Previous literature has extensively investigated the brain activity during response inhibition in adults with addiction. Inconsistent results including both hyper- and hypo-activities in the fronto-parietal network (FPN) and the ventral attention network (VAN) have been found in adults with addictions, compared with healthy controls (HCs).

Voxel-wise meta-analyses of abnormal task-evoked regional activity were conducted for adults with substance dependence (SD) and behavioral addiction during response inhibition tasks to solve previous inconsistencies. Twenty-three functional magnetic resonance imaging studies including 479 substance users, 38 individuals with behavioral addiction and 494 HCs were identified.

Compared with HCs, all addictions showed hypo-activities in regions within FPN (inferior frontal gyrus and supramarginal gyrus) and VAN (inferior frontal gyrus, middle temporal gyrus, temporal pole and insula), and hyper-activities in the cerebellum during response inhibition. SD subgroup showed almost the same activity patterns, with an additional hypoactivation of the precentral gyrus, compared with HCs. Stronger activation of the cerebellum was associated with longer addiction duration for adults with SD. We could not conduct meta-analytic investigations into the behavioral addiction subgroup due to the small number of datasets.

This meta-analysis revealed altered activation of FPN, VAN and the cerebellum in adults with addiction during response inhibition tasks using non-addiction-related stimuli. Although FPN and VAN showed lower activity, the cerebellum exhibited stronger activity. These results may help to understand the neural pathology of response inhibition in addiction.

People living in precarious housing or homelessness have higher than expected rates of psychotic disorders, persistent psychotic symptoms, and premature mortality. Psychotic symptoms can be modeled as a complex dynamic system, allowing assessment of roles for risk factors in symptom development, persistence, and contribution to premature mortality.

The severity of delusions, conceptual disorganization, hallucinations, suspiciousness, and unusual thought content was rated monthly over 5 years in a community sample of precariously housed/homeless adults (n = 375) in Vancouver, Canada. Multilevel vector auto-regression analysis was used to construct temporal, contemporaneous, and between-person symptom networks. Network measures were compared between participants with (n = 219) or without (n = 156) history of psychotic disorder using bootstrap and permutation analyses. Relationships between network connectivity and risk factors including homelessness, trauma, and substance dependence were estimated by multiple linear regression. The contribution of network measures to premature mortality was estimated by Cox proportional hazard models.

Delusions and unusual thought content were central symptoms in the multilevel network. Each psychotic symptom was positively reinforcing over time, an effect most pronounced in participants with a history of psychotic disorder. Global connectivity was similar between those with and without such a history. Greater connectivity between symptoms was associated with methamphetamine dependence and past trauma exposure. Auto-regressive connectivity was associated with premature mortality in participants under age 55.

Past and current experiences contribute to the severity and dynamic relationships between psychotic symptoms. Interrupting the self-perpetuating severity of psychotic symptoms in a vulnerable group of people could contribute to reducing premature mortality.

Heritability estimates from twin studies of the multi-faceted phenotype of nicotine dependence (ND) range from moderate to high (31–60%), but vary substantially based on the specific ND-related construct examined. The current study estimated the aggregate role of common genetic variants on key ND constructs.

Genomic-relationship-matrix restricted maximum likelihood (GREML) was used to decompose phenotypic variance across multiple ND indices using 796 125 polymorphisms from 2346 unrelated ‘lifetime ever smokers’ of European ancestry. Measures included DSM-IV ND and Fagerström Test for Nicotine Dependence (FTND) summary measures and constituent constructs (e.g. withdrawal severity, tolerance, heaviness of smoking and time spent smoking). Exploratory and confirmatory factor models were used to describe the covariance structure across ND measures; resulting factor(s) were the subject(s) of GREML analyses.

Factor models indicated highly correlated DSM-IV and FTND factors for ND (0.545, 95% confidence interval 0.50–0.60) that could be represented as a higher-order factor (NIC DEP). Additive genetic influence on NIC DEP was 33% (s.e. = 0.14, p = 0.009). Post-hoc analyses indicated moderate genetic effects on the DSM-IV (34%, s.e. = 0.14, p = 0.008) and FTND (26%, s.e. = 0.14, p = 0.032) factors, both of which were influenced by the same genetic effects (rG-SNP = 1.00, s.e. = 0.09, p < 0.00001).

Overall, common single nucleotide polymorphisms accounted for a large proportion of the genetic influences on ND-related phenotypes that have been observed in twin studies. Genetic contributions across distinct ND scales were largely influenced by shared genetic factors.

To our knowledge, there are no universal screening tools for substance dependence that (1) were developed using a population-based sample, (2) estimate total risk briefly and inexpensively by incorporating a relatively small number of well-established risk factors, and (3) aggregate risk factors using a simple algorithm. We created a universal screening tool that incorporates these features to identify adolescents at risk for persistent substance dependence in adulthood.

Participants were members of a representative cohort of 1037 individuals born in Dunedin, New Zealand in 1972–1973 and followed prospectively to age 38 years, with 95% retention. We assessed a small set of childhood and adolescent risk factors: family history of substance dependence, childhood psychopathology (conduct disorder, depression), early exposure to substances, frequent substance use in adolescence, sex, and childhood socioeconomic status. We defined the outcome (persistent substance dependence in adulthood) as dependence on one or more of alcohol, tobacco, cannabis, or hard drugs at ⩾3 assessment ages: 21, 26, 32, and 38 years.

A cumulative risk index, a simple sum of nine childhood and adolescent risk factors, predicted persistent substance dependence in adulthood with considerable accuracy (AUC = 0.80).

A cumulative risk score can accurately predict which adolescents in the general population will develop persistent substance dependence in adulthood.

Hypothalamic-pituitary-adrenal axis functioning, with cortisol as its major output hormone, has been presumed to play a key role in the development of psychopathology. Predicting affective disorders from diurnal cortisol levels has been inconclusive, whereas the predictive value of stress-induced cortisol concentrations has not been studied before. The aim of this study was to predict mental disorders over a 3-year follow-up from awakening and stress-induced cortisol concentrations.

Data were used from 561 TRAILS (TRacking Adolescents’ Individual Lives Survey) participants, a prospective cohort study of Dutch adolescents. Saliva samples were collected at awakening and half an hour later and during a social stress test at age 16. Mental disorders were assessed 3 years later with the Composite International Diagnostic Interview (CIDI).

A lower cortisol awakening response (CAR) marginally significantly predicted new disorders [odds ratio (OR) 0.77, p = 0.06]. A flat recovery slope predicted disorders with a first onset after the experimental session (OR 1.27, p = 0.04). Recovery revealed smaller, non-significant ORs when predicting new onset affective or anxiety disorders, major depressive disorder, or dependence disorders in three separate models, corrected for all other new onsets.

Our results suggest that delayed recovery and possibly reduced CAR are indicators of a more general risk status and may be part of a common pathway to psychopathology. Delayed recovery suggests that individuals at risk for mental disorders perceived the social stress test as less controllable and less predictable.

The extant major psychiatric classifications DSM-IV and ICD-10 are purportedly atheoretical and largely descriptive. Although this achieves good reliability, the validity of a medical diagnosis is greatly enhanced by an understanding of the etiology. In an attempt to group mental disorders on the basis of etiology, five clusters have been proposed. We consider the validity of the fifth cluster, externalizing disorders, within this proposal.

We reviewed the literature in relation to 11 validating criteria proposed by the Study Group of the DSM-V Task Force, in terms of the extent to which these criteria support the idea of a coherent externalizing spectrum of disorders.

This cluster distinguishes itself by the central role of disinhibitory personality in mental disorders spread throughout sections of the current classifications, including substance dependence, antisocial personality disorder and conduct disorder. Shared biomarkers, co-morbidity and course offer additional evidence for a valid cluster of externalizing disorders.

Externalizing disorders meet many of the salient criteria proposed by the Study Group of the DSM-V Task Force to suggest a classification cluster.

Although mental disorders have been shown to predict subsequent substance disorders, it is not known whether substance disorders could be cost-effectively prevented by large-scale interventions aimed at prior mental disorders. Although experimental intervention is the only way to resolve this uncertainty, a logically prior question is whether the associations of mental disorders with subsequent substance disorders are strong enough to justify mounting such an intervention. We investigated this question in this study using simulations to estimate the number of substance disorders that might be prevented under several hypothetical intervention scenarios focused on mental disorders.

Data came from the National Comorbidity Survey Replication (NCS-R), a nationally representative US household survey that retrospectively assessed lifetime history and age of onset of DSM-IV mental and substance disorders. Survival analysis using retrospective age-of-onset reports was used to estimate associations of mental disorders with subsequent substance dependence. Simulations based on the models estimated effect sizes in several hypothetical intervention scenarios.

Although successful intervention aimed at mental disorders might prevent some proportion of substance dependence, the number of cases of mental disorder that would have to be treated to prevent a single case of substance dependence is estimated to be so high that this would not be a cost-effective way to prevent substance dependence (in the range 76–177 for anxiety-mood disorders and 40–47 for externalizing disorders).

Treatment of prior mental disorders would not be a cost-effective way to prevent substance dependence. However, prevention of substance dependence might be considered an important secondary outcome of interventions for early-onset mental disorders.

Previous research indicates that alcohol and drug dependence constitute aspects of a general vulnerability to externalizing disorders that accounts for much of the parent-offspring resemblance for these and related disorders. This study examined how adolescent offspring risk for externalizing psychopathology varies with respect to parental alcoholism and illicit drug dependence.

Data from the Minnesota Twin Family Study, a community-based investigation of adolescents (age 17 years, n=1252) and their parents, were used. Lifetime diagnoses of alcohol and drug dependence (among both parents and offspring) and offspring attention deficit hyperactivity disorder, oppositional defiant disorder, conduct disorder, adult antisocial behavior, and nicotine dependence were assessed via structured interviews.

Parental alcohol dependence and parental drug dependence were similarly associated with increased risk for nearly all offspring disorders, with offspring of alcohol and drug-dependent parents having approximately 2–3 times the odds for developing a disorder by late adolescence compared to low-risk offspring. Compared to parental dependence on other illicit drugs, parental cannabis dependence was associated with weaker increased risk for offspring externalizing disorders.

Both parental alcohol and drug dependence are independently associated with an increased risk for a broad range of externalizing psychopathology among late-adolescent offspring.