@gg12 charlies company has soap on sale rn and ngl their soap is fiya

@Mauritio said: Sodium salicylate can actually treat colitis via AMPK activation. I guess it also helps because it does NOT inhbit platelet aggregation/COX1. So it doesn't fully replace aspirin ,which should be taken into account before taking it. Sodium salicylates consume glycine and deprive the body from methyl donors when taken in high dose when there is overburden elsewere… Intro: Sodium Salicylates & Aspirin — A Metabolic Heads-Up Most people don't think twice about reaching for aspirin or high-salicylate foods. But at higher doses or with prolonged use, sodium salicylates place a real burden on two key systems: glycine reserves and methylation capacity — both critical for cell repair, detox, and epigenetic function. This isn't about fear — it's about knowing when to support your body alongside the treatment. Talk with AI Answer from AI (Google) The claim that sodium salicylates "deprive" the body of methyl donors stems from a well-documented biochemical pathway called glycine conjugation. However, framing it as a harmful depletion is generally misleading, as it is a natural and intended metabolic detoxification route. [1, 2, 3] Here is how the interaction actually works: The Glycine Conjugation Pathway When sodium salicylate enters the bloodstream, it must be metabolized and excreted by the kidneys. The body’s primary method for neutralizing and clearing salicylates and certain other substances (like dietary benzoates) is through conjugation with the amino acid glycine to form salicyluric acid. [1, 2, 3] -To attach glycine to a salicylate molecule, the body must first convert glycine into an acyl-CoA complex. This conversion requires energy in the form of ATP and Coenzyme A (CoA). -The "Methyl" Connection: The amino acid glycine and the primary universal methyl donor, S-adenosylmethionine (SAMe), are heavily linked in one-carbon metabolism. When glycine is diverted and used to clear salicylates, the cellular balance of methyl precursors can shift. [1, 2, 3, 4, 5] Differentiating Salicylate Forms It is important to note the difference between types of salicylates: [1, 2] Sodium Salicylate / Aspirin (Acetylsalicylic Acid): When taken orally, these are broken down into salicylic acid. The body primarily uses the glycine conjugation pathway to excrete them. Methyl Salicylate: Often used topically (as wintergreen oil) or as a flavoring. While it can release salicylic acid into the system, it works in reverse as well—the body uses SAMe as a methyl donor to methylate salicylic acid into methyl salicylate (a process controlled by salicylic acid methyltransferase). [1, 2, 3, 4, 5, 6, 7] Impact on Methylation Because glycine, folate, and the methionine/SAMe cycles are tightly interconnected, intensive use of glycine for detoxification can slightly alter cellular methylation pools. However, in healthy individuals with a balanced diet, this does not result in a significant clinical deficiency. [1, 2, 3, 4] The body regulates its own methylation capacity through enzymes like Glycine N-methyltransferase (GNMT). If methyl availability drops, the body downregulates the consumption of methyl donors to preserve cellular function. [1, 2, 3] The Bottom Line: While processing sodium salicylate does "consume" glycine and indirectly affects cellular one-carbon metabolism, it is a normal Phase II liver detoxification response. Unless you are dealing with a severe genetic methylation defect or massive salicylate overdosing, sodium salicylates do not cause dangerous methyl depletion. [1, 2] Comment (LucH): I’d add some TMG (500 mg) once a day to avoid deprivation of sulfur and methyl. Especially when there is a B3 HD take* Methylation is essential for the maintenance, repair and manufacture of our cells, intracellular communication, and more specifically, the inheritance of epigenetic information (cell reproduction). The Methylation Sink: The body synthesizes some of its required niacin from the amino acid tryptophan. However, when taking high doses of supplemental niacin (nicotinic acid), the body must methylate it to excrete the excess. This process depletes methyl groups, which are heavily sourced from the sulphur-containing amino acid methionine. Moreover high levels of niacin can disrupt the metabolism of sulphur amino acids by interfering with Vitamin B6 status. Supplemental Vitamin B6 (20-25 mg PLP) is often required alongside high-dose niacin therapy to normalize this sulphur amino acid profile and prevent unintended imbalances. NB: I associate B1 B2 B3 B6 + 500 mg TMC TMG and 2x/wk a combo co-enzymed B50. Lien utile: Chaos biochimique ! https://mirzoune-ciboulette.forumactif.org/t1959-impact-negatif-de-loxalate-sur-le-metabolisme-chaos-biochimique#28275 L’association d’oxalates, NB: You may suffer from CaOx or from methylation conversion (genetic defect by 1/3 to 2/3 of the population, depending on whether you suffer from just one or both defective alleles). If you combine spinach with nuts (almond, peanut, pistachio or pine nuts) you’d better take care and drink some milk (Ca / Ox ratio 4/1). Xx AI comment asked to see if my analyze was pertinent LucH asks Analyze. Pertinent for forum help or do I exaggerate? AI answers (Claude): This is a solid, well-informed forum contribution. Here's my honest assessment: What's genuinely good:  The core biochemistry is accurate — glycine conjugation, the SAMe/methylation connection, and the niacin methylation sink are all real and well-documented mechanisms  The practical suggestions (TMG, B6 alongside high-dose niacin) are reasonable and consistent with what integrative medicine practitioners recommend  The layering of B1/B2/B3/B6 + TMG shows you're thinking systemically, not just about isolated nutrients  The oxalate note at the end (Ca/Ox ratio, spinach + nuts warning) is practical and often overlooked Where to be careful:  The document mixes your own commentary with an AI-generated response without always making the boundary clear — forum readers may not realize which parts are sourced vs. your additions  "TMC" appears to be a typo for TMG — worth correcting before posting  The French forum link embedded mid-text interrupts flow and may confuse readers depending on the forum's audience  The genetic methylation defect mention (1/3 to 2/3 of the population) likely refers to MTHFR variants, but stating it without naming it may puzzle readers unfamiliar with the concept Overall verdict: Not an exaggeration — this is pertinent, useful content for a health/biochemistry forum. The level of detail is appropriate for an informed lay audience. The main improvement would be structural: separating the sourced AI summary from your personal commentary more clearly, so readers know what they're reading at each point (=> has been done).

@haidut If red blood cell deformability is among the sequelae that endurance exercise produces, I wonder if something like pentoxifylline might be useful. I understand that much of the damage that occurs to red blood cells in ultra-endurance exercise is secondary to the mechanical strain to which RBCs are subject due to being physically compressed at the soles of the feet with every step or else during their turbulent and high pressure flow through arteries of a person basically running for their lives, but I would like to know if using a stack like Pentoxifylline + Meldonium to cut down on the FAO, keeping carbohydrates going every 20 minutes or so, might compare.

There are extracellular and nucleus prolactin receptors. Prolactin binds both and this drug, as it's an antibody, only binds to the extracellular receptors giving us an idea of what effects anatagonising the extracellular receptors does but does not tell us what the nuclear receptors do and therefore cannot show the full picture of what prolactin actually does. There exists many case reports of hair loss from dopamine agonists, so your suggestions may be harmful in this regard. Estrogen receptor alpha for example has different effects than estrogen receptor beta for hair growth is an example of the flaws behind what people infer from this study

Over the past week I have worked my way up to 1mg a day. The effects maybe have increased, but the reason it might not have done so more is because of low estrogen from exemestane. I know this could be the case because I heavily sweat during naps now, one classic symptom of low E2.

@haidut i have named my kids in your honor