The association of allostasis with alcohol use: A case-control study in males with and without alcohol use disorder.

BACKGROUND: Allostatic load (AL) is associated with a heightened predisposition to disease due to prolonged activation of biological stress-response systems. Alcohol use disorder (AUD) is known to activate these systems. The primary aim of the current study was to examine the relationship between AL and AUD. METHODS: Participants were males (100%) with DSM-IV Alcohol Dependence (n = 48) and healthy participants with no history of substance use disorder (n = 17). Participants with AUD were 4-6 weeks abstinent. The AL index used cortisol, interleukin-6 (IL-6), fibrinogen, tumor necrosis factor-alpha (TNFα), C-reactive protein (CRP), glucose, insulin, leptin, pulse, systolic blood pressure readings, diastolic blood pressure readings, and body mass index (BMI). Physiological dysregulation for each biological measure was determined based on values within the 25th or 75th percentiles; AL was calculated as the total number of physiologically dysregulated biological measures. RESULTS: No differences in mean AL scores between the cases and controls [t(63) = .48, p = .633] were observed. Among cases, AL was not associated with lifetime drinks per drinking day (F(2,42) = .42, p = .662), lifetime total drinks (F(2,42) = 0.48, p = .620), total drinks 6 months prior to participating in the study (F(2,43) = 0.58, p = .563), or drinks per drinking day at 3-month follow-up (F(2,35) = 1.93, p = .161). AL was negatively associated with drinks per drinking day 6 months prior to study participation (F(2,42) = 3.71, p = .033). CONCLUSIONS: The hypotheses were not supported. Given that alcohol is likely to lead to physiological dysregulation, the apparent absence of a relationship between biomarkers of cumulative stress as indicated by AL and drinking status was both unanticipated and remarkable. Based on the results, AL in the context of drinking status or drinking among males with AUD may not be applicable.

Exclusion of the non-English-speaking world from the scientific literature: Recommendations for change for addiction journals and publishers.

Background: While English is only the native language of 7.3% of the world's population and less than 20% can speak the language, nearly 75% of all scientific publications are English. Aim: To describe how and why scientific contributions from the non-English-speaking world have been excluded from addiction literature, and put forward suggestions for making this literature more accessible to the non-English-speaking population. Methods: A working group of the International Society of Addiction Journal Editors (ISAJE) conducted an iterative review of issues related to scientific publishing from the non-English-speaking world. Findings: We discuss several issues stemming from the predominance of English in the scientific addiction literature, including historical drivers, why this matters, and proposed solutions, focusing on the increased availability of translation services. Conclusion: The addition of non-English-speaking authors, editorial team members, and journals will increase the value, impact, and transparency of research findings and increase the accountability and inclusivity of scientific publications.

Addressing Structural Racism in Psychiatry With Steps to Improve Psychophysiologic Research.

Importance: The American Medical Association has acknowledged the public health threat posed by racism in medicine. While clinicians in psychiatry have echoed the sentiment, the research community has largely been silent. Current understanding of the biological domains that underlie psychiatric disorders was historically established by studying White populations, often leaving widely used treatments ineffective for Asian, Black, Hispanic, Indigenous, and other racial and ethnic minority individuals. This article addresses how undersampling of racial and ethnic minority individuals has led to overgeneralized physiological findings, the implications for development of psychiatric treatments, and steps to improve service to racially diverse communities. Observations: Three primary observations regarding differences associated with race and ethnicity have been addressed in the existing psychiatric research: misdiagnosis, medication nonadherence, and treatment efficacy and expression of adverse effects. While cultural factors have been discussed as potential factors associated with these differences, a lack of understanding of physiologic systems may be foundational to each of these issues. Recent evidence points to race differences in psychophysiological measures, likely attributed to factors including the lived experience of racism as opposed to inherent biological differences. This mounting evidence supports a reassessment of existing work to examine potential divergent patterns within racial and ethnic groups. The following strategies may improve understanding of the influence of racism on physiology, allowing clinicians to better address psychiatric symptoms and improve existing treatment approaches. Thus, psychiatric researchers need to (1) understand the historic and current terminology for race and ethnicity and use appropriate terms and categories as defined by sociologists, population health experts, and databases while respecting individuals' right to self-identify, (2) refine research questions, and (3) reexamine research data to determine whether patterns observed in largely White populations can extend to other groups. To appropriately implement these steps, researchers must accept the discomfort that accompanies growth, invite scientists from diverse backgrounds to participate, and use resources to increase diversity in recruitment of study participants. This will require a commitment from funding agencies to provide adequate support to recruit and investigate large, diverse samples. Conclusions and Relevance: To create more suitable medical treatments and improve the quality of care received by those with psychiatric conditions, further discussion is needed surrounding the physiologic toll that racism has had on multiple generations of racial and ethnic minority groups and how that may alter responsivity to biobehavioral interventions. To better inform psychiatric research, the resources provided must be expanded, basic physiologic studies should be replicated with more diverse samples and adequate analyses, and psychiatry scientists must reconsider approaches to clinical research.

Functional connectivity of dorsolateral prefrontal cortex predicts cocaine relapse: implications for neuromodulation treatment.

Relapse is one of the most perplexing problems of addiction. The dorsolateral prefrontal cortex is crucially involved in numerous cognitive and affective processes that are implicated in the phenotypes of both substance use disorders and other neuropsychiatric diseases and has become the principal site to deliver transcranial magnetic stimulation for their treatment. However, the dorsolateral prefrontal cortex is an anatomically large and functionally heterogeneous region, and the specific dorsolateral prefrontal cortex locus and dorsolateral prefrontal cortex-based functional circuits that contribute to drug relapse and/or treatment outcome remain unknown. We systematically investigated the relationship of cocaine relapse with functional circuits from 98 dorsolateral prefrontal cortex regions-of-interest defined by evenly sampling the entire surface of bilateral dorsolateral prefrontal cortex in a cohort of cocaine dependent patients (n = 43, 5 Fr) following a psychosocial treatment intervention. Cox regression models were utilized to predict relapse likelihood based on dorsolateral prefrontal cortex functional connectivity strength. Functional connectivity from only 3 of the 98 dorsolateral prefrontal cortex loci, one in the left and two in the right hemisphere, significantly predicted cocaine relapse with an accuracy of 83.9%, 84.6% and 85.4%, respectively. Combining all three loci significantly improved prediction validity to 87.5%. Protective and risk circuits related to these dorsolateral prefrontal cortex loci were identified that have previously been implicated to support 'bottom up' drive to use drug and 'top down' control over behaviour together with social emotional, learning and memory processing. Three dorsolateral prefrontal cortex-centric circuits were identified that predict relapse to cocaine use with high accuracy. These functionally distinct dorsolateral prefrontal cortex-based circuits provide insights into the multiple roles played by the dorsolateral prefrontal cortex in cognitive and affective functioning that affects treatment outcome. The identified dorsolateral prefrontal cortex loci may serve as potential neuromodulation targets to be tested in subsequent clinical studies for addiction treatment and as clinically relevant biomarkers of its efficacy. Zhai et al. identify three dorsolateral prefrontal cortex (dlPFC)-centric circuits that predict cocaine relapse with high accuracy, providing insights into the multiple roles of the dlPFC in brain functioning that affects treatment outcome and suggesting the dlPFC loci as potential neuromodulation targets for addiction treatment.

Alcohol Use Disorder Masks the Effects of Childhood Adversity, Lifetime Trauma, and Chronic Stress on Hypothalamic-Pituitary-Adrenal Axis Reactivity.

BACKGROUND: Individuals with alcohol use disorder (AUD) and those who have experienced traumas or chronic stress exhibit dysregulated hypothalamic-pituitary-adrenal (HPA) axis reactivity. Whether and how trauma and stress histories interact with AUD to affect HPA axis reactivity has not been assessed. METHODS: In the present study, 26 healthy male controls and 70 abstinent men with AUD were administered a pharmacologic probe [ovine corticotropin-releasing hormone (oCRH)] and psychosocial stressor to assess HPA axis reactivity. Plasma adrenocorticotropin hormone (ACTH) and cortisol were assessed every 10-20 minutes. Hierarchical clustering of multiple measures of trauma and stress identified 3 distinct clusters: childhood adversity, lifetime trauma, and chronic stress. General linear model procedures were used to examine main effects of group (AUD/control) and interaction effects of the 3 clusters upon net-integrated ACTH and cortisol response. RESULTS: We found that higher levels of childhood adversity, lifetime trauma, and chronic stress were each associated with blunted oCRH-induced ACTH reactivity in controls, but not in the AUD group. Recent chronic stress within the prior 6 months had the strongest influence upon ACTH reactivity in the control group, and lifetime trauma, the least. CONCLUSIONS: Childhood adversity, lifetime trauma, and chronic stress likely exert persistent, measurable effects upon HPA axis functioning in healthy controls. This association appears to be masked in individuals with AUD, potentially confounding studies examining the effects of stress, adversity, and/or trauma upon the HPA axis in this population during the protracted withdrawal phase of recovery. Future work targeting stress exposure and reactivity should consider the heightened effect of previous alcohol use relative to past adversity and trauma.

The Efficacy of Lidocaine in Disrupting Cocaine Cue-Induced Memory Reconsolidation.

RATIONAL: Cue-induced craving memories, linked to drug-seeking behaviors, require key molecular processes for memory reconsolidation. Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production. These processes are required for memory re-consolidation; inhibiting them may reduce cue-related craving memories in cocaine dependent subjects. OBJECTIVES: To assess the efficacy of lidocaine in decreasing cue-induced cocaine craving and cocaine use. METHODS: Treatment-seeking cocaine-dependent participants (n = 33, 25 men) were recruited. Personalized craving and relaxation scripts were developed. Participants were then randomly assigned in a double-blind design to either receive intravenous lidocaine immediately following a cocaine craving script (lidocaine/craving), saline following a craving script (saline/craving), or lidocaine following a relaxation script (lidocaine/relax). One week following the infusion, cue-induced craving was assessed in the same paradigm without an infusion. Cocaine use and craving were assessed for 4 weeks following infusion. RESULTS: The administration of lidocaine during craving induction (lidocaine/craving) did not decrease cue-induced craving during craving reactivation one week later or craving and cocaine use over the 4-week follow-up period compared to the saline/craving group. There were no significant differences in craving and cocaine use between the lidocaine/relax and saline/craving groups. CONCLUSION: Lidocaine administered following craving induction did not decrease subsequent cue-induced craving or cocaine use. Blocking the reconsolidation of craving-related memories with pharmacological agents remains an important area of investigation.

Brain activation and subjective anxiety during an anticipatory anxiety task is related to clinical outcome during prazosin treatment for alcohol use disorder.

BACKGROUND: Higher levels of anxiety, negative affect, and impaired emotion regulation are associated with alcohol use disorder (AUD) and contribute to relapse and worse treatment outcomes. Prazosin, while typically used to treat post-traumatic stress disorder (PTSD) and other anxiety disorders, has shown promise for treating AUD. In order to better understand these underlying neural processes in individuals with AUD, our aims in this study were to measure brain activation during an anticipatory anxiety task before treatment to determine whether observed patterns supported previous work. We then aimed to measure the effects of prazosin on patients with AUD and explore whether greater baseline anticipatory anxiety (as measured by subjective and neural measures) predicts better treatment outcomes. METHODS: Thirty-four individuals seeking treatment for AUD participated in a six-week placebo-controlled study of prazosin and underwent an anticipatory anxiety task during fMRI scans at baseline and three weeks. Alcohol use over six weeks was measured. RESULTS: Greater levels of subjective anxiety and deactivation in posterior cingulate cortex (PCC) and ventromedial prefrontal cortex (vmPFC) were observed during high-threat stimuli compared to low-threat stimuli. Compared to placebo, prazosin reduced subjective anxiety to high-threat stimuli but there were no observed significant effects of prazosin on brain activation during the task. However, AUD patients with greater vmPFC deactivation during high threat relative to low threat and patients with low baseline anticipatory anxiety during the task had worse clinical outcomes on prazosin. CONCLUSIONS: Deactivation in PCC and vmPFC to high-threat stimuli replicated previous work and shows promise for further study as a marker for AUD. Although prazosin did not affect brain activation in the regions of interest during the anticipatory anxiety task, subjective levels of anxiety and brain activation in vmPFC predicted treatment outcomes in individuals with AUD undergoing treatment with prazosin, highlighting individuals more likely to benefit from prazosin than others.

An insula-driven network computes decision uncertainty and promotes abstinence in chronic cocaine users.

The anterior insular cortex (AIC) and its interconnected brain regions have been associated with both addiction and decision-making under uncertainty. However, the causal interactions in this uncertainty-encoding neurocircuitry and how these neural dynamics impact relapse remain elusive. Here, we used model-based fMRI to measure choice uncertainty in a motor decision task in 61 individuals with cocaine use disorder (CUD) and 25 healthy controls. CUD participants were assessed before discharge from a residential treatment program and followed for up to 24 weeks. We found that choice uncertainty was tracked by the AIC, dorsal anterior cingulate cortex (dACC) and ventral striatum (VS), across participants. Stronger activations in these regions measured pre-discharge predicted longer abstinence after discharge in individuals with CUD. Dynamic causal modeling revealed an AIC-to-dACC-directed connectivity modulated by uncertainty in controls, but a dACC-to-AIC connectivity in CUD participants. This reversal was mostly driven by early relapsers (<30 days). Furthermore, CUD individuals who displayed a stronger AIC-to-dACC excitatory connection during uncertainty encoding remained abstinent for longer periods. These findings reveal a critical role of an AIC-driven, uncertainty-encoding neurocircuitry in protecting against relapse and promoting abstinence.

Implementing social justice in the transition from illicit to legal cannabis.

Background: The legalization of cannabis for adult use is being increasingly embraced in several countries and local entities. A driving force for these changes has been the individual, family, community, societal, and economic costs of cannabis prohibition, which have fallen most heavily upon disadvantaged minority populations.Objectives: In this review, we explore whether the legalization of cannabis has begun to correct the injustices of cannabis prohibition. Progress is assessed in five areas of social justice related to cannabis prohibition: expungement of previous arrests and convictions for cannabis-related crimes that are no longer illegal; consequences of cannabis-related offenses in a cannabis-legal environment; diversity of the cannabis-legal industry; funding of equity and/or restorative justice programs for those communities most affected by cannabis prohibition; and risks of cannabis legalization negatively impacting the populations that most suffered under the legacy of cannabis prohibition.Methods: Iterative and focused review.Results: There has been some progress in expunging previous cannabis-related convictions, particularly misdemeanors, and decreasing cannabis-related arrests. Encouraging diversity in the cannabis industry and the funding of equity programs has been very limited. There is no evidence to-date that populations that have suffered most as a result of cannabis prohibition are at increased risk from its legalization.Conclusions: Focused regulatory efforts and financial resources (from both cannabis revenue and savings from the abolition of cannabis prohibition) as well as more attentive data collection and analysis should be utilized to assure that all individuals experience the benefits, and avoid the consequences, of cannabis legalization.

Effect of Selective Serotonin Reuptake Inhibitors on Healthcare Utilization in Patients with Post-Traumatic Stress Disorder and Alcohol Use Disorder.

AIMS: The objective of this study is to address equivocation in estimates of selective serotonin reuptake inhibitor initiation (SSRI) effect on all-cause and alcohol-related ER visits, and medical or psychiatric admissions within 2 years of initial Post-Traumatic Stress Disorder (PTSD) diagnosis in patients with PTSD and Alcohol Use Disorder (AUD). METHODS: This study is a quasi-experimental, new-user-design cohort study of 3235 patients seen at the VA North Texas Healthcare System between January 1, 2000 and December 31, 2016. High dimensional propensity score (HDPS) techniques were used to estimate likelihood of SSRI initiation within 30 days of first PTSD diagnosis. Propensity scores were used to calculate weights for likelihood of SSRI initiation which were used to control for baseline covariates in estimations of SSRI medication effect on odds of each outcome occurring. RESULTS: Compared to those who did not receive SSRIs, patients prescribed an SSRI within 30 days showed significantly lower odds of alcohol-related ER visits (OR=0.668, 95%CI = 0.476 to 0.938, P = 0.02) and alcohol-related medical admissions (OR=0.583, 95%CI = 0.399 to 0.851, P = 0.005). LIMITATIONS: Inconsistent assessment of PTSD severity necessitated the use of HDPS models to control for baseline confounding. Our study design mimicked intent-to-treat trial design and therefore could not control for SSRI initiations after the 30-day grace period following initial PTSD diagnosis. CONCLUSIONS: SSRI initiation in patients with AUD and PTSD is associated with significantly reduced odds of alcohol-related medical hospitalization and alcohol-related ER visits within 2 years of first PTSD diagnosis. Additional studies are needed to verify these results.

Classification of cocaine-dependent participants with dynamic functional connectivity from functional magnetic resonance imaging data.

Static functional connectivity (FC) analyses based on functional magnetic resonance imaging (fMRI) data have been extensively explored for studying various psychiatric conditions in the brain, including cocaine addiction. A recently emerging, more powerful technique, dynamic functional connectivity (DFC), studies how the FC dynamics change during the course of the fMRI experiments. The aim in this paper was to develop a computational approach, using a machine learning framework, to determine if DFC features were more successful than FC features in the classification of cocaine-dependent patients and healthy controls. fMRI data were obtained from of 25 healthy and 58 cocaine-dependent participants while performing a motor response inhibition task, stop signal task. Group independent component analysis was carried out on all participant data to compute spatially independent components (ICs). Eight ICs were selected manually as relevant brain networks, which were used to classify healthy versus cocaine-dependent participants. FC and DFC measures of the chosen IC pairs were used as features for the classification algorithm. Support Vector Machines were used for both feature selection/reduction and participant classification. Based on DFC with only seven IC pairs, participants were successfully classified with 95% accuracy (and with 90% accuracy with three IC pairs), whereas static FC yielded only 81% accuracy. Visual, sensorimotor, default mode, and executive control networks, amygdala, and insula played the most significant role in the DFC-based classification. These findings support the use of DFC-based classification of fMRI data as a potential biomarker for the identification of cocaine dependence.

Systematic review of preclinical, clinical, and post-marketing evidence of bupropion misuse potential.

Background: Bupropion is a substituted cathinone compound widely used as a first line or add-on treatment for depression, smoking cessation, and more recently in combination with naltrexone for weight loss. As abuse of synthetic cathinone compounds has received more attention in recent years, concern about the misuse potential of bupropion has grown as well. Objectives: We review bupropion pharmacology and assessments of misuse potential including preclinical evidence, human studies, and post-marketing surveillance of bupropion misuse. Methods: This review reports the results of a systematic review of publications evaluating the potential for bupropion to be misused. Publications were identified using PubMed and Medline through Ovid® as well as iterative bibliographic searches. A summary of data from informal sources of information including substance-user experience from online forum entries is included. Results: Preclinical evidence demonstrates some potential for misuse based on psychomotor, discrimination, self-administration, and conditioned place preference tasks. However, this potential is less than that of commonly misused stimulants. Studies in human populations similarly indicate that bupropion shares interoceptive effects with other stimulants, but lacks some key reinforcing effects of other stimulants. In the real-world setting, misuse of bupropion occurs, but is uncommon. Adverse effects of bupropion misuse are frequently cited as significant barriers to obtaining any desired interoceptive effect. Conclusions: While bupropion demonstrates some potential for misuse, pharmacological differences from other structurally-related stimulants limit bupropion's reinforcing effects. Without additional data indicating susceptibility of specific populations to bupropion misuse, there is no empirical data suggesting a need to modify bupropion prescribing patterns.

Differences in pituitary-adrenal reactivity in Black and White men with and without alcohol use disorder.

BACKGROUND: Treatment-seeking men with alcohol use disorder (AUD) classically exhibit a blunted hypothalamic-pituitary-adrenal (HPA) axis response to pharmacologic and behavioral provocations during the early phases of abstinence from alcohol. Independent of alcohol, a significant muting of HPA axis reactivity is also observed among racial minority (e.g. Black) individuals. The effect of AUD upon the altered HPA axis response of racial minority individuals has not been explored. The current work represents a secondary analysis of race and AUD status among a sample of men. METHODS: Healthy male controls (17 White, 7 Black) and four-to six-week abstinent men with AUD (49 White, 13 Black) were administered a psychosocial stressor and two pharmacologic probes [ovine corticotropin releasing hormone (oCRH) and cosyntropin] to assess HPA axis reactivity. Plasma cortisol and adrenocorticotropin hormone (ACTH) were assessed at 10-20 min intervals prior to and following behavioral and pharmacological stimulation. Basal and net-integrated responses following provocations were analyzed to identify potential group differences. A measure of childhood adversity was also obtained to consider the implications of prior stressors upon HPA axis function. RESULTS: A three-fold increase in oCRH-induced ACTH was seen in Black men relative to White men regardless of AUD status. Adversity exerted a dampening effect on this pituitary sensitivity within Black controls only. Adjusted for adversity, a significant blunting effect of AUD status on ACTH reactivity was identified within White participants following oCRH. No group differences were present following cosyntropin administration. In response to the psychosocial stressor, White, but not Black, men with AUD experienced the expected blunting of cortisol reactivity relative to White controls. Rather, Black men with AUD exhibited greater cortisol reactivity relative to White men with AUD. CONCLUSIONS: Differences in HPA axis reactivity associated with race were present in men with and without AUD. Explanatory biological mechanisms of the relationship between alcohol use and/or stress, in both healthy and unhealthy populations, may require a reassessment in different racial populations.

A Multilevel Computational Characterization of Endophenotypes in Addiction.

Addiction is characterized by a profound intersubject (phenotypic) variability in the expression of addictive symptomatology and propensity to relapse following treatment. However, laboratory investigations have primarily focused on common neural substrates in addiction and have not yet been able to identify mechanisms that can account for the multifaceted phenotypic behaviors reported in the literature. To fill this knowledge gap theoretically, here we simulated phenotypic variations in addiction symptomology and responses to putative treatments, using both a neural model, based on cortico-striatal circuit dynamics, and an algorithmic model of reinforcement learning (RL). These simulations rely on the widely accepted assumption that both the ventral, model-based, goal-directed system and the dorsal, model-free, habitual system are vulnerable to extra-physiologic dopamine reinforcements triggered by addictive rewards. We found that endophenotypic differences in the balance between the two circuit or control systems resulted in an inverted-U shape in optimal choice behavior. Specifically, greater unbalance led to a higher likelihood of developing addiction and more severe drug-taking behaviors. Furthermore, endophenotypes with opposite asymmetrical biases among cortico-striatal circuits expressed similar addiction behaviors, but responded differently to simulated treatments, suggesting personalized treatment development could rely on endophenotypic rather than phenotypic differentiations. We propose our simulated results, confirmed across neural and algorithmic levels of analysis, inform on a fundamental and, to date, neglected quantitative method to characterize clinical heterogeneity in addiction.

Association of Biological Markers of Alcohol Consumption and Self-Reported Drinking with Hippocampal Volume in a Population-Based Sample of Adults.

AIMS: The current study examined a large community cohort to understand relationships between indicators of alcohol consumption and hippocampal volume. SHORT SUMMARY: Alcohol use measures were not associated with hippocampal volume in a population-based sample. However, alcohol consumption was associated with hippocampal volume reduction in subsets of the sample including subjects aged ≥50 years old, and those with none to moderate levels of depressive symptoms. METHODS: A total of 1848 adults with magnetic resonance imaging (MRI) and alcohol consumption data were included. Multiple linear regressions were performed with left or right hippocampal volume as dependent variables, and age, gender, race, education, body mass index, Quick Inventory of Depressive Symptomatology (QIDS-SR) scores, drinks per week (DPW), aspartate aminotransferase (AST), alanine aminotransferase (ALT), AST/ALT, γ-glutamyl transferase and mean corpuscular volume (MCV) as independent variables. Post hoc analyses were conducted to assess interactions of demographic factors and variables of interest (DPW, AST, ALT, AST/ALT, GGT and MCV). For statistically significant interactions, analyses were conducted in groups split by gender, depression (QIDS-SR scores ≥11 and <11) and age (≥50 and <50 years). RESULTS: Average alcohol consumption in the population was low (µ = 2.95 ± 6.7 DPW). Alcohol consumption measures were not significantly associated with hippocampal volume in the primary analysis. Exploratory analyses revealed significant associations between DPW and right hippocampal volume in participants with QIDS-SR scores <11 (B = -3.75, P = 0.02, CI = -6.97, -0.52) and in those aged ≥50 years (B = -4.844, P = 0.023 CI = -9.023 to -0.664). AST/ALT was significantly associated with right (B = -93.66, P = 0.022, CI = -173.64 to -13.68) and left hippocampal volume (B = -109.79 P = 0.008, CI = -190.97 to -28.61) in participants aged ≥50 but not <50 years. Gender differences were not observed. CONCLUSIONS: The findings suggest a relationship between alcohol use indicators and right hippocampal volume in non-depressed and older adults.

Brain intrinsic network connectivity in individuals with frequent tanning behavior.

BACKGROUND: Emergent studies suggest a bidirectional relationship between brain functioning and the skin. This neurocutaneous connection may be responsible for the reward response to tanning and, thus, may contribute to excessive tanning behavior. To date, however, this association has not yet been examined. OBJECTIVES: To explore whether intrinsic brain functional connectivity within the default mode network (DMN) is related to indoor tanning behavior. METHODS: Resting state functional connectivity (rsFC) was obtained in twenty adults (16 females) with a history of indoor tanning. Using a seed-based [(posterior cingulate cortex (PCC)] approach, the relationship between tanning severity and FC strength was assessed. Tanning severity was measured with symptom count from the Structured Clinical Interview for Tanning Abuse and Dependence (SITAD) and tanning intensity (lifetime indoor tanning episodes/years tanning). RESULTS: rsFC strength between the PCC and other DMN regions (left globus pallidus, left medial frontal gyrus, left superior frontal gyrus) is positively correlated with tanning symptom count. rsFC strength between the PCC and salience network regions (right anterior cingulate cortex, left inferior parietal lobe, left inferior temporal gyrus) is correlated with tanning intensity. CONCLUSION: Greater connectivity between tanning severity and DMN and salience network connectivity suggests that heightened self-awareness of salient stimuli may be a mechanism that underlies frequent tanning behavior. These findings add to the growing evidence of brain-skin connection and reflect dysregulation in the reward processing networks in those with frequent tanning.

The mixed message behind "Medication-Assisted Treatment" for substance use disorder.

The gap between treatment utilization and treatment need for substance use disorders (SUDs) remains a significant concern in our field. While the growing call to bridge this gap often takes the form of more treatment services and/or better integration of existing services, this perspective proposes that more effective labels for and transparent descriptions of existing services would also have a meaningful impact. Adopting the perspective of a consumer-based health-care model (wherein treatments and services are products and patients are consumers) allows us to consider how labels like Addiction-focused Medical Management, Medication-Assisted Treatment, Medication-Assisted Therapy, and others may actually be contributing to the underutilization problem rather than alleviating it. In this perspective, "Medication-Assisted Therapy" for opioid-use disorder (OUD) is singled out and discussed as inherently confusing, providing the message that pharmacotherapy for this disorder is a secondary treatment to other services which are generally regarded, in practice, as ancillary. That this mixed message is occurring amidst a nationwide "opioid epidemic" is a potential cause for concern and may actually serve to reinforce the longstanding, documented stigma against OUD pharmacotherapy. We recommend that referring to pharmacotherapy for SUD as simply "medication," as we do for other chronic medical disorders, will bring both clarity and precision to this effective treatment approach.