I know this is pretty basic for a Ray Peat forum but have you all tried consuming large amounts of coconut oil? I did some research on it, apparently it's more effective against fungus in vitro than antifungal drugs like fluconazole. It has a similar mechanism of action as antifungal drugs i.e. it targets the ergosterol in the fungal cell membranes. It's one of the most commonly mentioned natural candida remedies on forums like reddit. Popular anti-candida supplements like Now Candida Support contain caprylic acid which is abundant in and sourced from coconut oil. Coconuts evolved for their drupes to survive in humid tropical coastlines and to float on ocean currents so the fats are probably evolved to be resistant to fungi.

@jamezb46 said: I myself have been at a bit of a crossroads for how to regard AMPK since from a strict Peat perspective, AMPK is a signal of low energy availability and thus stress. It started when I researched low protein and FGF21. I realized most of these markers like AMPK, FGF21 and Sirtuins are strongly connected to peaty things like thyroid, klotho and overall health. Like you can't strictly separate them from each other and say one is bad and the other one is good. That's the Danny Roddy trap. He simultaneously says low protein is good, while FGF21 is bad. That's an illegal chess move Here's a list of peaty substances that activate AMPK. So either those substances are beneficial despite or because of AMPK activation. I tend towards the latter. @jamezb46 said: Question for you: Would you regard AMPK raising substances like berberine to be of net benefit? I think every substance has to be evaluated individually. Even if something has one seemingly bad MoA the overall net effect can still be good. Berberine could be such a substance but I haven't looked into it yet.

@dapose It varies, I don't take daily anymore as my body doesnt need it that much. Before I took powder so not exact dosages but approximately 300mg with a meal that doesnt have calcium and away from coffee. Genuinely life changing for me personally.

@sunsunsun Yeah, I personally haven't noticed a drop in strength though, despite losing 19lbs, but that is probably because I take tren. Though in all fairness, very little.

@AlphaZance said: Metabolic stress drives the formation of AGEs, but Ray Peat has not addressed existing AGEs in foods. yes, but you didn't find the right doc. The etymology of the word glycation doesn't only rely on sugar. You d' better take care of "lipid glycation" and not only from sugar sources. Request for IA: glycation doesn't only rely on sugar but much more on fat alteration. Google answer: You are on the right track! While sugar drives classic glycation, fat alteration (lipoxidation) is a massive, often underappreciated driver of Advanced Glycation End-products (AGEs). The Lipid-AGE ConnectionLipoxidation: When fats oxidize, they create reactive, unstable molecules (like dicarbonyls). These intermediate compounds then cross-link with proteins just as sugar molecules do, directly forming harmful AGEs.The Maillard Reaction: Heat processing (such as frying or grilling) animal foods high in both fat and protein yields the highest levels of dietary AGEs. The Interplay: Both pathways are deeply connected under "carbonyl stress". How to Manage Both Sugar and Fat Risks To minimize the buildup of AGEs and slow down cellular aging, you can focus on a few evidence-backed lifestyle and dietary strategies: Watch Your Cooking Methods: Avoid cooking foods—especially meats and fats—at high temperatures. Steaming, boiling, or poaching creates significantly fewer AGEs than frying, broiling, or grilling. Balance Dietary Fats: The type of fat you eat matters. Clinical trials suggest that increasing consumption of monounsaturated fats (MUFAs) and Omega-3 fatty acids can help control and beneficially affect your glycation markers. Maintain Stable Blood Sugar: Even though fat oxidation is crucial, reducing refined sugar and fructose intake lowers the available "fuel" for traditional sugar-protein glycation.Leverage Antioxidants: Oxidative stress is the catalyst for fat alteration. Consuming antioxidant-rich foods or using targeted anti-glycation interventions helps neutralize free radicals. Scientific Sources & Evidence To dive deeper into the science of how fats and sugars alter your cells and skin, review these authoritative resources: [1, 2] https://www.lifeextension.com/wellness/aging/glycation https://www.skinnutritioninstitute.com/blog/glycation-how-fat-ages-your-skin-and-destroys-collagen-clone Glycation & Oxidation: Explore the exact breakdown of how lipid damage forms AGEs through Advanced Glycation End-products (AGEs): an emerging ... - PMC. [1] https://pmc.ncbi.nlm.nih.gov/articles/PMC4648888/&ved=2ahUKEwjPyLaG4-iUAxXlkP0HHRf_BQEQy_kOegoIAggACAEIJxAC&opi=89978449&cd&psig=AOvVaw2nBJNpgaZPrk0yj1bOffN0&ust=1780497191863000 Lipoxidation Pathways: Read about how both carbohydrates and lipids drive carbonyl stress at Glycation, oxidation, and lipoxidation in the development of ... Ibidem Cellular & Skin Impact: Understand how these molecular processes affect your skin's health and elasticity in Sugar is altering your skin in ways no anti-ageing serum can ... Ibidem

This guy is a born liar and a fraud. His 'expert' research is incredibly sloppy and cherry picked. He has a raging ego, extremely thin skin and a tedious need to be the singular guru on ALL life matters. I challenged him on his claims on his blog about how much vitamin C he takes. He claims he only uses natural, acerola-based vitamin C, and claims he typically takes 4 grams a day for a few days and then settles on 2-3 grams a day. I found the brand he takes, crunched the numbers and worked out that if he was telling the truth, he'd be spending up to $400 a MONTH on this one supplement. I pointed this out to him and he wrote back calling me a "dumbass" and saying "of course I don't spend that much money on Vitamin C". Which means he out-and-out lied. He's also now making vague claims in his updated book that he had leukemia in the past. Previously he only mentioned the thyroid cancer. But now, leukemia too, because his WBC was slightly off. He is desperate to convince people he was at death's door and single-handedly fixed his multiple life threatening diseases. He's a dishonest loser, who loves to throw in comments implying he's hot af. He isn't. He's vain, preachy and profoundly wide of Ray Peat's mark.

@jamezb46 The links for Fat Loss Agents (and their considerable downsides): DNP, GLP-1 Agonists and Meldonium, EPO, and Advanced Performance Protocols were pointing to the wrong place. I've fixed them. Fat Loss Agents (and their considerable downsides): DNP, GLP-1 Agonists -> https://dinkov-distilled.vercel.app/7d35b1da-57db-11f0-bef1-11c2aded3be7 Meldonium, EPO, and Advanced Performance Protocols -> https://dinkov-distilled.vercel.app/4cfd75bc-5307-11f0-8501-fb369bf0f4ea Please let me know if you find anymore and I'll fix those too. I took 5 years of notes and used AI to put the unsorted notes into topics. There are 87 topics to go through and I haven't proof read the whole thing yet so there are bound to be some mistakes. If you found some errors your welcome to go in and make a pull request to update them or send me exactly what I should change and I'll go in and do it. My goal was to take all the nuggets Georgi and Brad have given out over the years and put it in one place.

alfredoolivas said: "Interestingly, potent anabolic steroid trenbolone bound to the glucocorticoid receptor with an affinity almost as high as that of corticosterone, the endogenous glucocorticoid in the rat " [image: 1780232719779-0b15ecd0-f7da-4623-b05e-1ff7e885b4b9-image.jpeg] Corticosterone binds to the GR in hepatoma cells as MORE than cortisol. So at least in rat liver cancer cells, trenbolone has an equal affinity as cortisol on the GR, antagonising it.

Combined inhibition of dopamine D1/D2 receptors induces cognitive and emotional dysfunction through oxidative stress and dopaminergic neuron damage Results: Low-dose co-DR1/2I significantly increased MAO-B and ROS levels (p < 0.01) and decreased SOD activity (p < 0.01) in the substantia nigra, striatum, and hippocampus. MAO-B activity positively correlated with ROS (r = 0.916, p < 0.001) and negatively correlated with SOD (r = −0.685, p < 0.001), whereas ROS negatively correlated with SOD (r = −0.661, p < 0.001) in co-DR1/2I-treated mice. The medium- and high-dose groups exhibited spatial memory impairment (longer escape latency, p < 0.05) in the water maze and more anxiety-like behavior (reduced central zone time, p < 0.01) in the open field test; however, no abnormalities in motor coordination were observed in the rotarod test (p > 0.05). Immunofluorescence and WB confirmed a reduction in the dopaminergic neuron count after co-DR1/2I.

@bio3nergetic said:What one most likely witnesses is big med making matters worse, but walking away silently pointing at made-up villains. >> Sounds like Finasteride and Dutasteride

@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