amanita and opioids

[jacky]

On a hunch that amanitas and opioids might at least go well together I ordered an ounce of pantherina amanitas. I am also interested in a few experience reports that liken the low dose amanita effect to analgesia created by codeine. I also figure that the amanitas may create favorable effect of either potentiating opiates, or lessening withdrawl effect of opiate detox. I took 10 grams of pantherina and cooked them up with a dash of mushroom tea extract that I bought in japan town seattle. I had taken my normal opiate dose earlier that day, but at the time I normally re-dose with some type of opiate I consumed a portion of the amanita extract instead. all in all I consumed around 7 grams of the mushroom over a 4 hour period. the effect came on in the form of sleepiness initially, so I slumbered for several hours. upon awakening I found myself experiencing mostly physical effects. slight body shock type flashes were felt, causing me to sometimes drop objects, or I would twitch, this is a normal side-effect of consuming amanitas. I suffered no hot or cold flashes, no extreme salivation. the effect seemed more like a barbituate or valium type effect. I took my nightly opiate dose much later than usual, and suffered no ill effect from doing so. It seems that having opiates in your system prior to consuming these mushrooms may blunt some of the visionary or entheogenic qualities. I am going to experiment further with combining tonic dosages of the mushroom with opiates, and on a day off, completely forego any opiate dosage while taking the tonic dose of amanitas. my hunch is that amanitas in small doses may help reduce withdrawl, and that the mushroom seems to potentiate opiates consumed. the reports of people using tonic doses that are comnpared to codeine list pain relief and a type of energetic support. I was sort of bummed the mushroom didnt have a pronounced entheogenic effect, as I have taken low doses of this same type of amanita before and experienced definite euphoric and visionary type effects. I would equate my experience recently as more of a debilitating polydrug combination, as my balance and dexterity was definitely compromised. I think a lower dose in combination with opiates may lend to a more euphoric experience. I have roughly 20 grams of amanitas left so I can approach this from several different ways. low dose opiate/amanita combinations, and higher dose amanita alone in place of usual opiate dosage .

[jacky]

its the day after my amanita experience, all day I have felt really good, cept for a mild case of nausea that has been hangin around. seems to me that the opiates I took today are affecting me stronger than usual, as I am taking poppy seeds though it is hard to predict dosage effects, as poppy seeds can vary greatly in strength. there are so many different variables with this type of conjecture/experimentation that I think the more experience the better. after 10 or more spererate dosings on any given substance I usually have a good idea of how the substance is going to affect me.

[jacky]

do I really expect amanitas to help with withdrawl, or to potentiate opiates? well in any given "direction" I would expect the chances to be 30% for either no activity, positive effect or negative effect

[deepinsyn]

Wow, Jacky can I come over to your pad...i bet you have the most interesting kitchen Cabinet stocked with plants and pods and seeds I can't even pronounce much less probably reach being that I am a shorty..lol......I promise I am a great cook, and can probably cook up a good concoction that will take us on some kind of fucken high....the only thing is when I cook, I never write down my ingredients and sometimes I regret that.....cause the cocktail was that good!
Respectfully,

[peacefulwarrior]

Here is a bunch of info on what seems like some very powerful potentiators. This seems like a gold-mine to me. Anyone every try proglumide, tagamet, hydroxyzine, or naltrexone for potentiation? read...

Tolerance, Addiction, and Effective Pain Management
by K. Trout

A major problem faced by narcotics users and abusers is the well-known development of tolerance when an opiate is given repeatedly over a period of time. This is directly responsible for a number of the problems associated with narcotic use and abuse since increasing tolerance requires that steadily larger doses be used to achieve the same effects or degree of pain relief.

This also underlies much of the crime associated with street addiction as the cost of maintaining a habit also escalates along with the dosage, often leading addicts to turn to drug dealing, prostitution or criminal activities to enable them to afford their daily dose.

Many experienced junkies, especially if heroin users, address this problem by taking regular breaks from their drug of choice, allowing their tolerance to diminish and their effective dosage to also be decreased. Due to the unpredictable quality of unregulated black-market street drugs this can actually be potentially dangerous if they then acquire material of greater potency than they were expecting. (Junkies who relapse after recovery face a similar risk when they return to use.)

Some users employ materials like cimetidine (Tagamet) [R.A.H. 2000] to retard drug metabolism and thereby maximize their effectiveness. [An interesting but unrelated point worthy of further investigation is the report of Peterson et al. 1983 indicating that use of cimetidine one hour before and after administration of large amounts of cocaine to rodents prevented hepatic toxicity and liver damage. Pellinen et al. 1994 also reported a prevention of “metabolism-related hepatotoxicity” by use of Cytochrome P450 3A inhibitors.]

Other users recommend grapefruit juice (Anonymous 2000) to interfere with the metabolism of the opiates by the liver and small intestinal Cytochrome P450 enzyme CYP3A and thus attempt to maximize their per dose effects, blood concentration and duration. While this has been reported by many users to be effective at maximizing per dose results this does not affect the development of tolerance.

Presently many questions remain, as there is also been some conjecture made that administration of grapefruit juice might interfere with the conversion of codeine to morphine due to its lesser inhibition of some CYP subfamilies. This does not seem to be the case; Caraco et al. 1996 reported (in animals) that if codeine was coadministered with selective inhibitors of CYP3A4 this could result in increased morphine production and enhanced effects due to “shunting into the CYP2D6 pathway” (as CYP2D6 would NOT be affected).

It is worth noting that I can thus far locate NOTHING in the *scientific* literature specifically supporting the use of grapefruit juice to increase the general effectiveness of opiates or even that CYP3A is responsible for the metabolism of heroin. Although, it is certainly reasonable to assume that CYP3A is responsible for its metabolism since it is proven as such for other opioids such as codeine (Caraco et al. 1996) and fentanyl (Feierman & Lasker 1996)

Reports of successful application, circulating orally among users (Anonymous 2000 & 2001) and posted on web-based bulletin boards, are common enough that this should be investigated further.

It is important to keep in mind that grapefruit juice can also prove problematic due to the elevated levels of bioavailable drug, requiring a reduction of the dosage. Sometimes it can even be dangerous if certain other drugs are being used. The combination of grapefruit juice with some specific pharmaceuticals has produced many serious problems and even some deaths. (Ameer & Weintraub 1997; Dresser et al. 2000)

Another practice reportedly employed by some narcotic users is combining hydroxyzine with opiates to potentiate their effects. This is said to produce a rough doubling of intensity with the addition of unwanted side effects like a dry mouth. [Anonymous 2000] It appears to have no effect on the development of tolerance.

An interesting approach is the combination of opiates with the opiate antagonists naloxone or naltrexone in miniscule amounts. The combination of less than 0.001% of what would be a normal dose of the antagonist with an opiate allows a far greater response (“at least 50%”) to the opiate which in turn permits a much lower effective dose to be used. It is also said to prevent respiratory depression, tolerance and addiction. This approach has apparently been patented (Crain & Shen 1996) and is being commercially developed by Pain Therapeutics. [R.A.H. 2000; Crain & Shen 2000]

Another interesting comment was made by Karl Jansen (2001) concerning the administration of small oral doses of ketamine being found to be of use in chronic pain clinic for “greatly reducing” the development of tolerance (via blockade of NMDA receptors).

However, many people are unaware that both enhanced effectiveness of narcotic analgesics AND prevention or reversal of tolerance is readily achievable through the oral use of up to 200-250 mg of Proglumide [(DL)-4-Benzamido-N,N-dipropylglutaramic acid]. [See Ott 1999; Watkins et al. 1984]

The work of Watkins suggests there may be a therapeutic dosage window with diminished results above it but more detailed work to define this is apparently lacking.

Rather than simply augment the action of the opiates, proglumide actually interferes with the anti-opioid activity of the neuropeptide CCK.

The chronic administration of opiates, or spinal cord and other CNS injuries, elevates the level of Cholecystokinin (CCK) that is present. Such elevated levels exert an antagonistic effect on opioid activity resulting in significantly diminished analgesic effects. (Watkins et al. 1984; Xu et al. 1993 & 1994)

It is this rise in CCK levels that directly leads to the condition known as drug tolerance and the corresponding increase in its anti-opioid activity that requires the opiate user to use increasingly larger amounts to achieve the same effects.

This anti-opiate effect can be prevented or even reversed through the administration of CCK inhibitors such as proglumide. (Watkins et al. 1984)

Besides just interfering with the adverse action of CCK on opiate activity, proglumide is also known to augment the analgesic effect of opiates. Often this can provide a higher quality of analgesia for those patients who suffer from an incomplete response to pain medications.

Watkins & coworkers reported that proglumide reversed morphine tolerance and also 1) hastened the onset of analgesia, 2) increased the peak levels, and 3) prolonged the duration.

They suggested that not simply did this indicate that effective narcotic doses could be decreased but it also indicated that proglumide might be able to enhance the effects of other procedures, such as acupuncture, which involve endogenous opiates. (Watkins et al. 1984)

Proglumide is a nonselective CCK inhibitor that was formerly employed as an anti-ulcer medication (Hahne et al. 1981). It shows NO analgesic effects of its own.

Although proglumide is now considered to be an obsolete pharmaceutical due to changes in our understandings of ulcer etiology, it has already seen extensive pharmacological and toxicological testing proving its safety and has been approved for use in humans.

It has largely fallen into disuse but is still available in bulk via chemical houses or as a pharmaceutical in Europe and Africa sold under the trade name Milid and Milide.

Other CCK inhibitors show similar properties (Idänpään-Heikkilä et al. 1997; Xu et al. 1993). However, beyond simply having seen previous use in humans, proglumide is both inexpensive and nontoxic. (Ott 1999)

Proglumide is not some sort of magic bullet for completely eliminating the risk of tolerance development and addiction as its effects are only effective for a limited duration before tolerance to IT begins to develop. (After 8 days its effectiveness begins to wane) The work of Kellstein & Mayer 1990 suggests that successful therapeutic/maintenance applications will probably require its discontinuation for a week after each week of use. More work is needed to better define the precise parameters of its effective use for this purpose.

Despite this, proglumide has already demonstrated itself to be of value both in pain management and as an adjunct to maintaining a narcotic addiction within a larger program of harm reduction (Anonymous 2000; Ott 1999).

What is fascinating is how few drug educators, drug treatment facilities or even drug users are aware of this despite it being readily available information for nearly 20 years.

If development of tolerance and the high price of a sustained addiction are truly as serious of a problem as we all agree that they are, one can only wonder how it is that, despite the tools existing to remove or at least reduce this problem, there seems to be no interest or research except on a limited scale related to specific small areas of chronic pain management and understanding.

The current misguided approach of substituting methadone is commonly reported to actually cause MORE perceptual and thinking problems than the opiates it replaces PLUS methadone is known to cause physical damage to internal organs that are not encountered with opiate use itself.

Harm reduction approaches would benefit greatly by using proglumide as a cornerstone and making it readily available to both narcotic users and abusers.

Those who will most certainly object include organized crime and drug dealers who enjoy the obscene profits reaped from escalating drug tolerances, and possibly also the so-called “drug educators” that sadly often seem to be the ones most in need of some factual education.

There are many problems associated with opiate use and abuse. While the majority of these are legal in origin, the most sensible approach would be to ameliorate [or mitigate] those that aren’t.

Increased analgesic effectiveness and prevention of tolerance are two obvious areas where harm reduction is readily possible TODAY. Both sufferers of chronic pain and narcotic addicts stand to benefit from having their needs met and their health risks simultaneously decreased.

As this is first and foremost a health problem, the current approach of harm maximization is both counterproductive and unacceptable. To a rationale or caring mind it might even be perceived of as unethical and amoral.

Not only do sufferers of chronic pain and narcotic addicts stand to benefit from such harm reduction approaches but, by decreasing drug-associated crimes, a significant area of the true “drug problem” can be directly addressed, thereby benefiting society as a whole.

[deepinsyn]

Fuck, you know how many times I had to read what you wrote peacefulwarrior??.....I think I'm gonna go back and read it again just to make sure I understood, what it is I understood the 2nd time I read it......Thank you, however, a little knowledge goes a long, long, way....the better informed we are the better we can better ourselves, well I better stop here, my eyes hurt, and my brain is starting to feel sore.....lol.....besides I'm being redundant with this better word, that it sounds like I was making a joke, and its a lil funny, but it wasn't my intention...so now I know I need some zzz's......Where is everybody???....Fuck!
Respectfully,

[jacky]

I have tried the naltrexone potentiation, and It works!! but it left me sick, as in TOO much potentiation, and my ears rang for three or four days. poppy seeds may have amounts of naloxone that aid in potentiation of the small amounts of agonist compounds.....grapefruit juice and CATS CLAW herb (which contains chemicals similiar to the kratom akaliod profile) also cause a build up of opiates in the users system, some labeled medications actually warn of grapefruit interaction. there are plenty of other substances that potentiate opiates, though many are prescription only. I have not tried tagamet as of yet, but have read a little about it in the pages of the Entheogen Review, especialy in interviews with Jonathan Ott. this K Trout fellow is an amazing entheogens explorer and competent chemist who has authored about the best literature describing mescaline and psychoactive cacti. he has also written this peice on opiates, and hopefully will have more to say in the future about entheogenic and other opioids...................

[jacky]

oh yeah, DXM is already approved by the FDA for lowering numbers of or reducing withdrawl sideeffects. I have used it extensively for a year inconjunction with opiates. It does have some very potent and in my opinion amazing effects with opioid combinations....but it addictive in its own rite. I would only use it occasionally in low doses (under 150 milligrams) myself anymore, and I am NOT trying to encourgae anyone to do this. It is also only used with chronic and terminal patients to my knowledge....a drug called Morphidex mixes morphine and DXM milligram to milligram, they have a pretty cool website.

[doctor diesel]

I'm going off at a tangent here on this thread, but on the subject of potentiators, I have one technical query for you guys, that you might be able to help me with. About a year ago, in my ongoing, desperate search for pain relief for my wife, I put together a concoction of Darvon and Tramadol. It was 3x65mg Darvon with 200mg IR Tramadol. I tried it on myself first, because I like to be the guinea pig. To my amazement within half an hour I started feeling blissfully euphoric, and continued to do so for the best part of six hours.

So I tried it on the missus, and the same thing happened to her - complete with the requisite total pain relief. A few days later I repeated the exercise on both of us, with the same result, and maybe two weeks later, I had a third go that also worked a treat.

However, to my disbelief, these results were never again repeatable - try as I might. I would use the same source of Darvon and of Tramadol, I'd try and starve us both of other meds for a couple of days leading up to another trial... and it has simply never worked again, although the combination now raises my pulse and prevents me sleeping, and it does still provide her with good pain relief. But where did the euphoria disappear to? Even waiting about three months to try it again produced nothing.

So I got to thinking that on those days when the formula worked, we might have inadvertently been taking some potentiator. Try as hard as I could to think what it might have been, I could only come up with a nine-hour proton pump inhibitor (heartburn relief) tablet that we'd both been having daily at the time. So I got hold of some more (ranitidine) and tried taking it a long time before, a short while before... but nothing. Then much later I read that Tagamet (cimetidine) was a known potentiator, and thought that maybe I'd been using that but had forgotton and confused it for some other pill. But can I now find Tagamet OTC in the UK? No, I think it must have been withdrawn.

Still, I don't think that was the explanation anyway, so can any of you guys suggest why the combination might have worked successfully on two people three times, but never, ever again worked to produce this euphoria? I know there are better ways of getting a high, but I don't have access to them... besides which, I'm really curious about this from a scientific standpoint.

Thanks,


Diesel.