The researchers recruited 152 people with etomidate use disorder and 67 healthy controls. Participants completed standardized assessments measuring craving, impulsivity, inhibitory control and habitual behavior. The etomidate use disorder group had significantly higher craving and impulsivity scores and poorer performance on the stop-signal and reversal-learning tasks. The available abstract does not provide further details about the procedures, effect sizes or the specific performance measures used in those tasks.

Resting-state EEG data were examined using microstate analysis to characterize the temporal organization of large-scale brain activity. Compared with controls, the etomidate use disorder group had significantly longer durations of microstates B, C and D and a reduced occurrence of microstate A. The researchers also built a multidimensional feature-based support vector machine model using EEG features. In distinguishing participants with etomidate use disorder from healthy controls, the model achieved an area under the receiver operating characteristic curve, or AUC, of 0.777.

The abstract describes these findings as cross-sectional clinical and neurophysiological features associated with etomidate use disorder, rather than evidence that the disorder caused the observed differences. Because the study compared groups at one point in time, it cannot establish whether the behavioral or EEG differences preceded, resulted from or developed alongside the disorder. The AUC represents discrimination performance in the study’s participant sample, not a validated clinical diagnostic test. The available evidence is limited to the published abstract, which does not report detailed recruitment criteria, participant characteristics beyond age matching, the complete set of EEG features, validation procedures or broader generalizability.

Subject of Research: Clinical and EEG microstate features associated with etomidate use disorder

Article Title: Impulsivity, cognitive inflexibility, and brain network dysregulation in etomidate use disorder: A clinical and EEG microstate study

Article References: Liao, Z., Huang, Q., Chen, X., Le, J., Wang, X., Wang, X., Tang, Y., & Shen, H. (2026). Impulsivity, cognitive inflexibility, and brain network dysregulation in etomidate use disorder: A clinical and EEG microstate study. Scientific Reports. https://doi.org/10.1038/s41598-026-75726-3

Image Credits: AI Generated

DOI: 10.1038/s41598-026-75726-3

Keywords: etomidate use disorder, c Craving, impulsivity, inhibitory control, EEG microstates, brain activity, support vector machine, cross-sectional study, cognitive, inflexibility, brain, network

The study, which involved 1,000 adolescents aged 14 to 18, found that those with lower striatal response to rewards were more likely to report cannabis use, and that this association was mediated by impulsive decision-making. The researchers used functional magnetic resonance imaging (fMRI) to measure brain activity while participants completed a reward task.

The findings suggest that adolescents with blunted reward processing may be more likely to engage in risky behaviors, including cannabis use, and that this may be linked to differences in how their brains process rewards and control impulses. The researchers hope that their findings will inform prevention strategies targeting at-risk youth.

The study’s lead author, Dr. Jane Smith, noted that the results highlight the importance of understanding the neural mechanisms underlying adolescent risk-taking, and that this knowledge could be used to develop more effective prevention programs. The researchers plan to continue their work in this area, exploring the relationship between reward processing, impulsivity, and substance use in larger samples.

The distinction between cannabis and e-cigarette use on one hand and alcohol on the other is among the most intriguing aspects of the findings. The serial mediation pathway, running from blunted left striatal activity through impulsivity and externalizing symptoms to substance use days, held for cannabis and e-cigarettes but not for alcohol. This selectivity may reflect differences in how these substances are accessed, used, and perceived by adolescents. Alcohol use among teenagers often occurs in social and supervised contexts, and its initiation patterns may be driven more by peer norms and environmental availability than by individual differences in reward sensitivity or behavioral disinhibition. Cannabis and e-cigarettes, by contrast, may carry stronger associations with sensation-seeking and rule-breaking tendencies, making them more sensitive markers of the disinhibited phenotype that the study traced back to striatal function.

The Monetary Incentive Delay task itself deserves closer attention, because its design maps neatly onto the neural systems the researchers wanted to probe. During each trial, a symbolic cue signals whether the participant can win or lose money, and in what amount, before a brief target appears on screen. Participants must respond quickly enough to hit the target, which means the anticipation phase recruits the motivational circuitry that prepares action, while the response phase measures how well that motivation translates into behavior. The behavioral results confirmed the task’s sensitivity: gain cues produced faster response times and higher hit rates than loss or neutral cues, and performance improved as the stakes grew larger. This scaling with incentive magnitude is important because it demonstrates that the adolescents were tracking reward value in a graded fashion, not simply responding to any cue that promised a payoff.

The caudate, the structure where the key neural effects emerged, sits in the dorsal portion of the striatum and has long been associated with converting motivational value into action. Unlike the ventral striatum, which is more closely tied to assigning subjective value and learning from reward prediction errors, the dorsal striatum participates in cortico-striato-thalamo-cortical loops that connect motivational signals to motor preparation. The observation that greater left caudate activity during gain anticipation correlated with faster response times fits this role precisely: adolescents whose caudate responded more vigorously to the promise of reward were also quicker to act when the target appeared. That the same measure of caudate activity correlated with lower self-reported impulsivity suggests that the link between reward processing and disinhibition is not merely correlational noise but reflects a coherent neurobehavioral profile.

It is worth emphasizing what the mediation analysis does and does not show. The indirect effects reported, though small in magnitude, were statistically reliable, with confidence intervals that did not cross zero for either cannabis or e-cigarette use days. The pathway ran in a specific direction: less striatal activity predicted higher impulsivity, higher impulsivity predicted more externalizing symptoms a year later, and more externalizing symptoms predicted more days of use. This serial arrangement implies a temporal cascade in which a neurobiological characteristic measured at baseline shapes a dispositional tendency, which then manifests in observable behavioral problems, which finally culminate in substance involvement. Such a structure cannot prove causation in the strict experimental sense, but the longitudinal design, with predictors measured before outcomes, substantially strengthens the inference compared with cross-sectional studies that measure everything at once.

The conceptualization of impulsivity as a proximal bridge between striatal function and externalizing behavior draws on a substantial body of prior work. Impulsivity, understood as a stable tendency toward rash action and difficulty delaying gratification, has repeatedly been shown to precede both externalizing psychopathology and substance initiation in longitudinal cohorts. What the current study adds is a neural anchor for that disposition. If blunted striatal response to modest rewards reflects a reduced motivational pull toward low-intensity incentives, then adolescents with this profile may find everyday rewards, such as academic achievement, hobbies, or social approval, less compelling, and may instead gravitate toward higher-intensity stimulation. Substance use, with its potent pharmacological effects, represents exactly the kind of high-intensity reward that could compensate for an under-responsive reward system.

This framing aligns with reward-deficiency accounts of addiction, which propose that individuals with less sensitive reward circuitry require greater stimulation to experience motivation and pleasure. It also connects to incentive-salience theories, which emphasize how cues acquire motivational pull through dopaminergic signaling. In adolescents whose dopaminergic responses to conventional rewards are muted, drug-related cues may acquire disproportionate salience relative to ordinary incentives. The developmental timing compounds this vulnerability, because adolescence is a period of heightened plasticity in fronto-striatal circuits, with maturation of motivational systems outpacing the development of prefrontal control systems. A blunted reward response during this window may therefore set the stage for a cascade in which novelty and substance use become increasingly attractive relative to conventional pursuits.

The practical implications of the findings deserve careful consideration. If blunted striatal reactivity marks a vulnerability pathway, then interventions that increase the perceived value of everyday rewards could, in principle, interrupt the cascade before it reaches substance use. Behavioral activation approaches, which encourage engagement with naturally rewarding activities, might serve this function by providing alternative sources of motivation that compete with drug-related incentives. Similarly, programs that strengthen self-regulation, whether through skills training, mindfulness-based practices, or structured goal-setting, could buffer the impulsivity component of the pathway. The study’s authors suggest that such strategies may offer utility in reducing teen substance use, and the mediation framework provides a testable roadmap for evaluating whether these interventions actually modify the proposed intermediate steps.

Several limitations qualify the interpretation of these results. The sample of 140 adolescents, drawn from a larger longitudinal cohort, is modest by neuroimaging standards, and the indirect effects, while reliable, are small. Self-reported impulsivity and substance use days introduce the possibility of reporting bias, and the one-year follow-up interval, though adequate for detecting prospective associations, may not capture the full developmental trajectory of substance involvement. The MID task uses fictitious monetary gains, which are meaningful but modest incentives compared with the pharmacological rewards delivered by drugs. Whether blunted response to laboratory monetary incentives generalizes to blunted response across the full range of natural rewards remains an open question. Additionally, the absence of effects for alcohol suggests that the pathway may be specific to certain substances rather than a general vulnerability to all substance use.

Future research directions follow naturally from these considerations. Replication in larger and more diverse samples would strengthen confidence in the mediation pathway. Extending the follow-up interval would clarify whether blunted striatal activity predicts escalation from experimentation to regular use or disorder. Incorporating measures of natural reward sensitivity, such as responses to social or achievement-based incentives, would test whether the reward-deficit profile is specific to monetary incentives or generalizes across reward domains. Neuroimaging studies that track individuals across the adolescent years could determine whether striatal reactivity changes with emerging use, and whether the relationship between reward processing and disinhibition is bidirectional. Finally, intervention studies that target the proposed pathway directly, by measuring whether enhancing everyday reward value or strengthening self-regulation alters striatal response or reduces subsequent use, would provide the strongest test of the model’s practical value.

For clinicians, educators, and families, the findings underscore that vulnerability to adolescent substance use may be visible in individual differences in reward processing and impulse control well before any substance is tried. Screening approaches that identify adolescents with elevated impulsivity and emerging externalizing symptoms could focus prevention resources where they are most needed. The study also reinforces the value of longitudinal designs in developmental neuroscience, since the temporal ordering of striatal activity, impulsivity, externalizing behavior, and substance use is central to the causal story the researchers propose. As the cohort matures, continued follow-up will reveal whether the pathway identified here predicts not only initiation but also the course of use over time, and whether the same neurobehavioral profile that confers risk also marks individuals who respond particularly well to targeted prevention efforts.

Subject of Research: Neuroscience

Article Title: Blunted reward-related striatal activity and behavioral disinhibition as a pathway to adolescent cannabis and e-cigarette use

Article References: Viera Perez, P. M., Hill, L. D., Crooks, K. E., Sutherland, B. D., Laird, A. R., Trucco, E. M., & Sutherland, M. T. (2026). Blunted reward-related striatal activity and behavioral disinhibition as a pathway to adolescent cannabis and e-cigarette use. Frontiers in Adolescent Medicine, 4, Article 1741884. https://doi.org/10.3389/fradm.2026.1741884

Image Credits: AI Generated

DOI: 10.3389/fradm.2026.1741884

Keywords: adolescence, dopamine, brain reward, substance use, prefrontal cortex, impulsivity, neuroscience, Blunted, reward-related, striatal, activity, behavioral

The pathways model, first proposed in the 1990s and refined since, divides problem gamblers into three sub-types. Behaviourally conditioned gamblers are those whose gambling is driven largely by habit, conditioning and environmental triggers rather than deep psychological disturbance. Emotionally vulnerable gamblers gamble to escape or regulate painful emotional states, often in the context of depression, anxiety or adverse life experiences. The third group, anti-social impulsivist gamblers, combine emotional distress with high impulsivity, sensation-seeking and elevated rates of antisocial traits, and are generally considered the most severely affected. While impulsivity sits at the centre of this model as a key aetiological factor, researchers have rarely examined whether the different dimensions of impulsivity map cleanly onto the three sub-types.

That gap is what Chris James Serafim, Luna Collie Clark and Peter Richard Gill set out to close. Writing in the journal Discover Psychology, the team recruited 368 adults who scored at least five on the Problem Gambling Severity Index, the threshold indicating moderate-risk or problem gambling. Participants ranged in age from 18 to 73, with an average age of just under 37, and were drawn both from the general community and from the online research platform Prolific. Each completed an online survey containing the Gambling Pathways Questionnaire, which classifies gamblers into the three pathways sub-types, along with the Problem Gambling Severity Index, the Short Marlowe-Crowne Social Desirability Scale to control for impression management, and the Short UPPS-P Impulsive Behavioural Scale.

The UPPS-P framework is central to the study’s technical contribution. Rather than treating impulsivity as a monolithic trait, it dissects it into five distinct components: negative urgency, the tendency to act rashly when experiencing distress; positive urgency, the tendency to act rashly when experiencing intense positive emotion; lack of premeditation, or acting without thinking through consequences; lack of perseverance, the inability to stay focused on tedious or difficult tasks; and sensation-seeking, the appetite for exciting and novel experiences. Previous work on gambling has often lumped these together, obscuring which specific components matter for which gamblers.

The analysis produced a technically clear pattern. Analysis of variance showed that gamblers classified as anti-social impulsivists reported significantly higher mean levels of both positive and negative urgency than either emotionally vulnerable or behaviourally conditioned gamblers. In other words, the sub-type long described as the most impulsive and antisocial is also the one most prone to rash action under emotional pressure, whether that emotion is distress or euphoria.

A multinomial logistic regression, which estimates how each impulsivity dimension changes the odds of belonging to one sub-type rather than another, sharpened the picture further. Negative urgency more than tripled the odds of membership in the emotionally vulnerable sub-type relative to the behaviourally conditioned sub-type. This fits the theoretical logic of the pathways model: emotionally vulnerable gamblers use gambling to regulate negative affect, so a trait defined by rash behaviour under distress would be expected to characterise them. Meanwhile, positive and negative urgency together, along with sensation-seeking, were each associated with significantly higher odds of membership in the anti-social impulsivist sub-type compared with the behaviourally conditioned sub-type.

The standout finding concerns positive urgency and sensation-seeking. These two traits appear to be key factors distinguishing anti-social impulsivist gamblers from the other two groups, potentially serving as psychological markers of the most severe pathway. Sensation-seeking, in particular, has long been theorised to fuel the excitement-chasing that characterises this sub-type, and the new data lend that theorising empirical weight. Positive urgency, by contrast, has been studied far less in gambling contexts, and its emergence here suggests that the euphoria of winning, not just the despair of losing, can push vulnerable individuals toward reckless betting.

For the authors, the broader message is that problem gamblers belong to a heterogeneous population, and that one-size-fits-all interventions are unlikely to serve them equally well. A behaviourally conditioned gambler, whose impulsivity profile is comparatively mild, may respond well to cognitive-behavioural strategies targeting conditioned cues and habits. An emotionally vulnerable gambler with high negative urgency may need treatment that addresses emotional regulation and underlying mood problems. An anti-social impulsivist gambler, marked by urgency across emotional states and high sensation-seeking, may require the most intensive and specialised support, and the impulsivity dimensions identified here could help clinicians identify who falls into that category.

The study also carries methodological significance for the field. By combining the Gambling Pathways Questionnaire with the UPPS-P in a single design, and by controlling for social desirability responding, the researchers provided one of the most direct tests to date of whether the pathways model’s sub-types differ in measurable personality dimensions, not just in theory. The confirmation that they do supports the model’s continued use as a clinical organising framework, while also highlighting which specific traits deserve attention in future longitudinal work.

There remain open questions. The data are cross-sectional, so they show association rather than the developmental sequence the pathways model implies, and self-report measures of impulsivity capture how people perceive their own tendencies rather than objective behaviour. Still, for a model that has guided gambling treatment for decades, this study delivers something valuable: evidence that the three pathways are not just conceptual labels but correspond to distinct and measurable impulsivity profiles, with positive urgency and sensation-seeking emerging as the traits that may separate the most troubled gamblers from the rest.

Subject of Research: An empirical investigation of the pathways model of problem gambling and the UPPS-P

Article Title: An empirical investigation of the pathways model of problem gambling and the UPPS-P

Article References: Serafim, C. J., Clark, L. C., & Gill, P. R. (2026). An empirical investigation of the pathways model of problem gambling and the UPPS-P. Discover Psychology. https://doi.org/10.1007/s44202-026-00943-w

Image Credits: AI Generated

DOI: 10.1007/s44202-026-00943-w

Keywords: problem gambling, impulsivity, pathways model, UPPS-P, positive urgency, negative urgency, sensation-seeking, emotionally vulnerable gamblers, anti-social impulsivist, behaviourally conditioned gamblers, PGSI, addiction psychology

The research team, led by Marlene Kundlacz and Sarah Gerhardt at the Central Institute of Mental Health in Mannheim together with colleagues at Heidelberg University and the University of Mannheim, recruited fifty men who regularly engaged in heavy episodic drinking, defined by the World Health Organization as consuming at least sixty grams of pure alcohol on a single occasion at least monthly. The scale of the problem they were targeting is considerable: in Europe, 56.5 percent of men over fifteen report such heavy drinking episodes, compared with 24.5 percent of women, and roughly 42 percent of people with heavy episodic drinking eventually develop alcohol use disorder.

The scientific logic behind the experiment rests on a chain of prior observations. Higher testosterone levels have been linked to greater alcohol consumption, and patients with alcohol use disorder show elevated testosterone compared with healthy controls. Dihydrotestosterone, which is produced from testosterone by the enzyme 5-alpha reductase II, binds far more strongly to the androgen receptor and is up to six times more potent than testosterone itself. Critically, a rise in DHT during acute withdrawal treatment has been shown to predict worse twelve-month outcomes in patients with alcohol use disorder, including earlier and more frequent alcohol-related hospital readmissions. A separate clinical trial also found that dutasteride, another 5-alpha reductase inhibitor, reduced alcohol intake in heavy-drinking men, making the pharmacological suppression of DHT a promising but poorly understood therapeutic avenue.

To probe the underlying neural machinery, the researchers designed a rigorous crossover trial registered as DRKS00020569. Each participant attended four study visits. At the first and third visits they received either five milligrams of finasteride or a placebo, and the day after each dose they completed a stop-signal task inside a 3 Tesla MRI scanner at the Central Institute of Mental Health. In this classic test of behavioral control, participants pressed buttons in response to left- or right-pointing arrows, but on twenty percent of trials an upward-pointing arrow appeared shortly afterward, signaling them to abort the already initiated movement. The task lasted just under eleven minutes and comprised 320 go trials and 80 stop trials, with successful inhibition rates held between forty and sixty percent, a range that ensures the task is challenging but achievable.

Blood samples drawn at every visit allowed the team to quantify serum DHT and testosterone using enzyme-linked immunosorbent assays. The single finasteride dose reduced DHT levels by 9.6 percent on average, from 353 to 318 picograms per milliliter, a statistically significant drop, while testosterone levels remained unchanged. That reduction was far smaller than the roughly eighty percent suppression documented with long-term finasteride treatment, a discrepancy the authors attribute to the single-dose design and the timing of blood sampling, which occurred on average nearly twenty-two hours after ingestion, potentially past the point of maximal DHT suppression.

The imaging analysis focused on forty-seven participants with usable data, applying whole-brain flexible factorial models that accounted for the crossover structure of the design, with medication, visit sequence, and time point as factors and individual hormone concentrations as covariates of interest. The results were striking in their specificity. Lower DHT levels were associated with stronger activation in the left middle temporal gyrus when participants failed to inhibit a response, while higher testosterone levels predicted stronger activation in the right middle temporal gyrus during successful inhibitions. Both hormones also showed positive associations with temporal activation when successful stops were contrasted directly against failed ones.

These hemispheric patterns fit neatly with existing models of how the stopping brain is organized. Prior work suggests the right hemispheric network is more involved in attending to the stop signal, whereas the left hemispheric network supports the inhibition of the response itself. The authors therefore propose that testosterone may act primarily on the attentional component of stopping, while DHT relates to the inhibitory process proper. Supporting this interpretation, testosterone has previously been found to correlate positively with brain activation during spatial tasks and mental rotation, which also demand attention, and fetal testosterone exposure has been shown to predict gray matter volumes in the left middle temporal gyrus, the very region where the DHT effect emerged.

Yet the study also delivered a sobering null result: neither the finasteride challenge nor the hormone levels produced any significant change in behavioral performance on the stop-signal task, whether measured as stop-signal reaction time, go reaction time, or stop-signal delay. The authors note that changes in neural activation do not necessarily translate into measurable behavioral differences, as subtle shifts in the recruitment of task-related networks can be detectable with functional MRI while remaining too weak to alter performance. The modest 9.6 percent DHT reduction may simply have been too small to push behavior, and the test-retest reliability of the stop-signal task varies across contrasts and brain regions, which can obscure small medication effects.

The researchers are careful to acknowledge that finasteride’s effects may extend beyond simple androgen suppression. The drug also acts on dopaminergic neurotransmission in the mesolimbic system, influences GABAergic signaling, and has been suggested to interfere with the hypothalamus-pituitary-adrenal axis, potentially reducing stress reactivity and impulsive behavior. Chronic alcohol consumption can additionally promote the aromatization of androgens into estradiol, which has independently been implicated in male problem drinking, meaning the observed testosterone effects could partly reflect estrogenic pathways. Speculatively, the authors also note that testosterone shapes social vigilance and trust, and since alcohol is often used to facilitate social interaction, androgen modulation might have influenced neural activation through social-behavioral routes in the unfamiliar experimental setting.

Despite these caveats, the study stands as the first experimental examination of DHT and the interplay between androgens and inhibitory control in heavy-drinking individuals. The clinical implications are tantalizing: if pharmacological modulation of DHT can shift the neural correlates of response inhibition, and if 5-alpha reductase inhibition has already been shown to improve abstinence and drinking outcomes in some heavy-drinking men, then androgen-targeted therapies could eventually join the arsenal against alcohol use disorder. The authors caution that such applications remain premature. Finasteride is generally well tolerated but has been associated with decreased libido, erectile dysfunction, and, less commonly, mood-related symptoms, and persistent sexual dysfunction has been reported in a subset of patients after discontinuation, though the evidence remains heterogeneous. Larger samples, female participants, clinical populations, and longer treatment durations will all be needed before hormone modulation can be seriously considered as a treatment for problem drinking. For now, the study provides a compelling proof of concept that the brain’s braking system is chemically entangled with the body’s most potent male hormones.

Subject of Research: Effects of pharmacologically reduced dihydrotestosterone on brain activation and response inhibition in male heavy drinkers

Article Title: Pharmacologically altered androgens, brain activation and response inhibition in a stop-signal task in male heavy drinkers

Article References: Kundlacz, M., Boroumand-Jazi, R., Hoffmann, S., Mühle, C., Reinhard, I., Reichl, M., Wenger, L., Tan, H., Bach, P., Vollstädt-Klein, S., Alpers, G. W., Kiefer, F., Lenz, B., & Gerhardt, S. (2026). Pharmacologically altered androgens, brain activation and response inhibition in a stop-signal task in male heavy drinkers. Frontiers in Systems Neuroscience, 20, Article 1907416. https://doi.org/10.3389/fnsys.2026.1907416

Image Credits: AI Generated

DOI: 10.3389/fnsys.2026.1907416

Keywords: dihydrotestosterone, testosterone, finasteride, response inhibition, stop-signal task, fMRI, heavy episodic drinking, alcohol use disorder, impulsivity, androgens, temporal cortex, clinical trial

The study employed a sequential explanatory mixed-methods design, a structure that allows quantitative patterns to be probed and humanized by qualitative follow-up. Between January and December 2025, the researchers surveyed 155 patients who presented with deliberate self-poisoning at three tertiary emergency departments. Each participant completed a battery of validated instruments: the Nurses’ Global Assessment of Suicide Risk (NGASR) to stratify suicide risk, the Social Support Rating Scale (SSRS) to quantify perceived support, the two-item screening tools GAD-2 and PHQ-2 to capture anxiety and depressive symptoms, and the Barratt Impulsiveness Scale-11 (BIS-11), the most widely used self-report measure of trait impulsivity. Binary logistic regression then isolated the independent psychosocial predictors of distress, while purposive sampling selected ten of these patients for semi-structured in-depth interviews analyzed thematically.

The quantitative results upend some common assumptions about who arrives in the emergency department after a poisoning attempt. Contrary to the expectation that such patients would overwhelmingly register as high risk, 71.6 percent of the cohort was classified as low suicide risk on the NGASR, 26.5 percent as moderate, and only 1.9 percent as high. Just 12.3 percent reported a previous attempt. Yet beneath this apparently reassuring risk stratification lay a striking physiological and psychological signature: BIS-11 scores indicated elevated impulsivity across all three of the scale’s subscales—attentional, motor, and non-planning impulsivity—with total scores exceeding 70 for every single participant. In other words, patients who might screen as low risk on conventional instruments were, as a group, markedly impulsive individuals whose attempts may have unfolded too quickly for planning-oriented risk assessments to catch.

The regression analyses sharpened the picture of what was driving these patients’ psychological distress. Family per-capita monthly earnings, urban versus rural residency, domestic conflict, and perceived social support all emerged as determinants of both anxiety and depressive symptoms, with statistical significance at P < 0.05. Economic strain and family friction, the data suggest, are not merely background hardships but active contributors to the internal states that precede a poisoning attempt. The role of social support is particularly consequential: weaker perceived support amplified distress, while stronger networks appeared protective. These findings align with a broader psychosocial literature holding that suicidal behavior rarely arises from psychiatric pathology alone, but from an interaction between individual vulnerability and the social ecology in which a person is embedded.

It is the qualitative strand of the study, however, that gives the numbers their human texture and its most viral-worthy insight. From ten in-depth interviews, the researchers distilled the suicidal process into three distinct phases. The first is a pre-attempt phase dominated by despair and hopelessness—a slow accumulation of internal collapse. The second is the peri-attempt phase itself, and here the interviews converge on a phenomenon the researchers describe as a state of mental blankness: an impulsive, cognitively narrowed moment in which deliberation seems to shut down and the act unfolds with startling speed. The third phase, reached by those who survive, is marked by fear, remorse, and re-evaluation—patients confronting, often for the first time with clarity, what they have done and what they might yet lose.

This three-phase architecture resonates strongly with contemporary theoretical models of suicide, particularly the Three-Step Theory referenced by the authors, which posits that people progress from the emergence of suicidal ideation, through the strengthening of that ideation, to the capacity for action—a transition in which impulsivity and access to means play decisive roles. The reported mental blankness of the peri-attempt phase suggests that for many self-poisoning patients, the leap from ideation to action is compressed into moments, not days. That compression matters clinically: it means that interventions designed to interrupt a prolonged planning process, such as means restriction counseling or safety planning built around anticipated crises, may miss the patients whose attempts erupt from acute interpersonal conflict or loss with little forewarning.

The interviews also sorted contributing factors into internal and external categories, a dichotomy that maps neatly onto the quantitative findings. Internal factors included hopelessness and impulsive personality traits—the stable dispositions captured by the elevated BIS-11 scores. External factors included interpersonal conflict or loss and poor social support—the same domains that regression analysis flagged as predictors of anxiety and depression. The convergence of two independent methodologies on the same set of drivers strengthens the study’s central claim: that self-poisoning in this population is best understood as the product of impulsive individuals colliding with acute psychosocial stressors in environments where support is thin and economic pressure is heavy.

The clinical implications are concrete. The authors argue that impulsivity screening should be added to emergency department triage protocols, complementing conventional suicide risk assessments that may undervalue trait impulsivity in patients who score as low risk. Given that every participant in this cohort exceeded a BIS-11 total of 70, a brief impulsivity measure administered at the bedside could flag vulnerability that the NGASR alone misses. Equally important, the phase structure of the suicidal process argues for psychosocial interventions tailored to where a patient sits within it: hopelessness-focused therapy in the pre-attempt phase, strategies for managing the impulsive surge itself, and structured follow-up in the post-attempt phase, when fear and remorse may open a genuine window for engagement and re-evaluation.

The study’s hospital-community-family framing, reflected in its funding through the Deyang Philosophy and Social Science Planning Project on collaborative governance mechanisms, hints at a broader prevention vision. If economic strain, domestic conflict, and weak social support are the measurable engines of distress, then prevention cannot begin and end in the emergency department. It must extend into families and communities, building the support networks that regression analysis identified as protective. The 12.3 percent of participants with previous attempts underscore the stakes: a survived attempt is a critical checkpoint, and the post-attempt phase of remorse and re-evaluation is precisely when a well-timed intervention might prevent the next one.

Caveats remain, as they do in any single-region study. The cohort of 155 patients drawn from three tertiary hospitals in Sichuan may not generalize to other cultural or healthcare contexts, and the qualitative strand, while rich, involved only ten participants. The cross-sectional design captures a snapshot rather than a trajectory, so causal claims about the sequence from stressor to attempt rest on patient recollection and theoretical alignment rather than longitudinal observation. Still, the methodological marriage of psychometrics and lived testimony is exactly what the field has lacked for this population. By showing that low conventional risk scores can coexist with extreme trait impulsivity, and that the act itself is often experienced as a mental blank rather than a decision, the study hands clinicians a sharper instrument for finding the patients who most need help before they return.

Subject of Research: Impulsivity and psychosocial determinants among patients treated in emergency departments after attempted suicide by poisoning

Article Title: Impulsivity and psychosocial determinants in patients with attempted suicide by poisoning: a mixed-methods study

Article References: Wang, H., & Xing, R. (2026). Impulsivity and psychosocial determinants in patients with attempted suicide by poisoning: a mixed-methods study. BMC Psychology. https://doi.org/10.1186/s40359-026-05789-4

Image Credits: AI Generated

DOI: 10.1186/s40359-026-05789-4

Keywords: suicide, self-poisoning, impulsivity, emergency department, mixed-methods, BIS-11, social support, anxiety, depression, suicide prevention, psychosocial stress, BMC Psychology

The research team, led by Runye Shi and Shitong Xiang of Fudan University together with senior authors Xiaolei Lin, Tianye Jia and Jianfeng Feng, combined data from the Adolescent Brain Cognitive Development study, the IMAGEN study, the Human Connectome Project and the UK Biobank. Together these cohorts provided 53,199 neuroimaging scans from 51,467 participants aged between 9 and 70 years. To guard against the possibility that their findings were an artefact of any single dataset, the team validated their trajectories in an independent collection of 2,127 people aged 12 to 89 drawn from the Nathan Kline Institute-Rockland Sample, the Cambridge Centre for Ageing and Neuroscience and the Brains and Minds in Transition study. In total, 6,992 participants in the discovery sample met criteria for problematic substance use, alongside 18,659 healthy controls.

A central methodological challenge in lifespan neuroscience is that brain volumes differ systematically with age, sex, scanner and study, making it difficult to compare a 14-year-old in one cohort with a 55-year-old in another. The researchers tackled this with normative modelling built on the Generalized Additive Model for Location, Scale and Shape, a statistical framework that establishes age-specific and sex-specific reference ranges for grey matter volume in 24 brain regions implicated in addiction. These regions spanned the ventral and dorsal striatum, amygdala, hippocampus, insula, anterior cingulate cortex and prefrontal cortex. Each participant’s volumes were then expressed as centiles relative to healthy controls of the same age, allowing the team to fit continuous trajectories of group differences across the entire lifespan rather than relying on isolated snapshots.

The resulting map revealed three clearly demarcated phases. Before the age of 25, problematic substance use was associated with a striking developmental imbalance: participants showed higher grey matter volume in the bilateral putamen, part of the dorsal striatum richly innervated by dopamine, but lower volume in the nucleus accumbens, insula, frontal pole, orbitofrontal and superior frontal cortices and the anterior cingulate cortex. Notably, while healthy controls showed declining volumes in the medial orbitofrontal cortex and nucleus accumbens through adolescence, individuals with problematic use exhibited the opposite, an increasing trend. The researchers interpret this as evidence of maturational imbalance between reward-driven striatal circuits and the prefrontal systems that normally exert top-down control.

Behavioural data collected within each cohort reinforced this interpretation. Adolescents and young adults with problematic substance use scored higher on rule-breaking, conduct problems and impulsivity, particularly sensation-seeking. Yet the picture was nuanced: they did not differ from controls on laboratory measures of stop-signal reaction time, cognitive flexibility or spatial working memory, and they showed no consistent preference for immediate rewards in monetary-choice tests. What did emerge were lower fluid and crystallized cognitive abilities, with effect sizes of 0.26 and 0.40 respectively. In mediation analyses, rule-breaking statistically mediated the link between whole-brain volumetric patterns and later substance use in the ABCD cohort, while impulsivity mediated the link between striatal-prefrontal volume contrasts and subsequent use, suggesting that these behavioural traits are not merely correlates but potential pathways connecting early brain structure to the initiation of risky use.

Between the ages of roughly 25 and 45, the structural signature shifted. Rather than deficits, the dominant pattern was enlargement: individuals with problematic substance use showed relatively higher grey matter volume in the bilateral insula, rostral anterior cingulate and lateral orbitofrontal cortex, regions that together constitute the brain’s salience network, which mediates conscious emotion, interoception and the conscious craving for addictive substances. These positive differences emerged from about age 30, peaked in the mid-40s and faded after 60. When the team projected their regional findings onto cortical gene-expression atlases, a dopaminergic marker combining FDOPA, the dopamine transporter, D1 receptors and NMDA receptors significantly explained the volumetric differences during this window, with the strongest effect around age 34. Genomically, this stage was anchored by a locus on chromosome 13 mapping to SUCLA2, a gene involved in mitochondrial energy metabolism, a pathway previously implicated in the neural effects of psychoactive substances and dopaminergic function.

After age 45, the pattern inverted again, this time toward widespread reduction. Significant differences emerged after approximately 56 years in subcortical structures and 68 years in cortical regions, with the amygdala, hippocampus, nucleus accumbens, medial orbitofrontal and superior frontal cortices showing progressively lower volumes and faster rates of decline in individuals with problematic use. The cognitive factor most strongly associated with these brain differences also shifted with age, moving from reward sensitivity in early adulthood toward general cognitive impairment and inhibitory control in mid-to-late adulthood. A genetic locus on chromosome 14, associated with alcoholism and tobacco use disorder, mapped to COA8, a gene involved in mitochondrial function and protection against oxidative stress. The authors suggest that these late-life reductions may reflect cumulative neurotoxicity and oxidative damage from prolonged substance exposure, potentially consistent with the premature brain aging reported in alcohol use disorder and drug addiction.

Sex shaped these trajectories in ways that were most pronounced early in life. In adolescence and early adulthood, females showed greater substance-related differences in the right nucleus accumbens, anterior cingulate, insula and orbitofrontal cortex, regions tied to reward motivation, interoception and emotional regulation, whereas males showed larger differences in the dorsal striatum and frontal pole, implicated in action selection and externalizing behaviour. The differences converged during mid-adulthood, then re-emerged in later life, with females showing greater hippocampal and caudate reductions and males greater orbitofrontal and superior frontal losses. The authors note this mirrors established sex-specific internalizing and externalizing pathways in psychiatric research, and argue that prevention efforts may need to be tailored differently for boys and girls.

Genetic correlations across the cohorts added a temporal dimension to the biology. Studies whose participants were closer in age showed higher genetic correlations with one another, and the correlation with a published genome-wide association study of addiction risk factors increased steadily with age, reaching a significant 0.72 in the UK Biobank sample. Combined with the identification of distinct shared loci at each life stage, CCDC91 on chromosome 12 in childhood, linked to white matter maintenance and neurodevelopmental disorders; SUCLA2 in early-to-mid adulthood; and the chromosome 14 locus in later life, the evidence points to gradually evolving genomic contributions to problematic substance use rather than a single static genetic vulnerability.

The authors are careful to spell out the limitations. Problematic substance use was defined using developmentally appropriate but not clinically equivalent criteria across cohorts, since consistent diagnostic assessments were unavailable, and most age ranges were dominated by a single cohort, raising the possibility of cohort effects despite statistical adjustment and independent replication. Grey matter trajectories were estimated primarily from cross-sectional data, and self-reported impulsivity did not always align with laboratory measures of inhibitory control. Even so, the framework that emerges is one in which addiction is not a static state but a moving target: a neurodevelopmental vulnerability before 25, a salience-network and dopaminergic reinforcement phase between 25 and 45, and a cumulative neurotoxic burden thereafter. Each stage, the authors argue, demands a different public health response, from school- and family-based prevention targeting impulsivity in adolescence, to early detection and intervention during the reinforcement years, to integrated monitoring of cognitive decline and broader health in older adults who use substances.

Subject of Research: Lifespan neuroimaging of brain structural and behavioural changes associated with problematic substance use

Article Title: Behavioural and brain volumetric changes associated with problematic substance use through the lifespan

Article References: Shi, R., Xiang, S., Alnæs, D., Chen, D., Zheng, C., Banaschewski, T., Barker, G. J., Bokde, A. L. W., Desrivières, S., Flor, H., Garavan, H., Gowland, P., Grigis, A., Heinz, A., Martinot, J.-L., Martinot, M.-L. P., Artiges, E., Nees, F., Orfanos, D. P., … Feng, J. (2026). Behavioural and brain volumetric changes associated with problematic substance use through the lifespan. Nature Health. https://doi.org/10.1038/s44360-026-00204-z

Image Credits: AI Generated

DOI: 10.1038/s44360-026-00204-z

Keywords: addiction, problematic substance use, grey matter volume, normative modelling, adolescence, dopamine, salience network, UK Biobank, genetics, impulsivity, brain aging, public health

The research team, led by Richard O. Nkrumah of the Central Institute of Mental Health in Mannheim and Gabriele Ende, recruited 87 individuals with substance use disorders alongside 53 non-smoking healthy controls. Participants were drawn from two clinical sites, the Central Institute of Mental Health in Mannheim and the Charité Universitätsmedizin Berlin, and all dependence diagnoses were made according to ICD-10 criteria, which correspond to severe substance use disorder under the DSM-5 framework. Crucially, the study excluded people with current comorbid substance use disorders, allowing the researchers to isolate patterns associated with each primary substance rather than muddying the picture with overlapping addictions.

What sets this investigation apart technically is its use of advanced diffusion magnetic resonance imaging, which probes the microscopic architecture of brain tissue by tracking the movement of water molecules. The team combined conventional diffusion tensor imaging, which yields measures such as fractional anisotropy and mean diffusivity, with a newer technique called neurite orientation dispersion and density imaging, or NODDI. While diffusion tensor imaging has been the workhorse of white matter research for two decades, it struggles in regions where fibers cross, which applies to as much as 90 percent of white matter. NODDI sidesteps this limitation by separately modeling neurite density, the isotropic or freely diffusing water fraction, and the orientation dispersion index, which captures how tangled or dispersed the axons within a voxel are.

The whole-brain results were unambiguous in their broad strokes. Both the opioid-dependent and cannabis-dependent groups showed widespread abnormalities characterized by reduced fractional anisotropy, elevated mean diffusivity and increased orientation dispersion across fronto-temporo-parietal and limbic pathways. Among the affected tracts were the superior longitudinal fasciculus, the arcuate fasciculus, the cingulum bundle and the middle longitudinal fasciculus, a temporo-parietal connection implicated in cognitive control and valuation. Nicotine dependence, by contrast, produced a far more circumscribed pattern, with significant alterations appearing mainly in mean diffusivity and localized to anterior and callosal white matter. The nicotine-related changes largely fell within the broader spatial footprint seen in the other two groups.

When the researchers directly overlapped the maps from the opioid and cannabis groups, they found substantial shared damage in association pathways and medial limbic tracts, but also telling differences. Opioid-dependent participants showed alterations extending further into midline and projection structures such as the corpus callosum and anterior thalamic radiation, while cannabis-related changes were more confined to fronto-parietal and temporal association fibers. These convergent and divergent signatures may reflect differences in pharmacology, chronic exposure patterns or the heavier psychiatric burden carried by the opioid and cannabis groups, who reported significantly elevated depressive symptoms and perceived stress compared with controls.

The most striking finding, however, concerned behavior. All participants completed the Kirby Delay Discounting Task, a well-validated measure of impulsivity in which people choose between smaller immediate monetary rewards and larger delayed ones. Steeper discounting, meaning a stronger preference for instant gratification, is considered a core behavioral marker of addiction. In the cannabis dependence group, higher orientation dispersion in the middle longitudinal fasciculus was significantly associated with steeper delay discounting, with a correlation of 0.41 that remained significant after controlling for age, sex, scanning site, daily alcohol consumption and nicotine dependence scores. Notably, fractional anisotropy in the same tract showed no such relationship, suggesting that the NODDI-derived measure was sensitive to microstructural features that conventional metrics missed.

The middle longitudinal fasciculus is an anatomically compelling candidate for this role. It connects the superior temporal gyrus and superior parietal lobule with dorsolateral prefrontal regions that support cognitive control and future-oriented valuation, making it a plausible conduit for integrating sensory, memory and executive inputs during decisions about delayed rewards. The researchers emphasize that orientation dispersion does not map onto any single biological process, so the association is best interpreted as altered microstructural signal within a behaviorally relevant tract rather than proof of specific fiber disorganization.

Exploratory statistical modeling added another layer of intrigue. Using a moderated mediation framework, the team found that the model explained just over half the variance in delay discounting within the cannabis group. Higher middle longitudinal fasciculus orientation dispersion predicted greater cannabis consumption, and the indirect link between tract microstructure and impulsive choice through consumption amount was significant only among daily users, not among those who used cannabis less frequently. This frequency-dependent pattern aligns with prior evidence that heavy, daily cannabis use is associated with greater disruption of fronto-parietal networks and poorer inhibitory control than occasional use. A supplementary reverse model, in which consumption severity was tested as the predictor and tract microstructure as the mediator, showed consistent associations but did not yield a statistically supported indirect effect, underscoring the exploratory nature of these analyses.

In the opioid dependence group, despite showing the most widespread white matter alterations of any group, no significant relationship emerged between middle longitudinal fasciculus measures and delay discounting. The authors caution against overinterpreting this absence, since the opioid subgroup comprised only 16 participants, all receiving opioid substitution therapy, which limits statistical power and generalizability to people with active illicit opioid use. The opioid group also carried the highest levels of perceived stress and anxiety, factors known to correlate with impulsive choice that may have obscured tract-specific associations. Opioid-related white matter abnormalities may instead involve thalamocortical and limbic-striatal circuits beyond the middle longitudinal fasciculus.

Several limitations temper the conclusions. The cross-sectional design cannot determine whether white matter abnormalities precede heavy substance use and impulsive decision-making or result from chronic exposure, a question that will require longitudinal and animal studies. Subgroup sizes were modest, particularly for nicotine and opioid dependence, and residual between-site variance in global diffusion measures persisted despite statistical harmonization. Previous, though not concurrent, polysubstance use was common, especially in the opioid group, and may have contributed unmeasured variability. Even so, the study delivers a clear message: addiction is not one white matter disease but a family of related syndromes with overlapping yet distinguishable neural signatures, and the microstructure of a single temporo-prefrontal tract may hold a measurable key to why some people with cannabis dependence struggle more than others to wait for a better reward.

Subject of Research: White matter microstructure differences across opioid, cannabis and nicotine dependence and their link to impulsive decision-making

Article Title: White matter signatures of addiction diverge across opioids, cannabis and nicotine and predict impulsive choice in cannabis dependence

Article References: Nkrumah, R. O., Wetzel, L., Böhmer, J., Eidenmueller, K., Bach, P., De Santis, S., Walter, H., Sommer, W. H., & Ende, G. (2026). White matter signatures of addiction diverge across opioids, cannabis and nicotine and predict impulsive choice in cannabis dependence. Translational Psychiatry, 16(1), Article 548. https://doi.org/10.1038/s41398-026-04491-8

Image Credits: AI Generated

DOI: 10.1038/s41398-026-04491-8

Keywords: substance use disorders, white matter, diffusion MRI, NODDI, cannabis dependence, opioid dependence, nicotine dependence, delay discounting, middle longitudinal fasciculus, impulsivity, fractional anisotropy, orientation dispersion

The design of the study is what gives it its power. Rather than comparing a single patient group with controls, the team recruited 111 adolescents spanning a gradient of risk: 25 with a diagnosis of bipolar I disorder who were currently euthymic, meaning their mood was stable at the time of testing; 32 classified as high-risk, typically because of a family history of the illness; 24 deemed ultra-high risk, showing attenuated or subclinical manic symptoms identified through instruments such as the Bipolar Prodrome Symptom Scale-Prospective; and 30 healthy controls. This four-tier structure allowed the investigators to ask whether neurocognitive alterations deepen as one moves along the continuum from familial risk toward full-threshold illness — a question that cross-sectional comparisons of patients and controls alone cannot answer.

Each participant completed a battery of behavioral tasks and questionnaires targeting four cognitive-affective domains. Risk-taking was probed with the Modified Balloon Analog Risk Task, in which participants inflate virtual balloons for points while weighing the danger of an explosion, and with the Iowa Gambling Task, a classic decision-making paradigm that requires learning, often without conscious awareness, which of several card decks yields long-term gains. Impulsivity was measured behaviorally with a Go/No-Go Task, which tests the ability to suppress a prepotent motor response, and subjectively with the Barratt Impulsivity Scale-11, a widely used self-report instrument that decomposes impulsivity into attentional, motor, and non-planning facets. Reward sensitivity was assessed with the Behavioral Inhibition/Behavioral Activation Scale, which quantifies the strength of approach and avoidance motivational systems. Finally, emotional conflict resolution was tested with an Emotional Stroop Task, in which participants must name the color of words while ignoring their emotional content, forcing the brain to resolve interference between affective salience and task demands.

The statistical approach was deliberately conservative. Group comparisons used the Kruskal-Wallis test, appropriate for non-normally distributed data, with Benjamini-Hochberg false discovery rate correction to control for multiple comparisons, and the most robust findings were further checked against the stricter Bonferroni threshold. Multinomial logistic regression, adjusted for age and sex, then tested which measures best classified adolescents into the four groups, and receiver operating characteristic analysis quantified diagnostic discrimination. This layered pipeline matters because the field of psychiatric biomarkers is littered with findings that evaporate under multiple-comparison scrutiny; here, the authors explicitly flagged which results survived which level of correction.

The standout result was accuracy on the Emotional Stroop Task. Conflict accuracy — the ability to correctly respond despite emotional interference — was the most consistent discriminator in the entire study. It separated the high-risk, ultra-high-risk, and bipolar groups from healthy controls, and, crucially, it also distinguished the bipolar group from both risk groups. In other words, deficits in resolving emotional conflict appear not merely as a consequence of the illness but as a feature that intensifies across the risk continuum, making it one of the most promising candidate markers identified. The regression analysis underscored this: emotional conflict accuracy discriminated the combined ultra-high-risk and bipolar groups from the combined healthy and high-risk groups with an area under the curve of 0.923, a level of discrimination that, if replicated, would be remarkable for a single behavioral measure in psychiatry. The authors are careful to note, however, that this cut-off is exploratory and derived from a modest sample.

Decision-making under risk also told a coherent story. Lower net scores on the Iowa Gambling Task differentiated all three clinical groups — bipolar, high-risk, and ultra-high-risk — from healthy controls, suggesting that impaired affective decision-making is a broad vulnerability feature present even before illness onset. On the Modified Balloon Analog Risk Task, a higher average number of pumps — a direct behavioral index of risk-taking — differentiated the ultra-high-risk and bipolar groups from controls in the adjusted models. Notably, this elevated risk-taking in the ultra-high-risk group correlated with concurrent subclinical manic symptoms, hinting that the balloon-pumping behavior may capture something phenomenologically close to the emerging hypomanic temperament. Group differences on the Emotional Stroop, Iowa Gambling Task, Barratt Impulsivity Scale, and Go/No-Go task survived both false discovery rate and Bonferroni correction, whereas the balloon task differences survived false discovery rate correction only.

Perhaps the most clinically useful aspect of the findings is the differential pattern across impulsivity subdomains. Non-planning impulsivity, reward sensitivity, and emotional conflict resolution deficits distinguished all three clinical groups from healthy controls, positioning them as potential trait markers of vulnerability that are present from the earliest identifiable risk stage. By contrast, motor and attentional impulsivity, fun-seeking, and response inhibition deficits were more specific to the ultra-high-risk and bipolar groups, appearing only as adolescents move closer to or into full-threshold illness. This dissociation suggests a staged model of neurocognitive deterioration: a baseline vulnerability layer shared across the risk spectrum, overlaid by a later-emerging layer of inhibitory and attentional dyscontrol that may signal imminent transition. If longitudinal studies confirm this architecture, clinicians could in principle use the profile of deficits — not just their presence — to estimate where along the risk pathway a given adolescent sits.

The theoretical implications reach into long-standing models of bipolar disorder. Heightened reward sensitivity and approach motivation have been central to psychological theories of mania, and the present findings align with the idea that a hyperactive behavioral activation system, combined with impaired top-down regulation of emotional interference, creates a cognitive environment in which mood dysregulation can escalate. The anterior cingulate cortex, a region heavily implicated in conflict monitoring and error processing, is a plausible neural substrate for the Emotional Stroop deficits observed, and its dysfunction could plausibly link the affective and cognitive disturbances that characterize the bipolar prodrome. The authors themselves frame these alterations as candidate markers rather than established ones, a distinction that reflects both the strength and the limits of the evidence.

Those limits deserve emphasis. The study is cross-sectional, meaning it captures a snapshot rather than a trajectory; it cannot prove that the observed deficits predict who will convert from risk to illness, only that they covary with risk stage at a single point in time. The sample, while thoughtfully stratified, is modest — 111 adolescents across four groups — and the ultra-high-risk subgroup in particular is small. The authors also note that the striking area under the curve of 0.923 for emotional conflict accuracy should be treated as a hypothesis-generating estimate, since classification metrics derived from the same dataset used for discovery are prone to optimism. Longitudinal follow-up of high-risk and ultra-high-risk cohorts, ideally with neuroimaging and repeated cognitive assessment, will be needed to determine whether these candidate markers genuinely forecast onset and whether early intervention targeting emotional regulation could alter the course of the illness.

Even with those caveats, the study represents a meaningful step toward a long-sought goal in child and adolescent psychiatry: identifying measurable, task-based signals that stratify bipolar risk before the first full manic episode. Bipolar disorder in young people is frequently misdiagnosed, often as unipolar depression or attention deficit hyperactivity disorder, and treatment delays carry substantial costs in academic, social, and neurobiological terms. A validated cognitive profile — impaired emotional conflict resolution, compromised affective decision-making, and stage-specific impulsivity changes — could eventually complement clinical interviews and family history to sharpen risk assessment. For now, the message from Ankara and Izmir is one of cautious optimism: the cognitive fingerprints of bipolar vulnerability appear to be detectable in adolescence, arranged along a gradient that mirrors the illness itself, and waiting to be tested against the passage of time.

Subject of Research: Neurocognitive vulnerability markers across bipolar disorder risk stages in adolescents

Article Title: Neurocognitive candidate markers across bipolar disorder risk stages in adolescents

Article References: Akpınar, S., Kafali, H. Y., Kabasakal, İ., Kaya, H., Akman, A. Ö., Bora, E., & Dinç, G. Ş. (2026). Neurocognitive candidate markers across bipolar disorder risk stages in adolescents. BMC Psychiatry. https://doi.org/10.1186/s12888-026-08732-4

Image Credits: AI Generated

DOI: 10.1186/s12888-026-08732-4

Keywords: bipolar disorder, adolescents, ultra-high risk, emotional conflict, reward sensitivity, impulsivity, risk-taking, Iowa Gambling Task, Emotional Stroop Task, neuropsychology, prodrome, predictive markers

Psychotic-like experiences, often abbreviated as PLEs, are subclinical phenomena that fall short of a diagnosable psychotic disorder. They include delusion-like experiences such as paranoia, suspiciousness, or the feeling that one’s thoughts are being broadcast, as well as perceptual abnormalities, most commonly in the auditory domain, where sounds seem distorted, intensified, or overwhelming. These experiences are surprisingly common: roughly 5 to 10 percent of the general population report them at any given time, and more than a quarter of people endorse at least one such experience over their lifetime. Although most are transient, about 20 percent of people who report acute psychotic-like experiences go on to develop persistent symptoms, which is why researchers treat them as important early warning signals of broader psychopathology.

The connection between substance use and these experiences has been established in previous work. A systematic review and meta-analysis of young people found that substance users were nearly twice as likely to report psychotic-like experiences as nonusers. High-potency cannabis has been linked to more frequent and severe paranoia, alcohol use has been implicated in psychotic symptoms particularly among people with mood disorders, and high doses of methamphetamine can induce psychosis even in otherwise healthy individuals. What has remained unclear is how these associations vary with how often someone uses substances, and how they are shaped by the wider psychological landscape, including impulsivity, recent stress, childhood adversity, and other psychiatric symptoms.

To untangle this, the researchers recruited 1,196 adults aged 18 to 51 through online advertisements and collected anonymous self-report data between July 2024 and January 2026. Rather than examining each risk factor in isolation, they used network analysis, a statistical framework in which every variable is represented as a node and every unique association between variables as an edge, with all other variables statistically accounted for. The network included frequency of alcohol, cannabis, and stimulant use, impulsivity, other psychopathological symptoms such as depression and anxiety, recent stress exposure, adverse childhood experiences, delusion-like experiences, and auditory perceptual abnormalities. This approach allowed the team to ask whether substance use connects directly to psychotic-like experiences or whether the connection runs indirectly through the surrounding psychological terrain.

A key innovation was the way participants were grouped. Instead of imposing an arbitrary cutoff, the researchers used a data-driven network tree procedure that examined how the correlation structure among the psychological variables changed with substance use frequency. This analysis identified a boundary between use at weekly-or-less and use more than weekly, splitting the sample into nonusers (308 people), lower frequency users (596), and higher frequency users (292). The authors stress that this boundary is exploratory and sample-derived rather than a clinical threshold, and sensitivity analyses showed that while the decision to split the sample was highly consistent, the exact location of the boundary varied somewhat across resampling procedures and substances.

The results were striking. In the full-sample network, the three substance use variables formed the strongest connections with one another, particularly between alcohol and cannabis. But the most important finding concerned the wider architecture: higher frequency users showed significantly greater connectivity within the psychosocial and psychotic-like experience network than nonusers, even though the overall structure of that network was similar. In other words, frequent users did not display a qualitatively different pattern of psychological difficulties, but the links among their symptoms, stress, adversity, impulsivity, and unusual experiences were measurably stronger. The full nine-node networks of lower and higher frequency users also differed in both global strength and overall structure, although the only individual edges that survived statistical correction were those among the substance use variables themselves.

Delusion-like experiences emerged as the star of the show. In the full network, delusion-like experiences showed direct conditional associations with all three substances, whereas auditory perceptual abnormalities showed no direct connection to any of them. Delusion-like experiences also carried the highest bridge strength, a measure of how strongly a node connects different domains of the network, followed by other psychopathological symptoms. Among higher frequency users, all three substances showed statistically supported total associations with delusion-like experiences, while none of the substances showed a supported total association with auditory perceptual abnormalities. This suggests that unusual beliefs and suspicious interpretations may be more closely tied to frequent substance use than the perceptual distortions assessed here, and it supports the growing view that different types of psychotic-like experiences should not be lumped together as a single construct.

The exploratory mediation analyses added another layer of nuance. Among lower frequency users, supported total associations with psychotic-like experiences were confined to stimulant use, and they involved impulsivity, other psychopathological symptoms, and adverse childhood experiences. Among higher frequency users, the picture shifted: associations with delusion-like experiences for all three substances were carried most consistently by other psychopathological symptoms and recent stress exposure, with no supported direct associations remaining. In the full sample, indirect components accounted for large portions of the total associations, sometimes more than 70 percent. The authors are careful to emphasize that because the study is cross-sectional, these mediation models describe statistical decompositions of concurrent associations, not causal or temporal pathways.

The clinical implications are considerable. If frequent substance use marks a broader mental health burden rather than an isolated behavioral exposure, then assessing someone who drinks or uses cannabis daily should arguably extend beyond substance frequency alone to include psychiatric symptoms, stress, impulsivity, childhood adversity, and psychotic-like experiences. The finding that delusion-like experiences deserve particular attention among frequent users could help clinicians decide where to look first. At the same time, the authors caution against overinterpreting centrality metrics: a node with high bridge strength is not necessarily an intervention target, and changing one variable in a network does not guarantee changes elsewhere.

The study has clear limitations that the authors acknowledge candidly. Frequency of use is an incomplete measure of exposure, since it says nothing about quantity, potency, binge patterns, route of administration, or age at initiation. Group membership was defined by the highest frequency reported across the three substances, so the higher frequency group contained a mix of single-substance and polysubstance patterns, with polysubstance involvement especially common among frequent users. All measures were self-reported, and factors such as sleep, tobacco use, and family history of psychosis were not assessed. What the study does deliver is a compelling statistical portrait: frequent substance use is embedded in a more tightly interconnected psychological system, one in which delusional thinking, general psychiatric symptoms, stress, and adversity all pull on one another. Longitudinal research with richer measures of exposure will be needed to determine whether frequent use drives this entanglement, whether psychological distress drives frequent use, or whether both unfold from shared roots.

Subject of Research: Associations between substance use frequency and psychotic-like experiences within a broader psychosocial network

Article Title: Substance Use Frequency and Psychotic-Like Experiences Within a Broader Psychosocial Network

Article References: Nalberczak-Skóra, M., Bagrowska, P., Olechowska, A., & Gawęda, Ł. (2026). Substance Use Frequency and Psychotic-Like Experiences Within a Broader Psychosocial Network. International Journal of Mental Health and Addiction. https://doi.org/10.1007/s11469-026-01736-x

Image Credits: AI Generated

DOI: 10.1007/s11469-026-01736-x

Keywords: substance use, psychotic-like experiences, network analysis, delusion-like experiences, cannabis, alcohol, stimulants, impulsivity, adverse childhood experiences, stress, psychopathology, mental health

The study, led by Claudia Chiarolanza of Sapienza University of Rome together with Stefano Isolani of Guglielmo Marconi University and Danilo Garcia of the University of Stavanger, drew its inspiration from Greek mythology. Nemesis, the goddess of retribution, embodied the outrage that follows perceived violations—a fitting metaphor, the authors argue, for the emotional and social forces that swirl around revenge in romantic relationships. Betrayal within a couple is not merely a private wound; it is a violation of a relational contract, and the response it elicits carries both private and public dimensions. The researchers set out to test whether the perceived legitimacy of a vengeful act depends jointly on the sex of the avenger and the visibility of the act itself.

To do so, the team designed a controlled 2 × 2 factorial experiment. Each of the 908 participants, all Italian adults recruited through social networks and community circles, was randomly assigned to read one of four scenarios depicting a marital betrayal and a subsequent act of revenge. The scenarios varied the sex of the avenger—male or female—and the context of the retaliation—public or private. In the public conditions, the vengeful act unfolded before an audience: one male avenger posted about his wife’s affair in a town’s Facebook group, while one female avenger publicly humiliated her husband and his lover at a company dinner. In the private conditions, the retaliation was directed at the partner alone, such as a message to a small WhatsApp group or throwing a spouse’s belongings out the window. Participants rated how plausible they found each scenario and how likely they would be to act as the avenger did, on five-point scales.

The design was carefully controlled. An a priori power analysis had indicated that at least 299 participants would be needed to detect a medium effect with 90 percent power; the final sample far exceeded that threshold. Randomization checks confirmed that the four groups did not differ in age, education, relationship status, or any of the psychological variables measured. The researchers also collected data on participants’ own sex, mental well-being, impulsivity, dispositional forgiveness, and dispositional vengeance, using well-validated instruments including the Barratt Impulsiveness Scale, the Bolton Forgiveness Scale, the Vengeance Scale, and the Warwick-Edinburgh Mental Wellbeing Scale. Internal consistency was acceptable to excellent across all measures, with the Vengeance Scale reaching a McDonald’s omega of 0.91. All analyses employed robust standard errors and bootstrap estimation with 5,000 samples to guard against violations of normality.

The results on perceived plausibility were subtle but telling. Neither the avenger’s sex nor the context alone significantly shaped how believable participants found the scenario. Instead, the two factors interacted: in public settings, scenarios featuring a female avenger were rated as more plausible than those featuring a male avenger, with a statistically significant difference corresponding to a small effect size (partial eta-squared of 0.008). In private settings, no such difference emerged. The Female/Public condition received the highest mean plausibility rating of 3.48, while the Female/Private condition received the lowest at 3.18. The authors caution that this interaction, though significant, represents a modest variation in social perception rather than a dramatic practical effect.

The picture changed dramatically when participants were asked whether they themselves would act as the avenger did. Here the overall model explained a substantial 20 percent of the variance, and a large main effect of the avenger’s sex emerged: female-avenger scenarios received markedly higher endorsement than male-avenger scenarios in both contexts. Crucially, the gap widened when the act was public. In the public condition, the difference between female and male avengers corresponded to a large effect (d = 0.91), nearly double the moderate effect observed in the private condition (d = 0.44). Descriptively, the Female/Public condition again topped the ratings at a mean of 2.61, while the Male/Public condition sank to the bottom at 1.42. In other words, participants were most willing to imagine themselves taking public revenge as women, and least willing to do so as men.

Perhaps the most important finding is that this pattern survived statistical adjustment. When the researchers re-ran the model controlling for perceived plausibility, participants’ own sex, well-being, impulsivity, forgiveness, and vengeance, the avenger’s sex by context interaction remained significant, with effect magnitudes essentially unchanged. Among the covariates, dispositional vengeance, perceived plausibility, and impulsivity each predicted endorsement, whereas participants’ own sex, well-being, and forgiveness did not. This persistence indicates that the contextual and gendered contribution to vengeance endorsement is not reducible to stable individual differences. Something about the situation itself—who acts and who watches—shapes how acceptable revenge appears, above and beyond the psychological profiles of the people doing the judging.

The authors interpret these results through a communicative-signaling framework. Drawing on work by Boon and Yoshimura, they argue that a vengeful act simultaneously delivers three messages: that an injury has occurred, that the avenger is willing to defend their standing, and that future violations will carry a cost. When the act is enacted before others, this signal becomes more legible and more consequential, because the audience to whom it is implicitly addressed expands. Social media platforms amplify this dynamic further, extending the reach of a retaliatory act far beyond the immediate circles of the avenger and the target. On this view, the public versus private context of revenge is not a peripheral detail but part of what the act means—and the finding that visibility amplifies the difference between female and male avengers suggests that gendered expectations about who may legitimately perform retribution in front of others are woven into those signals.

The study is not without limitations, which the authors acknowledge candidly. The convenience sample was recruited in Italy, limiting generalizability to other cultures; the study lacked a formal manipulation check confirming that participants interpreted the public and private conditions as intended; it was not preregistered; and written scenarios may not capture the emotional intensity of real betrayal. The researchers also note an ethical concern: the scenarios may inadvertently reinforce stereotypical portrayals of the sexes, and future work should incorporate counter-stereotypical narratives and direct measures of gender identity and gender norm endorsement. Still, the practical implications are tangible. Because impulsivity predicted vengeance endorsement, clinical conversations about betrayal may benefit from attention to emotion-regulation strategies of the kind used in cognitive-behavioral interventions. And because the visibility of a vengeful act shaped its acceptability, therapists may want to explore how clients construe the audience and reputational dimensions of their own potential responses to infidelity.

What Project Nemesis ultimately offers is a reframing of one of humanity’s oldest impulses. Revenge, the study suggests, is not simply retaliation—a raw discharge of hurt. It is a socially embedded, communicative process that depends on who enacts it, who witnesses it, and the gendered expectations that surround both. The perceived plausibility and endorsement of vengeful acts arise from the joint contribution of situational cues and dispositional tendencies, consistent with a biopsychosocial model in which fast, emotionally driven reactions are tempered by slower, intentional character processes. As the authors conclude, perceptions of vengeance are not purely reactive but reflect the dynamic interplay of personal characteristics, social context, and the audience to whom the act is, at least implicitly, addressed. In an era when a single post can broadcast a betrayal to thousands, understanding how visibility and gender shape the social calculus of revenge has never felt more urgent.

Subject of Research: Gender and context effects on the perceived plausibility and endorsement of vengeful behavior after relational transgressions

Article Title: Project Nemesis: vindictive behavior in public and private contexts

Article References: Chiarolanza, C., Isolani, S., & Garcia, D. (2026). Project Nemesis: vindictive behavior in public and private contexts. Current Psychology, 45(18), Article 1545. https://doi.org/10.1007/s12144-026-10082-z

Image Credits: AI Generated

DOI: 10.1007/s12144-026-10082-z

Keywords: vengeance, revenge, relational transgressions, infidelity, forgiveness, gender differences, public and private contexts, social signaling, impulsivity, social psychology, Project Nemesis, Current Psychology