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  • BDD Moderators: Keif’ Richards | negrogesic

Codiene + Plugging + GFJ = Really Good time?

nekointheclouds

Bluelight Crew
Joined
Aug 23, 2009
Messages
12,847
Okay, so I have searched around, and I know some basic facts.

GFJ will poteniate Codiene orally.

Plugging Codiene has a better Bio availability.

So can I do both?

I mean, will drinking GFJ still potientiate codiene even if its plugged?
 
I don't think so, because you're bypassing your liver role when you're plugging. No dope going through the liver = no GFJ potentiation.
 
I don't think so, because you're bypassing your liver role when you're plugging. No dope going through the liver = no GFJ potentiation.

Exactly. For potentiators in the liver to work it cant skip the liver, so IV, IM SC, Snorting(unless some drips down your esophagus and plugging wont work.
 
Hmm, I have read around the site conflicting reports.

But I thought that even if you plug stuff, it still goes to the liver. Its just taking a different route.

Perhaps that is the real question, when plugging a substance, does it still go through the liver?
 
Okay, so after doing some more research around BL, I found this thread which addresses ROA and the liver. In case anyone else is wondering, you can read about First Past Metabolization here:

http://bluelight.ru/vb/showthread.php?t=482162

So according to what folks are saying here, if I plugged codiene, it would make a pass through my liver, but only one pass. But that still gives my body a chance to boost the amount that is converted to morphine.

So I think I am gonna give this a try, but with a lower dose of codiene then I might normally try just in case. Seems to me that Drinking some GFJ an hour before plugging could still have a good effect.

I'll get back to this thread on my experience. But if anyone else has any thoughts on this topic, please share!
 
Only use the grape fruit juice at the peak of the high, or else it will slow the metabolism of codeine to a crawl.

It inhibits the enzyme to break codeine into morphine. But it stops morphine from being broken down so fast.

You have to time it right, or you could fuck it all up.

Now if you have CWE some codeine, you can drink a couple of shots 30-60min before the codeine, then drink one more shot after to greatly boost the metabolism of codeine to morphine.
 
it seems like plugging codeine would be silly. it is gonna pass through your liver multiple times, no matter what ROA you use. if you use one besides oral, it will hit your BBB before your liver, but that should not matter with codeine, which needs to be metabolized into active chemicals.
 
Only use the grape fruit juice at the peak of the high, or else it will slow the metabolism of codeine to a crawl.

It inhibits the enzyme to break codeine into morphine. But it stops morphine from being broken down so fast.

You have to time it right, or you could fuck it all up.

Now if you have CWE some codeine, you can drink a couple of shots 30-60min before the codeine, then drink one more shot after to greatly boost the metabolism of codeine to morphine.

This. You need to allow the codeine to convert into morphine before using grapefruit juice.
 
Only use the grape fruit juice at the peak of the high, or else it will slow the metabolism of codeine to a crawl.

It inhibits the enzyme to break codeine into morphine. But it stops morphine from being broken down so fast.

You have to time it right, or you could fuck it all up.

Now if you have CWE some codeine, you can drink a couple of shots 30-60min before the codeine, then drink one more shot after to greatly boost the metabolism of codeine to morphine.

But this is what I read about Grapefruit juice in the ADD thread on Codiene:

"A Note on Codeine & Oxycodone
Codeine is metabolised by both CYP3A4 and CYP2D6. CYP3A4 metabolised codine into norcodine which isn't very active, while CYP2D6 metabolises codiene into morphine which is responsible for codiene's effect. When the CYP3A4 enzyme is inhibited by grapefruit juice, more codiene may be metabolised by CYP2D6. This is theoretical and is not supported by literature at this time.

Like codeine, oxycodone is metabolized by both CYP3A4 and CYP2D6, with the more potent metabolite, oxymorphone, produced by CYP2D6. When the CYP3A4 pathway is blocked, more oxycodone may be metabolised by CYP2D6.

Grapefruit Juice and Cimetidine (Tagamet)
Cimetidine acts on a different enzyme than grapefruit juice, specifically CYP2D6. CYP2D6 metabolises many opiates and opiods, but grapefruit juice has no effect on CYP2D6."

So GFJ should allow more codiene to turn to morphine, while Cimetidine is the one that inhibits codiene to turn to morphine.

I always drink GFJ before drinking PST, and I notice a huge difference if the PST's strength.
 
But this is what I read about Grapefruit juice in the ADD thread on Codiene:

"A Note on Codeine & Oxycodone
Codeine is metabolised by both CYP3A4 and CYP2D6. CYP3A4 metabolised codine into norcodine which isn't very active, while CYP2D6 metabolises codiene into morphine which is responsible for codiene's effect. When the CYP3A4 enzyme is inhibited by grapefruit juice, more codiene may be metabolised by CYP2D6. This is theoretical and is not supported by literature at this time.

Like codeine, oxycodone is metabolized by both CYP3A4 and CYP2D6, with the more potent metabolite, oxymorphone, produced by CYP2D6. When the CYP3A4 pathway is blocked, more oxycodone may be metabolised by CYP2D6.

Grapefruit Juice and Cimetidine (Tagamet)
Cimetidine acts on a different enzyme than grapefruit juice, specifically CYP2D6. CYP2D6 metabolises many opiates and opiods, but grapefruit juice has no effect on CYP2D6."

So GFJ should allow more codiene to turn to morphine, while Cimetidine is the one that inhibits codiene to turn to morphine.

I always drink GFJ before drinking PST, and I notice a huge difference if the PST's strength.
Grapefruit juice will not make more convert period. The only way to truly boost the metabolism is through inducing. Gf juice is not the ideal thing for either of these.
 
No matter the route of administration, your body will break down the drug into its constituent parts and excrete them. It is myth that the drug somehow follows a totally different metabolic process based upon the ROA. I'm not giving anyone shit, but I've heard this information spread around in multiple instances on the forums. It's simply not how things work. When you take the drug orally, more of it is destroyed through first-pass metabolism, but I can assure you that I'm quite positive that the same mechanism at-play, being enzyme inhibition, will function similarly regardless of the route.

I'm open for debate on the subject but I would like to nip this in the bud if possible, whether I'm right or I'm wrong.
 
Plugging would raise the bioavailability so using this roa would probably get you higher.
 
Whoops accidentally deleted my last post when I tried to edit. I'm just sick of people saying GFJ won't potenate codeine, yet it inhibits the enzymes that break it down into inactive metabolites (CYP3A4) and doesn't inhibit the enzyme that turns it into morphine (CYP2D6). Paracelsus tried to clear this up but people keep spreading misinformation.
 
this is an old thread, but seeing as it's back, this is not accurate ...

So according to what folks are saying here, if I plugged codiene, it would make a pass through my liver, but only one pass. But that still gives my body a chance to boost the amount that is converted to morphine.

first pass metabolism is when a drug passes through your liver before the rest of your circulatory system including your brain. this is the route orally ingested substances enter the body. plugging a drug reduces the amount of the drug that is subject to first pass metabolism. beneficial with a drug like morphine that's already active. i'm far from sure, but what i understand of codeine means it would not benefit from avoiding first pass metabolism.
 
Whoops accidentally deleted my last post when I tried to edit. I'm just sick of people saying GFJ won't potenate codeine, yet it inhibits the enzymes that break it down into inactive metabolites (CYP3A4) and doesn't inhibit the enzyme that turns it into morphine (CYP2D6). Paracelsus tried to clear this up but people keep spreading misinformation.

That's an important bit of information. I should've included the specific enzymes at play here. Not all Opioids are metabolized by the same groups of enzymes and many, like Methadone for instance, are broken down in a substantial way, by several different enzyme systems.

I'm in agreement with TrippyZebra in regards to his point about misinformation, which is what I was scratching at in my last post in this thread. We all need to be as sure as possible before interjecting into a debate about this sort of thing. Sure, it may seem like small potatoes, dealing with a drug as seemingly mild as Codeine, but Codeine is capable of and does kill, all the time. To say that a 10% potentiation through enzyme changes via GFJ or what have you couldn't kill is very optimistic thinking.

For the record, all available information seems to imply that Codeine is made more potent by administration with substances like GFJ. What is the rate of said potentiation? - This is the more difficult question to answer. There are myriad substances which effect the functioning of our body's enzymes though ranging from OTC medication, prescription medication, nutritional/herbal supplements and as we've seen here, even food. For instance, coadministration of the SSRI-type antidepressant Fluvoxamine (Luvox) in patients or users of Methadone has been documented in plurarlity to lead to potentially fatal overdose and toxicity in individuals that previously experienced minimal side effects i.e. sedation/drowsiness.

It's my personal opinion that Codeine has become mired in misinformation about its range of effects because it has never really "caught on" by use of any route other than oral. For those needing more powerful analgesia, the logical jump has always been Morphine, as opposed to further administration of Codeine. This has left us and the medical community with little need to understand the drug by varying ROA's. I'm not saying we know nothing, but I think it's safe to say we know more about parenteral administration of Morphine than we do for Codeine.

Also, further for the record, Codeine has historically been distributed in virtually all forms, Intravenous being contradindicated by virtue of the potential for deadly anaphalaxysis. There have been Codeine injectables (IM/SC) and suppositories in the past, when it would seem that the drug was more in vogue. It wasn't so long ago that Codeine was treated in the States like it is in Europe and Canada, as an OTC medication, generally considered outside the bounds of a "full Opioid narcotic". I'm sure this played a role when disucssing cases of celebrities like Howard Hughes who was addicted to the shit as a Drug of Choice. As doctors have desired greater control over analgesia, agents like the shorter-acting Hydromorphone (Dilaudid) have become the new(er) gold standard. Something like Codeine just isn't appropriate given its range of bioavailability and not to mention the plethora of varying levels of metabolization from person to person and race to race.
 
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