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Thats what the Harvard study found, too: High intake of vitamin B12 alone was not associated with increased fracture risk

At the N-terminus, the Tyr1 of Tirzepatide makes Van der Waals contact with the receptor residues, the Glu3 forms an ionic bond with Arg183 and a network of hydrogen bonds with Tyr145 and Ser381 of the receptor

Although we performed multivariate adjustments, residual confounding may persist due to unmeasured factors such as dietary habits (e.g., irregular intake of animal-derived foods or B12-fortified products), unrecorded use of nutritional supplements, and genetic predispositionsparticularly MTHFR polymorphisms, which are known to influence homocysteine metabolism and folate cycling, thereby potentially altering the functional demand for vitamin B12

Simply because the ingredients used in these treatments are derived from natural sources, which means they have a significantly lower risk of unintended side-effects