At São Paulo State University in Marília, researchers have upended a widespread assumption held by millions of gym-goers and competitive athletes: that creatine, one of the fitness world's most popular supplements, reduces inflammation in the body. A systematic review and meta-analysis of eight randomized, placebo-controlled clinical trials published in Frontiers in Immunology found no consistent evidence to support this belief—a finding that challenges years of marketing claims and athlete testimonials.
Since the 1990s, creatine has earned its reputation through solid science. The supplement genuinely improves physical performance, helping athletes train harder, generate more strength, resist fatigue longer, and recover faster. That much is clear. But the supplement's rising popularity has bred a secondary myth: that it also calms inflammation—a notion that Vitor Engrácia Valenti, the group coordinator and study advisor, traces to a common mistake. "Many people claim that creatine is anti-inflammatory based on the results of studies done on animals or isolated cells in a lab," Valenti explains. "The problem is that these basic research findings don't always translate into clinical effects in humans."
The UNESP researchers examined the most reliable human studies on the subject, looking specifically at inflammatory biomarkers—measurable signals that inflammation is occurring in the body. What they found was messier than a simple yes or no. Some studies suggested that athletes who took high-dose creatine supplements (about 20 grams per day for five days) showed reductions in inflammatory markers like prostaglandin E2 and tumor necrosis factor alpha after intense endurance events such as long-distance runs and triathlons. These findings suggested a protective effect against the muscle damage that follows extreme exertion. But this benefit vanished when researchers looked at other populations. Studies involving patients with osteoarthritis and older adults showed no significant reductions in inflammatory markers such as C-reactive protein, even after weeks of supplementation.
When the researchers looked at the most commonly measured biomarkers across all the trials—C-reactive protein and interleukin-6—the picture became even clearer. The average reduction in C-reactive protein was just 0.41 mg/dL, and the reduction in interleukin-6 was smaller still. "The magnitude of the difference was small," Valenti notes, emphasizing that these decreases fell short of what would be considered statistically or clinically meaningful. In some instances, improvements in strength or muscle recovery were traced directly to the exercise itself rather than to the creatine, suggesting that the supplement received undeserved credit.
This is not a final verdict against creatine, Valenti cautions. The absence of evidence in human trials doesn't necessarily mean the anti-inflammatory effect doesn't exist—it may simply require better-designed studies, larger sample sizes, or investigation of specific subgroups where the effect is real. What the research does show is that athletes and gym-goers should update their mental model. Creatine works for what it was designed to do: boost training capacity and strength. But the promise of taming inflammation, at least for most people in most conditions, remains unproven and likely overstated.