Successful use of pure cannabidiol for the treatment of super-refractory status epilepticus.

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Epilepsy & Behavior Case Reports

“We present the case of a child with long-standing, super-refractory status epilepticus (SRSE) who manifested prompt and complete resolution of SRSE upon exposure to pure cannabidiol. SRSE emerged in the context of remote suspected encephalitis with previously well-controlled epilepsy. We discuss the extent to which response may be specifically attributed to cannabidiol, with consideration and discussion of multiple potential drug-drug interactions. Based on this case, we propose that adjunctive cannabidiol be considered in the treatment of SRSE.”

https://www.ncbi.nlm.nih.gov/pubmed/30596011

“Adjunctive cannabidiol may be effective in the treatment of super refractory status epilepticus. Given the paucity of evidence-based therapies for SRSE as well as the prompt and enduring response that accompanied the adjunctive administration of CBD in this patient, CBD should be a consideration in the treatment of SRSE.”

https://www.sciencedirect.com/science/article/pii/S2213323218300513?via%3Dihub

The Misclassification of Medical Marijuana.

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Journal of the American Academy of Psychiatry and the Law

“Marijuana has a complicated legal, social, and economic history in the United States, as well as an uncertain future. Marijuana has been consistently tied to racial minority groups since its arrival in the United States in the 1900s, and former Attorney General Jeff Sessions further propagated that notion. AG Sessions even recently wrote a memo that directly contradicted Obama-era policy, demonstrating that the current legal status of marijuana in both state and federal government is currently up for debate. While several states have legalized marijuana for medical or even recreational purposes, federal law still categorizes cannabis as a drug with no currently accepted medical use and a high potential for abuse. The comparison between marijuana, opioids, and ketamine in this article demonstrates that marijuana has been unnecessarily withheld and stigmatized by the federal government. Also reviewed is the impact of stringent marijuana-based legal policies upon the racial makeup of prison populations. The implications of current policy upon potential and future research are also discussed, with the determination that current policy has stymied research and prevented a more accurate determination of the risks and benefits of medical marijuana.”

https://www.ncbi.nlm.nih.gov/pubmed/30593477

“Cannabis was initially marked as Schedule I for reasons related to race and class. The federal government has restricted access to marijuana on the basis of its unknown risks and lack of proven benefits despite the fact that synthetic cannabinoids have been demonstrated to elicit FDA-approved benefits. This article demonstrates that marijuana should be removed from the Schedule I listing, as would be consistent with the labeling of ketamine and opioids, and reclassified as a Schedule III or Schedule II drug. Given the beneficial medical use, possible side effects, and potential for abuse and addiction of each drug, medical cannabis has been unfairly kept from the public through its unnecessary classification as a Schedule I drug.”

http://jaapl.org/content/46/4/472.long

Theoretical Explanation for Reduced Body Mass Index and Obesity Rates in Cannabis Users

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“Obesity is treatment-resistant, and is linked with a number of serious, chronic diseases. Adult obesity rates in the United States have tripled since the early 1960s. Recent reviews show that an increased ratio of omega-6 to omega-3 fatty acids contributes to obesity rates by increasing levels of the endocannabinoid signals AEA and 2-AG, overstimulating CB1R and leading to increased caloric intake, reduced metabolic rates, and weight gain. Cannabis, or THC, also stimulates CB1R and increases caloric intake during acute exposures. The present meta-analysis reveals significantly reduced body mass index and rates of obesity in Cannabis users, in conjunction with increased caloric intake. We provide for the first time a causative explanation for this paradox, in which rapid and long-lasting downregulation of CB1R following acute Cannabis consumption reduces energy storage and increases metabolic rates, thus reversing the impact on body mass index of elevated dietary omega-6/omega-3 ratios. Evidence suggests that, in the United States, many people may actually achieve net health benefits from moderate Cannabis use, due to reduced risk of obesity and associated diseases.” https://www.liebertpub.com/doi/10.1089/can.2018.0045?_ga=2.221453528.1791159238.1546024140-1083808004.1546024140

“Reduced Body Mass Index and Obesity Rates in Cannabis Users”  https://www.genengnews.com/insights/reduced-body-mass-index-and-obesity-rates-in-cannabis-users/?fbclid=IwAR3a0wbfGoPwAR-pYQGCeLz-KYUFdiLJoj6Ja7rTTNGBYwkjIGw1fUjf5LI

 
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n-3 polyunsaturated N-acylethanolamines are CB2 cannabinoid receptor-preferring endocannabinoids

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 Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids“Anandamide, the first identified endogenous cannabinoid and TRPV1 agonist, is one of a series of endogenous N-acylethanolamines, NAEs. We have generated novel assays to quantify the levels of multiple NAEs in biological tissues and their rates of hydrolysis through fatty acid amide hydrolase. This range of NAEs was also tested in rapid response assays of CB1, CB2 cannabinoid and TRPV1 receptors. The data indicate that PEA, SEA and OEA are not endocannabinoids or endovanilloids, and that the higher endogenous levels of these metabolites compared to polyunsaturated analogues are a correlate of their slow rates of hydrolysis. The n-6 NAEs (AEA, docosatetraenoyl and docosapentaenoyl derivatives) activated both CB1 and CB2 receptors, as well as TRPV1 channels, suggesting them to be ‘genuine’ endocannabinoids and ‘endovanilloids’. The n-3 NAEs (eicosapentaenoyl, docosapentaenoyl and docosahexaenoyl derivatives) activated CB2 receptors and some n-3 NAEs (docosapentaenoyl and docosahexaenoyl derivatives) also activated TRPV1 channels, but failed to activate the CB1 receptor. We hypothesise that the preferential activation of CB2 receptors by n-3 PUFA NAEs contributes, at least in some part, to their broad anti-inflammatory profile.” https://www.ncbi.nlm.nih.gov/pubmed/30591150 https://www.sciencedirect.com/science/article/pii/S1388198118302026?via%3Dihub
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