Good questions. Yes, adenosine could join back with homocysteine and turn back into SAH, but SAH can not turn back into SAMe, so ultimately, SAH needs to break into homocysteine and adenosine to metabolize through the pathway.
Supporting the movement of the Methylation cycle through the use of methylfolate/B12 can lower SAH by helping it metabolize to homocysteine and adenosine (SAH is made of adenosine and homocysteine linked and it gets split by the SAHH enzyme).
I don't see how Methylfolate/B12 would lower adenosine. However, increasing methylation pathways in those who are deficient can help with serotonin, dopamine, epinephrine, and norepinephrine production, which can help with alertness and mood (this is likely why SAMe works for depression).
As far as ways to lower adenosine. After looking at the literature, I think Inosine balances out the action of adenosine more than inhibiting its production. In fact, Inosine inhibits the Adenosine Deaminase Enzyme, so taking too much of it, while balancing the action of adenosine, could also increase adenosine (
ref). Maybe that is why those of us experimenting with inosine feel like it both helps and harms us at the same time.
So back to lowering adenosine, the Self-Hacked posts give the following suggestions:
- Zinc is the only cofactor necessary for ADA activity, so adequate zinc is needed for the enzyme to work well [2].
- Estradiol is one of the few inducers of adenosine deaminase [13].
- IGF-1 is another inducer of adenosine deaminase [14].
- Simvastatin (and probably other statins) increases ADA production when it’s suppressed by IL-13 [15].
The other input pathway to adensoine is from AMP (via the 5-nucleotidase enzyme), which is something we haven't explored, maybe a project for tomorrow.
@Violeta noted earlier that Caffeine inhbits Phosphodiesterase and she found somewhere that boron does too.