Concussion Recovery

Concussion Recovery: A Nutritional and Natural-Health Reference

1. Definition, Clinical Presentation, and Body Systems Involved

Definition

The 2022 6th International Conference on Concussion in Sports defines concussion as "a traumatic brain injury caused by a direct blow to the head, neck or body resulting in an impulsive force being transmitted to the brain that occurs in sports and exercise-related activities." More broadly, the expert Concussion in Sport Group defined concussion as "a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces," and agreed that concussion typically involves temporary impairment of neurological function that heals by itself within time, and that neuroimaging normally shows no gross structural changes to the brain as the result of the condition.

A concussion is a brain injury associated with rapid brain movement and characteristic clinical symptoms, with no associated objective biomarkers or overt pathologic brain changes, thereby making it difficult to diagnose by neuroimaging or other objective diagnostic tests. 70–90% of the over 50 million estimated global TBI cases per year are thought to reflect concussion, or mild TBI (mTBI).

Clinical Presentation

Early and late clinical symptoms, including impairments of memory and attention, headache, and alteration of mental status, are the result of neuronal dysfunction mostly caused by functional rather than structural abnormalities. Most concussion symptoms are transient and resolve within 1–2 weeks. However, between 10% and 20% of adults who are diagnosed with a concussion have symptoms that persist beyond 3 months post-injury. This persistent condition is referred to as post-concussion syndrome (PCS) or prolonged post-concussion symptoms (PPCS).

Neurometabolic Cascade and Body Systems Involved

Concussion is a complex brain injury affecting neurons and nonneuronal cells such as astrocytes, oligodendrocytes, microglia, and endothelial cells, leading to acute neurometabolic disturbances such as ionic imbalance and energy crisis.

Concussions share similar acute pathophysiologic perturbations to more severe TBI: there is a rapid release of neurotransmitters, which causes ionic disequilibrium across neuronal membranes. Re-establishing ionic homeostasis consumes energy and leads to dynamic changes in cerebral glucose uptake.

The mechanical insult initiates a complex cascade of metabolic events leading to perturbation of delicate neuronal homeostatic balances. Starting from neurotoxicity, energetic metabolism disturbance caused by the initial mitochondrial dysfunction seems to be the main biochemical explanation for most postconcussive signs and symptoms.

These biomechanical differences may yield distinct early injury phenotypes but converge on shared downstream cascades involving ionic disequilibrium, excitotoxicity, mitochondrial dysfunction, inflammation, and impaired cerebral blood flow regulation.

The neuroinflammatory system is heavily engaged: resident immune cells in the central nervous system, primarily microglia, become activated and release many inflammatory mediators, including cytokines and chemokines, that permeate brain tissues and potentially contribute to ongoing neuronal damage. Inflammation may persist for days to weeks, causing secondary injury cascades that impair neuronal function and potentiate neurodegeneration.

The glymphatic system has also emerged as a key structure in concussion pathophysiology: the glymphatic system has emerged as a potential mechanistic bridge between acute injury and chronic symptomatology. Experimental and clinical studies demonstrate altered aquaporin-4 polarization, increased perivascular space burden, impaired solute clearance, elevated inflammatory markers, and tau pathology following mTBI. Increased perivascular space burden has been linked to persistent cognitive deficits and overall post-concussive symptom burden, suggesting a role of glymphatic dysfunction in long-term outcomes.

The autonomic nervous system and cardiovascular system are also implicated: the coupling of the autonomic nervous system and the cardiovascular system is typically reflected in heart rate variability (HRV). High HRV is a marker of better health and indicates an improved ability of the body to adapt to many different changes. Increased sympathetic nervous system activity results in less heart rate variability.

Furthermore, concussed cells enter a peculiar state of vulnerability, and if a second concussion is sustained while they are in this state, they may be irreversibly damaged by the occurrence of swelling. This condition of concussion-induced brain vulnerability is the basic pathophysiology of the second impact syndrome.

2. Contributing and Associated Factors

Injury-Level Factors

Short-term predictors of prolonged recovery and PCS vary across studies but appear to include older age (adolescent versus child), high initial symptom load, initial presenting symptoms of amnesia and loss of consciousness, and some evidence to support premorbid conditions as contributing to symptom persistence (e.g., previous concussion, learning difficulties, psychiatric difficulties).

Mild brain injury-related factors that increase the risk for persisting post-concussion symptoms include an injury associated with acute headache, dizziness, or nausea; an acute Glasgow Coma Score of 13 or 14; and having another head injury before recovering from the first.

Demographic and Premorbid Factors

For risk factors of concussion, history of prior concussion and female sex have the most supporting evidence. Premorbid psychiatric conditions, pre-injury health system usage, and older age were associated with increased risk of a prolonged recovery from concussion.

A multitude of risk factors for developing PCS have been identified in the literature including severity of initial symptoms, prolonged headache, subjective concentration deficits, female gender, referral to a concussion rehabilitation program, history of prior concussion, dizziness, vestibulo-ocular dysfunction and younger age. Others have also reported history of psychological (e.g., depression, anxiety) or neurodevelopmental (e.g., attention-deficit/hyperactivity disorder [ADHD], learning disability) disorders as risk factors for developing PCS.

Nutritional and Metabolic Context

In the contact sports population, the syndrome of reduced brain resilience leads to increased susceptibility to concussions. This syndrome is a particular physiological state corresponding to functional nutrient deficits and disturbances of certain mechanisms that normally maintain metabolic homeostasis in brain tissue. The brain is a very special tissue with exceptional metabolic constants compared to other tissues. For example, it uses 20% of all ingested calories and requires more than 40 different nutrients to function properly.

Concussions cause overconsumption of nutrients by the brain. This creates a state of heightened nutritional vulnerability during the recovery period, an observation that has driven research into nutritional strategies for support.

3. Nutrients, Herbs, and Natural Ingredients

Overview of the Research Landscape

The injury triggers a complex neurometabolic cascade involving multiple mechanisms. There are pharmaceutical treatments that target one mechanism, but specific nutrients have been found to impact several pathways, thus offering a broader approach. This has prompted intensive research into the use of nutrient supplements as a concussion prevention and treatment strategy.

While many athletes and clinicians incorporate vitamins and supplements into concussion recovery plans, human-based studies specific to sports concussion remain limited. The main finding of one systematic review was the lack of interventions conducted to date, and a quality assessment of the included studies was found to be fair to good. Notably, all studies reported a positive effect of the interventions on recovery outcomes, which may indicate possible publication bias.

The following compounds are categorized by best available evidence, with traditional use and scientific evidence separated where applicable.

Omega-3 Polyunsaturated Fatty Acids (DHA and EPA)

Scientific Evidence

Omega-3 fatty acids play a crucial role in neuronal integrity and function, aiding TBI recovery by reducing oxidative stress and inflammation. There is evidence that the amount of DHA in brain tissue is decreased after mTBI, suggesting an elevated need for DHA in mTBI recovery. DHA is likely more effective than EPA in addressing the pathophysiologic events related to concussion.

Preclinical data are substantial: rats pretreated with DHA showed significant reductions in anatomical damage after TBI, as measured by β-amyloid precursor protein counts within injured axons, axonal bulbs, and enhancement of cell survival. The effects of DHA on these cellular responses translated into cognitive resiliency, where rats pretreated with DHA showed similar memory function after TBI compared to sham rats, whereas untreated rats showed significant cognitive declines after TBI.

In terms of human evidence: preclinical studies suggest that administering DHA during both the acute (1 day) and subacute (14 days) time frame following TBI may enhance cognitive recovery and improve learning and memory. Most clinical studies of omega-3 fatty acids have investigated their prophylactic use; however, some have begun to investigate the use of these fatty acids for treating post-concussive symptomology. Some studies have reported faster mild TBI symptom resolution and return-to-play after omega-3 supplementation than after placebo treatment.

One double-blind placebo-controlled trial found that DHA supplementation significantly increased plasma DHA in a dose-dependent manner and led to an attenuated increase in serum neurofilament light (NFL), a biomarker of axonal injury. However, the current state of the science regarding LCPUFA supplementation for the treatment of concussion is based primarily on animal models and these animal models have specific limitations that preclude their ability to be adequately generalized to the human condition. There is a growing body of strong preclinical evidence and clinical experience that suggests that benefits may be possible from aggressively adding substantial amounts of n-3FA to optimize the nutritional foundation of TBI, concussion, and postconcussion syndrome patients, though further clinical trial research is needed.

Evidence strength: Strong preclinical (animal) evidence; limited but emerging human clinical evidence. Randomized controlled trials in sports concussion populations are ongoing. No definitive clinical recommendations yet exist.

Creatine Monohydrate

Scientific Evidence

Concussions not only impact neurocognitive function but also lead to metabolic disruptions, including decreased cerebral creatine concentrations. Given creatine's critical role in energy metabolism within neural tissue, its supplementation may support recovery by stabilizing these metabolic alterations.

Evidence from experimental models in rats demonstrates that pre-emptive supplementation with creatine may reduce damage following TBI by 36–50% in a "moderate" severity controlled cortical impact model that results in significant tissue loss.

Several small clinical studies provide compelling evidence that creatine supplementation for a week or more may improve or accelerate outcomes following a mild TBI, but to date, there have been no large prospective placebo-controlled randomized trials to establish the efficacy of this treatment.

Patients suffering from TBI experience mitochondrial dysfunction, neuropsychological burden, and deficits in cognitive performance due to malperformance of brain creatine levels, diminished brain ATP levels, glutamate toxicity, and oxidative stress. Results from a systematic review are only clinically significant after a month of supplementation. Creatine shows efficacy as a neuroprotective agent in battling the chronic manifestations which lead to oxidative stress and cognitive decline post brain injury.

Evidence strength: Strong rationale from biochemistry and animal models; limited small clinical studies; no large RCTs specific to sports concussion. Evidence is preliminary.

Riboflavin (Vitamin B2)

Scientific Evidence

Vitamin B2 or riboflavin is important in the mitochondrial respiratory chain to produce ATP and helps to maintain a major antioxidant enzyme, glutathione. Riboflavin's physiologic actions as an energy producer and antioxidant are naturally tailored to the metabolic mismatch found at the cellular level in sport-related concussions. Several animal studies have reported on the impact of riboflavin in concussed rat models showing an improvement in behavioral function, a reduction in brain edema, and a decrease in glial fibrillary acidic protein around the brain contusion site.

Riboflavin is a powerful antioxidant acquired from meat and dairy dietary sources. It is readily absorbed, required for normal cellular functioning, and has strong antioxidant effects. Riboflavin rapidly reduces oxidized iron, high levels of which lead to free radical damage and lipid peroxidation.

A randomized placebo-controlled trial in sport-related concussion (listed in the Cochrane Central Register of Controlled Trials) found that riboflavin shortens duration of sport-related concussion. This represents one of the few human RCTs directly targeting concussion with a nutritional supplement. Riboflavin has also been studied in the context of concussion-related headache due to its established role in migraine prophylaxis: data previously published shows potential benefit of certain vitamins in the management of migraine headache, including Vitamin B2 (Riboflavin), Magnesium, Co-Enzyme Q-10, and Omega-3 fatty acids, at dosages described in the literature, used based on the migraine literature findings to help treat complaints of headache in concussion management.

Evidence strength: Mechanistic rationale is strong; positive animal data; at least one human RCT with positive findings specific to sports concussion. Evidence is still early-stage but more direct than many other compounds in this field.

Magnesium

Scientific Evidence

Magnesium also shows promise in reducing inflammation and enhancing recovery in TBI models, although further clinical research is needed. Magnesium plays a critical role in hundreds of enzymatic reactions, and its depletion is a known consequence of TBI. A small pilot study examined acute magnesium oxide supplementation post-concussion/mTBI: the effects of acute magnesium oxide supplementation post-concussion/mTBI were examined for improving symptoms and resulting in a return to functional baseline time in pediatric adolescents (n = 17).

Magnesium has also been investigated in clinical trial registries alongside riboflavin and CoQ10 for concussion-related headache management, based on its established evidence base in migraine prophylaxis.

Evidence strength: Strong mechanistic rationale; limited direct human concussion-specific RCT evidence; broader evidence from migraine literature. Evidence is preliminary and largely preclinical for the concussion-specific context.

Vitamin D

Scientific Evidence

A vitamin D deficiency primes patients for poorer recovery post-mTBI, leading to unregulated inflammatory and immune responses, reduced neuroprotection, and increased risk of cell death. In addition, deficiency can affect testosterone levels and increase patients' post-traumatic stress disorder (PTSD) risk, resulting in chronic fatigue outcomes post-TBI.

Findings from clinical research were positive, highlighting that vitamin D supplementation following mild to moderate TBI may improve patients' long-term performance and cognitive outcomes. Animal studies have also shown that combined vitamin D and progesterone has been found to reduce inflammatory markers (cytokines), decrease brain oedema, blood-brain barrier disruption, and cell death when tested on TBI models.

Evidence strength: Observational and mechanistic evidence is strong, particularly relating to deficiency worsening outcomes. Intervention evidence in humans is limited. No large RCTs specific to concussion exist.

Melatonin

Scientific Evidence

Melatonin is a hormone produced in the brain that binds to melatonin-specific receptors on neuronal membranes in several brain regions. Its documented neuroprotective properties, low toxicity, and ability to cross the blood-brain barrier have led to its evaluation for patients with traumatic brain injury, a condition for which there are currently no FDA-approved therapies.

Melatonin supplementation may improve some of the sleep disturbances often experienced post-TBI. Sleep disruption is among the most commonly reported post-concussion symptoms, and melatonin's role in circadian regulation provides a biological basis for its use. In the PMC systematic review on nutritional interventions in chronic mTBI, melatonin was identified as safe and well-tolerated, and these nutritional interventions including melatonin may improve cognitive failures and sleep disturbances following mTBI.

There remains a significant gap in the literature pertaining to the role of therapeutic melatonin after TBI.

Evidence strength: Mechanistically plausible with good safety profile; some human data in the chronic mTBI phase supporting sleep and cognitive outcomes; larger controlled trials are lacking. Evidence is preliminary but among the more clinically studied of the natural interventions for this indication.

N-Acetylcysteine (NAC)

Scientific Evidence

Emerging evidence from experimental trials and systematic reviews suggests that certain micronutrients and biological compounds, including N-Acetylcysteine (NAC), may have beneficial effects both before and after the occurrence of TBI and concussion by targeting specific neuropathological mechanisms such as inflammation and oxidative stress. NAC is a precursor to glutathione, the brain's primary endogenous antioxidant, which is substantially depleted following concussive injury. Research in animal ischemia-reperfusion models has demonstrated reduced oxidative stress injury when NAC is administered.

Evidence strength: Strong mechanistic rationale; animal and in vitro evidence; human clinical trial evidence specific to sports concussion is limited. Classified as preliminary/investigational.

Branched-Chain Amino Acids (BCAAs)

Scientific Evidence

Animal studies have shown that branched-chain amino acids may improve neurophysiological outcomes after TBI. The most current evidence regarding supplements with emerging data in concussion management includes branched-chain amino acids; other supplements such as vitamins C, D, and E, and taurine are discussed based on findings in animal models and moderate-to-severe traumatic brain injury.

Evidence strength: Predominantly animal model evidence; very limited direct human RCT data for concussion specifically. Investigational.

Choline

Scientific Evidence

Choline is among the prophylactic and/or therapeutic compounds under investigation for TBI-related outcomes. Choline is an essential nutrient involved in the synthesis of acetylcholine, a neurotransmitter critical for memory and learning, and is a structural component of neuronal phospholipid membranes. TBI has been shown to alter choline metabolism, and a nutritional approach focused on compounds available in the diet that may mitigate the effects of impact includes choline among compounds whose levels or requirements are potentially modified by the accumulation of multiple smaller impacts over time.

Evidence strength: Mechanistic rationale established; direct human RCT evidence for concussion is lacking. Investigational.

Boswellia serrata

Traditional Use

Boswellia serrata (Indian frankincense) has been used for centuries in Ayurvedic medicine for conditions involving inflammation, including joint disease, neurological conditions, and inflammatory bowel disease. Traditionally the oleoresin is extracted and administered as an oral preparation. Its active constituents, boswellic acids, have been the subject of modern phytochemical investigation for anti-inflammatory properties.

Scientific Evidence

Boswellia serrata downregulates the production of inflammatory cytokines, an action relevant to the neuroinflammatory cascade implicated in concussion pathophysiology. Boswellia serrata is among the prophylactic and/or therapeutic compounds under investigation in the context of TBI-related outcomes.

Evidence strength: Well-established traditional use in anti-inflammatory contexts; modern mechanistic data are promising; direct human RCT evidence specific to concussion or mTBI is currently lacking. Preliminary/investigational.

Enzogenol (Pine Bark Extract)

Scientific Evidence

The systematic review on nutritional interventions in the chronic phase of mTBI identified Enzogenol® as safe and well-tolerated. Enzogenol is a proanthocyanidin-rich extract of New Zealand pine bark with antioxidant and anti-inflammatory properties. It was among the six nutritional areas identified in a 2023 systematic review and these nutritional interventions may improve cognitive failures, sleep disturbances, anxiety, physical disability, systolic blood pressure volume and sport concussion assessment tool scores following mTBI.

Evidence strength: Some human data in the chronic mTBI phase, but from small studies with heterogeneous populations. Evidence is preliminary.

Berry Anthocyanins

Traditional Use

Berries rich in anthocyanins (e.g., blueberries, elderberries, bilberries) have a long cross-cultural history of use for cognitive support and as general tonics. In folk traditions throughout Europe and North America, berries were consumed to support vision, memory, and general brain health.

Scientific Evidence

Berry anthocyanins are among the prophylactic and/or therapeutic compounds under investigation for TBI-related outcomes. Emerging evidence from experimental trials suggests that certain compounds, including anthocyanins, may have beneficial effects by targeting specific neuropathological mechanisms such as inflammation and oxidative stress. Research remains primarily in cell and animal models, with mechanistic evidence showing neuroprotective effects including reduction of oxidative stress, inflammation, and neuronal apoptosis.

Evidence strength: Primarily animal and in vitro evidence; no direct human RCTs specific to concussion. Investigational.

Ketones and the Ketogenic Diet

Scientific Evidence

Ketogenic diets and circulating ketones have purported signaling properties, reduce oxidative stress, decrease systemic inflammation, and promote mitochondrial function. The ketogenic diet has been further shown to be neuroprotective in animal models of several central nervous system (CNS) disorders, including Alzheimer's disease, Parkinson's disease, hypoxia, glutamate toxicity, ischemia, and traumatic brain injury.

A human feasibility study of an 8-week ketogenic diet in patients with PCS symptoms examined cognitive and self-reported symptoms. A recent study examined the ketogenic diet and medium chain triglyceride supplementation in post-concussion syndrome and reported improvements in visual memory and post-concussion syndrome symptomology. The rationale connects directly to the neurometabolic crisis of concussion: in animal TBI models, ketosis-inducing nutritional approaches have been demonstrated to have neuroprotective benefit. Acutely post-TBI, cerebral ketone concentration is elevated and can be modulated through administration of ketosis-inducing nutrition, which could be indicative of a metabolic adaptation to ketone metabolism in the early stages of TBI.

There is an absence of information on which forms of TBI—mild/concussion, moderate, severe, and penetrating—might benefit from such therapy. Another consideration is the feasibility of prescribing such a strict diet when treating nonhospitalized patients. Although ensuring compliance with any nutrition intervention may present a challenge, this is especially true when the whole diet needs to be altered.

Evidence strength: Mechanistic rationale is strong; animal evidence is well established; human feasibility data are encouraging but limited to small, uncontrolled or pilot studies. Further controlled trials are needed.

Phytocannabinoids

Scientific Evidence

The systematic review on nutritional interventions in chronic mTBI identified phytocannabinoids as safe and well-tolerated, and these nutritional interventions may improve cognitive failures and sleep disturbances following mTBI. The term phytocannabinoids in this research context refers primarily to cannabidiol (CBD) and related hemp-derived compounds. Research in TBI/mTBI is at an early stage, with most evidence derived from animal models or small clinical observations.

Evidence strength: Preliminary. Human safety data exist, but efficacy in concussion specifically is not yet established in large controlled trials.

Zinc

Scientific Evidence

Zinc also shows promise in reducing inflammation and enhancing recovery in TBI models, although further clinical research is needed. Zinc is among the nutrients reviewed as nutraceutical treatments for brain injury in experimental models. Zinc is essential for antioxidant enzyme function and is a co-factor for numerous neurochemical processes. Depletion of brain zinc has been observed following TBI.

Evidence strength: Mechanistic rationale and animal model evidence; human clinical trial evidence for concussion specifically is limited. Investigational.

Coenzyme Q10 (CoQ10)

Scientific Evidence

Coenzyme Q10 also shows promise in reducing inflammation and enhancing recovery in TBI models, although further clinical research is needed. CoQ10 functions as a critical electron carrier in the mitochondrial respiratory chain and is a potent fat-soluble antioxidant. Given the role of mitochondrial dysfunction in concussion pathophysiology, CoQ10 has been proposed as an investigational supplement. It has also been studied in migraine prevention, providing secondary rationale for its investigation in concussion-related headache.

Evidence strength: Mechanistic rationale; limited direct concussion evidence. Investigational.

Ginseng and Ginkgo biloba (Traditional Medicines)

Traditional Use

Both Panax ginseng and Ginkgo biloba have been used for millennia in Traditional Chinese Medicine (TCM) for cognitive enhancement, fatigue, and recovery from illness. Ginseng was classically employed as an adaptogenic tonic to restore vitality and mental clarity, while ginkgo leaf preparations were used for circulation and memory. Both are still widely employed in global herbal traditions for brain-supportive effects.

Scientific Evidence

Ginseng and ginkgo biloba are among the herbs and traditional medicines reviewed as nutraceutical treatments for brain injury in experimental models. Preclinical studies have demonstrated antioxidant, anti-inflammatory, and neuroprotective effects for both botanicals in various brain injury contexts. However, direct human clinical evidence in concussion or sports-related mTBI populations remains absent. Evidence is confined to general neuroprotective and cognitive literature, and extrapolation to concussion recovery is speculative.

Evidence strength: Long traditional use history; mechanistic animal evidence for neuroprotection; no direct human RCT evidence in concussion populations. Traditional and preliminary investigational.

4. Dietary and Lifestyle Factors

The Gut-Brain Axis and Microbiota

Gut microbiota is an important factor in concussion recovery, pointing to a potential benefit of probiotics and prebiotics. Research has highlighted the bidirectional gut-brain-microbiota axis as a potential nexus between traumatic brain injury, inflammation, and disease. Disruptions in gut microbial composition following mTBI may perpetuate neuroinflammation and impair recovery.

A narrative review of nutrition in mild TBI rehabilitation specifically covered the topic of gut microbiota among nine key nutritional topics relevant to mild TBI outcomes.

Alcohol and Caffeine

A literature review in PubMed and Google Scholar on nutritional interventions in mild TBI specifically examined caffeine and alcohol as factors of interest in mild TBI outcomes. Alcohol is broadly recognized as a factor that may impair recovery processes in concussion, while the evidence on caffeine is more nuanced, given its widespread use and potential interactions with concussion-related headache and sleep disruption.

Weight Management and Energy Status

Weight management was specifically identified as one of the nine nutritional topics with primary focus on mild TBI in a narrative review on nutrition in mild TBI rehabilitation. The brain's exceptional energy demands during recovery make systemic metabolic status—including body composition and overall nutritional adequacy—potentially relevant to healing outcomes.

The MIND Diet

A literature review on nutrition and mild TBI rehabilitation covered the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet as a topic of interest in mild TBI outcomes. The MIND diet, which emphasizes green leafy vegetables, nuts, berries, beans, whole grains, fish, poultry, olive oil, and wine (moderate), while limiting red meat, butter, cheese, pastries and sweets, and fried/fast food, has been associated with reduced neurodegenerative risk in aging populations and may provide a rationale for investigation in concussion recovery, though direct RCT evidence in mTBI is not yet established.

Sleep and Circadian Health

Immediately post-impact, a focus on physiological parameters and sleep is likely to assist in recovery. Sleep is essential for glymphatic clearance of metabolic waste from the brain—a process directly implicated in concussion pathophysiology. Disruptions in sleep following concussion are common and may perpetuate the neuroinflammatory environment.

Exercise Timing

While not a dietary factor per se, graduated aerobic exercise is discussed in the broader rehabilitation literature as an important physiological factor. Some preclinical studies have also suggested that the combination of exercise with a DHA-enriched diet may improve cognition following head injury, underscoring the interaction between lifestyle and nutritional factors in the concussion recovery context.

Overall Nutritional Approach

A full health assessment to screen for and address nutritional and metabolic health markers that may be associated with worse outcomes after TBI is recommended, along with consideration of a "left of bang" nutritional approach focused on compounds available in the diet that may mitigate the effects of impact or whose levels or requirements are potentially modified by the accumulation of multiple smaller impacts over time (e.g., creatine, choline, omega-3s).

As clinical evidence in this research field is rapidly emerging, a comprehensive approach including appropriate nutritional interventions has the potential to mitigate some of the physical, neurological, and emotional damage inflicted by TBIs, promote timely and effective recovery, and inform policymakers in the development of prevention strategies.

5. Evidence Limitations and Research Gaps

All the research included in several systematic reviews recruited adults, and thus findings should not be assumed to generalize to children or adolescents. Similarly, participants were in the chronic phase of mTBI, and additional research is required to investigate whether the same findings would apply during the acute phase of such injury.

Further research of higher quality is needed to investigate the role of nutrition in recovery from mTBI to reduce the burden of chronic outcomes following mTBI. Heterogeneity may have impacted the strength of evidence. Differences included population variability, different dosage of nutrients, diversity of injury and outcome measurements.

Numerous supplements, including n-3 polyunsaturated fatty acids, sulfur amino acids, antioxidants and minerals, have shown promising results as aids to concussion recovery or prevention in animal studies, most of which use a fluid percussion technique to cause brain injury, and in a few human studies of severe or moderate traumatic brain injury. The translation of these findings to mild traumatic brain injury and sport-related concussion specifically remains an important research frontier.

References

• Purcell LK et al. "The pathophysiology of concussion." PubMed / Journal of Clinical Sport Medicine, 2012.
• Giza CC, Greco T, Prins ML. "Concussion: pathophysiology and clinical translation." PubMed / Handbook of Clinical Neurology, 2018.
• Clinics in Sports Medicine. "The Pathophysiology of Concussive Brain Injury," 2025.
• ScienceDirect. "The Pathophysiology of Concussion," Current Sports Medicine Reports, 2011.
• ScienceDirect. "Concussion pathophysiology: From biomechanical insult to clinical phenotype," 2026.
• Medscape. "Concussion: Background, Epidemiology, Sport-Specific Biomechanics," 2025.
• Walrand S et al. "Nutritional factors in sport-related concussion." PubMed / Nutrition Reviews, 2021.
• The Role of Nutritional Supplements in the Treatment of Sport-Related Concussion. PubMed, 2025.
• Clifford T et al. "A Potential Role Exists for Nutritional Interventions in the Chronic Phase of Mild Traumatic Brain Injury, Concussion and Sports-Related Concussion: A Systematic Review." PMC, 2023.
• Monti K et al. "The role of nutrition in mild traumatic brain injury rehabilitation for service members and veterans." PMC / Neurorehabilitation, 2024.
• Oliver JM et al. "ω-3 Fatty Acid Supplementation as a Potential Therapeutic Aid for the Recovery from Mild Traumatic Brain Injury/Concussion." ScienceDirect / Advances in Nutrition, 2014.
• Lewis M et al. "Concussions, Traumatic Brain Injury, and the Innovative Use of Omega-3s." PubMed / Military Medicine, 2016.
• U.S. Department of Defense / Defense and Veterans Brain Injury Center. "Information Paper on Omega-3 Supplements for Mild Traumatic Brain Injury," 2025.
• MDPI Nutrients. "Omega-3 Fatty Acids and Traumatic Injury in the Adult and Immature Brain," 2024.
• Rawlings GH et al. "Mitigating Traumatic Brain Injury: A Narrative Review of Supplementation and Dietary Protocols." PMC / Nutrients, 2024.
• Rawlings GH et al. "Mitigating Traumatic Brain Injury: A Narrative Review of Supplementation and Dietary Protocols." MDPI Nutrients, 2024.
• Defense and Veterans Brain Injury Center. "Information Paper on Creatine and TBI," 2025.
• Dolan E et al. "Potential for use of creatine supplementation following mild traumatic brain injury." PMC / Nutrients, 2018.
• Neuroprotection and Therapeutic Implications of Creatine Supplementation for Brain Injury Complications. PubMed, 2023.
• Journal of the International Society of Sports Nutrition. "Neuroprotective effects of creatine supplementation in mild TBI management among contact sport athletes: A scoping review," 2025.
• Frontiers in Nutrition. "Nutritional interventions to support acute mTBI recovery," 2022.
• Bhatt D et al. "Melatonin as a Therapy for Traumatic Brain Injury: A Review of Published Evidence." PMC, 2018.
• Kent JB et al. "The impact of riboflavin on the duration of sport-related concussion: A randomized placebo-controlled trial." SAGE Journals / Journal of Science and Medicine in Sport, 2023.
• Shao A et al. "Vitamins and Nutrients as Primary Treatments in Experimental Brain Injury: Clinical Implications for Nutraceutical Therapies." PMC, 2016.
• D'Alton F et al. "The Ketogenic Diet in the Treatment of Post-concussion Syndrome—A Feasibility Study." PMC / Frontiers in Nutrition, 2021.
• Frontiers in Neurology. "The Therapeutic Potential and Limitations of Ketones in Traumatic Brain Injury," 2021.
• National Academies of Sciences / NCBI Bookshelf. "Treatment and Management of Prolonged Symptoms and Post-Concussion Syndrome — Sports-Related Concussions in Youth," 2014.
• Mollayeva T et al. "Prediction of risk of prolonged post-concussion symptoms: TRICORDRR score." PMC / PLOS Medicine, 2021.
• Leong DF et al. "Risk Modifiers for Concussion and Prolonged Recovery." PMC / Sports Health, 2013.
• NCBI Bookshelf / Institute of Medicine. "Ketogenic Diet — Nutrition and Traumatic Brain Injury," 2011.
• Nutritional Neuroscience. "Supplement and nutraceutical therapy in traumatic brain injury," 2024.
• PMC. "Clinical examination factors that predict delayed recovery in individuals with concussion," 2020.
• PMC / PLOS One. "Investigating omega-3 fatty acids' neuroprotective effects in repetitive subconcussive neural injury: Study protocol for a randomized placebo-controlled trial," 2025.
• Scientific Reports. "Ketogenic Diet as a potential treatment for traumatic brain injury in mice," 2021.