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☠ WARNING ☠ *WARNING* Chronic ketamine/dissociative use causes bladder/organ damage

Well if you're all cartilage and are into yoga.. :p


Edit: no but seriously, just lying down still has a drip.
You need to let the head hang over the rim of a sofa or sumn, and then it just places perfeKtly.

Try to get in the mindset that a drip just shouldn't be a thing to begin with. Could save you a kidney transplant..
 
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@Chris Timothy
Yea I meant lying on your front, with your head hanging over the edge. Missed that comment even though I aparantly liked it haha.
I used to lie on my bed with my head hanging off the tail end, plate of 10 or more massive 0.5g+ lines on the floor, and do as many as I could (norm all of them lol) until it was literally pouring out my nose. Then plug both nostrils with tissue balls.
Hahaha. Good times
 
DXM does not appear to share the same issues. It seems to have to do with metabolites of acrylyclohexylamines, as far as I can tell. So the -phenidines, nitrous, and DXM don't count.
 
As for the urinary tract and bladder issues, its my understanding this is caused by Ketamines primary metabolite- norketamine crystal buildup. The popular myth that "ketamine recrystallises in the bladder" is derived from this. This, however, infers that only the bioavailable portion is actually causing the problem as its metabolite is the issue. Spitting the drip (contrary to it often being touted as good risk mitigation) IS NOT AN ADEQUATE SAFEGUARD to the development of ketamine aquired cystitis. Ketamine has only 20-30% bioavailability orally. The amount you swallow from a drip, minus the absorbed intranasal portion, then accounting for the lack of availability, results in very little extra norketamine ending up in your bladder. The appropriate harm reduction is to consume less ketamine in the first place. If the contents of a drip is particularly measurable in terms of the harm its doing, then your habit is already beyond the point of problematic or you need to adjust your insufflation technique.

Its extremely inconsistent though, it seems to take literal grams a day for years for some, and others not quite near that as evidenced in this thread. Theres a medical report (ill grab it if needed) citing that there are patients on~600mg of ketamine daily for pain with no signs of KAC developing.
 
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Ketamine has only 20-30% bioavailability orally. The amount you swallow from a drip, minus the absorbed intranasal portion, then accounting for the lack of availability, results in very little extra norketamine ending up in your bladder. The appropriate harm reduction is to consume less ketamine in the first place.
I won't disagree with the general sentiment but I think that this oft-quoted low figure for oral bioavailability is somewhat misleading. Bioavailability is a measure of how much of a substance gets into the bloodstream unchanged - with oral ketamine, a significant portion is metabolised into norketamine before this happens - but the net bioavailability of ketamine and first pass metabolites is higher. I referenced a study which appeared to show this in my post above, which I will link again for you here: https://academic.oup.com/painmedicine/article/7/5/469/1855020

The combined bioavailability of ketamine and norketamine here was found the be around 59%. This being the case, it's possible to demonstrate, at least theoretically, that not swallowing the drip could make a far more significant difference than one might assume. Granted, it might turn out that the difference is similar to smoking filtered cigarettes versus unfiltered cigarettes... and for sure, taking less ketamine is the superior option, but there might still be something to it, it seems to me.

Additionally -
its my understanding this is caused by Ketamines primary metabolite- norketamine crystal buildup
Do you have a source for this you could share? Because I see people saying this all the time but as I mentioned earlier in the thread, again, although there might be a theoretical basis for this idea, I never see anyone reference a primary source.
 
I won't disagree with the general sentiment but I think that this oft-quoted low figure for oral bioavailability is somewhat misleading. Bioavailability is a measure of how much of a substance gets into the bloodstream unchanged - with oral ketamine, a significant portion is metabolised into norketamine before this happens - but the net bioavailability of ketamine and first pass metabolites is higher. I referenced a study which appeared to show this in my post above, which I will link again for you here: https://academic.oup.com/painmedicine/article/7/5/469/1855020

The combined bioavailability of ketamine and norketamine here was found the be around 59%. This being the case, it's possible to demonstrate, at least theoretically, that not swallowing the drip could make a far more significant difference than one might assume. Granted, it might turn out that the difference is similar to smoking filtered cigarettes versus unfiltered cigarettes... and for sure, taking less ketamine is the superior option, but there might still be something to it, it seems to me.

Additionally -
Do you have a source for this you could share? Because I see people saying this all the time but as I mentioned earlier in the thread, again, although there might be a theoretical basis for this idea, I never see anyone reference a primary source.


You raise a good point with regard to combined bioavailability there actually. I'll grab papers for you after I'm out of work today. iirc there was one from '14 and one from '17 that I touted last time someone asked me for my reasoning on this but for now [citation needed]. Ill grab the paper that talks aboit medical patients too.
 
Additionally -
Do you have a source for this you could share? Because I see people saying this all the time but as I mentioned earlier in the thread, again, although there might be a theoretical basis for this idea, I never see anyone reference a primary source.

I see where im getting my info from in general here but i may have polarised the point slightly on further review. I admittedly have a chip on my shoulder about spitting the drip being touted as appropriate HR as although there may be some minmaxing involved the issue is the habit and doing tertiary things like this tends to lull people into a false sense of security about the root of the issue.


"The pathogenesis of bladder dysfunction under this condition is still not clear. It has been proposed that it may result from the two active metabolites of ketamine: norketamine and hydroxynorketamine.7 Recent studies have shown that ketamine and its active metabolites can be measured in high quantities in the urine of patients using ketamine.14 It is conceivable that ketamine and its active metabolites may accumulate in the urine and induce significant bladder irritation. Chu et al7 postulated the following pathophysiological mechanisms that might account for the urinary tract damage: (1) the high concentration of ketamine and its metabolites in the urine might cause direct toxic effects on the bladder interstitial cells, causing a significant chronic submucosal inflammatory response; (2) ketamine and its metabolites might induce microvascular changes in the bladder and possibly the kidney, causing endothelial cell injury of microvessels and leading either to compromised intrinsic microcirculation, or decreased microvascular density in the subendothelium; (3) an autoimmune reaction to the bladder urothelium and submucosa triggered by the presence of circulating ketamine or urinary ketamine and its metabolites; and (4) bacteriuria as the possible cause for the cystitis and papillary necrosis is unlikely in these patients, compared with other possible causes as described above. "

_________________


The study above actually cites ketamine and its primary metabolite being equally toxic so that puts weight to what youre saying.

Im still trying to find the paper where i specificaly read about norketamine crystal buildup though (positive i did not imagine this one lol), its possible its old science iv been running on these assumptions for some time. Will get back to you if i find it.

_________________

Turns out the 600mg thing is just the max reccomended daily dosage in healthcare for pain. im not sure on periods of use though, i would have assumed 600mg daily for a moderate or long period would induce some aspects of the symptomology:


"The actual mechanism is not well known yet, but these could be secondary to the toxic effect of ketamine and its metabolites, immune reaction or change in microvasculature.2 The minimum dose of ketamine associated with LUTS and/or cystitis is not known yet, but there are no symptoms reported with the 600 mg daily dose for pain management, at least in our pain management clinic which leads to the conclusion, and replicates what others had found: it is dose and frequency related. Future malignant transformation remains unknown and needs follow-up of all similar cases. However, we had one case of metaplasia which is a premalignant condition. "

_____________

Also apologies for missing your more lengthy comment above gave it a read now. I only read thru like 4 pages of the thread before commenting initially.
 
My main concern with DXM use was all the sorbitol and other additives in the syrups/gels. It was the main reason that I had to stop attempting to gain something from that substance. My first time with it was amazing and a lot of fun but going back two more times just provided more and more body load as my body refused and rejected the substance. I would try it again if I ever got pure DXM but considering all the other options I don't think I'll ever buy any. I never took DXM often enough to notice bladder/organ problems like I did with MXE. I don't understand how some folks are able to take DXM in cough syrup regularly.
Thats like rikodeine with me.cant go near that shit anymore.last time I had it
I felt so sick from all the other shit in it not to mention that fucking strawberry flavouring.
 
^^ @LabRat74, thanks for taking the time to look up that stuff. For sure, I think there is a lot of "minmaxing" going on, as you put it (had to urbandictionary that term lol :giggle:) and there is a danger of relying too much on (potentially) minor things like not swallowing the drip. I had also seen this technique touted often as I said but purely anecdotally and it wasn't until I tried crunching the bioavailability numbers that I started to think maybe there was something to it. This is pure theory of course though and there might well be an element of wishful thinking on my part, wanting to find some analytical reason that this should actually help and isn't just wishful thinking on the part of ketamine's fanbase.

On topic, I recently did about 130mg of MXE and in the days afterwards I had minor bladder symptoms, increased urination frequency, and just general bladder awareness that I don't usually have. Admittedly on the day I was not careful with hydration, even had a few beers and mixed with another dehydrating stimulant I had taken earlier in the day (armodafinil). I did take my EGCG supplements like a good dissociative (ab)user, but did not take cranberry extract or some other bladder stuff I forget the name of now but which I usually take on ketamine binges. I also ate like shit the day after. So, basically I did a lot of things wrong and am therefore not too surprised on the one hand to experience negative effects - but on the other hand, I would not expect to experience these same effects if I was entirely ACH-naive, even if I had been just as careless, especially given the quite low dose. So in my own experience there seems to be a definite kindling going on with regards to negative bladder effects. Prior to this I had not used any ketamine in about 40 days, I had used some 3-HO-PCP, although less than 100mg over about a week, and did not experience any apparent bladder side effects from that.
 
^ i don't think its so much a kindling effect as cumulative damage. i have no scientific ground to base that on. I can tell you that in my experience that some minor "bladder awareness" progresses quite quickly to "i'm going to fucking kill myself from the level of pain I have." This is pain that heroin won't touch..

I often question how much damage or how fucked up drugs have to make my life for me to quit them. I don't wonder that about ketamine even for a second, because the severity of that bladder pain left no question in my mind that i will never touch that drug again, maybe on my death bed ;)

its been about 2 years since my bladder blowout and its still fucked. Not suicidal levels of pain 24/7 anymore, but i still can't eat most foods
 
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Sorry to hear that LucidSDreamer - in my own experience though, the issues do seem go fairly quickly. At least the subjective ones. I guess I could be considered a lighter user than some, though. What I'd really like is to get some kind of deep high fidelity 3D scan of my bladder and have someone talk me though if I have indeed done any permanent damage.

I have read a study that suggested in the absence of continuing to use ACHs, things do generally return to nornaml within about a year, although I guess the cut off point is hard to predict or perceive, when too much is too much.

A good rule of thumb for sure is quit forever at first alerts, advice I did not personally heed, although I'm going to do my very bust not to do a single ACH for at least a year now.
 
Also ^ have you ever tried BPC-157? I suggest this to people all the time but I'm not sure anyone's ever taken my advice. It seems to be a universal soft tissue healer or sorts though and there is scant evidence that these healing effects might extend to the bladder... in fact I think I posted such reference further up in this very thread.

Edit, here we go:
The discussion of peptides in that other thread just reminded me of something - I remember thinking a while ago that there might be some potential for BPC-157 to be useful in reversing ketamine-induced bladder damage.

For anyone not aware this is an interesting peptide which is stable in human gastric juices (and therefore, supposedly, orally active) and seems to have quite wide effectiveness in promoting various forms of soft-tissue healing. So far most people using it are using it primarily for muscular or tendon injuries, but it has also shown some promise in treatment of bowel conditions like ulcerative colitis and other inflammatory bowel diseases. It appears to have anti-ulcer properties and there are a lot of anecdotal reports of people using it to clear up digestive issues. I wondered if it's healing properties would also extend to the bladder... and in fact, there is some early indication that they do indeed!

Novel Approach in Therapy of Internal Fistulas: The Stable Gastric Pentadecapeptide BPC 157 in Therapy of Vesicovaginal Fistulas in Rats


A "vesicovaginal fistula" apparently, is a hole in the bladder which allows fluids to leak continuously into the vaginal cavity - the study above seems to indicate that BPC-157 made a marked difference to the controls and essentially completely closed these fistulas! I would say despite the fact that this study was done in rats, coupled with the evidence of BPC-157's effectiveness in healing other tissues in humans, this is a very good sign!

I think I recommended a while back to another member here that they give BPC-157 a try, although I have no idea if they did. I forgot but I actually used BPC-157 myself shortly after my first bladder scare - I have no idea if it was effective or not really because I also abstained for maybe as long a 6 months and probably my symptoms were fairly minor... but this does look very promising, I would really urge anyone with persistent bladder related problems from ketamine abuse to give it a try and report back - it seems to be very well tolerated overall so the worst that can happen is probably that it just doesn't work - especially if you go the oral route (I believe it should be active sublingually too, given it's resistance to human digestive enzymes... or possibly nasally, I know there are a few places offering it as a nasal spray).
 
Sorry to hear that LucidSDreamer - in my own experience though, the issues do seem go fairly quickly. At least the subjective ones. I guess I could be considered a lighter user than some, though. What I'd really like is to get some kind of deep high fidelity 3D scan of my bladder and have someone talk me though if I have indeed done any permanent damage.

I have read a study that suggested in the absence of continuing to use ACHs, things do generally return to nornaml within about a year, although I guess the cut off point is hard to predict or perceive, when too much is too much.

A good rule of thumb for sure is quit forever at first alerts, advice I did not personally heed, although I'm going to do my very bust not to do a single ACH for at least a year now.

interstitial cystitis is considered a permanent condition, the bladder wall does not grow back - this is what I've read, but I am not a urologist. My use was quite light. I had friends using absurd amounts more than me that didn't develop problems. The only diagnostic that can make a definitive finding is a cystoscopy.

In my case, there were minor sensations and feelings for a year or two when they first started, that would only appear when using NMDA antagonists. Then i started to notice them when doing other drugs (kratom and stimulants in particular).

I went from not thinking I had much bladder damage to enduring months and months of pain that was the worst pain imaginable. It all happened very quickly in how it escalted. We can tell ourselves all day that using a little won't hurt or that taking breaks allows the bladder to heal. The truth is that these drugs (the RCs) are all new and we don't know a damn thing about them.

Just because bladder pain subsides does not mean your bladder has healed it self. I have periods with no pain whatsoever that last for weeks or months even. One spicy dish, one wrong drug...a world of pain is unleashed. The damage is permanent just because the pain isn't.
 
Interesting stuff. Funny that I have a urologist friend who I tend to get my K from. Guess it's just good business to him... 😉🤔

I will have to pick his brain over this stuff next time we're together.

In other related notes, I haven't seen any mention of Olney's lesions also known as NMDA receptor antagonist neurotoxicity (NAN), are a form of potential brain damage due to drugs that have been studied experimentally and have produced neuronal damage, yet are administered by doctors to humans in the settings of pharmacotherapy and of anesthesia.


This study revealed the lesions in many regions of the brain of ketamine addicts. These lesions appeared as minute patches in the first year and became larger sites of atrophy by 4 years of addiction. The majority of the addicts was on dosage of 1 g per day and used ketamine daily for several years. In this work, since the volunteers were mostly below 30 years old and only 2 individuals above 30 years old, a comparison of the effect of age upon addiction was not conclusive in this stage, even though we had seen no worse in the aged group (above 30 years old) when compared with the slightly younger old. A study of age response would definitely be conducted in future. However, it is well-known that ketamine addicts were usually young as represented in this cohort. The brain regions affected were prefrontal, parietal, occipital, limbic, brainstem, and corpus striatum. The lesions affected both the gray and white matter, i.e., neurons and nerve fibers in the human; these were similar to those reported earlier by us in the mice and the monkey (Yu et al., 2012). This MRI study also collated with the work by Morgan and Curran suggesting a loss of memory via psychological examination in chronic ketamine abuses (Morgan and Curran, 2006). In animals, prefrontal cortex apoptosis, mutated tau aggregation, brainstem chemical changes, and cerebellar apoptosis had been reported (Mak et al., 2010; Yeung et al., 2010b; Sun et al., 2011, 2012; Tan et al., 2011b, 2012; Yu et al., 2012; Wai et al., 2013). In fact, in the mice model, it had been documented both neurons and fibers (white matter) were both targets like in this report consisting of human subjects (Mak et al., 2010; Yeung et al., 2010b). Along with structural changes, fMRI and functional studies confirmed functional and cognitive derangements (Morgan and Curran, 2006; Sun et al., 2011, 2012; Chan et al., 2012; Yu et al., 2012). This human MRI brain imaging on the ketamine addicts thus consolidated that the areas of lesion in mice, monkey, and human were essentially similar. We now have clear and unequivocal proof of damages in the CNS upon chronic use of ketamine in human



This shit scares the piss out of me (pun intended 🤫) but I still love me some dissos, although it's been over a year now.

Did anyone else ever notice the brain damage / concussed feel that others often refer to as "afterglow" from some dissos (specifically DXM). Its been almost 20 years since I last touched that stuff, but I know for a fact it was seriously fucking up my brain.
 
interstitial cystitis is considered a permanent condition, the bladder wall does not grow back - this is what I've read, but I am not a urologist. My use was quite light. I had friends using absurd amounts more than me that didn't develop problems. The only diagnostic that can make a definitive finding is a cystoscopy.

In my case, there were minor sensations and feelings for a year or two when they first started, that would only appear when using NMDA antagonists. Then i started to notice them when doing other drugs (kratom and stimulants in particular).

I went from not thinking I had much bladder damage to enduring months and months of pain that was the worst pain imaginable. It all happened very quickly in how it escalted. We can tell ourselves all day that using a little won't hurt or that taking breaks allows the bladder to heal. The truth is that these drugs (the RCs) are all new and we don't know a damn thing about them.

Just because bladder pain subsides does not mean your bladder has healed it self. I have periods with no pain whatsoever that last for weeks or months even. One spicy dish, one wrong drug...a world of pain is unleashed. The damage is permanent just because the pain isn't.
Damn... that is concerning. I guess I'm not overly surprised though. I'm at the point right now seemingly that even doing small amounts of MXE (~100mg in a night) will give me bladder pain and urinary retention during, or at least, as soon as the immediate dissociation wears off, and maybe the day after. Larger amounts of ketamine can cause more persistent uncomfortable sensations but I haven't touched that stuff in just over 2 months (65 days to be exact). Hopefully I've managed to call time on ACHs in time... I do wonder sometimes if my bladder capacity has reduced slightly, but just not to the point of clinical significance... I'd be very interested to get a cystoscopy but I suppose it wouldn't be easy to get without more persistent symptoms, and maybe not worth it anyway because it sounds a fairly unpleasant procedure!
 
Interesting stuff. Funny that I have a urologist friend who I tend to get my K from. Guess it's just good business to him... 😉🤔

I will have to pick his brain over this stuff next time we're together.

In other related notes, I haven't seen any mention of Olney's lesions also known as NMDA receptor antagonist neurotoxicity (NAN), are a form of potential brain damage due to drugs that have been studied experimentally and have produced neuronal damage, yet are administered by doctors to humans in the settings of pharmacotherapy and of anesthesia.






This shit scares the piss out of me (pun intended 🤫) but I still love me some dissos, although it's been over a year now.

Did anyone else ever notice the brain damage / concussed feel that others often refer to as "afterglow" from some dissos (specifically DXM). Its been almost 20 years since I last touched that stuff, but I know for a fact it was seriously fucking up my brain.
Pretty sure it's generally assumed Olney's Lesions are a fabricated/inaccurate portrayal of NMDA action in the brain; however, DXM abuse I bet might still cause some sort of long term issues. I only ever abused MXE and I feel none the worse for it and never think twice about Olney. DXM is a crazy one though, it's like booze, a shotgun to the brain.
 
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