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However, in contrast to the situation with anandamide, acute and chronic stress cause a protracted increase in brain 2-AG levels that is preceded by increases in corticosterone resulting from increased HPA axis activityReference 167. Furthermore, elevations in brain 2-AG levels are associated with HPA axis response termination, HPA axis habituation, modulation of synaptic hemp oil for pain plasticity, decreased memory retrieval and a decrease in painReference 167. The ECS therefore appears to be both a target and a regulator of stress-induced activation of the HPA axisReference 167. A small randomized clinical trial of nabilone (0.03 mg/kg) in seven patients with PD found that nabilone reduced levodopa-induced dyskinesiaReference 254.

Fear-conditioning experiments in animals suggest a role for the amygdala-hippocampal-cortico-striatal circuit as a key brain circuit responsible for processing and storing fear-related memories and for coordinating fear-related behavioursReference 1048. Additional evidence in humans suggests that PTSD is characterized by over-activity or hyper-responsiveness of the amygdala, with deficient regulation of prefrontal cortical structures as well as abnormal hippocampal and basal ganglia functionsReference 1048.

In fact, it appears that CB1 receptors are expressed more abundantly in skeletal sympathetic nerve terminals in close proximity to osteoblastsReference 922. Besides the receptors, the endocannabinoids 2-AG and anandamide have been detected in mouse trabecular bone and in cultures of mouse osteoblasts and human osteoclastsReference 921Reference 923Reference 924. Taken together, these findings suggest the existence of a functional ECS in bone.

For information on other diseases with an inflammatory component such as the arthritides or IBD, please consult Sections 4.8 and, respectively, of this document. Pre-clinical studies suggest the ECS protects against excitotoxicity, oxidative stress, and inflammation – all key pathological events associated with the development of ADReference 1153.

Dystonia involves overactivity of muscles required for normal movement, with extra force or activation of nearby but unnecessary muscles, and is often painful in addition to interfering with functionReference 938. Dystonia can be primary, including torticollis and blepharospasm/orofacial dyskinesias or dystonias (Meige syndrome) or part of another condition such as HD, and tardive dyskinesia after dopa-blocking drugsReference 938. CB1 and CB2 receptors have been detected in mouse osteoblasts and osteoclasts, although CB1 is expressed at very low levels compared to CB2Reference 20Reference 920Reference 921.

There have also been some case-reports of contact urticaria following exposure to cannabis flowers, and extreme sensitization to Δ9-THC and CBN has also been observed in an animal model of contact dermatitisReference 1182Reference 1183 (and see Section 7.3 for additional information on hypersensitivity/allergy to cannabis). The role of the ECS in inflammation is complex as this system has been implicated in both pro- and anti-inflammatory processesReference 1149. Endocannabinoids, such as anandamide and 2-AG, are known to be produced and released by activated immune cells and to act as immune cell chemoattractants promoting or directing the inflammatory responseReference 1169. On the other hand, cannabinoids can also suppress the production of pro-inflammatory cytokines and chemokines and thus may have therapeutic applications in diseases with an underlying inflammatory componentReference 1169Reference 1170.

As similarities exist between the expression of fear and anxiety in humans suffering from phobias, PTSD, or other anxiety disorders, and the expression of conditioned fear in animals, the use of certain animal behavioural models to study PTSD is feasible and relevantReference 1040Reference 1049. Taken together, the weight of the evidence suggests that the ECS functions as a homeostatic mechanism for buffering stress, inhibiting unnecessary HPA axis activation and promoting the recovery of the HPA axis once the stressful stimulus has passedReference 1010Reference 1011. Dysfunction of the ECS both increases sensitivity to stress and prolongs maladaptive responses to stress in the absence of any further stress stimulusReference 1010Reference 1011. Importantly, chronic stress appears to reduce the ability of the ECS to buffer stress effectively and can contribute to precipitation of psychopathology including anxiety and depressionReference 1010Reference 1011.

Pharmacological interventions that function to raise endocannabinoid tone such as inhibition of the endocannabinoid degradative enzymes FAAH and MAGL appear to have anxiolytic and anti-depressive effects, at least in animal models of anxiety and depressionReference 167Reference 177Reference 1011. Emerging evidence suggests substrate-selective inhibition of COX-2 also increases brain endocannabinoid levels and may have anxiolytic effectsReference 167Reference 1012Reference 1013. Chronic stress also generally appears to produce reductions in anandamide similar to those seen with acute stressReference 167.

The ECS links stress exposure to changes in synaptic plasticity contributing to activation and feedback regulation of the HPA axis, and facilitates the activation of resilience factors during and/or after stress exposureReference 1047. It has been hypothesized that chronic stress creates a "hypocannabinergic state" that results in impaired fear extinction (as is seen in PTSD) and this state can be alleviated with CB1 receptor agonistsReference 1047.

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