The evidence summarized in this article demonstrates the potential cannabis has to ease opioid withdrawal symptoms, reduce opioid consumption, ameliorate opioid cravings, prevent opioid relapse, improve OUD treatment retention, and reduce overdose deaths. Cannabis’ greatest potential to positively impact the opioid epidemic may be due to its promising role as a first line analgesic in lieu of or in addition to opioids. The comparative efficacy of cannabis alone or in conjunction with current medication-assisted OUD therapies is not well characterized. However, no other intervention, policy, pharmacotherapy, or treatment paradigm has been as impactful as cannabis legislation has been on the rates of opioid consumption, overdose, and death.
Regular use of full or partial opioid agonists can block or reduce the euphoria derived from the use of additional illicit opioids and the prescription of MOUD has been shown to have anti-craving effects [16, 17, 22]. Furthermore, the implementation of these regimens has led to far-reaching societal benefits, including a significant reduction in opioid-related mortality as well as a reduction in social adversity in the form of reduced crime and incarceration rates (8, 12). Growing pre-clinical and clinical evidence appears to support the use of cannabis for these purposes.
Undergoing behavioral therapy can help you understand your addictions and motivations better. With a primarily psychological drug like marijuana, it is also crucial to implement cognitive behavioral therapy as well as other therapeutic methods. Many people who develop a marijuana habit are able to quit without entering a full-scale treatment center since the substance is not as harsh on the brain and body as other, “harder” drugs. However, for those in an environment that makes it seemingly impossible to stop using marijuana, an inpatient treatment center may help cut out proximity to non-ideal settings and circumstances or daily triggers. Those who receive treatment for a marijuana addiction are predominantly individuals who have chronically used marijuana on a daily basis.
It bears noting, however, that there are no scientific or long-term studies to back up these methods. The current choices are acetaminophen (which does very little for pain but certainly can harm your liver), opioids (which have obvious dangers), or non-steroidal anti-inflammatory medications (NSAIDS). Increasingly, we are becoming aware of how dangerous daily NSAIDS use truly is, causing bleeding ulcers, chronic gastritis, heart attacks, and often resulting in permanent kidney damage. In follow up studies, they further showed that this robust effect was minimized among mice bred with genetic mutations leading to the under production of CREB.
A given patient half-year was categorized as exposed (coded as 1) to a policy—medical marijuana legalization or comprehensive PDMP mandate—if the policy took effect in the patient’s residential state before the start of the patient half-year and as not exposed (coded as 0) otherwise. Changes in the outcome from before to after policy implementation in implementing states were compared with concurrent changes in states that had not yet implemented the policy. Association of medical marijuana legalization with an outcome may differ by the patient’s previous exposure to opioids; thus, we included interaction terms between each policy indicator and an indicator of recent opioids, defined as having 1 or more opioid prescriptions during the 12 months before the new cancer diagnosis. As already noted in this review, epidemiological and observational studies have highlighted the potential of medicinal cannabis as a therapeutic for opioid addiction, or as an adjuvant analgesic with prescription opioid to reduce dosage, and by extension, minimising the propensity of developing OUD. Although limited, our search of the literature highlighted key MCRPs of interest in clinical trials for this two-pronged potential in ameliorating the opioid crisis.
One obstacle to this is that health insurance doesn’t often cover medical marijuana and patients can find it difficult to afford. While their work is convincing that nicotine can serve as a gateway drug to cocaine in mice models, it cannot speak directly to the possible role of cannabis as a gateway drug for opioids in adolescent humans. However several lines of research are suggestive that similar processes may occur for a subset of individuals with genetic risk. It is these processes and the extended period of time it takes for a human brain to fully myelinate that are thought to confer additional risk for addiction with younger ages of trauma exposure, adverse events, and drug use-because the brain is still actively developing and more vulnerable to environmental exposures. For instance, one study published by the American Academy of Pediatrics documents findings from one analysis that adolescents who use cannabis are 104 times more likely to use cocaine than adolescents who never use cannabis.7 There are significant differences between these two populations of adolescents predating the onset of cannabis use.
Alongside the many components and derivatives of the cannabis plant (Cannabis sativa), an increasing number of synthetic cannabinoids (SCBs) have been formulated that have different effects and potency at cannabinoid receptors [69]. Similarly, drugs acting within the endocannabinoid system to mediate levels of endogenous cannabinoids have also been developed [90]. While this variability can make it difficult to interpret existing research findings (particularly when participants are taking recreational cannabis with unclear components), it also opens many avenues for future research, with the potential to develop cannabinoid formulations to target specific indications. In this case, cannabinoids with maximal impact on withdrawal suppression and minimal adverse effects would be most useful in targeting OUD outcomes.
Long derided by drug policy reformers, the “gateway hypothesis” posits that a drug, such as cannabis, could “lower the threshold for addiction” to other substances, such as opioids. Behaviorally and developmentally it is clear that many of the shared root causes (e.g. genetic predisposition, trauma, unstable psychiatric symptoms, how to overcome alcoholism thrill seeking, impulsivity, delay discounting, environmental exposures) that increase an individual’s likelihood of using cannabis also increase the same individual’s likelihood of opioid use. In another sub-group analysis, we estimated the effect of MML on opioid utilization among chronic non-cancer pain patients.
Neurodevelopment of the adolescent brain continues through young adulthood with ongoing pruning and remodeling which is affected by cannabis use and directly implicates key pathways that are also involved in the neuropathophysiology of substance use disorders. Cannabis use affects adolescent emotion and cognition circuits through disruption of signaling, decreased neurogenesis, and impaired memory formation during key periods of development. Genetic studies have found that genes can predict the impact of cannabis use on subsequent heroin in animal models and that cannabis can also change adolescent gene expression suggesting individual variation in risk of cannabis’ effects on adolescent brain maturation based on gene by environment interactions. Finally, there are many reasons to believe endogenous cannabinoid and opioid systems interact in complex ways; there may be multiple mechanisms by which the use of one class of substances could affect self-administration of the other.