Smoking Cessation Pharmacotherapy Utilization and Costs to a Medicaid Managed Care Plan.

BACKGROUND: Medicaid coverage for smoking cessation medications has expanded; however, little research has been conducted to evaluate patient-level changes in medication use over time and its associated economic impact on health plans. OBJECTIVE: The aim of this study was to characterize trends in smoking cessation medication utilization between 2006 and 2017 within a Medicaid population and estimate per-member per-month (PMPM) costs to the health plan. METHODS: This study was a retrospective longitudinal analysis conducted among adult members of a Medicaid managed care plan in California. Pharmacy claims data from January 1, 2006 to December 31, 2017 were analyzed to estimate utilization and cost of smoking cessation medications. Additionally, data from 3164 members who filled prescription(s) for cessation medication(s) in 2017 were evaluated to quantify quit attempts and use of combination therapy. For members who had been prescribed bupropion SR, varenicline, or the nicotine patch, the extent to which the durations of therapy were consistent with the manufacturers' recommended minimum duration of therapy were also assessed. RESULTS: The average PMPM expenditures for smoking cessation medications were approximately US$0.15 in 2017, compared with US$0.01-US$0.03 between 2006 and 2013. In 2017, a total of 3164 members initiated an estimated 3850 quit attempts, most commonly using the nicotine patch (57.5%) or varenicline (32.8%). Combination therapy accounted for 2.9% of quit attempts. The median therapy duration for the nicotine patch, varenicline, and bupropion SR was 28, 30, and 33 days, respectively, and for each of these medications, fewer than half of members filled prescriptions for the minimum recommended duration of therapy. CONCLUSIONS: Pharmacy claims data suggest that despite comprehensive coverage, most beneficiaries are underutilizing smoking cessation agents and are not completing the recommended treatment durations.

Enhancement of Anandamide-Mediated Endocannabinoid Signaling Corrects Autism-Related Social Impairment.

Introduction: We recently uncovered a signaling mechanism by which the endocannabinoid anandamide mediates the action of oxytocin, a neuropeptide that is crucial for social behavior, to control social reward. Oxytocin signaling has been implicated in autism spectrum disorder (ASD), and social reward is a key aspect of social functioning that is thought to be disrupted in ASD. Therefore, as a proof of principle for the core component of ASD-social impairment-we tested an endocannabinoid-enhancing compound on two widely studied mouse models of ASD, the BTBR and fmr1-/- (model of Fragile X Syndrome). Methods: We used the established three-chambered social approach test. We specifically increased the activity of anandamide by administering the compound URB597, a selective inhibitor of fatty acid amide hydrolase (FAAH), the hydrolytic enzyme for anandamide. Results: Remarkably, we found that FAAH blockade completely reversed the social impairment in both mouse models. CB1 receptor blockade prevented the prosocial action of FAAH inhibition in BTBR mice. These results were likely independent of effects on anxiety, as FAAH inhibition did not alter the performance of BTBR mice in the elevated plus maze. Conclusions: The results suggest that increasing anandamide activity at CB1 receptors improves ASD-related social impairment and identify FAAH as a novel therapeutic target for ASD.