Models Of Addiction Research Articles

A non-human primate model of cocaine addiction: interpreting associations with increased vs. decreased dopamine function.

A non-human primate model of cocaine addiction: interpreting associations with increased vs. decreased dopamine function.

Sex- and age-specific effects on the development of addiction and compulsive-like drinking in rats

BackgroundBiological factors are known to influence disease trajectories and treatment effectiveness in alcohol addiction and preclinical and clinical evidence suggests that sex is an important factor influencing disease dynamics in alcohol dependence. Another critical factor is age at first intoxicating drink, which has been identified as a risk factor for later alcohol binging. Preclinical research allows prospective monitoring of rodents throughout the lifespan, providing very detailed information that cannot be acquired in humans. Lifetime monitoring in rodents can be conducted under highly controlled conditions, during which one can systematically introduce multiple biological and environmental factors that impact behaviors of interest.MethodsHere, we used the alcohol deprivation effect (ADE) rat model of alcohol addiction in a computerized drinkometer system, acquiring high-resolution data to study changes over the course of addictive behavior as well as compulsive-like drinking in cohorts of adolescent vs. adult as well as male vs. female rats.ResultsFemale rats drank more alcohol than male rats during the whole experiment, drinking much more weak alcohol (5%) and similar amounts of stronger alcohol solutions (10%, 20%); female rats also consumed more alcohol than male rats during quinine taste adulteration. Increased consumption in females compared to males was driven by larger access sizes of alcohol. Differences in circadian patterns of movement were observed between groups. Early age of onset of drinking (postnatal day 40) in male rats had surprisingly little impact on the development of drinking behavior and compulsivity (quinine taste adulteration) when compared to rats that started drinking during early adulthood (postnatal day 72).ConclusionsOur results suggest that there are sex-specific drinking patterns, not only in terms of total amount consumed, but specifically in terms of solution preference and access size. These findings provide a better understanding of sex and age factors involved in the development of drinking behavior, and can inform the preclinical development of models of addiction, drug development and exploration of options for new treatments.

Cell type-specific expression of the molecular players in mouse prefrontal cortex during cocaine addiction

Cocaine addiction is an issue that affects more than 5 million people in America per year. Although there has been much research into the genes and chemicals responsible for cocaine addiction, there are many specific questions left unanswered. Our experiment attempts to further previous research into certain molecular players. We follow up with their use of single-cell RNA sequencing on the prefrontal cortex cells of mice undergoing cocaine intravenous self-administration. Data of 12 samples from both saline and cocaine treated mice which are found on the Gene Expression Omnibus public database were retrieved. Using the Seurat function of RStudio, the data was merged into objects, normalized, clustered, and labeled into one of eight cell types. What resulted was a detailed UMAP plot displaying the clusters, their gene expression level, expression frequency, and their cell type. With this plot, we were able to determine the specific cell types that express the genes encoding the pre-established molecular players (∆FosB, MeCP2, and BDNF). When the analysis was expanded to a cell-type specific level, it was discovered some of these genes were selectively expressed in excitatory neurons and non-neuronal cells. Going further into the analysis, we determined the 6 genes with the most varied gene expression over the 3 stages of cocaine addiction for each of the 8 cell types. Overall, our computational analysis of publicly available transcriptome datasets from mouse addiction model provides new insights into the molecular basis of cocaine addiction.

The Role of Metabotropic Glutamate Receptor Subtype 5 in Mouse Models of Cocaine Addiction

Cocaine is a psychostimulant that is one of the most widely used illicit drugs, particularly in America. Cocaine addiction is a chronic relapsing disease that is characterized by drug craving and loss of inhibitory control. Animal models of psychiatric diseases are essential to identify underlying neural circuitry and to test the effectiveness of novel pharmacotherapies to prevent relapse. Current research using animal models indicates that type 5 metabotropic glutamate receptors may be of particular importance to the onset and maintenance of cocaine addiction. This literature review provides a general overview of the glutamate system, and the animal models frequently used in the study of addiction and summarizes peer-reviewed research focused on cocaine-induced adaptations to the type 5 metabotropic glutamate receptors in mice. Cocaine administration in mouse models induces a range of neural changes in the brain, reflecting the neuroadaptations associated with cocaine addiction. Cocaine-induced adaptations to type 5 metabotropic glutamate receptor vary by brain region and by methodological constraints. Key neural changes that occur in the mouse brain following cocaine administration include adaptations in the dopaminergic and glutamatergic systems. The interplay between mGluR5 and the dopamine system plays a significant role in the neurobiological adaptations that drive cocaine addiction. Lastly, we cover the potential efficacy of targeting this receptor as a novel therapeutic option to prevent cocaine relapse. Selective antagonists of this receptor have been studied for their potential therapeutic effects in mouse models of cocaine addiction. These compounds reduce the conditioned responses to drug-associated cues and reduce the motivation to seek cocaine, thereby inhibiting relapse-like behavior, and have been found to modulate synaptic plasticity in brain regions involved in addiction, such as the nucleus accumbens and prefrontal cortex. Overall, these compounds demonstrate promising effects in mouse models of cocaine addiction.

Multiple Risk Factors Precipitate Smoking Relapse: a Demonstration Using a Rat Model of Nicotine Addiction

Relapse to drug addiction behavior in abstinent subjects could be attributable to re-exposure to relevant environments (i.e., environmental cues), drug priming, and stressful life events. In particular, it is common for the abstinent subjects to be imposed with more than one risk factors at any social circumstance. Using a rat model of nicotine addiction, we demonstrated the behavioral effect of exposure to a combination of risk factors on relapse to nicotine-seeking behavior. Male Sprague-Dawley rats were trained to press a level to intravenously self-administer nicotine at a unit dose of 0.03 mg/kg/infusion. In the daily 60-min session, an auditory/visual stimulus was paired with each nicotine infusion so that the stimulus become a nicotine-conditioned cue. After the administration responses were extinguished without nicotine infusion, the reinstatement tests were conducted under five conditions: cue representation, nicotine priming, stress, cue/priming, and cue/stress. The results showed that nicotine priming, pharmacological stressor and re-presentation of the cue respectively reinstated lever responses. The combined presentation of these factors seemed to produce stronger effect. These laboratory findings confirmed the motivational effect of re-exposure to nicotine-associated environmental cues, nicotine priming and confrontation with stressful life events in abstinent smokers. This work would support for behavioral management, in addition to medications, to eliminate exposure to these risk factors.

The Stage-Based Model of Addiction-Using Drosophila to Investigate Alcohol and Psychostimulant Responses.

Addiction is a progressive and complex disease that encompasses a wide range of disorders and symptoms, including substance use disorder (SUD), for which there are few therapeutic treatments. SUD is the uncontrolled and chronic use of substances despite the negative consequences resulting from this use. The progressive nature of addiction is organized into a testable framework, the neurobiological stage-based model, that includes three behavioral stages: (1) binge/intoxication, (2) withdrawal/negative affect, and (3) preoccupation/anticipation. Human studies offer limited opportunities for mechanistic insights into these; therefore, model organisms, like Drosophila melanogaster, are necessary for understanding SUD. Drosophila is a powerful model organism that displays a variety of SUD-like behaviors consistent with human and mammalian substance use, making flies a great candidate to study mechanisms of behavior. Additionally, there are an abundance of genetic tools like the GAL4/UAS and CRISPR/Cas9 systems that can be used to gain insight into the molecular mechanisms underlying the endophenotypes of the three-stage model. This review uses the three-stage framework and discusses how easily testable endophenotypes have been examined with experiments using Drosophila, and it outlines their potential for investigating other endophenotypes.

Twisted memories: Addiction-related engrams are strengthened by desire thinking

Associative learning plays a central role in addiction by reinforcing associations between environmental cues and addiction-related information. Unsupervised learning models posit that memories are adjusted based on how strongly these representations are coactivated during the retrieval process. From a different perspective, clinical models of addiction posit that the escalation and persistence of craving may depend on desire thinking, a thinking style orienting to prefigure information about positive addiction-related experiences. In the present work, we tested the main hypothesis that desire thinking is a key factor in the strengthening of addiction-related associations. A group of adult smoking volunteers (N = 26) engaged in a period of desire thinking before performing an associative learning task in which neutral words (cues) were shown along with images (smoking-related vs. neutral context) at different frequencies. Two retrieval tests were administered, one immediately after encoding and the other after 24 h, to test how the recall of associations changed as a function of retention interval. Two control groups, smokers (N = 21) and non-smokers (N = 22), performed a similar procedure, with a neutral imagination task replacing desire thinking. Participants who engaged in desire thinking increased their performance from the first to the second retrieval test only for the most frequent smoking-related associations. Crucially, this selective effect was not observed in the two control groups. These results provide behavioral evidence in support of the idea that desire thinking plays a role in strengthening addiction-related associations. Thus, this thinking process may be considered a target for reconsolidation-based conceptualizations of, and treatments for, addiction.

Synaptic remodeling of GluA1 and GluA2 expression in the nucleus accumbens promotes susceptibility to cognitive deficits concomitant with downstream GSK3β mediated neurotoxicity in female mice during abstinence from voluntary oral methamphetamine

Stimulant-use disorders can present with long-term cognitive and mental health deficits. Little is known about the underlying molecular mechanisms perpetuating sex differences in cognitive and behavioral deficits in preclinical models of addiction to stimulants such as methamphetamine (MA). The current study investigated the neurochemical shifts underlying sex disparities in MA-induced working memory deficits and an addictive phenotype following abstinence from chronic MA abuse. We used our previously reported mouse model of voluntary oral methamphetamine administration (VOMA) consisting of an acquisition phase (days 1–14) characterized by escalating doses of MA and a binge phase (days 14–28) characterized by static doses. Female VOMA mice exhibited sustained MA consumption during the binge phase, demonstrating sex-specific vulnerabilities to the maintenance of MA addiction. The 8-arm radial maze was used to test spatial working memory performance following abstinence from VOMA. Results indicate working memory deficits correlated to higher MA consumption in females only. Hippocampal and accumbal tissue were collected and analyzed by immunoblotting. Female VOMA mice had decreased GluA1, but not GluA2, in the hippocampus, which may perpetuate synaptic destabilization and working memory deficits. Female-specific increases in GluA1 and p-GSK3β expression in accumbal tissue suggest vulnerability toward abstinence-induced drug craving and heightened downstream neurotoxicity. Our study reveals female-specific neurochemical shifts in hippocampal and accumbal AMPA receptor signaling following abstinence from chronic MA consumption that may perpetuate female susceptibility to MA-induced cognitive deficits. These data demonstrate a novel molecular pathway that would exacerbate memory deficits and perpetuate an addictive phenotype in female populations following MA abuse.

An empirical analysis of e-cigarette addiction

ABSTRACT This paper examines the role of addiction in influencing the demand for e-cigarettes using the Nielsen Retail Scanner Data and the Nielsen Consumer Panel Data between 2012 and 2017. With a comparison of a myopic addiction model, a forward-looking model, and a rational addiction model, this paper tests whether the consumption of e-cigarettes is addictive and rational. Results from both the macro data and the microdata support the rational addictiveness of e-cigarettes. Applying an OLS method and an instrumental variable method in causal inference, results show that the long-run price elasticity estimates are larger than the estimates of the short-run price elasticity of demand for e-cigarettes. Estimates of both long-run and short-run elasticities are greater than one, −1.50 and −1.05, suggesting e-cigarette demand is elastic in both the long run and short run.

Discussing evidence on the components model of addiction. A commentary on Fournier et al. (2023)

Fournier and colleagues have recently examined whether the components model of addiction includes peripheral features of addiction not indicative of a disorder. The authors conducted factor analyses and network analyses of responses (N = 4,256) to the Bergen Social Media Addiction Scale. Their results showed that a bidimensional solution best fitted the data and that two items examining salience and tolerance loaded on a factor not associated with symptoms of psychopathology signifying salience and tolerance as peripherical features of addiction to social media.A reanalysis of the data (focused on the internal structure of the scale) was believed necessary considering that previous studies consistently demonstrated the one-factor solution of the scale and that four independent samples were analysed as a single sample potentially limiting the results of the original study.Findings of the reanalyses of Fournier and colleagues’ data provided additional support for a one-factor solution of the scale. Potential explanations of the findings and suggestions for future research were elaborated.

BAY 11-7085 attenuates alcohol dependence induced spontaneous withdrawal syndrome in mice

Upregulation of nuclear factor kappa B plays a prominent role in drug addiction. The current study explored the neuroprotective effect of BAY 11-7085, a selective nuclear factor kappa B inhibitor, on the spontaneous alcohol withdrawal syndrome in mouse model of alcohol addiction. Administration of Alcohol (2g/kg, 10%, v/v, oral), once daily for 7 days. Assessment of behavioral parameters and exploratory parameters was done on 7 day after 8 hr. of the last ethanol administration for a period of 120 minutes. Various behavioural parameters were conducted like wall climbing test, composite withdrawal severity score, anxiety like behaviour assessed in open field and elevated plus test. Treatment with BAY 11-7085 markedly and dose dependently (p<0.05) attenuated spontaneous alcohol withdrawal syndrome in mice measured in terms of withdrawal severity score, wall climbing, locomotor sensitization by open field test and anxiety. Thus, it is suggested that activation of nuclear factor kappa B pathway is involved in the development of alcohol dependence induced withdrawal syndrome. Modulation of NFK-β may be used as therapeutic agent to overcome the problems related with alcohol dependence.

Toluene-Induced Behavioral Sensitization is Attenuated by Voluntary Physical Exercise and Social Interaction

Toluene-based inhalants found in some common products, such as paint thinner or glues, may be used to induce intoxication. Though addiction may be one of its most detrimental consequences, treatment options are insufficient or limited. Environmental enrichment (EE) refers to housing conditions that enhance sensory, cognitive, and motor stimulation. This paradigm induces beneficial effects in a variety of animal models of brain disorders, and also in animal models of drug addiction. Previous studies have shown that toluene induces behavioral sensitization and that EE treatment can reduce this response. Since EE comprises a variety of elements, the aim of the present study was to group mice into five different types of EE-shaping housing conditions (4 weeks) and to identify which of them are key elements in attenuating toluene-induced behavioral sensitization. The experimental groups were: Standard housing with conspecifics; EE with conspecifics; Toys stimulation with conspecifics; Exercise wheels with conspecifics; and Wheel and toy isolated. Mice in Standard housing and previously exposed to toluene exhibited high locomotor activity, suggesting behavioral sensitization. When animals were exposed to toluene and then housed in EE with conspecifics or Exercise wheels with conspecifics conditions an attenuation of behavioral sensitization was observed ( p < 0.001; 100% and 75% effectiveness, respectively). Toy with conspecifics housing also reduced behavioral sensitization, but in a less proportion than the two previous mentioned treatments ( p < 0.002; 33.5% effectiveness). Mice in the Wheel and toy isolated housing did not show significant changes in the assessed behavior ( p = 0.061; 12.4% effectiveness). We suggest that exercise and social interaction are the key enriched main elements to attenuate toluene-induced behavioral sensitization. Our results advise preclinical strategies for inhalant abuse interventions based on social interactions and physical exercise. Also, they provide guidelines to develop experimental models with diverse environments and groups that lead us to understand the complexity of environmental enrichment.

Optimal Consumption Under a Habit-Formation Constraint: The Deterministic Case

We formulate and solve a deterministic optimal consumption problem to maximize the discounted constant relative risk aversion utility of an individual’s consumption-to-habit process assuming they only invest in a riskless market and that they are unwilling to consume at a rate below a certain proportion of their consumption habit. Increasing increases the degree of addictiveness of habit formation, with (respectively, ) corresponding to nonaddictive (respectively, completely addictive) model. We derive the optimal consumption policies explicitly in terms of the solution of a nonlinear free-boundary problem, which we analyze in detail. Impatient individuals (or, equivalently, those with more addictive habits) always consume above the minimum rate; thus, they eventually attain the minimum wealth-to-habit ratio. Patient individuals (or, equivalently, those with less addictive habits) consume at the minimum rate if their wealth-to-habit ratio is below a threshold and above it otherwise. By consuming patiently, these individuals maintain a wealth-to-habit ratio that is greater than the minimum acceptable level. Additionally, we prove that the optimal consumption path is hump-shaped if the initial wealth-to-habit ratio is either (1) larger than a high threshold or (2) below a low threshold and the agent is more risk seeking (that is, less risk averse). Thus, we provide a simple explanation for the consumption hump observed by various empirical studies.

Effects of different iodine levels on the DNA methylation of intrinsic apoptosis-associated genes and analysis of gene-environment interactions in patients with autoimmune thyroiditis.

Iodine is an essential nutrient that may change the occurrence of autoimmune thyroiditis (AIT). Apoptosis and DNA methylation participate in the pathogenesis and destructive mechanism of AIT. We detected the methylation and the expression of mRNA of intrinsic apoptosis-associated genes (YWHAG, ING4, BRSK2 and GJA1) to identify the potential interactions between the levels of methylation in these genes and different levels of iodine. 176 adult patients with AIT in Shandong Province, China, were included. The MethylTargetTM assay was used to verify the levels of methylation. We used PCR to detect the mRNA levels of the candidate genes. Interactions between methylation levels of the candidate genes and iodine levels were evaluated with multiplicative and addictive interaction models and GMDR. In the AIT group, YWHAG_1 and six CpG sites and BRSK2_1 and eight CpG sites were hypermethylated, whereas ING4_1 and one CpG site were hypomethylated. A negative correlation was found between methylation levels of YWHAG and mRNA expression. The combination of iodine fortification, YWHAG_1 hypermethylation and BRSK2_1 hypermethylation was significantly associated with elevated AIT risk. A four-locus model (YWHAG_1 × ING4_1 × BRSK2_1 × iodine level) was found to be the best model of the gene-environment interactions. We identified abnormal changes in the methylation status of YWHAG, ING4 and BRSK2 in patients with AIT in different iodine levels. Iodine fortification not only affected the methylation levels of YWHAG and BRSK2 but also interacted with the methylation levels of these genes and may ultimately increase the risk of AIT.

Preventive Education Model Based on Multiculturalism and Local Wisdom for Reducing the Impact of Drugs among School Students in Madura

This study aims to investigate the implementation of a preventive education model based on multiculturalism and local wisdom for dealing with the effects of drugs among school students in Madura. This research uses a qualitative approach with a case study method. The research participants were students from two schools in Madura who had been exposed to or were at risk of being exposed to drugs. Data was collected through interviews and analyzed using the thematic analysis technique. The research results showed that forms of drug control among students in Madura are carried out in 3 ways, namely medical rehabilitation is carried out using screening results data which is used as a reference for assessment and followed up by administering doses of drugs in the form of methadone pills and buprenorphine; non-medical rehabilitation is carried out using a psychological approach which includes counselling services, community therapy and spiritual therapy with talqin al dzikr through the qadiqah qadir naqsyabandiyah; and further rehabilitation is carried out using the Disease Model of Addiction through the development of vocational-based skills and activity management. The development of a model for overcoming the effects of drugs among students in Madura based on multiculturalism and Madurese local wisdom consists of three categories, namely: spiritual collaboration with certain amaliyah, spirituality collaboration with local wisdom of the koteka'an type, and collaboration of various types of local wisdom in the form of koteka'an.

Rhynchophylline inhibits methamphetamine dependence via modulating the miR-181a-5p/GABRA1 axis

Ethnopharmacological relevanceUncaria rhynchophylla (Miq.) Miq. ex Havil. is a plant species that is routinely devoted in traditional Chinese medicine to treat central nervous system disorders. Rhynchophylline (Rhy), a predominant alkaloid isolated from Uncaria rhynchophylla (Miq.) Miq. ex Havil., has been demonstrated to reverse methamphetamine-induced (METH-induced) conditioned place preference (CPP) effects in mice, rats and zebrafish. The precise mechanism is still poorly understood, thus further research is necessary. Aim of studyThis study aimed to investigate the role of miRNAs in the inhibitory effect of Rhy on METH dependence. Materials and methodsA rat CPP paradigm and a PC12 cell addiction model were established. Microarray assays were used to screen and identify the candidate miRNA. Behavioral assessment, real-time PCR, dual-luciferase reporter assay, western blotting, stereotaxic injection of antagomir/agomir and cell transfection experiments were performed to elucidate the effect of the candidate miRNA and intervention mechanism of Rhy on METH dependence. ResultsRhy successfully reversed METH-induced CPP effect and the upregulated miR-181a-5p expression in METH-dependent rat hippocampus and PC12 cells. Moreover, suppression of miR-181a-5p by antagomir 181a reversed METH-induced CPP effect. Meanwhile, overexpression of miR-181a-5p by agomir 181a in combination with low-dose METH (0.5 mg/kg) elicited a significant CPP effect, which was blocked by Rhy through inhibiting miR-181a-5p. Finally, the result demonstrated that miR-181a-5p exerted its regulatory role by targeting γ-aminobutyric acid A receptor α1 (GABRA1) both in vivo and in vitro. ConclusionThis finding reveals that Rhy inhibits METH dependence via modulating the miR-181a-5p/GABRA1 axis, which may be a promising target for treatment of METH dependence.

A serial mediation model of social media addiction and college students’ academic engagement: the role of sleep quality and fatigue

BackgroundIt has been documented that social media addiction (SMA) has a detrimental effect on college students’ academic engagement. However, the mechanisms underlying this association are not well understood. This study aimed to determine the serial mediation effects of sleep quality and fatigue on the relationship between SMA and academic engagement among college students.MethodsA cross-sectional survey was conducted with 2661 college students (43.3% males, mean age = 19.97 years). The participants completed the Bergen Social Media Addiction Scale, the Utrecht Student Work Engagement Scale for Students, the Pittsburgh Sleep Quality Index, and the Fatigue Assessment Scale. The serial mediation effects were examined using Model 6 in the Hayes’ PROCESS macro for SPSS.ResultsThe results showed that SMA among college students had a direct negative relationship with their academic engagement (Effect = − 0.051, 95% CI: −0.087 to − 0.015). In addition, sleep quality and fatigue mediated the relationship between SMA and academic engagement both independent and serially, with the independent mediation effect of sleep quality being − 0.031 (95% CI: −0.048 to − 0.016), the independent mediation effect of fatigue being − 0.109 (95% CI: −0.133 to − 0.088), and the serial mediation effect of sleep quality and fatigue being − 0.080 (95% CI: −0.095 to − 0.066). The total indirect effect of the three mediation paths was 80.9%.ConclusionsDecreased academic engagement caused by SMA can be aggravated by poor sleep quality and fatigue. Strengthening supervision and intervention in social media use among college students, supplemented by attention to psychosomatic health, including sleep quality and fatigue could promote their engagement in academic work.

Neurotensin and Alcohol Use Disorders: Towards a Pharmacological Treatment.

Harmful alcohol use is responsible for a group of disorders collectively named alcohol use disorders (AUDs), according to the DSM-5 classification. The damage induced by alcohol depends on the amount, time, and consumption patterns (continuous and heavy episodic drinking). It affects individual global well-being and social and familial environments with variable impact. Alcohol addiction manifests with different degrees of organ and mental health detriment for the individual, exhibiting two main traits: compulsive drinking and negative emotional states occurring at withdrawal, frequently causing relapse episodes. Numerous individual and living conditions, including the concomitant use of other psychoactive substances, lie in the complexity of AUD. Ethanol and its metabolites directly impact the tissues and may cause local damage or alter the homeostasis of brain neurotransmission, immunity scaffolding, or cell repair biochemical pathways. Brain modulator and neurotransmitter-assembled neurocircuitries govern reward, reinforcement, social interaction, and consumption of alcohol behaviors in an intertwined manner. Experimental evidence supports the participation of neurotensin (NT) in preclinical models of alcohol addiction. For example, NT neurons in the central nucleus of the amygdala projecting to the parabrachial nucleus strengthen alcohol consumption and preference. In addition, the levels of NT in the frontal cortex were found to be lower in rats bred to prefer alcohol to water in a free alcohol-water choice compared to wild-type animals. NT receptors 1 and 2 seem to be involved in alcohol consumption and alcohol effects in several models of knockout mice. This review aims to present an updated picture of the role of NT systems in alcohol addiction and the possible use of nonpeptide ligands modulating the activity of the NT system, applied to experimental animal models of harmful drinking behavior mimicking alcohol addiction leading to health ruin in humans.

Does working hard really pay off? Testing the temporal ordering between workaholism and job performance

AbstractIs workaholism an antecedent or a product of job performance? Or is there a reciprocation between workaholism and job performance? To address this issue, we collected data from 352 employees using a two‐wave panel design in Study 1, and 247 employee–supervisor dyads using a three‐wave panel design in Study 2. In Study 1, job performance had a negative effect on working compulsively but not working excessively, whereas, in Study 2, job performance had a positive effect on working compulsively and working excessively. Across the two studies, working compulsively and working excessively had no lagged effect on job performance. Collectively, these findings suggest that job performance causes workaholism rather than the other way around, challenging the traditional view. The inconsistent effects of job performance across working excessively and working compulsively underscore the importance of separating workaholism dimensions. Collectively, our findings challenge the validity of the reinforcement theory of learning and the psychological model of addiction in explaining the development of workaholism. We encourage future research to address when job performance has a positive, negative or null effect on workaholism to further improve our understanding of the causal relationship between workaholism and job performance.

Sexual minority stress and substance use: An investigation of when and under what circumstances minority stress predicts alcohol and cannabis use at the event-level.

Sexual minority women and gender diverse (SMWGD) individuals are at elevated risk for alcohol and cannabis use disorders compared with cisgender, heterosexual women. This has been attributed to the unique stressors that SMWGD experience (i.e., sexual minority stress); however, recent studies have found mixed evidence for a link between sexual minority stress and substance use. The current manuscript introduces and tests a novel theoretical model derived from integrating minority stress theory and the multistage model of drug addiction to explain these mixed findings. We used data from a 30-day ecological momentary assessment (EMA) study of substance use among SMWGD to determine whether event-level associations between enacted stigma (bias from others) and same-/next-day alcohol and cannabis use are dependent on an individual's typical pattern of substance use (e.g., frequency, quantity, motives, and substance use disorder [SUD] symptoms). Findings indicate that enacted stigma predicted an increased likelihood of alcohol and cannabis use among those who used frequently and those who had a probable alcohol or cannabis use disorder and predicted a decreased likelihood of use among those who used less frequently. Enacted stigma also predicted cannabis (but not alcohol) use among those who reported high coping motives for use. Findings provide initial evidence in support of an integrated model of minority stress theory and the multistage model of drug addiction. Findings suggest that alcohol and cannabis use disorder interventions for SMWGD would benefit from addressing sexual minority stress and coping skill-building. (PsycInfo Database Record (c) 2023 APA, all rights reserved).