Eat oats for β-glucan and resistant starch

This 2021 review highlighted effects of processing oat products:

“Starch contents in oats ranges from 51% to 65%. Resistant starch (RS) accounts for 29.31% of starch content in raw granular form of oat starch.

RS in raw oat starch is RS2 starch, where its slow digestion is mainly due to the compact nature of starch granules making starch less accessible to enzymes. Since amylose–lipid complex is resistant to enzymatic breakdown, high lipid content in oats (3–7%) may be another reason why oat has a relatively high level of RS starch. This type of RS is called RS5.

Although RS2 occurs naturally, most starch needs to be cooked for consumption. RS3 that is formed due to recrystallization of gelatinized starch is more commonly consumed by processing via gelatinization and retrogradation.

β-glucans are found in cell walls of endosperm and aleurone layers of oats, accounting for 1.73-5.70% of oat grains dry basis. Oat β-glucans are not digested in the upper gastric tract, but instead can be consumed by gut microbiota in the colon. This kind of prebiotic can be fermented by colonic microbiota, resulting in production of short chain fatty acids (SCFA) metabolites.

From field to table, oats are processed into various foods for consumption, and these foods exhibit high variability of GI values:

  • β-glucan dose and molecular weight are crucial determinants affecting viscosity and gastric emptying rate; and
  • Higher content of protein in oats is an important factor that deserves attention.”

https://www.mdpi.com/2304-8158/10/6/1304/htm “Oat-Based Foods: Chemical Constituents, Glycemic Index, and the Effect of Processing”


Didn’t care for this focus on one dimension of health, glycemic index. Why not focus on healthy individuals’ behaviors? See An oats β-glucan clinical trial for more human in vivo evidence regarding β-glucan molecular weight.

I eat oats three times a day, and it’s worked out alright.

PXL_20210825_100824154

An IBD trigger?

Three papers on interactions of the virus and inflammatory bowel disease, beginning with a 2021 review:

“Analysis signaling pathways of innate and adaptive immunity components during SARS-CoV-2 infection in IBD (inflammatory bowel disease) patients through a putative alternative route – the gastrointestinal tract, with virus attachment to ACE2 (angiotensin-converting enzyme 2) expressed on IECs (intestinal enterocytes) – allows identifying some molecular pathways and establishing possible mechanisms of immune response formation.

In general, any virus infecting intestinal tissues and/or entering the host’s body through receptors located on intestinal IECs, may be a trigger for the onset of IBD in individuals.”

https://link.springer.com/article/10.1007%2Fs11033-021-06565-w “Pathogenesis of the inflammatory bowel disease in context of SARS-COV-2 infection”


A second 2021 review continued:

“Patients with COVID-19 may develop various gastrointestinal symptoms, which may be pre-existing or not accompanied by respiratory symptoms. Positive detection of SARS-CoV-2 in stool specimens was a breakthrough because it demonstrated that the virus could replicate and exist in the digestive tract. Duration of viral nucleic acid in feces is longer than that in respiratory specimens, and the peak of viral load is later.

COVID-19 induces an acute inflammatory response which accelerates consumption of nutrients. Gastrointestinal symptoms caused by SARS-CoV-2 further impacted nutrition absorption and exacerbated malnutrition. Patients’ anxiety and poor appetite were also potential contributors to malnutrition.”

https://www.wjgnet.com/1007-9327/full/v27/i24/3502.htm “COVID-19 and its effects on the digestive system”


I found the above two papers by their citing a 2020 review:

“Based on data on over 1400 patients with IBD from an international registry, compared with TNF monotherapy, thiopurine monotherapy and combination thiopurines with TNF antagonists are associated with significantly increased risk of severe COVID-19. Mesalamine/sulfasalazine may be associated with an increased risk, particularly when compared with TNF antagonists. There are no significant differences between biological classes (TNF, interleukin-12/23 and integrin antagonists) on the risk of severe COVID-19.”

https://gut.bmj.com/content/70/4/725 “Effect of IBD medications on COVID-19 outcomes: results from an international registry”


I rated these three papers as requiring more work because they didn’t address an individual’s preparation for originating causes. Managing symptoms isn’t an appropriate response for what all of us face.

Instead, take personal responsibility for your own one precious life.

Looking forward, looking back

PXL_20210817_095643714.NIGHT

Don’t count on broccoli compounds bailing out a high-fat diet’s effects on gut microbiota

Two rodent studies of mature broccoli and broccoli sprouts’ effects on a high-fat diet, with the first from 2021 investigating broccoli florets and stalks:

“Addition of broccoli florets to a HFD ameliorated insulin sensitivity. Florets further promoted gut microbiota diversity and low-grade inflammatory-associated strains.

Stalk supplementation also altered gut microbiota, leading to increased Bacteroidetes/Firmicutes ratio and levels of communities that preserve mucus layer and gut integrity while simultaneously decreasing levels of potentially harmful species.

Addition of broccoli to a HFD did not ameliorate body and tissues weight gain or food intake. Both broccoli stalks and florets did not affect fat accumulation, carbohydrate, or lipid metabolism-related parameters.”

https://www.frontiersin.org/articles/10.3389/fnut.2021.680241/full “Broccoli Florets Supplementation Improves Insulin Sensitivity and Alters Gut Microbiome Population – A Steatosis Mice Model Induced by High-Fat Diet”


A 2020 study cited by this first study investigated compounds extracted from 1-day-old broccoli sprouts:

Bioaccessibility of aliphatic glucosinolates was shown to 76.2 ± 0.6%:

aliphatic glucosinolate bioavailability

Glucoraphanin was the predominant glucosinolate with the highest bioaccessibility in broccoli, and could effectively prevent HFD-induced body weight gain in mice, especially increases in liver weight and the accumulation of lipids in adipocytes. Furthermore, supplementation with glucoraphanin reduced the level of oxidative stress, regulated genes of FAS, PPARα, CPT1 and ACOX associated with lipid metabolism, and might be associated with changes in composition of gut microbiota.”

https://www.frontiersin.org/articles/10.3389/fnut.2021.680241/full “Effect of glucoraphanin from broccoli seeds on lipid levels and gut microbiota in high-fat diet-fed mice”

This study’s title was “Effect of glucoraphanin from broccoli seeds..” although its Materials and methods section disclosed:

“1 day after germination from broccoli seeds, sprouts were boiled in water for 30 min. The resulting aqueous extract was processed by liquid solid separation and condensation and was subsequently spray-dried to yield an extract powder containing 249 mg glucoraphanin.”


Eat broccoli sprouts every day and its predecessor study demonstrated that broccoli intake every day had beneficial effects during shorter periods than either of these studies.

Both studies had many “may”, “could”, and “might” statements. Not sure that broccoli compounds / gut microbiota relationships are adequately investigated by choosing a few out of tens of thousands of gut microbiota species as both studies attempted to do.

There are too many additive / antagonistic / synergistic combinations to analyze even before reaching twenty gut microbiota species. But researchers aren’t often sponsored for studies unless they conform to existing research.


I haven’t made headway in understanding my top 10 of 42,156 gut microbiota species’ exact causes, effects, and interactions. The top three by themselves are considered beneficial:

top 1-10 species

Uncertainty is fine for now, though, with a 40-hour work week interfering. Finding out what my gut microbiota generally want and giving that to them has been a productive approach this year.

If you aren’t where you want to be, change yourself

This 2021 human study evaluated associations among epigenetic clocks and socioeconomic status:

“We conducted a comprehensive, comparative analysis of associations between various dimensions of socioeconomic status (SES) (education, income, wealth, occupation, neighbourhood environment, and childhood SES) and eight epigenetic clocks in two well-powered US ageing studies:

  • The Multi-Ethnic Study of Atherosclerosis (MESA); and
  • The Health and Retirement Study (HRS).

We found robust associations between SES measures in adulthood and the GrimAge and DunedinPoAm [Dunedin New Zealand (P)lace (o)f (A)ging (m)ethylation clock)] clocks. In the HRS, significant associations with the Levine and Yang clocks were also evident.

These associations were only partially mediated by smoking, alcohol consumption, and obesity, which suggests that differences in health behaviours alone cannot explain the SES gradient in epigenetic ageing in older adults. Further analyses revealed concurrent associations between polygenic risk for accelerated intrinsic epigenetic ageing, SES, and the Levine clock, indicating that genetic risk and social disadvantage may contribute additively to faster biological aging.”

https://www.medrxiv.org/content/medrxiv/early/2021/03/02/2021.03.01.21252660.full.pdf “The Socioeconomic Gradient in Epigenetic Ageing Clocks: Evidence from the Multi-Ethnic Study of Atherosclerosis and the Health and Retirement Study”


This study had a lot of squishy data. Didn’t see peer review comments, but I’d require evidence for several of these categorizations and subsequent findings.

For example, I quit smoking on February 5, 1985, the day I left my third submarine. This study would have categorized me 36 years later as a former smoker.

This categorization defied human cell turnover, with exceptions of our:

  • Cerebrum and cerebellum neurons;
  • Eye inner lens cells; and
  • Heart muscle cells.

Neither these cells nor other cells are associated with current status and quitting smoking four decades earlier. Consider that “associated” relationships don’t necessarily have any causal origins.

Another example from this study. My parents’ educational achievements of Masters degrees were during the 1950s. Pretty sure they weren’t causal to my degrees during the 1980s when I focused on advancing in the U.S. Navy.

Your responses to life events and subsequent behaviors are up to you, when and where you need them to be.

Do you feel a need to be consciously aware of who you really are? If not, unconsciously move along with the herd.


980604-N-7726D-002

PTSD susceptibility?

This 2021 rodent study investigated post-traumatic stress disorder (PTSD) susceptibility:

“PTSD is an incapacitating trauma-related disorder, with no reliable therapy. We show distinct DNA methylation profiles of PTSD susceptibility in the nucleus accumbens (NAc). Data analysis revealed overall hypomethylation of different genomic CpG sites in susceptible animals.

Is it possible to treat PTSD by targeting epigenetic processes? Such an approach might reverse genomic underpinning of PTSD and serve as a cure.

To test plausibility of such an approach, a reliable animal (rat) model with high construct validity is needed. Previously, we reported one such model, which uses predator-associated trauma, and cue reminders to evoke recurring trauma. This simulates clinical PTSD symptoms including re-experiencing, avoidance, and hyperarousal.

Individual PTSD-like (susceptible) behavior is analyzed, enabling identification of susceptible animals separately from those that are non-PTSD-like (resilient). This model captures salient features of this disorder in humans, in which only a fraction of trauma victims develop PTSD, while others are resilient.

experimental model

Sprague–Dawley rats were exposed to trauma and to three subsequent trauma-associated reminders. Freezing behavior was measured under conditions of:

  • Exploration;
  • Social interaction (with a companion); and
  • Hyperarousal.

Controls were exposed to identical conditions except for the traumatic event.

PTSD-like behavior of each animal was compared with baseline and with the population. Two unambiguous sub-populations were identified, resilient and susceptible.

After exposure to trauma and its reminders, susceptible animals showed an increase from baseline in freezing behavior, and over time in all three behavioral tests, as opposed to resilient and control groups.

DMRs

Differentially methylated sites in susceptible and resilient animals compared to control group.

Although we focused in this study on DNA methylation changes that associate with susceptibility, we also report unique changes in DNA methylation that occur in resilient animals. Inhibition of critical genes that are downregulated in susceptible animals convert resilient animals to become susceptible.”

https://www.researchgate.net/publication/353192082_Reduction_of_DNMT3a_and_RORA_in_the_nucleus_accumbens_plays_a_causal_role_in_post-traumatic_stress_disorder-like_behavior_reversal_by_combinatorial_epigenetic_therapy “Reduction of DNMT3a and RORA in the nucleus accumbens plays a causal role in post-traumatic stress disorder-like behavior: reversal by combinatorial epigenetic therapy” (registration required)


Rodents with the same genetics and environment displayed individual differences in their responses to traumatic events. Please provide evidence for that before venturing elsewhere.

Not sure why it took 3+ years for this study received in November 2017 to finally be published in July 2021. Sites other than https://doi.org/10.1038/s41380-021-01178-y are more transparent about their peer review and publication processes.

No causes for PTSD susceptibility were investigated. PTSD effects and symptoms aren’t causes, notwithstanding this study’s finding that:

“Our results support a causal role for the NAc as a critical brain region for expression of PTSD-like behaviors, and a role for programming genes by DNA methylation in the NAc in development of PTSD-like behaviors.”

Can’t say that I understand more about causes for PTSD susceptibility now than before I read this study. Researchers attaching significance to gene functional groups seemed like hypothesis-seeking efforts to overcome limited findings.

Will this study’s combination of a methyl donor with a Vitamin A metabolite address PTSD causes in humans? If it only temporarily alleviates symptoms, what lasting value will it have?


Several brain and body areas that store traumatic memories other than the nucleus accumbens were mentioned in The role of recall neurons in traumatic memories. A wide range of epigenetic memory storage vehicles is one reason why effective human therapies need to address each individual, their whole body, and their entire history.

PXL_20210714_095056317

Osprey breakfast

Gut and brain health

This 2021 human review subject was interactions of gut health and disease with brain health and disease:

“Actions of microbial metabolites are key for appropriate gut-brain communication in humans. Among these metabolites, short-chain fatty acids (SCFAs), tryptophan, and bile acid metabolites / pathways show strong preclinical evidence for involvement in various aspects of brain function and behaviour.

Dietary fibres, proteins, and fats ingested by the host contain components which are metabolized by microbiota. SCFAs are produced from fermentation of fibres, and tryptophan-kynurenine (TRP-KYN) metabolites from dietary proteins. Primary bile acids derived from liver metabolism aid in lipid digestion, but can be deconjugated and bio-transformed into secondary bile acids.

1-s2.0-S0149763421001032-gr1

One of the greatest challenges with human microbiota studies is making inferences about composition of colonic microbiota from faeces. There are known differences between faecal and caecal microbiota composition in humans along with spatial variation across the gastrointestinal tract.

It is difficult to interpret microbiome-host associations without identifying the driving influence in such an interaction. Large cohort studies may require thousands of participants on order to reach 20 % explanatory power for a certain host-trait with specific microbiota-associated metrics (Shannon diversity, relative microbial abundance). Collection of metadata is important to allow for a better comparison between studies, and to identify differentially abundant microbes arising from confounding variables.”

https://www.sciencedirect.com/science/article/pii/S0149763421001032 “Mining Microbes for Mental Health: Determining the Role of Microbial Metabolic Pathways in Human Brain Health and Disease”


Don’t understand why these researchers handcuffed themselves by only using PubMed searches. For example, two papers were cited for:

“Conjugated and unconjugated bile acids, as well as taurine or glycine alone, are potential neuroactive ligands in humans.”

Compare scientific coverage of PubMed with Scopus:

  • 2017 paper: PubMed citations 39; Scopus citations 69.
  • 2019 paper: PubMed citations 69; Scopus citations 102.

Large numbers of papers intentionally missing from PubMed probably influenced this review’s findings, such as:

  1. “There are too few fibromyalgia and migraine microbiome-related studies to make definitive conclusions. However, one fibromyalgia study found altered microbial species associated with SCFA and tryptophan metabolism, as well as changes in serum levels of SCFAs. Similarly, the sole migraine-microbiota study reported an increased abundance of the kynurenine synthesis GBM (gut-brain module).
  2. Due to heterogeneity of stroke and vascular disease conditions, it is difficult to make substantial comparisons between studies. There is convincing evidence for involvement of specific microbial genera / species and a neurovascular condition in humans. However, taxa were linked to LPS biosynthesis rather than SCFA production.
  3. Several studies suggest lasting microbial changes in response to prenatal or postnatal stress, though these do not provide evidence for involvement of SCFA, tryptophan, or bile-acid modifying bacteria. Similar to stress, there are very few studies assessing impact of post-traumatic stress disorder on microbiota.”

These researchers took on a difficult task. Their study design could have been better.


PXL_20210628_095746132

Wildlife

PXL_20210710_100826663

Eat mushrooms for a longer life?

Two papers, starting with a 2021 meta-analysis of mushroom intake:

“Mushroom consumption was associated with a lower risk of total mortality in this nationally representative sample of US adults.

median mushroom intake

15,546 participants were included, mean age 44.3 years. During a mean follow-up duration of 19.5 years, a total of 5,826 deaths were documented.

Participants who reported consuming mushrooms had lower risk of all-cause mortality compared with those without mushroom intake after adjusting for demographic, major lifestyle factors, overall diet quality, and other dietary factors including total energy.”

https://nutritionj.biomedcentral.com/articles/10.1186/s12937-021-00691-8 “Association of mushroom consumption with all-cause and cause-specific mortality among American adults: prospective cohort study findings from NHANES III”


A 2019 review with two of the same coauthors:

“Mushrooms are inherently, or can easily be made to be, excellent dietary sources of 4 important bioactive compounds that decrease in humans as they age:

  • Selenium;
  • Vitamin D2;
  • Glutathione; and
  • Ergothioneine (Ergo).

All of these except for Ergo can be found in significant amounts in other foods, and mushrooms are by far the best human dietary source.

Humans produce a highly specific transport protein for Ergo that makes it highly bioavailable and avidly retained. Such specific transporters are rarely present for nonnutrient bioactive compounds.

mushroom ergothioneine glutathione

Mushrooms are a valuable source of protein, fiber, B vitamins, phenolic compounds, potassium, and β-glucans. An Ergo increase of 3 mg/d can be accomplished by consumption of about 100 g of fresh button mushrooms per day, or around 25 g of fresh specialty mushrooms such as shiitake, oyster, or maitake mushrooms.

One potential way to add fresh button mushrooms to the diet would be to embrace the meat-blend approach in which about 30% to 40% ground, fresh button mushrooms are blended with 60% to 70% ground beef to replace pure ground beef in burgers or other common commonly consumed dishes. Another approach could be to use small amounts of Ergo-rich specialty mushroom dried powder as a new food ingredient into current or new food products.”

https://journals.lww.com/nutritiontodayonline/Abstract/2019/01000/Micronutrients_and_Bioactive_Compounds_in.5.aspx# “Micronutrients and Bioactive Compounds in Mushrooms: A Recipe for Healthy Aging?” (not freely available)


I doubt that mushroom intake was a cause of more than a third of this meta-analysis’ participants dying before they reached age 64. The first study of The amino acid ergothioneine had better methodological approaches that related mushroom intake to mortality.

I’ve eaten more than triple the first graphic’s 72 grams for over a year, not because I knew of health effects, but because I like mushrooms. The second graphic is nice to know, but probably won’t go out of my way for ergothioneine content.

Does sulforaphane treat autism?

A 2021 human study investigated sulforaphane treatments of autistic 3-to-12-year-olds:

“Sulforaphane (SF) led to non-statistically significant changes in the total and all subscale scores of the primary outcome measure. Several effects of SF on biomarkers correlated to clinical improvements. SF was very well tolerated and safe and effective based on our secondary clinical measures.

13229_2021_447_Fig1

Clinical response to SF was associated with changes in mitochondrial function, and large intrasubject variability in this study was linked to underlying biological responses. The increase in ATP [adenosine triphosphate]-Linked Respiration associated with improvement in ABC [Aberrant Behavior Checklist] scores suggests that those individuals who showed improvements in behavior also had improved mitochondrial capacity to produce ATP.

Individuals who showed an improvement in ABC scores also showed a decrease in Proton Leak Respiration, suggesting that their mitochondria were better able to regulate oxidative stress. It is also possible that the increase in ATP production was related to improvement in the ability of mitochondria to handle oxidative stress.

SF had significant positive effects on oxidative stress, cytoprotective markers and cytokines, as well as mitochondrial function. These were promising findings that require further investigation of both clinical effects and mechanisms of action of SF.”

https://molecularautism.biomedcentral.com/articles/10.1186/s13229-021-00447-5 “Randomized controlled trial of sulforaphane and metabolite discovery in children with Autism Spectrum Disorder”


Differences between this clinical trial and its pilot study curated in Autism biomarkers and sulforaphane included:

“HO-1 [heme oxygenase 1] functions to couple activation of mitochondrial biogenesis to anti-inflammatory cytokine expression. It was initially increased in the pilot study, then paradoxically decreased in the main study, on continued treatment for longer periods with SF.

Increased HO-1 is consistent with decreases in proinflammatory cytokines we observed initially in IL-6, IL-1β and TNF-α. Decreased levels of cytokines continued after HO-1 returned to baseline with longer duration of treatment and suggest a decreased inflammatory state.

These cytokines are usually elevated in children with ASD, but were decreased on treatment with SF: IL-6 and TNF-α at 15 (but not 30) weeks.”

This study made a good effort with autistic children. Its insignificant effects of sulforaphane treatments pointed toward an understanding that human experiences when we are fetuses can override many subsequent events, treatments, and life experiences.

Your bones influence your brain

This 2020 review subject was brain-bone crosstalk:

“Multiple stress, mood and neurodegenerative brain disorders are associated with osteoporosis. Skeletal diseases display impaired brain development and function.

Along with brain and bone pathologies, trauma events highlight strong interaction of both organs. While brain-derived molecules affecting bone include central regulators – transmitters of the sympathetic, parasympathetic and sensory nervous system – bone-derived mediators altering brain function are released from bone cells and marrow.

ijms-21-04946-g001

Osteoblast-derived hormone osteocalcin (OCN) exerts neuroprotective effects. Studies revealed a bidirectional dependence of brain and bone through bone cell-derived modulators that directly affect behavioral and cognitive function.

The main bone-derived mediator affecting the brain is OCN, which is exclusively synthesized by osteoblasts. OCN was recently discovered to transverse the BBB to enter the CNS, where it promotes spatial learning and memory while preventing anxiety-like behavior or even depression.

Cognitive function and circulating levels of OCN are proposed to inversely correlate with age. Maternal osteocalcin regulates embryonic brain development by enhancing monoamine neurotransmitters and their synthesis.

Clinical observations provide key evidence for a bidirectional communication between brain and bone tissue, which is strongly supported by experimental studies that unraveled underlying mechanistic pathways and identified molecular mediators involved in this crosstalk.”

https://www.mdpi.com/1422-0067/21/14/4946/htm “Crosstalk of Brain and Bone-Clinical Observations and Their Molecular Bases”


The first paper of Vitamin K2 – What can it do? said:

Osteocalcin γ-carboxylation is the main mechanism of action through which Vitamin K2 improves bone health.”

This paper didn’t mention Matrix Gla Protein (MGP) carboxylation, and said a contrary:

“Undercarboxylated, bioactive OCN, initially considered as an inhibitor of bone mineralization, participates in systemic body regulation and homeostasis.”

The 2019 paper cited was Osteocalcin‑GPRC6A: An update of its clinical and biological multi‑organic interactions (Review):

“Osteocalcin is a small protein present in two forms: Carboxylated (cOC) and undercarboxylated (ucOC). Only ucOC can signal as a hormone while cOC cannot.”

It went on to downplay cOC, and also didn’t mention MGP carboxylation.

I think it’s a question of balance. cOC stays in your bones. Carboxylated MGP influences calcium to go into your bones instead of your blood vessel walls. Two good things.

Eat broccoli sprouts daily, and manage weight

This 2018 human study found:

“The objective of this study was to determine whether daily broccoli consumption alters absorption and metabolism of isothiocyanates derived from broccoli glucosinolates. We conducted a randomised cross-over human study (n = 18) balanced for BMI and glutathione S-transferase μ 1 (GSTM1) genotype in which subjects consumed a control diet with no broccoli (NB) for 16 d or the same diet with 200 g of cooked broccoli and 20 g of raw daikon radish daily for 15 d (daily broccoli, DB) and 100 g of broccoli and 10 g of daikon radish on day 16.

On day 17, all subjects consumed a meal of 200 g of broccoli and 20 g of daikon radish. Plasma and urine were collected for 24 h and analysed for sulphoraphane (SF) and metabolites of SF and erucin (ER). (a) BMI < 26 (b) BMI > 26.

sulforaphane and erucin metabolites

db-nb

Plasma AUC [area under the curve] and urinary excretion rates were higher on DB diet than on NB diet. Daily consumption of broccoli interacted with BMI to affect plasma concentrations and urinary excretion of glucosinolate-derived compounds.

Plasma and urinary levels of SF and mercapturic acid pathway products of SF and ER following a broccoli challenge meal were altered when preceded by 16 d of daily broccoli ingestion, and the effect depended on BMI.”

https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/absorption-and-metabolism-of-isothiocyanates-formed-from-broccoli-glucosinolates-effects-of-bmi-and-daily-consumption-in-a-randomised-clinical-trial/ “Absorption and metabolism of isothiocyanates formed from broccoli glucosinolates: effects of BMI and daily consumption in a randomised clinical trial”


Humans are the same, yet we’re each individually unique. These researchers could have explored individual differences, but that wasn’t part of this study’s design.

So we’re left with BMI as a discriminator. I don’t think that’s evidentiarily sufficient.

Eat broccoli sprouts every day. You’ll figure it out.

Astaxanthin bioavailability

By request, research on astaxanthin bioavailability. I used a “astaxanthin” “bioavailability” “quinone reductase” 2021 search term, and read citing papers.

“The bioaccessibility, bioavailability, and antioxidative activities of three astaxanthin geometric isomers were investigated using an in vitro digestion model.

  • 13Z-Astaxanthin showed higher bioaccessibility than 9Z- and all-E-astaxanthins during in vitro digestion, and
  • 9Z-astaxanthin exhibited higher transport efficiency than all-E- and 13Z-astaxanthins.

These might explain why 13Z- and 9Z-astaxanthins are found at higher concentrations in human plasma than all-E-astaxanthin.

9Z- and 13Z- astaxanthins exhibited a higher protective effect than all-E-astaxanthin against oxidative stress.”

https://pubs.acs.org/doi/10.1021/acs.jafc.7b04254 “Bioaccessibility, Cellular Uptake, and Transport of Astaxanthin Isomers and their Antioxidative Effects in Human Intestinal Epithelial Caco-2 Cells” (2017, not freely available)


jf1c00087_0005

“Astaxanthin with a high proportion of Z-isomer (especially rich in 9Z- and 13Z-isomers) was prepared from (all-E)-astaxanthin by thermal treatment and solid–liquid separation. Z-isomer-rich astaxanthin diet resulted in higher levels of astaxanthin in blood and many tissues (in particular, skin, lung, prostate, and eye) compared to all-E-isomer-rich diet.

Z-isomer-rich diet enhanced the level of 13Z-isomer in blood and tissues rather than that of 9Z-isomer. (13Z)-astaxanthin would have higher bioavailability and tissue accumulation than other isomers.”

https://pubs.acs.org/doi/10.1021/acs.jafc.1c00087Z-Isomers of Astaxanthin Exhibit Greater Bioavailability and Tissue Accumulation Efficiency than the All-E-Isomer” (2021, not freely available)


“Astaxanthin is highly susceptible to light, oxygen, and heat stress degradation. In addition, poor water solubility and bioavailability limit its efficacy in vivo. Investigating novel astaxanthin delivery systems is necessary in order to solve these drawbacks.”

https://www.mdpi.com/1420-3049/24/14/2640/htm “The Neuroprotective Effects of Astaxanthin: Therapeutic Targets and Clinical Perspective” (2019)


“Astaxanthin Z-isomers potentially have greater bioavailability and biological activity than (all-E)-astaxanthin. However, stability of Z-isomers is lower than all-E-isomer, which is a serious problem affecting its practical use.

In this study, we investigated impacts of different suspension media (oils and fats) and additives on astaxanthin isomer stability.

  • Z-isomers of astaxanthin isomerized to all-E-isomer during storage.
  • When soybean and sunflower oils were used as the suspension medium, astaxanthin isomers were hardly degraded. However the total Z-isomer ratio decreased from ~80% to ~50% during 6-week storage at 30 °C.
  • (9Z)-astaxanthin showed higher stability than 13Z- and 15Z-isomers.”

https://www.sciencedirect.com/science/article/abs/pii/S0308814621003770 “Evaluation and improvement of storage stability of astaxanthin isomers in oils and fats” (2021, not freely available)


I looked for but didn’t find a graph similar to this one that comparatively plotted astaxanthin:

OMCL2019-2716870.006

I also didn’t find recent human studies.

It seems that a special delivery system is required for taking astaxanthin as a supplement. It would require investigating manufacturers’ claims about isomer content and stability.

Eating colorful seafood is another way to get astaxanthin. Don’t know about eating raw or dried algae.

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 (one teaspoon) 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.

Measuring bioavailability

This 2017 review challenged snapshot measurements of biological availability:

“There is a general belief that anthocyanins, flavanones, and other polyphenols are poorly bioavailable with only relatively small amounts of ingested dose entering systemic circulation in the form of metabolites. When lower molecular weight phenolic and aromatic ring-fission catabolites produced primarily by colonic microbiota are taken into account, it is evident that anthocyanins and flavanones are much more bioavailable than previously envisaged.

Although plasma pharmacokinetic measurements provide a snapshot of absorbed circulating metabolites, 0–24-h urinary excretion of both metabolites absorbed in the small intestine and catabolites of distal gastrointestinal (GI) origin that are products of bacterial processing provide a more quantitative reflection of polyphenol absorption. Overall 0–48-h urinary recovery of phenolic compounds – after baseline subtraction – was 43.9 ± 8.0 μmol, which is equivalent to 15% of ingested anthocyanins.

raspberries

With orders of magnitude higher plasma/serum Cmax levels and significantly longer half-lives, evidence points toward lower molecular weight phenolic and aromatic catabolites being the primary bioavailable products of anthocyanin consumption. Gut-derived catabolites can often exert higher bioactivity than their precursor flavonoid structures.”

https://www.annualreviews.org/doi/full/10.1146/annurev-food-030216-025636 “Anthocyanins and Flavanones Are More Bioavailable than Previously Perceived: A Review of Recent Evidence” (not freely available)


Much of this review’s anthocyanin section was dedicated to a coauthor’s 9-person study where they ate a huge amount of raspberries. Its flavanone section was similarly influenced by another coauthor’s human orange juice studies.

I’d like to see stronger evidence before reviewer statements become faits accomplis, elevated through citations to become indisputable facts. Its underlying point that studies could take more and varied measurements over extended periods seems amenable to evidence.

I arrived at this review through its citations in Colorize your diet and Red cabbage pigments and the brain.

Colorize your diet

This 2020 review subject was anthocyanins in Brassicaceae species:

“Anthocyanins provide red to blue colors in Brassicaceae plants, have nutritional value, and pharmaceutical potential. This review summarizes chemical composition, stability, bioavailability, and health benefits.

Edible sprouts are good sources of anthocyanins. Even within the same species, content of anthocyanins may vary with cultivar, growing season, growth condition, and plant organ.

Acylated anthocyanins were more stable than non-acylated anthocyanins. Bioavailability is the proportion of nutrient reaching systemic circulation.

Brassicaceae anthocyanins

Large amounts of unabsorbed anthocyanins reached the large intestine, where they were extensively metabolized by microbiota, forming simple anthocyanins, which were much more bioavailable. Degradation products can also be absorbed.

When these events are taken into account, Brassicaceae anthocyanins might be more bioavailable than previously perceived.

Stability of Brassicaceae anthocyanins may be beneficial in preventing certain chemical degradation in the gastrointestinal tract. Anthocyanins reaching blood circulation may be different from original food compounds.

Brassicaceae anthocyanins possess potential:

  • Antioxidant;
  • Anti-cancer;
  • Anti-inflammatory activities;
  • Protection against hepatic andrenal damage; and
  • Cardiovascular disease.

Most evidence is based on in vitro studies. More studies are necessary to further understand health benefits, as well as levels of consumption to maximize benefits, and mechanisms involved.”

https://www.tandfonline.com/doi/abs/10.1080/10408398.2020.1852170 “Anthocyanins in Brassicaceae: composition, stability, bioavailability, and potential health benefits” (not freely available)


I found this review as a fourth-order citation of related papers.

Chew it!

This 2020 human study examined associations between food consumption and chewing difficulty:

“Masticatory function influences not only control of chewing frequency and pressure, but also quality of life through food intake. Reduced food intake caused by chewing difficulty results in loss of eating pleasure and nutritional imbalance.

Chewing difficulty (DC) has been related to brain-related diseases such as cognitive impairment, cerebrovascular disorder, and Parkinson’s disease, increase in occurrence of diseases such as muscular dystrophy, aging acceleration, stomach, and kidney dysfunction due to reduced digestive enzyme secretion, and depression.

Subjects were divided into not difficult in chewing (NDC) and DC groups, with 24.17% being classified into DC. Average age of all subjects (n = 20,959 adult subjects aged between 19 and 64 yrs plus older) was 50.67 yrs. Average age of DC (60.5 yrs) was about 13 yrs older than NDC (47.5 yrs old).

Males and females consumed 35 and 37 items less frequently than the other sex, respectively:

nrp-14-637-g001

Subjects over 65 yrs who had chewing difficulty were 45.4% whereas that of adults was 24.3%. Items known to contain relatively high dietary fiber content or a high content of connective tissues were considered as foods to avoid by those with chewing difficulty due to strong or hard texture.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7683204/ “Food consumption frequency of Korean adults based on whether or not having chewing difficulty using 2013–2016 KNHANES by sex-stratified comparative analysis”


I’d like to know more about subjects who had unresolved dental problems. This study focused on age and sex, but I’ve known twenty-somethings who had problems such as false teeth and dentures.

I go to a dentist twice a year. Don’t think I’d make my gut microbiota happy with Avena nuda oats, broccoli and oat sprouts, and AGE-less chicken vegetable soup if I had dental problems.