Genetic factors

A compelling review of epigenetic transgenerational inheritance

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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?

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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?

See Part 3 to follow up.

Eat broccoli sprouts for DIM

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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 30 grams of broccoli super 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 metabolizing more DIM.

That Day 35 data point didn’t have an asterisk next to it to indicate a statistically significant decrease. But the overweight postmenopausal women group’s next Day 50 significant “steady decrease” finding supported an interpretation that eating broccoli sprouts supplied them 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 super sprout indolic compounds were as follows:

indolic glucosinolates

Assuming that only glucobrassicin is a precursor to DIM, subjects’ DIM bioavailability can be calculated as μmol DIM / 21.61 μmol. For example, overweight postmenopausal women Day 35 average of 0.5544 μmol DIM that ranged from 0.1771 to 0.8034 μmol DIM represented an average 2.57% DIM bioavailability with a range of 0.82% to 3.72% DIM bioavailability.

See Part 2 for DIM follow-up.

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

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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.

IL-6 2020

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.” [Zinc and broccoli sprouts – a winning combination]
  • “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 estimated 52 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 = 21.4 g x 30 days = .642 kg or 1.42 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.

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

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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. I eat 131 grams daily as calculated in Estimating daily consumption of broccoli sprout compounds.
  3. 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.
  4. I immerse 3-day-old broccoli sprouts in 100 ml distilled water, then microwave them on 1000W full power for 35 seconds to ≤ 60°C (140°F) per Microwave broccoli to increase sulforaphane levels.
  5. 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, indole-3-carbinol, 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’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

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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 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 52 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. Connections within our brains become less inhibited, and external connections concordantly become more apparent.

A review of sulforaphane and aging

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This 2019 Mexican review stated:

“We describe some of the molecular and physical characteristics of SFN, its mechanisms of action, and the effects that SFN treatment induces in order to discuss its relevance as a ‘miraculous’ drug to prevent aging and neurodegeneration. SFN has been shown to modulate several cellular pathways in order to activate diverse protective responses, which might allow avoiding cancer and neurodegeneration as well as improving cellular lifespan and health span.

NF-κB is in charge of inflammatory response regulation. Under basal conditions, NF-κB is sequestrated into the cytosol by IκB, but when pro-inflammatory ligands bind to its receptors, the IKK protein family phosphorylates IκB to degrade it via proteasome, so NF-κB is able to translocate into the nucleus and transcript several inflammatory mediators. Sulforaphane is capable to inhibit IκB phosphorylation and NF-κB nuclear translocation.

SFN upregulated Nrf2 expression by reducing DNA demethylation levels of the Nrf2 promoter. In another model using the triple-transgenic mouse model of Alzheimer’s disease (3 × Tg-AD), the use of SFN regulates the expression of the Brain-derived neurotrophic factor (BDNF) via HDAC inhibition, thus increasing H3 and H4 acetylation on the BDNF promoter. Enhancing BDNF expression as an effect of SFN treatment increased the neuronal content of several synaptic molecules like MAP 2, synaptophysin, and PSD-95 in primary cortical neurons of 3 × Tg-AD.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6885086/ “Sulforaphane – role in aging and neurodegeneration”

I came across this review while searching PubMed for sulforaphane commonalities with presentation topics in Part 2 of Reversal of aging and immunosenescent trends with sulforaphane. The review outlined some aging aspects and presented relevant sulforaphane studies. Others such as eye and muscle decline weren’t addressed.

Since sulforaphane’s “a ‘miraculous’ drug” in the Abstract, I expected but didn’t see corresponding excitement in the review body. Just phrases like “it is known” and non-specific “more research is needed.”

Other papers published after this review were found by a PubMed “sulforaphane signal aging” search:

Part 2 of Reversal of aging and immunosenescent trends with sulforaphane

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Reversal of aging and immunosenescent trends with sulforaphane covered only the first 13 minutes of a super informative presentation by the lead researcher of clinical trial Reversal of aging and immunosenescent trends.  Commonalities with sulforaphane research were found by PubMed searches of sulforaphane and each presentation topic, and used a 1/1/2015 publication date cutoff.

Continuing presentation topics from the 13:40 mark:

Cancer

Lymphocyte/monocyte ratio

CD38 monocytes

  • NQO1-induced activation of AMPK contributes to cancer cell death by oxygen-glucose deprivation

    “NQO1 plays a key role in AMPK-induced cancer cell death in OGD through the CD38/cADPR/RyR/Ca2+/CaMKII signaling pathway. Expression of NQO1 is elevated by hypoxia/reoxygenation or inflammatory stresses through nuclear accumulation of the NQO1 transcription factor, Nrf2 (NFE2-related factor 2). Activation of the cytoprotective Nrf2 antioxidant pathway by sulforaphane protects immature neurons and astrocytes from death caused by exposure to combined hypoxia and glucose deprivation.”

Thymus – no recent sulforaphane studies

Renal function

  • Rapid and Sustainable Detoxication of Airborne Pollutants by Broccoli Sprout Beverage: Results of a Randomized Clinical Trial in China

    “Rapid and sustained, statistically significant increases in levels of excretion of glutathione-derived conjugates of benzene (61%), acrolein (23%), but not crotonaldehyde were found in those receiving broccoli sprout beverage compared with placebo. Excretion of benzene-derived mercapturic acid was higher in participants who were GSTT1-positive compared to the null genotype, irrespective of study arm assignment. Measures of sulforaphane metabolites in urine indicated that bioavailability did not decline over the 12-week daily dosing period. Intervention with broccoli sprouts enhances detoxication of some airborne pollutants, and may provide a frugal means to attenuate their associated long-term health risks.”

Hair rejuvenation

Epigenetic clocks – There are no sulforaphane studies that use epigenetic clocks, although broccoli compounds have epigenetic effects on aging, as reviewed in 2019:

  • Sulforaphane – role in aging and neurodegeneration

    “SFN has been shown to modulate several cellular pathways in order to activate diverse protective responses, which might allow avoiding cancer and neurodegeneration as well as improving cellular lifespan and health span.”

Both biomarker (Lymphocyte / monocyte ratio) and epigenetic clock (GrimAge) measurements done 6 months after the clinical trial ended suggested trial subjects’ aging phenotypes had been reset:

An environmental signaling paradigm of aging explained:

“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.

This is not so much a principle as an application of principle that the environment determines age-phenotype.”

There wouldn’t be a potential payoff for a company to study any broccoli compound / aging connections. People can achieve clinically relevant, daily doses of broccoli sprouts for < $500 a year.

What sponsor would be interested enough to put sulforaphane research on the clock?

Presentation topics are continued in Uses of the lymphocytes to monocytes ratio and A review of sulforaphane and aging. This pilot trial’s follow-on clinical trial was updated in The next phase of reversing aging and immunosenescent trends.

Reversal of aging and immunosenescent trends with sulforaphane

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Sulforaphane research findings have commonalities with a super informative presentation by the lead researcher of clinical trial Reversal of aging and immunosenescent trends. I did a PubMed search of sulforaphane and each presentation topic, and used a 1/1/2015 publication date cutoff.

Presentation topics through the first 13 minutes were:

Thymus – no recent sulforaphane studies

Treatments

PSA

C-reactive protein and IL-6

Bone marrow fat – no recent studies

T cells

PD-1 / PD-L1

Treatment cost

I estimate the annual cost of the non-prescription treatments of the clinical trial to be $100. The estimated annual cost of eating broccoli sprouts every day is < $500 for the broccoli seeds.

broccoli seed label

The above image isn’t an endorsement although it’s what I’ve used. It’s buzzword marketing to put “sprouts” and “sulforaphane” but not “seeds” on the label of a broccoli seeds package. For another thing, broccoli sprouts don’t “abound with phytochemical sulforaphane.”

Repeating a point from Estimating daily consumption of broccoli sprout compounds, broccoli seeds and 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.

Continue presentation topic commonalities with sulforaphane research at A pair of broccoli sprout studies and Part 2 of Reversal of aging and immunosenescent trends with sulforaphane.

Do broccoli sprouts treat migraines?

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While rereading a review in Eat broccoli sprouts today, it occurred to me that I haven’t needed to take migraine medicine during the 9 weeks I’ve been eating broccoli sprouts every day. Since 14 weeks of lockdown overlap this period, it’s also possible that I’ve avoided triggering conditions. I look at brightly-lit screens all day, but don’t have cold air blowing on my head that’s the other half of my most common triggering condition.

I started having intermittent ~monthly episodes about ten years ago. I wouldn’t take sumatriptan unless I have a half-day-long headache that doesn’t respond to acetaminophen. It stops a headache from turning into a 3-day-long migraine.

I went over to PubMed and did a “sulforaphane migraine” search, which turned up exactly 1 (!!) result. A 2016 Chinese rodent study Activation of the nuclear factor E2-related factor 2/anitioxidant response element alleviates the nitroglycerin-induced hyperalgesia in rats found:

“Activation of the Nrf2/ARE pathway inhibited the activation of TGVS [trigeminovascular system] and prevented the induction of hyperalgesia. Sulforaphane might therefore be an effective agent for hyperalgesia.”

Plausible conclusion. Nitroglycerin definitely jolts a monster headache.

Two of the eleven papers citing this study were:

There wouldn’t be any potential payoff for a company to be interested in studying a sulforaphane-migraine connection. What sponsor would be interested enough to double the number of studies in this area?

See Part 2 of Do broccoli sprouts treat migraines? for a follow up.

Reevaluate findings in another paradigm

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It’s challenging for people to change their framework when their paychecks or mental state or reputations depend on it not changing.

I’ll use The hypothalamus and aging as an example. This review was alright for partial fact-finding up through 2018. Its facts were limited, however, to what fit into the reviewers’ paradigm.

The 2015 An environmental signaling paradigm of aging provided examples of findings that weren’t considered in this 2018 review. It also presented a framework that better incorporated what was known in 2015.

Here’s how they viewed the same 2013 study, Hypothalamic programming of systemic ageing involving IKK-β, NF-κB and GnRH (not freely available).

Paradigm: “The hypothalamus is hypothesized to be a primary regulator of the process of aging of the entire body.”

Study assessment:

“Age-associated inflammation increase is mediated by IκB kinase-β (IKK-β) and nuclear factor κB (NF-κB) in microglia and, subsequently, nearby neurons through microglia–neuron interaction in the mediobasal hypothalamus. Apparently, blocking hypothalamic or brain IKK-β or NF-κB activation causes delayed aging phenotype and improved lifespan.

Aging correlates with a decline in hypothalamic gonadotropin-releasing hormone (GnRH) expression in mice. Mechanistically, activated IKK-β and NF-κB significantly down-regulates GnRH transcription. GnRH therapy through either hypothalamic third ventricularor or subcutaneous injection leads to a significant recovery of neurogenesis in the hypothalamus and hippocampus, and a noticeable improvement of age-related phenotype in skin thickness, bone density, and muscle strength when applied in middle-aged mice.”

Paradigm: Environmental signaling model of aging

Study assessment:

“A link between inflammation and aging is the finding that inflammatory and stress responses activate NF-κB in the hypothalamus and induce a signaling pathway that reduces production of GnRH by neurons. GnRH decline contributes to aging-related changes such as bone fragility, muscle weakness, skin atrophy, and reduced neurogenesis. Consistent with this, GnRH treatment prevents aging-impaired neurogenesis, and decelerates aging in mice.

Zhang et al. report that there is an age-associated activation of NF-κB and IKK-β. Loss of sirtuins may contribute both to inflammation and other aspects of aging. But this explanation, also given by Zhang et al., merely moves the question to why there is a loss of sirtuins.

The case is particularly interesting when we realize that the aging phenotype can only be maintained by continuous activation of NF-κB – a product of which is production of TNF-α.

Reciprocally, when TNF-α is secreted into the inter-cellular milieu, it causes activation of NF-κB. In their study, Zhang et al. noted that activation of NF-κB began in microglia (the immune system component cells found in the brain), which secreted TNF-α, resulting in a positive feedback loop that eventually encompassed the entire central hypothalamus.

The net result of this is a diminution in production of gonadotropin-releasing factor which accounted for a shorter lifespan. Provision of GnRH eliminated that effect, while either preventing NF-κB activation (or that of the IKK-β upstream activator) or by providing gonadotropin-releasing factor directly into the brain, or peripherally, extending lifespan by about 20%.

In spite of the claim of Zhang et al. that the hypothalamus is the regulator of lifespan in mice, their experiments show that only some aspects of lifespan are controlled by the hypothalamus, as preventing NF-κB activation in this organ did not stop aging and death. Similar increased NF-κB activation with age has been seen in other tissues as well, and said to account for dysfunction in aging adrenal glands.

It was demonstrated that increased aging occurred as a result of lack of gonadotropin-releasing hormone, and that increased lifespan resulted from its provision during aging. In this manner:

  1. Aging of hypothalamic microglia leads to
  2. Aging of the hypothalamus, which leads to
  3. Aging elsewhere in the body.

So here we have a multi-level interaction:

  1. Activation of NF-κB leads to
  2. Cellular aging, leading to
  3. Diminished production of GnRH, which then
  4. Acts (through cells with a receptor for it, or indirectly as a result of changes to GnRH-receptor-possessing cells) to decrease lifespan.

So the age state of hypothalamic cells, at least with respect to NF-κB activation, is communicated to other cells via the reduced output of GnRH.”

Not using the same frameworks, are they?

In 2015, this researcher told the world what could be done to dramatically change the entire aging research area. He and other researchers did so recently as curated in Part 3 of Rejuvenation therapy and sulforaphane which addressed hypothalamus rejuvenation.

Tailoring measurements for broccoli sprouts

gettingwell4 4-5 stars Advanced knowledge, Epigenetics

To follow up two points of Lab analyses of broccoli sprout compounds:

3. Without knowing the broccoli sprouts’ cultivar, could a person infer from a glucoraphanin amount how much sulforaphane they would consume?

No. The 2014 Iron Man 5.2 μmol per g glucoraphanin wasn’t that different from the 2015 Sirtaki 5.4 amount. But Iron Man vs. Sirtaki differences of 0.3 vs. 0.6 μmol per g sulforaphane amounts and 5% vs. 11% hydrolyzed showed Sirtaki cultivar had double or more those of Iron Man.

4. Could a person infer from a mature broccoli glucoraphanin amount anything about its broccoli sprout glucoraphanin amount, or vice versa?

No. The Sirtaki 8.0 μmol per g sprout glucoraphanin amount was the highest cultivar, but its fully developed head was lowest at 0.27.

Studies often tailor their measurements to interests of either their sponsor or audience. This tailoring may leave gaps in what people outside of their target audience want to know.

Item 3 showed that sprout glucoraphanin amount can’t be relied upon to infer sprout sulforaphane amount because the hydrolysis process may be cultivar specific. The 3-day-old broccoli sprouts have the optimal yields study showed this result was also true using seed glucoraphanin and sulforaphane measurements.

Item 4 showed cultivar comparative measurements of glucoraphanin and sulforaphane made with broccoli florets may be the opposite of broccoli seed and sprout measurements. We should use studies that measured compounds in broccoli seeds and / or sprouts because we’re interested in eating broccoli sprouts.

A problem arises when studies compare cultivars using seed or sprout glucoraphanin but not also sulforaphane. We can’t ignore Item 3’s findings and automatically prefer a cultivar that has a higher glucoraphanin amount.

Repeating a point from Estimating daily consumption of broccoli sprout compounds, broccoli seeds and 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.

So if a study’s processing is what creates sulforaphane, what can we do with study findings if researchers didn’t bother to also measure that sulforaphane? I’ll guess that substantial differences in glucoraphanin seed or sprout amounts could be used as rough guides for sulforaphane amounts.

Looking at the above 2014 sprout amounts, a Iron Man 5.2 vs. Marathon 4.0 μmol per g glucoraphanin difference didn’t result in their 0.3 sulforaphane amounts being different. As a rough guide for home gardens, a 1.3 (5.2 / 4.0) ratio could be used as a threshold.

Broccoli seed glucoraphanin amounts in this 2004 table from Glucoraphanin and 4-Hydroxyglucobrassicin Contents in Seeds of 59 Cultivars of Broccoli, Raab, Kohlrabi, Radish, Cauliflower, Brussels Sprouts, Kale, and Cabbage (not freely available) are sorted by higher-to-lower glucoraphanin (GR) amounts per cultivar. Marathon can be found at 59.81 μmol per g. A threshold of 78 μmol per g (59.81 x 1.3) would roughly guide planting cultivars Premium Crop down to Monterey, depending on their availability 16 years later in 2020.

We’d like to plant broccoli cultivars that have laboratory results so we could expect comparatively higher sulforaphane from their seeds and sprouts. I’ve contacted broccoli seed suppliers for commercial growers and home gardeners, and asked them for lab evidence of their offered cultivar’s sulforaphane contents. Haven’t received responses yet. When they respond, we’ll have to clarify whether those lab results are from seeds or tailored to mature plant’s florets in order for us to reliably use them.

Broccoli seeds intended for commercial growers and home gardeners are prohibitively expensive for home sprouting. If such a supplier did sell in bulk at much lower prices, unless otherwise specified, seeds are expected to be treated with insecticides, fungicides, dyes or bulking agents.

Home sprouting has to deal with unknown cultivar, unknown glucoraphanin, and unknown sulforaphane. Even so, I’ve documented good results from eating broccoli sprouts every day for 8 weeks. A worst-case estimate of 52 mg sulforaphane with microwaving 3-day-old broccoli sprouts exceeds:

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

Current growing and preparation processes of microwaving to achieve 60° C, transferring broccoli sprouts to a strainer, and allowing further myrosinase hydrolization of glucoraphanin into sulforaphane compensate for some degree of these uncertainties. It would still be better, though, to know which cultivar is purchased along with lab reports of its compounds’ characteristics.

Let’s say that one day, bulk broccoli seed suppliers start advertising cultivated variety (and Calabrese isn’t a cultivar). We have Marathon in both a lab analysis and a seed glucoraphanin list to help inform our decisions.

Would I pay extra for seeds of cultivars substantially below Marathon in the glucoraphanin list like common cultivars DeCicco and Waltham 29? No, I’m doing fine changing my phenotype despite unknowns. The advertised cultivar would have to be substantially above Marathon to consider a purchase.

A hair color anecdote

gettingwell4 2-3 stars Required further work, Epigenetics, Hypothalamus, Immune system, Limbic system, Memory, Stress

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 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

gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Immune system, Memory, Stress ,

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, 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 a worst-case estimate in Estimating daily consumption of broccoli sprout compounds of 52 mg sulforaphane with microwaving 3-day-old broccoli sprouts. This exceeds:

“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 and glucoraphanin.

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.

Lab analyses of broccoli sprout compounds

gettingwell4 2-3 stars Required further work, Epigenetics

To follow up Estimating daily consumption of broccoli sprout compounds, the main point of which was: how can a person guide their actions with evidence when a broccoli cultivated variety’s beneficial characteristics aren’t known?

I focus on broccoli sprout lab analyses of 3 cultivars made in a 2017 German study Isothiocyanates, Nitriles, and Epithionitriles From Glucosinolates Are Affected by Genotype and Developmental Stage in Brassica oleracea Varieties. Here are rounded numbers from the supplementary material:

1. What happened in 2015 to lessen all broccoli cultivars’ sprout compound values by 2015 / 2014 percentages?

I read and reread, and didn’t come up with a satisfactory answer. Maybe it’s a language difference, but this was an insufficient explanation:

“Decreased myrosinase activity probably was the reason for the low levels of hydrolysis products formed in broccoli cv. Sirtaki in 2015 compared to 2014, while 70% [67%] of the GLS concentration of 2014 was present.”

What caused “decreased myrosinase activity?” And why would that be explanatory for just one cultivar when two others also experienced “low levels of hydrolysis products?”

Greenhouse-grown broccoli sprouts clearly varied between batches. Temperatures and sun radiation were tossed in but not shown to have been explanatory variables.

2. Could a person infer from one cultivar’s 2014 lab report how much sulforaphane they would consume from that cultivar in 2015?

No.

3. Without knowing a broccoli sprouts’ cultivar, could a person infer from a glucoraphanin amount how much sulforaphane they would consume?

No. The 2014 Iron Man 5.2 μmol per g glucoraphanin wasn’t that different from the 2015 Sirtaki 5.4 amount. But Iron Man vs. Sirtaki differences of 0.3 vs. 0.6 μmol per g sulforaphane amounts and 5% vs. 11% hydrolyzed showed Sirtaki cultivar’s unrounded numbers had double or more those of Iron Man.

4. Could a person infer from a mature broccoli glucoraphanin amount anything about its broccoli sprout glucoraphanin amount, or vice versa?

No. The Sirtaki 8.0 μmol per g sprout glucoraphanin amount was the highest cultivar, but its fully developed head was lowest at 0.27.

5. Could differences be explained by the broccoli sprout batches’ one-day age difference?

6. Did both years use the same seed lot? If so, could a one year aging of seeds explain differences?

Here’s a graphic of the 2014 batch major broccoli sprout compounds. Glucoraphanin is red 4MSOB in A, and sulforaphane is red 4MSOB-ITC in C:

This study demonstrated that there are many unknowns even with lab analyses. It would seem that not much could be accurately inferred past knowing that broccoli sprouts of one cultivar produced more sulforaphane than another.

Would similar lab reports help current purchase decisions? I haven’t come across a broccoli seed bulk supplier who had lab reports for products they’re selling. When pressed on Amazon they at best say Calabrese, which has described hundreds of cultivars. Such as Iron Man and Marathon, which are also named Calabrese Iron Man F1 and Calabrese Marathon F1.

Obtaining information for each batch would probably cost them a lot of money, which would be passed on to their customers. Lab reports for a different batch than the broccoli seed offered may have limited utility to consumers.

It would assist broccoli seed consumers to at least know the cultivar. This study’s genotypes had a greater effect than did environmental influences.

See follow up Tailoring measurements for broccoli sprouts.