A nationwide pharmacy chain responds to the opioid epidemic.

OBJECTIVES: To describe the 3-pronged approach taken by a large national retail pharmacy chain to address the opioid epidemic and associated overdoses. SETTING: Large national retail pharmacy chain with more than 8200 stores in 50 states. PRACTICE DESCRIPTION: Eight million customer interactions daily through in-store and digital settings. This is a company with a long history of responding to public health crises. PRACTICE INNOVATION: Initiated 3 programs to respond to the opioid crisis: 1) provide safe medication disposal kiosks; 2) expand national access to naloxone; and 3) provide education on the risk and avoidance of opioid overdose. Used the RE-AIM framework to evaluate and enhance the quality, speed, and public health impact of the interventions. EVALUATION: Not applicable. RESULTS: Early results are safe medication disposal kiosks in more than 43 states, naloxone-dispensing program in 33 states, and patient and support system education using the Opioid Overdose Toolkit from the Substance Abuse and Mental Health Services Administration. CONCLUSION: The availability of safe drug-disposal kiosks, naloxone dispensing at pharmacies, and patient education are key prevention initiatives to address the opioid epidemic and reduce the increasing national burden of opioid overdose. Early results are quantitatively and qualitatively promising.

Are there common familial influences for major depressive disorder and an overeating-binge eating dimension in both European American and African American female twins?

OBJECTIVE: Although prior studies have demonstrated that depression is associated with an overeating-binge eating dimension (OE-BE) phenotypically, little research has investigated whether familial factors contribute to the co-occurrence of these phenotypes, especially in community samples with multiple racial/ethnic groups. We examined the extent to which familial (i.e., genetic and shared environmental) influences overlapped between Major Depressive Disorder (MDD) and OE-BE in a population-based sample and whether these influences were similar across racial/ethnic groups. METHOD: Participants included 3,226 European American (EA) and 550 African American (AA) young adult women from the Missouri Adolescent Female Twin Study. An adaptation of the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) was administered to assess lifetime DSM-IV MDD and OE-BE. Quantitative genetic modeling was used to estimate familial influences between both phenotypes; all models controlled for age. RESULTS: The best-fitting model, which combined racial/ethnic groups, found that additive genetic influences accounted for 44% (95% CI: 34%, 53%) of the MDD variance and 40% (25%, 54%) for OE-BE, with the remaining variances due to non-shared environmental influences. Genetic overlap was substantial (rg = .61 [.39, .85]); non-shared environmental influences on MDD and OE-BE overlapped weakly (re = .26 [.09, .42]). DISCUSSION: Results suggest that common familial influences underlie MDD and OE-BE, and the magnitude of familial influences contributing to the comorbidity between MDD and OE-BE is similar between EA and AA women. If racial/ethnic differences truly exist, then larger sample sizes may be needed to fully elucidate familial risk for comorbid MDD and OE-BE across these groups.

Is the relationship between binge eating episodes and personality attributable to genetic factors?

Aspects of disordered eating and personality traits, such as neuroticism, are correlated and individually heritable. We examined the phenotypic correlation between binge eating episodes and indices of personality (neuroticism, extraversion, openness to experience, agreeableness, conscientiousness, and control/impulsivity). For correlations ≥|0.20|, we estimated the extent to which genetic and environmental factors contributed to this correlation. Participants included 3,446 European American same-sex female twins from the Missouri Adolescent Female Twin Study (median age = 22 years). Binge eating episode was assessed via interview questions. Personality traits were assessed by self-report questionnaires. There was a significant moderate phenotypic correlation between binge eating episode and neuroticism (r = 0.33) as well as conscientiousness (r = -0.21), while other correlations were significant but smaller (r ranging from -0.14 to 0.14). Individual differences in binge eating episodes, neuroticism, and conscientiousness were attributed to additive genetic influences (38% [95% CI: 21-53%], 45% [95% CI: 38-52%], and 44% [95% CI: 0.33-0.55%] respectively), with the remaining variance attributed to individual-specific environmental influences. Covariance was attributable to genetic (neuroticism r g = 0.37; conscientiousness r g = -0.22) and individual-specific environmental (neuroticism r e = 0.28; conscientiousness r e = -0.19) influences. Personality traits may be an early indicator of genetic vulnerability to a variety of pathological behaviors, including binge eating episode. Furthermore, prior research documenting phenotypic correlations between eating disorder diagnoses and personality may have stemmed from etiological overlap between these personality traits and aspects of disordered eating, such as binge eating episode.

Preliminary evidence for the role of HTR2A variants in binge eating in young women.

We examined the association between 15 single nucleotide polymorphisms (SNPs) in HTR2A and characteristics of disordered eating, including weight/shape concerns, binge eating (with or without loss of control), and compensatory behaviors (purging and nonpurging). Whether a lifetime history of major depressive disorder (MDD) moderated or mediated this association was also investigated. A sample of 1533 twin women of White descent that were part of the Missouri Adolescent Female Twin Study was used. Data were collected using self-report responses to a semistructured interview. Logistic regression analyses were used to examine the association between weight/shape concerns, binge eating, and compensatory behaviors and SNPs (where carriers of the minor allele were coded as 1). Two SNPs, rs6561333 and rs2296972, showed a protective influence against binge eating, with rs2296972 being significant at a trend level after application of the false discovery rate. The SNP was not associated with MDD nor did MDD moderate its putative relation with binge eating. Pending replication, our analyses provide preliminary evidence for intronic SNPs in HTR2A and their association with binge eating. Given the well-documented role of serotonergic dysfunction in eating psychopathology, this report warrants considerable further study.