How much sulforaphane is suitable for healthy people?

This post compares and contrasts two perspectives on how much sulforaphane is suitable for healthy people. One perspective was an October 2019 review from John Hopkins researchers who specialize in sulforaphane clinical trials:

Broccoli or Sulforaphane: Is It the Source or Dose That Matters?

Since these researchers didn’t give a consumer-practical answer, I’ve presented a concurrent commercial perspective to the same body of evidence via an October 2019 review from the Australian founder of a company that offers sulforaphane products:

Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease


1. Taste from the clinical trial perspective:

“The harsh taste (a.k.a. back-of-the-throat burning sensation) that is noticed by most people who consume higher doses of sulforaphane, must be acknowledged and anticipated by investigators. This is particularly so at the higher limits of dosing with sulforaphane, and not so much of a concern when dosing with glucoraphanin, or even with glucoraphanin-plus-myrosinase.

The presence and/or enzymatic production of levels of sulforaphane in oral doses ranging above about 100 µmol, creates a burning taste that most consumers notice in the back of their throats rather than on the tongue. Higher doses of sulforaphane lead to an increased number of adverse event reports, primarily nausea, heartburn, or other gastrointestinal discomfort.”

Taste wasn’t mentioned in the commercial review. Adverse effects were mentioned in this context:

“Because SFN is derived from a commonly consumed vegetable, it is generally considered to lack adverse effects; the safety of broccoli sprouts has been confirmed. However, the use of a phytochemical in chemoprevention engages very different biochemical processes when using the same molecule in chemotherapy; the biochemical behaviour of cancer cells and normal cells is very different.”

2. Commercial products from the clinical trial perspective:

“Using a dietary supplement formulation of glucoraphanin plus myrosinase (Avmacol®) in tablet form, we observed a median 20% bioavailability with greatly dampened inter-individual variability. Fahey et al. have observed approximately 35% bioavailability with this supplement in a different population.”

Avmacol appeared to be the John Hopkins product of choice, as it was mentioned 15 times in the clinical trials table. A further investigation of Avmacol showed that its supplier for broccoli extract, TrueBroc, was cofounded and is still run by a John Hopkins coauthor! Yet the review stated:

“The authors declare no conflict of interest.”

Other products were downgraded with statements such as:

“5 or 10 g/d of BroccoPhane powder (BSP), reported to be rich in SF, daily x 4 wks (we have assayed previously and found this not to be the case).”

They also disclaimed:

“We have indicated clinical studies in which label results have been used rather than making dose measurements prior to or during intervention.”

No commercial products, not even the author’s own company’s, were directly mentioned in the commercial perspective.

3. Dosage from the clinical trial perspective:

“Reporting of administered dose of glucoraphanin and/or sulforaphane is a poor measure of the bioavailable / bioactive dose of sulforaphane. As a consequence, we propose that the excreted amount of sulforaphane metabolites (sulforaphane + sulforaphane cysteine-glycine + sulforaphane cysteine + sulforaphane N-acetylcysteine) in urine over 24 h (2–3 half-lives), which is a measure of “internal dose”, provides a more revealing and likely consistent view of the delivery of sulforaphane to study participants.

Only recently have there been attempts to define minimally effective doses in humans – an outcome made possible by the development of consistently formulated, stable, bioavailable broccoli-derived preparations.”

Dosage from the commercial perspective:

“Of the available SFN clinical trials associated with genes induced via Nrf2 activation, many demonstrate a linear dose-response. More recently, it has become apparent that SFN can behave hormetically with different effects responsive to different doses. This is in addition to its varying effects on different cell types and consequent to widely varying intracellular concentrations.

A 2017 clinical pilot study examined the effect of an oral dose of 100 μmol (17.3 mg) encapsulated SFN on GSH [the endogenous antioxidant glutathione] induction in humans over 7 days. Pre- and postmeasurement of GSH in blood cells that included T cells, B cells, and NK cells showed an increase of 32%. The researchers found that in the pilot group of nine participants, age, sex, and race did not influence the outcome.

Clinical outcomes are achievable in conditions such as asthma with daily SFN doses of around 18 mg daily and from 27 to 40 mg in type 2 diabetes. The daily SFN dose found to achieve beneficial outcomes in most of the available clinical trials is around 20-40 mg.”

The author’s sulforaphane products are available in 100, 250, and 700 mg capsules of enzyme-active broccoli sprout powder. From Eat broccoli sprouts today:

“The bioavailability of sulforaphane in a broccoli sprout extract with the myrosinase enzyme 100 μmol gelcap was 36.1% which weighed 6.4 mg.”

The author’s products convert to 36, 90, and 253 mg sulforaphane dosages. Since only the first is in the review’s recommended “20-40 mg” range, I don’t see a readily apparent conflict.

4. Let’s see how the perspectives treated a 2018 Spanish clinical trial published as Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects.

From the commercial perspective:

“In a recent study using 30 grams of fresh broccoli sprouts incorporated daily into the diet, two key inflammatory cytokines were measured at four time points in forty healthy overweight [BMI 24.9 – 29.9] people. The levels of both interleukin-6 (Il-6) and C-reactive protein (CRP) declined over the 70 days during which the sprouts were ingested.

These biomarkers were measured again at day 90, wherein it was found that Il-6 continued to decline, whereas CRP climbed again. When the final measurement was taken at day 160, CRP, although climbing, had not returned to its baseline value. Il-6 remained significantly below the baseline level at day 160.

The sprouts contained approximately 51 mg (117 μmol) GRN, and plasma and urinary SFN metabolites were measured to confirm that SFN had been produced when the sprouts were ingested.”


The clinical trial perspective added that the study dosage was “1.67 (GR) μmol/kg BW.” This wasn’t accurate, however. It was assumed into existence by:

“In cases where the authors did not indicate dosage in μmol/kg body weight (BW), we have made those calculations using the a priori assumption of a 70 kg BW.”

117 μmol / 1.67 μmol/kg = 70 kg.

The study provided the subjects’ mean weight in Table 1 as “85.8 ± 16.7 kg.” So the study’s actual average dosage per kg body weight was 117 μmol / 85.8 kg = 1.36 μmol/kg. Was making an accurate calculation too difficult?

The clinical trial review included the study in the informative Section “3.2. Clinical Studies with Broccoli-Based Preparations: Efficacy” subsection “3.2.8. Diabetes, Metabolic Syndrome, and Related Disorders.” However, this was somewhat misleading, as it was grouped with studies such as the 2012 Iranian Effects of broccoli sprout with high sulforaphane concentration on inflammatory markers in type 2 diabetic patients: A randomized double-blind placebo-controlled clinical trial (not freely available).

The commercial perspective pointed out substantial differences between the two studies:

“Where the study described above by Lopez-Chillon et al. investigated healthy overweight people to assess the effects of SFN-yielding broccoli sprout homogenate on biomarkers of inflammation, Mirmiran et al. in 2012 had used a SFN-yielding supplement in T2DM patients. Although the data are not directly comparable, the latter study using the powdered supplement resulted in significant lowering of Il-6, hs-CRP, and TNF-α over just 4 weeks.

It is not possible to further compare the two studies due to the vastly different time periods over which each was conducted.”


The commercial perspective impressed as more balanced than the clinical trial perspective. The clinical trial perspective also had an undisclosed conflict of interest!

A. The commercial perspective didn’t specifically mention any commercial products. The clinical trial perspective:

– Effectively promoted one commercial product whose supplier was a coauthor’s company;

– Downgraded several other commercial products; and

– Tried to shift responsibility for the lack of “minimally effective doses in humans” to commercial products with:

“Only recently have there been attempts to define minimally effective doses in humans – an outcome made possible by the development of consistently formulated, stable, bioavailable broccoli-derived preparations.”

Unless four years previous is “recently,” using commercial products to excuse slow research progress can be dismissed. A coauthor of the clinical trial perspective was John Hopkins’ lead researcher for the November 2015 Sulforaphane Bioavailability from Glucoraphanin-Rich Broccoli: Control by Active Endogenous Myrosinase, which commended “high quality, commercially available broccoli supplements” per:

“We have now discontinued making BSE [broccoli sprout extract], because there are several high quality, commercially available broccoli supplements on the market.”

B. The commercial perspective didn’t address taste, which may be a consumer acceptance problem.

C. The commercial perspective provided practical dosage recommendations, reflecting their consumer orientation. These recommendations didn’t address how much sulforaphane is suitable for healthy people, though.

Practical dosage recommendations are what the clinical trial perspective will eventually have do after they stop dodging their audience – which includes clinicians trying to apply clinical trial data – with unhelpful statements such as:

“Reporting of administered dose of glucoraphanin and/or sulforaphane is a poor measure of the bioavailable / bioactive dose of sulforaphane.”

How practical was their “internal dose” recommendation for non-researcher readers?


Here’s what I’m doing to answer how much sulforaphane is suitable for healthy people.

I’d like to posthumously credit my high school literature teachers Dorothy Jasiecki and Martin Obrentz for this post’s compare-and-contrast approach. They both required their students to read at least two books monthly, then minimally write a 3-page, single-spaced, compare-and-contrast paper.

You can see from their linked testimonials that their approach was in a bygone era, back when some teachers considered the desired outcome of public education to be that each individual learned to think for themself. My younger brother contributed:

“I can still remember everything Mr. Obrentz ever assigned for me to read. He was the epitome of what a teacher should be.”

Microwave broccoli to increase sulforaphane levels

This 2020 Chinese/USDA study investigated effects on sulforaphane amount from heating broccoli in water and microwaving at different power settings to different temperatures:

“Microwave treatment causes a sudden collapse of cell structure due to the increase in osmotic pressure difference over vacuole membrane. Mild heating could increase SFR [sulforaphane] level, possibly explained by the increased activity of MYR [the enzyme myrosinase] which can hydrolyze GLR [glucoraphanin] into SFR at high temperature (up to 60°C).

Microwave‐cooked broccoli had higher levels of these two compounds compared to broccoli heated in water. The broccoli sample without cooking as a control showed the least amount of GLR, indicating that microwave heating did help to release more GLR from the cell.

In the temperature range of 50–60°C, a positive correlation was observed between GLR or SFR contents and temperature. However, these two physiochemical contents were negatively correlated with temperature when it increased to 70°C.

The glucoraphanin (GLR) and sulforaphane (SFR) contents (μmol/g DW) in florets of broccoli during microwaving at 40, 50, 60, and 70°C using low power level (LL) or high power level (HL). Data are reported as the mean ± SD (n = 3). Values with different letters are significantly (p < .05) different.

[For example, sulforaphane levels of the control (raw), LL40, LL70, and HL40 conditions weren’t significantly different, and the HL70 level was significantly lower than those levels.] The microwave using high level at 60°C showed the greatest SFR level (2.45 µmol/g DW).”

Table S1 from the supporting material:

Temperature

(°C)

Time

(S)

Power level

(W)

Heating in water 40 185 NA
50 230
60 262
70 290
Microwave (HL) 40 65 950
50 90
60 108
70 120
Microwave (LL) 40 115 475
50 148
60 178
70 200

https://onlinelibrary.wiley.com/doi/10.1002/fsn3.1493 “Microwave cooking increases sulforaphane level in broccoli”


The study demonstrated a more effective method of increasing sulforaphane than did the cited and widely discussed 2004 Heating decreases epithiospecifier protein activity and increases sulforaphane formation in broccoli (not freely available). The older study methods were difficult to implement in kitchens, and evaluated heating temperature as the only factor.

The present study added microwave power level irradiation effects as a factor, and simplified heating temperature implementation. People can use Table S1 to maximize broccoli florets / broccoli sprout sulforaphane content in their kitchens.

The next time I eat broccoli, for example, I’ll put 16 oz. of water and broccoli into a casserole dish, then cook in my 1000W microwave on full power for 95 seconds. I’ll immediately dump the broccoli into a colander and spray it with cold water, since a linear interpolation of Table S1 would place its temperature close to the 60° goal:

(1000W / 950W) x (((108s -90s) / (60° – 50°)) * (95s – 90s))) + 50° = 59.5°


Reminders from Eat broccoli sprouts today:

  1. A 1 mg sulforaphane weight equals a 5.64 μmol sulforaphane amount.
  2. “Content of glucoraphanin in extract from broccoli sprouts was 16.6 μmol per gram of fresh weight. In contrast, mature broccoli extract contained 1.08 μmol per gram of fresh weight.”
  3. The bioavailability of sulforaphane in a broccoli sprout extract with the myrosinase enzyme 100 μmol gelcap was 36.1% which weighed 6.4 mg.
  4. The question of how much sulforaphane is suitable for healthy people remains unanswered.

The current study provided the optimal sulforaphane end result of “(2.45 µmol/g DW)” but didn’t provide the measurements needed to understand how that was calculated. I’ve asked a study author for the data.

The study also measured broccoli stems:

“GLR and SFR were hardly detected in stems. Less than 52% of GLR was detected in the [50/50] mixture of florets and stems compared to florets.

Microwaved at 60°C, the florets had a concentration of GLR and SFR at 2.78 and 2.45 µmol/g DW, respectively, which was significantly higher than the levels detected in mixture of florets and stems (1.21 and 0.82 µmol/g DW, respectively).”

The 50% florets / 50% stems mixture’s glucoraphanin amount of 1.21 µmol was roughly comparable with the 1.08 µmol glucoraphanin amount of mature broccoli extract in item 2 above.

The evidence says..

Three items to follow up yesterday’s The UK downgraded COVID-19 a week ago:

1. From March 24, 2020:

Oxford Epidemiologist: Here’s Why That Doomsday Model Is Likely Way Off

“Fewer than one in a thousand who’ve been infected with COVID-19 become sick enough to need hospitalization, leaving the vast majority with mild cases or free of symptoms.”

However, that was based on “my model’s better than yours” arguments rather than sufficient evidence.

2. From March 26, 2020:

Dr. Deborah Birx Shreds Media For Salacious Claims: ‘We Don’t Have Evidence Of That’

“Birx began by highlighting the study in the U.K. that dramatically revised its projections of the total number of deaths projected in the U.K. from ‘half a million to 20,000.’

‘When people start talking about 20% of a population getting infected,’ Birx later added. ‘It’s very scary, but we don’t have data that matches that based on the experience.'”

3. From March 25, 2020: the panic model’s lead researcher offered a long non-apology to UK Parliament, which they accepted uncritically:

Witness: Professor Neil Ferguson, Director, MRC Centre for Global Infectious Disease Analysis, Imperial College London


Still don’t know exactly who is herding the US population. While we wait at home for headlines to emphasize evidence:

Image from Whatfinger.

The UK downgraded COVID-19 a week ago

From https://www.gov.uk/guidance/high-consequence-infectious-diseases-hcid:

“As of 19 March 2020, COVID-19 is no longer considered to be a high consequence infectious diseases (HCID) in the UK.

The 4 nations public health HCID group made an interim recommendation in January 2020 to classify COVID-19 as an HCID.  Now that more is known about COVID-19, the public health bodies in the UK have reviewed the most up to date information about COVID-19 against the UK HCID criteria. They have determined that several features have now changed; in particular, more information is available about mortality rates (low overall), and there is now greater clinical awareness and a specific and sensitive laboratory test, the availability of which continues to increase.

Definition of HCID

  • acute infectious disease
  • typically has a high case-fatality rate
  • may not have effective prophylaxis or treatment
  • often difficult to recognise and detect rapidly
  • ability to spread in the community and within healthcare settings
  • requires an enhanced individual, population and system response to ensure it is managed effectively, efficiently and safely.”

Who is herding the US population, with demands that businesses be shut down, for a disease that the UK recognizes as not the most serious health threat?

Will their scorched earth agenda not be satisfied until the remains of US businesses are in a pile like this?

Image from Rare Historical Photos

Waiting to be officially denied

Three items to follow up yesterday’s What’s next?:

1. A view from a Singapore gold dealer:

LBMA colludes with the COMEX – To lockdown the global gold market?

“LBMA [London Bullion Market Association] market-makers have a duty and obligation to make a market in gold. So where were these market makers as the spot price seized up, and why would these market makers not be making a market and providing liquidity for gold?

Is it just a management of perceptions exercise with no gold bars involved, to try to coax back the spot and futures prices by telegraphing that the gold that is backing the spot price (which is actually unallocated non-existent gold) is now also backing COMEX gold futures. While neither of the two can be delivered, the same non-gold now backs both, so voila, there is no need for any price divergence!”

2. Concurrently, from the Wall Street Journal, a new form of US currency may or may not be part of the coronavirus bailout package:

Fed Digital Dollars Are Part of Debate Over Coronavirus Stimulus

“While it may not make it to the finished coronavirus economic stimulus and support package now being weighed in Congress, there is a push from some legislators to give the Federal Reserve a new tool some believe could radically reshape how it conducts monetary policy.

At issue are so-called digital dollars and the accounts that would hold them.”

3. Private equity eyes industries crippled by coronavirus: ‘They have been waiting for this’

“‘Vulture investors, especially in private equity, are waiting in the wings to scoop up scores of struggling businesses on the cheap,’ tweeted Rohit Chopra, an FTC commissioner.”


Still no idea about exactly who are the herders. Getting a better picture of who benefits from the herd’s demise.


Charles M. Russell “Driving Buffalo Over the Cliff” 1914

Eat broccoli sprouts today

This 2020 Korean letter to a journal editor cited 23 recent papers in support of sulforaphane’s positive effects, mainly in anti-cancer treatments:

“Gene expression is mediated by chromatin epigenetic changes, including DNA methylation, histone modifications, promoter-enhancer interactions, and non-coding RNA (microRNA and long non-coding RNA)-mediated regulation. Approximately 50% of all tumor suppressor genes are inactivated through epigenetic modifications, rather than by genetic mechanisms, in sporadic cancers. Accumulating evidence suggests that epigenetic modulators are important tools to improve the efficacy of disease prevention strategies.

Because sulforaphane (SFN) induces the nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element pathway that induces the cellular defense against oxidative stress, SFN has received increased attention because it acts as an antioxidant, antimicrobial, anti-inflammatory, and anticancer agent.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7068201/ “A recent overview on sulforaphane as a dietary epigenetic modulator”


Letters to the editor aren’t peer-reviewed, though. One of the cited papers was a 2018 Czech mini-review that included metabolism, preparation and processing evidence:

“Sulforaphane is a phytochemical that occurs in plants in the form of biological inactive precursor glucoraphanin. This precursor belongs to the group of phytochemicals – glucosinolates – that are rapidly converted to the appropriate isothiocyanate by the enzyme called myrosinase.

The process of transformation takes place after a disruption of plant tissues by biting, chewing, slicing, and other destruction of tissues, when the enzyme myrosinase is released from plant tissues. When the enzyme myrosinase is destroyed during meal preparation (during cooking, steam cooking, or microwave treatment), a likely source of isothiocyanates is the microbial degradation of glucosinolates by the intestinal microflora. However, the hydrolysis by the microflora has been reported to be not very efficient, and in humans it is very diverse and variable.

Content of glucoraphanin in extract from broccoli sprouts was 16.6 μmol per gram of fresh weight. In contrast, mature broccoli extract contained 1.08 μmol per gram of fresh weight. The total amount of glucosinolates in the young broccoli sprouts is 22.7 μmol per gram of fresh weight and 3.37 μmol per gram of fresh weight for mature broccoli.

Percentage amount of sulforaphane formed from its precursor glucoraphanin in broccoli which had not been heat treated and had been lyophilized [freeze-dried] was 22.8%. Broccoli steaming (5 min) and its lyophilization decrease the amount of sulforaphane formed to 4.2%.”

https://www.liebertpub.com/doi/full/10.1089/jmf.2018.0024 “Isothiocyanate from Broccoli, Sulforaphane, and Its Properties (not freely available)


Information about 43 completed sulforaphane clinical trials is here. Among them, the 2014 Effect of Broccoli Sprouts on Nasal Response to Live Attenuated Influenza Virus in Smokers: A Randomized, Double-Blind Study was of particular interest, stating:

“Nutritional interventions aimed at boosting antioxidants may be most effective in individuals who are relatively antioxidant-deficient at baseline, a condition likely to be more prevalent in smokers.”

I didn’t notice regular supplement dosage studies. Maybe I didn’t read the control group information carefully enough?


For those who don’t want to tend a broccoli sprout garden, a 1 mg sulforaphane broccoli sprout extract capsule is available for $.20/day. https://pubchem.ncbi.nlm.nih.gov/compound/sulforaphane lists sulforaphane’s molecular weight as 177.3 g/mol. A 1 mg sulforaphane capsule weight equals a 5.64 μmol sulforaphane amount (.001 / 177.3).

From the 2015 Sulforaphane Bioavailability from Glucoraphanin-Rich Broccoli: Control by Active Endogenous Myrosinase:

  • Figure 4 showed the bioavailability of sulforaphane in a broccoli sprout extract with the myrosinase enzyme 100 μmol gelcap was 36.1% which weighed 6.4 mg (36.1 / 5.64).
  • Figure 3 showed that the bioavailability of sulforaphane in freeze-dried broccoli sprouts in pineapple-lime juice was 40.5% in 50, 100, and 200 μmol amounts and 33.8% with 100 μmol gel caps. You do the weight math.
  • Figure 2 showed that if the broccoli sprout extract didn’t have the enzyme, the bioavailability of sulforaphane was 10.4% whether the amount was 69 or 230 μmol, weighing 1.27 mg (69 x .104) / 5.64 and 4.24 mg (230 x .104) / 5.64.

It makes sense to add broccoli sprouts to a sulforaphane capsule to potentially increase bioavailability from the worst case of Figure 2’s 10.4% to the best case of Figure 4’s 36.1%. Eating sprouts at least increases the sulforaphane consumed. But the question of how much sulforaphane is suitable for healthy people remains unanswered.