Tolerance breaks are infamous strategies for cannabis consumers and medical patients to rejuvenate their experience. A different strain of medical cannabis might be a strategy to make THC stronger compared to a tolerance break, though.
Perhaps the required dose of THC has become outrageous. Otherwise, the effect can simply become bland after enough time despite the dose. Or, more simply, it’s time for a reset. Regardless of why THC has lost its medical prowess, a tolerance break can be useful. As an alternate option, switching the type of cannabis, or cannabinoid profile can help bring THC’s therapeutic potential back to normal.
Why quit when you have a different strain?
Other cannabinoids and terpenes in cannabis’s genetic quiver help protect the endocannabinoid system. Utilizing the full cannabimimetic library can avoid complete abstinence. A docket of nine clinical trials now wrapped in one review concluded that medical cannabis can help treat any withdrawal symptoms from, well, cannabis. The University of Duisburg-Essen — located in Germany — funded the review. (1)
Some clinical trials accepted in the review tested the efficacy of Naboximols — an oral spray containing a one-to-one ratio of CBD and THC. A synthetic form of THC known as dronabinol only treated some withdrawal effects. A more beneficial cannabinoid, however, is CBD. Tolerance breaks can at least become easier without needing to abstain from regular consumption with the addition of CBD.
Inhibitors of an enzyme known as Fatty Acid Amide Hydrolase (FAAH), including CBD, protect the fatty acid and endocannabinoid known as anandamide. As a biased and partial agonist of CB1 receptors, the uptick of anandamide by a FAAH inhibitor can maintain a regular endocannabinoid tone. Otherwise, anandamide regulates cell signalling (via ERK 1 and 2) and might stop CB1 receptor desensitization during THC consumption.
Medical cannabis that regulates THC and the ECS
The German review highlighted the treatment of cannabis use disorder (CUD). As previously documented, CUD can be explained as a form of cannabis seeking. Symptoms of excessive THC consumption include interim internalization and desensitization of the CB1 receptor. Whereas CB2 receptors temporarily morph to adapt to microbial cells. But the drive causing one to seek cannabis is deeper within the core of mammalian biology. Receptors and ligands make up a matrix known as the endocannabidiome, consisting of the EC system. And it’s this naturally active matrix that drives one person to cannabis more than someone else.
Natural levels of this system must be maintained by everyday routines, such as diet and exercise, to maintain its function. Or, genetic disorders can chronically degrade the system and cause illnesses. Excessive THC consumption, however, turns down the system. Therefore, heavy use of unregulated THC can deplete the ECS over time and lead to tolerance. But it’s only temporary since receptors comprising the system restore once THC leaves the body after four days or up to one month for consistent consumers.
Cannabis Use Disorder or Bad ECS Tone
Professor Shana Augustin, a pharmacologist for the National Institute on Alcohol Abuse and Alcoholism, co-authored a different review published this month. Collaborating with Augustin was her colleague, David Lovinger, Ph.D. Despite a focus on the ECS, the NIAA, an arm of the National Institute of Health (NIH), also focused on the condition of Cannabis Use Disorder. (2) Specific changes in the CB1 receptor after chronic THC consumption were noted. That said, the clinical importance of CB1 receptor agonists for malignancies that deplete the ECS was understated.
Let us know in the comments if you have had any luck with CBD during a tolerance break.
- Vuilleumier C, Scherbaum N, Bonnet U and Roser P (2022) Cannabinoids in the Treatment of Cannabis Use Disorder: Systematic Review of Randomized Controlled Trials. Front. Psychiatry 13:867878. doi: 10.3389/fpsyt.2022.867878
- Augustin SM, Lovinger DM. Synaptic changes induced by cannabinoid drugs and cannabis use disorder. Neurobiol Dis. 2022;167:105670. doi:10.1016/j.nbd.2022.105670