@Insomniac I wasn't clear... Do you agree with his conclusions about proper nutrition and excellent health?

@haidut Yeah. I ask about Georgi a few hours ago, and BOOM. He posts!

@Lejeboca - thank you for taking the time to respond. I got things twisted around in my mind and it is embarrassing. I think of the relationship between the eNOS and iNOS isoforms of nitric oxide synthase as being analogous to Dr. Jekyll and Mr. Hyde. The "i" in iNOS is related to inflammation, ischemia and intoxication all of which are generally bad. Whereas the "e" is related to the endothelium and is very healthy to have on board. Caldwell Esselstyn had his cardiac patients eat greens all day to maintain high levels of eNOS as part of his successful plan to reverse heart disease. In 1998, the Noble Prize in Medicine was awarded to 3 people for their work on NO (see press release). This encouraged people to supplement with L-arginine to lower their blood pressure. The excessive iNOS from the supplementation had long term consequences that were not good. Incidentally, aspirin releases eNOS. Aspirin induces nitric oxide release from vascular endothelium: a novel mechanism of action (2009)

The role of melatonin in bone regeneration: A review of involved signaling pathways Abstract Increasing bone resorption followed by decreasing bone mineralization are hallmarks of bone degeneration, which mostly occurs in the elderly population and post-menopausal women. The use of mesenchymal stem cells (MSCs) has raised many promises in the field of bone regeneration due to their high osteoblastic differentiation capacity and easy availability from abundant sources. A variety of compounds, including growth factors, cytokines, and other internal factors, have been combined with MSCs to increase their osteoblastic differentiation capacity. One of these factors is melatonin, whose possible regulatory role in bone metabolism and formation has recently been suggested by many studies. Melatonin also is a potential signaling molecule and can affect many of the signaling pathways involved in MSCs osteoblastic differentiation, such as activation of PI3K/AKT, BMP/Smad, MAPK, NFkB, Nrf2/HO-1, Wnt, SIRT/SOD, PERK/ATF4. Furthermore, melatonin in combination with other components such as strontium, vitamin D3, and vitamin K2 has a synergistic effect on bone microstructure and improves bone mineral density (BMD). In this review article, we aim to summarize the regulatory mechanisms of melatonin in osteoblastic differentiation of MSCs and underling involved signaling pathways as well as the clinical potential of using melatonin in bone degenerative disorders. https://www.sciencedirect.com/science/article/abs/pii/S0300908422002127 Melatonin-micronutrients Osteopenia Treatment Study (MOTS): a translational study assessing melatonin, strontium (citrate), vitamin D3 and vitamin K2 (MK7) on bone density, bone marker turnover and health related quality of life in postmenopausal osteopenic women following a one-year double-blind RCT and on osteoblast-osteoclast co-cultures https://pubmed.ncbi.nlm.nih.gov/28130552/

tea is very high in fluoride. The more expensive teas are harvested from young shoots, which are much lower in fluoride due to less time growing to accumulate it. But that is the issue, the cheaper assam teas can have 2mg per cup.

@Lejeboca - I did not know that one could search Sci-Hub by ISBN. Thanks.

Pantethine Because of pantothenic acid’s role in triglyceride synthesis and lipoprotein metabolism, experts have hypothesized that pantothenic acid supplementation might reduce lipid levels in patients with hyperlipidemia [19]. Several clinical trials have shown that the form of pantothenic acid known as pantethine reduces lipid levels when taken in large amounts [20], but pantothenic acid itself does not appear to have the same effects [1]. A 2005 review included 28 small clinical trials (average sample size of 22 participants) that examined the effect of pantethine supplements (median daily dose of 900 mg for an average of 12.7 weeks) on serum lipid levels in a total of 646 adults with hyperlipidemia [20]. On average, the supplements were associated with triglyceride declines of 14.2% at 1 month and 32.9% at 4 months. The corresponding declines in total cholesterol were 8.7% and 15.1%, and for low-density lipoprotein (LDL) cholesterol were 10.4% and 20.1%. The corresponding increases in high-density lipoprotein (HDL) cholesterol were 6.1% and 8.4%. A few additional clinical trials have assessed pantethine’s effects on lipid levels since the publication of the 2005 review. A double-blind trial in China randomly assigned 216 adults with hypertriglyceridemia (204–576 mg/dl) to supplementation with 400 U/day CoA or 600 mg/day pantethine [21]. All participants also received dietary counseling. Triglyceride levels dropped by a significant 16.5% with pantethine compared with baseline after 8 weeks. Concentrations of total cholesterol and non-HDL cholesterol also declined modestly but significantly from baseline. However, these declines might have been due, at least in part, to the dietary counseling that the participants received. Two randomized, blinded, placebo-controlled studies by the same research group in a total of 152 adults with low to moderate cardiovascular disease risk found that 600 mg/day pantethine for 8 weeks followed by 900 mg/day for 8 weeks plus a therapeutic lifestyle change diet resulted in small but significant reductions in total cholesterol, LDL cholesterol, and non-HDL cholesterol compared with placebo after 16 weeks [19,22]. Increasing the amount of pantethine from 600 to 900 mg/day did not increase the magnitude of reduction in the lipid measures. Additional studies are needed to determine whether pantethine supplementation has a beneficial effect on hyperlipidemia independently of, and together with, eating a heart-healthy diet. Research is also needed to determine the mechanisms of pantethine’s effects on lipid levels. https://ods.od.nih.gov/factsheets/PantothenicAcid-HealthProfessional/#h9

@Mauritio said in Glycine is an anti-biotic, restores sensitivity to antibiotics: In light of this thread, the findings of this old thread by haidut are even more interesting. https://lowtoxinforum.com/threads/gut-bacteria-overgrowth-drives-cocaine-addiction-glycine-can-reverse-it.48285/ I'm puzzled. How can glycine be helpful if it feeds the bacteria? Aren't we supposed to deprive the bacteria of its food source to have an antibiotic effect such that the bacteria would just not be able to multiply and become a thriving colony by being deprived of its food source? How is providing more gelatin going to help?

@yerrag Yes, although this study shows rapamycin has thymus weight lowering effect in mice. Although there was clearly a dose dependant effect and the HEDs were like 15-60mg per day which is really high, so I'm not sure if there would be any such effect if you were to take just 1-5mg / week . So the weekly dose of this study was about 30-100 times higher than what most humans take. https://pmc.ncbi.nlm.nih.gov/articles/PMC9360838/

@sneedful said in vitamin k2 mk4 levels elevated in covid patients, k2 mk7 and k1 depleted: is it because k2 mk7 and k1 are being rapidly converted into k2 mk4 which is then detected at high levels in blood? No, I don't think so. K2 MK7 is preferably used for clotting problems. More soluble and also "reactive". Reactive to ox-agression. But mind the peremption of K2 MK7: very fragile (3 months) if not well encapsulated and protected by e.g. rosmarinus. Source: Chris Masterjohn There is reason to think MK-7 would be better at supporting blood clotting. “MK-7 is not just three times better than K1 at reaching bone; it’s also five times better at supporting blood clotting (Schurgers, 2007). This may be because the greater fat-solubility of MK-7 makes it hold on more tightly to the membranes within liver cells, making it stay active in the liver much longer rather than being released and broken down (Shearer, 2008). The liver is where clotting proteins are made, so more extended activity in the liver would explain why MK-7 could better support blood clotting. If this is correct, other long-chain MKs such as MK-8 and MK-9 probably share this property as well.” https://chrismasterjohnphd.com/blog/2016/12/09/the-ultimate-vitamin-k2-resource/ It's advised not to take vitamin E at the same time as vitamin K when taking high dose. Since I take 1 mg (1 000) K2 MK4 at breakfast, I never take vit E at the same time. 2x/wk for 400 UI mix toco.

Where do ppl buy it from?

@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.