Month: August 2025

Oats sprouts treat gut inflammation

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

A 2025 rodent study investigated differing effects of regular oats and oat sprouts to treat induced colitis:

“This study aims to test our hypothesis that germinated oats exert stronger anti-inflammatory effects than raw oats due to their higher levels of bioactive phytochemicals. First, the nitric oxide (NO) production assay was used to screen [22] commercially available oat seed products and identify the product with the highest anti-inflammatory activity after germination [for five days]. The selected oat seed product was then produced in larger quantities and further evaluated in an in vivo study using the dextran sulfate sodium (DSS)-induced colitis mouse model to compare the anti-inflammatory effects of phytochemical extracts from germinated and raw oats.

The guideline states that for a healthy U.S.-style dietary pattern at a 2000 calorie level, a daily intake of 6 ounces of grains is recommended, with at least 3 ounces (84 g) coming from whole grains (WGs). For a 60 kg human, consuming 3 ounces of WGs per day translates to a 17.2 g/kg daily dose in mice. Given that the daily food intake of a 20 g mouse is approximately 2.5 g, the 17.2 g/kg daily dose corresponds to 14% of the total diet as WGs. Therefore, the 7 and 21% WG equivalent doses used in this study are relevant to human consumption.

Germination led to an overall increase in the content of all avenanthramides (AVAs) and avenacins (AVCs) as well as some avenacosides (AVEs):

  • For AVAs, the compounds 2c, 2p, 2f, 2cd, 2pd, and 2fd significantly increased by 10.0-, 6.3-, 9.6-, 20.7-, 10.6-, and 4.6-fold, respectively, which is consistent with previous reports.
  • This study is the first to report an increase in AVCs after germination, with AVC-A2, B2, A1, and B1 contents significantly increasing by 2.5-, 2.2-, 3.6-, and 4.2-fold, respectively.
  • Although germination resulted in a decrease in certain AVEs, it significantly increased the levels of AVE-C, Iso-AVE-A, AVE-E, and AVE-F by 1.8-, 3.3-, 3.3-, and 5.0-fold, respectively. Notably, AVE-E has been previously reported to have the strongest anti-inflammatory activity among all of the major AVEs.

In summary, germination enhances the anti-inflammatory properties of oats in both cells and DSS-induced colitis in mice by increasing levels of bioactive phytochemicals. Correlation analysis showed a significant inverse relationship between pro-inflammatory cytokines and phytochemical content in feces, especially AVAs and their microbial metabolites.

The observation of a stronger anti-inflammatory effect in the low-dose germinated oat group compared with the high-dose group is intriguing and warrants further investigation. One possible explanation is the phenomenon of hormesis, where low doses of bioactive compounds can exert beneficial effects, while higher doses may lead to diminished efficacy or even adverse effects. Further studies involving a broad range of doses would be valuable to define the effective intake range and provide insight into the underlying mechanisms.

It is possible that AVAs, AVEs, and AVCs act synergistically to enhance the overall anti-inflammatory efficacy, potentially by targeting different inflammatory pathways or modulating each other’s bioavailability and activity. Further investigation into the synergistic interactions among these compounds is warranted.”

https://pubs.acs.org/doi/10.1021/acs.jafc.5c02993 “Phytochemical-Rich Germinated Oats as a Novel Functional Food To Attenuate Gut Inflammation”

I’ve eaten 3-day-old Avena sativa oat sprouts (started from 20 grams of groats) every day for 4.5 years now, and haven’t had gut problems. Here’s what they looked like this morning:

Get a little stress into your life, Part 2

gettingwell4 5+ stars Premium, Cortisol, Epigenetics, Hypothalamus, Immune system, Limbic system, Memory, Neurochemicals, Stress , , , , ,

A 2025 reply to a letter to the editor cited 56 references to elaborate on Part 1 and related topics:

“A positive effect does not necessarily mean benefit, and positive effects on individual organisms may mean adverse effects on other coexisting organisms. However, a vast literature shows that hormetic stimulation can result in benefits depending on the context, for instance, clear growth, yield, and survival improvement.

There is some energetic cost to support hormetic stimulation, with a likely positive energy budget, which might also have negative consequences if there is insufficient energy substrate, especially under concurrent severe environmental challenges. Moreover, hormetic preconditioning could be particularly costly when there is a mismatch between the predicted environment and the actual environment the same individuals or their offspring might face in the future.

Hormesis should not be unilaterally linked to positive and beneficial effects without considering dose levels. For any research to answer the question of whether a stimulation represents hormesis and whether it is beneficial, robust dose–response evaluations are needed, which should be designed a priori for this purpose, meeting the requirements of the proper number, increment, and range of doses.

Both additivity and synergism are possible in the hormetic stimulatory zone, depending also on the duration of exposure and the relative ratio of different components. This might happen, for example, when a chemical primes stress pathways (e.g., heat shock proteins and antioxidants), thus enabling another chemical to trigger hormesis (defense cross-activation) and/or because combined low subtoxicity may modulate receptors (e.g., aryl hydrocarbon receptor and nuclear factor erythroid 2-related factor 2) differently than individual exposures (receptor binding synergy).

Moreover, even when stimulation occurs in the presence of individual components, stimulation may no longer be present when combined, and therefore, effects of mixtures cannot be accurately predicted based on the effects of individual components. There may be hormesis trade-offs; hormesis should be judged based on fitness-critical end points.

While often modeled mathematically, hormesis is fundamentally a dynamic biological process and should not be seen as a purely mathematical function, certainly not a linear one. Much remains to be learned about the role of hormesis in global environmental change, and an open mind is needed to not miss the forest for the trees.”

https://pubs.acs.org/doi/10.1021/acs.est.5c05892 “Correspondence on ‘Hormesis as a Hidden Hand in Global Environmental Change?’ A Reply”

Reference 38 was a 2024 paper cited for:

“Hormetic-based interventions, particularly priming (or preconditioning), do not weaken organisms but strengthen them, enhancing their performance and health under different environmental challenges, which are often more massive than the priming exposure.

The catabolic aspect of hormesis is primarily protective whereas the anabolic aspect promotes growth, and their integration could optimize performance and health. The concept of preconditioning has also gained widespread attention in biomedical sciences.”

https://www.sciencedirect.com/science/article/abs/pii/S1568163724004069 “The catabolic – anabolic cycling hormesis model of health and resilience” (not freely available)

Reference 40 was a 2021 review that characterized hormesis as a hallmark of health:

“Health is usually defined as the absence of pathology. Here, we endeavor to define health as a compendium of organizational and dynamic features that maintain physiology.

Biological causes or hallmarks of health include features of:

  • Spatial compartmentalization (integrity of barriers and containment of local perturbations),
  • Maintenance of homeostasis over time (recycling and turnover, integration of circuitries, and rhythmic oscillations), and
  • An array of adequate responses to stress (homeostatic resilience, hormetic regulation, and repair and regeneration).

Disruption of any of these interlocked features is broadly pathogenic, causing an acute or progressive derailment of the system.

A future ‘medicine of health’ might detect perilous trajectories to intercept them by targeted interventions well before the traditional ‘medicine of disease’ comes into action.”

https://www.sciencedirect.com/science/article/pii/S0092867420316068 “Hallmarks of Health”

Sulforaphane as a senotherapy, Part 2

gettingwell4 4-5 stars Advanced knowledge, Brain development, Cerebrum, Hippocampus, Limbic system, Memory, Stress , ,

A 2025 rodent study by the same group as Part 1 investigated similar subjects from a different experimental angle of senotherapy effects on brain and behavior rather than cardioprotective effects of dasatinib / quercetin (a senolytic combination) and sulforaphane (senomorphic):

“This is the first study to analyze the effect of senotherapy in the brain of a model of chronic obesity in middle-aged female rats. D + Q reduced the pro-inflammatory cytokines evaluated in the obesity model. It did not improve memory and learning nor the expression of molecules associated with the maintenance of synapses.

In contrast, sulforaphane (SFN), which without eliminating senescent cells, decreased pro-inflammatory factors, increased IL-10, as well as brain-derived neurotrophic factor BDNF, synaptophysin (SYP), and postsynaptic density protein 95 (PSD-95), which, in turn, were associated with an improvement in behavioral tests in obese rats. This suggests that modulating the senescence-associated secretory phenotype (SASP), rather than eliminating senescent cells, might have better effects.”

https://www.sciencedirect.com/science/article/pii/S0014488625001955 “Senotherapy as a multitarget intervention in chronic obesity: Modulation of senescence, neuroinflammation, dysbiosis, and synaptic integrity in middle-aged female Wistar rats”

Treating a stomach infection with sulforaphane

gettingwell4 4-5 stars Advanced knowledge, Epigenetics

A 2025 rodent study integrated metabolomics and lipidomics analyses to investigate how sulforaphane treats a Helicobacter pylori infection:

“Helicobacter pylori (H. pylori) is a microaerobic Gram-negative bacterium that colonizes the gastric mucosa. Approximately half of the global population is infected with this bacterium, and it is classified as a group 1 carcinogen.

However, H. pylori infection does not typically present with obvious symptoms in the early stages, making it difficult to detect. Daily dietary interventions may be a relatively effective method for its prevention and treatment.

This study established an H. pylori-infected mouse model, to which sulforaphane was orally administered. H. pylori-low-dose and H. pylori-high-dose represent 4 weeks of gavage with 5 mg/kg/d and 20 mg/kg/d of sulforaphane after H. pylori colonization.

Metabolomics and lipidomics analysis of the effects of sulforaphane treatment on mouse serum. Stacked bar chart of the metabolites regulated by (A) low-dose and (B) high-dose sulforaphane treatment compared to the differential metabolites between the control group and H. pylori group.

Results showed that H. pylori infection significantly altered host amino acid and lipid levels, specifically manifested as abnormal serum glycerophospholipids and metabolic imbalances of amino acids, bile acids, glycerophospholipids, ceramides, and peptides in the liver. Sulforaphane treatment reversed these metabolic abnormalities, with high-dose sulforaphane exhibiting more prominent regulatory effects.

High-dose sulforaphane effectively restored hepatic metabolic disorders of amino acids, bile acids, and lipids, and ameliorated abnormal serum glycerophospholipid profiles. Regulation of key pathways such as glycine metabolism and glutathione metabolism constitutes an important basis for sulforaphane’s anti-H. pylori infection effects.

This study provides a comprehensive metabolic basis for understanding the role of sulforaphane as a dietary intervention in preventing and managing H. pylori-associated gastric diseases and lays a foundation for subsequent clinical translational research.”

https://www.mdpi.com/1422-0067/26/16/7791 “Therapeutic Effects of Sulforaphane on Helicobacter pylori-Infected Mice: Insights from High-Coverage Metabolomics and Lipidomics Analyses of Serum and Liver”

A human equivalent to this study’s low sulforaphane dose is (5 mg x .081) x 70 kg = 28 mg, which is achievable by eating broccoli sprouts every day. Quadrupling 28 mg to a human equivalent of the study’s high sulforaphane dose would involve additional supplementation.

Another way to support this study’s glycine metabolism findings without high-dose sulforaphane is to supplement betaine (trimethylglycine) so that the body requires less choline-to-glycine synthesis. A synergistic effect can be achieved with taurine supplementation that enhances cysteine availability for the tripeptide (glutamate, cysteine, and glycine) glutathione synthesis by requiring less cysteine-to-taurine synthesis.

Inulin vs. FOS

gettingwell4 2-3 stars Required further work, Epigenetics

A 2025 clinical trial compared inulin glycemic effects with FOS effects. I won’t curate its gut microbiota results as these have unresolved measurement problems:

“In this study, we conducted a randomized, double-blind investigation to examine the impact of inulin and fructooligosaccharides (FOS) on glycemic metabolism in overweight/obese and healthy adults.

Inulin and FOS are both fructans composed of fructose units, but they differ in their degree of polymerization (DP) and chain length, which lead to differences in their physicochemical properties and physiological effects. Inulin typically has a longer chain length, with a DP ≥ 10, resulting in lower solubility and slower fermentation in the distal colon. FOS consists of shorter chains, with a DP 2 to 9, presenting higher solubility and undergoing rapid fermentation in the proximal colon. These differences affect their impact on short-chain fatty acid (SCFA) production, gut microbiota modulation, and subsequently results in different effects on host metabolism.

131 participants were recruited and randomized into three groups: inulin (N = 44), FOS (N = 43), and control (N = 44). Each group was conducted with a daily supplement of 15 g FOS, inulin, and maltodextrin as placebo and lasted for 4 weeks. Dosage was determined based on our previous clinical trials in the healthy young population, which reported using 16 g/day has no risk of adverse effects. Subjects were still recommended to take a half dose in the first 2 days to promote adaptation to the prebiotics and minimize gastrointestinal symptoms. Products were suggested to add to drinks such as coffee, tea, or milk.

Inulin significantly reduced glucose levels at 1 h and 2 h during oral glucose tolerance test (OGTT), increased fasting insulin, and lowered homocysteine (HCY) levels in overweight/obese individuals. These effects were not observed in healthy individuals.

In contrast, although FOS significantly decreased HCY, it did not improve glycemic metrics in either group.”

https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-025-04189-6 “Differential effects of inulin and fructooligosaccharides on gut microbiota composition and glycemic metabolism in overweight/obese and healthy individuals: a randomized, double-blind clinical trial”

Prior research found:

“A 2010 gastrointestinal tolerance of chicory inulin products study indicated that 10 g/day of native inulin were well-tolerated in healthy, young adults. Over this dose would induce mild gastrointestinal symptoms.”

So a lead-in half-dose probably wouldn’t be needed for people to start a 10 gram inulin dose.