@user73636 Di Bella method is very successful in many difficult cancers It usues somatostatin and melatonin. http://www.metododibella.org/it/Archivio-Newsletter.html https://www.metododibellaevidenzescientifiche.com/2022/05/03/mdb001-di-bella-et-al-2018/ Il sinergismo di somatostatina, melatonina, retinoidi, vitamin E, D3, C, inibitori prolattinici ed estrogenici, microdosi metronomiche di ciclofosfamide, ha incrementato sopravvivenza, risposte obiettive, performance status, in 297 casi di carcinomi del seno – The Synergism of Somatostatin, Melatonin, Vitamins Prolactin and Estrogen Inhibitors Increased Survival, Objective Response and Performance Status In 297 Cases of Breast Cancer

@sunsunsun facts

@user73636 1 cup of chocolate chips has 15.691g of stearic acid. I think this fusion is just the result of fixing a deficiency. there are lots of foods with decent amounts of stearic acid in them.

@Luke dang rip. I bet they had that anti-socmed epiphany/mid-life-crisis to finally do something good with their life hahahaha

Hass avocado vs le Fuerte Hass avocado has a black or brown grainy skin The Fuerte avocado has a smooth, green skin, with yellow flesh. A much bigger fruit too. (See the picture). The total amount fat could be quite different. How much (proportion)? Why the difference matter The Fat Breakdown Hass avocados have a lower water content. The "Hass Advantage": Because it’s proportionally about 25-30% higher in fat than the Fuerte, it mashes better. On average, here is how the two compare in terms of fat proportion: Feature - Hass Avocado - Fuerte Avocado Total Fat Content ~18–22% / ~12–15% Texture Rich, creamy, and buttery. / Lighter, thinner, and "cleaner" Water Content / Low / High Flavor Profile - Nutty and intense - Mild and slightly grassy

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

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

In case you're not familiar with saddle chairs, they're elevated stools with a better seat, not intended for full relaxation. Yet, they can improve hip positioning, spinal alignment, and reduce leg compression. Sitting pressure distribution for different chair types How to use your saddle chair ⠀ Salli Story Saddle chairs have been on the market for years and are popular with professionals who need to sit actively for long periods (such as dentists, tattoo artists, aestheticists). Some models include a modest backrest, but it's meant for stretching on occasion rather than constant support. So, if you perceive discomfort with your chair or want sitting variety, give these a try. Some companies offer satisfaction guarantees. Desks with adjustable height carry the LITEK seal (Licensed to Exist by Kvothe), but you can improvise and slip a block under each leg to reach the desired height and match the stool.

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#