Mulberry I recently got introduced to mulberries by the great saint Hildegard von Bingen. She had an astounding knowledge on plants and medicine. Mulberry is one of the things she recommended for improving liver health. And indeed, there is a bunch of studies showing benefits on the liver, corroborating what she said already 800 years ago. On top of that mulberries taste really good, I could see them pair well with yogurt and honey. [image: 1772815177825-1000027188.webp] Liver: It ameliorates NAFLD, Increasing ATP, endogenous antioxidants, michondrial complex I + II. While lowering triglycerides, liver weight, FFAs and SCD1. https://pubmed.ncbi.nlm.nih.gov/30643537/ Mulberry extract lowers liver damage induced by the fungal toxin AflatoxinB1. It increases antioxidants, phase 2 liver detox enzymes and SCFAs in the gut. https://pubmed.ncbi.nlm.nih.gov/41046554/ It inubits liver inflamamtion in diabetes model. Lowers TLR4. Seems therapeutic for diabetes too. https://pubmed.ncbi.nlm.nih.gov/35845591/ Mulberry leaves extract ameliorates alcohol-induced liver damages through reduction of acetaldehyde toxicity and inhibition of apoptosis caused by oxidative stress signals https://pubmed.ncbi.nlm.nih.gov/33390773/ Hormonal: It strongly increases StAR in diabetic mice, to values even above the control group. [image: 1772814519576-1000027187.jpg] https://pubmed.ncbi.nlm.nih.gov/24644381/ Metabolism/Weight loss It lowers weight on a HFD by over 5%. Decreases leaky gut and intestinal endotoxin. https://pubmed.ncbi.nlm.nih.gov/41645603/

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

@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%