CBD has been suggested as a beneficial drug for treating drug-resistant epilepsy in
pediatric population (Cortesi and Fusar-Poli 2007). Study by Luszczki et al.
demonstrated the synergistic effect of CB1 receptor agonist ACEA (arachidonyl-
20 chloroethylamide) on valproate by increasing its anticonvulsant action (Luszczki
et al. 2006). Despite these hints from various studies, use of cannabinoids has not
gained therapeutic status in the treatment of epilepsy (Kogan and Mechoulam 2007).
12.5.3 Respiratory Disorders
12.5.3.1 Asthma
Asthma is a chronic inflammatory lung disease, characterized by elevation of IgE
and various cytokines (Interleukins 4, 5, 9, and 13) locally in the airway or systemi-
cally in blood. In this disease there is reversible constriction of the small bronchioles
with excessive mucus production. Inhaled corticosteroids and bronchodilators rep-
resent the mainstay treatments for asthma (Global Initiative for Asthma 2020;
Colodenco et al. 2018). Most patients with asthma, however, can overcome
limitations in daily activities and impairments in overall quality of life by using
appropriate pharmacological interventions. Still, there is a need for therapies that
target IgE and cytokine production. Asthmatic patients have shown increased
expression of CB1 receptor mRNA and elevated levels of AEA (Martin-Fontecha
et al. 2014; Zoerner et al. 2011). The first evidence of cannabinoids as a therapeutic
agent in airway was reported in the 1970s. The use of THC as a bronchodilator has
been identified in a study by Vachon et al. (1973). THC attenuated allergic inflam-
mation by decreasing the cytokine production, mucus secretion, and IgE levels in
CB1- and CB2-independent manner (Braun et al. 2011; Jan et al. 2003). Addition-
ally, it was investigated that CBD activates both CB1 and CB2 receptors. These
receptors modulate the release of chemical messengers and inflammatory cytokines.
Thus, cannabinoids may be beneficial agents for the treatment of asthma according
to the available literature.
12.5.4 Cancer
12.5.4.1 Antiemetic
Patients undergoing chemotherapy experience acute nausea and vomiting. Emesis is
a devastating side effect of chemotherapeutic drugs. It occurs due to the production
of serotonin (5-hydroxytryptaminergic; 5-HT) through the enterochromaffin cells,
which are found to be distributed across the GI tract. Standard treatment of
chemotherapy-induced nausea and vomiting (CINV) includes 5-HT3 receptor
antagonists and neurokinin 1 (NK1) receptor antagonists. Cannabinoid system
interacts with 5-HT system to control CINV. Use of cannabinoids cause inhibition
of nausea and emesis related to chemotherapy or radiotherapy. CB1 receptors are
localized in this region of the brain (Cannabinoids 2003). Thus, administration of
CB1 agonist can reduce the release of 5 HT (Hu et al. 2007). The US FDA approved
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