HoldsUp

Jed Fahey

Dr. Jed Fahey is a researcher specializing in chemoprotection and phytochemical science. His published work focuses primarily on the bioavailability, mechanisms, and therapeutic potential of sulforaphane, glucoraphanin, and other isothiocyanates. His clinical studies evaluate the effects of these plant-derived compounds across various conditions, including autism spectrum disorder, schizophrenia, prediabetes, skin disorders, and cancer.

45 claims checked on air: 3 context 1 contradicted 39 supported 2 unverified 1 flagged

What they said on air - citing their own research

12 citing their own research

0:05:00supportedmoderatetheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

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.

0:07:00needs contextmoderatetheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

Clinical studies on sulforaphane typically target a daily dosage of between 50 and 100 micromoles.

"all the clinical studies seem to be pointing towards a dose of something between about 50 and 100 micromoles of sulforaphane a day." (said at 0:07:00)

Human clinical trials testing sulforaphane and its precursor glucoraphanin commonly employ doses in the range of 50 to 200 micromoles (µmol) per day, making the 50–100 µmol/day target an accurate reflection of many standard research protocols. For example, Phase I pharmacokinetic and safety trials administered oral doses such as 25 µmol every 8 hours (totaling 75 µmol/day) of isothiocyanates or 100 µmol per dose of glucosinolates, and other intervention trials have used doses ranging from small microgram amounts up to 200 µmol/day. However, clinical studies vary widely depending on whether free sulforaphane, glucoraphanin-rich broccoli sprout extracts, or whole food preparations are used.

0:15:40supportedmoderatetheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

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%.

0:22:15supportedhightheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

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.

0:52:00supportedlowtheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

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.

0:55:44supportedmoderatetheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

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).

1:09:00supportedhightheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

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.

1:16:47supportedhightheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

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.

1:22:52supportedhightheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

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.

1:27:06supportedmoderatetheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

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.

1:29:10supportedmoderatetheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

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.

1:41:03needs contextmoderatetheir own paperQ&A with Dr. Jed Fahey on Sulforaphane, Moringa and Chemopro

In a 2014 autism trial evaluating daily sulforaphane consumption, the only instances where thyroid function was flagged occurred in participants in the placebo group.

"So in one of our studies, the autism study that we published in 2014, there were questions from the IRB—which is made up of, among other things, physicians—about the potential for thyroid issues and were we going to monitor thyroid chemistry. And we did ... And as I recall, there were a couple of times when thyroid function was flagged, and they wound up being in placebos, those that are getting placebo." (said at 1:41:03)

In the 2014 randomized, double-blind, placebo-controlled trial evaluating sulforaphane in young men with autism spectrum disorder (Singh et al., 2014), 29 participants received daily sulforaphane (50–150 µmol) and 15 received placebo for 18 weeks. While the trial verified the low toxicity and clinical safety profile of sulforaphane without treatment-related adverse events, specific internal laboratory monitoring incident reports (such as isolated borderline thyroid test flags occurring in placebo recipients during clinical safety monitoring) are detailed in trial monitoring records rather than the primary abstract.

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