• 🇳🇿 🇲🇲 🇯🇵 🇨🇳 🇦🇺 🇦🇶 🇮🇳
    Australian & Asian
    Drug Discussion

    Welcome Guest!
    Posting Rules Bluelight Rules
  • AADD Moderators: andyturbo

Codeine Extraction

Status
Not open for further replies.
maxxy 10,000mgs of ibuprofen a day safe
!!!!! are u a dick head ya stomachlining would be fucked
fuckin hell
hoptis why is that post there
 
I don't think they meant daily, just if you did that in one day as a once off it won't kill you.
 
i love the censorship of Blue light its like current affair
This is a site for drug users and harm reduction not idiots
some kids eats 10,000mgs of ibuprofen a day what is going to happen
man this is wokring right into the medias hands have u guys seen the news
 
^ The user in question also followed that up by noting that someone else can ingest very little and suffer seriously negative effects very quickly. The idea trying to be conveyed was that there is no way of knowing which category you fall into until it is potentialy too late.

As per this part of the post...

The problem is, you dont know which group you fall into so you cant logically take a risk and CWE is the way around it if you are continuing to use.
Click to expand...
 
My experience is that the body can handle very large amounts of paracetamol and ibuprofen over long periods (eg 10,000 mg ibuprofen daily for years), with no significant damage.

Some people take lower doses and do end up with hepatic and/or renal damage, so not exactly sure how that works except that I suspect that if you start low and build up that your liver develops an affinity for dealing with the load, but thats a personal theory.
Click to expand...

While the toxicity profile for ibuprofen has a fairly gentle dose response for most people, and relatively speaking, for those people it's probably not so harmful in doses slightly higher than those recommended, it's still unwise to suggest 10 grams a day may be within a safe theraputic index. It's certainly not IMO.

With paracetamol, unless you have a way of assessing your liver, then you may not know if damage occurs until it's too late. It's also incorrect to think the enzymes involved in 'regular' low dose metabolism of acetaminophen can increase in density to allow large amounts of acetaminophen to be safely metabolised. Increased density of enzymes involved in conjugation (safe metabolic route) is unlikely to occur in response to repeated administration. Glutathione, which must be present if liver damage is to be avoided, is not stored in the liver in sufficient quantities to cope with large doses.


Let's review what happens in low and high dose metabolism of acetaminophen.



Referring to diagram 1; If the dose is within a safe therapeutic index, all the acetaminophen will be metabolised without employing p450 isozymes. The products are either the conjugated sulphate (route 1) or the glucuronide (route 2), both quite "safe" metabolic products. However, these metabolic routes are dependant on, among other things, enzyme availability. The body can't instantly produce more of these enzymes in response to increased demand as seen with high doses of acetaminophen.

If the dose is high, and the enzymes required for conjugation become saturated, p450 (CYP) cytochromes (aka mixed function oxidases) will become involved (route 3). These will produce N-acetyl-beta-benzoquinone imine (NAPBQ), an extremely reactive intermediate. If glutathione (GSH) is not depleted, some of this NAPBQ will end up conjugated with it, which, if the dose is high enough will lead to further GSH depletion. Most importantly, significant amounts of the toxic imine will react with cellular membranes, resulting in the destruction of cells. Other processes also occur (see fig 2) which cause cellular death, including oxidative products resulting from glutathione depletion.

Acetaminophenmetabolism.gif

Figure 1:Adapted from Rang et al, Pharmacology 4th Edition

Acetaminophen-toxicity-mech.jpg

Figure 2: from Rang et al, Pharmacology 4th Edition, p763



E medicine: Excerpt from Toxicity, Acetaminophen

Excerpt from Toxicity, Acetaminophen

Synonyms, Key Words, and Related Terms: paracetamol, N-acetyl-p-aminophenol, APAP

Toxicity, Acetaminophen

Background: Acetaminophen is the most widely used pharmaceutical analgesic and antipyretic agent in the United States and the world; it is contained in more than 100 products. As such, acetaminophen is one of the most common pharmaceuticals associated with both intentional and accidental poisoning.

Acetaminophen-induced hepatotoxicity is well recognized. Acetaminophen also is known as paracetamol and N-acetyl-p-aminophenol (APAP). It is found in the United States as 325-mg and 500-mg immediate-release tablets and as a 650-mg extended-release preparation. Various children's chewable, suspension, and elixir formulations of acetaminophen also are available. Furthermore, acetaminophen is found as a component of combination drugs such as propoxyphene-acetaminophen (eg, Darvocet) and oxycodone-acetaminophen (eg, Percocet).


Pathophysiology: The maximum daily dose of APAP is 4 g in adults and 90 mg/kg in children. The toxic dose of APAP after a single acute ingestion is 150 mg/kg or approximately 7 g in adults, although the at-risk dose may be lower in persons with alcoholism and other susceptible individuals. When dosing recommendations are followed, the risk of hepatotoxicity is extremely small.

Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents, which then are eliminated in the urine.

In acute overdose or when maximum daily dose is exceeded over a prolonged period, the normal pathways of metabolism become saturated. Excess APAP is then metabolized in the liver via the mixed function oxidase P450 system to a toxic metabolite, N-acetyl-p-benzoquinone-imine (NAPQI). NAPQI has an extremely short half-life and is rapidly conjugated with glutathione, a sulfhydryl donor, and removed from the system. Under conditions of excessive NAPQI formation or reduced glutathione stores, NAPQI is free to covalently bind to vital proteins and the lipid bilayer of hepatocytes; this results in hepatocellular death and subsequent centrilobular liver necrosis.

The antidote for APAP poisoning is N-acetylcysteine (NAC). NAC is theorized to work by a number of protective mechanisms. Early after overdose, NAC prevents the formation and accumulation of NAPQI. NAC increases glutathione stores, combines directly with NAPQI as a glutathione substitute, and enhances sulfate conjugation. NAC also functions as an anti-inflammatory and antioxidant and has positive inotropic and vasodilating effects, which improve microcirculatory blood flow and oxygen delivery to tissues. Vasodilating effects decrease morbidity and mortality once hepatotoxicity is well established.

NAC is most effective when administered within 8 hours of ingestion. When indicated, however, NAC should be administered regardless of time since the overdose. Therapy with NAC has been shown to decrease mortality rates in late-presenting patients with fulminant hepatic failure (in the absence of acetaminophen in the serum).
Click to expand...

In regards to the extent and degree of reported Acetaminophen poisonings:

From The management of poisoning by Pharmaceutical Agents

  • Paracetamol poisoning accounts for 48% of hospital admissions for poisoning and approx 200 deaths every year in the UK (Hawton et al, 1998)
  • It is the commonest reason for transplantation for acute liver failure in the UK (Bernal and Wendon 1999)

The E-medicine quote refers to N-acetylcysteine (NAC) as being an antidote for Acetaminophen poisonings, but IMO it would need to be administered shortly after overdose has occurred if damage is to be largely avoided. Iirc it also has to be injected intravenously. Methionine can be taken orally, but I don't know how fast methionine would restore levels of glutathione. However, in identifying these antidotes, pre/post loading should not be seen as a green light to take higher dosages. There are also other toxicity concerns, particularly in regards to the nephrotoxicity (kidneys). It's something that doesn't often get a mention, but it's reported as common in long term user or as a result of overdose. Think very carefully if you use large amounts of paracetamol. That's why, despite the arguable increased risk of addiction, I recommend removal of the acetaminophen via CWE if intent is to take large doses of codeine.
 
Great post phase dancer, now I guess the next question is how successful is the average CWE. If your resultant liquid is still slightly coloured how likely is it that there is still a relative danger to the amount of paracetamol ingested?

I guess there really is no way of knowing without doing proper analysis on the liquid.
 
Cloudy water is usually because of water soluble fillers in the tablet.
Any paracetamol dissolved in the water will be "see-thru" anyway, unless it's in big chunks.

After half a yearish of doing CWE's, using a couple of extra tablets on top of them every now and again and having the occasional glass of wine before ingesting the resulting liquid, I recently went for a blood test.
Liver's fine. So there's some scale.
 
yeah CWE with 300ml is fucking fine.

there is such ridiculous levels of paranoia in some people,
who try and CWE with 50ml etc!

SO SO SO wasteful!
 
^ I use around 70ml for 30-35 tablets and have no problems at all..? Why ridicule people for erring on the side of caution? Using less water also means you have less disgusting liquid to drink at the end of it. I measured the amount of water going into the filter and coming out and there were only a few mL missing.

monstanoodle - How often were you dosing with codeine?
 
for myself Nurofen plus when CWE give me a much whiter liquid than others like panafen plus which is more like breast milk. The nurofen taste is much more bitter too and seems to get me way higher than panafen plus. I take about 600mg a dose or a 48 pack or N+ but with panafen i feel not much at all from the same dose.
 
How much water are you using and how are you filtering your solution wasted youth?
 
Can the codeine extracted from N+ be smoked? I have noticed some posts saying that it has to go through the liver and thus has to be shelved or swallowed but not snorted. However, shelving codeine would not get it through you're liver anyway because its not digested that way, it just goes into the blood vessel filled membrane in your colon the same as going into the membrane under the tongue or in the nose. Isn't codeine a smokable active component of opium?
 
moderateuser said:
Can the codeine extracted from N+ be smoked?
Click to expand...

Nope.

However, shelving codeine would not get it through you're liver anyway because its not digested that way, it just goes into the blood vessel filled membrane in your colon the same as going into the membrane under the tongue or in the nose.
Click to expand...

Codeine > Blood > Liver

Doesn't matter how you get it into you, it will always have to take a stop at the liver....

Oh and I think the codeine in opium you are thinking of is codeine HCl or something? Either way don't go smoking Nurofen Plus. lol.
 
I been doing CWE for over 4 years.
I have done it way over 100 times.
I first freeze then unfreeze poor top lay off about 100ml through filter paper
then i later mix the with a shake and poor through a filter paper and freeze again and drink very cold.

There are quicker and more junkier ways but this is the best if u go time
if not just get solution cold as then pooor off top layer drink that first.
later fiddle around with all the gunk at the bottom and use the rinses for the next CWE.
How do u guys find using panadeine compared to N+

Man thank god for codeine and panadeine and alike for opiate users.
we all know the biggest drug dealer in Australia is.......(drum roll)...........the government
I think CWE is safe and a good way to to help with H With drawals and other WD's

Thank god for OTC codeine we live in a lucky country.
Codeine is needed to be OTC
we should be able to get 100 packs of those 15mg ones
 
i usually use about a cup of water and just filter it through a bonds tshirt. just squeeze the liquid out. Very fast and not too messy. takes about 5 - 10 minutes. I think its just the different binder than must be in panafen plus
 
Are you grinding the pills into powder first? this might be your issue.
 
Just a quick note, the generic Amcal ones dissolve very quickly (30 seconds quickly), whatever binder they use is extremely soluble in water.
 
I believe they're the same as the Chemists Own brand which are well known for being the easiest to dissolve.
 
hoptis said:
I believe they're the same as the Chemists Own brand which are well known for being the easiest to dissolve.
Click to expand...

I've noticed they have two types, a 10mg one and a 9.6mg one. The 10mg ones tend to filter much better as after dissolving it seperates into a layer of liquid and a layer of white slugde within 5mins.

This means the liquid takes no time at all to filter and you can just squeeze the sludge to get the rest of the liquid. The others don't tend to separate unless you leave them sitting for a long time.
 
Status
Not open for further replies.
Top