Opioids The Ultimate Opiate Potentiation Thread

[Kebil]

I think that people are getting confused because they are thinking of different things when they talk of "potentiation". Really, there are three separate things that we are confusing with each other, name; Potentiation: Increased Bioavailablity; lastly, Inhibition of Metabolism/Drug Accumulation.

Potentiation occurs when two drugs work synergistically (or additively) with each other, acting in unique ways to increase the total effect, resulting in a higher effect than what you would get if you added the result of using each seperately. I never really thought of combing other drugs with opiates as potentiation, rather, the opiate should just always be there, and then I mixed in various drugs as I got my hands on them, etc. I guess one good (great) potentiator is benzodiazepines. I know this field as I used to collect and sample them like delicacies when I used to be a pharmacist. I was always partial to chlordiazepoxide (note - methadone with benzo's can be very dangerious - benzo's are usually invovled in most methadone overdoses, and usually have caused respiratory depression.)
Marijuana is very good, as is DXM, ketamine. Some people use stimulants , cocaine/crack, meth, or hallucinogens such as psilocybin. I guess the question you need to answer first is what is about opiates you want to potentiate.

NO SIMPLE ANSWERS Drugs which in inhibit the metabolism of opiates (such as cimetidine, many SSRI's, some antifungals, etc - are generally inhibitors of cytochrome P450 isoenzymes in the liver (and there are as many types of these as you can count)). The list of these interactions is large and can be complicated and I won't go into it here as it is available in many other sources/references.

One class of drugs commonly encountered is SSRI's class of antidepressants. Several of these drugs inhibit various and sundry different P450 enzymes - different SSRI's inhibit different enzymes, and different enzymes are responsible for the metabolism of different opiates. Consult such a table for specific details. I know that for methadone, each of fluvoxamine, fluoxetine, and sertraline can inhibit the metabolism of methadone by inhibition of various P450 isoenzymes. When the metabolism of drugs is inhibited in the liver (and/or the gut, drug levels can increase in two ways. Increased availability, and decreased elimination

Increased Bioavailability - Drugs taken orally that are usually metabolized extensively by first past metabolism in the liver (or gut) during absorption, can have sudden, possible large, increases in bioavailability if the enzyme responsible for its metobolism is inhibited. When grapefruit juice is drunk before (about an hour) taking a dose of methadone, the amount of methadone absorbed can increase between 5 to 15, sometimes even up to 30%. This is the equivalent of taking an additional 5 to 15% methadone. This is not really potentiation, more like addition. Of course, the ultimate ways to increase bioavailability is to change the route - to IV if possible, to a lesser degree but still highly effective is the newly popular method of insuffulation (snorting). Growing up, I never would have dreamed I would one day prefer to snort my tablets.

Decreased Elimination Opiates metabolized in the liver (all of them (that I can think of)) can also have their metobolism inhibited (we are no longer talking about first pass metobolism) by drugs which directly inhibit some of the enzymes that metabolize (and inactivate) our precious dose. SSRI's love to do this for us, as well as cimetidine, and 3.5 trillion other drugs (however, a great many of these interactions have no clinical relevance and are barely perceivable, if at all, other than for a placebo effect). Again, various drugs affect various opiates, but their are patterns to the madness (but they are a secret). This inhibition does not result in a higher dose absorbed (all though it could do that in addition), nor dose it alter the peak levels achieved following a single dose opiate (their are exceptions to every opiate rule). However, enzyme inhibition can result in prolonged activity (yeah for more nodding off), usually to a moderate extent. Most of these interactions are not clinically relevant, but some combinations can have dramatic effects (personal experience as cited below) generally as the result of drug accumulation.

Methadone is notorious for this, as its usually half life is between 12 and 36 (to 48 to 60 or more hours, it varies a little bit). Because of this, there is always still a lot of drug remaining from the previous dose (typically half the previous dose when methadone is dosed daily)when it is time for the next dose. Slowing the metabolism of methadone can result in a gradual but pronounced increase in drug levels, reaching it's peak in 5 half-lives (i.e. 2.5 to 7 to even more DAYS). For me, it was fluvoxamine and methadone (a mistake I allowed my doctor to make twice). Fluvoxamine inhibits cytochrome 2D6 in the liver, one of the main enzymes that deactivate methadone. This resulted in a longer half life, resulting in more drug left over when the next dose is due, resulting in slowly climbing blood levels, followed by a 1 month stupor where I wandered the winter landscape of northern BC walking an hour through storms everyday for one hour to get my daily dose of sunshine. This eventually led to me in the the psych ward for 2 weeks over Christmas (I don't remember most of it. This was all due to drug induced delirium via methadone (I was only 31 years old (and it was Christmas))),

(of course, remember, 5 half lives to peak levels, 5 half lives to eliminate 98% of the opiates from your body (you may need to know that if you have a drug test coming up).

 

[Kebil]

Oh, and Grapefruit juice only inhibits enzymes in the gut wall - it does nothing for the liver. Therefore it has effects only on drugs taken orally, and only has effects on first pass metabolism, thus it increased bioavailablity of some drugs, and has no effects on the duration of action (except as far as the increased amount of drug absorbed changes the duration of action. It does not change the half life

 

[El Commandante]

Are there any herbals (apart from Cat's Claw) which might go well with Methadone? Kava, Valerian, Skullcap and others spring to mind.

 

[v4lium]

I think I've said this already in the thread(not sure, too lazy to check through 26 pages to find out)... doxylamine is great opiate potentiator IME, a lot of painkillers here are prepared with x dose of opiate and like 5 or 10mg of doxylamine, good stuff.

Good for countering the itches and improving the general sedation of opiates.

 

[El Commandante]

Few more points I wanted to bring up.
On the first page of this thread there is a methadone user who says he doesn't take cimetidine until 1hr after he's taken his Done, then reloads his cimetidine every half hr or so for the next couple of hours. This seems to go against most of the info i've read relating to cimetidine and methadone, but he seemed confident that it worked for him. I thought it should be taken an hour before taking Done, and that reloading on cimitidine would make little difference.
Secondly can anyone make the following quote a little easier for me to understand?

A dose of Tagamet an hour before a hydrocodone/oxycodone session will make the drug last longer and have a better effect. Antacids should be taken at least 45 minutes after the Tagamet otherwise absorption of the Tagamet will be impaired. Grapefruit juice also has the same type of impact on liver enzymes; use a Maalox chaser to neutralise any systemic acidification effect from the grapefruit juice. Tagamet should not be taken with codeine because it impairs the metabolism into morphine necessary for it to have any real effect.

Would it relate to Methadone as well?
Thirdly, in terms of methadone, how does nicotine and caffeine interact. When taking poppy pods, a cigarette used to noticeably intensify the opiate effects, often causing me to lie down for a few minutes. However, from what i've read nicotine actually decreases methadone blood levels! Any thoughts? And will drinking a few cups of tea, increase or decrease the euphoria?

 

[El Commandante]

Would the best way to boost a drug like methadone be to take several potentiators that work in different ways? Say, cimitidine and/or GFJ, cat's claw and diazapam all together?

 

[Kebil]

It makes little sense to take the cimetidine after methadone. It will still work to inhibit the metabolism of methadone, just as it would do if you took it an hour before the methadone, but when you take it an hour after methadone then you are allowing the first part of the absorbed methadone dose to be metabolised at its normal rate. The confusing part for some is that it takes a minimum of 2 hours, and up to 4 hours, before the bulk of the dose is absorbed and kicks in. It would be hard for most people to notice this after one dose because methadone is an already very long acting drug. After a week of doing this the methadone levels will rise to its new maximum amount and by then you may or may not notice a dose. Remember that 70 to 90% of a methadone dose is already absorbed, and it has a half life of between 12 and 36 hours, depending on how your body handles the drug.

Of course, I have been on methadone for a year and a half now, and even if I take two doses at once I don't really notice anything - that is just the way tolerance works after continuous use. I take grapefruit juice with every dose - partly because I am now "addicted" to grape fruit juice (I love that shit).

I don't believe that caffeine would interact with interact with opiates in any way other than to help increase the pain relief by a small amount. Nicotine, in general, stimulates the liver, inducing enzymes and in general speeding up the metabolism of many drugs so I doubt it would potentiate them at all.

I have not really tried to try to potentiate other opiates. When I was using them, I would just use more if I wanted to get higher. I don't do other opiates much anymore and just stick with the methadone. The opiate buzz is not really worth losing my life over anymore.

 

[KFINN]

Wow.... Well, i've scanned this entire thread and am feeling somewhat hopeful that i might perhaps get better effect from my pain medications. Grapefruit juice, Benadryl and NyQuil will be on my grocery list tomorrow! I so desperately need more relief, and would much rather drink a little grapefruit juice than ask my doctor to increase my doses (which at this point i believe is not even an option anyway).

Thank you so much for all your information and sharing your experiences!

Aloha nui loa,

~Suffering Beach Girl %)

 

[El Commandante]

Sorry to keep banging on about Methadone potentiation, and thanks to everyone who has attempted to answer my many questions, but can anyone advise me on Cat's Claw and Methadone? It was mentioned on the list of opioids at the start of this thread as being a definate potentiator of methadone (and was the only one listed actually).
I have a bottle of 500mg capsules of Cat's Claw, but am unsure as to how much and at what time to use them in relation to my daily methadone dose. The only other post that mentions an experience with the two recommends 300mg 1 hour before, and 200mg 1 hour after. I can't do this because i've got 500mg capsules, so what's the best way for me?

 

[Kebil]

Cat's claw, just like cimetidine, many SSRI's, and other drugs just inhibits the metabolism of methadone. Methadone is an already very long acting drug, taking enzyme inhibitors with it just increases its duration of action, and upon repeated methadone and cats claw administration, slowy the blood leves of methadone will rise, slowly over the course of the next 5 to 10 days probably. How much it rises depends on who much it can inhibit liver enzymes. Grape fruit is another good enzyme inhibitor, but it.

However, in my own opinion, I wish people would just back away from getting off on methadone, non-methadone maintanence patients are usually the ones that end up dieing and giving all of us actual patients a very bad name.

 

[El Commandante]

Well Kebil, i too am a methadone maintenance patient, so i'm not trying to "get off" on methadone. I happen to be on a low dose (35mg) which I feel does not equate to my previous opiate usage. However, my drugworkers are very hesitant to raise it by too much, so here i am trying to boost its effectiveness by any means possible. I have not come close to OD'ing, whatever potentiator i've used as I have a tolerance.
I appreciate your explanation as to the workings of Cat's Claw, but am still unsure as to whether i should be taking it before, with or after my methadone, and whether i need more than 1 500mg capsule. Can anyone offer advice about this?

 

[Kebil]

Sorry, meine Commandante, we must have misunderstood each other a little bit. I was not talking about you specifically, nor did I have any one individual in mind when I complained about people misusing methadone and giving MM patients and methadone a bad name. When used appropriate in selected patients, methadone can be very safe. When people who are only occasional users of opiates take methadone, there lack of familiarity with the drug is what leads to their death. They take a dose that is generally to large to start with, and wait half an hour. Not getting much effect (methadone peaks in 2 to 4 hours p.o.) they take the rest of whatever they have, and we know what happens next .

I just spent 45 minutes writing a response, only to somehow press a wrong button and all that text disappeared. I have it when that happens and I will try to rewrite it all later.

I will just quickly attempt an answer to the Cat's Claw (CC) question you just sent. You would want to take the CC before you take your methadone. You want it to be circulating in your body so that it will be inhibiting the P450 isozymes in the liver when the methadone is taken.. I don't know how long CC stays in the body, but once it is gone the enzyme inhibition would end. P450 inhibition is almost always a reversible reaction. It requires that the enzyme inhibiting compound (from Cat's Claw, or from cimetidine) binds to an allosteric binding site on the enzyme. When this site is occupied, a conformational change takes place in the enzyme. This change in the structure of the enzyme has an effect on the catalytic ability of the enzyme, virtually ALWAYS results in a decreasing in activity.

The occupation of the allosteric site by itself does not have an effect on the body. It is only when a substrate for a particular enzyme finds its way into the catalytic site of the enzyme WHILE the enzyme inhibitor is also present, at the allosteric site. When this set of circumstances occurs, the enzymatic reaction is slowed down, inhibited, maybe even temporarily blocked. The enzyme is not totally inactivated and metabolism can still occur, but with less efficacy and efficiency.

As soon as the enzyme inhibiting compound is released from the allosteric site, the enzyme springs back to in's original conformation. It is now no longer inhibited and can return to it's rapid catalysis of whichever particular reaction it is responsible for. P450 enzyme inhibition is almost never irreversible, although I am sure there are substances that could permanently block these enzymes, such as some chemotherapy drugs, etc, but that would be an incredibly stoopid thing to do just for a fix of methadone. Inhibition of p450 does not decrease the amount of enzyme present in the liver, they do not get degraded quicker nor is less of the enzyme produced, that is how they DO NOT work.

Thus, it becomes clear that we would want both the enzyme inhibitor (Cat's Claw or cimetidine (Tagamet)) and the enzyme substrate (methadone) present at the same time, otherwise they won't have any effect on each other. I don't know what compound in Cat's Claw is responsible for this enzyme inhibition, nor do I know how quickly it is absorbed, how long it stays in the body, nor do I know how much of this substance is in 1500mg, nor how long it lasts. That is a lot of unknown factors (which is why I would recommend cimetidine over CC, but again, I have never tried Cat's Claw, and I am going to give it a try this week!

I would recommend taking your CC 1 to 2 hours before your methadone so that is present and actively inhibiting P450 when the methadone is being absorbed, and as it passes through the liver on it's first pass. This should decrease the amount of first pass metabolism by the liver, and therefore increase methadones bioavailability (which would give the same effect as an increase in dose.

Take another dose 1 to 2 hours, maybe 3 hours after your dose of methadone later. I don't know what the effects of CC is on the human body, or what effects would occur if you took a high dose of it, that is up to whoever wants to use this information to figure out. Any dose taken after you have taken methadone is not going to have much of an effect on first pass metabolism or bioavailability (as most of the methadone will already be absorbed. Rather, these doses will decrease the overall rate of methadone metabolism, thus increasing the half life. This will not result in any more methadone appearing in your body the first day you do this. However, it will obviously mean that at any given time, your methadone blood levels will be a little higher than they would be if you did not take CC (or cimetidine).

When the time comes for your next dose, you may notice that you are not feeling as "sick" as usual. This is because not as much of the methadone has been broken down. Now when you take your dose of methadone, following the same schedule of CC (or cimetidine), your blood methadone levels will rise to a slightly higher level than the level you used to reach. This is just because blood levels are additive. When you take your methadone dose, you are adding that dose to a baseline level that is higher than usual, thus adding up to a higher level than usual.

Don't be surprised when you realize that you don't really notice much of a difference, maybe a small difference, but I always find it hard to notice small increase in my dose. Don't despair or come on here to call me an idiot (I already know that), continue with your scheduled doses of CC (or cimetidine) for the rest of the week. Each day your blood levels will rise a little bit higher than the day before - from the increase in BA, but mostly as a result of reduced elimination of your methadone. Remember, anytime a drug you take regularly is increased in dose, it takes 5 half lives to reach steady state (well, 95 or 98 percent of steady state). The half life of methadone varies from person to person (as does every drug), but is usually around 24 hours (estimated range of half life in opiate addicts is between 12 and 36 hours, occasionally up to 72 hours). That means that it will take about 5 days for this strategy to reach its maximum effect, but you should be able to notice some effects in 3 or 4 days. Hepatic enzyme inhibition will increase the half life of drug metabolized by the liver, I don't have any numbers for this effect. If anybody else know, I would like to hear.

Grapefruit juice is similar yet different. GJ only inhibits the enzymes in your gut and gut wall. It has no known effect on hepatic P450 isoenzymes. Thus, the main effect of GJ is to decrease the amount of methadone metabolized before it reaches the circulatory system. The effect is basically the same as taking a slightly higher dose every day (about 17% higher, with a range between 3% and 25%). There is a maximum effect that enzyme inhibition in the gut can have, and it is easy to understand why. Only about 15 to 40 percent of methadone is typically metabolized in the gut wall (by bacteria I think). So obviously the most you can change the amount absorbed is by this amount, 15 to 35%. GJ increases the oral BA of methadone, but has no effect on the half life of methadone.

When you instead focus on inhibiting hepatic metabolism, there is theoretically no limit to the level of inhibition of metabolism (well, I guess the max is 100%, if you could block every route of methadone degradation, as well as blocking excretion by the kidneys). Cat's Claw alone, or cimetidine alone, will never achieve a true 100% inhibition because they only inhibit a few of the thousands of p450 isoenzymes, and several distinct subtypes of P450 enzymes can break down methadone.

Obviously you would not want to inhibit all of your hepatic enzymes. They are not just there to metabolize drugs (although they mostly do metabolize exogenous substance) but other toxins and waste products as well. If you want to feel really sick, turn green, start vomiting constantly , and risk going into a coma, yes, you could probably block almost all of the P450 enzymes, but you would probably die from an overdose of whatever you are using to block these enzymes.

Something you should also consider is enzyme induction. This is different from inhibition not just in the direction of change, but also in the mechanism of change. There are a number of substances, most of them also metabolized in the liver, that will signal the liver to produce more copies of p450 enzymes. Drugs such as rifampin, barbiturates, many anti-epileptic drugs, St Johns Wort, cigarette smoking, et al induce the production of p450 enzymes. If you take any prescription or non-prescription drugs, it may be worthwhile to check if they have any effect on hepatic enzymes.

Lastly, I still think that cimetidine is a better choice as an enzyme inhibitor than Cat's Claw. For one thing, cimetidine is a single chemical entity, so it is obvious what is responsible for inhibition. It has reliable effects, has been shown to be safe (who knows what the long term effects of CC is, lots of herbal medications, some of them very poplular in their day, were eventually shown to be potent hepatotoxins, nobody realized this because the time between consumption and the onset of symptoms can be many, many years, and besides, most people died from other causes before chronic disease could set in.

The most complicated part of trying to create a strategy for inhibiting the metabolism of your Daily Dose of Sunshine is figuring out which enzymes are most involved in methadone metabolism, and what substances will inhibiti those isoenzymes. There are voluminous lists of cytochrome P450 drug interactions.

I remember it was 2 years ago that I ended up in the psych ward over Christmas. I was on methadone back them as well, and I was also on fluvoxamine (Luvox). Now, since I had been a practicing pharmacist for 8 years, I did realize that Luvox can inhibit the metabolism of methadone. Unfortunately, I was the only one who realized this, my methadone doctor did not know, by psychiatrist did not know, nor did my family doctor (I am very lucky to live in a country with free health care.The only reason I was escorted to the hospital by my doctor (I had an appointment at the clinic that morning) was because he could not understand anything I said. I was feeling just fine.

I had been on methadone for 2 months, and it was my 3rd time in a maintenance program. I honestly thought I was doing okay, as I had been able to almost completely stop smoking crack (which was hard as my wife was smoking crack constantly) I would later learn that everybody around me had been watching me slowly decline over the course of 2 months, but of course, crack heads don't make very good caregivers.

I had also lost about 50 lbs, so their was not much left of me to contain the methadone. The really fucked up thing is that I was only getting 35mg a day. While in the the hospital they slowly tried to step down all my meds, including my methadone. Towards the end I was down to 18 mg, and still living in a dream world. I don't think it was only methadone affecting me, but that was a big part of it.

And then there was the matter of the fluvoxamine (Luvox). I have been on and off treatment for depression since I was 19 years old. And when I say depressed, I don't mean I had a little blues, or a broken heart from my girlfriend leaving me, I had a really deep depression, and their would be entire months where all I wanted to do was just kill myself, and the only reason I did not was because I did not want to upset and hurt my parents again. When, 1 year earlier, I had lost my pharmacy job and was planning on going on methadone, I asked my head doctor to switch me to Luvox, I made up some reason to switch and he had no problem with it. Of course I choose Luvox because of its enzyme inhibitionhttp://i.bluelight.ru/s/biggrin.gif

By they time I made it to the hospital, I was basically living in my own little dream world. I spent the majority of my time on the nod., nobody could understand a thing I said, which was fine with me cause I was not in the mood to talk to anybody. I must have looked like a total mess, walking around town, with my 4 sweaters on (that was my winter jacket because we could not afford a real jacket., but now I have gotten ahead of myself

Our car had burnt down a month earlier, so I had to walk to the pharmacy everyday, which was a 2 1/2 miles one way, in the middle of a very cold winter (we were living in Fort St John, far nothern BC). I would leave our apartment at 11 am, then wander all over town, wherever I want to go. One day I decided to go shoplifting at Canadian Tire. (Important Note: Do not try to shoplift when you are so doped up you don't notice people all around you watching). I was stuffing plumbing pipes and parts in my pants, I put some things in my socks, some behind my sweater, I was all laden down with parts to make a crack pipe. I was about to go out the front door, when I almost bumped into a women with a walkie talkie, one of the employees. Up till know I had been extremely UNPARANOID, so much so that I was not even looking around when I was stuffing my clothes with all this stuff. Anyways, I heard a crackling voice on the walkie talkie, and I heard a mans voice asking "can you see him, do you know where he is", and she, now 3 feet away from me, staring right at me, said "yup, he is right here".

Now, had I bin a bit smarter, I would have put all the stuff back, as as long as I had not tried to leave the building, I could not be charged with theft. But I needed those pipe parts. Amazingly, I came up with a pretty good plan. I was walking around the plumbing section more, making sure nobody on the floor could clearly see me. I made a few abrupt and unexpected corners down the aisles, and then, being near the automotive shop, I walked to the front desk of the autoshop, there was nobody there, and without a second thought I very quickly went through the door and into the auto shop.

I looked around and there was nobody around. Nobody could see me, or I could not see anybody, not that I stood looking long. I immediately went out the side door, and started to head across the parking lot.

Of course, stupid stoned me, I walked across the parking lot in the open. Suddenly I noticed a group of people standing out in the parking lot, somebody shouting "well, where is he". I think realized that I did not want to talk to these people, so I turned, and as I did, I saw the group break out in chase. I hightailed it, running as fast as I could (in University I was a national level 50 and 60 meter sprinter, I was 7 fastest in Canada in my freshman year, and the second of only two caucasian sprinters. However, I had never tried to run with a soldering iron up one sock, pipe parts in the other sock, hands full, sweaters full, I had stolen a lot more than I could easily carry. It did not take more than 8 steps and I was flat on my face, I heard them approaching, and I just lay there. I could not have cared less.

I spent the next 12 hours in the drunk tank, charged with shoplifting, etc. The only think I was concerned about was making it home before I was due for my next dose. It was 2 weeks later that I ended up in hospital.

I did have a reason for telling that story, but it is time for my Saturday afternoon nap., but just take that as proof positive that enzyme inhibition can sometimes have very very strong effects , and sometimes it is easy to slowly slip into that wonderful opiated daydream state for months at a time. Yes, it was my fault to a large extent, but I don't know why nobody said anything sooner. My wife and friends (my crack "friends") did not say anything. The pharmacists at my methadone pharmacy never said anything, and it is part of their job to not dose people who seem intoxicated. I had many several visits with my methadone doctor and my counselor, and my nurse, and my social worker (I was unemployed at the time, and trying to figure out how I could extricate myself from the situation I was in without having to leave my wife. Even in my haze, I realized I did not want to live the life of a crack head anymore.) So I had all these people trying to help me help myself, and none of them said a word about me going on the nod regularly, nobody said anything about my half closed droopy eyes, nobody mentioned that I was frequently make no sense at all.. Not until my doctor finally asked me to be admitted to the hospital did I start to realize just how fucked up I was.

So be careful, potentiation can be more effective than you might realize, especially as it sets in so slowly, and because methadone has such a long half life.

I have a few things to say about potentiation with benzos, and myabe I will dig up a list of enzyme inhibitors, etc if anybody wants.

 

[El Commandante]

Thanks for all the info and the warning story as well. It's hard to believe that 35mg can screw someone up to that extent, and I suppose the self-destructive side of me would actually like to be closer to that level of intoxication rather than worrying each day whether I will even notice ANYTHING from my 35mg, but you tell a very poignant tale. I'm on 40mg Paroxetine ATM, and am hoping to have it increased as high as poss, as i believe it has some kind of potentiating effect on methadone. Let's hope it is not as drastic as that!! I'm also on 5mg Olanzapine which may or may not reduce Paroxetines' effect. We'll have to see.
One thing i'm a bit confused about with the Cat's Claw is that i had read it was an NDMA(?) antagonist, so worked a bit differently to cimitidine when used with methadone. Is this correct? Just that i thought that's why it potentiated methadone. I may be wrong.
Interesting that you say cimitidine has to be taken for 5 days or so before having much effect, which would explain why i felt nothing from it the 1st time i took it. I usually take it along with my usual GFJ dose. Is this a good idea?
Would be pleased to hear any more of your thoughts regarding benzos and meth, and enzyme inhibitors. I have found diazapam very effective, although its effectiveness decreases quite quickly.

 

[PottedMeat]

Dramamine is dimenhydrinate. Benadryl is diphenhydramine. Both should increase the tendencies to "nod" but not necessarily the euphoric effects. Both should also reduce any itchiness. In fact, if I don't take a small dose of Benadryl (or the OTC sleep medication Unisom, it is also diphenhydramine) I will start itching almost as soon as the heroin is up my nose and into my bloodstream, if it is any good. Furthermore, more often than not the stuff I find around a certian really-big midwestern urban area is cut with diphenhydramine in the form of "Dormin." It is used because the Dormin capsules contain a fine white powder that is easily used as a cutting agent. When I get stuff in anything greater than $10 bags (like, say, a gram), I usually get a few Dormin capsules "in case you want to cut it up, man." Needless to say, I don't want to cut it as I'll most certainly be doing it myself, and I would much rather snort the purer, tannish powder. The $10 bags are typically cut and therefore contain a much whiter powder, though the mix is so homogeneous it looks like it's all one thing. I do save a Dormin or two, nonetheless, as like I said before, it does help with the itchiness!

Careful. Unisom gel caps contain a different active ingredient than the pills.

 

[Thorn105]

I hope I am in the right section here. I've been a member awhile, but don't post that often. I just wanted to share something on the poppy pod tea. To me, that taste is AWFUL, and smells like nasty ass. I was using ground up tums to potentiate as per suggestion from another member, and it has worked for me. Over the week-end, I found a new tums flavor in our store called BERRY flavor. I use about one and a half cups of pod material (yes, I know that's a lot, I have been on prescription pain meds for years and have a high tolerance), and ground up 6 extra strength BERRY FLAVOR tums in my mortar and pestle and add to the water, then let it boil, then remove from the heat and put in the pod material, steep for 1-2 hours. I swear, I have finally found a way to disguise the taste of the stuff enough so I don't gag when I am drinking it. The tums take away most of the bitter taste and it is SO much easier to get down. I don't know how or why, but seriously, most of the bitterness is gone. It still isn't a delightful taste or anything, but I can taste mostly berries with just a hint of that bitter crappy taste, so not hard to get down anymore at all. Before I made the berry discovery, I chased the tea with pomegranate juice. The juice immediately takes away the bitter aftertaste. However, with the berry tums, I don't even need a juice chaser. Hope this is a bit useful to someone else, because I use and appreciate so much information I have found on bluelight and would like to think I can contribute a little something in return. I like the poppy pod tea for pain relief because it has no acetemenophen in it, and lasts all day for me. Again, I apologize if this is in the wrong section, but since the tums potentiate it IME, I thought this was the place to post. Cheers!

 

[El Commandante]

Have you ever thought of just swallowing the poppy powder with water, in a slurry, rather than making a tea every time. You would probably find that you need a lower dose of powder this way, and would also experience better results, in terms of effects and duration. Just a thought!

 

[Thorn105]

I have considered that, and wondered how much I should try this way. Like maybe, half my usual dose, or even less than that? Am I to understand you have tried it successfully this way? If so, could I get a few more details, mainly, how could you choke it down? When the powder hits my throat at the end of the cup of tea, it gags me, but I'll bet I could choke it down if I had to. Just curious as to what your experience is, and thank you for the suggestion. Any tips on reducing the amount I have to use is greatly appreciated.

 

[tadfish]

Is mixing tagamet with DHC a good way to make it stronger or not?
I heard tagamet is great for morphine orally but not codeine i think.

If u take the tagamet at same time or after codeine it makes it stronger as the morphine stays around longer is that true. I am trying to recall i think it does but can't be for sure.
My theory its takes a while fro tagamet to work in stomach and by the time it does codeine has turned into morphine is this corrected or am i fried?

Also what opiates does it potentate? I know it does for most benzos if not all.

I recall but from past use that DHC is potentated by tagamet. true or false and when is best time to take tagamet (Cimetidine)?

some info on tagamet

from MIMS: (Oral absorption studies carried out using a 200 mg dose have resulted in blood levels averaging 2.8 micromol/L (0.7 mg/L), occurring at times ranging from 45 to 75 minutes after dosing. Up to 34% of the drug was recovered from the urine two hours after dosing, and after 24 hours 70% of the dose was recovered.)

Interactions
Cimetidine has the potential to affect the absorption, metabolism or renal excretion of other drugs, which is particularly important when drugs with a narrow therapeutic index are administered concurrently. The altered pharmacokinetics may necessitate dosage adjustment of the affected drug or discontinuation of treatment (see Precautions).

Interactions may occur by several mechanisms including the following.

1. Inhibition of certain cytochrome P450 enzymes (including CYP1A2, CYP2C9, CYP2D6 and CYP3A3/A4, and CYP2C18). Inhibition of these enzymes may result in increased plasma levels of certain drugs including warfarin type coumarin anticoagulants (e.g. warfarin), tricyclic antidepressants (e.g. amitriptyline), class I antiarrhythmics (e.g. lidocaine (lignocaine), quinidine), calcium channel blockers (e.g. nifedipine, diltiazem), oral sulfonylureas (e.g. glipizide), phenytoin, theophylline and metoprolol.

2. Competition for renal tubular secretion. This may result in increased plasma levels of certain drugs including procainamide, quinidine, metformin, cyclosporin, tacrolimus and dofetilide (see Contraindications).

3. Alteration of gastric pH. The bioavailability of certain drugs may be affected. This can result in either an increase in absorption (e.g. atazanavir) or a decrease in absorption (e.g. some azole antifungals, e.g. ketoconazole, itraconazole or posaconazole).

4. Unknown mechanisms. Cimetidine may potentiate the myelosuppressive effects (e.g. neutropenia, agranulocytosis) of chemotherapeutic agents, e.g. carmustine, fluorouracil, epirubicin, or therapies, e.g. radiation. Isolated cases of clinically relevant interactions have been documented with narcotic analgesics (e.g. morphine).

ok what opiates does tagamet potentiate? it seems
Also is there anything that makes suboxone, subutex, bupe stronger if take subliminally not IV. I know bupe doesn't work if u shallow it at all is there anyway of changing that? cause i always worried when i get my bupe dose some of it is shallow by my spit and not absorbed in my mouth.

 

[fluckimissed420]

Hm Sleepinal or maybe sleepinex ive heard seems to work ok. For boost skip it for one day if you can and deal with minor methadone w/d Then dose next morning immediately on an empty stomach ofr best results

 

[morphonorconic]

^^Unless I'm mistaken, Cimetidine should potentiate Dihydrocodeine. But Tagamet inhibits the conversion of Codeine to Morphine and Norcodeine and any other metabolites are responsible for it's effects.

If you are worried about wasting Buprenorphine from swallowing it, perhaps you might try taking your dose in fractions, so you would be less likely to build up a lot of saliva, or as much as you would from a whole or half suboxone. Also, that would increase the surface area that is to come into contact with your sublingual palate.