A hair color anecdote

Will you excuse a poorly-evidenced observation that’s a positive development I left out of Week 8 of Changing to a youthful phenotype with broccoli sprouts?

I got a haircut last weekend after waiting for Governor Klan Robes Blackface to not arrest barbershop and hair salon owners for the crime of earning a living. A thirty-something tattooed barber wearing a face mask and face shield said my last haircut had been on February 1, 2020, so it had been 14 weeks. She used a #4 clipper to cut everything to about 1/2 inch.

I’d eaten broccoli sprouts every day for 7 weeks at that point. Post-haircut visible hair was all from that period, probably since Week 3, which was also when broccoli sprouts’ effects on inflammation became noticeable.

One evening as I brushed my teeth, I noticed overall hair appearance was mainly dark brown again, an unexpected phenomenon. Maybe white hair will show up as it gets longer?

Feedback on hair color from a back-of-the-head picture was mixed, ranging from “Yes. Definitely!” to Unsupported non-evidence since before and after pictures weren’t taken under the same lighting conditions. Even if validated, other factors could be in play, such as working from home without the stress of going into work.


While eating my usual steel cut oats for breakfast this morning, I remembered a super informative presentation by the lead researcher of clinical trial Reversal of aging and immunosenescent trends. I rewatched it, pausing after two minutes to reabsorb when he said:

“There’s a collapse that takes place somewhere between the ages of sixty to eighty in which you lose 98% of your ability to recognize foreign antigens.”

You will have forgotten why I drew your attention to this super interesting presentation by the 21:25 mark. But pause for the “Hair Rejuvenation?” slide with before and after photos:

“A couple of guys came to us and said they seemed to notice that their hair was growing in darker again. It’s an anecdote. It didn’t apply to most of the guys. But it’s a sign that maybe something interesting is going on.”

That’s followed by epigenetic clock findings using four different clocks. Note that no significant effects on biological age were found until the trial’s 9-month point, and those weren’t as strong as improvements by 12 months.

Improvements accelerated between 9 and 12 months, and at 12 months, subjects had increased their life expectancies by 2 years. The GrimAge clock showed the subjects’ predicted lifespan and health span was unchanged 6 months after the trial ended.


I started and have continued four lifestyle “interventions” since last summer:

  1. In July I dramatically reduced 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 this trial’s non-prescription daily treatments of Vitamin D, zinc, and DHEA.
  3. Also in September, I started non-prescription intermittent quercetin treatments of Preliminary findings from a senolytics clinical trial.
  4. Eight weeks ago I started eating broccoli sprouts every day per clinical trial Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects.

In a month or so I should be able to say whether or not my hair really is growing in darker. One way to find out which “intervention” had the largest effect may be to stop one or more of them. That might happen anyway because:

  1. Consistently eating AGE-less food is boring.
  2. I’m leery of taking more than RDAs.
  3. Ehh.
  4. I still sadly hope against reality that we’re past the Madness of Crowds phase and can accelerate the “recover their senses slowly, one by one” phase. It would be harder to take care of my broccoli sprout farm if I have to go into work every day.

Or maybe An environmental signaling paradigm of aging is correct, and at a certain point, clocks are reset and none of these “interventions” will be needed? What do you think?

 

Week 8 of Changing to a youthful phenotype with broccoli sprouts

To follow up Week 7 of Changing to a youthful phenotype with broccoli sprouts:

1. I changed practices per Enhancing sulforaphane content. After microwaving to achieve 60°C, I now transfer broccoli sprouts to a strainer, and allow further myrosinase hydrolization of glucoraphanin and other glucosinolates into sulforaphane and other healthy compounds. I previously cooled them immediately.

They taste better, too, and I stopped putting mustard in them to make them more palatable. What does letting 3-day-old broccoli sprouts cool down by themselves to increase sulforaphane do that makes them more agreeable?

Despite improving yields two weeks ago, 3-day-old broccoli sprouts started from two tablespoons of broccoli seeds still fit into a Corning Ware 16 fl. oz. / 473 ml container:

2. I made worst-case estimates in Estimating daily consumption of broccoli sprout compounds of 20.71 mg sulforaphane without microwaving and 29.86 mg sulforaphane with microwaving in 3-day-old broccoli sprouts. They fit within:

“The daily SFN [sulforaphane] dose found to achieve beneficial outcomes in most of the available clinical trials is around 20-40 mg.”

The post’s point was: how can a person guide their actions with evidence when a broccoli cultivated variety’s beneficial characteristics aren’t known? I’ll repeat a sulforaphane yields graphic from the 3-day-old broccoli sprouts have the optimal yields study for examples of unknowns:

A. If sulforaphane content was a consumer’s overriding concern. the above evidence suggests that it would be better to always eat the seeds of an unknown cultivar. A tablespoon seems like a good choice, but be sure to chew the broccoli seeds thoroughly (try for five minutes) to release myrosinase.

The first minute goes alright. Sometime after that, your mouth and the back of your throat starts to burn. That will be a reminder of an evolved function that protects plants from predators.

I haven’t successfully swallowed a mouthful of thoroughly chewed broccoli seeds without also eating something else or drinking more than just water. That might not go along with your plan for a snack or eating before bedtime.

B. The study recommended consuming 3-day-old sprouts because:

Although germination reduces SF [sulforaphane] yield to some extent, it is beneficial to the formation and accumulation of total phenol and flavonoids, ensuring the health properties of sprouts.”

Fine, but if your unknown cultivar’s sulforaphane characteristics look like the third cultivar’s 3-day-old sprouts, you’ll have a 53% reduction in the sulforaphane weight. Should you take a 1-in-6 chance with Day 5 sprouts? Or stick with Day 3, guessing that they may still yield more sulforaphane than 3 of the 5 other cultivars’ Day 3 broccoli sprouts?

C. What if you can’t stomach the appearance of 3-day-old broccoli sprouts per the above photo, and you prefer microgreens? Should you wait until Day 7, and take a 1-in-6 chance that your unknown cultivar’s characteristics are like the highest Day 7 of the fourth cultivar? When you roll the die, does it come up 4?

Broccoli seed bulk suppliers aren’t providing evidence for their products and educating customers. Their marketing strategy depends more on buzzwords and price.

3. I compared lab reports of 3 broccoli sprouts’ cultivars in Lab analyses of broccoli sprout compounds to see if they helped rationally deal with these unknowns. It turned out that not much could be accurately inferred from lab reports, past knowing that broccoli sprouts of one cultivar produced more sulforaphane than another.

I haven’t found studies of cultivar characteristics for items I could actually purchase in bulk. I contacted five small US and Canadian suppliers to ask “Do you sell broccoli seeds that have lab evidence of the cultivar’s sulforaphane content?” Two said no so far. I contacted another supplier for the home garden business who has two dozen cultivars listed for sale and asked them the same question.

None of the broccoli seed bulk suppliers specified the cultivar on their offering. When pressed on Amazon they at best said Calabrese, which has described hundreds of cultivars. Such as two in this study, Iron Man and Marathon, which are also named Calabrese Iron Man F1 and Calabrese Marathon F1.

4. I’ve had only sporadic inflammation, and I’m tempted to write anecdotes of positive things. But self-reports are better evidence for emotions than for other internal events.

See Week 9 of Changing to a youthful phenotype with broccoli sprouts for follow ups.

Enhancing sulforaphane content

This 2020 Chinese study experimented with enhancing sulforaphane content of broccoli florets in a range of conditions:

“For direct water blanching at 60°C, the sulforaphane yield increased with treatment time from 1698.0 ± 121.9 μmol per kg DW (0 min) to 2833.3 ± 118.6 μmol per kg DW (1 min) and then steadily decreased to the lowest value of 2345.8 ± 57.7 μmol per kg DW for 5 min.”

The sulforaphane yield was 503.7 ± 23.8 μmol per kg DW of broccoli after 5 min thermal treatment at 65 °C, which was even lower than the value obtained for raw broccoli. The reason could be the leaching of glucoraphanin into the blanching water coupled with partial inactivation of myrosinase resulting in low yield of sulforaphane.

For direct water blanching, the best treatment temperature for maximizing sulforaphane yield was 60 °C, which is similar to the best treatment temperature for maximizing sulforaphane yield reported previously.

Sulforaphane yield depends on the relative activity of myrosinase and ESP in the broccoli matrix and 3 min treatment at 65 °C during in-pack processing in this study was found to be the best condition that favours conversion into sulforaphane instead of sulforaphane nitrile. This indicates that the condition favours the inactivation of ESP to a larger extent while maintaining sufficient myrosinase activity resulting in optimal conversion into sulforaphane.

Under this condition, it seems that all of the extractable glucoraphanin is converted to sulforaphane assuming 1 to 1 conversion, since the glucoraphanin content of the broccoli samples were determined to be 3141.2 μmol per kg DW whereas the sulforaphane yield was 3983 μmol per kg DW. The slightly higher sulforaphane yield than would be predicted from the level of glucoraphanin in raw broccoli requires further investigation.”

https://pubs.rsc.org/en/content/articlehtml/2020/fo/c9fo02089f “Mild heat combined with lactic acid fermentation: a novel approach for enhancing sulforaphane yield in broccoli puree”


1. The study presented evidence for kitchen practices:

  • Per the above graphic’s point a, I’ve changed to let broccoli sprout heating continue for 1 minute after microwaving to achieve 60°C. This allows further myrosinase hydrolization of glucoraphanin into sulforaphane. My practice had been to immediately cool them down, which was suboptimal point c on the 60°C line. I still transfer the broccoli sprouts to a strainer immediately after microwaving.
  • The 60°C (140°F) cliff finding of Microwave broccoli to increase sulforaphane levels was confirmed.

2. I didn’t view this study’s in-pack or lactic acid bacteria fermentation findings as having practical kitchen use. Maybe it’s a cultural difference?

3. Poor performance at 65°C after 5 minutes was partially attributed to “leaching of glucoraphanin into the blanching water.” But poor 65°C performance was evident at the 1 minute point compared with good 60°C performance.

“Partial inactivation of myrosinase” at 65°C was more likely to be the dominant factor.

4. Regarding:

“The slightly higher sulforaphane yield than would be predicted from the level of glucoraphanin in raw broccoli requires further investigation.”

The microwaving study author was on a productive investigation track with:

“Microwave irradiation might help to release more conjugated forms of glucosinolates and then get hydrolyzed by released myrosinase.”

That track developed in part from finding that broccoli florets microwaved on full power to 60°C increased glucoraphanin past control (raw) levels:

“The control GLR amount was 2.18 µmol/g DW, while the HL60 GLR amount was 2.78 µmol/g DW.”

Not to mention the coincident 1,114% increase in sulforaphane content of ordinary broccoli purchased at a grocery store!


I arrived at this study through it being referenced in the enjoyable 2020 Spanish review Functional Ingredients From Brassicaceae Species: Overview and Perspectives. The reviewers noted that this study’s 2019 predecessor Fermentation for enhancing the bioconversion of glucoraphanin into sulforaphane and improve the functional attributes of broccoli puree (not freely available) found:

“Preferential formation of SFN-nitrile (less potential as inducer of phase II detoxification enzymes than SFN) instead of SFN.”

Estimating daily consumption of broccoli sprout compounds

Rainy day thought for the 13th week of lockdown: What are methods of estimating the minimum contents of broccoli sprouts for those of us who aren’t willing to turn their kitchen into a laboratory?

With the 3-day-old broccoli sprouts have the optimal yields study as a reference, minimum values of the six broccoli cultivated varieties studied were:

  1. Lowest weight of 100 seeds: .33 grams.
  2. 100 of that cultivar’s 3-day-old sprouts weighed 1.55 grams.
  3. A different cultivar had the lowest total phenolics (gallic acid equivalents): 0.94 mg per gram of 3-day-old sprouts.
  4. That second cultivar also had the lowest total flavonoids (rutin equivalents): 1.02 mg per gram of 3-day-old sprouts.
  5. A third cultivar had the lowest weight of sulforaphane in its seeds: 2.43 mg per gram of seeds.
  6. Reduction of sulforaphane content during germination from seeds to 3-day-old sprouts is evident from the below chart. The only 3-day-old sprout chart number the study provided was the best case, though. I requested the study data, but in the meantime..I enlarged the chart, measured the worst cultivar as a 8.5 cm bar where the seed bar was 16 cm. Its 3-day-old sprout sulforaphane yield was ~53% of its seed yield.

sprout ages 1B

Another caveat for contents: Researchers had to process broccoli seeds and 3-day-old broccoli sprouts in order to make measurements. Total phenolics and total flavonoids may not have been affected by processing. However, processing generated sulforaphane.

Broccoli seeds and 3-day-old broccoli sprouts contain little or no sulforaphane. They have glucoraphanin and myrosinase enzyme which are structurally separated. Disturbing their cells mixes the two, and the enzyme hydrolyzes glucoraphanin and other glucosinolates into sulforaphane and other healthy compounds.


I start out each daily batch with two tablespoons of broccoli seeds of an unknown cultivar. I counted 812 broccoli seeds in a teaspoon (yes, I did), and multiplied by 6 for 4,872 total seeds.

Runt-of-the-litter calculations for the six broccoli cultivars studied are:

  • (4,872 / 100) x .33 g = 16.08 g broccoli seeds
  • (4,872 / 100) x 1.55 g =75.52 g 3-day-old broccoli sprouts
  • 75.52 x 0.94 mg per gram of 3-day-old sprouts = 70.99 mg total phenolics
  • 75.52 x 1.02 mg per gram of 3-day-old sprouts = 77.03 mg total flavonoids
  • 16.08 g broccoli seeds x 2.43 mg per gram of seeds = 39.07 mg sulforaphane
  • 39.07 mg x 53% = 20.71 mg sulforaphane in 3-day-old broccoli sprouts without microwaving them.

I’ll use the Microwave broccoli to increase sulforaphane levels study as a reference for an alternate sulforaphane calculation. The cultivar wasn’t mentioned, only that it was ordinary broccoli purchased in Silver Spring, Maryland, grocery stores.

One assumption is that microwaving broccoli sprouts will have the same effects as microwaving broccoli florets to increase sulforaphane content. Are the similarities between broccoli floret and broccoli sprout characteristics enough to say whether or not that’s a valid assumption?

Another assumption is that there’s no beginning amount of sulforaphane in 3-day-old broccoli sprouts. Microwaving them on full power to 60°C produces all of the sulforaphane.

A third assumption is that the sulforaphane increase from .22 to 2.45 µmol / g of the tested cultivar fairly represents other broccoli cultivars.

Combining this with the worst-case calculated weight of 3-day-old broccoli sprouts in the first study:

((2.45 – .22 µmol / g)

x 75.52 g 3-day-old broccoli sprouts)

/ 5.64 μmol conversion of amount to weight

= 29.86 mg sulforaphane


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

“The daily SFN [sulforaphane] dose found to achieve beneficial outcomes in most of the available clinical trials is around 20-40 mg.”

I’ll guess that my daily consumption of broccoli sprout compounds is at least in this clinical trial range with worst-case calculations of 20.71 mg sulforaphane without microwaving and 29.86 mg sulforaphane with microwaving in 3-day-old broccoli sprouts. I’ll include this estimate in Week 8 of Changing to a youthful phenotype with broccoli sprouts.

Broccoli seed suppliers are missing a marketing opportunity by not specifying their cultivars. They could be advertising specific benefits, etc.

The first study showed that sulforaphane contents vary widely among broccoli cultivars, from the 2.43 mg used above to 12.07 mg per gram of seeds. If your product was almost 5 times better than a competitor’s, why wouldn’t you advertise it?

Week 7 of Changing to a youthful phenotype with broccoli sprouts

To follow up Week 6 of Changing an inflammatory phenotype with broccoli sprouts:

1. I changed the title of this week’s update as a result of reading the study in A rejuvenation therapy and sulforaphane. The study wasn’t about sulforaphane, but its clinical findings had commonalities with this broccoli sprouts effort. It’s become the blog’s most popular post, read by people in 50+ countries.

A close second is An environmental signaling paradigm of aging. The study’s lead laboratory researcher presented his view five years ago on where aging evidence was pointing.

Part 2 of Rejuvenation therapy and sulforaphane better curated the study’s innovative epigenetic clock results. There are no sulforaphane clinical trials that also use epigenetic clocks.

What are the effects that broccoli sprouts and their compounds may have on human aging? With this new human-rat relative biological age clock, researchers can get reliable answers from rat studies, with human clinical trials needed only to confirm those findings!

2. This week I found out that exercising control over my charges to protect them from disease was counterproductive. I exposed them to harm, destroyed their community, and stunted their growth by forcing them to distance from each other for their own good.

Am I a politician, an unelected bureaucrat, or some other form of busybody? No. I admit my mistakes right away, I apologize, then I immediately try to do better.

A proper context:

  • In Week 2 I switched from sprouting trays with 1/16″ high ridges in the bottom to Russian-doll bowls. That solved a problem of excess moisture, with which broccoli sprouts don’t do well but bacteria do.
  • In Week 3 I rotated in the next larger sized bowl to replace the smallest bowl. My thought was that Day 3 broccoli sprouts were too crowded to dry in the smallest bowl.
  • At the end of Week 5 I doubled the starting amount of broccoli seeds from one to two tablespoons. To accommodate that increase, I again rotated in the next larger size bowl to replace the smallest bowl.

Starting in Week 6, I had uneven batch yields. The two larger bowls yielded noticeably fewer sprouts than did batches in the two smaller bowls.

What did bowl size have to do with yield? Nothing, it was me. It turned out I’d neglected Plant Care 101 instructions to provide adequate moisture.

After rinsing, straining, and wicking out excess moisture with a paper towel twice daily, I then spread out the seeds and sprouts to prevent problems with excess moisture. The broccoli seeds and sprouts in the two larger bowls were more separated than in the two smaller bowls.

All of which led to moisture levels that were inadequate for broccoli seeds and sprouts. All batches sprouted less well than their potential yield. The larger the bowl, the more my behavior adversely affected the batch.

Here’s what Day 2 and Day 3 yields were with my previous practices.  The batch volume of Day 2 in the smaller bowl was larger than Day 3’s:

I changed practices to group broccoli seeds and sprouts together at the step where I used to spread them out. Here’s the same bowl with my current practice, but at Day 2. The photo may not show it well, but it’s a larger volume than the previous practice’s Day 2:

I’ll guess that batch yield volumes have improved by 60% 75%. I increased distilled water from 100 ml to 160 175 ml before microwaving since 100 ml no longer completely immersed the increased Day 3 broccoli sprout volume. My 1000W full power microwave time concomitantly increased from 45 seconds to 70 seconds to achieve 58°C.

The better-developed batches also taste better. I still mix in mustard and eat Day 3 broccoli sprouts with other food.

3. My sulforaphane intake has probably decreased with the current practice. The 3-day-old broccoli sprouts have the optimal yields study said:

Although germination reduces SF [sulforaphane] yield to some extent, it is beneficial to the formation and accumulation of total phenol and flavonoids, ensuring the health properties of sprouts. SF contents in sprouts were 46% – 97% of seeds, whereas TP [total phenolic] and TF [total flavonoid] contents in sprouts were 1.12 – 3.58 times higher than seeds among [broccoli] varieties.”

I’m not concerned about less sulforaphane with a two tablespoons starting amount of broccoli seeds. Even a one tablespoon starting amount yields 60 g of broccoli sprouts, twice that of the model clinical trial, Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects. See our discussion in Understanding a clinical trial’s broccoli sprout amount.

4. Another week of no inflammatory problems after four-to-six-mile-long beach walks. I’m not pushing myself, just walking often, and working out my upper body every fourth day.

I emphasize the eccentric motion in upper body workouts. I haven’t curated the below 2019 papers although they’re informative:

I don’t expect recovery times from workouts to shorten. What’s an appropriate exercise recovery time? found with 26.5 ± 6.5 year-old male subjects that even three days wasn’t enough time for the biceps brachii to fully recover from eccentric exercise.

5. During Friday’s walk I accidentally startled a large turkey hen who was on the ground, and she flew up on a fence. Can you see her moments before she hopped down to the other side?

Don’t have any idea what bugs a turkey found attractive near a beach.

See Week 8 of Changing to a youthful phenotype with broccoli sprouts for follow ups.

An environmental signaling paradigm of aging

To follow up A rejuvenation therapy and sulforaphane, the study’s lead laboratory researcher provided evidence for an environmental signaling paradigm of aging in this 2015 paper:

“The age-phenotype of a cell or organ depends on its environment and not its history.

Organ dysfunction is not the cause of aging, but is the result of its milieu. Therefore, the aged milieu is the cause. Though it has been thought that the aging immune system is the cause of aging, it can seen to be the result of aging.

The systemic milieu of an organism sets the age-phenotype of its cells, tissues and organs. Cells and organs secrete factors into the blood, which are determined by the age-phenotype and repair-states of those cells and organs. The presence and concentrations of these blood-borne factors determine the age-phenotype of cells and organs.

Interactions between disparate levels of the body’s hierarchy establish a consensus age-phenotype for cells and organs, and this largely occurs via the bloodstream. There appear to be positive factors that promote youthful age-phenotypes and negative factors that promote the aged phenotypes.

We readily consider development as a ‘program’, and it seems clear that we must consider post-adult development as ‘programmed’ as well. But if there is a program it is neither in the genes nor the chromatin, but in the interaction of complex, interconnected systems spanning the hierarchical levels.

If these aforementioned principles are correct, it should be easy to verify. If so, then whole organism rejuvenation might require little more than changing the concentrations of all age-determining molecules of the bloodstream and the various stem cell niche environments to youthful levels for a time sufficient to cause rejuvenation at the cellular level.

Once cells start secreting factors appropriate to their new, younger age-phenotypes, cognate changes should propagate through the hierarchical levels.

The analogy to the workings of a mechanical clock is not very exact. ‘Gears’ represent the individual aging clocks, both cellular and organic (shown at different levels within the mechanism) which interact, ultimately resulting in the organismic age, i.e. the ‘body clock’, represented by the ‘hour hand’ (no minute hand is shown).

In mammals, the readout of the clock corresponds to the age-related composition of the blood plasma. In this model, moving the hour hand backwards should result in a turning back of the composite clocks as well – a result obtain[ed] when induction to pluripotence is used to reset the cellular clocks.

Apart from being slowed down or sped up, the body clock can also be reset. Organisms, organs, and their cells can be reset to different age-phenotypes depending on their environment.

We know that old transplanted tissues and organs can regain function and live for the entire life of the younger host at least in rodents. We must suppose that age-phenotype changes must have taken place at the cellular level to allow this.

Rejuvenation cannot be explained on the basis that aging represents the accumulation of irreparable cellular damage.”

http://www.eurekaselect.com/130538/article “Towards an Evidence-based Model of Aging”


Here are some of his responses to comments on the blog post that first curated his current research:

“We’ve (scientists), spent the past 70 years trying to definitively prove the commonsense ‘wear and tear’ theories and have not succeeded. So I tried something different, looking at the results of experiments.

This is not based on ‘theory’ (say mitochondrial aging or ‘wear and tear’) but on experimental evidence. Theory comes in explaining our results, not achieving them. There is a theory becoming clear, one very different from the commonsense view of ‘wear and tear’ aging.

We haven’t examined the immune response. All that we know for sure is that the chronic inflammation of aging stopped. I can definitively say that chronic inflammation due to aging can be reversed with factors present in young blood.

There are amazing things that Big Pharma won’t touch as there’s not enough profit in them (they can’t be patented). So I guess we’re somewhat the same, but we know what to do and have proven it – for us, it’s not the money. However, money allows you to do things.

Being 75 myself puts a time-frame around the project. We plan to propose its use for the diseases of aging – eventually, everyone will use it. It will end up changing humanity. As people already seem to have too much free time to begin with, what will people do with those extra years they will be given?”


Sections 3 “Aging Manifestations that Have Hitherto Been Proposed as the Causes of Aging are the Consequences of Aging” and 10 “Several Factors ‘Conspire’ to Promote Inflammation in Old Mammalian Bodies, Inflammation Leads to Several Diseases of Aging and Perhaps to Aging Itself” were especially informative.

The former section discussed cells that were capable of making repairs but didn’t make repairs, with aging being the consequence of this behavior. The latter reviewed topics of the current study such as senescence, IL-6, NF-κB, and C-reactive protein in terms of feedback loops.

See Reevaluate findings in another paradigm for comparisons with another view of hypothalamic aging.

Week 6 of Changing an inflammatory phenotype with broccoli sprouts

To follow up Week 5 of Changing an inflammatory phenotype with broccoli sprouts:

1. I had an informative exchange with an author of Microwave broccoli to increase sulforaphane levels. The study provided an optimal sulforaphane end result of “(2.45 µmol/g DW)”. I asked a study author for additional data, and they replied:

“The control GLR and SLR amount was 2.18 and 0.22 µmol/g DW, respectively, while the HL60 GLR amount was 2.78 µmol/g DW.”

Microwaving broccoli florets to 60°C (140°F) increased the sulforaphane amount by 1,114% (2.45 / .22)! That also increased the glucoraphanin amount by 27% (2.78 / 2.18) for further processing into sulforaphane after eating.

I replied: That’s an exciting result, increasing sulforaphane more than 11 times, while also increasing glucoraphanin! I haven’t found similar experiments with broccoli sprouts. Would you expect similar results?

The study author responded:

“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. Further studies are being carried out.”

2. I stopped panning out spent broccoli seed coats. The 3-day-old broccoli sprouts have the optimal yields study didn’t directly address coats, and coats were presumably discarded before broccoli sprout analyses.

However, since broccoli seeds were ground, coats were part of broccoli seed analyses. Broccoli seeds had higher sulforaphane weights than did broccoli sprouts. So 3-day-old spent broccoli seed coats probably don’t reduce sulforaphane amounts.

“The SF [sulforaphane] contents were calculated and expressed by mg SF per gram of seeds or fresh sprouts. Furthermore, to be comparable with the seeds, the contents of SF and the following bioactive compounds in 100 fresh sprouts were divided by the weight of 100 seeds and then the contents of bioactive compounds in fresh sprout were expressed as mg per gram of seeds.

Although germination reduces SF yield to some extent, it is beneficial to the formation and accumulation of total phenol and flavonoids, ensuring the health properties of sprouts. SF contents in sprouts were 46% – 97% of seeds, whereas TP [total phenolic] and TF [total flavonoid] contents in sprouts were 1.12 – 3.58 times higher than seeds among varieties.”

3. Doubling the starting amount of broccoli seeds from one to two tablespoons is going well. My wonderful woman’s latest measurement of the yield for a batch of 3-day-old broccoli sprouts was 84.6 grams. She immersed the broccoli sprouts in 350 ml water and microwaved them on full 1000W power for 2 minutes to achieve 61°C.

I put daily batches in 100 ml distilled water, and microwaved on full 1000W power for 45 seconds to achieve 58°C. For comparison with the 3-day-old point of starting with one tablespoon of broccoli seeds, that took 35 seconds to achieve 57°C.

Two tablespoons of broccoli seeds produce a lot of broccoli sprouts for me to eat in a single serving. I mix in spicy brown mustard after microwaving and cooling them down. It complements the taste and makes them more palatable. The mixture goes better with a meal than eating it by itself.

4. Not sure what went on with last week’s inflammatory problems after four-to-six-mile-long beach walks. I did similar walks on Thursday and Saturday, and didn’t have those problems afterwards.

Did a small amount of running in Weeks 3 and 4 trigger something? Did my body adapt to a one tablespoon starting amount of broccoli seeds dosage, such that it wasn’t effective anymore?

Did raising the starting amount of broccoli seeds to two tablespoons cause the problems to quiet down this week? Or was the quiescence because I didn’t run even a short distance? This week’s occasional left ankle / left knee twinge makes me think that running, like golf, may not be a future activity.

5. I intend to follow the model clinical trial Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects curated in How much sulforaphane is suitable for healthy people? and measure IL-6 and C-reactive protein after Week 10. These two weren’t among the 50+ measurements taken during last June’s annual physical, so I’ll request them along with HbA1c.

6. I credit my son for getting me started on the current investigation into broccoli sprouts. He repeatedly asked me for evidence of minimum effective sulforaphane dosage. Still haven’t found complete answers.

The treatments mentioned in Week 1, and the unmentioned months of physical therapy and years of periodic cortisone injections hadn’t worked. I could have been doing more to better address the causes of a long-term problem rather than just treat the symptoms. Now I am, thank you.

See Week 7 of Changing to a youthful phenotype with broccoli sprouts for follow ups.