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PCE
PCE may cause psychosis and mania at a significantly higher rate than other dissociatives.[1][2]
It is strongly discouraged to use this substance in high doses or multiple days in a row. Please see this section for more details.
WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.
DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.
PCP was marketed in the 1950s as an anesthetic pharmaceutical drug but was taken off the market in 1965 due to the high prevalence of dissociative hallucinogenic side effects, which was also discovered of PCE. Soon after, ketamine was discovered by Parke-Davis researchers as a better-tolerated derivative for use as an anesthetic pharmaceutical drug. Since this time, a number of synthetic derivatives of PCP have been sold as dissociative drugs for recreational and non-medical use.[6]
Today, PCE is typically taken as a recreational drug or more rarely, for entheogenic purposes alongside its popular contemporary relatives 3-MeO-PCP and 3-MeO-PCE. PCE may be ingested orally, smoked, insufflated or injected.[9] It has been noted for its potency, diversity in effects, long-lived effects, and abuse liability. Notably, PCE is slightly more potent than PCP and has similar effects, but its unpleasant taste and tendency to cause nausea made it less accepted by users, making it relatively obscure.
PCE, or Eticyclidine, is a synthetic dissociative of the arylcyclohexylamine class. PCE contains cyclohexane, a six-member saturated ring, bonded to a ring and -ethyl group at R1. One of these rings is a piperidine ring, a nitrogenous six member ring, bonded at its nitrogen group. The other constituent at the nitrogen is not a full cyclohexane ring like with PCP, but an ethyl group. As with PCP, PCE is an initialism named from the first letters of the three constituent rings phenyl, cyclohexane and ethyl.
NMDA receptors (a subtype of receptors for glutamate, which are the principle excitatory neurotransmitters in the nervous system) allow for electrical signals to pass between nerve cells in the brain and spinal column; for the signals to pass, the receptor must be open. NMDA receptor antagonists have been shown to disrupt this signaling by blocking these receptors. This disconnection of information flow in the nervous system leads to loss of sensation (anesthesia), difficulty moving (motor discoordination), and eventually this substance's equivalent of a “"hole"-like state that is most associated with that experienced on ketamine, although of a qualitatively different nature.”[citation needed]
PCE is slightly more potent than PCP and has similar effects, but its unpleasant taste and tendency to cause nausea has made it less accepted by users.[10]
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWikicontributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.
Visual disconnection - This eventually results in PCE's equivalent of the "k-hole" or more specifically, holes, spaces and voids alongside of structures. However, unlike ketamine, PCE does not immobilize the user at this level, which can lead to unpredictable psychotic behavior.
At high doses, PCE can produce a full range of high-level hallucinatory states in a fashion that is less consistent and reproducible than that of many other commonly used psychedelics. These effects include:
The general head space of PCE is often described as particularly stimulating, euphoric and clear-headed in comparison to that of DXM and ketamine. The specific cognitive effects can be broken down into several separate subcomponents which are listed and described below:
There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:
The long-term use of PCE may lead to schizophrenia-like psychotic episodes, severe lasting memory loss, disorganized thinking, depression, weight loss, liver abnormalities and rhabdomyolysis (skeletal muscle breakdown).[12]
Some studies have found that, like other NMDA receptor antagonists, PCE can cause brain damage called Olney's lesions in rats.[13][14] Studies conducted on rats showed that high doses of the NMDA receptor antagonist dizocilpine caused reversible vacuoles to form in certain regions of the rats' brains. All studies of Olney's lesions have only been performed on non-human animals and may not apply to humans.
PCE has also been shown to cause schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate levels in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.[15] It also induces symptoms in humans that mimic schizophrenia.[16]
It is strongly recommended that one use harm reduction practices, such as volumetric dosing, when using this substance to ensure the administration of the intended dose.
Tolerance and addiction potential
The chronic use of PCE can be considered highly addictive with a high potential for adverse side effects such as psychosis. In comparison to other dissociatives, PCE has been reported to be more addictive than MXE, diphenidine, ephenidine, and ketamine. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage. There have been multiple reports across the internet of people becoming seriously addicted daily users of this substance so serious precautions and considerations should be taken before trying this substance.
Tolerance to many of the effects of PCE develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). PCE presents cross-tolerance with [[Cross-tolerance::all dissociatives]], meaning that after the consumption of PCE, all dissociatives will have a reduced effect.
Psychosis
PCE is reported to cause psychosis and mania at a significantly higher rate than other dissociatives such as ketamine, diphenidine, or MXE. Multiple scientific papers describe states of psychosis, mania, and/or delirium occurring after moderate to large doses of the drug were ingested. In one initial human trial, it was reported that one-sixth of the patients who had received anesthetic doses became psychotic. In some cases, it took up to a week or more to resolve. Similar results (although less severe) were reported during trials using subanesthetic doses of PCE for pain relief.[11]
It is strongly recommended that one use extreme caution and harm reduction practices when using this drug.
Users should avoid taking the drug multiple days in a row or becoming addicted to it as this increases the risk of severe adverse effects.
The recommended dosage range should not be exceeded as high doses can trigger adverse effects.
Users should start with extremely low doses and work their way up as slowly as possible. Volumetric liquid dosing should preferably be used due to the drug's potency; most standard milligram scales cannot accurately weigh out doses below 10-15mg.
Compulsive redosing before one has fully sobered up is not recommended and can result in too high of a dose.
Due to the risk of psychosis, it is not recommended to combine this drug with other substances, especially stimulants, psychedelics, or other dissociatives like MXE. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.
Urinary tract effects
In terms of its long-term health effects when used repeatedly and excessively for extended periods of time, PCE seems to exhibit similar extreme bladder and urinary tract problems to those found with other arylcyclohexylamines like ketamine or PCP.
Urinary frequency - Urinary frequency is the need to empty the bladder every few minutes.
Urinary urgency - This can be described as a sudden, compelling need to urinate.
Urinary pressure - This is experienced as a constant sensation of fullness in the bladder that is unrelieved by urination.
Pelvic and bladder pain - Pain can develop suddenly and severely, particularly as the bladder fills with urine.
Hematuria - Hematuria is visible blood in the urine.
Incontinence - This is the leakage of urine.
A large body of anecdotal evidence suggests that these symptoms can be minimized by not using PCE on a regular basis (daily or weekly at the bare minimum) and carefully monitoring and limiting one's usage of the substance, although general usage of this substance is still discouraged due to its observed toxic properties.
Dangerous interactions
Warning:Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
Psychedelics - This combination is not advised because PCE has been reported to cause extreme psychological disturbances such as psychosis and mania at a significantly higher rate than other dissociatives.
Stimulants - Both stimulants and dissociatives carry the risk of adverse psychological reactions like anxiety, mania, delusions and psychosis and these risks are exacerbated when the two substances are combined.
Depressants - Because both depress the respiratory system, this combination can result in an increased risk of suddenly falling unconscious, vomiting and choking to death from the resulting suffocation. If nausea or vomiting occurs, users should attempt to fall asleep in the recovery position or have a friend move them into it.
As such, it may contain incomplete or wrong information. You can help by expanding it.
Internationally, PCE is a Schedule I substance under the Convention on Psychotropic Substances.[17]
Canada - PCE is controlled under CDSA schedule III making it illegal to sell, possess and manufacture without a license or prescription.[citation needed]
Germany: PCE is controlled under BtMG Anlage I, making it illegal to manufacture, import, possess, sell, or transfer it without a license.[18]
New Zealand - PCE is Schedule I (class A) in New Zealand.[citation needed]
Poland - PCE is Schedule II (II-P group) in Poland.[citation needed]
Portugal - Effective July 2001, personal use of PCE was decriminalized by Law 30/2000. Possession of less than 100 mg is not regarded as a criminal offence, although the substance is liable to be seized and the possessor can be referred to mandatory treatment. Sale or possession of quantities greater than the personal possession limit are criminal offences punishable by jail time.[citation needed]
Switzerland: PCE is a controlled substance specifically named under Verzeichnis D.[19]
United Kingdom - PCE is a class A in the U.K., making it illegal to buy or possess without a prescription.[citation needed]
United States - PCE is a Schedule II controlled substance.[citation needed]
Morris, H., & Wallach, J. (2014). From PCP to MXE: A comprehensive review of the non-medical use of dissociative drugs. Drug Testing and Analysis, 6(7–8), 614–632. https://doi.org/10.1002/dta.1620
↑ 6.06.1Morris, H., Wallach, J. (August 2014). "From PCP to MXE: a comprehensive review of the non-medical use of dissociative drugs". Drug Testing and Analysis. 6 (7–8): 614–632. doi:10.1002/dta.1620. ISSN1942-7611.
↑McKim, W. A. (2000). Drugs and behavior: an introduction to behavioral pharmacology (4th ed ed.). Prentice Hall. ISBN9780130831460.CS1 maint: Extra text (link)
↑Olney, J. W., Labruyere, J., Price, M. T. (16 June 1989). "Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs". Science (New York, N.Y.). 244 (4910): 1360–1362. doi:10.1126/science.2660263. ISSN0036-8075.
↑Hargreaves, R. J., Hill, R. G., Iversen, L. L. (1994). "Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology". Acta Neurochirurgica. Supplementum. 60: 15–19. doi:10.1007/978-3-7091-9334-1_4.
↑Reynolds, L. M., Cochran, S. M., Morris, B. J., Pratt, J. A., Reynolds, G. P. (1 March 2005). "Chronic phencyclidine administration induces schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in rat brain". Schizophrenia Research. 73 (2–3): 147–152. doi:10.1016/j.schres.2004.02.003. ISSN0920-9964.
↑Murray, J. B. (May 2002). "Phencyclidine (PCP): a dangerous drug, but useful in schizophrenia research". The Journal of Psychology. 136 (3): 319–327. doi:10.1080/00223980209604159. ISSN0022-3980.
