# DXM - The Opiate Addicts's Miracle Drug, PLEASE READ



## StrappingYoungLad

Hey guys a little intro here, this post is about DXM and I was hoping someone could shed a little light on how it has managed to temporarily cure my opiate tolerance and everything that came with it. Part of this message is copied from something I sent to an ex girlfriend whos attending Harvard in the hopes that she could do some published research on the topic and spread the word. 

The reason I'm posting it here is because in the past 2 or 3 years of opiate addiction bluelight has given me an amazing resource for harm reduction and drug information and I want to share this with opiate addicts seeking help on this forum.

By the way, before I paste the edited version of what I sent her, I am currently experiencing no withdrawal symptoms thanks to DXM and I was sick as a dog yesterday with no oxycodone left to save my ass. (Took about 4.5 hours after taking my 55mg dose of DXM for withdrawal to cease entirely)
Here's my account of DXM and its effects on reversing opiate tolerance that I sent to my ex: 



> This drug DXM stands for dextromorphan or something.  I need you to research its effects on the brain and the nervous system.  This is insane.
> 
> Let me try to explain a little bit.  It's known as robotussin and its used for coughs and its a dissociative which means it fucks with the central nervous system, but I tried taking 3 times the normal dose in some sort of attempt to reverse my opiate tolerance as ive been going into withdrawal and this is what happened:
> 
> Last night it worked and i got high off a dose of oxycodone i havent been able to feel even since last year.
> 
> But this is even more INSANE like seriously Alicia I want to jump and shout.  It's unlocked memories and removed what I can only describe as a brain fog and has unlocked my personality and I feel like a NORMAL HUMAN BEING I feel like MYSELF for the first time in a long time since I started using opiates.
> 
> My theory is that it deactivates the glial cells in the CNS that are responsible for producing whats called 'tolerance' to opiates and the endogenous opiods produced by the brain. In other words, the 'brain damage' (aka tolerance) i've incurred with long term opiate use has been temporarily removed by this otc dissociative drug, DXM.  I can FEEL my brains natural pleasure chemicals again and it feels so great.  But the thing is NO ONE UNDERSTOOD.  After long term opiate abuse at school I was suffering from constant depression and my parents put me in rehab counseling/psychologist/psychiatrist.  the psychiatrist gave me SSRI's and they did jack shit but THIS WORKS.
> I was depressed and fiending for opiates because I was so overly tolerant to the family of neurotransmitters known as opioids.  Apparently these chemicals are as much involved with long term memory and basically EVERYTHING as they are with pleasure.
> I cannot believe this, but at the same time, the body builds its own tolerance to DXM, so it's not like I can feel like myself unless I start abusing DXM to reverse opiate tolerance which obviously won't work after a long period of time.
> 
> I feel excitement and all kinds of other emotions I haven't known for a year at least.  It's insane, it's like I just woke up out of a coma.



Thanks Bluelight. if a mod wants this to be in journals or trip reports I'd ask them to please wait to move it until some users with advanced knowledge of chemistry have read my anecdotal account and possibly verified it with accurate info, thanks!!!


----------



## pofacedhoe

ketamine is known to reverse tolerance to opiates/amphetamines and more

dxm works on the same receptors as ketamine (nmda, glutamate system)- this is not that shocking


----------



## MeDieViL

http://www.bluelight.ru/vb/showthread.php?t=501875

Ive made a thread about this a while ago.


----------



## MurphyClox

^...which looks absolutely amazing. Good work!


----------



## MeDieViL

Thx murphy

Still need to update a few things, some ppl that say they prevented tolerance did end up tolerant but much later, regarding memantine the only long term reports i saw used doses of 30/40mg, 10mg etc likely works short term but tolerance can still creep up later, so its definatly no wonder antidote that makes you immume, NMDA antagonists help a ton, but some caution is adviced (take a week break once and awhile, take 1 or 2 days off in the weekend etc).

Also regarding benzo's, (ive accidently deleted the benzo section while updating) it appears that they work against tolerance to the sedative effects but another study found that tolerance to the anxiolytic effects did occur, on the other hand ive found 3 reports of ppl saying memantine reversed tolerance to the anxiolytic effects of benzo's, but offcourse take with a grain of salt.


----------



## StrappingYoungLad

sick thread MeDieViL.  im forwarding the anecdotal accounts to most of my friends because almost all of them are on an opiate or amphetamine. very nice collection.

what i've found is:

dxm reverses tolerance temporarily depending on how high your tolerance is.  it appears to reverse it permanently as well in small amounts so if you take dxm daily you will chip away at your tolerance.

HOWEVER, opiate tolerance returns quickly. in order to prevent this, DO NOT take any opiates without first letting DXM take effect on your nervous system, else your tolerance will jump back up to previous levels in leaps and bounds.


----------



## MeDieViL

Yeah you should stay on the NMDA antagonist while taking opiates.


----------



## MeDieViL

Personally i take 20mg of memantine a day and augment with occasional small ket bumps when i'm on something (k on its own will most likely not work due ot its half life and possible rebound, but the memantine should cover most of the rebound and i have some extra nmda antagonism going on when i'm on other stuff.)


----------



## fastandbulbous

NMDA antagonist tolerance will also increase and it's a bitch to get down again. After months off dissociatives, a little try revealed that I'm still horribly tolerant to their effects, so they're no wonder drugs


----------



## MeDieViL

fastandbulbous said:


> NMDA antagonist tolerance will also increase and it's a bitch to get down again. After months off dissociatives, a little try revealed that I'm still horribly tolerant to their effects, so they're no wonder drugs



Tolerance to the recreational effects is a big issue, but it appears that there's no tolerance to the anti tolerance effects.


----------



## StrappingYoungLad

MeDieViL said:


> Tolerance to the recreational effects is a big issue, but it appears that there's no tolerance to the anti tolerance effects.



hey medievil, if this is true, that is very good knowledge to have; hella thanks for sharing it man.  that was the only flaw i assumed using dxm for tolerance would have: that after a time of use i would quickly develop tolerance to dxm, but if what you say is true, that kicks so much ass.

i couldnt appreciate this drug more.  i was telling my boy who has tried and enjoys it that it was like we went to a doc and said, "doc im having problems with tolerance," and he prescribed dxm.  fucking exactly what i asked for!


----------



## MagickalKat777

I'm curious about the effect of NMDA antagonists during rapid benzodiazepine withdrawal. Obviously this is a harm reduction site but couldn't high-dose ketamine or DXM prevent the seizures and most of the unpleasant side effects that happen when withdrawing from benzos by keeping glutamate in check?

From what I've been reading it seems like the main problem (grossly simplified mind you) with benzodiazepine withdrawal is that when GABA gets down-regulated, NMDA becomes up-regulated and the up-regulation is what causes most of the nastiness... If you could down-regulate NMDA as well while the brain repairs itself on the GABA side, wouldn't that potentially be an easy way to withdraw from benzodiazepines?


----------



## MeDieViL

AMPA receptors also play a big role in withdrawal guys, NMDA is the major player in tolerance but for proper withdrawal supression i would combine a ampa antagonist (like topiramate) with a NMDA antagonist like memantine.


> Topiramate in opiate withdrawal.
> Zullino DF, Cottier AC, Besson J.
> 
> Division of Substance Abuse, University Department of Adult Psychiatry, Prilly-Lausanne, Switzerland. Daniele.Zullino@inst.hospvd.ch
> Abstract
> The alpha2-adrenergic agonist clonidine is the mainly used drug for the opiate withdrawal. Its efficacy and tolerance in treating withdrawal symptoms is, however, suboptimal. The pharmacological profile of topiramate suggests it could be rather valuable for opiate withdrawal, as there is some evidence that topiramate acts, among others, through inhibition of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors, which play an important role in the withdrawal-induced activation of the locus coeruleus (LC) by glutamate. Three patients undergoing an inpatient opiate detoxification program were treated with topiramate, which achieved a nearly complete control of withdrawal symptoms.


There's another case report somewhere of topi supressing benzo withdrawal. It should also prevent seizures (something memantine wont do, unless the seizures are mediated trough NMDA).


----------



## MagickalKat777

Dope-a-max? Ugh. Everybody that I know who takes topiramate are quite frankly, stupid, until they get off of it - and then they still remain stupid for weeks or months before they finally recover.

What about oxcarbazepine for seizures? There are studies that show carbamazepine and oxcarbazepine to both be effective in managing benzo withdrawal and oxcarbazepine in particular interests me because of the lesser side effect profile compared to carbamazepine. Memantine is new for me, never heard of it, I would need to look it up...

EDIT: Memantine seems rather benign - I'd be curious what dose I would need. Particularly since I'm a smoker. My insurance covers it under the brand name Namenda although its not cheap...


----------



## MeDieViL

> Dope-a-max? Ugh. Everybody that I know who takes topiramate are quite frankly, stupid, until they get off of it - and then they still remain stupid for weeks or months before they finally recover.


Its just temporary untill the withdrawals are over man, wouldnt take it long term myself Memantine should be taken daily with the drug your taking for reduction in tolerance.

Yeah there's other stuff that works againt seizures, but topi is special because it actually helps with the withdrawal symptons itself too (besides preventing seizures).


----------



## MagickalKat777

I don't know if I could handle Topamax - for one, I'm already on Wellbutrin, which has almost entirely suppressed my appetite as it is (and I'm already about 30 pounds under recommend weight for my build and height) and two, if there are side effects, I'm likely to get all of them.

So with memantine, is it a once daily thing? I noticed there are 5 and 10mg doses available... Ideally I would like to taper off my 2mg Klonopin at a rate of 25% per week... but with no other drugs in my system but Wellbutrin, I couldn't even handle 1.75mg after the second day and had to take an extra milligram to get under control... Funny considering I cut 1mg flat-out in December with no withdrawal issues.

I was dead serious about trying to use K to suppress NMDA by keeping myself at 2nd plateau levels - not really psychedelic but just enough out there to not care and just chill - but if memantine can do it and I still function, that's even better.


----------



## IHateOpiophobes

Good to hear you feel better  I would not do opies anymore if i had your chance.  they have ruined enough shit for 6 lifetimes.....
I dont believe glial cells/neurons can be "deactivated".  Activated brain areas create neurons to form networks to tighten response, but die off if not used.  Short term memory is the best example.  
Possibly antagonism, but I would look into the memory centers of the brain.

Go borrow a fMRI machine from a hospital.  jk 

   I was hoping someone could shed a little light on how it has managed to temporarily cure my opiate tolerance and everything that came with it. Part of formthis message is copied from something I sent to an ex girlfriend whos attending Harvard in the hopes that she could do some published research on the topic and spread the word. 

The reason I'm posting it here is because in the past 2 or 3 years of opiate addiction bluelight has given me an amazing resource for harm reduction and drug information and I want to share this with opiate addicts seeking help on this forum.

By the way, before I paste the edited version of what I sent her, I am currently experiencing no withdrawal symptoms thanks to DXM and I was sick as a dog yesterday with no oxycodone left to save my ass. (Took about 4.5 hours after taking my 55mg dose of DXM for withdrawal to cease entirely)
Here's my account of DXM and its effects on reversing opiate tolerance that I sent to my ex: 



Thanks Bluelight. if a mod wants this to be in journals or trip reports I'd ask them to please wait to move it until some users with advanced knowledge of chemistry have read my anecdotal account and possibly verified it with accurate info, thanks!!![/QUOTE]


----------



## VFORV4AN1

I'd hate to break it to you (even though it seems it's already been broken) but Dextromethorphan (or any NMDA antagonists for that matter) will play about as big of a role in alleviating opiate/oid withdrawal symptoms as Diphenhydramine, Naproxen and Loperamide do.  On a relief factor, it *may* lie somewhere between the OTC remedies and Benzodiazepines/Barbituates.

Someone with a very mild Codeine addiction would probably benefit from a combination of DXM with the other remedies listed, but a Heroin addict that injects 2+ grams a day for years will not think of it as a 'miracle drug' at all.

Back when I was that Heroin addict I just spoke of, I tried DXM, Ketamine, PCP, all the OTC methods, Benzos, Barbituates, Clonidine, etc; trying to find the *right* combination for making withdrawal at least somewhat tolerable.  Even throwing a Methadone taper into the mix didn't work.  The only thing that got me off of Heroin was making my first visit to my PCP (not to be confused with Phencyclidine) in order to get on Suboxone maintenance.  When he saw that I was in severe withdrawals 6 hours after injecting 7 'Philly' bags, he put me on 32mg of Suboxone instantly.  I went through a pretty nasty withdrawal for about 48 hours, but got back to baseline at around 72 hours.  That was 13 months ago and now I am down to 8mg once per day with zero relapses.  The only time(s) I've ever felt a craving were after I'd get done with an intense workout and I'd see a vein that originally had collapsed suddenly re-appear, sort of announcing to the monkey in me, "Hey, I'm back! Whatcha got for me?"... anyways, I'll leave it at that.

Sorry for the long post.  I just don't want anybody to see this thread title and get their hopes up without diving deep into the data and personal experiences and go lock themselves in a room with a couple of bottles of cough syrup thinking they'll be "cured" by a "miracle drug".

By the way, hello everyone.  I recognize a few names and posting styles from the old BL, the bee's nest, PhreeX's old board, etc.  My account got canned back when BL had the "re-boot" or whatever around 2005(?), so unfortunately I can't access it/it doesn't exist anymore, and I've just been lurking for years.

Peace!


----------



## MeDieViL

Thx for your reply, any other that tried DXM for opiate withdrawal WITHOUT succes? We need as many anecdotal reports as possible to see what looks promosing and what does not.

The reports on NMDA antagonism and tolerance do seem consistent, withdrawal is mediated by differend mechanism, the case reports ive posted above seem to indicate that glutamate induced ampa activation plays a major role in that, but thats only 3 case reports.

The ones reporting succes usually post but those that do not usually dont mention it, wich can give a biased perspective.


----------



## VFORV4AN1

MeDieViL said:


> Thx for your reply,



No problem.



> The ones reporting succes usually post but those that do not usually dont mention it, wich can give a biased perspective.



You hit the nail on the head there.  I probably wouldn't have even mentioned it if the title didn't read "DXM - The Opiate Addict's Miracle Drug, PLEASE READ".  In all honesty I think the title should be changed to something regarding research of DXM and other dissociatives as possible aids in alleviating certain withdrawal symptoms in mild Opiate/oid users.  But that's just me.  

Too many people will just glance at a topic like this/read the first post and then go buy a bunch of DXM and try to kick and will either have no results and no money to go get their fix since it didn't work, or end up in a level 5 (What was that called again, Sigma?) plateau DXM trip *while* going through Opiate withdrawals.  I know it sounds asinine, but it's true.


----------



## MeDieViL

Lets see what research we got:



> The NMDA antagonist memantine attenuates the expression of opioid physical dependence in humans.
> Bisaga A, Comer SD, Ward AS, Popik P, Kleber HD, Fischman MW.
> 
> Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York, USA. bisagaa@pi.cpmc.columbia.edu
> Abstract
> RATIONALE: Preclinical observations suggest that NMDA receptor-mediated glutamatergic neurotransmission is involved in the expression and maintenance of opioid dependence.
> 
> OBJECTIVE: The present study evaluated whether memantine, the clinically available non-competitive NMDA receptor antagonist, decreases naloxone-precipitated withdrawal in morphine-dependent humans.
> 
> METHODS: Eight heroin-dependent, non-treatment seeking, inpatient participants were stabilized on a fixed dose of morphine (30 mg PO qid). Subsequently, they received a series of challenges with naloxone (0.4 mg, IM) and the severity of opioid withdrawal was monitored. Either placebo or memantine (60 mg PO) was given 6 h before each naloxone challenge. A modified multiple baseline, across-participants design was used to evaluate the effects of memantine on the severity of naloxone-precipitated opioid withdrawal.
> 
> RESULTS: Naloxone increased ratings and produced physical changes consistent with opioid withdrawal. Memantine attenuated the severity of opioid withdrawal as assessed with the Clinical Institute for Narcotic Withdrawal Scale scale. Withdrawal was significantly reduced when naloxone was administered at 6 and 52 h after memantine, but not when administered 126 h (5 days) after memantine. Medication effects, assessed 5 h after memantine administration and before naloxone administration, included significant increases in ratings of "strong" and "good" drug effect, and "I feel sedated", "mellow", and "high".
> 
> CONCLUSIONS: Memantine attenuated the expression of opioid physical dependence in humans, indicating that glutamatergic neurotransmission at the NMDA receptor site contributes to the maintenance of opioid dependence. This finding suggests that memantine may be a useful adjunct in the treatment of opioid dependence.





> Objectives: There is a growing body of evidence suggesting that N-methyl-D-aspartate (NMDA) receptor antagonists effectively counteract somatic and behavioral symptoms of the opioid withdrawal syndrome in humans and in laboratory animals. NMDA receptor blockade also reduces the development and expression of drug-conditioned behaviors. At present, there is only one NMDA receptor antagonist, memantine, registered for clinical use in Russia. Memantine is used in Europe for the treatment of Parkinson's disease and senile dementias. Most of heroin addicts soon after the termination of withdrawal syndrome are suffering from protracted withdrawal (syndrome of anhedonia [SA]), which includes affective disorders (depression and anxiety) and craving for heroin. SA is viewed as a major factor contributing to the relapse to heroin use.
> 
> The aim of this study was to evaluate efficacy of memantine in the treatment of protracted withdrawal (SA) in recently detoxified heroin addicts.
> 
> Methods: Following standard detoxification procedures (7-10 days), 67 heroin addicts were randomly assigned to 1 of 3 treatment groups: memantine (n = 21), amitriptyline (n = 24) or placebo (n = 22). While inpatients, subjects received one of the following medications: memantine (initial dose of 10 mg/day was gradually increased to the final dose of 30 mg/day over a period of 1 week), amitriptyline (75 mg/day), or placebo for a period of three weeks. Patients from all treatment groups received standard psychotherapy and counseling and were required to attain abstinence from heroin by providing a heroin-free urine toxicology screen prior to starting medications and at the end of each treatment week. The study design was single blind. Outcome measures included treatment retention, heroin craving (Visual Analog Scale), depression (Zung's scale), anxiety (Spielberger's scale) and anhedonia (Anhedonia syndrome scale) scores.
> 
> Results: Both memantine and amitriptyline significantly reduced heroin craving, depression, state and trait anxiety, and anhedonia scores at the end of the three-week treatment period; placebo did not have any significant effects. The dropout rate in the memantine group was significantly lower than that in either placebo or amitriptyline groups. The average number of side effects was higher in the amitriptyline group compared with other groups.
> 
> Conclusions: Memantine appears to be an effective and safe medication for protracted withdrawal (SA) and relapse prevention in recently detoxified heroin addicts. These data provide a rationale for further studies on the use of memantine in heroin dependence treatment.





> Memantine produces modest reductions in heroin-induced subjective responses in human research volunteers
> 
> Rationale
> Previous studies have demonstrated an interaction between opioids and noncompetitive antagonists at N-methyl-d-aspartate (NMDA) receptors, but few studies have examined the utility of these medications for treating opioid dependence.
> Objective
> In this 8-week inpatient study, participants were maintained on the low-affinity, noncompetitive NMDA receptor antagonist memantine (0, 30, and 60 mg per day, PO) and under each maintenance dose condition, the effects of intranasal heroin (0, 12.5, and 50 mg, IN) were examined.
> Methods
> During the first week after admission to the hospital, participants were detoxified from heroin. All of the volunteers received all of the memantine and heroin dose combinations. Participants (N = 8) first sampled a dose of heroin and $20. During a subsequent choice session, participants could self-administer heroin and/or money. Responses, which consisted of finger presses on a computer mouse, were made under a modified progressive ratio schedule (PR 50, 100, 200, 400, 800, 1,200, 1,600, 2,000, 2,400, and 2,800) during a ten-trial self-administration task. Subjective, performance, and physiological effects were measured repeatedly during laboratory sessions.
> Results
> Memantine produced modest reductions in subjective ratings of drug quality, liking, willingness to pay for the drug, and craving for heroin. However, memantine produced few changes in the reinforcing effects of heroin.
> Conclusions
> These data demonstrate that memantine was well tolerated and modestly effective in reducing the subjective but not the reinforcing effects of heroin. Although it is unlikely that memantine will be useful as a stand-alone maintenance medication for opioid dependence, it may have some utility as an adjunct treatment medication.



So looks like there are some indications it may help, but definatly not a miracle med.


----------



## StrappingYoungLad

my original post was not so much about withdrawal but more like tolerance reduction.  it was pretty poorly cropped together thought because i was in a strange state of mind for sure haha


----------



## pharmman

*DXM and glial cells*

dex has no effect on glial cells except maybe sigma mediated.  Tolerance however is mediated via the NMDA receptor with dex blocking the influx of CA thus lowering intracellular CA levels.


----------



## negrogesic

Yes.....that original post is of little value. 

Having experience mega-dose opioid withdrawal, I agree entirely with F&B.......no miracle....

Also, as a note of caution; some of those anecdotal accounts discuss the use of DXM, amphetamines and serotonergic anti-d's. This is a potentially dangerous interaction at high doses; technically, it can be fatal. 

My anecdotal experience: While experiencing cold-turkey withdrawal to a 600mg/day IV morphine habit, I found significant but transient 'relief' from IV sub-anesthetic doses of ketamine (10-30mg); it did not shorten the withdrawal, nor did relieve all symptoms upon dosing, but it provide short-lived acute relief. If you do not know what you are doing, or are not with a capable 'sitter', IV ketamine can be rather dangerous. And ultimately, it didn't do much more than take me away from the horror for 10 or so minutes. 

Nitrous oxide helps....and is much safer. The relief is not nearly as profound as the IV ket, but is far less dangerous. The is no free ticket ultimately. 

Methadone, being an NMDA-antagonist of sorts, is honestly the best way to get off of serious habits. I have found this to be true not only in my own case, but clinically.


----------



## ampakine

Interesting shit, thanks for sharing.


----------



## jasonmp321

MeDieViL said:


> Thx for your reply, any other that tried DXM for opiate withdrawal WITHOUT succes? We need as many anecdotal reports as possible to see what looks promosing and what does not.
> 
> The reports on NMDA antagonism and tolerance do seem consistent, withdrawal is mediated by differend mechanism, the case reports ive posted above seem to indicate that glutamate induced ampa activation plays a major role in that, but thats only 3 case reports.
> 
> The ones reporting succes usually post but those that do not usually dont mention it, wich can give a biased perspective.



I've tried DXM a couple times when i was in opiate withdrawal and it just made me feel awkward and shitty.  Really didnt help at all.  Loperamide was more effective.


----------



## 80mg

BUMP

So. I found this thread after researching DXM for w/d.

For me, this came to be by accident. I miscalculated my subs I had left and somehow over did it to the point that I would have to go 6 whole days with none. At first, I figured "no biggy. Ill borrow a few bucks from friends, get a few blues fronted to me...itll all be good"

BUT...it seems that the "friends" that I wouldnt even think twice about giving a bag of H or a blue or two when I have alot are not so fast to return the favor. The only person I could really count on is a friend we'll just call TJ. TJ is a good guy. If he has enough, and your sick, hell help you out....but this time he didn't. So then  like a dirtbag I asked my mom for money...she got hit with a 1600 dollar mechanic bill and honestley din't have it. So what was a man to do?

12 hours after last sub- This aint that baddd...Im just being a puss. Let me just suck it up and chill out

18 - ok...maybe this aint as easy as I thought...

20- Depression comes on strong. That trade mark warm fuzzy feeling from opiates has me feeling the COMPLETE opposite right now. Its almost like someone stabbed me in the chest. Im watering eyes, starting to sweat, RLS coming on now...wheres my kick kit? -goes to bathroom- Ok Benedryl, Ibprofen, a hot bath....waith Tussin? Heh...I remember reading somewhere the Tussin has helped with W/D in doses 100-300mg. Fuck it -gulps 1/4 of bottle

21.5 - The DXM did the trick! I still have extreme fatigue and depression but all physical w/d besides the fatigue is basically gone!

I am now in my 60th hour of complete absence just using tussin and benedryl every few hours. Id deffinedley recommend this to anyone w/d. This is the most sobure I been in  5 years atleast.


----------



## 'medicine cabinet'

There is def something to this at least from what i have found in my experience. A few years back when i was at my heaviest point of using heroin IV, i was doing about 80$ or a half-g of really strong "raw" dope every day, more if i could afford it....how i got the $ looking back i have no idea, but if i had enough money i could shoot well over a gram a day.

When i decided i didnt want to be strungout and homeless anymore, i stayed with my cousin and said im going to kick this w/o any other opiates or opioids, all i had was some booze (gross, i know) crappy muscle relaxers, i mean really crappy like robaxin or something and dxm. at the peak of the WD i was basically in a state of psychotic delirium, shaking, sweating, vertigo ect ect. i said fuck it ill take some dxm and see if it will help any, so i downed a few gulps and a few hours later when i had my head burried in the toilet puking, i started to almost hallucinate from the intensity of the WD and the dxm, but for some reason after that insane experience, the WD seemed to end quicker than normal and be less severe. it was almost like the dxm kicked my receptors back on. It was pretty unpleasant the effect of the DXM while WDing, but it def did something.


----------



## synergistic.affect

MagickalKat777 said:


> From what I've been reading it seems like the main problem (grossly simplified mind you) with benzodiazepine withdrawal is that when GABA gets down-regulated, NMDA becomes up-regulated and the up-regulation is what causes most of the nastiness... If you could down-regulate NMDA as well while the brain repairs itself on the GABA side, wouldn't that potentially be an easy way to withdraw from benzodiazepines?



The known mechanisms behind opiate addiction are extremely diverse, multifaceted, and complicated.  withdrawal is the result of a cascade of neurological changes.  NMDA receptors are known to play a significant part, tho without many years of focused high-level education, it seems that it is very difficult to make accurate inferences.  NMDA receptors themselves seem to be particularly complex and somewhat poorly understood in comparison to many other types.  I mean, to me It would make sense that nmda antagonists might modulate those symptoms of drug withdrawal that are created by the overactivity of gutamate at NMDA sites, But i think it would also logically follow that the antagonism of those receptors would ultimately cause thier own up-regulation too, no?  It might... then again there might be 100 other mechanisms in place that make for a different outcome.  

I found 2 articles that seem relevant to creating a working picture of some the possible actions of these receptors.  Both articles are quite fascinating to me; one pertains to a super-sensitivity to excitotoxicity that's found in the wake of administration of NMDA antagonist MK-801(tho it must pointed out that this study used neonatal rats resulting in limited application of the study's results), and the second uses PCP as the antagonist and studies the apoptotic epigenetic damage it causes upon interaction with different receptor subtypes/proteins.  Both of these studies support the idea of NMDA receptor up-regulation due to exposure to NMDA antagonists, and also illustrate the coorelation between receptor density and excitotoxic brain damage.  I do hope that there are no major errors in my comprehension of the material... but, of course, it is possible.

Here are the links for the MK-801 and the Phencyclidine articles, respectively: 
http://www.sciencedirect.com/science/article/pii/S0165380698000844
http://www.sciencedirect.com/science/article/pii/S000629520500122X

Currently, i've been doing some reading on the action of nitric oxide(NO) in addiction.  I don't know if it actually plays one, but its been repeatedly turning up in readings.  Perhaps it's relevant, perhaps not;  I suppose it(NO) could be integral in one of the larger mysteries that's been on my mind:  In my experience, i have found GBL to be the better than ANYTHING else at alleviating opiate withdrawal; by leaps and bounds, head and shoulders above, and other body-part related colloquialisms.  Just how it does this has intrigued me for years...

To further describe, there has been many occasions where i have found myself sweating thru devastating morphine withdrawal more times than i'd like to admit.  Symptoms include horrible depression, gooseflesh, terrible agitation, anxiety/panic, runny nose, eyes, and ass, hot flashes, more hot flashes, vomiting, etc.  
If i take a 2ml dose of GBL i experience almost full remediation of nearly all of my symptoms; usually left with transient and relatively minimal skin discomfort, a greatly attenuated runny nose, and some gurgling from my intestines.  Although uncomfortable, all of this equates to almost nothing when compared to the way i would otherwise experience the withdrawal. CAN ANYONE TELL ME WHY?  I cannot find anything concrete about why this happens nor, surprisingly, anyone else doing this.  The only study i found only had like 10 participants and was completely ignored presumably due to the studies 100% recidivism rate.

Of course nothing is perfect and using GBL to quit opiates presents with it's own set of problems.  The short duration of action requires redosing every 3 hours or so around the clock to hold w/ds at bay.  It is EXTREMELY easy to trade dependencies instead of just treating negative symptoms.  On the bright side, it seems that, while treating with chronic GBL to block symptoms, my body is effectively withdrawing beneath them.  I can successfully taper the GBL somewhere between the 3rd and 7th day without too much discomfort depending on severity of the opiate addiction and how much of a vagina im feeling like.

Once again, I DO NOT RECOMMEND THIS route for opiate addiction due to the myriad of effects that severe abuse of GBL can cause.  I have taken GBL around the clock for months and months at a time in my past and i'm still here, but i would be lying if i said that ive sustained no lasting damage from such stupidity.  Opiate addiction can, however, be a devastating, life wrecking issue that pushes us to extremes.  So if you find yourself pulling out the scale to weigh such options, please view it as if you were weighing a whale against a dinosaur; not to be taken lightly.  

I welcome any speculation regarding the mechanisms of action behind GBL's merciful effect on opiate addiction.


----------



## negrogesic

^^^Woah...hold on there....I can't say I read even half of the above, but the logic appears to be to 'questionable'. Can you briefly reiterate what mechanism is deserved of elucidation?


----------



## synergistic.affect

Sure, and i'd welcome any corrections of my logic.  Honestly tho, my post is really raising questions more than it is determining anything.  

Initially i hit google looking for support for the idea that NMDA antagonists block w/d symptoms caused by excess glutamatergic activity.  Instead, however, i ended up finding studies that point toward the idea that use of antagonists causes a glutamatergic rebound in thier wake, or at least MK-801 and and pcp seem to, likely, i think, do to an upregulation of receptors. However, it would then logically follow that one would become less and less tolerant to the effects of antagonist drugs with time and we all know that that doesn't happen at all.  I assume this is the questionable logic you were refering to.  ItIf anyone can shed some light on this i welcome it.  Again tho, it must be said that antagonism of NMDA receptors and the resultant cascades of neurochemical processes is extremely complex relative to catecholamine and other better charecterized receptor sites.

Like i said, i'm offering no answers, rather posing particular questions and trying to get inside of if and why NMDA antagonists seem to help many people thru opiate withdrawal (myself included).  And also, why the hell GBL seems to so thuroughly attenuate w/d symptoms.


----------



## Comma MD

Hello people, first posting here, figured it's time to finally register. I won't get into any formal or informal introductions here, as I only intend to address a specific topic, for now at least. I certainly do not intend to bore you all. Yet before I chime in, I would like to mention, as my username boastfully screams (sarcasm ladies and gents), I am indeed a licensed health care clinician aka MD aka physician aka doctor aka pompous self entitled douche (that damn sarcasm again). I'm sure you get the pic. I mention this only bc I've been browsing these forums from time to time, albeit when time permits, and I've never come across any other docs willing to "chime in", was a little shocked, since as we all know, the incidence of chemical dependency within the health care arena (specifically docs) is not one in nine as in the general population, but two in nine... nifty. Seriously though, I hope to offer as much as I can since this site alone has offered a plethora of vital knowledge for me. So please feel free to ask questions, especially those nit gritty ones in which you are expecting feedback that takes into account evidence based clinical medicine. Bow. I'm here to serve..

Nuff of the bullshit, on to my $0.02. As I stated earlier, I only wanted to address a specific topic and I'll try my best to do so as briefly as possible. I've been reading a lot of comments and responses surrounding the topic of opiate withdrawal, dextromethorphan's possible clinical efficacy, NMDA receptor antagonists, and our good friend glutamate. I only wanted to make a clarification; please understand, I'm doing so in a very general and broad manner. If anyone would like specifics, again, feel free to ask. In my attempt to offer some clarification regarding opiate withdrawal, please acknowledge that there have been no concrete clinical trials concluding the role of NMDA receptor antagonists, glutamate, and DXM with respect to their "connection" to opiate withdrawal syndrome. In actuality, alcohol withdrawal more precisely correlates with these topics, however DXM has been shown via evidence based medicine to effect "tolerance" and "dependence" to opiates, however not so much regarding w/d. Now allow me to mention that via my own experience, as both patient and doctor, DXM has demonstrated profound impacts on cessating those relentlessly horrible w/d symptoms. 

Here's a nice way of looking at the big picture when it comes to our central nervous system and the concept of withdrawal. I'm going to focus on alcohol (or benzodiazepine) w/d though. Here's what happens, at the most broadest of levels: one consumes ethanol chronically over a number of years. Aside from contracting severe hepatic malfunction, chronically over time there manifests a global increase in the levels of GABA within the brain. GABA's inhibitory effects on the CNS up regulate glutamate's activity within the CNS, since the body is trying to compensate for this over secretion of GABA. Ultimately a balance is achieved, equilibrium, although the body is physiologically dependent upon the ethanol (the irony hungh). Now what happens? You take away the alky, say cold turkey, after chronically ingesting for years, and we all know the result... Withdrawals. The body's equilibrium is effed, dramatically. During the acute phase, the body is still kicking out shit loads of glutamate, an excitatory neurotransmitter, since those neurons that release it have been trained to do so due to balance the hypersecretion of GABA, an inhibitory neurotransmitter. It takes some time for the body to realize that oh shit, I guess no more alky is coming in, meaning no more outrageous GABA levels, maybe we should kick back our secretion of glutamate? This acute off balance in the most broadest of senses equals withdrawals. All the unopposed glutamate activity is the actual culprit for all the signs and symptoms of alcohol and benzo w/d, hence the DTs, tremors, seizures, etc. Neat hungh.. K, time for tea. 

Nice meeting all of you btw; cheers.


----------



## ProducedRaw

You'd probably also benefit from Magnesium and Zinc supplements. Both are NMDA antagonists and won't have the long term problems associated with DXM usage but at the same time won't be anywhere near as efficient. Most people are deficient in Magnesium anyway so it's a good idea to take it whether you're a junkie or not.


----------



## negrogesic

As to the GBL 'approach' mentioned, I am reminded of an individual who did the following: 

In order to 'break' his sublimaze (don't ask) dependency, he would employ barbiturates and nitrous oxide in a very methodical process to mask the distress of acute withdrawal. Note that I used the work 'break', as this man was so depraved that he did this use this as an attempt to resolve an addiction, he simply did it so he could continue on getting 'high' on the sublimaze.


----------



## Darksidesam

What an interesting thread. Could be some vital information here, perhaps more news of this would be very helpful for certain people.


----------

