Clinical Endocannabinoid Deficiency Reconsidered: Current Research Supports the Theory in Migraine, Fibromyalgia, Irritable Bowel, and Other Treatment-Resistant Syndromes
Reference: Russo EB (2016) Clinical endocannabinoid deficiency reconsidered: current research supports the theory in migraine, fibromyalgia, irritable bowel and other treatment-resistant syndromes, Cannabis and Cannabinoid Research 1:1, 154–165, DOI: 10.1089/can.2016.0009.
Migraine and CED
Migraine is an extremely prevalent headache syndrome affecting 14% of Americans, with a 3:1 female:male ratio and $20 billion annual cost in that country. This author has previously reported on migraine's treatment by cannabis and two major reviews have recently appeared. Migraine is far more complex than merely cranial pain. It has a genetic predilection and female predominance and presents as a predominantly hemicranial beating headache associated with unusual associated manifestations: nausea, photophobia, and phonophobia, with hormonal and environmental triggers.
The possible relationship of migraine with the ECS is highlighted by numerous findings. Anandamide produced serotonin receptor responses consisting of 89% potentiation of 5-HT1A and 36% inhibition of 5-HT2A, findings that have been associated with profiles of effective pharmacological migraine interventions that would seem to support respective activity in acute and chronic migraine (CM), respectively. The migraine epiphenomena of photophobia and phonophobia suggest an overactive sensory hyperalgesia, just the kind of homeostatic imbalance that the ECS tends to correct in central nervous system (CNS) function.5 The periaqueductal gray matter is a putative migraine generator in which AEA is tonically active, producing analgesia when administered or hyperalgesia when CB1 is pharmacologically blocked.
Various strategies to treat CED conditions are possible. A direct approach with CB1 agonists must recognize the fact that the ECS operates as a homeostatic regulator that sometimes requires a gentle pharmacological nudge, rather than a forceful shove, by synthetic full agonists. Thus, small doses of a weak partial agonist (e.g., THC) should be considered, which would not induce tolerance and may jump-start the ECS. Even THC alone is poorly tolerated or appreciated by patients and standardized whole cannabis extracts that contain additional synergistic and buffering components, such as CBD and cannabis terpenoids, are certainly preferable.
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