Recovery After Stroke

Recovery After Stroke

A Community And Podcast For Stroke Survivors And Carers

  1. 4d ago

    Brad Pitzele – How Exercise With Oxygen Therapy Brings Hyperbaric-Style Benefits Home

    EWOT for Stroke Recovery: The Affordable Alternative to Hyperbaric Oxygen Therapy Brad Pitzele did not set out to become an oxygen therapy equipment maker. He set out to survive. After years of battling significant health challenges, conventional medicine had given him answers that kept failing him. He tried around 200 treatments. Some helped. Many did not. Then he found EWOT Exercise With Oxygen Therapy, and something finally shifted. Brad’s journey is not the same as a stroke. But what he discovered about oxygen, inflammation, and cellular energy maps directly onto one of the most stubborn obstacles stroke survivors face: the feeling that the brain has gone offline, that the body is running on empty, and that the path back is either impossibly expensive or simply does not exist. In Episode 407 of the Recovery After Stroke podcast, Brad shares what EWOT is, why it works, and why he now makes affordable EWOT systems through his company, One Thousand Roads, specifically so survivors do not have to remortgage their homes to access oxygen-driven recovery. What Is EWOT? EWOT stands for Exercise With Oxygen Therapy. The concept is straightforward: you breathe high-concentration oxygen through a mask while exercising even lightly, and that combination pushes oxygen into parts of the body that normal breathing cannot reliably reach. Most people assume oxygen therapy means a hyperbaric chamber: a pressurized tube, a clinic, a course of treatments costing tens of thousands of dollars. Hyperbaric oxygen therapy (HBOT) is effective. Brad describes it as “a heroic treatment.” But it is also inaccessible for most survivors, financially and logistically. EWOT operates on a related principle without the chamber. The key mechanism is not about oxygenating red blood cells; they are already carrying close to their maximum load under normal breathing. The target is the blood plasma. Plasma does not carry oxygen efficiently under resting conditions, but during exercise, even light exercise, blood pressure and circulation increase enough to force dissolved oxygen into the plasma. That plasma can then reach the micro-capillaries, the tiny vessels that feed tissues deep in the body, including areas of the brain that become inflamed and oxygen-starved after a stroke. The Post-Stroke Energy Problem One of the most commonly reported and least-explained symptoms after stroke is fatigue that does not go away, no matter how much a survivor rests. Most survivors are told that is just part of it. Brad’s framework centres on mitochondrial dysfunction. Mitochondria are the energy-producing structures inside cells. After stroke, the cells in and around the affected area are often not dead; they are in a kind of low-power state. Brad describes it as a “brownout”: the lights are on, but dimly. The mitochondria are not producing energy at full capacity, and one significant reason for that is insufficient oxygen supply to the tissue. “The cells that are offline after a stroke are not all dead. Some of them are just starving. Oxygen is part of what feeds them back.” — Brad Pitzele, Episode 407 When EWOT increases plasma oxygen during exercise, it can reach those inflamed, under-oxygenated micro-capillaries that larger vessels cannot access. The result, for some survivors, is a gradual improvement in energy, cognition, and physical capacity, not because the therapy is miraculous, but because it addresses a specific physiological deficit that conventional post-stroke care often does not target. EWOT vs. Hyperbaric: What’s the Real Difference? The honest answer is that EWOT and hyperbaric oxygen therapy are not equivalent. HBOT delivers oxygen under pressure, which drives it into tissue more forcefully. For certain conditions, particularly in acute or severe cases, hyperbaric oxygen has a stronger evidence base.  But for many stroke survivors in the subacute or chronic phase of recovery, access is the defining variable, not theoretical ceiling. A home-based hyperbaric unit costs $50,000 to $75,000. A clinical course can run to $60,000 or more. EWOT systems are available for under $2,000.  The question Brad puts to survivors is not “which is better in a lab?” It is: “Which one can you actually do, consistently, at home, over the months and years that brain recovery requires?” Consistency matters more than peak intensity in long-term neurological recovery.  Starting EWOT With Deficits EWOT does not require running on a treadmill. The exercise component can be a stationary bike, a recumbent bike, or simple seated leg movements with one limb strapped in. The goal is to raise circulation enough to push oxygen into the plasma, not to hit a cardiovascular fitness target. For survivors exploring this option, Brad’s team has built a specific resource at onethousandroads.com/stroke-recovery with a listener discount of $100 to $500, depending on the package. There is also a broader introduction to EWOT at onethousandroads.com/pages/exercise-with-oxygen-therapy. Recovery Is Possible — And It Does Not Have to Be Expensive If this episode resonated with you or if you want to explore more conversations about recovery options that do not require a second mortgage, Bill’s book, The Unexpected Way That A Stroke Became The Best Thing That Happened, is available at recoveryafterstroke.com/book. And if the Recovery After Stroke podcast has been useful to you, you can support it financially at patreon.com/recoveryafterstroke. Every contribution helps keep the show going and these conversations accessible to survivors around the world. This blog is for informational purposes only and does not constitute medical advice. Please consult your doctor before making any changes to your health or recovery plan. EWOT for Stroke Recovery: The Affordable Alternative to Hyperbaric Oxygen Therapy Why pay $60,000 for hyperbaric oxygen? EWOT brings oxygen therapy into your living room — and could help the brain cells that are only offline. One Thousands Roads Exercise With Oxygen Therapy (EWOT) YouTube Channel Highlights: 00:00 Introduction and Background 05:37 Challenges in Stroke Recovery and Treatment Options 13:45 Understanding Oxygen Therapy and Its Mechanism 15:51 Oxygen Toxicity Explained 19:24 The Importance of Oxygenating Blood Plasma 24:53 Oxygen and Mitochondrial Function 31:16 Adapting Exercise for Stroke Survivors 38:27 Cost and Accessibility of Oxygen Therapy Devices Transcript: Introduction – EWOT for Stroke Recovery Brad Pitzele (00:00) like many of your listeners, when you have a medical issue that isn’t treated by traditional medicine and you’re desperate to get your life back, you’ll try just about anything. You, the lens it goes through is like, Well, how bad can this hurt me? BIll Gasiamis (00:15) Welcome back to Recovery After Stroke. I’m your host, Bill Gassiamas. Today’s guest is Brad Pitzele, founder of 1000 Roads, who overcame significant health challenges of his own and along the way discovered the science behind exercise with oxygen therapy. In this conversation, we get into how increasing oxygen saturation in the blood, specifically in the blood plasma, can help reach the inflamed microcapillaries. That are blocking oxygen delivery to cells in the recovering brain. We talk about mitochondrial dysfunction, post-stroke fatigue, and why Ewatt is worth understanding as an accessible alternative to hyperbaric oxygen therapy. Before we get into it, if you’ve found value in this podcast and want to support it financially, you can do that at patreon.com/slash recovery after stroke. And if you haven’t yet read my book, The Unexpected Way That a Stroke Became the Best Thing That Happened, it is available at recovery after stroke dot com slash book. Here’s my conversation with Brad. BIll Gasiamis (01:19) Brad Pitsley, welcome to the podcast. Brad Pitzele (01:22) Thank you so much. BIll Gasiamis (01:24) Thanks for reaching out and ⁓ connecting with me to educate me on another thing that I can bring to stroke survivors that could potentially help them in the rehabilitation side of their brain. The the thumbnail that people found on YouTube is probably gonna have E W O T on it somewhere. E what. And it sounds something like something out of that ⁓ space war out of out of what is it? Brad Pitzele (01:53) Star Wars. Star Wars. BIll Gasiamis (01:54) Star Wars. Like the Ewok, right? And it doesn’t really mean anything to me. But before we descri tell people what Ewok is, ⁓ tell me a little bit about your background, the work that you do and how it is you came to be on the podcast today is for s for for the specific discussion that we’re gonna have. Brad Pitzele (01:58) Yep. Sure. ⁓ yeah, so I ⁓ I I’m an e recovering engineer. I like to joke. I spent my first decade of my life engineering. later on in life, I left engineering and went into different pursuits and I became chronically ill, had a variety of medical issues, ⁓ cancer, autoimmunity, and eventually Lyme disease. And I was in really bad shape. And a doctor recommended I look into either hyperbaric oxygen or this exercise with oxygen therapy, EWAT, that almost no one had heard of, and I’d never heard of it. ⁓ I I I had tried like everything to get better at this point. I was many years in special diets, ⁓ all sorts of supplements and ⁓ all sorts of modalities and things. And nothing really worked. There was nothing in a matter of fact, some of the medications I took actually gave me cancer. So it kind of forced me on this road to try something different. ⁓ and eventually I found my way back to health through exercise with oxygen when so many things weren’t working. ⁓ and actually later paired that with ⁓ red light therapy. ⁓ and along the way I started because I’m an engineer and I’m inquisitive, I like It was Lyme disease is kind of a do-it-yourself disease.

    53 min
  2. Jun 5

    Plastics in Your Arteries: The Stroke Risk Study You Must Know

    Microplastics and Stroke Risk: What a Landmark 2024 Study Found Inside Human Arteries In 2024, a team of Italian researchers published a study in the New England Journal of Medicine that stopped the cardiovascular science community in its tracks. They found microplastics, tiny synthetic fragments embedded inside the carotid artery plaque of more than half the patients they examined. And the patients who had them faced more than four and a half times the risk of a serious cardiovascular event compared to those who didn’t. This isn’t a distant, theoretical risk. These are living people who had already been identified as having carotid artery disease, and plastics were found inside their arterial walls. For stroke survivors and those at elevated risk of stroke, this study raises important questions that the medical system has not yet caught up with. What the Research Found The study by Marfella et al., published in the New England Journal of Medicine (2024), enrolled 304 patients who were undergoing carotid endarterectomy, a surgical procedure to remove plaque from the carotid arteries. Researchers analysed the excised plaque for the presence of microplastics and nanoplastics. Their findings: 58% of patients had detectable levels of polyethylene, polyvinyl chloride (PVC), or polystyrene in their arterial plaque. This was not contamination from the surgical procedure; it was already there. Over a 34-month follow-up period, patients with microplastics in their plaque had a 4.53 times higher risk of a combined endpoint: non-fatal myocardial infarction, non-fatal stroke, or death from any cause. Inflammatory markers were significantly elevated in the microplastics-positive group. IL-18 and TNF-alpha proteins associated with systemic vascular inflammation were markedly higher in plaque samples that contained plastics. This suggests the mechanism is not simply physical obstruction, but an inflammatory cascade triggered by the presence of synthetic material in arterial tissue. What This Means for Stroke Survivors The carotid arteries are the primary conduits supplying oxygenated blood to the brain. Plaque accumulation in these vessels is one of the leading causes of ischaemic stroke, and carotid artery disease is a condition many stroke survivors are already living with. “The patients with microplastics in their plaque had a 4.53 times higher risk of stroke, heart attack, or death over the 34-month follow-up. That’s not a marginal finding. That’s a signal the research community needed to take seriously.” The NEJM study doesn’t yet tell us whether removing microplastic exposure after the fact reduces risk. It doesn’t confirm that healthy individuals with no existing carotid disease are accumulating plastics at the same rate. And it cannot tell us which plastic sources are most responsible because we’re exposed to microplastics through drinking water, food packaging, air, and a dozen other vectors simultaneously. But what it does tell us clearly and with high statistical significance is that microplastics in arterial plaque are associated with dramatically worse cardiovascular outcomes. What the Research Does Not Yet Tell Us Science at the frontier moves in one direction at a time. This study establishes association, not causation. It cannot yet answer: Whether people without existing carotid disease are accumulating microplastics at comparable rates. Whether reducing exposure actively reverses or slows plaque-associated risk. Which types of microplastics are most biologically harmful? Whether there will be a clinical screening tool for this in the near future. These are the questions the next generation of research will need to answer. In the meantime, it’s reasonable to act on what we do know. Practical Steps to Reduce Exposure No clinical screening currently exists for microplastics in arterial plaque. There is no blood test, no imaging, no biomarker that your GP can order today. What you can do is reduce your ongoing exposure, particularly through food and water contact with plastics. Evidence-informed steps worth discussing with your treating team: Use glass, stainless steel, or ceramic containers rather than plastic for food and drink storage. Avoid microwaving food in plastic containers; heat accelerates the leaching of plastic particles. Filter your drinking water; some filters (carbon block and reverse osmosis) reduce microplastic levels significantly. Reduce consumption of highly processed foods in plastic packaging. Bring this study to your vascular neurologist, cardiologist, or GP and ask whether it’s relevant to your personal risk profile. This is not a recommendation to take a supplement or start a treatment. It’s an invitation to have an informed conversation with the people responsible for your care using the best available evidence. If you found this useful, my book walks through the science of stroke recovery in the same evidence-first, no-hype way. Find it at recoveryafterstroke.com/book. Want to go deeper and support the channel? Join the community at patreon.com/recoveryafterstroke. The post Plastics in Your Arteries: The Stroke Risk Study You Must Know appeared first on Recovery After Stroke.

    9 min
  3. Jun 1

    Sent Home Mid-Stroke: CEO of Optometry Canada on Vision Loss and Recovery – Francois Couillard

    Stroke Symptoms Dismissed – What Happens When the CEO of Canada’s Optometry Body Has a Stroke Stroke Symptoms Dismissed: François Couillard has spent his career protecting people’s vision. As the CEO of Optometry Canada, the national body representing every optometrist in the country, he understands better than almost anyone how much vision matters, what threatens it, and how to preserve it. Then he had a stroke. And it only attacked his eyes. The irony is not lost on François. But what makes his story essential listening for every stroke survivor and caregiver isn’t the cruel symmetry of it; it’s what happened at the emergency department before his stroke even reached its worst point. His symptoms were dismissed. He was sent home. When Stroke Symptoms Are Dismissed François arrived at the ER with symptoms. He was assessed and sent home. What the medical team didn’t know and what François didn’t yet know was that he was mid-stroke. He walked home alone in the middle of the night. This is not an isolated story. Stroke symptoms dismissed at the emergency department are more common than most people realise, particularly when the presentation is atypical. Symptoms that don’t match the classic FAST criteria, such as facial drooping, arm weakness, speech difficulties, and time to call, can be overlooked, minimised, or misattributed. Visual disturbances, in particular, are frequently missed. For François, the consequences became clear the next morning. Waking Up With Vision Loss After Stroke François woke up having lost the right visual field in both eyes permanently. The condition is called homonymous hemianopia: a stroke-related vision loss that removes the same portion of the visual field from each eye simultaneously. Here is what makes it disorienting: the brain doesn’t show you the gap. It fills it in. You don’t see darkness where the vision is missing, you see what your brain invents to complete the picture. You look normal. You appear, in many ways, almost normal. But you are not. The Hidden Cost of Stroke Vision Loss What François describes and what many survivors with stroke-related vision changes will recognise is the extraordinary cognitive load of compensating for what you can no longer see. The brain works continuously to fill in the missing visual field. That work is invisible to everyone around you. There’s no cast, no limp, no obvious marker. But the fatigue it generates is profound and relentless. This is the invisible disability that follows many stroke survivors: the gap between how they appear and the effort required to simply exist in a world that assumes full function. Stroke vision loss recovery is rarely straightforward, and the fatigue accompanying it is one of the least-discussed consequences of stroke. François knows this intimately. He continues to live it. One Week Post-Stroke: 100km on the Bike One week after his stroke, François completed a 100km cycling event. One week. 100 kilometres. This isn’t recklessness, it’s the character of the man. A pragmatist who processes by doing, who defines himself not by what has been taken but by what remains. His approach to his stroke carries a dark honesty: he hasn’t minimised what happened, but he hasn’t surrendered to it either. The 100km ride is not a metaphor. It happened. Returning to Lead a National Health Organisation François returned to his role as CEO of Optometry Canada. He leads a national health organisation while navigating permanent vision loss, invisible fatigue, and the ongoing adaptation that stroke demands. He also carries the particular weight of professional identity intersecting with personal experience. The man who has advocated for Canadians’ vision health now lives with the consequences of a stroke that targeted exactly that. He has become, in a specific and irreversible way, both the professional and the patient. That dual perspective, the insider who became the survivor, gives his voice a precision that very few stroke stories carry. What This Episode Is Really About Episode 406 of the Recovery After Stroke podcast is not simply about vision therapy after stroke, although François discusses that too. It is about what happens when stroke symptoms are dismissed and the cascade that follows. It is about the invisible burden of neurological fatigue. It is about identity, adaptation, and the kind of resilience that doesn’t announce itself. If your stroke symptoms were dismissed, or you know someone whose were, François’s story will feel familiar in a way that is both validating and important. If you are navigating stroke vision loss and wondering whether the fatigue you feel is real, it is, and François names it plainly. Listen to Episode 406 with François Couillard available now on all major podcast platforms. Bill’s book – The Unexpected Way That A Stroke Became The Best Thing That Happened Support the show: https://www.patreon.com/recoveryafterstroke Sent Home Mid-Stroke: CEO of Optometry Canada on Vision Loss and Recovery – Francois Couillard When François Couillard, CEO of Optometry Canada, went to the ER with stroke symptoms, he was sent home. By morning, he had permanently lost part of his vision. In this episode, he shares his experience with stroke-related vision loss, invisible fatigue, and the resilience required to adapt and move forward. Highlights: 00:00 Introduction 01:13 The Stroke Experience 04:14 Diagnosis and Aftermath 13:05 Navigating Recovery and Support 17:13 Vision Challenges and Cycling Safety 23:10 The Impact of Stroke on Daily Life 29:47 Finding New Connections and Balance 37:40 The Importance of Downtime 46:08 Impact of Stroke on Daily Life 51:05 Understanding Stroke and Its Misconceptions 56:18 Mindset and Recovery After Stroke Transcript: Introduction – Stroke Symptoms Dismissed François Couillard (00:00) I had no other symptoms. Everything else was functioning. I could touch my nose. I could do everything. So they said you had that episode, you zapped a piece of your brain and now go home. Bill Gasiamis (00:00) What a nerd he is. François Couillard (00:14) it’s ironic that I worked in the field of the eyes of vision. And the only thing that got affected on my stroke was my vision. BIll Gasiamis (00:25) Hello everyone, welcome to the Recovery After Stroke Podcast. I am your host, Bill Gassiamas. My guest today is Francois Couliard, the former CEO of Optometry Canada, the national body that represents every optometrist in the country. Francois has spent his career at the intersection of vision health and leadership at the highest level. And then he had a stroke. His only symptom was visual. He went to the emergency department and was sent home. And what happened in the months, hours, days and months that followed is a story about the gap between how you look and how you feel, about the invisible cost of neurological damage, and about what it means to keep leading an organization dedicated to the very thing your stroke attacks. The Stroke Experience Bill Gasiamis (01:13) Francois Coulard, welcome to the podcast. François Couillard (01:16) Thank you, Bill. It’s a pleasure to be here. Bill Gasiamis (01:18) Thank you for coming to me all the way from sunny Canada, it looks like through your window there. François Couillard (01:24) It’s very sunny, but it’s cold. was like a few days ago, it was 29 Celsius and then yesterday morning was plus two Celsius. So it’s still a little nippy in the morning. Bill Gasiamis (01:34) Ugh. It was 29 Celsius and plus two. François Couillard (01:42) Yeah, it went from 29 to plus two in 24 hours. That’s my part of the world. Bill Gasiamis (01:46) Wow, I thought Melbourne was crazy like that. Often we have 40 Celsius days in summer and then the next day it will be 20 Celsius. but I think I prefer the 20 Celsius one than the plus two Celsius one. François Couillard (02:02) Yeah, and we go in winter, we get to minus 30. So this is not bad. We don’t complain at plus two. Still nice. Bill Gasiamis (02:11) Whereas I would definitely complain. Tell me, tell me a little bit about what happened to you. François Couillard (02:16) So a few years ago, I was sitting at the kitchen table with my wife on Halloween and I’d worked all day at my desk. I’d done some strenuous exercise in the morning. Like I do a lot of exercise. ⁓ And my wife is sitting on my left. There’s just the two of us around the table. And I turned to her and I say, it’s funny. I don’t see you that well. I can see the world, but you’re a little bit, I can’t describe it. It’s just difficult to explain, but I just don’t see you well. Now I happened, and she said, you look fine and everything. happened to, at that point I was working with the Canadian Association of Optometrists. My role was CEO of the Canadian Association of Optometrists. So anything site related, I’m gonna call an optometrist. I’m not an optometrist myself. Diagnosis and Aftermath So I called the president of the association. had just talked to him an hour or two ago. I said, hey, ⁓ I’m having this thing there. Should I worry? And he said, well, it could be one of two things. You’re either having a ⁓ migraine headache or you’re having a stroke. So go lie down for half an hour. And if it’s still there, head to emergency. So that’s why I did not lie down for half an hour. I stood up and told my wife and that’s still there. We live five minutes from the hospital from a nice large tertiary care hospital. So she took me straight there. I was full of energy just like I am now bubbly, no pain, just this funny thing. So I walk in the emerge and I tell them, you know apparently I’m having a stroke with the looking at me and it’s like, you don’t look like you’re having a stroke, but okay. ⁓ So they got me through fairly quickly, maybe half an hour. They tri

    1h 3m
  4. May 25

    Greg Graham – AVM Superhero: How He Rebuilt Life After Losing Everything

    Rebuilding Life After Stroke: Why You Can’t Go Back – And Why That’s the Point There’s a moment in stroke recovery that almost every survivor reaches. You look at the person you used to be. Your job, your relationships, your body, your identity, and you realise something that nobody prepared you for: you can’t get that person back. The question is what you do next. Greg Graham knows this moment intimately. An AVM (Arteriovenous Malformation), a rare tangle of blood vessels in the brain, changed the course of his life in an instant. What followed wasn’t just physical recovery. It was the hardest work of rebuilding everything from the ground up. What an AVM Stroke Takes From You An arteriovenous malformation stroke happens when a cluster of abnormal blood vessels ruptures in the brain. Unlike ischaemic strokes caused by a clot, AVM strokes involve bleeding into the brain. The consequences depend heavily on where the bleed occurs, and for Greg, the impact was severe. In the immediate aftermath, Greg found himself isolated. Six weeks of recovery largely alone. Relationships fractured under the weight of what had happened. The losses were not just physical; they were existential. The life he had built, piece by piece, was no longer available to him. “I’ve lost everything. I don’t see a way forward.” This is the thought that lives underneath so much of early stroke recovery. It’s not self-pity. It’s the honest reckoning that comes when the gap between who you were and who you now are becomes impossible to ignore. Why “Getting Back to Normal” Is the Wrong Goal The dominant narrative around stroke recovery in hospitals, in rehabilitation settings, in well-meaning conversations with family is built around return. Return to work. Return to independence. Return to your life. But for many survivors, this framing creates a wall they can never climb. The person they’re trying to return to doesn’t exist anymore. The brain has changed. The body has changed. The world has shifted in ways that can’t be reversed. Greg’s insight, hard-won through the kind of experience that can’t be faked, is that rebuilding life after a stroke isn’t about restoration. It’s about construction. Not returning to a previous blueprint, but laying new foundations with the materials you actually have. What Rebuilding Actually Looks Like Rebuilding after a stroke is rarely dramatic. It’s the accumulation of small decisions made under enormous pressure. It’s choosing to engage with rehabilitation when nothing in your body wants to cooperate. It’s finding a reason to get out of bed when the reasons that used to work have stopped working. For Greg, the path through began with a fundamental shift in framing. Instead of measuring recovery by what had been lost, he began to ask a different question: what is actually possible from here? That question is deceptively simple. But it’s the foundation on which real recovery is built. Because once you stop trying to recreate the past, you free up everything you have to build something new. The Identity Question Nobody Asks One of the least-discussed dimensions of stroke recovery is identity. Who are you now? Not in a philosophical sense, in a practical, daily, operational sense. If your work defined you, and stroke took your ability to do that work, who are you on a Tuesday morning? Greg’s experience speaks directly to this. The construction of a new identity after a stroke doesn’t happen overnight. It isn’t a single breakthrough moment. It’s a slow, deliberate process of discovering what you still are and what you’re becoming. This is why Greg Graham calls himself the AVM Superhero. Not because recovery was easy, but because naming what you’ve survived and choosing to carry it with you rather than hiding from it is itself a form of strength. Listen to the Full Conversation Episode 405 of the Recovery After Stroke podcast is available on all major platforms. Greg’s story is one that will resonate with anyone who has faced the impossible question of rebuilding when going back is not an option. You can also find more resources at Bill’s book, The Unexpected Way That A Stroke Became The Best Thing That Happened, a practical guide to recovery and personal transformation written from lived experience. If this show has helped you on your recovery journey, you can support it at patreon.com/recoveryafterstroke. This blog is for informational purposes only and does not constitute medical advice. Please consult your doctor before making any changes to your health or recovery plan. The post Greg Graham – AVM Superhero: How He Rebuilt Life After Losing Everything appeared first on Recovery After Stroke.

    1h 7m
  5. May 19

    GABA, Sleep, and Brain Health – Neurological Recovery

    Does GABA Actually Help With Sleep? What the Research Says for Brain Injury Recovery Someone in our community recently asked me about GABA for sleep. They’d seen it recommended online, understood that sleep was critical for their recovery, and wanted to know whether the supplement was worth exploring or just noise. It’s a genuinely good question. And it deserves a proper answer. In this post, I’m going to walk you through what GABA is, what the clinical research actually shows about its effect on sleep, why the blood-brain barrier debate matters (and why it might not derail the whole argument), and what the evidence says about the relationship between sleep and brain recovery. By the end, you’ll have enough to have an informed conversation with your medical team. I’m not a doctor. I’m a three-time haemorrhagic stroke survivor who has spent years researching the science of brain recovery and interviewing hundreds of clinicians and survivors on the Recovery After Stroke podcast. What I offer is a careful read of the evidence, not a clinical prescription. What Is GABA and Why Does It Matter for Sleep? GABA (gamma-aminobutyric acid) is the brain’s primary inhibitory neurotransmitter. If your nervous system were a car, GABA is the brake pedal. It reduces neuronal excitability, quiets cortical arousal, suppresses the brain’s primary arousal centre (the locus coeruleus), and modulates the HPA axis, the stress-response system that drives cortisol. Most sedative medications work by amplifying GABA activity. Benzodiazepines, for instance, bind to GABA-A receptors to increase chloride channel opening, producing their calming effect. GABA isn’t doing something unusual here – it’s doing something fundamental. The question with supplemental oral GABA is more specific: Does taking GABA as a capsule or powder actually produce meaningful neurological effects? What Does the Research Show? Finding 1 — Oral GABA Reduces Sleep Latency (and EEG Can Measure It) A 2015 clinical trial published in the Journal of Nutritional Science and Vitaminology by Yamatsu and colleagues used EEG measurement, actual brainwave monitoring, rather than self-reported sleep questionnaires. One hundred milligrams of oral GABA shortened sleep latency (time to fall asleep) by 5.3 minutes compared to placebo. That might sound modest. But for someone lying awake for 30–40 minutes each night, it’s a meaningful shift. Crucially, this was objective neurophysiological data, not a survey response. (PMID: 26052150) Finding 2 — A 90-Day RCT Showed Improved Sleep Efficiency and Mood A 2024 randomised double-blind placebo-controlled trial published in the Journal of Dietary Supplements (Guimarães et al.) gave 200 mg of GABA daily for 90 days to sedentary overweight women also undergoing an exercise program. The GABA group showed significantly improved Pittsburgh Sleep Quality Index (PSQI) scores, significantly reduced depression scores, and improved heart rate variability, a marker of parasympathetic nervous system activity. The HRV finding is particularly interesting. It suggests GABA may be doing something broader than simply reducing sleep latency – it appears to support the overall physiological state that makes rest restorative. (PMID: 38321713) Finding 3 — But a High-Dose RCT Found No Effect Here’s where intellectual honesty matters. A 2023 Dutch RCT (de Bie et al.) published in the American Journal of Clinical Nutrition gave participants 500 mg of GABA three times daily, 1,500 mg/day total, and found no significant effect on self-reported sleep quality. Fasting plasma GABA wasn’t significantly elevated either, raising real bioavailability questions at that dose. This isn’t a reason to dismiss GABA entirely. It is a reason to pay attention to the dose. The evidence base supports 100–300 mg, not 1,500 mg. Higher is not better, and the non-linear dose response is clinically important. (PMID: 37495019) The Blood-Brain Barrier Debate — and Why the Gut May Be the Point The most common objection to oral GABA supplementation is this: GABA is a zwitterion at physiological pH, meaning it has low lipophilicity and poor predicted ability to cross the blood-brain barrier via passive diffusion. So if it can’t get into the brain directly, how does it produce neurological effects? The emerging explanation involves the gut-brain axis. The enteric nervous system, your gut’s own neural network, has GABA receptors. When oral GABA activates these enteric receptors, it can signal the brain via vagal afferents without needing to cross the BBB at all. Think of it as a side door rather than the front entrance. Supporting this: a 2024 RCT (Li et al.) found that a probiotic strain engineered to increase gut GABA production significantly improved objective sleep duration as measured by wearable devices, alongside reduced cortisol and suppressed HPA axis activity. The mechanism wasn’t direct CNS access – it was gut-brain signalling. (PMID: 39385735) The BBB debate doesn’t negate the clinical effect. It changes how we understand the mechanism. Why Sleep Is Not Optional in Brain Recovery This is the part that I think gets underweighted in recovery conversations — and the research is unambiguous. A 2026 large retrospective cohort study (Muhtar et al., Sleep Medicine) matched over 35,000 stroke patients and found that post-stroke insomnia was associated with a 29% higher risk of post-stroke cognitive impairment and a 30% higher risk of all-cause dementia. The association with Alzheimer’s disease was also significant. (PMID: 41924789) A 2024 observational study from Monash University and Alfred Health (Smith et al.) found that in stroke rehabilitation patients, poor sleep quality was significantly associated with higher fatigue severity and lower salivary BDNF gene expression. BDNF (brain-derived neurotrophic factor) is one of the primary molecular drivers of neuroplasticity. Less BDNF means a less receptive environment for the neurological rewiring that rehab is trying to build. (PMID: 38802847) And then there’s the glymphatic system: the brain’s waste-clearance mechanism that is most active during deep sleep. Poor sleep means reduced clearance of metabolic byproducts, including proteins associated with neurodegeneration. This is not a theoretical risk. It is an active, ongoing process. Sleep is not passive recovery. It is one of the primary mechanisms of recovery. What to Do With This Information Here are three practical steps if you’re exploring GABA for sleep: 1. Measure your sleep baseline first. Use the Pittsburgh Sleep Quality Index (freely available online) before you make any changes. Understanding whether you’re struggling with latency, duration, or quality will determine what you actually need to address. 2. If you trial GABA, choose the right form and dose. Look for PharmaGABA — naturally fermented GABA, derived from Lactobacillus hilgardii, which has the strongest clinical evidence base. A dose of 100–300 mg taken 30–60 minutes before bed is consistent with the positive studies. Avoid very high doses; the null result at 1,500 mg/day is important context. Important drug interaction note: If you are taking benzodiazepines, anticonvulsants (gabapentin, pregabalin, valproate), or any other GABAergic medication, discuss GABA supplementation with your prescriber before adding it. The additive sedative effect is a real risk. The same applies if you drink alcohol regularly. 3. Don’t skip the foundation. Sleep hygiene interventions, consistent sleep and wake times, a dark and cool room, and no screens in the 60 minutes before bed, are consistently among the highest-leverage sleep interventions in the literature. GABA may provide a genuine incremental benefit. But it cannot compensate for a fundamentally disrupted sleep environment. The Bottom Line The evidence for GABA and sleep is more substantive than I expected when I started researching it. The EEG data is real. The 90-day RCT showed meaningful clinical outcomes. The gut-brain axis mechanism is biologically plausible and now has direct RCT support. And the consequences of poor sleep in neurological recovery are not trivial – they are quantifiable, significant, and, to a degree, addressable. GABA is not a guaranteed fix. Individual responses vary. The research is not yet definitive at the level of large multi-centre trials in neurological populations. But as one tool in a comprehensive approach to sleep quality alongside good sleep hygiene, appropriate medical support, and consistent rehabilitation, the case for cautious exploration is reasonable. The next step is a conversation with your neurologist, GP, or rehab physician. Take the research with you if it’s useful. Research References All studies cited in this post are retrievable via PubMed: Yamatsu et al. — GABA sleep latency EEG clinical trial (2015) — PMID: 26052150 Guimarães et al. — GABA 200mg RCT, sleep efficiency + mood (2024) — PMID: 38321713 de Bie et al. — GABA high-dose RCT, null sleep result (2023) — PMID: 37495019 Li et al. — Gut-brain GABA axis and sleep RCT (2024) — PMID: 39385735 Muhtar et al. — Post-stroke insomnia and cognitive decline cohort (2026) — PMID: 41924789 Smith et al. — Sleep, BDNF, and fatigue in stroke rehabilitation (2024) — PMID: 38802847 This post is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making changes to your supplementation or treatment plan. If you or someone you care about is recovering from a stroke, brain injury, or any neurological condition, the Recovery After Stroke podcast and this blog exist for you. Subscribe on YouTube @BillGasiamis, or visit Recovery After Stroke to find episodes, resources, and community. The post GABA, Sleep, and Brain Health – Neurological Recovery appeared first on Rec

    10 min
  6. May 18

    The Laser That Restarts Brains – Dr. Robert Hedaya on Photobiomodulation, QEEG, and Whole Psychiatry After Stroke

    Photobiomodulation Stroke Recovery: How Laser Therapy Is Restarting Damaged Brains After Stroke For seven years, a woman lived unable to remember faces. She had developed prosopagnosia, a condition that turned every person she met into a stranger, no matter how many times they had been introduced. She kept notes. She took photographs. She built systems to compensate for what her brain could no longer do on its own. Then she sat down for a single laser therapy session with Dr. Robert Hedaya. One session later, the problem was gone. “I can remember the face of the person I worked with this morning and his wife and the dimple on his face,” she told him, describing something she hadn’t been able to do in nearly a decade. What Dr. Hedaya witnessed that day and what he now works to replicate for stroke survivors, people living with aphasia, early dementia, and Parkinson’s, is the result of a therapy called photobiomodulation. And the principle behind it may fundamentally change how you understand your own recovery ceiling. Your Neurons May Not Be Dead. They May Just Be Stuck When a stroke occurs, conventional medicine draws a clear line. Tissue that is destroyed is gone. Deficits that persist beyond the early recovery window are considered permanent. Survivors are told, sometimes gently, sometimes bluntly, that they have plateaued. Dr. Hedaya challenges that directly. In his clinical experience, there is often a population of neurons that survived the stroke intact but are no longer functioning. They are alive. Their cellular architecture is preserved. But they have lost their energy supply, specifically, the ability to produce ATP, the molecule that powers every cellular process in the body. Without energy, these neurons go quiet. They stop firing. From the outside, this looks like permanent damage. But it isn’t. It is dormancy. This mirrors the concept of the chronic penumbra explored in hyperbaric oxygen therapy research, where viable tissue sits in a suspended state, waiting for conditions to change. Dr. Hedaya’s approach is different in method but identical in premise: the brain has not finished recovering. It is waiting for the right signal. Photobiomodulation provides that signal. What Photobiomodulation Actually Does “After the first laser treatment, the problem was gone. Gone. She told me — I can remember the face of the person I worked with this morning.” — Dr. Robert Hedaya Photobiomodulation, also called transcranial laser therapy, delivers precise wavelengths of near-infrared light to targeted areas of the scalp. The photons penetrate through the skull, meninges, and tissue to reach dormant neurons, where they act on the fourth complex of the mitochondrial electron transport chain, the site where nitric oxide accumulates and blocks ATP production. The photons dislodge that nitric oxide. The mitochondria resume normal energy output. The neuron now has what it needs to resume its function. The downstream effects are significant: new synapses form through a process called synaptogenesis, brain-derived neurotrophic factor (BDNF) is produced, inflammation decreases, and misfolded proteins associated with cognitive decline begin to clear. Given energy, the brain begins repairing itself, not because the laser forces it to, but because the cells already know what to do. They were just waiting for the fuel. How QEEG Makes It Precise Not every stroke survivor responds to the same laser parameters or needs treatment in the same regions. This is where Dr. Hedaya’s approach clearly separates from consumer LED helmets or generic light therapy devices. Before any laser is applied, he conducts a quantitative EEG, a brain mapping process that measures electrical activity at 19 points across the scalp. Unlike a standard EEG, which relies on a clinician reading scrolling waveforms visually, QEEG uses AI to analyse thousands of data points and reverse-engineer the source. The result is a functional map: which networks are underperforming, which are overactive, and where pathways between regions have broken down. This is paired with a neuroquant MRI that measures 30 to 40 distinct brain structures volumetrically. Together, they function as a GPS triangulating exactly where the laser should be directed, at what wavelength, power, pulse frequency, and joule delivery for each individual patient. These parameters are adjusted as the patient responds, session by session. This level of precision is what distinguishes clinical photobiomodulation from anything available over the counter. A half-watt LED helmet delivering diffuse light through hair and scalp is not the same intervention. Depression After Stroke – And the Whole-Body Connection Roughly 30% of stroke survivors experience depression in the aftermath. This is not simply an emotional response to a difficult event – it is a physiological outcome with identifiable drivers that conventional psychiatry often does not investigate. Dr. Hedaya’s model, which he calls whole psychiatry, treats post-stroke depression as a downstream expression of broader disruption: hypothyroidism, hormonal imbalance, B12 deficiency, elevated mercury from dietary sources, gut dysbiosis, chronic inflammation, and unresolved neurological stress all play measurable roles. In one of his current stroke cases, treating low thyroid function triggered seizure sensitivity because post-stroke tissue is more vulnerable to excitatory input. That kind of complexity is precisely why a comprehensive functional evaluation must precede treatment. For survivors too depleted to engage with lifestyle changes, Dr. Hedaya will now often begin with laser therapy directly. Once cellular energy is restored, the motivation and capacity to make further changes typically follow. The jump-start, he has found, enables everything else. Is Recovery Still Possible After a Plateau? If you have been told you have reached your ceiling, the core message of this episode is worth sitting with: the plateau is often not a biological fact. It is frequently the consequence of underlying conditions that haven’t been identified, and dormant tissue that hasn’t been activated. “The brain is incredibly plastic,” Dr. Hedaya says. “When you challenge it and give it everything it needs, nutrients, light, hormones, and remove the toxins, great things can happen. There is hope. There is so much hope.” His practice, the Whole Psychiatry and Brain Recovery Center, offers initial consultations via Zoom for those who cannot travel to New Jersey. For survivors with a local physician willing to collaborate, educational consultation is also available. Reach Dr. Hedaya at wholepsychiatry.com. If this episode opened something up for you, Bill’s book – The Unexpected Way That A Stroke Became The Best Thing That Happened follows the full arc of what recovery can become when you stop accepting the ceiling and start questioning it. Find it at recoveryafterstroke.com/book. If the Recovery After Stroke podcast has supported your journey, you can support the show at patreon.com/recoveryafterstroke. This blog is for informational purposes only and does not constitute medical advice. Please consult your doctor before making any changes to your health or recovery plan. The Laser That Restarts Brains – Dr. Robert Hedaya on Photobiomodulation, QEEG, and Whole Psychiatry After Stroke A laser pointed at the right spot in your brain can restart neurons that stopped working. Dr. Robert Hedaya explains how and who it can help. Hyperbaric Oxygen Therapy – Dr. Amir Hadanny Highlights: 00:00 Introduction – Photobiomodulation Stroke Recovery 01:09 Dr. Hedaya’s Medical Journey 07:55 Transition to Functional Medicine 10:31 Photobiomodulation Stroke Recovery Applications 19:21 Understanding Laser Mechanisms 24:36 Jumpstarting Healing with Laser Therapy 29:48 Understanding EEG vs. QEEG 34:10 Addressing Depression Post-Stroke 39:38 Holistic Approaches to Recovery 46:20 Patient-Centered Care and Follow-Up 51:38 The Role of Spirituality in Healing Transcript: Introduction – Photobiomodulation Stroke Recovery Dr Bob Hedaya (00:00) After the first laser treatment, the problem was gone. Gone. She told me, she said, my God, I can remember the face of the person I worked with this morning and his wife and the dimple on the face. And I said, what are you talking about? She says, have prosopagnosia. I said, says, can’t remember faces. I have to write down everything that I do and take pictures of everything and every person. I said, my God, it’s gone, gone. that’s when I went home that night and I was like, this doesn’t make any sense. How could this be? There’s nothing about a neurological condition being turned around in one minute. It makes no sense. Dr. Hedaya’s Medical Journey Bill Gasiamis (00:41) Welcome everyone to the Recovery After Stroke podcast. I’m Bill Gasiamis and my guest today is Dr. Robert Hedaya, a board-certified psychiatrist, functional medicine practitioner, and the founder of the Hull Psychiatry and Brain Recovery Center in New Jersey. Dr. Hedaya trained at Georgetown and the National Institute of Mental Health. And over the course of his career, he moved from conventional psychopharmacology into functional medicine after discovering of what was driving his patient’s symptoms had nothing to do with their medications and everything to do with their biology. In more recent years, Dr. Hedaya has added a tool that very few practitioners anywhere in the world are using, QEEG, guided transcranial photobiomodulation. That’s laser therapy, precisely using a functional brain map to reactivate neurons that survived the stroke but stopped working. In this conversation, we get into the science behind photobiomodulation and what it actually does inside the cell. How QEEG brain mapping removes the guesswork from treatment, why post-stroke depression is so ofte

    1h 8m
  7. May 4

    EECP Therapy and Stroke Recovery: Can a Cardiac Treatment Help Grow New Blood Vessels?

    EECP Therapy and Stroke Recovery: Can a Cardiac Treatment Help Grow New Blood Vessels? When I first heard about EECP therapy in the context of stroke recovery, I was skeptical. It’s a cardiac device approved in Australia for stable angina and congestive heart failure. Stroke is not on the label. So why are we talking about it on a stroke recovery podcast? Because the mechanism is fascinating. And the research, while still emerging, is pointing somewhere worth paying attention to. In this episode, I sat down with Jack Clifford, a heart disease patient who discovered EECP therapy and began exploring its potential beyond its approved indications. What started as a cardiac conversation quickly became one of the most scientifically interesting discussions I’ve had on the show. What Is EECP Therapy? EECP stands for Enhanced External Counterpulsation. The treatment involves a set of pneumatic cuffs fitted around the calves, thighs, and buttocks. These cuffs inflate and deflate in precise synchrony with the heartbeat, inflating during the heart’s resting phase (diastole) to push blood back toward the heart, and deflating just before the heart contracts. The result is an increase in blood flow and a specific type of fluid shear stress on blood vessel walls. It’s that shear stress that makes things interesting. The Biology: Arteriogenesis and Angiogenesis To understand why EECP therapy might be relevant to stroke survivors, you need to understand two terms: angiogenesis and arteriogenesis. Angiogenesis is the sprouting of entirely new capillary vessels — the body builds small blood channels where none existed before. Arteriogenesis is different: it’s the remodelling of pre-existing, dormant collateral vessels into functional bypass channels. Think of it like upgrading a dirt track into a highway. The track was always there; the body just wasn’t using it. When blood flow is obstructed, whether by a blocked coronary artery or a stroke, the body can, under the right conditions, activate these collateral pathways. The shear stress produced by EECP therapy appears to be one of the triggers that stimulate arteriogenesis. By generating repeated waves of increased blood flow, the treatment creates the mechanical signal that tells blood vessel walls to grow and remodel. This is why cardiac researchers originally developed EECP for heart patients. But it raises a legitimate scientific question: could the same mechanism support blood flow recovery in the brain after stroke? What Does the Research Say? A 2026 meta-analysis published in the QJM: An International Journal of Medicine examined 15 randomized controlled trials involving 506 participants, looking specifically at EECP’s effects on functional outcomes in stroke patients. The results showed statistically significant improvements, with EECP outperforming control conditions on standard functional recovery measures. This is preliminary evidence, not a settled clinical consensus. The studies are relatively small, the methodology varies across trials, and EECP remains off-label for stroke in Australia. But for a therapy with a well-understood safety profile and an existing approval framework, 15 studies and 506 participants is not nothing. It’s enough to warrant serious discussion. What I Discussed with Jack Clifford Jack came to EECP as a patient, not a researcher. His experience with heart disease led him to explore the therapy, and he’s spent considerable time understanding the evidence base and connecting with practitioners. He’s not a clinician, and neither am I, but what we can do together is examine what the research actually says, what the mechanism actually is, and what questions remain unanswered. In our conversation, we discussed: How Jack first encountered EECP therapy and what led him to investigate it further The difference between approved and off-label use, and why that distinction matters What the shear stress mechanism actually looks like in practice The existing network of EECP practitioners and how stroke survivors might access the therapy The questions both of us still have about where the research needs to go Important Disclaimers   EECP therapy is approved in Australia by the TGA for stable angina pectoris and congestive heart failure (ARTG Entry 376470). Stroke is NOT an approved indication. This article and podcast episode are not medical advice. Speak with your treating physician before pursuing any treatment. This episode is not medical advice. It is a conversation about an area of emerging research that I find scientifically credible and worth understanding. The goal is to help you ask better questions, not to tell you what treatment to pursue. Where to Learn More ecplocator.com a directory of EECP therapy providers eecpbook.com is a dedicated resource on the treatment and its evidence base recoveryafterstroke.com for stroke survivors looking for a broader community Research cited: Zhao et al. (2026). Enhanced external counterpulsation for ischaemic stroke: a systematic review and meta-analysis. QJM: An International Journal of Medicine. DOI: 10.1093/qjmed/hcag010. Therapy and Stroke Recovery: Can a Cardiac Treatment Help Grow New Blood Vessels? Bill Gasiamis sits down with Jack Clifford to explore EECP therapy, a TGA-approved cardiac treatment that may stimulate the growth of new blood vessels. Together, they examine the emerging research on angiogenesis, arteriogenesis, and whether this off-label approach holds promise for stroke survivors seeking to improve blood flow to the brain. Highlights: 00:00 Introduction – EECP Therapy 06:06 Recognizing Health Issues and Seeking Help 09:50 Hospital Experience and Heart Health 12:12 Decisions Against Medical Advice 16:28 Exploring Alternative Treatments 18:06 Understanding Enhanced External Counter Pulsation (EECP) 21:58 The Mechanism of EECP 27:03 Personal Transformation Through EECP 30:29 Lifestyle Changes and Holistic Health 34:35 The Impact of Stress on Health 38:30 The Journey of Writing a Book 43:29 The Role of EECP in Heart Health 48:21 Raising Awareness for EECP Therapy 56:05 Exploring the Future of EECP Therapy Transcript: Introduction – EECP Therapy Jack Clifford (00:00) Mine was really severe. 100 % blocked in my widow maker, the left anterior descending. I’m 95 in my left coronary artery and in my right main, I am 80%. And I’m still that way today, but I can run a sub seven mile. Bill Gasiamis (00:16) Welcome to the Recovery After Stroke podcast. I am your host, Bill Gassiamus. Before we get into today’s interview, I need to share something important. The topic we’re exploring today involves a medical device called an EACP, Enhanced External Counterpulsation Machine. In Australia, EACP is registered with the Therapeutic Goods Administration for the treatment of stable angina and congestive heart failure. It is not approved for stroke. What we are discussing today is emerging off-label research, not a treatment recommendation. Everything in this episode is for informational purposes only. This is not medical advice. Please speak with your treating physician before pursuing any treatment, therapy or intervention discussed here. With that said, let’s talk about something that genuinely fascinated me when I started reading the research. Your body has the capacity to grow new blood vessels, not just small capillaries, but to remodel dormant pre-existing channels into functional bypass routes. Scientists call this arteriogenesis. There’s also angiogenesis, the sprouting of entirely new Both processes matter deeply for stroke because stroke is fundamentally a blood flow problem. Now here’s where it gets interesting. A cardiac therapy developed for heart patients, not stroke patients, trigger exactly this kind of vascular remodeling. And in 2026, a meta-analysis published in the QJM across 15 randomized controlled trials and 506 participants found that EECP produced statistically significant improvements in functional outcomes for ischemic stroke patients. Now, that’s not proof. That’s not a green light to go and get an EECP, but it is worth a serious conversation. My guest today is Jack Clifford. Jack is a heart disease patient who discovered EECP therapy while managing his own cardiac condition and who has since spent considerable time investigating its potential. beyond cardiac care. I should tell you, I was skeptical going into this conversation, but I’ve learned that skepticism without curiosity isn’t really skepticism. It’s just closed mindedness. So I read the research and then I sat down with Jack. So if you find this episode valuable, I’d love for you to grab a copy of my book, The unexpected way that a stroke became the best thing that happened at recoveryafterstroke.com/book. And if you want to support the show, you can join Patreon at patreon.com/recoveryafterstroke. And I want to thank everyone who is supporting me on Patreon, especially the people that have been around for a long time and the people who have just recently signed up. I very much appreciate it. And now here’s my conversation with Jack Clifford. Bill Gasiamis (03:19) Welcome to the podcast. Jack Clifford (03:22) Thanks, Bill. Great to be here. Bill Gasiamis (03:24) Let’s give the listeners a bit of a background understanding of why you’re on the podcast. You’re not a stroke survivor, but we have something in common as ⁓ somebody who has been unwell before myself and you in the past. Tell me a little bit about your journey to the podcast So we just kind of give people an understanding as to how it is that somebody who’s not a stroke survivor. Jack Clifford (03:34) We do. Bill Gasiamis (03:51) how we ended up chatting together? Jack Clifford (03:54) Yeah, absolutely. So the quick version here is ⁓ I was on the brink five years ago of having ⁓ unsentable emergency triple bypass surgery. And ⁓ I chose a different

    1h 9m
  8. May 1

    Near-Infrared Light Therapy After Stroke: Does the Science Hold Up?

    Near-Infrared Light Therapy After Stroke: Does the Science Hold Up? A viewer reached out recently with a question I have been getting more frequently: Does near infrared light therapy actually help the brain recover after stroke? It is a fair question — the claims circulating online range from cautiously promising to outright extraordinary. In this post, I am going to cut through the noise and look at what the peer-reviewed research actually shows. What is Near-Infrared Light Therapy? Near infrared (NIR) light therapy — also called photobiomodulation (PBM) or transcranial photobiomodulation (tPBM) when applied to the head — uses specific wavelengths of light (typically 630-1100 nm) to penetrate tissue and interact with cells at a biological level. This is not a tanning lamp or a heat lamp. The mechanism is specific: NIR light at the right wavelengths is absorbed by cytochrome c oxidase, a key enzyme in mitochondrial energy production. When stimulated, cytochrome c oxidase increases ATP synthesis — essentially giving cells more energy to carry out repair and function. For neurons recovering from ischaemic or haemorrhagic stroke, the theory is compelling: damaged brain cells that are energy-starved might benefit from an additional energy stimulus. The Mechanism: What the Biology Says The cytochrome c oxidase pathway is well-established in photobiology. What is less settled is whether light at therapeutic intensities can penetrate the skull deeply enough to reach relevant brain structures. Skull and scalp tissue absorb and scatter light substantially. Transcranial delivery requires sufficient power density (irradiance) at the source and long enough exposure to accumulate meaningful fluence (energy dose) at depth. Studies using ex vivo human skull specimens suggest that only 1-3% of surface irradiance reaches cortical tissue at clinically relevant depths — and deeper subcortical structures receive even less. This does not make tPBM ineffective — it means dosing is everything. And most consumer devices do not disclose their irradiance or fluence specifications, which makes comparing them to clinical trials nearly impossible. What the Research Shows Animal Studies: Encouraging Signals Several well-designed rodent studies have demonstrated that tPBM applied within hours to days of stroke onset reduces infarct volume, improves functional recovery, and modulates neuroinflammation. A 2019 study by Thunshelle et al. found tPBM reduced lesion size in ischaemic stroke models and improved neurobehavioural scores. Animal models are useful for mechanistic insights. However, rodent skulls are thinner and brain structures are more superficial than in humans — so translational accuracy is limited. Human Clinical Trials: More Complicated The human evidence is where the story becomes nuanced. The NeuroThera Effectiveness and Safety Trial (NEST-1 and NEST-2) were the most prominent early RCTs. NEST-1 (2007) reported positive outcomes for acute ischaemic stroke patients treated within 24 hours. However, NEST-2 (2009), a larger double-blind RCT with 660 patients, failed to replicate those results on its primary outcome measure. NEST-3 was halted early in 2013 after an interim analysis showed it was unlikely to meet its primary endpoint. What went wrong? Researchers identified several issues: heterogeneous stroke populations, inconsistent dosing protocols, and the fundamental challenge of transcranial light delivery in adults with varying skull thickness and tissue composition. More recent work has shifted focus. A 2023 review by Zomorrodi et al. examined pulsed tPBM and found preliminary evidence for cognitive and neurological benefits in traumatic brain injury and neurodegeneration — but noted the absence of large, well-powered RCTs in stroke specifically. The Consumer Device Problem Here is where I have to be direct with anyone considering purchasing a NIR device for home use. Clinical studies use medical-grade devices with precisely calibrated irradiance, typically 10-700 mW/cm2 at the source, with controlled exposure times to achieve specific fluence targets (often 0.9-36 J/cm2). Consumer devices vary enormously — and most do not publish their specifications at all. Buying a NIR cap or helmet marketed for brain wellness is not equivalent to receiving the protocol used in clinical research. This does not mean it is harmful. It means we do not know whether you are getting a therapeutic dose, a sub-therapeutic dose, or anything in between. The Stakes If you are in recovery from a stroke or brain injury and you are exploring every option — which I completely understand — the risk here is not primarily financial. The risk is investing hope, time, and energy into something that may or may not be delivering what clinical trials suggest is therapeutic. The opportunity, on the other hand, is real: the underlying biology is sound, and the research pipeline is active. This is an area worth watching closely. Three Actionable Steps Talk to your neurologist or rehab physician before purchasing any device. Ask specifically whether tPBM has been considered in your care plan and what the current clinical guidance is. If you want to explore the evidence yourself, search PubMed (pubmed.ncbi.nlm.nih.gov) for transcranial photobiomodulation stroke — filter for systematic reviews and RCTs published after 2018 for the most current picture. Check ClinicalTrials.gov (clinicaltrials.gov) for active trials recruiting stroke survivors for tPBM studies. Participation in a trial gives you access to a properly calibrated protocol and contributes to the evidence base. What Recovery Can Look Like When the brain is given the right conditions — adequate sleep, nutrition, rehabilitation, reduced inflammation, and potentially adjunct therapies that the evidence supports — healing happens in ways that can surprise both patients and clinicians. I have spoken with hundreds of stroke survivors on this channel who found approaches that contributed meaningfully to their recovery. Not a single one found a shortcut. But many found tools — used thoughtfully, in partnership with their medical team — that made a genuine difference. That is what this channel is about: doing the work so you can make informed decisions. References Lampl Y et al. Infrared laser therapy for ischemic stroke: a new treatment strategy. Stroke. 2007;38(6):1843-9. PMID: 17463313. pubmed.ncbi.nlm.nih.gov/17463313 Zivin JA et al. Effectiveness and Safety of Transcranial Laser Therapy for Acute Ischemic Stroke (NEST-2). Stroke. 2009;40(4):1359-64. PMID: 19233936. pubmed.ncbi.nlm.nih.gov/19233936 Thunshelle C, Hamblin MR. Transcranial Low-Level Laser (Light) Therapy for Brain Injury. Photomed Laser Surg. 2016;34(12):587-598. PMID: 27854434. pubmed.ncbi.nlm.nih.gov/27854434 Zomorrodi R et al. Pulsed Near Infrared Transcranial and Intranasal Photobiomodulation Significantly Modulates Neural Oscillations. Sci Rep. 2019;9(1):6309. PMID: 31004089. pubmed.ncbi.nlm.nih.gov/31004089 Bill Gasiamis is a stroke survivor and the host of the Recovery After Stroke podcast. He is not a medical professional. Nothing in this post constitutes medical advice. Always consult your treating physician before starting any new therapy. The post Near-Infrared Light Therapy After Stroke: Does the Science Hold Up? appeared first on Recovery After Stroke.

    7 min
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