Yes, these might interest you: Oxidation of hydrogen sulfide by Quinones: How polyphenols initiate their Cytoprotective effects ‘Antioxidant’ berries, anthocyanins, resveratrol and rosmarinic acid oxidize hydrogen sulfide to polysulfides and thiosulfate: A novel mechanism underlying their biological actions Alteration of the Gut Microbiome in Inflammatory Bowel Disease

@alfredoolivas cannabis, full spectrum oil, and lanolin.

Compounds that inhibit lactate overproduction are usually beneficial, but relying on oxaloacetate for this is not ideal. Pyruvate carboxylase is required for glutamine-independent growth of tumor cells (PC synthesizes oxaloacetate) In case of oxaloacetate supplementation, delivery is the first challenge because most of the dose is metabolized in the liver after absorption. For esterified forms, the fraction that reaches target cells is likely overestimated, especially when tissue circulation is poor. Malate dehydrogenase (MDH) interconverts malate and oxaloacetate, and this enzyme is also part of the malate-aspartate shuttle (MAS) that you mention. [image: 1772751634940-d34ce921-acea-4633-9653-639c96f9838f-image.png] ⠀(10.1101/cshperspect.a040543) The figure shows some potential concerns: Cytosolic NAD reoxidation by MDH can promote glycolysis, but without reliably improving mitochondrial metabolism for further oxidation. Increased demand for NAD+ relative to ATP drives aerobic glycolysis Extra oxaloacetate (OAA) may not convert into malate as expected. Aspartate is another component of the shuttle and is a reaction away from oxaloacetate (GOT/AST is bidirectional). [image: 1772751647814-4f7a93ec-7e75-4c6a-a1ad-ae54d314276c-image.png] ⠀(10.1016/j.ymgmr.2023.100967) An Essential Role of the Mitochondrial Electron Transport Chain in Cell Proliferation Is to Enable Aspartate Synthesis Supporting Aspartate Biosynthesis Is an Essential Function of Respiration in Proliferating Cells Oxaloacetate enters mitochondria hydrogenated as malate. Recovering oxaloacetate on the mitochondrial side depends on sufficient NAD⁺ (also shown on the figure), which may be scarce and prioritized for other reactions, such as that of KGDHc. Recovery of oxaloacetate from malate in mitochondria doesn't guarantee its reaction with acetyl-CoA. It may instead support glutamate metabolism by accepting its amino group, yielding ketoglutarate for KGDHc (↻) or IDH (↺). One route doesn't exclude the other, as a fraction of ketoglutarate can undergo oxidative decarboxylation (releasing CO₂) and the other reductive carboxylation (incorporating CO₂), Supporting glutamate metabolism in forward function: Oxaloacetate + glutamate ←{GOT}→ Aspartate + Ketoglutarate Ketoglutarate –{KGDHc}→ Succinyl-CoA ←{STK}→ ATP + Succinate A portion of oxaloacetate-derived malate can also be converted to fumarate in reverse TCA cycle operation. Oxaloacetate → Malate → Fumarate → Succinate [image: 1772751671369-3224a3ed-9ba4-4586-bbab-57e75c344b76-image.png] ⠀(10.3389/fendo.2012.00022) This way, oxaloacetate helps to generate ketoglutarate to support mitochondrial fermentation and non-respiratory ATP synthesis with minimal oxidation. In addition, fumarate may be used as a substitute to deficient oxygen, accepting electrons from the respiratory chain sourced from ketoglutarate itself, dihydro-orotate, etc. (Oxaloacetate +) Glutamate → Ketoglutarate → Succinate ← Fumarate ← Oxaloacetate Succinate accumulation becomes comparable to lactate. Both metabolites are exported as fermentation end-products together with an extra H⁺, contributing to extracellular acidification. [image: 1772751690253-15d16b6b-0813-45e0-8bb1-7fecd96f1d33-image.png] ⠀(10.1080/17590914.2024.2422268) "Succinate-stabilized HIF-1a" reinforces PDHc inhibition, giving another reason not to assume that extra oxaloacetate and CoA release will serve PDHc, because they may just as well promote fatty acid oxidation. If oxaloacetate condenses with acetyl-CoA, that doesn't commit it oxidation either; oxaloacetate can serve as a carrier to export excess acetyl groups to support lipid synthesis. As for pyruvate and its multiple metabolic fates, even discounting lactate and oxaloacetate in this context, we can't assume that pyruvate routing to the chronically inhibited PDHc will prevail over supporting an upregulated pathway, such as in metabolizing abundant glutamate via GPT/ALT, which remains expressed outside the liver. Pyruvate + H⁺ + CoA + NAD⁺ –{PDHc}→ Acetyl-CoA + CO₂ + NADH + H⁺ Pyruvate + ⇈Glutamate ←{GPT}→ Alanine + Ketoglutarate This is another potential route that would supply ketoglutarate without depending on glutamate oxidation, sparing oxidative capacity to keep KGDHc running.

[image: 1772655639415-injust.jpg] Adjustment to what.

@Mauritio i have not but planning on it

@lobotomize - Thanks, another reason to proceed with caution.

Dihydromyricetin in the management of diabetes and its complications: a narrative review Managing diabetes mellitus (DM) and its long-term complications remains a major global health challenge. Dihydromyricetin (DHM), a natural flavonoid abundant in Ampelopsis grossedentata and Hovenia dulcis, has attracted increasing attention for its multi-target anti-diabetic properties. Growing evidence indicates that DHM improves glucose metabolism, alleviates oxidative stress and inflammation, regulates autophagy and cell death, and exerts beneficial effects in DM and a range of related complications, including diabetic nephropathy, cardiomyopathy, cognitive impairment, and wound healing impairment, and other related complications. Overall, this review provides an overview of preclinical research on DHM in DM and its main complications, emphasizing its therapeutic benefits and underlying molecular mechanisms.

silicon chelates aluminum *edit posted that b4 reading your whole post

Propolis extract (ethanolic) Appears to have significant effects on healing of upper gastrointestinal tract mucosa (gastric & duodenal ulcers), especially as treatment enhancement of antibiotics against H. pylori, as well as for promoted healing thereafter (gastritis only slowly subsides over the course of at least 6 months up to a couple of years even after successful H. pylori eradication) Using human equivalent conversion from rat trials, generous daily propolis doses seem to be required: Ideally 3600mg. Certainly not below 1800mg. Synergistic combinations with olive leaf extract (OLE) and/or L. rhamnosus and/or L. reuteri. However, propolis monotherapy fails for H. pylori eradication. There's initial inhibition, but then the infection and bacterial evasion catches up. Propolis and Its Potential to Treat Gastrointestinal Disorders, 2018, review Propolis in the Treatment of Oral Mucositis ** Propolis shown effective. Propolis in the Therapeutic Management of Ulcerative Colitis ** "the studies developed with kaempferol, luteolin, and naringenin stood out" ** yet "these studies do not translate to human application, remaining to be explored its efficacy and safety in clinical trials." Propolis and Its Potential to Treat Gastrointestinal Cancers ** Various effects in vitro Antiulcer Activity of Propolis ** "propolis has been used in folk medicine to treat gastric ulcer" ** Dose-dependent protective effects (preventative), but also healing effects ** Effects of propolis mirrored in part by oral caffeic, ferulic, and cinnamic acids ** "100% of the tested extracts inhibited the H. pylori growth" Evaluating the Inhibitory Effects of Probiotic Bacteria and Propolis Extracts on the Growth and Histopathological Changes in Gastric Tissues of Helicobacter pylori Challenged Wistar Rats, 2024 "In vivo, the findings demonstrated that oral administrations of propolis and probiotics [L. rhamnosis, L. reuteri], either separately or in combination, led to significant increases in body weight and amelioration of histopathological changes in gastric tissue samples, particularly in terms of erosion depth, hemorrhagic inflammation, and apoptosis in the infected animals" Effects were dose-dependent and highest at 300mg/KG per day (HED = 48mg/KG, ie 3600mg@75KG). The yellow positive control received antibiotic triple therapy: [image: ijpr-23-1-148158-i001.jpg] "Propolis generally exhibits bacteriostatic properties against various bacterial genera; however, it may demonstrate bactericidal effects at elevated concentrations" "Propolis contains caffeic acid phenethyl ester (CAPE), which inhibits the enzyme peptide deformylase, a critical factor for the survival of H. pylori." "The antibacterial activities of propolis are dependent on the concentration of biologically active compounds, including phenolic acid esters and flavonoids such as pinocembrin and galangin" "During the study, a significant enhancement in the antibacterial activity was observed in the prepared propolis mixture (combination of all four propolis extracts). " "In the gastric tissue samples of the animals treated with propolis and/or probiotics, reduced bacterial load comparable to the antibiotic-treated group animals was observed. " "polyphenol compounds of propolis have significant enhancing effects on the eradication rate of H. pylori in rats with gastritis and peptic ulcers, suggesting that propolis supplementation may enhance the effectiveness of conventional H. pylori treatment" Anti-inflammatory and anti-oxidative effect of Korean propolis on Helicobacter pylori-induced gastric damage in vitro, 2020 "These findings indicate that the use of Korean propolis, which has anti-inflammatory and anti-oxidative effects, can be promising for the prevention of H. pylori-induced gastric damage. South African Propolis: Anti-Helicobacter pylori Activity, Chemistry, and Toxicity, 2025 Of 27 geographically distinct South African propolis sources tested, only 7 propolis compositions exhibited a MIC of >6.25 mg/mL against H. pylori. Many sources were as dose-effective as amoxicillin. "Propolis from northern Spain was investigated against H. pylori with ethanolic and propylene glycol extracts which were found to have MIC values ranging between 6.00 and 14.00 mg/mL" "The compounds pinocembrin, 3‐O‐acetylpinobanksin, and pinobanksin were found to be the most abundant." "Antimicrobially active South African propolis was reported to be primarily comprised of pinocembrin, galangin, and chrysin" Potential Efficacy of Propolis in Treating Helicobacter pylori Infection and Its Mechanisms of Action, 2025 "Propolis demonstrates dual functionality by inhibiting the release of inflammatory mediators and suppressing H. pylori growth" [image: nutrients-17-02803-g005.jpg] "The combined use of propolis with other natural extracts demonstrates superior efficacy. Studies indicate that propolis complexes, when used in combination with olive leaf and licorice extracts, more effectively inhibit H. pylori-induced gastric mucosal ulcers, reduce bacterial colonization, and alleviate gastric mucosal inflammation" "A trial involving 18 infected participants showed that after seven consecutive days of oral administration of Brazilian green propolis extract (3 times daily, 20 drops per dose), 50% of participants experienced a decrease of over 20% in their urea breath test values, indicating an initial inhibitory effect; However, after a 40-day treatment cycle, 83% of participants failed to achieve complete eradication of H. pylori, suggesting that while propolis monotherapy has some activity, it is insufficient for effective eradication and may require optimization of the dosing regimen, such as increasing the dose or frequency, to achieve sufficient antimicrobial concentrations."

@user73636 Quoting Wikipedia: https://en.wikipedia.org/wiki/Diisopropylamine_dichloroacetate#:~:text=DADA is formed by combining diisopropylamine with dichloroacetic acid. It is chemically related to pangamic acid (formerly known as "vitamin B15")%2C which may convert to DADA and diisopropylamine in the body.[4] Pangamic acid = ester of D-gluconic acid (the sugar-acid part) N,N-dimethylglycine (DMG) (the amino-acid part) Pangamic acid, stomach acid quickly breaks the ester bond and you get free DMG + free gluconic acid.

I believe a stack of B5 + carnitine + OAA/malate High carb low fat Eating leaner meat cuts Lower bcaa intake And focusing on odd chain fats (produce less acetyl coa) would be a great way to lower the acetyl coa/coa ratio further increasing the activity of pyruvate dehydrogenase Also eat foods rich in nad precursors as the nad/nadh ratio is also important for pdh/pdk ratio malate and OAA can not only help pull acetyl-CoA into the TCA cycle (Krebs cycle) to make energy, which frees up CoA. They also help turn NADH back into usable NAD+. (TCA Cycle Pull) OAA mixes with acetyl-CoA to start the cycle, releasing free CoA each turn . Malate turns into OAA inside mitochondria, keeping OAA stocked so the cycle keeps running smoothly.

Get your eggs in! Spinach also is rich in lutein. Interestingly, cooking it doesn't degrade the lutein content. And having calcium with the spinach is two-fold beneficial: block oxalate absorption enhance lutein absorption by 30 to 40%