When taken orally, plain riboflavin is one enzymatic step ahead of FMN, as FMN cannot be absorbed until after it has been degraded to plain riboflavin. (1-4) In order for FMN to reach our cells, it must first be converted to plain free riboflavin, which normally occurs in the intestine during absorption, but may not take place in various medical conditions. In this case, it cannot be absorbed well and instead, riboflavin-5-phosphate (FMN), which cannot be degraded to riboflavin, ends up in the toilet.

Forms of riboflavin

In our food, vitamin B2 is present as free riboflavin, FMN (ribofalvin-5-phosphate) and FAD (may also occur in supplements as free riboflavin or as the sodium salt of FMN). FMN and FAD must first be converted to plain (free) riboflavin before they can be absorbed. (1-4) To do this, we first need to hydrolyze the FMN/FAD bound to the protein, and then the FMN/FAD must also be hydrolyzed by various enzymes (alkaline phosphatases and pyrophosphatases) to release the free riboflavin. The problem is the same as I discussed in B1: Low levels of these enzymes are found in, among others, hypothyroidism, cardiovascular disease, (7) people taking contraceptives, (14) small bowel problems, persistently high cortisol levels, (15) zinc/magnesium deficiency (8-10, 12) and many other conditions. For people with these conditions, plain riboflavin overcomes this problem, while in healthy people both forms are equally good (except for the money wasted on FMN, which is more expensive but at best only as good as plain riboflavin). 

The good news is that the kinase that converts riboflavin to FMN (riboflavin-5-phosphate) does not appear to be genetically defective in anyone [4], so it is practically safe to say that anyone is able to convert plain riboflavin to FMN properly, if there is no zinc deficiency, which is required for the kinase enzyme to work. However, when riboflavin-5-phosphate (FMN) is supplemented, it is uncertain how useful it is in the aforementioned conditions with low levels of the enzyme alkaic phosphatase, and who knows how many other conditions with insufficient levels of other non-specific digestive enzymes, that would also play a role in converting FMN to riboflavin for absorption.

Absorption of vitamin B2 is excellent up to 30mg, but above that its transporters become saturated, so more than that cannot be absorbed, or can only be absorbed to a very limited extent.[4] As a result, it is hardly worth taking more than 20-30mg a day, at least at one time. Vitamin B2 is a very important vitamin, as in many cases it plays a more important role in the status of B6 and B9, among others, than they do. This is because we need vitamin B2 to convert B6 and B9 into their active forms.

As a point of interest, I provide a link to a short video by Christopher Masterjohn on B2 absorption. Maybe it's not new information, but it's nice to see that a well-known, sort of celebrity nutritionist has come to this realization more than 3 years ago (I don't necessarily recommend his other videos, but he's mostly pretty good and typically thorough – I suspect the same with vitamin K – he's due for some realization, I plan to look him up on this as soon as we have a quiet period...)

If not on the topic of vitamin K (I recommend my new paper on that), I can highly recommend Masterjohn on the topic of B2; he recently had a great insight that MTHFR gene mutation is likely to be problematic only if B2 deficiency is present. It seems to work well even in homozygotes, given adequate B2 supply. (In this sense, folic acid may be appropriate for anyone without a B2 deficiency. Of course, I would stick to methylfolate just to be on the safe side.