Posted by undopaminergic on May 4, 2008, at 21:36:34
In reply to Re: A few Cyprenil (liquid selegiline citrate) ?s, posted by Alucard on May 4, 2008, at 15:16:10
> just make sure to always take them with a meal that's got a decent amount of fat in it because that increases bioavailability by a factor of 3 - 4 times, a huge difference for getting your money's worth.
>That does increase the bioavailability of selegiline itself, but it has the opposite effect as far as the metabolites are concerned. The reason why some people find ingestion to be more effective than sublingual absorption may be the metabolism of selegiline to L-methamphetamine and L-amphetamine in the liver. With regard to neuroprotection, the formation of desmethylselegiline is also of relevance.
I would be very interested in learning about comparative experiences with selegiline and the other selective MAO-B inhibitor, rasagiline, which does not give rise to amphetamine metabolites - this would help clarify the relative roles of the different chemical entities.
> For motivational/antidepressant purposes (the same reason I'm taking the stuff) you might want to take some phenylalanine or tyrosine (NOT tyramine) with it, or maybe a Mucuna pruriens extract. That's just educated speculation on my part, however, and a big thing to keep in mind on this forum seems to be: "Your mileage may vary".
>
> Related questions: Anybody have personal experience with L-phenylalanine vs. the racemic DL form (DLPA)? I've read the opinions of many people who swear that only the L form by itself works, but just as many who swear that DLPA is far more effective for our purposes. And what about skipping the phenylalanine and going straight to the L-tyrosine? Or both? Thoughts anyone?
>The reason for using L- or D,L-phenylalanine rather than tyrosine or L-dopa (including Mucuna pruriens) is that it serves as a precursor to phenylethylamine (PEA). PEA is the preferred substrate of MAO-B, which selegiline inhibits, and is similar to amphetamine in its pharmacological actions: it releases dopamine (DA) and noradrenaline (NA) from storage vesicles into the cytoplasm, and reverses the direction of the DA and NA transporters, resulting in the massive efflux of the neurotransmitters into the synaptic cleft. Unless one has advanced Parkinson's disease, the effect of PEA on synaptic DA concentrations is far more substantial than that of L-dopa or other DA precursors. D-phenylalanine is more effective as a PEA precursor than the L-isomer as it is not subject to hydroxylation (to tyrosine), but personally, I found both inadequate, and had to resort to using PEA directly.
Eventually, I found the use of PEA and selegiline not to be very productive. Alternatives that I've since taken up in preference include methylphenidate, modafinil, memantine and some amisulpride or sulpiride.
poster:undopaminergic
thread:825078
URL: http://www.dr-bob.org/babble/20080430/msgs/827239.html