Sulforaphane

Evidence Fact Sheet

Sulforaphane (SFN), an isothiocyanate from broccoli sprouts and its precursor glucoraphanin, is one of the most potent natural NRF2/ARE activators studied. Human RCTs cover Phase II detox-enzyme induction, pollutant excretion, autism, liver and glucose markers — with prominent null findings (COPD NRF2, hypertension). Sold as a supplement; no authorized health claim.

Also known as: Sulforaphane · SFN · Broccoli Sprout Extract · Glucoraphanin (precursor)

Overview

Sulforaphane (SFN) is a sulfur-containing isothiocyanate generated when the broccoli-sprout precursor glucoraphanin meets the enzyme myrosinase; it is one of the most potent known natural activators of the NRF2/Keap1/ARE pathway, which coordinately up-regulates Phase II cytoprotective and detoxification enzymes (GST, NQO1, HO-1). Research-context mechanisms also include NF-kB suppression and HDAC inhibition. Most human studies use broccoli-sprout extract or glucoraphanin with active myrosinase co-delivery, with research doses commonly in the 30-60 mg SFN/day range (roughly 100-200 g fresh sprouts) over a few weeks. It is sold as a dietary supplement (the precursor glucoraphanin/Truebroc holds self-affirmed GRAS), but as of 2026 neither FDA nor EFSA has authorized any sulforaphane health claim, and all disease claims are red-lined; in the EU, CN and BR concentrated extracts may require novel-food or case-by-case assessment.

Mechanism of Action

NRF2/ARE pathway activation (modifies Keap1 cysteine residues Cys151/273/288 -> NRF2 nuclear translocation -> up-regulates >200 cytoprotective genes); in a research context sulforaphane is one of the most potent known natural NRF2 activators · Phase II detox-enzyme induction: coordinated up-regulation of GST / NQO1 / HO-1 / GCL / TrxR (research context; relevant to carcinogen/pollutant conjugation and glutathione synthesis) · NF-kB signaling suppression (down-regulating IL-6 / TNF-alpha / COX-2 pro-inflammatory pathways; research-stage mechanism) · Epigenetic modulation: HDAC (histone deacetylase) inhibition · Mitochondrial protection / autophagy-mitophagy-related signaling (preclinical plus some human research)

Body systems: Liver & Detoxification · Immune System · DNA & Epigenetic · Cellular Renewal · Endocrine & Metabolic

Evidence-Based Benefits

Each benefit below is anchored to a specific PubMed-indexed study. Effect sizes, sample sizes, and p-values are reported as published; no values are inferred. Honest negatives and null results are kept alongside the positive findings, and disease-research populations are described as such — Sulforaphane is not characterized as a treatment for any disease.

Airborne-Pollutant Detoxification (NRF2 / Phase II Excretion)

RCT supported
  • benzene 61%excretion increase · P≤0.01
  • acrolein 23%excretion increase · P≤0.01
  • 291participants · 12-week RCT

In a 12-week randomized trial in a heavily polluted region of Qidong, China, a broccoli-sprout beverage delivering glucoraphanin and sulforaphane raised urinary excretion of the glutathione-derived conjugates of inhaled pollutants, consistent with accelerated Phase II detoxification of carcinogens. The effect was significant for benzene and acrolein but, honestly, not for crotonaldehyde. This is a biomarker-excretion endpoint, not a disease outcome.

Reported effect: Statistically significant (P ≤ 0.01) increases in excretion of conjugates of benzene (61%) and acrolein (23%), but not crotonaldehyde, in the broccoli-sprout group vs placebo; n=291.

“Rapid and sustained, statistically significant (P ≤ 0.01) increases in the levels of excretion of the glutathione-derived conjugates of benzene (61%), acrolein (23%), but not crotonaldehyde, were found in those receiving broccoli sprout beverage compared with placebo.”

Source: PMID 24913818 · Egner 2014 · Cancer Prev Res (Phila)

NRF2 Target-Gene Induction in COPD (Honest Null)

Null / no benefit RCT supported
  • 0.79 to 1.45NRF2 gene change · ns
  • 89patients randomized

A prominent honest negative: in a three-center phase 2 RCT, oral sulforaphane at 25 or 150 micromoles/day for four weeks did NOT consistently raise NRF2 target-gene expression (NQO1, HO1, AKR1C1/3) in the airway cells of COPD patients, despite measurable plasma absorption, and did not change inflammation or lung function. It illustrates that mechanistic NRF2 potency seen in vitro does not always translate to a target-tissue response in patients.

Reported effect: Changes in NRF2 target gene expression relative to baseline ranged from 0.79 to 1.45 with no consistent pattern among the three groups; changes were not statistically significant; n=89.

“Changes in Nrf2 target gene expression relative to baseline ranged from 0.79 to 1.45 and there was no consistent pattern among the three groups; the changes were not statistically significantly different from baseline.”

Source: PMID 27832073 · Wise 2016 · PLoS One

Autism Spectrum Disorder (Social Responsiveness Scale)

Meta-analysis supported
  • 6 trialsRCTs pooled
  • 333participants

A 2025 meta-analysis pooling six randomized controlled trials reported that both 4-5 week and 8-10 week sulforaphane supplementation significantly lowered Social Responsiveness Scale scores versus placebo in children with autism spectrum disorder, with no significant difference in adverse-event incidence. The abstract reports the direction and significance but does not state a numeric pooled effect size, and the authors note efficacy across this literature remains controversial. Framed as a research finding, not a treatment.

Reported effect: Six trials involving 333 participants; both 4-5 weeks and 8-10 weeks of supplementation significantly decreased Social Responsiveness Scale scores vs placebo; no significant difference in adverse events (no numeric pooled effect size reported in abstract).

“Six trials involving 333 participants were included in the meta-analysis. Pooled results demonstrated that both 4-5 weeks and 8-10 weeks of sulforaphane supplementation significantly decreased the scores on the Social Responsiveness Scale compared to placebo controls. No significant difference was observed in the incidence of adverse events.”

Source: PMID 41275316 · Long 2025 · BMC Pharmacol Toxicol

Liver-Function Markers (Fatty Liver)

RCT supported
  • ALT 54.0→48.5 IU/Lmedian · P<0.05
  • 8-OHdG 6.66→5.49ng/mg-creat · P<0.05
  • 24 vs 28extract vs placebo

In a randomized, double-blind, placebo-controlled trial in Japanese men with fatty liver, two months of sulforaphane-precursor (glucoraphanin) broccoli-sprout extract significantly reduced serum ALT and gamma-GTP and lowered the oxidative-stress marker urinary 8-OHdG, while placebo did not. The 8-OHdG reduction correlated with the fall in liver enzymes, consistent with an oxidative-stress mechanism.

Reported effect: ALT median 54.0 (IQR 34.5-79.0) before vs 48.5 (33.3-65.3) IU/L after, P < 0.05; urinary 8-OHdG 6.66 (5.51-9.03) vs 5.49 (4.89-6.66) ng/mg-creatinine, P < 0.05; n=24 extract vs n=28 placebo.

“Dietary supplementation with BS extract containing SF precursor GR for 2 mo significantly decreased serum levels of liver function markers, ALT [median (interquartile range), before: 54.0 (34.5-79.0) vs after supplementation: 48.5 (33.3-65.3) IU/L, P < 0.05] ... The urinary level of 8-OHdG ... was significantly reduced in participants who had received BS capsules but not the placebo [before: 6.66 (5.51-9.03) vs after: 5.49 (4.89-6.66) ng/mg-creatinine, P < 0.05].”

Source: PMID 26604653 · Kikuchi 2015 · World J Gastroenterol

LDL Cholesterol (High-Glucoraphanin Broccoli Diet)

RCT supported
  • -7.1%LDL-C · study 1 · p=0.011
  • -5.1%LDL-C · study 2 · p=0.001

Two independent double-blind RCTs (130 volunteers total) found that eating 400 g/week of high-glucoraphanin broccoli for 12 weeks significantly reduced plasma LDL cholesterol versus standard broccoli. Important caveat: this signal comes from a glucoraphanin-rich whole-food broccoli diet, not from a free-sulforaphane supplement, so it should not be read as a free-SFN lipid claim.

Reported effect: Study 1 (n=37): LDL-C reduced 7.1% (95% CI -1.8% to -12.3%, p=0.011); Study 2 (n=93): LDL-C reduced 5.1% (95% CI -2.1% to -8.1%, p=0.001); combined reduction greater than standard broccoli (p=0.031).

“the HG broccoli diet reduced plasma LDL-C by 7.1% (95% CI: -1.8%, -12.3%, p = 0.011) ... the HG broccoli diet resulted in a reduction of 5.1% (95% CI: -2.1%, -8.1%, p = 0.001) ... When data from the two studies were combined the reduction in LDL-C by the HG broccoli was significantly greater than standard broccoli (p = 0.031).”

Source: PMID 25851421 · Armah 2015 · Mol Nutr Food Res

Endothelial Function / Blood Pressure in Hypertension (Honest Null)

Null / no benefit RCT supported
  • FMD 4%→5.8%not significant
  • 40hypertensive adults

A clean honest negative: in 40 adults with essential hypertension, four weeks of 10 g/day dried broccoli sprouts did not significantly improve flow-mediated dilation, blood pressure, or blood markers, and the small FMD shift was driven mainly by two participants. The authors conclude broccoli sprouts do not improve endothelial function in hypertension — so this card carries no blood-pressure claim.

Reported effect: FMD rose from 4% to 5.8% in the intervention group vs stable in controls but was not statistically significant; systolic BP showed only a small non-significant 9 mmHg decrease (from 153 mmHg); n=40.

“In the interventional group overall FMD increased from 4% to 5.8% ... The observed differences were not statistically significant. Likewise significant changes in blood pressure or blood samples were not detected between or within groups ... the systolic blood pressure showed a small non significant decrease (9 mm Hg) in the interventional group from a value of 153 mm Hg at start.”

Source: PMID 20805984 · Christiansen 2010 · PLoS One

Glucose / Insulin Resistance (NAFLD)

RCT supported

A 2024 study combined rat experiments with a human arm of 36 volunteers with abnormal glucose given a broccoli-seed tablet (42 mg/day sulforaphane) for 12 weeks. In the human arm, sulforaphane raised GLP-1, which correlated with reductions in blood glucose and HOMA-IR, proposed to act via a gut Bacteroides/Lactobacillus-SCFA-GLP1 axis. The abstract reports the direction for the human arm but no standalone numeric effect size, so the human glucose effect size is not extracted here.

Effect size: this study reports the direction of the finding but does not state a specific numeric effect size, so none is given here rather than estimated.

“SFN intervention increased the level of GLP1 in NAFLD patients, which was positively correlated with the reduction of blood glucose and HOMA-IR.”

Source: PMID 39045769 · Tian 2024 · Food Funct

Dosage (research context · not a recommendation)

30-60 mg sulforaphane/day (roughly equivalent to 100-200 g fresh broccoli sprouts); most RCTs fall in the 25-300 micromol SFN/day range over 2-18 weeks. The precursor glucoraphanin needs active myrosinase co-delivery to convert efficiently into active SFN. Educational reference, not a dosing recommendation.

Regulatory Status · 4 Markets

US · FDA
Sold as a dietary supplement (e.g. Avmacol, Prostaphane, BroccoMax, BrocElite); the broccoli-derived precursor glucoraphanin (Truebroc) holds a self-affirmed GRAS no-objection, while sulforaphane products are marketed via the DSHEA structure/function-claim pathway (30-day notification + FDA disclaimer) as a manufacturer self-determination, not an FDA-authorized health claim. All disease claims are red-lined (cancer/autism/diabetes/H. pylori eradication prohibited). 'Detox' is a high-sensitivity term and should be expressed indirectly as supports the body's natural detoxification processes.
EU · EFSA
Broccoli-sprout extract is sold as a supplement in member states such as France and Italy (Prostaphane precedent); highly concentrated/purified SFN may trigger Novel Food assessment. As of 2026 EFSA has authorized no sulforaphane health claim, so no authorized claim exists (science-education / brand context only).
CN · China
Broccoli is unrestricted common food and sprout powder is sold as vegetable powder; concentrated standardized sulforaphane/glucoraphanin extract has no novel-food approval and needs case-by-case assessment.
BR · ANVISA
Broccoli as food is unrestricted; concentrated extract is not on the IN no 28/2018 positive list, has no specific functional claim, and requires case-by-case technical assessment. Only a food-grade 'contains cruciferous-vegetable active compounds' description is safe.

Safety

The broccoli source has a long dietary-use history; a single oral 200 micromol (~35 mg) SFN dose was well tolerated and long-term RCTs at 68 mg glucoraphanin/day showed no serious adverse effects. The common effect is transient, dose-related mild GI upset (bloating, gas, mild nausea). Theoretically, large doses of isothiocyanates could affect iodine uptake (a goitrogenic effect), though no significant effect is seen at clinical doses; people with thyroid dysfunction should consult a doctor. NRF2-induced Phase II enzymes may mildly affect some drug metabolism (e.g. increased acetaminophen conjugation). Caution in people allergic to cruciferous vegetables; no safety data in infants; no dedicated pregnancy/lactation trials, so consult a professional before using concentrated extracts. Labels should clearly distinguish glucoraphanin (precursor) from sulforaphane (active) doses.

Goals: longevity-stack · inflammation-relief

Lifestyles: senior-60-plus

References

PubMed-indexed citations anchoring the benefit findings above. Effect sizes are reported as published.

  1. PMID 24913818 · Egner 2014 · Cancer Prev Res (Phila) — Airborne-Pollutant Detoxification (NRF2 / Phase II Excretion)
  2. PMID 27832073 · Wise 2016 · PLoS One — NRF2 Target-Gene Induction in COPD (Honest Null)
  3. PMID 41275316 · Long 2025 · BMC Pharmacol Toxicol — Autism Spectrum Disorder (Social Responsiveness Scale)
  4. PMID 26604653 · Kikuchi 2015 · World J Gastroenterol — Liver-Function Markers (Fatty Liver)
  5. PMID 25851421 · Armah 2015 · Mol Nutr Food Res — LDL Cholesterol (High-Glucoraphanin Broccoli Diet)
  6. PMID 20805984 · Christiansen 2010 · PLoS One — Endothelial Function / Blood Pressure in Hypertension (Honest Null)
  7. PMID 39045769 · Tian 2024 · Food Funct — Glucose / Insulin Resistance (NAFLD)

Frequently Asked Questions

1. What is sulforaphane and where does it come from?

Sulforaphane (SFN) is a sulfur-containing isothiocyanate produced when the precursor glucoraphanin in broccoli and broccoli sprouts is acted on by the plant enzyme myrosinase. In research it is studied as one of the most potent natural activators of the NRF2/Keap1/ARE pathway, which up-regulates Phase II detoxification and antioxidant enzymes such as GST, NQO1 and HO-1. Most human studies use broccoli-sprout extract or glucoraphanin with active myrosinase rather than pure SFN.

2. What is the strongest human evidence for sulforaphane?

Among the better-controlled findings, a 12-week RCT in 291 people in polluted Qidong, China showed broccoli-sprout beverage significantly raised urinary excretion of conjugates of benzene (61%) and acrolein (23%), a Phase II detox biomarker endpoint (Egner 2014, PMID 24913818). A 2025 meta-analysis of 6 trials (333 participants) found sulforaphane significantly lowered Social Responsiveness Scale scores in autism (Long 2025, PMID 41275316). A fatty-liver RCT lowered ALT from a median of 54.0 to 48.5 IU/L (Kikuchi 2015, PMID 26604653). These are research findings in studied populations, not treatments.

3. Are there negative or null sulforaphane studies?

Yes, and they matter. A three-center COPD RCT (89 patients) found oral sulforaphane did not consistently raise NRF2 target-gene expression (changes ranged 0.79 to 1.45, not significant) and did not change inflammation or lung function (Wise 2016, PMID 27832073). Separately, a trial in 40 adults with hypertension found broccoli sprouts did not significantly improve endothelial function (FMD 4% to 5.8%, not significant) or blood pressure (Christiansen 2010, PMID 20805984). So mechanistic potency in the lab does not always translate to a clinical signal.

4. Does the cholesterol finding mean sulforaphane supplements lower LDL?

Not exactly. The LDL reduction of about 7.1% and 5.1% (across 130 volunteers) came from eating high-glucoraphanin broccoli as a whole-food diet, not from a free-sulforaphane supplement (Armah 2015, PMID 25851421). That distinction is important: the evidence supports the broccoli diet, and it should not be read as a free-SFN lipid claim. This is an evidence-reporting page, not dosing or clinical guidance.

5. What is sulforaphane's regulatory status?

It is sold as a dietary supplement, and the broccoli-derived precursor glucoraphanin (Truebroc) holds a self-affirmed GRAS no-objection in the US, where SFN products use the DSHEA structure/function-claim pathway. As of 2026 neither FDA nor EFSA has authorized any sulforaphane health claim, and all disease claims (cancer, autism, diabetes, H. pylori) are red-lined. In the EU, China and Brazil, concentrated or purified extracts may require novel-food or case-by-case assessment, while broccoli as a food is unrestricted.

Last evidence review: 2026-06-13

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