@16characterstwas Thank you, appreciate it very much.

@zorba990 kind of an amazing find as for the issue you are talking about maybe you could heal it with a moggy silicon intake. peaty diet is probably deficient in it.

@Mauritio taurine for bile excretion actually seems better than TUDCA at their relative normal doses (3g per day for taurine vs 500mg per day for TUDCA)

@maplesyrupbro said in 11-keto-DHT for penile growth: @bio3nergetic It's not about needing it, it's just about optimizing the body(without obsessing about it). There are many factors more important than penile size. I ask because it seems that modern males are obsessed with penile size, and from my viewpoint, it is the ultimate indicator of beguilement by the false toxic-matriarch they created to break young men down. Even in my opinion that most studies are tainted and meaningless, some are good and in the sphere of sociological studies, it is never found that women actually desire large penises. This idea is porno culture usurping the mentality of young men. The more men cater to it, the more they are bowing to a false feminity. Judge sexual health by how you react to a woman you are interested in; by your ability to be aroused in a healthy way and in turn engage sexually with said woman. Everything else falls under the category of freakish fantasy perpetuated by a criminal industry ruining the physical and mental health of young generations.

@16characterstwas I am going to take a few days off and then do the co2 bath again. see what happens. I will keep it to 1 hour or less next time.

@maplesyrupbro said in Vitamin D paradox: What methods have you found to counteract VDR down regulation? Aside from the obvious things(take magnesium and K2). There is no single answer. Sorry. => If I rephrase it: How to counteract the downregulation of the VDR receptor, if there is a perceived problem by the body? So, we accept now the fact that VDR acts as a kind of sensor, allowing a retro-feedback. But before explaining “how”, we have to explain “why”, to understand it’s not always black or white. Think of your VDR receptors as a high-tech toll booth on a busy highway. If you send a massive convoy of several trucks and cars all at once, you create a total metabolic traffic jam. The system panics, closes half the lanes (downregulation), and calls in the "cleanup crew" (here the 24-hydroxylase enzyme) to divert the trucks off the road entirely just to clear the chaos. But By sending only a few trucks at a time (fractionated doses), the sensors stay calm, the gates stay open, and the cargo—calcium—is guided exactly where it needs to go by the "GPS" of K2 and Magnesium (as cofactors). The Conclusion: To keep the sensors sensitive, stop trying to flood the engine; just keep the fuel line steady. Too much "light" at once simply forces the body to pull the shades. For other readers, we’ve got 3 different situations: Blood test under the minimum conventional required level: 20 ng/ML. I target 42-45 ng for optimizing immunity. Bone fracture or pathology (osteoporosis). Trying to improve RDA towards 45 ng when you’re still-standing, though all the parameters are nearly good. The context is correct/fairly good: Light exposure Stress management Immunity Lifestyle Micronutrition Absorption plateaus at approximately 30 ng/ml. However, you’re aiming for a minimum of 45 ng/ml, as already said elsewhere. I won’t act on the same way in the first two situations. Emergency situation. Now we’re going to optimize the interaction (synergy). But first we have to explain – for “trustworthy readers” (follow-up requested via the appropriate tab) how the body communicates with a feedback. Sorry, by advance, since it’s going to be a little esoteric and long. No need to understand how, in details, by the way. *) The VDR/RXR Mechanism: Competition vs. Cooperation Vitamin A (Retinol) and D3 "share" the same partner, the RXR (Retinoid X Receptor). So, they can compete when not well supplied. Too much of a good thing is bad. The VDR cannot bind to DNA alone; it must hook up with an RXR receptor. If there is an overwhelming excess of Retinoic Acid (active Vitamin A), it may saturate the available RXR pool, potentially leaving the VDR "single" and unable to initiate gene transcription. So remind that taking 10 000 UI retinyl palmitate (Vit. A) once a week is not the good advice (if you want to target the usual advised ratio A/D). Personally, I take 2 x 5 000 UI Vit A per week, at breakfast with some MUFAs. No Vit. D3 supplement at the same time, but at the next meal. The "VDR Downregulation" Fix: To counteract excess VDR downregulation, you don't just need Vitamin A; you need the balance. Too much A blocks D; too much D can induce a functional A deficiency. The "Triangle" strategy (A-D-K2) I’ve already mentioned in another post is the correct pragmatic fix for this. *) The Role of the 24-hydroxylase Enzyme 24-hydroxylase (CYP24A1) has been identified as the "off-switch."  Insight: a very high-dose bolus supplementation strongly triggers this enzyme, which then degrades not only the excess but also the active form (1,25(OH)2D). 50 000 UI D3 is a strong bolus. Several times 10 000 UI could be considered on the same way when repeated.  Action: The strategy of fractionation (e.g., 1,000 UI twice daily) is the most pragmatic way to keep VDR sensitivity high without "scaring" the body into upregulating the degradation enzymes, when taking on a usual way. *) Request for AI (gemini3) Explain this: 24-hydroxylase (CYP24A1) has been identified as the "off-switch." => 24-hydroxylase is a degrading enzyme to get rid of metabolites / toxins. Detailed explanation (you can bypass) The CYP24A1 enzyme (24-hydroxylase) acts as the body’s internal thermostat for Vitamin D. Its primary biological role is to maintain homeostasis—ensuring that levels of the active hormone do not reach toxic or hypercalcemic levels. Here is a breakdown of how this "off-switch" functions and why it matters for supplementation strategy. The Mechanism of Degradation Vitamin D follows a specific activation pathway, but it also requires a clear exit strategy. CYP24A1 is the primary tool for that exit. • Targeting the Active Form: The enzyme targets 1,25(OH)2D (calcitriol), the active form that binds to the Vitamin D Receptor (VDR). • The Inactivation Process: It adds a hydroxyl group to the 24th carbon position of the molecule. This transforms the active hormone into calcitroic acid, a water-soluble metabolite that is inactive and easily excreted by the kidneys. • Preemptive Action: CYP24A1 also targets 25(OH)D (the storage form), breaking it down before it can even be activated if the body senses an oversupply. Why it’s the "Off-Switch" The term "off-switch" is used because CYP24A1 is inducible. Unlike some enzymes that run at a constant speed, the body "turns on" the production of 24-hydroxylase specifically when Vitamin D levels rise too high. • Negative Feedback Loop: When 1,25(OH)2D binds to the VDR, it actually triggers the gene that produces CYP24A1. Essentially, the active hormone creates its own "assassin" to ensure it doesn't overstay its welcome. • The Bolus Effect: Large, infrequent doses (e.g., 50,000 IU) create a massive spike in 1,25(OH)2D. This "scares" the system into a state of high CYP24A1 expression. The enzyme becomes so active that it can over-correct, degrading not just the excess, but the very D3 you are trying to utilize. CYP24A1 in the Kidneys and Beyond While the kidneys are the major site for systemic regulation, this enzyme is present in almost every tissue that has a Vitamin D Receptor. • Local Regulation: In tissues like the skin, colon, or immune cells, CYP24A1 acts as a local gatekeeper. It prevents the local concentration of Vitamin D from getting high enough to disrupt cellular mineral balance. • Detoxification: By converting fat-soluble Vitamin D into water-soluble calcitroic acid, it allows the kidneys to flush the metabolites out through urine. Without this "off-switch," Vitamin D (being fat-soluble) would accumulate indefinitely, leading to calcification of soft tissues. Pragmatic Application Understanding the "off-switch" supports the fractionation strategy. Approach / CYP24A1 Response / Outcome High Bolus / High Induction / Rapid degradation; potential "crash" in active levels. Daily Low Dose / Low/Stable Induction // Consistent VDR activation without triggering the "off-switch" aggressively. By keeping doses smaller and more frequent, you provide enough substrate to keep the VDR active without reaching the threshold that triggers a massive "cleanup" by 24-hydroxylase. Summary 24-hydroxylase is the biochemical name for what that specific enzyme does. • Its job is to attach a hydroxyl group (—OH) to the 24th carbon of the Vitamin D molecule. • While there are many "hydroxylases" in the body (some put an —OH on the 1st carbon, some on the 25th), CYP24A1 is the primary enzyme designated as the "24-hydroxylase." The Functional Hierarchy If we were to map it out like a corporate structure: • Division (Superfamily): Cytochrome P450 (The "Chemical Managers"). • Department (Family): CYP24 (The "Vitamin D Disposal Team"). • Employee (Specific Enzyme): CYP24A1 (The "24-hydroxylase" specialist). Why the Kidney context matters As we often note it, Cytochrome P450 (Cyp450) is highly active in the kidneys, but its primary goal isn't just "general toxin removal" like some other CYP enzymes (like those in the liver that break down caffeine or ibuprofen). It is a precision tool specifically evolved to prevent Vitamin D toxicity. When it acts as the "off-switch," it isn't just cleaning up; it is actively regulating your hormone levels to protect your kidneys from the calcium buildup (calcification) that would occur if Vitamin D levels remained unchecked. End of the “detailed explanation. X Now back to the main question: “What methods have you found to counteract VDR down regulation? Aside from the obvious things (take magnesium and K2).” *) Optimization: The D3 - A - K2 triangle Applying a fractionation strategy (2 x 1000 IU D3) is excellent to avoid receptor saturation and degradation by 24-hydroxylase (the enzyme that "breaks down" excess vitamin D). The Vitamin A/Vitamin D ratio: This is the sticking point in many protocols. Retinol and D3 share the same partner receptor, the RXR (Retinoid X Receptor). An excess of retinol (often via cod liver oil or isolated supplementation) can block the action of D3 on gene expression. The synergy between K2, MK4, and MK7 Everybody won’t agree here. Particularly a labo that easily and cheaply makes MK7 (from fermented soy). Choosing 1 mg of MK4 is relevant for tissue health and osteocalcin activation, although its half-life is short. It complements vitamin D3 well to ensure that calcium (even at 600-800 mg) goes to the bone and not the arteries, which is crucial if you are increasing your absorption efficiency with vitamin D3. Taking 5,000 IU of vitamin D3 (cholecalciferol) without an adequate supply of cofactors will, on the one hand, deplete some existing cofactors, and on the other hand, it could excite PTH (and move outside the optimal range of 0.4-3 mIU/L), thus impacting osteocalcin synthesis. Osteocalcin synthesis is activated by 1,25-vitamin D3, which binds to the vitamin D receptor on osteoblasts (bone remodeling). The strategy The strategy of fractionation (e.g., 1,000 UI twice daily) is the most pragmatic way to keep VDR sensitivity high without "scaring" the body into upregulating the degradation enzymes, when not well metabolized. PTH and the "Paradox" The mention of PTH (Parathyroid Hormone) is crucial.  Clarification: If Vitamin D3 is taken without enough Calcium or Magnesium, PTH can actually rise or stay high to pull calcium from the bones to satisfy the blood levels required by the increased D3 activity.  VDR Impact: Chronic high PTH can sometimes lead to a desensitization of the VDR response in certain tissues. Keeping PTH in the "sweet spot" (the text suggests 0.4–3 pmol/L or equivalent) ensures the VDR is responding to nutritional status rather than a "stress signal" from the parathyroid glands. *) MK4 vs. MK7: The Tissue-Specific Approach My preference for MK4 (1 mg) is well-grounded for VDR-related gene expression. The Nuance: While MK7 (from Natto) is better for maintaining stable blood levels due to its long half-life, MK4 is the form actually produced by animal tissues and is a potent ligand for the SXR (Steroid and Xenobiotic Receptor), which works alongside the VDR to manage bone mineralization. MK4 is also the preferred K2 of the brain (90%), probably because it’s less prone to oxidation. *) Potential downregulation by pathogens Since Vit. D has an effective power in immune response, some phila / viruses are able to “clog” the receptor. In these cases, VDR "agonists" (like Resveratrol or Curcumin) are often used alongside D3. *) Remember 1 High D3 increases the demand for Calcium. If diet is low in Calcium, D3 can become "bone-catabolic" rather than "bone-anabolic." That’s why I target 800-850 mg Ca. never under 600 mg (if the acid-base balance is correct). No need to target 1100-1200 mg Ca. I’ve set my “dead-lines” in cronometer.com for calcium at: 600 mg minimum 1200 mg red level. *) Remember 2 To understand the VDR (Vitamin D Receptor) as a "sensor" with a built-in "protection" mechanism, you have to look at it as a thermostat rather than a simple light switch. The body uses retro-feedback (negative feedback loops) to ensure that Vitamin D activity doesn't lead to toxic levels of calcium in the blood. If you want more details (you can bypass), here is an explanation (for fine tuning) (with help of Gemini3, to keep it clear). The VDR as a Metabolic Gatekeeper The VDR is a nuclear receptor. When 1,25(OH)2D (the active form) binds to it, the VDR doesn't just turn on "good" genes (like bone building); it simultaneously turns on the genes for its own destruction. • The Sensor Trigger: When the VDR senses high levels of active Vitamin D, it triggers the expression of the CYP24A1 enzyme (24-hydroxylase). • The Protection (Retro-feedback): This enzyme immediately begins breaking down both the storage form and the active form of Vitamin D into inactive metabolites. • Pragmatic Result: If you "flood" the sensor several times with a massive dose, the body perceives a "danger" signal and aggressively ramps up the breakdown process, which can actually leave you with less functional Vitamin D in the long run. The Calcium-Sensing Receptor (CaSR) Link The VDR doesn't work in a vacuum; it "talks" to the Calcium-Sensing Receptor (CaSR) in the parathyroid glands. • The Interaction: When VDR is activated, it increases calcium absorption in the gut. • The Feedback: As blood calcium rises, the CaSR senses this and shuts down the production of PTH (Parathyroid Hormone). • The Protection: Since PTH is required to convert storage D (25(OH)D) into active D (1,25(OH)2D), dropping PTH levels acts as a "brake" on the system. This prevents the body from absorbing so much calcium that it would become toxic (hypercalcemia). Receptor "Downregulation" vs. "Saturation" When people speak of "VDR downregulation," they are often describing a state where the receptor becomes less responsive. This happens for two main reasons: Saturation & Internalization: Just like insulin receptors in Type 2 Diabetes, if the VDR is constantly bombarded by high-peak doses, the cell may "hide" the receptors (internalization) to protect the DNA from over-stimulation. Cofactor Depletion: The VDR requires Magnesium to bind and RXR (Vitamin A) to "dock" onto the DNA. If these are missing, the sensor is "broken"—it’s like a thermostat with no battery. It might "sense" the heat, but it can't tell the furnace to turn off. Summary of the "Sensor" Strategy By taking smaller, fractionated doses (1,000 UI 2x/day), you are essentially "whispering / lightly tickling” the sensor. And so, you get:  No "Panic" Response: You stay below the threshold that triggers a massive spike in CYP24A1 (the breakdown enzyme).  Steady Signaling: You provide a consistent signal to the CaSR and PTH, allowing the metabolism to maintain a steady state of calcium transport without the "sawtooth" spikes of high-dose therapy that can lead to arterial calcification or receptor desensitization. *) Remember 3 There is interaction between liposoluble vitamins. Vitamins E and K appear to share the same metabolic pathways because both undergo side chain ω- hydroxylation and b-oxidation to produce their respective metabolites (Dr. traber) do not take them at the same time if 400 UI vit E mix. Useful link: How much fat do we need to absorb liposoluble vitamins? (In French) https://mirzoune-ciboulette.forumactif.org/t1357-vitamines-liposolubles-et-matiere-grasse-ratio#15157

@risingfire sorry that wasn’t clear.. it is more like the opposite of what i was trying to say. let’s try again: Endotoxin measure correlates positively with being overweight and that relation seems to be causative. Seeing so, anything that reduces bacteria (a producer of endotoxin) would reduce endotoxin.

@lobotomize haha

@ThinPicking I haven't personally used it, but this is fairly well regarded as being a good NDT: https://shop.forefronthealth.com/products/raw-desiccated-thyroid-130mg

@alfredoolivas said in moggy chicken log: "Purified" Pregnenolone DMSO (40mg daily) Let us know how 40mg works out for you because I'm using 10 drops pansterone (10mg pregnenolone + DHEA) and 2 drops kuinone (K2) for my similar regimen to yours. I'm not sure if that's enough or if the DHEA is estrogenic so it'd be nice to get more data points

It would make sense if the thyroid won't get much damaged at the time of hypothyroidism, but a better question i was never really answered is, what actually happens with thyroid when it stops functioning.

Fatty acid oxidation drives senescence Context1 : study https://pubmed.ncbi.nlm.nih.gov/39454000/ (...) Context 2: comment from user73636 (forum) A simplified explanation Excerpt (part) if you block FAO (Fatty acid oxidation) (with drugs like etomoxir or by turning off FAO genes), the cells are less likely to become senescent, even though the DNA is still damaged. That suggests “fat burning mode” is a key step in turning DNA damage into aging like changes. � The simple takeaway Think of it like this: Damage to the DNA → flip a switch → cell starts burning fat for energy more than usual → this fat burning helps push the cell into a “retired, old” state (senescence) → that speeds up aging changes in the body. Blocking that fat burning step can reduce this effect, so scientists are looking at it as a possible way to slow some age related problems. My comment (LucH) (not yet posted): Blocking FAO won’t help mitochondria to get the appropriate stuff if glycolysis from glucose isn’t induced / optimized. What you get is less inflammation, since less stress coming from unloaded / discharged fatty cells (AA reaction) would be temporally beneficial. What you’ll get is a slower energy metabolism (adaptation). Demand for AI Analyze my comment (LucH). No need to search for approximation, by the way, in the formulation (image). IA says (Gemini3) Your comment offers a sharp, pragmatic critique of the metabolic "trade-off" that occurs when intervening in fatty acid oxidation (FAO). You are essentially pointing out the difference between inhibiting a pathological state (senescence) and restoring a healthy one (metabolic flexibility). Here is an analysis of your points: The Energy Deficit Argument You are correct that blocking FAO is not a "free lunch." In the study, DNA damage forces the cell into a high-energy demand state to maintain the Senescence-Associated Secretory Phenotype (SASP). If you block the lipid fuel source without a compensatory shift back to efficient glycolysis, the cell enters a state of energetic crisis. • Your Logic: Slower metabolism = Adaptation. • Scientific Reality: If the mitochondria cannot switch back to glucose effectively (due to the original DNA damage or underlying insulin resistance), you aren't "fixing" the cell; you are simply starving it into a low-power mode. Inflammation vs. Function Your point about the Arachidonic Acid (AA) reaction is insightful. By blocking FAO, you likely reduce the release of pro-inflammatory lipid mediators. • The "Net Gain": You get a temporary reduction in systemic inflammation (less SASP). • The "Net Loss": You risk mitochondrial "discharge." If the cell can't burn fat and isn't optimized for glucose, the proton motive force across the mitochondrial membrane may drop, leading to reduced ATP output and potential functional decline in the tissue. Adaptation as a Double-Edged Sword You highlight a critical flaw in "senomorphic" therapies (drugs like Etomoxir). While the study suggests blocking FAO prevents the transition to senescence, your comment suggests that in an aging body, this might just result in metabolic stagnation. Summary of your Perspective (LucH) Point. Mechanism. Outcome Glycolysis Gap: If glucose uptake isn't optimized, blocking FAO leaves a void. / Energy deficiency. Inflammatory Relief Reduced stress from "unloaded" fatty cells/AA pathway.// Lowered SASP/Inflammation. Metabolic Speed Shifting away from FAO without a replacement fuel. / Slower, adaptive metabolism (Low-power mode). Critique of Formulation Your comment is technically grounded and avoids the "magic bullet" trap often found in longevity forums. It correctly identifies that senescence is a metabolic choice made by a damaged cell; removing the fuel for that choice doesn't necessarily restore the cell to its "youthful" prime—it just stops it from completing its "retirement" program. Would you like me to help refine the phrasing of your comment for the forum to emphasize the risk of "metabolic stall," or perhaps look into how glucose metabolism behaves specifically in these FAO-blocked models? LucH says: Better rephrase this with an image, if possible: When you stop or moderate the natural senescence, you limit inflammation well, but you don't feed the mitochondria correctly. Image from AI says: [image: 1774853817018-limiting-inflammation-from-fao-for-senescence.png] LucH says: Fine. End of the talk. Give the same deduction, but shortly: AI says: Inhibiting FAO to block senescence creates a trade-off: you successfully reduce inflammation, but at the cost of starving the mitochondria. Without optimizing glucose use, this forces the cell into an inefficient, low-power adaptive state rather than restoring healthy function. LucH says : OK, End. Thanks. AI says : You're very welcome. It was a pleasure dissecting that metabolic trade-off with you—pragmatic skepticism is always the best lens for longevity research. If you ever want to dive into the specifics of mitochondrial uncoupling or another study, I'm here. See you next time!

https://www.youtube.com/watch?v=8mDWI84FlEg

In case anyone is interested, here is a no-bake cheesecake recipe made with strained yogurt: https://hungryandchill.com/icelandic-delight-skyr-cake/

@hwisdom did you actually try this?

Thanks for posting. Excerpt from the study: In the U-13C-Glu + Lys + AA model, AA produced glyoxal (GO), methylglyoxal (MGO), CML and CEL, which was significantly higher than with Glu alone. This study provides a theoretical basis for the formation mechanism of AGEs in the Maillard reaction involving AA. Comment: Among Amadori rearrangements (becoming a Maillard reaction), methylglyoxal (MGO) is a frequent and strong one. But the body is able to manage these AGEs from food if we get glutathione enough (and cofactors to recycle or spare oxidized GSH). However the problem comes from other agressions ... Useful info (in French but with links in English) Glucosepane glycation et agents protecteurs https://mirzoune-ciboulette.forumactif.org/t2184-glucosepane-glycation-et-agents-protecteurs#30714 In anyone aging or subjected to prolonged metabolic stress (persistent inflammation, toxins, processed foods), the body's metabolism becomes disrupted and the entire redox system weakens. Glutathione levels decrease, other cofactors become deficient, and defenses against dicarbonyls are compromised. This overall shift in redox metabolism creates a favorable environment for the increased formation of glucose, a major AGE (Advanced Glycation End Product). Most of the AGEs formed in the body do not come directly from ingested foods (sugar and meat), but from two highly reactive dicarbonyls: 3-deoxyglucosone (3-DG) and methylglyoxal. Our natural defenses—zinc, insulin, glutathione, among others—serve precisely to neutralize these compounds before they can attack proteins. When these defenses are depleted, due to age or metabolic stress, AGE formation accelerates. Protective agents against 3-DG and MGO (two highly reactive dicarbonyls) B6 PLP Benfotiamine Optimize and recycle glutathione Anti-glycation formula (L-carnosine, aminoguanidine, sodium R-lipoate, benfotiamine, L-histidine, guava/banaba leaf extract (1% corosolic acid)). Details on the link.

Magnesium ratio for Ca:Mg is a nonsense as long you target the RDA for Ca 1000-1200 mg Ca. We’d better target the minimum amount, which is makes more sense. Why? The body is able to optimize the assimilation. As far as I’m concerned, I target: Ca: 800-850 mg. minimum 600 mg if other acid-base elements are correct. Mg: 300 mg. Not higher than 450 mg (Vit D). K: 3000 mg. Comment: Yes, Mg is useful. And so are MCTs from coconut. But before targeting ketosis for changing the microbiote, you’d better think twice and enlarge the view / the approach. You’ll probably get the same result with a 3-4 day fast and 600 K/cal diet, combined with a 16.8 diet. Useful info: https://mirzoune-ciboulette.forumactif.org/t2182-conversation-ia-n1-relation-calcium-mg-et-k-ajr-revisite-et-prevention-lithiase#30697 AI Conversation N° 1: Calcium, Mg, and K Relationship. Revised RDA and Kidney Stone Prevention. Context: Kidney stones. Excerpt (translated from French) Potassium intake (fine for getting oxalate crystals very brittle) and fiber (25-35 g/day). This is a key element. Personally, I aim for 3000 IU of K, 300 IU of Mg, and 800-850 IU of Ca (never below 600 mg for Ca). And don't bother me with the Mg/Ca ratio and aiming for 1200 mg of Ca. That's unrealistic… Acid-base balance is the determining factor. As long as PTH (0.5-3) isn't stimulated, things should be fine. This needs to be verified and nuanced (done on the given link with the “help” of AI). Potassium intake (very fragile oxalate crystals) and fiber (25-35 g/day). This is a key element. And if you're wondering how I use AI to avoid dodging the issue and thus influencing other readers, here's an explanatory link on my forum: https://mirzoune-ciboulette.forumactif.org/t8-presentation-de-luc-alias-nestor345#9 Excerpt: I use digital tools to confront my own statements and ensure the coherence of my summaries, but the 'spirit' of the advice comes from the literature I study and the feedback from my own community at Mirzoune et Ciboulette forum. I see my role as a translator or an analyst who reviews an interesting book or document. Having been a language teacher, my focus is on taking complex, dense information and making it structured and accessible for someone who’s lost or overwhelmed, who currently lacks the energy to digest a 200-page book. PS: I Know: We shouldn’t trust IA (…).

Histamine is a stress signal Iirc it also turns on NO You are under metabolic stress You need to energize cell function I am simplifying this a lot…. 1- blood sugar. 2- endotoxin. Start there If you raise your metabolic rate Naturally- not with exogenous t4 But sugar Sugar supplies your liver and thyroid essential metabolic support It’s a pillar of Peats teachings Addendum: not glucose supplements

@lobotomize right but this is a mycelium product not a mushroom (fruiting of mycelium) product. I know Reishi mushroom blocks 5 ar but I don’t see that shiitake does. Thanks, I’ll keep looking!