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Kevin J. Tracey posted thisNovember 15, 2011 is a date I won't forget. That day in Mostar, Bosnia and Herzegovina, I met the first patient ever treated with a method I had invented. He was a young man whose autoimmune disease had taken away his ability to work, to play with his children, and to move through the world without pain. And he had volunteered to be the first person in a clinical trial led by SetPoint Medical, a company Shaw Warren and I co-founded in 2007 to test the idea that a vagus nerve stimulating device could treat RA, IBD, and other inflammatory conditions. After spending years with my colleagues in the lab at the Feinstein Institutes, and with others in their labs around the world, I asked him what it felt like to be treated with this therapy. He said, "the pain is gone. The pain I had for years disappeared." His inflammation was under control, and he returned to a life playing with his children and working as a truck driver. This day was built on a foundation of discoveries showing that the brain and immune system speak to each other through the vagus nerve. Brilliant engineers at SetPoint had configured the device, defined the stimulation parameters within a narrow therapeutic window (now only 1 minute daily), and designed and sponsored the clinical trials that would lead to FDA approval. But nothing had prepared me for what it felt like to actually meet him. As I sat in a quiet conference room in a hospital a few miles from the historic medieval arched Stari Most (Old Bridge), I listened to his story about getting his life back. I was witnessing how neuroimmunology offers a path where scientists and physicians, working together for many years, can bring a new idea across time from a hypothesis (which some perhaps thought crazy) to a smiling fellow human being living fully. That is what makes it all worthwhile. We may still be early in the bioelectronic medicine journey, but that morning in 2011 made the direction unmistakable.
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Kevin J. Tracey reposted thisKevin J. Tracey reposted thisAre you attending #SXSW? Feinstein Institutes’ president and CEO Kevin J. Tracey will offer his expert advice on vagus nerve stimulation in a critical discussion with Wim Hof and Dr. Geoffrey Ling, moderated by Erica Berenstein. Attend his session "#TikTok vs. Real Doc? Doctor Approved #Biohacking Tips": https://bit.ly/4rrpI0T #SXSWBiohack #SXSW #vagusnerve #bioelectronicmedicine #SXSW2026
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Kevin J. Tracey posted thisDoes cold exposure stimulate your vagus nerve? It's one of the questions I'm asked most frequently. The direct answer requires more explanation than is typically provided on social media posts and corporate webpages. The vagus nerve carries signals from the skin, airways, and internal organs to the brain. Some of these signals respond to temperature. Cold exposure can produce physiological changes that involve the vagus nerve: heart rate slows, certain reflexes activate, the dive response engages. These observations are real, their mechanisms are well studied, and the underlying physiology has been honed by millions of years of adaptation to the changing environment of the internal and external world. But inherent in the one question are two answers that require distinction. The first is mechanistic: can cold exposure activate vagal pathways? The answer is yes, under certain conditions of temperature and timing. The second is therapeutic: do cold-activated vagus pathways produce specific health outcomes as claimed: does it reduce inflammation? improve mood? optimize "vagal tone"? The answers here demand well-controlled, appropriately sized randomized clinical trials. Unfortunately, for most of the claims circulating online and in the ether, we don't yet have those trials. The gap between a plausible mechanism and a proven therapy is real and consequential. Health care providers are accountable, meaning their recommendations to their patients need to be backed by both mechanisms and RCT data. Perhaps cold exposure is not worthless, but there is a requirement to be factual and honest about where the evidence actually sits. And to be skeptical of those who speak (or shout) with certainty about things where the mechanisms are uncertain, and the RCT data unavailable. In The Great Nerve, I work through these concepts in the context of cold exposure, breath-work, meditation, and exercise and discuss what looks genuinely promising, what remains speculative, and where we simply don't know yet.
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Kevin J. Tracey posted thisDoes cold exposure stimulate your vagus nerve? It's one of the questions I'm asked most frequently. The direct answer requires more explanation than is typically provided on social media posts and corporate webpages. The vagus nerve carries signals from the skin, airways, and internal organs to the brain. Some of these signals that respond to temperature. Cold exposure can produce physiological changes that involve the vagus nerve: heart rate slows, certain reflexes activate, the dive response engages. These observations are real, their mechanisms are well studied, and the underlying physiology has been honed by millions of years of adaptation to the changing environment of the internal and external world. But inherent in the one question are two answers that require distinction. The first is mechanistic: can cold exposure activate vagal pathways? The answer is yes, under certain conditions of temperature and timing. The second is therapeutic: does cold-activated vagus pathways produce specific health outcomes as claimed: does it reduce inflammation? improve mood? optimize "vagal tone"? The answers here demand well-controlled, appropriately sized randomized clinical trials. Unfortunately, for most of the claims circulating online and in the ether, we don't yet have those trials. The gap between a plausible mechanism and a proven therapy is real and consequential. Health care providers are accountable, meaning their recommendations to their patients need to be backed by both mechanisms and RCT data. Perhaps cold exposure is not worthless, but there is a requirement to be factual and honest about where the evidence actually sits. And to be skeptical of those who speaks (or shout) with certainty about things where the mechanisms are uncertain, and the RCT data unavailable. In The Great Nerve, I work through these concepts in the context of cold exposure, breath-work, meditation, and exercise and discuss what looks genuinely promising, what remains speculative, and where we simply don't know yet.
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Kevin J. Tracey posted thisFor most of the history of medicine, the immune system and the nervous system were studied as if they operated independently. Immunologists worked on immunity. Neurologists worked on the brain. Two fields, fire-walled, with nary a reason to talk to each other. But my colleagues and I found, in the late 1990s, that this separation was a mirage. They were actually intertwined, speaking a commons language for a shared purpose: recognizing infection and injury, coordinating the response, and learning. In the lab we discovered that the brain monitors and regulates inflammation in real time through a reflex circuit in the vagus nerve. Calling it "the inflammatory reflex," we proposed that inflammation, which we now understand to be the root cause of dozens of major diseases, wasn't purely an immune phenomenon. The vagus nerve and brain are active and direct participants . The implications took years to work through. But the central idea is this: if the nervous system governs inflammation through an electrical to chemical circuit, then stimulating that circuit can suppress inflammation. And since this reflex was honed and perfected by millions of years of evolutionary adaptation, it does not cause immunosuppression. This is the foundation of bioelectronic medicine. Now FDA-approved vagus nerve stimulators from SetPoint Medical are being implanted in rheumatoid arthritis patients. And an extensive and deep scientific understanding is now extending these results into preclinical and clinical trials for multiple sclerosis, inflammatory bowel disease, hemorrhage, diabetes, and other conditions. The field of neuroimmunology, the nervous and immune systems together, has arrived. Stimulating "The Great Nerve" is happening now just in time to start helping patients who need something besides the current standards of expensive, invasive, potentially toxic, immunosuppressive drugs.
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Kevin J. Tracey reposted thisKevin J. Tracey reposted thisLet's inspire the next generation of women scientists. 🔬 🧪 🥼 Betty Diamond, MD, Feinstein Institutes' Director of the Institute of Molecular Medicine shares her encouraging words for young women interested in a career in research: "Do it, and don’t be deterred by microaggressions or those who say a career in science is not compatible with a family life... Talk with women in science who will advocate for you. It's an exciting, worthwhile career." Join our Feinstein Institutes scientists in celebrating International Day of Women and Girls in Science on February 11. More info: https://lnkd.in/e4as4Fc #WomenInScience #STEM #11February #science #medicalresearch
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Kevin J. Tracey reposted thisKevin J. Tracey reposted thisThank you Rachel Spicer, Ph.D. Peder Olofsson and Fiona Harrison for the nice commentary about our paper using percutaneous #vagus nerve stimulation (pVNS) as a potential novel avenue to treat postoperative neuroinflammation in #delirium superimposed on dementia. https://lnkd.in/euTA_HewExploring vagus nerve stimulation in postoperative delirium and dementia - Bioelectronic MedicineExploring vagus nerve stimulation in postoperative delirium and dementia - Bioelectronic Medicine
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Kevin J. Tracey shared thisBrain neurons encode specific inflammatory experiences, as if making memories of specific cytokines. In a new paper just published in the Journal of Experimental Medicine, we tagged the neurons responsible. CRH-expressing neurons in a brain region that integrates threat and stress encode IL-1β signals and store them. When we reactivated those same neurons chemogenetically, without any inflammatory stimulus present, the animals launched a precise physiological program: IL-6 production, tachycardia, adrenergic signaling. The full signature of inflammation as if recalled from memory. Here is what makes this discovery important for patients. Psychological stress activates the same neurons. This provides a mechanistic explanation for two observations that clinicians have known for decades but could never fully explain: why inflammatory diseases are so often associated with depression and anxiety, and why psychological stress worsens conditions like rheumatoid arthritis, Crohn's disease, and lupus. The brain does not merely respond to inflammation. It records it. And stress can replay it. It may be possible to modulate these circuits to break the link between stress and inflammatory disease. Sincere congratulations to Okito Hashimoto, Tyler Hepler, Aisling Tynan, Alejandro Torres, Jian Hua Li, Michael Brines, and Sangeeta Chavan on this remarkable discovery from our team at the Feinstein Institutes for Medical Research. https://lnkd.in/gNPMjNxm
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Kevin J. Tracey posted thisSearch "vagus nerve" on any social platform and you'll find hundreds of millions of posts. Written confidently, shared widely, and repeated and reposted until it sounds like dogma. Most are misleading, and a significant number are flat-out wrong. Not misleadingly incomplete. Not slightly exaggerated, but factually incorrect. I've spent decades with my colleagues studying this nerve. We’ve co-invented different devices to stimulate the vagus nerve to treat inflammation, obesity, bleeding and autoimmune diseases. So I understand why the misinformation spread. The vagus nerve is complex, mysterious, and fascinating. Its’ 200,000 fibers connect the brain to nearly every organ in your body. It carries signals to regulate your heart, your lungs, your gut, and your immune system. The idea that you can "activate it” to improve your health is appealing and partially true. But what is “activate?” and equally important, what is “it?” The problem is that the wellness industry latched onto partial truths and now run into territories where mechanistic knowledge is incomplete. That would be okay if well controlled, appropriately sized, randomized clinical trial results supported their claims. But we don’t have more than a few RCTs either. I wrote "The Great Nerve" because patients with serious inflammatory diseases, and people genuinely trying to take care of their health, deserve accurate information. Not hype. Not false certainty about things we don't know yet. The science is remarkable enough on its own. We don't need to make things up.
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Kevin J. Tracey liked thisKevin J. Tracey liked thisLast week's Gun Violence Prevention Forum was powerful. It takes profound courage for survivors of gun violence to rise after unimaginable loss. Lesley, a mother who lost her young son, Pierce, to gun violence, is an example of survivors who refuse to let tragedy have the last word. Her pledge ensures family law attorneys ask about firearms in custody cases, removing guns temporarily from the home and away from dangerous situations. That's why Northwell Health is proud to sponsor Pierce's Pledge across New York and Connecticut. Northwell stood up to reframe gun violence for what it is, a public health crisis, and we’ve seen progress. The energy in that room, with clinicians, researchers, community leaders, and business owners coming together for this cause, proved that we have the collective resolve to accelerate this movement.
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Kevin J. Tracey liked thisKevin J. Tracey liked thisIs there an “on” and “off” switch for stress and inflammation? Feinstein researchers just found a major clue. Dr. Sangeeta Chavan and her team published new findings in the Journal of Experimental Medicine, that reveals specific neurons within the brain's Bed Nucleus of the Stria Terminalis (BNST) act as a primary responder and when activated by inflammatory signals, they precisely trigger the body's full stress response–from increased heart rate to stress hormones. This understanding could provide a common pathway for bioelectronic medicine to control vital bodily functions and offer potential drug-free therapies to precisely 're-tune' these circuits. Find out more about this “master switch”: https://bit.ly/4l0xw7B #neuroscience #immunology #bioelectronicmedicine #Inflammation #medicalresearch #FeinsteinInstitutesFeinstein Institutes’ scientists discover brain circuit that links inflammation and stress responseFeinstein Institutes’ scientists discover brain circuit that links inflammation and stress response
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Kevin J. Tracey liked thisKevin J. Tracey liked thisWe tell our students that the results should not be expressed to more decimals than the error of the measurement. If your uncertainty is ±0.1, you do not report 0.1234. Every weekend, when we watch football we are shown VAR (video-assisted refereeing) drawing surgical-looking lines and declare a player offside by 2 or 3 centimeters. Let’s slow this down and look at the physics. First: the “moment” the ball is played is not a mathematical instant. The foot touches the ball first, the ball deforms, it re-expands, and then it leaves the foot. The process lasts about 10 milliseconds. Second: broadcast video runs at 60 frames per second. That means one frame every 17 milliseconds. The true contact event can occur anywhere within that interval. The VAR is then limited by that temporal resolution. A realistic running speed of a striker can be around 6 m/s. Now let’s convert time uncertainty into spatial uncertainty: Distance error ≈ running speed × timing uncertainty. 6 m/s × 0.01-0.017 s ≈ 0.06-0.10 m. We are talking 6-10 centimeters of error. So when we see an offside decision presented with a margin of 2-3 cm…especially when the striker was running at full speed… we cannot be certain if the offside call was real, or influenced by measurement error. VAR may be displaying more precision than the system can realistically support. Perhaps football could benefit from the same intellectual discipline we expect from first-year students: do not report more precision than your method justifies.
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