Take taurine for your mitochondria

This 2021 review summarized taurine’s beneficial effects on mitochondrial function:

“Taurine supplementation protects against pathologies associated with mitochondrial defects, such as aging, mitochondrial diseases, metabolic syndrome, cancer, cardiovascular diseases and neurological disorders. Potential mechanisms by which taurine exerts its antioxidant activity in maintaining mitochondria health include:

  1. Conjugates with uridine on mitochondrial tRNA to form a 5-taurinomethyluridine for proper synthesis of mitochondrial proteins (mechanism 1), which regulates the stability and functionality of respiratory chain complexes;
  2. Reduces superoxide generation by enhancing the activity of intracellular antioxidants (mechanism 2);
  3. Prevents calcium overload and prevents reduction in energy production and collapse of mitochondrial membrane potential (mechanism 3);
  4. Directly scavenges HOCl to form N-chlorotaurine in inhibiting a pro-inflammatory response (mechanism 4); and
  5. Inhibits mitochondria-mediated apoptosis by preventing caspase activation or by restoring the Bax/Bcl-2 ratio and preventing Bax translocation to the mitochondria to promote apoptosis.

taurine mechanisms

An analysis on pharmacokinetics of oral supplementation (4 g) in 8 healthy adults showed a baseline taurine content in a range of 30 μmol to 60 μmol. Plasma content increased to approximately 500 μmol 1.5 h after taurine intake. Plasma content subsequently decreased to baseline level 6.5 h after intake.

We discuss antioxidant action of taurine, particularly in relation to maintenance of mitochondria function. We describe human studies on taurine supplementation in several mitochondria-associated pathologies.”

https://www.mdpi.com/1420-3049/26/16/4913/html “The Role of Taurine in Mitochondria Health: More Than Just an Antioxidant”


I take a gram of taurine at breakfast and at dinner along with other supplements and 3-day-old Avena sativa oat sprouts. Don’t think my other foods’ combined taurine contents are more than one gram, because none are found in various top ten taurine-containing food lists.

As a reminder, your mitochondria come from your mother, except in rare cases.

Part 2 of Improving epigenetic clocks’ signal-to-noise ratio

Another excellent blog post by Josh Mitteldorf, A New Approach to Methylation Clocks, that curated the same study:

“The Levine/Horvath PhenoAge epigenetic clock was calibrated using a combination of metabolic factors that correlate with health, including inflammation, DNA transcription, DNA repair, and mitochondrial activity.

Evolution is not an engineer. Living things are not constructed out of parts that are separately optimized for exactly one function.

Every molecule has multiple functions. Every function is regulated by multiple pathways.

For clock technology, using individual CpGs for a starting point may not be optimal. We suspect that CpGs, like other biological entities, work together closely in teams.

CpGs on a team might vary slightly from one individual to the next. But the team has a function and an identity and a signature that is robust. We expect the team to function more consistently than any of its individual members.

The peer-reviewed version of her paper will be published shortly. Full details of algorithms will be available on GitHub, and script in the R programming language will be released for use of other researchers. If principal component analysis clocks correlate well with previously validated clocks but offer tighter uncertainties, we’ll know we’re on the right track.”


Best wishes for Josh to recover from a bike accident.

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Choosing appropriate dietary fibers

This 2021 rodent study investigated effects of dietary fibers on Type 2 diabetes:

“Nine types of dietary fibers were used to investigate and evaluate their effects on type-2 diabetic rats via physiology, genomics, and metabolomics.

In human clinical trials, supplementation with dietary fibers was found inversely associated with risks of diabetes, along with improvement on glycemic control, lipid profiles, and host homeostasis. However, mixed fibers with diverse types from dietary sources are generally used for treatment intervention in clinical trials, and effects of individual dietary fibers on T2D are seldom discussed.

We found that supplementation with β-glucan, arabinogalactan, guar gum, and apple pectin had favorable effects on alleviating T2D:

upset plot

Non-bioactive dietary fibers (NBDF) were glucomannan, arabinoxylan, carrageenan, xylan, and xanthan gum.

dietary fibers effects

Relatively high viscosity was an important driving factor of dietary fibers for hypoglycemic effects. Supplementation with β-glucan, arabinogalactan, guar gum, and apple pectin tended to restore gut microbiota composition.

Our study uncovered effects of different dietary fibers on T2D, along with their potential mechanisms. Different dietary fibers influenced host metabolism via different metabolic pathways.”

https://pubs.acs.org/doi/10.1021/acs.jafc.1c01465 “Bioactive Dietary Fibers Selectively Promote Gut Microbiota to Exert Antidiabetic Effects” (not freely available). Thanks to Dr. Yonggan Sun for providing a copy.


I eat oat β-glucan three times a day – Avena nuda whole oats for breakfast, and twice daily 3-day-old Avena sativa hulled 3-day-old oat sprouts. Not to be confused with training my immune system with daily yeast cell wall β-glucan.

I recommend “Section 6. Biological functions” of the 2021 Plants arabinogalactans: From structures to physico-chemical and biological properties (not freely available), which reviewed:

  • ACE inhibitory;
  • Anti-cancer;
  • Anti-complementary;
  • Anti-diabetic;
  • Anti-ulcer;
  • Antiaging;
  • Antinociceptive;
  • Antioxidant;
  • Antitumor;
  • Antitussive;
  • Antiviral;
  • Complementary system;
  • Complement fixation;
  • Gastrointestinal-protective;
  • Hepatoprotective;
  • Hypoglycemic;
  • Immunomodulating;
  • Immunostimulatant;
  • Immune enhancing;
  • Intestinal immune system;
  • Phagocytosis stimulating; and
  • Prebiotic activities

properties of different arabinogalactans. Thanks to Professor Michaud for providing a copy.

Arabinogalactans were favored in both papers, yet few are commercially available. In January 2021 I used an arabinogalactan supplement, but it was too expensive to continue. Maybe multiple processing steps were a cost factor?

arabinogalactan processing

Changing your immune system / gut microbiota interactions with diet

This 2021 human clinical trial investigated associations between gut microbiota and host adaptive immune system components:

“Diet modulates gut microbiome, and gut microbes impact the immune system. We used two gut microbiota-targeted dietary interventions – plant-based fiber or fermented foods – to determine how each influences microbiome and immune system in healthy adults. Using a 17-week randomized, prospective study design combined with -omics measurements of microbiome and host and extensive immune profiling, we found distinct effects of each diet:

  • Those in the high-fiber diet arm increased their fiber consumption from an average of 21.5±8.0 g per day at baseline to 45.1±10.7 g per day at the end of the maintenance phase.
  • Participants in the high-fermented food diet arm consumed an average of 0.4±0.6 servings per day of fermented food at baseline, which increased to an average of 6.3±2.9 servings per day at the end of the maintenance phase.
  • Participants in the high-fiber diet arm did not increase their consumption of fermented foods (Figure 1.C dashed line), nor did participants consuming the high-fermented food diet increase their fiber intake.

fiber vs fermented

Fiber-induced microbiota diversity increases may be a slower process requiring longer than the six weeks of sustained high consumption achieved in this study. High-fiber consumption increased stool microbial protein density, carbohydrate-degrading capacity, and altered SCFA production, indicating that microbiome remodeling was occurring within the study time frame, just not through an increase in total species.

Comparison of immune features from baseline to the end of the maintenance phase in high-fiber diet participants revealed three clusters of participants representing distinct immune response profiles. No differences in total fiber intake were observed between inflammation clusters. A previous study demonstrated that a dietary intervention, which included increasing soluble fiber, was less effective in improving inflammation markers in individuals with lower microbiome richness.

In both diets, an individual’s microbiota composition became more similar to that of other participants within the same arm over the intervention, despite retaining the strong signal of individuality.

Coupling dietary interventions to longitudinal immune and microbiome profiling can provide individualized and population-wide insight. Our results indicate that fermented foods may be valuable in countering decreased microbiome diversity and increased inflammation.”

https://www.cell.com/cell/fulltext/S0092-8674(21)00754-6 “Gut-microbiota-targeted diets modulate human immune status” (not freely available). See https://www.biorxiv.org/content/10.1101/2020.09.30.321448v2.full for the freely available preprint version.


Didn’t care for this study’s design that ignored our innate immune system components yet claimed “extensive immune profiling.” Not.

There was sufficient relevant evidence on innate immunity cells – neutrophils, monocytes, macrophages, natural killer cells, and dendrites – when the trial started five years ago. But maybe this didn’t satisfy study sponsors?

This study found significant individual differences in the high-fiber group. These individual differences failed to stratify into subgroup p-value significance.

I won’t start eating fermented dairy or fermented vegetable brines to “counter decreased microbiome diversity and increased inflammation.” I’m rolling the die with high-fiber intake (2+ times more grams than this clinical trial, over a 3+ times longer period so far).

Changing to a high-fiber diet this year to increase varieties and numbers of gut microbiota is working out alright. No worries about “increased inflammation” because twice-daily 3-day-old microwaved broccoli sprouts since Day 70 results from Changing to a youthful phenotype with broccoli sprouts have taken care of inflammation for 15 months now.

What effects have this year’s diet changes had on my adaptive and innate immune systems? 2021’s spring allergy season wasn’t pleasant. But late summer’s ragweed onslaught hasn’t kept me indoors – unlike other years – despite day after day of readings like today’s:

ragweed

Regarding an individual’s starting point and experiences, those weren’t the same as family, friends, significant other, identified group members, or strangers. Each of us has to find our own way to getting well.

Agenda-free evidence may provide good guidelines. So does how you feel.

Your pet’s biological age

This 2021 cat study developed human-comparable epigenetic clocks:

We aimed to develop and evaluate epigenetic clocks for cats, as such biomarkers are necessary for translating promising anti-aging interventions from humans to cats and vice versa. We also provided the possibility of using epigenetic aging rate of cats to inform on feline health, for which a quantitative measure is presently unavailable. Specifically, we present here DNA methylation-based biomarkers (epigenetic clocks) of age for blood from cats.

Maximum lifespan of cats is 30 years according to the animal age data base (anAge), but most cats succumb to diseases before they are 20 years old. Age is the biggest risk factor for a vast majority of diseases in animals, and cats are no exception.

Interventions to slow aging are being sought. Ideally, testing should occur in species that are evolutionarily close to humans, similar in size, have high genetic diversity, and share the same environment as humans. It has been recognized that domestic dogs fulfill these criteria.

Investigations have yet to be extended to cats although they share similar environments and living conditions with their human owners. Identification of environmental factors and living conditions that affect aging, as well as potential mitigation measures, can be achieved by proxy with cats.

The human-cat clock for relative age exhibited high correlation regardless of whether analysis was applied to samples from both species or only to cat samples. This demonstrated that relative age circumvented skewing that is inherent when chronological age of species with very different lifespans is measured using a single formula.

Evidence is compelling that epigenetic age is an indicator of biological age. These results are consistent with the fact that epigenetic clocks developed for one mammalian species can be employed – to a limited extent – to other species, and reveal association of DNA methylation changes with age.

Human epigenetic age acceleration is associated with a wide array of primary traits, health states, and pathologies. While it is still unclear why age acceleration is connected to these characteristics, it does nevertheless suggest that extension of similar studies to cats may allow for development of epigenetic age acceleration as a surrogate or indicator of feline biological fitness.”

https://link.springer.com/article/10.1007%2Fs11357-021-00445-8 “Epigenetic clock and methylation studies in cats”


As noted earlier this summer in Smoke and die early, while your twin lives on, Dr. Steve Horvath is on a torrid publishing streak this year. He’s made it questionable for study designs based on published science to omit epigenetic clocks.

I titled this post Your pets because I’m too allergic to have cats, dogs, etc. live with me. Maybe this year’s focus on making my gut microbiota happy will change that?

My pets live free:

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Seeds vs. sprouts: red cabbage and broccoli

This 2021 study compared properties of red cabbage and broccoli seeds and sprouts:

“Antioxidant and antidiabetic properties and metabolite profiling of ethanol extracts of red cabbage (RC) and broccoli (BR) seeds and sprouts were investigated:

  • BR seeds had the highest total phenolic and flavonoid contents;
  • BR sprouts had the highest saponin content;
  • RC sprouts demonstrated the highest antioxidant capacity;
  • BR and RC sprouts showed the most potent inhibition against α-glucosidase and pancreatic lipase; and
  • BR seeds demonstrated the lowest AGE inhibition.

RC and BR seeds vs sprouts

In vitro assessment of antidiabetic potential of extracts revealed that sprouts demonstrated better potential as antioxidant, α-glucosidase, and pancreatic lipase inhibitors compared to raw seeds. Amino acids and phenolic compounds were the most improved metabolites in the germination process.

Germination not only enhanced levels of metabolites, but also synthesized new compounds in seeds. Germination effectively enhanced functional properties and metabolite profiles of broccoli and red cabbage seeds, making their sprouts more applicable as functional ingredients.”

https://www.mdpi.com/2076-3921/10/6/852/htm “UHPLC-ESI-QTOF-MS/MS Metabolite Profiling of the Antioxidant and Antidiabetic Activities of Red Cabbage and Broccoli Seeds and Sprouts”


I asked coauthors for sprout ages and pertinent growing conditions for the above-pictured sprouts. I’ll guess > 3-days-old, temperature 25° C, and relative humidity 90%. What would you guess?

Update: Two coauthors replied:

“Red Cabbage and Broccoli were germinated for 6 and 7 days respectively. Temperature ranged between 20-23 °C in the dark.”

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It’s pawpaw season!

“In this episode we speak with Neal Peterson, who has devoted over 40 years to breeding pawpaws (Asimina triloba). We talk about how he first fell in love with this delicious fruit, how he tracked down remnants of the early 20th century pawpaw collections just in time, and selected 7 superior pawpaw cultivars out of 1,500 seedlings.”

Go to https://anchor.fm/plantcunning/ and episode 46.


I first ate a pawpaw while on a Capital Area Hiking Club September 2015 hike on the Susquehanna River. Our hike leader loaded up his backpack and was willing to share when we finished. Didn’t take a photo, but here’s what I picked a year later from a farm:

IMG_20160924_185415

Ugly looking, but beautiful inside.

In subsequent seasons, I found pawpaws in national and state parks. Can’t find pawpaw fruit sales online that I previously bought from, so may revisit these parks next month.

My son and I engaged in Guerrilla Planting. Maybe it’s time to check on those trees’ progress, too?

Stay out of the hospital with Vitamin K

This 2021 study investigated Vitamins K1 and K2 associations with hospitalization for atherosclerotic cardiovascular disease (ASCVD):

“In this prospective cohort study, both dietary vitamin K1 intake and vitamin K2 intake were inversely related to ASCVD hospitalization risk, and very low vitamin K1 was associated with a higher risk of ASCVD hospitalizations. Given very different food sources, these data support an independent protective effect for both subtypes of vitamin K.

u-shape

Relatively higher vitamin K2 intake in our cohort permitted discovery of a nonlinear, more U‐shaped association between vitamin K2 intake and ASCVD risk, which, to the best of our knowledge, has not previously been described. This may reflect a competing increase in ASCVD risk associated with overconsumption of vitamin K2‐rich foods (ie, cheese, eggs, butter).

Our study comes with some limitations common to nutritional epidemiology, and has significant strengths:

  • A large sample size with up to 23 years of follow‐up, allowing for accumulation of a high number of events;
  • Availability of important participant characteristics, enabling appropriate methods to be employed to reduce residual confounding; and
  • Minimal loss to follow‐up (<0.3%).”

https://www.ahajournals.org/doi/10.1161/JAHA.120.020551 “Vitamin K Intake and Atherosclerotic Cardiovascular Disease in the Danish Diet Cancer and Health Study”


I came across this study through a 2021 video:

Twice-daily broccoli / red cabbage / mustard sprouts for Vitamin K1, and a supplement for Vitamin K2 is what I do. Expect more than staying out of hospitals, but don’t know whether previous damage can be repaired.

Looking forward

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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.

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Preventing human infections with dietary fibers

This 2020 review covered interactions of gut microbiota, intestinal mucus, and dietary fibers. I’ve outlined its headings and subheadings, and ended with its overview:

“I. Dietary fibers and human mucus-associated polysaccharides: can we make an analogy?

I.1 Brief overview of dietary fibers and mucus polysaccharides structures and properties

I.I.1 Dietary fibers

  • Dietary fiber intake and health effects

I.I.2 Intestinal mucus polysaccharides

  • Structure
  • Main functions

I.2 Similarities and differences between dietary fibers and mucus carbohydrates

  • Origin and metabolism
  • Structure

II. Interactions of dietary fibers and mucus-associated polysaccharides with human gut microbiota

II-1 Substrate accessibility and microbial niches

  • Dietary fibers
  • Mucus polysaccharides

II-2 Recognition and binding strategies

  • Dietary fibers
  • Mucus polysaccharides

II-3 Carbohydrate metabolism by human gut microbiota

II-3.1 Specialized carbohydrate-active enzymes

II-3.2 Vertical ecological relationships in carbohydrate degradation

  • Dietary fibers
  • Mucus polysaccharides

II-3.3 Horizontal ecological relationships in carbohydrate degradation

II.4 Effect of carbohydrates on gut microbiota composition and sources of variability

II.4.1 Well-known effect of dietary fibers on the gut microbiota

II.4.2 First evidences of a link between mucus polysaccharides and gut microbiota composition

III. Gut microbiota, dietary fibers and intestinal mucus: from health to diseases?

[no III.1]

III.2 Current evidences for the relationship between dietary fibers, mucus and intestinal-inflammatory related disorder

III.2.1 Obesity and metabolic-related disorders

  • Dietary fibers
  • Mucus polysaccharides

III.2.2 Inflammatory bowel diseases

  • Dietary fibers
  • Mucus polysaccharides

III.2.3 Colorectal cancer

  • Dietary fibers
  • Mucus polysaccharides

IV. How enteric pathogens can interact with mucus and dietary fibers in a complex microbial background?

IV.1 Mucus-associated polysaccharides: from interactions with enteric pathogens to a cue for their virulence?

IV.1.1 Pathogens binding to mucus

  • Binding structures
  • Sources of variations

IV.1.2 Mucus degradation by pathogens

  • Bacterial mucinases
  • Glycosyl hydrolases

IV.1.3 Mucus-based feeding of pathogens

  • Primary degraders or cross-feeding strategies
  • Importance of microbial background

IV.1.4 Pathogens and inflammation in a mucus-altered context

IV.1.5 Modulation of virulence genes by mucus degradation products

IV.2 How can dietary fiber modulate enteric pathogen virulence?

IV.2.1 Direct antagonistic effect of dietary fibers on pathogens

  • Bacteriostatic effect
  • Inhibition of cell adhesion
  • Inhibition of toxin binding and activity

IV.2.2 Indirect effect of dietary fibers through gut microbiota modulation

  • Modulation of microbiota composition
  • Modulation of gut microbiota activity

IV.2.3 Inhibition of pathogen interactions with mucus: a new mode of dietary fibers action?

  • Binding to mucus: dietary fibers acting as a decoy
  • Inhibition of mucus degradation by dietary fibers

V. Human in vitro gut models to decipher the role of dietary fibers and mucus in enteric infections: interest and limitations?

V.1 Main scientific challenges to be addressed

V.2 In vitro human gut models as a relevant alternative to in vivo studies

V.3 In vitro gut models to decipher key roles of digestive secretions, mucus and gut microbiota

V.4 Toward an integration of host responses

V.5 From health to disease conditions

dietary fibers prevent infections

Overview of the potential role of dietary fibers in preventing enteric infections. Reliable and converging data from scientific literature are represented with numbers in circles, while data more hypothetical needing further investigations are represented with numbers in squares.

  1. Some dietary fibers exhibit direct bacteriostatic effects against pathogens.
  2. Dietary fiber degradation leads to short-chain fatty acids (SCFAs) production that can modulate pathogens’ virulence.
  3. By presenting structure similarities with receptors, some dietary fibers can prevent pathogen adhesin binding to their receptors.
  4. By the same competition mechanism, dietary fibers can also prevent toxins binding to their receptors.
  5. Dietary fibers are able to promote gut microbiota diversity.
  6. Dietary fibers may promote growth of specific strains with probiotic properties and therefore exhibit anti-infectious properties.
  7. Suitable dietary fiber intake prevents microbiota’s switch to mucus consumption, limiting subsequent commensal microbiota encroachment and associated intestinal inflammation.
  8. Dietary fibers may prevent pathogen cross-feeding on mucus by limiting mucus degradation and/or by preserving diversity of competing bacterial species.
  9. By preventing mucus over-degradation by switcher microbes, dietary fibers can hamper pathogen progression close to the epithelial brush border, and further restrict subsequent inflammation.”

https://doi.org/10.1093/femsre/fuaa052 “Tripartite relationship between gut microbiota, intestinal mucus and dietary fibers: towards preventive strategies against enteric infections” (not freely available)


There were many links among gut microbiota studies previously curated. For example, Go with the Alzheimer’s Disease evidence found:

“Akkermansia cannot always be considered a potentially beneficial bacterium. It might be harmful for the gut–brain axis in the context of AD development in the elderly.”

The current review provided possible explanations:

“Akkermansia muciniphila could be considered as a species that fulfills a keystone function in mucin degradation. It is a good example of a mucus specialist.”

Points #7-9 of the above overview inferred that insufficient dietary fiber may disproportionately increase abundance of this species. But Gut microbiota strains also found that effects may be found only below species at species’ strain levels.

These reviewers provided copies in places other than what’s linked above. Feel free to contact them for a copy.


Moon bandit

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No magic bullet, only magical thinking

Consider this a repost of Dr. Paul Clayton’s blog post The Drugs Don’t Work:

“The drug industry has enough funds to:

  • Rent politicians;
  • Subvert regulatory agencies;
  • Publish fake data in the most august peer-reviewed literature; and
  • Warp the output of medical schools everywhere.

Their products are a common cause of death. Every year, America’s aggressively modern approach to disease kills over 100,000 in-hospital patients, and twice that number of out-patients.

In 1900, a third of all deaths occurred in children under the age of 5. By 2000 this had fallen to 1.4%. The resulting 30-year increase in average life expectancy fed into the seductive and prevailing myth that we are all living longer; which is manifestly untrue. Improvements in sanitation were far more significant in pushing infections back than any medical developments.

There is currently no pharmaceutical cure for Alzheimer’s or Parkinsonism, nor can there be when these syndromes are in most cases driven by multiple metabolic distortions caused by today’s diet. The brain is so very complex, and it can go wrong in so many ways. The idea that we can find a magic bullet for either of these syndromes is ill-informed and philosophically mired in the past.

It is also dangerous. There is a significant sub-group of dementia sufferers whose conditions are driven and exacerbated by pharmaceuticals. Chronic use of a number of commonly prescribed drugs – and ironically, anti-Parkinson drugs – increases the risk of dementia by roughly 50%.

Big Pharma’s ability to subvert regulatory authorities is even more dangerous. The recent FDA approval of Biogen’s drug aducanumab is a scandal; not one member of the FDA Advisory Committee voted to approve this ineffective product, and three of them resigned in the aftermath of the FDA’s edict. This ‘anti-Alzheimer’s’ drug, which will earn Biogen $56,000 / patient / year, was licensed for financial reasons; it reduced amyloid plaque but was clinically ineffective.

So did the eagerly awaited gantenerumab and solanezumab. But they, too, failed to produce any significant clinical benefit.”


A knee-replacement patient enduring her daily workout

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Eating sprouts prevents AGEs

This 2021 in vitro study found:

“Prolonged and chronic hyperglycemia is a leading factor in inducing formation of advanced glycation end-products (AGEs) generated by reaction of free amino groups of proteins and carbonyl groups in reducing sugars, especially glucose and fructose. Metabolism of glucose via the glycolysis pathway also produces the most reactive compounds such as methylglyoxal (MG), a potent precursor of AGEs.

Previous studies reported that red cabbage extract could decrease glycated hemoglobin concentration in streptozotocin-induced diabetic rats and oxidative stress makers including protein carbonyl content and malondialdehyde in red blood cells. Emerging evidence supports that inhibition of protein glycation and oxidative damage may be attributed to free radical scavenging activity of plant extracts.

three brassicae

Extracts of Brassica vegetables cauliflower, cabbage and Chinese cabbage:

  • Inhibited formation of AGEs;
  • Prevented loss of protein thiol group; and
  • May act as a MG-trapping and antioxidant agent.

Phenolic acids, particularly sinapic acid and p-hydroxybenzoic acid, were commonly found in Brassica vegetables. These findings suggest that Brassica vegetables may be promising antiglycation and antioxidant agents for preventing formation of AGEs.”

https://link.springer.com/article/10.1007/s11130-021-00903-w “Phytochemical Composition, Antiglycation, Antioxidant Activity and Methylglyoxal‑Trapping Action of Brassica Vegetables” (not freely available)


Regarding this study’s sinapic acid findings, Broccoli sprout compounds include sinapic acid derivatives found with 6-day-old broccoli sprouts:

“Sprouting in darkness results in overall decrease in total content of sinapic acid derivatives with growth time, but promotes replacement of relatively low active constituents, such as sinapine, by stronger antioxidants. These structural changes are beneficial for total antioxidant capacity of broccoli sprouts, and are correlated with their increasing ability to scavenge free radicals, reduce transition metal ions, and inhibit lipid peroxidation.”

Regarding this study’s p-hydroxybenzoic acid findings, Advantages of 3-day-old oat sprouts over oat grains found with 3-day-old oat sprouts:

“Six hydroxybenzoic acids were found in greater amounts in sprouts, whereas two were reduced or lost.”


Getting onboard before sunrise

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Gut reaction

Two papers on broccoli compounds and gut microbiota relationships, with the first a 2021 article:

“We provide a supportive environment and a supply of nutrition and, in return, the microbiome delivers benefits to our health. What exactly are those benefits, and how can we maximise them?

Fibre component of food was thought to be completely indigestible roughage, but we now know that there is a digestible (a.k.a. soluble) component that can be fermented by bacteria resident in the large intestine, providing them with nutrition. There is also non-digestible fibre (a.k.a. insoluble fibre), which is not fermented by gut bacteria and includes plant cell walls formed from cellulose and lignin.

However, when cell walls remain intact, they encapsulate starch contained within cells and physically protect it from full digestion in the small intestine, ensuring that more passes into the large intestine where it can then be fermented by bacteria.

A bioactive is any chemical found in plant-based food that affects biological processes in the body, promoting better health or reducing risk of disease. Unlike macronutrients, such as carbohydrates and proteins, bioactive compounds are usually found in small amounts.

One class of bioactives where this has been known for some time is glucosinolates. For some compounds, including glucosinolates, we have identified particular bacteria that perform this task. For others, we still do not know which microbes are responsible.

S-methylcysteine sulphoxide (SMCSO) is found in brassicas but also in garlic and its relatives. Its metabolic breakdown products have been associated with protective effects against prostate and colon cancer, diabetes, and cardiovascular disease.

SMCSO-derived compounds are highly bioactive, so understanding how they affect the body’s central metabolic pathways could explain some of their health benefits. Only recently have we found clues to bacteria responsible.”

https://ifst.onlinelibrary.wiley.com/doi/10.1002/fsat.3501_6.x “Gut reaction”


The 2020 study cited for SMCSO was an in vitro 2020 study by their coworkers:

“We examined effects of a broccoli leachate (BL) on composition and function of human faecal microbiomes of five different participants under in vitro conditions. Bacterial isolates from these communities were then tested for their ability to metabolise glucosinolates and SMCSO.

We believe that this is the first study that shows reduction of dietary compound SMCSO by bacteria isolated from human faeces. Microbial communities cultured in vitro in BL media were observed to have enhanced growth of lactic acid bacteria, such as lactobacilli, with a corresponding increase in levels of lactate and short-chain fatty acids (SCFAs).

lactate

These results would have been strengthened by analysing soluble fibre content of BL media. As such, it is difficult to relate these results to in vivo SCFA production following consumption of broccoli.”

https://link.springer.com/article/10.1007/s00394-020-02405-y “Effects of in vitro metabolism of a broccoli leachate, glucosinolates and S-methylcysteine sulphoxide on the human faecal microbiome”


Which one of this pair is a male? I’ll guess on the right, as it subsequently turned to face me – a threat – when I walked passed them at a distance.

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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