Both mucuna and Dopamine Agonists supply dopamine, so why did the DAs work for me (till augmentation) but not mucuna pruriens? Any ideas?

[grandpianoman]

Dopamine agonists supply dopamine--at night, even--but the problem isn't inadequate dopamine, it's inadequate dopamine receptors, right? So then why did the dopamine agonists work for me (till augmentation), and why doesn't mucuna pruriens work for me now that I'm off the DAs? Can't make sense of that.

[Hidden]

You're right, RLS isn't due to a lack of dopamine, it's due to a dysfunction and/or lack of dopamine receptors.

Dopamine "agonists" do increase dopamine levels, but that's not really why they work.

They work because they stimulate the receptor sites. Any substance that does that is called an "agonist". The converse is that anything that blocks a receptor is called an "antagonist".

The problem is that raised dopamine levels can cause "down-regulation" of the receptors, i.e. even less receptors working.

So. dopamine agonist= higher dopamine = less receptors = worse RLS = augmentation.

L Dopa is even worse for causing augmentation.

Mucuna pruriens raises dopamine levels, but it's not a dopamine agonist and doesn't stimulate receptors, so if it works at all, like L Dopa it's likely to cause augmentation, quite quickly.

I hope that helps.

[bill54321]

Because, the American Academy of Sleep is run by a bunch of amateurs.