@ThinPicking things are good. Launching a new product and developing v2 of Healthkeeper. Thanks for asking.

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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.

@gg12 high in silicon to get moggy. lots of oxalates so good call on milk

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

@Mauritio i have not but planning on it

@Ecstatic_Hamster said in Ended snacking between meals: I am starting to reduce my calories just a bit. Ok if you manage to keep 80 % of your required calories. Or you try sth like 2 days (not continuous) with only 600 K/ cal. from a green soup and a white fish. The type of diet you choose is going to postpose problems: You need fiber (30 g) for transit and microbiota. If you lack polyphenols, mainly from vegetables and fruit, you are going to selection a type of phylum. Some species are going to take the lead ... And you won't like the way they act.

@cookielemons Only 2 minerals are used in bone mineralization: calcium or phosphorus. As metabolism decreases, bone mineralization via phosphorus increases. For a brief correlation: older people have a higher phosphorus to calcium ratio in the bones than young people (who have higher calcium in the bones), and older people also have more bone fractures than young people. For the amount of phosphorus naturally occuring in the diet, it's actually pretty hard to balance it on a 1:1 parity with calcium, which is a way more important balance than with magnesium. High dietary calcium does not cause a problem, you urinate out excess. PTH causes all kinds of problems with calcium metabolism, tho. PTH raises when dietary calcium is low, and this forces calcium rich tissues to dump calcium into the blood, and for calcium uptake everywhere. It's an emergency response and redistribution by the body because of how vital calcium is for metabolism and the heart. If dietary calcium is not present, supplemental vitamin D can place higher demand on calcium, which will raise PTH to get it, and this cause the afformentioned problems. This is not Peat's crazy ideas he just made up. I can't remember the Japanese researcher, but he got a nobel prize for his research on calcium metabolism. Peat referenced his work. Peat is on the ball with calcium metabolism. While it's totally possible to be so low in magnesium, and metabolism be so retarded, you could possibly cause problems, it's possible you just weren't eating magnesium rich foods. Kidney stones are actually created by elevated PTH -- this is paradoxically caused by low dietary calcium. Toying with mineral balances is mostly what it sounds like: playing wackamole -- because minerals can never be regulated effectively until thyroid is addequate. the body doesn't feel the presence of a high calcium food and go "oh no, need more magnesium." Storage, utilization, and/or discarding of nutrients, is a constant automatic process. Either the metabolism is functioning to do this, or it's retarded. hand-selecting the nutrients to attempt to bypass this has little basis in reality as far as I understand it. Sodium and calcium are the only minerals you really have to conciously consume in accute weigh-able amounts, the rest come from a nutrient dense diet. They function like a chemical, directly impacting physiological processes. Sodium turns off aldosterone, a vasoconstricting hormone. Calcium lowers PTH, a calcium leaching hormone. Both of these are stress hormones. Between coffee, milk, OJ, oysters, and liver, you should hit your other mineral intakes decently well.

Update I'm feeling just fine again at rest like before taking the thiamine. Hooray!

@LucH said in Limit blue light with a software?: For what wavelength does lutein provide protection? Same question for blue light. => Lutein, zeaxanthin, anthocyanin. [image: 1772481782012-addf12df-1d7f-41e9-944c-194a4424c2d4-image.png] https://healthjade.net/what-is-lutein/ https://www.mdpi.com/2072-6643/13/9/3239#

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

You’d better listen to the signals of your body and accept them. Perhaps temporally though the body has memory (immune system). Perhaps not yet too late if you are very cautious with dairy. Nothing to do with lactose intolerance. 50 % intolerant with gluten are intolerant to milk. Mimicry. We don’t need dairy to get the appropriate amount of calcium even if it’s easier or if you like it. E.g. broccoli is very rich in available calcium. You don’t need 1200 mg calcium. The amount 550 or 850 mg Ca depends on how you deal with the acid-base balance (Na, Ca, K, Mg versus Phosphorus and Sulfur). To help balancing you’ll probably need: bisglycinate magnesium phophocalcium (+ calcium citrate when there is oxalate in veggies) potassium bicarbonate. I track my balance with cronometer.com (I’ve changed the targets). I repeat: you can’t force the body to accept sth when the intestinal linen are fragile / irritated. The sooner you accept it (100 % or it won’t never heal completely), the quicker you can get / optimize the tightness of the brush border of the stomach. I can give a link if interested, if you accept the fact you won’t heal “over the next 2 weeks”! To optimize the motility, get inform on MMC (interprandial motility). But you’ll probably need to heal the integrity and the thickness of the stomach linen before adding fibbers (with glutamine). A last advice: If you wait too long, you’ll get problem with the microbiota and perhaps / probably with candidiasis. There, no glutamine advisable or you’ll feed the beast. Act before you suffer from SIBO/ SIFO too much to tolerate what you can eat. Much more restrictive then. See my answer here to Samyo: Key information for SIBO / SIFO https://bioenergetic.forum/post/50601

@cookielemons I was eating a shit ton of them, probably 0.5 kg every evening, but yeah, I agree they were not my only issue back then

I have had the same issue with not just B vitamins but also any pro metabolic supplement like pyrucet. The trick is to both take the vitamins with lots of carbs and to also increase carb intake in the hours after, since your glucose oxidation will be ramped up and your blood sugar will plummet easier, leading to the fatigue you describe.

@engineer The surplus comes from grannies I think my dopamine/serotonin ratios and amounts itself aren't the issue, but rather dopamine tone/receptors are INHIBITED probably by higher serotonin/its receptor signaling Direct dopaminergic stuff like coffee/concentric exercise/carbs/protein/light don't improve the post-olanzapine anhedonia/other symptoms even 0.1% NO CHANGE at all So something is rewired, inhibiting brain centers related to pleasure/sense vividness Keep in mind I only got this AFTER olanzapine My nutrition/lifestyle was the same before The drug changed something and it isn't going away on its own so far

Another quick update. Just took a shower and removed a large quantity of earwax from my left ear. My left TMJ feels much better now, though not completely. I might go to an ENT in a month to get a professional ear cleaning. Even if you can hear, you could have earwax that is affecting TMJ symptoms.

Soon to be replaced by the Open AI brain chip. Zog planted right in your gray matter.