@Mauritio Appreciate your thoroughness. It will be interesting to see what effect they have on you. I don't like the taste and feel of chia seeds, but maybe they could be used as a food supplement, like I do with liver.

What I have to say about the studies on “essential fatty acid deficiency (EFAD)” is that they are all incomplete, and it is necessary to piece the studies together like a puzzle, in addition to seeking out others that may not specifically address EFAD. 1. The overwhelming number of symptoms attributed to EFAD actually stems from the high metabolic rate caused by TEWL, which activates thermogenesis. If you neutralize TEWL in an EFAD-affected animal by increasing the humidity in the laboratory, it grows and develops normally without any symptoms. In many studies on EFAD, researchers mention “spontaneous recovery”—usually in the summer, lasting for long periods—followed by a worsening of symptoms, which they attribute to the seasons and their fluctuations in humidity. [image: 1783716841140-c2beaeab-cd4b-4280-893f-15ed7932ef46-image.jpeg] 2- The body is a dissipative system; if you remove n-3/n-6, the body changes the way it handles various processes that previously relied on them. It is a mistake in these studies to remove n-6 while keeping the diet essentially the same. I’ll give an example using zinc, a deficiency of which causes similar skin symptoms: [image: 1783716910557-18db4162-345c-48b3-8870-f9e63651d26c-image.jpeg] This table shows an EFAD (HCO) diet and a non-EFAD (corn oil) diet, and both have versions supplemented with zinc (C-2 and D-2); the key point here is that the protein source is casein (this detail will be important later): [image: 1783716961668-e9846a0d-82e0-4480-8775-ccff5e0a2872-image.jpeg] Now, in this table, it's the same thing, but supplemented with egg albumin instead of casein: [image: 1783717008090-135a94d7-db40-4a08-b637-c8e7375a8dae-image.jpeg] It can be seen from these two tables that EFAD causes skin problems if: There is a zinc deficiency The proteins are casein-based, rather than egg albumin. I was curious as to why the type of protein would influence the symptoms, so I remembered this: [image: 1783717055701-1fcf7b00-75a5-49ff-b33f-950b0a9deb48-image.jpeg] Egg albumin is rich in sulfur-containing amino acids. [image: 1783778512118-7b99813c-70e6-4d66-8021-ea93b7d1b7e9-image.jpeg] I considered the possibility of contamination with PUFA, but they also use soy protein, which I think theoretically poses a greater risk: [image: 1783717093452-c1514880-eaeb-428f-ada3-bac7bcafde56-image.jpeg] Is it possible that, with enough zinc, they could live indefinitely on an EFAD diet? Who knows... Well, if the problem is humidity, people who live by the beach can easily follow a diet like this and reap the benefits of the EFAD (resistance to endotoxins, inflammation, autoimmune diseases, snake venom, etc.). And btw, it is possible for a human to live well in EFAD, without skin problems, in a city as well. [image: 1783718698155-ec41016c-25cb-4832-b2a5-490f5885f41b-image.jpeg] (not mine) Thanks to learnmyhelpless at X for reminding me of zinc and EFAD relationship haha

I've been reconsidering past supplements and their effects in the face of fungus and biofilm. work in progress • All the B vitamins and also vitamin E quite strongly feed Candida glabrata (Caveat crucial differences to C. albicans). • Magnesium feeds it too and the ambivalence is enhanced by its much stronger osmotic effect when mucosal absorption is impaired. • Calcium significantly stabilizes biofilms, explaining possible initial symptom relief at the cost of long-term worsening. Perhaps even more effective against systemic effects of C. albicans than glabrata as it could temporarily "clog-up" the candidalysin etc toxins of C. albicans within the biofilm. • Zinc and iron supplemenation feed it and greatly strengthen its biofilms. On the other hand zinc can significantly raise mucosal immune responses so it's quite double-edged; good for prolonging and intensifying any suffering even though most people need more zinc for many bodily functions. • Copper, in contrast, is a disruptor and also raises defence mechanisms. It's quite a burden on the system but at least doesn't help out the fungus. • Butyric acid and lactic acid act as topical biofilm disruptors and can therefore aggravate local symptoms. Nice to have endogenously as naturally prophylactic countermeasures. • Alpha lipoic acid, interestingly, causes fungal membrane permeabilization at its subinhitory concentrations achievable by oral or iv. administration. I.e. it weakens fungal cells and makes them more sensitive to penetration by azoles and other antifungals or destruction by host immunity. On the other hand, orally administered ALA exerts significant chelation of the metals and minerals like zinc and iron in the GI lumen and topically. Such sequestration significantly disrupts fungal biofilms and has the potential to aggravate local symptoms especially in the duodenum, jejunum and, if mucosal absorption is impaired by biofilms, further beyond. Talk of ALA in the context of fungi is dominated by its half-time and redistribution issues (Cutler protocol) of toxic metals like cadmium and mercury and it is being argued by quite a few folks that these heavy metals were at the base and enablers of any chronic fungal infection. But from the aforementioned, ALA obviously has possible (over)straining impact also in the absence of pathological levels of Cd or Hg. • EGCG binds iron, therefore a powerful biofilm disruptor especially topically; potential to aggravate local symptoms. EGCG weakens growth and resilience of Candida by inhibiting their endogenous folate synthesis. • The major importance of (divalent) metals/minerals in biofilm composition and stability brings up the potential of oral EDTA administration as a more powerful chelation tool against intestinal fungal pools. EDTA's meagre oral absorption is of very good benefit and of relative merit over ALA's worrisome systemic heavy metal redistribution in this context. • Enzymes: I've again been considering beta-glucanases against fungal biofilms and cell walls. Chitinases/(Hemi)-cellulases are of secondary importance. IMO the two only proper oral enzyme products against Candida are the Biofase by D & G Industries and the Ther-Biotic Interfase Plus by SFI Health / Klaire Labs. They are pricey and for some reason I keep skimping on them. I don't see great use of nattokinase or serrapeptase or fibrin targeting against fungal biofilms. However, I'm reconsidering bromelain in the face of strong past aggravating reactions to this compound. By what I can find the direct antibiofilm activity of bromelain is not so clear but most of its promises are shown against candidal adhesins. I.e. the extracellularly placed proteins used by Candida to attach themselves to surfaces and tissues. In the face of bromelain's excellent systemic uptake and distribution I'm thinking that it may help weaken the apical attachment of fungus from the host's side at the base of their biofilms (rather than attacking the exterior layers). Bromelain appears to cover pretty much the same targets as papain: Maybe one is slightly more effective than the other but I see no need to take both. It will always somewhat irritate the mucosa, of course. Perhaps of extra benefit over papain is the dilution and degradation of mucus viscosity to increase its transmucosal cleavage of adhesins. IME the disruptors are an everlasting pain without concurrent antifungals. And the antifungals are (besides mostly underdosed) greatly insufficient if not combined with proper biofilm disruptors. Current tools to use: Nystatin, an azole, hesperitin, NAC, bromelain. No or minimal supplemental minerals. Must look into EDTA (otherwise EGCG or ALA on an empty stomach). Addendum 1: There's tetrasodium EDTA/edetate which is alkaline and disodium edetate which is slightly acidic. The disodium form would seem to be more sensible to pass through the stomach. It's freely and cheaply available. In contrast, for i.v. use it's always calcium disodium EDTA as it is supposed to release its pre-loaded calcium ion upon facing the greater binding affinity of a heavy metal ion. Quite necessary for i.v. use to lower acute cardiovascular risk and bone loss but it makes no sense for oral use against biofilm as one would explicitely want to sequester also calcium. There was one poster one reddit 8years ago reporting on using disodium EDTA and feeling initial symptoms already from a mere 50mg before eventually creeping it up to 300mg once per day. Better to start humbly then. Addendum 2: Definitely encapsulate any oral disodium EDTA. It's not very acidic but obviously readily grabs calcium. If you know how freshly mineralized teeth feel: Having drunk Na2-EDTA dissolved in a glass of water, even after an immediate extra rinse, feels like the opposite of that.

@springsnow check DMs

@alfredoolivas What is androstane?

Talk with AI (Claude) to try to understand Crumblecooking’s comment. Some info to move the Schmilblick forward (to move things along). Context: Weak ground: researchers focused on patients diagnosed with either ADRD or mild cognitive impairment (MCI). A widely used supplement marketed for joint pain relief may be linked to faster progression of Alzheimer's disease, according to new research from the University of Florida. Researchers found that glucosamine significantly increased the attachment of sugar molecules to proteins within cells. Mice receiving glucosamine also showed worsening deficits in social memory, which is the ability to recognize and remember other individuals. When scientists chemically reduced this sugar-tagging activity, memory performance improved. "In the United States, there are about 7 million people living with Alzheimer's and millions more with related dementias such as Lewy body or frontotemporal dementia," said senior author Ramon Sun, Ph.D., director of the Center for Advanced Spatial Biomolecule Research and associate director for innovation of UF's McKnight Brain Institute. "A lot of these people actively take an over-the-counter supplement that could be making their disease progression worse." Comment from the forumer Crumblecooking: Add linoleic acid to this—the prostaglandin E₂ precursor—and you then have a powerful yeast➝hyphal transducer—more commonly known as potato chips, bread, and granola bars. Comment from LucH (me) (not yet posted): I know we have here a weak ground: already inflamed cells behind BBB by ROS perturb the cohesion, weakening the balance behind BBB: There is inflammation (via ROS) and perturbation in the brain cells as far as the homeostatic balance is concerned: Detailed explanation: The blood-brain barrier (BBB) is composed primarily of cerebral microvascular endothelial cells and astrocytes linked by tight junctions (TJs) and adhesion molecules (AMs). This system maintains the homeostatic balance between the brain parenchyma and the extracellular fluid. => Not a proof, OK. But more and more studies take this direction... How to Help a Leaky BBB before it’s too late (usual process for ¾ people above 80ies) a) Which useful molecules can cross the BBB: Aspirin (mind the platelet impact) Caffeine (coffee and tea) EGCG (green tea) Resveratrol Taurine Vitamin E Vitamin C Etc. See detailed information on reference 2. b) How to Heal a Leaky Blood-Brain Barrier Which Supplements Repair the Blood-Brain Barrier? Several B vitamins support blood-brain barrier health: a vitamin B1 (thiamine) deficiency disrupts the blood-brain barrier, and supplementation can restore it. Vitamins B12, B5, and B9 (folate) can restore the integrity of the blood-brain barrier. (4) Magnesium, as a cofactor in over 300 biochemical processes, affects brain neurotransmitters, enzymes, and hormones. Magnesium L-threonate is often used for its potential brain benefits and may help manage certain brain disorders, such as depression, Alzheimer's disease, and age-related memory loss. To be continued on the reference 1. Sources and references Useful link: Alzheimer's Cognitive Decline and Inflammation (In French but with links in English) https://mirzoune-ciboulette.forumactif.org/t2067-declin-cognitif-dans-alzheimer-et-inflammation#29882 What can get through the BBB? https://my.clevelandclinic.org/health/body/24931-blood-brain-barrier-bbb The list of what can make it through your BBB is extremely lengthy, so here are some examples … Antocyanins can cross the BBB Phenolic compounds that cross the blood–brain barrier exert positive health effects as central nervous system antioxidants. 2021 Food & Function. Dafne Velásquez-Jiménez et al. What supplements repair the blood-brain barrier? https://thefnc.com/research/nutrients-to-help-repair-your-blood-brain-barrier/#:~:text=B vitamins.,restore blood-brain barrier integrity Glutamine et cancer Un lien intéressant : https://www.julienvenesson.fr/glutamine-cancer/ A natural compound, EGCG from green tea, also shows promise. It counteracts the action of glutamate dehydrogenase, which converts glutamate into α-ketoglutarate, leading to the death of cancer cells. https://www.julienvenesson.fr/la-quercetine-ameliore-les-effets-du-the-vert-sur-la-sante/ Glutamine is the preferred amino acid of cancer cells, required for their growth. But if you try to limit this intake, the cancer will destroy muscle tissue to obtain it. You can try to ration it, but never eliminate it. Therefore, you limit it, you don't eliminate it. NB: Whenever I suffer from a weak / a thin layer of stomach mucin, I associate ¼ tsp glutamine and ¼ tsp taurine powder (+ 1.5 g magnesium bisglycinate). Take one hour before bedtime. Always associate both to dampen the possible glutamate pathway. Question for AI (Claude) I don’t want a comment or an analyze of my answer but I’d like an explanation for Crumblecooking’s comment: “Add linoleic acid to this—the prostaglandin E₂ precursor—and you then have a powerful yeast➝hyphal transducer—more commonly known as potato chips, bread, and granola bars.” => What is the mechanism? Asparagine becoming nitrosamine? Short answer for IA (summarized because in French and 2 pages A4 long) No, not linked to nitrosamine. Vocabulary: the yeast→hyphal morphological transition. Hyphal: Adjective derived from “hypha”, describing anything related to this filamentous form. We have a morphological change from the yeast form (isolated round cell) to the invasive filamentous form. So, ultra-processed foods rich in omega-6 oils potentiate the pro-Alzheimer's effect of glucosamine via a dual mechanism: local inflammation (PGE₂) + fungal dysbiosis, promoting a compromised intestinal mucosa/BBB. The hyphal transition of Candida increases epithelial permeability, exacerbating precisely the leaky BBB problem you describe (LucH talking with Claude). LucH said: Okay, I get it. It's a stimulant on already fragile ground. IA says: Exactly. That's the most accurate wording. A stimulator—not a primary cause—on an already weakened foundation: • Compromised BBB • Chronic low-grade inflammation • Already disrupted O-GlcNAcylation Glucosamine + PGE₂ don't initiate the disease; they accelerate what's already underway. That's why the study refers to aggravated progression, not a trigger. This ties in with your notion of a weak ground from the introduction—the underlying condition precedes it, the stimulator amplifies it.

@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.

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