ASD (Autism Spectrum Disorder) is an idiopathic brain disorder that can affect the general population. Patients diagnosed with ASD tend to also suffer from adjacent diseases such as epilepsy, mood, and anxiety disorders which affect negatively their life quality and their overall life survival. Pharmacological treatments to treat ASD are currently incapable of targeting precisely the root of the disease making it a painful and tedious process for the patients.
In the past couple of decades, researchers started to pay close attention to cannabinoids as a potential therapy for ASD patients as a result of a series of successful anecdotal experiences and single case studies. However, the exact mechanism of action by which different cannabinoids interact with the brain to ameliorate ASD symptoms remains to be elucidated.
In a randomized, placebo-controlled, cross-over study led by the King’s College London in the UK, the effect of 600 mg of orally administered CBD (cannabidiol) on brain activity was evaluated in 17 neurotypical (neurologically typical) and 13 ASD patients. Researchers employed fMRI evaluations to measure low-frequency activity and functional connectivity in the brain while the subjects were resting.
Herein, they found that patients suffering from ASD displayed higher brain activity in the vermis of the cerebellum, an area known to be responsible for movement, language, and social processing. Also, the brains of adults with ASD displayed higher low-frequency activity in the right fusiform area, an area known to be responsible for the visual processing of words and parts of the body.
Both of these areas are also known to display irregular behaviors in ASD patients. Finally, although limitations such as sample size and lack of task-oriented evaluations dim an accurate interpretation of the results in the study, the authors were able to conclude that CBD acts as a neuro-balancing agent for the brain in ASD patients.
Meanwhile, a retrospective study led by a collaboration of several academic and non-academic institutions in Israel examined the safety and efficacy of medical cannabis oil as a treatment for children suffering from ASD. Herein, 93 patients and their parents responded to structural questionnaires after 6 months of sublingual administration of CBD-rich (30% CBD and 1.5% THC) cannabis oil.
Analysis of the results showed that common symptoms concomitant with ASD, such as restlessness, rage attacks, and seizures, were significantly improved in the majority of the patients. While side effects such as sleepiness, psychoactive effects, and digestion problems were apparent in less than 10% of the patients, all of them reported them as tolerable. Overall, more than 80% of the parents reported a significant or moderate improvement in their child’s symptoms.
In the last 3 decades, there has been a three-fold increase in people being diagnosed with ASD. Previous studies have shown that ASD patients suffer from GABAergic and glutamatergic (neuro-signaling systems crucial for brain development and regular functioning) dysregulation in the brain.
Also, previous studies have shown the capability of the endocannabinoid system to modulate imbalances in both the GABAergic and glutamatergic signaling systems, providing a plausible mechanism of action for the therapeutic improvement in ASD-associated symptoms. Given the safety and efficiency profile of cannabis-based therapies, ongoing clinical trials are researching the effect of cannabis/CBD treatments in patients suffering from ASD.
Bar-Lev Schleider, L., Mechoulam, R., Saban, N. et al. Real life Experience of Medical Cannabis Treatment in Autism: Analysis of Safety and Efficacy. Sci Rep 9, 200 (2019). https://doi.org/10.1038/s41598-018-37570-y
Pretzsch, C. M., Voinescu, B., Mendez, M. A., Wichers, R., Ajram, L., Ivin, G., Heasman, M., Williams, S., Murphy, D. G., Daly, E., & McAlonan, G. M. (2019). The effect of cannabidiol (CBD) on low-frequency activity and functional connectivity in the brain of adults with and without autism spectrum disorder (ASD). Journal of Psychopharmacology, 33(9), 1141–1148. https://doi.org/10.1177/0269881119858306
