How Ketones Help the Brain Recover From Concussions

Summary

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Podcast Summary: How Ketones Help the Brain Recover From Concussions

Podcast: The Metabolic Classroom with Dr. Ben Bikman
Host: Insulin IQ
Episode Date: November 3, 2025

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Episode Overview

This episode focuses on the metabolic consequences of concussions, specifically how traumatic brain injuries impair glucose metabolism in the brain and the crucial, overlooked role of ketones in supporting brain recovery. Dr. Ben Bikman breaks down the metabolic crisis triggered by concussions, the science of how ketones can bridge the energy gap, and practical strategies—ranging from ketogenic diets to exogenous ketone supplementation—for optimizing brain resilience and recovery.

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Key Discussion Points and Insights

1. Concussions as a Metabolic Problem

[02:38–04:20]

• While typically considered mechanical injuries resolved by rest, concussions create a significant metabolic disturbance in the brain.
• "When the brain is injured, its ability to generate energy from glucose declines, creating a temporary but profound and relevant energy crisis." — Dr. Ben Bikman [03:15]

Key Facts:

• A concussion is a mild traumatic brain injury (TBI) caused by physical impact that temporarily disrupts brain function.
• Symptoms may include headaches, dizziness, concentration issues, and mood changes.
• Up to 30% of individuals may experience lingering symptoms—post-concussion syndrome.

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2. The ‘Energy Crisis’ in the Injured Brain

[04:21–07:40]

• The brain accounts for only 2% of body mass but consumes roughly 20% of total energy expenditure.
• After a concussion, the main energy pathway—glucose metabolism—becomes impaired at multiple stages:
  • Reduced Glucose Transport: GLUT1 (on the blood-brain barrier) and GLUT3 (on neurons) decrease after injury, restricting glucose entry.
  • Enzymatic Bottlenecks: Key enzymes in glycolysis (hexokinase, PFK) and mitochondrial entry (pyruvate dehydrogenase) are inhibited by increased calcium and oxidative stress following TBI.
• This leads to reduced ATP (cellular energy) production and increased vulnerability of neurons.
• "There's a bottleneck of glycolysis, which of course is going to sharply reduce the ability of the brain cells to produce energy in the form of ATP." — Dr. Ben Bikman [06:40]

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3. Knock-on Effects: Oxidative Stress and Inflammation

[07:41–09:12]

• Disrupted mitochondrial function leads to increased oxidative stress (ROS), prompting inflammation.
• Microglia (brain immune cells) are activated, escalating the inflammatory response and exacerbating injury.

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4. Ketones: The Brain’s Backup Fuel

[09:13–12:30]

• The brain can adapt by shifting to ketones—specifically, beta hydroxybutyrate (BHB) and acetoacetate—produced by the liver during fasting or carbohydrate restriction.
• Ketones cross the blood-brain barrier efficiently via monocarboxylate transporters (MCTs).
• Unlike glucose pathways, ketone metabolism operates independently, bypassing glycolytic bottlenecks.
• "It's the glucose transport that's compromised, not ketone transport. It's the breakdown of that glucose that's compromised, not the breakdown of the ketones." — Dr. Ben Bikman [10:55]
• Classic fasting studies (e.g., by Dr. George Cahill) demonstrate that the brain can derive more than two-thirds of its energy from ketones when available.

Notable Insight:

• Most people on a standard, carbohydrate-heavy diet rarely generate meaningful ketone levels due to frequent eating and elevated insulin—leaving the brain unable to access this protective fuel after injury.

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5. Animal and Human Evidence Supporting Ketone Therapy

[12:31–13:18]

• Animal models show that ketogenic diets or exogenous ketones can increase brain ketone uptake by ~50%, restoring ATP and aiding neuron survival post-injury.
• Human studies (e.g., Bernini et al, 2018) confirm that blood ketone levels closely track brain ketone levels following TBI, demonstrating rapid ketone availability to the injured brain.
• "Collectively, these findings and more suggest that ketones do serve as an efficient compensatory substrate when glucose metabolism is impaired." — Dr. Ben Bikman [13:10]

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6. Mechanisms: How Ketones Support Brain Recovery

[14:18–17:41]

A. Energy Provision

• Ketones sustain ATP production even when glucose metabolism is disrupted.
• Animal studies: ketones reduce lesion volume by up to 50% compared to glucose-fed counterparts.

B. Oxidative Stress Reduction

• BHB inhibits Class 1 histone deacetylase, promoting antioxidant gene expression.
• Ketogenic diets attenuate post-injury oxidative stress by boosting antioxidant defenses.

C. Inflammation Control

• Ketones dampen inflammatory responses by inhibiting the NLRP3 inflammasome (pro-inflammatory master switch).
• This modulates cytokines, shifting the brain environment from pro- to anti-inflammatory.

D. Enhanced Neuroplasticity

• BHB elevates brain-derived neurotrophic factor (BDNF), supporting neurogenesis and repair.
• Animal models indicate ketogenic adaptation improves motor recovery and preserves cell health markers (telomere length).

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7. Practical Strategies for Individuals at Risk

[17:42–19:47]

• Metabolic preparedness is critical, especially for those in contact sports or with recurrent concussion risk.
• Dr. Bikman advocates for maintaining a mild state of nutritional ketosis as a preventative measure, but acknowledges that strict ketogenic diets are impractical for many athletes.
• "I submit that maintaining some level of nutritional ketosis during play or during that work may offer some preventative protection." — Dr. Ben Bikman [18:16]

Exogenous Ketones:

• Exogenous ketone supplements (particularly those with BHB or GO BHB) offer a practical solution for real-time brain fuel before, during, and after potential concussions.
• Not all ketone supplements are equal—look for “GO BHB” or “straight BHB acid.”
• Clean Form Nutrition now offers NSF-certified ketone supplements suitable for athletes.

Discount Mention:

• Dr. Bikman shares a discount code: "You can use the code BEN10… and you can get a 10% discount." [19:36]

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8. Takeaway Message

[20:15–21:02]

• Concussions trigger a metabolic crisis in the brain by shutting down glucose pathways, but ketones present a safe and effective backup energy source.
• Ensuring ketones are available—through diet or supplementation—can support resilience and recovery.
• "As Dr. George Cahill demonstrated decades ago, the brain is very metabolically adaptable. It will use whatever fuel is present. Our task…is to ensure that ketones are available when the brain needs it most." — Dr. Ben Bikman [20:35]

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Notable Quotes & Memorable Moments

• “When the brain is injured, its ability to generate energy from glucose declines, creating a temporary but profound and relevant energy crisis.” [03:15]
• “There's a bottleneck of glycolysis, which of course is going to sharply reduce the ability of the brain cells to produce energy in the form of ATP.” [06:40]
• “It's the glucose transport that's compromised, not ketone transport. It's the breakdown of that glucose that's compromised, not the breakdown of the ketones.” [10:55]
• “Maintaining some level of nutritional ketosis during play or during that work may offer some preventative protection.” [18:16]
• “As Dr. George Cahill demonstrated decades ago, the brain is very metabolically adaptable. It will use whatever fuel is present. Our task…is to ensure that ketones are available when the brain needs it most.” [20:36]

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Important Timestamps

• [03:33] – Introduction to concussion and metabolic lens
• [04:21] – Explanation of glucose transport impairment
• [07:41] – Description of oxidative stress and inflammation
• [09:13] – Introduction to ketones as alternative brain fuel
• [12:31] – Evidence for ketone therapy in brain injury
• [14:17] – Ketones, energy, oxidative stress and inflammation
• [17:42] – Practical strategies for at-risk individuals
• [19:36] – Exogenous ketone supplement recommendation
• [20:15] – Summary and core takeaway

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Final Thoughts

Dr. Ben Bikman delivers a compelling scientific breakdown of why ketones are vital for brain recovery after concussion, elevating the conversation beyond rest and mechanical repair. The episode equips listeners—from athletes to health professionals and caregivers—with a clear understanding of the underlying metabolic crisis in concussion and actionable strategies to support brain resilience.

Class dismissed. Until next time—more knowledge, better health!

Transcript

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[Professor Benjamin Bickman]

Welcome to the Metabolic Classroom Podcast. I'm Ben Bickman. Thanks for letting me be your guest professor for the next few minutes. Don't worry about any pop quizzes. I'm here to simply make the science of metabolism clear, practical and engaging. Hey everyone. Before we get started today, I want to tell you about something brand new that our team has created called Dr. Bickman's Digital Mind. It's an AI version of me that can help answer your questions about the science behind metabolic Health. It's been trained using nearly 3 million of my own words from my lectures, published research, my books, interviews and even unpublished books. Private Q and A sessions. You can chat with it or even talk with it, using your voice to try it out. You'll get five complimentary responses and five minutes of voice conversation time just to see how it works. After that, you can decide whether or not you'd like to have unlimited access by becoming an insider. You can find it right now on my website and there's a direct link below at the top of the show. Notes welcome to the Metabolic Classroom. I'm Professor Benjamin Bickman, a biomedical scientist and professor of Cell Biology in today's mini lecture, we'll examine concussions through a metabolic lens. While concussions are often viewed as mechanical injuries caused by impact and resolved with rest, the underlying damage is deeply metabolic. When the brain is injured, its ability to generate energy from glucose declines, creating a temporary but profound and relevant energy crisis. Fortunately, of course, the body has a backup fuel system, namely ketones. By understanding how concussions disrupt brain metabolism and how ketones can restore it, we gain insight into prevention, recovery, and even the broader resilience of the human brain. Now, to get things started, let's define a concussion. Of course, you probably already know this, but a concussion is considered a mild traumatic brain injury, or tbi. Resulting from a physical impact temporarily disrupts normal brain function. The injury does not always involve loss of consciousness. It can occur from something as seemingly mild as a header in soccer or hitting the ball with your head. Even a minor collision, or, of course, an impact in many other sports, or a fall. During impact, the brain shifts within the skull. It literally moves, leading to stretching of axons. It can also cause some electrolyte disturbances or ion imbalances. And of course, as we're going to focus, focus on metabolic disturbance as well. The most common symptoms of a concussion include things like headaches, dizziness, difficulty concentrating, and even mood changes. While most individuals recover within days or weeks, up to 30% experience some lingering effects, a condition known as post concussion syndrome. In the midst of focusing on the hit or impact, few realize that a concussion causes an energy crisis that matters in the brain because the brain is hungry. Even though it accounts for only about 2% of body mass, the brain consumes roughly 20% of total energy expenditure with carbohydrate heavy diets, which of course, is the global diet. At this point. Glucose acts as the brain's primary fuel after a concussion. Unfortunately, glucose metabolism becomes compromised. This impairment begins at the cellular entry point. Glucose transporters, particularly glucose transporter 1, or GLUT1, which exists on the blood brain barrier and GLUT3 on the neurons, show reduced expression and activity within hours of the injury. Even when glucose is available in the bloodstream, and it always is, its delivery into the brain becomes compromised. It becomes restricted because of the lower levels of those glucose transporters. But the problem does not stop inside the cell. Several of the enzymes involved in glycolysis, these glycolytic enzymes, including hexokinase and phosphofructokinase, sometimes just abbreviated as pfk, are inhibited. This happens because of elevations in calcium and increased oxidative stress. Of course, those are direct results of the TBI itself. Also a very important enzyme called pyruvate dehydrogenase, which is the enzyme that determines enzyme entrance into the mitochondria at the end of glycolysis, is further inhibited. So altogether, these create a bit of a bottleneck, these effects, these inhibited enzymes. There's a bottleneck of glycolysis, which of course is going to sharply reduce the ability of the brain cells to produce energy in the form of ATP. ATP is that energy currency. It's the money with which the brain cells, or any cells, purchase some kind of work or some effect. Well, in the glucose fueled brain, when glucose can't work well, the brain is running out of fuel in the acute phase after the injury. So this is minutes to hours. There's actually a marked increase in energy demand, and glucose would normally fuel that demand, but the glucose transport and the loss of those glycolytic enzymes makes it so that the energy cannot be met. The energy demand can't be met with glucose. So the metabolic dysfunction that happens here, in fact doesn't end there. It can persist for several days, even in mild cases. Ultimately, this leaves the neurons to be very vulnerable to going hungry. And the disordered mitochondrial function, where the mitochondria aren't fueled well and, and they can end up creating more oxidative stress, which in turn can increase inflammation. And that oxidative stress, I note the mitochondria, that's because the mitochondria can start leaking electrons which then bind to oxygen, creating the first of the reactive oxygen species. So you have more ROs, accumulating ROs, and that in turn, in turn can start under forcing oxidative damage on other things in the cell, like lipids and proteins. Further, we have microglia which can amplify. These are immune cells or inflammatory cell in the brain. They can become active and further amplify the inflammatory response. And what was meant to be a help becomes a hindrance, and that can ultimately extend neuronal injury. Thankfully, in the midst of all of this compromised glucose use and further consequences, the brain can adapt. Ketones, namely beta hydroxybutyrate and its mother molecule acetoacetate, serve as efficient alternative fuels for the brain. Produced in the liver during fasting or carbohydrate restriction, these ketones can easily cross the blood brain barrier via monocarboxylate transporters, or MCTs, aptly named. And it then allows the ketones to enter the citrate cycle directly so BHB can just go straight in. It becomes acetyl CoA, and we are right into the citrate cycle. All of this bypassing the compromised glycolytic pathways. It's the glucose transport that's compromised, not ketone transport. It's the breakdown of that glucose that's compromised, not the breakdown of the ketones. This metabolic adaptability was elegantly demonstrated in the classic fasting studies by the famous George Cahill and his colleagues. When both glucose and ketones are available, the human brain derives the majority of its energy from ketones, even to the point where it's exceeding two thirds of its total ATP production now coming from ketones. So it can be more than 2 to 1 in a ratio that the brain is using ketones over glucose when it has access to both. The brain, in other words, is not loyal to any particular fuel. It is opportunistic. It will use whichever substrate is most available and importantly, in this context, can be adequately metabolized. The challenge for most modern individuals is that ketones are almost never available. Frequent eating of high carbohydrate diets and the subsequent elevated insulin suppresses ketone production, leaving the brain metabolically reliant on glucose. But of course, in the case of concussion, it is forced to use or rely on glucose, but it can't actually metabolize it. In other words, the brain goes hungry. In animal models of tbi, ketogenic diets and exogenous ketones can increase cerebral or brain ketone uptake by as much as 50%. Of course, that allows the brain to restore its ATP production and help these neurons survive. Human and preclinical data together indicate that the injured brain can rapidly shift toward ketone use when ketones are available. Within hours after injury, the expression of those MCTs, those monocarboxylate transporters that carry the ketones into the brain increases. And in experimental models, bhb, the main ketone, beta hydroxybutyrate. When it's infused, it markedly, of course, increases ketone uptake and oxidation, so helping to prevent ATP depletion. So if the brain can't make enough ATP because of its compromised glycolysis, all the more reason to give it some kind of ketone. Collectively, these findings and more suggest that ketones do serve as an efficient compensatory substrate when glucose metabolism is impaired. When the brain is impaired. Now, the vast majority of what we know about brain metabolism in brain injury experiments comes from animal models, and that is not surprising. Ethically, it would be difficult to get approval and have people agree to undergo some traumatic brain injury. So most of our mechanistic insights come from controlled experiments in rodents. Nevertheless, a few careful clinical studies do provide some valuable windows into the human condition. One of the most informative comes from Bernini and colleagues. In 2018, they used a technique of cerebral microdialysis in patients with moderate to severe tbi. They found that brain ketone levels closely tracked with blood ketones, which isn't surprising, rising during fasting and falling with carbohydrate feeding. So this just demonstrated that circulating ketones easily and readily reach the injured brain. That's important because remember, glucose won't Ultimately, this work highlights the need for direct BHB delivery, either orally or even infused if needed, to reinforce the concept that the human brain, after injury can use ketones when they are available, providing a strong rationale for exogenous ketones as both preventative and therapeutic interventions. It's third down.

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[Professor Benjamin Bickman]

Now I want to expand on that topic because with all of this in mind, and to summarize some of this so far, ketones influence several key processes relevant to brain recovery. The first, as I have mentioned, I think a few times now, is the energy provision. When glucose uptake and use declines, ketones sustain mitochondrial function by providing energy. In the models that I've already mentioned, mostly rodent, but even some human ketones can reduce lesion volume by approximately 50% compared to glucose fed controls, indicating a very important role for energy control. And the smaller the lesion size, of course, the Greater the neuronal preservation and the faster the recovery. Number two is a reduction in oxidative stress. Following a concussion, ROS generation increases rapidly and robustly. Ketones can counteract this through multiple mechanisms. BHB inhibits a molecule or an enzyme called class 1 histone deacetylase which can then promote the expression of antioxidant genesis. In rodent models of tbi. A ketogenic diet can attenuate post injury oxidative stress by increasing the expression and activity of antioxidant defenses. Number three is inflammation control. Concussion induced inflammation involves a significant increase in elevated pro inflammatory cytokines. These are molecules like TNF alpha. Ketones modulate this response and instead promote a shift from pro inflammatory to anti inflammatory states. Remember ketones. BHB in particular inhibits the central molecule called the NLRP3 inflammasome. This master switch that when it's turned on it increases the production of myriad other pro inflammatory molecules. Now, beyond fuel, ketones also promote neuroplasticity and this again goes beyond the basic energy support because BHB has been shown to enhance bdnf, brain derived neurotrophic factor and this can then in turn encourage neurogenesis and even the repair of synapses or the connections between neurons. In adolescent animal models of brain injury, prior ketogenic adaptation has been shown to improve motor recovery and even preserved telomere length, of course, which is a marker of the longevity or the health of a cell. From a practical standpoint, metabolic preparedness, if you will, matters for individuals engaged in contact sports or at higher risk of any kind of head injury. I submit that maintaining some level of nutritional ketosis during play or during that work may offer some preventative protection. Of course a ketogenic diet can do this, but in the case of athletics, many athletes don't want such dietary restrictions and I would even say metabolically, they don't need it. Not to say they might not benefit from it, but how else then can they keep their ketone levels elevated? Well, of course at that point it becomes clear that there is an obvious role for exogenous ketones and I think they should be considered as both a preventative and immediate. In other words, in real time therapeutic strategy, providing ketones before and during activity ensures that the brain has access to an alternative energy source even in the event of injury. After a concussion, exogenous ketones can help bridge that metabolic gap while the glucose metabolism remains impaired. I've mentioned this a few times, but the most effective exogenous ketone and indeed the most bioavailable is beta hydroxybutyrate or bhb. So when it comes to finding an exogenous ketone supplement that you want, just look for anything that has just BHB in it. This is generally going to take the form of of a patented molecule called GO bhb. That's what you can find on the label somewhere. This is directly usable by the brain and of course any other tissue with mitochondria. But other supplements labeled as ketone products might not be based on bhb and in fact they may have some complications because they have to be converted to BHB in the liver and in the process may actually provide or create some harm in the liver if the BHB is not already available through diet because of an exogenous because of a ketogenic diet. Rather then supplementation with bhb, I would suggest in the form of GO BHB or a straight BHB acid in the L or D form that can provide an immediate and a very practical way to deliver this critical fuel right when the brain is demanding fuel post injury. Now, to my delight, if you'll allow me to add this for especially for you athletes, the first NSF certified ketone supplement is now available. This is a problem because you have professional or collegiate athletes who can't or the university or the organization cannot openly encourage or provide the ketone supplement because it might not meet this NSF certification. Well, you can go to cleanformnutrition.com cleanformnutrition.com is now or just a clean form version of BHB. Or there go BHB is NSF certified so you can go there. In fact, I know these guys. I have a discount code. You can use the code BEN10B E N10 and you can get a 10 discount. CleanForNutrition.com the first NSF certified ketone supplement. Let's end, let's wrap it up. So in. Over the course of this mini lecture, we've examined how concussions trigger a metabolic crisis and how ketones offer a protective alternative energy source that can stabilize the brain's energy and thus facilitate the recovery process. As Dr. George Cahill demonstrated decades ago, the brain is very metabolically adaptable. It will use whatever fuel is present. Our task, if you will, is to ensure that ketones are available when the brain needs it most. Thanks for joining me in the metabolic classroom. Class dismissed. Until next time. More knowledge, better health.

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