• BASIC DRUG
    DISCUSSION
    Welcome to Bluelight!
    Posting Rules Bluelight Rules
    Benzo Chart Opioids Chart
    Drug Terms Need Help??
    Drugs 101 Brain & Addiction
    Tired of your habit? Struggling to cope?
    Want to regain control or get sober?
    Visit our Recovery Support Forums
  • BDD Moderators: Keif’ Richards

Codeine End of the Line?

Zoeylynn said:
Some people respond to codeine some don't. You have to have a specific enzyme in your body to break it down. Once all the enzymes are saturated, you can not get any higher. It has a platoe (sp?) or ceiling that you reach and it won't do anything else. Say the platoe is 400mg and you take 1000mg you will feel no different. The rest is just wasted.
Click to expand...

This is absolutely incorrect.

Ignore.
 
Zoeylynn said:
Some people respond to codeine some don't. You have to have a specific enzyme in your body to break it down. Once all the enzymes are saturated, you can not get any higher. It has a platoe (sp?) or ceiling that you reach and it won't do anything else. Say the platoe is 400mg and you take 1000mg you will feel no different. The rest is just wasted.
Click to expand...

It is incorrect because the ceiling dosage is for the amount of codeine your liver can process into morphine at anyone point in time.

"80 percent of codeine is conjugated with glucuronic acid to codeine-6-glucuronide. Only 5% of the dose is O-demethylated to morphine, which in turn is immediately glucuronidated at the 3- and 6-position and excreted renally. Based on the structural requirement of the opiate molecule for interaction with the mu-receptor to result in analgesia, codeine-6-glucuronide in analogy to morphine-6-glucuronide must be the active constituent of codeine. Poor metabolisers of codeine, those who lack the CYP450 2D6 isoenzyme for the O-demethylation to morphine, experience analgesia from codeine-6-glucuronide. Analgesia of codeine does not depend on the formation of morphine and the metaboliser phenotype."
 
About 70-80% of the administered dose of codeine is metabolized by conjugation with glucuronic acid to codeine-6-glucuronide (C6G) and via O-demethylation to morphine (about 5-10%) and N-demethylation to norcodeine (about 10%) respectively.

UDP-glucuronosyltransferase (UGT) 2B7 and 2B4 are the major enzymes mediating glucurodination of codeine to C6G. Cytochrome P450 2D6 is the major enzyme responsible for conversion of codeine to morphine
and P450 3A4 is the major enzyme mediating conversion of codeine to norcodeine.


Morphine and norcodeine are further metabolized by conjugation with glucuronic acid.
The glucuronide metabolites of morphine are morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G). Morphine and M6G are known to have analgesic activity in humans.
The analgesic activity of C6G in humans is unknown. Norcodeine and M3G are generally not considered to possess analgesic properties.


If you don't possess these enzymes you can not make morphine in your body. Codeine is a prodrug. It is ingested and then converted to something else. That's why some people can not take it and feel the effect. And once all the enzymes are saturated you can not convert any more codeine into morphine and others.
 
You just explained that different enzymes deal with C6G and Morphine metabolisation from codeine.

C6G is the main reason for codeines analgesia. There is not thought to be a ceiling for this process.

I can personally vouch for codeine increasing above the ceiling dose for morphine conversion.
 
I have the ceiling effect to codeine. :( Then they switched me to hydrocodone. Employers look at you different when you say you take Hydrocodone vs tylenol 3.
 
I have never read about genetic disposition to undermetabolize codeine, but I have heard of rapid metabolizers who can OD on normal codeine doses to to rapid conversion to morphine.

To the OP: codeine is weak. 800mg codeine is about 80mg oxycodone. If you switched you'd probably catch a great trip from 40-60mgs oxycodone.

I hate APAP. It is an unnecessary additive to far too many medications. A CWE is a smart move.
 
Last edited by a moderator:
SPC this is a HR website. Please keep comments such as "it may be bad, but not as bad as..." to yourself.

You don't want people thinking it's perfectly ok to consume large quantities of APAP.
 
True, but should we over estimate the dangers to scare people into doing what we consider safe? Everything I said other than my analogy I can back up with citations to accepted medical literature. I suffer from anxiety disorder, and the last time I took a bit too much APAP I was scared half to death based on what I read on Bluelight, and ended up driving myself to the ER at 100mph in my panic. True harm reduction can only take place when people are honestly informed. I know I'm not the only anxious hypochondriac who reads these boards.....
 
The fact is that taking large doses of APAP is toxic for you is not something to shrug off. Just because your liver will heal itself like you originally stated doesn't mean that it isn't bad in the first place.

Not to mention you left out the excrutiating pain that comes with an APAP OD.

I also know someone who has completely fucked up her internals from APAP abuse and TBPH she didn't use it for a long time. A couple of months tops.
 
Jacko123 said:
In a UK hospital you won't be adminsitered NAC with a single ingestion of less thant 10gm. So I think there is a littel bot of ignorance generally about prolonged use of APAP as it is often used daily on a prescribed basis and is evidenced as being fine for prolonged use in safe limits. Just like a glass of wine a night is ok, a bottle and you'll pay for it.
Click to expand...

I will simply add "I agree" and leave it at that then.
 
You must log in or register to reply here.
Top