Dissociatives The Big & Dandy 3-MeO-PCE Thread

[higherconciousness]

I start outpatient in a couple of weeks because I got my 3rd DUI 2 weeks ago with multiple possession charges. Lost over a grand in drugs to the cops. I’m going fucking hard til then.

 

[higherconciousness]

Is there no 3-ho-pce mega thread? Well, I just got a sample of that my gram of the MEO this coming. Popped 10 mg of 3-ho-pce with lil amphetamine sulfate. Feeling good. Oral is def better. I would always snort it. Think the amine group is more effectively metabolized orally. It’s like a mix between 3-meo-pce and 3-ho-pcp.

 

[higherconciousness]

Finally got my g of 3-meo-pce today. I’m too drunk and coked out to even think about touching it. Thankfully I don’t have any needles around because when I get going I want to take it all the way.

Either tomorrow or the next day I plan on combining lsd, MDA, 4-ho-mipt, and 3-meo-pce. I’m doing my last pull on my MHRB solution and hope to get enough for a couple blast offs. I recall a similar combo except there was no mipt and I had 3-ho-pcp instead. I was able to explore hyperspace for a good 20-30 min.

 

[4DQSAR]

On closer examination I checked my own vital signs and note that 3-MeO PCE significantly increased my blood-pressure, heart rate and respiration rate.

I note that as well as NMDA and DAT activity, 3-MeO PCE also has significant α2A adrenoceptor affinity. This is the same as cocaine.

I am entirely unsurprised that even without a person consuming other compounds, we have seen fatalities attributed to '3-MeO PCE Intoxication'.

 

[SuperPsych]

On closer examination I checked my own vital signs and note that 3-MeO PCE significantly increased my blood-pressure, heart rate and respiration rate.

I note that as well as NMDA and DAT activity, 3-MeO PCE also has significant α2A adrenoceptor affinity. This is the same as cocaine.

I am entirely unsurprised that even without a person consuming other compounds, we have seen fatalities attributed to '3-MeO PCE Intoxication'.

I never took my heart rate while consuming 3-MeO-PCE so I don't have exact numbers to back it up, but that was the red flag for me with that compound. There would be times where my heart rate and BP felt like it got real wonky out of nowhere. At times it was a bit concerning and I'd have to take a clonidine.

It can be a great compound when used in moderation but it is not a chemical suited for binging

 

[higherconciousness]

On closer examination I checked my own vital signs and note that 3-MeO PCE significantly increased my blood-pressure, heart rate and respiration rate.

I note that as well as NMDA and DAT activity, 3-MeO PCE also has significant α2A adrenoceptor affinity. This is the same as cocaine.

I am entirely unsurprised that even without a person consuming other compounds, we have seen fatalities attributed to '3-MeO PCE Intoxication'.

Yeah it def does more so than 3-ho-pcp or even 3-ho-pce and I tend to combine it with amphetamines. Well today it’s been 3 hits of lsd throughout the day, sniffed rest of my 4-ho-mipt, 12mg or so 3–meo-pce, bumps of amphetamine sulfate, and a mix of low doses of etiz, flualp, and bromoethylazolam, oh and 200mg of Lyrica. Thankfully, I have loads of clonidine as well

 

[higherconciousness]

Bummed I’m out of dmt. Got about 1.2 g of dmt via stb from 100g bark. I did it with missing equipment so not too bad but damn I miss it. One psychedelic I could do and it never gives me a bad trip.

 

[4DQSAR]

Yeah it def does more so than 3-ho-pcp or even 3-ho-pce and I tend to combine it with amphetamines. Well today it’s been 3 hits of lsd throughout the day, sniffed rest of my 4-ho-mipt, 12mg or so 3–meo-pce, bumps of amphetamine sulfate, and a mix of low doses of etiz, flualp, and bromoethylazolam, oh and 200mg of Lyrica. Thankfully, I have loads of clonidine as well

Yeah - be very careful when mixing up all those things. I mean, I know doctors only flag single interactions so heavens alone knows what the potential interactions that could be going on with all that.

Don't want to see your name in the Bluelight Shrine. Take good care of yourself.

 

[SuperPsych]

Yeah it def does more so than 3-ho-pcp or even 3-ho-pce and I tend to combine it with amphetamines. Well today it’s been 3 hits of lsd throughout the day, sniffed rest of my 4-ho-mipt, 12mg or so 3–meo-pce, bumps of amphetamine sulfate, and a mix of low doses of etiz, flualp, and bromoethylazolam, oh and 200mg of Lyrica. Thankfully, I have loads of clonidine as well

That is a hell of a combo. Good thing you aren't driving lol. It does sound fun. Never been one to mix stimulants with psychedelics but I can see it being fun with benzos

 

[higherconciousness]

That is a hell of a combo. Good thing you aren't driving lol. It does sound fun. Never been one to mix stimulants with psychedelics but I can see it being fun with benzos

I have quite a tolerance to amphetamines and I find it less taxing than taking MDA or some other compound in that family. The 3-meo-pce seems to complicate things more than anything in regards to heart rate, but as long as the dose isn’t too high it seems manageable. The benzos and clonidine seem to offset any side effects produced by such a mix as well.

Just woke up and took 50mg 2-FMA as I’m out of my normal amp sulfate. May take 12 mg of 3-meo-pce. As long as it’s used within reasonable doses it’s a great substance, but over that threshold is crossed it can get messy. This one is to be used with extreme caution more so than the others. Getting quite pricey lately but a g should last one quite some time.

 

[4DQSAR]

I have quite a tolerance to amphetamines and I find it less taxing than taking MDA or some other compound in that family. The 3-meo-pce seems to complicate things more than anything in regards to heart rate, but as long as the dose isn’t too high it seems manageable. The benzos and clonidine seem to offset any side effects produced by such a mix as well.

Just woke up and took 50mg 2-FMA as I’m out of my normal amp sulfate. May take 12 mg of 3-meo-pce. As long as it’s used within reasonable doses it’s a great substance, but over that threshold is crossed it can get messy. This one is to be used with extreme caution more so than the others. Getting quite pricey lately but a g should last one quite some time.

I suggest to you that while your consciousness may become tolerant to certain compounds, it's in no way certain that the body will equally evolve tolerance.

3-MeO PCP is a high risk compound in my experience. I've just spent the last week exploring it until last night I didn't sleep a wink and even moderate exercise showed that my vital signs were still elevated some 18 hours after the last dose.

So I've put it down for a while. I don't like stimulants but it appears that 3-MeO PCE produces diminishing returns in terms of pseudopsychedelic effects and essentially you are left with a long-acting nasty stimulant. Not as bad as desoxypipradrol, but still pretty bad. Why not the much safer (based on very little proper in vivo testing) CMXE (2-(2-chloro-5-methoxyphenyl)-2-(ethylamino)cyclohexan-1-one)? I presume because although more potent than K, it's more akin to K than to PCP derivatives thus less potent and shorter acting.

BTW if someone really feels it VITAL to produce a pure stumulant based on the ACA (aryl cyclohexylamine) class, benocyclizine (BTPC) briefly turned up as an RC and as with 3-MeO PCP, the dose/response curve is steep, the duration long and it would appear that consumers avoided it in droves. It ended up being sold in fake MDMA tablets. What does that tell us? Just because we can doesn't mean we should, I suspect.

 

[higherconciousness]

I read an article, granted a single article, on mice claiming,

“Agmatine potentiates antidepressant and synaptic actions of ketamine: Effects on dendritic arbors and spines architecture and Akt/S6 kinase signaling”​

I’m wondering if the combination of agmatine and low doses of 3-meo-pce could potentially exert some of the same effects. This is highly speculative of me and perhaps I’m out of my depth here because 3-meo-pce is a whole other beast when compared to ketamine, yet it’s still an NMDA antagonist. The article purposes that the combination of agmatine resulted an increase in the post formation of dendritic spines, leading to a higher number of dendrites formed.

https://www.sciencedirect.com/science/article/pii/S0014488620302296

 

[4DQSAR]

I can't answer that. Nobody can. My feeling is no.

 

[Allylbenzene]

I’m wondering if the combination of agmatine and low doses of 3-meo-pce could potentially exert some of the same effects. This is highly speculative of me and perhaps I’m out of my depth here because 3-meo-pce is a whole other beast when compared to ketamine, yet it’s still an NMDA antagonist. The article purposes that the combination of agmatine resulted an increase in the post formation of dendritic spines, leading to a higher number of dendrites formed.

Yes, agmatine shares a similar primary MOA as (S)-ketamine (AMPA, mTOR) = neurogenesis (probably involving BDNF & 5-HT2A), with additional α2-adrenergic, 5-HT2A, sigma and imidazoline activity. Agmatine also increases allopregnanolone which is a potent endogenous anti-depressant hormone.

Agmatine is used as an all around drug potentiator, anti-addiction aid, and even antidepressant/psychedelic.

Agmatine produces antidepressant-like effects by activating AMPA receptors and mTOR signaling​

Agmatine, an endogenous amine, has been proposed as a neuromodulator in the CNS, since it is taken up by presynaptic axon terminals, stored in synaptic vesicles, and released through membrane depolarization (Piletz et al., 2013). Moreover, it may be co-localized with other neurotransmitters, particularly with glutamate in nerve cell bodies and synaptic terminals (Seo et al., 2011). Also, it is an agonist for the α-2-adrenergic and imidazoline receptors and an antagonist for the NMDA receptor (Piletz et al., 2013).

These results indicate that the antidepressant-like effect of agmatine in the TST may be dependent on the activation of AMPA and TrkB receptors, PI3K and mTOR signaling as well as inhibition of GSK-3β, and increase in synaptic proteins. The results contribute to elucidate the complex signaling pathways involved in the antidepressant effect of agmatine and reinforce the pivotal role of these molecular targets for antidepressant responses.

https://www.sciencedirect.com/science/article/abs/pii/S0924977X16300074

The fact that the concentration of agmatine in brain was comparable to that of classic neurotransmitters suggested that agmatine might be a neurotransmitter.

As a result of its ability to inhibit both hyperalgesia and tolerance to, and withdrawal from, morphine, and its neuroprotective activity, agmatine has potential as a treatment of chronic pain, addictive states and brain injury.

Chronically, agmatine prevents tolerance to morphine dosing for ten days, blocking tolerance to the delta opioid peptide receptor ligand [d-Pen,d-Pen]enkephalin but not to the kappa κ3 opioid peptide receptor agonist naloxone benzoylhydrazone. Most interestingly, agmatine dose-dependently and significantly attenuates all of the behavioral signs of the morphine abstinence syndrome that is precipitated in morphine-addicted rats by naloxone.

https://www.sciencedirect.com/science/article/abs/pii/S0924977X16300074

 

[4DQSAR]

This strikes me as something @Smyth2 would likely know a lot more about.

I notice a site called https://www.geneticlifehacks.com/ is writing a lot of copy on the subject of agmatine. But call me Mr. Suspicious, but if someone is charging for membership, there is a potential conflict of interest.

I'm sure I must have bored @Smyth2 to death by pointing out that animal models are known to be really poor at modelling depression in man. I only mentioned the above site because I searched for human study and it took me to that page which as I mentioned, has a conflict of interest.

Sci-Hub | | 10.1111/j.1601-5215.2012.00675.x

It's certainly interesting. My first goal is always to ask the author but in this case, that isn't possible since the author passed away some years ago. But I'm just a little surprised that if a paper was publiched in 2012 (and publicattion generally takes years), I can't find any double-blind studies. But that could be me simply not finding it - which happens.

Please don't get me wrong - I commend everyone to read every academic paper they can, but be aware that their is an adage of 'if it looks too good to be true probably isn't true'.

I note it's being sold as a food supplement but that the recommended doses are an order of magnitude lower than the amounts used in that pilot study.

Sci-Hub | | 10.1089/jmf.2014.0026

I did find the above case study at higher doses but if you sell a product, clearly their is a conflict if interest which to be fair, they DO state.

 

[Allylbenzene]

I note it's being sold as a food supplement but that the recommended doses are an order of magnitude lower than the amounts used in that pilot study.

People tend to use a wide range doses, depending on their intention. I've seen reccomended doses range from 250mg to 1000mg. My nutricost agmatine powder says 1g. This person used 2-6g daily.

Agmatine has recreational and therapeutic value. Taken alongside opiates/stimulants/benzos it appears to reduce tolerance build-up & potentiates most drugs. Taken whilst tapering those drugs it appears to reduce withdrawal symptoms.

Anecdotal report on benzo taper

I'm using to get through a benzodiazipine taper I used it the last 5 days amazing relief! I was shocked!

Heres an example of someone taking 2.6g fairly regularly for it's psychedelic and introspective qualities.



2021 review:

Agmatine, a natural polyamine disregarded almost for over 100 years, was discovered in year 1910. Almost after a decade, several researches on Agmatine indicated its modulatory action at multiple molecular targets such as, nitric oxide synthesis, neurotransmitter systems, and polyamine metabolism unbolt the new avenues for extensive therapeutic applications which includes neurotrauma and neurodegenerative diseases, antidepressant, cognitive disorders. Agmatine exerts its varied biological characteristics and therapeutic potential in diverse arena. Agmatine has been extensively researched for its neuroprotective effect in various types of neurological diseases, including stroke and trauma brain injury along with Parkinson's disease, Alzheimer's disease, Hypoxia /Ischemia. In the present review we have summarized the therapeutic potential of agmatine as protective and regenerative properties in the CNS.

View of Agmatine: A potential Neurotherapeutic Agent | Journal of Drug Delivery and Therapeutics

@50shadesofDave

 

[Allylbenzene]

Agmatines benefits for using opioids sustainably, potentiating their analgesic effects and tapering/reducing their dose.

I theorise that many of agmatines benefits arise from it's anti-cortisol and pro-allopregnanolone effects. Allopregnanolone is a potent GABA-A PAM. Cortisol causes excitatory effects via adrenaline, glutamate and acetylcholine (iirc), leading to mental stimulation and anxiety.

Our results indicate that cotreatment of agmatine with morphine produces antinociceptive enhancement via an α2-adrenergic receptor-mediated mechanism and agmatine–morphine combination may be an effective therapeutic strategy for medical treatment of pain.

Agmatine Potentiates the Analgesic Effect of Morphine by an α2-Adrenoceptor-Mediated Mechanism in Mice - Neuropsychopharmacology

The effects of agmatine, which is an endogenous polyamine metabolite formed by decarboxylation of L-arginine, and a combination of agmatine and morphine on tail-flick test have been investigated in mice. Adult male Swiss–Webster mice were used in the study. Agmatine (10, 20 and 40 mg/kg)...

www.nature.com

This review, mainly based on our research work in the past decade, focused on the modulations by agmatine action on imidazoline receptors to opioid analgesia, tolerance and dependence, and its possible neurochemical mechanisms. We went on to propose that agmatine and imidazoline receptors constitute a novel system of modulating opioid functions.

Agmatine and imidazoline receptors: their role in opioid analgesia, tolerance and dependence - PubMed

Agmatine is an endogenous amine that is synthesized following the decarboxylation of L-arginine by arginine decarboxylase. Agmatine exists in mammalian brain and has been proposed as a neurotransmitter and/or neurotransmodulator. Agmatine binds to several targets and is considered as an...

pubmed.ncbi.nlm.nih.gov

The ability of agmatine to inhibit the acquisition and re-acquisition of intravenous morphine self-administration suggests a possible use of agmatine in the treatment of opioid dependence.

Agmatine blocks acquisition and re-acquisition of intravenous morphine self-administration in rats - PubMed

Our previous studies showed that agmatine inhibits morphine-induced conditioned place preference, locomotor sensitization and drug discrimination in rats. In the present study, we investigated the effects of agmatine on intravenous morphine self-administration in rats. At a dose of 80...

pubmed.ncbi.nlm.nih.gov

Systemically or centrally administered agmatine (decarboxylated arginine) prevents, moderates, or reverses opioid-induced tolerance and self-administration, inflammatory and neuropathic pain, and sequelae associated with ischemia and spinal cord injury in rodents.

Immunoneutralization of Agmatine Sensitizes Mice to μ-Opioid Receptor Tolerance - PMC

Systemically or centrally administered agmatine (decarboxylated arginine) prevents, moderates, or reverses opioid-induced tolerance and self-administration, inflammatory and neuropathic pain, and sequelae associated with ischemia and spinal cord ...

pmc.ncbi.nlm.nih.gov

 

[4DQSAR]

I just walked to the shop and wondered if the human diet has changed so that we no longer consume agmatine as part of out diets. If nothing else, there is that famous pair of sketches by William Hogarth comparing the health and wellness provided by beer contrasted by the degradation found in areas where gin was the alcoholic beverage of choice.

Even a small child I can remember my mother quoting an early 18th century saying common around London that said of gin 'drunk for a penny, dead drunk for tuppence'. I just checked and a quarter pint of overproof (60-80% alcohol) gin cost a penny. So tuppence for a pint of modern gin (usually 40% alcohol).

My point being - are most people simply not consuming a compound we may actually need to be well?

I was only able to find small studies of just one claimed benefit (depression) and while it's certainly of value, reading the papers showed that people sort of volenteered so I for one would like to see a larger study which is designed to elimnate any biases that may exist. No study is perfect but you do at least need to double-blind the stufy and use a larger cohort so dosing can be optimized.

 

[Allylbenzene]

I just walked to the shop and wondered if the human diet has changed so that we no longer consume agmatine as part of out diets.

Agmatine is produced from decarboxylated arginine, so what foods contain high levels of arginine, and what dictates arginine decarboxylation?

I could rephrase your pondering as follows...

I wondered if the human diet has changed so that we no longer endogenously produce sufficient protective hormones and ATP.

To which I'd reply:

What causes reduced cellular oxidative respiration?
What causes reduced cholesterol synthesis?
What causes reduced thyroid activity?
What causes the liver to produce less active thyroid hormone (T3) and more of the inactive form (T4/rT3)?

My point being - are most people simply not consuming a compound we may actually need to be well?

I'd agree, but specifically for other compounds in the human diet. Look at the composition of traditional fats, then compare them with cheap modern day fats. Animal feed also influences the animals fat composition. What is the most popular animal feed used today? - soy & corn I think, cheap...

I could also rephrase this pondering as...

My point being - are most people consuming a compound(s) that is unknowingly harming the integrity of our metabolic system?

Some potential answers...

At birth, the baby’s mitochondria contain a phospholipid, cardiolipin, containing palmitic acid, but as the baby eats foods containing polyunsaturated fatty acids, the palmitic acid in cardiolipin is replaced by the unsaturated fats. As the cardiolipin becomes more unsaturated, it becomes less stable, and less able to support the activity of the crucial respiratory enzyme, cytochrome oxidase.

The respiratory activity of the mitochondria declines as the polyunsaturated oils replace palmitic acid, and this change corresponds to the life-long decline of the person’s metabolic rate.

The mitochondria are responsible for the efficient production of energy needed for the functioning of complex organisms, and especially for nerves. The enzyme in the mitochondria that reacts directly with oxygen, and that is often rate limiting, is cytochrome oxidase.

This enzyme is dependent upon the thyroid hormone and is inhibited by nitric oxide, carbon monoxide, estrogen, polyunsaturated fatty acids, serotonin, excess or free iron, ionizing radiation, and many toxins, including bacterial endotoxin...

The German demonstration that spontaneous cancer was eliminated on a fat free diet preceded the really awful, incompetent study that supposedly demonstrated the essentiality of polyunsaturated fatty acids, and in the 75 years since the German study a tremendous amount of information has accumulated showing both the toxicity and the non-essentiality of the polyunsaturated fatty acids. But there has been no financial support for publicizing the protective effect of not eating vegetable oils or fish oils. To the contrary, vast amounts of money are being spent in the promotion of the various polyunsaturated fats as foods.

The editorial boards of many of the journals are packed with industry flacks who are apparently willing to publish any junk that helps to sell soy oil, canola, waste fish oil, or algae oils. And researchers have to get grants to stay in business.

As early as 1951, it was known (Kunkel and Williams, J. BioI. Chern.) that the polyunsaturated fatty acids strongly inhibit the crucial respiratory enzyme, cytochrome oxidase, and that inhibition of this enzyme has a very important effect on the whole animal suppressing its metabolic rate, reducing the number of calories it can burn. It is now known that polyunsaturated fats interfere with thyroid hornone in just about every conceivable way.

 

[4DQSAR]

We have somewhat drifted OT so I suggest it more appropriate to begin a new thread. I mean, mods can do that but I can't.