@LucH ty

@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.

@user73636 said in A Thereotical combination for inhibition of warburg effect: Pyrroloquinoline quinone I quite like Pyrroloquinoline quinone, and it does make me ravenous.

Walking continuously for 15 minutes is actually a minimum amout of activity. According Dr, Mercola there are additonal benefits for liver fat reduction. this begins at about 20 to 25 minutes of moderate activity five days weekly, with the strongest efficiency gains occurring around 150 to 160 minutes per week. https://articles.mercola.com/sites/articles/archive/2026/02/12/optimal-exercise-dose-reducing-fatty-liver.aspx?ui=f75a5a937074cc5b2fe8c56ad7c8da4175c90f9af39afe799ad679ff096c9372&sd=20050420&cid_source=dnl&cid_medium=email&cid_content=art1HL&cid=20260212&foDate=false&mid=DM1883713&rid=500975687

@LucH said in Toward a Better Understanding of Reactive Oxygen Species: @Amazoniac said in Toward a Better Understanding of Reactive Oxygen Species: The ROS linked to fat metabolism can arise partly from parallel effects, such as structural or functional perturbations and up-regulation of alternative ROS-producing enzymes (NOX, XO, COX, LOX, CYP2, etc.). I suppose that here we're mainly talking about excess PUFA loaded in adipocytes (AA cascade). When we stress or have a diet (fat loss). If we remain under 10 g PUFA/day, preferably 5-6 g, it would be OK. Edit: fine, the picture on ROS effects. (downloaded) ROS concentration & deleterious effects on cells. The next question is: What about when corn / soy food (from real food) is eaten, with LPS by-side load. Otherwise, it remains a theory. 1° In presence of ALA (thiol antioxidant) or a lipoprotection (A D3 K2 + vit E). 2° The same with aspirin or WWB. Parallel effects can also come from saturated fatty acids. Yet another example: Deleterious action of FA metabolites on ATP synthesis: possible link between lipotoxicity, mitochondrial dysfunction, and insulin resistance (Cyt c received fewer electrons overall, and pyruvate (oxaloacetate precursor) didn't normalize.) Impairing ATP synthesis limits electron consumption, which favors leakage from affected sites. On a related note, whether an imported fatty acid is saturated or not, the first stage of each β-oxidation cycle involves creating or dealing with an unsaturated intermediate (enoyl-CoA), and it's the hydrating reaction by enoyl-CoA hydratase* (ECH) that resolves the double bond by adding water, which also introduces the oxygen atoms that lack in fatty acids. *Synonym: unsaturated acyl-CoA hydratase This temporary double bond adds to any existing fatty acid double bonds outside of the segment being oxidized. After hydration, the NAD-dependent dehydrogenase (HADH) and the CoA-dependent thiolase (KAT) conclude a β-oxidation cycle. [image: 1770837140988-3a06059b-f0ac-452e-943e-35dceaf24dae-image.png] ⠀(10.1016/B978-0-12-382163-8.00022-0) Proper ECH activity relies on functional HADH and KAT, especially when the three enzymes form a supercomplex (the mitochondrial trifunctional protein, MTP) and work together to metabolize longer-chain fatty acids. Control of mitochondrial β-oxidation: sensitivity of the trifunctional protein to [NAD+]/[NADH] and [acetyl-CoA]/[CoA] Inhibitory effect of 3‐hydroxyacyl‐CoAs and other long‐chain fatty acid β‐oxidation intermediates on mitochondrial oxidative phosphorylation Pathophysiology of fatty acid oxidation disorders and resultant phenotypic variability Despite the experiment suggesting that inhibition is unlikely at healthy NADH/NAD⁺ and acetyl-CoA/CoA ratios, any factor that compromises one enzyme can affect the others. Local ratio perturbations or failure of backup systems may still lead intermediates to accumulate, including enoyl-CoA (the supercomplex's primary substrate). Given that some enzymes related to β-oxidation generate ROS, enoyl-CoA accumulation might place this unsaturated intermediate near ROS sources and start lipid peroxidation that then spreads to other lipids, such as cardiolipin. But it's a speculation.

@alfredoolivas the purpose of PT-141 is specifically to increase NO similarly to the PDE5 inhibitors like sildenafil/tadalafil, and it seems to be great at doing that. The benefit of melanotan II would be the added tanning which would be good if that's what you're looking for with the androgenicity/GR antagonism as a bonus. I personally have no need for that extra NO but in small quantities I think it wouldn't be a problem unless there's evidence otherwise. For the "symptom free cushing" thing it appears that if there are truly no symptoms, then the actual cause could be a faulty test where it's getting triggered by something else or had some manufacturing defect. Actually, the fact that the result was off the charts with no symptoms and that this was one case drastically increases the probability of a testing error. I am so curious about MT II's tanning and androgenicity that I'm thinking of grabbing some vials and trying something like 50ug/d. Anybody else thinking the same?

@AL said in Vitamin E Source in Europe: You also have this one , mixed tocopherols. I tried this one. Had a pretty rancid taste. Didn't like it at all.

3 meals each with 100g of carb and 36g lean protein and 15g of fat give 2000calories a day and thats not even counting vegetable side dishes. so you're exaggerating on how low the calorie count of 500 if you eat clean. I would do 3 meals with 200-250g of veg per meal and some pineapple and eggshell. some c8/c10 mct oil might clean out the gut. your comment about how "all" the food around you has fuing st in it is hitting that you have some sort of neuroticism and thats probably causing more issues than a SIBO which will probably resolve after digestion speeds up.

@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.

@evan.hinkle I will try that — thanks. I have been meaning to use it with coffee as a sweetener as well. And maybe I'll try it in jello instead of sugar: adding even more glycine to the gelatin.

@engineer How's your experience with this setup going so far? I just moved into a house that receives very little natural light coming in through the windows, as it's squeezed tightly in between two other shotgun-style houses, and I'm looking into my various options for tackling the problem. I've got plenty of chicken clamp-lamps, and a red light panel that I use for spot treatment directly on my body, but I need a broader solution that'll cover an entire room and make working from home without adequate natural sunlight tolerable.

using Mg topically is the only way it really works for me. I hate the feeling so I spray it on and rinse it off about 15-20 minutes later. I use it at nigh and mostly on my legs. If I'm lazy I just wipe it off with a wet cloth. If I don't do it I also get a nasty rash. I don't get a rash on my legs either but I do on my stomach and arms, even for a shorter time. Just my experience.

Get some trees in your home! Shefflera are easy, ficus do well and ponytail palms!

@cs3000 My thought chain goes like… supplementing D3 raises T4 production in the gut. And not T3. Maybe you are getting too much t4 production going and maybe you have a sluggish liver, not converting to excess t4 to t3, so it gets converted to reverse t3 and your feeling a peculiar form of hypothyroidism. https://www.frontiersin.org/journals/veterinary-science/articles/10.3389/fvets.2025.1559608/abstract Do you take magnesium as well? https://medicalxpress.com/news/2025-09-magnesium-inhibits-colorectal-cancer-carcinogenesis.html

The alibaba stuff will need to be analysed with a CoA provided by the seller/producer of their previous batch before ordering, and again of your batch before shipping, of course. Just as with the US company you've found. To double-check you could then order an additional non-GMP IR-spectrography or NMR or LC/MS for a couple to few hundred bucks after you've received the product. If the substance is neither listed on any prohibited compound lists nor within the registry of pharmaceuticals the chances of it passing through should be good but always subject to the general degree of arbitrariness.

@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

@Kilgore that was probably me tbh

a teaspoon of grain alcohol in a 355ml coca cola