Unravelling the role of the gut microbiome in antipsychotic-induced weight gain and metabolic dysfunction in humans and rodents: A systematic review.
Maximilian Tufvesson-Alm, Louise Walsh, Sinead Pierce et al.
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In 30 seconds
This systematic review examined whether gut microbiota changes are involved in weight gain and metabolic dysfunction associated with second-generation antipsychotics, drawing on 24 clinical and preclinical observational and intervention publications in humans and rodents. Across studies, antipsychotic-related weight and metabolic effects were accompanied by microbiota alterations, including reduced diversity, a higher Firmicutes/Bacteroidetes ratio, and fewer Akkermansia species. The review found no consensus on the mechanisms or causal role of the microbiome. Microbiota-targeted interventions generally had weak effects in clinical cohorts, while some probiotics and microbiota metabolites showed promise in preclinical studies.
Key findings
- The review included 24 publications spanning clinical and preclinical observational and intervention studies.
- Commonly reported microbiota patterns included reduced diversity, an increased Firmicutes/Bacteroidetes ratio, and reduced Akkermansia species.
- Microbiota-targeted interventions generally had weak effects on weight gain and metabolic dysfunction in clinical cohorts.
- Specific probiotic strains and microbiota metabolites showed promise in preclinical studies.
Why it matters
Antipsychotic-associated weight and metabolic effects are accompanied by gut microbiota changes, making the microbiome a potential avenue for understanding these adverse outcomes. However, the review does not establish that microbiota alterations cause them. The contrast between limited clinical intervention effects and promising preclinical findings highlights the need for evidence that clarifies mechanisms before microbiota-targeted approaches can be relied upon.
What to keep in mind
The included studies were heterogeneous, and the review found no consensus on mechanisms or the microbiome’s causal role. Clinical intervention effects were generally weak.