This study examined whether intermittent fasting (IF) could relieve neuropathic pain, cognitive deficits, and anxiety across multiple chronic pain models (including the CCI model in mice), and dissected the gut microbiota–metabolite–neuroimmune mechanism driving these effects.
IF reduced mechanical allodynia, thermal hyperalgesia, cognitive deficits, and anxiety-like behavior; effects were recapitulated by supplementation with *Alistipes finegoldii* or systemic hippuric acid administration. Mechanistically, both IF and hippuric acid downregulated the STING neuroimmune pathway, and pharmacological STING activation abolished hippuric acid's therapeutic effects.
All experiments were conducted in rodent models (CCI and others); translation to human chronic pain patients is unproven. The genomic link between *A. finegoldii* and hippuric acid biosynthesis is based on homolog annotation, not direct enzymatic confirmation. Sample sizes and specific statistical outcomes are not reported in the abstract.
While still preclinical, these findings suggest that dietary IF and microbiota-targeted strategies (e.g., *A. finegoldii* supplementation) may offer non-pharmacological routes to address both pain and its cognitive comorbidities. The STING pathway and hippuric acid are highlighted as potential therapeutic targets worth investigating in translational studies.
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