@Chris2401 Of what I understand. They make a supposition. Ovarian removal operation (OVX) induces a lack of estrogen, like in age-old-years, pretending it induces a decline and a neurodegenerative process. They make a correlation: iron accumulates with time. Excess iron is creating ROS. Female rats have showed decreased dihydroorotate dehydrogenase (DHODH) expression when getting under OVX. However DHODH supports a vital role in neuronal ferroptosis. But E2 alleviates ferroptosis induced by erastin and ferric ammonium. So, if we try to link: a) OVX + neuro-decline + lack of estrogen b) Excess iron in menopause + lack of estrogen => If A induces B, and if C induces B, A should equal C. If excess iron induces ROS and lipid peroxidation, take the way back and get estrogen to cancel the decreased DHODH induced by ovarian removal operation (OVX). How does iron cause ferroptosis? Taken together, excess iron in both the cytosol and mitochondria significantly contributes to the development of ferroptosis in neurodegenerative diseases, and this occurs primarily through its promotion of oxidative stress and lipid peroxidation. Note1: One correlation seems to give an analogy but not an equivalence. Expressed differently, pharma tries to find positive effect to supplementing E2, event by arranging or inventing improvements. Note2: Estrogen is not directly linked to ROS. Iron is linked to ROS and ROS induce membrane peroxidation.

Here's a guy with some horse-sense when his dog is bitten by a cottonmouth. He blockaded the serotonin and adrenalin. https://www.youtube.com/shorts/O5WmPFSVVcg

@haidut it’s funny how most of the k2 studies youve posted recently are of mk7

My poll was voted on and I forgot to check: https://lowtoxinforum.com/threads/oxidized-cholesterol-vs-pufa.28333/ Which one is worse? Oxidized Cholesterol vs Polyunsaturated Fatty Acid Oxidized Cholesterol Votes: 2 Polyunsaturated Fatty Acid Votes: 7

@A-Former-User said in Restoration of the Biofield topic: @ThinPicking I'll try to explain: I posted the original post to this thread. I mentioned "biofield" and I also wrote about Dr. Robert Young. @yerrag responded that yes, the biofield is a real thing. @yerrag also said that Dr. Robert Young is not a credible source and listed reasons why. I responded to @yerrag and wrote a little about the biofield/aura/chi. I also wrote that I agree with @yerrag that Dr. Robert Young is not a good source and that I regret that I linked to his site. Note that I posted several times at the beginning of this thread and have provided multiple links to sources other than Dr. Robert Young in these posts. I could have and should have simply left Dr. Young out of the topic entirely for the sake of clarity. Dr. Robert Young makes some good points on his blog and in his videos. However your own discernment abilities must be activated when reading/watching him. Simply opening up the top of one's head and pouring Dr. Young's (or anyone else's) ideas in unabated can be hazardous to one's own well being. Discernment abilities can be thought of as "intuition" or "spidey senses" which ties back into qualities of an activated biofield and why it is important to have one. Ray has mentioned something similar to a biofield, although it is more about how health practitioners in the middle ages (I would associate the notable ones like Avicenna or Ibn Senna) approach healing in a way that isn't mechanistic. This aligns a lot with the thinking of Tom Cowan even, as he is influenced as much in his thinking by Rudolf Steiner. These names are outside the western approach to healing. Even in his book Mind and Tissue, which I only read halfway through, Ray talks as much about the 'active field' which is more compatible with the Eastern mind (Eastern as in Greek and Russian orthodoxy) which is less influenced by the materialistic philosophy of Descartes, which I gather puts forever into the Western educated mind a reductionistic approach to seeing things. And this is clear when you waddle in between hospitals and alternative healers, and find experts talking over each other because of the philosophical divide.

@haidut I suspect that 5-HT is high in babies because constipation/impaction of the gut would be life threatening for a baby. 5-HT keeps things moving along in the intestine; it increases/intensifies peristalsis. Serotonin Deficiency Is Associated With Delayed Gastric Emptying I suspect that the issue of serotonin (5-HT) getting through the intestinal wall and into the blood stream is the primary concern; so long as the 5-HT remains inside the intestine (along with the endotoxin) things should be fine. If the integrity of the intestinal wall is compromised and endotoxin and 5-HT are able to seep through into the blood stream major problems happen (sepsis, high serotonin symptoms). The health of the epithelial cells that line the intestine are important because if they fail, leaky gut happens. Thiamine is believed to be important for the epithelial cell function. See here: Dietary supplementation of thiamine enhances colonic integrity and modulates mucosal inflammation injury in goats challenged by lipopolysaccharide and low pH "The results show that dietary thiamine supplementation could improve the colon epithelial barrier function and alleviate mucosal inflammation injury in goats after lipopolysaccharide and low pH challenge." Another important body part that requires excellent epithelial cell function is the blood/brain barrier. Thiamine deficiency compromises the blood/brain barrier too. Thanks for all you do! I always appreciate your posts.

@haidut is leucomethylene blue safe to take? It is what is left over after turning ascorbic acid ----> dehydroascorbic acid with MB. You've said before the mixture can be left out after the LMB and DHAA are produced and the LMB will oxidize back to MB, yet I'm unsure if the DHAA degrades in the meantime. I've thought of bubbling air back into the solution to get it to go blue again. And then again, I have the suspicion that the redox state of MB/LMB is pretty much inconsequential as it cycles between the forms relatively rapidly once ingested. My urine still changes color wether I take MB by itself or LMB + DHAA. I like taking it during winter.

No thanks Lurking.

@SpicyPeater said in screenshot of T3 Uncoupled post RE Coffee testosterone: https://u.pcloud.link/publink/show?code=XZMyuc0ZdjYs4iDfpEBp7h6mvqwkxRQzJHKX Reductionist BS...aka Twitter.

@pannacottas No but Ive tried memantine, and I prefer to amantadine on every metric except the long half life (makes sleep impossble for me). Bromantane might be my saving grace though since its half life is not as much and I heard is more dopaminergic than either memantine or amantadine.

@calvinklein21101 said in Vitamin A may prevent/treat motor neuron diseases, including the lethal ALS: something going wrong in their metabolism I read Poisoning for Profits and my first inclination wasn't to start rattling on about my liver while chomping rice and beans all day. Something about it seems to ring with them.

@Serotoninskeptic The values above need to be revised. The doses of calcium needed in practice to complex with oxalate are higher than expected, and how calcium interacts with phosphate is relevant: "The degree of interference reported here (~166 mg phosphorus for every 500 mg ingested calcium—0.4 mmol phosphorus for every mmol calcium) is substantially less than might have been predicted from simple stoichiometry. A 1:1 molar ratio for CaHPO4 would predict binding of 388 mg phosphorus by 500 mg calcium and, for Ca3(PO4)2 at a Ca:P molar ratio of 1.5:1.0, 258 mg phosphorus would be bound per 500 mg calcium. A molar ratio of 1:1 seems more likely at digestate pH values below 7.0. Even at the upper end of the confidence interval for the regression model—210 mg (6.8 mmol)—binding would still be substantially less than the lowest stoichiometric prediction. This discrepancy may be partly due to rapid absorption of phosphorus in the duodenum well before calcium and phosphorus complexes can form in the chyme. In any event it undoubtedly reflects the complexity and multiplicity of the interactions within the digestive residue." (10.1080/07315724.2002.10719216) Compare them: Predicted: Ca 1:1 P Practical: Ca 2.5:1 P For oxalate: Predicted: Ca 1:1 Oxa Practical: Ca ?:1 Oxa If we treat the interaction with oxalate as that with phosphorus (2.5:1) and adjust for mass (2.5:2), we would need 125 mg of calcium for every 100 mg of soluble oxalate. One problem is guessing how much is soluble from the total oxalate content of a food. Based on the last two 'Cooked' columns (⇈), it's all over the place. Another problem is the additional confounders. Member 'blabla' posted this elsewhere: [image: 1727908046169-cab6428c-10ca-4047-a0e4-08d21350c5b1-image.png] ⠀(10.1097/01.asn.0000127864.26968.7f) Up to 800 mg: dietary calcium alone More than 800 mg: dietary calcium and supplements (400 mg and 1000 mg) Only the supplements were dosed with the labeled oxalate, suggesting that indirect interference is possible, but notice the degree of variations at low intakes. If you must supplement, it's preferable to dose in the same meal: [image: 1727908061457-edacf8d3-917e-41a6-b44f-6a24525a3abb-image.png] ⠀(10.4065/79.1.91) But when the diet contains enough calcium (1000 mg), adding more seems unnecessary because a further reduction is minimal.

@thyroidchor27 P5P can help to reduce homocysteine.

@mikeyd So if you can’t tolerate wheat and have SIBO, what foods would you recommend? I too, have issues with many fruits. I try to peel the skin off of most fruits before I eat them. I think this helps but I still feel inflamed. I skin dates, peaches etc. I can’t eat apples or pears at all. Please help, like you I’ve had it probably for 10 years but only heard of term SIBO this year.

Elevated fructose in the brain is a sequester to protect it because of AD. Much like the protein plaques, which have been erroneously blamed as a result of AD.

The rationale was: carbon dioxide goes through cells' lipids and releases a proton inside once hydrated. Then, let's find another compound that's also not barred by lipids and releases even more protons. This led to 2,6-DHBA. It overlooks that the very property that makes the selected compound a greater acidifier is also what makes it extraordinarily prone to deprotonate prematurely. The ability to pass through lipids is likely to be compromised with the early proton release. If it could be injected into the tumor, it would still be uncertain if it could be taken up by target cells. Healthy Cancerous Extracellular pH 7.4 ↓6.5 Intracellular pH 7.1 ↑7.5 For direct internal acidification, it would be more fitting to seek weak rather than strong acids, those that can take advantage of the bump in transitioning from the extracellular to intracellular compartment (6.57.5) to deprotonate the molecule where intended.

Relevant for many and thank you as always. This info will be passed on.

Also, if b.i. progesterone actually maintained or reduced the size of a meningioma.