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 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 more palatable. Seeds that have 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 that have soaked for at least two hours:

  • 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.

I’ll guess that using 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 after ingesting a 200 μmol (35 mg) sulforaphane supplement dose. Row 2’s time was at the study’s first of three measurement intervals (3, 6, and 12 hours), and peak time probably took place earlier.

There’s much variation among individual responses to sulforaphane supplements. The 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 – demonstrate how a sulforaphane supplement metabolic profile was different than a fresh broccoli sprout profile:

My metabolic profile resulting from current practices is probably in between the Sprout and BSE divided-dose statistics in the above graphic:

  • My sulforaphane intake is greater than eating raw broccoli sprouts because I microwave 3-day-old broccoli sprouts to create an increased amount of sulforaphane in them before eating.
  • Sulforaphane is metabolized more quickly because I don’t depend upon my metabolism to create broccoli sprout hydrolization compounds like sulforaphane.
  • My 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 one minute through five minutes to be leaching caused by leaving the broccoli sample immersed in water. So I strain water from broccoli sprouts after microwaving, the Time 0 mark of the above graphic.

The divided dose part of the first of the pair studies 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.”

Sulforaphane supplements are readily metabolized, blood plasma levels peak by two hours, and dissipate by eight hours. To the extent my metabolism is closer to a sulforaphane supplement profile than a raw broccoli sprouts profile, maybe that leaves the door open to a broccoli seed dose at lunch time? My beautiful woman thinks so.

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.

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.

Week 10 of Changing to a youthful phenotype with broccoli sprouts

To follow up Week 9 of Changing to a youthful phenotype with broccoli sprouts:

1. I increased three of eight upper body exercises by 50% through adding another set. I did it because I didn’t feel muscle exhaustion after two sets like I’d previously felt. 🙂

Cognitively, see A claim of improved cognitive function and its follow on Upgrade your brain’s switchboard with broccoli sprouts.

2. It’s been inspirational at times, and at other times, dull, duller, dullest, to do what’s necessary and keep on track. But the efforts paid off when Week 9 was unlike any previous week!

I expressed appreciation in Our model clinical trial for Changing to a youthful phenotype with broccoli sprouts because scientific evidence provides great bases for intentional behavior. It’s still up to me to voluntarily carry out my part. And why wouldn’t I act when my healthspan and lifespan are the consequences? Except…

What if I’d been:

  • Tired of the hassle, or bored with self-imposed discipline, or lazy, and quit?
  • Projecting personal problems onto others, such that improving my present and future became less important than act-outs?
  • Distracted by, or believed propaganda, or participated in Madness of Crowds behavioral contagion, and missed day after day of required actions?

I may not have ever experienced Week 9’s intermediate-term benefits!

If I keep going past ten weeks, what long-term benefits could be expected?

Our model clinical trial didn’t say how researchers decided on a ten-week period for subjects to consume broccoli sprouts every day. I asked a study coauthor about trial duration, but no answer yet.

A few of the same coauthors answered generally in Reviewing clinical trials of broccoli sprouts and their compounds:

Biomarkers of effect are early stage end-points, for instance the modulation of phase 2 enzymes by glucosinolates. They need more time than biomarkers of exposure to be influenced by the dietary treatment.

Hence, length or duration of the study must be defined according to the biomarker measured to be modified, that is, to define perfectly the time of exposure to observe changes in relevant parameters. Gene expression is one important target for glucosinolates, and it requires a sufficient period of exposure to (de)activate signaling pathways involved.

It is crucial to find appropriate biomarkers of effect that are linked to later disease outcomes, and more investigation is needed in this sense. Post-study follow-up can be of great value in assessing the persistence of certain effects, or in discovering those that appear more long-term.

3. I’ll go into a clinic on Sunday for Day 70 truth tests. Here they are: Day 70 results from Changing to a youthful phenotype with broccoli sprouts!

Our model clinical trial for Changing to a youthful phenotype with broccoli sprouts

The further I get into a daily regimen of eating broccoli sprouts for ten weeks, the more I appreciate “Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects.”

“This study represents an advance in intervention studies as the broccoli sprouts were included in a daily dietary pattern in quantities that reflect a real consumption. The hypothesis of our research is that broccoli sprouts are able to reduce the inflammatory status in overweight subjects due to their content in phytochemicals, mainly glucosinolates.

Total concentration of aliphatic glucosinolates was 80.50 mg/30 gf.w. This concentration was two-fold higher than indolic glucosinolates. Volunteers consumed an average of 51 mg (117 μmol) and 20 mg (42 μmol) of glucoraphanin and neoglucobrassicin, respectively, on a daily basis, during the 70 days of the dietary intervention. Considering an amount of GRA [glucoraphanin] of 117 μmol by serving, a 4% on average was metabolized through mercapturic acid pathway.

No significant changes were observed in weight and BMI. By contrast, body fat mass slightly decreased significantly after 70 days of broccoli [sprout] consumption and returned to basal levels at day 90, a state that was maintained until day 160.

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].

The possible synergistic interaction of both SFN and 3,30-DIM and the isothiocyanates erucin and sulforaphane are interconvertible, so that the anti-inflammatory effects observed with broccoli sprouts intake are likely due to the combined effects of all the hydrolysis products of glucosinolates.

https://www.sciencedirect.com/science/article/abs/pii/S0261561418301183 (Not freely available, better format) and https://researchonline.lshtm.ac.uk/id/eprint/4647168/ (freely available)


Modifications I’ve made to the clinical trial’s protocols include:

  1. I start new broccoli sprout batches twice a day with one tablespoon of seeds per A pair of broccoli sprout studies.
  2. Per 3-day-old broccoli sprouts have the optimal yields, I consume broccoli sprouts when they’re 3 days old. The clinical trial subjects ate broccoli sprouts that were at least a week old.
  3. 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.
  4. Per Enhancing sulforaphane content, 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.

I use the above studies as guides to create broccoli sprout hydrolysis compounds just before eating them. I don’t depend on my metabolism to create sulforaphane, DIM, erucin, and other hydrolysis compounds as did the clinical trial. But then again, those subjects ate super sprouts:

“We used the elicitor methyl jasmonate (MeJA) by priming the seeds as well as by spraying daily over the cotyledons from day 4-7 of germination. We observed that MeJA at concentrations of 250 μmol 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 a 70% and similar increases were observed with glucoiberin or glucobrassicin. In this way, we improved the content of these health-promoting compounds.”

I don’t have a scale in my kitchen, and don’t have a measured weight of broccoli sprouts consumed daily. It’s probably more than twice the clinical trial’s 30 grams:

  • My most recent broccoli seed purchase was a 5 pound can (2,268 grams). Its volume by the formula height x π x (diameter / 2)2 with 17 cm height and 15 cm diameter is 1,767 cubic centimeters.
  • With 1 tablespoon = 14.79 cc, (14.79 cc / 1,767 cc) x 2,268 grams = 19 grams per serving. Broccoli seed weight of two servings is 19 x 2 = 38 grams a day.
  • The lowest weight gain for 3-day-old broccoli sprouts in Item 2 above was 4.32 times the seed weight. That was in laboratory conditions, though.
  • Let’s guess that 3-day-old broccoli sprouts only gain twice as much weight in my kitchen, 38 g x 2 = 76 grams. A comparable worst-case Estimating daily consumption of broccoli sprout compounds calculation was 75.52 grams.

I’ve referenced our model clinical trial in 15 previous blog posts. They are, in date descending order:

  1. A pair of broccoli sprout studies
  2. Reversal of aging and immunosenescent trends with sulforaphane
  3. A hair color anecdote
  4. Week 7 of Changing to a youthful phenotype with broccoli sprouts
  5. Part 2 of Rejuvenation therapy and sulforaphane
  6. A rejuvenation therapy and sulforaphane
  7. Week 6 of Changing an inflammatory phenotype with broccoli sprouts
  8. Week 3 of Changing an inflammatory phenotype with broccoli sprouts
  9. Broccoli sprouts oppose effects of advanced glycation end products (AGEs)
  10. Reviewing clinical trials of broccoli sprouts and their compounds
  11. Understanding a clinical trial’s broccoli sprout amount
  12. Week 2 of Changing an inflammatory phenotype with broccoli sprouts
  13. Changing an inflammatory phenotype with broccoli sprouts
  14. Growing a broccoli sprouts Victory Garden
  15. How much sulforaphane is suitable for healthy people?

Upgrade your brain’s switchboard with broccoli sprouts

Further investigating A claim of improved cognitive function, Part 3 of Rejuvenation therapy and sulforaphane offered:

“Improving brain function does not depend on neurogenesis as much as it does on synapse formation and factors such as NMDA receptors which decline in density with age.”

A PubMed “sulforaphane NMDA receptors” search turned up a 2019 cell study The glutathione cycle shapes synaptic glutamate activity:

Sulforaphane is a potent inducer of the Nrf2 transcription factor, has blood–brain barrier penetration, and might expand the size of the glutathione reservoir by our observation that it increases expression of GCL [glutamate cysteine ligase], the rate-limiting step in glutathione biogenesis. Our recent study in human subjects revealed that sulforaphane elevates peripheral glutathione levels and those of other brain metabolites.”

The referenced study was a 2017 Sulforaphane Augments Glutathione and Influences Brain Metabolites in Human Subjects: A Clinical Pilot Study:

“We found that the naturally occurring isothiocyanate sulforaphane increased blood GSH [reduced glutathione] levels in healthy human subjects following 7 days of daily oral administration. In parallel, we explored the potential influence of sulforaphane on brain GSH levels in the anterior cingulate cortex, hippocampus, and thalamus via 7-T magnetic resonance spectroscopy.

A significant positive correlation between blood and thalamic GSH post- and pre-sulforaphane treatment ratios was observed, in addition to a consistent increase in brain GSH levels in response to treatment. The sulforaphane response in brain GSH levels is not influenced by age, sex, or race.

The participants were given 100 µmol sulforaphane as standardized broccoli sprout extract in the form of 2 gel capsules, and instructed to ingest the extract each morning for 1 week.

Following sulforaphane administration, the increase in blood GSH was positively correlated with GABA, Gln [glutamine], Glu [glutamate], and GSH in the THAL [thalamus]. Although these correlations were not significant following multiple comparison, they remain suggestive. Power analysis calculations suggest that a sample size of n = 50 would yield a significant result, and this will be the focus of a future study.

As has been reported for cardiovascular and cerebrovascular diseases, longer treatment duration and/or higher dosages may be warranted. In a submitted study, we will report that peripheral GSH levels may be correlated with cognitive functions.”


One week of consuming sulforaphane wasn’t long enough to achieve much. Not enough subjects and “higher dosages may be warranted” were also thrown in to explain the lack of significant results.

Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease estimated the “100 µmol sulforaphane” dosage to be 17.3 mg. Worst-case estimates made in Estimating daily consumption of broccoli sprout compounds are that since doubling the starting amount of broccoli seeds from one to two tablespoons in Week 6, I’ve consumed 30 mg sulforaphane with microwaving 3-day-old broccoli sprouts every day.

Something happened where the promised “In a submitted study, we will report that peripheral GSH levels may be correlated with cognitive functions” either wasn’t performed or wasn’t published. The follow-on 2019 study became a cell study instead of a 50+ person study.


The study’s thalamus findings provided plausible explanations for why eating a clinically relevant amount of broccoli sprouts every day since at least Week 6, Week 9 was so much different from the others. Sulforaphane changed a blood antioxidant which may have changed four thalamus metabolites.

The thalamus part of our brain is analogous to a switchboard. Signals pass through it to and from other brain areas.

Signals can be routed better when we clean up and upgrade wiring, and lower circuit resistance.