OH JESUS HERE IS ONE OWNING ON THE SAME SUBJECT.
Quote from: suckmymuscle on October 25, 2009, 05:58:53 PM
You apparently didn't know that, given that you think ampetamines are harmless. And more catecholamines being expelled from the synaptic gap via agonism of the transporter protein by amphetamine's structural similarity to norepinephrine and other phenyethlamines + decreased dopamine production due to decreased tyrosine hydroxlase and l-dopa carboxylase = depletion of the pre-synaptic stores of catecholamines. No cathecholamines equal atrophy and death of the neuron due to neurochemical understimulation.
Apples and oranges. The physiology of the testes and that of specific neurons are quite different. Leydig cells are not destroyed by exogenous testosterone except if the doses are massive and taken over extremely long periods of time. In most cases, testosterone production resumes after exogenous androgenic steroids are discontinued. This does not seem to happen in the case of exogenous phenylethylamines being taken and then discontinued: permanent damage to neurons result.
Actually, the original study of amphetamine neurotoxicity was done back in Germany in the 1940s by the Nazis and it was regarding racemic(d,l) amphetamine and not methylated amphetamine which was only in use at that time in Japan.
You are confusing that with serotonin. At low doses, only methamphetamine causes serotonin release and not amphetamine. Both amphetamine and methamphetamine cause dopamine release at any dose, although of course higher doses result in more of this cateholamine being released. Don't confuse catecholamines with indolamines.
I hardly think you can mitigate neurotoxicity from amphetamines, although a monoamine oxidase B inhibitor like selegiline might work. There is an easier solution: don't take them at all. There are alternatives to increase attention span than don't involve destroying parts of your brain, like taking l-theanine and pyridoxine.
SUCKMYMUSCLE
again you try to obsfurcate the argument by using distraction and straw men. Where did i say "amphetamine was harmless", go have a look at my post, i dont think you'll find it. My correlation bt test lowring LH is just an analogy, anybody with a basic understanding would realize that tyrosine hydroxylase would be downregulated, maybe you should see if the enzyme is low in people with ADHD.
Also, you are wrong dextroamphetamine does not induce dopamine release until high doses are reached, you are wrong as usual.
oh, l-theanine and a b vitamin treat a disorder with known structural differences and different brain metabolism do they? Why is the crazy idea of alpha waves that go rushing through your body after ingestion of the amino acid? is the the calm tranquility you get from a cup of white tea. No they do not treat ADHD.
"You are confusing that with serotonin. At low doses, only methamphetamine causes serotonin release and not amphetamine. Both amphetamine and methamphetamine cause dopamine release at any dose, although of course higher doses result in more of this cateholamine being released. Don't confuse catecholamines with indolamines."
no im not, you are confusing your lack of knowledge.
http://en.wikipedia.org/wiki/Dextroamphetamine
"Because dextroamphetamine is a substrate analog at monoamine transporters, at all doses, dextroamphetamine prevents the re-uptake of these neurotransmitters by competing with endogenous monoamines for uptake.[41] .At higher doses, when the concentration of dextroamphetamine is sufficient,[41] the drug can trigger direct release of norepinephrine and dopamine from the cytoplasmic transmitter pool, that is, dextroamphetamine will cause norepinephrine and dopamine efflux via transporter proteins, functionally reversing transporter action, which triggers a cascading release of catecholamines"
all the references i have see show dopamine release at higher doses, unlike methamphetamine that does this at all doses. You are right about 5-HT, but i didn't comment on that, trying to make yourself look smart perhaps?
