Below are the excerpts of the 2010 American Society of Addiction Medicine (ASAM) white paper republished by The Journal of Global Drug Policy and Practice about The Basis For Cannabinoid Therapeutics:
Momentum for developing cannabinoid medications gained force only after the discovery of endocannabinoid receptors and the brain’s endogenous cannabinoid ligands in the late 1980s and early 1990s. These monumental discoveries, parallel in their basic framework to the discovery of the brain’s endogenous morphine-like neural system (the endorphins), transformed the focus of research from marijuana to the brain itself. These discoveries marked the dawn of cannabinoid neuroscience.
We now understand that an extensive system of the nerves within the brain communicate with each other using the same basic chemistry found in marijuana. While we are only beginning to unravel the role the endocannabinoid system plays in overall brain function, Raphael Mechoulam has declared that “The cannabinoid receptors are found in higher concentrations than any other receptor in the brain.”
Cannabinoid type 1 (CB1) receptors are distributed throughout the brain, where they are concentrated in the hippocampus, amygdala, basal ganglia, cerebellum, nucleus accumbens, and cortex (anterior > posterior). Cannabinoid type 2 (CB2) receptors are generally located peripherally. Tonic activity within the endocannabinoid system is continuously modulating a huge variety of physiological and brain functions, including short-term memory, learning, appetite, anxiety/fear, pain, and spontaneous motor activity.
THC and similar molecules in marijuana are able to affect the brain only because they mimic our natural neurotransmitters, flooding receptor sites with stimulation. All the cannabinoid-based areas of the brain are subsequently activated beyond normal physiological levels. This is generally enjoyable for most people, but not without consequences for many. Smoking marijuana essentially reaches into the brain and increases the activity of the one specific subset of neuronal activity – like turning up a rheostat that controls the brain’s endocannabinoid activity.
The question of whether there is medicinal value in stimulating, or reducing activity in cannabinoid-based portions of the brain depends on three things:
1.) Specific areas of the brain where cannabinoid chemistry is concentrated and the functions served by these areas;
2.) The specific disease and symptoms being treated; and
3.) Side effects produced by the treatment – essentially a “medical cost/benefit analysis.”
In addition, there are also CB2 found throughout the body, on nerves, blood cells, on organs, and throughout all stages of embryonic development. The potential for cannabinoid therapeutics must also look at the direct impact of stimulating or antagonizing these receptors as well.
The potential value of any cannabinoid medication depends on modifying physiologic functions that are naturally controlled by our body’s internal cannabinoid system. Given all the functions that are modulated by endocannabinoid chemistry, it is likely that either stimulating or blocking portions of this ubiquitous neuronal subsystem has the potential for relieving the suffering caused by the disease. The basic neuroscience of our endocannabinoid system thus provides the American Society of Addiction Medicine’s (ASAM) perspective on the most effective framework for medicalizing cannabinoid therapeutics.