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Antibiotic Administration and Risk of Multiple Sclerosis: a Systematic Review and Meta-Analysis
Abdorreza Naser Moghadasi1, Mohsen Rastkar2,3, Maryam Feili4
1Multiple Sclerosis Research Center, Neurosciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Maedica
|December 17, 2025
Summary
Antibiotic use, except for penicillin, may increase the risk of multiple sclerosis (MS). This systematic review and meta-analysis examined the gut-brain axis and antibiotic effects on MS risk.
Area of Science:
- Neuroscience
- Microbiology
- Epidemiology
Background:
- The gut-brain axis describes bidirectional communication between the gut and nervous system.
- Antibiotics can disrupt this crucial gut-brain axis.
- The potential impact of antibiotic exposure on neurological conditions like multiple sclerosis (MS) warrants investigation.
Purpose of the Study:
- To conduct a systematic review and meta-analysis.
- To determine if antibiotic administration is associated with an increased risk of developing multiple sclerosis (MS).
Main Methods:
- A comprehensive literature search was performed across six major databases (PubMed, Scopus, EMBASE, PsycINFO, Web of Science, Google Scholar).
- Data extraction was conducted by two independent researchers, including study details, participant demographics, and antibiotic types used.
- Six studies met the inclusion criteria for the systematic review and meta-analysis.
Main Results:
- The meta-analysis included data on penicillin, tetracycline, sulfonamides, macrolides, and quinolones.
- Penicillin use showed no significant association with MS risk (OR=1.01, 95% CI: 0.84-1.22).
- Significant associations between increased MS risk and the use of tetracycline (OR=1.20), sulfonamides (OR=1.30), macrolides (OR=1.19), and quinolones (OR=1.24) were found.
Conclusions:
- Antibiotic use, with the exception of penicillin, may be linked to an elevated risk of multiple sclerosis (MS).
- Further research is needed to elucidate the mechanisms underlying the gut-brain axis and antibiotic impact on MS pathogenesis.
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