So I was responding to this post:
http://www.longecity...alize/?p=726670
I felt what I was talking about definitely deserved its own thread. This is because this way of increasing DA and 5HT is vastly different from SRI and DAT Inhibitors, and could help some people in ways they may not expect.
So with OTC products, you can significantly increase dopamine and serotonin levels. This is one of many reasons I see the distinction between supplements and traditional pharmaceuticals as a largely cultural distinction (Don't believe me? Try Rhodiola + Caffine or 18g/day of Inositol if you have OCD). This is one of the few ways you can increase Dopamine in a non stimulant way, and increase Serotonin without an SRI or SRA (Serotonin releasing agent, the fun stuff like MDMA. It's extremely fascinating how vastly different SRIs and SRAs are, where DRIs and DRAs (dopamine) have largely the same effect, the latter simply being more potent). You can do this with OTC 5-HTP, L-Dopa, and very importantly, EGCG:
http://www.ncbi.nlm....les/PMC2916818/
http://www.ncbi.nlm....pubmed/22107329
EGCG seems to act like a combined version of Carbidopa (an L-Amino Acid Dexcarboxylase Inhibitor, almost always given with L-Dopa), and Entacapone, a COMT-Inhibitor. The LAADI prevents the conversion of L-Dopa to dopamine and 5-HTP to serotonin before it gets to the brain. The COMT Inhibitor extends the effect of L-Dopa in the brain significantly and also prevents unhealthy metabolites. EGCG is about half as strong per dose as Entacapone, which is quite potent or an OTC supplement (IC50 = 174.9(EGCG) 76.8(Entacapone), and there's that cultural distinction). The mechanisms and potency of the LAADI is a little more unclear, but it does seem at least somewhat comparable to Carbidopa, though it's unclear right now just how strong it is per dose.
As I said, L-Dopa and EGCG or Entacapone/Carbidopa is one of the few ways of increasing dopamine in a non-stimulant way. The only other ones I can think of are MAOIs and 5HT2c antagonists. DAT inhibitors like cocaine and amphetamines cause stimulation with dopamine release, and I don't think we know yet why these two things differ, but it fascinates the hell out of me.
Why increase both DA and 5-HTP? Increasing levels of dopamine can decrease serotonin and vice versa, which is why many recommend that if one takes L-Tryptophan (the precursor to 5-HTP, btw) or L-Tyrosine (the precursor to L-DOPA), they take them together. Serotonin lowers dopamine in the Ventral Tegmental Area (and perhaps the Substantia Nigra), a major pleasure center of the brain, through the 5HT2c receptor. The mechanisms through which dopamine lowers serotonin appears to be more complicated, but there is good evidence that this occurs. A great study:
http://www.gatsby.uc...apers/dkd01.pdf
The reason for 5-HTP and L-Dopa over Tryptophan and Tyrosine is that your body has a mechanism that regulates the conversion of Tryptophan & Tyrosine to 5-HTP and L-Dopa. Your body does not have a mechanism to regulate the conversion of 5-HTP and L-Dopa to Serotonin and Dopamine. This allows you to increase the respective neurotransmitters simply based on the dose you're taking (and of course, given this, you should be careful with the dosage).
I take the 5-HTP and L-Dopa, w/ EGCG, because of my Vyvanse. It's a higher dose, and I often feel depleted the next day, especially if I take the full 70mg. This helps a lot in countering that.
I hope this helps someone. Feel free to ask any questions if you want a more in-depth explanation.
Edited by OneScrewLoose, 07 May 2015 - 07:35 AM.
