Suboxone – A New Treatment Paradigm Part Two

Suboxone is made up of two medications: buprenorphine and naloxone. If the addict takes the drug correctly, naloxone is meaningless, but if the tablet is diluted in water and ingested, naloxone will cause involuntary withdrawal. Naloxone is destroyed in the liver immediately after absorption from the intestines and has no therapeutic benefit when suboxone is used appropriately. Have a look at Glen Allen Suboxone for more info on this. Buprenorphine is the active substance; if swallowed, it is absorbed under the tongue (and all over the mouth) but killed by the liver. There is a non-naloxone buprenorphine formulation called subutex; this formulation was used when the patient had obvious complications with naloxone, including headaches after suboxone dosing. I have treated gastric bypass addicts, where the first part of the intestine is bypassed and the contents of the stomach empty into the more distal part of the small intestine. In such situations, naloxone escapes the ‘first pass metabolism,’ the normal anatomical phase in which the drug is taken up by the duodenum and passed by the portal vein directly to the liver, where it is rapidly and completely destroyed. Naloxone may be taken up by parts of the intestine that are not served by the portal system after gastric bypass, triggering blood levels of naloxone that are sufficient to cause brief, relatively mild symptoms of withdrawal.

The drug’s narcotic effect increases with increasing doses of up to around one or two mg, but then the effect plateaus and higher levels of buprenorphine do not increase narcosis. Buprenorphine has a ‘ceiling effect.’ The typical patient typically takes 12-24 mg of suboxone a day, and the effects of buprenorphine are easily absorbed (buprenorphine does have significant narcotic potency, but the potency usually pales in comparison to the degree of tolerance found in active opiate addicts).. Opiate receptors are completely bound to buprenorphine in the addict’s brain, and the effects of any other opiate drug are blocked. As soon as the abuser is tolerant of the right dose of suboxone, the buprenorphine added to their opiate receptors decreases cravings and eliminates the effects of other opiates—and hence the use of them. Suboxone is very effective in preventing relapse; the problem of ‘choose to use’ is essentially eliminated by the fact that use will enable the addict to go through several days of withdrawal in order to remove the blockade of the receptor and encourage the effect of other opiates. The appeal of this ‘option’ is very poor, considering the attitudes of addicts towards withdrawal. The only real concern with treatment with suboxone relates to specificity. The abuser remains off the opiates with suboxone, but there is little to avoid alcohol replacement. On the other hand, through blocking opiate receptors, naltrexone decreases alcohol cravings, and it is very possible that suboxone, by its similar mechanism, will also reduce alcohol cravings. Such an effect was reported to me by a number of patients with suboxone, but was not reported at this point in the literature. Suboxone patients transitioning from one drug to another are likely to need an approach that requires full sobriety. But other advantages of suboxone for pure opiate lovers are that only moderate (and likely medicated) withdrawal is necessary to start treatment, the drug is typically covered by insurers, medication requirements are minimal, and there are less maintenance-related stigmas than there are for methadone.