Codeine Receptors bindings

Codeine  is a known mu full agonist.  But it is not as strong as morphine in its effects.  However it is more complex than this, as there is some evidence of minor delta and kappa binding.  This is not surprising as codeine in the plant is a precursor to morphine, so one would expect the bindings to be similar.  Once inside your body codeine is metabolised with about

5-10% converted to morphine
70% converted to codeine-6-glucuronide
less than 10% converted to norcodeine
and less than 1% to hydromorphone

This makes C6G the primary active compound.

The 6-glucuronides possess a decreased selectivity for mu-receptors over delta-receptors.  In effect the ratio changes in our bodies and we are likely to get more pain relief from the delta effects.   In contrast the 6-glucuronides possess an increased selectivity for mu- over kappa-receptors.  So the overall effect is that of a mu and delta agonist.

Approximately 6–10% of the Caucasian population, 2% of Asians, and 1% of Arabs are "poor metabolizers".  Conversely, 0.5-2% of the population are "extensive metabolizers".  Two selective serotonin reuptake inhibitors, paroxetine (Paxil) and fluoxetine (Prozac) as well as the antihistamine diphenhydramine and the antidepressant, buproprion (Wellbutrin, also known as Zyban) block the metabolisation of codeine.  Conversely Rifampicin and dexamethasone, increase the metabolism.  So the extent to which the mu and delta effects kick in is very dependent on the other drugs you are taking as well as your own body make-up.

Note that, as codeine is metabolized in part to morphine, morphine can be passed through breast milk in potentially lethal amounts, fatally depressing the respiration of a breastfed baby

So what are likely to be the overall effects?

Like all opioids, continued use of codeine induces physical dependence and can be psychologically addictive.  Withdrawal symptoms are also the same but not as severe, as codeine is not as strong as morphine.  But they are still pretty grim.