Rationale of the use of Archaeato deplete TMA in the intestine / pTMAO in plasma
How to correct this?
There are various (hypothetical) targets to avoid either TMAO in plasma / intestine in TMA. Most of them are either very complex to develop, unrealistic or dangerous. For example, N-methyl coumponds supplied by the diet are needed for the correct physiolog and their deficiency would lead to severe consequences. Also, antibiotics use could be year efficient way to avoid bacteria / N-methyl compounds converting bacteria in the gut, but the consequences of a long-term therapy by antibiotics would be also very dangerous. Also, acting on the (human) disrupted FMO3 enzyme activity would avoid TMAO in plasma, but would lead to TMA in blood / body fluids, like Trimethylaminuria patients, which is not again.