@war4512 "Low X/A ratio for the European doesn’t mean more genetic distance from Africans or bonobos." there's articles about this and a response from the paper authors after it was posted on stormfront.

Nobiletin for fatty liver: Helps with fatty liver and fibrosis via increasing adiponectin and SOD while lowering MDA https://pubmed.ncbi.nlm.nih.gov/38073108/ Helps via modulating Nrf2 https://pubmed.ncbi.nlm.nih.gov/38073108/ Helps via altering the gut microbiome https://pubmed.ncbi.nlm.nih.gov/37139957/ Helps via lowering oxidative stress and lipid peroxidation and increasing ATP. https://pubmed.ncbi.nlm.nih.gov/34695558/ Helps via increasing cholesterol to bile acids conversion ( increasing CYP7A1, and CYP27A1), increasing SCD1 and LXRa and lowering FAS. So should be good for people with high cholesterol ,low bile production/flow. https://pubmed.ncbi.nlm.nih.gov/36985541/

Why not make an impartial compilation of experiments on cancer and group them according to the effect of extra glucose (without additional factors) on cancer cells: supporting versus hindering proliferation? We can't go by the majority, but it's a starting place to question. The line of thought would not be far from the idea that more glutamine should be delivered to cancer cells because they overconsume it to the point of depletion. Deficiencies can promote a more aggressive behavior, but it's not that we need the encouragement to load up on glutamine to compensate. Regional Glutamine Deficiency in Tumours Promotes De-differentiation through Inhibition of Histone Demethylation A condition of generalized scarcity is common, and this would call for the replenishment of many compounds. For example, immune cells can also compete with cancer cells for glucose, but also glutamine and other nutrients that may be rapidly used up. Gerson's approach consisted of a moderate caloric intake, better distributed in smaller and more frequent meals, which leans in favor of a controlled exposure. If I was against dietary toxins, I wouldn't mention him often because the original therapy asked for minimal fats. Sometimes tumors have a person attached to them, and the person must be fed on occasion. Looking for potential downsides helps to identify and counteract them, but also avoids cults*. In case anyone knows superior dietary therapies to that of Gerson, I wouldn't mind relegating it, no matter how unconventional. *Reflected on a thread such as our "Can glucose loading cure everything?" It would be good to know how relevant fructose-1-phosphate would be on tissues that don't express ketohexokinase or glucokinase (a variant of hexokinase). Also, how high uric acid levels have to be to affect aconitase. But it makes more sense to seek local nutrient repletion when you can target the misbehavior or exploit it. In the previous experiment, they first manipulated Hypoxia-inducible Factor (HIF) to lift some of the metabolic inhibitions and only then pound glucose with insulin, intending to provoke oxidative stress. Otherwise, the effect was insignificant. It's not difficult to picture glucose lessening the oxidative burst from vitamin C therapy when not much else is done to manipulate the fermentation pattern. NADPH homeostasis in cancer: functions, mechanisms and therapeutic implications [image: 1733183560593-3d3cb85c-f336-4445-96cf-f87243fd64f8-image.png] NADPH-producing enzyme Origin of main substrate G6PDH Glucose PGDH Glucose ME Glutamine, glucose IDH Glutamine MTHFDH Glucose ALDH Glucose GDH Glutamine NNT Glutamine, fatty acids, glucose Glucose may also spare glutamine in antioxidation. By the great Matthew Vander Heiden and Sophia Lunt: Aerobic Glycolysis: Meeting the Metabolic Requirements of Cell Proliferation [image: 1733183823555-2b5e1401-54ee-435e-8890-af3d87f7344e-image.png] All of the carbons that occur in nucleotides can conceivably come from glucose. It's absurd. Carbon source Derivation Carbons donated Ribose Glucose →→ ribose 5 Aspartate Glucose →→ pyruvate → oxaloacetate → malate → asp 3 Formyl-THF Glucose →→ serine →→ formyl 2 Glycine Glucose →→ serine → glycine 2 Hydrocarbonate Glucose →→ carbon dioxide → hydrocarbonate 1 Methylene-THF Glucose →→ serine →→ methylene 1 Cancer Cells Tune the Signaling Pathways to Empower de Novo Synthesis of Nucleotides [image: 1733183911508-1f4542ae-d2c5-43e4-a791-3056033c728d-image.png] It's also evident that the base of phospholipids and triglycerides can be derived from glucose in the form of glycerol. Ceramide needs serine, which can come from glucose as well. In addition, serine accepts the sulfur from homocysteine to yield cysteine, and then glutathione. Expanding on the fates of glucose, pyruvate kinase (PK) is the last enzyme of glycolysis, responsible for the following simplified reaction: Phosphoenol-pyruvate (PEP) + ADP –(PK)→ pyruvate + ATP PK has 4 variants: Pyruvate Kinase M2 and Cancer: The Role of PKM2 in Promoting Tumorigenesis [image: 1733184025045-f7b87222-6593-4a89-b935-fe72fb1efbab-image.png] The PK-M2 prevails in tumor cells and can occur as a dimer or as a tetramer: [image: 1733184057517-472de7e3-36b0-4f8a-8f7e-a4a9984f6b79-image.png] PK-M2 dimer is hypoactive → Less pyruvate and ATP But the lower rate of conversion creates a metabolite congestion that spills over to the branches of glycolysis → More biosynthesis and antioxidation ⠀ PK-M2 tetramer is hyperactive → More pyruvate and ATP They differ in low and high affinity for the substrate PEP and give (tumor) cells more flexibility to rely on either state depending on needs for biosynthesis or energy. Excess ATP inhibits multiple metabolic steps and can be counterproductive. Oxidative stress inhibits the enzyme, which is a convenient way to recreate the hypoactive situation above. Inhibition of Pyruvate Kinase M2 by Reactive Oxygen Species Contributes to Cellular Antioxidant Responses Expressing PK-M2 is an advantage, not a requisite. No evidence for a shift in pyruvate kinase PKM1 to PKM2 expression during tumorigenesis M2 isoform of pyruvate kinase is dispensable for tumor maintenance and growth The cell can adopt different strategies in diverting glucose from glycolysis: Glucose 6-P Dehydrogenase—An Antioxidant Enzyme with Regulatory Functions in Skeletal Muscle during Exercise [image: 1733184525448-d7b70fa2-a7a1-4bdd-b986-8651c9ecf9a7-image.png] Modes 1 and 2 result in sudden loss of carbons as ribose for nucleotides, without or with decrapoxylation. Mode 3 represents a cycle for continuous production of NADPH until complete decrapoxylation. It may be an overlooked source of carbon dioxide. Note that it bypasses a reaction that's treated as irreversible (F6P ↶ F1,6P). Only mode 4 yields pyruvate with the net gain of regenerated ATP. Rather than serving to normalize the redox state of cancer cells, glucose metabolism can easily go from redox neutral in straightforward fermentation to reductive in case of diversion with return. If we arrive on pyruvate [3C]: The metabolic fates of pyruvate in normal and neoplastic cells [image: 1733184596221-f3c7d2e9-5cc9-491e-9da9-e5fb86a31029-image.png] Enzyme Reaction description Main changes Km [low value: high affinity] 'PDC' Oxidation to acetyl(CoA) [2C] –2H –CO₂ 0.02 mM (0.005-0.043 mM) LDH Reduction to lactate [3C] +2H 0.1 mM (0.034-0.630 mM) PC Crapoxylation to oxaloacetate [4C]* +HCO₃⁻ (+ATP) 0.265 mM (0.23-0.30 mM) ME Crapoxylation to malate [4C] +2H +HCO₃⁻ 0.75 mM (GPT or) ALT Amination to alanine [3C] +NH₄ 2.8 mM (0.07-12.50 mM) N/A Oxidation to acetate [2C] ? +H₂O₂ Each has cytosolic and mitochondrial forms, with the exception of PDC. Pyruvate import (and not just its oxidation) may be impaired, and pyruvate is formed in amounts that are only comfortably processed by LDH. Glutamate can be oxidized (through GDH) or transaminate to produce ketoglutarate. Pyruvate (through ALT (⇈)) can accept the amino group of glutamate to become alanine and yield ketoglutarate. So, pyruvate offers an alternative way to metabolize glutamate. Lactate is known to be elevated in cancer, but we now know that alanine is somewhat elevated too. I'm aware of the ethyl-pyruvate experiments, but the picture is more complicated than apparent, in special for pyruvate derived from glucose. Exogenous pyruvate facilitates cancer cell adaptation to hypoxia by serving as an oxygen surrogate Conversely (and beyond acidification): Lactic acidosis switches cancer cells from aerobic glycolysis back to dominant oxidative phosphorylation But to get to this condition naturally, you'd need disturbing levels and the associated concerns to achieve it. I have to stress that this is not vilify dextructose or levilose, but to put things into perspective. If we are extra cautious with folate to the point of discouraging its use preventively (!), we can't brush these aspects off, including the fact that glucose is a major carbon donor that keeps the folate cycle running, with glycolysis and its branches being overactive in cancer. And if we have antifolates as cancer therapies, folate should be present in enough quantities to matter as a carrier.

@Ena - I do not believe that you can determine if a post is automatically posted just by looking at it here on the forum. Haidut posts at http://haidut.me/ and the content is automatically copied on this site. This particular post is at http://haidut.me/?p=2714 There are no comments there. From reading his post, it indicates that it is also posted at twitter, facebook and linkedin. If you post a reply here, Haidut may not answer but others will. It takes a critical mass of users and their comments to keep this forum lively.

This is the interview with Ray where he really goes into what he knows about William F Koch’s work. https://youtu.be/9NJgekVDbZo

I find this a classic example of misinterpretation of scientific studies. And there are way too many to discuss each one of those in their wrong conclusions. D3 metabolism in rodents is known to be crucially different from D3 metabolism in humans. It's beyond poor science to even directly convert these rodent findings to human equivalent doses. This just feels like science-spam. The findings themselves and the priorly known implications of hypothyroidism may be valid. The conclusions (and motives for funding such studies) with regard to "vitamin D prevents it" are not.

Histological and biochemical study of the superficial abdominal fascia and its implication in obesity Abstract The advancement of liposculpturing and fascial flaps in reconstructive surgery has renewed interest in the superficial fascia of abdomen. Its histological and biochemical composition may play a vital role in maintaining strength and elasticity of the fascia. Hence, study of abdominal fascia for the elastic, collagen, and hydroxyproline contents is desirable to understand asymmetrical bulges and skin folds and in improving surgical treatment of obesity. Samples of superficial fascia were collected from of upper and lower abdomen from 21 fresh cadavers (15 males and 6 females). Samples were stained using Verhoeff–Van Gieson stain. Digital images of superficial fascia were analyzed using TissueQuant software. The samples were also subjected to hydroxyproline estimation. The superficial fascia was formed by loosely packed collagen fibers mixed with abundant elastic fibers and adipose tissue. Elastic contents and collagen contents of superficial fascia were significantly more in the upper abdomen than that in the lower abdomen in males. Hydroxyproline content of superficial fascia of upper abdomen was significantly more than that of lower abdomen in both males and females. The elastic, collagen and hydroxyproline contents of superficial fascia of upper abdomen were higher compared to the lower abdomen. This may be a reason for asymmetric bulging over abdomen and more sagging fold of skin in the lower abdomen than in the upper abdomen. This study may therefore be helpful in finding new ways to manage obesity and other body contour deformities. https://pmc.ncbi.nlm.nih.gov/articles/PMC5052227/ Muscle Pain: It May Actually Be Your Fascia Ways to Relieve Fascia Pain There are various strategies that work to loosen up painful knots, such as: Heat therapy: Apply a heating pad to the affected area or take a warm shower or bath. Yoga therapy: See a highly trained yoga therapist to get a regimen of yoga poses targeted to treat your area of pain. (Yoga therapy works in the same manner as physical therapy — the therapist creates a routine and you practice it at home between visits.) Foam rolling: Try a foam roller, a cylinder of hard foam that you roll your body over to release tension. It’s a form of self-massage. You can also do this with a lacrosse ball. Massage therapy: Schedule multiple therapeutic massage sessions with an experienced therapist who can find and apply pressure to release knots. Acupuncture: The insertion of acupuncture needles into trigger points can cause tense tissue fibers to relax. https://www.hopkinsmedicine.org/health/wellness-and-prevention/muscle-pain-it-may-actually-be-your-fascia Yoga Poses for Myofascial Release | 5 Poses to Try https://www.acefitness.org/resources/everyone/blog/5667/yoga-poses-for-myofascial-release-5-poses-to-try/

@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.