Clinical Endocannabinoid Deficiency (CED)
A theoretical condition proposed by Ethan Russo in which insufficient endocannabinoid system tone contributes to conditions including migraine, fibromyalgia, and irritable bowel syndrome.
In Depth
The CED hypothesis suggests that some chronic conditions characterized by pain, sleep disturbance, and mood dysregulation may result from deficient endocannabinoid signaling. Supporting evidence includes reduced anandamide levels in CSF of migraine patients and altered ECS markers in fibromyalgia. The hypothesis provides a rationale for cannabinoid therapy in these conditions. However, CED remains a theoretical framework rather than an established clinical diagnosis, and direct measurement of ECS tone in humans is technically challenging.
Related Terms
More in Pharmacology
Endocannabinoid System (ECS)
A lipid-based retrograde neurotransmitter system comprising endogenous cannabinoids (endocannabinoids), their receptors (CB1, CB2), and metabolic enzymes.
CB1 Receptor
Cannabinoid receptor type 1. A G protein-coupled receptor (GPCR) primarily expressed in the central nervous system. The primary target of THC's psychoactive effects.
CB2 Receptor
Cannabinoid receptor type 2. A GPCR primarily expressed in immune tissues and peripheral organs. Less abundant in the CNS than CB1.
Anandamide (AEA)
N-arachidonoylethanolamine. The first endocannabinoid identified. A partial agonist at CB1 and CB2 receptors, named from the Sanskrit word "ananda" meaning bliss.
2-Arachidonoylglycerol (2-AG)
The most abundant endocannabinoid in the brain. A full agonist at both CB1 and CB2 receptors.