Posted by undopaminergic on April 12, 2008, at 17:53:56
In reply to Re: PEA or PLA with Selegiline?? » undopaminergic, posted by Amigan on April 12, 2008, at 7:16:08
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> I see. Interestingly, eating chocolate or drinking 3 cups of hot cocoa while taking Selegiline, didn't have much effect on me. While drinking hot milk i notice a gentle activation and increased heart beat. I read that milk is phenylalanine-rich, although i can't be sure that it was phenylalanine responsible for this.
>I haven't noticed anything from cocoa either, but some people get reactions even with low doses (less than 5 mg/day) of selegiline. Also, some people taking non-selective MAOIs have had hypertensive reactions from dark chocolate.
Some people can easily get too much central dopaminergic stimulation, with paranoia, anxiety, psychosis and other unpleasant reactions as a result. You're probably not one of them, but it's nevertheless a good idea to test whether phenylalanine (PA) is sufficicent before moving on to PEA. PA should be smoother and longer lasting, and can also help replenish DA (and NA) via conversion to tyrosine (and hence L-dopa), but excessive PA can also competitively inhibit tyrosine hydroxylation. The D-isomer of PA cannot be converted to tyrosine, so more of it will be metabolised to PEA.
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> > I may possibly have a pathologically low dopamine/noradrenaline ratio and ëxcessive dopamine beta-hydroxylase (DBH) activity, and others may be less sensitive to noradrenergic side-effects than I am. It may be interesting to test the effects of a alpha2-agonist like guanfacine, as it might improve the ratio in favour of dopamine, and seems to be the next best thing after DBH-inhibitors, which aren't clinically available.
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> If only Carbidopa was able to cross the BBB..Excuse me? Carbidopa is primarily useful *because* it doesn't cross the BBB. As a peripheral inhibitor of aromatic amino acid decarboxylase (AADC) it helps greater amounts of L-dopa and 5-HTP (and other aromatic amino acids) cross the BBB before they are decarboxylated to dopamine and serotonin, which can't cross the BBB and hence have no CNS effect and furthermore cause unpleasant side effects like nausea, vomiting, diarrhoea, etc.
DBH converts dopamine to noradrenaline, and can be inhibited with research compounds like nepicastat and fusaric acid (while these may be worth trying, there are higher risks of unknown and potentially serious side effects).
I actually tried L-dopa with a peripheral AADC inhibitor (benserazide), but it didn't seem to work, even with methylphenidate and selegiline, and with amisulpride there seemed to be increased side effects like muscle stiffness. I had expected that the stimulant effect of methylphenidate would be potentiated, but little or no such effects were noted.
poster:undopaminergic
thread:822660
URL: http://www.dr-bob.org/babble/20080412/msgs/822926.html