Sulforaphane supplements

Most sulforaphane supplements are glucoraphanin supplements. Glucoraphanin is the stable precursor that broccoli stores, and sulforaphane is what forms when an enzyme cuts it. Which of those two a capsule holds, and whether it also holds the enzyme, decides how much of the label amount reaches your blood. This page covers what human studies have measured for each arrangement, and which comparisons between products are worth making.

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What is actually inside the capsule?

Three arrangements cover almost everything on the market. The first supplies glucoraphanin alone, from broccoli seed or sprout extract. The second supplies glucoraphanin together with active myrosinase, the plant enzyme that converts it. The third supplies sulforaphane itself, chemically stabilized so it survives storage.

Sulforaphane is reactive and degrades, which is why the third arrangement is uncommon and why the other two exist at all. The practical consequence is that a label figure often describes a precursor, and the conversion step sits outside the manufacturer's control.

Does the myrosinase on the label change anything?

By the available measurements, yes, and by a large margin. A group at Johns Hopkins dosed volunteers with glucoraphanin preparations and collected 24-hour urine, measuring sulforaphane metabolites as dithiocarbamates by cyclocondensation with 1,2-benzenedithiol, read by HPLC at 360 nm against a recrystallized standard.

Preparations lacking active myrosinase gave back roughly 10 percent of the dose, a figure the authors draw from their own earlier studies. When active myrosinase came with the dose, recovery rose to almost 40 percent, and the variation both within and between subjects narrowed. When the glucoraphanin was hydrolyzed in advance, so that subjects swallowed sulforaphane rather than making it, recovery was about 90 percent.

Read the numbers alongside the design. Most of the comparisons in that paper used five adults, four women and one man, mean age 53.8 years. A separate comparison of commercial supplements used twenty. Five people is enough to show a difference this size and not enough to put a confident percentage on it, and the authors present the figures as approximate throughout.

The same paper reports that when broccoli sprouts or seeds were given whole, with their own enzyme intact, sulforaphane was 3 to 4 times more bioavailable than from glucoraphanin delivered without active plant myrosinase. It also found that a commercially prepared glucoraphanin supplement gave urinary output equivalent to an equimolar dose in a boiled, freeze-dried sprout extract. Neither contained active enzyme, and neither did better than the other. The loose equivalent of those two, a sulforaphane powder, has been measured separately in four men, where an air-dried sprout powder that kept its enzyme returned 74 percent of its dose in urine against 19 percent for a glucoraphanin-rich powder without one.

What does "stabilized sulforaphane" mean?

It means the sulforaphane has been put in something that stops it reacting, most often a molecular cage. One study tested two such preparations: sulforaphane held in an alpha-cyclodextrin inclusion, and a commercial sulforaphane-rich supplement. Both were more stable than pure sulforaphane and, in the authors' assessment, comparably bioavailable. The cyclodextrin preparation reached peak serum concentrations at 2 hours.

Two findings in that paper deserve more attention than they get. Six of the ten volunteers taking the cyclodextrin preparation reported mild stomach upset. And applied to the skin of SKH1 mice, it failed to switch on the cytoprotective enzymes that pure sulforaphane did switch on, so stabilizing the molecule did not leave every one of its effects intact.

That stomach upset is the pattern across the trials rather than a quirk of one preparation. In a crossover trial of 49 smokers, 29 reported at least one mild adverse event and every one of the 29 was gastrointestinal, with abdominal pain and diarrhea significantly more frequent at 296 µmol of glucoraphanin daily than at 148 µmol. The groups with a reason to ask a doctor first, and the laboratory heart finding that circulates without its concentrations attached, are set out under sulforaphane side effects.

The claim that both preparations matched pure sulforaphane in potency rests on cultured cells, not on people. Cells in a dish and a person who has swallowed a capsule are different measurements, and this topic blurs them constantly. The published abstract also names no assay for the serum concentrations and the full text sits behind a paywall, so no absorption percentage from it appears here.

One stabilized preparation has gone much further than that. A synthetic sulforaphane held in alpha-cyclodextrin has been through three randomized placebo-controlled trials, which makes stabilized sulforaphane the only form taken into a trial with a clinical endpoint rather than a laboratory marker. In its phase 1 study, 18 healthy men reached peak blood concentrations of 0.43 to 2.12 µmol/L by validated LC-MS/MS, and 17 of the 18 recorded an adverse event against none of the 6 on placebo. The two trials that measured a clinical outcome, after subarachnoid hemorrhage and in pneumonia, both found nothing. It is an investigational drug rather than a supplement, so no product on a shelf carries that evidence.

What human studies measured, by preparation

Every row below comes from people rather than cells or animals. Recovery figures are not comparable across assays, so each row names its own, and says so where the method was never published.

Does any of this activate Nrf2?

Copy for these products almost always arrives at Nrf2, a transcription factor that switches on a group of antioxidant and detoxification genes. Sulforaphane induces it in cells and in animals, consistently enough that the mechanism is usually written about as established. In people it has been looked for once, at a dose of preformed sulforaphane above what a glucoraphanin capsule delivers, and it was not found.

Long and colleagues gave 300 mg of a stabilized synthetic sulforaphane once daily for 14 days to 65 patients hospitalized with pneumonia, against 68 on placebo, and measured 45 serum cytokines and messenger RNA from blood leukocytes on days 1, 8 and 15. Expression of Nrf2 target genes was not significantly changed. Neither were interleukin-6, interleukin-1 beta or tumor necrosis factor alpha. The trial was stopped early for futility with 133 patients enrolled.

The dose is what makes that relevant to a label rather than only to a drug. A 300 mg unit of that preparation supplies 46.2 mg of preformed sulforaphane, about 260 micromoles, needing no conversion at all. A glucoraphanin capsule starts from the precursor and, without active enzyme, gives back around a tenth of it. So the pathway claim printed on a bottle is being made for a dose well below the one that was tested and missed.

The same reasoning limits what the trial proves. One study, in patients who were acutely ill, over two weeks, says little about a healthy person taking a smaller dose for a year, and nobody has run that study. The trial and the ten others in people are set out under sulforaphane benefits.

What a label does not tell you

Four things, and the first is the one that matters most. A label states a quantity of something, and that something may be glucoraphanin, total glucosinolates, extract weight or sulforaphane. Only the last is the compound the research is about, and the four are not interchangeable.

Second, a stated myrosinase content is not a stated myrosinase activity. The enzyme is a protein and it can be denatured by heat or time while still being present to assay by weight.

Third, conversion is incomplete even under laboratory control. When the Johns Hopkins group deliberately hydrolyzed glucoraphanin before dosing and checked the result by cyclocondensation just before the subjects swallowed it, the 50, 100 and 200 µmol glucoraphanin doses yielded mean dithiocarbamate levels of 23.5, 49.6 and 97.4 µmol. About half the starting glucoraphanin had converted, in a tube, with the enzyme added on purpose.

Fourth, no label can tell you about your gut bacteria, and without active plant enzyme they do much of the converting. That is the mechanism behind the 1 to 40 percent spread, and it is specific to you rather than to the product.

What follows from all this is narrow. You can compare which compound a label names, whether active enzyme is supplied, and whether the product has been through a human study. The doses human trials have used, and how each was measured, are on the how much sulforaphane per day page. The food and sprout comparison sits with broccoli sprouts.