Stress could increase delay discounting in subjects with bulimia nervosa and alcohol use disorder (AUD), meaning that the short-term benefits of coping through eating or drinking outweigh the long-term negative consequences. Therefore, this study explores differences in delay discounting between patients and healthy controls, the impact of stress on food and alcohol delay discounting and associated changes in brain activity.

A total of 102 female participants (AUD, 27; bulimia nervosa, 25; healthy controls, 50) underwent repeated functional magnetic resonance imaging scanning. Initially, all participants performed a monetary delay discounting task (DDT), followed by a food or alcohol DDT before and after stress induction. Specifically, those with bulimia nervosa completed a food DDT, those with AUD completed an alcohol DDT and healthy controls were randomly allocated to one or either DDT.

Participants with AUD, but not healthy controls, displayed a higher discounting of alcohol after stress. Healthy controls, but not those with bulimia nervosa, had nominally higher discounting rates of food following stress, although not significant following multiple testing correction. Participants with AUD displayed a lower activity of the right supplementary motor area while discounting alcohol after stress. Healthy controls showed a lower activity of the frontal cortex and a higher activity of the motor cortex while discounting food after stress, while those with bulimia nervosa displayed a higher activity of the occipital cortex.

The results suggest that, in subjects with AUD, stress induces neurobiological changes that cause them to prefer more immediately available alcohol. However, the results observed in participants with bulimia nervosa suggest a more complex relation between stress and food.

DNA methylation plays a crucial role in gene regulation and has been implicated in various neuropsychiatric disorders, including alcohol use disorder (AUD). The rs27072 polymorphism within the SLC6A3 gene has been studied in addictive disorders; however, its role in epigenetic modifications remains unclear. This study investigates the methylation levels of CpG sites near rs27072 and their potential associations with AUD, personality traits, and environmental stressors.

One hundred twenty-four male participants (66 patients with AUD and 58 controls) were analyzed for DNA methylation at CpG islands proximal to the rs27072 locus. The personality traits and life stress events were assessed in all participants.

AUD patients had a lower methylation level than healthy controls (p = 0.003 for total average). However, the results changed to borderline significance after adjusting for clinical covariates in the analysis (p = 0.042), and the genotype at rs27072 did not modulate the methylation levels. There is high novelty seeking (p < 0.001), and more bad life events in patients with AUD than healthy controls (p < 0.001). Additionally, no significant correlations were found between methylation levels and personality traits or life stress scores (p > 0.05).

The methylation of the SLC6A3 gene may be marginally associated with AUD; however, the rs27072 genotype, personality, and life stress may not be directly linked to epigenetic modifications. Cross-sectional epigenetic studies may not establish causality; future studies with larger, more diverse cohorts and longitudinal designs are warranted to elucidate the complex interplay in AUD pathophysiology.

Alcohol use disorder (AUD) is a major global health concern associated with limited treatment efficacy and high relapse rates. Recent research highlights the gut microbiota as a critical modulator of AUD pathophysiology through its influence on the gut–brain axis. Chronic alcohol consumption induces gut dysbiosis, characterised by reduced microbial diversity, impaired gut barrier function and systemic inflammation, which perpetuate neuroinflammation, stress dysregulation and neurotransmitter imbalances. These disruptions exacerbate addiction-related behaviours, contributing to the cycle of dependence and relapse. This critical review synthesises current evidence on the role of gut microbiota in AUD, examining the mechanisms linking dysbiosis to addiction and evaluating therapeutic interventions such as probiotics, prebiotics, faecal microbiota transplantation (FMT), psychobiotics and dietary modifications.

The strategies evaluated show significant potential in restoring microbial homeostasis and improving AUD outcomes, but challenges remain, including gaps in mechanistic understanding, variability in methodologies, and barriers to clinical translation.

There is a need for multi-omics research, personalised medicine approaches and integrated treatment models to advance microbiota-based therapies. Gut microbiota-targeted strategies might then transform AUD management, offering innovative and personalised solutions for addiction recovery.

Understanding the factors influencing alcohol use disorder (AUD) treatment outcomes is essential. More knowledge about patient characteristics that predict treatment outcomes can help personalise interventions, improve treatment planning and address the needs of specific subgroups. The frequency of treatment attendance may also affect drinking outcomes after treatment. Despite research efforts, uncertainty remains about how patient factors and treatment attendance influence treatment outcomes.

To examine how patient factors and treatment attendance predict high- or low-risk drinking at the end of treatment.

We used data (N = 92) from a multisite observational study of treatment-seeking individuals with AUD attending group treatment. Sociodemographic measures, alcohol and substance use measures, cognitive functioning, psychological distress, personality functioning and quality of life were screened in univariate analyses. Significant variables were entered into a binary logistic regression model.

Individuals with a higher percentage of treatment attendance (odds ratio 0.96 [95% CI 0.93, 0.96]) and with greater responsiblity scores on the Severity Indices of Personality Functioning (odds ratio 0.30 [95% CI 0.14, 0.64]) had a decreased likelihood of high-risk drinking at treatment end. Substance use, psychological distress and cognitive functioning were not associated with drinking levels at the end of treatment.

A higher percentage of treatment attendance has a minor effect on drinking levels. Being more responsible, as reflected in higher scores on the responsibility domain, reduces the likelihood of high-risk drinking at the end of treatment. Clinicians are encouraged to screen and assess personality functioning when planning treatment for individuals with AUD.

This study examines the prospective associations of alcohol and drug misuse with suicidal behaviors among service members who have left active duty. We also evaluate potential moderating effects of other risk factors and whether substance misuse signals increased risk of transitioning from thinking about to attempting suicide.

US Army veterans and deactivated reservists (N = 6,811) completed surveys in 2016–2018 (T1) and 2018–2019 (T2). Weights-adjusted logistic regression was used to estimate the associations of binge drinking, smoking/vaping, cannabis use, prescription drug abuse, illicit drug use, alcohol use disorder (AUD), and drug use disorder (DUD) at T1 with suicide ideation, plan, and attempt at T2. Interaction models tested for moderation of these associations by sex, depression, and recency of separation/deactivation. Suicide attempt models were also fit in the subgroup with ideation at T1 (n = 1,527).

In models controlling for socio-demographic characteristics and prior suicidality, binge drinking, cannabis use, prescription drug abuse, illicit drug use, and AUD were associated with subsequent suicidal ideation (AORs = 1.42–2.60, ps < .01). Binge drinking, AUD, and DUD were associated with subsequent suicide plan (AORs = 1.23–1.95, ps < .05). None of the substance use variables had a main effect on suicide attempt; however, interaction models suggested certain types of drug use predicted attempts among those without depression. Additionally, the effects of smoking/vaping and AUD differed by sex. Substance misuse did not predict the transition from ideation to attempt.

Alcohol and drug misuse are associated with subsequent suicidal behaviors in this population. Awareness of differences across sex and depression status may inform suicide risk assessment.

Externalizing and internalizing pathways may lead to the development of substance use behaviors (SUBs) and substance use disorders (SUDs), which are all heritable phenotypes. Genetic correlation studies have indicated differences in the genetic susceptibility between SUBs and SUDs. We investigated whether these substance use phenotypes are differently related to externalizing and internalizing problems at a genetic level.

We analyzed data from genome-wide association studies (GWAS) of four SUBs and SUDs, five externalizing traits, and five internalizing traits using the bivariate causal mixture model (MiXeR) to estimate genetic overlap beyond genetic correlation.

Two distinct patterns were found. SUBs demonstrated high genetic overlap but low genetic correlation of shared variants with internalizing traits, suggesting a pattern of mixed effect directions of shared genetic variants. Conversely, SUDs and externalizing traits exhibited considerable genetic overlap with moderate to high positive genetic correlation of shared variants, suggesting concordant effect direction of shared risk variants.

These results highlight the importance of the externalizing pathway in SUDs as well as the limited role of the internalizing pathway in SUBs. As MiXeR is not intended for the identification of specific genes, further studies are needed to reveal the underlying shared mechanisms of these traits.

The prevalence of alcohol use disorder among older adults is increasing, with this population being particularly vulnerable to alcohol’s detrimental effects. While knowledge of preventative factors is scarce, physical activity has emerged as a potential modifiable protective factor. This study aimed to examine associations between alcohol consumption and physical activity in a large-scale, multi-national prospective study of the older adult population.

Longitudinal data from the SHARE study on physical activity, alcohol consumption, demographic, socioeconomic, and health variables, were analyzed in older adults. Individual-level data were examined using logistic regression models. Both cross-sectional and longitudinal models were calculated to account for potential latency in the association between physical activity and alcohol consumption.

The study included 3133 participants from 13 countries. Higher physical activity levels were significantly associated with higher alcohol consumption in cross-sectional (p = 0.0004) and longitudinal analyses (p = 0.0045) over a median follow-up of 6 years. While the presence of depressive symptoms and higher educational attainment were associated with higher alcohol consumption, female sex and persons with lower perceived health showed lower frequency of alcohol consumption. Additionally, the country of residence also proved to be a relevant factor for alcohol consumption.

Higher levels of physical activity showed an association with higher alcohol consumption in older adults. Future research should investigate whether this association is causal and underpinned by neurobiological, social, or methodological factors.

Extant literature implicates the role of glucagon-like peptide-1 (GLP-1) and GLP-1 receptor agonists (GLP-1RAs) on modulating alcohol-associated behaviours, with a particular emphasis of these agents on neural circuits subserving reward and appetite control. Herein, we explore the potential effects of GLP-1RAs on alcohol-associated behaviours in brain regions implicated in reward processing facilitating the repurposing of these agents for the treatment and prevention of problematic drinking. Understanding how GLP-1’s analogues interact with alcohol-related behaviours may underscore the development of therapeutic strategies for alcohol use disorder (AUD) and those with comorbid metabolic disorders.

A systematic review was conducted, wherein relevant literature was identified through Web of Science, PubMed, and OVID (MedLINE, Embase, AMED, PsycInfo, JBI EBP) from database inception to October 27th, 2024. Preclinical and clinical studies examining the association between GLP-1RAs and alcohol-related behaviours were assessed.

Preclinical studies (n = 19) indicate that GLP-1RAs attenuate alcohol-related behaviours, with exenatide demonstrating significant dose-dependent effects in high alcohol-consuming phenotypes. Semaglutide and liraglutide are associated with reduced alcohol intake, though their effects were often transient. In human studies (n = 2) with AUD, semaglutide significantly reduced alcohol consumption, while exenatide showed mixed results, with reductions in alcohol drinking within high BMI subpopulations.

Extant preclinical and clinical literature provides preliminary support for the potential therapeutic role of GLP-1RAs in attenuating alcohol consumption and preference. There is a need for large well controlled studies evaluating the effect of GLP-1RAs as a treatment strategy for behavioural modifications in individuals living with alcohol use disorder.

Associations between childhood trauma, neurodevelopment, alcohol use disorder (AUD), and posttraumatic stress disorder (PTSD) are understudied during adolescence.

Using 1652 participants (51.75% female, baseline Mage = 14.3) from the Collaborative Study of the Genetics of Alcoholism, we employed latent growth curve models to (1) examine associations of childhood physical, sexual, and non-assaultive trauma (CPAT, CSAT, and CNAT) with repeated measures of alpha band EEG coherence (EEGc), and (2) assess whether EEGc trajectories were associated with AUD and PTSD symptoms. Sex-specific models accommodated sex differences in trauma exposure, AUD prevalence, and neural development.

In females, CSAT was associated with higher mean levels of EEGc in left frontocentral (LFC, ß = 0.13, p = 0.01) and interhemispheric prefrontal (PFI, ß = 0.16, p < 0.01) regions, but diminished growth in LFC (ß = −0.07, p = 0.02) and PFI (ß = −0.07, p = 0.02). In males, CPAT was associated with lower mean levels (ß = −0.17, p = 0.01) and increased growth (ß = 0.11, p = 0.01) of LFC EEGc. Slope of LFC EEGc was inversely associated with AUD symptoms in females (ß = −1.81, p = 0.01). Intercept of right frontocentral and PFI EEGc were associated with AUD symptoms in males, but in opposite directions. Significant associations between EEGc and PTSD symptoms were also observed in trauma-exposed individuals.

Childhood assaultive trauma is associated with changes in frontal alpha EEGc and subsequent AUD and PTSD symptoms, though patterns differ by sex and trauma type. EEGc findings may inform emerging treatments for PTSD and AUD.

Machine learning could predict binge behavior and help develop treatments for bulimia nervosa (BN) and alcohol use disorder (AUD). Therefore, this study evaluates person-specific and pooled prediction models for binge eating (BE), alcohol use, and binge drinking (BD) in daily life, and identifies the most important predictors.

A total of 120 patients (BN: 50; AUD: 51; BN/AUD: 19) participated in an experience sampling study, where over a period of 12 months they reported on their eating and drinking behaviors as well as on several other emotional, behavioral, and contextual factors in daily life. The study had a burst-measurement design, where assessments occurred eight times a day on Thursdays, Fridays, and Saturdays in seven bursts of three weeks. Afterwards, person-specific and pooled models were fit with elastic net regularized regression and evaluated with cross-validation. From these models, the variables with the 10% highest estimates were identified.

The person-specific models had a median AUC of 0.61, 0.80, and 0.85 for BE, alcohol use, and BD respectively, while the pooled models had a median AUC of 0.70, 0.90, and 0.93. The most important predictors across the behaviors were craving and time of day. However, predictors concerning social context and affect differed among BE, alcohol use, and BD.

Pooled models outperformed person-specific models and the models for alcohol use and BD outperformed those for BE. Future studies should explore how the performance of these models can be improved and how they can be used to deliver interventions in daily life.

Problematic drinking frequently co-occurs with depression among young adults, but often remains unaddressed in depression treatment. Evidence is insufficient on whether digital alcohol interventions can be effective in this young comorbid population. In a randomized controlled trial, we examined the effectiveness of Beating the Booze (BtB), an add-on digital alcohol intervention to complement depression treatment for young adults.

Participants were randomized to BtB + depression treatment as usual (BTB + TAU, n = 81) or TAU (n = 82). The primary outcome was treatment response, a combined measure for alcohol and depression after 6-month follow-up. Secondary outcomes were number of weekly drinks (Timeline Follow-back) and depressive symptoms (Center for Epidemiologic Studies Depression scale). Treatment response was analyzed using generalized linear modeling and secondary outcomes using robust linear mixed modeling.

Low treatment response was found due to lower than expected depression remission rates. No statistically significant between-group effect was found for treatment response after 6-month follow-up (odds ratio 2.86, p = 0.089, 95% confidence interval [CI] 0.85–9.63). For our secondary outcomes, statistically significant larger reductions in weekly drinks were found in the intervention group after 3-month (B = −4.00, p = 0.009, 95% CI −6.97 to −1.02, d = 0.27) and 6-month follow-up (B = −3.20, p = 0.032, 95% CI −6.13 to −0.27, d = 0.23). We found no statistically significant between-group differences on depressive symptoms after 3-month (B = −0.57, p = 0.732, 95% CI −3.83 to 2.69) nor after 6-month follow-up (B = −0.44, p = 0.793, 95% CI −3.69 to 2.82).

The add-on digital alcohol intervention was effective in reducing alcohol use, but not in reducing depressive symptoms and treatment response among young adults with co-occurring depressive disorders and problematic alcohol use.

Pre-registered on October 29, 2019 in the Overview of Medical Research in the Netherlands (OMON), formerly the Dutch Trial Register(https://onderzoekmetmensen.nl/en/trial/49219).

Although the link between alcohol involvement and behavioral phenotypes (e.g. impulsivity, negative affect, executive function [EF]) is well-established, the directionality of these associations, specificity to stages of alcohol involvement, and extent of shared genetic liability remain unclear. We estimate longitudinal associations between transitions among alcohol milestones, behavioral phenotypes, and indices of genetic risk.

Data came from the Collaborative Study on the Genetics of Alcoholism (n = 3681; ages 11–36). Alcohol transitions (first: drink, intoxication, alcohol use disorder [AUD] symptom, AUD diagnosis), internalizing, and externalizing phenotypes came from the Semi-Structured Assessment for the Genetics of Alcoholism. EF was measured with the Tower of London and Visual Span Tasks. Polygenic scores (PGS) were computed for alcohol-related and behavioral phenotypes. Cox models estimated associations among PGS, behavior, and alcohol milestones.

Externalizing phenotypes (e.g. conduct disorder symptoms) were associated with future initiation and drinking problems (hazard ratio (HR)⩾1.16). Internalizing (e.g. social anxiety) was associated with hazards for progression from first drink to severe AUD (HR⩾1.55). Initiation and AUD were associated with increased hazards for later depressive symptoms and suicidal ideation (HR⩾1.38), and initiation was associated with increased hazards for future conduct symptoms (HR = 1.60). EF was not associated with alcohol transitions. Drinks per week PGS was linked with increased hazards for alcohol transitions (HR⩾1.06). Problematic alcohol use PGS increased hazards for suicidal ideation (HR = 1.20).

Behavioral markers of addiction vulnerability precede and follow alcohol transitions, highlighting dynamic, bidirectional relationships between behavior and emerging addiction.