380mg DHC safe?
- Thread starter Biak12345
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Bella Figura
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What's your codeine tolerance like?
Don't mix in any other depressants such as benzos or alcohol and you'll be ok. You might feel nauseous but I don't think you're at risk of anything serious like an overdose.
380mg isn't a crazy dose or anything, it is on the upper end but if you've got a bit of a tolerance / some opiate experience I think you'll be alright.
Don't mix in any other depressants such as benzos or alcohol and you'll be ok. You might feel nauseous but I don't think you're at risk of anything serious like an overdose.
380mg isn't a crazy dose or anything, it is on the upper end but if you've got a bit of a tolerance / some opiate experience I think you'll be alright.
kleinerkiffer
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If you feel like your breathing is slowed down and shallow at least get a friend over to monitor you
What's your tolerance like?
What's your tolerance like?
It's a high dose if you're opioid naive dhc is about 1.5 times stronger than codeine i think you'll be ok and able to ride it out though cause your not opiod naive
In 1898, Bayer launched diacetylmorphine as a nonaddicting alternative to morphine for treating cough, headache, and morphine and cocaine addiction. Within a dozen years, it was recognized that diacetylmorphine, marketed as heroin, is a prodrug of morphine. However, the term "prodrug" was not introduced until about 50 years later with its originator, Adrien Albert, acknowledging in hindsight that "predrug" would have been a more appropriate term.[1]
By definition, a prodrug is inactive or significantly less active than its metabolite. Activity is initiated in vivo when the prodrug is chemically or enzymatically converted to an active metabolite.[1]About 10% of marketed drugs are prodrugs, but this percentage is increasing as drug developers use prodrugs to improve drug formulation and pharmacokinetics.[1,2]Unlike the pharmaceutical blunder diacetylmorphine, currently marketed prodrugs are more often intentional. Fosphenytoin was designed to overcome the instability of phenytoin in intravenous fluid; oseltamivir was designed to increase oral bioavailability; proton pump inhibitors are all prodrugs designed to improve site selectivity in the low pH of the stomach.[1,2]
The downside of prodrugs is potential for drug interactions and differences in metabolism due to genetic polymorphisms. The activity of prodrugs may be diminished or eliminated in the absence of bioconversion to the active metabolite, or greatly enhanced by increased production of the active metabolite.[1]Several analgesics are prodrugs and require special attention to ensure adequate pain relief and avoidance of adverse effects.
Codeine
The majority of the analgesic effect of codeine, which has low affinity for opioid receptors, is attributed to its conversion to morphine by cytochrome P-450 2D6 (CYP2D6). CYP2D6 inhibitors, such as quinidine or fluoxetine, can reduce the conversion of codeine to morphine, resulting in reduced analgesia. Genetics may also affect codeine metabolism. So-called poor metabolizers may convert no or lower amounts of codeine to morphine. Ultra-rapid metabolizers have CYP2D6 gene duplication and may convert toxic quantities of codeine to morphine.[1,3]Multiple case reports of opioid toxicity have been reported in ultra-rapid metabolizers, including death in a breastfed baby of an ultra-rapid-metabolizing mother receiving codeine for postpartum pain.[4-8]
Tramadol
Like codeine, tramadol is a prodrug. Tramadol is converted by both CYP3A4 and CYP2D6 to O-desmethyltramadol, which is also metabolized by CYP2D6.[9]Patients with deficiencies in CYP2D6 production may experience decreased analgesia; those who produce increased quantities of CYP2D6 may experience increased pharmacologic and adverse effects. Drug interactions with CYP2D6 inhibitors may also reduce the analgesic efficacy of tramadol.[10-12]
Hydrocodone
Hydrocodone (dihydrocodeinone) is a relatively weak analgesic, but it has greater antitussive potency than codeine.[3]CYP2D6 converts much of hydrocodone to hydromorphone. Preliminary research suggests that genetic CYP2D6 polymorphisms might affect hydrocodone.[13]One case report suggests that pharmacogenetics may have played a role in a fatal hydrocodone overdose in a child.[14]
Oxycodone
Oxycodone is metabolized by CYP3A4 to noroxycodone, which is a weakly active opioid agonist, and by CYP2D6 to oxymorphone, which has significant opioid activity. Although the parent drug oxycodone appears to be responsible for the majority of analgesic activity in most patients (so it is not a true prodrug), some research suggests that patients with CYP2D6 abnormalities might have altered analgesic response to oxycodone.[3,15,16]Respiratory depression has been reported in neonates breastfed by mothers receiving oxycodone for postpartum pain, but the contribution of oxycodone metabolites is unclear.[17]
Conclusion
Genetic variations and drug interactions may result in reduced or increased response to prodrug analgesics. Antidepressants, such as fluoxetine, paroxetine, sertraline, bupropion, and duloxetine, as well as some over-the-counter drugs such as cimetidine, inhibit CYP2D6 and may affect prodrug metabolism. Particular vigilance for clinically significant effects of interacting drugs and genetic polymorphisms on analgesic prodrugs is prudent for very old or young patients or patients with impaired hepatic or renal function.
In 1898, Bayer launched diacetylmorphine as a nonaddicting alternative to morphine for treating cough, headache, and morphine and cocaine addiction. Within a dozen years, it was recognized that diacetylmorphine, marketed as heroin, is a prodrug of morphine. However, the term "prodrug" was not introduced until about 50 years later with its originator, Adrien Albert, acknowledging in hindsight that "predrug" would have been a more appropriate term.[1]
By definition, a prodrug is inactive or significantly less active than its metabolite. Activity is initiated in vivo when the prodrug is chemically or enzymatically converted to an active metabolite.[1]About 10% of marketed drugs are prodrugs, but this percentage is increasing as drug developers use prodrugs to improve drug formulation and pharmacokinetics.[1,2]Unlike the pharmaceutical blunder diacetylmorphine, currently marketed prodrugs are more often intentional. Fosphenytoin was designed to overcome the instability of phenytoin in intravenous fluid; oseltamivir was designed to increase oral bioavailability; proton pump inhibitors are all prodrugs designed to improve site selectivity in the low pH of the stomach.[1,2]
The downside of prodrugs is potential for drug interactions and differences in metabolism due to genetic polymorphisms. The activity of prodrugs may be diminished or eliminated in the absence of bioconversion to the active metabolite, or greatly enhanced by increased production of the active metabolite.[1]Several analgesics are prodrugs and require special attention to ensure adequate pain relief and avoidance of adverse effects.
Codeine
The majority of the analgesic effect of codeine, which has low affinity for opioid receptors, is attributed to its conversion to morphine by cytochrome P-450 2D6 (CYP2D6). CYP2D6 inhibitors, such as quinidine or fluoxetine, can reduce the conversion of codeine to morphine, resulting in reduced analgesia. Genetics may also affect codeine metabolism. So-called poor metabolizers may convert no or lower amounts of codeine to morphine. Ultra-rapid metabolizers have CYP2D6 gene duplication and may convert toxic quantities of codeine to morphine.[1,3]Multiple case reports of opioid toxicity have been reported in ultra-rapid metabolizers, including death in a breastfed baby of an ultra-rapid-metabolizing mother receiving codeine for postpartum pain.[4-8]
Tramadol
Like codeine, tramadol is a prodrug. Tramadol is converted by both CYP3A4 and CYP2D6 to O-desmethyltramadol, which is also metabolized by CYP2D6.[9]Patients with deficiencies in CYP2D6 production may experience decreased analgesia; those who produce increased quantities of CYP2D6 may experience increased pharmacologic and adverse effects. Drug interactions with CYP2D6 inhibitors may also reduce the analgesic efficacy of tramadol.[10-12]
Hydrocodone
Hydrocodone (dihydrocodeinone) is a relatively weak analgesic, but it has greater antitussive potency than codeine.[3]CYP2D6 converts much of hydrocodone to hydromorphone. Preliminary research suggests that genetic CYP2D6 polymorphisms might affect hydrocodone.[13]One case report suggests that pharmacogenetics may have played a role in a fatal hydrocodone overdose in a child.[14]
Oxycodone
Oxycodone is metabolized by CYP3A4 to noroxycodone, which is a weakly active opioid agonist, and by CYP2D6 to oxymorphone, which has significant opioid activity. Although the parent drug oxycodone appears to be responsible for the majority of analgesic activity in most patients (so it is not a true prodrug), some research suggests that patients with CYP2D6 abnormalities might have altered analgesic response to oxycodone.[3,15,16]Respiratory depression has been reported in neonates breastfed by mothers receiving oxycodone for postpartum pain, but the contribution of oxycodone metabolites is unclear.[17]
Conclusion
Genetic variations and drug interactions may result in reduced or increased response to prodrug analgesics. Antidepressants, such as fluoxetine, paroxetine, sertraline, bupropion, and duloxetine, as well as some over-the-counter drugs such as cimetidine, inhibit CYP2D6 and may affect prodrug metabolism. Particular vigilance for clinically significant effects of interacting drugs and genetic polymorphisms on analgesic prodrugs is prudent for very old or young patients or patients with impaired hepatic or renal function.
Bella Figura
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I'd say so - it's got a half life of 4 hours.
In future try not to consume first and ask questions later! Saves you stressing out / something unwanted happening
In future try not to consume first and ask questions later! Saves you stressing out / something unwanted happening