*) Additional info Vit E: sparing effect and recycling (In French; translator needed) http://mirzoune-ciboulette.forumactif.org/t30-vitamine-e-plus-qu-une-vitamine#60 "Vitamin C regenerates vitamin E, and vitamin E protects β-carotene—a process aided by polyphenols. With β-carotene supplementation, vitamin C regenerates both vitamin E and β-carotene, and β-carotene appears to protect vitamin E, although the actual mechanism behind this phenomenon remains unexplained." Savings effect Vitamin E is not just a vitamin. Vitamin C makes it possible to recycle oxidized vitamin E and thus prolong its lifespan. The same goes with glutathione which is thus saved for other more useful functions (detox). Glutathion is our antioxidant master. Vitamin E protects against the deleterious effects of polyunsaturated fatty acids when the latter are excess. And this is quickly done! English corner: How Does Vit E Regulate Redox interactions? Breaking the ROS chain-reaction from PUFA https://mirzoune-ciboulette.forumactif.org/t2081-english-corner-how-does-vit-e-regulate-redox-interactions#29973 RP advised 100 UI Vit E (+/ 150 mg) though our requirement increases with age, as our tissue iron stores increase… Since vitamin E has a half-life of about 48 hours, it could be advisable to take 75 IU - 100 IU orally when there suspicion of Sars-Cov-2. This study also found that alpha-tocopherol (vitamin E) was about 100-fold more potent/effective than Remdesivir against SARS-CoV-2 and other coronaviruses! https://www.news-medical.net/news/20210715/Water-soluble-vitamin-E-compounds-directly-inhibit-SARS-CoV-2-replication-and-synergize-with-remdesivir.aspx NB: vitamin E appear to be one of the substances having the ability to inhibit the proliferation / replication as well as the infection once it has already occurred. So do zinc, glycine, naringening, quinine and vitamin D. Too much of a good thing is bad There is no real danger with high dose vitamin E. But high repeated doses of vitamin E inhibit platelet aggregation. Need to be compensate with K1. Not taken at the same meal (transporters). Alpha-tocopherol is preferably stocked in the liver. (Kayden and Traber, 1993; Traber et al., 1990). Every 72 hours would be fine with 400 UI (at least 2 toco). 20-25 UI are needed per day, according to Chris Masterjohn. Note: As the mechanism by which phylloquinone (K1) is converted to K2 MK-4 is unknown, we cannot readily speculate how vitamin E supplementation influences the concentrations of these forms of vitamin K in extrahepatic tissue. While it is plausible that less MK-4 is produced because vitamin E supplementation reduces phylloquinone as a substrate in the extrahepatic tissue, vitamin E may also decrease MK-4 concentrations independently of phylloquinone. NB: Vit E and K use the same transporter. So don’t take these supplements at the same time. More info on Vit E https://mirzoune-ciboulette.forumactif.org/t30-vitamine-e-plus-qu-une-vitamine#60 Excerpt 1 (translator needed, in French): Most studies show a beginning of preventive efficiency at doses of 100 IU /d in degenerative diseases. Braking of oxidative stress which is underlying the phenomena of senescence and the appearance of all degenerative pathologies: cardiovascular, cancers, osteoarthritis, osteoporosis, presbyacousis, cataract, macular degeneration, Parkinson and Alzheimer's diseases, etc… Excerpt 2: Optimal contribution, without pathology, if under 40 years old: 100 IU per day. Contribution in case of supplementation in polyunsaturated fatty acids 100 IU per gram of EPA. - Therapeutic contribution: 400 - 500 IU every 5 days. Mg/ UI conversion: 100 mg = 150 IU. Personally, it’s 400 UI mixed toco every 3 days (+/ twice a week). 3x if inflammation. Now Foods – E 400 – with mixed tocopherols. Softgels. + Once a week K1 (mix K1 and K2). Vit K2 MK7 must be encapsulated (oxidation).

@alfredoolivas i eat under 3g of PUFA daily, ive been avoiding PUFA for long time so i think my fat is pretty much saturated fats atp. idk what is EFA ill look into it. im not doing low protein just 0.7-0.9g/lb protein. i will try out this stack that im going to do and report back here about my results but just looking for some additional info on what im doing or what else to do. Also what do u suggest i restrict my calories to?

If I try to decode: During the TCA cycle (energy for mitochondria), mi-infrared photons are released, at 87 THz frequency, derived from the reduction of NAD+. At this frequency light particles enter in vibration when meeting CH2 (carbon-hydrogen bonds) in membrane lipids. This “coupling” share a 𝐂𝐎𝟐 connection (called polariton). The researchers hypothesize that this arrangement boosts TCA cycle and add a 10% energy gain. Haidut said: “Red / infrared light forms a quantum system with the lipids present inside the mitochondria and CO2, which results in boosting ATP synthesis when cells are exposed to red/infrared light and enough CO2 is present. I suspect most of the effect are driven by the lipids composing cardiolipin, and the effect can probably be modulated (up or down) based on the nature of those lipids – i.e. PUFA, MUFA or SFA.” => Importance of cardiolipin connected with IR light. Cardiolipin is a unique phospholipid located exclusively in the inner mitochondrial membrane. It plays a structural role (featuring an inverted-cone curvature), acting as a waveguide (a quantum phenomenon). Naturally, it is important to ensure an intake of MUFAs (e.g., oleic acid) to maintain membrane fluidity, while keeping PUFA levels low. AI says: "Enriching mitochondrial membranes with monounsaturated fatty acids stabilizes cardiolipin against free-radical damage. By protecting the physical integrity and curvature of the cristae, these lipids maintain the strict structural conditions that allow polaritons to exist and catalyze ATP production via a quantum effect. Cellular nutrition and quantum physics converge to lock in the energy efficiency of living systems." — (1-2) DOI: 10.1186/s12944-019-0990-y (Double bonds of unsaturated fatty acids differentially regulate mitochondrial cardiolipin remodeling) 2019. Scientists propose a light-matter quantum state inside living cells https://www.thebrighterside.news/post/scientists-propose-a-light-matter-quantum-state-inside-living-cells/ Excerpt: • Researchers report an unexplained 71-terahertz vibration in living cells, mouse tissues and isolated mitochondria that disappears when mitochondrial structure is disrupted. • A theoretical model proposes that the signal could arise from a quantum hybrid state, or polariton, created by coupling infrared light with collective vibrations of lipid molecules inside mitochondrial cristae. • Weak infrared illumination at 71 and 87 terahertz increased ATP production by about 10% in cultured human cells, but the preprint has not been peer-reviewed and does not directly prove that mitochondria use a functional quantum state.

@haidut said: ... it may very well be helpful for cancer too. The reason to use B3 in this study was explained, in part, by its prior use for skin cancer prevention: "In a phase III randomized, placebo-controlled trial by Chen et al, [8] oral nicotinamide administered at 500 mg BD for 12 months was safe and effective in reducing the incidence of nonmelanoma skin cancer and actinic keratoses in individuals who were at high risk. " [8] Chen AC, Martin AJ, Choy B, et al. A phase 3 randomised trial of nicotinamide for skin-cancer chemoprevention. N Engl J Med 2015; 373(17):1618–1626. doi: https://doi.org/10.1056/NEJMoa1506197

@haidut Interesting find -- thankss! Yet another reason to keep the glucose uptake high and to avoid metabolic stess. From this paper's concluding passages [bold-facing is mine]: "These results also have implications for therapeutic strategies that manipulate cyst(e)ine availability. Intracellular cysteine became toxic at concentrations of approximately 1–1.5 mM (Extended Data Fig. 4l), substantially above its normal systemic abundance. In fasting human plasma, free cysteine and cystine are present at approximately 10 µM and 80 µM, respectively, with total cyst(e)ine reaching ~250 µM (refs. 31,32). Thus, the toxic threshold is unlikely to be reached through bulk plasma exposure but may be approached in cells with unusually high cyst(e)ine uptake or impaired cysteine disposal. One such example would be cancers with constitutive NRF2 activation that accumulate cysteine beyond biosynthetic demand through upregulation of SLC7A11, promoting the formation of cysteine-derived conjugates that may serve as a detoxification route [33]. Cysteine or NAC has also been reported to induce cell death in glioblastoma and other cellular contexts, particularly during metabolic stress¹¹,³⁴. Our study suggests that, when this buffering capacity is exceeded, or under conditions of metabolic stress such as glucose limitation, excess cysteine becomes deleterious. Conversely, cystine supplementation can enhance tissue regeneration and stem-cell function in some settings.³⁵. Such findings are therefore likely to depend on the capacity of the receiving cells to metabolize or safely dispose of the resulting cysteine. Cysteine damages the mitochondrial electron transport chain via iron–sulfur protein loss, leading to cells relying more on glycolysis for ATP production and trying to uptake more glucose (Extended Data Fig. 4b). This would explain why glucose starvation is synthetically lethal with high cyst(e)ine as exemplified by disulfidptosis, although this death cannot be rescued by iron chelation [10]. Although this process shares features with ferroptosis, it occurs despite elevated GSH and suppressed lipid peroxidation, defining a distinct form of mitochondrial iron-dependent cell death (Extended Data Fig. 4m). Together, these results position thiol imbalance as a central metabolic vulnerability and underscore the importance of both limiting cysteine accumulation and promoting its safe disposal to maintain cellular homeostasis. "

The functional difference between an isoprenoid motif and a bis-allylic motif comes down to double-bond spacing, C–H bond strength, and how effectively the molecule stabilizes free radicals. Structural Spacing The arrangement of double bonds determines whether a methylene carbon (CH2) is allylic or bis-allylic: Bis-Allylic Motif: A single methylene carbon is sandwiched directly between two double bonds (-CH=CH-CH2-CH=CH-). The double bonds are separated by one single bond on either side. Isoprenoid Motif: Isoprene repeating units (-CH2-C(CH3)=CH-CH2-) place double bonds farther apart (-CH=C(CH3)-CH2-CH2-CH=C(CH3)-). The double bonds are separated by an ethylene bridge of two single-bonded carbons. Chemical Comparison Feature Bis-Allylic Motif Isoprenoid (Allylic) Motif Chemical Structure -CH=CH-CH2-CH=CH- -CH=C(R)-CH2-CH2-CH=C(R)- Double-Bond Spacing Separated by 1 carbon Separated by 2 carbons C–H Bond Energy (BDE) ~ 75-80 kcal/mol (Extremely weak) ~ 85-90 kcal/mol (Moderately strong) Radical Resonance Pentadienyl radical (Delocalized across 5 carbons) Allylic radical (Delocalized across 3 carbons) Lipid Peroxidation Risk Very High (Primary initiator of chain reaction) Low (Resistant under biological conditions) Biological Examples PUFAs (Linoleic acid, EPA, DHA) Tocotrienols, Coenzyme Q10, Squalene Why Bis-Allylic Carbons Are Vulnerable When a radical attacks a bis-allylic carbon, it extracts a hydrogen atom to form a pentadienyl radical: R• + -CH=CH-CH2-CH=CH- -> R-H + [-CH...CH...CH...CH...CH-]• Because this radical is delocalized across five carbon atoms, the activation energy required to break the original C–H bond is low (~ 75-80 kcal/mol). This makes polyunsaturated fatty acids (PUFAs) susceptible to spontaneous lipid peroxidation in the presence of reactive oxygen species (ROS). Why Isoprenoid Carbons Resist Peroxidation In an isoprenoid tail (like that of tocotrienols), the two-carbon bridge (CH2-CH2) prevents pentadienyl resonance. Abstracting a hydrogen from either carbon produces a standard allylic radical: R• + -CH=C(R')-CH2-CH2- -> R-H + [-CH...C(R')...CH-]• + -CH2- Because the resulting radical is delocalized across only three carbon atoms, the C–H bond dissociation energy is significantly higher (~ 85-90 kcal/mol). Under physiological conditions, reactive oxygen species lack the thermodynamic drive to extract hydrogens from isoprenoid tails, leaving the tail intact while the molecule's chromanol head group quenches free radicals.

I managed to get the device before the price hike and with a bit of a discount. Now I use it daily. Still just for a few minutes at about 3% of CO₂. Noticed better sleep (remember dreams better and consistently get about 7 hours of sleep). Inhaling CO₂ also helped clear my migraine. (It was a mild, albeit annoying, case of migraine.) Here is an interesting paper on the CO₂ for migraines: STUDIES ON HEADACHE1. Effects of Carbon Dioxide—Oxygen Mixtures Given During Preheadache Phase of the Migraine Attack 2. Further Analysis of the Pain Mechanisms in Headache From the Summary and Conclusions section: A series of patients were given a 10 per cent carbon dioxide-90 per cent oxygen mixture by face mask during the preheadache or early headache phase. This mixture abolished the preheadache phenomena and aborted the headache in most of the trials. Ten per cent carbon dioxide in air was less effective, having a shorter and more transient effect.

I applied her protocol when I suddenly started to have cavities in my front teeth and thinning of enamel. This came after years of no cavities at all, probably decades. I did not change anything else in my daily routine. After just a month 2 of my small cavities had completely disappeared and I did not get any new ones.

@AnomPhen Thank you so much for your advice.I also think it's hypothyroidism, My mother was recently diagnosed with it and she's taking T4.

I was experimenting with various solid foods recently (I was eating mostly liquid or blended food until now) and it made me realize that I'm not digesting my food at all. My stool is indistinguishable from the food I eat. My stool is a lump of bits of food with absolutely no change in size, shape, texture or color, and very little change in smell (sorry for TMI). What goes in leaves my body almost unchanged, undigested.

I was experimenting with various solid foods recently (I was eating mostly liquid or blended food until now) and it made me realize that I'm not digesting my food at all. My stool is indistinguishable from the food I eat. My stool is a lump of bits of food with absolutely no change in size, shape, texture or color, and very little change in smell (sorry for TMI). What goes in leaves my body almost unchanged, undigested. That would explain the lack of weight gain I guess.

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@RandomUser I though the whole point of Haidut’s method was that the c02 accumulates and stays there after each use? So if you did it regularly you wouldn’t have to wait at all. I’ve been wanting to try it for a while now but I’ve been put off of it by having to breathe through the mouth, which I find gives me anxiety. I was wondering if anyone had experimented with adding an oxygen mask or altering the mouth of the jug to allow you to breathe through your nose instead.