Fueling a gut fire

This 2022 article commented on a human / rodent study of gut dysbiosis:

“Crohn’s disease (CD) is a chronic disease that causes inflammation in the gastrointestinal track. Together with ulcerative colitis, another major type of inflammatory bowel disease (IBD), these intestinal disorders affect millions of people in the U.S. and worldwide.

Excessive T helper 1 (Th1) and Th17 cell responses have been documented to act as important mediators of CD pathogenesis. An imbalance between regulatory T (Treg) cells and effector T cells in the intestinal tissue microenvironment is crucial to promote gut inflammation in CD.

Lysophosphatidylserine (LysoPS) exaggerates intestinal inflammation by fueling IFNγ-producing Th1 cells via metabolic reprogramming and chromatin modification (panel A). While this work has provided novel functional insights into dysbiotic microbiota–derived LysoPS in CD pathogenesis (panel B), it also raises several questions. 

m_jem_20220723_fig2

By employing multiple animal colitis models, the authors have shown that administration of LysoPS was detrimental in T cell–driven colitis, while having no significant impact on pathogenesis of T cell–independent dextran sodium sulfate–induced colitis.

Considering the complex nature of LysoPS in regulating responses of different immune cell types in a given tissue environment under a particular physiological or pathological condition, more research is needed to elucidate the precise role of LysoPS in CD before targeting these multifunctional bioactive lipids to treat human gastrointestinal disorders becomes a reality.”

https://doi.org/10.1084/jem.20220723 “Fueling the fire in the gut”


The referenced study:

  • “We identified key metabolites derived from dysbiotic microbiota that induce enhanced Th1 responses and exaggerate colitis in mouse models.
  • Patients with CD showed elevated LysoPS concentration in their feces, accompanied by a higher relative abundance of microbiota possessing a gene encoding the phospholipid-hydrolyzing enzyme phospholipase A.
  • Our findings elaborate on the mechanism by which metabolites elevated in patients with CD harboring dysbiotic microbiota promote Th1-mediated intestinal pathology.”

https://doi.org/10.1084/jem.20211291 “Lysophosphatidylserines derived from microbiota in Crohn’s disease elicit pathological Th1 response”


When standard DSS and TNBS models of colitis don’t account for observed effects, other avenues need to be investigated. Relationships with our gut microbiota are complicated.

PXL_20220529_183842508

Food combination effects

Two 2022 studies, starting with “Increasing bound antioxidant compounds through their reaction with soluble phenolic compounds”:

“Wheat, oat, rye, and rice bran samples were reacted with different concentrations of beverages (green tea infusion, black tea infusion, espresso, and red wine) rich in various soluble phenolic compounds.

  • Green tea infusion was found to be the most effective beverage.
  • pH rather than time and temperature had significant effects on the reaction.
  • Neutral or slightly alkaline conditions (pH 7.0-7.9) and mild temperature (at about 50 °C) were found to be optimum to increase antioxidant capacity of cereal bran samples.
  • Total antioxidant capacity of oat bran treated with green tea infusion at optimum conditions (53.3 °C, pH 7.4, 60.0 min) reached 226.42±0.88 mmol.
  • Free amino groups in cereal bran were also found to decrease 32–95% after treatment.”

https://onlinelibrary.wiley.com/doi/10.1002/jsfa.12017 “Optimization of reaction conditions for the design of cereal based dietary fibers with high antioxidant capacity” (not freely available)

Hadn’t thought about purposely combining oats with green tea before. I eat whole oats, though, not oat bran.


The same coauthors earlier used an in vitro digestion procedure to investigate combinations of 20 foods purchased from local markets:

“Individual antioxidant capacity of a single compound is not adequate to assess antioxidant potential of food or human plasma. Compounds always present as natural mixtures, and may possess similar, overlapping, or different but complementary effects.

Certain types of foods co-existing in daily diet were investigated in terms of their combined total antioxidant capacity (TAC) determined by the QUENCHER method, which allows physiological evaluation without any extraction procedure. Hydroxyl radical scavenging capacity was also determined in bioaccessible fractions of foods.

Interaction types were determined at each step:

  • Synergism refers to a greater overall effect in the combination of two samples compared to simple addition of their individual effects, which means that TACmeasured is greater (p < 0.05) than TACestimated.
  • The phenomenon in which a lower (p < 0.05) net interactive effect than the sum of their individual effects (TACmeasured < TACestimated), is known as antagonism.
  • Additive interaction occurs when a net interactive antioxidant effect is as same (p > 0.05) as the sum of individual effects.

1-s2.0-S2665927122000351-ga1_lrg

  • Seeds and nuts interacted antagonistically with other foods due to the pro-oxidant potential of transition metals on lipid rich system.
  • Protein-phenol interactions masking TACs of phenol-rich foods before digestion could stabilize and regenerate phenolic compounds under gastrointestinal digestion conditions, providing a synergistic interaction.
  • Intestinal conditions promoting reaction between antioxidant compounds and radicals resulted in increases in TACs of foods.
  • Enzymatic colonic digestion caused significant increases in TACs of certain foods.

These findings provide a basis to increase antioxidant activity in daily diet and new food formulations.”

https://www.sciencedirect.com/science/article/pii/S2665927122000351 “Effect of food combinations and their co-digestion on total antioxidant capacity under simulated gastrointestinal conditions”


View this second study as representative or hypothesis-generating, but not specifically definitive. No research group will use its resources to investigate even the 190 pairwise combinations of 20 foods, much less all 616,645 combinations.

Also, since food is digested all in the same place and time, contexts for each combination’s synergistic, antagonistic, or additive activities may be influenced by other combinations’ results. See the second study of Dietary contexts matter for a similar investigation.

PXL_20220519_213057647

Oat product biological effects

Two oat species studies, starting with Avena nuda:

“Oats are a good source of carbohydrates and fibers. They contain more proteins and fats than other grains, and they are packed with vitamins (vitamin E, thiamine, etc.), minerals (Ca, Fe, Mn, etc.), and antioxidants (avenanthramides, ferulic acid, caffeic acid, flavonoids, etc.).

β-glucan contained in naked oats has multiple health benefits, including improving insulin sensitivity, lowering blood sugar levels, reducing risk of type II diabetes, and reducing low-density lipoprotein and total cholesterol levels.

There are two key enzymes in the hydrolysis of starch: α-amylase and α-glucosidase. Inhibiting activity of these enzymes can delay degradation of starch and absorption of glucose, thereby inhibiting rapid rise of postprandial blood glucose levels. α-amylase and α-glucosidase inhibitors are often used in treatment of type II diabetes.

This study investigated inhibitory effects of free and bound bioactive extracts from naked oats on amylase and glucosidase activity.

1-s2.0-S0023643821010550-gr1

α-amylase inhibition by free (A) and bound (B) compound extracts from naked oats. The half maximal inhibitory concentrations (IC50) of free and bound compound extracts were 0.09 and 1.33 mg/mL, respectively, higher than that of acarbose (0.03 mg/mL), the positive control.

Low digestibility of naked oats will help facilitate development of low-glycemic foods.”

https://www.sciencedirect.com/science/article/pii/S0023643821010550 “Endogenous bioactive compounds of naked oats (Avena nuda L.) inhibit α-amylase and α-glucosidase activity”

“Low digestibility of naked oats” referred to human capabilities, not to those of our gut microbiota. See A healthspan improvement for more on acarbose.


A second study investigated uses for Avena sativa hull and bran by-products:

“β-Glucan is mainly found in oat bran (OB) along with various phenolic compounds. Oat husk (OH) is a by-product produced during oat processing for food purposes, about 25–33% of its weight.

Ultrafine grinding or micronization is a new technique used for making a super fine powder with a particle size of 1–100 μm and good surface properties. This very fine powder is characterized by higher solubility, dispersibility, and water absorption, which improves quality of target food products. Micronization considerably enhances efficiency of extraction of phytochemicals, and is widely employed to extract natural polysaccharides from different bioresources.

OH is especially rich in insoluble fiber such as cellulose, hemicelluloses, and lignin, whereas both soluble and insoluble fiber occurs in OB in a ratio of 1:5. OB has a higher soluble dietary fiber content than wheat or rice bran.

The optimal composition, 60–70% of OH and 30–40% of OB, allows for obtaining a product with 60–70% fiber and enhanced antioxidant activity due to bioactive substances and their synergistic effect. The resulting product can be a valuable additive to various food and dietary supplements.”

https://www.mdpi.com/1420-3049/27/9/2621/htm “Fiber Preparation from Micronized Oat By-Products: Antioxidant Properties and Interactions between Bioactive Compounds”


See Oat species comparisons of the good stuff for more comparisons of their hulls.

PXL_20220520_150215836

Take β-glucan for new blood vessels

This 2022 cell study investigated yeast cell wall β-glucan’s effects on angiogenesis:

“Angiogenesis, the formation of new blood vessels, is essential for embryonic development and physiological damage repair, such as wound healing and post-ischemic tissue restoration. It is also essential for pathological processes, such as diabetic retinopathy, rheumatoid arthritis, and atherosclerosis.

We evaluated physical and functional interactions of β-glucan with HDAC5, including the scratched wound, tube formation, and rat aortic ring assays. β-glucan-induced HDAC5 pathway mediates cell migration and formation of tubes and microvessels in vitro and ex vivo.

β-glucan angiogenesis

Our findings demonstrate that β-glucan-induced HDAC5 phosphorylation is important in endothelial cell angiogenesis. Further investigations into how β-glucan phosphorylates HDAC5 are required. There is also a need to identify a receptor that specifically binds to β-glucan in vascular endothelial cells.

β-glucan could be useful in developing new strategies in therapeutic angiogenesis for conditions such as cardiovascular disease and diabetes.”

https://www.sciencedirect.com/science/article/abs/pii/S0141813022010273 “Yeast beta-glucan mediates histone deacetylase 5-induced angiogenesis in vascular endothelial cells” (not freely available). Thanks to Dr. Chan-Gi Pack for providing a copy.


PXL_20220521_133100360

Young gut, young eyes

I’ll highlight this 2022 rodent study findings of effects on eye health:

“We tested the hypothesis that manipulating intestinal microbiota influences development of major comorbidities associated with aging and, in particular, inflammation affecting the brain and retina. Using fecal microbiota transplantation, we exchanged intestinal microbiota of young (3 months), old (18 months), and aged (24 months) mice.

Transfer of aged donor microbiota into young mice accelerates age-associated central nervous system inflammation, retinal inflammation, and cytokine signaling. It promotes loss of key functional protein in the eye, effects which are coincident with increased intestinal barrier permeability.

These detrimental effects can be reversed by transfer of young donor microbiota.

young and aged fmt

We provide the first direct evidence that aged intestinal microbiota drives retinal inflammation, and regulates expression of the functional visual protein RPE65. RPE65 is vital for maintaining normal photoceptor function via trans-retinol conversion. Mutations or loss of function are associated with retinitis pigmentosa, and are implicated in age-related macular degeneration.

Our finding that age-associated decline in host retinal RPE65 expression is induced by an aged donor microbiota, and conversely is rescued by young donor microbiota transfer, suggests age-associated gut microbiota functions or products regulate visual function.”

https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-022-01243-w “Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain”


PXL_20220517_190954606

Blood pressure and brain age

This 2021 human study investigated associations between blood pressure and MRI measurements:

“We estimated how a validated measure of brain health related to changes in BP over a period of 12 years. The main findings of this study were:

  • All BP measures were associated with older BrainAGE;
  • Associations were stronger in men than women;
  • Associations were not only detected in hypertensive individuals but across the whole BP range; and
  • Individuals with optimal blood pressure (110/70) presented with the lowest BrainAGE.

These findings support the view that maintaining blood pressure in an optimal range (SBP < 115, DBP < 75) across the lifespan starting before mid-life (i.e., in early adulthood and before) is essential to maintain good cerebral health.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8523821/ “Optimal Blood Pressure Keeps Our Brains Younger”


I’m making progress on a New Year’s resolution. Here’s how I started 2022:

bp 2021

Current readings show both lower averages and variability:

bp 2022

~12% decreases in average systolic (111 – 126)/126 and diastolic (69 – 78)/78 pressures over 135 days. 🙂 I measure blood pressure every day right after I wake up.

What caused these decreases? Continuing what I was already doing. The top factor is probably that at lunch every day I take 600 mcg of Vitamin K2 MK-7 along with a gram of flax oil.

I started taking K2 this time last year per Vitamin K2 – What can it do? Apparently its effects are gradual and develop slowly. Vitamin K2 and hypertension may also be relevant.

I came across this study from its mention in today’s video:

Coffee improves information’s signal-to-noise ratio

This 2022 rodent study investigated caffeine’s effects:

“A majority of molecular and neurophysiological studies explored the impact of acute rather than repeated exposure to caffeine. We show that, in bulk tissue analysis, chronic caffeine treatment reduced metabolic processes related to lipids, mitochondria, and translation in mouse hippocampus. In sharp contrast to what was observed in bulk tissue, we found that caffeine induced a neuronal autonomous epigenomic response related to synaptic plasticity activation.

149371-JCI-RG-RV-3_ga_591026

Regular caffeine intake exerts a long-term effect on neuronal activity/plasticity in the adult brain, lowering metabolic-related processes, and simultaneously finely tuning activity-dependent regulations. In non-neuronal cells, caffeine decreases activities under basal conditions, and improves signal-to-noise ratio during information encoding in brain circuits, contributing to bolster salience of information.

Overall, our data prompt the novel concept that regular caffeine intake promotes a more efficient ability of the brain to encode experience-related events. By coordinating epigenomic changes in neuronal and non-neuronal cells, regular caffeine intake promotes a fine-tuning of metabolism in resting conditions.”

https://www.jci.org/articles/view/149371 “Caffeine intake exerts dual genome-wide effects on hippocampal metabolism and learning-dependent transcription”


PXL_20220514_181401668

Eat broccoli sprouts for stress

This 2022 review subject was aspects of sulforaphane regulating stress:

“Sulforaphane (SFN) shows great versatility in turning on different cellular responses. This isothiocyanate acts as a master regulator of cellular homeostasis due to its antioxidant response and cytoplasmic, mitochondrial, and endoplasmic reticulum (ER) protein modulation. SFN acts as an effective strategy to counteract oxidative stress, apoptosis, and ER stress, among others as seen in different injury models.

The ER is a complex membrane system, involved in several cellular processes including lipid synthesis and distribution, and Ca2+ storage and signaling. The ER is highly dynamic and changes according to cellular demand (e.g., hypoxia, mitochondrial dysfunction, or oxidative stress), leading to accumulation of unfolded or misfolded proteins in ER lumen, known as ER stress.

ER stress is buffered by unfolded protein response (UPR) activation, a homeostatic signaling network that orchestrates recovery of ER function by decreasing the burden of misfolded proteins. If stress signals continue it could lead to apoptosis activation.

Studies highlight a close interrelationship between ER stress and oxidative stress, two events driven by the accumulation of reactive oxygen species. Responses to stress inevitably perpetuate, and act as a vicious cycle that triggers development of different pathologies, such as cardiovascular diseases, neurodegenerative diseases, and others.

The PERK/Nrf2 pathway communicates oxidative stress and ER stress:

1-s2.0-S0024320522002545-ga1_lrg

SFN couples oxidative and ER stress to promote cellular redox homeostasis. Further studies in animal and human models are required to elucidate pathways and proteins involved in differential responses orchestrated by SFN, emphasizing that responses will depend on cell type and kind of pathology, as well as SFN concentration.”

https://www.sciencedirect.com/science/article/abs/pii/S0024320522002545 “Role of sulforaphane in endoplasmic reticulum homeostasis through regulation of the antioxidant response” (not freely available) Thanks to Dr. Alejandro Silva for providing a copy.


Every hand’s a winner, and every hand’s a loser has more on UPR.

Brain changes

This 2022 human study investigated healthy young adult brain changes using MRI and epigenetic clock technologies:

“We aimed to characterize the association of epigenetic age (i.e. estimated DNA methylation age) and its acceleration with surface area, cortical thickness, and volume in healthy young adults. It is largely unknown how accelerated epigenetic age affects multiple cortical features among young adults from 19 to 49 years. Prior findings imply not only that these dynamic changes reveal different aspects of cortical aging, but also that chronological age itself is not a reliable factor to understand the process of cortical aging.

accelerated epigenetic age vs brain features

Seventy-nine young healthy individuals participated in this study. Findings of our study should be interpreted within the context of relatively small sample size, without older adults, and with epigenetic age assessed from saliva.

Additional and unique regional changes due to advanced and accelerated epigenetic age, compared to chronological age-related changes, suggest that epigenetic age could be a viable biomarker of cortical aging. Longitudinal and cross-sectional studies with a larger sample and wider age range are necessary to characterize ongoing effects of epigenetic cortical aging, not only for healthy but also for pathological aging.”

https://doi.org/10.1093/cercor/bhac043 “The effects of epigenetic age and its acceleration on surface area, cortical thickness, and volume in young adults” (not freely available) Thanks to Dr. Yong Jeon Cheong for providing a copy.

A healthspan improvement

Two 2022 publishments, starting with an excerpt from an informative interview with the Director of one of the three Interventions Testing Program centers:

“A paper submitted this week is one in which we tried a combination of rapamycin plus acarbose. Rapamycin works very well in male and female mice, while acarbose works significantly in both sexes but has a much stronger effect in males.

What we found in males is that when you give rapamycin and acarbose together, you do better than either rapamycin by itself or acarbose by itself. That combination of drugs together gives male survival a 29% boost.

That’s the largest percentage increase we’ve seen in males or females. This combination is the best thing we’ve ever had for either sex.

When you give acarbose and rapamycin together to females, they don’t do any better or any worse than on rapamycin alone. This is not too surprising because acarbose gives only a small effect in females. We expected it wouldn’t have a big boost over rapamycin alone in female animals, and that’s what we found.”

https://www.lifespan.io/news/prof-richard-miller-on-the-intervention-testing-program/


The study mentioned above:

“C57BL/6 mice were fed a cocktail diet containing one-half the dose of each drug compared to full dose cocktail diet and control diet. Half-dose drug cocktail was just as effective as full dose in preventing age-related cognitive impairment, but was less effective in other physical performance tests. Half-dose cocktail also had no effect on reducing pathological lesions.

Rapamycin was the major contributor for the cocktail’s effect on suppressing cognitive impairment. Decreased neuronal activation and impaired cognitive performance during aging occurs in both humans and rodents. Chronic mTOR attenuation by rapamycin has shown benefits of restoring deficits in neurovascular coupling response and cerebrovascular dysfunction in aging rodent models.

C57BL/6 female mice fed chow with acarbose performed equally well in grip strength as females fed chow with cocktail. That this sex-dependent result in strength performance was not seen in cocktail treated mice suggests that rapamycin and phenylbutyrate contributed in some way.

grip strength

HET3 4-way cross is a useful strain to help validate effects of the cocktail on aging parameters in C57BL/6 mice. HET3 mice were tested in the same manner, age, and timing as C57BL/6 mice, but only with the drug cocktail compared to control chow.

grip strength het3 mice

Grip strength force was normalized by body weight measured on the testing date so that peak force was expressed relative to body weight.

The drug cocktail was very effective in delaying progression of age-related pathology in all organs examined. We view this as a vital component of the study since mice were treated for only three months.

Administration of a cocktail has a major advantage over any individual drug tested in this study. A combination of three drugs previously shown to enhance lifespan and health span in mice is able to delay aging phenotypes more effectively and more robustly than any individual drug in the cocktail when started at middle age and given for a short period of time.”

https://www.nature.com/articles/s41598-022-11229-1 “Short term treatment with a cocktail of rapamycin, acarbose and phenylbutyrate delays aging phenotypes in mice”


It makes evolutionary sense for male mice to benefit more from anti-aging treatments than females.  Per How well do single-mother rodent studies inform us about human fathers?

“The Rattus and Mus genera used in almost all rodent research aren’t part of the 6% in which fathers also provide offspring care.”

There probably isn’t an evolutionary advantage for male mice to live much longer after sperm donation. Female mice don’t cache sperm.

It’s similar to studies in which treatments only benefited subjects who started out deficient. This interview hinted at how females’ healthspans and lifespans were already evolutionarily protected, with only male mice benefiting from 17α-estradiol treatment.

Female protection may have limits in humans. For example, most whale species don’t experience menopause. In those that do, like Orca, menopause is thought to be evolutionarily determined in order to keep females’ children from competing for resources with females’ grandchildren and great-grandchildren. That’s a hypothesis, though, as those species’ male lifespans aren’t adequately measured.

Rodent research and development on interventions and doses continues. 37 months is a human equivalent to this study’s 3-month treatment. What will effective anti-aging treatments be for humans?


More strange birds

PXL_20220507_193018118

Young immune system, young brain

This 2022 study investigated brain aging:

“We aimed to explore key genes underlying cognitively normal brain aging and its potential molecular mechanisms. Cellular and molecular mechanisms of brain aging are complex and mainly include:

  1. Dysfunction of mitochondria;
  2. Accumulation of oxidatively damaged proteins, nucleic acids, and lipids in brain cells;
  3. Disorders of energy metabolism;
  4. Impaired ‘waste disposal’ mechanism (autophagosome and proteasome functionality);
  5. Impaired signal transduction of adaptive stress response;
  6. Impaired DNA repair;
  7. Abnormal neural network activity;
  8. Imbalance of neuronal Ca2+ processing;
  9. Stem cell exhaustion; and
  10. Increased inflammation.

mrna brain expression

Expression of CD44, CD93, and CD163 mRNA detected by qPCR in hippocampal tissue of cognitively normal aged and young mice.

Underlying molecular mechanisms for maintaining healthy brain aging are related to decline of immune-inflammatory responses. CD44, CD93, and CD 163 are potential biomarkers.”

https://www.frontiersin.org/articles/10.3389/fnagi.2022.833402/full “Identification of Key Biomarkers and Pathways for Maintaining Cognitively Normal Brain Aging Based on Integrated Bioinformatics Analysis”


PXL_20220506_184430747

Thyroid function

This 2022 review subject was thyroid function changes:

“Circulating concentrations of thyrotropin (TSH) and thyroxine (T4) are tightly regulated. Each individual has setpoints for TSH and free T4 which are genetically determined, and subject to environmental and epigenetic influence.

What is normal for one individual may not be normal for another, even within conventional definitions of euthyroidism. Notably, circulating TSH exists in several different isoforms with varying degrees of glycosylation, sialylation, and sulfonation which affect tissue availability and bioactivity. This is not reflected in immunoreactive TSH concentrations determined by routine laboratory assays.

enm-2022-1463f2

TSH and free T4 relationship analyzed by age in 120,403 patients who were not taking thyroxine treatment. Median TSH for each free T4 integer value (in pmol/ L) was calculated, then plotted as 20-year age bands in adults. Dotted horizontal and vertical lines mark the TSH reference range (0.4 to 4.0 mU/L) and free T4 reference range (10 to 20 pmol/L), respectively.

Mild TSH elevation in older people does not predict adverse health outcomes. In fact, higher TSH is associated with greater life expectancy, including extreme longevity.

In older people, TSH increases with aging without an accompanying fall in free T4. Clinical guidelines now recommend against routine levothyroxine treatment in older people with mild subclinical hypothyroidism.”

https://e-enm.org/journal/view.php?doi=10.3803/EnM.2022.1463 “Thyroid Function across the Lifespan: Do Age-Related Changes Matter?”


PXL_20220427_190457415

Reinvigorated

A follow-on to Beginning of the cure for aging:

“So, I rubbed a small sample of E5 on my right hand and after three days the results were visible. The skin on the treated hand is visibly thicker and lighter. Certainly not a definitive test, but wow, my hand looks decades younger. Dr. Harold Katcher

maos

Hi all,

I applied a little bit of an old freeze-dried prep – there’s no trick here Jay (how could there be), my right-hand looks 30 years younger, even my veins are narrower and less prominent, (I wonder if they’ve let go of their calcification) they also seem less visible because the skin appears thicker

Obviously, the experiment needs to be tried on many people, but I’m certain their reaction will be the same as mine. The interesting thing is, as you noted Jay that the E5 used was essentially just the precipitate, (so therefore crude), but if only for external use, it would not have to meet the same criteria for use as something used internally.

I’m looking at my hands right now and am amazed, a real miracle. I suppose it will fade (as my blood contains pro-aging factors) – but surprisingly, we now have real evidence that E5 works on people. Yesterday Kavita said it doesn’t look like both hands could belong to the same person).

I only applied a small bit to the upper surface of my right hand, nothing more. It was actually historic.

Best to all, Harold


One thing I remember about my father’s parents was spots on their hands and forearms. As a child, I didn’t understand how that happened. After growing up in Miami, and visiting dermatologists 2-3 times a year decades later, it’s apparent.

PXL_20220502_185746582

Estimating bioavailability of oat compounds

Two papers on oat compounds’ bioavailability, starting with a 2022 review:

“There are many nutrients and bioactive chemical compounds exerting beneficial properties in oats. Results indicated that oats and their extracts possessed essential roles in preventing chronic diseases.

However, most studies focused on Avns’ [avenanthramides] functions were performed using cell models. In animal models, one disadvantage of Avns was low bioavailability.

Avns were also metabolized in the gastrointestinal tract in a gut microbiota (especially Faecalibacterium prausnitzii) dependent or independent manner. Administration of Avns usually ranged from 100−300 mg/ kg, which was much higher than that for cell treatment.

After eating cookies with 9.2 mg or 0.4 mg (control) Avns for 8 weeks, plasma level of TNF-α after exercise was significantly reduced in young women (16 women aged 18−30 years). Similar results were obtained in a study enrolling postmenopausal women (16 women aged 50−80 years), and Avns supplementation (9.2 mg in cookies) dramatically reduced plasma levels of IL-1β and C-reactive protein after exercise.

More attention should be given to studying preventative effect of Avns on chronic diseases and underlying molecular mechanisms, and further revealing potential roles of small molecules with powerful regulatory activity, such as miRNAs.”

https://pubs.acs.org/doi/full/10.1021/acs.jafc.1c05704 “The Progress of Nomenclature, Structure, Metabolism, and Bioactivities of Oat Novel Phytochemical: Avenanthramides” (not freely available)


This first paper’s Reference 25 was a 2018 paper on oat compounds’ bioaccessibility that used an in vitro digestion system without microbiota:

“Malting was performed for 5 days, from M0 (non-malted oat grains) to M5 (oat grains malted for 5 days), using the following: steeping at 20 °C for 24 h, germination in the dark at 15 °C, and kilning in an air oven at 100 °C for 12 h.

The cookie formulation with lowest phenol concentration showed highest bioaccessibility. This result was surprising, as we expected an increase in SP [soluble phenols] bioaccessibility, in parallel with increasing SP concentration of cookies.

bioavailability avena nuda avn sp

A portion of 5B cookies provides 4.8 mg of AVNs, which is more than double a maximal daily AVN intake in oat consumers.”

https://ifst.onlinelibrary.wiley.com/doi/10.1111/ijfs.14020In vitro bioaccessibility of avenanthramides in cookies made with malted oat flours” (not freely available)


Every day I eat Avena nuda oats that start out as 82 grams of seeds, and two servings of 3-day-old Avena sativa oat sprouts that each start out as 20 grams of seeds. Using this second paper’s 50 gram Avena nuda methods to develop estimates:

avena nuda avn sp

  • (82 g / 50 g) x 42 µg = 69 µg total AVNs; and
  • (82 g / 50 g) x 660 µg = 1,082 µg soluble phenols.

My Avena nuda whole oat grain total AVNs and soluble phenol weights aren’t much. They aren’t bioavailability estimates. Their species and growing conditions are different from this second paper, etc.

That’s all okay with me. I eat Avena nuda oats primarily to make my trillion+ gut microbiota partners happy with indigestible-to-me whole grain contents, expecting that they will reciprocate.

Plugging in the study’s 3-day figures to estimate Avena sativa oat sprouts:

  • (40 g / 50 g) x 324 µg = 259 µg total AVNs; and
  • (40 g / 50 g) x 1350 µg = 1,080 µg soluble phenols.

Using the first graphic’s 3-day relative bioaccessibility percentages:

  • 259 µg x .28 = 72 µg total bioavailable AVNs; and
  • 1,080 µg x .41 = 442 µg bioavailable soluble phenols.

Both papers cited studies that found with eccentric exercise, “9.2 mg per day AVNs are sufficient to provide effects on exercise induced inflammation.” I exercise at least 30 minutes every day, but don’t perform eccentric exercises more frequently than every five days per Eat broccoli sprouts for your workouts.

Advantages of 3-day-old oat sprouts over oat grains provided methods comparable to my Avena sativa 3-day-old oat sprouts intake, although it didn’t assess bioavailability. Sprouts’ beneficial effects compared with seeds “were mainly related to their high content of avenanthramides A (2p), B (2f), and C (2c), quercetin 3-O-rutinoside [rutin], kaempferol, sinapoylquinic acid, and apigenin and luteolin derivatives.”

Couldn’t say whether I benefit more from bioavailability of 3-day-old oat sprouts’ directly soluble phenols, or from bioavailability of their phenolic breakdown byproducts provided by gut microbiota. For example, regarding oat sprouts rutin content, a 2019 review pointed out:

“Humans lack the enzyme needed to hydrolyze this bond. Consequently, microorganisms in the colon mediate hydrolysis of this rutinoside, resulting in minimal intestinal absorption, and production of phenolic acid metabolites in the colon.”


Osprey below a bird-like cloud

PXL_20220426_190518487