Bottom line: There is not very much evidence supporting the claim that CBN acts as a sleep aid. In fact, rather than arising from CBN levels, the sedative properties of aged cannabis may actually come from terpenes with low molecular weight, which tend to remain on cannabis as it ages and as THC oxidizes.
Similar to THC, CBN also binds to your body’s CB1 receptors. However, CBN interacts with these receptors with only around one-tenth the strength of THC. This is one of the primary reasons that the CBN cannabinoid does not give you the sensation of being high.
Bottom line: More research is needed to make any surefire claims about CBN’s effects on the human body and its potential benefits.
What is CBD and what does it do?
There is sparse research supporting the claim that CBN acts as a sleep aid. Photo by: Gina Coleman/Weedmaps
For example, a 2011 study published in the British Journal of Pharmacology found that THC in combination with CBN may produce a more sedated, “couch-locked” body high. This may be why older cannabis products or those exposed to a lot of heat and sunlight, such as Moroccan hashish, are said to produce more pronounced relaxing effects than other forms of marijuana.
In fact, cannabidiol is widely believed to have a regulatory effect, counteracting the potentially adverse effects of THC, such as anxiety and paranoia. Several studies support the finding that high doses of THC can cause anxiety or paranoia in otherwise healthy users and individuals with a predisposition for mental illness. However, the presence of CBD tends to mellow out these effects, producing a more manageable (and oftentimes more enjoyable) high.
Old cannabis or cannabis extracts left unrefrigerated or in the light will have higher levels of CBN. Photo by: Gina Coleman/Weedmaps
Several cannabinoids also interfered at mid-µM concentrations with enzymes catalyzing 2-AG biosynthesis via DAGLα, or with AEA inactivation via the putative membrane transporter or FAAH.
Efficacy and potency of pure cannabinoids and of most of their corresponding ‘botanical drug substance’ (BDS) as inhibitors of human recombinant DAGLα
The effects of the BDS at TRP channels reflected in many cases those of the corresponding pure cannabinoids. However, in some cases, these extracts were endowed with pharmacological actions of their own at the investigated targets, as in the case of the inhibitory effects observed on MAGL and NAAA, or with a capacity to inhibit AEA uptake, antagonize TRPM8 or activate TRPA1 that was stronger than that of the corresponding pure cannabinoids.
AEA and PEA are inactivated by enzymatic hydrolysis catalyzed by amidases, the best characterized of which is the FAAH (Cravatt et al., 1996). All compounds were therefore evaluated in assays of FAAH using [ 14 C]-AEA hydrolysis by rat brain membranes (which express FAAH as the only AEA hydrolyzing enzyme). The effects are shown in Table 7 . It is noteworthy that CBD was the only compound that inhibited FAAH, this effect having been already reported previously (Watanabe et al., 1998).
Inhibition of TRPM8-mediated elevation of intracellular calcium by cannabigerol (CBG), a CBG-botanical drug substance rendered free of CBG [denoted as botanical extract (BDS)] and the reconstituted CBG-BDS (denoted as CBG-BDS reconstituted). Experiments were carried out in HEK-293 cells stably over-expressing the rat recombinant TRPM8 channel and are means of at least n = 3 separate experiments. ‘CBG-BDS reconstituted’ was obtained by mixing the amount of CBG present in a given amount of CBG-BDS and the remaining amount of the ‘CBG-free’ BDS. The concentrations tested of ‘CBG-BDS reconstituted’ were calculated to contain equimolar concentrations of CBG as in pure CBG. The potency of ‘CBG-BDS reconstituted’ was slightly lower than that shown in Table 2 for CBG-BDS but still higher than that of CBG. SEM are not shown for the sake of clarity and were never higher than 10% of the means.
The extent and duration of AEA actions are determined by its extracellular concentration, controlled in turn by the rate of AEA synthesis and degradation. As the hydrolytic enzymes are intracellularly located, an efficient transport system allowing for the rapid trafficking of AEA through these topographically separated sites was proposed. Although this putative ‘carrier’ has yet to be cloned, some indirect biochemical and pharmacological evidence suggests its existence (Di Marzo et al., 1994; Ligresti et al., 2004; 2010;). The 21 cannabinoid preparations were therefore evaluated for their activity on [ 14 C]-AEA uptake by intact RBL-2H3 cells. Eleven were found to be active ( Table 9 ), and interestingly none of the most potent preparations inhibited FAAH ( Table 7 ). CBC = CBG > CBD inhibited AEA uptake most efficaciously and potently (IC50 = 11.3–25.3 µM), but some BDS (i.e. those of THCVA, CBGV, CBDA, THCA) were even more potent (IC50 = 5.8–12.5 µM) than the corresponding pure compounds in this assay ( Table 9 ).
In summary, non-psychotropic cannabinoids might contribute to several therapeutic benefits ascribed to Cannabis. On the other hand, the therapeutic use of THC is limited by its psychoactivity and potential for inducing dependence and tolerance, thus drawing further attention towards non-THC cannabinoids. The aim of the present study was to investigate the effects of 11 such compounds on TRPA1, TRPM8, TRPV1 and TRPV2 channels, as well as on DAGLα, FAAH, MAGL, NAAA and AEA cellular uptake (ACU). Apart from CBD, CBG, CBN and CBC, we also tested several cannabinoid propyl analogues and acids. For almost every cannabinoid tested, we also evaluated the activities of the corresponding cannabinoid extracts [‘botanical drug substance’ (BDS)]. The comparison between the effects observed with pure cannabinoids and the corresponding BDS might reveal the presence of potentially important synergistic effects that might be useful from a therapeutic point of view.
Potency of pure cannabinoids and of most of their corresponding ‘botanical drug substance’ (BDS) as functional antagonists at TRPM8 channels
Data are means ± SEM of at least n = 3 separate experiments in which various concentrations (1, 10, 25, 50 or 100 µM) of the pure compounds/BDS were incubated. Efficacy was calculated as % of FAAH inhibition at the maximal concentration tested (which is shown in the first line of the cell).