Prostate research is where sulforaphane has been tested in humans most seriously, and it is also where the results are most frequently overstated. Three separate trials have given sulforaphane or glucoraphanin-rich broccoli to men with prostate cancer concerns, measuring PSA behavior and gene expression in prostate tissue. All three produced interesting secondary findings. None of them met its primary endpoint. Both halves of that sentence matter.
Key Takeaways
- A randomized, double-blind, placebo-controlled trial in 78 men with rising PSA after prostatectomy did not meet its primary endpoint, but PSA doubling time was 86 percent longer in the sulforaphane group (28.9 vs 15.5 months) [1].
- In that trial, 44.4 percent of men on sulforaphane had a PSA increase greater than 20 percent at six months, compared with 71.8 percent on placebo [1].
- A single-arm phase II study in 20 men with recurrent prostate cancer also missed its primary endpoint, with only one man achieving a 50 percent PSA decline, but on-treatment PSA doubling time was significantly longer than pre-treatment [2].
- The ESCAPE trial gave men on active surveillance glucoraphanin-rich broccoli for 12 months and examined gene expression changes in prostate tissue [3].
- PSA doubling time is a surrogate marker. No trial has shown sulforaphane changes survival, metastasis, or the need for treatment.
The Randomized Trial: Cipolla 2015
This is the strongest study in the set, because it is the only one that is both randomized and placebo-controlled. Seventy-eight men, mean age 69, all with rising PSA after radical prostatectomy, took either 60 mg per day of stabilized free sulforaphane or placebo for six months, followed by two months off treatment [1].
The primary endpoint was a specified reduction in the log PSA slope, and the trial did not reach it. That is the headline result and it should be stated first. The secondary findings were more encouraging. Mean PSA change from baseline to month six was significantly lower with sulforaphane than placebo (+0.099 vs +0.620 ng/mL, p = 0.0433). PSA doubling time, the interval over which PSA doubles and a widely used marker of how fast a recurrence is progressing, was 28.9 months on sulforaphane versus 15.5 months on placebo, an 86 percent difference. Men whose PSA rose by more than 20 percent at six months made up 44.4 percent of the sulforaphane arm and 71.8 percent of the placebo arm [1].
One further detail is worth attention. The effects were most pronounced between months three and six, and once treatment stopped, PSA slopes in the two arms became the same over the following two months. Whatever the compound was doing, it stopped doing it when the men stopped taking it.
The Single-Arm Study: Alumkal 2015
Twenty men with recurrent prostate cancer took 200 micromoles per day of sulforaphane-rich broccoli sprout extract for up to 20 weeks. The primary endpoint was a PSA decline of at least 50 percent, achieved by one man out of twenty, so the trial missed its target. Seven men had smaller declines. On-treatment PSA doubling time was significantly longer than pre-treatment doubling time (9.6 vs 6.1 months, p = 0.044), and there were no grade 3 adverse events [2].
The obvious limitation is that this was single-arm and open-label. Without a placebo group, a change in PSA doubling time is hard to attribute confidently to the intervention. The authors themselves framed the result as a reason to study higher doses rather than as a demonstration of efficacy.
The ESCAPE Trial: Active Surveillance
ESCAPE took a different approach, working with men on active surveillance rather than men with recurrence. Participants ate glucoraphanin-rich broccoli for 12 months, and researchers examined transcriptional changes in prostate tissue rather than PSA alone [3]. Looking directly at gene expression in the target organ is methodologically stronger than inferring activity from a blood marker, and it is one of the few sulforaphane studies to run for a full year.
What PSA Doubling Time Actually Tells You
All three trials converge on the same secondary signal: PSA rises more slowly. This is worth understanding precisely. PSA doubling time correlates with prostate cancer outcomes in observational data, which is why clinicians track it. But a compound that slows a marker has not been shown to change what the marker predicts. Slowing PSA rise could reflect slowed disease, or it could reflect a direct effect on PSA production that leaves the underlying disease unchanged. Distinguishing between those requires trials with clinical endpoints, and those trials have not been run.
This distinction is not academic for a man deciding whether to take a supplement. A 28.9-month doubling time instead of 15.5 months sounds like a large effect, and it may be. It has not been demonstrated to translate into fewer men needing salvage treatment, fewer metastases, or longer survival.
Where This Fits
Prostate is one of the better-studied applications of sulforaphane in humans, alongside the air pollution detoxification trials. Anyone with a prostate cancer diagnosis, a rising PSA, or an active surveillance plan should treat sulforaphane as a question for their urologist or oncologist, not a decision to make alone, particularly given that our article on chemotherapy interactions covers real reasons some cancer treatments and antioxidant supplements need coordinating.
A Note on the Evidence
Two of the three trials described here missed their primary endpoints, and the third measured gene expression rather than clinical outcomes. PSA doubling time is a surrogate marker, not a demonstrated clinical benefit. This article is informational and is not medical advice. Anyone with prostate cancer should make supplement decisions with their oncology team.
Frequently Asked Questions
Does sulforaphane lower PSA?
In the randomized trial, PSA still rose in both groups, just more slowly on sulforaphane (+0.099 vs +0.620 ng/mL over six months) [1]. In the single-arm study, only 1 of 20 men had a 50 percent PSA decline [2]. Sulforaphane slowed PSA rise in these trials rather than reducing PSA.
What dose was used in the prostate trials?
The randomized trial used 60 mg per day of stabilized free sulforaphane for six months [1]. The phase II study used 200 micromoles per day of sulforaphane-rich broccoli sprout extract for up to 20 weeks [2].
Did the trials succeed?
No. Both PSA trials missed their pre-specified primary endpoints. The positive findings on PSA doubling time were secondary outcomes, which carry less weight than a primary endpoint result.
Does the effect last after stopping?
Apparently not. In the randomized trial, PSA slopes in the sulforaphane and placebo arms were the same over the two months after treatment stopped [1].
Should someone with prostate cancer take sulforaphane?
That is a decision for their oncology team. The trials showed good tolerability, but sulforaphane has not been shown to change survival or disease progression, and antioxidant supplements can interact with some cancer treatments.
References
- Cipolla BG et al. Effect of Sulforaphane in Men with Biochemical Recurrence after Radical Prostatectomy. Cancer Prevention Research (2015). PMID 25968598
- Alumkal JJ et al. A phase II study of sulforaphane-rich broccoli sprout extracts in men with recurrent prostate cancer. Investigational New Drugs (2015). PMID 25431127
- Traka MH et al. Transcriptional changes in prostate of men on active surveillance after a 12-mo glucoraphanin-rich broccoli intervention, results from the ESCAPE randomized controlled trial. American Journal of Clinical Nutrition (2019). PMID 30982861
These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease. Content is for informational purposes only and is not medical advice; consult a qualified healthcare provider before starting any supplement. As an Amazon Associate we earn from qualifying purchases.
