If people don’t stand up for their rights, their rights will be forgotten

Here’s an interview last week with a German epidemiologist, Professor Wittkowski, who isn’t on a government payroll:

“First of all the elderly and fragile should be separated from the population where the virus is circulating. Everyone else, especially the children, should keep going to school, because they will be the primary impetus for herd immunity.

Flattening the curve prolongs the time a virus stays in the population. People staying indoors keeps the virus healthy.

Like every other respiratory disease, without government intervention, the pandemic would already be over like it’s over in China and South Korea. Except, both in China and South Korea, social distancing started very close to the peak. By keeping the virus from running its course, they are now having a second wave of cases. It will keep on if we don’t let it complete.

There’s nothing to be scared about. This is a flu epidemic like others, maybe more severe. What’s changed is the internet. People get their information in a few seconds, rather than a week.

Tracking a respiratory disease is impossible. Even in times of social distancing. Nature has ways to make sure we survive.

The standard for AIDS reporting, i.e., the date of infection separated from the date of reporting, is not being followed.

If we had herd immunity now, we wouldn’t have a second wave in the fall. Herd immunity typically lasts for a couple of years. If we prevent herd immunity, it is certain that a second wave will occur.

Testing doesn’t stop anything. Antibody testing will give us estimates of herd immunity, which would be useful. We don’t die of the virus. We die of pneumonia.

The downside of starting containment is that we should not believe that we are more intelligent than mother nature when we were evolving. Mother nature was pretty good at making sure we were a good match for the diseases that we happened to see virtually every year.

I think people, especially in the United States, are more docile than they should be. People should talk with their politicians, question them, ask them to explain. Because if people don’t stand up to their rights, their rights will be forgotten.”

Changing an inflammatory phenotype with broccoli sprouts

This follow up to Growing a broccoli sprouts Victory Garden is what’s gone on during Week 1 of starting to grow broccoli sprouts for a “30 grams of fresh broccoli sprouts incorporated daily into the diet” [1] program.

Day 0 – I’ve tried many things to cure chronic inflammation over the years, basing most of my actions on what’s proven to work for other people. These treatments have helped but haven’t completely worked for me. I’ve continued them with the hypothesis that they may have positive synergistic interactions with daily eating 30 grams of broccoli sprouts / 17 mg of sulforaphane.

Day 0 treatments included two dozen supplements I’ve taken since turning 50, a diet low in advanced glycation end products started last year [2], and naproxen (a nonsteroidal anti-inflammatory drug). The chronically inflamed spots are the left thumb base (arthritis), tendons outside the left ankle (peroneal tendinosis), and left knee tendonitis, all probably consequences of playing golf for 40+ years.

Day 1 – The vertical farming equipment is a Deluxe Kitchen Crop 4-Tray Seed Sprouter Model VKP1200 made by VICTORIO Kitchen Products. I soak one tablespoon of organic broccoli seeds for 12 hours. Take them out of the stackable trays for a twice-daily rinsing, which is counter to directions of pouring water into the tower top. Microwave the Day 3 broccoli sprouts daily per [3]. Run its tray through the dishwasher (but no heat cycle). Put the tray back in rotation for Day 0.

Day 2 – Threw away one of my crutches, naproxen, as taking it had become more of a habit than a necessity. I’d been taking 220 mg twice daily for years until two weeks ago, when I switched to once daily.

Sulforaphane increases “several endogenous antioxidant compounds via the transcription factor Nrf2 [nuclear factor erythroid 2-related factor 2, discovered in 1994]. Of the phytochemicals with Nrf2 inducer capacity, Brassica-derived SFN [sulforaphane] is the most potent naturally occurring biomolecule known at this time.

Another transcription factor, NF-κB, which is associated with inflammatory pathways is downregulated by SFN. This dual action of SFN is especially intriguing in that Nrf2 and NF-κB interact via their own ‘cross talk’.” [4]

Day 3 – Stopped taking 2 mg of sulforaphane in the form of a broccoli sprout extract capsule, and 200 mg of a diindolyl methane (DIM) capsule daily. DIM was raised 195% from Day 0 to Day 70 after daily intake of broccoli sprouts in [1], noting: “The anti-inflammatory effects observed with broccoli sprouts intake are likely due to the combined effects of all the hydrolysis products of glucosinolates.” Don’t need either supplement when broccoli sprouts supply them.

The next supplement I might drop is N-Acetyl-Cysteine (NAC), the precursor to our endogenous antioxidant glutathione. I take a 600 mg capsule twice daily.

[4] goes on and on about sulforaphane / glutathione interactions. For example: “Several well-studied Nrf2-dependent target genes of possible relevance are those encoding synthesis of glutathione (GSH)” in Section 5.2. SFN as a Redox Modulator that included Figure 6 below, and in Section 6. SFN: Its Redox-Modulating Effects:

Day 4 – I’d seen studies of broccoli sprouts that ranged from 3-days old (the most frequent age) to 8-days old. Before [5], I hadn’t found analyses of broccoli sprout age differences in sulforaphane contents, and only a few studies of sulforaphane differences among broccoli sprout cultivated varieties.

Day 5 – I’ve eaten sprouts at 3 – 5 days old, and haven’t noticed a taste difference after microwaving per [3]. Here’s what they look like at Days 0, 1, 2, and 3:

Day 6 – Are you ready to change your phenotype?


References in order of citation:

[1] 2018 Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects

[2] 2016 Dr. Vlassara’s AGE-Less Diet: How a Chemical in the Foods We Eat Promotes Disease, Obesity, and Aging and the Steps We Can Take to Stop It

[3] 2020 Microwave cooking increases sulforaphane level in broccoli curated in Microwave broccoli to increase sulforaphane levels

[4] 2019 Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease

[5] 2020 3-day old broccoli sprouts have the optimal yields

Growing a broccoli sprouts Victory Garden

To follow up How much sulforaphane is suitable for healthy people? I’ve started growing broccoli sprouts, and a “30 grams of fresh broccoli sprouts incorporated daily into the diet” [1] program. I loosely follow [2]‘s sprouting guidelines. One preparation difference is microwaving per [3]‘s findings as follows:

I put broccoli sprouts into a small casserole dish, add enough water to cover them, then cook in my 1000W microwave on full power for 90 seconds. I immediately dump the broccoli sprouts into a colander and spray with cold water to stop heating at the desired temperature. A linear interpolation of Table S1 would place its temperature after 95 seconds on full 1000W power close to but not exceeding the 60°C goal:

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

The first batch of broccoli sprouts was a mild, cabbage-tasting side dish to the home-style chicken soup on page 238 of [4].

The a priori hypotheses:

    1. 30 grams of fresh broccoli sprouts will not have “51 mg (117 μmol)” of glucoraphanin [1] because they “Used the elicitor methyl jasmonate (MeJA) by priming the seeds as well as by spraying daily. MeJA at concentrations of 156 μM act as stressor in the plant and enhances the biosynthesis of the phytochemicals glucosinolates. Compared to control plants without MeJA treatment, the content of compounds as the aliphatic glucosinolate glucoraphanin was enhanced up to 70%.” 117 μmol / 1.70 = 69 μmol is the expected glucoraphanin amount in 30 grams weight of fresh broccoli sprouts.
    2. One measurement [5] of how much sulforaphane is present in fresh broccoli sprouts before microwaving is 100 μmol / 111 g = .9 μmol / g. (.9 x 30 g) = 27 μmol is the expected sulforaphane amount in 30 grams of fresh broccoli sprouts.
    3. Microwaving the raw broccoli sprouts will convert the 69 μmol of glucoraphanin to 69 μmol of sulforaphane. Last week a [3] coauthor agreed to make the data available to facilitate calculations. While I’m waiting…The study said the Figure 3 HL60 sulforaphane amount was 2.45 μmol / g. Eyeball estimates of the below Figure 3 control (raw broccoli florets) are a sulforaphane amount of .2 μmol / g and a glucoraphanin amount of 2.2 μmol / g. I assume that the broccoli florets and sprouts glucoraphanin-to-sulforaphane conversions would be the same. A roughly 1-to-1 glucoraphanin-to-sulforaphane conversion of ~2.2 μmol / g + a sulforaphane amount of ~.2 μmol / g is ~2.4 μmol / g of sulforaphane. Note the Figure 3 detrimental effects that continuing cooking for a few more seconds to HL70 (70°C), had on its sulforaphane contents, dropping it below even the control (raw) content!
    4. The estimated sulforaphane amount would be 96 μmol (27 from item 2 + 69 from item 3). This would be a 17 mg weight of sulforaphane (96 / 5.64) [6]. This dosage is comparable to a 2017 clinical pilot study [7] and seven other completed clinical trial dosages of 100 μmol (17.3 mg) listed in [8].
    5. I’ve been sitting around a lot since returning from Milano, Italy, on February 24, 2020, and probably weigh around 75 kg. The estimated dosage represents 96 μmol / 75 kg = 1.28 μmol / kg, which is comparable to the 1.36 μmol / kg average of [1]. (The study provided the subjects’ mean weight in Table 1 as “85.8 ± 16.7 kg.” The average dosage per kg body weight was 117 μmol / 85.8 kg = 1.36 μmol / kg.)
    6. Don’t have a practical estimate of the amount of sulforaphane I metabolize from post-microwave glucoraphanin. Both [7] and [8] cited a 2012 study that found: “Some conversion of GRN to SFN can occur in response to metabolism by the gut microflora; however, the response is inefficient, having been shown to vary ‘from about 1% to more than 40% of the dose.’”
    7. Don’t have a practical estimate of the “internal dose.” [8]

I don’t have a laboratory in my kitchen 🙂 and won’t have quantified results.


References in order of citation:

[1] 2018 Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects

[2] 2017 You Need Sulforaphane – How and Why to Grow Broccoli Sprouts

[3] 2020 Microwave cooking increases sulforaphane level in broccoli curated in Microwave broccoli to increase sulforaphane levels

fsn31493-fig-0003-m

[4] 2016 Dr. Vlassara’s AGE-Less Diet: How a Chemical in the Foods We Eat Promotes Disease, Obesity, and Aging and the Steps We Can Take to Stop It

[5] 2016 Effect of Broccoli Sprouts and Live Attenuated Influenza Virus on Peripheral Blood Natural Killer Cells: A Randomized, Double-Blind Study

[6] 2020 https://pubchem.ncbi.nlm.nih.gov/compound/sulforaphane lists sulforaphane’s molecular weight as 177.3 g / mol. A 1 mg weight of sulforaphane equals a 5.64 μmol sulforaphane amount (.001 / 177.3).

[7] 2019 Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease

[8] 2019 Broccoli or Sulforaphane: Is It the Source or Dose That Matters? Note that a coauthor didn’t disclose their business’ conflict of interest for an effectively promoted commercial product.

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.

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.


Train your immune system every day!

This 2019 US review subject was β-glucan:

“β-1,3-Glucans (hereafter referred to as glucan) are natural molecules able to significantly improve our health. In human studies, the tested (and suggested) daily dose remains in the range of 100–500 mg for stimulation of the immune system, whereas for a decrease in cholesterol levels a daily dose of 3 g is recommended.

Glucan does not represent essential nutrients, but it might be successfully used not only for improvement of immune functions but also to improve the general quality of life via improvements of immune status, lowering cholesterol, improving blood glucose levels and reduction of stress. ClinicalTrials.gov summarizes 177 [now 199 with 103 completed] β-glucan clinical trials, mostly in cancer, gastrointestinal tract therapy, lowering cholesterol and improvements of immune reactions.

The question is not if glucans will move from food supplement to widely accepted drug, but how soon.

Reactions known to be influenced by glucan are represented in white, reactions where glucan has no confirmed effects are shown in black. The first defensive body response to infection results from formation of the anorexia cytokines (IL-1, IL-6, IL-8, and TNF-α).”

https://www.mdpi.com/1420-3049/24/7/1251/htm “Beta Glucan: Supplement or Drug? From Laboratory to Clinical Trials”

The review is also indexed at https://www.betaglucan.org/i-p/ under “Immunomodulator”


I’m curating this review on Day 12 of a self-quarantine after coming back from Milano, Italy, Monday, February 24, 2020. The previous Friday into Saturday I flew to Milano sitting with a group of elderly Italians who were returning from vacation.

On Saturday my wonderful woman and I used the Milano rail and subway system to go downtown. On Sunday we used the rail, bus, and ferry systems to visit Como, Bellagio, and Menaggio. I don’t think we could have mixed in more with people during transits, touristing, and Carnevale celebrations.

After returning to our hotel Sunday evening, we heard about the coronavirus outbreak south of Milano and the closing of ten towns. We changed flights and departed for the US early Monday morning.

Neither of us have had any signature symptoms of COVID-19 (fever, shortness of breath, dry cough). Our daily diet the past few years included β-glucan from steel-cut oats (~3 g) and from a 1/3, 1/6 yeast supplement (400 mg).

Coincidence?

Moonrise at sunrise with Venus