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.”
