FYI I don’t take sulforaphane, I remember Rhonda mentioned it many years ago and was interested at some point before I was scientifically minded.
The benefits page on Nootropicsdepot like many of their other products seems like mechanistic speculation. But I posted it since I appreciate the CEO’s & brand credibility, gravitas and long winded posts to random customers, and for those who take it.
I also sprouted for a few weeks. I was inspired after watching an engaging video featuring Doug Evan’s, the sprout guy! He was even so kind as to PM with me to offer some tips.
I plan to start again… it’s on my long list of things to do!!!
https://www.nature.com/articles/s41598-026-39389-4
Exogenous myrosinase from mustard seed increases bioavailability of sulforaphane from a glucoraphanin-rich broccoli seed extract in a randomized clinical study
Strikingly, the addition of exogenous Myr to GR with vitamin C resulted in a dramatic increase in the conversion rate compared to GR with vitamin C only, as measured in the first 0–8-hour urine collection. Differences did not persist in the 8–24-hour urine collection. Furthermore, four documented GR-converting genes identified in fecal samples from study subjects were correlated with GR conversion, and bacterial entrainment is hypothesized to contribute to increase conversion efficiency.
I just had a Fable session prior to pulling the trigger on the $$$ ND sulforaphane product… I won’t bury the lead, I won’t be buying it.
One ‘man’s’ opinion:
Not marketing, not old wives’ tale — real chemistry that got inflated into a superfood. And yes: nice to have, not needed.
Why sprouts got the reputation (from memory, flagged): Johns Hopkins chemists in the 1990s found sulforaphane was one of the strongest natural activators of the body’s own antioxidant switch (Nrf2), and that 3-day-old broccoli sprouts carry something like 20–50× more of its precursor than grown broccoli. That’s a legitimate lab finding. The press turned “potent in a dish” into “superfood.”
What the human evidence actually shows (from the 2025 Cambridge review of clinical trials, fetched earlier): real results in glucose control and a few niche conditions. For cancer prevention, the trials mostly show it changes biomarkers — nobody has shown fewer cancers or fewer heart attacks in people. So the gap is between “does something measurable” and “does something you’d notice or that changes your outcomes.” Mechanistic-strong, outcome-weak.
Is it a nutrient? No. There’s no sulforaphane deficiency. Your body doesn’t need it the way it needs iodine or B12. It’s a plant chemical that nudges a pathway you already have. You can live a full life eating zero cruciferous vegetables. Nitrate, fiber, folate — those have real “you’re short on this” states. This doesn’t.
Why previous Fable said take it: I can’t see its reasoning. My best read is it followed the same logic I’d have followed a week ago: greens are good → sulforaphane is the famous thing in greens → supplement it. The mistake is treating one celebrity molecule as the reason greens are good. They aren’t good because of any single compound; that’s why every “greens in a pill” product underdelivers.
your instinct is right. Eat the arugula, skip the sprouts, and let the BROQ run out without replacing it — unless you want an antioxidant hedge for your GPX1 gene, which is the one angle where it’s a defensible “lean helps.” Even there, NAC is already doing that job.
Your move: Nothing.
Open question: None.
me too.
https://pubmed.ncbi.nlm.nih.gov/42641715/
In patients with T2D and moderate CKD, 12 weeks of treatment with BSE with progressing dose (50 to 150 μmol/day BSE) did not result in statistically significant changes in measures related with glycemic control.
https://pubmed.ncbi.nlm.nih.gov/27832073/
Sulforaphane administered for four weeks at doses of 25 μmoles and 150 μmoles to patients with COPD did not stimulate the expression of Nrf2 target genes or have an effect on levels of other anti-oxidants or markers of inflammation.
https://pubmed.ncbi.nlm.nih.gov/38089924/
Although glucoraphanin intake produced a marginally significant statistical result for ALT at 24 weeks ( = 0.041), the absolute change was clinically meaningless (a mere 1 U/L median difference vs. placebo), while failing to show any significant improvement in secondary endpoints including AST, gamma-GTP, or serum glutathione
Sulforaphane is by no means a reliable anti-aging compound right now. It might help a subset of people in very poor health, but it does almost nothing for healthy people. You just need to eat cruciferous vegetables. Epidemiological studies have already shown that this reliably reduces all-cause mortality, partly due to hormesis. Taking supplements may actually backfire. If you asked me to grade it, it gets a Z.
Another update. I found that cruciferous sprouts like broccoli sprouts and kale sprouts have very high erucic acid levels, and even after 7 days of sprouting, it only drops by about 50%. I’ll just stick with regular broccoli.
I asked Claude Opus 5 about this and here is what it recommended:
For individuals cultivating Brassicaceae sprouts specifically to extract sulforaphane (a potent Nrf2 activator, antioxidant, and potential senolytic), erucic acid dictates the dose-response safety limit:
NootropicsDepot found 0.14 mg sulforaphane formed with BroccoMax by dumping the capsule in plain water, which is the ideal condition, similar to BROQ’s test. It’s a dud.
“Simulated gastric fluid followed by simulated intestinal fluid: Resulted in 0.00mg.”
This statement is incompetent, if not irresponsible, because it doesn’t mention how long the capsule was submerged. I don’t believe they submerged it for a long enough time to account for Broccomax’s possible thicker or multi-layered polymer coatings and longer lag time, just like BROQ failed to do so (only 2 hours).
When Broccomax added calcium ascorbate to its capsules not too long ago, to improve the conversio to sulforaphane, we see BROQ’s test result of Broccomax change from 2.07 mg as shown up above, to <.1 mg. Must be because Broccomax’s capsule changed.
The capsule contents was dumped, ND didn’t test with the capsule. Either way you really think they’re going to test the water when they see a capsule floating in it?
It was tested in optimal conditions - without capsules.
Gastric acid destroys myrosinase which is the enzyme that forms sulforaphane from glucoraphanin. It’s why some companies tries to use special capsules to bypass it.
No companies really have any preformed sulforaphane.
ND skips gastric acid by sprinkling powder in plain water and let it form there, before drinking.