Giving children allergies with pets

This 2021 human study investigated development and persistence of allergies:

“Allergic rhinitis (AR) is a common IgE-mediated disorder involving troublesome symptoms of nasal congestion, nasal itch, sneezing, and associated eye symptoms. Like many chronic health conditions, AR stems from complex gene–environment interactions.

130 subjects with AR were recruited. Control population included 154 healthy children who underwent a regular physical examination in the same ear, nose and throat clinic as AR patients. Individuals with history of asthma or atopic dermatitis were excluded.

AR analysis

Plenty of contradictory associations exist as whether furred pet exposure (cats and dogs) may be a risk or a protective factor for AR development. Discrepancies are likely due to the ubiquitous nature of pet allergens, while pet owners are more concerned about sanitation and many other hygiene-related reasons.

Interaction of early-life pet exposure with methylation level of ADAM33 increased the risk for AR onset 1.423 times more in children. This study provides evidence that:

  • Early-life pet exposure and low methylation level of ADAM33 increase AR risk in children; and
  • The interaction between pet exposure and methylation level of ADAM33 may play an important role in development of AR.”

https://aacijournal.biomedcentral.com/articles/10.1186/s13223-021-00526-5 “Interaction between early-life pet exposure and methylation pattern of ADAM33 on allergic rhinitis among children aged 3–6 years in China”


There’s nothing children can do about who their parents were. Exposing them to pet allergens, though, may be another example of early-life experiences causing lifelong effects.

Happy Mothers Day

This 2021 rodent study investigated effects on offspring of maternal high-fat diet (HFD) during gestation and lactation, and offspring HFD during young adulthood:

“We found that gestation was the most sensitive period to induce obesity in late life, and there was no difference between sexes in chance of obesity. Furthermore, we found that lactation and administration of a HFD post‐weaning increased incidence of lipid metabolism disorders and obesity in offspring.

gestational hfd effects on offspring

There are different windows of opportunity for programming epigenetically labile genes. Some studies support the alteration of epigenetic status during development as an important cause induced adult obesity.

Gestation is considered as the most sensitive period because high DNA synthesis and DNA methylation patterns are established for normal tissue development during the embryonic period. These two programming events are the times when the epigenetic state changes most widely in the life cycle.”

https://onlinelibrary.wiley.com/doi/10.1111/jcmm.16551 “Gestational high-fat diet impaired demethylation of Pparα and induced obesity of offspring”


Hey mothers! Do what you please. But don’t turn around and deny consequences of your behavior and choices on your descendants’ physiology and behavior, and possibly those of further descendants.

Gestation, birth, infancy, and early childhood are critical periods for humans. There’s no going back to correct errors and problems.

Does skin improvement cause overall effects?

This 2019 human skin study found:

“We demonstrated in aged mice that epidermal dysfunction largely accounted for age-associated elevations in circulating cytokine levels, and that improving epidermal function reduced circulating cytokine levels. We performed a pilot study to determine whether improving epidermal function reduces circulating proinflammatory cytokine levels in aged humans.

Both aged human and mouse skin display sustained abnormalities in epidermal permeability barrier homeostasis, stratum corneum (SC) hydration, and elevations in SC pH 4-6, each of which has been shown to independently provoke cutaneous inflammation. Disruption of the epidermal permeability barrier provoked an increase in:

  1. Cutaneous cytokine production; and
  2. Serum cytokine levels, independent of hepatic or T cell involvement.

We assessed whether improving epidermal function with an emollient, containing a mixture of lipids that mimics components of normal SC, lowered circulating levels of these same pro-inflammatory cytokines in aged humans.

skin treatment

After 30 days of twice-daily topical treatments, circulating levels of IL-1β and IL-6 decreased significantly in the treated aged cohort vs. untreated aged controls. Topical treatments reduced circulating levels of IL-1β and IL-6 to levels comparable to young controls. Though levels of TNF-α declined by over 40% in comparison to untreated aged humans, the difference did not attain statistical significance.

Results of this preliminary study suggest that a larger clinical trial should be performed to confirm whether improving epidermal function also can reduce circulating proinflammatory cytokine levels in aged humans, while also possibly attenuating downstream development of chronic inflammatory disorders.”

https://onlinelibrary.wiley.com/doi/abs/10.1111/jdv.15540 “Topical applications of an emollient reduce circulating pro‐inflammatory cytokine levels in chronically aged humans: a pilot clinical study” (not freely available)


I discussed enrolling in a trial whose objective would be to test this study’s findings. No big deal, just have to take IL-6 and TNF-α measurements in an upcoming annual physical. Then apply that trial’s skin treatment for 30 days per this study’s twice-daily protocol.

Day 70 results from Changing to a youthful phenotype with broccoli sprouts provided some of last year’s measurements. IL-6 was already at a negligible 1.0 pg / ml, one-fifth of the above Baseline Young group’s 5.1 ± 0.9.

IL-6 2020

Probably won’t want my data, since their treatment wouldn’t be expected to lower an already very low inflammation marker.

Weight loss for the lazy

At the risk of becoming Dr. Paul Clayton’s echo chamber, another great blog post, Falling Down:

“When lab rats or mice are weighted down with lead pellets they lose substantial amounts of weight, almost exclusively adipose tissue. Unlike dieting, there is little if any loss of muscle mass, making lead an ideal weight loss strategy for the lazy.

A clinical trial generated the same result. Their paper concludes, ‘Increased weight loading reduces body weight and fat mass in obese subjects in a similar way as previously shown in obese rodents. These findings demonstrate that there is a loading-dependent homeostatic regulation of body weight, the gravitostat, also in humans.’

Polyphenol resveratrol protects against damaging effects of de-loading by acting as an exercise mimetic, and does so by activating AMP-K directly. Other nutrients which do the same thing include polyphenol quercetin, sapogenin dammaranes, and omega 3 fatty acid EPA.”


The doctor still doesn’t mention sulforaphane, although it activates the AMPK pathway on the way to its primary effect of Nrf2 activation. First time I’d seen the term covidiots.

“You can fool some people sometimes
But you can’t fool all the people all the time
And now you’ve seen the light
Stand up for your rights”

Part 2 of Broccoli sprouts activate the AMPK pathway

This 2021 review subject was metformin’s role in autophagy:

“Metformin had been used as the first choice for treating diabetes for almost a century. Autophagy is responsible for recycling and degrading cellular components, which significantly affects cell functions in physiology and pathology.

Effects of metformin on autophagy mainly depend on corresponding signaling pathways in specific organs or tissues. Metformin can induce autophagy in cells of many organs and tissues via affirmed signaling pathways, such as AMPK-related signaling pathways.

1-s2.0-S0753332221000718-gr5_lrg

Different signaling pathways (alone or in combination) mediated the process of metformin affecting autophagy in different organs or tissues. It is necessary to combine effects of metformin on autophagy with pharmacological effects on pathologies in different organs or tissues, which would provide indications for future metformin applications.”

https://www.sciencedirect.com/science/article/pii/S0753332221000718 “The effects of metformin on autophagy”


I characterized this review as Part 2 of Broccoli sprouts activate the AMPK pathway because that study’s experimental evidence showed sulforaphane activation of the AMPK pathway was a predecessor to sulforaphane’s main effects of Nrf2 pathway activation. This review didn’t even mention Nrf2 activation.

Do all of metformin’s cited effects apply to daily intake of broccoli sprouts? Probably not, but most people who take metformin every day aren’t healthy.

Grow your 3-day-old sprouts in darkness

This 2021 study examined light frequency effects on Chinese kale sprouts’ development of glucosinolates:

“We investigated sprout growth and secondary metabolite glucosinolates (GSs) accumulation under white or combined red-and-blue (RB) light sources. Most GSs in sprouts are stored in seeds, which is gradually degraded to provide nutrients for other metabolic functions.

Phenotype of 3-day-old Chinese kale sprouts grown with different photoperiods condition under white or RB light:

capital A was grown in darkness

Sprouts grown under dark conditions showed only elongation of hypocotyls [shoots]. Sprouts grew with shorter hypocotyls and wider cotyledons [first leaves] irrespective of whether a white or combined RB light source was used.

Growth indicators (including plant height, cotyledon length, fresh weight, and dry weight) under different photoperiodic treatments were measured on days 2, 3, 6, and 9. Consistent with the phenotype presented, plant height and cotyledon length responded rhythmically to illumination time.”

https://www.frontiersin.org/articles/10.3389/fpls.2020.589746/full “Effect of Photoperiod on Chinese Kale (Brassica alboglabra) Sprouts Under White or Combined Red and Blue Light”


Circadian rhythms rule. Accept and adjust.

Week 56 of Changing to a youthful phenotype with sprouts

1. Per Improving healthy compounds of broccoli sprouts and Broccoli sprouts’ immune effects, this week I added mustard sprouts and red cabbage sprouts to my twice-daily routine of eating 3-day-old microwaved broccoli sprouts.

At first, I started mustard and red cabbage seeds with the same 10.7 gram weight (one tablespoon) of seeds. They grew well such that after three days, mustard sprouts weighed an average 61.2 g, and red cabbage sprouts weighed 60.3 g average. Both of these were slightly less than broccoli sprouts’ 65.5 g average.

3-day-old mustard sprouts substantially mellowed out from mustard seeds’ effects. After microwaving mustard sprouts to ≤ 60°C (140°F) and letting them sit for five minutes, I still felt constant nose burn while eating them. 3-day-old red cabbage sprouts were milder than broccoli sprouts, so no difficulties.

The main problem with doing one tablespoon seed weights of all three Brassicaceae species consistently was that 61.2 + 60.3 + 65.5 = 187 g (6.6 ounces) twice a day was too much for me. I eat a lot of low-calorie fibrous food everyday to make my gut microbiota happy. An extra 4+ oz increase at the same time as twice-daily broccoli sprouts put my stomach over the top.

I changed to make equal contents of these three Brassicaceae species be the 10.7 g (one tablespoon) that I started sprouting twice a day.

2. I haven’t seen relevant mustard and red cabbage 3-day-old sprout studies, only 7+ day microgreen and mature plant studies. Evidence is limited in determining effects of cutting my estimated 52 mg of daily sulforaphane intake from broccoli sprouts by two-thirds starting this week.

A. I’ve eaten a clinically-relevant amount of sulforaphane every day for 4+ times longer than any clinical trial. I’ve experienced many positive effects described in studies, and look forward to further improvements.

Reducing sulforaphane intake from broccoli sprouts to 17 mg is still within boundaries of measurable effects. As an example, Upgrade your brain’s switchboard with broccoli sprouts found effects from a daily sulforaphane 17.3 mg (100 µmol) intake.

B. Mustard’s main glucosinolate, sinigrin, hydrolyzes to allyl isothiocyanate, and is in the same aliphatic group as broccoli’s glucoraphanin, which hydrolyzes to sulforaphane. An example of their similar effects was in a citation of Eat broccoli sprouts for DIM:

“Isothiocyanates are both inducers and substrates for Phase II enzymes as glutathione-S-transferases, and polymorphisms of these enzymes have a significant impact.”

Mustard’s myrosinase enzyme activities over and above broccoli myrosinase were highlighted in cited studies of Does sulforaphane reach the colon? Pretty sure that mustard sprouts’ myrosinase ≤ 60°C increases broccoli sprouts’ sulforaphane.

C. Red cabbage’s main glucosinolate is also glucoraphanin. Here’s a graphic from a 2010 study RED CABBAGE, A VEGETABLE RICH IN HEALTH-RELATED GLUCOSINOLATES which compared its glucoraphanin content with white cabbage:

red cabbage glucoraphanin vs white cabbage

The seeds I received were an “Agnostic” variety. In clarification correspondence with my supplier, I received a response “It means in this use ‘Generic’ or Variety not stated. Meaning it is just whatever variety of Red cabbage we bought and we don’t know the exact specifics.” 🙄

Red cabbage anthocyanins have a larger extent than broccoli anthocyanins, which was highlighted in Colorize your diet, Red cabbage pigments and the brain, and Measuring bioavailability. Figure 5 of Lab analyses of broccoli sprout compounds had analysis of three red cabbage cultivars’ 9-day-old sprouts. Glucosinolates are on top, hydrolysis products on the bottom. Glucoraphanin is red 4MSOB in A, and sulforaphane is red 4MSOB-ITC in C:

red cabbage 9-day-old sprouts

D. In summary, I don’t think I’ve significantly reduced broccoli sprouts’ effects by substituting two-thirds weight with two other Brassicaceae species. I haven’t noticed that growth characteristics / compounds interfered with each other.

Still looking for mustard and red cabbage 3-day-old sprout studies. My current Brassicaceae species composite is tasty, and doesn’t cause mustard nose burn.

3. This Brassicaceae species composite isn’t photogenic:

PXL_20210502_214348538

Red cabbage sprouts by themselves are pretty.

PXL_20210504_212505224

4. I still eat 3-day-old oat sprouts twice a day per Sprouting hulled oats. I don’t eat them with Brassicaceae species, but wait at least an hour later with Avena nuda oats in the morning, and AGE-less chicken vegetable soup in the evening.

One aspect of research on short-chain fatty acids

To further understand An overlooked gut microbiota product, a 2018 rodent study found:

“Microbial metabolites short-chain fatty acids (SCFAs) have been implicated in gastrointestinal functional, neuroimmune regulation, and host metabolism, but their role in stress-induced behavioural and physiological alterations is poorly understood

SCFAs are primarily derived from fermentation of dietary fibres, and play a pivotal role in host gut, metabolic and immune function. All these factors have previously been demonstrated to be adversely affected by stress.

Administration of SCFAs to mice undergoing psychosocial stress alleviated enduring alterations in anhedonia and heightened stress-responsiveness, as well as stress-induced increases in intestinal permeability.

experimental design

SCFA treatment alleviated psychosocial stress-induced alterations in reward-seeking behaviour, and increased responsiveness to an acute stressor and in vivo intestinal permeability. In addition, SCFAs exhibited behavioural test-specific antidepressant and anxiolytic effects, which were not present when mice had also undergone psychosocial stress.”

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/JP276431 “Short-chain fatty acids: microbial metabolites that alleviate stress-induced brain–gut axis alterations”


One way researchers advance science is to relate aspects of their findings to previous studies. That approach works, but may miss items that weren’t covered in previous research.

This study fed specific quantities of three SCFAs – acetate, butyrate, and propionate – apparently due to previous research findings. If other SCFAs produced by gut microbiota were ignored – like crotonate (aka unsaturated butyrate) – how would that approach advance science?

I found this study from its citation in Harnessing endogenous defenses with broccoli sprouts.

An overlooked gut microbiota product

This 2021 review subject was histone crotonylation:

“Histone crotonylation is a newly identified epigenetic modification that has a pronounced ability to regulate gene expression. It belongs to an expanding group of short chain lysine acylations that also includes the extensively studied mark histone acetylation.

Histone Kcr was first identified in 2011 where it was found to be mainly associated with active chromatin. Kcr occurs on the ε-amino group of the lysine side chain, where it neutralizes the positive charge of this residue. The loss in positive charge on histone Lys residues weakens DNA interaction, thus making chromatin less compact and accessible to DNA-binding factors.

Crotonate, like other short chain fatty acids (SCFAs), is mainly produced by gut microbiota during fermentation of partially and nondigestible carbohydrates. Circulating SCFAs (acetate, crotonate, butyrate, and propionate) can be taken up by tissues and converted into their cognate short-chain acyl-CoAs, the direct donors of histone Lys acylations.

fcell-09-624914-g001

Crotonyl-CoA is generated as a by-product of fatty acid and amino acid metabolism. Synthesis of crotonyl-CoA can occur in mitochondria or the cytoplasm. Evidence suggests that histone acylations are directly sensitive to changes in concentrations of their corresponding acyl-CoA metabolites, and therefore can act as indicators of cellular metabolic state.

Only a small number of Kcr sites in human histones have been identified so far. This is in part due to a lack of commercially available Kcr site-specific antibodies, which has meant much of the research in this field has focused on studying total histone crotonylation. This is likely to limit our understanding of the importance of histone Kcr, as functional impact of modification at specific sites cannot be readily assessed.”

https://www.frontiersin.org/articles/10.3389/fcell.2021.624914/full “The Regulation and Function of Histone Crotonylation”


At first I thought I had missed recent studies of gut microbiota producing crotonate. Searching again for “crotonate” “microbiota” 2020 2021, I didn’t find any that weren’t cited by this paper.

A lack of research could be due to factors mentioned above. It may also be that researchers just don’t look for evidence of the circulating SCFA crotonate.

Broccoli sprouts’ immune effects

Two 2021 papers, with the first’s subject being sulforaphane’s immune effects:

“Effects of sulforaphane (SFN) on immune response generate scientific interest because of its bioavailability, which is much higher than other phytochemicals, and its capacity to induce Nrf2 target genes. Clinical trials suggest that sulforaphane produces favorable results in cases where pharmaceutical products fail.

SFN exhibits the highest bioavailability among well-known antioxidant phytochemicals, such as quercetin (20-fold higher) and curcumin (80-fold higher). SFN confers a high potential to be used either as a nutraceutical to improve health status, or as pharmaceutical to treat disease states.

molecules-26-00752-g001

Sulforaphane exerts a pleiotropic effect on immunological response, and the final effect depends on cell type.

  • In lymphocyte T-cells, SFN induces ROS production, GSH depletion, and repression of inflammatory cytokines, resulting in suppression of immune and inflammatory responses.
  • In monocytes and macrophages, SFN stimulates immune response by inducing Nrf2, thus triggering antioxidant and anti-inflammatory responses.”

https://www.mdpi.com/1420-3049/26/3/752/htm “Potential of Sulforaphane as a Natural Immune System Enhancer: A Review”


A second study was Fertilization and Pre-Sowing Seed Soaking Affect Yield and Mineral Nutrients of Ten Microgreen Species:

“Ten tested microgreen species [amaranth, arugula, basil, broccoli, red cabbage, Daikon radish, kale, kohlrabi, mustard, and green pea] in this study varied in fresh and dry shoot weights, shoot height, and mineral nutrient concentrations.”

This study grew sprouts for 6 – 18 days before harvesting. Its study design didn’t require sampling along the way to discover informative compositional changes, as did 2020’s 3-day-old broccoli sprouts have the optimal yields and Broccoli sprout compounds include sinapic acid derivatives.

Their supplier was the same as I used for broccoli and red cabbage seeds. No endorsement is intended.

I’d rather use an unknown broccoli variety than this study’s broccoli cultivar, Waltham 29. It was found to be relatively glucoraphanin-deficient when measured in a 2004 study referenced in Tailoring measurements for broccoli sprouts, 32nd of 34 tested.

Received these today:

PXL_20210424_191628875

I’ve asked for clarification of the red cabbage seed variety I received. Not sure what “Agnostic” means in a “Red Cabbage Microgreen – Agnostic” context. 🙂

Mustard and red cabbage sprouting will follow Improving healthy compounds of broccoli sprouts efforts, minus that study’s laboratory setup and duration. I expect synergistic effects from handling both species’ sprouts with my protocol for microwaved 3-day-old broccoli sprouts.

Benefits of eating fermentable fiber

This 2021 review subject was effects of short-chain fatty acids produced by gut microbiota:

“SCFAs are the main players in the interplay between diet, microbiota, and health. SCFAs contribute to intestinal homeostasis and regulation of energy metabolism.

SCFAs regulate the blood–brain barrier and neuroimmunoendocrine functions. During gestation, SCFAs can cause epigenetic imprinting and protect against allergic airway disease.

gr3_lrg

Fiber reaching the colon is anaerobically fermented by gut bacteria, which produce SCFAs. Nondigestible polysaccharides are found in plant cell walls, and are further classified into soluble and nonsoluble dietary fibers.

A role for SCFAs in histone modification of tissues in the body was definitively shown by dietary supplementation of germ-free mice with microbially produced acetate, propionate, and butyrate. These SCFAs increased acetylation of histone H4 and H3 in a tissue-specific fashion.

Most research to date has focused on butyrate but unlike acetate and propionate, it is typically present in undetectable or very low concentrations in the body. SCFAs appear to influence health through three principal mechanisms:

  1. Altering levels of HAT [histone acetyltransferase] and HDAC [histone deacetylase] activity;
  2. Signaling by specific fatty acid-sensing GPCRs [G-protein-coupled receptors]; and
  3. Anti-inflammatory mechanisms in the periphery and tissues due to the first two mechanisms.”

https://www.cell.com/trends/microbiology/fulltext/S0966-842X(21)00035-4 “Microbial Regulation of Host Physiology by Short-chain Fatty Acids”


PXL_20210412_104327851

Effects of another broccoli sprout compound

This 2020 rodent study investigated effects of broccoli sprout hydrolysis compound indole-3-carbinol:

“I3C metabolites act as ligands of the aryl hydrocarbon receptor (AhR), an important sensor for environmental polyaromatic chemicals. We investigated how dietary AhR ligand supplementation influences AhR target gene expression and intestinal microbiota composition.

Environmental signals, such as dietary, microbial, or xenobiotic factors, are sensed in intestinal tissue AhR, an important regulator of metabolism. It influences immune cell homeostasis and immune activation in the intestine.

AhR activation plays an important role in intestinal immunity, contributing to intestinal homeostasis, inflammation, and host defense:

  • AhR activation through high affinity AhR ligands has been shown to stimulate production of antimicrobial peptides.
  • AhR has been shown to be an important regulator of T cell immunity.

This indicates a major role of AhR in resolving intestinal inflammation.

High fat diet and control diet lead to reduced expression of Ahrr in intestinal immune cells.

High fat diet and control diet lead to reduced expression of Ahrr in intestinal immune cells.

Mucosal surface area of the gut represents an enormous area in direct contact with the environment. In addition to occasional pathogen encounters, the intestinal immune system is constantly exposed to antigens from diet or microbiota.

Gut-associated immune cells maintain a balance between protection against harmful infections and tolerating harmless food-derived antigens and commensals.

Our findings are in agreement with reports that dietary I3C supplementation restored AhR activation in intestinal mucosa under conditions of malnutrition and deprivation of natural AhR ligands. In humans, such malnutrition may result from a severely reduced consumption of vegetables and fruit in favor of a carbohydrate rich, high fat diet.”

https://www.mdpi.com/1422-0067/21/9/3189/htm “Dietary AhR Ligands Regulate AhRR Expression in Intestinal Immune Cells and Intestinal Microbiota Composition”


Our gut microbiota outnumber our human cells. Treat them well with broccoli sprout compounds, resistant starch, and fermentable fibers, and expect reciprocity.

Every hand’s a winner, and every hand’s a loser

Another great blog post Know When To Fold ‘Em by Dr. Paul Clayton:

“Newly formed proteins entering the endoplasmic reticulum must be correctly folded to achieve their final form and function. This is a complex procedure with a failure rate of over 80%.

When metabolism is sufficiently skewed, accuracy of protein folding in the endoplasmic reticulum falls below an already low baseline of 20%. Accumulation of misfolded or unfolded proteins in the endoplasmic reticulum then triggers stress.

Integrated Stress Response (ISR) is something that cells do when they are affected by major stressors:

  • ISR turns down global protein synthesis, which is designed to kill virally infected or cancerous cells. If it kills the cancer cell or virally infected cell, that is the end of it.
  • If the stressor is in the heat / hypoxia / nutrient group, however, ISR effectively puts a cell into dark mode until hard times are over. Once the stressor has passed, a cell can then start to recover and return to homeostatic health.
  • But if the stressor is sustained, a low-grade ISR continues to smolder away, causing long-term impairment locally and ultimately systemically. Accumulation of misfolded or unfolded proteins activates ISR, leading to a down-regulation of protein synthesis, and increasing protein folding and degradation of unfolded proteins.

This is analogous to inflammation. Acute inflammatory responses to a pathogen or to tissue damage are entirely adaptive, and essential. Chronic inflammation, on the other hand, causes local and eventually systemic damage if left unchecked for long enough.”


A 2020 rodent study was cited for “reversing age-related cognitive decline”:

“This suggests that the aged brain has not permanently lost cognitive capacities. Rather, cognitive resources are still there, but have been somehow blocked, trapped by a vicious cycle of cellular stress.

Our work with ISR inhibition demonstrates a way to break that cycle, and restore cognitive abilities that had become walled off over time.

stress response inhibitor effects

If these findings in mice translate into human physiology, they offer hope and a tangible strategy to sustain cognitive ability as we age.”

https://elifesciences.org/articles/62048 “Small molecule cognitive enhancer reverses age-related memory decline in mice”


I’m curious as to why sulforaphane hasn’t been mentioned even once in Dr. Paul Clayton’s blog, which started three years ago. Do hundreds of sulforaphane studies performed in this century not contribute to his perspective? Polyphenols are mentioned a dozen times, yet they are 1% bioavailable compared with 80% “small molecule” sulforaphane.

Advice from the song depends on your definition of money:

“Know when to walk away
Know when to run
Never count your money
When you’re sitting at the table”

Pigs and glucosinolates

This 2020 porcine study subject was improving healthy aspects of canola-oil-processing by-products:

“We hypothesized that inclusion of high-amylose cornstarch (HA-starch) in canola co-products-based diets for pigs can reduce hindgut pH, leading to increased degradation of glucosinolates present in hindgut of pigs into non-goitrogenic products. Most dietary myrosinases [enzymes] are inactivated by heat during cooking, pressing and toasting of canola seeds during oil extraction, implying that microorganisms that reside in the hindgut of pigs are a major source of myrosinase that degrade glucosinolates into various metabolites.

Negative effects of dietary cold-pressed canola cake (CPCC) on thyroid gland functions of nursery pigs were alleviated by dietary HA-starch. Composition of glucosinolate degradation products was dependent on parent glucosinolate type and pH conditions.

Dietary resistant starch for nursery pigs reduced cecal digesta pH from 6.07 to 5.37. Resistant starch escaped enzymatic digestion in the small intestine, and was highly fermented in hindgut of pigs.

total canola gluconisolates

Since dietary HA-starch at 40% reduced growth performance of pigs in the current study, there is a need to identify optimal dietary level of HA-starch that does not compromise growth performance of pigs fed canola co-product-based diet, or to identify alternative strategies that can be used to reduce pH in the hindgut of pigs fed canola co-product-containing diet without compromising growth performance.”

https://academic.oup.com/jas/article-abstract/98/5/skaa111/5817019 “Toxicity of canola-derived glucosinolates in pigs fed resistant starch-based diets” (not freely available)


Pig metabolism is similar to humans. Glucosinolate compound effects weren’t similar to those in sulforaphane studies because their contexts were different. Regarding resistant starch, read Eat oats to prevent diabetes which provided evidence for what dietary resistant starch and β-glucan can achieve.

Found this study through a search term “indole-3-carbinol” restricted for 2021. It was cited in Toxicity of Canola-Derived Glucosinolate Degradation Products in Pigs—A Review coauthored by the same researchers.

Improving healthy compounds of broccoli sprouts

This 2020 study investigated known and experimental effects on sprouted broccoli, white mustard, red radish, and red cabbage compounds:

“We planned development of cruciferous sprouts in hydroponics elicited with LED lighting and Methyl-Jasmonate (MeJA) to bio-stimulate production of glucosinolates, comparing effects of two types of LEDs designed for indoor food production systems.

We aimed to gain knowledge on response (germination rate, biomass yield) and phytochemical composition of fresh edible sprouts of cruciferous varieties (broccoli, radish, cabbage and mustard) under these conditions for future food production recommendations:

  • Use of LED lights to grow edible cruciferous sprouts was positive in terms of biomass production and phytochemical content (glucosinolates) without any negative effects.
  • Use of MeJA was positive, confirming previous results. Intensity of response for different species is useful to focus production of sprouts for specific purposes.

3-day old sprouts were placed in a growth chamber with controlled conditions (Photoperiod 18/6 h; temperature 24/18 °C; and relative humidity 60/80%), irrigated every other day to maintain enough humidity in substrate, using 1% bleach in distilled water, and collected on day 7. Trays of germinating seeds were evenly sprayed daily with 10 mL of solution for 4 days.

4 sprouts glusosinolates affected by LED and MeJa

Total Glucosinolates (mg/100 g fresh weight) of White Mustard, Broccoli, Red Cabbage and Red Radish sprouts, under two different LED lightings, and elicited with MeJA (250 μM).

Combining MeJA spraying with different LED light treatment showed clear increases in total glucosinolate contents for all studied sprouts when sprayed for 4 days with MeJA 250 μM.”

https://www.mdpi.com/2504-3900/70/1/67 “The Quality and Glucosinolate Composition of Cruciferous Sprouts under Elicitor Treatments Using MeJA and LED Lights”


The research group of Our model clinical trial for Changing to a youthful phenotype with broccoli sprouts keep ramping it up. They’ve published studies of MeJA effects and LED effects on sprouts separately, but not combined like this one did.

I ordered a pound of red cabbage seeds to see how I like their 3-day-old sprouts. I started soaking mustard seeds purchased from a grocery store’s spice section last year to see if they’ll sprout.

Although effects in the above graphic are compelling, I don’t want to turn my kitchen into a laboratory with LED lights and MeJA treatments. I’ll first see if red cabbage and mustard sprouts are tolerable.