Sulforaphane powder

A powder is a processing step rather than an ingredient, which is why the category is so uneven. Two pouches can both hold dried broccoli and differ by nearly four to one in how much sulforaphane you absorb from them. What separates them is whether the drying left the plant enzyme alive, and two small studies from the University of Illinois put numbers on the difference.

What is sold as sulforaphane powder?

Almost always a glucoraphanin powder. Glucoraphanin is the stable precursor that broccoli stores, and sulforaphane is what forms when myrosinase cuts it. Sulforaphane itself is reactive and does not keep well, so putting it in a pouch and expecting it to survive a year on a shelf is hard. Drying the precursor is easy.

Three kinds of dried material end up in the same aisle. A glucoraphanin-rich powder made from broccoli seed or floret, concentrated and with the enzyme gone. An air-dried sprout powder, where the drying was gentle enough to leave myrosinase working. And a boiled or blanched sprout extract, where it was not. The label rarely tells you which of the three you have bought, and the three behave differently in people.

How much of a powder dose did people absorb?

Between a fifth and three quarters of it, depending on the enzyme. Cramer and Jeffery ran the comparison twice, both times in four healthy men, and both times by feeding each man every arm of the study.

In the first study, each man ate four meals of dry cereal and yogurt: one with 2 g of air-dried broccoli sprouts, one with 2 g of the glucoraphanin-rich powder, one with both, and one with neither. Recovery of sulforaphane metabolites in 24-hour urine was 74 percent of the dose from the sprouts, 19 percent from the powder, and 49 percent from the two together.

The second study swapped the air-dried sprouts for fresh ones, on the reasoning that fresh sprouts are what people can actually buy. Doses were set by sulforaphane equivalent rather than by weight: sprouts at 70 µmol, powder at 120 µmol. Recovery of sulforaphane-N-acetylcysteine was 60 percent from the sprouts, 24 percent from the powder, and 65 percent from the combination.

Read the right-hand columns before the numbers. Four men is four men, and a percentage from four people carries no confidence interval worth quoting. Neither abstract names the platform used to measure the metabolites, so these recoveries cannot be set against figures from a study that did name one. And every value is a percentage of the dose ingested rather than an absolute amount, which matters in the second study because the powder supplied about 1.7 times the sulforaphane equivalent of the sprouts. The powder delivered a smaller share of a larger dose.

The two studies also disagree about the combination, which is worth saying out loud. In 2011 the pair recovered 49 percent, below the sprouts alone at 74. In 2012 the pair recovered 65 percent, just above the sprouts alone at 60. What both agree on is narrower and more useful: adding a myrosinase source raised what came back from the glucoraphanin powder about two and a half times, in both studies.

Why was the powder slower as well as weaker?

Because the conversion happened somewhere else in the body. A preparation carrying live myrosinase starts hydrolyzing as soon as it is chewed, so sulforaphane is available for absorption in the small intestine. A preparation without the enzyme has to reach the colon, where bacteria do the cutting, and that takes hours.

Both Illinois studies recorded that delay in plasma and in urine. The same pattern shows up in a crossover trial that gave 12 adults fresh sprouts at 150 µmol glucoraphanin and, on another occasion, six capsules of a broccoli supplement at 121 µmol: the plasma peak came at 3 hours on the sprouts and 6 hours on the capsules. Bacterial hydrolysis is also less complete and far less consistent between people, which is the mechanism behind the 1 to 40 percent spread in recovery that the Johns Hopkins group has reported across individuals.

Does drying always destroy the enzyme?

No, and Cramer's 74 percent figure shows why. The best-performing preparation in either study was itself a powder: air-dried sprouts, not fresh ones. Gentle drying keeps myrosinase working.

Heat is what kills it, and the threshold has been measured. In laboratory work on frozen broccoli, blanching at 86 °C and above inactivated myrosinase entirely, while 76 °C cost only about 18 percent of sulforaphane formation. The consequence turns up in people: 18 volunteers given soup made from commercial frozen broccoli absorbed roughly a tenth as much sulforaphane as from soup made with lightly cooked fresh broccoli, and the authors traced it to the enzyme destroyed during commercial blanching and freezing. The glucoraphanin was still in the frozen florets. Nothing was left to cut it.

So "freeze-dried" and "air-dried" are not interchangeable words on a pouch, and "broccoli sprout extract" usually means the enzyme has been through a boiling step. The Johns Hopkins group fed volunteers a boiled, freeze-dried sprout extract and found it gave the same urinary output as an equimolar commercial glucoraphanin supplement. Neither carried active enzyme, and neither beat the other.

Has a powder been tested on anything beyond absorption?

One trial has, in 81 people, and the reporting of it is easy to miscount. A group in Tehran randomized 81 patients with type 2 diabetes to 10 g a day of broccoli sprout powder, 5 g a day, or a placebo, for four weeks. Seventy-two completed and 63 were included in the analysis.

Taking the powder at either dose lowered malondialdehyde, oxidized LDL cholesterol and a calculated oxidative stress index, and raised total antioxidant capacity. At 10 g a day specifically, serum triglycerides and the oxidized LDL to LDL ratio fell and HDL cholesterol rose, and fasting insulin and HOMA-IR fell at p = 0.05 for the treatment effect, which sits on the edge of conventional significance.

Those results were published as three separate papers between 2011 and 2012. They are three reports of one randomization, not three trials, and a reader counting citations will get the wrong impression of how much evidence exists. Every outcome is a blood marker rather than a diagnosis or a symptom.

The larger constraint is what the papers do not say. None of the three abstracts states the sulforaphane or glucoraphanin content of the powder used, and none names an assay for it. So the dose can be reported only as 10 g or 5 g of powder a day. Whether that powder had active myrosinase, and therefore whether a reader buying a different powder is taking anything comparable, cannot be read from the published record. The doses that can be stated in micromoles, each with its measurement, are collected on how much sulforaphane per day.

Two bigger trials used dried preparations that were not powders sold to consumers, and their numbers agree with Cramer's enzyme-free arms. Forty-nine smokers took a broccoli seed and sprout extract at 148 and 296 µmol glucoraphanin daily, two weeks each with a washout between, and mean bioavailability was 11 and 10 percent. In Qidong, 291 people drank a sprout-derived beverage supplying 600 µmol glucoraphanin and 40 µmol sulforaphane daily for 12 weeks, and the urinary metabolite levels showed no fall in bioavailability across the three months.

What a powder label leaves out

Four things, and only the first is specific to powders. Whether the drying left myrosinase active, which no label states and which decides most of the outcome. Which compound the stated milligram figure describes, since glucoraphanin, total glucosinolates, extract weight and sulforaphane are not the same substance. What the powder was made from, because seed, floret and sprout differ by more than an order of magnitude in glucoraphanin, as the content by food figures show. And your own gut bacteria, which do the converting when the plant enzyme is gone.

One practical point does follow from the absorption work, and it is the only one the data supports. If a powder has no active enzyme, eating it with a source of myrosinase raised recovery substantially in both Illinois studies. Fresh broccoli sprouts worked in the 2012 trial, and in laboratory work on frozen broccoli, 0.25 percent added daikon radish restored formation that blanching had stopped. That second result has never been tested in a person.

What nobody has done is compare a myrosinase-active sprout powder against a glucoraphanin powder on an outcome rather than a urine sample, or feed the same people a sprout powder and fresh sprouts of matched content in one study. The absorption evidence for this whole category rests on two studies of four men. How the capsule versions of the same material behave is covered under sulforaphane supplements, and what a daily amount of the fresh article looks like is on how much broccoli sprouts per day.