Still coughing Over the night my tube fills up with mucus so I start to cough because of that then once that clears out I have a more dry type of cough I think. Either way it usually turns into a fit and it takes me some time to calm down and stop. Will try sodium bicarb rn.

Talk with AI (Claude) How efficient is the intake of a MK4 supplement, (with enough fat, hereby 25 g fat with some MUFAs), when taking 1 mg (1 000 mcg) K2 MK4? Question of vehicle only? No intermediate change into menadione, I suppose, since there is no digest process. Need a confirmation, whenever there is a target amount limited to 2-3 mg K2 supplement. Note: 2 takes of 1 mg MK4 at breakfast and midday meal, with 1 000 UI D3 (both at the same time, AKA 2 x 1 000 UI D3). Brain target. AI says (Claude): Summary: A moderate amount of D3 and K2 are co-absorbed in the same chylomicron pathway; so simultaneous intake is fine. Brain target and dose adequacy: 2 mg/day total is a reasonable range for a brain-focused protocol. Step 1 — Chylomicrons (intestinal phase, 0–4h postprandial) Step 2 — Chylomicron remnants → liver (4–6h) Step 3 — VLDL → IDL → LDL (hepatic re-export, hours to days) A possible route for extra-hepatic tissue supply is that part of the K-vitamins are re-packed into LDL, which forms a major transport system from the liver to peripheral tissues. ScienceDirect This is the key insight for your brain target — the liver processes the chylomicron-delivered MK4 and re-exports it via VLDL, which is then progressively remodeled into IDL and LDL for peripheral tissue delivery. Agarose gel electrophoresis of lipoprotein fractions after K2 supplementation revealed distinct chylomicron bands and variations in VLDL and HDL mobility, influenced by dietary lipids and VK2 supplementation. Wiley Online Library

@Ray-Peat-Fanboy no politics allowed in my Christian ray peat forum

@bio3nergetic this is reasonable, but hear ye, hear ye, some dudes are deeply, keanly, eagerly, needy, of healing an exceedingly teeny weeny thingy, albeit a bigly hearted beefy meany Peeny, by any means necessary. speaking for a friend.

@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 (whenever there is no chicken liver (2x) at the menu, once a week). 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

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"The evidence from history, as well as animal experiments, is that you can produce it (homosexuality) by stress during gestation. And everyone is abnormal in some way - that isn't something that I think law should be involved in regulating in any way. But I think the evidence is clear that it's a particular product of both prenatal and early life stresses." - Ray Generative Energy #70 https://www.youtube.com/live/Pdb_xOl3GJY?si=_3Fu5-5xKBxoovp1&t=5933

@John-Smithra I dealt with this while stuck living in a moldy house for two years. Along with the loud explosion noise I was also experiencing hypnic jerks where I would lurch forward involuntarily, or an arm or leg would whip into the air, as I attempted to drift off into sleep; this would violently jolt me awake. Sometimes they were accompanied by a flash of light in my vision. I would regularly go through 40-50 of those in a row or more, forced to stay awake for hours before my body became so exhausted that it was able to push over the threshold into sleep, for a short while at least. Needless to say it was torturous; once I got out of that house, my life and health got so much better.

Here's a concrete example of where the information came from and how I used AI, in relation to microglia and inflammation. I don't master everything https://mirzoune-ciboulette.forumactif.org/t2174-neuropathologie-comment-attenuer-la-fibrose-en-cas-d-algodystrophie-et-de-fibromyalgie#30632 Excerpt Neuropathology & how to mitigate fibrosis in complex regional pain syndrome (CRPS) and fibromyalgia. Key ideas • Improve nerve conduction and limit hyperalgesia. • Limit fibrosis (dermal sclerosis) by modulating TGF-β1 stimulation. • Combined approach to fibrogenesis, the extracellular matrix (ECM), and inflammation. • Tactics to counteract fibrosis & optimize conduction – Practical aspects. Antifibrotic action of curcumin & dexamethasone. Anti-excitotoxic action of magnesium bisglycinate Neurotropic mechanism of action of thiamine (B1), pyridoxine (B6), and vitamin B12 in cases of heightened neurosensitivity and as modulators of inflammation PEA to stabilize mast cells and limit microglial activation. By stabilizing mast cells, PEA reduces the sensitization of peripheral and central nerves.

@ThinPicking yes - no glorifying violence or illegal behavior. Thank you.

I'm going to end up with useful nutrients to protect lipid directly 1. Antioxidants That Protect Lipids Directly Vitamin E (tocopherols + tocotrienols) • Acts as the primary lipid-phase antioxidant, protecting membrane phospholipids from peroxidation. • Gamma-tocotrienols add stronger chain-breaking antioxidant activity in membranes. Dose: 400 IU mixed tocopherols (with gamma tocotrienols) 2–3×/week, or 20–25 mg/day. Note: More is not better; excess can disrupt redox balance. Beta-carotene (from food) • Quenches singlet oxygen and supports antioxidant recycling. • Best obtained from diet (carrots, sweet potatoes, leafy greens). Astaxanthin • A potent carotenoid that embeds across the lipid bilayer and protects both sides of the membrane from ROS. • Particularly effective in mitochondrial membranes. 2. Water-Soluble Antioxidants and Cofactors Vitamin C • Regenerates oxidized vitamin E. • Supports collagen, immune function, and general redox balance. Magnesium • Key mechanism: Magnesium inhibits PLA₂, the enzyme that releases arachidonic acid (AA) from membrane phospholipids. • Mg²⁺ stabilizes phospholipid bilayers, reduces Ca²⁺-dependent PLA₂ activation, and lowers eicosanoid production. Dose: 350–420 mg/day elemental magnesium. Form: Magnesium bisglycinate (≈2.5 g/day split into 2–3 doses to reach ~450 mg). Note: Higher needs after stress; do not “preload” before stress. Zinc • Protects thiol groups and stabilizes membrane proteins. • Inhibits NADPH oxidase–induced lipid peroxidation, reducing the arachidonic acid cascade. Dose: 10–15 mg/day. Mechanism: o ↓ membrane peroxidation o ↓ PLA₂ activation o ↓ free AA release o ↓ PGE₂ formation (independent of COX inhibition) Key references: • Prasad, Am J Clin Nutr, 2009 • Ho et al., Free Radic Biol Med, 2008 Selenium • Required for GPx4, the enzyme that repairs lipid hydroperoxides directly in membranes. • GPx4 is the only enzyme that can detoxify oxidized phospholipids inside the bilayer. Dose: 100 mcg 2–3×/week; more if inflammation is present. Note: Excess selenium causes fatigue and organ stress — more is not better. 3. Structural Lipid Support Phosphatidylcholine (PC) • The primary phospholipid of cell membranes. • Essential for maintaining bilayer structure, fluidity, and repair. • Supports ER–mitochondria lipid exchange, which is required for cardiolipin remodeling. Stearic Acid • A saturated fatty acid that “solidifies” and stabilizes membranes without promoting peroxidation. • Helps maintain the optimal balance between membrane fluidity and rigidity. Sources: Cocoa butter, dark chocolate, beef tallow. Why This Matters for Mitochondria • PC stabilizes the outer mitochondrial membrane and supports lipid trafficking. • PE (phosphatidylethanolamine) shapes the inner membrane and allows cardiolipin to organize respiratory complexes. • Cardiolipin anchors the electron transport chain and is extremely sensitive to oxidation. • GPx4, vitamin E, astaxanthin, zinc, and magnesium protect cardiolipin and PC from peroxidation and enzymatic degradation. • Stearic acid and low-PUFA intake prevent fragile, oxidation-prone lipids from entering mitochondrial membranes. Together, these nutrients maintain membrane integrity, mitochondrial efficiency, and resistance to oxidative stress.

@Corngold said in Unbelievable Reddit thread: I think male hair has been sexualized by the non-committing hypergamous modern female and baldness was always the norm for at least 50% of dudes after like 25-30. "Unconsciously" they probably know what actually causes it. I don't, so I can't say anything more about this. They're all adorable. Also the shape of a Hamilton-Norwood is not suspicious at all.

@sunsunsun said in Vitamin C Role in Blocking Nitrosamine: u eat seed oil chips??? Yes, I eat Lays’ pepper and salt chips, only when I “crave” for, not as a snack. I know they use sunflower oil, rich in PUFAs, which I shouldn't be using. It’s rather once a month, and even less. Nothing is forbidden if you limit the impact (quantity and frequency). Because we only "need" a tiny amount of Omega-6 (around 1-2% of calories) for essential functions, our modern intake (often 10-20%) sends a constant signal of "inflammation and storage" to the body. The Bottom Line: You can't just "burn off" a bad type of fat the next day. It stays in your system, influencing your inflammatory markers for years. This is why a small amount of "bad" fat is more disruptive long-term than a large amount of "good" fat. I know. By keeping the chips to once a month, I ensure that these "fragile" fats never become the primary building blocks of my cells. This is where the quantity vs. type debate is settled. I know fat isn't just stored energy; it’s a signaling molecule. Nobody is perfect Useful info (in French, translator needed, but with English links): Les besoins réels en AG polyinsaturés surestimés ? (Are the actual needs for polyunsaturated fatty acids overestimated?) https://mirzoune-ciboulette.forumactif.org/t1581-les-besoins-reels-en-ag-polyinsatures-surestimes#18738

a teaspoon of grain alcohol in a 355ml coca cola

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@Corngold ah so I wasn't referencing the video I was sharing when I said I didn't think women were at fault, I was referencing your comment, that part I disagree with I think women get blame kinda like a child is to be blamed for their bad decision. Yes, they made the choice, but who built the environment. And that's why I'll forever be a masculinist in my assessment of the dynamics of the sexes -- it's always man's responsibility at the end of the day, women have cunning and deception, but like a child trying to trick a parent with even clever lies, a parent's best guard is to be unwavering in stable and wise conduct, and they will weather conflict well -- this requires a discipline, most parents, indeed men, don't have. On to the point of the types of feminine, I'm always one for some classical skull calipers and their categorizations, but I feel like it's back seat to man with huge balls going apeshit on the opp. I think women (and men) have changing charactar traits according to circumstance/environment. I don't believe it's set in stone... For instance, which came first: Hitler, or WW1 and it's consequences?

@LucH said in How to get Vit C from potatoes milk and meat: @sunsunsun said in How to get Vit C from potatoes milk and meat: have you considered an orange? I suppose you're asking for "histamine problems". If you want to know if there is some DHA in orange juice or in the fruit, it's not pertinent. Mostly AA in the fruit. DHA is present in fresh and processed orange juice, where the enzyme ascorbate oxidase can catalyze its formation, especially at temperatures above 30°C. Stability: The total ascorbic acid (AA) content (ascorbic acid + DHA) decreases over time and with exposure to air/oxygen. Histamine Orange is H3, like most citrus fruits. Clementine is H2. I do not eat H3 nor L3 at breakfast (histamine). No orange when in crisis. Now under control. Ok for one orange a day, but still with 1 000 0000 unit DAO enzyme every other day. Naturdao. No need to take the one with useful nutrients (Mg & B6) as I already follow them with cronometer.com Note: When leaving fresh orange juice for 2-3 days in a frigde with some "peel", there is a fermentation, and we got new DHA. So drop after 36 hours, then higher at 72 hours. All that commun claim that oranges/citrus fruits inherently increase histamine therefore it can be bad or is bad isnt true, most oranges simply arnt optimally ripe so it wont make people feel optimal, if a person eat enough optimally ripe oranges, it would increase relaxation significantly, more than most foods

One month later: I'm using more protein powder and whenever I don't, the Nurri shakes take its place, along with Super Coffee in the morning.

@Sugar said in I will teach you to grow taller: Frankfurt plane Is it fun to be this crazy?? I kind of wish I would be like this when my mental health is down the drain.