What Can be Done to Reduce the Impact of a Concussion Before One Occurs?
Building neurological resilience before injury - the evidence for prehabilitation in concussion risk mitigation
Baseline Testing - a Crucial Gap
In elite sport and increasingly in recreational contact sport, pre-season or pre-participation baseline testing is now standard practice. Physios, osteopaths, and exercise physiologists routinely establish pre-injury reference points for cognitive function (through tools like ImPACT or the SCAT6), vestibular and oculomotor status, cervical spine range of motion and muscular strength, aerobic fitness, and reaction time. The rationale is sound: you cannot meaningfully assess the impact of a concussion without knowing what that person looked like before it happened.
This kind of baseline work is genuinely valuable as it gives clinicians a reference point for return-to-play decisions, helps identify athletes who may be under-reporting symptoms, and flags individuals with prior vulnerabilities that might influence their recovery. The practitioners doing this work are doing important things.
But the baseline testing that currently exists, comprehensive as it is within its scope, is entirely focused on the neurological and physical outputs of the brain and body. It measures how the brain performs. It does not measure the physiological terrain that will determine how well the brain responds to injury and recovers from it.
None of it measures the gut microbiome. None of it assesses intestinal permeability. None of it evaluates the abundance of butyrate-producing bacteria, or the presence and activity of indole-producing species, or the thickness and integrity of the mucosal layer, or the baseline level of LPS-driven systemic inflammation. And yet these factors, collectively, are among the most powerful determinants of how severe a concussion becomes and how long it persists.
If we accept that baseline neurological testing matters before contact sport exposure, the question becomes: why is the most physiologically significant baseline of all not being taken?
The Answer: Because Nobody Has Connected the Dots Yet
Well, I have, and this is not a criticism of the practitioners doing baseline testing in its current form because that work is essential. The gut-brain axis in concussion is a research area that has matured significantly over the past decade, but its translation into standard pre-season or pre-participation practice has not yet happened. The neurological side of concussion management has a well-developed clinical infrastructure. The gut-brain side does not feature in standard practices by those in high risk for head impact situations - yet.
That is the gap this post is addressing. Not what to do after a concussion, but what to optimise before one, specifically through the gut-brain axis, because the state of that axis at the moment of impact is one of the most powerful and most modifiable determinants of what follows.
Why the Gut Microbiome Determines Concussion Severity
To understand why the gut microbiome matters before a concussion occurs, you need to understand what happens in the gut within hours of the injury because it is that event, and how severely it unfolds, that determines much of what follows.
A concussion triggers an immediate inflammatory cascade that disrupts intestinal barrier integrity within hours of injury. Tight junction proteins are degraded and intestinal permeability increases causing a shift in the microbial balance. Beneficial microbial species can significantly decline and gram-negative bacteria have the opportunity to proliferate. Lipopolysaccharide (LPS) enters systemic circulation and binds to TLR4 receptors throughout the body, including in the brain. The gut then becomes a driving force of the very neuroinflammation the brain is trying to manage.
This cascade does not unfold with the same severity in every person. Its magnitude depends directly on the baseline state of the gut microbiome at the time of injury. A gut-brain axis with high microbial diversity, strong populations of butyrate-producing bacteria, adequate IPA-producing species, intact intestinal barrier function, and a well-maintained mucosal layer has substantially more reserve and resilience when the concussion hits. A gut-brain axis that was already under strain before the injury has almost none. In the instance of repetitive head trauma, such as those in contact sports, damage in the gut, and therefore the brain worsens with each impact.
A review in Frontiers in Immunology examining gut microbiota and acute central nervous system injuries concluded that the altered composition of gut microbiota after acute CNS injury aggravates secondary brain injury, cognitive impairments, and motor dysfunction and that manipulating the gut microbiota through targeted therapeutic approaches has potential to alleviate secondary brain injury and facilitate functional outcomes (Yuan et al., 2022). The corollary holds in the pre-injury direction: a more resilient, diverse, and well-populated microbiome before injury is a gut-brain axis with greater capacity to limit that secondary cascade.
“The concussion hits in a moment. But it is the gut microbiome, established a lifetime before that moment that determines how the damage perpetuates” ~ Louise Cork
The Species That Matter Most
Butyrate-producing bacteria: the keystone community
Butyrate is the short-chain fatty acid most critical to gut barrier integrity, immune regulation, and the gut-brain axis. It is the primary energy source for intestinal epithelial cells, the fuel that maintains the tight junction proteins that prevent intestinal permeability, and a potent modulator of intestinal and systemic inflammation. Butyrate-producing bacteria such as Faecalibacterium prausnitzii, Eubacterium rectale, Roseburia intestinalis, and related Lachnospiraceae species form a strong foundation for a resilient gut.
Research in Nutrients reviewing gut commensals and intestinal barrier function identified Faecalibacterium prausnitzii and related butyrate producers as among the most clinically promising species for restoring intestinal health by reducing inflammation, strengthening the epithelial barrier, and modulating the immune response through HDAC inhibition and down-regulation of TLR4-mediated inflammatory signalling (Hiippala et al., 2018). A 2024 review in Nature Reviews Immunology confirmed that butyrate exerts direct effects on intestinal epithelial cell differentiation, phagocyte function, T-cell regulation, and systemic immune control including at extra-intestinal sites, specifically the brain (Mann et al., 2024).
In TBI specifically, butyrate has been shown to suppress microglia-mediated neuroinflammation through the GPR109A/PPAR-gamma/TLR4-NF-kB signalling pathway, restore intestinal tight junction integrity, reduce LPS translocation, and improve cognitive and behavioural outcomes in animal models (Wei et al., 2023). Adequate butyrate-producing bacterial populations protect the gut barrier before injury and reduce the neuroinflammatory amplification loop after it.
Indole-3-propionic acid: the tryptophan metabolite protecting both barriers
Indole-3-propionic acid (IPA) is a tryptophan-derived metabolite produced by specific gut bacteria, most notably Clostridium sporogenes. It is one of the most biologically potent microbial metabolites for neuroprotection. IPA crosses the blood-brain barrier, where it acts as a direct antioxidant, reduces neuroinflammatory signalling, and exerts barrier-stabilising effects on the blood-brain barrier itself. At the intestinal level, IPA stabilises the mucosal barrier by activating pregnane X receptor (PXR) signalling in enterocytes.
A 2026 review in the Journal of Neuroimmunology identified IPA, alongside butyrate and urolithins (bioactive metabolites produced by the gut from dietary polyphenols - but more on that later) as among the most important neuroprotective microbial metabolites governing the gut-brain axis, with specific roles in preserving gut integrity, suppressing inflammation, upregulating BDNF (Brain Derived Neurotrophic Factor) for synaptic plasticity, and enhancing mitophagy (Lahariya et al., 2026). The review drew a clear clinical distinction between microbial communities that produce these protective compounds and those that produce neurotoxic indole derivatives -- specifically indoxyl sulphate and p-cresyl suphate which activate microglia, promote neurodegeneration, and worsen neurological outcomes.
“Cultivating the bacterial populations that produce IPA and avoiding the conditions that suppress them is targeted neuroprotection in advance of a potential injury” ~ Louise Cork
Akkermansia muciniphila: the guardian of the mucosal layer
Akkermansia muciniphila is a mucus-degrading bacterium that is one of the most important species for maintaining mucosal layer thickness and integrity. By degrading the outer mucus layer it stimulates continuous mucin production by goblet cells, maintaining a dynamic, thick, well-renewed mucosal barrier. Akkermansia also modulates intestinal permeability, immune function, and metabolic signalling. Low Akkermansia abundance is consistently associated with increased intestinal permeability, dysbiosis, and elevated systemic inflammation. Maintaining healthy Akkermansia populations supports the ecological conditions in which butyrate-producing and IPA-producing species thrive.
The Mucosal Layer: The Gut's First Physical Defence
The intestinal mucosal layer is composed of mucins secreted by goblet cells, embedded with secretory IgA and antimicrobial peptides and is the physical barrier between the luminal microbiome and the epithelial cells beneath it. It is not static, it is dynamically maintained and requires ongoing microbial and nutritional support to remain intact.
A review in Gut Microbes on commensal and pathogenic interactions with the mucus layer found that homeostasis between the microbiota and mucus layer is easily disrupted by diet, medications, and other environmental factors and that disruption creates conditions in which pathogens can penetrate to the epithelial surface and intestinal permeability increases (Cai et al., 2020). When the mucosal layer is thin or compromised before a concussion, the tight junction disruption that follows has less of a buffer. The LPS that would have been captured in a healthy mucosal layer reaches the epithelium and enters systemic circulation faster, and in greater amounts.
Intestinal Permeability and Systemic Inflammation: Why Baseline Matters
If the gut-brain axis is already under strain before a concussion occurs, the injury does not arrive into a neutral physiological environment. It arrives into one that is already primed for a larger, longer inflammatory response.
Someone who already has elevated intestinal permeability, a depleted microbial community, or chronic low-grade systemic inflammation before their injury is essentially starting the post-concussion cascade from a worse position. The inflammatory loop that the concussion triggers neuroinflammation causing gut disruption → feeding neuroinflammation → neuroinflammation feeding further gut disruption, runs harder and runs longer when the baseline terrain offers less resistance to it.
The key microbial metabolites that would normally buffer that response, butyrate and other short-chain fatty acids produced by the beneficial bacterial species discussed above, play a direct role in keeping the gut's immune response calibrated toward resolution rather than escalation. When those metabolites are abundant, the gut is better positioned to contain and resolve the inflammatory signal. When they are depleted, the same signal produces a larger, more sustained response.
This is why the state of the gut microbiome before a concussion is not a novel consideration. It is part of the injury itself, it is shaping the severity of the cascade from the moment it begins and it is crucial to reducing the long-term risks of head trauma and repetitive head impacts - particularly those seen in contact sports.
What Pre-Injury Gut Baseline Assessment Would Actually Involve
Just as a physio establishes a neurological and physical baseline before the season starts, a gut-brain baseline would establish the microbiome terrain before contact sport exposure begins. Metagenomic sequencing of the gut microbiome can identify the specific species present and in what abundance, measure functional metabolite-producing capacity including butyrate output and IPA production, assess microbial diversity, and flag the presence of LPS-producing and other species that would amplify any future inflammatory cascade.
That baseline data has direct clinical benefit and tangible outcomes for individuals. It identifies whether a person is going into their season with adequate butyrate-producing populations or a deficiency that could be corrected before first contact. It reveals whether IPA-producing bacteria are present or absent. It shows whether Akkermansia is supporting mucosal integrity or has been depleted by diet, antibiotic use, or chronic stress. And it provides a reference point against which post-injury gut changes can be compared giving the same clinical grounding that neurological baseline testing provides for cognitive recovery.
This kind of baseline assessment is currently not part of any pre-season concussion programme I am aware of and I strongly believe it should be. This missing piece of baseline testing has the potential to significantly change the trajectory for so many people, not just in injury and recovery, but for their long term health outcomes - microbiome testing and target interventions to optimise the integrity of the gut and the microbial population,
References
Yuan B, Lu XJ, Wu Q. Gut Microbiota and Acute Central Nervous System Injury: A New Target for Therapeutic Intervention. Front Immunol. 2022;12:800796. https://doi.org/10.3389/fimmu.2021.800796
Hiippala K, et al. The Potential of Gut Commensals in Reinforcing Intestinal Barrier Function and Alleviating Inflammation. Nutrients. 2018;10(8). https://doi.org/10.3390/nu10080988
Mann ER, Lam YK, Uhlig HH. Short-chain fatty acids: linking diet, the microbiome and immunity. Nat Rev Immunol. 2024;24(8):577-595. https://doi.org/10.1038/s41577-024-01014-8
Wei H, et al. Butyrate ameliorates chronic alcoholic central nervous damage by suppressing microglia-mediated neuroinflammation and modulating the microbiome-gut-brain axis. Biomed Pharmacother. 2023;160:114308. https://doi.org/10.1016/j.biopha.2023.114308
Lahariya R, et al. Postbiotics and the gut-brain axis: A mechanistic review on modulating neuroinflammation and cognitive aging. J Neuroimmunol. 2026;413:578870. https://doi.org/10.1016/j.jneuroim.2026.578870
Parada Venegas D, et al. Short Chain Fatty Acids (SCFAs)-Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases. Front Immunol. 2019;10:277. https://doi.org/10.3389/fimmu.2019.00277
Zhang D, et al. Short-chain fatty acids in diseases. Cell Commun Signal. 2023;21(1):212. https://doi.org/10.1186/s12964-023-01219-9
Cai R, et al. Interactions of commensal and pathogenic microorganisms with the mucus layer in the colon. Gut Microbes. 2020;11(4):680-690. https://doi.org/10.1080/19490976.2020.1735606
Cotoia A, et al. The Role of Macronutrients and Gut Microbiota in Neuroinflammation Post-Traumatic Brain Injury. Nutrients. 2024;16(24). https://doi.org/10.3390/nu16244359
Hanscom M, Loane DJ, Shea-Donohue T. Brain-gut axis dysfunction in the pathogenesis of traumatic brain injury. J Clin Invest. 2021;131(12). https://doi.org/10.1172/JCI143777