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cannabinoid treatment

A growing number of clinical trials are studying a medicine made from an extract of Cannabis that contains specific amounts of cannabinoids. This medicine is sprayed under the tongue.

Stimulating appetite

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For details on the cannabinoid preparations, randomization process, important changes to methods after trial commencement, anchoring instructions for rating the CGI-S and CGI-I, and the CONSORT checklist, see Additional file 2.

Bearss K, Johnson C, Smith T, Lecavalier L, Swiezy N, Aman M, et al. Effect of parent training vs parent education on behavioral problems in children with autism spectrum disorder: a randomized clinical trial. JAMA. 2015;313(15):1524–33.

Baseline evaluations

Iannotti FA, Hill CL, Leo A, Alhusaini A, Soubrane C, Mazzarella E, et al. Nonpsychotropic plant cannabinoids, cannabidivarin (CBDV) and cannabidiol (CBD), activate and desensitize transient receptor potential vanilloid 1 (TRPV1) channels in vitro: potential for the treatment of neuronal hyperexcitability. ACS Chem Neurosci. 2014;5(11):1131–41.

Epidiolex is a cannabis-derived pure CBD compound which was approved by the U.S. FDA in 2018 for the treatment of two severe forms of epilepsy [13]. This may be relevant for patients with ASD, as 10–30% also have epilepsy, and several pathophysiological pathways are implicated in both disorders [11, 14].

Cannabinoids might affect behavior and communication through several mechanisms. THC activates CB1R and has been associated with enhanced social behavior in multiple studies [42, 43]. CBD is a 5-HT1A receptor agonist, which might facilitate anxiolytic effects. Its presumed antipsychotic effect is attributed to partial agonism at dopamine D2 receptors, similar to the antipsychotic action of aripiprazole [44].

Cannabis use for medicinal purposes dates back at least 3,000 years.[1-5] It was introduced into Western medicine in 1839 by W.B. O’Shaughnessy, a surgeon who learned of its medicinal properties while working in India for the British East India Company. Its use was promoted for reported analgesic, sedative, anti-inflammatory, antispasmodic, and anticonvulsant effects.

Patients often experience mood elevation after exposure to Cannabis, depending on their previous experience. In a five-patient case series of inhaled Cannabis that examined analgesic effects in chronic pain, it was reported that patients who self-administered Cannabis had improved mood, improved sense of well-being, and less anxiety.[70]

Laboratory/Animal/Preclinical Studies

Seventy-four patients with newly diagnosed head and neck cancer self-described as current Cannabis users were matched to 74 nonusers in a Canadian study investigating quality of life using the EuroQol-5D and Edmonton Symptom Assessment System instruments.[71] Cannabis users had significantly lower scores in the anxiety/depression (difference, 0.74; 95% CI, 0.557–0.930) and pain/discomfort (difference, 0.29; 95% CI, 0.037–1.541) domains. Cannabis users were also less tired, had more appetite, and better general well-being.

An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors. CBD inhibited the survival of both estrogen receptor–positive and estrogen receptor–negative breast cancer cell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic mammary cells.[18] Other studies have also shown the antitumor effect of cannabinoids (i.e., CBD and THC) in preclinical models of breast cancer.[19,20]

Preclinical research suggests that emetic circuitry is tonically controlled by endocannabinoids. The antiemetic action of cannabinoids is believed to be mediated via interaction with the 5-hydroxytryptamine 3 (5-HT3) receptor. CB1 receptors and 5-HT3 receptors are colocalized on gamma-aminobutyric acid (GABA)-ergic neurons, where they have opposite effects on GABA release.[35] There also may be direct inhibition of 5-HT3 gated ion currents through non–CB1 receptor pathways. CB1 receptor antagonists have been shown to elicit emesis in the least shrew that is reversed by cannabinoid agonists.[36] The involvement of CB1 receptor in emesis prevention has been shown by the ability of CB1 antagonists to reverse the effects of THC and other synthetic cannabinoid CB1 agonists in suppressing vomiting caused by cisplatin in the house musk shrew and lithium chloride in the least shrew. In the latter model, CBD was also shown to be efficacious.[37,38]