Disclaimer: I can't guarantee the information in this topic is 100% accurate. Also, I'm not trying to hate on Mr. Lindsay's creation; I'm simply stating that if you have DP, you might want to think twice before taking it long-term.
CILTEP is a nootropic stack, designed to Chemically Induce Long-Term Potentiation.
To quote wiki:
The inventor of the stack states the following:
Which, indeed, is true.
However, to quote from "The many faces of CREB":
Simplified translation:
CREB transcription factor activation in the Nucleus Accumbens increases Dynorphin expression, thus KOR activation, (also stated in this article from the same author(s)), which is responsible for dysphoria, anxiety and depression. On the other hand, hippocampal CREB activation causes the opposite.
However, KOR (Kappa Opioid Receptor) activation has been extensively documented to induce depersonalization, derealization, visual distortions, and more in humans. Thus, regardless of the observation that hippocampal CREB activation elicits anti-depressive effects, nucleus accumbens CREB activation would ultimately contribute to more dissociation. CILTEP would cause this.
Anyway, this has been a quick write up, so I might've missed some things, in which case; please do let me know if I'm wrong.
One more interesting (and lengthy) article about Dynorphin and KOR
Lastly, one highly interesting feature that nearly every drug of abuse has in common, is that they increase Dynorphin in one way or the other, and nearly every drug of abuse has been documented to be able to induce DP.
CILTEP is a nootropic stack, designed to Chemically Induce Long-Term Potentiation.
To quote wiki:
It consists of a PDE4 inhibitor, which would inhibit the degradation of cAMP. Another ingredient is Forskolin, which raises cAMP levels.
The inventor of the stack states the following:
source
Which, indeed, is true.
However, to quote from "The many faces of CREB":
Some more work of the same author(s):
source
Simplified translation:
CREB transcription factor activation in the Nucleus Accumbens increases Dynorphin expression, thus KOR activation, (also stated in this article from the same author(s)), which is responsible for dysphoria, anxiety and depression. On the other hand, hippocampal CREB activation causes the opposite.
However, KOR (Kappa Opioid Receptor) activation has been extensively documented to induce depersonalization, derealization, visual distortions, and more in humans. Thus, regardless of the observation that hippocampal CREB activation elicits anti-depressive effects, nucleus accumbens CREB activation would ultimately contribute to more dissociation. CILTEP would cause this.
Anyway, this has been a quick write up, so I might've missed some things, in which case; please do let me know if I'm wrong.
One more interesting (and lengthy) article about Dynorphin and KOR
Lastly, one highly interesting feature that nearly every drug of abuse has in common, is that they increase Dynorphin in one way or the other, and nearly every drug of abuse has been documented to be able to induce DP.