Sulforaphane dosage and evidence

Overview

Mechanism of action

Sulforaphane modifies cysteine residues on KEAP1, which releases the transcription factor NRF2 to enter the nucleus and drive a large battery of phase 2 detoxification and antioxidant genes, including glutathione S-transferases and NAD(P)H quinone dehydrogenase 1. This is why its most reproducible human effect is on the conjugation and excretion of electrophilic toxicants rather than on any disease process: the pathway it activates is literally a disposal system. Separate work identified sulforaphane by matching a type 2 diabetes liver gene expression signature against a library of 3,800 drug signatures, and found it suppressed hepatic glucose production through NRF2 nuclear translocation with reduced expression of gluconeogenic enzymes. In the plant it does not exist. Broccoli stores the stable glucosinolate glucoraphanin in one compartment and the enzyme myrosinase in another, and sulforaphane is generated when the tissue is damaged, which is the relevance of chewing, chopping and of whether a capsule contains active enzyme.

Human evidence

Unusually large for a supplement: multiple randomised placebo-controlled trials across detoxification, glycaemia, prostate cancer recurrence and autism, several publicly funded. The consistent pattern is that biomarker endpoints move and prespecified primary endpoints do not.

• Qidong, China, 170 adults, 10 days: urinary benzene mercapturic acids up 63.2 percent on the full dose, not significantly different from placebo at half and one fifth doses.
• Prostate biochemical recurrence, 78 men, 6 months at 60 mg daily: primary endpoint not reached. PSA doubling time 28.9 against 15.5 months as a secondary outcome.
• Prediabetes, 74 adults, 12 weeks: prespecified 0.3 mmol/L fasting glucose target not met, overall effect 0.2 mmol/L.
• Autism, 44 young men, 18 weeks: 34 percent improvement on the Aberrant Behavior Checklist against under 3.3 percent on placebo, with scores returning toward baseline after discontinuation.
• Autism replication, 45 children analysed, 15 weeks: primary outcome not significant; a secondary caregiver-rated scale did improve.
• Bioavailability: sprouts and seeds with active myrosinase delivered 3 to 4 fold more sulforaphane than an equimolar glucoraphanin dose without it.
• No human trial has measured lifespan, mortality, cancer incidence or any ageing endpoint.

What this does not tell you: Every positive result above is a surrogate. Raised urinary excretion of a benzene conjugate is evidence that a disposal pathway was switched on, not evidence that anybody got less cancer, and the authors describe it as a strategy that portends reduced risk rather than one shown to reduce risk. The two autism trials point in different directions on their primary measures, and the earlier one carries a patent and licensing conflict of interest that the paper discloses. The prostate result is a doubling time, which is a rate of change in a marker, in men whose disease had already recurred.

Reading the research record

The evidence, charted

Key studies & citations

• Human2019
  Dose-dependent detoxication of the airborne pollutant benzene in a randomized trial of broccoli sprout beverage in Qidong, China.

  Only the strongest dose did anything, and what it shifted was a chemical in urine. 170 adults in a polluted part of China were split by chance to a dummy drink or one of three strengths of broccoli sprout beverage, for 10 days. The top dose raised benzene clearance by 63.2 percent. The half dose and the fifth dose were no different from the dummy. The thing measured is a detoxification marker, not illness and not cancer. NIH funded.

  170 adults randomised to placebo (n = 55) or one of three concentrations of broccoli sprout beverage for 10 consecutive days. Urinary benzene mercapturic acids rose significantly only in the high dose group, by 63.2 percent. The one half dose (+11.3 percent) and one fifth dose (-6.4 percent) were not significantly different from placebo. Median 24 hour urinary sulforaphane metabolite output was 24.6, 10.3 and 4.3 micromol across the three doses. The endpoint is a urinary detoxification biomarker, not a cancer rate. NIH funded, registered as NCT02656420.

  PMID 31268126 American Journal of Clinical Nutrition
• Human2015
  Effect of Sulforaphane in Men with Biochemical Recurrence after Radical Prostatectomy.

  It missed the one thing the trial was built to test, and the rest looked good. 78 men whose PSA was climbing after prostate surgery took 60 mg of free sulforaphane daily or a dummy for six months. The paper states plainly that the main test was not met. PSA took 28.9 months to double on sulforaphane against 15.5 on the dummy, and rose above a fifth by month 6 in 44.4 percent against 71.8 percent. Once treatment stopped, PSA climbed at the same rate in both groups.

  78 men, mean age 69, with rising PSA after radical prostatectomy, randomised double blind to 60 mg free sulforaphane daily for 6 months. The paper states plainly that the primary endpoint was not reached. Secondary results favoured sulforaphane: PSA doubling time 28.9 months against 15.5 on placebo, and PSA rises above 20 percent at month 6 in 44.4 percent against 71.8 percent. PSA slopes were the same in both arms once treatment stopped.

  PMID 25968598 Cancer Prevention Research
• Human2025
  Effect of broccoli sprout extract and baseline gut microbiota on fasting blood glucose in prediabetes: a randomized, placebo-controlled trial.

  It missed the target the researchers set in advance, and the effect it did produce was smaller. 74 adults with prediabetes who were on no diabetes drugs took broccoli sprout extract or a dummy for 12 weeks, 35 and 39 of them. They had said beforehand they needed fasting blood sugar to drop by 0.3 units to count. It dropped 0.2. Stomach side effects occurred and nothing severe happened. A group of apparent responders was picked out afterwards, which raises a question rather than answering one.

  74 drug-naive adults with prediabetes randomised to broccoli sprout extract (n = 35) or placebo (n = 39) for 12 weeks. The authors report that the extract did not meet the prespecified primary outcome of a 0.3 mmol/L fall in fasting blood glucose; the overall effect was 0.2 mmol/L (95 percent CI -0.44 to -0.01, p = 0.04). Gastrointestinal side effects, no severe adverse events. A responder subgroup was identified in exploratory analysis, which is hypothesis generating rather than confirmatory.

  PMID 39929977 Nature Microbiology
• Human2014
  Sulforaphane treatment of autism spectrum disorder (ASD).

  A clear improvement in young men with autism, from a study with a conflict attached. 44 young men aged 13 to 27 with moderate to severe autism took sulforaphane or a dummy for 18 weeks. Behaviour ratings improved 34 percent against under 3.3 percent on the dummy, and social responsiveness by 17 percent. Scores drifted back toward where they started once treatment stopped. Johns Hopkins holds patent applications here and licensed sprouts to a company run by the son of one of the authors.

  44 young men aged 13 to 27 with moderate to severe autism, 29 on sulforaphane at 50 to 150 micromol daily and 15 on placebo for 18 weeks. Aberrant Behavior Checklist scores improved 34 percent against under 3.3 percent on placebo (p < 0.001) and Social Responsiveness Scale 17 percent (p = 0.017); scores rose back toward baseline after stopping. The declared conflict of interest states that Johns Hopkins holds patent applications and has licensed glucosinolate-rich sprouts and seeds to a company whose chief executive is the son of one of the authors.

  PMID 25313065 Proceedings of the National Academy of Sciences
• Human2021
  Randomized controlled trial of sulforaphane and metabolite discovery in children with Autism Spectrum Disorder.

  The attempt to repeat it in children failed on the measure that mattered. 57 children aged 3 to 12 were assigned by chance and 45 were analysed. On the main clinical scale, treatment made no difference at 7 weeks or at 15. A behaviour scale filled in by caregivers did improve at 15 weeks. The authors say the effects were less notable in children than in their earlier trial in young men. Funded by the US Department of Defense.

  The attempted replication in children, 57 randomised and 45 analysed, aged 3 to 12. Treatment effects on the primary outcome, the Ohio Autism Clinical Impressions Scale, were not significant at 7 or 15 weeks (Cohen's d 0.21 and 0.10, both confidence intervals crossing zero). A secondary caregiver-rated measure, the Aberrant Behavior Checklist, did improve significantly at 15 weeks. The authors state that clinical effects were less notable in children than in their earlier trial in young men. US Department of Defense funded.

  PMID 34034808 Molecular Autism
• Human2015
  Sulforaphane Bioavailability from Glucoraphanin-Rich Broccoli: Control by Active Endogenous Myrosinase.

  What is printed on the label does not tell you what you absorb. Volunteers were given broccoli sprouts or seeds with the plant's own enzyme still alive. They produced three to four times more usable sulforaphane than the same amount of the raw ingredient delivered without that enzyme. A commercial supplement performed no better than boiled, freeze-dried sprout extract. Whether the plant enzyme survived processing decides how much of the active compound ever reaches your blood, and no dose on a bottle captures that.

  Human volunteers given broccoli sprouts or seeds with endogenous myrosinase still active produced 3 to 4 fold more bioavailable sulforaphane than the same molar dose of glucoraphanin delivered without active plant enzyme. A commercial glucoraphanin supplement gave urinary sulforaphane metabolite output equivalent to a boiled and lyophilised sprout extract. This is the reason a label dose of glucoraphanin does not tell you the delivered sulforaphane dose.

  PMID 26524341 PLoS One
• Human2017
  Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes.

  The human part of this much-cited paper is the smallest part of it. Sulforaphane was picked out by computer, by matching a diabetic liver pattern against 3,800 drug patterns. It cut sugar production in liver cells. In diabetic animals it improved glucose handling about as much as metformin. Finally, in a small human group, obese patients with poorly controlled type 2 diabetes took concentrated sprout extract and their fasting and average blood sugar came down. A later prediabetes trial could not confirm that human piece.

  A multi-part paper. Sulforaphane was identified computationally by matching a type 2 diabetes liver disease signature against 3,800 drug signatures; it suppressed glucose production in hepatic cells via NRF2 nuclear translocation, attenuated glucose intolerance in diabetic animals by a magnitude similar to metformin, and in the final human component, given as concentrated broccoli sprout extract, reduced fasting blood glucose and HbA1c in obese patients with dysregulated type 2 diabetes. The human arm is the smallest part of the paper and is the part that the later prediabetes trial did not confirm on its primary endpoint.

  PMID 28615356 Science Translational Medicine

What users report

Self-reported experiences, not evidence. Nothing below was measured under controlled conditions, and reports like these cannot separate a real effect from placebo, from the training or diet change that accompanied it, or from what the product actually contained. They are here because knowing what people describe, including what goes wrong, is worth reading alongside the studies.

• Two separate conversations run in parallel and barely meet. One is about standardised supplements rated in milligrams of sulforaphane per serving, with people describing taking several capsules to reach roughly 75 mg daily and naming a European product they describe as considerably more expensive. The other is about growing broccoli sprouts, which is almost entirely about seed variety and brief steaming and carries no experience reports at all.
• Heat degradation is the most practical thing discussed. People describe a product shipped in warm months needing several times the number of capsules to produce what a winter batch produced, and that instability is also offered as the explanation whenever someone reports inconsistent results.
• What people describe noticing is anxiety and mood rather than any of the longevity claims the compound is usually sold on, and the timeframe described is days to about a week rather than months.
• Against that, other people in the same discussion describe increased anxiety, irritability and disrupted sleep from it, and the thread leaves the contradiction standing rather than resolving it. Individual variation is the explanation offered, which explains nothing.
• The volume of genuine first-hand discussion is small relative to how much attention the compound gets, so this pattern rests on a narrow base.

Sources: Sulforaphane threads on LongeCity covering supplement products, mood reports and home grown sprouts, found by site-restricted search and read directly, September 2026. Nothing above is attributed to any specific post and no post is reproduced.