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PostPosted: Fri Dec 10, 2010 2:42 pm 
I dont realy feel its neccessary for this post to be in this forum because I dont consider it "still messing around" but I figured some people might. I have a real hard time affording staying on subs and am on way to low of a dose but its the most I can afford. I started drinking a glass of grapefruit juice 2 hours before i take me dose and to my suprise it actualy does increase the half life of it significantly. I am not doing it to get high (which isnt possible anyway) I am only doing it to stretch my dose and get the most out of it that i possibly can. Before I did this I would usualy start to feel antsy at night and feel my dose wearing off but now I feel maintained well into the next morning its pretty unbelievable how well it works. I knew it worked with other opiates but wasnt sure about subs but it sure does. Im not condoning people to use this method because I honestly dont know if its unhealthy for the liver but it works very well for me and until I can afford to go back to 8mgs Im gonna stick with doing it.


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PostPosted: Fri Dec 10, 2010 4:12 pm 
You know, i remember doing this. Not with bupe but a long time ago when i wouldnt be able to get enough of my DOC and i would wanna do something to try to increase the effects, i would drink grapefruit juice. I never did understand why it worked but it definitely does increase the effects somehow. I had really forgotten all about that but i bet it would work for the reason you are mentioning. Thanks for sharing that. Like i said, i had forgotten all about that. It may not be for my particular situation because i am at a stable dose but it could definitely help someone who isnt or someone who is in the boat you are.


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PostPosted: Fri Dec 10, 2010 4:55 pm 
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I’m just lost on this one grapefruit juice and opiates?


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PostPosted: Fri Dec 10, 2010 5:25 pm 
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It sounds wierd but its true mostley with Benzos it can be dangeres with Benzos just be carefull thats all do wha you have to do to fill normal filling like shit depressed just not right sucks. I support you 100 % if it keeps you feeling normal and not like shit. Just don't do it with Benzos think it canne be very bad.

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PostPosted: Fri Dec 10, 2010 5:27 pm 
Bboy:

I know it sounds crazy but its something in it. It does seem to increase the effects and i really wish i could explain it but like i said, i've never fully understood it. I've only experienced it and it does actually work or at least i know it did with other opiates. So, it only makes sense that it would work with this also. However, i had completely forgotten about it. It would be kool if somebody could explain how this works cuz i did use to wander.


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PostPosted: Fri Dec 10, 2010 6:52 pm 
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It has an enzyme that breaks down the benzos faster/ more efficiently or something like that. not a scientist or doctor here. on a valium bottle it says "do not consume grapefruit while on this med"

maybe dr. J will see this topic


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PostPosted: Fri Dec 10, 2010 11:09 pm 
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lifesaver wrote:
Bboy:

I know it sounds crazy but its something in it. It does seem to increase the effects and i really wish i could explain it but like i said, i've never fully understood it. I've only experienced it and it does actually work or at least i know it did with other opiates. So, it only makes sense that it would work with this also. However, i had completely forgotten about it. It would be kool if somebody could explain how this works cuz i did use to wander.


YYea i saw this thread and was like WHAT? But wow thats crazy shit and with all the Technology today im suprised they cant figure a way to prevent this if it can be dangerous or harmfull to someone on a certain medication ya know. I could be wrong but i think its safe to say not every person on a benzo knows this and just per say they have a large glass of grape fruit juice and something happens then what. But thankyou for shareing this now ill never have a glass of grapefruit juice again thats for sure.


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PostPosted: Sat Dec 11, 2010 12:20 am 
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I have never heard of this before in my life but it certainly is interesting. It does remind me of a story though. When I first moved to NY and got a new doctor (took FOREVER with my WA state insurance card) I was given vicodin and clindamycin (antibiotic) for my HS (see other posts if you are curious and no that doesn't stand for herpes simplex). This was way before any drug addiction. I had been on the vicodin off and on already and on Keflex but then they changed the antibiotic. I always drank grapefruit juice throughout the day. Loved it. So I started taking the vic and clinda and within about 1/2 hr to an hr. I was so ill I thought I would die. At first I thought maybe the vicodin was making me sick to my stomach so I was avoiding it. Then I just started puking - horribly. Of course I was also pissed because every time I took the vicodin, I just friggin' puked it up anyways. This happened for two days straight and I just kept throwing up. I finally called my doctor and told her I was really sick and needed to go in. I thought maybe over time I became allergic to the vicodin or that maybe I was allergic to the clindamycin. So I get there and am explaining things and casually mentioned that I drank grapefruit juice. She just got this wide eyed look and repeated me inquisitively. I was like "yea - grapefruit juice. I drink it all day long". She started laughing and told me to stop and said she never would have figured it out if I hadn't mentioned it. Anyways....I find it funny because if this grapefruit thing is true, she probably thought I was a druggy anyways and that is why I was drinking it. Especially because I asked for a refill on the vicodin since I had puked a bunch of it up.

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PostPosted: Sat Dec 11, 2010 9:11 am 
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I found something online that describes how and why this works. I won't post a link to the site because I think it's an inappropriate web site in the context of THIS message board, but here's the article copied and pasted:

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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.

==========================================================================


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PostPosted: Sat Dec 11, 2010 2:40 pm 
To put it in a nutshell, grapefruit juice inhibits an enzyme (CYP34A) involved in the metabolism of opiates (and some other drugs). Slowing the drug's metabolism = higher blood levels and increased duration.
However, as the article mentions, some drugs NEED to be partially metabolized to work, ie codeine is converted to morphine in the liver. I know that buprenorphine is converted to norbuprenorphine, but I don't know if the enzyme in question affects this process.


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PostPosted: Sat Dec 11, 2010 4:28 pm 
Yeah with bupe it def doesnt effect anything other than making it last longer and feel like you took a little more. Im guessing my 4mgs with grapefruit juice would be = to 6-8mgs without it. With time tho Im sure this effect will diminish as my liver becomes more tolerant to the effect and over compensates. I probably wont do it for long periods of time but for now its keeping me more maintained.


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PostPosted: Tue Jun 28, 2011 2:10 pm 
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I drank Grapefruit juice on Suboxone one night. I woke up three hours vomiting up every last thing in my body. Miserable for hours. Went to the hospital still vomiting in the parking lot and on the car ride. It went away in the afternoon. I hardly ever vomit. Either that was the biggest coincidence ever or grapefruit juice and Suboxone was a terrible mix for me.


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PostPosted: Thu Nov 17, 2011 6:04 pm 
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[b]I dont think this is considered "still messing around" at all. My doctor suggests this to me all the time to maximize my dose and my absorption. She said patients swear by this. Ive never tried it but I dont think its still messing around if it's recommended by some doctors, besides it's grapefruit juice not another drug. Some ppl due to money troubles would probably benefit from this alot.

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PostPosted: Thu Nov 17, 2011 6:13 pm 
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I thought this sounded kinda crazy.......when I first read it.

I actually love grapefruit juice. I normally drink it in the evenings anyways. So, one night I drank it about 30min after my dose.

To my surprise, I DID notice that the juice seemed to intensify my Sub.

I dont know if this will work for everyone, but I definitely noticed a difference.


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PostPosted: Thu Nov 17, 2011 6:44 pm 
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I think its great, people found out a HEALTHY way to maximize their dose. Some ppl using this method might require less so it could be cheaper as well which is always a good thing. Theres nothing wrong with doing this, Its not using other drugs or anything like that. I hope the ppl that do try this that it works because they're alot of benefits in alot of ways. Good Luck and I hope alot of ppl see this thread and get use out of it.

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 Post subject: grapefruit juice
PostPosted: Thu Nov 17, 2011 10:43 pm 
I used to drink grapefruit juice before I was a daily benzodiazepine user to intensify the effects, which it totally did. I do drink grapefruit juice on occasion to this day and I have never noticed it interact with my buprenorphine but like we all know, once on a maintenence dose above X mg's, no 'greater' effect is going to be noticed. Cheers to those using it to save money on buprenorphine, though! Good idea!

-Travis


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PostPosted: Sat Nov 08, 2014 4:29 pm 
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Even OTC loperamide anti diahrrea medication is a weak opiate, but one that does not cross the blood brain barrier. Something about the acidic property of grapefruit juice has an effect that allows opiates to cross the BBB or blood brain barrier that normally would not get through and as a result more of the opiate is absorbed into the brain and a larger percentage of the opiate receptors are satisfied. So if you're ever in a serious bind, try taking about 20 loperamide, some Tagamet, and wash it down with about a liter of grapefruit juice. Trust me, it will alieviate just about every symptom. :D


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PostPosted: Thu Nov 27, 2014 6:12 pm 
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Lol in a way I think we addicts are ever the mad scientists. We like knowing chemical effects on the brain and how they work, from pills to natural remedies. I'm not saying that's a bad thing in this case, if it prevents cravings and keeps you stable at your given dose then I don't see a big issue.


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PostPosted: Fri Nov 28, 2014 1:44 am 
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"Lilly" describes the mechanism accurately a few posts back. Grapefruit juice blocks the liver enzyme CPY3A4, which destroys buprenorphine. The effect is much greater than simply prolonging the halflife of orally-absorbed buprenorphine. By blocking first-pass metabolism, grapefruit juice allows even SWALLOWED buprenorphine to become active, increasing buprenorphine levels several-fold.

Talk to your doctor about any plans to deliberately change drug delivery. The combination may be dangerous-- especially in the presence of other CNS depressants.


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PostPosted: Fri Nov 28, 2014 6:56 am 
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My guess is that we shall see
an uptick in the sales of grapefruit. .i hate the stuff, but thought has now come to mind that maybe it isnt so bad after all..ha..

interesting. ..


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