Because it is not uncommon to prescribe moclobemide or low dose selegiline with stimulants anymore? Akathasia is the result of low dopamine, not high dopamine, hence why it's a common side effect of antipsychotics. Those are dopamine receptor antagonists, if you weren't aware.
So, say, if these dopaminergic neurons were to die or become severely damaged due to the neuron being overactive, such as
in the event of mixing an MAOI with an amphetamine, it would cause akathisia which is also caused when there is a lack of dopamine or in the use of dopamine antagonists, is that correct Professor Hammilton?
That's your personal theory, but there's no evidence that your are correct. Evidence is research, not more theory, just to make things clear. Doses of the l-amphetamines are too low to cause any problems. This is why you don't see selegiline described negatively by those taking it.
This refers to your comments about how selegiline is so terribly closely related to the amphetamines. If it doesn't have similar effects (it might, but considering that primates won't self administer it, it can't to any significant degree) then the structural similarities are irrelevant. But then again, everything in that post was irrelevant.
It's binding to MAO-B irreversibly refutes the next section. Because it binds irreversibly and completely, very little selegiline is metabolized into l-meth. What is bound to the enzyme is not available for metabolism.
Right, we're talking about a few hundred micrograms administered locally. Compared to a few hundred micrograms present systemically. Were the level of l-meth or l-amp present at physiologically active levels, you would not see hypotension, you'd have hypertension.
Ahh I see! So because the signs of hypertension are outweighed by hypotension, which makes the net result show signs of only hypotension, then that means that
there is no hypertension at all, after all
if you can't see something happening then that means it isn't happening. Much like how if I were to take a gallon of milk and add a teaspooon of urine to the milk, then pour a glass for an unsuspecting victim, that person would still only taste the milk because he didn't know that I put urine in it, and because he didn't know that there was urine in it, the urine magically disappeared upon entering his mouth. It makes perfect sense Professor Hammilton, thank you for enlightening me with your logic.
You don't understand why it's complete binding and that it produces hypotension makes all your nonsense about l-meth metabolism irrelevant? Really it comes down to this: because of those, it's obvious (and proven) that the levo-amphetamine metabolites are present at physiologically irrelevant levels. These are major misunderstandings and they seem to be the crux of your argument against selegiline.
Ah, sorry professor for questioning your almighty logic.
Wait professor, Selegiline can yield a false positive result for amphetamine in a drug test because of the presence of l-methamphetamine. The cut-off level of amphetamines for most urinary most drug tests is 1000ng/ml to 200ng/ml. Just for shits and giggles, lets see how much l-methamphetamine is in that urine if the test is set for 200ng/ml (more precise than 1000ng/ml) as a cut-off level. Lets say he pissed out about 500ml of urine. 500*200 is 100,000. There are 1000ng in 1mg, so that means... oh shit, wait... that means there was
at least 100mg of l-methamphetamine that went through that persons system, which is far more than whats needed to produce peripheral effects... well, I guess all those drug testers were faulty,
because you are always right Professor Hammilton.
Right, because in a thread about MAOIs + Stimulants, I'd of course be referring to an amino acid.
The vast majority of "Selegiline + something else" that was prescribed mutually to treat parkinsons disease is selegiline and L-Dopa. It just seemed like common sense for me to connect the two, and exclude the 1 out of 5,000 Segeline prescriptions that were "Selegiline + Amphetamine" written by doctors who cheated off the asian guy in med school and didn't read "AMPHETAMINE+MAOI=BAD".
If you don't believe me, call up Poison Control and say "I accidentally took my mothers Selegiline thinking that it was my prescribed amphetamine, then realized this so I took my prescribed amphetamine afterwards, and now I don't feel too good, was this a bad interaction?". See what they tell you.
Did you actually read the original post? The OP makes no reference to any such thing. He was talking about using an MAOI to reduce the side effects caused by oxidation of dopamine resulting in subsequent dopamine depletion and formation of pro-oxidant species.
Amazing. You can't even keep the conversation straight.
So "using an maoi to stop the oxidation of neurons" isn't just a shorter way of saying "using an MAOI to reduce the side effects caused by oxidation of dopamine resulting in subsequent dopamine depletion and formation of pro-oxidant species"?
You claimed that selegiline + L-dopa was given to parkinson's patients so that they could 'enjoy' the last few years of normal functioning. That's absolutely not what it is given for, it's given because it eradicates symptoms and substantially slows the worsening of symptoms.
Dopamine Dysregulation Syndrome is quite common to be provoked in those treated with L-Dopa, and it is due to the fact that as more and more L-Dopa is needed to maintain effectiveness (the tolerance to L-Dopa increases very rapdily) the destruction of dopaminergic receptors results.
They might alleviate a few symptoms during the initial stages of treatment, but then they will rapidly become worse off than before.
If you can't keep your own comments straight, you should consider restraining yourself to OD where your almost intelligent comments might pass.
Ahah, so now the
real matter at hand reveals itself - a matter of territorial ego. Quite similar to a prepubescent girl in a school cafeteria saying "umm you can't sit here, this table is reserved for cool girls".
Very primitive of you! But instead of an actual tangible object such a lunch table, you are defending something far more embarassing, a section of an internet forum (a "virtual" lunch table). But, just like a prepubescent girl who eventually realizes that "spots at the lunch table" don't mean shit in life, you will also learn that your 'reputation' on an online forum will have little to no impact on your near future (i.e., when you decide to turn your computer off and do something productive).
You're arguing against a now fairly commonly employed regiment. Selegiline / Moclobemide (but apparently not phenelzine or tranylcypromine or other non-selective irreversible MAOIs) I'm not suggesting that this be done in the absense of psychiatric care, but with careful dosing and the appropriate drugs, it's definitely something that can be done safely and with measurable benefit. Certainly not something to be undertaken by the uninformed or anyone who might be prone to rapid dose escalation.
MAOI interaction concerns are grossly overstated, and this is being corrected now. PI sheets are being updated, though the PI sheets for a 2.5mg tablet of selegiline I read yesterday stated that anyone taking anything more than one 2.5mg tablet per day must observer dietary restrictions. Insane. You could be eating four of those per day and not have any reason to observe dietary restrictions.
Is that last sentence just personal opinion? Or is it the same logic that is used by a person saying "4g of APAP a day can cause liver damage? Thats insane! I could easily eat four times that amount and not have any reason to observe liver health!"
) and slightly reverses the reuptake of norepinephrine in the CNS causing all the bad feelings of a "crash". Another mistake everyone has been making was relating dopamine as the primary neurotransmitter responsible for a crash, when it is actually norepinephrine. I DID NOT SAY IT INCREASED DOPAMINERGIC ACTIVITY
