Context: Successful long-term weight loss is challenging. Brain endogenous opioid systems regulate associated processes; however, their role in the maintenance of weight loss has not been adequately explored in humans. Objective: In a preliminary study, the objective was to assess central μ-opioid receptor (MOR) system involvement in eating behaviors and their relationship to long-term maintenance of weight loss. Design: This was a case-control study with follow-up of the treatment group at 1 year after intervention. Setting: The study was conducted at a tertiary care university medical center. Participants: Lean healthy (n = 7) and chronically obese (n = 7) men matched for age and ethnicity participated in the study. Interventions: MOR availability measures were acquired with positron emission tomography and [¹¹C]carfentanil. Lean healthy men were scanned twice under both fasted and fed conditions. Obese men were placed on a very low-calorie diet to achieve 15% weight loss from baseline weight and underwent two positron emission tomography scans before and two after weight loss, incorporating both fasted and fed states. Main Outcome Measures: Brain MOR availability and activation were measured by reductions in MOR availability (nondisplaceable binding potential) from the fed compared with the fasted-state scans. Results: Baseline MOR nondisplaceable binding potential was reduced in obese compared with the lean and partially recovered obese after weight loss in regions that regulate homeostatic, hedonic, and emotional responses to feeding. Reductions in negative affect and feeding-induced MOR system activation in the right temporal pole were highly correlated in leans but not in obese men. A trend for an association between MOR activation in the right temporal pole before weight loss and weight regain 1 year was found. Conclusions: Although these preliminary studies have a small sample size, these results suggest that obesity and diet-induced weight loss impact central MOR binding and endogenous opioid system function. MOR system activation in response to an acute meal may be related to the risk of weight regain.

Antipsychotics are an important pharmacotherapy option for the treatment of many mental illnesses. Unfortunately, selecting antipsychotics is often a trial-and-error process due to a lack of understanding as to which medications an individual patient will find most effective and best tolerated. Metabolomics, or the study of small molecules in a biosample, is an increasingly used omics platform that has the potential to identify biomarkers for medication efficacy and toxicity. This systematic review was conducted to identify metabolites and metabolomic pathways associated with antipsychotic use in humans. Ultimately, 42 studies were identified for inclusion in this review, with all but three studies being performed in blood sources such as plasma or serum. A total of 14 metabolite classes and 12 lipid classes were assessed across studies. Although the studies were highly heterogeneous in approach and mixed in their findings, increases in phosphatidylcholines, decreases in carboxylic acids, and decreases in acylcarnitines were most consistently noted as perturbed in patients exposed to antipsychotics. Furthermore, for the targeted metabolomic and lipidomic studies, seven metabolites and three lipid species had findings that were replicated. The most consistent finding for targeted studies was an identification of a decrease in aspartate with antipsychotic treatment. Studies varied in depth of detail provided for their study participants and in study design. For example, in some cases, there was a lack of detail on specific antipsychotics used or concomitant medications, and the depth of detail on sample handling and analysis varied widely. The conclusions here demonstrate that there is a large foundation of metabolomic work with antipsychotics that requires more complete reporting so that an objective synthesis such as a meta-analysis can take place. This will then allow for validation and clinical application of the most robust findings to move the field forward. Future studies should be carefully controlled to take advantage of the sensitivity of metabolomics while limiting potential confounders that may result from participant heterogeneity and varied analysis approaches.

Refugees experience high rates of post-traumatic stress disorder (PTSD), anxiety, and depression due to exposure to civilian war trauma and forced migration. Inflammatory products may offer viable biological indicators of trauma-related psychopathology in this cohort, promoting rapid and objective assessment of psychopathology. Incoming Syrian and Iraqi refugees (n = 36) ages 18–65 completed self-report measures of PTSD, anxiety, and depression and provided saliva samples during an assessment at a primary care clinic within the first month of resettlement in the United States. Interleukin 1β (IL-1β) and C-reactive protein (CRP) differentially correlated with symptom severity by domain, and there was a non-significant trend for sex moderating the relation between inflammation and PTSD symptoms. Our findings show unique relations between trauma-related psychopathology and inflammation. There is a need for further research in diverse ethnic cohorts with differential trauma exposures for inflammation to be considered a biological indicator of psychopathology.

Background: Prenatal exposure to maternal metabolic conditions associated with inflammation and steroid dysregulation has previously been linked to increased autism risk. Steroid-related maternal serum biomarkers have also provided insight into the in utero steroid environment for offspring who develop autism. Objective: This study examines the link between autism among offspring and early second trimester maternal steroid-related serum biomarkers from pregnancies enriched for prenatal metabolic syndrome (PNMS) exposure. Study design: Early second trimester maternal steroid-related serum biomarkers (i.e., estradiol, free testosterone, total testosterone, and sex hormone binding globulin) were compared between pregnancies corresponding to offspring with (N = 68) and without (N = 68) autism. Multiple logistic regression analyses were stratified by sex and gestational duration. One-way ANCOVA with post hoc tests was performed for groups defined by autism status and PNMS exposure. Results: Increased estradiol was significantly associated with autism only in males (AOR = 1.13 per 100 pg/ml, 95% CI 1.01–1.27, p = 0.036) and only term pregnancies (AOR = 1.17 per 100 pg/ml, 95% CI 1.04–1.32, p = 0.010). Autism status was significantly associated with decreased sex hormone binding globulin (AOR = 0.65 per 50 nmol/L, 95% CI 0.55–0.78, p < 0.001) overall and when stratified by sex and term pregnancy status. The inverse association between sex hormone binding globulin and autism was independent of PNMS exposure. Limitations: The relative racial and ethnic homogeneity of Utah’s population limits the generalizability of study results. Although significant differences by autism status were identified in concentrations of sex hormone binding globulin overall and of estradiol in participant subgroups, differences by PNMS exposure failed to reach statistical significance, which may reflect insufficient statistical power. Conclusion: Both elevated maternal serum estradiol in males only and low maternal serum sex hormone binding globulin in both sexes are associated with increased autism risk. Further investigation is merited to identify how steroid, metabolic, and inflammatory processes can interact to influence neurodevelopment in early second trimester.

Scholarly productivity is a critical component of pharmacy faculty effort and is used for promotion and tenure decisions. Several databases are available to measure scholarly productivity; however, comparisons amongst these databases are lacking for pharmacy faculty. The objective of this work was to compare scholarly metrics from three commonly utilized databases and a social networking site focused on data from research-intensive colleges of pharmacy and to identify factors associated with database differences. Scholarly metrics were obtained from Scopus, Web of Science, Google Scholar, and ResearchGate for faculty from research-intensive (Carnegie Rated R1, R2, or special focus) United States pharmacy schools with at least two million USD in funding from the National Institutes of Health. Metrics were compared and correlations were performed. Regression analyses were utilized to identify factors associated with database differences. Significant differences in scholarly metric values were observed between databases despite the high correlations, suggestive of systematic variation in database reporting. Time since first publication was the most common factor that was associated with database differences. Google Scholar tended to have higher metrics than all other databases, while Web of Science had lower metrics relative to other databases. Differences in reported metrics between databases are apparent, which may be attributable to the time since first publication and database coverage of pharmacy-specific journals. These differences should be considered by faculty, reviewers, and administrative staff when evaluating scholarly performance.