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The National Institute on Drug Abuse (NIDA) contracts with the University of Mississippi, the only facility in the country registered with the Drug Enforcement Agency (DEA) to grow and supply the cannabis that scientists are allowed to study. However, these strains are often not the ones widely distributed to the public in states that have legalized medical cannabis.
17. Wei D, Lee D, Cox CD, et al. Endocannabinoid signaling mediates oxytocin-driven social reward. Proc Natl Acad Sci U S A. 2015;112(45):14084-14089.
Effects of cannabinoids on the developing brain of children with and without ASD have also demonstrated the potential for adverse effects such as depressive-like symptoms and an increased risk for psychotic symptoms as an adult [20, 68, 83]. In addition, the impact of cannabis on cognition (specifically, learning, memory, and attention) have also been cited as concerns . Evaluations of studies conducted by the National Academies of Sciences, Engineering, and Medicine illustrate moderate evidence of effects of cannabis on learning, memory, and attention impairment [60, 84], which can impact academic, employment, and social outcomes .
Thus far, only five research studies to the best of our knowledge exist which have examined the direct effects of medical cannabis in individuals with ASD. The most recently published study conducted in Israel, examined the safety and efficacy of medical cannabis use amongst 188 patients with ASD. Most patients were treated using cannabis oil (1.5% THC and 30% CBD), and functional activities of daily living, mood, and quality of life were assessed using structured. Only 93 parents of 155 active participants participated in the six-month follow-up, but a third of participants reported a significant improvement on the three endpoints. Side effects were experienced by approximately 25% of patients, with the most common side effects reported as restlessness followed by sleepiness and psychoactive effects. This study is limited by the follow-up attrituion at the one and six-month follow-up, which was not explained in the publication .
Existing literature highlights potentially promising areas of research, suggesting correlations between the pathogenesis of ASD and the ECS. For example, mutations of neuroligin-3 (a primary protein required for tonic secretion of eCBs) interrupt eCB signaling . Among the effects of such a mutation is the potential for decreased capacity for regulating symptoms of ASDs, such as gastrointestinal function [35,36,37]. Furthermore, Kerr et al.,  reported decreased levels of DAGL and MAGL in rats exposed to valproic acid (2-propylpentanoic acid; VPA) Previous studies have found that prenatal exposure to VPA may increase risk of ASD  and these findings indicate a possible mechanism by which VPA leads to ASD with respect to altered levels of 2-AG and the corresponding behavioral responses. Additionally, a clinical study completed by Siniscalco et al.,  demonstrated high expression levels of CB2 in peripheral blood mononuclear cells (PBMCs) of children diagnosed with ASD, indicating the eCBs receptor as a potential target for treatment purposes. Human neuroimaging studies have evaluated the role of the ECS in ASD by measuring responses to social rewards. The studies reported associations between CB1 polymorphisms and ventral striatal cluster activity that suggest a possible link between CB1 polymorphisms and sensitivity to social rewards, a common endophenotype of ASD [41, 42].
A third study is currently ongoing and examining behavioral effects of cannabidivarin (with weight-based dosing of 10 mg/kg/day for 12 weeks) versus placebo on children with ASD. The clinical trial is funded by a $1.3 million grant from the United States Department of Defense [57, 58].
While research on medicinal uses of cannabinoids continues to expand and some co-occurring disorders of ASD such as epilepsy have been evaluated extensively with cannabinoids; equivalent evidence is not currently available to evaluate the efficacy of cannabinoids in treating other multiple conditions associated with ASDs. Given reports suggesting a dysfunctional endocannabinoid system in ASD, the pharmacologic potential of CBD to impact the symptoms and comorbidities affecting individuals with ASD is significant . Medical cannabis may provide the urgent support needed to address the unique core symptoms of ASD and improving quality of life. Further research, as a result, is necessitated to understand this line of treatment option and to expand the generalizability of results.
The mechanism by which cannabinoids could be utilized for treating ASD and its associated disorders, including epilepsy, may possibly be through the synthetic modulation of the ECS, which can help regulate social responses, pleasure, cognition, concentration, body movement, gastrointestinal function, pain, seizures, and the five senses [7, 43]. Unlike THC, CBD is a serotonin (5-hydroxytryptamine) receptor agonist, which is a non-cannabinoid receptor, but may explain the facilitation of the anxiolytic effect . Its antipsychotic effect is attributed to partial agonism at dopamine D2 receptors [45,46,47], similar to the antipsychotic action of aripiprazole . Additionally, CBD modulates glutamate-GABA systems that may be altered in ASD . Importantly, CBD inhibits the enzyme FAAH that degrades AEA, one of the main endocannabinoids. The modulation of the ECS is primarily targeted to CB1R and CB2R, and synthetic introduction of cannabinoids facilitates a process that mimics natural eCBs signaling to affect physiological factors . THC is more effective in binding to CB1R when compared to binding to CB2R . A high density of CB1R can be found in the basal ganglia, hippocampus, neocortex, hypothalamus, and limbic cortex. These neuron terminals affect motor activity, motor coordination, thinking, appetite, and sedation respectively. CB2R can be found on immune cells and tissues, which affect inflammation and immunosuppression , as well as the tonsils and spleen, the central nervous system, and in glial and neuronal cells . These interactions, potentiated by cannabinoid treatment, may offer a prospective treatment option for management of ASD related symptoms in the future. Though CB2R is not expressed in neurons under normal conditions, it is highly expressed under pathological conditions (i.e. psychiatric and neurological diseases) , and this warrants further investigation. At this time, although still controversial, immune system dysregulation is beginning to receive attention as having a possible role in ASD . The role of CB2R in regulating the immune system and inflammation offers a potentially promising therapeutic mechanism for managing the symptoms associated with ASD etiology [40, 51]. Previous studies have noted an upregulation of CB2R density and an increase in CB2R protein levels in the PBMC of all of the subjects with ASD, while there were no reported differences in CB1R, nor FAAH levels . No significant intragroup variances were also reported for the control group. These results indicate an endocannabinoid-CB2 signaling dysregulation in ASD, though CB2R has not shown good cannabinoidergic activity . Despite this, there is a hypothesized treatment opportunity for synthetic eCBs manipulation via CBD administration. CBD thus, could offer a therapeutic potential for improving motor skill and sleep, while also supporting anxiolytic, antipsychotic , and anticonvulsant symptoms .
There is currently insufficient evidence for cannabis use in ASD, which creates an urgent need for additional large-scale controlled studies to increase understanding of risks and benefits and also to examine the impact of “entourage effects.” This will support discussions of treatment options between health care providers and ASD patients and their families. Evidence may lead to a desired new line of treatment or prevent adverse outcomes from unsubstantiated use amongst families aiming for symptom reduction.
The effect of CBD oil begins at different rates for different people depending on dosage and product. Vaping/smoking can produce effects the quickest, sublingual tinctures may take 20-40 minutes, and edibles can take 1-2 hours to move through the digestive system. CBD taken topically in a cream or salve can also take an hour to get into the bloodstream, but their effects can last up to 6 hours.
Thanks for the info Molly. I’m an OTA and my husband is an OTR. Our young son is severely Autistic and we have been researching CBD as a means to regulate his behaviors.
Is it effective for autism andAsperger’s?
The syndromes have impacts that grossly affect the child’s development and overall quality of life. This news is huge for the medical and autism community; as this is the first time the FDA has approved a marijuana-derived substance.
A pediatric neurologist in Israel began research last year with 60 children on the autism spectrum and while still to be published, some preliminary results have been released. These qualifying study subjects had not responded to previous conventional drug therapies. 80% of participants who were treated for 7 months with 20:1 ratio of CBD to THC saw improvements. After the study, parents were asked about communication, behavior, and anxiety. 80% of parents noted a decrease in problem behavior, with 62% reporting significant improvement in behavior. Additionally, 50% noted an improvement in communication, 40% reported a decrease in anxiety (2/3 of the participants began the study with anxiety).
Thanks for your article….very interesting information as I am considering trying CBD with my 14 year old daughter who has Autism. I appreciate the link to the company/product you recommended, however I have not yet been able to get my daughter to swallow pills. Any other recommendations or suggestions other than a pill? Thanks in advance for your help ! Sincerely, Linda