I'm not sure if anyone else experiences this, but whenever I've plugged O-DSMT dissolved in pure PG, I'd get this pretty uncomfortable sensation. It's something I've experienced with a couple other drugs as well. Dissolving in a mixture of PEG-400 and PG however, no discomfort.

Anybody have experience with using different solvents? Is this discomfort experience just me or it common? my doses are like 70mg btw

I know it may be a stupid question but u never know

This post is a bit messy, but from what I read substituted cathinones can cause a pattern of brain damage almost indistinguishable from schizophrenia. I'm writing this post because this is with a very high probability what happened to me.

I have a schizophreniform psychotic disorder resulting from frequent and high dose abuse of synthetic cathinones / pyrovalerones. My first psychosis appeared after months of use, first intranasal but the last month entailed vaping my subsstances.

My first psychosis cleared up spontaneously after a few days, my second required medication but did not come back after cessation of medication, but I was stupid and continued abusing pyrovalerones and my third psychosis is still active, and has been active for more than 1.5 years. I have auditory and tactile hallucinations, like demons are terrorizing me. The auditory hallucinations are always negative in character, with two females and one male voice interfering in every thought process and practicing brain washing techniques by repeating things a lot and at times promising improvement but then holding off the improvement (fake goodbyes). The tactile hallucinations feel like a demon is torturing my feet with hot embers and knives, cutting off bits of skin, and there is a strange clicking, warping and tightening sensation as if someone is rewiring the sensory neurons in my feet.

I have no underlying succeptibility for schizophrenia. I am 39 and I have used a lot of drugs, from LSD to ketamine to all kinds of amphetamines to cocaine to heavy marijuana use, for two-and-a-half decades, and never went psychotic - except once where I combined many stimulant drugs in much too high dosages but it was only a few hours and directly relatable to the combined drugs in my system duration of action.

As I do not wish this type of psychosis on anyone I did some digging on what substituted cathinones do in the brain and what damage they probably leave behind. I was surprised to find that the pattern of damage (glutamate excitotoxicity and dopaminergic neurotoxicity) is very much in line with what is seen in schizophrenia.

So I have put this here as a harm reduction post, to make people think twice before experimenting with substituted cathinones / pyrovalerones. You give these substances one hand and they take your whole arm, and then your soul. You'll be hooked in no time and stopping a binge is impossible for most. And then psychosis with these substances is very common.

Substituted cathinones

The number of synthetic derivatives of cathinone, the primary psychoactive alkaloid found in Catha edulis (khat), has risen exponentially in the past decade. Synthetic cathinones (frequently referred to as “bath salts”) produce adverse cognitive and behavioral sequelae, share similar pharmacological mechanisms of action with traditional psychostimulants, and may therefore trigger similar cellular events that give rise to neuroinflammation and neurotoxicity. Synthetic cathinones produce varying effects on markers of monoaminergic terminal function, and can increase the formation of reactive oxygen and nitrogen species, induce apoptotic signaling, and cause neurodegeneration and cytotoxicity. Like their traditional psychostimulant counterparts, synthetic cathinones appear to induce neurocognitive dysfunction and cytotoxicity, which are dependent on drug type, dose, frequency, and time following exposure. There is some evidence for an ability of MDPV to down-regulate expression of the glutamate transporter GLT-1, which is responsible for clearance of the majority of extracellular glutamate, and as a result this down-regulation of GLT-1 raises extracellular glutamate levels, potentially leading to excitotoxicity. (https://pmc.ncbi.nlm.nih.gov/articles/PMC6486871/#R116).

Dopamine, glutamate and schizophrenia

Glutamate and dopamine systems play distinct roles in terms of neuronal signalling, yet both have been proposed to contribute significantly to the pathophysiology of schizophrenia. Converging evidence indicates that genetic and environmental risk factors for schizophrenia underlie disruption of glutamatergic and dopaminergic function. However, while genetic influences may directly underlie glutamatergic dysfunction, few genetic risk variants directly implicate the dopamine system, indicating that aberrant dopamine signalling is likely to be predominantly due to other factors. Schizophrenia is a severe mental disorder characterized by positive symptoms such as delusions and hallucinations, negative symptoms including amotivation and social withdrawal, and cognitive symptoms such as deficits in working memory and cognitive flexibility. The finding that antagonists of a specific glutamate receptor, the N‐methyl‐D‐aspartate (NMDA) receptor, induce psychotic symptoms has led to a wealth of research implicating the glutamate system in the pathophysiology of schizophrenia (https://pmc.ncbi.nlm.nih.gov/articles/PMC6953551/).

Dopamine related neurotoxicity

Abnormally high levels of dopamine cause high levels of DA-o-quinone, a metabolic product of dopamine that is neurotoxic and causes degeneration and dysfunction in dopaminergic neurons. For instance, oxidative stress shortens cellular lifespan. The expansive nature of oxidative damage includes mitochondrial dysfunction, DA autooxidation, α-synuclein aggregation, glial cell activation, alterations in calcium signaling, and excess-free iron (https://pmc.ncbi.nlm.nih.gov/articles/PMC4684895/). In neurons, mitochondria are the major sites for energy production, generation of reactive oxygen species (ROS), calcium signaling, developmental and synaptic plasticity, and the arbitration of cell survival and death. Many gene products are localized in the mitochondria, and mutations of these genes have been linked to neurological and psychiatric diseases. Mitochondria-mediated oxidative stress perturbs Ca2+ homeostasis, and apoptosis also contributes to the pathogenesis of prominent neurological diseases, including AD, PD, Huntington’s disease, stroke, amyotrophic lateral sclerosis (ALS), and psychiatric disorders (https://pmc.ncbi.nlm.nih.gov/articles/PMC9676987/). DA-o-quinone causes mitochondrial dysfunction, inflammation, oxidative stress, and dysfunction of the ubiquitin-proteasome system (https://link.springer.com/article/10.1007/s11064-008-9843-1).

Proline related neurotoxicity and enhancement of glutamate neurotransmission

Proline dehydrogenase, mitochondrial is an enzyme that in humans is encoded by the PRODH (proline dehydrogenase) gene. The protein encoded by this gene is a mitochondrial proline dehydrogenase which catalyzes the first step in proline catabolism (https://en.wikipedia.org/wiki/Proline_oxidase). Proline metabolism is especially important in nutrient stress because proline is readily available from the breakdown of extracellular matrix (ECM), and the degradation of proline through the proline cycle initiated by PRODH, a mitochondrial inner membrane enzyme, can generate ATP. This degradative pathway generates alpha-ketoglutarate and glutamate (https://en.wikipedia.org/wiki/Proline_oxidase). Proline catabolism resulting in glutamate production adds to the already excessive levels of glutamate in the case of glutamate excitotoxicity.

Proline disrupts GABAergic transmission through glutamate decarboxylase blockade, leading to higher levels of glutamate and exacerbating glutamate excitotoxicity (https://pmc.ncbi.nlm.nih.gov/articles/PMC9676987/). High levels of proline increase prefrontal dopamine signaling through interference with glutamatergic pathways, normally reducing vulnerability to an otherwise prefrontal hypodopaminergic state, but exacerbating abnormally high levels of dopamine if present. High levels of proline alter glutamate and dopamine signaling, including an enhancement of glutamatergic synaptic transmission and prefrontal dopamine transmission, exacerbating the already high levels of both neurotransmitters (https://pmc.ncbi.nlm.nih.gov/articles/PMC5048199/).

There is a mechanistic link of PRODH gene dysfunction to dopaminergic neurotransmission, a notion that is supported by recent imaging genetics findings that show a convergent effect on prefrontal-subcortical interactions (https://pmc.ncbi.nlm.nih.gov/articles/PMC2838993/). High levels of dopamine lead to high levels of proline bacause dopamine stimulates proline biosynthesis by upregulating PYCR1 (pyrroline-5-carboxylate reductase 1), a key enzyme in proline synthesis, via activation of the PI3K/Akt/mTOR signaling pathway (ChatGPT).

Glutamate excitotoxicity

Synaptic glutamate is taken up by astrocytes expressing EAAT2/GLT-1. These transporters are down regulated in a number of pathologic processes (https://pmc.ncbi.nlm.nih.gov/articles/PMC4640931/). Substituted cathinones also down-regulate the GLT-1 glutamate transporter, which is responsible for clearance of the majority of extracellular glutamate, and as a result this down-regulation of GLT-1 raises extracellular glutamate levels, potentially leading to excitotoxicity (https://pmc.ncbi.nlm.nih.gov/articles/PMC6486871/#R116). Down-regulation of GLT-1 makes it harder for astrocytes to remove excess glutamate from the synaptic cleft (https://pmc.ncbi.nlm.nih.gov/articles/PMC4912874/). The transporters act first to buffer glutamate away from the synapse, and transport glutamate into glia at a slower rate (https://pmc.ncbi.nlm.nih.gov/articles/PMC6033743/). Excess glutamate over-excites the NMDA-receptor, causing increases in intracellular Ca2+ by directly opening ion channels and secondarily affecting calcium homeostatic mechanisms. The decreased sodium gradient across the cell membrane caused by the glutamate receptor–coupled channels reduces the ability of the sodium gradient–dependent antiporter to remove intracellular calcium. The ATP-dependent calcium transporters as well as the energy-dependent sodium potassium pump are adversely affected (https://pmc.ncbi.nlm.nih.gov/articles/PMC7973850/). Stimulation of the GluN2B-containing NMDA receptor in the extrasynaptic sites triggers excitotoxic neuronal death via PTEN, cdk5, and DAPK1, which are directly bound to the NMDAR, nNOS, which is indirectly coupled to the NMDA receptor via PSD95, and calpain, p25, STEP, p38, JNK, and SREBP1, which are further downstream (https://pubmed.ncbi.nlm.nih.gov/24361499/). Changes in GABA-A subunit expression lead to changes in the phasic inhibition of the presynaptic pyramidal cell and deficits in membrane repolarization, ultimately leading to GABA interneuron cell-death (https://pmc.ncbi.nlm.nih.gov/articles/PMC4640931/).

21q11.2 deletion syndrome

Chromosome 22 contains a region named 21q11.2, that codes for both the COMT (catechol-O-methyltransferase) gene and the PRODH gene. COMT codes for proteins that break down dopamine, PRODH codes for proteins that break down proline. Schizophrenia occurs in about one in four individuals with 22q11.2 deletion syndrome. In 21q11.2 deletion syndrome, COMT is expressed 50% less compared to controls, leading to a reduced ability to break down dopamine. Dopamine transporters are relatively sparse in the prefrontal cortex, and the removal of dopamine there may be more impacted by COMT activity and the interaction with proline, as compared with subcortical regions (https://pmc.ncbi.nlm.nih.gov/articles/PMC5048199/). When PRODH is knocked out in mice, high proline levels lead to an under-expression of COMT in the prefrontal cortex as a compensatory measure to prevent a hypodopaminergic state. Subjects with reduced expression of PRODH show increased neurotransmitter release at glutamatergic synapses (https://www.nature.com/articles/nn1562).

Signal-to-noise ratio

Dopamine is thought to modulate the signal-to-noise ratio of neurons in the prefrontal cortex (https://pmc.ncbi.nlm.nih.gov/articles/PMC7575248/). Due to neurotoxic dopamine and glutamate levels, neurons in the prefrontal cortex experience a decrease in the signal-to-noise ratio in relation to afferent signals coming from diverse brain regions including sensory neurons. This leads among other behavioral effects, to aberrant salience, which underlies visual, auditory, olfactory, gustatory, tactile, proprioceptive, equilibrioceptive, nociceptive, thermoceptive and chronoceptive hallucinations. (https://pmc.ncbi.nlm.nih.gov/articles/PMC7575248/).

TLDR;

Substituted cathinones can cause a syndrome that is practically indistinguishable from schizophrenia.

Substituted cathinones downregulare glutamate GLT-1 transporters, lowering astrocyte ability to remove extracellular glutamate. There’s a combination of high levels of dopamine being metabolised into DA-o-quinone causing damage and cell death to dopaminergic neurons and inhibited activity of glutamate GLT-1 transporters causing glutamate excitotoxicity, leading to dysfunction and death of GABA neurons in the hippocampus, prefrontal cortex and superior temporal lobe, damage that contributes to hallucinations. Furthermore, compensatorial decrease of dopamine activity in the prefrontal cortex in response to heightened proline levels lead to a reduced signal to noise ratio (increased entropy) in the prefrontal cortex with regard to afferent signals from sensory neurons as well as the superior temporal lobe and the hippocampus, further contributing to hallucinations.

Hello guys,

Is it dangerous to take 4 fma and 25E NBOH together ?

Did it taste kind of like gasoline to you?

Update: So I am definitely getting lots of warm, happy, euphoric feelings. Body feels good. It's light Molly 'lite' lol. Definitely not one i can take and go to work on... Shit might get weird in the office real quick! My body wants to move and stretch and be touched - yup i am officially high 😂

I've been apprehensive about using any of the NBOH and NBOMe substances since I first heard about them due to their perceived danger

But recently whilst stocking up on acid I noticed 25E-NBOH and its insanely cheap price. 25 1.2mg tabs for almost a euro per tab? How could I resist?

I took half a tab an hour 1/2 ago and felt the comeup with half an hour. I then immediately redosed the other half a tab because it felt fucking amazing.

This feels like psychedelic speed, but it's not pushy! I want to move but I don't feel compelled to keep moving. Already at 1 hour the visuals are mild but entertaining! Colour looks simply fantastic and my TV has this cool really far depth of field effect. Like I could almost reach into it.

I legit cannot stop laughing at the show I'm watching. My headspace is crystal clear as well! I might actually try making some music because it's making me feel a little inspired

The taste isn't that bad either! I hardly even noticed it but it my tongue felt a bit numb for around 20 minutes.

Also, I haven't felt any vasoconstriction nor nausua despite having a full meal less than 2 hours ago. My BPM is also well within my comfortable range. Far less than other stimulants

EDIT: 3 hours in, and it feels like I'm just past the peek, but the visuals are still beautiful.

One interesting thing to note, however, is that this is the first psychedelic I've used that feels "morish." This drug really has a stimulant backbone to it that feels fantastic. However, it also seems to have a short duration. I'm going to redose half a tab and lock the rest away.

EDIT: 5 hours in, I forgot to refose the half a tab I mentioned earlier 😅

The strong visuals are gone, but colours still look so beautifully vibrant. There's a wonderful warm body high still present.

Everything I've read about this substance says it makes you crazy nauseous, but this trip has me STARVING rn. Gonna get some 🍕

Is there any reason to keep them sublingually before swallowing, like you would a tab of acid, considering it has to be absorbed in the intestine to convert to a benzo?

Also, I’ve taken 3mg around 2 hours ago, although on a full stomach, and I can’t say I’m really feeling anything? I read that it was a relatively chill and underwhelming benzo and of course there’s the classic delusions of sobriety, but I haven’t taken any benzos in a year or more so I shouldn’t have any tolerance (although I do drink pretty regularly), this lack of effect seems kinda weird.

Just wondering about anyone else's experience with the substance really, or if I should just try again with 4 on an empty stomach

Anyone using this for functional purposes? It's convenient how fast, rapid and cheap it is. Perfect if you don't want to commit to a full use of an amphetamine/phenidate. Recent post a user mentioned he preferred it to them for his work, gave him nice stimulation without the robotic focus of the others.

I don't do the whole gigadegen vaping/stimfap thing, I know it's a factor for many but don't bother warning me about this. I have a 1g pack on my shelves for a couple months now and never had any problems, still haven't finished it. Problem is it's not as productive as amphetamines/phenidates actually, trades robotic feeling for scatterbrain-ness for me, and it gives me an anxious heart even in small doses, so the returns diminish extremely fast.

Anyone here using NEP (or similar non-serotonergic cathinones) for productivity purposes please report your regimen or any tips to improve effects.

Yeah, basically planning on taking a decently small dose of 5-MAPB near the end of the 2-FA effects (which are going to be soon).

Not considerned about the "don't combine stims, it's bad for your heart", I know they are and all stimulants are, not just these. I'm just wondering about the synergy and anecdotal reports. If any of you have tried this and if so, how was it synergy-wise

Thanks

Did someone ever try this?

What is it like figured it would be great against the side effects nep can give?

Hello guys.

I'm about to take 2c-b-fly 10 mg pill and I have two questions about it.

I was testing 2c-b-fly once 2 years ago with my good friend. And it felt amazing. After long break from this compound it's finally in my hands again. I'm experienced in psycho's I ate many of acids, mdma and tryptamines in my life. But year after year every psycho hits me stronger than before for some reason. My last psycho trip was on ~15 mg 4-aco-met. And it was to intense in my head space that I had to rescue my self with small portion of benzo's to fight anxiety. Friend of mine who took estimated 5 mg of 4-aco was feeling heavy on head too. Maybe pills was over dosed or sth. That's why my eyes stopped on 2c-b-fly

Any way.

I still have some of 4-aco-met. Is it a good idea to take small dose like 5mg of 4-aco with 10 mg 2c-b-fly? I'm curious cause on 2c my head space was very light but visuals was weak on the other hand 4-aco have strong mindfuck but strung visuals. Is it possible it's gonna by good synergy od completely disaster ?

And second questions is re dosing 2c-b-fly have sense ? Let's say I'm about to take second 10 mg pill during peak. Or maybe it's just better to take 20 mg at once/stay with 10 mg

And by revolutionary I mean something thats not necessarily "good" for you like LSD but something that gets popular because they hit home in your brain so fcking hard. Something like Mephedrone and APVP with each's analogues from the latest drugs that were found or at least commercialized.

Ofc they always synth new analogues from every substance there is but I wouldn't be surprised if we already hit the peak so to say.

Hi,

as Pemoline RC derivatives, Cyclazodone and NMC are touted to exert some liver toxicity effects, as studies in students in the 1970's showed Pemoline to induce liver toxicity in at least 2% of subjects.

Therefore it is popularly assumed that the Cyclazodone should theoretically exert adverse effects on the liver,

do you have experience with thise compounds and liver health ?

There at least doesn't seem to be any consensus on the issue online.

Thanks !

Hi i’ve been experimenting with rcs for the last year and honestly its kinda getting out of my hand. I started using every weekend for last half year sometimes even in the middle of week. I use mainly dissos, emphactogens and psychedelics. I think i need to set some limits so i wanted to ask how often do you use and how big impact it has on your life and health?

I have stimulant naive and I ordered it on a whim. Any have experiences with it?

i have obly experience with snorted 5-meo-dmt and it was fun

Sup

Last days I felt a pretty annoying sensation: when I am coming down from 3FA, I am getting a heavy chest and out of breath sensation. Together with some anxiety (this is normal and a sign of the comedown). But the fatigue and the trouble breathing is worrying me. I already had a cardiologist planned anyway, but still, anyone has any insights?

The thing is that while 3FA is working I am getting no high bp (measured, 125, 30 over 70 or so). HR is also ok at 60, sometimes 70

Havent measure it when coming down, but it almost feel like low BP.

Sometimes palpitations too but this one is more normal, ,have had that in the past when coming down.

What could this be?

I only tried 2c-b a couple of times and high doses gave me nausea, and were much more physical than classical psychedelic (psilocybin, LSD, etc.). I would like to try MAL one day for sure, but wanted to know your opinion, compared to what I already know (2c-b). Thanks!

I was just wondering if there was any point to combining the two at the same time. I'm aware It's not as simple as the two drugs countering each other and I'm not sure how diazepam would feel on a decent dose of mph so I ended up trying it myself today,

Setting:

• M21 - Anxiety/ADHD
• 135 lbs
• 5'10
• Medium-Low GABA tolerance
• Medium-High dopaminergic tolerance (daily use)
• Commuting home from university after class
• Depressed and exhausted

T+0:00 – 40 mg methylphenidate XR (Biphentin) to start the day

T+5:00 – 3mg of Rilmazafone (Rhitmy) on the bus ride home after university classes

T+5:30 - Deep relaxation in my shoulders and back muscle. I can feel the tension in my body starting to release. Still very functional.
The methylphenidate sharpness is taking a step back and I'm even considering engaging in conversations with strangers.

T+6:00 - Complete suppression of stress response and able to communicate with strangers without overbearing dread. Judgment of others doesn't cross my mind at all. Not very sleepy and my motor skills aren't too impaired.

T+6:30 - I wish I could be in this state forever. I feel normal at this stage 1:30 after dosage of Rhitmy.
Perfection. Reached normalcy.

T+7:30 – 30 mg of Avizafone (Pro-Diazepam) once home with a small quantity of 5% alcohol beer.

In conclusion, dosing the GABA tabs past the mph peak has allowed a smooth transition into deep relaxation while remaining functional. Good experience overall. I think I'll continue to use Rilmazafone as needed on occasion to deal with my anxiety. I'll have to consider lowers doses to prevent trouble concentrating but I feel like the ability to not be anxious even at lower doses is worth at least attempting it.

About Avizafone preservation and bacteria growth prevention

I will add this here in relation to my previous post about preservation of Avizafone:
The plastic containing the 20% alcohol and Avizafone solution started Yellowing and this could be indicative of degradation of the plastic and of the product according to a study about Avizafone stability. I have now switched the solution into an amber glass container stored in the fridge.

The solution lets precipitates form at the bottom after sitting for a while but after mixing it again before use it seems to dissolve completely again for proper dosing. No other issues to report.

So if I have to pick between 2F-DCK, O-PCE or DMXE which one would be the mist fun for a night of videogames?

So tomorrow ill be meeting some friends after having stayed inside for a month. Two weeks ago i ended my diazepam taper. So tomorrow the plan is to go to dinner, afterwards were going out to party. I struggle with extreme anxiety so if it was up to me i wouldnt go, but u gotta socialize from time to time right? My problem is that im never at ease. I Just wanna have a good time. So at this moment i have pyrazolam, bromazoalm and 2f ketamine. Been using 2f ketamine for like 9 days straight now. I will probably be drinking tomorrow but which one of the three rc's i mentioned will help me the most? Small sidenote: ive abused the f out of benzos and also opioids while combining them with liquor so im aware of the risks if i mix them. My idea would be to take the bromazolam. But then again, i hear that a lot of people use ketamine to party. Any advice is welcome

Title pretty much. Been loving BDO so far and have a day off soon that I plan to spend tripping on acid. Can I safely mix these together? Are they even worth mixing?

Just tried 5-meo-mipt for the first time at around 5mg and noticed I've been "crying" for the last hour despite not feeling sad or having even thought of anything emotional.

Just feeling like euphoric melty wax and got my eyes wet for no apparent reasons.

Unless I just didn't notice it before other psychedelics only make me cry occasionally by amplifying my emotions but not like that producing tears without any reason

So I read a few reviews of DMNPC and was extremely interested due its positive effects profile

So I did a little research and wouldn't you know it, this stuff is made using arecoline!

What's that, you've never heard of arecoline? It's the active ingredient in betel nut, a very popular plant in asia with stimulant properties due to arecoline.

I actually made a post about betel nuts ages ago when I first heard about the ban and was told it wasn't worth investigating further.

And yet here we are, the active compound in betel nut lead to an actually worth while stimulant that's legal!

But here's the interesting part, DMNPC doesn't have a phenylethylamine backbone, it's a piperidine derivative meaning it's not explicitly covered by the upcoming NL ban nor any previous legislation.

In fact, there's likely quite a few more potentially interesting substances that can be made from arecoline!

So don't be too disappointed about the ban, even with stupid legislation there's still a whole world of interesting compounds to fuel your multi day stim fap sessions :>

Hey all, I am a bit of a benzo enthusiast and have tried most ofthe rc and rx benzos that have been available over the past 5-10 years at some point. A reliable vendor of mine has just started offering nifoxipam, and while i did use the search bar in this sub and others, i’ve seen lots of contradictory results, especially pertaining to dosage/source (things being under/over dosed).

I’m curious if anyone here has any experience with nifox and could share that experience and how it compares to other rc and rx benzos.

I'm looking to buy nb dmt and I heard to consume it, you should heat it. I don't have currently neither a way vape nor a pipe and I don't know which one is the best. For around 45€ I can get the Yocan Orbit or for under 10€ a pipe. And another question, do I have to mix it with soda or another base e before consuming for good effects?

Disclaimer: i do not advocate use of any psychodelics in any shape or form.

So I was wondering, since they say the psychedelics like lsd and what not can have a "healing" effect on some people that suffer from depression or ptsd. I was just wondering if there are any people here with autism/adhd that have experienced benefits from psychedelics on the long term. Like did it fix some of the problems you had? Did it clear up some doubts/internal struggles? Im actually curious about the potential of such substances of such psychedelics. Also, did you do micro dosing or just a "regular" dosage?

Hi i am going to rave within two weeks and i am thinking about combining 6 apb and 5 mapb. I think 70mg of 6apb and 50mg of 5mapb can be nice. I am pretty experienced with both substances separetly. What do you think about combining those two? I will maybe add some bumps of 3fa :)