The king of cruciferous vegetables. Its sulforaphane content activates your body's own detox and antioxidant systems. Provides glucoraphanin that converts to sulforaphane, activating your Nrf2 antioxidant pathway and upregulating Phase II detoxification enzymes.
Reviewed March 2026
These words describe the research, not the molecule's worth. Research strength is how much work stands behind one claim, and it is never a product score.
A pairing appears on this page only when a trial gave both ingredients together and measured the result. Broccoli has none that clears that bar.
Stitching two separate single-ingredient studies into a pairing is the one thing this engine will not do. When a study of the combination itself holds up at source, it lands here with its citation.
No invented synergy. Where actives were studied on their own rather than together, the record shows each on its own evidence, never a combined effect no trial measured.
Research strength. Research strength says how much work stands behind the combination. It is never a product score.
Independent record. Every finding is cited to a named trial, dated, and never written by the brand.
20 pairings are live across the library today. Checked 20 July 2026.
No study gave these as a pair, so they are not in the card above. But the reason they belong together is settled biochemistry, not a guess, so it is worth knowing.
Sprouts carry many times the glucoraphanin of mature broccoli, so the two supply the same precursor at very different densities. Combining them loads one pool.
Broccoli carries glucoraphanin, the inert storage form, which becomes sulforaphane only after myrosinase hydrolysis. Preformed sulforaphane skips that step.
Cooking inactivates the myrosinase naturally present in broccoli, leaving glucoraphanin dependent on gut bacteria for conversion. Added myrosinase restores hydrolysis in the upper gut.
Ascorbate raises myrosinase activity as a cofactor, which favours conversion of broccoli glucosinolates to their isothiocyanates. Broccoli also carries meaningful vitamin C of its own.
Broccoli glucobrassicin yields indole-3-carbinol on hydrolysis, which condenses in stomach acid to DIM. Supplying DIM directly enters the same pathway further along.
Cruciferous isothiocyanates induce phase II conjugating enzymes, while calcium D-glucarate lowers gut beta-glucuronidase activity that would uncouple glucuronide conjugates. The two act at successive points of the same clearance route.
Silymarin and cruciferous isothiocyanates both influence Nrf2-driven antioxidant enzyme expression, by different chemistry acting on the same transcriptional route.
Isothiocyanates upregulate antioxidant enzymes, and several of those enzymes are selenoproteins that need selenium to be built. Induction without the trace element gives less finished enzyme.
Glucosinolate breakdown yields thiocyanate, which competes with iodide for uptake at the sodium-iodide symporter in thyroid tissue. Large habitual cruciferous intakes therefore raise the value of adequate iodine, and this is settled physiology.
Broccoli is one of the densest dietary sources of phylloquinone, so it adds to any vitamin K1 already in a formula. The combined intake matters for anyone tracking a steady vitamin K load for normal clotting factor activity.
Sulforaphane from broccoli is metabolised through the mercapturic acid pathway, beginning with glutathione S-transferase conjugation. Nrf2 activation in turn increases transcription of glutamate cysteine ligase, the rate-limiting enzyme of glutathione synthesis. Glutathione is therefore both the vehicle for sulforaphane clearance and one of the outputs of the pathway it switches on.
N-acetylcysteine supplies cysteine, the limiting amino acid for glutathione synthesis. Isothiocyanates from broccoli are excreted as N-acetylcysteine conjugates after passing through the same pathway. The two intersect at cysteine supply rather than acting on separate targets.
Alpha-lipoic acid cycles between its dithiol and disulfide forms and participates in regenerating other cellular reductants. Sulforaphane acts upstream by modifying Keap1 cysteines and increasing transcription of thiol-handling enzymes. One acts as a redox couple, the other changes how much enzyme is present.
Quercetin is present in broccoli itself and, like sulforaphane, has been described as an inducer of Nrf2-regulated genes in cell systems. The two reach that pathway by different chemistry, one through electrophilic cysteine modification and one through phenolic redox behaviour. Most of this work is cellular, so it is mechanism rather than a measured human outcome.
EGCG and sulforaphane are both described as activators of Nrf2-regulated transcription in cell models, arriving there through different chemistry. Combining them in a blend is common. The combined effect in people has not been measured in the material available here.
Curcumin carries a Michael-acceptor group and modifies sensor cysteines in a way conceptually similar to sulforaphane, though the two differ in potency and in how well they reach tissues. Formulators pair them for that reason. Human combination data are not present here.
Broccoli is a notable food source of ascorbate, which reduces ferric iron and improves non-heme iron uptake in the same meal. The same vegetable also contributes calcium and fibre, which work in the opposite direction. The net effect on any given meal depends on which of those dominates, so it is a modulating relationship rather than a straightforwardly helpful one.
Broccoli carries phylloquinone, and both phylloquinone and MK-7 serve as the cofactor for gamma-glutamyl carboxylase, the enzyme that carboxylates glutamate residues on vitamin K dependent proteins. Total vitamin K intake from food and a supplement adds up at that enzyme. Anyone whose clotting is being managed pharmacologically should keep their vitamin K intake steady and discuss it with their clinician rather than change it unannounced.
Glucoraphanin is a stable glucosinolate and is inert until a thioglucosidase cleaves its glucose, after which the aglycone rearranges to sulforaphane. Cooking inactivates the plant's own myrosinase, leaving gut bacterial thioglucosidase as the route. Standard pancreatic digestive enzyme blends do not carry myrosinase activity, so they do not substitute for it.
When plant myrosinase has been destroyed by heat, colonic bacteria carry out the thioglucosidase step that releases isothiocyanates, so the gut community influences how much sulforaphane a person actually forms. One randomised study compared probiotic or broccoli supplementation added to a clinician-prescribed antibacterial regimen in adults and reported the clearance rates observed. The conversion mechanism is established; the clinical combination result belongs to that single study.
Some Lactobacillus strains have been shown in culture to hydrolyse glucosinolates and release isothiocyanates. That gives a plausible route for improving conversion when dietary myrosinase has been cooked away. Strain differences are large and this has been characterised mainly in vitro.
Inulin is fermented in the colon and shifts the composition and activity of the resident bacteria. Because those bacteria are what convert glucoraphanin when plant myrosinase is absent, a prebiotic can indirectly affect conversion. The link is indirect and has not been quantified in the material here.
Broccoli carries lutein alongside beta-carotene, and both are absorbed from mixed micelles with dietary fat. A supplemental xanthophyll simply adds to what the vegetable contributes. Cooking with some fat improves how much of either becomes bioaccessible.
Broccoli contributes beta-carotene, which needs a lipid phase to reach the enterocyte. Adding a supplemental carotenoid raises total intake through the same micellar route, where the carotenoids compete with one another for space in the micelle. High single doses of one carotenoid can lower the uptake of another.
Broccoli supplies naturally occurring folates as polyglutamates, which are deconjugated at the brush border before absorption. Supplemental folate or methylfolate adds to the same one-carbon pool. Food folate is less completely absorbed than the synthetic form, which is why intakes are expressed as dietary folate equivalents.
Unlike spinach, broccoli is low in oxalate, so the calcium it carries is not locked into an insoluble complex and is absorbed comparatively well for a vegetable source. A calcium supplement adds to that intake. Calcium in the same sitting also works against non-heme iron uptake, which is the trade-off to note.
Metallothionein transcription is among the responses downstream of Nrf2 activation, and the protein requires zinc to fold around its metal centre. Copper and zinc superoxide dismutase likewise needs its metals. Broccoli-derived isothiocyanates change how much enzyme is made; the metal supply decides how much of it is functional.
Cruciferous vegetables carry an unusually high sulfur load in their glucosinolates, and the sulfur that comes off in catabolism is handled in part by sulfite oxidase, a molybdenum cofactor enzyme. Molybdenum requirements are small and normally met by diet. The relationship is a cofactor one, described here for completeness.
Viscous fibre thickens gut contents and slows the transit of everything dissolved in them. For a compound whose conversion depends on where in the gut it meets bacterial enzymes, that timing shift can go either way. Broccoli also carries its own insoluble fibre load, so adding a bulking fibre compounds the effect on tolerance.
Chlorella and broccoli powders appear together in green blends as sources of chlorophyll and plant micronutrients. There is no measured interaction between them in the material available here, and the pairing rests on the blend category rather than on chemistry. It is included as a formulation observation only.
Talk to a doctor before taking Broccoli if any of these apply to you: Supplement doses vary wildly in sulforaphane content, Myrosinase enzyme needed for conversion (often destroyed in processing). These are flags to check first, not effects Broccoli is known to cause.
Not medical advice. Show the label to your pharmacist.The whole-food sources on file. A supplement closes the gap, it does not replace dinner.
A gram-for-gram figure (how much of each you would eat to match a dose) will appear here once it is sourced and reviewed. This page will not print a number it cannot cite.
These are the studies our verdict leans on, chosen from the 5,399 we read for Broccoli. The full linked list is below.
11 sources behind our Broccoli verdict: peer-reviewed studies and registered clinical trials. Every one links straight to PubMed, the journal, or ClinicalTrials.gov. Read them yourself.
Evidence surfaced via Semantic Scholar (Allen Institute for AI) and ClinicalTrials.gov. Ranked by study type and citation weight, not cherry-picked.
Read this carefully. These are 91,068 voluntary, unverified reactions reported to the FDA (openFDA). The number mostly reflects how popular Broccoli is, not how risky it is. A report is not proof Broccoli caused anything. It is a signal of what to watch for, nothing more.
Source: openFDA adverse-event reports. Voluntary reporting, not an incidence rate.
FDA Disclaimer: These statements have not been evaluated by the Food and Drug Administration. This information is for educational purposes only and is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider before starting any supplement regimen.