Author Topic: Marijuana, Synthetic Exogenous Cannabinoids (Spice, K2) treatment modalities ?  (Read 243 times)

Offline Chip (OP)

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source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3091262/

my EDIT: I suggest taking Spice addicts and moving them slowly across to Bupe via GHB/GBL and slowly adding Naltrexone to the mix, prorata titration to detox. Sustain on Sodium Oxybate or Baclofen ... AND OBSERVE !


the salient bits:

Quote
Discussion

The proportion of patients who smoked cannabis following detoxification was significantly lower among those receiving VLNTX in addition to methadone taper. Cannabis use after discharge from inpatient detoxification was clinically significant in this sample because it was associated with increased opioid use and reduced engagement in outpatient treatment. These associations were not influenced by differences in socio-demographic and drug use characteristics.

Several factors may explain the effects of VLNTX treatment on cannabis use. Increased cannabis use was associated with more severe opioid withdrawal and craving at discharge. Cannabinoids attenuate the sympathetic hyperactivity associated with opioid withdrawal,8 and opioid addicts may have attempted to mitigate withdrawal by using cannabis.2,9 Activation of the cannabinoid CB1 receptor facilitates the reinforcing effects of opioids.10 Thus, reduced cannabis use could promote abstinence from opioids. Conversely, opioid receptor activity may influence reduced cannabis use. It has been suggested that agonist action at the μ-opioid receptor increases cannabis reward and seeking behavior.11 NTX reduces the reinforcing effects of cannabis in non-human experiments12 However, 50 mg NTX enhances subjective and reinforcing effects of cannabis in chronic users.13, although a lower dose of naltrexone (12 mg) blunts these effects.4 Thus, addition of VLNTX during detoxification may indirectly reduce cannabis use by reducing μ-opioid receptor activity, thereby reducing cannabis reward. There are indications that VLNTX may also act directly at the cannabinoid receptor. In preclinical studies, VLNTX increases analgesic and anticonvulsant effects of cannabis by acting at the CB1 receptor,14,15 similar to effects observed with the CB1 receptor antagonist rimonabant.16

This study has several limitations. Cannabis use was not taken into account in the prospective randomization of subjects. It is possible that the association between VLNTX administration and reduced use of cannabis is accounted for by unmeasured confounds, although this likelihood is reduced by the randomized assignment to treatment groups.

Confounding by socio-demographic, drug use, or treatment variables is unlikely because cannabis users and non-users did not significantly differ in such characteristics. Another potential confounder is the high attrition rate observed during the study, which could have led to selection bias.

Such bias is unlikely because the patients lost to follow-up did not differ significantly in socio-demographic characteristics or drug use history from those who participated in this follow-up study. We also limited the sensitivity of our analyses by dichotomizing cannabis use as present or absent. However, this approach does not detract from the validity of the results.

In spite of these limitations, this study supports the validity of our earlier findings, the first to show that opioid manipulation significantly reduced cannabis use in a clinical setting. Further investigations are needed to confirm the efficacy of VLNTX in reducing secondary cannabis use, improving the outcome of outpatient treatment, and as possible treatment for primary cannabis abuse and dependence.

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