Jen Hatz, MS, RD, CSSD, LDN, CSCS
Head injuries, concussions, and TBI tend to take an interesting variety of perspectives as a topic to discuss in the sports and performance world. These perspectives can range from prevention strategies, to diagnostic criteria, to treatment protocols, and to potential long-term effects. What is most interesting however, is the reality of what altered neurological functioning appears as in our day to day physiological functioning and potential long-term effects with our brain metabolism, our trauma and stress response, and therefore our resilience. If all else is controlled for in trying to prevent an injury, yet an uncontrollable event occurs, we stand to benefit from that adversity through a sound understanding of how our internal environment is impacted, and what is within our control to support our own recovery and healing processes, so that we can regain functioning and neural pathways, and emerge as a newly adapted form that may now require a different process of care and attention to accommodate for this newly developed, healed, and adapted structure and function. It is therefore imperative that we gain an increased awareness of the physiology at play, the factors that contribute and correlate, the potential downstream effects, and determine what is within our control for the most realistic, comprehensive, and safe preventative, diagnostic, and treatment options for the health and safety of our athletes.
We have a poor understanding of what a concussion actually is and so we instead understand it as a deviation from the norm of our own individualized index of cognitive and neurological functioning with comparisons made against population standards. Due to this complexity and individuality, research is limited but substantially growing in our understanding of how to assess, diagnose, treat, and potentially prevent cellular damage, neuroinflammation, oxidative stress, and downstream neurological effects from concussive events.
Notably, the emphasis in concussion-related research has been on:
Preventing direct head contact (with rule changes, coaching new movement patterns, increased safety standards, etc)
Preventing or limiting force-based impact trauma to the athlete (with advancing equipment design, neck strengthening and spinal stability, viewing angles of force production, etc)
Immediate assessment post-contact with a concussion protocol (to quickly diagnose and begin treatment)
However, there is more to the story of how our brains function in the variety of trials and tribulations we may be put through that extends beyond physical impact, and so there is essentially a world unknown if we view the effects of a concussion based entirely on the impact of the event itself. We alternately need to turn our focus towards the effects, the residual, long-term, ongoing effects after the impact as well as the underlying, lingering, or predisposing stressors before the impact in order to truly understand the overall trauma of it.
Trauma is not an isolated event but rather the effects, the aftermath, and the continued response that the body and brain experience as a presence of danger even when the environment or situation presents otherwise, or the presence of danger that is beyond our ability to handle. Trauma therefore carries a wider definition that translates into our physiology. and may be seen as a blueprint for our prevention, recovery, and resilience from impactful events.
What is needed then in order to expand on gaining awareness, improving control of what we can, and building resilience:
Comprehensive diagnostic protocol with assessment methods and devices (with biomarkers collected and non-invasive assessment of fluid and electrolyte shifts, neuroinflammation, BBB integrity, brain metabolism and oxidative stress to provide evidence of degree of severity and physiological impact)
Individualized index of trauma and stress responses and sources (continuous data collection of psychological and physiological responses to lifestyle factors including sleep patterns, nutrition and hydration intake and behaviors, medications, supplements, and substances including alcohol, nicotine, natural and synthetic THC, CBD, and caffeine to name a few, BBB integrity and gut lining integrity, and neuroendocrine signaling)
Equitable approach to a needs analysis (developing equitable model for assessing and delivering all elements, including basic needs for physiology and safety, relational, community and belonging, and individualized motivation and self-actualization)
For our focus in this piece, we are looking specifically at what existing research shows with nutrition factors playing a potential role in prevention and treatment. Future posts will dive into details across the different pieces of this puzzle to round out this picture.
It is suggested that nutrition could play a role in BOTH prevention and the immediate post-concussive treatment.
Prevention strategies with nutrition tend to focus on prophylactic use/supplementation of:
Creatine
Omega 3 fatty acids
Immediate post-injury treatment strategies may include:
Possibly short-term fasting or ketogenic diet
Continued creatine and omega 3 fatty acid supplementation
Emphasis of anti-inflammatory and antioxidant-rich foods
The MAJOR limitation for concussion-related findings and recommendations is the fact that MOST of these studies are conducted in ANIMAL TRIALS, or are based on mechanisms of action.
But first, let's get into the brain...
The brain, while only contributing 2% to total body weight, requires approximately 20% of the body's energy for functioning to where adequate energy production is essential for maintaining neurological functions, especially during times of stress or tissue damage. (Erdman, et al. 2011) More than half of those energy requirements are devoted entirely to maintaining the sodium-potassium pumps within our cells which are responsible for maintaining the integrity, and therefore structure and function of the cells. This devotion of energy to maintaining proper fluid and electrolyte balance amidst metabolic processes is a key piece in understanding where to focus our assessments. During times of stress or under conditions of trauma, these energy demands increase in an effort to stabilize and maintain function when all else feels unstable. Some of the most universally accepted post-injury treatment recommendations emphasize short-term REST (from both physical AND mental activity) where these increased neurologic energy requirements can be prioritized. *Increased requirements due to the hypermetabolic brain tissue and sites of trauma.
Under NORMAL conditions...
With adequate blood flow and under 'normal' energy demands and neurologic functioning, the primary source of energy production, particularly in the brain, is derived from glucose.
During acute brain injury however...
There may be vascular changes leading to reduced neural blood flow and autoregulation, impacting the oxygen availability for energy production to where AEROBIC respiration is impaired. (Ainsley Dean, et al. 2017) As well, intracellular calcium is INCREASED to the extent that mitochondrial function is impaired. (Ainsley Dean, et al. 2017) In the immediate time following an acute brain injury, prolonged mitochondrial dysfunction (from increased calcium) is associated with increased oxidative damage, increased enzyme activity that degrades ion channels, axon structural breakdown, and even axon disconnection and cell death. (Ainsley Dean, et al. 2017)
With this REDUCED oxygen availability and mitochondrial dysfunction...
There is instead a shift to relying on anaerobic glycolysis for energy production (i.e. producing energy without the demands for oxygen and mitochondrial functioning). (Ainsley Dean, et al. 2017) Now, anaerobic glycolysis (using glucose as the primary fuel source) leads to lactate production which could be utilized in energy production, yet this lactic acid utilization is NOT enough to meet the HIGH neural energy demands to where the utilization of creatine for immediate anaerobic energy production presents as a highly sought after solution. (Ainsley Dean, et al. 2017) *It is during this time of cellular energy crisis, when blood flow and oxygen is reduced, and mitochondrial function is impaired, that creatine is relied upon for cellular energy production. (Ainsley Dean, et al. 2017)
What is creatine?
Creatine is a naturally occurring amino acid that we already produce ourselves, but we can get it from eating meats, fish, and poultry as well. Primarily contributing to energy production, creatine supplementation is most popularized for increasing strength, muscle mass, and it's ergogenic effects with improving power and sprint performance. (Erdman, et al. 2011) There are no dietary recommendations for creatine intake but with increased LOSSES (like highly active and younger populations) or potentially inadequate intake (like in vegetarians and vegans), supplementing with creatine (~5g/day) is standardized as a SAFE protocol for anyone, of all ages, to be able to replenish their own creatine amino acid pool. (Erdman, et al. 2011) *Studies of creatine for brain injury are primarily limited to animal studies, but given the evidence of creatine effects and safety, it is safe to determine that daily supplementation is not only NOT harmful, but could pose a huge benefit.
In addition to energy production...
Creatine phosphate not only plays a major role in energy production, including shuttling energy between sites of ATP production, therefore buffering energy needs, but ALSO acting as an antioxidant and reducing reactive oxygen species. (Kreider, et al. 2017) Beyond it's ergogenic effects [increasing muscle mass, strength, sprint, and power performance] creatine supplementation has also been shown to aid in recovery, enhancing hydration status for hot and humid exercise tolerance, and offering neuroprotective effects. (Kreider, et al. 2017)
It is important to note: findings suggest that following a focal brain injury, there is an observed INCREASE in the neurotransmitter glutamate that reaches excitotoxic concentrations potentially leading to secondary brain damage. (Erdman, et al. 2011) Under these conditions, there is an observed increase in free fatty acids and lactate in the brain, notably as a result of an impaired glucose metabolism during this time of cellular stress and damage. (Erdman, et al. 2011) Creatine supplementation however was associated with decreased concentrations of free fatty acids and lactate during this post-injury window of time, indicating that the creatine is predominantly being utilized for energy production, and potentially decreasing that risk of secondary brain damage. (Erdman, et al. 2011) *In this sense, creatine can contribute to immediate energy production and thereby reduce the potential of further oxidative damage from high glucose metabolism post-stress, as well as act as an antioxidant and influencing edema (fluid retention), inflammation, and hyper or hypo-osmosis through it's water retention effects. (Ainsley Dean, et al. 2017)
In rat studies, the use of creatine supplementation reduced the extent of cortical damage following a traumatic brain injury, likely due to the creatine maintaining the integrity and bioenergetics of the neuronal mitochondria. (Kreider, et al. 2017) Additional rat studies suggested the creatine supplementation IMPROVED locomotor function and DECREASED scar tissue after spinal surgery, and decreased brain infarct size after a stroke. (Kreider, et al. 2017) Creatine supplementation was suggested to reduce a loss of gray matter and helped to improve brain bioenergetics to minimize the impact of brain ischemia, i.e. may limit damage from concussions and TBI. (Kreider, et al. 2017)
When it comes to dosing...
Studies of creatine supplementation have been limited to animal studies, and post-injury supplementation in children and adolescents, to where 0.4g/kg body weight of creatine for six months, helped to reduce post-traumatic amnesia and improved recovery, cognitive function, dizziness, headaches and fatigue. (Ainsley Dean, et al. 2017) *Post-injury in adolescents: 0.4g/kg body weight starting within 4 hours after injury, and continuing once a day for 6 months. (Erdman, et al. 2011) **Take note: This is a comparatively VERY high daily dose, equivalent to ~20g/day for a 110lb individual vs 5g/day for supporting performance.
Interestingly, studies of former NFL players experiencing symptoms related to repeated head impacts showed a correlation between an index of repetitive head impacts and DECREASED creatine in the parietal white matter of the brain. (Alosco, et al. 2019) There were also some correlations noted with glutamate, glutathione, and myo-inositol concentrations and behavior or mood symptoms. (Alosco, et al. 2019) Given the slow rate of neural creatine uptake, it is suggested that prophylactic supplementation may be best warranted for mitigating the effects of mild traumatic brain injury with neuroprotective effects and improving cognitive and somatic symptoms post-stress. (Ainsley Dean, et al. 2017)
And not just for concussions...
Creatine is notably associated with brain functioning and health where disruptions in creatine synthesis or transport are associated with cognitive disabilities and deficits, language and speech impairments, epilepsy, and brain atrophy. (Erdman, et al. 2011) Creatine supplementation has therefore been studied and has shown improvements for some neurologic disorders and neurodegenerative diseases (like Parkinson's and Alzheimer's), potential improvements in psychiatric disorders (like depression, PTSD, schizophrenia) and even simply improved memory and cognitive functions in other healthy, but sleep-deprived populations (like military personnel in acute sleep deprivation). (Erdman, et al. 2011)
But enough about creatine...
Additionally, the administration of omega 3 fatty acids for at least 4 weeks prior to repeated head injuries was associated with improved cognitive performance, with the omega 3 supplementation continuing for another 2 weeks post-injury. (Prins & Matsumoto, 2014)
Omega 3 fatty acids can be found in the diet as plant-based a-Linolenic acid (which can convert into EPA and then DHA in the body) or you can obtain high DHA itself from animal foods like fish and seafood. (Prins & Matsumoto, 2014) In the body, the brain is primarily composed of DHA due to it's flexible structure and function in neural and synaptic membranes. (Prins & Matsumoto, 2014) Study findings show that preventative supplementation with omega 3 fatty acids, particularly DHA like from fish, seafood, and fish oils, for at least 30 days was associated with decreased cell damage and cell death, and improved cognitive and behavioral performance. (Prins & Matsumoto, 2014) Pretreatment of omega 3 fatty acids was also noted to preserve white matter in the brain with a decreased inflammatory response to injury, improved concentrations of myelin proteins and fibers, and subsequently improved conduction velocity of localized action potentials. (Prins & Matsumoto, 2014)
When it comes to an immediate treatment...
As mentioned in previous posts regarding the ketogenic diet and the use of intermittent fasting, there are clinically relevant findings of dietary protocols impacting neurologic disorders and potentially brain health and functioning. The most studied dietary approach in this regard is the ketogenic diet, primarily for it's utility as a treatment protocol for refractory epilepsy (where there may be impaired glucose metabolism and increased oxidative stress under hyper-excitatory and hypermetabolic neurologic demands).
Based on this notion, it has been theorized that there MAY be utility in a temporary cessation from a high intake of glucose during the immediate post-injury window of time when glycolytic metabolism is impaired. (Prins & Matsumoto, 2014) It has been suggested that in the immediate post-injury window of time, there is an increase in cerebral glucose uptake, termed 'hyperglycolysis', for up to 8 days post-injury. (Prins & Matsumoto, 2014) This state of hyperglycolysis is reportedly then followed by a period of glucose metabolic depression with a subsequent decrease in ATP energy supply, increased free radical production with DNA damage, and a decrease in glycolytic energy production alluding to the notion that glucose may not be the most favorable fuel source in this period of time. (Prins & Matsumoto, 2014) Under this premise, the utilization of endogenously produced ketone bodies (ketones that you produce from being in a ketogenic state...NOT from a ketone supplement that you drink) as an alternative fuel source is deemed an acceptable, and possibly beneficial, energy source that may reduce free radical formation as a post-injury therapeutic agent. (Prins & Matsumoto, 2014) In rat studies, administering a ketogenic diet (where the ratio of fat: carbs+ protein was as much as 4:1) as a method to induce early endogenous ketosis, was associated with significantly DECREASED volume of brain lesions and neurodegenerative cells with improved motor and cognitive function within one week post-injury. (Prins & Matsumoto, 2014) Fasting has been suggested to induce similar effects with regards to ketone formation, decreasing oxidative stress, and decreasing mitochondrial calcium loading, primarily following moderate brain injury vs severe injury. (Prins & Matsumoto, 2014) However there are mixed results on a neuroprotective effect compared to a therapeutic ketogenic diet. (Prins & Matsumoto, 2014) *Take note however, maintaining adequate energy and protein intake to meet increased energy demands is still important, especially during this immediate post-injury window. The act of RESTING (both physically and psychologically) could balance out where a temporary decrease in energy intake compared to usual intake will still meet energy demands.
Study findings suggest that there is a cumulative nature of repeated head injuries but where some findings show administration of a ketogenic diet immediately following the first head injury is associated with improved cognitive function following the second injury, indicating a potential neuroprotective effect. (Prins & Matsumoto, 2014) It should be noted that some study findings suggest endogenous ketone formation secondary to a fasted state or short term ketogenic diet was associated with less problematic side effects compared to exogenous ketone administration (i.e. taking a ketone supplement). (Prins & Matsumoto, 2014) *In this case, the utilization of an immediate post-injury fasting period following by a short-term ketogenic diet may be a beneficial post-concussive dietary treatment protocol.
One big takeaway to keep in mind: following a ketogenic diet for therapeutic benefits during an acute recovery timeframe is not synonymous with following a ketogenic diet as a lifestyle. Due to the high necessity for appropriate glucose metabolism and stable blood glucose concentrations across normal dietary intake and lifestyle, the general recommendations for regular lifestyle eating patterns is to maintain an intake of carbohydrate foods within your recommended requirements based on your individual body composition and activity level. Maintaining steady and stable blood glucose concentrations is the goal across lifestyle patterns and is especially relevant to monitor and mitigate any exacerbation of cellular damage and oxidative stress in the presence of acute metabolic stress.
In summary:
Everyone can benefit from creatine, 5g/day everyday. Potentially** increase it during windows of time post-injury up to 0.4g/kg body weight for up to 6 months.
Get Omega-3 fatty acids in your diet through fish, seafood, and fish oil supplements, as well as plant-based sources like chia seeds, flaxseeds, and walnuts
Maintain stable blood glucose concentrations; avoid drastic changes in blood glucose by avoiding high concentrations of simple sugars like juices, sweetened drinks, sports drinks, and low-fiber refined carbohydrate foods. Eat enough high-fiber carbohydrate foods to meet your carbohydrate and fiber needs while limiting simple sugars or high concentration carbohydrates. Use of ketogenic diet practices may be helpful during the acute recovery window of time.
References:
Ainsley Dean P, Arikan G, Opitz B, et al. Potential use of creatine supplementation following mild traumatic brain injury. Concussion. 2017; 2(2): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6094347/
Alosco M, Tripodis Y, Rowland B. A magnetic resonance spectroscopy investigation in symptomatic former NFL players. Brain Imaging and Behavior. 2019; https://link.springer.com/article/10.1007%2Fs11682-019-00060-4
Erdman J, Oria M, Pillsbury L. Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel. Institute of Medicine Committee on Nutrition, Trauma, and the Brain. 2011; https://www.ncbi.nlm.nih.gov/books/NBK209321/
Kreider R, Kalman D, Antonio J, et al. International Society of Sports Nutrition position stand: safety and efficacy of creatine supplementation in exercise, sport, and medicine. Journal of the International Society of Sports Nutrition. 2017; 14:18. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5469049/
Prins M, Matsumoto J. The collective therapeutic potential of cerebral ketone metabolism in traumatic brain injury. The Journal of Lipid Research. 2014; 55(12): 2450-2457. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242438/