“Social characteristics, such as socioeconomic status and race/ethnicity, play a role in the treatment and outcomes of patients with epilepsy (PWE), but little is known about how these factors affect patients receiving cannabidiol (CBD) to treat seizures. This exploratory study examined the sociodemographic profile of patients treated with CBD (n=80) and associations between social factors and patient-centered outcomes – overall health status, Quality of Life in Epilepsy-89 (QOLIE-89), and Profile of Mood States (POMS) – in this population. Associations were examined using Pearson correlations and multiple ordinary-least-squares regression (alpha=0.1). The sample was predominantly white (96%) and non-Hispanic/Latino (96%); 76% of patients had family incomes of $40,000+/year. Some patients/families reported experiencing food scarcity (13%), not being able to make ends meet (6%), or not being able to afford antiepileptic medications (8%). The patients’ health ratings declined with age and income (p≤0.014), and there was a statistically significant interaction (p<0.055) between these variables: for example, a higher-income 10-year-old had a predicted health rating of 3 (“very good”), followed by a higher-income 40-year-old with a rating of 2 (“good”), a low-income 10-year-old with a rating of 1 (“fair”), and a low-income 40-year-old with a rating of 0 (“poor”). This is the first study reporting the social profile of patients taking pharmaceutical grade CBD for the treatment of epilepsy. The results suggest that despite free access to this treatment some patients may not be accessing CBD because of their socioeconomic situation or race/ethnicity. Larger, diverse samples and longitudinal data are needed to more accurately model social factors and patient-centered outcomes in PWE receiving CBD.” https://www.ncbi.nlm.nih.gov/pubmed/28236578]]>
Concise review of the management of iatrogenic emesis using cannabinoids: emphasis on nabilone for chemotherapy-induced nausea and vomiting.
“Chemotherapy-induced nausea and vomiting (CINV) is a prevalent, distressing, and burdensome side effect of cancer chemotherapy. It is estimated to affect the majority of patients receiving certain anti-cancer drug regimens and can be treatment-limiting, even for life-saving medications. Despite seemingly numerous options, such as antimuscarinic anticholinergics, antihistamines, 5-HT3 receptor antagonists, dopamine receptor antagonists, and neurokinin-1 receptor antagonists, preventative therapies are often inadequately effective, particularly for “delayed CINV”-leaving an important unmet clinical need.
Cannabinoid receptor agonists, by virtue of their unique mechanism of action and efficacy and safety data reported in clinical trials, appear to offer a useful additional option.
The mechanistic value of cannabinoids has been well known for many years, but these agents may have been underutilized in the past because of the notoriety and legal status of marijuana. While botanical marijuana contains nearly 500 components, including the psychoactive tetrahydrocannabinol (THC), nabilone is an established, single-entity synthetic cannabinoid receptor agonist that has become the focus of renewed interest. We review the basic pharmacology and clinical trial data of nabilone for use in prophylaxis and treatment of CINV.”
Chronic and acute adenosine A2A receptor blockade prevents long-term episodic memory disruption caused by acute cannabinoid CB1 receptor activation.
“Cannabinoid-mediated memory impairment is a concern in cannabinoid-based therapies. Caffeine exacerbates cannabinoid CB1receptor (CB1R)-induced memory deficits through an adenosine A1 receptor-mediated mechanism. We now evaluated how chronic or acute blockade of adenosine A2A receptors (A2ARs) affects long-term episodic memory deficits induced by a single injection of a selective CB1R agonist. The finding that CB1R-mediated memory disruption is prevented by antagonism of adenosine A2ARs, highlights a possibility to prevent cognitive side effects when therapeutic application of CB1R drugs is desired.” https://www.ncbi.nlm.nih.gov/pubmed/28235548]]>
FAAH inhibition produces antidepressant-like efforts of mice to acute stress via synaptic long-term depression.
“Recent studies have shown that inhibition of fatty acid amide hydrolase (FAAH), the major degradative enzyme of the endocannabinoid N-arachidonoylethanolamine (AEA), produced antidepressant behavioral responses, but its underlying mechanism is not clear. Here we find that a systemic administration of the FAAH inhibitor PF3845 or an intra-CA1 application of AEA elicits an in vivo long-term depression (LTD) at excitatory glutamatergic CA3-CA1 synapses of the hippocampus. The PF3845- and/or AEA-elicited LTD are abolished by the LTD-blocking peptide Tat-GluR2. PF3845 significantly decreases passive behavioral coping of naïve mice to acute inescapable stress, which is also abolished by Tat-GluR2 peptide. However, PF3845 does not significantly affect sucrose assumption ratio of mice receiving chronic administration of corticosterone. These results suggest that FAAH inhibitors are able to produce antidepressant effects in naïve animals in response to acute stress through LTD at hippocampal glutamatergic CA3-CA1 synapses.” https://www.ncbi.nlm.nih.gov/pubmed/28193523]]>
Fatty acid amide hydrolase inhibitors produce rapid anti-anxiety responses through amygdala long-term depression in male rodents.
“It has recently been recognized that anandamide (arachidonylethanolamide), which is an endogeneous-
“Obesity is a risk factor for increased severity of acute