to feel the spike and convinced myself that it was still there.

    GROSS: Are there any medications that exist or that are in development that could turn on the body’s natural opioid system and release more endorphins?

    GUPTA: What we’ve done is basically try to give endorphins, right? We’ve – instead of saying exactly what you said, which is can you harness the body’s own EOS, endogenous opioid system? Instead, we said, oh, the body makes endogenous morphine. Let us synthesize this molecule on our own. Let us create a drug that essentially attaches to the same receptors that these endorphins do, the mu receptors in the body. And that was sort of the genesis of opioids. You know, so many techniques and medications that we use in real life take their inspiration from our human body, and that’s one of them.

    So we give opioids, probably more so than focusing on teaching the body to release its own opioid system. And while they both may have opioid in the name, they’re very different. One thing is that with your own opioid system, it is very, very sensitive. So it can turn on and it can turn off really, really well. So instead of having the lingering sort of side effects of opioids and sedation and all these other things, the opioids that you make yourself can just be washed away very, very quickly. The second thing is that impact on mood. It can actually make you euphoric. It can really improve your mood. And the third thing is that people with opioids, often it does not suppress their memory. In fact, it may actually worsen it. And worsen it, in this case, means over-remembering. So people who take opioids long term might actually start to have more pain because they become increasingly challenged to forget their pain.

    GROSS: Right. So in answer to our researchers trying to develop an external form of endorphins, your answer is, yeah, morphine, and it didn’t work out very well. But that’s why pleasure is kind of like a prescription right now.

    GUPTA: Yeah. I think pleasure, savoring – we know these things will release more opioids. People tend to feel better. Their pain tolerance goes up, and their remembering of unpleasant things goes down.

    GROSS: Right.

    GUPTA: So all these things sort of happen. I always say, if the endogenous opioid system didn’t exist, women would probably never have more than one child. You know, it can be a painful experience, but those opioids help with the pain. They help with the mood. And then that memory component is so fascinating to me. It can actually inhibit your memory. Like, I talked to my wife about this, Rebecca. We have three girls. And she’s like, yeah, you know, I had the baby. I, you know, just – by time we’re having the second one, it wasn’t, like, something she reflected on and was traumatized by. That’s, like, one of the most significant things that happens in your life. How could you possibly forget that? And maybe it’s – forgetting’s not the right word, but how could you not remember it really vividly? And I think that’s not by accident. I think that’s really our own endorphins sort of doing their job in terms of pain, mood and memory.

    GROSS: OK. We need to take another break here, but there’s plenty more to talk about. If you’re just joining us, my guess is Dr. Sanjay Gupta, CNN’s chief medical correspondent and author of the new book “It Doesn’t Have To Hurt.” We’ll talk more about pain and pain relief after a short break. I’m Terry Gross, and this is FRESH AIR.

    (SOUNDBITE OF SAINT SINNA AND CREEBO LODI SONG, “REAL FLOW”)

    GROSS: This is FRESH AIR. I’m Terry Gross. Let’s get back to my interview with Dr. Sanjay Gupta. His new book, “It Doesn’t Have To Hurt” is about pain, how the brain sounds the alarm through pain and how the brain sometimes misinterprets the signals it gets and sends alarms that are unnecessarily loud and misleading. He also writes about treating pain from over-the-counter standbys like Tylenol, Advil and Motrin to new non-opioid medications, including electric medicine, new medications and how meditation and other techniques can help you retrain how your brain and how you process pain.

    Let’s talk about the latest understanding of inflammation and anti-inflammatories, and that would include medications like Advil and Motrin. Inflammation is an essential part of healing after an injury. It protects the injury. It’s like putting a protective covering over the injury. But after a while, it seems like part of the problem is the inflammation itself. Sometimes it just won’t go away, or it just lingers too long or gets too large.

    GUPTA: I think, for the most part, inflammation has sort of gotten a bad rap. I think that the idea that I don’t want to have inflammation, I’ll do everything I can to get rid of inflammation if I have some sort of injury, that has been, I think, the prevailing wisdom for a long time. And I think it’s understandable. I think when you look at a sprained ankle, for example, and it looks swollen and red, the idea that I want to get rid of that that’s associated with my pain makes intuitive sense. I think the idea that that inflammation serves a real purpose, that not only is it sort of helping protect the site of injury but also sending all these various molecules to the site of injury to help with the healing, I think, is also what’s happening at that point.

    So there was a study that came out that basically was trying to figure out who is most likely to have chronic pain after injuries. So if you look at the sprained ankle example, who is most likely to still have pain three months later? And interestingly – and the researchers weren’t looking for this – what they found was that people who had the lowest levels of inflammation at the time of injury were the most likely to have chronic pain. So low levels of inflammation were linked to chronic pain, not high levels of inflammation. And it was really relevant, I think, for people, especially in the sports world and orthopedic surgeons and physical therapists to sort of look at the guidance that had typically been given to people, which was do everything you can to decrease inflammation.

    GROSS: So some researchers are recommending now not taking anti-inflammatories right after an injury. When do researchers suggest that you do take anti-inflammatories?

    GUPTA: I think it’s if you can’t tolerate it. That’s the thing about pain is that everyone’s threshold is going to be a little bit different. Again, if you haven’t broken it, I’m telling you it’s better to mobilize and not try and decrease inflammation. I think for a lot of people, they think they need to take anti-inflammatories. Oh, this is bad. I got to treat that. That inflammation’s not good. It’s hurting my body. But if I flip the script on you and I say, it’s not bad for your body. That is exactly how your body is supposed to work. This is your body doing its job.

    GROSS: This may be a good time to mention that acetaminophen, for example, Tylenol, is not an anti-inflammatory.

    GUPTA: That’s right.

    GROSS: In your book, in describing what kinds of problems could be treated with acetaminophen, like Tylenol or ibuprofen, like Advil and Motrin, you have under both categories, under both types of pills that they’re really not for nerve pain. Why not?

    GUPTA: Nerve pain or neuropathic pain tends to be a different sort of pain. Again, with anti-inflammatories, I guess it’s inherent in the name, the way that it works – Tylenol can help decrease inflammation, but in a totally different mechanism. It’s very good at reducing fever. Nerve pain really seems to be something that has to do with an abnormality of the way the nerve’s actually conducting signals. So, for example, when someone herniates a disc in their back or their neck and it puts pressure on the nerve, the nerve is not conducting the same way. It may be over-sending some signals or under-sending other signals. And what you’re really trying to do in that situation is take certain meds that might balance out that nerve conduction again. And that’s a different class of medications. There are several classes that can do this, but not typically anti-inflammatories.

    GROSS: You know what I sometimes wonder? Can a numbing agent like lidocaine train the brain to think like, oh, there’s no longer pain, so I can turn the pain signals – like…

    GUPTA: Yeah.

    GROSS: …The unnecessary pain signals, from chronic pain. I can turn them off now. Can you trick a brain with a numbing agent?

    GUPTA: This is a – it’s a really interesting question. And lidocaine is a good example of this. So Lidocaine is what’s called a sodium channel blocker. You know, whenever there’s signals being transmitted in the body, the way those signals move is through changes in ions – sodium, potassium. Ions like that. If you can block certain – a certain of those sodium channels, you can inhibit certain sensations. In this case, pain or sensation overall because lidocaine makes you numb. It’s not just taking away pain. I don’t know that there’s any indication that they will necessarily train your brain in some way to have any benefit beyond the time that the lidocaine is there in terms of chronic pain.

    You can get rid of it for a period of time, and we use lidocaine to basically convince ourselves as surgeons that something that we’re about to do is going to be beneficial. So someone who has trigeminal neuralgia, I don’t know if you’ve ever heard of that, but it’s lancinating face pain. Tic douloureux, it’s called, and it’s one of the worst pains I think a human can actually feel. Just these lightning bolts of pain in your face. But anyways, one of the things that we’ll do is we might inject the root of the nerve with some numbing agent like lidocaine and basically see if that takes away the pain. And if it does, that gives us an indication that it may be OK to heat up that area of the nerve or to use chemicals to sort of make that nerve not conduct anymore. But that’s what those types of numbing agents are good for.

    GROSS: Well, it’s time for another break, so let me reintroduce you. If you’re just joining us, my guest is neurosurgeon Dr. Sanjay Gupta, CNN’s chief medical correspondent. His new book is called “It Doesn’t Have To Hurt.” We’ll talk more after a break. This is FRESH AIR.

    (SOUNDBITE OF LOOP 2.4.3’S “ZODIAC DUST”)

    GROSS: This is FRESH AIR. Let’s get back to my interview with CNN chief medical correspondent Dr. Sanjay Gupta. He’s a neurosurgeon, and his new book is about pain and ways to control it. It’s called “It Doesn’t Have To Hurt.”

    While you were writing your new book, a non-opioid pain medication was approved by the FDA. Tell us about it.

    GUPTA: Yeah. The medication is called suzetrigine. It is a new pain medication. And interestingly enough, it is the first new pain medication that was approved by the FDA in the United States since 1998, which I found really remarkable. I mean, the last one was Celebrex. And just to give some context, the FDA will typically approve 40 to 50 new drugs a year. But for pain, which is a condition, chronic pain, that affects 20% of the population and, according to some of the statistics we saw, is the fastest-growing condition now in the United States, faster than cancer, diabetes and dementia – it’s pretty remarkable that we hadn’t had a new option for pain. But suzetrigine is that new option, and it is a fascinating story of how it came about.

    There were these families of circus performers in Karachi, Pakistan, that got the attention of researchers, whatever, 25, 30 years ago. And they saw that these circus performers were able to do all these remarkable things. Like, they could put sharp things through their appendages, and they could walk on hot coals and do all that sort of stuff. But what they found was that when they were doing this, they could feel the coals on their feet, and they could feel that they were hot. They just didn’t have pain. And that’s very different than what we were just talking about with lidocaine, which basically numbs you. So when you’re numb, you just have no sensation. Here, they had sensation. They just didn’t have pain. And that was pretty striking because it gave these researchers a clue as to which sodium channel blocker may be important when it came to just targeting pain and not sensation overall. They studied this family. They found that they had a gene in common. I think it’s called SCN9. And basically, for 25 years, these researchers tried to replicate what that gene was doing in the body.

    Now, one of the big challenges of creating a medicine like that is something you alluded to earlier, which is that you didn’t want to take away pain forever. Pain has utility. It can keep you safe. It can teach you lessons. So they wanted to create a half-life for the drug. So they basically now have an oral formulation. I think it’s twice-a-day formulation to basically try and treat pain, something that, you know, they hadn’t had a new therapy for in over 25 years.

    GROSS: Let’s talk about cannabis as a pain medication. You’ve done extensive reporting on cannabis as medicine. What are some of your takeaways about the use of it for pain?

    GUPTA: We spent a lot of time looking at the literature around cannabis. And I walked into it thinking that if I really examined all this literature, there was going to be a pretty compelling case made for using cannabis for all sorts of different pains but mostly neuropathic pain, this type of pain where the nerve’s just not conducting well and either over- or under-conducting, and that’s causing pain. And I walked away not as impressed, to be quite honest, as I thought I would be. And this is just the data talking. I will say it’s hard to collect this data when you’re dealing with a substance that has been a Level 1 substance in the United States for a long time. It’s just really hard to get good studies.

    GROSS: It’s hard to get funding probably, too, right?

    GUPTA: Yeah. And then there’s a lot of stigma attached to it, so people don’t volunteer for the trials, whatever it might be. But having said that, the best available data seemed to suggest that for about a third of people, it could be pretty effective and maybe, in some cases, as effective as the best other options for that neuropathic pain. Terry, for about two-thirds of people, it really did not seem to be that effective. And this is the case, I think, for about a third of people. They get significant benefit, and we don’t quite know who those third of people are. We don’t know what makes them different than the other two-thirds that they’re getting that kind of relief.

    GROSS: Is there any evidence that it might be the placebo effect?

    GUPTA: Yeah. I think that they’re looking at all sorts of different things, including placebo effect. I think one of the researchers that I talked to – I think it was Julie Holland. She kept making this point that I thought was a really good point, that expectations and experience are inextricably linked, especially when it comes to pain, and the idea that if you really expect something to work, it’s more likely to work. And that isn’t necessarily your body or your brain playing tricks on you. That is probably, again, harnessing that endogenous opioid system. You think it’s going to work. Your body’s like, oh, yeah, I’m about to get relief. Wow, I’m already feeling it, you know? And that, in part, could be those endorphins starting to really ramp up.

    GROSS: Another way of kind of retraining the brain is deep brain stimulation, which uses electric impulses in parts of the brain, in relevant parts of the brain. It’s used now for Parkinson’s disease. There’s, like, a little device that’s implanted in the appropriate part of the brain, and there’s a remote control. You can turn it up or turn it down. So how is that being used in pain relief, or is it just in the real beginning stages?

    GUPTA: Deep brain stimulation’s been around for a long time. And, you know, Parkinson’s was one of the things, but they also treat things like obsessive compulsive disorder now, even with – Tourette’s, things like that, with deep brain stimulation. It’s pretty fascinating. The idea of using it for pain sort of came about in a very interesting way.

    I think one of the big questions neuroscientists have been percolating on for a long time is, we know pain is processed in the brain. Is there a way to figure out where and how it’s processed in the brain and also to measure it in some way? Right now, we’re primarily relying on, you know, smiley or frowny faces for patients to tell us how much pain they have. But is there a way to objectify that in some way?

    And I think that’s really how these researchers, Prasad Shirvalkar and others at UCSF started approaching this, was to say, OK, these patients who have pain – and these were the worst of the worst patients. They had pain that was so refractory. They’d had sometimes dozens of operations, spinal cord stimulators, taking many generations of pain medications, and they just weren’t getting relief. They were the ones who qualified for the trial. And the trial basically consisted of putting a bunch of stimulators all over the brain, left side and right side, and basically just listening to the brain. When the person had pain, they recorded it, and they would do this for months. And they would basically say, OK, whenever the patient has pain, what happened in the brain at that point? Was there a transfer of energy somewhere? Is there something to see?

    And using, you know, machine learning now, being able to analyze a lot of that data – because it’s a lot of data. You have 84 billion neurons in the brain. They were able to find those areas, in some ways measure them, seeing how much energy was actually changing in that part of the brain, which gave some sort of correlation with the significance of pain or the severity of pain. And they even got to the point where they could start to predict that change of energy before the patient felt it. And they even got to the point where they could then interrupt it, much like you do with Parkinson’s.

    You gave a little jolt of electricity at that point, and you basically interrupt that pain signaling at that point in the brain. It was proof of concept, I think, to your fundamental question, which is, not only is this the formative stages, this isn’t something that’s ever going to be, you know, for the masses. No one is suggesting that brain surgery, which is what these patients had, is going to be the answer. But I think what it has proven is that pain is very much in the brain. And we can objectify it in ways that we did not fully appreciate before.

    GROSS: That’s fascinating. Is AI being used as part of this to process the data?

    GUPTA: Yes. I think if you talk to these researchers, I don’t think they could’ve done this probably without at least these large machine learning models. It is so much data. I mean, they had some idea where pain processing is likely to occur. There are some areas of the brain that are more likely to process pain than others, but there is no single pain processing center. So they needed to look all over the brain and then just spend this time correlating lots and lots of data with all these energy transfers that are happening in the brain, because your brain is constantly communicating.

    And I got to tell you, I got to spend time with a patient who got tremendous success with this strategy that I’ve described. And he’s had terrible pain for decades. You know, it’s the kind of pain I’m not sure I could’ve tolerated in my own life the way he described it. Just like these snakes constantly biting his feet and razor blades all the time. He had a condition known as CRPS, chronic regional pain syndrome.

    And he’s in the hospital, and he’s got the stimulator in. And he’s, you know, in the middle of a patient visit. And all of a sudden, he goes, whoa. And they said, what? He goes, I don’t have pain. The veil of pain just went away. I’ve had this veil over my face and over my, you know, brain for decades, and it just got lifted. I don’t have pain. It was the wildest thing. I don’t know where the research goes in terms of what this is going to mean for the masses. But it was really, really amazing to see that kind of relief.

    GROSS: Well, on that note, Sanjay Gupta, thank you so much for talking with us.

    GUPTA: Thanks, Terry. I always look forward – I write books just so I can have these conversations with you.

    (LAUGHTER)

    GUPTA: I really appreciate your time.

    GROSS: I appreciate yours. Thank you so much and be well. Thank you.

    Sanjay Gupta is a neurosurgeon and CNN’s chief medical correspondent. His new book about pain is called “It Doesn’t Have To Hurt.”

    After we take a short break, TV critic David Bianculli will review the new HBO crime series, “Task,” by the creator of “Mare Of Easttown.” It stars Mark Ruffalo. This is FRESH AIR.

    (SOUNDBITE OF THE BENNIE MAUPIN QUARTET’S “PROPHET’S MOTIFS”)

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  • Seroconversion of SSA and the Development of Inflammatory Myositis in a Patient With Chronic Joint Pain: A Potential Overlap Connective Tissue Disease

    Seroconversion of SSA and the Development of Inflammatory Myositis in a Patient With Chronic Joint Pain: A Potential Overlap Connective Tissue Disease


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  • Sanjay Gupta talks pain and why ‘It Doesn’t Have to Hurt’ : NPR

    Sanjay Gupta talks pain and why ‘It Doesn’t Have to Hurt’ : NPR

    CNN Chief Medical Correspondent Sanjay Gupta vividly remembers the day he impaled himself on a wrought iron fence. He had just turned 12, and he was running through the neighborhood when he spontaneously decided to vault over a fence that he usually ran around. Except he didn’t quite make it.

    “One of the spikes caught me on my side and went in the back area of my side and out the front,” Gupta says. “It was the skin, thankfully, as opposed to going into the chest or into the abdomen, which would have been much worse, but it was sort of a classic in-out sort of injury.”

    Gupta says he was impaled for several minutes before his mother arrived to help hoist him off the fence. Looking back now, he remembers feeling a strange sense of euphoria when it happened, which he attributes to his body’s natural pain relief system.

    “For some people, it reacts really vigorously — like really, really churns out a bunch of endorphins,” he says. “And so you could have this really sort of ironic situation where you’ve got a terrible injury and you’re almost laughing. It’s a very protective sort of response from the body. And not everyone responds the same way.”

    In his new book, It Doesn’t Have to Hurt: Your Smart Guide to a Pain-Free Life, Gupta, a trained neurosurgeon, writes about pain — what causes it, and the various medications that can be used to treat it. He also reflects on ways to train the mind to minimize certain kinds of pain, using distraction and meditation.

    “With pain, people are usually hyper-focused on a particular sensation. Being able to take them out of that hyper-focus can be really helpful,” he says. “The idea [is] that you could take someone’s pain score from really terrible pain to a zero out of 10 … for the 30 minutes that they are meditating. … I think the brain can be trained that way.”

    Interview highlights

    It Doesn't Have to Hurt, by Sanjay Gupta

    It Doesn’t Have to Hurt, by Sanjay Gupta

    Simon & Schuster


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    Simon & Schuster

    On mistakes the brain makes in processing pain

    One of the best examples of how the brain can make a mistake is phantom limb pain … It was amputated, and yet it still hurts. I think that’s one of those sort of insights about the brain that I think led to a lot of learning about what exactly the brain’s role was with pain. If the brain’s the decider of pain, can it create pain as well? And the answer is yes.

    Referred pain is another sort of mistake. So some people may be having what should be chest pain from a heart attack, but instead of having chest pain, they may have jaw pain. They may have just left arm pain. … And then there’s sorts of things where whatever the reason may be, the brain continues to play the loop of pain over and over again. I guess that’s not so much a mistake as it is maybe some sort of glitch, where the pain loop doesn’t stop and it just gets recycled over and over again, and that’s chronic pain. So those are some of the ways that the brain can sort of either mistake or misinterpret the signals and the pain.

    On how pleasure can rewire brain

    What I think is really interesting is that we have this system within our body, the endogenous opioid system. … This is like our internal morphine system, endorphin system. We can activate this system in all sorts of different ways. And by activating, I mean exactly what it sounds like. You just basically release a lot of these endorphins, these basically personalized morphine molecules all throughout your body. And one of the ways that they have shown can really facilitate that is to not just practice gratitude, but to actively practice gratitude. Meaning, actually savor something. I’m not just grateful for this ice cream cone. I’m so enjoying this ice-cream cone. I’m just not grateful for being able to look at this sunset. I am gazing at every different color in the sky and just taking it all in. It’s a very active form of gratitude. And it seems to be very associated with basically activating the endogenous opioid system, which is really fascinating to me.

    On opioid drugs compared to the body’s natural opioid system

    So many techniques and medications that we use in real life take their inspiration from our human body, and that’s one of them. … With your own opioid system, it is very, very sensitive. So it can turn on and it can turn off really, really well. So instead of having the lingering sort of side effects of opioids and sedation and all these other things, the opioids that you make yourself can just be washed away very, very quickly. …

    I always say if the endogenous opioid system didn’t exist, women would probably never have more than one child. It can be a painful experience, but those [natural] opioids help with the pain. They help with the mood, and … [they] can actually inhibit your memory.

    On how inflammation serves a purpose

    I think for the most part, inflammation has sort of gotten a bad rap. … I think when you look at a sprained ankle, for example, and it looks swollen and red, the idea that I want to get rid of that. That’s associated with my pain makes intuitive sense. I think the idea that that inflammation serves a real purpose, that not only is it sort of helping protect the site of injury, but also sending all these various molecules to the site of injury to help with the healing. …

    The thing about pain is that everyone’s threshold is going to be a little bit different. … I think for a lot of people, they think they need to take anti-inflammatories. Oh, this is bad, I gotta treat that, that inflammation’s not good, that’s hurting my body. But if I flip the script on you and I say, “It’s not bad for your body, that is exactly how your body is supposed to work. This is your body doing its job.”

    On a new FDA approved non-opioid pain medication

    The medication is called Suzetrigine. … It is a fascinating story of how it came about. There were these families of circus performers in Karachi, Pakistan. That got the attention of researchers, whatever, 25, 30 years ago. And they saw that these circus performers were able to do all these remarkable things, like they could put sharp things through their appendages and they could walk on hot coals and do all that sort of stuff. But what they found was that when they were doing this, they could feel the coals on their feet and they could feel that they were hot, they just didn’t have pain. … And that was pretty striking because it gave these researchers a clue as to which sodium channel blocker may be important when it came to just targeting pain and not sensation overall. They studied this family. They found that they had a gene in common. … And basically for 25 years, these researchers tried to replicate what that gene was doing in the body. … Now, one of the big challenges of creating a medicine like that is you didn’t want to take away pain forever. Pain has utility. It can keep you safe. It can teach you lessons. So they wanted to create a half-life for the drug. So they basically now have an oral formulation.

    On Cannabis for pain

    I walked into it thinking that if I really examined all this literature, there was going to be a pretty compelling case made for using cannabis for all sorts of different pains … and I walked away not as impressed, to be quite honest, as I thought I would be. And this is just the data talking. I will say it’s hard to collect this data when you’re dealing with a substance that has been a level one substance in the United States for a long time. It’s just really hard to get good studies.  …

    But having said that, the best available data seem to suggest that for about a third of the people, it could be pretty effective, and maybe in some cases as effective as the best other options for that neuropathic pain. … For about two-thirds of people, it really did not seem to be that effective. And this is the case, I think, for about a third of people, they get significant benefit. And we don’t quite know who those third of the people are. We don’t know what makes them different than the other two-thirds that they’re getting that kind of relief.  

    Monique Nazareth and Susan Nyakundi produced and edited this interview for broadcast. Bridget Bentz and Molly Seavy-Nesper adapted it for the web.

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  • Ebola Outbreak Is Declared in Kasai Province of Congo – The New York Times

    1. Ebola Outbreak Is Declared in Kasai Province of Congo  The New York Times
    2. Democratic Republic of the Congo declares Ebola virus disease outbreak in Kasai Province  WHO | Regional Office for Africa
    3. 15th Ebola Outbreak Declared in Africa  Vax-Before-Travel
    4. New Ebola outbreak in DRC kills 15 people  TRT Français
    5. Ebola Returns to Congo as 28 Suspected Cases Reported  Modern Diplomacy

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  • Fast-growing brains may explain how humans — and marmosets — learn to talk

    Fast-growing brains may explain how humans — and marmosets — learn to talk

    image: 

    Could a baby’s still-growing brain help set the stage for learning language? Princeton neuroscientists find surprising clues from chatty monkeys who share the power of babble.


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    Credit: Francesco Veronesi, “Family of Common Marmoset”, Flickr (2014). Licensed under CC BY-SA 2.0

    PRINCETON, N.J. — When a baby babbles and their parents respond, these back-and-forth exchanges are more than adorable-if-incoherent chatter — they help to build a baby’s emerging language skills.

    But it turns out this learning strategy makes humans an oddity within the animal kingdom.

    Only a handful of other species — including a few songbirds such as cowbirds and zebra finches — learn to “talk” by noting their parents’ reactions to their initial coos and gurgles.

    How did humans become adept at learning language this way? A new study across multiple members of the primate family tree suggests the answer may lie, in part, in newborn babies’ fast-growing brains.

    Published August 19 in the journal Proceedings of the National Academy of Sciences, the findings come from research on a squirrel-size monkey called the marmoset.

    Babbling beyond humans

    In the wild, marmosets use their high-pitched calls to stay in touch when they’re out of sight of one another in the thick dense forests of northeastern Brazil.

    Just over a decade ago, while studying marmoset vocalizations, Princeton professor of neuroscience and psychology Asif Ghazanfar and colleagues noticed that baby marmosets go through a babbling phase, just like humans do.

    As newborn marmosets grow, their first sputtering cries transform into the more whistle-like calls of adults. The researchers also found that baby marmosets who received more frequent adult feedback during their babbling bouts were quicker to catch on. They learned to produce adult-like calls significantly faster than the controls.

    “That was a pretty big ‘aha!’ moment,” Ghazanfar said.

    These studies, published in 2015 and 2017 by Ghazanfar with his then-postdoc Daniel Takahashi, now at the Federal University of Rio Grande do Norte in Brazil, were some of the first evidence of what appeared to be vocal learning in another primate.

    But humans and marmosets last shared a common ancestor some 40 million years ago. Even our closest living relatives, chimpanzees, need very little tutoring to make the sounds of their kin.

    “So that kind of presents a puzzle,” Ghazanfar said. 

    Since then, the researchers have been trying to figure out why humans and marmosets arrived at such similar learning strategies despite being so distantly related.

    Neural growth spurt supports learning

    In the new study, led by Princeton Ph.D. student Renata Biazzi, the researchers collected and analyzed previously published data on the brain development of four primate species including humans, marmosets, chimpanzees and rhesus macaques, from conception to adolescence.

    The results suggest that, in early infancy, the brains of humans and marmosets are growing faster than those of other primates. Importantly, most of that growth happens not in the confines of the womb, as is the case for chimpanzees and macaques, but right around the time they are born and first experience the outside world.

    In marmosets, as in humans, this also happens to be an incredibly social time, Ghazanfar said. That’s because marmoset moms, like human mothers, don’t raise their offspring without help. Babies interact with multiple caregivers who respond to every cry.

    “They are a handful,” Ghazanfar said.

    And because their brains are still developing, “that means that the social environment an infant is born into has a tremendous influence” on their learning, he added.

    Using a mathematical model, the researchers were able to show how these early interactions, when coupled with rapid brain growth, set the stage for vocal skills to develop later on.

    Baby talk

    Next, the team plans to look into whether adult marmosets use specific sounds when interacting with infants, much like human adults use “baby talk” to communicate with our babies.

    By looking at the only other primate whose infants are capable of using feedback to learn sounds, scientists hope to better understand how a child goes from cooing and babbling to, say, negotiating their way out of chores or joining the debate team.

    This doesn’t mean that other primates can’t change up their calls later in life.

    “We’re only talking about vocal learning during infancy,” Ghazanfar said. “This is the period when their brains are especially malleable.”

    This work was supported by a grant from the National Institute of Health (R01NS054898).

    CITATION: “Altricial brains and the evolution of infant vocal learning,” Renata B. Biazzi, Daniel Y. Takahashi, and Asif A. Ghazanfar. Proceedings of the National Academy of Sciences, Aug. 19, 2025. https://doi.org/10.1073/pnas.2421095122

    # # #

    About the Princeton Neuroscience Institute (PNI)

    Founded in 2005, the Princeton Neuroscience Institute brings together researchers across disciplines at Princeton University to investigate how the brain gives rise to perception, cognition, and behavior. Led by Director Mala Murthy, PNI has built internationally recognized strengths in computational and quantitative neuroscience, advanced neurotechnology, and integrative approaches that connect molecular, cellular, and systems-level analyses with human cognitive studies. For more information, please visit: https://www.pni.princeton.edu


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  • Congo declares new Ebola outbreak three years after last – Reuters

    1. Congo declares new Ebola outbreak three years after last  Reuters
    2. Ebola outbreak kills 15 in DR Congo  BBC
    3. Democratic Republic of the Congo declares Ebola virus disease outbreak in Kasai Province  WHO | Regional Office for Africa
    4. 15th Ebola Outbreak Declared in Africa  Vax-Before-Travel
    5. New Ebola outbreak in DRC kills 15 people  TRT Français

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  • New study explores how childhood social determinants impact young adult cardiovascular health

    New study explores how childhood social determinants impact young adult cardiovascular health

    Cardiovascular disease (CVD) remains the leading cause of death and disability for adults in the U.S. Recent projections from the American Heart Association suggest that by 2050, more than 45 million American adults will have clinical CVD and more than 184 million will have hypertension. As a result, inflation-adjusted direct health care costs related to CVD risk factors are projected to triple between 2020 and 2050, to $1.34 trillion annually, and direct costs related to clinical CVD conditions are projected to rise from $393 billion to $1.49 trillion. Thus, understanding early-life determinants of cardiovascular health behaviors and health factors are of particular interest.

    In the first prospective study of social determinants from birth, and how they impact young adult cardiovascular health, researchers from Boston University Chobanian & Avedisian School of Medicine and colleagues are investigating the upstream causes of cardiovascular disease – the factors that drive poor diet, a sedentary lifestyle, nicotine exposure, poor sleep, obesity, and adverse blood cholesterol, blood pressure and blood glucose levels. Known as the Future of Families Cardiovascular Health Among Young Adults (FF-CHAYA) Study, a new paper describes the rationale, study design, methods and characteristics of the FF-CHAYA cohort, a novel longitudinal study designed to examine associations of childhood social determinants with young adult cardiovascular health and early arterial injury.

    In recent years, social determinants of health (SDoH) have received significant attention as upstream societal and structural factors that drive the propensity for beneficial or adverse health outcomes. While data on SDoH among middle-aged adults is increasingly available, as are longitudinal associations with downstream health outcomes, investigations examining the full array of SDoH in children and prospective associations with health outcomes is rare.”


    Donald Lloyd-Jones, MD, ScM, corresponding author, professor of medicine at Boston University Chobanian & Avedisian School of Medicine and director of the Framingham Heart Study

    Using the largest and longest running study of a representative group of children born between 1998-2000, the researchers examined more than 2,000 young adults (average age 23 years) from 22 cities across the U.S. who had been followed since birth. Families provided information on socioeconomic status, neighborhood conditions, environmental exposures, schools, behavior and other psychosocial factors up to seven times during early life. As young adults, all participants answered detailed questions about health status and health behaviors, and three-quarters of them had in-person examinations with checks on height, weight, body shape, blood pressure and blood drawn for clinical measures. Those same young adults also underwent sophisticated ultrasound imaging of the carotid arteries in the neck to look for signs of early arterial injury. The researchers are now linking their detailed sociological data with state-of-the-art, quantitative measures of cardiovascular health in young adulthood.

    According to the researchers, detailing childhood social determinants helps target those factors that drive poor cardiovascular health across the life course. “Ultimately we hope it will guide pediatricians, family practitioners and even public health policy makers to those things that will launch children into better lifelong health trajectories,” adds Lloyd-Jones.

    These findings appear online in the Journal of the American Heart Association.

    Funding for this study was provided by grant R01 HL149869 from the National Heart, Lung, and Blood Institute and supported by institutional funding from Princeton University and Northwestern University Feinberg School of Medicine.

    Source:

    Boston University School of Medicine

    Journal reference:

    Lloyd‐Jones, D. M., et al. (2025). Future of Families: Cardiovascular Health Among Young Adults Cohort Study: Rationale, Key Questions, Study Design, and Participant Characteristics. Journal of the American Heart Association. doi.org/10.1161/jaha.125.042030

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  • No advantage found in modulating antiplatelet therapy intensity after complex stenting

    No advantage found in modulating antiplatelet therapy intensity after complex stenting

    There was no benefit to modulating the intensity of antiplatelet therapy compared with standard antiplatelet therapy in high-risk patients who had undergone complex stenting procedures, according to late-breaking research presented in a Hot Line session today at ESC Congress 2025.

    Dual antiplatelet therapy (DAPT) consisting of aspirin plus a P2Y12 receptor inhibitor, such as clopidogrel, is generally given to patients after coronary stenting (percutaneous coronary intervention [PCI]) to prevent ischemic events, such as heart attacks (myocardial infarction). Principal Investigator, Professor Duk-Woo Park from Asan Medical Center, Seoul, South Korea, explained why the TAILORED-CHIP trial was carried out: “The optimal antiplatelet therapy is not well established for patients who have undergone complex PCI procedures and are at high risk of ischaemic events. We hypothesized that modulating the intensity of antiplatelet therapy over time, i.e. stronger inhibition in the early phase to reduce ischaemic events and weaker inhibition in the later phase to mitigate bleeding, may be beneficial in this high-risk population. The TAILORED-CHIP trial was designed to study whether early escalation with low-dose ticagrelor plus aspirin and late de-escalation with clopidogrel alone would be better than standard clopidogrel plus aspirin.”

    The open-label randomized TAILORED-CHIP trial was conducted at 24 sites in South Korea. Patients with high-risk anatomical or clinical characteristics undergoing complex PCI were enrolled and were randomized 1:1 to receive tailored antiplatelet strategy consisting of early escalation (low-dose ticagrelor at 60 mg twice daily plus aspirin for 6 months) then late de-escalation (clopidogrel monotherapy for 6 months) or standard DAPT (clopidogrel plus aspirin for 12 months).

    The primary outcome was net adverse clinical events, defined as a composite of death from any cause, myocardial infarction, stroke, stent thrombosis, unplanned urgent revascularization and clinically relevant bleeding (BARC type 2, 3, or 5) at 12 months. Prespecified secondary outcomes included major ischemic and clinically relevant bleeding events.

    In total, 2,018 patients were enrolled. The mean age was 64.0 years and 17.1% were women. Most patients (93.7%) had PCI conducted in at least two major heart vessels during the same procedure.

    At 12 months, the primary of outcome of net adverse clinical events was not significantly different between the groups, occurring in 10.5% of patients assigned to tailored antiplatelet therapy and in 8.8% of patients assigned to standard DAPT (hazard ratio [HR] 1.19; 95% confidence interval [CI] 0.90 to 1.58; p=0.21).

    There was no significant difference in the incidence of major ischaemic events at 12 months between the tailored-therapy and DAPT groups (3.9% vs. 5.0%, respectively; HR 0.78; 95% CI 0.52 to 1.19; p=0.25). However, the incidence of clinically relevant bleeding at 12 months was significantly higher in the tailored-therapy group (7.2%) compared with the DAPT group (4.8%; absolute difference 2.45%; 95% CI 0.37% to 4.53%; p=0.002). The incidence of major bleeding was similar in the tailored-therapy group (1.7%) and the DAPT group (1.5%; absolute difference 0.21%; 95% CI −0.89% to 1.31%; p=0.70).

    Summarizing the findings, Professor Park said: “Our results suggest that a tailored strategy in patients undergoing complex high-risk PCI does not provide a net clinical benefit. We observed an increase in bleeding complications without a significant reduction in ischaemic events. This challenges the notion that ‘more is better’ even in carefully selected patients at high ischemic risk undergoing complex PCI procedures. Standard 12-month DAPT remains appropriate.”

    Source:

    European Society of Cardiology (ESC)

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  • Air pollution can drive devastating forms of dementia, research suggests | Air pollution

    Air pollution can drive devastating forms of dementia, research suggests | Air pollution

    Fine-particulate air pollution can drive devastating forms of dementia by triggering the formation of toxic clumps of protein that destroy nerve cells as they spread through the brain, research suggests.

    Exposure to the airborne particles causes proteins in the brain to misfold into the clumps, which are hallmarks of Lewy body dementia, the second most common form of dementia after Alzheimer’s disease.

    The finding has “profound implications” for preventing the neurodegenerative disorder, which affects millions worldwide, with scientists calling for a concerted effort to improve air quality by cutting emissions from industrial activity and vehicle exhausts, improving wildfire management and reducing wood burning in homes.

    “Unlike age or genetics, this is something we can change,” said Dr Xiaobo Mao, a neurologist at Johns Hopkins University in the US and the study’s lead investigator. “The most direct implication is that clean air policies are brain health policies.”

    The researchers began by analysing hospital records of the 56.5 million US Medicare patients. They looked at those who were admitted for the first time between 2000 and 2014 with the protein damage. Armed with the patients’ zip codes, the scientists estimated their long-term exposure to PM2.5 pollution, airborne particles that are smaller than 2.5 thousandths of a millimetre. These can be inhaled deep into the lungs and are found in the bloodstream, brain and other organs.

    They found that long-term exposure to PM2.5 raised the risk of Lewy body dementia, but had less of an impact on rates of another neurodegenerative brain disease that is not driven by the toxic proteins.

    Lewy bodies are made from a protein called alpha-synuclein. The protein is crucial for healthy brain functioning, but can misfold in various ways to produce different kinds of harmful Lewy bodies. These can kill nerve cells and cause devastating disease by spreading through the brain.

    To see if air pollution could trigger Lewy bodies, the team exposed mice to PM2.5 pollution every other day for 10 months. Some were normal mice, but others were genetically modified to prevent them making alpha-synuclein. The results were striking: in normal mice, nerve cells died off, leading to brain shrinkage and cognitive decline. The genetically modified mice were largely unaffected.

    Further work in mice showed that PM2.5 pollution drove the formation of aggressive, resilient and toxic clumps of alpha-synuclein clumps that looked very similar to Lewy bodies in humans. Although the work is in mice, the findings are considered compelling evidence.

    “Putting the two together, to me, indicates that there’s a pretty strong association with air pollution causing Lewy body dementia. We think it’s a very important driving factor for dementia,” said Ted Dawson, a senior author on the study and a professor in neurodegenerative diseases at Johns Hopkins. “There needs to be a concerted effort to keep our air clean.”

    The work, published in Science, builds on previous studies that have found PM2.5s in people’s brains where damage has been linked to Alzheimer’s disease and reductions in intelligence.

    “Our findings have profound implications for prevention because they identify air pollution as a modifiable risk factor for Lewy body dementia,” Mao told the Guardian. “By lowering our collective exposure to air pollution, we can potentially reduce the risk of developing these devastating neurodegenerative conditions on a population-wide scale.”

    Last year, researchers at University College London and the Francis Crick Institute in London launched a project called Rapid, for Role of Air Pollution in Dementia, to investigate how the air we breathe may harm the brain.

    “This is an important and compelling study that deepens our understanding of how air pollution can drive neurodegenerative disease,” said Prof Charles Swanton, a co-leader of the Rapid project and deputy clinical director at the Crick.

    “By linking fine-particulate matter exposure to the biology of Lewy body dementia, it provides a mechanistic bridge between environmental exposure and disease pathology. More broadly, the work underscores the urgent need to understand and mitigate the impact of air pollution on dementia and disease risk more broadly, given its enormous and growing public health burden.”

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  • Raw cat food tests positive for H5N1

    Raw cat food tests positive for H5N1

    After a cat located in San Fransisco, California, tested positive for H5N1 highly pathogenic avian influenza (H5N1), the FDA, state and local public health and agriculture partners, and federal partners suggest that after further testing, there a link between the strain detected in the cat and certain lots of RAWR Raw Cat Food Chicken Eats, a product the cat ate prior to falling ill.

    Frank Gärtner/stock.adobe.com

    According to the FDA, the San Francisco Department Public Health (SFDPH) was notified a cat ate Lot CC 25 093 before becoming ill with H5N1 and euthanized.1 An initial PCR testing of the open product was conducted and detected H5N1. Subsequent whole genome sequencing (WGS) of a diagnostic sample from the cat and the open sample from Lot CCS 25 093 were performed by the USDA National Veterinary Service Laboratories.

    The FDA then collected and tested 2 retail samples of the same RAWR Chicken Eats product with a different lot number (CC 25 077) and Sell By Date (09/18/26), each testing positive for Influenza A Virus, and a WFS performed on one sample was also positive for H5N1.1 WGS results also indicated that H5N1 from all 3 samples were within the same WGS cluster, indicating relatedness. This cluster involves a virus lineage that was detected from around November to December 2024, and is no longer circulating, supporting that the infected cat became ill from eating the Lot CCS 25 093 of the Chicken Eats product.1

    RELATED: Additional cat food company announces recall over H5N1 concerns

    NVSL testing of the cat, Lot CCS 25 093, and Lot CCS 25 077 identified the H5N1 as genotype B3.13. This genotype virus was found in other brands of raw poultry-based pet foods before that were associated with the illness or death of cats.1

    The RAWR Raw Cat Food Chicken Eats, Sell by 09/18/26, and RAWR Cat Food Chicken Eats, Sell by 10/03/26, are sold in 2.5-pound resealable frozen plastic bags that have 40 1 ounce sliders in them in retail stores nationwide and online. The bags are white and yellow with black lettering, and have the lot code CCS 25 077 and CCS 25 093 printed in the center of the back of each bag.

    At this time, the FDA is not aware of any human cases of HPAI contracted through exposure to contaminated food.

    H5N1 in dogs and cats

    The H5N1 virus can result in illness and death in birds and mammals such as domesticated cats and large felids as well as dogs. For dogs however, their cases usually present with mild clinical signs and low mortality in comparison to cats. Currently, there are no known dogs with highly pathogenic avian influenza in the United Sates, but other countries have seen fatal cases. There is a list of animals that have tested positive for the virus on the USDA’s APHIS website.

    Animals who have weak immune systems or are very old or young are especially at risk of contracting the virus. Animals with the virus typical present with the following signs, according to the American Veterinary Medical Association2:

    • Discharge from the eyes and nose
    • Difficulty breathing
    • Fever
    • Lethargy
    • Low appetite
    • Neurologic signs such as blindness, incoordination, seizures, and tremors
    • Reddened or inflamed eyes.

    While there have been no identified cases of H5N1 infections among anyone handling raw pet food products, humans are still at risk of being infected if an active virus gets into their eyes, nose, our mouth. Because of this, it is crucial for people to wash their hands after handling any pet food products as well as sanitize contact surfaces.

    References

    1. FDA Notifies Pet Owners That Tests Show H5N1 Contamination in Certain Lots of RAWR Raw Cat Food Chicken Eats. News release. US Food and Drug Administration. September 3, 2025. Accessed September 4, 2025. https://www.fda.gov/animal-veterinary/cvm-updates/fda-notifies-pet-owners-tests-show-h5n1-contamination-certain-lots-rawr-raw-cat-food-chicken-eats?utm_medium=email&utm_source=govdelivery
    2. American Veterinary Medical Association. Avian influenza in companion animals. American Veterinary Medical Association. Published 2025. https://www.avma.org/resources-tools/animal-health-and-welfare/animal-health/avian-influenza/avian-influenza-companion-animals

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