Vitamin B1 (thiamine) supplementation prevents/treats osteoarthritis (OA)
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Actual conclusion of the study itself and a very strong claim, considering medicine considered OA to be incurable and progressive. While the study claims that reduced inflammation is the main mechanism of action of vitamin B1 supplementation, I think the much more likely explanation is the simple fact that B1 is a crucial factor for the oxidative metabolism of glucose and the generation of CO2. In fact, vitamin B1 is often given clinically as a supplementat to lower lactate and raise CO2. While medicine considers CO2 as little more than “metabolic waste”, a well-known fact is that the deposition of calcium into the bones depends on the carboxylation (i.e. using CO2) of various bone building proteins such as osteocalcin. Thus, elevated CO2 levels directly result in denses, bigger, stronger bones while lower CO2 levels (which means higher lactate) result in bone resorption, and elevated serum calcium and excretion. Thus, in the context of elevating CO2 the effects of vitamin B1 make perfect sense, and in fact can be further increased by adding niacinamide and biotin, both of which have also been shown to lower lactate and raise CO2 levels. Btw, this CO2-raising, synergistic effect of B1, B3, and B7 (biotin) is one of the main reasons I chose those vitamins for the cancer studies I am currently running.
https://pubmed.ncbi.nlm.nih.gov/39024114/
“…As the primary cause for chronic pain and disability in elderly individuals, osteoarthritis (OA) is one of the fastest-growing diseases due to the aging world population. To date, the impact of microenvironmental changes on the pathogenesis of OA remains poorly understood, greatly hindering the development of effective therapeutic approaches against OA. In this study, we profiled the differential metabolites in the synovial fluid from OA patients and identified the downregulation of vitamin B1 (VB1) as a metabolic feature in the OA microenvironment. In a murine destabilization of medial meniscus-induced OA model, supplementation of VB1 significantly mitigated the symptoms of OA. Cytokine array analysis revealed that VB1 treatment remarkably reduced the production of a pro-OA factor-C-C Motif Chemokine Ligand 2 (CCL2), in macrophages. Further evidence demonstrated that exogenous CCL2 counteracted the anti-OA function of VB1. Hence, our study unveils a unique biological function of VB1 and provides promising clues for the diet-based treatment of OA.”
“…Additionally, Fursultiamine, a VB1 derivative, was found to improve the therapeutic effect of glucosamine hydrochloride plus chondroitin sulfate in OA (11). In this study, we systemically profiled the metabolic changes in the OA microenvironment and identified VB1 as one of the most dramatically changed metabolites. The anti-OA function of VB1 is at least partially attributed to its capacity to suppress CCL2 expression. Compared to other chemokines, CCL2 plays a particularly crucial role in OA progression. OA patients exhibited increased CCL2 production in the synovial fluid compared to healthy controls (12). Mechanistically, CCL2 may exacerbate OA by mediating the recruitment of peripheral monocytes (13), inducing the expression of MMPs and VCAM-1 (12, 14), increasing the activity of collagenase (15), or promoting cartilage damage (16) or facilitating the production of inflammatory cytokines (17). As a natural and water-soluble vitamin, VB1 has relatively higher safety and lower costs compared to traditional anti-OA drugs, potentially enhancing patient compliance. Thus, increasing the intake of VB1-rich food (such as whole grains, beans, nuts, and fish) is a potentially beneficial dietary approach in OA patients. Taken together, in this study, we identified a safe, natural nutrient (VB1) that prevents the pathological processes of OA, thereby providing unique perspectives on dietary interventions for OA.”
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@haidut What was the HED for Vitamin B1 in this study?
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@haidut said in Vitamin B1 (thiamine) supplementation prevents/treats osteoarthritis (OA):
B1 is a crucial factor for the oxidative metabolism of glucose and the generation of CO2.
Apart from seeing my lactate levels under controls (cramps) with 100 mg thiamin HCL (3x/d),
Mostlylurking has seen side effects when taking high dose Thiamin (B1) without supplementing riboflavin (B2). Not necessarily every day.Marked temporary increase of riboflavin excretion was not observed by all subjects (period not above 8 days).
Does thiamine deplete riboflavin?
Klopp, Abels, and Rhoads found a transitory increase in riboflavin excretion in men treated with large doses of thiamine. Pro- longed administration of thiamine, however, failed to produce any clinical evidence of riboflavin deficiency.
Source: ScienceDirect.com
https://price-pottenger.org/pdfs/LF009_2.pdf (See & “Effect of Overloading with B”). -
Just my simplified take on arthritis, as more and more I am swayed to think that there is only arthritis, and that arthritis is caused by low metabolism, and very much so because CO2 deficiency from low mitochondrial metabolism makes the ecf acidic, enough so that some salts, urate salts being one, precipitate, and cause the formation of crystals that cause wear and tear on our joints.
I profess ignorance though, on the matter of the different forms of arthritis, as when I attempt to understand the different forms of arthritis, the explanations given in the literature always lead to draw blanks, which makes me either an embecile thet fails to comprehend or simply that the literature is just playing on words and terms that give different names to a banana. The added complexity is a ploy to distract from the one true cause of arthritis, if I may dare say so.
Which is why Ray points to hypothyroid as the cause of arthritis, which I first thought of as a rather simplistic explanation. But if I can relate to cause and effect, and dig deeper into it, it is not as complicated as it appears to be.
The key is acid base balance. As simple as that. When we have an abundance of CO2 because our body makes a lot of it at our disposal, we have the best pH buffer available for our lungs and kidneys to manage acid base balance. When alkaline, it can turn into an acid called carbonic acid, and when acidic, CO2 can turn into bicarbonate. This is based on Le Chatelier's principle, where the direction of a reaction is in the direction of the stress that it relieves.
What better way to provide a surfeit of CO2 in our body than to be producing energy using mitochondrial oxidation. Vitamin B1 is a crucial link in a chain of nutrients and substances and processes that enable mitochondrial oxidation. Simply being deficient in one link makes rhe chain broken, and a broken chain only leads to low metabolism, and the resulting imbalance in pH, usually acidic, will just cause the formation of salt crystals that irritate and inflame and destroy tissues.
I know enough how to monitor my acid base balance, so I know what remedial actions to take to keep my acid base balance from being chronically in an imbalanced state. Many bad things happen in a chronic state of acid base imbalance.
I have high uric acid, yet I don't have any arthritis, much less gout. Only because my optimal acid base balance keeps uric acid crystals from forming.
I don't have tachycardia (high heart rate) because my heart muscle pumps well and isn't strained because the muscle contracts and relaxes effortlessly because of good acid base balance.
I don't fear cancer because I believe that an acidic ecf is what causes regulatory and harmless and commensal microbes to turn into virulent parasites that cause cancer to develop.
Yes, vitamin B1 is important, but such studies are subordinate to putting all the pieces of rhe puzzle together to form a whole picture. This is where we need work on, as without this perspective one can end up taking one supplement after another and not progressing from his poor state of health.
