Investigating the clinical efficacy, safety and molecular mechanism of sulforaphane in autism spectrum disorder: an integrated study combining meta-analysis, network pharmacology, and computational biology.
Level 1 - systematic review of randomized trials
Systematic review and meta-analysis of randomized controlled trials
PubMed 41275316 · doi:10.1186/s40360-025-01052-5
What was done
Systematic review and meta-analysis of randomized controlled trials from PubMed, Web of Science, Embase, and Cochrane Library evaluating sulforaphane supplementation in autism spectrum disorder. Clinical efficacy on the Social Responsiveness Scale and adverse event rates were pooled using Review Manager 5.4. Network pharmacology, Mendelian randomization, GEO transcriptomics, molecular docking, and molecular dynamics simulations were conducted to explore molecular mechanisms.
What was found
Six trials involving 333 participants were included. Sulforaphane significantly decreased Social Responsiveness Scale scores compared to placebo at both 4-5 weeks and 8-10 weeks; exact numerical effect sizes, confidence intervals, and p-values were not reported in the abstract. Adverse event incidence showed no significant difference compared to placebo. Ten core targets were identified with binding energies all -4.0 kcal/mol or lower, and Mendelian randomization showed an inverse association between STAT1 levels and autism risk.
Why it matters
This review aggregates limited trial evidence suggesting sulforaphane may safely offer short-term improvements in social responsiveness for individuals with autism spectrum disorder.
Limits
The total human sample size is small at 333 participants across six trials, and treatment duration was limited to 10 weeks or less. The abstract does not provide numerical effect estimates or confidence intervals for the clinical outcomes. Biological mechanisms were derived from in silico and transcriptomic modeling rather than direct clinical bioassays.