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There is preliminary data suggesting that methylcobalamin by itself can cause an increase in SAH, leading to incomplete reconstitution of the methionine cycle

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Moreover, microbial transplantation studies in germ-free mice with human commensals containing a functional (but not a deletion mutant) microbial cutC gene (responsible for cholineTMA transformation) (23) and genetic manipulation (both gain of function and loss of function) of host hepatic flavin monooxygenase 3 have been shown to modulate host TMAO levels, platelet responsiveness, and thrombosis potential in vivo (24)

Repeated injections in the same area can also lead to increased irritation over time