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Creatine protected hippocampal structure, inflammatory measures and electrical function in rats with chronic gut inflammation. The finding, reported online in Brain, Behavior, and Immunity on 28 July 2026, adds to evidence that intestinal inflammation can disturb the creatine–phosphocreatine energy system in both the gut and brain. It does not yet show that creatine prevents brain fog, neuroinflammation or neurological injury in people with Crohn’s disease or ulcerative colitis.
What the new rat study found
The model
Ruiz-Calero and colleagues used male and female rats with chronic dextran-sulfate-sodium (DSS) colitis. DSS is a chemical model that produces ulcerative-colitis-like intestinal inflammation in rodents; it is not the same disease as human inflammatory bowel disease (IBD).
The researchers examined the hippocampus, including CA1 pyramidal neurons, a region involved in memory and learning. They measured inflammatory activity, microglial activation, neuronal injury, electrical function and hippocampal creatine levels.
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Creatine’s effects
Oral creatine supplementation prevented the measured colitis-associated abnormalities in both sexes. Treated rats showed protection against hippocampal neuroinflammation, excessive microglial activation, neuronal damage and abnormal electrical excitability. Supplementation also restored hippocampal creatine levels.
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The study’s abstract describes the result this way: Significantly, creatine supplementation was highly effective in both sexes and prevented colitis-induced hippocampal neuroinflammation, microglial activation, neuronal damage, and electrophysiological dysfunction.
A sex difference in untreated disease
Male rats had more severe baseline hippocampal inflammation, neuronal injury and electrophysiological dysfunction than female rats after chronic DSS exposure. That difference describes this animal model; it does not establish that men with IBD suffer greater brain injury, or that women are protected, in clinical practice.
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- PERFORMANCE SUPPORT DURING TRAINING:Formulated to support performance in explosive movements, maximal effort lifts, and intense exercise sessions. Helps support training capacity and volume so you can take on more reps and sets during demanding workouts.
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- QUALITY TESTED: Optimum Nutrition Creatine Powder is banned substance tested and part of the informed choice program which is regularly tested for banned substances, so you feel comfortable and safe down to the last capsule!
Why gut inflammation could affect brain energy metabolism
Creatine and phosphocreatine act as a rapidly available energy buffer. Cells can use the system to help maintain ATP when energy demand changes. The supporting studies suggest that intestinal inflammation may disrupt this energy pathway and that restoring phosphocreatine availability can improve gut-barrier biology in experimental models.
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|---|---|---|---|
| Creatine-kinase deficiency study | Mice exposed to DSS colitis | Deficient mice were more susceptible to colitis. | Supports a role for the creatine-kinase system in intestinal energy handling. |
| 2025 phosphocreatine study | Deficient intestinal epithelial models and colitic mice | Phosphocreatine normalized ATP levels, cell proliferation and barrier formation in epithelial models, and improved disease activity in mice. | Connects phosphocreatine availability with epithelial repair and barrier function. |
| Metabolomics study | DSS-treated rodents | Creatine was lower in colonic contents and hippocampi after DSS treatment. | Shows an association between colitis and altered creatine levels in gut and brain compartments. |
| 2026 theasinensin C study | Mice on a high-fructose diet | A protocol using 150 mg/kg/day for eight weeks increased serum and brain creatine and reduced neuroinflammation. | Provides related mouse evidence, but the dose belongs only to that experiment and is not a human recommendation. |
These studies do not prove a single pathway from intestinal inflammation to human neurological symptoms. They do, however, provide a biologically plausible explanation for why chronic gut inflammation and brain energy metabolism might change together.
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Does this explain brain fog in Crohn’s disease or ulcerative colitis?
Not yet. The rat study measured hippocampal inflammation, neuronal injury and electrical activity, not concentration, memory performance or patient-reported brain fog. No human study identified for this result demonstrates that creatine prevents cognitive symptoms, fatigue or neurological injury in people with IBD.
Several distinctions matter:
- Species: The direct evidence comes from rats, with additional support from mice and laboratory intestinal cells.
- Inflammation model: DSS is an experimentally induced chemical colitis model, not Crohn’s disease or ulcerative colitis as diagnosed in people.
- Timing: The reported protection was tested in an experimental setting. It does not establish whether creatine can reverse established neurological problems or treat an IBD flare.
- Outcome: Changes in hippocampal tissue and electrical measures are not the same as a demonstrated improvement in daily cognition.
Is creatine safe if you have IBD?
This study cannot establish safety, an effective dose or a suitable treatment plan for people with IBD. The exact creatine dose used in the rat experiment is not stated in the available report, and no validated human dose for IBD-related brain inflammation has been established.
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The intervention tested was oral creatine. If a clinician and patient decide to discuss supplementation, the evidence-based product description is creatine monohydrate, with the explicit understanding that the cited brain-protection result is preclinical. Phosphocreatine is relevant to laboratory research in this context, not a routine consumer treatment recommendation.
Anyone with IBD should review a supplement decision with the treating gastroenterology team, particularly when kidney disease, dehydration, abnormal laboratory results or multiple medicines are involved. A supplement should not replace prescribed anti-inflammatory or biologic treatment, and it should not be used to delay evaluation of new neurological symptoms.
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What researchers need to test next
Human randomized trials would be required before creatine could be presented as a treatment for IBD-related neuroinflammation. Useful studies would need to report:
- Whether participants have Crohn’s disease, ulcerative colitis or another defined condition, and how active the intestinal inflammation is.
- Creatine formulation, dose, treatment duration and adherence.
- Gut-barrier measures alongside blood and tissue inflammatory markers.
- The brain region examined and whether creatine or phosphocreatine levels change there.
- Clinical outcomes such as validated cognitive testing, fatigue or brain-fog scores, and electrophysiological measurements.
- Whether supplementation is preventive, added during active disease, or tested after neurological symptoms have appeared.
- Results by sex and other factors that could alter creatine metabolism or IBD severity.
What readers can conclude now
Creatine prevented several hippocampal consequences of chronic DSS colitis in rats, and related animal and epithelial studies support a possible gut-energy mechanism. That is a meaningful preclinical signal, not proof of a human treatment effect. For now, there is no established evidence that taking creatine prevents brain inflammation or relieves brain fog caused by Crohn’s disease or ulcerative colitis.
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