Microwave broccoli seeds to create sulforaphane

Two sulforaphane topics came up in discussions with my wonderful woman. The first was an inference:

  1. 3-day-old broccoli sprouts have the optimal yields found that broccoli sprout sulforaphane content (after processing for analysis) ranged from 46% to 97% of broccoli seeds.
  2. Microwave broccoli to increase sulforaphane levels found that microwaving broccoli florets to 60°C (140°F) increased the sulforaphane amount from .22 to 2.45 µmol / g (1,114%!!).
  3. Wouldn’t broccoli seeds’ sulforaphane be more than broccoli sprouts by microwaving seeds up to 60°C in the same amount of water?

The 3-day study broccoli sprout measurements were relative to each variety’s seeds:

“To be comparable, the content of these bioactive compounds from 100 fresh sprouts was divided by the weight (gram) of 100 seeds, and then this value was compared with their content from one gram seeds.”

Broccoli compounds are similar among broccoli florets, sprouts, and seeds. A major difference is that broccoli sprouts and seeds have no initial sulforaphane content because hydrolization hasn’t occurred yet. The above graphic’s seed and sprout sulforaphane content was created by processing for analysis.

I’ll reason that sulforaphane would be created by:

  • Microwaving one tablespoon of broccoli seeds with a 1000W microwave in 100 ml of distilled water for 30 seconds to achieve up to 60°C; then
  • Straining out the water; then
  • Allowing further myrosinase hydrolization of glucoraphanin and other glucosinolates into sulforaphane and other healthy compounds.

Broccoli seeds are dry, and microwaving acts directly on a material’s water content. The 3-day study methods “immersed [broccoli seeds] in distilled water and soaked at 30°C for 2 h” to start germination. I’ll stipulate two hours as a minimum broccoli seed soaking time before microwaving.

I’ve tried microwaving broccoli seeds five times so far to see if they’re palatable. Seeds soaked for at least two hours then microwaved for 30 seconds swell to almost twice their dry size. They’re easier to strain, chew, and swallow. I don’t have to pulverize them with my molars for five minutes like non-microwaved dry broccoli seeds.

The 3-day study also found “total phenolic and flavonoid contents in sprouts were 1.12 to 3.58 times higher than seeds.” I won’t stop eating broccoli sprouts, but sometimes it may be expedient to reduce a 72-hour preparation time to 2 hours and still benefit from sulforaphane and other healthy broccoli compounds.

Let’s use Estimating daily consumption of broccoli sprout compounds runt-of-the-litter calculations and assumptions to make a worst-case estimate of sulforaphane content in one tablespoon of broccoli seeds:

  • Minimum broccoli seed weight of one tablespoon (2,436 seeds / 100) x .33 g = 8.04 g.
  • Minimum sulforaphane weight in one tablespoon of broccoli seeds (8.04 g x 2.43 mg sulforaphane per gram of seeds) = 19.54 mg.

I won’t calculate a worst-case sulforaphane weight after microwaving because part of the 3-day study processing for analysis was:

“Broccoli seeds were comminuted by analysis grinder. Seed powder (0.5g) was immersed in distilled water at 55 °C for 5 min to inactivate the epithiospecifier protein.”

Grinding seeds into powder then heating it probably incorporates any effects of microwaving intact broccoli seeds up to 60°C.

The 3-day study varieties’ least weight of seeds multiplied by the least weight of sulforaphane adequately estimates a worst case of 19.54 mg sulforaphane from one tablespoon of broccoli seeds after microwaving.


The second discussion topic came by gathering study data from Broccoli or Sulforaphane: Is It the Source or Dose That Matters?

Assessing these 200 μmol amount / 35 mg weight sulforaphane supplement dose studies:

  1. Peak plasma statistics ranged from 0.5 μmol in Row 2 (n = 20) to 2.15 (n = 4) μmol in Row 1. Row 4 (n = 10) statistics don’t show it, but its individual peak plasma ranges per the below graphic were 0.359 μmol to 2.032 μmol. Coincidentally, the Row 4 subject (#2) who had the lowest peak plasma amount also had the lowest urinary % of dose excreted (also termed bioavailability) of 19.5%, and the Row 4 subject (#8) who had the highest peak plasma amount also had the highest sulforaphane bioavailability of 86.9%.
  2. From the Row 4 study: “The half-life of SF in the body was 2.07 ± 0.26 h as calculated from serum area-under-the-curve determinations.” Its Subject #2 had the longest sulforaphane half-life at 2.709 hours.
  3. The peak time after dose ranged from Row 1’s 1 hour to Row 2’s 3 hours. Not sure why Row 4 didn’t calculate a peak time, but eyeballing the above graphic showed that all subjects peaked between 1 and 2 hours. Row 2’s time was at the study’s first of three measurement intervals (3, 6, and 12 hours). Comparing it to other 200 μmol amount / 35 mg weight sulforaphane supplement dose studies, Row 2’s peak time after dose probably took place earlier than 3 hours.

These four studies showed that there’s wide variation among individual responses to sulforaphane supplements. Row 4 study’s Concluding Remarks ended with:

“Innate metabolic differences must not be discounted when assessing the metabolism of SF alone, delivered in supplements.”


The first of A pair of broccoli sprout studies was Row 2 (n = 20) above. Its sulforaphane supplement statistics – repeated in the below graphic’s BSE (broccoli sprout extract) column – demonstrated how humans’ sulforaphane supplement metabolic profiles were different than our fresh broccoli sprout metabolic profiles:

The divided dose was twelve hours apart at breakfast and dinner times. Also, its first measurements weren’t taken until 3 hours after ingesting, which explains its later times with lesser amounts than other 200 μmol amount / 35 mg weight sulforaphane supplement studies’ earlier times with greater amounts.

I changed my practices to eat microwaved broccoli sprouts at breakfast and dinner times from its finding:

“In sprout consumers, plasma concentrations were 2.4-fold higher after consuming the second dose than after the first dose.”

A metabolic profile resulting from current practices is probably between the Sprout and BSE divided-dose statistics:

  • Sulforaphane intake is greater than eating raw broccoli sprouts because microwaving 3-day-old broccoli sprouts creates an increased amount of sulforaphane in them before eating.
  • Sulforaphane uptake is quicker than eating raw broccoli sprouts because it doesn’t primarily depend upon metabolism.
  • Sulforaphane metabolism may not be as immediate as ingesting a sulforaphane supplement, though.

The microwaving study processed 10 grams of broccoli florets immersed in 500 ml water with a 950W microwave on full power for 108 seconds to achieve 60°C. I microwave a worst-case 38 grams of 3-day-old broccoli sprouts immersed in 100 ml water with a 1000W microwave on full power for 35 seconds to achieve 60°C.

After microwaving I transfer broccoli sprouts to a strainer, and wait five minutes to allow further myrosinase hydrolization of glucoraphanin and other glucosinolates into sulforaphane and other healthy compounds. Enhancing sulforaphane content provided evidence that myrosinase hydrolization peaks at one minute after achieving 60°C per the below graphic:

I interpret the above sulforaphane degradation from minutes 1 to 5 to be leaching caused by leaving the broccoli sample immersed in water. I strain water from broccoli sprouts after microwaving – the Time 0 mark of the above graphic – because without leaching water, further hydrolization may increase sulforaphane.

Sulforaphane supplements:

  • Are readily metabolized,
  • Blood plasma levels peak by two hours, and
  • Blood plasma levels dissipate by eight hours.

To the extent a metabolism resulting from current practices is closer to a sulforaphane supplement profile than a raw broccoli sprouts profile, maybe that leaves the door open to a microwaved broccoli seed dose at lunch time? My beautiful woman thinks so. What do you think?

Measuring sulforaphane plasma compounds

This 2020 Australian human study investigated methods of measuring sulforaphane plasma compounds:

“A simplified methodology to allow high-throughput LC–MS [Liquid Chromatography-Mass Spectrometry] analysis of plasma samples for the measurement of sulforaphane and its metabolites is described. Analysis time is greatly reduced by employing fast chromatography and simple plasma extraction procedure.”

“The participants were observed consuming four Broccomax capsules, each containing 30 mg of broccoli seed extract and a dose of 8 mg of sulforaphane, as per manufacturer certificate of analysis, resulting in a total dose of 32 mg of sulforaphane (120 mg of broccoli seed extract).

The mean peak of combined metabolites from our study (0.9 and 1 μM) using 120 mg of broccoli seed extract (~32 mg of SFN) was similar to work by Fahey et al. who investigated the pharmacokinetics of 350 mg of purified broccoli seed powder (mean 1.3 μM ± 0.5 μM), though our dose was almost three-times less. The pharmacokinetic profiles of our study mirrored those of Fahey et al. in that excretion was complete 8 hrs after consumption. Our intervention peaked slightly later (~2hrs), than that of Fahey (~1 hr), likely due to our use of a capsule rather than liquid.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7070302/ “Measuring Sulforaphane and Its Metabolites in Human Plasma: A High Throughput Method”


The study was thin on comparing their 2-person results to previous work. I filled in other comparables from Broccoli or Sulforaphane: Is It the Source or Dose That Matters?


The current study set up a strawman by stating a false comparison:

“Our dose was almost three-times less.”

The compared study was the n = 10 subjects row above, which stated its dose as:

“200 μmol of SF was contained in about 350 mg of SF-αCD powder dissolved in 25 mL of distilled water, which subjects were given to drink upon arrival at the clinic.”

If the current study wanted a true comparison, they would measure and compare sulforaphane dose weights or amounts:

  • https://pubchem.ncbi.nlm.nih.gov/compound/sulforaphane lists sulforaphane’s molecular weight as 177.3 g / mol.
  • A 5.64 μmol sulforaphane amount (.001 / 177.3) equals a 1 mg weight of sulforaphane.
  • 200 μmol / 5.64 μmol = 35 mg sulforaphane used in the compared study.

But these researchers couldn’t even do that. They asserted a 32 mg sulforaphane dose “per manufacturer certificate of analysis” when they had the resources to do otherwise.

Why would a study that went to all the trouble of measuring sulforaphane not test their process by measuring their dose? Had they closely read the compared study, they may have also noticed that its commercial supplement, Prostaphane, was tested to verify stated dosage.

Are sulforaphane supplements better than microwaved broccoli sprouts?

Armando asked a good question in Upgrade your brain’s switchboard with broccoli sprouts:

“Is there any way to consume sulphorafane in a supplement form? Rather than have to jump so many hops to consume it from broccoli.”

The relevant 2017 study’s sulforaphane amount was:

“100 µmol [17.3 mg] sulforaphane as standardized broccoli sprout extract in the form of 2 gel capsules.”

One answer in A pair of broccoli sprout studies was No:

  • “Plasma and urinary levels of total SFN [sulforaphane] metabolites were ~3–5 times higher in sprout consumers compared to BSE [broccoli sprout extract] consumers.
  • In sprout consumers, plasma concentrations were 2.4-fold higher after consuming the second dose than after the first dose.
  • Calculated SFN bioavailability from broccoli sprouts exceeded 100%.”

That study was from 2015, though. Are better products than broccoli sprout extracts available now?


Image from the US Library of Congress

During Week 5 of Changing an inflammatory phenotype with broccoli sprouts, back in May when I still believed impossible things like we would:

I contacted a distributor of a dried broccoli sprout powder for evidence of their claim:

“Independent assays confirm that EnduraCELL yields more Sulforaphane per gram and per dose than any other broccoli sprout ingredient available! These assays showed that EnduraCell yields around 3.5 times more SULFORAPHANE than the next highest broccoli sprout product.”

I’ve asked three times for the lab assays. They declined each time to provide the data.

The company founder has written several reviews, one of which is entitled Sulforaphane and Other Nutrigenomic Nrf2 Activators: Can the Clinician’s Expectation Be Matched by the Reality? In Section 6.5 Sulforaphane it stated:

“By calculation, MYR [myrosinase]-active whole broccoli sprout supplement yielding 1% SFN could deliver 10 mg SFN per gram of powder, corresponding to ~12 grams of fresh broccoli sprouts (dried powder retains ~8% moisture).

The 2017 study’s dosage of “100 µmol [17.3 mg] sulforaphane as standardized broccoli sprout extract” weighed a gram or less, for a 1.73% sulforaphane yield. A broccoli sprout powder that could deliver “3.5 times” may have a 3.5 x 1.73% = 6.1% sulforaphane yield.

Using worst-case calculations from Estimating daily consumption of broccoli sprout compounds and Our model clinical trial for Changing to a youthful phenotype with broccoli sprouts, I eat at least 76 grams of 3-day-old broccoli sprouts daily. That would be 76 g / 12 = 6.3 grams of a “whole broccoli sprout supplement yielding 1% SFN” or ≈ 1 gram of a powder yielding 6.1% sulforaphane.

I immerse 3-day-old broccoli sprouts in 100 ml distilled water, then microwave them on 1000W full power for 35 seconds to achieve up to but not exceeding 60°C (140°F) per Microwave broccoli to increase sulforaphane levels. Worst-case estimates are 21 mg sulforaphane without microwaving and 30 mg sulforaphane with microwaving. The equivalent weight of a broccoli sprout powder yielding 6.1% sulforaphane for the worst case of microwaved broccoli sprouts is (30 mg / 21 mg) x 1 g powder = 1.4 grams of powder.

This 30 mg / 21 mg worst-case ratio could also be used to calculate a best case. If it’s true that:

  1. “Whole broccoli sprout supplement yielding 1% SFN could deliver 10 mg SFN per gram of powder” and
  2. The equivalent weight of microwaved broccoli sprouts is at least (30 mg / 21 mg) x 1 g powder = 1.4 grams of a broccoli sprout powder yielding 6.1% sulforaphane,

then my daily sulforaphane dosage is at least 10 mg x 6.1 x 1.4 = 85 mg.


My answer to Armando’s question would be No for sulforaphane supplements. I’d consider a whole broccoli sprout powder after lab assays were personally verified.

Microwave broccoli to increase flavonoid levels

This 2019 USDA study investigated representative broccoli cooking methods for their impact on kaempferol and quercetin levels:

“Understanding cooking effects on flavonoids is crucial to accurately estimate their daily intake and further investigate their health benefits. The purpose of this study was not to compare different conditions of each cooking methods, but to focus on retentions of the individual flavonoids under common cooking conditions in the US:

  • For boiling, we chose to use 85 seconds.
  • A 5-minute steaming time was used.
  • Microwave treatment was carried out in a 1200W microwave at full power for 1 minute.

Seven kaempferol (Km) glycosides and one quercetin (Qn) glycoside were identified and quantified in raw and cooked broccoli by HPLC-MS:

Boiling resulted in significant loss of all flavonoids, while steaming and microwaving led to minor losses or even increases of the flavonoids.

Microwaving without water or with small amount of water tended to retain or increase total phenolics and/or flavonoids. When a large amount of water was added during microwaving, to some extent resembling boiling, total phenolics and/or flavonoids decreased.

Different agriculture practices may affect flavonoids’ existence and their interactions with other compounds, which in turn alter their sensitivity to heat treatments.

Retention of nutrients in cooked foods can be calculated as apparent retention (AR) based on dry form, or true retention (TR) based on fresh/wet form. TR represents the actual consumption forms and also takes the weight change after cooking into consideration.

The possible explanation for TR over 100% is that the thermal processing may increase the extractability and/or the release from binding to other compounds as a result of matrix softening.”

https://www.cell.com/heliyon/fulltext/S2405-8440(19)30568-7 “Effects of domestic cooking on flavonoids in broccoli and calculation of retention factors”


The Material and methods section didn’t state that heated products’ temperatures were measured. So there wasn’t sufficient evidence for a solely thermal explanation of only microwaving achieving percentages over 100 per:

“The possible explanation for TR over 100% is that the thermal processing..”

A more plausible explanation similar to Microwave broccoli to increase sulforaphane levels may account for microwaving’s increased percentages:

“Microwave treatment causes a sudden collapse of cell structure due to the increase in osmotic pressure difference over vacuole membrane.

We didn’t expect this result, and think microwave irradiation might help to release more conjugated forms of glucosinolates and then get hydrolyzed by released myrosinase.”


I immerse 3-day-old broccoli sprouts in 100 ml distilled water, then microwave them on 1000W full power for 35 seconds to achieve up to but not exceeding 60°C (140°F). After microwaving I transfer broccoli sprouts to a strainer, and allow further myrosinase hydrolization of glucoraphanin and other glucosinolates into sulforaphane and other healthy compounds.

Myrosinase deactivation above 60°C apparently wasn’t a consideration, since boiling, steaming, and a 1200W microwave on full power for one minute may have produced temperatures above 60°C. I’ll guess that an active enzyme wasn’t a requirement for flavonoid contents of broccoli purchased in a Beltsville, Maryland, grocery store.

The microwave tests used:

“Broccoli florets (150 g) were put in a microwave safe bowl with a 1 tablespoon [15 ml] of water.”

I use:

  • A lesser weight of 3-day-old broccoli sprouts;
  • A greater volume of distilled water;
  • A less powerful microwave operated on full power for a lesser duration.

Before microwaving, I would expect a worst-case estimated 77 mg total flavonoids from eating 3-day old broccoli sprouts every day. This study’s findings lead me to expect that current practices with microwaving would improve flavonoid levels.

Don’t overcook broccoli

This 2020 US / Korea study set a low bar and jumped over it by finding:

“The abundance of GSL [glucosinolate] hydrolysis products in cooked samples was lower compared to the raw samples.

Regardless of different cooking methods and durations, the total GSL amount in MeJA [methyl jasmonate]-treated broccoli was still higher than in the non-treated broccoli. This suggests that the increased GSL concentration in broccoli samples was solely affected by MeJA treatment, and the effect of MeJA was not affected by cooking methods.

Effect of cooking and 250 µM MeJA treatment on (A) total aliphatic glucosinolates, (B) total indole glucosinolates, and (C) total glucosinolates in ‘Green Magic’ broccoli. * = detected significant different by Student’s T-test (p ≤ 0.05, n = 3) with a significant interaction between MeJA treatment and cooking treatment.”

https://www.mdpi.com/2304-8158/9/6/758/htm “Methyl Jasmonate Treatment of Broccoli Enhanced Glucosinolate Concentration, Which Was Retained after Boiling, Steaming, or Microwaving”


Did it advance science to only replicate mistakes in consumer broccoli cooking methods with:

“The abundance of GSL hydrolysis products in cooked samples was lower compared to the raw samples.”

No.

Did the study design have tests to provide cooking method guidance for:

“To date, methods of delivering cooked broccoli without losing its nutritional benefits are still lacking in the literature, although consuming cooked broccoli is the most common practice for consumers.”

No.

Were there cooking method and temperature recommendations to avoid:

“Cooking also inactivates myrosinase, the enzyme converting GSL into hydrolysis products, and then hinders the formation of hydrolysis products.”

No.

Were there cooking method tests to further enhance either control samples or:

“Exogenous methyl jasmonate (MeJA) treatment was known to increase the levels of neoglucobrassicin and their bioactive hydrolysis products in broccoli.”

No.

Why omit temperature measurements since:

“The major research questions of this study were to evaluate how MeJA application to broccoli plants will affect GSL concentration, myrosinase activity, GSL hydrolysis product amounts..”

Maybe Microwave broccoli to increase sulforaphane levels wasn’t yet published when this study’s design decisions were made. Still, why would a study:

  • Test microwave half power without also testing full power?
  • Select microwaving time as the sole measurement without also measuring temperature?

Table S1 and Figure 3 of the Chinese / USDA study showed a two-minute microwaving time at 50% power wouldn’t be expected to have any sulforaphane content significantly different from uncooked broccoli. Also, temperatures of a five-minute microwaving time at 50% power were guaranteed to completely deactivate myrosinase.

Supplementary material confirmed that this study’s microwaving parameters didn’t show anything of value for how to use your microwave to increase broccoli compound levels. Did the study’s findings provide much more than what not to do?

Poor design decisions created a large gap between what could have been studied and what was studied. Let’s hope there will be better use of resources next time.

One of these numbers is not like the others

117622 / 330937295 = 0.000355

or 0.0355%

.133 x 330937295 = 44,014,660

So 44+ million people were thrown out of work in the US to justify and accompany a cover story of a disease that would have to triple its death rate to reach one-tenth of one percent?

Are we a nation of math illiterates? This makes sense only to those who are impelled to gain power over people’s lives for no reason other than to have power.

No wonder the narrative changed four weeks ago to race.

What topics have your conversations been obsessed with the past four weeks? Are you running with the herd? Take caution of the herd’s destination.

A compelling review of epigenetic transgenerational inheritance

This 2020 review by coauthors of 2019’s A transgenerational view of the rise in obesity and Epigenetic transgenerational inheritance extends to the great-great-grand offspring summarized:

“The prevalence of obesity and associated diseases has reached pandemic levels.

Ancestral and direct exposures to environmental toxicants and altered nutrition have been shown to increase susceptibility for obesity and metabolic dysregulation. Environmental insults can reprogram the epigenome of the germline (sperm and eggs), which transmits the susceptibility for disease to future generations through epigenetic transgenerational inheritance.

During the 1950s, the entire North American population was exposed to high levels of the pesticide DDT, when the obesity rate was < 5% of the population. Three generations later, the obesity frequency in North America is now ~45% of the population.”

https://www.sciencedirect.com/science/article/abs/pii/S1043276020300515 “Epigenetic Transgenerational Inheritance of Obesity Susceptibility” (not freely available)


Do any of us have accurate and complete medical histories of our parents back to our great-great-grandparents? Did any of our ancestors record their exposures to environmental toxicants?

The research community has been conditioned to not trust research done primarily from one source. Dr. Michael Skinner’s labs at Washington State University are suspect by this preconception.

A researcher there addressed the situation when I asked. Their answer in A self-referencing study of transgenerational epigenetic inheritance ended with:

“We hope to see other labs contributing to this particular field and we will be delighted to cite them. In the meantime, our only option is to reference our previous work.”

It’s especially time for toxicologists to overcome their behavioral conditioning. If they don’t understand how epigenetic transgenerational inheritance impacts their field now, will they ever get a clue?

Our ancestors’ experiences have much to do with our physiologies. The biological evidence is compelling, yet it continues to be ignored and misconstrued.

Part 2 of Do broccoli sprouts treat migraines?

To follow up Do broccoli sprouts treat migraines? which used a PubMed “sulforaphane migraine” search, a PubMed “diindolylmethane” search came across a 2020 Czech human cell study Antimigraine Drug Avitriptan Is a Ligand and Agonist of Human Aryl Hydrocarbon Receptor that Induces CYP1A1 in Hepatic and Intestinal Cells that had this informative Introduction:

“The aryl hydrocarbon receptor (AhR) transcriptionally controls a wide array of genes. AhR is a critical player in human physiology (e.g., hematopoiesis) and also in many pathophysiological processes such as diabetes, carcinogenesis, inflammation, infection or cardiovascular diseases.

Suitable candidates for off-targeting AhR could be the antimigraine drugs of triptan class, which have an indole core in their structure. Indole-based compounds were demonstrated as ligands of AhR, including dietary indoles (e.g., indole-3-carbinol and diindolylmethane).”

Adding AhR to the search showed:

Changing the PubMed search to “icz migraine” pulled up a 2013 review Biomedical Importance of Indoles that described sumatriptan as an indole, and:

“Since DIM accumulates in the cell nucleus, it likely contributes to cell nuclear events that have been ascribed to I3C.”

Widening the search to “i3c ahr” added:

Changing the search to “i3c migraine” picked up a 2011 UK human study Effect of diindolylmethane supplementation on low-grade cervical cytological abnormalities: double-blind, randomised, controlled trial:

“In the study reported here, there was no statistically significant difference in serious adverse events between groups; in fact a higher proportion of women in the placebo group reported a serious adverse event. Although this study did not have sufficient power to study migraines, we did find a non-significant increase in reported headaches (18% on DIM, 12% on placebo, P=0.12).”

Returning to the original PubMed “sulforaphane migraine” search, Bioavailability of Sulforaphane Following Ingestion of Glucoraphanin-Rich Broccoli Sprout and Seed Extracts with Active Myrosinase: A Pilot Study of the Effects of Proton Pump Inhibitor Administration included one subject who took migraine medication. They weren’t a study outlier, however.


Although indole chemistry indicates a broccoli sprouts – migraine connection, I haven’t found relevant research. Maybe the known properties and actions of broccoli sprout compounds provide enough to affect causes of migraines?

Eat broccoli sprouts for DIM

This 2019 Spanish human study ran in parallel with Our model clinical trial for Changing to a youthful phenotype with broccoli sprouts. I’ll focus on the aspect of diindolylmethane (DIM) from eating broccoli sprouts:

“The aim of this study is to evaluate the effect of gender or hormonal status (menopause) on the bioavailability of broccoli sprouts in different cohorts of overweight adult subjects: men, non-menopausal women and post-menopausal women.

3,3′-diindolylmethane (DIM) was detected and quantified in all volunteers. It increased significantly during broccoli [sprouts] ingestion in men. However, a steady decrease of its urinary concentration was observed in post-menopausal women that was significant at day 50. No significant changes were observed in premenopausal women. Albeit this different behaviour, no significant differences between the three groups were detected by the different statistical tests performed.

High increases observed in SFN-metabolites in the three cohorts confirm that the fresh product is a good source of bioactive compounds bioavailable in the organism. We detected high amounts of 3,3-DIM in urine samples, which can be related to the metabolism of glucobrassicin derivatives from our broccoli sprouts.

Post-menopausal women seem to metabolize isothiocyanates in a greater extension. Hormonal status and differences in gut microbiota may influence the bioavailability of isothiocyanates from broccoli sprouts but more studies are needed to support this statement.”

https://www.sciencedirect.com/science/article/abs/pii/S1756464619303147 “Bioavailability of broccoli sprouts in different human overweight populations” (not freely available)


“Post-menopausal women seem to metabolize isothiocyanates in a greater extension. A steady decrease of its [DIM] urinary concentration was observed in post-menopausal women that was significant at day 50.”

Subjects ate broccoli sprouts every day through Day 35, then stopped, and were measured again at Day 50. The only example of measurements where Day 35 was less than Day 0 was postmenopausal women retaining more broccoli sprout indolic compounds’ metabolite, DIM, than excreting it.

That Day 35 data point didn’t have an asterisk next to it to indicate a statistically significant decrease. But the group’s next Day 50 significant “steady decrease” finding supported an interpretation that eating broccoli sprouts supplied those overweight postmenopausal women with DIM that they especially needed.

Regarding the huge percentage changes above, our model clinical trial found in a longer time frame:

The decrease in IL-6 levels was significantly related to the increase in 24 h urine SFN [sulforaphane] levels. In case of C-reactive protein, the decrease was significantly related to the increases in 24 h urine SFN-NAC [SFN-N-acetylcysteine] and SFN-CYS [SFN-cysteine].

I’ll guess that these parallel trial subjects also experienced similar benefits from eating broccoli  sprouts every day for five weeks. See Day 70 results from Changing to a youthful phenotype with broccoli sprouts for another guess that even shorter time frames would be effective.


Broccoli sprout indolic compounds that metabolize to DIM:

Day 70 results from Changing to a youthful phenotype with broccoli sprouts

Here are my Day 70 measurements* to follow up Our model clinical trial for Changing to a youthful phenotype with broccoli sprouts, which had these findings:


Keep in mind that I’m not in the population represented by the clinical trial sample:

  1. My chronological age is above their inclusion range;
  2. My BMI is below their inclusion range; and
  3. I take supplements and meet other exclusion criteria.

I also didn’t take Day 0 measurements.

June 2019 BMI: 24.8

June 2020 BMI: 22.4

2020 IL-6: 1.0 pg / ml. See Part 2 of Rejuvenation therapy and sulforaphane for comparisons.

2020 C-reactive protein: < 1 mg / l.

2019 and 2020 No biological age measurements. Why aren’t epigenetic clocks standard and affordable?


I’ve made four lifestyle “interventions” since last summer:

  1. In July 2019 I started to reduce my consumption of advanced glycation end products after reading 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.
  2. In September I started non-prescription daily treatments of Vitamin D, zinc, and DHEA per clinical trial Reversal of aging and immunosenescent trends.
  3. Also in September, I started non-prescription intermittent quercetin treatments of Preliminary findings from a senolytics clinical trial.
  4. I started eating broccoli sprouts every day eleven weeks ago.

1. Broccoli sprouts oppose effects of advanced glycation end products (AGEs) provided examples of Items 1 and 4 interactions.

2. Two examples of Item 2 treatment interactions with Item 4 are in Reversal of aging and immunosenescent trends with sulforaphane:

  • “The effects of the combined treatment with BSE [broccoli sprout extract] and zinc were always greater than those of single treatments.”
  • “Vitamin D administration decreased tumor incidence and size, and the co-administration with SFN [sulforaphane] magnified the effects. The addition of SFN decreased the activity of histone deacetylase and increased autophagy.”

3. How broccoli sprout compounds may complement three supplements I take was in a 2020 review Central and Peripheral Metabolic Defects Contribute to the Pathogenesis of Alzheimer’s Disease: Targeting Mitochondria for Diagnosis and Prevention:

“The nutrients benefit mitochondria in four ways, by:

  • Ameliorating oxidative stress, for example, lipoic acid;
  • Activating phase II enzymes that improve antioxidant defenses, for example, sulforaphane;
  • Enhancing mitochondrial remodeling, for example, acetyl-l-carnitine; and
  • Protecting mitochondrial enzymes and/or stimulating mitochondrial enzyme activities, for example, enzyme cofactors, such as B vitamins and coenzyme Q10 .

In addition to using mitochondrial nutrients individually, the combined use of mitochondrial nutrients may provide a better strategy for mitochondrial protection.”

The review provided a boatload of mitochondrial multifactorial analyses for Alzheimer’s. But these analyses didn’t include effective mitochondrial treatments of ultimate aging causes. I didn’t see evidence of why, after fifteen years of treating mitochondrial effects with supplements, treating one more effect could account for my Week 9 vastly different experiences.


I nod to An environmental signaling paradigm of aging explanations. Its Section 10 reviewed IL-6, C-reactive protein, senescence, and NF-κB in terms of feedback loops, beginning with:

“It is clear that the increasing number of senescent cells depends on the post-adult developmental stage rather than chronological age. The coincidence that these processes result in particular forms of impairment in old age does not seem to be random as it is present in all mammals, and may be causative of many aspects of aging.”

A derived hypothesis: After sufficient strength and duration, broccoli sprout compounds changed my signaling environment, with appreciable effects beginning in Week 9.

I offered weak supporting evidence in Upgrade your brain’s switchboard with broccoli sprouts where a study’s insufficient one week duration of an insufficient daily 17.3 mg sulforaphane dosage still managed to change a blood antioxidant that may have changed four thalamus-brain-area metabolites. For duration and weight comparisons, I doubled my daily amount of broccoli seeds from one to two tablespoons just before Week 6 (Day 35), and from that point onward consumed a worst-case estimated 30 mg sulforaphane with microwaving 3-day-old broccoli sprouts every day.

Maybe a promised “In a submitted study, we will report that peripheral GSH levels may be correlated with cognitive functions” will provide stronger evidence? I’m not holding my breath for relevant studies because:

  • There wouldn’t be potential payoffs for companies to study any broccoli sprout compound connections with research areas such as aging, migraines, etc. Daily clinically-relevant broccoli sprout dosages can be grown for < $500 a year.
  • Sponsors would have to change paradigms, a very-low-probability event. They’d have to explain why enormous resources dedicated to current frameworks haven’t produced effective long-term treatments.

What long-term benefits could be expected if I continue eating broccoli sprouts every day?

The longest relevant clinical trial I’ve seen – referenced in Part 2 of Reversal of aging and immunosenescent trends with sulforaphane – was twelve weeks. Part 2 also provided epigenetic clock examples of changes measured after 9 months, which accelerated from there to the 12-month end-of-trial point.

Reviewing clinical trials of broccoli sprouts and their compounds pointed out:

“Biomarkers of effect need more time than biomarkers of exposure to be influenced by dietary treatment.”


A contrary argument: Perhaps people don’t require long durations to effectively change their signaling environments?

I apparently didn’t start eating an effective-for-me daily broccoli sprouts dosage until Day 35, when I changed from one to two tablespoons of broccoli seeds a day. If so, Weeks 6 through 8 may account for my substantial responses during Week 9.

Could eating broccoli sprouts every day for four weeks dramatically change a person’s signaling environment?

Do you have four weeks and $38 to find out? Two tablespoons of broccoli seeds = 38 g x 30 days = 1.14 kg or 2.5 lbs.

This is what twice-a-day one-tablespoon starting amounts of broccoli seeds look like through three days:


Maintaining the sprouting process hasn’t been a big effort compared with the benefits.

In the absence of determinative evidence, I’ll continue eating broccoli sprouts every day. Several areas of my annual physical have room for improvements. Extending my four lifestyle “interventions” a few more months may also provide hints toward inadequately researched connections.

* Results may not be extrapolatable to other people, to any specific condition, etc.