Posted by Elroy on March 29, 2005, at 6:44:45
In reply to RE: PEA, posted by gromit on March 27, 2005, at 21:03:06
Probaby should have noted this earlier, but the problem with PEA is that it has a ridiculously low half-life in the brain. Larry H. probably knows it more accurately, but it is something like just a minute or two. So it is gone that quickly (which is why one craves more chocolate or runs for miles and miles - if one is the type that easily gets the PEA release from running).
And that is the theory behind the LOW DOSE levels of Selegiline - but combined with DLPA (or variation thereof). The Selegiline inhibits the breakdown of PEA, keeping it active longer (also dopamine, etc. if you are taking the L-Phenylalanine or DLPA).
BTW, the LOW DOSE levels of Selegiline (15mg and under) are NOT considered MAO Type A Inhibitor. At those levels Selegiline is a selective MAO type B inhibitor with minimal side effects and no dietary restrictions. It is also minimally effective (as an Anti-depressent) by itself at those low dosage levels - although used extensively as a life extension agent at very low doses. Anyway, clinical tests show that ut seems to be very effective at those LOW DOSE levels when used in combination with DLPA or simply D-Phenylalanine.... or with L-Phenylalanine if one's problem consists of low levels of dopamine as a brain neurotransmitter.
See:
http://www.deprenyl.net/Deprenyl/deprenyl-14.htm
http://www.deprenyl.net/Deprenyl/deprenyl-61.htm
http://www.deprenyl.net/Deprenyl/deprenyl-27.htm
http://www.deprenyl.net/The last site has some interesting text explaining deprenyl (or selegiline) action... and why this would NOT be a good selection if one has primarily an anxiety problem....
QUOTE: Knoll discovered that deprenyl (and its “cousin”, PEA) are “catecholamine activity enhancers”. Catecholamines refers to the inter-related neurotransmitters dopamine, noradrenalin, and adrenalin. Catecholamines are the transmitters for key activating brain circuits... What Knoll and colleagues discovered through their highly technical experiments is that deprenyl and PEA act to more efficiently couple the release of neurotransmitters to the electrical impulse that triggers their release.... In other words, deprenyl (and PEA) cause a larger release of transmitters in response to a given electrical impulse. It’s like “turning up the volume” on catecholamine nerve cell activity. And this may be clinically very useful in various contexts - such as Parkinson’s disease and Alzheimer’s disease, where the nigrostriatal tract and mesolimbic-cortical circuits under-function, as well as in depression, where they may be under-activity of both dopamine and noradrenalin neurons.... END QUOTE
In primary anxiety states, there is too much "brain circuit transmitting" going on (which is why Xanax, a GABA enhancer, is so effective as GABA tends to calm down that neurotransmitting activity). Also, persons with primary anxiety states tend to have excessive levels of "Catecholamines" (the inter-related neurotransmitters of dopamine, noradrenalin, and adrenalin) in the system already. Therefore (as I quickly came to find out through trial), the selegiline - and especially as combined with DLPA - is not a good protocol for primary anxiety states.
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> > Sorry, I've read only the last few posts on this thread, so perhaps I shouldn't be responding, but I wanted to mention that I've read that vigorous physical exercise increases levels of phenylethylamine (PEA).
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> You would think so. I used to run quite a bit when I was younger and I've never had this "runner's high" that others get. I've had this discussion with my PCP and the new pdoc and they both agree my endorphines are messed up. They didn't mention any treatment though. My former pdoc was a runner and couldn't believe it, 1 of 100 reasons he is my FORMER pdoc.
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> I think for whatever reason my body either can't produce PEA or produces very little of it.
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> Thanks
> Rick
>
poster:Elroy
thread:452259
URL: http://www.dr-bob.org/babble/alter/20050323/msgs/477084.html