Well it all started back in December around this time last year. He took 80mgs 3c-p, ingested meth earlier in the day, and 60 micrograms of acid, and that was all. I watched him go unconscious first, he was still breathing for 12 hours in the recovery position. I kept checking his breathing, and trying to wake him up. Thinking he just crashed hard from meth

I go to sleep on lyrica, and all of a sudden. I wake up and he’s still alive. I’m talking to discord friends trying to figure out if he’s okay. When all of sudden I watched his last breathes. I cried so much, and I immediately missed him. His face blue life less, me just hoping he got past the death of my mother, and saw the sacred geometry. Of course I try to take a pulse, and call 911 but he’s gone :(

I just had to come by to ask you guys, that have maybe even done similar dosages. What he would’ve saw, and how it changed your perception. I almost tried the batch myself. But my traumas wouldn’t let me I feared it was another analog. So I threw it away, if I knew it was only that of course I would try it. I might not do 80 but my heart wants to just to know that he wasn’t in pain.

I’m sure there’s many people it has helped. I’d love to be one of them myself. I have an open mind, and a positive attitude. A lot of people try to make me feel guilt for what happened. But I know ultimately I only wanted his best interests. I wanted to help him work through his traumas. I can’t let this negative experience stunt my growth as a person. Especially with strong psychedelics, and psychedelic phenethylamines.

O-DSMT isn't doing it for me anymore, and I would like to try something stronger. Which one is the most euphoric in your experience?

Cychlorphine HCl,

Isotonitazepyne HCl,

Methiodone IC-26,

N-Desethylisotonitazene,

Metonitazepyne,

Protonitazepyne

Any opinions are welcomed and thank you in advance

So will any new cathiones like 2-mmc etc comeout or all the possible combinations of chemicals have been done and marketed ?

I know it's possibly neurotoxic but that's all that was available. Does anyone know what it's like or has tried it? Also what would be the best ROA? Thanks

I don’t have a super high tolerance, but once in a blue moon i get oxy and just pound thru 450 mg in a single night. Id say i do that twice a month. Anyways though, i have never tried meto and ofc i hve heard all the horror stories but my friend has the fake oxy pills containing it, which he tried and did not overdose. I took a small dose orally and am enjoying it a lot but i don’t want to do it again cuz i love oxy and I am set on stone on that being the opiate i’ll typically do. My question, is hypothetically i don’t get addicted to it and continue to do it, will doing it this once fuck my tolerance to the point where I can’t do oxy anymore?

I have had it once. I got high but didn't really notice. Other people did though. I just bought 5 grams of it. And want to know more. I'm also considering buying isotonizypene next month.

Specifically JWH-210,.

Tried to find some info on this combination but it's very hard to find anything, is it a good combo?

Both insufflated and oral, what is the best dose for studying and which one is most euphoric?

I'm writing this as I'm coming down from a trip of DPT and ketamine and it's with enormous sadness that I can say that it is over for me.

With DPT I truly experienced the most pristine form of pure cosmic psychedelia, stargazing fantasy and euphoria in mythical realms of the mind, got lost in magmatic abyss of the psyche and met the most pure form of joy and freedom.. a spark of what I then understood to be God, or at least for what I recognize God in: the power, the energy of life, the joy.

But to touch the sky also mean you gotta fuck with the ground at some point, and the truth is that it's too much for me now, now I'm growing, now what once was an uncertain future my young punk ass wouldn't care about is becoming the today, and DPT sometimes is truly a beast.

It's now too much of a commitment, once I realized how harsh is for my body, or at least for what I feel like is doing to my body, it's kind of hard to enjoy it, it just put all your senses and nervous system in such an otherworldly and high energy state that It makes me feel like a short-circuit could happen and fuck me forever (heart attack). How this drug alters your body is totally different from any other psychedelic I tried (I tried all of them) and sometimes feels like it's stressing me too much wich kind of compromise my ability to let go, and with DPT you truly gotta be able to let the fuck go and relax or you gonna dive in the deepest nightmare of your life, it happened once to me and only God knows how I made it through it.

DPT is the most potent psychedelic and entheogen in the world and it will forever have a special place in my heart, for the most profound and fulfilling experiences of my life.. but as an old psychonaut used to say: when the message is received is time to hang up the phone.. or something like that ahah

Acetylcholine and Sigma receptors - ligands and pathways to address therapeutic outcomes underutilized?

Sigma-1, Nicotinic, Downstream Pathways, etc, being a relevant way to assess biological impact on behaviors and physiology of various types of species including humans is relevant for mental health.

https://www.nature.com/articles/35077000

Because nicotine can activate AKT via PI3K, we examined the protein levels of Bcl-2 and Bcl-x. We found that treatment with nicotine for 24 h increased the levels of Bcl-2 and Bcl-x, and this was inhibited by LY294002, which indicates the involvement of the PI3K pathway in nicotine-induced Bcl-2 and Bcl-x upregulation.

overexpression of Sig-1Rs significantly up-regulated Bcl-2. Overexpression of Bcl-2 member Mcl-1 in neurons enhanced surface expression of endogenous α7 nAChRs. Furthermore, the activity of several other neuronal nAChR subtypes is also enhanced by NACHO17. Biochemical studies show that NACHO mediates α7 pentamer formation, as NACHO is required for receptor labeling by α-bungarotoxin (α-Bgt)16, which binds at the interface between assembled α7 subunits4,18. Interestingly, resistance to inhibitors of cholinesterase-3 (Ric-3) protein, which is required for nAChR function in Caenorhabditis elegans19, synergizes with NACHO to promote receptor assembly and function16. https://www.nature.com/articles/s41467-019-10723-x

In this manuscript, we demonstrate that S1R is required for biosynthesis of the Atg8 family proteins LC3B, GABARAP, and GABARAPL2. Cells lacking SIGMAR1 show reduced levels of many Atg8-family proteins and impaired autophagic flux.

The intra-α subunit ECD-TMD interface is important to channel function in both human adult and Torpedo nAChR. The transmembrane domain (TMD) of α7nAChR has been identified as a target for positive allosteric modulators (PAMs). https://www.nature.com/articles/s41467-024-46028-x

demonstrating that Nkcc1 overexpression in adult mice restored plasticity to a similar level as observed in the juvenile brain. Activation of TRPV1 by exogenous agonists can increase the expression and function of NKCC1 protein in DRG, which is mediated by activation of PKC/p-ERK signaling pathway. Sigma-1 σ-1 receptor activation inhibits glutamate release from rat cortical nerve terminals. This effect is linked to a decrease in Ca²⁺ caused by Ca²⁺ entry through presynaptic voltage-dependent Ca²⁺ channels and the suppression of the PKC signaling cascade. Furthermore,results suggest that DRG NKCC1 may participate in the inflammatory pain induced by TRPV1. Pursuant to its local anesthetic properties we have shown, for the first time, that nicotine inhibits TTX-resistant sodium channels. In addition, we have also shown, for the first time, that nicotine sensitizes responses to TRPV1 receptors. https://journals.physiology.org/doi/full/10.1152/jn.00922.2003

In all types of nAChRs, agonists such as ACh itself or nicotine-induced ion channel opening and evoke influx of Na+ and Ca2. Sodium-Channel literature results are consistent with the idea of a sigma-1 protein behaving like either a "chaperone" or a regulatory subunit associated with nNav1.5. Increasing sigma-1 expression to the cells reduced the surface expression of nNav1.5 protein. https://pubmed.ncbi.nlm.nih.gov/23139844/

It is unlikely that nicotine-induced protection against glutamate neurotoxicity is due to its direct action on NMDA receptors though there are some reports indicating that nicotine partially inhibits NMDA receptors. The sigma-1 receptor modulates NMDA receptor synaptic transmission and plasticity via SK channels in rat hippocampus. Overall, results indicate that Ca2+influx through post-synaptic NMDARs is required for the σR-1 activation to exert the enhancement of the NMDAR currents.

nAChRs, especially α7 nAChRs, generate specific and complex Ca2+ signals that include adenylyl cyclase, protein kinase A, protein kinase C, Ca2+-calmodulin-dependent kinase, and phosphatidylinositol 3-kinase (PI3K). Sigma-1, residing mainly at the mitochondria-associated Endoplasmic-Reticulum (ER) membrane (MAM), where it chaperones IP3R3 to ensure proper Ca2+ signaling from the endoplasmic reticulum into mitochondria.

The nuclear pore complex (NPC) has been coined “The gate to neurodegenerative diseases”58. Here we report the existence of the first molecular chaperone at the NPC and show that this chaperone, the Sig-1R(Sigma-1 Receptor), being therapeutic for ALS patients. Firstly, we used a human cell line here in the present study. Secondly, we have shown in the past that results from cell lines perfectly mimic the results from rodent brain39,59. https://www.nature.com/articles/s41467-020-19396-3

Immunohistochemistry showed marked loss of nuclear TDP-43, was accompanied by reduction of choline acetyltransferase (ChAT). Choline O-acetyltransferase) is an important enzyme catalyzing the transfer of acetyl group from Acetyl-CoA to choline for synthesis of acetylcholine (ACh), which is a major neurotransmitter in the brain. SIGMAR1 was consistently shown to be co-localized with neuronal nuclear inclusions in TDP-43 proteinopathy, five polyglutamine diseases and INIBD, as well as in intranuclear Marinesco bodies in aged normal controls.

Young hippocampal neurons in α7 nicotinic KO mice have a prolonged period of GABAergic excitation because of delayed appearance of the mature chloride transporter KCC2 and extended presence of the immature chloride transporter NKCC1.

These results suggest that antinociceptive effects of α7 nAChR PAM are associated with downregulation of hippocampal BDNF and p-NKCC1 and upregulation of KCC2 in a mouse model of inflammatory pain. Respectively, nicotine and neurotrophins show similar properties in terms of time-course and signal pathways of neuroprotection. https://www.ncbi.nlm.nih.gov/books/NBK543551/ Results suggest that activation of cholinergic pathway(both muscarinic and nicotinic) restores GABAergic driving force and temporal order recognition deficits in Ngfr−/− (NERVE GROWTH FACTOR KNOCKOUT) mice. Stimulation at sigma-1 receptors by sigma-1 receptor agonists and subsequent interaction with IP3 receptors are involved in the mechanism underlying the potentiation of NGF-induced neurite outgrowth by sigma-1 receptor agonists. Https://pubmed.ncbi.nlm.nih.gov/18647636/

PC12 Mutagenized cell variants reveal striking differences in the expression of Sodium channels and Nicotinic receptors when compared to wild-type PC12 cells. Even in the absence of nerve growth factor (NGF), the mutant cells express functional Na channels and Na channel mRNA at levels exceeding those in wild-type PC12 cells differentiated with NGF. In contrast, acetylcholine-induced currents were evident in only a small proportion of cells, presumably due to the altered pattern of expression of mRNAs encoding individual nAChR subunits. The altered ion channel expression in these variants provides an avenue for analyzing Na channel and nAChR channel function, as well as for identifying mechanisms governing their expression. https://link.springer.com/article/10.1007/BF00238418

Interactions in Dynamic reciprocity of sodium and potassium channel expression in a macromolecular complex involve Sigma-1 receptors. Such as Sigma-1 mediated regulation of ion currents interacting with various channels, like Kv1.2 channels, increasing their surface expression. Sigma-1 also inhibit Kv1.3, Kv1.4, and Kv1.5 channels. While regulating Kv2.1 channels, and inhibiting L-type voltage-gated calcium channels. Also inhibiting N-type Ca2+ channels currents. And inhibit voltage-gated sodium ion channels: Nav1.2/1.4 and Nav1.5. Sigma-1 regulate hERG channels while inhibiting acid-sensing ion channels (ASIC1a). https://www.sciencedirect.com/science/article/pii/S0149763421004796

NGF-dependent increase in phosphoinositide hydrolysis in PC12 cells is due to selective phosphorylation of PLC-gamma by serine and tyrosine protein kinases associated with the NGF receptor. https://www.sciencedirect.com/science/article/pii/S0021925818522997

Dose-Response Curve Stimulation by ATP gamma S of phospholipase C(PLC) was shifted to the right by the presence of UTP, indicating that both compounds act on the same receptors. Neuronal “nucleotide” receptor linked to phospholipase C and phospholipase D.

The lipase activity of PLCβ is not required for C3PO inhibition, and C3PO does not inhibit PLCβ. C3 Protein reduces neurite outgrowth and neuronal viability in vitro and restricts axon regeneration in vivo, and demonstrate a novel, non-traditional role for this inflammatory protein in the central nervous system.

PLCβ1 is strongly activated by Gαq. NGF added to PC12 cells remarkably increased PLCβ1 (i.e. 2.5–2.7-fold) in first 24 h. This increase peaks to 4-fold at 48 h (Fig. 1A) and decreases thereafter. Although Gαq also showed a large increase in expression with differentiation (1.6-fold), the onset of this increase was delayed 24 h relative to PLCβ

Alpha-7 Nicotinic Agonists or PAM both increased RhoA activity and inhibited neurite outgrowth. G-Protein Coupling is necessary for Alpha-7 Nicotinic mediated activated of RhoA. https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.13660

Sigma-1 receptor agonist induces RhoA/ROCK activation. https://www.atherosclerosis-journal.com/article/S0021-9150(16)31056-5/abstract

Sigma-1 agonist significantly increased both β-catenin and ZO-1 levels. https://pmc.ncbi.nlm.nih.gov/articles/PMC7821090/

Wnt/β-catenin signaling plays an essential role in α7 nicotinic receptor-mediated neuroprotection. https://www.sciencedirect.com/science/article/abs/pii/S0006295217302848

Nicotinic ACh receptor activation decreases IL-1β secretion. stimulation of the evolutionarily ancient CHRNA7, CHRNA9, and/or CHRNA10 efficiently inhibit ATP-mediated secretion of IL-1β. The ATP-induced signaling cascade is regulated by nicotinic receptor stimulation. Phosphocholine and Phosphocholine-Modified Macromolecules modify many proteins and carbohydrates and reduce IL-1β. https://www.semanticscholar.org/paper/Phosphocholine-Modified-Macromolecules-and-Agonists-Hecker-Küllmar/e36c016ccf998540e4061f31581a91eae6feb780

Bromocytisine (3-BrCy) and 3-iodocytisine (3-ICy) exhibited increased binding affinity (especially at alpha7 nicotinic receptors; Ki approximately 0.1 microM) and functional potency. In addition, 3BrCy and 3-ICy increases intracellular Ca2+ in PC12 cells and inward currents in Xenopus oocytes expressing human alpha3beta4 nicotinic receptor (EC50 approximately 2 microM).

To examine the functional interaction between the sigma binding sites and nicotinic acetylcholine receptors, we investigated the effects of various sigma receptor ligands on nicotine-evoked Ca2+ uptake in differentiated PC12 cells. This study showed that PC12 cells express sigma 1-like sites and the inhibitory effect of sigma receptor ligands on the nicotine-evoked Ca2+ uptake was not directly coupled with either the sigma 1 or sigma 2 sites. https://www.sciencedirect.com/science/article/abs/pii/001429999600115X

I took to much 4-ho-met and feel off the next day. Will I be okay?

I want to make sure I’ll be okay and not feel off like this forever! I took 60mg.

I know I know, not an RC

But I feel like many of you (me included) search for a feeling similar to what pregabalin just gave me.

Honestly the fact that it could lift me today is just amazing because it really shouldn't be able to, considering not even strong stimulants work when I am like this. Benzos just sedate me, cognitively I am not there either. Opioids are great and make me feel warm and happy, but obv not functional or just barely so.

The best way I can describe it is clean. Completely clean elimination of anxiety, but not forced. I could still feel bad about stuff, I could even feel anxious if I pushed it. Is subtle but at the same time not, like pushing towards the best version of yourself. Cognitively it felt like a brain fog being lifted, and made me present and focused. Obviously being a gaba drug significantly improved my inhibition. I can see it the last being problematic if I was already close to a hypomaniac state before taking it. Anyway absolutely great socially.

The following data points are very interesting to me and I am super curious:

1. it feels very similar to how DHTs hormones make me feel. In fact by far the most similar. I have to be careful because is honestly something that I would like to feel more frequently than the stimulants feeling even.

2. I have tried phenibut and alcohol only in this class of drug: phenibut only worked in the beggining and it was great, but it made me more maniac and honestly I didnt like who I was on it. It stopped working altogether. Alcohol gives me a similar feeling to pregabalin but ofc shortly after stupidity settles in or I just become tired.

3. Is just as great, or better, for my brand of adhd than stimulants. This one is wild, and I know there is some research between gaba and adhd out there but is annoying that the only focus is on dopamine. Dont get me wrong, zero tolerance stimulants are obviously better, but that ship sailed long time ago and it doesn't matter how much of a break I give to stims, that effectiveness is not coming back. Pregabalin though, made me so damm present. You know that adhd feeling of "the action we are performing right now is not the right action and we will feel physically uncomfortable until you find that action"? Preg took it away. I could sit and do stuff and yeah I would be bored or even not motivated, but this disgusting feeling was not there

4. Repetitive, ocd-like behaviours and thoughts, were also gone. When I am in a low dopamine state (usually triggered by low estrogen + environment) I start having ocd-like behaviours and thoughts. Gone, just gone. It makes me suspect preg is dopaminergic, but then, why no crash? Why not the typical side effects of every single compound that raises dopamine?

5. There is a subtype of adhd called "sluggish cognitive tempo", is where many of the "inatentive" subtype actually belong to. Many in the subreddit report similar reactions to me: dht makes them feel much better, creatine and glycine makes them feel much better, gaba drugs too. Some believe sct is a type of extreme inhibition, so it makes sense a gaba drug would help. But why does inhibition fuck with executive function even for simple tasks?

6. An area where you can see a clear difference with stimulants is humor. With preg I am myself and I can take things lightly and crack jokes much more easily than with stimulants. Even if I dont become robotic on stims I am still leaning towards more serious

Anyway sorry for the long post. Does anyone else have similar reactions to this drug? Anyone with adhd feel like they benefit from gaba drugs to this high degree?

So i made 2 caps with 2 different doses so far: 250mg and 325mg. (I have a really high tolerance for stims... 10 years as a heavy tweaker, last 2-3 years a very massive crackhead.. like bigger than Bobby AND Whitney 😅😭 lol) And i have experience with drugs like ad2pv, apcyp, 3mmc, apvp too. Im 27 6'4 and about 200-210lb

Are these dosages good for a strong hard hitter or should I add or subtract from them.

Lemme know! Thank you 😊

Very weak stuff, 60mgs is the equivalent to roughly 1-2mg Bromazolam in my opinion. But regardless of its weakness it’s one of the most relaxing benzos I’ve ever tried.

I’ve only used Xanax, Bromazolam and Ativan but Avizafone was easily the most calm and best feeling. I can usually still feel some anxiety on benzos but with Avizafone it was completely gone. For a prodrug it also hits surprisingly fast within 30 minutes of oral dosing I could feel it.

Overall it’s the weakest benzo I’ve done but one of the best by far. Amazing for anxiety and extremely difficult to black out on.

Has anyone tried this combo? If so how was your experience, I was thinking about trying it this weekend

7-OH (7-hydroxymitragynine) is the quite extremely potent (and skyrocketing tolerance- inducing) alkaloid of Kratom. These days (because of course you can!), you can buy tablets that contain pure 7-OH (or some combo of mitragynine and 7-OH, or a powder of the 7-OH itself, even).

As aforementioned, tolerance hits the moon, quick, when dosing (and chasing the dragon of) 7-OH. Just like kratom/mitrygynine/etc. there is a ceiling due to the antagonistic properties alongside its agonistic ones.

I’m on a …well… pretty decent dose of 7-OH alone. I ordered some tablets as well as mixture extracts that contain both 7-OH and mitragynine. Two, to be exact. With the latter of the two containing much less 7-OH relative to the mitragynine, in an attempt an easier taper.

On to the O-DSMT. I’m looking at a vendor to order a few grams of the stuff.

My question would be as follows: does anyone know how tolerance would be between the two? As in, like, a rough estimate (random guess example: 15mg approx. equivalent to 100mg O-DSMT - again, this is a random example of what I’m looking for as far as how to compare doses in order to assess tolerance).

Thanks if any help can be put out there!

I vaped nep and this happened. I came back to reality on a coach in my gf's flat. Apparently I had been there for a few hours and she was giving me electrolytes in water to rehydrate me and consoling me when I was anxious. Last memory before that is vaping NEP and feeling like a boss.

I don't know what happened during these 4 days. I had 2 g of the substance I assume I vaped it all. I was pretty battered, apparently I tried to climb over a gate and fell (twice).

Worst of all, I want to repeat the experience, just not vaping it. I have a pretty strong craving. What did I do wrong? Is vaping that dangerous? I used a typical crack pipe which allowed it to melt prior to vaporization.

Thats not all. My gf had a full-blown delusion (when I was trip sitting her) after a few hour of consumption and mixing it with 3cmc. She believed she saw a chat with a girl on my computer and accused me of cheating - I laughed at first thinking its a prank. Then when I told her to show me proof she was confused and said I deleted it remotely somehow. She could even recall details from the non-existent conversation, even after sovering up. It wasnt our best night.

Still, if I repeat it, what RoA is the safest?

Heard it's got somewhat stoning couchcloecked effects and that's why people add a stim like 3-fma or whatever. Basically the same as real good MDMA where the setting is important as if you'd do MDMA crystals at the crib you don't mind just chilling and talking. 5-MAPB seems to be like this.

So what dose to take if just out chilling with mates? and can I insufflate a redose if it's not strong enough? Haven't tried it out yet. Was thinking aboit candyflipping on it too since I've got the crib to myself so it's perfect or simply add some 2c-EF to it.

I also got 6-apb, would that be better in a chill setting and to potentially add LSD to it or later (I was thinking at the start due to similar duration and all that.

I'm an experienced drug user btw, have used MDMA with trips a lot, have tripped a lot, just never been much of a fan of stims except benzofurans and MDMA, my friend said 6-apb was awesome when gaming with his friends at a LAN party so I dunno which one to start with.

I also know you should take a substance alone to get a feel for it if you haven't done it before but honestly only have like 0,5g of 6-apb succinate, 0,25g of 5-MAPB, and then 10-20mg 2C-EF and about 3 LSD tabs I think.

Perhaps I could take one of the benzofurans first and see how I feel and add in the LSD later? And if the benzofuran wears off when the LSD is in full force still, just snort a redose or something?

Thanks for the replies in advance

Has anyone thought about this? A UV dye would be perfect! I binged 5 grams of NEP in 3 days and somehow got this stuff EVERYWHERE, plus I was snorting hugeee lines while carpet/floor surfing so I pretty much surfed for several hours feeling like I'm some treasure hunter finding El Dorado and picking up gold nuggets off the ground. Turns out, a lot of stuff looks like NEP, and dust is disgusting.

What tool do you guys use for carpet surfing cz a lot of things just break the brittle crystals and my fingertips r too sweaty.

I ordered a gram of NEP. Did small doses 1-2 hours in between, but then BOOM!. I was convinced people were trying to kill me. Ran out with my Katana being ready to kill "those people". At some point i've fell sleep with my Katana next to me.

I know this isn’t optimal as a solvent but it is difficult for me to get this right using vodka. Can anyone walk me through it? I have 100ml 37.5% organic vodka and .1g bromaz

Update: 2 hours of shaking and warm bathing in a glass bottle until it dissolved and it feels exactly like 2mg broz. Thanks guys

Anyone experience o-dsmt causing skin issues? It has been causing my face to turn red, then the next day I get flaky skin coming off in parts of my face and a sensation that feels as if I got sunburned. It didn't used to happen so I am wondering if maybe something is wrong with the batch

I’ve been wanting to start doing mentioned drug, and want to know how a doses usually goes.

I’ve used 3mmc for almost a year (most times daily use), and then stopped completely for a few months already.

I know (not sure about) 3mmc is both serotonergic and dopaminergic, but 2mmc is mostly or completely dopaminergic.

Can it be functional?

What would be the light / common insufflated dosage?

I recently got a hernia and might have to undergo an operation with anesthesia soon. I do have some tolerance to nmda-antagonists. Have been taking 3-ho-pcp and 3-meo-pcp quite regularly over the past three years.

My doses are not astronomical though. Up to either 10 mg of 3-meo-pcp or 15 mg of 3-ho-pcp taken orally I am still functional and it is only obvious to people who know me well, that I am on something.

I take that dose range around 3 times a week, combined with benzodiazepines, which I also have a moderate tolerance to. (Say I take 15 mg of 3-ho-pcp with 3mg of etizolam 3 times a week)

I really really really don't want to talk to the anaesthesiologist about my drug use.

Has anyone been in a similar situation or works in the field and can give me advice?

I stopped using 3mmc for few months already but I bought 5g of 2mmc.

I’m feeling really shit, although I didn’t use, but I’m feeling like I failed as a person. I know drugs are not good, and I do not really want to use, but I feel so lost sometimes, lonely, and being far away from my family for more than a year and receiving a lot of "no" responses from interviews I do with big companies make me feel bad.

I want to use, not to solve my problems, but to "distract" myself a bit in some moments, enhance the music, for the time do not pass so long.

I cannot afford therapy atm but I really wanted.

i basically have about 2 g of nep did two 0.1 lines feeling nothing special, have a feeling i ll snort the whole pack in a few hours. any recoms on dosing? am i wasting if i do 0.4 lines? should i smoke it?