Can Diet and Supplements Aid Traumatic Brain Injury Recovery?

In today’s episode of Daily Value, we explore the complex and ever-evolving topic of Traumatic Brain Injuries (TBIs), with a focus on new findings related to nutritional support and recovery. TBIs are often referred to as "invisible injuries" due to their [at times] subtle presentation, but they can have long-lasting effects on brain health and function. Recent research suggests that targeted supplementation may aid in recovery and even mitigate some of the long-term impacts of TBIs. 

Episode Talking Points:

*Mechanisms of TBI pathology, including primary and secondary injury phases that affect brain metabolism, neuroinflammation, and energy production.

*Highlighting a recently published narrative review paper (PMID: 39125311) suggesting nutritional interventions that may offer neuroprotection if used peri-TBI.

*The role of creatine supplementation in maintaining ATP levels during recovery.

*How omega-3 fatty acids in certain doses, particularly DHA, may promote brain repair/recovery.

*Other nutrient strategies that show promise in supporting brain health post-TBI.

https://www.mdpi.com/2072-6643/16/15/2430

Transcript

Speaker 1: 0:00

Hello everyone, welcome to Daily Value. I'm William Wallace and today we're tackling a serious and complex topic traumatic brain injuries of which I will occasionally abbreviate to TBIs in this episode. Tbis affect millions of people globally each year and are one of the leading causes of disability, particularly among athletes of all ages and military personnel. Today, we're going to be exploring briefly the mechanisms associated with TBI pathology how baseline nutrient status can affect TBI outcomes for better or worse. How certain supplemental compounds and dietary protocols may help mitigate the effects of TBIs by either promoting brain recovery and or reducing the long-term impact of these injuries. Lastly, I'll be talking about the dosages of nutrients or dietary compounds that might be suggested, if they've shown positive effects in clinical data, for addressing TBI. This topic was spurred by a narrative review paper of supplementation and dietary protocols for mitigating traumatic brain injury that was published in July of this year in the journal Nutrients. I will note that this episode will largely cover supplementation and dietary protocols for traumatic brain injury and not go too deeply into any other areas that include photobiomodulation and the like. Before we dive in, remember that this podcast is for educational purposes only and is not intended to replace medical advice. Please do not use this episode to diagnose yourself with ATBI. If you are on medication being treated for a diagnosed illness or a traumatic brain injury, please consult with your primary healthcare practitioner before beginning any supplement-based protocols that we may discuss here. A traumatic brain injury please consult with your primary health care practitioner before beginning any supplement-based protocols that we may discuss here.

Speaker 1: 1:48

A traumatic brain injury, as defined by the Centers for Disease Control and Prevention, occurs when a sudden trauma, such as a blow, jolt or penetration to the head, disrupts normal brain function. According to the CDC, tbis contribute to about 30% of all injury-related deaths in the United States and, as of 2016, 1-2% of the population lives with a chronic impairment due to TBI. It's been suggested that most TBIs are not accompanied by any change in physical appearance that can easily be detected and, as such, tbi is often referred to as the invisible injury. The severity of TBIs can range from mild concussions to severe ones. Mild are the most common, where there is a brief, if any, change in mental state or consciousness that lasts no longer than 30 minutes. Confusion can also present in mild TBI and last for hours to less than a day. Moderate TBIs are characterized by loss in consciousness and amnesia lasting from 30 minutes to 24 hours. Common symptoms of moderate TBIs include headaches, dizziness, confusion, memory problems, nausea and sensitivity to light. Nausea and sensitivity to light. Lastly, severe TBIs can cause a loss of consciousness and amnesia lasting 24 hours up to 7 days. Any severity in TBI can result in injury-related structural abnormalities when undergoing brain imaging.

Speaker 1: 3:18

As mentioned just a minute ago, tbi is a signature injury in contact sport athletes, but it's also a signature injury of modern warfare. It's here that the invisible injury aspect of the condition can come into play in a pernicious and harmful way. As the Department of Defense reported that up to 83% of TBIs in military members are mild, suggesting that there is a high likelihood of many going uninvestigated or undetected entirely. Now there are two general phases of a TBI where injury occurs. The primary injury occurs at the time of the trauma, when intracranial contents experience damage resulting in lacerations, hemorrhages or contusions. What can potentially be more damaging, depending on the severity of TBI and if left untreated and unattended, is the second phase of injury, which occurs in the aftermath of an incident which is characterized by excitotoxicity neuroinflammation leading to alterations in neurometabolism and blood flow.

Speaker 1: 4:22

Excitotoxicity, in this case describes an overactivation of glutamate receptors in the central nervous system. Glutamate is the brain's most abundant excitatory neurotransmitter, too much of which can lead to overstimulation, which can damage neurons. When glutamate is elevated in the case of traumatic brain injury, it can lead to increased calcium and sodium influx into cells, which increases the activity of proteins and reactive oxygen species, leading to cell death. This in turn affects how well mitochondria in the brain are able to make energy in the form of ATP, so mitochondrial energy output goes down. To compensate for a loss in mitochondrial energy production, the brain increases energy production through anaerobic glycolysis pathway. Anaerobic glycolysis is the process where cells break down glucose to produce energy without using oxygen. We typically hear about this process in the context of exercise, when muscles need more energy quickly and oxygen supply is limited. The this process is fast, but it's less efficient compared to aerobic respiration because it produces far less ATP. In the context of TBI, atp from this pathway is exhausted very quickly. This leads to DNA damage, which leads to further cell death. Stemming from all of this, an inflammatory cascade that leads to an overactivation of immune cells in the brain, which contributes to damage to the blood-brain barrier, which again contributes to changes in metabolism and blood flow. This secondary phase of TBI can last for weeks to months.

Speaker 1: 6:01

It's important to note that not all characteristics and mechanisms of TBIs outlined are relevant to all injuries or all head impacts. While the immediate care for TBI often involves medical interventions like imaging and monitoring, research is emerging that shows how specific nutrients and supplemental compounds can support recovery and protect the brain during the post-injury period if used in a prophylactic manner before injury occurs, or if used after injury to support the recovery process, depending on the compound in question. Firstly, it's important to state that there's strong evidence to suggest that baseline nutrient status plays a large role in the prognosis after TBI. As such, criteria number one when dealing with people at risk for TBI should be fulfilling micronutrient requirements under normal conditions and, as best you can, through regular dietary practices. The very first food-derived nutritive compound that the narrative review from Conti et al mentions is creatine, and for good reason.

Speaker 1: 7:10

Creatine's most characterized and well-known function in the body is helping maintain ATP levels in high-energy turnover cells like the brain. After TBI, as I had discussed just a minute or two ago, the brain undergoes an energy crisis of sorts due to low oxygen blood flow and a reduced ability to produce energy. Low oxygen blood flow and a reduced ability to produce energy. Research in rodents has shown that creatine supplementation reduced damage following a TBI by up to 50%. In a TBI model, the protective effect was thought to be due in part to creatine's ability to preserve ATP levels, which helps to maintain the membrane integrity of a cell. Now, interestingly, a study in 2017 found that there was a significant decline in brain creatine levels in football players over the course of a season. Animal research does show that creatine levels drop in concentration following head trauma. As such, it would seem that creatine supplementation to raise or maintain brain creatine levels before head trauma were to even occur is a useful preventative strategy. Dosing strategies to increase creatine in the brain include creatine in doses of 20 grams or 0.3 grams per kilogram of body weight for 5 to 7 days, or using over 4 grams of creatine a day for months at a time.

Speaker 1: 8:32

The next compound or groups of compounds that we're discussing are omega-3 fatty acids, those being EPA and DHA specifically. Both of these omega-3 fatty acids may interfere with the inflammatory cascade by decreasing the expression and the activation of inflammatory genes following a TBI. Actually, they may help, through multiple mechanisms, as they've been shown, to improve blood flow in the brain of hypertensive adults, but also their metabolites, known as pro-resolving mediators, are responsible for resolving inflammation and repair after an injury. I'd have to dedicate a whole episode to pro-resolving mediators, because those are some very interesting compounds and it takes some time to explain. There are actually supplements available now that have these concentrated omega-3 metabolites that could be quite useful for pre and post-TBI. Anyways, the review suggests that omega-3 fatty acids should be taken in doses of 2 to 4 grams per day, with 2 of those grams coming from DHA at the higher end of dosing. 2 grams of DHA has been shown in the past to reduce neurofilament light chain levels in college football players. Neurofilament light chain can be a marker for brain injury.

Speaker 1: 9:48

Riboflavin, otherwise known as vitamin B2, is the next nutrient of interest. Riboflavin is a major coenzyme involved in ATP synthesis in the electron transport chain. For this reason, it's been used in high doses to treat migraines in past clinical research. A study published in 2023 so very recently found that 400 milligrams a day of riboflavin for two weeks given to people post-TBI significantly reduced recovery days by over a week compared to people taking a placebo. Now, 400 milligrams is a very large dose, but has been shown to be well tolerated in the migraine research I mentioned before.

Speaker 1: 10:26

This TBI research, magnesium is up next. Mechanistically, magnesium inhibits NMDA receptors, which again are known for driving excitotoxicity after head trauma. In addition to that, in rodent models there is a well-documented depletion in neuronal magnesium levels following head trauma. The extent of magnesium depletion coincides with the severity of head trauma and the level of behavioral abnormalities that animals experience. In those models, when magnesium is resupplied, behavioral abnormalities, memory and motor function return more quickly compared to when it's not given A 2021 study in humans giving 400 milligrams of magnesium twice a day improved concussion severity scores 48 hours post-injury. That probably will lead some people to ask well, what form of magnesium is best? To which we can mention that, acutely, some forms of magnesium will preferentially accumulate more neural tissue compared to others, those being magnesium, threonate, taurate, acetyltaurate and possibly glycinate. However, there's currently no hard evidence that any one form of magnesium definitively works best for TVI protocol outcomes.

Speaker 1: 11:44

There are a few other compounds the review mentions, but in the interest of time, I will mention three things with more evidence compared to the remaining that I have not covered, one of which is the botanical Boswellia serrata. Mechanistically active constituents of Boswellia, known as Boswellic acids, inhibit an enzyme called 5-lipoxygenase. This enzyme is involved in producing leukotrienes, which are inflammatory lipid-based molecules. By reducing leukotriene levels, among other things, boswellia helps lower inflammation in the brain. There are three trials in humans that have used Boswellia with some success in those recovering from head injury or stroke. As it stands, it would seem that 400 milligrams of Boswellia taken three times daily would yield the best effects. I would also make sure the extract was standardized to 20 to 30% Boswellic acids. Extracts standardized to acetyl-11-keto-beta Boswellic acid may also be suitable, and that standardization you'd like to see at 10% or higher. Boswellia, when used effectively, was done. So post-brain injury. A brief note on the next compound, melatonin. Melatonin has been used in doses of 2-5 mg in people post-TBI to improve sleep quality, which is known to suffer post-TBI Melatonin though there's not a lot of evidence in this area, for it can be considered post-TBI to support what is routinely disturbed sleep, which would obviously contribute to recovery time.

Speaker 1: 13:21

Now a nutrient of possible concern after TBI, as is mentioned in the review. Concern after TBI, as is mentioned in the review, is caffeine. The totality of research does not entirely suggest that one removes caffeine entirely around TBI. However, it does suggest that caffeine intake be moderated as it could potentially worsen some of the symptoms following head trauma. Caffeine, under normal circumstances, is known to cause cerebral vasoconstriction, reducing blood flow, and although that does not alter brain oxygen levels under normal circumstances, it should be monitored under conditions of TBI. I will reiterate there is strong rationales to support the notion that improving nutrient status at baseline may mitigate the effects of later KPIs.

Speaker 1: 14:08

Supplementation should come after one notes the level of nutrient intake they are getting from their diet. That being said, supplementation can provide concentrated levels of key nutrients like creatine or omega-3s that many people are getting in from food because it's simply too difficult, as is the case for creatine, or because getting that amount of nutrient from food can be cost prohibitive, as is the case with omega-3s. If you or someone you know is at risk for TBI, whether through sports, military service or other high-risk activities, it's worth exploring supplements like omega-3 fatty acids, creatine, monohydrate, magnesium and melatonin as part of a comprehensive recovery strategy. It's important to consult a healthcare provider to ensure that these supplements are appropriate for your individual situation as, again, these situations can be serious and quite complex.

Speaker 1: 15:05

Traumatic brain injuries and their effects can be long-lasting. However, by incorporating targeted nutritional interventions, we may be able to reduce damage caused by TBIs and promote faster, more effective recovery. Omega-3s, creatine, magnesium and melatonin are just a few of the promising nutritive tools. More research is needed to fully understand their potential here. Thank you for tuning in to Daily Value. If you found today's episode helpful, be sure to subscribe and share this podcast with anyone who could benefit from this information. Until next time, stay safe, take care of your brain and stay healthy.