Medical marijuana is a viable alternative to opioids

"Do no harm" is more than just a motto:

A bipartisan effort to legalize marijuana for medical use in North Carolina got a legislative committee hearing on Wednesday. But it's unclear whether enough legislators are ready now to alter their views on pot to make it law.

With nearly three-quarters of states already allowing medical marijuana, senators who unveiled their framework told colleagues the measure takes health and safety seriously while offering palliative care for those with painful or life-threatening illnesses such as cancer.

If you listen to NPR on a regular basis, you may have heard a segment recently about medical marijuana, where they talked about doctors not being exposed to education about the palliative properties of cannabis, even those physicians who were supportive of it. There is a misconception that research in this area is thin and/or not conclusive, but in fact the NIH has compiled the results from several studies:

In 1988, the first cannabinoid receptor was identified (CB1) (Howlett et al 1988) and in 1993, a second was described (CB2) (Munro et al 1993). Both are 7-domain G-protein coupled receptors affecting cyclic-AMP, but CB1 is more pervasive throughout the body, with particular predilection to nociceptive areas of the central nervous system and spinal cord (Herkenham et al 1990; Hohmann et al 1999), as well as the peripheral nervous system (Fox et al 2001; Dogrul et al 2003) wherein synergy of activity between peripheral and central cannabinoid receptor function has been demonstrated (Dogrul et al 2003). CB2, while commonly reported as confined to lymphoid and immune tissues, is also proving to be an important mediator for suppressing both pain and inflammatory processes (Mackie 2006).

Following the description of cannabinoid receptors, endogenous ligands for these were discovered: anandamide (arachidonylethanolamide, AEA) in 1992 in porcine brain (Devane et al 1992), and 2-arachidonylglycerol (2-AG) in 1995 in canine gut tissue (Mechoulam et al 1995) (Figure 1). These endocannabinoids both act as retrograde messengers on G-protein coupled receptors, are synthesized on demand, and are especially active on glutamatergic and GABA-ergic synapses. Together, the cannabinoid receptors, their endogenous ligands (“endocannabinoids”) and metabolizing enzymes comprise the endocannabinoid system (ECS) (Di Marzo et al 1998), whose functions have been prosaically termed to be “relax, eat, sleep, forget and protect” (p. 528).

In short, contrary to popular belief, we actually do know a lot about how cannabinoids interact with human physiology, and many of the effects (and side-effects) of its usage. It does more than just make you "feel good," it is a very effective pain management tool:

The endocannabinoid system is tonically active in control of pain, as demonstrated by the ability of SR141716A (rimonabant), a CB1 antagonist, to produce hyperalgesia upon administration to mice (Richardson et al 1997). As mentioned above, the ECS is active throughout the neuraxis, including integrative functions in the periacqueductal gray (Walker et al 1999a; Walker et al 1999b), and in the ventroposterolateral nucleus of the thalamus, in which cannabinoids proved to be 10-fold more potent than morphine in wide dynamic range neurons mediating pain (Martin et al 1996). The ECS also mediates central stress-induced analgesia (Hohmann et al 2005), and is active in nociceptive spinal areas (Hohmann et al 1995; Richardson et al 1998a) including mechanisms of wind-up (Strangman and Walker 1999) and N-methyl-D-aspartate (NMDA) receptors (Richardson et al 1998b). It was recently demonstrated that cannabinoid agonists suppress the maintenance of vincristine-induced allodynia through activation of CB1 and CB2 receptors in the spinal cord (Rahn et al 2007). The ECS is also active peripherally (Richardson et al 1998c) where CB1 stimulation reduces pain, inflammation and hyperalgesia. These mechanisms were also proven to include mediation of contact dermatitis via CB1 and CB2 with benefits of THC noted systemically and locally on inflammation and itch (Karsak et al 2007). Recent experiments in mice have even suggested the paramount importance of peripheral over central CB1 receptors in nociception of pain (Agarwal et al 2007)

I've read this whole thing as a layman, and one thing that I noticed was, the higher the THC level, the more effective the pain remediation was. CBDs that don't contain THC (or have very little) had questionable effects on pain, but they did help curb nausea fairly well.

Everybody should bookmark the link above, especially clinicians who could prescribe them (MDs, PAs, DNPs) when they become available.

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