This article about positive effects of cannabinoids is exceptional only because it was published by “drugabuse.gov”, site of the National Institute on Drug Abuse (NIDA).
This is truly revolutionary because, as of now (July 2016) cannabis is still classified a Schedule I drug by “DEA.gov” (defined as drugs with no currently accepted medical use and a high potential for abuse. Schedule I drugs are the most dangerous drugs of all the drug schedules with potentially severe psychological or physical dependence.)
The stance of the DEA is inconsistent with science, society, and even other government agencies. This enforcement agency has stifled research, intimidated politicians, and determined legislation far too long.
Chronic cannabinoid receptor 2 activation reverses paclitaxel neuropathy without tolerance or cannabinoid receptor 1-dependent withdrawal.
The treatment of cancer pain is often among the approved uses of medical cannabis in states where it is legal.
∆9-THC, the active ingredient in cannabis, acts on both of the cannabinoid receptors CB1 and CB2 and is associated with negative side effects such as dizziness, psychoactive effects, and dependence, which are thought to result from the activation of the CB1 receptor.
While the majority of cannabis-like molecules have some activity at both CB1 and CB2 receptors, one that is selective for CB2 could potentially exhibit therapeutic properties without the side effects associated with ∆9-THC.
In this study, the authors looked at whether the CB2-selective molecule AM1710 could reduce neuropathic pain caused by the chemotherapy drug paclitaxel, while avoiding unwanted side effects
Mice that were given ∆9-THC to treat paclitaxel-induced pain developed tolerance to the drug, so its pain-relieving properties diminished. After discontinuing ∆9-THC, the mice also experienced withdrawal symptoms, indicating the development of drug dependence
In contrast, AM1710 was able to relieve neuropathic pain, but without inducing either tolerance or withdrawal
This ideal clinical profile of pain-suppression in the absence of tolerance or dependence risk suggests that CB2 receptors could be a viable target for development of pain-management drugs that avoid adverse outcomes of cannabis use.
For a list of scheduled drugs, see DEA Drug Scheduling