Treating (acute)/post-acute opioid w/d with psychostimulants?

[splenda]

During opioid w/d there is a pronounced decrease of DA/DAT in the nucleus accumbens with a postulated theory that opioid tolerance/dependence increases DA receptor sites.

Knowing this, some people use psychostimulants, such as cocaine and amphetamine, to attenuate certain aspects of both acute and post-acute withdrawal.

Certain symptoms of w/d that I've seen attenuated from amphetamine (acute w/d):

Less restless legs
Less runny eyes/nose/yawning
More energy (Less of that "down and out drained" feeling.)
Minor happiness (albeit in high doses this could be different.)
Less aches and pains (Lower sensitivity to pain probably due to NE/NET effects that psychostimulants cause.)
Less cold/hot flashes

Symptoms that WORSEN by taking psychostimulants during acute w/d:
Insomnia
Anxiety/Paranoia
Restlessness
Doesn't help much with motivation if at all (so it doesn't fully get rid of the depression, but gets rid of most of the dysphoria.)
Diarrhea
Urination
Sweating
HR/BP
Elevated temperature (not hyperthermia, but it causes your body to heat up more than normally.)

At least these are my observations. And here is an interesting study to back up what I've seen during opioid w/d and stimulant-use:

Monoaminergic drugs can modify opioid withdrawal in nonhumans, and cocaine is reported to attenuate opioid withdrawal in humans. Drug discrimination was used to examine whether s.c. cocaine or other indirect-acting monoamine agonists attenuate morphine (3.2 mg/kg/day) withdrawal induced by naltrexone and by 27 h of morphine deprivation. Naltrexone-precipitated withdrawal was attenuated not only by morphine but also by cocaine, amphetamine, and imipramine. However, reversal of naltrexone-precipitated withdrawal was greater for morphine than for any of the indirect-acting monoamine agonists. Attenuation of the naltrexone discriminative stimulus by indirect-acting monoamine agonists was pharmacologically selective insofar as drugs lacking affinity for monoamine transporters (ketamine and triazolam) were without effect. Twenty-seven hours of morphine deprivation occasioned naltrexone-lever responding and decreased response rate, and both effects were reversed by morphine, cocaine, and amphetamine and not by imipramine, desipramine, ketamine, and triazolam. Thus, indirect-acting monoamine agonists attenuate some (e.g., discriminative) aspects of naltrexone-precipitated withdrawal, whereas only indirect-acting agonists with high affinity for dopamine transporters attenuate deprivation-induced withdrawal. These results suggest that dopamine is differentially involved in naltrexone- and deprivation-induced withdrawal and support the notion that opioid-dependent individuals use stimulants, in part, to attenuate withdrawal.

http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

What are your thoughts?

 

[Tchort]

I made a thread along these lines in OD not long ago.

http://www.bluelight.ru/vb/showthread.php?t=400031&highlight=aet

AET & Opioid Withdrawal

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Shulgin writes in TiHKAL:


Quote:
One property has been mentioned more than once in anecdotal reports. It appears to serve well, with short term dosage regimens, as an effective tool in kicking dependency on opiates. In chronic use, there is a rather rapid tolerance built up over four or five days, that allows a dosage escalation to a daily load of a gram or more. There might be some discomfort such as sores in the softer tissues of the mouth, but apparently the withdrawal from heroin is easy and effective. Here is a potential tool in addiction treatment that might warrant closer investigation.


Wikipedia says:


Quote:
It is structurally related to α-methyltryptamine but its pharmacological effects are very different. α-ET is not a hallucinogenic drug, its effects resemble more that of the empathogen-entactogens like MDMA (Ecstasy).


AET was an early RC, and an early trial of the Federal Analogue Act. In the trial involving AET and the Analogue Act, the judge ruled that AET was not an analogue of DMT or DET under the language of the act, because the language is 'unconstitutionally vague'. AET then was de facto decriminalized, as a judge had ruled the government could not prosecute cases of AET possession or sale under the Analogue Act: so the DEA made it Schedule I a year later in 1993.

There are some reports on the internet from the late '60s of a doctor in the Haight-Ashbury area of San Fransisco who was prescribing injectable Methamphetamine ampoules to treat Heroin withdrawal.

Has anyone heard about or tried to use euphoric stimulants or any empathogens, or any Phenethylamine or Tryptamine to aid withdrawal? If so, what were the results?

 

[fastandbulbous]

It's a definite 2 edged sword as opiate withdrawl symptoms are in part due to overactivity of the sympathetic nervous system, so any psychostimulant is likely to make those symptoms worse. If you're going to use one, it's best to get one that is mostly dopaminergic in action with minimal noradrenergic activity - best bet is probably something like methylphenidate or desoxypipradrol (amphetamine has far too much noradrenergic activity, as exemplified by the symptoms increased by it mentioned by the O/P).

Actually using ketamine in conjuction with whatever you use will help lessen the symptoms by a fair degree

 

[Jamshyd]

^ I agree about both points. IMO, Stims are a very bad idea during opioid withdrawal. Ketamine, on the other hand, is a godsend.

As for AET, remember that shulgin was trying as hard as he could to find as many wonder-drugs as possible in his stash. Another example is 2C-D being "nootropic".

 

[negrogesic]

From my experiences, cocaine and d-MPH proved far superior to the amphetamines during opioid withdrawal. However, during opioid withdrawal, problems can occur as these stimulants wear off. Strangely enough (or perhaps not strangely at all), oral cocaine works quite well for opioid withdrawal...

Also, I noticed that IV ketamine was quite effective in temporarily relieving opioid withdrawal symptoms, however I found that IM ketamine was less analgesic and significantly more psychedelic (which could be bad during severe opioid withdrawal).

 

[Tchort]

The short term benefits of using a euphoriogenic stimulant of any type during WD is paid for ten fold when it wears off as others have noted. IV Cocaine being my candidate for worst of the worst as far as this is concerned (an old dealer called me almost in tears, saying he was sick but had .5g of blow stashed, shot it all, and once it wore off he said he had never felt that dreadful before. He and I had a falling out some time before, and I was on Suboxone at the time, which he pleaded for. Remembering my own experience with IV coke comedown while very dopesick I drove an hour away to give him a few for free. It's hard not to sympathize with someone despite your opinion of them if they are experiencing that).

I've read of people trying to use Meth to tweak all the way through the 5-10 days of IV Heroin WD (none successfully that I know of), to keep the good effects going and ward off the comedown until after detox. This is just as bad if not worse than the old 'Sleep Cure' Burroughs wrote about in Junky, where you're given supratherapeutic doses of Chloral Hydrate and/or Barbiturates for a week to keep you asleep during the entire detox; but of course it doesn't work out that way (and was described by Burroughs as the most painful WD he had ever done). I don't know of anyone trying it, but I am sure it has been done in some manner, using dissociatives to stay anaesthetized while conscious through WD. Sounds dreadful.

So, the article the op quoted is right, addicts do use stimulants to alleviate WD, but that doesn't mean that it works well, or at all, they/we just do it in a desperate attempt to make it go away for any amount of time and deal with the consequences when they happen. The only time I can see this actually working is the beginning of WD, between 12-24 hours without dope, and using speed to keep you stimulated and "euphoriated" until you can make a connection, at which point the Heroin/opioid would kill the stimulation and the sickness at once. Still a very bad idea to put your body through all of that.

 

[splenda]

I think "attenuate" and "some aspects of withdrawal" are keywords here, heh.

During acute w/d, psychostimulants can screw up other things such as increase aggression (endocrine adrenal imbalance caused by w/d increased by psychostimulants; HTPA axis messed up, etc.)

But, for some people, if they don't take high doses of amphetamine (less than 60mg/day; pharmaceutical preparation as opposed to street speed/crystal meth), it provides not necessarily "euphoria" (if you even want to call it that), but moreso alleviates the aches/pains, mental horribleness, and lack of energy/overall malaise which I believe should be the worst of withdrawal.
And with low doses, you shouldn't come down too hard either.

I guess there are a lot of variables, heh.

 

[rangrz]

perhaps the atypical stimulant modafinil?

It has some mood brighting effect and general stimulant like properties, but its fairly mild and I've noticed little/no come down from it, and very little PNS stimulation.

 

[Hammilton]

I don't think modafinil has any 'mood brightening' properties. It's a great drug though, don't get me wrong. Just not mood elevating.

I'd probably be good for relieving the feeling of death though- by providing a little mild energy.

 

[rangrz]

Hmm, I find it somewhat mood brighting...not in the super acute way methamphetamine is, but in a subtler way, along the lines of the SNRI effects from tramadol kind of mood brighting.

maybe its just me or me mistaking alertness and enegry for enhanced mood. But I think it has some mood lifting abilities.