Zimmerman · Molecular autism 2021 · randomized double-blind placebo-controlled trial · n=57

Randomized controlled trial of sulforaphane and metabolite discovery in children with Autism Spectrum Disorder.

Cited 109 times in the scientific literature.

Level 2 - randomized trial

Individual randomized double-blind placebo-controlled trial

PubMed 34034808 · doi:10.1186/s13229-021-00447-5 · record verified 2026-08-26

What was done

A 15-week randomized, parallel, double-blind, placebo-controlled trial with an additional 15-week open-label phase and 6-week washout evaluated oral sulforaphane in 57 children (aged 3–12 years) with Autism Spectrum Disorder (ASD). Twenty-eight children were randomized to sulforaphane and 29 to placebo. Clinical effects were evaluated using the clinician-rated Ohio Autism Clinical Impressions Scale (OACIS; primary outcome) and secondary caregiver measures (Aberrant Behavior Checklist [ABC] and Social Responsiveness Scale-2 [SRS-2]), along with biomarker assays for glutathione redox status, mitochondrial respiration, inflammatory markers, and heat shock proteins.

What was found

Data were analyzed for 45 children (22 sulforaphane, 23 placebo). The primary outcome (OACIS) showed no statistically significant difference between groups at week 7 (Cohen's d = 0.21; 95% CI: -0.46 to 0.88) or week 15 (Cohen's d = 0.10; 95% CI: -0.52 to 0.72). Caregiver ratings on the secondary ABC measure improved significantly in the sulforaphane group at 15 weeks (Cohen's d = -0.96; 95% CI: -1.73 to -0.15), whereas SRS-2 did not differ significantly between groups. Biomarkers of glutathione redox status, mitochondrial respiration, inflammation, and heat shock proteins showed significant changes with sulforaphane compared to placebo. Sulforaphane was well tolerated, with rare, non-serious adverse events including insomnia, irritability, and taste/smell intolerance.

Why it matters

Sulforaphane reliably engages cellular antioxidant and mitochondrial pathways in children with ASD and improves some secondary caregiver-reported behavioral measures, but failed to show a statistically significant benefit on the primary clinician-rated autism scale.

Limits

The sample size was small (45 completed/analyzed out of 57 randomized) and no missing data imputation was performed. The primary clinical outcome was negative. Later phases were open-label and unblinded, introducing caregiver expectation and placebo bias.

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