Intermittent fasting appeared to reduce pain sensitivity in mice with chronic pain

For 38 days, mice with chronic pain alternated 24 hours without food with 24 hours of unrestricted feeding. Other mice ate freely throughout. In the fasting group, the animals appeared less sensitive to normally harmless touch and heat, performed better on simple tasks and showed fewer anxiety-like behaviors.

The experiment was run by researchers at Zhengzhou University and its First Affiliated Hospital across several mouse models involving injury, inflammation and other controlled causes of chronic pain. The team assessed pain sensitivity, memory, anxiety-like behavior, the intestinal barrier, gut bacteria and circulating metabolites. Chronic pain, defined as pain lasting or returning for more than three months, can also affect concentration, memory and emotional well-being; existing treatments do not relieve every associated symptom for every patient.

The biological trail led from the gut to the brain. Intermittent fasting changed the gut microbiota — the community of bacteria living in the digestive tract — and appeared to strengthen the intestinal barrier while reducing neuroinflammation. One species, Alistipes finegoldii, consistently increased. The researchers also identified hippuric acid, a molecule produced by gut microbes, and STING, an immune-signaling pathway, as parts of what they call an intermittent fasting–Alistipes finegoldii–hippuric acid–STING neuroimmune axis.

The team then supplemented mice with Alistipes finegoldii or hippuric acid and manipulated STING signaling with drugs. Adding the bacterium reproduced the pain-relieving and cognitive effects seen with fasting, supporting the idea that the gut changes were involved rather than merely accompanying the result. The findings were published in Brain, Behavior, and Immunity.

So what changes in practice? Not a treatment plan for people yet. The work offers a possible route toward non-drug interventions, microbiota-based therapies or metabolite supplements for chronic pain and related cognitive or emotional symptoms, but the evidence currently comes from mice. Kenji Hashimoto and colleagues say their next steps include identifying the specific cells affected by STING signaling, examining sex differences and testing the pathway in larger, longitudinal clinical studies.