Nutritional Approach to Preventing & Treating Brain Injuries Tutorial Recording
Summary
This on-demand teaching session delves deep into the realm of preventive and therapeutic nutritional approaches for brain injuries. The session begins with an overview of brain injuries, particularly traumatic brain injuries (TBI) often caused by sports and recurrent subconcussive blows. The speaker will discuss the short-term and long-term implications of TBI, describing in detail the pathophysiology involved.
Further, the spotlight is on nutritional supplementation for brain health, focusing on Omega-3 fatty acids (EPA and DHA), creatine monohydrate, riboflavin choline, branched-chain amino acids, and anthocyanins. Emphatic discussions on the protective mechanisms of Omega-3 and their beneficial effects on TBI are included, citing various studies.
The speaker also explores the preventative and post-injury benefits of creatine monohydrate to the brain. This comprehensive talk could provide invaluable insights for medical professionals seeking knowledge on protective nutritional approaches for brain injuries.
Learning objectives
- The learners will be able to understand the causes and effects of traumatic brain injuries (TBIs), specifically in sports.
- The participants will learn about specific nutritional supplements like fatty acids, creatine monohydrate, riboflavin choline, branch chain amino acids, and anthocyanins, and their role in helping prevent and treat brain injuries.
- By the end of the session, the attendees will develop a knowledge of how Omega-3 factors into brain health, and how this can be managed through diet or supplementation.
- Participants will be equipped with an understanding of how creatine monohydrate, while often associated with muscle development, also plays a significant role in brain health.
- Attendees will be able to then apply the gathered knowledge on nutritional approaches to both preventative measures against traumatic brain injuries and treatment plans for those already affected by such injuries.
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Computer generated transcript
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The following transcript was generated automatically from the content and has not been checked or corrected manually.
All right. Um I think I'm gonna make you start now. So thanks again for joining me today. Today. We're gonna be looking at nutritional approaches for preventing and treating brain injuries. Um Now, the format is gonna be slightly different to previous times. Um I'm gonna give a brief overview of brain injuries in sport and then we're gonna dive right into nutritional supplementations. So looking at fatty acids, creatine, monohydrate, riboflavin choline, this will involve a critical analysis, then branch chain amino acids. And finally, we'll have a look at anthocyanins. Um Right. So brain related injuries. So often we refer to these as traumatic brain injuries or TBI S and there are about 1.7 to 3.8 million traumatic brain injuries in the US every year, 10% of which are due to sports and recreational activities. And this proportion is representative to more or less what we see worldwide. Now, a mild traumatic brain injury or M TBI is defined as an injury resulting from either direct or indirect biomechanical forces acting on the head or neck. And this to be classified as a mild TBI, you would see loss of consciousness of no more than 30 minutes. And that is why a concussion classifies as an MTB. Um I do wanna draw your attention to the second Impact syndrome as well, which is where you get repeated subconcussive blows to the head. And so often this can occur, for example, in contact sports like martial arts where you will get blows to the head, but you don't feel any significant effects of it, but it's still a blow to the head. And if you get repeat these repeatedly over time, actually the consequences can be um quite dramatic as well. So implications of TBI short term, you can see disturbances of the brain, fossil lipid metabolism and degradation of neuronal and astrocytic membrane, fossil lipids. Um and just to clarify neurons, astrocytes are all cells that we see in within the brain matter and they're involved for brain and cell signaling. And there are also long term health consequences like an increased risk of dementia. Now to explain the pathophysiology, I want you to imagine the brain to be like an accordion. Essentially when you get a blow to the head, the matter compresses and then expands again. And the pressure waves that are sent through the brain because of that cause damage to the internal portions of the brain. And because of that, the damage that we see with brain impact injuries can vary immensely because you can't really control for how it's gonna contract and expand. And that's where you can see injuries to blood vessels, you can see injuries to the axons. You can any portion of the brain really can be injured. And it's difficult to predict how. Now this is a slightly more detailed overview of the pathophysiology, which is where if you look at the top, you have the concussive injury and then to the right, you can get inflammation. So microglia activation, microglia or like immune cells of the brain and macrophage recruitment, which macrophages are also immune cells which are in the whole body and then they can get protruded to the site of injury. This then leads to cellular damage, causing cell apoptosis or cell death. Um again, going back to the concussive injury to the left, you can get external damage. So the neurons themselves get injured, you can get membrane disruption and excited toxicity. So if the membrane of the cells and of the neurons gets damaged, um the flow of ions across the membrane gets disrupted and therefore the signal propagation does not work properly. This can lead to apoptosis of cells again or to metabolic dysfunctions like that of the mitochondria, um causing oxidative stress, which again can cause cellular damage. And this can also actually increase the susceptibility to further injuries. So it's a whole cascade of events, really one feeding into the other. Now, the cons of cos of this are, well, firstly, you have the structural damage, something is getting damaged from the impact, but this then leads to energy deficits because of the inability to produce energy. So we just saw that mitochondria, for example, can get impaired. And if mitochondria don't function, we can't really produce energy for the brain. And as a result of this as well, you can get um a prolonged inflammatory response which can further damage the brain tissue. Now, functionally, this means that you can have problems in things like temperature control metabolism. You can get inflammation within the brain and you can get structural damage to the brain. And here this image depicts necrosis of cell death in the brain. And the consequences are also dependent on whether it was one big impact like a car accident or whether the individual suffered many subconcussive events like in martial arts or uh any other contact sports. Really? So how can we intervene on a nutritional level? Well, firstly, we have Omega threes and these are particularly relevant because of their EPA and DH A content. And Omega threes are vital for the mammalian brain because they have structural functions as well as um involvements in cell signaling. Now, DH A makes up about 10% of the brain and it is critical for neurological function, injury risk. So, preventing external injury of the neurons metabolic rate and prevention of neurodegeneration and aging. An epa is mainly involved in vascular function, inflammation, oxygen delivery and delivery of nutrients to brain. Now, because of this function, the protective mechanisms of omega threes are that they can increase the ischemic tolerance and reduce neurodegeneration. Ischemia is when the blood flow is um severed or reduced. And so that particular organ or tissue is not receiving enough oxygen supply. That's what we call ischemia. And in brain injury because you can get external damage. For example, parts of the brain can lack oxygen supply. And so because omega threes help with oxygen delivery, help with vascularization, um they can help prevent this severe damage to the oxygen supply. Now, this is also in part because they decrease cyclooxygenase activity, which is involved in the inflammatory cascade as well as inhibiting the formation of proinflammatory sinos and cytokines. And again, acting on the inflammatory pathway. They can modulate inflammation, post injury by regulating reactive oxygen species. And they do this by actually cutting off inflammation at a genetic level by preventing the transcription of IL one TNF alpha and NF KB um which are all involved in the inflammatory pathway. Again. Now, a study by Hong et al in rats showed that DH a therapy on its own diminished blood brain barrier damage and attenuated infarct volume and accelerated behavioral recovery in rats. So it seemed to reduce the damage and enhance recovery in the rat models. In terms of clinical evidence or looking at human studies. Pal et al showed that 2 to 3 g per day of omega three supplementation was associated with a larger hippocampus. Now, this was done in healthy individuals. So the relevance of this is that actually in TBI S, we see atrophy of the hippocampus and this is associated with the detriments in learning and memory functions. And so if we kind of reverse apply this, if you're taking omega threes, which seem to increase the hippocampus size, maybe thereby we're able to offset the atrophy that we see with TBI S. Um So trying to get it back to or some level of baseline homeostasis, essentially. Now another study gave again a combination of EPA DH A and this resulted in a greater accuracy and speed of recall tasks, again, functions that are impaired with traumatic brain injuries. Now, this is an interesting study because they looked at the omega three index, the omega three index is essentially just a measure of the amount of EPA and DH A per red blood cell. And they showed that having a better omega three index. So a high percentage of omega three when going into injury resulted in less severe injuries. And to put this into context, an optimal omega three index seems to be around 8 to 12%. Whereas the average athlete and to be honest, probably average person has an omega three index of less than 5% usually. So there really is a huge room for supplementation to actually have um a beneficial effect. And this was again, put into evidence by the study where they looked at American footballers. So, again, contact sport and they gave them either DH a supplementation or a placebo for the entire duration of their training and competition season. And what they showed is that the placebo group had an increase in serum neurofilament light concentration changes. I'll explain in a second over the season, whereas the DH A group remained relatively constant. Now, the serum neurofilament light concentration is a measure of neuro external damage. And so what we're seeing is that actually the DH A seems to have a protective effect of the subconcussive or concussive impacts that the footballers are experiencing over the training and competition seasons, they seem to have less neuronal damage. Um So again, speaking to the protective effects of DH A, so in terms of recommendations, this can be gotten through food sources or supplements. Um DH A in particular can be used both as a preventative measure and after TBI and I say DH A because more studies have been done particularly on the beneficial effects of DH A. Um but Omega three supplements are the way to go about getting the DH A and the EPA has positive effects as well. And this is where taking it prior. So pre loading in a sense, um taking it consistently before impacts, gives a protective mechanism against the acute effects of TBS by enhancing the omega three content, the DH A content of the brain and this can be done by 2 to 4 g a day. Um for brain related injury. So for protection against brain related injury and this honestly has very little adverse risk except some people may get slightly looser stool. Um, but yes, this can be very easily gotten through fish oil supplements, which are usu usually in the form of capsules or liquid form, you can get it through food. It is a bit more difficult. I think it would require daily effort. Um, for example, 100 g serving of salmon has about 1.5 g of DH A. So that's a lot of salmon every day. Um but it it's possible. Um Yeah, and yes, the timing doesn't matter, but obviously it would be good to be taking it before the injury to kind of have that pre loading effect, that protective um benefit going into the injury and then after the injury to then accelerate the recovery, um moving on to creatine monohydrate, which we've talked a lot about with regards to muscle. Um but it also has beneficial effects in the brain. So creating monohydrate is the most largely studied sports supplement and it is as in muscle also used in the brain as a quick fuel source. It is not the best nootropic sometimes of like acutely enhancing cognitive function. It's not like coffee in that sense, but it's very effective and safe in the long term. Now, before I dive into the protective mechanisms of creatine, some of you have been with me since the start of the series and others may have some insights about this as well. So I created a poll and I'd like you to just um select one of the answers um about why you think? Oh, sorry, that's the wrong pole. Sorry. Um Yeah. OK. Hold on. Sorry. Are you still able to pull? I think I mess it up one second. I think I might have no. OK. It seems to be working. Ok, thank you. So, yeah, just have a go. Ok. I think we've got more or less most people voting now. Um So the majority of votes um went for the that it allows maintenance of cellular ATP um and thereby limiting ischemic damage. We did have a few votes as well for the fact that it incorporates into some membranes to prevent them getting damaged during impact. So let's have a look at the actual roles of creatine um both very um reasonable and good answers. Um So based on the mechanism of creatine and what we just saw the previous side as well is that creatine, it can, it will increase the brain levels of phospho creatine just like it does in muscle and therefore it acts as an immediate source of ADP as we just saw. Um So that was the primary correct answer I was looking for. So more than 66%. Um it also seems to increase the uptake of glutamate and glucose now, because of its um immediate it's increasing phosphocreatinine levels in the brain and thereby acting as an immediate source of ADP this maintenance of cellular ADP levels is what how it confers its um protective benefit because this reduces the formation of reactive oxygen species because they are primarily formed or amongst other times, they are formed in instances of um energy, acute energy um deficiency in a sense um because of the injury to the mitochondria, for example, with traumatic brain injury, and therefore, if we're having decreased levels of ros creatine indirectly acts as an antioxidant. Um which means we are reducing the downstream effects of inflammation on the brain. Now again, because of the maintenance of cellular ATP levels, it can maintain the calcium concentration and the membrane potential protecting from neurotoxicity and neurotoxicity is when essentially the neurons don't fire as they should be. We're having bronch signals, we're having over fring of certain neurons. And that just like too much of anything can be toxic. And finally, because again, so at P levels are maintained, mitochondria retain a healthy function. And this reduces the mental fatigue you would feel because the mental fatigue comes from the fact that your brain doesn't have enough energy to supply the thinking and improve cognitive function as a result of that as well. Now, because of this creatine also prevents the decrements of synaptic homeostasis and the loss of brain parenchyma after TBI because again, we're maintaining the calcium and membrane homeostasis, we're preventing to a certain degree ischemic damage and um inflamma inflammatory damage and mitochondrial function is maintained to a certain degree. Of course, it all depends on how severe the actual injury is. Creatine is a mile drug. Um But yeah, now because repeated head blows can cause more damage over time. And this has particularly been seen if creatine is depleted prior to the next impact. This is where creatine supplementation prior to an impact and making sure the creatine source are always filled is really important, especially when athletes are competing in impact sports. Because the problem is with the secondary impact syndrome is that often athletes don't realize that the first impact has occurred. You have a slight, you know, hit to the head, you don't, your functions are impaired, nothing's really wrong, you keep running, but that counts as an impact. And if these accumulate over time, even over the course of the game that can have detrimental effects. And so that's why creatine um loading prior is really important to make sure that the creatine stores, fossil creatine stores in the brain are filled and able to essentially buffer the impacts that the athletes will get. Um and indeed, Sullivan, it all showed in rats that creatine reduced the cortical damage from TBS by up to 50% which is huge. And this was associated with enhancements in sleep cognition and mood, all of which are downstream effects of traumatic brain injuries. And as we just saw this is probably by preventing mitochondrial dysfunction, maintaining membrane health and fending off the ross cascade. In terms of human studies, um this study showed that creatine monohydrate improved cognitive function both in brain injury, abnormal aging and the thing with aging is that it's a physiological model of brain injury almost because you get the neurodegeneration, you get, get the losses in cognition and memory in recall tasks. All these things which are also impacted by TBI I so often these are models that are used to inform decision made about injuries in the brain. Um What's interesting is that this recent study published this year actually, um when giving 0.35 g per kilogram, which is quite a high dosage, but given acutely after sleep deprivation, they showed that it was in enough to attenuate the drop in cognitive function. And so this is actually the first paper showing that creatine can have acute benefits. So far, we've only ever looked at creatine loading and its long term effects in brain health and muscle same. But um being able to prevent the drop in going to function after sleep deprivation actually showed that creatine might have benefits when maybe super dosing to a certain extent after injury. Now, this is the only real study done so far. So a lot more research in this field is warranted, but obviously it bodes well for the future. So in terms of recommendations, the benefits of creatine seem to be both acute and chronic. With obviously a lot more evidence being in the field of chronic, in terms of prophylaxis, 5 to 10 g of creatine per day should be enough to fill the brain fos of creatine stores. But when leading up to a high risk situation, like a competition, it may be worth increasing it up to about 20 g per day for the week prior to the competition to really um maximally load it. And also to just make sure that you're able to refill the stores as soon as some kind of impact has occurred. Some people do experience gastrointestinal disturbances even at very low doses. It is rare but obviously make sure you test the supplements and um know whether you tolerate it or not moving on to riboflavin or vitamin B2. This can be found in most animal products, meats, especially organ meats, eggs, milk, Vitamin D is required for proper DH a incorporation into the membranes and it's important for energy production and the prevention of inflammation. And that's because it's a coenzyme for ATP production and it's highly responsible for glutathione. Glutathione is the major antioxidant module in the human body pretty much. Um so very important molecule and vitamin b2 helps um form regulate glutathione in terms of clinical evidence. Um shouldn't it all show that 400 mg per day was safe and well tolerated for migraines and a follow up study done in 2023 provided 400 mg twice a day and this was done post injury. So, starting 24 hours after injury and this was shown to half the recovery time required. So, in terms of recommendations, we're looking at about 400 mg a day. Um and this is especially interesting in folate deficiency because they tend to have elevated homocysteine levels, which is associated with oxidative stress and therefore inflammation. Um and because vitamin b2 can um act on the glutathione pathway or it does. Um this is especially in these instances of a more inflammatory state, it becomes more relevant. It's quite easy to maintain vitamin B2 levels as long as your Vitamin B status in general is good. So just make sure that is um kept well. But after injuries, extra supplementation can have an extra beneficial effect. Now, moving on to Choline choline is critical for blood brain barrier maintenance as a wards off the membrane breakdown. Um It's a precursor to acetylcholine and glutathione and increased dietary choline has been associated with decreases in biomarkers for Alzheimer's dementia and pretty much all other neurodegenerative diseases. Now, in football players brain cline, especially in the primary motor cortex was shown to diminish during the season and this is probably due to recurrent head impacts and therefore, it might also contribute to second impact syndrome. So the thought that having after each impact, even if it's sub subconcussive reduces brain calling, you reduce the protective mechanisms of colline. And therefore every subsequent impact will have a greater effect than the prior. Um Yeah, in terms of evidence, G et al showed that 100 mg per kilogram per day immediately after injury significantly improved the spatial memory performance in rats and a dose dependent reduction in blood brain barrier breakdown and edema as well as reduced hippocampal neuronal death following brain injury was shown in rats as well. So it seemed that the higher dose of um choline, the greater the protective effect in terms of clinical evidence, 1 g per day for 30 days in humans. After mild TBI, I showed significant improvements in recognition, memory. Bye. The cot analysis published 20 years later, actually found no benefit for cognitive function 90 days post injury with two rounds per day. So they used double the dosage and three times the amount of time. Now, the question is why are we seeing this difference? And because you've been doing this for a couple of weeks now, I thought I'd ask you. So we just got one more pull. Um There are technically no wrong answers. They are all possible reasons for discrepancies. Um I think it's just good to have a look through different options and think about them. Um For these, these particular studies, one of them will be the right answer, but they're all things to look out for whenever you're looking at a paper, whenever you're trying to critically analyze papers and the literature, these are all things that you could be looking out for. So I'll just give you a couple of minutes. Um I hope the pul is working. Yes, it is. OK. So right now, we look to be a 5050 split between different types of c being taken and different definitions or measures of quality of function or participants having different severities of TBI and differences in adherence to treatment. Um So let's have a look. Um So adherence to treatment in the cot study in particular is of interest because they defined adherence as taking acetylcholine 75% of the time. And let's see, more striking is that only 44% of the participants met the adherence criteria, but all of them were included in the study analysis. So um only 44% or taking tycho only 75% of the time. So I don't know how many were actually taking it all of the time. But that's a very important thing to consider when um looking at the results. Now, the other thing is that the sample size and composition was different. So in the 11 study that did find beneficial effects of Choline, they were looking at 14 patients, most of which had mild TBI. Now the Cobert meta analysis who found no benefit of Choline looked at 996 patients. But of these patients, two thirds had complicated mild TBI S and one third had moderate TBI S. So the co analysis looked at far more complex brain injuries than the 11 study. And there comes a threshold where supplementation isn't gonna i it's not gonna protect you from everything and it's not gonna heal every injury. It can help prevent injuries, it can help recover from injuries, but there's a certain certain threshold where, you know, even medical interventions can salvage the brain. So that is a very important consideration. Now, for those who um selected the different types of co are taken and different definitions or measures of cognitive function, those are very valid points. Um So again, as I said, there were no wrong answers. Just in this instance, these were the two criteria that um really made a big difference. Um But all four answers could be correct in a different context. I think some of them probably weren't some of my previous um analyses. So yeah, thank you for participating. So in terms of recommendations, the supplements are actually usually in the form of alpha GPC or Phosphatidylcholine. So again, slightly different to the ones used in the studies. Um But those are the ones that you get most access to Choline is more used for research purposes, but they have more or less the same effects really um negligible differences, 500 mg per day prophylactically is what you should be aiming for and then increasing that to 1 to 2 g per day. If a direct head injury has been suffered, this is quite easy to get through meat and eggs. Um, so many people may not even need supplementation unless obviously it's the post injury or you're following a vegan diet, vegetarian diet where it might be slightly more difficult. Um, and it is rather safe and well tolerated. Um, although it can have a nootropic effect, so it's better to take it in the morning so that it doesn't kind of interfere with sleep too much. Right. Um, P CAA S uh we were miss if I didn't mention amino acids of some sort in this talk. Um branch chain amino acids, these are isoleucine, leucine and valine. And it seems that the sev severity of TBI symptoms correlate with the degree of BCA suppression in the brain kinda like with most other supplements we've been seeing so far. Now, the benefits of BCA S range from cognitive deficits to sleep, wake abnormalities. Um Well, correcting the deficits or sleep with abnormalities. And the main benefits actually come by their correction of excited toity and other Gaba and glutamate abnormalities, which I will talk about now. So PCA S are nitrogen donors and nitrogen is used for the synthesis of glutamate and Gaba. Now this is important because in traumatic brain injuries, it's the excessive release of neurotransmitters like glutamate that lead to excitotoxicity. Now, excitotoxicity, I talked briefly at the start about neurotoxicity and this is a type of neurotoxicity where you get too much excitatory signals. Glutamate is the main excitatory neurotransmitter in the central nerve system. So it just sends signals for activation. Now, Gabaa has opposing actions. It's the main inhibitory neurotransmitter in the central nerve system. So it shuts things down. It inhibits things. Now, although obviously you need glutamate because I wouldn't be moving my hands if there wasn't some excitatory pathway activating this, I wouldn't be able to talk if I didn't have some excitatory pathway allowing me to protect my voice. But too much of anything is a bad thing. And I think one example to put this into simple terms is if you're trying to charge your computer, you're gonna plug in your charger into a socket and you need the electricity to charge your computer without the electricity, you're not charging computer and it's gonna die. But if the voltage is too high, then that's too much signal, too much electricity and it's gonna fry your computer and the computer is dead too. So you need the perfect balance and in the brain to counter the balance of the excitation, you have Gaba that provides inhibition now because you get excessive release of neurotransmitters like glutamate. So the more excitatory ones in TBI S, what B CAA S can do by being nitrogen donors is that they can increase the synthesis of Gaba, thereby allowing for a new homeostasis to be established where Gaba can still kind of tune down the ex excitatory signal sent by glutamate. Now, another beneficial effect of BCA S is their transportation interference across the blood brain barrier. Um BCA S, they share a transporter through the blood brain barrier with tyrosine and tryptophan, which are two other um amino acids. Now, tyrosine and tryptophan are precursors for serotonin, which in turn is a precursor for catecholamines. So what happens when you have more BCA S in the blood is that they essentially reduce the uptake of trip five and tyrosine into the brain because they compete for the transporter and thereby they reduce the concentrations of the, the formation of serotonin in the brain and thereby reduce the formation of catecholamines. And yes. So this is what I was just saying. So we have reduced serotonin and reduced catecholamines. Now, the reason why this is important is because catecholamines like noradrenaline can exacerbate damage from traumatic brain injuries by their involvement in the inflammatory response and by increasing BP and cerebral edema. So, by preventing trip tyrosine uptake or limiting their uptake in through the blood brain barrier, BCA S actually reduce the damage by acting on the catecholamine level of the equation. There's a clinical evidence. Um Corned all showed that BCA supplementation decreased the symptoms of concussion, allowed for faster and better return to baseline and found no adverse effects. And they actually showed a dose dependent improvement with the greatest benefit at 54 g per day. And el um showed that 30 g twice a day, improved insomnia and other latency associated issues in veterans with chronic TB. And so in terms of recommendations, this can be managed quite simply with adequate protein intake, looking at around 1 g per kilogram. Um but supplementation to reach higher levels, post TBI I may be relevant. We don't know exactly what more research, more studies are warranted in this field. But current evidence suggests around 60 g per day. Um again, following vegan vegetarian diets, it may be more important to suffer with PCA S. Um And yes, and the reason why we want to supplement post TBI as well is because obviously, protein sources like animal sources that have a full profile of amino acids will also contain tryptophan tyrosine amongst some sources. And so the issue is obviously that since you're competing for a transporter, you want the BCA concentration to be higher than the tryptophan tyrosine concentration so that they can outcompete and reduce the uptake of tryptophan and tyrosine. Um And that's why post injury supplementation becomes more important so that you can really increase the proportion of the leucine isen and um valine compared to the tyrosine and tryptophan concentrations. Now, the final one we're looking at are anthocyanins. These are phytochemicals in the flavonoid family. And so the mechanism is not quite certain, but they're primarily known about um being in high concentrations in blueberries. But as you can see here, they're quite readily available in any purple, red bluish fruit and vegetables. Um they protect against oxidative stress and because of that they are involved in protection against pretty much, I mean, most dis diseases you can think of, especially the metabolic and the inflammatory ones. Um The clinical evidence um shows that here, the study by Krishna et al in animals show that blueberry extracts or supplements post injury improved BDNF. Now, BDNF or brain derived neurotropic factor is involved in the survival growth and um the maintenance of nerve cells and the spinal cord. And as a result of this, um improving BDNF was shown to be increasingly correlated with the indirect markers of memory performance and cognition. So these extracts seem to help with these um cognitive deficits seen with traumatic brain injuries too. Um There are unfortunately no randomized controlled trials yet on blueberries and TBI S. But studies on brain health in general have shown that um alignments help with attention, memory and executive function and that they improve sports performance. Um Now, this study actually showed that a six month supplementation with Mieno twice a day in elderly, improved episodic memory performance and reduced cardiovascular disease. Now, Momen is a patented polyphenol rich grape and blueberry extract. So essentially what we're looking at here is lots of anthocyanins and again, elderly are an interesting cohort to be studying even when looking at brain injuries because they are physiological memory of cognitive dysfunction, a lot of which has similar etiology um or similar pathophysiology as that seen TBS again, a great variety in terms of um age related neurodegeneration and injury related neurogen degeneration, both of which still very ill defined. But in any case, they are a good physiological model for us to use. And um given that they seem to help in the elderly, there's no reason to think that they could not have a potential benefit in injuries as well. So as I said, recommendations, these are honestly very easy to get through simply a cup of blueberries a day, um or any other berries or purple, red fruit and vegetables. So the take home points, routine impacts during contact sport are subconcussive and result in brain damage that can have long term effects on brain health. Obviously, acute severe impacts also have long-term consequences on brain health, nutritional supplementation has the potential to target multiple pathways in the complex secondary events that occur following an injury. There is very strong evidence for supplementation with epa DH A. So Omega threes as well as creatine monohydrate and there is relatively strong evidence for the consumption of riboflavin choline, branch chain, amino acids and anthocyanin. And this can be done through foods or through supplements and that is it. So, thank you again for your attention and for your interaction with the polls. Um It's time for questions now if anybody has any. Um And if not, thank you again for joining me today, please do fill out the feedback survey that I sent out and um I do try to take all feedback on board. Um And yeah, next week, the final tutorial on relative energy deficiency syndrome in sport. So I look forward to seeing some of you there. Ok. There's a question in the chat. Going back to what you said about aging being quite a good model for TBI S. Do you think the supplements would be beneficial for an older person to take to ward off some of the cognitive effects of aging? Um There are definitely a lot of the studies actually done on these supplements for brain injuries are done on aging to help ward off neurodegeneration. Um There is definitely a protective mechanism, especially things like creatine monohydrate which are involved in energy generation in the brain. Um That is one of the um main ones really that has been shown to have predictive benefit benefits. Again, we're only a few decades in to creatine studies. So a lot more research is so warranted, we need more longitudinal studies. But because the a lot of the cognitive um deficits seen with aging with neurodegeneration are linked to the fact that we have certain energy deficits in certain parts of the brain. Um especially things like creatine monohydrate that can increase this ADP generation. Um actually do definitely seem to have a um pro not necessarily protective benefit in the sense that you're never gonna get it, but it slows down the progression and can delay the onset of certain um characteristics of neurodegenerative diseases. Um Other ones like omega threes, like choline may be more um directly applicable to injuries. But again, a lot, the, the problem of course is that a lot of neurodegenerative diseases are not well characterized yet. It's difficult to know exactly what is happening, but a lot of them do have an inflammatory element to them as well. Um So yes, any of these supplements that seem to act on the inflammatory pathway, um like riboflavin, for example, as well could possibly have beneficial effects in that sense. Um I think creatine monohydrate is one where supplementation would be required for the brain benefits. Um because although there's some creatine in food, it's unlikely if you're a carnivore that you will get more than maybe 3 g a day on a good day. Um So to reach the 5 to 10 g, it really is worth supplementing. Um Yeah, I have to answer your question. And again, the same is true for things like Omega threes difficult to get really sufficient amounts from the diet itself to have a neuroprotective effect. Um But then there are things like Ocys that honestly, you probably do not need to supplement it unless you're allergic to all purple foods.