The reason that Zembrin is better from a PDE4 inhibition perspective is that it has higher mesembrenone content. Mesembrenone is the strongest PDE4 inhibiting component of Sceletium Tortuosum. The other psychoactive component of the plant, Mesembrine, is weak PDE4 inhibitors and acts in an SSRI like way by blocking the activity of the 5-HT transporter. Subjectively, the raw extract puts me in a good mood and makes me tell a lot of funny jokes but isn't as good for studying or mental work as Zembrin is.
Here's some of my earlier analysis on the topic:
http://www.longecity...260#entry572326
IMO, the developers have done a very good job on this product and I'll continue purchasing it.
I don't want to risk getting another heavy SSRI on my hands. They're absolutely awful for getting anything done.
It's also interesting to see that the product has so many synergistic actions that orchestrate its effect. (AChE, GABA, 5-HT, PDE3, 10A, 7A, 11...)
I'm going to continue experimenting with an extended version of CILTEP to also increase hormonal health.
PDE-4 inhibition (or inhibition of other PDE's, accomplished by Artichoke and Zembrin) clearly potentiates the effect of LH/HcG in the Leydig cells and increase hormonal production.
That means a good LH-agonist is the missing link, which leads me to the only convenient and studied alternative:
D-aspartic acid (DAA).
DAA accomplishes LH-release by acting as an NMDA agonist. And it's already used widely for exactly this purpose.
If anyone is interested, the following formula could probably work very effectively for both LTP and hormonal health.
Besides making you feel incredibly cool, the hormonal release will also contribute to the nootropic effect of CILTEP.
Zembrin (1x) + Forskolin + 3-5g D-aspartic acidThe stack utilizes the following pathway:
NMDA agonism -> LH-release from pituitary gland -> cAMP-activation in Leydig cells by LH -> Cholesterol uptake from HDL during steroidogenesisDAA will stimulate LH production, Forskolin potentiates the action of LH, and Zembrin provides the necessary PDE-inhibition to stop cAMP degradation in Leydig cells.
I also recommend consuming a diet high in monosaturated fats (nuts, seeds, animal fats) to elevate HDL-levels.
For potentiation of steroidogenesis, the literature has indicated that PDE-4 and PDE-8 are the desired targets of inhibition.
PDE-8 inhibition could be accomplished by some prescription medications, but this would be very inconvenient and the potential side-effects are too many.
Besides, the simple addition of DAA to the morning routine of Zembrin + Forskolin is just so cheap and effortless.
http://www.ncbi.nlm....pubmed/19860889
In humans and rats, sodium D-aspartate induces an enhancement of LH and testosterone release.
http://www.pnas.org/...3/52/19925.full
Leydig cells produce testosterone in the testes under the pulsatile control of pituitary luteinizing hormone (LH). cAMP is the intracellular messenger for LH action on steroidogenesis, and pharmacological evidence indicates that the response to LH can be modulated by cyclic nucleotide phosphodiesterases (PDEs).
http://molpharm.aspe...t/81/4/556.full
These results suggest that the pool(s) of cAMP regulating androgen production are controlled by PDE8s working in conjunction with PDE4.
I'll also include Sulbutiamine, since there are some indications that it acts as an nmda-agonist and subsequent LH-release agent.
http://www.ncbi.nlm....pubmed/15951087
Dizocilpine (NMDA-antagonist), impaired both acquisition and retention of the DNMTS task in the saline-treated group, but not in the two sulbutiamine-treated groups, suggesting that sulbutiamine may counteract the amnesia induced by a blockade of the N-methyl-D-aspartate glutamate receptors.[8]
Edited by chung_pao, 03 July 2013 - 02:58 PM.