Marijuana has historically been a favorite villain in anti-drug campaigns across the United States. It has been given the status as a Schedule I drug, meaning that it has a high potential for abuse, no accepted medical benefit, and that there is a lack of accepted safety measures for its use. Although marijuana is not nearly as addictive as the majority of other drugs in this Schedule (such as heroin), it must remain in that schedule until information supporting two important areas is discovered: 1) its role as a medicine and 2) its possible potential for abuse. However, recent research and political activity have made the topic of marijuana use one to look into more deeply. There has been much concern and interest associated not only with its safety as a recreational drug but also pertaining to its usefulness as a form of medicine.
The compounds in marijuana responsible for the high it produces are known as cannabinoids; endogenous cannabinoid (or endocannabinoid) receptors found in the body are what enable people to experience this feeling. The existence of these receptors indicates that the body creates its own cannabinoids. This is similar to how receptors for endorphins (endogenous morphine-like compounds, which create the feeling of a runner’s high) allow people to feel the effects of opiates such as morphine. The body’s endocannabinoid system is mainly responsible for regulating many important processes. This wide scope of activity is part of the reason it is so difficult to fully understand the complexity of its specific roles in the body.
There are two known cannabinoid receptors in the body: CB1 and CB2. While CB1 is more often found in the brain than in the rest of the body, CB2 is most present in cells of the immune system. The separate locations of these receptors throughout the body highlight their separate but related functions. THC has a higher affinity for CB1 than for CB2, which makes sense given its brain-related effects. Only two endocannabinoids (AEA and 2-AG) have been identified so far and both have a higher affinity for CB1. Although they will both bind to CB2, they do so weakly. 2-AG, which is more prevalent in the brain than AEA and does a slightly better job of binding to CB2, can induce cell death in some pathways. It has been implicated to have other neuromodulatory functions, but these have yet to be exactly defined. AEA plays a role in pain relief, motor activity, and stimulation of appetite. In addition to the endocannabinoid receptors, AEA can also bind to a vanilloid receptor (TRPV1R). When capsaicin (an actual vanilloid meant to bind here) signals via TRPV1R, it can reduce local inflammation and inflammation-induced pain. This has positive implications for the involvement of AEA (and, similarly, THC) in immune response.
The health claims being currently made about marijuana may seem too good to be true. While it may not treat every ailment it claims to, it is due to the wide-reaching modulatory role of cannnabinoids that THC can be useful in many instances. It is difficult to pinpoint which receptors endocannabinoids may have a hand in regulating (either directly or indirectly) and how they do this, but current research is getting us closer to an answer.