48 Supported by research
Human gut bacteria contain the enzyme myrosinase, which hydrolyzes glucoraphanin to form sulforaphane.
"myrosinase is an enzyme found in the plants and in your body, your microbiome, and they react and they form sulforaphane." (said at 0:05:00)
Published literature confirms that glucoraphanin (a glucosinolate found in cruciferous vegetables like broccoli) is converted into sulforaphane by myrosinase enzymes present both in the plants themselves and through myrosinase-like enzymatic activity of the human gut microbiota. When plant myrosinase is inactivated (e.g., through cooking), human intestinal bacteria possess functional enzymes that hydrolyze glucoraphanin to yield bioavailable sulforaphane, although the conversion rate via microbial activity is typically lower and more variable than plant-derived myrosinase.
- supports: Microbiota: a mediator to transform glucosinolate precursors in cruciferous vegetables to … (Journal of the science of food and agriculture 2018) · cited 82x in the literature
"They normally exist as glucosinolates (GLSs) in cruciferous vegetables, which are not themselves bioactive until they are degraded by myrosinase to form ITCs... However, studies using animal models and population trials have suggested that human gut bacteria might act like an 'organ' in that they can secrete their own myrosinase. In this review, the hydrolysis of GLS by myrosinase is discussed, with an important focus on the gut microflora and their myrosinase-producing roles." (abstract, background)
pubmedfull study (doi) - supports: Exogenous myrosinase from mustard seed increases bioavailability of sulforaphane from a gl… (Scientific reports 2026) · cited 3x in the literature
"Inactive glucoraphanin (GR) in broccoli is converted to the antioxidant, anti-inflammatory, and anti-bacterial sulforaphane (SF) by cruciferous vegetable enzyme myrosinase (Myr), or similar enzymes from specific gut bacteria; both sources have variable efficiency." (abstract, background, passage verified)
pubmedfull study (doi)
A 100-gram serving of broccoli sprouts yields between 5 to 6 milligrams and 60 milligrams of sulforaphane.
"with broccoli sprouts, 100 grams would give you somewhere between, I don't know, about five milligrams and 350—sorry, between about 5 or 6 milligrams and about 60 milligrams of sulforaphane." (said at 0:08:30)
Broccoli sprouts are widely recognized as rich sources of the glucosinolate glucoraphanin, which hydrolyzes into sulforaphane (SFN). Because sulforaphane content varies significantly based on seed cultivar, sprout age, cultivation conditions, and preparation methods (such as degree of mastication, heating, or blanching), the yield from 100 grams of fresh broccoli sprouts spans a wide range that typically falls between ~5–6 mg (or ~30–40 µmol) under modest conditions up to ~60 mg or higher under optimal conversion/high-yielding sprout cultivars (sprouts contain roughly 5–50+ µmol SFN per gram dry weight or substantial fractions thereof per fresh weight). The stated range accurately reflects the literature's observed variation in fresh sprout sulforaphane yield.
- supports: Maximization of Sulforaphane Content in Broccoli Sprouts by Blanching. (Foods (Basel, Switzerland) 2022) · cited 23x in the literature
"The optimum conditions were blanching at 61 °C for 4.8 min, resulting in 54.3 ± 0.20 µmol SFN/g dry weight, representing a 3.3-fold increase with respect to untreated sprouts." (abstract, results, passage verified)
pubmedfull study (doi) - context: Formation, immunomodulatory activities, and enhancement of glucosinolates and sulforaphane… (Critical reviews in food science and nutrition 2024) · cited 32x in the literature
"One of hydrolysates-sulforaphane from glucoraphanin is positively associated with the attenuation of inflammatory, which could reduce diabetes, cardiovascular and cancer risk. In recent decades, the great interest in natural bioactive components especially for sulforaphane promotes numerous researchers to investigate the methods to enhance glucoraphanin levels in broccoli sprouts" (abstract, passage verified)
pubmedfull study (doi)
Cooking broccoli or broccoli sprouts destroys the plant enzyme myrosinase.
"Cooking destroys myrosinase, so if you're cooking broccoli or broccoli sprouts, then you're just counting on the bacteria in your gut." (said at 0:08:55)
Cooking broccoli or broccoli sprouts leads to the thermal denaturation and inactivation of the endogenous plant enzyme myrosinase. When cooked brassica vegetables lacking active plant myrosinase are consumed, glucosinolates (such as glucoraphanin) pass into the colon, where conversion to isothiocyanates (such as sulforaphane) relies on hydrolysis by the resident gut microbiota.
A serving of approximately 60 grams of broccoli sprouts contains as much glucoraphanin as 1/4 to 1/2 pound of market-stage broccoli.
"a serving of, say, something like a couple of ounces, 60 grams or so, of broccoli sprouts gave you as much glucoraphanin as, um, you know, a quarter of a pound or a half a pound of market-stage broccoli." (said at 0:10:05)
Phytochemical analyses show that young (3-day-old) broccoli sprouts contain 10 to 100 times higher concentrations of glucoraphanin (the glucosinolate precursor to sulforaphane) by weight than mature market-stage broccoli heads. Consequently, a 60-gram (~2 ounce) serving of broccoli sprouts easily provides as much glucoraphanin as 1/4 to 1/2 pound (approximately 113 to 227 grams) of mature broccoli, and depending on cultivar and growing conditions, can equal the amount found in several pounds of mature broccoli.
Human gut microbial conversion efficiency of ingested glucoraphanin ranges from a few percent up to 60 to 70 percent.
"our best knowledge of the range of conversion efficiencies that you as a person might do ranges from a few percent of what you ingest to up to maybe about 60 or 70 percent." (said at 0:15:40)
Human pharmacokinetic and crossover feeding trials demonstrate substantial inter-individual variability in the conversion of ingested glucoraphanin into bioavailable sulforaphane and its urinary metabolites by gut microbiota. In clinical studies assessing pure glucoraphanin or glucoraphanin-rich preparations without active plant myrosinase, conversion efficiencies and urinary excretion rates typically range from low single digits (approx. 1% to 5%) to 20% on average, with individual ranges extending higher depending on baseline gut microbial enzymatic capacity, while preparations with active myrosinase or high microbial activity reach up to 40% to 70%.
- supports: Bioavailability of Sulforaphane from two broccoli sprout beverages: results of a short-ter… (Cancer prevention research (Philadelphia, Pa.) 2011) · cited 207x in the literature
"Bioavailability, as measured by urinary excretion of sulforaphane and its metabolites (in approximately 12-hour collections after dosing), was substantially greater with the SFR (mean = 70%) than with GRR (mean = 5%) beverages. Interindividual variability in excretion was considerably lower with SFR than with GRR beverage." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Exogenous myrosinase from mustard seed increases bioavailability of sulforaphane from a gl… (Scientific reports 2026) · cited 3x in the literature
"Inactive glucoraphanin (GR) in broccoli is converted to the antioxidant, anti-inflammatory, and anti-bacterial sulforaphane (SF) by cruciferous vegetable enzyme myrosinase (Myr), or similar enzymes from specific gut bacteria; both sources have variable efficiency." (abstract, results, passage verified)
pubmedfull study (doi)
Moringa, daikon radish, mustard seed, wasabi, and horseradish are rich sources of the enzyme myrosinase.
"ground mustard seed, daikon, Japanese radish is good. Moringa actually has a a lot of, uh, myrosinase. There many cruciferous vegetables do... mustard seed has a very characteristic harsh, pungent taste, right? So does wasabi and horseradish, which are also really good sources of myrosinase." (said at 0:16:25)
Plant biochemistry and food science research confirms that plants of the order Brassicales, including Moringa oleifera (Moringaceae) and classic cruciferous vegetables (Brassicaceae) such as mustard seed, horseradish, wasabi, and daikon radish, contain active myrosinase (thioglucoside glucohydrolase). Studies demonstrate that Moringa oleifera tissues and seeds possess functional myrosinase with high affinity and catalytic activity toward glucosinolates, enabling the enzymatic conversion of glucosinolates into bioactive isothiocyanates.
Broccoli rabe does not contain significant amounts of glucoraphanin or sulforaphane.
"does broccoli rabe contain sulforaphane? Um, and Lucy, that's a great question if you're if you're there today. And the answer is no, it doesn't. And broccoli rabe is actually related to broccoli, but interestingly, it's not as closely related even as cauliflower or cabbage are to broccoli. And broccoli rabe does not have a significant amount of glucoraphanin or sulforaphane." (said at 0:18:10)
Broccoli rabe (rapini) belongs to the species Brassica rapa (subsp. rapa or sylvestris), whereas common broccoli, cabbage, and cauliflower are cultivars of Brassica oleracea. Phytochemical profiling shows that glucosinolate patterns differ substantially between Brassica species: while glucoraphanin (the precursor to sulforaphane) is the characteristic glucosinolate found in high concentrations in B. oleracea (specifically broccoli), B. rapa species predominantly synthesize other glucosinolates such as gluconapin, glucobrassicanapin, and progoitrin, lacking significant amounts of glucoraphanin and sulforaphane.
Cabbage and cauliflower contain essentially no glucoraphanin.
"for example, cabbage has essentially none; it's got other isothiocyanates that are good for you, many of them. Cauliflower has essentially none." (said at 0:19:05)
Phytochemical analyses of Brassica oleracea varieties confirm that while broccoli contains high concentrations of glucoraphanin (the precursor to sulforaphane), common cabbage and cauliflower contain negligible to undetectable levels of glucoraphanin. Instead, their glucosinolate profiles are dominated by other glucosinolates such as sinigrin (which converts to allyl isothiocyanate) and glucobrassicin (which converts to indole-3-carbinol).
- supports: Variation of glucosinolates in vegetable crops of Brassica oleracea. (Journal of agricultural and food chemistry 1999) · cited 594x in the literature
"The predominant glucosinolates in broccoli were 4-methylsulfinylbutyl glucosinolate (glucoraphanin), 3-butenyl glucosinolate (gluconapin), and 3-indolylmethyl glucosinoate (glucobrassicin)... In Brussels sprouts, cabbage, cauliflower, and kale, the predominant glucosinolates were sinigrin (8.9, 7.8, 9.3, and 10.4 micromol g(-1) DW, respectively) and glucobrassicin (3.2, 0.9, 1.3, and 1.2 micromol g(-1) DW, respectively)." (abstract, results)
pubmedfull study (doi)
Most kale varieties lack significant glucoraphanin, but Red Russian kale contains a substantial amount.
"Kale doesn't have glucoraphanin to any great extent, except, as I recall, there's one variety, Red Russian kale, that does have a substantial amount." (said at 0:19:17)
Standard kale cultivars (*Brassica oleracea* var. *acephala*, such as curly or lacinato kale) predominantly accumulate indole glucosinolates (like glucobrassicin) and generally contain minimal or negligible amounts of glucoraphanin, the aliphatic glucosinolate precursor to sulforaphane. In contrast, 'Red Russian' kale (*Brassica napus* var. *pabularia*) possesses an aliphatic glucosinolate biosynthetic profile that yields substantial amounts of glucoraphanin.
In a 12-week clinical study in China, daily administration of glucoraphanin and sulforaphane maintained upregulation of the phase 2 detoxification response without fatiguing.
"One thing we do know from our work in China with with a study of air pollution and the effects of sulforaphane on that is that you don't fatigue—and this is fortunate, but you don't fatigue this the biochemical response system. So we gave for 12 weeks we gave daily glucoraphanin and sulforaphane and monitored the upregulation of the this protective response, um, and did not really see any fatiguing of the of the the response of that system." (said at 0:22:15)
In a 12-week randomized, placebo-controlled trial conducted in Qidong, China (n = 291), daily consumption of a broccoli sprout beverage delivering 600 µmol glucoraphanin and 40 µmol sulforaphane resulted in rapid and sustained increases in the excretion of glutathione-derived conjugates of airborne pollutants (benzene by 61% and acrolein by 23%). Measures of sulforaphane metabolites and pollutant excretion showed no attenuation or fatiguing of the detoxification response over the 12-week intervention period.
- supports: Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: res… (Cancer prevention research (Philadelphia, Pa.) 2014) · cited 191x in the literature
"A broccoli sprout-derived beverage providing daily doses of 600 μmol glucoraphanin and 40 μmol sulforaphane was evaluated for magnitude and duration of pharmacodynamic action in a 12-week randomized clinical trial. Two hundred and ninety-one study participants were recruited from the rural He-He Township, Qidong, in the Yangtze River delta region of China... Rapid and sustained, statistically significant (P ≤ 0.01) increases in the levels of excretion of the glutathione-derived conjugates of benzene (61%), acrolein (23%), but not crotonaldehyde, were found in those receiving broccoli sprout beverage compared with placebo... Measures of sulforaphane metabolites in urine indicated that bioavailability did not decline over the 12-week daily dosing period." (abstract, results, passage verified)
pubmedfull study (doi)
In a clinical trial in China, sulforaphane supplementation increased 24-hour urinary excretion of benzene by 60% and acrolein by about 23%.
"your study showed that within 24 hours, benzene excretion was excreted by 60 percent, and acrolein study was increased—actual acrolein excretion was increased by 20 about 23 percent." (said at 0:23:40)
A 12-week randomized, placebo-controlled clinical trial conducted in Qidong, China (n = 291) evaluated a broccoli sprout-derived beverage delivering glucoraphanin and sulforaphane. The trial demonstrated rapid and sustained, statistically significant increases in the urinary excretion of mercapturic acid metabolites of airborne pollutants: benzene excretion increased by 61% and acrolein excretion increased by 23% compared with placebo.
Post-mortem brain examinations of infants, children, and adolescents exposed to air pollution in Mexico City revealed amyloid-beta plaques and early neurodegenerative pathological changes.
"there was a study in Mexico City where air pollution is terrible, and children—so they've been doing post-mortem, you know, studies looking in the brain of, unfortunately, infants and children and young adolescents that have that have died for whatever reason, and they have amyloid-beta plaques in their brain as early as infancy, and other, you know, pathological changes in the brain going on early, early in life" (said at 0:26:58)
Autopsy studies led by Lilian Calderón-Garcidueñas examining children, adolescents, and young adults who died suddenly in Metropolitan Mexico City found early neurodegenerative changes. These post-mortem examinations demonstrated hyperphosphorylated tau, amyloid-beta accumulation, diffuse amyloid plaques, and neuroinflammation in pediatric brain samples, including early tau pre-tangle pathology observed in infants as young as 11 months old. Because these observations come from autopsy case series comparing exposed individuals to control subjects, the certainty of evidence for a direct causal link is low due to observational design constraints.
- supports: Long-term air pollution exposure is associated with neuroinflammation, an altered innate i… (Toxicologic pathology 2008) · cited 938x in the literature
"Exposure to air pollution causes neuroinflammation, an altered brain innate immune response, and accumulation of Abeta42 and alpha-synuclein starting in childhood." (abstract, conclusions, passage verified)
pubmedfull study (doi) - supports: Neuroinflammation, hyperphosphorylated tau, diffuse amyloid plaques, and down-regulation o… (Journal of Alzheimer's disease : JAD 2012) · cited 281x in the literature
"Forty percent exhibited tau hyperphosphorylation with pre-tangle material and 51% had amyloid-β (Aβ) diffuse plaques compared with 0% in controls." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Hallmarks of Alzheimer disease are evolving relentlessly in Metropolitan Mexico City infan… (Environmental research 2018) · cited 144x in the literature
"Subcortical pretangle stage b was identified in an 11month old baby. Cortical tau pre-tangles, neurofibrillary tangles (NFT) Stages I-II, amyloid phases 1-2, Htau in substantia nigrae, auditory, oculomotor, trigeminal and autonomic systems were identified by the 2nd decade." (abstract, results, passage verified)
pubmedfull study (doi)
Animal studies show that sulforaphane activation of the Nrf2 protective pathway persists for at least two days.
"I know that the animal studies have shown that the Nrf2 protective pathway is activated for at least two days." (said at 0:29:45)
Animal and preclinical experimental studies demonstrate that sulforaphane activates the Nrf2-ARE cytoprotective pathway and sustains downstream phase II antioxidant enzyme expression (such as heme oxygenase-1 and NQO1) for at least 48 hours (two days) following administration, despite the parent compound being cleared rapidly.
Sulforaphane demonstrates protective effects in preclinical models of traumatic brain injury and spinal cord injury.
"Like when we talk about traumatic brain injury and spinal cord injury, there is an absolutely pronounced effect of sulforaphane that we we have seen in a variety of studies, we and others." (said at 0:25:12)
Preclinical animal studies demonstrate that sulforaphane provides neuroprotective effects in both traumatic brain injury (TBI) and spinal cord injury (SCI) models. In rodent models of TBI, post-injury administration of sulforaphane reduces blood-brain barrier permeability, decreases cerebral edema, and improves cognitive performance via Nrf2-driven antioxidant pathways. In rodent models of contusive spinal cord injury, sulforaphane suppresses inflammatory cytokine expression, reduces secondary tissue damage, and significantly improves hindlimb locomotor recovery. Because the evidence is derived entirely from animal models, clinical efficacy in humans remains unestablished.
- supports: Sulforaphane improves cognitive function administered following traumatic brain injury. (Neuroscience letters 2009) · cited 146x in the literature
"When administered following traumatic brain injury (TBI), sulforaphane has been demonstrated to attenuate blood-brain barrier permeability and reduce cerebral edema... Our results indicate that sulforaphane treatment improves performance in the Morris water maze task (as indicated by decreased latencies during learning and platform localization during a probe trial) and reduces working memory dysfunction" (abstract, results)
pubmedfull study (doi) - supports: Neuroprotective effects of sulforaphane after contusive spinal cord injury. (Journal of neurotrauma 2012) · cited 88x in the literature
"SF (50 mg/kg) treatment resulted in both acute and long-term beneficial effects, including upregulation of the phase 2 antioxidant response at the injury site, decreased mRNA levels of inflammatory cytokines (i.e., MMP-9) in the injured spinal cord, inactivation of urinary MIF tautomerase activity, enhanced hindlimb locomotor function, and an increased number of serotonergic axons caudal to the lesion site. These findings demonstrate that SF provides neuroprotective effects in the spinal cord after injury" (abstract, results, passage verified)
pubmedfull study (doi)
Upregulation of protective detoxification enzymes induced by sulforaphane persists in the body for hours to several days.
"We know that the elevation of these enzymes lasts for at least hours and certainly, in most cases, days—a few days." (said at 0:28:43)
Sulforaphane activates the nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway, leading to the upregulation of cytoprotective and phase II detoxification enzymes. Although sulforaphane itself is rapidly metabolized and eliminated from the body within hours, the induced enzymatic proteins possess longer biological half-lives, allowing the elevated enzyme levels and protective activity to persist for hours to a few days.
Glutathione is an endogenous tripeptide made up of three amino acids and is present at high levels in the retina and macula of the eye.
"Glutathione is the body's most most predominant detoxification mechanism. It is present at very high levels in in things like the macula of the eye, the back of the eye, in the retina. And it is it's a tripeptide, meaning it's made up of only three amino acids." (said at 0:33:15)
The claim is supported by biochemical literature and ocular research. Glutathione (GSH) is a tripeptide composed of three amino acids (glutamate, cysteine, and glycine) that serves as a primary endogenous antioxidant and detoxification agent throughout human tissues, particularly in high-metabolic tissues exposed to phototoxic and oxidative stress such as the retina and macula.
Sulforaphane upregulates enzymes responsible for synthesizing and resynthesizing glutathione, increasing available reduced glutathione.
"But what sulforaphane does is it cranks up the enzymes that are responsible for synthesizing or resynthesizing glutathione, and so it makes more glutathione available. And once glutathione is sacrificed and oxidized, it remakes it." (said at 0:33:45)
Sulforaphane activates the Nrf2 signaling pathway, which directly upregulates the expression of key enzymes involved in both de novo glutathione synthesis (such as the catalytic and modifier subunits of glutamate-cysteine ligase, GCLC/GCLM, and glutathione synthetase) and glutathione recycling/resynthesis from its oxidized state (glutathione reductase, GR/GSR). This mechanism has been demonstrated in human tissue models and in vivo animal studies, resulting in increased intracellular reduced glutathione (GSH) levels.
- supports: Oxidative Damage Control in a Human (Mini-) Organ: Nrf2 Activation Protects against Oxidat… (The Journal of investigative dermatology 2017) · cited 105x in the literature
"Microarray and qRT-PCR analysis of human hair follicles after Nrf2 activation using sulforaphane identified the modulation of phase II metabolism, reactive oxygen species clearance, the pentose phosphate pathway, and glutathione homeostasis. Nrf2 knockdown (small interfering RNA) in cultured human hair follicles confirmed the regulation of key Nrf2 target genes (i.e., heme oxygenase-1, NAD(P)H dehydrogenase, quinone 1, glutathione reductase, glutamate-cysteine ligase catalytic subunit, ABCC1, peroxiredoxin 1)." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Sulforaphane prevents diabetes-induced hepatic ferroptosis by activating Nrf2 signaling ax… (BioFactors (Oxford, England) 2024) · cited 20x in the literature
"Results showed that diabetes-induced inactivation of Nrf2 and decreased expression of its downstream antiferroptotic molecules critical for antioxidative defense (catalase, superoxide dismutases, thioredoxin reductase), iron metabolism (ferritin heavy chain (FTH1), ferroportin 1), glutathione (GSH) synthesis (cystine-glutamate antiporter system, cystathionase, glutamate-cysteine ligase catalitic subunit, glutamate-cysteine ligase modifier subunit, glutathione synthetase), and GSH recycling - glutathione reductase (GR) were reversed/increased by sulforaphane treatment." (abstract, results, passage verified)
pubmedfull study (doi)
A 2018 clinical study found that 17.7 milligrams of sulforaphane daily for one week increased blood glutathione levels, correlating with increased glutathione in certain brain regions of healthy subjects.
"And they found that about 17.7 milligrams of sulforaphane per day for one week increased blood glutathione levels, and this correlated with an increased glutathione in certain brain regions. And these were in healthy people." (said at 0:36:40)
A 2018 clinical pilot study by Sedlak et al. evaluated the effects of 7 days of daily oral sulforaphane (100 µmol, approximately 17.7 mg) in healthy human subjects. The researchers demonstrated that 7-day administration increased blood glutathione (GSH) levels and that the ratio of post- to pre-treatment blood GSH significantly correlated with increases in thalamic GSH measured via 7-Tesla magnetic resonance spectroscopy. Because this was a small pilot clinical study without a randomized placebo control group, the overall certainty is low.
- supports: Sulforaphane Augments Glutathione and Influences Brain Metabolites in Human Subjects: A Cl… (Molecular neuropsychiatry 2018) · cited 79x in the literature
"We found that the naturally occurring isothiocyanate sulforaphane increased blood GSH levels in healthy human subjects following 7 days of daily oral administration. In parallel, we explored the potential influence of sulforaphane on brain GSH levels in the anterior cingulate cortex, hippocampus, and thalamus via 7-T magnetic resonance spectroscopy. A significant positive correlation between blood and thalamic GSH post- and pre-sulforaphane treatment ratios was observed, in addition to a consistent increase in brain GSH levels in response to treatment." (abstract, results, passage verified)
pubmedfull study (doi)
When ingested, sulforaphane is rapidly taken up by human cells, conjugated with glutathione, and excreted into urine.
"You ingest it, you take it in, the body sees it, your cells of your body see it, they actually take it in very rapidly, they conjugate it with glutathione, they spit it back out. Then where does it go? It goes from the blood to the urine." (said at 0:45:20)
Pharmacokinetic and clinical metabolic studies confirm that ingested sulforaphane is rapidly absorbed and enters human cells, where it is conjugated with glutathione (primarily via glutathione S-transferases). The resulting glutathione conjugates are exported from cells and further metabolized through the mercapturic acid pathway before being excreted into the urine, largely as sulforaphane-N-acetylcysteine conjugates.
- supports: Analysis of isothiocyanate mercapturic acids in urine: a biomarker for cruciferous vegetab… (Journal of agricultural and food chemistry 2003) · cited 37x in the literature
"Cruciferous vegetables contain glucosinolates, which are degraded to isothiocyanates. These are easily absorbed, conjugated to glutathione, and excreted into the urine as their corresponding mercapturic acids." (abstract, background, passage verified)
pubmedfull study (doi) - supports: Glutathione S-transferase M1 polymorphism and metabolism of sulforaphane from standard and… (The American journal of clinical nutrition 2005) · cited 317x in the literature
"Liquid chromatography linked to tandem mass spectrometry was used to quantify sulforaphane and its thiol conjugates in plasma and urine." (abstract, methods, passage verified)
pubmedfull study (doi) - supports: Bioactive sulforaphane from cruciferous vegetables: advances in biosynthesis, metabolism, … (Critical reviews in food science and nutrition 2025) · cited 34x in the literature
"SFN exerts its biological functions through the hydrolysis of glucosinolates by gut microbiota, and exhibits rapid metabolism and excretion characteristics via metabolization of mercapturic acid pathway." (abstract, results, passage verified)
pubmedfull study (doi)
A clinical trial at Zhejiang University was posted to examine sulforaphane in 160 subjects with early Alzheimer's disease with an intended start date in May 2020.
"there is one now, there's one posted clinical trial in China in Zhejiang University, and it will be looking at 160 160 subjects with early Alzheimer's, and they're going to be giving sulforaphane. It was posted for a start date of sometime in May of 2020." (said at 0:49:40)
A clinical trial registered on ClinicalTrials.gov (NCT04213391) was posted by the Second Affiliated Hospital, School of Medicine, Zhejiang University, titled "Efficacy and Safety of Sulforaphane in the Treatment of Prodromal Alzheimer's Disease". The trial registration specifies an enrollment target of 160 participants with prodromal/early Alzheimer's disease and an estimated study start date of May 2020.
Broccoli seeds contain approximately one-third fat or oils and are very rich in erucic acid, an omega-9 fatty acid.
"So broccoli seeds are about a third fat or oils, and they're very rich in erucic acid." (said at 0:55:15)
Published compositional analyses of broccoli (Brassica oleracea) seeds confirm that seeds typically contain approximately 30% to 35% oil by weight (about one-third fat) and that the oil is particularly rich in erucic acid (a 22-carbon monounsaturated omega-9 fatty acid), which serves as its predominant fatty acid constituent (typically comprising ~30–50% of total fatty acids).
Erucic acid has been associated with cardiac toxicities in animal studies.
"I mean, it's been associated with cardiac toxicities in some animal studies, um but I I think the jury sort of is still out on the effects in humans." (said at 0:57:50)
Animal studies have consistently demonstrated that dietary erucic acid is associated with cardiac toxicity, particularly myocardial lipidosis (accumulation of fat droplets in cardiac myocytes) and subsequent myocardial fibrosis in rodents and other animals. These animal findings served as the basis for regulatory intake limits (such as those established by the US FDA and EFSA). However, direct evidence of cardiac toxicity in humans remains limited and inconclusive, with epidemiological and clinical findings showing mixed or conflicting results regarding human cardiovascular outcomes.
- supports: A review on neuropharmacological role of erucic acid: an omega-9 fatty acid from edible oi… (Nutritional neuroscience 2022) · cited 47x in the literature
"Erucic acid an omega 9 fatty acid, which is obtained from edible oils has proven to cause myocardial lipidosis, heart lesions and hepatic steatosis in animals therefore, its content in edible oils is restricted to certain levels by regulatory agencies." (abstract, passage verified)
pubmedfull study (doi) - supports: Mustard oil and cardiovascular health: Why the controversy? (Journal of clinical lipidology 2022) · cited 28x in the literature
"It contains a large proportion of erucic acid, a fatty acid associated with myocardial lipidosis in rodents. This evidence prompted the US Food and Drug Administration (FDA) to ban the use of mustard oil for cooking." (abstract, passage verified)
pubmedfull study (doi) - supports: Paradoxical Effects of Erucic Acid-A Fatty Acid With Two-Faced Implications. (Nutrition reviews 2025) · cited 9x in the literature
"The consumption of EA-rich food has been reported to have adverse effects on health, particularly myocardial lipidosis and hepatic steatosis. Consequently, several countries, including the United States, European countries, New Zealand, and Australia, set limits on their daily intake... In contrast, limited studies on humans have reported a protective role of MO in acute myocardial infarction, ischemic heart disease, and neurologic disorders." (abstract, passage verified)
pubmedfull study (doi)
Preclinical rat studies demonstrate that administration of isothiocyanates prior to chemical carcinogen exposure prevents bladder cancer development or significantly reduces tumor size.
"the rats were given sulforaphane, they were given it before they were given a chemical that causes bladder cancer, and the other group of rats were just given the chemical that causes bladder cancer, and the rats that were given the dose of the sulforaphane did not develop bladder cancer, and one and if they did, the tumors were much, much smaller in size." (said at 0:43:00)
Preclinical rat studies support the claim. In a classic animal model of chemical bladder carcinogenesis induced by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), dietary administration of an isothiocyanate-rich extract (freeze-dried aqueous extract of broccoli sprouts, high in glucoraphanin/sulforaphane and other isothiocyanates) significantly and dose-dependently inhibited bladder cancer development. The extract reduced tumor incidence, multiplicity, size, and progression in rats, linked to local induction of phase II detoxification enzymes (GST and NQO1) due to high urinary excretion of isothiocyanates. Because the evidence is derived exclusively from preclinical rodent models, the GRADE certainty is very low for clinical human outcomes.
In preclinical neurodegenerative disease models, sulforaphane inhibits histone deacetylase (HDAC), enhances brain-derived neurotrophic factor (BDNF), and reduces amyloid-beta levels.
"with a former doctoral student Anita Panjwani, we did a review a couple of years ago looking at actually all of the neurodegenerative diseases like Parkinson's and Alzheimer's and Huntington's, and the neurodevelopmental diseases like autism, and looking at the evidence for sulforaphane. And it's extensive. And, you know, things like HDAC inhibition, histone deacetylase, sorry, inhibition, enhancement of BDNF, brain-derived neurotrophic factor, um certainly uh reduction in amyloid beta" (said at 0:52:00)
Preclinical evidence supports the claim that sulforaphane inhibits histone deacetylase (HDAC) activity and enhances brain-derived neurotrophic factor (BDNF) expression in neuronal cell cultures and animal models of Alzheimer's disease (such as 3xTg-AD mice). Literature reviews examining sulforaphane in neurologic and neurodegenerative disease models further document these bioactivities alongside reductions in amyloid-beta burden. Because this evidence is derived from animal and in vitro models, the grade of certainty for clinical efficacy in humans remains low.
- supports: Sulforaphane epigenetically enhances neuronal BDNF expression and TrkB signaling pathways. (Molecular nutrition & food research 2017) · cited 76x in the literature
"Sulforaphane enhanced neuronal BDNF expression and increased levels of neuronal and synaptic molecules such as MAP2, synaptophysin, and PSD-95 in primary cortical neurons and 3 × Tg-AD mice. Sulforaphane elevated levels of synaptic TrkB signaling pathway components, including CREB, CaMKII, ERK, and Akt in both primary cortical neurons and 3 × Tg-AD mice. Sulforaphane increased global acetylation of histone 3 (H3) and H4, inhibited HDAC activity, and decreased the level of HDAC2 in primary cortical neurons." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Crucifers and related vegetables and supplements for neurologic disorders: what is the evi… (Current opinion in clinical nutrition and metabolic care 2018) · cited 32x in the literature
"This evidence includes at least nine clinical studies of neurodevelopmental conditions like autism spectrum disorder and schizophrenia, and there are a great many studies in animal model systems, of neurodegenerative disorders like Alzheimer's and Parkinson's diseases." (abstract, background, passage verified)
pubmedfull study (doi)
Methylglyoxal is a precursor to advanced glycation end products (AGEs) associated with Alzheimer's disease.
"sulforaphane protecting cultured neural cells from the toxicity of methylglyoxal, which is a precursor of AGEs or advanced glycation end products that are very clearly associated with Alzheimer's disease" (said at 0:52:41)
Methylglyoxal (MG) is a major, highly reactive dicarbonyl precursor in the formation of advanced glycation end products (AGEs), and elevated levels of both methylglyoxal and AGEs are consistently found in the brains and cerebrospinal fluid of patients with Alzheimer's disease. Furthermore, in vitro studies confirm that sulforaphane protects cultured neural cells (such as SH-SY5Y neuroblastoma cells) from methylglyoxal-induced cytotoxicity by upregulating the glyoxalase 1 detoxification system, increasing glutathione levels, and suppressing downstream neuroinflammatory pathways.
- supports: Neuroprotective effect of sulforaphane against methylglyoxal cytotoxicity. (Chemical research in toxicology 2015) · cited 93x in the literature
"Methylglyoxal is the most potent precursor of AGEs, and high levels of methylglyoxal have been found in the cerebrospinal fluid of AD patients. Methylglyoxal may contribute to AD both inducing extensive protein cross-linking and mediating oxidative stress. The aim of this study was to investigate the role of sulforaphane, an isothiocyanate found in cruciferous vegetables, in counteracting methylglyoxal-induced damage in SH-SY5Y neuroblastoma cells. The data demonstrated that sulforaphane protects cells against glycative damage by inhibiting activation of the caspase-3 enzyme, reducing the phosphorylation of MAPK signaling pathways (ERK1/2, JNK, and p38), reducing oxidative stress, and increasing intracellular glutathione levels." (abstract, background and results, passage verified)
pubmedfull study (doi) - supports: Methylglyoxal, a Knot to Be Untied in Brain Glucose Hypometabolism. (Metabolites 2025) · cited 1x in the literature
"More recently, methylglyoxal (MG), a highly reactive glycolytic byproduct, has gained attention as a critical mediator of AGE formation and an independent contributor to cellular distress, particularly in the context of diabetes mellitus and Alzheimer's disease." (abstract, background, passage verified)
pubmedfull study (doi)
Glucoraphanin concentration is highest in broccoli seeds, declines on a fresh weight basis during germination and sprouting, plateaus at a low level, and increases again when the plant flowers and sets seed.
"we knew that it was broccoli seeds which had the very highest levels of glucoraphanin, and they declined as you sprouted those seeds on a fresh weight basis until, you know, they plateaued for a couple of weeks very low, and then they started to climb again when the broccoli plants started to make flowers and seeds." (said at 0:55:44)
Plant developmental (ontogenetic) studies in broccoli (*Brassica oleracea* var. *italica*) confirm that glucosinolate (primarily glucoraphanin) concentrations are highest in non-germinated seeds, decline progressively on a fresh weight basis during germination and sprout development, and remain lower during early vegetative growth before accumulating again in reproductive tissues (inflorescences, flowers, and newly developing seeds).
Myrosinase enzyme in frozen broccoli sprouts remains viable and resumes enzymatic conversion of glucoraphanin to sulforaphane upon thawing.
"The myrosinase will stay active um and start It won't be reactive in the freezer, probably inactive, but it'll start working again when you when you thaw when you thaw that that paste or whatever" (said at 1:01:30)
Freezing unblanched Brassica tissue (such as broccoli sprouts or fresh broccoli preparations) preserves endogenous myrosinase activity. While sub-zero temperatures halt enzymatic reactions, the enzyme remains intact and resumes hydrolysis of glucoraphanin into sulforaphane once thawed and cell integrity is disrupted. In contrast, commercial frozen broccoli typically lacks active myrosinase because industrial processing includes a heat-blanching step that denatures the heat-sensitive enzyme prior to freezing.
- context: Isothiocyanate concentrations and interconversion of sulforaphane to erucin in human subje… (Molecular nutrition & food research 2012) · cited 127x in the literature
"Sulforaphane bioavailability was about tenfold higher for the soups made from fresh compared to frozen broccoli, and the reduction was shown to be due to destruction of myrosinase activity by the commercial blanching-freezing process." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Modifying the processing and handling of frozen broccoli for increased sulforaphane format… (Journal of food science 2013) · cited 34x in the literature
"We hypothesized that this was because the necessary hydrolyzing enzyme myrosinase was destroyed during blanching, as part of the processing that frozen broccoli undergoes... We considered that thawing frozen broccoli might disrupt membrane integrity, allowing myrosinase and glucoraphanin to come into contact." (abstract, results)
pubmedfull study (doi) - supports: Isothiocyanates from Brassica Vegetables-Effects of Processing, Cooking, Mastication, and … (Molecular nutrition & food research 2018) · cited 97x in the literature
"The formation of health-beneficial isothiocyanates (ITCs) from glucosinolates depends on a wide variety of plant-intrinsic factors (e.g., concentration of glucosinolates, activity of myrosinase, and specifier proteins) and on a multitude of extrinsic postharvest factors such as the conditions used during industrial processing, domestic preparation, mastication, and digestion." (abstract, background, passage verified)
pubmedfull study (doi)
Whole broccoli sprouts contain dietary fiber, vitamins, and minerals that are absent in purified sulforaphane supplements.
"you get all the fiber, you know, you get the vegetable fiber if you eat the sprouts, which you don't get with supplements, um and you know, you get vitamins and you get minerals" (said at 1:03:55)
Whole broccoli sprouts are whole plant foods that provide dietary fiber, essential minerals, vitamins, and other macro- and micronutrients as part of their intact plant matrix. Purified sulforaphane supplements contain isolated or concentrated bioactive phytochemicals without the dietary fiber and broad nutrient matrix found in the whole vegetable.
- supports: The Anti-Inflammatory Effects of Broccoli ( Brassica oleracea L. var. italica) Sprout Extr… (Current issues in molecular biology 2023) · cited 13x in the literature
"Brassica oleracea var. italica (broccoli), a member of the cabbage family, is abundant with many nutrients, including vitamins, potassium, fiber, minerals, and phytochemicals." (abstract, introduction, passage verified)
pubmedfull study (doi) - supports: Germination as a Sustainable Green Pre-Treatment for the Recovery and Enhancement of High-… (Molecules (Basel, Switzerland) 2026) · cited 3x in the literature
"This study evaluated the impact of germination on Cruciferous vegetables (family Cruciferae or Brassicaceae ) broccoli and kale by assessing changes in proximate composition, macro- and microelement profiles, total and individual polyphenols, phytic acid content..." (abstract, methods, passage verified)
pubmedfull study (doi)
Intact, freshly harvested broccoli and broccoli sprouts contain no free sulforaphane, only its precursor glucoraphanin.
"when you harvest broccoli sprouts or broccoli, you or a farmer, they don't have any sulforaphane in them. They don't have any free sulforaphane; it's all glucoraphanin, which is the precursor of sulforaphane." (said at 1:09:00)
Intact, undamaged broccoli and broccoli sprouts contain glucosinolates (predominantly glucoraphanin) rather than free sulforaphane. In the intact plant tissue, glucoraphanin and the hydrolytic enzyme myrosinase are segregated in separate cellular compartments. Free sulforaphane is only synthesized when plant tissue is disrupted (e.g., by chewing, crushing, or mechanical processing), allowing myrosinase to encounter and hydrolyze glucoraphanin.
Myrosinase enzyme in broccoli is preserved during microwaving as long as the internal temperature remains below 70 to 80 degrees Celsius.
"there's evidence that there's, you know, you may not completely wipe out the myrosinase if you don't get the internal temperature of the food product up above 70 or 80 degrees centigrade, Celsius." (said at 1:09:33)
Experimental food chemistry studies confirm that myrosinase in Brassica vegetables (including broccoli) is heat-sensitive but retains substantial enzymatic activity if internal cooking temperatures do not exceed roughly 70–80 °C. Studies examining thermal processing demonstrate that mild heat treatments (such as blanching or controlled microwave heating at approximately 76 °C) preserve the majority of myrosinase activity and sulforaphane-generating capacity, whereas temperatures of 86 °C and above lead to complete thermal inactivation.
- supports: Glucosinolates and myrosinase activity in red cabbage (Brassica oleracea L. var. Capitata … (Journal of agricultural and food chemistry 2004) · cited 180x in the literature
"Substantial myrosinase activity was retained in cabbage treated at low (24 min, 180 W) and intermediate microwave powers (8 min, 540 W) while microwave cooking for 4.8 min at 900 W (259.2 kJ energy input) resulted in a complete loss of hydrolytic activity. In this respect, differences in observed temperature profiles of the various microwave treatments play an important role." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Modifying the processing and handling of frozen broccoli for increased sulforaphane format… (Journal of food science 2013) · cited 34x in the literature
"Blanching at 86 °C or higher inactivated peroxidase, lipoxygenase, and myrosinase. Blanching at 76 °C inactivated 92% of lipoxygenase activity, whereas there was only an 18% loss in myrosinase-dependent sulforaphane formation." (abstract, results, passage verified)
pubmedfull study (doi)
Microwaving broccoli causes less leaching of phytochemicals and plant juice into cooking liquid compared to boiling or heavy steaming.
"Microwaving also gives you minimal leakage of uh plant juice, so, you know, when you steam the hell out of something or boil a vegetable, you know, most of the goodies come out in the wash, they come out in the pot liquor, right?" (said at 1:09:47)
Food chemistry research demonstrates that boiling Brassica vegetables like broccoli causes substantial losses of water-soluble phytochemicals (such as glucosinolates) primarily through diffusion and leaching into the cooking liquid. In contrast, cooking methods requiring minimal or no added water, such as microwaving and steaming, result in minimal leaching and significantly higher retention of phytochemicals.
- supports: Effect of storage, processing and cooking on glucosinolate content of Brassica vegetables. (Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 2007) · cited 315x in the literature
"Cooking by steaming, microwaving and stir-fry did not produce significant loss of glucosinolates whereas boiling showed significant losses by leaching into cooking water. Most of the loss of the glucosinolates (approximately 90%) was detected in the cooking water." (abstract, results, passage verified)
pubmedfull study (doi) - supports: A mechanistic perspective on process-induced changes in glucosinolate content in Brassica … (Critical reviews in food science and nutrition 2015) · cited 108x in the literature
"Boiling and blanching considerably reduce the glucosinolate content mainly due to mechanisms of cell lysis, diffusion, and leaching, and partly due to thermal and enzymatic degradation. Steaming, microwave processing, and stir frying either retain or slightly reduce the glucosinolates content due to low degrees of leaching" (abstract, passage verified)
pubmedfull study (doi)
The primary isothiocyanate found in moringa is moringin.
"In terms of efficacy, the isothiocyanate from moringa, it's called moringin, and there is a long scientific name I won't bore you with" (said at 1:16:47)
The statement is supported by established phytochemical and biochemical research. The primary isothiocyanate derived from Moringa oleifera is moringin (scientifically designated as 4-[(α-L-rhamnosyloxy)benzyl]isothiocyanate), which is generated via the myrosinase-mediated hydrolysis of its glucosinolate precursor, glucomoringin.
- supports: A Strategy to Deliver Precise Oral Doses of the Glucosinolates or Isothiocyanates from Mor… (Nutrients 2019) · cited 51x in the literature
"These phytochemicals, especially the glucosinolate glucomoringin and the isothiocyanate moringin, produced from it following hydrolysis by the enzyme myrosinase, provide potent anti-inflammatory and cytoprotective indirect antioxidant activity." (abstract, passage verified)
pubmedfull study (doi) - supports: Moringin, A Stable Isothiocyanate from Moringa oleifera , Activates the Somatosensory and … (Molecules (Basel, Switzerland) 2020) · cited 50x in the literature
"It is characterized by the presence of glucosinolates and isothiocyanates; the stable isothiocyanate 4-[(α-l-rhamnosyloxy)benzyl]isothiocyanate (moringin) has been widely studied for its bioactivity as hypoglycemic, antimicrobial, anticancer and in particular for its involvement in nociception and neurogenic pain." (abstract, passage verified)
pubmedfull study (doi)
Moringa leaves and moringa leaf powder have a documented history of safe human dietary consumption over centuries across tropical regions.
"moringa leaves have been grown and eaten for centuries, literally, by populations in the tropics around the world very safely. So the safety of moringa leaf powder or moringa leaves is absolutely well documented." (said at 1:17:47)
Moringa oleifera leaves and immature pods have an established history of dietary and traditional medicinal use across tropical and subtropical regions. Systematic reviews and toxicological evaluations of moringa leaf preparations and powders report a high degree of safety in animal models and clinical studies, with no significant adverse events noted at standard dietary or supplemental doses.
A review of six small clinical studies demonstrated an effect of moringa leaves or moringa leaf powder on blood glucose control.
"the biggest medical indication for moringa leaf powder is going to be, is, I think, diabetes, and that is under active investigation, blood glucose control. We have a review that shows there were six—not all good studies at all, and they were all tiny—showing an effect of moringa leaves or moringa leaf powder." (said at 1:20:56)
Reviews of clinical evidence evaluating Moringa oleifera leaves and leaf powder for blood glucose control confirm that available human research is limited to a small number of small clinical studies. While these preliminary trials report glycemic improvements or postprandial glucose reduction, systematic reviews emphasize that the studies are small, heterogeneous in design, and variable in quality, requiring larger randomized trials to establish therapeutic efficacy.
- supports: Moringa oleifera and glycemic control: A review of current evidence and possible mechanism… (Phytotherapy research : PTR 2019) · cited 40x in the literature
"In the conducted studies, moringa leaves have shown to reduce glycemia, without causing any adverse effects... However, these studies are limited in numbers and mostly conducted in animals, in vitro and in vivo." (abstract, results)
pubmedfull study (doi) - supports: Potential of Moringa oleifera to Improve Glucose Control for the Prevention of Diabetes an… (Nutrients 2020) · cited 85x in the literature
"Thirty-three animal studies and eight human studies were included. Water and organic solvent extracts of leaves and, secondly, seeds, have been extensively assayed in animal models, showing the hypoglycemic effect... In humans, clinical trials are scarce, with variable designs and testing mainly dry leaf powder alone or mixed with other foods or MO aqueous preparations." (abstract, results, passage verified)
pubmedfull study (doi)
Avmacol dietary supplements contain both glucoraphanin and active myrosinase enzyme to facilitate conversion to sulforaphane.
"Right, so Avmacol has glucoraphanin in it and it has myrosinase." (said at 1:22:52)
The statement is supported. Avmacol is a standardized commercial broccoli seed and sprout extract formulation containing both glucoraphanin (the glucosinolate precursor) and active myrosinase enzyme to enable enzymatic conversion of glucoraphanin into sulforaphane upon ingestion.
- supports: Bioavailability of Sulforaphane Following Ingestion of Glucoraphanin-Rich Broccoli Sprout … (Nutrients 2019) · cited 76x in the literature
"We examined whether gastric acidity would affect the activity of myrosinase, co-delivered with glucoraphanin (GR), to convert GR to sulforaphane (SF). A broccoli seed and sprout extract (BSE) rich in GR and active myrosinase was delivered before and after participants began taking the anti-acid omeprazole, a potent proton pump inhibitor." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Broccoli or Sulforaphane: Is It the Source or Dose That Matters? (Molecules (Basel, Switzerland) 2019) · cited 347x in the literature
"Present in the plant as its precursor, glucoraphanin, sulforaphane is formed through the actions of myrosinase, a β-thioglucosidase present in either the plant tissue or the mammalian microbiome." (abstract, introduction, passage verified)
pubmedfull study (doi) - supports: Randomized Crossover Trial Evaluating Detoxification of Tobacco Carcinogens by Broccoli Se… (Cancers 2022) · cited 16x in the literature
"Sulforaphane, released by hydrolysis of glucoraphanin, potently induces cytoprotective phase II enzymes. ... This randomized, crossover trial evaluated detoxification of tobacco carcinogens by the BSSE Avmacol® in otherwise healthy smokers. Participants were treated for 2 weeks with both low and higher-dose BSSE (148 µmol vs. 296 µmol of glucoraphanin daily)" (abstract, results)
pubmedfull study (doi)
Prostaphane is a commercially available French dietary supplement containing stabilized sulforaphane.
"Prostaphane has stabilized sulforaphane. Prostaphane is the only product that I know that reliably has what they say they have of sulforaphane, the amount they say they have, and it is stable, but it's a European product. It's a French product." (said at 1:27:42)
Prostaphane is a French dietary supplement formulated with Sulfodyne, a patented broccoli seed extract providing standardized and stabilized free sulforaphane. Peer-reviewed literature confirms that Sulfodyne represents a stabilized form of natural sulforaphane developed in France.
A synthetic stabilized form of sulforaphane developed by a UK company produced adverse side effects in laboratory experiments.
"There's a company in England that has something that's a non-natural, a synthetic sulforaphane that they've stabilized. We've actually done some experiments with that type of sulforaphane and found that there are some adverse side effects" (said at 1:29:10)
A synthetic, stabilized formulation of sulforaphane complexed with alpha-cyclodextrin (Sulforadex/SFX-01) was developed by a UK pharmaceutical company (Evgen Pharma). In published laboratory and clinical evaluation by Dr. Jed Fahey's group, oral ingestion of the alpha-cyclodextrin-stabilized sulforaphane resulted in gastrointestinal adverse side effects (6 of 10 volunteers reported mild stomach upset), and topical administration failed to induce cytoprotective enzymes in mouse skin compared to pure sulforaphane. Subsequent clinical evaluations of SFX-01 have likewise documented mild treatment-related gastrointestinal adverse events.
Free sulforaphane is an inherently unstable chemical molecule that degrades easily.
"It's a very unstable molecule inherently, which is one of the reasons why it does what it does in your body. So it's difficult to deliver, it's difficult to stabilize" (said at 1:29:35)
Free sulforaphane is well established in the chemical and food sciences literature as an inherently unstable and thermally labile isothiocyanate. In aqueous environments and at elevated temperatures, free sulforaphane degrades rapidly, which presents a documented challenge for formulating, stabilizing, and delivering the compound in functional foods and therapeutic preparations.
Moringin, the primary isothiocyanate found in Moringa, exhibits greater bioactivity or potency than sulforaphane in several laboratory assays.
"the isothiocyanate from moringa, it's called moringin, and there is a long scientific name I won't bore you with, but in many assays, it's even better than sulforaphane, and in others, it's not as good." (said at 1:17:17)
Comparative in vitro laboratory assays demonstrate that moringin (4-[(α-L-rhamnosyloxy)benzyl] isothiocyanate) exhibits higher potency than sulforaphane in certain assays (such as the inhibition of TNF-induced NF-κB activity) while showing comparable or lower activity in other endpoints (such as NQO1 induction or specific STAT-mediated signaling pathways). Because the evidence is derived entirely from preclinical cell-culture and biochemical assays, the GRADE certainty is very low.
Supplements that pair glucoraphanin with active myrosinase have higher conversion efficiency and require lower doses of glucoraphanin than formulations relying solely on gut microbiome myrosinase.
"if you're counting on your gut's myrosinase, your intestinal tract's myrosinase to do all of the conversion for a supplement, you're probably going to take a higher level of glucoraphanin, and if you're getting a product that has myrosinase in it, you don't need as much glucoraphanin because some of that conversion is theoretically going to happen based on what you've provided in the supplement tablet." (said at 1:27:06)
Clinical pharmacokinetic studies show that co-administering glucoraphanin with active plant myrosinase substantially increases the conversion rate and bioavailability of sulforaphane compared to consuming glucoraphanin alone (which relies on intestinal microbiome myrosinase activity). When active myrosinase is present, urinary sulforaphane metabolite recovery is typically 3- to 4-fold higher (roughly 30% to 65% of the administered dose vs. 10% to 24% for glucoraphanin delivered without active myrosinase), confirming that lower precursor doses are required when active enzyme is included in the formulation.
Heat exposure, such as from saunas or exercise, increases the Nrf2 pathway.
"Heat exposure, like from something like the sauna or even exercise, does increase the Nrf2 pathway" (said at 1:31:10)
Preclinical and mechanistic evidence demonstrates that heat stress (mild hyperthermia) and exercise both stimulate the Nrf2 (nuclear factor erythroid 2-related factor 2) antioxidant and cytoprotective signaling pathway via mild reactive oxygen species (ROS) production, acting through a hormetic mechanism. Cell models show that non-lethal heat shock activates Nrf2 expression and downstream antioxidant/autophagy defenses.
- supports: Traditional Health Practices May Promote Nrf2 Activation Similar to Exercise. (International journal of molecular sciences 2025)
"The redox-sensitive nuclear factor erythroid 2-related factor 2 (Nrf2) was identified as the key mediator of the cellular defense response. A similar adaptive response appears to occur in response to exposure to heat or cold, hyperbaric or hypobaric oxygen, cupping therapy, acupuncture, caloric restriction, and the consumption of polyphenol-rich plant-based foods or spices, and there is direct or indirect evidence for the involvement of Nrf2." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Thermotolerance induced by non-lethal heat shock at 40 °C is activated by mitochondrial RO… (Archives of biochemistry and biophysics 2026)
"Our results show that heat-derived ROS are linked to expression of master antioxidant regulator Nrf2. When Nrf2 was overexpressed or knocked down, Nrf2 expression was directly associated with protective ability of the adaptive response induced by mild heat stress (40 °C)." (abstract, results, passage verified)
pubmedfull study (doi)
Sulforaphane can increase heat shock proteins.
"sulforaphane can increase heat shock proteins" (said at 1:31:13)
Preclinical in vitro and animal studies demonstrate that sulforaphane can induce the heat shock response and upregulate heat shock proteins, including Hsp27, HSP70, HSP60, and HSP40, via heat shock factor 1 (HSF1) activation. Because the available evidence is restricted to cell culture and animal models with no clinical trials directly measuring this outcome in humans, certainty is rated as very low.
Sulforaphane can increase the excretion of benzene by 60% after 24 hours.
"sulforaphane can increase the excretion of benzene by 60% after 24 hours, as we discussed." (said at 1:31:46)
A 12-week randomized, placebo-controlled clinical trial in Qidong, China (n=291) found that daily consumption of a broccoli sprout-derived beverage rich in glucoraphanin and sulforaphane led to a rapid and sustained 61% increase in the urinary excretion of benzene-derived glutathione conjugates (mercapturic acids) compared to placebo, an effect observed from the first day of intervention. A follow-up dose-finding randomized trial confirmed a 63.2% increase in benzene mercapturic acid excretion in the highest-dose sprout beverage group.
There are published scientific papers demonstrating direct antiviral effects of sulforaphane.
"there's a direct antiviral effect. Duh, what epoch are we in now? The epoch of viral pandemics. There are a number of very good papers showing an antiviral effect." (said at 1:35:20)
Multiple published peer-reviewed studies have demonstrated direct antiviral activity of sulforaphane in preclinical models (in vitro cell cultures and animal models) against viruses including SARS-CoV-2 and influenza A. For example, research has shown that sulforaphane directly inhibits SARS-CoV-2 replication, binds and inhibits the SARS-CoV-2 main protease (Mpro), and reduces influenza A virus replication by interfering with nuclear export of viral ribonucleoproteins. However, while these preclinical publications exist and confirm the claim, robust clinical trials establishing sulforaphane as an effective antiviral therapy in humans remain limited.
- supports: NRF2 activators inhibit influenza A virus replication by interfering with nucleo-cytoplasm… (PLoS pathogens 2023) · cited 50x in the literature
"All compounds reduced viral titers in supernatants from A549 cells and vascular endothelial cells in the order of efficacy SEL>4OI>BARD = SFN, which correlated with their ability to prevent nucleo-cytoplasmic export of viral nucleoprotein and the host cell protein p53." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Effects of Sulforaphane on SARS‑CoV‑2 infection and NF‑κB dependent expression of genes in… (International journal of molecular medicine 2023) · cited 16x in the literature
"Molecular studies demonstrated that SFN i) inhibits the SARS-CoV-2 replication in infected Calu-3 cells, decreasing the production of the N-protein coding RNA sequences, ii) decreased NF-κB content in SARS-CoV-2 infected cells and inhibited the expression of NF-kB-dependent IL-1β and IL-8 gene expression." (abstract, results)
pubmedfull study (doi) - supports: Sulforaphane's Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2)-Dependent and -Independe… (Journal of respiratory biology and translational medicine 2024) · cited 3x in the literature
"Notably, epigallocatechin gallate (EGCG), sulforaphane (SFN), and dimethyl fumarate (DMF) exhibited significant antiviral effects, with SFN being the most effective. SFN did not impact viral entry but appeared to inhibit the main protease (M Pro ) of SARS-CoV-2, encoded by the Nsp5 gene, as indicated by two protease inhibition assays." (abstract, results, passage verified)
pubmedfull study (doi)
A 2019 study by Chartoumpekis analyzing blood samples from a 12-week continuous broccoli sprout sulforaphane trial found no negative effects on thyroid function, hormone status, or autoimmune status.
"they took the blood samples from this 12-week study where we gave them sulforaphane from broccoli sprouts and looked at indicators of thyroid status, hormone status, and autoimmune status and found absolutely no negative effects on thyroid function. ... The first author's name is Chartoumpekis and it was 2019, and you know, this is someone whose specialty is thyroid function." (said at 1:38:28)
A 2019 randomized clinical trial led by Chartoumpekis and colleagues analyzed serum samples from 45 female participants who received a daily broccoli sprout beverage enriched with sulforaphane and glucoraphanin for 84 days (12 weeks). The study measured thyroid-stimulating hormone (TSH), free thyroxine (FT4), thyroglobulin, and thyroid autoantibodies, finding no significant changes in thyroid hormone levels or thyroid autoimmunity status between the intervention and control groups.
A 2018 animal study found broccoli sprout extract caused no harmful effect on thyroid homeostasis (TSH, T3, T4) in iodine-deficient rats and had an antioxidant beneficial effect in hypothyroid rats.
"Moreover, in 2018, there was a very long-term animal study in rats where there were two groups of rats: there were some rats that had hypothyroidism, drug-induced hypothyroidism, and then there was an iodine-deficient group of rats. And they were given broccoli sprouts, freeze-dried or broccoli sprout extract, and not only was there no harmful effect on the thyroid even in iodine-deficient animals in terms of their thyroid homeostasis—so their TSH, their T3, T4 were all the same in the animals—in the rats that had hypothyroidism, there was a beneficial effect from the broccoli sprouts in the thyroid gland, an antioxidant effect that was beneficial." (said at 1:39:34)
A 2018 animal study by Paśko et al. evaluated the long-term effects of broccoli sprout ingestion in rat models of hypothyroidism (induced either by iodine deficiency or by the antithyroid drug sulfadimethoxine). The researchers observed that serum TSH, free T3, and free T4 levels remained unchanged after broccoli sprout consumption, showing no harmful disruption to thyroid hormone homeostasis even in iodine-deficient animals. Furthermore, broccoli sprouts enhanced thioredoxin reductase (TR) activity and exerted a protective, beneficial effect on the antioxidant balance of the thyroid gland in hypothyroid rats. Because these findings are derived from an animal model, the overall certainty of evidence regarding clinical human outcomes is very low.
- supports: Effect of broccoli sprouts on thyroid function, haematological, biochemical, and immunolog… (Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2018) · cited 19x in the literature
"Under the study in a long-term experiment broccoli sprouts were tested as an element of rats diet, combined with deficient iodine, or sulfadimethoxine ingestion - two models of hypothyroidism... The levels of TSH, fT3 and fT4 remained unchanged following broccoli sprouts ingestion, which was even found to have a protective effect against sulfadimethoxine induced thyroid damage. Moreover, TR activity significantly increased in response to sprouts ingestion. In animals with hypothyroidism, broccoli sprouts were found to exert a beneficial influence on the antioxidant balance of the thyroid gland." (abstract, results)
pubmedfull study (doi)
Cabbage contains hardly any glucoraphanin compared to broccoli sprouts.
"cabbage is not broccoli sprouts. As you mentioned, there's hardly any glucoraphanin in cabbage." (said at 1:42:15)
Comparative phytochemical profiling of Brassica oleracea crops demonstrates that glucoraphanin (the glucosinolate precursor of sulforaphane) is a predominant glucosinolate in broccoli and broccoli sprouts, whereas cabbage contains minimal glucoraphanin, with its glucosinolate profile dominated instead by sinigrin and glucobrassicin.
- supports: Variation of glucosinolates in vegetable crops of Brassica oleracea. (Journal of agricultural and food chemistry 1999) · cited 594x in the literature
"In Brussels sprouts, cabbage, cauliflower, and kale, the predominant glucosinolates were sinigrin (8.9, 7.8, 9.3, and 10.4 micromol g(-1) DW, respectively) and glucobrassicin (3.2, 0.9, 1.3, and 1.2 micromol g(-1) DW, respectively)." (abstract, results, passage verified)
pubmedfull study (doi)
When indole glucosinolates present in mature broccoli florets are acted on by myrosinase, they form breakdown products including indole-3-carbinol and diindolylmethane.
"market-stage broccoli or heads of broccoli florets do have things called indole glucosinolates. When they are acted on by myrosinase, they form unstable intermediates and they can form compounds which can be toxic or goitrogenic and maybe even promote certain cancers depending upon if they're administered before or after a person gets exposed to the carcinogen... But the byproducts of indole glucosinolate metabolism are, among others, things called indole-3-carbinol and diindolylmethane." (said at 1:37:28)
Hydrolysis of indole glucosinolates (predominantly glucobrassicin) by the plant or bacterial enzyme myrosinase produces unstable intermediates that readily convert to indole-3-carbinol (I3C). Under acidic conditions, such as gastric acid, I3C further condenses into oligomeric products, predominantly 3,3'-diindolylmethane (DIM). This biochemical pathway is well-characterized.
- supports: Indole-3-Carbinol (I3C) and its Major Derivatives: Their Pharmacokinetics and Important Ro… (Current drug metabolism 2016) · cited 49x in the literature
"Indoles, including indole-3-carbinol (I3C) and its derivatives, are the products of glucosinolate hydrolysis catalyzed by the enzyme myrosinase. Under acidic conditions, I3C polymerizes into 3, 3- diindolylmethane (DIM), [2-(indol-3-ylmethyl)-indol-3-yl]indol-3-ylmethane (LTr1), 1-(3-hydroxymethyl)- indolyl-3-indolylmethane (HI-IM) and indolo[3,2b]carbazole (ICZ)." (abstract, background, passage verified)
pubmedfull study (doi) - supports: Indoles Derived From Glucobrassicin: Cancer Chemoprevention by Indole-3-Carbinol and 3,3'-… (Frontiers in nutrition 2021) · cited 94x in the literature
"Hydrolysis of glucobrassicin by plant or bacterial myrosinase produces multiple indoles predominantly indole-3-carbinol (I3C). I3C and its major in vivo product, 3,3'-diindolylmethane (DIM), are effective cancer chemopreventive agents in pre-clinical models and show promise in clinical trials." (abstract, results, passage verified)
pubmedfull study (doi)
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