Currently, only Oregon and Colorado have legalized psychedelic therapy for mental health treatment, with a licensing process in place. In other states, treatment facilities may explore partnerships with research organizations to participate in clinical trials. The research supporting psilocybin’s use in this context has been growing for a while now.

1. Neuroscientist Deborah Mash, professor of neurology and molecular and cellular pharmacology, Leonard M. Miller School of Medicine, has been studying the effects of ibogaine in substance-use disorders for more than three decades.
2. One explanation for the issuance of problematic patents for psychedelics may be a lack of expertise at the PTO.
3. Supplemental background information was gathered from references of retrieved and reviewed works.
4. No studies were identified evaluating the efficacy of psilocybin in patients with amphetamine (or derivatives) use disorder.
5. Studies were generally strong in essential reporting items, and variably limited by incomplete or lacking probability reporting, power analysis, blinding, randomization, and adjustment for confounding factors.

Ethically, leaders must ensure that all patients feel safe and informed about their treatment options. Considerations around the cultural significance of these substances, particularly within Indigenous communities, also warrant attention. It’s crucial that addiction treatment centers approach the use of psychedelics with respect for their cultural roots and aim to provide equitable access. Now a what are whippets? professional recovery coach, Guckel said psychedelics might hold a promise to treat addiction disorders. Given the partially overlapping adverse potential of cannabis and psychedelics, risks common to the two substances, and risks elevated in persons with chronic cannabis use, should be considered.

Building Diversity and Health Equity Into Psychedelic Treatment

A recent single-blind 6-week pilot study assessed the feasibility and tolerability of ketamine in eight participants with CUD. Participants received motivational enhancement therapy and mindfulness-based relapse prevention behavioral treatments in addition to a ketamine infusion of 0.71 mg/kg, with non-responders receiving a second infusion at 1.41 mg/kg. While there was no control group, compared to before treatment participants had a statistically significant reduction in cannabis use following treatment, and improvement in self-reported confidence in resisting the urge to use cannabis. The study additionally demonstrated the feasibility of integrating a psychedelic drug into behavioral treatment targeting CUD (33). Medications that have been shown to be effective for other SUDs, including naltrexone (alcohol and opioid use disorders) and bupropion (tobacco use disorder), or have demonstrated promise, such as topiramate (alcohol and cocaine use disorders), were without success (2). Trials of medications aimed at reducing cannabis use or cannabis withdrawal symptoms, including antipsychotics, antidepressants, and mood stabilizers among several others, have also been largely ineffective.

Quality assessment of studies

In this systematic review, we identified only one double-blind, placebo-controlled RCT, and three small clinical trials, of which three were conducted in the 21st century assessing the efficacy of psilocybin in patients with alcohol and tobacco use disorder. All four studies combined psilocybin with some form of psychotherapy and showed a beneficial effect of psilocybin-assisted therapy on SUD, but the risk of bias ranged from some concerns to critical. whats the legal drinking age in russia Future (double-blind, placebo-controlled) RCTs in patients with SUD need to evaluate whether psilocybin-assisted therapy is effective in this population. Recent years have seen a resurgence in psychedelic research, a development sometimes referred to as the psychedelic renaissance. Although these reviews provide an excellent overview of clinical trials published in the last 25 years, including multiple psychedelics and conditions, they may have missed clinical trials evaluating the efficacy of psychedelics that were conducted before the 1980s (19–21). As shown by Fuentes et al. (6), many trials have been conducted assessing the efficacy of LSD in SUD in these early decades, which may have been an important era for psilocybin research as well (6).

One of the most recent such studies, published in Scientific Reports on April 7, looked at data from 214,505 U.S. adults in the National Survey on Drug Use and Health (NSDUH) from 2015 to 2019, and found an association between past use of psilocybin—at any time in their lives—and a reduced risk of opioid use disorder. A case report of hallucinogen-persisting perception disorder (HPPD) in an individual with CUD provides an opportunity to consider the interaction and safety concerns of psychedelic use in those with CUD and comorbid disorders. A 16-year-old white female with a past psychiatric history of major depressive disorder, CUD, and social anxiety disorder tried LSD a total of four times over several months, each of which was a subjectively negative experience.

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In rats, the potent synthetic CB1/CB2 receptor agonist CP 55,940 caused a selective upregulation of 5HT2A receptors in prefrontal cortex via a cascade of CB2 binding, increased phospholipase C β activity, and increased ERK1/2 activation (57). In parallel, chronic administration of CP 55,940 led to downregulation of CB1 and CB2 receptors, consistent with imaging results in human with chronic cannabis use (58). In addition to providing links between development of psychosis and anxiety following cannabis use, this cannabinoid-induced upregulation of 5HT2A receptors provides a tantalizing link between the effects of chronic cannabis use and an essential target of psychedelic hallucinogens.

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MDMA, a stimulant with mixed pharmacological effect which include the increase of oxytocin, has shown tremendous promise as a novel treatment for posttraumatic stress disorder (PTSD), and therefore has undergone increasing study and scrutiny (41). Given the higher prevalence of cannabis use and CUD in those with PTSD compared to the general population (42), it should be anticipated that MDMA could be therapeutically administered in persons with co-morbid disorders. In a secondary analysis of a study of MDMA for PTSD which allowed inclusion of participants with mild CUD or alcohol use disorder (AUD) or moderate CUD or AUD in early remission, only two participants were identified with CUD (both mild) who were randomized to the placebo group. Thirteen of the 21 participants with past, but not current, AUD received MDMA and had significant reductions in comparison to the placebo group of self-reported AUD and at-risk symptoms, which correlated to improvements in PTSD symptoms. In combination with the CUD participants, eight of the additional 14 participants with past, but not current, SUD received MDMA and had no significant change in self-reported SUD and at-risk symptoms (35).

To date, treatments demonstrating the most promise in clinical studies are cannabinoid partial agonists (THC, nabiximols). However, significant barriers related to cost and access in addition to their abuse potential make these currently impractical strategies. N-acetylcysteine, which has been shown to reduce symptoms of obsessive-compulsive behavior, has shown promise in studies of adolescents, but not adults, with CUD. Some medications that, broadly speaking, have sedating or anxiolytic potential, namely zolpidem, gabapentin, and quetiapine, have demonstrated some potential for reducing cannabis withdrawal symptoms (26). Given the mixed research findings, it is important to proceed with care and focus on scientific rigor and transparency. There is a need to better establish which of these drugs are most effective, how they should be administered, and who is most likely to benefit.

As described in a retrospective observational study by Cox et al., psychedelics that target 5HT2A receptors appear to reduce the consumption of cannabis (28). Furthermore, when 5HT2A receptors are directly acted upon, they appear to enhance psychological domains noted above, such as insight, self-efficacy, and spirituality, suggesting potential for targeting serotonergic receptors for CUD treatment (29). This case is notable for the adverse effect of HPPD occurring after relatively few experiences with LSD, and the self-discontinuation of cannabis. While some or all of the LSD doses may have been above a range considered therapeutic, the number of reported experiences is close to that used in current clinical studies of other psychedelics (typically 1–3). While it remains unknown if this case represents an accelerated first break of an undeclared psychotic disorder, the reported history lacks clearly identifiable pre-morbid risk factors for psychotic disorders, and echoes long-identified concerns connecting LSD use to subsequent development blood alcohol content (bac) depends on of psychotic disorders (43–45).