Bile acid has more than one way of being absorbed, which includes passive forms of absorption when it is not bound to certain amino acids (e.g. glycine, taurine). (L. Reuteri is known to deal with taurine and bile acids.) Bile acid tends to be absorbed in the terminal ileum and that almost all of it is absorbed per day. This suggests that its absorption rate is very efficient. So, for its absorption to be hindered implies significant intervention. Arguably, to the point where you should probably consider other causes for any gut disorders before entertaining the microbiome in regards to BAM.
The first part of this is all true... there are multiple transporters, several of which have very broad specificity. There are two things that determine which transporter(s) are likely to be used, or whether the uptake is even passive, without a transporter at all:
1) Whether the bile acid is conjugated, e.g. to taurine or glycine. A number of gut microbes express bile acid DEconjugating enzymes, and other species conjugate new amino acids to the deconjugated bile acids that the host doesn't conjugate with.
2) The hydroxylation of the steroid nucleus itself, which is the determinant of it being a "primary" or "secondary" bile acid. Many species of gut microbes convert primary BAs, with more hydroxyl groups, to secondary BAs, with fewer, however few if any do the reverse. Of the transporter data I saw, there isn't a clear preference for primary over secondary or vice versa. Even within primary or secondary, the BAs differ in how high an affinity they have, about as much as between primary and secondary. However, secondary BAs are known to be more hydrophobic and "harsher" (in the detergent sense) than primary, so I suspect that more than affecting transport per se, the microbial balance influences the proportion of the total bile acids that are symptom-provoking. A slight to moderate slowdown in transport might not be a big deal if the BAs left behind in the gut are "milder" ones, whereas it may be a major issue if they're strongly irritant BAs.
Also worth mentioning here... if people are concluding that they have a bile acid problem
solely because they get temporarily better on bile acid sequestrants like cholestyramine, this may not necessarily be the case. Cholestyramine also binds protein toxins produced by some microbes, most notably C. difficile. When I had C. diff I was given cholestyramine and it made symptoms better while on it, though of course it didn't clear the infection and I still needed a FMT. When not having C. diff it didn't make a difference.
