Converging evidence has revealed both functional and structural abnormalities in adolescents with early-onset conduct disorder (EO-CD). The neurological abnormalities underlying EO-CD may be different from that of adolescent-onset conduct disorder (AO-CD) patients. However, the cortical structure in AO-CD patients remains largely unknown. The aim of the present study was to investigate the cortical alterations in AO-CD patients.

We investigated T1-weighted brain images from AO-CD patients and age-, gender- and intelligence quotient-matched controls. Cortical structures including thickness, folding and surface area were measured using the surface-based morphometric method. Furthermore, we assessed impulsivity and antisocial symptoms using the Barratt Impulsiveness Scale (BIS) and the Antisocial Process Screening Device (APSD).

Compared with the controls, we found significant cortical thinning in the paralimbic system in AO-CD patients. For the first time, we observed cortical thinning in the precuneus/posterior cingulate cortex (PCC) in AO-CD patients which has not been reported in EO-CD patients. Prominent folding abnormalities were found in the paralimbic structures and frontal cortex while diminished surface areas were shown in the precentral and inferior temporal cortex. Furthermore, cortical thickness of the paralimbic structures was found to be negatively correlated with impulsivity and antisocial behaviors measured by the BIS and APSD, respectively.

The present study indicates that AO-CD is characterized by cortical structural abnormalities in the paralimbic system, and, in particular, we highlight the potential role of deficient structures including the precuneus and PCC in the etiology of AO-CD.

As a neuroprogressive illness, depression is accompanied by brain structural abnormality that extends to many brain regions. However, the progressive structural alteration pattern remains unknown.

To elaborate the progressive structural alteration of depression according to illness duration, we recruited 195 never-treated first-episode patients with depression and 130 healthy controls (HCs) undergoing T1-weighted MRI scans. Voxel-based morphometry method was adopted to measure gray matter volume (GMV) for each participant. Patients were first divided into three stages according to the length of illness duration, then we explored stage-specific GMV alterations and the causal effect relationship between them using causal structural covariance network (CaSCN) analysis.

Overall, patients with depression presented stage-specific GMV alterations compared with HCs. Regions including the hippocampus, the thalamus and the ventral medial prefrontal cortex (vmPFC) presented GMV alteration at onset of illness. Then as the illness advanced, others regions began to present GMV alterations. These results suggested that GMV alteration originated from the hippocampus, the thalamus and vmPFC then expanded to other brain regions. The results of CaSCN analysis revealed that the hippocampus and the vmPFC corporately exerted causal effect on regions such as nucleus accumbens, the precuneus and the cerebellum. In addition, GMV alteration in the hippocampus was also potentially causally related to that in the dorsolateral frontal gyrus.

Consistent with the neuroprogressive hypothesis, our results reveal progressive morphological alteration originating from the vmPFC and the hippocampus and further elucidate possible details about disease progression of depression.

There is increasing evidence that certain environmental factors can modify genetic effects. This is an important area of investigation as such work will help to guide the development of new intervention programs. In this paper, we address whether rural environments moderate the genetic influence on adolescent substance use and rule-breaking behavior (i.e. externalizing psychopathology).

Over 1200 Minnesotan 17-year-old twins were classified as either urban or rural. Externalizing behavior was operationalized as the use and abuse of alcohol and drugs along with symptoms of conduct, oppositional defiant, and antisocial personality disorders. Biometric factor modeling estimated whether the relative contribution of genetic and shared environmental factors varied from urban to rural settings.

Residency effects reached statistical significance in the male sample only. In urban environments, externalizing behavior was substantially influenced by genetic factors, but in rural environments, shared environmental factors became more influential. This was apparent at both the individual-variable and factor levels.

These findings suggest a gene–environment interaction in the development of male adolescents' problem behaviors, including substance use. The results fit within an expanding literature demonstrating both the contextual nature of the heritability statistic and how certain environments may constrain the expression of genetic tendencies.

There is limited information about psychological predictors of cosmetic surgery and how cosmetic surgery influences subsequent changes in mental health and overall appearance satisfaction. To date, there is a lack of studies examining this issue, whereby representative population samples are assessed at an age before cosmetic surgery is typically conducted and followed up after such surgery has commonly been performed.

We obtained data from a survey study following 1597 adolescent females from a representative Norwegian sample over a 13-year period. Participants provided information on cosmetic surgery, appearance satisfaction, mental health, risky sexual behavior, drug use and conduct problems at two time-points (overall response rate 67%).

Of all participants, 78 (4.9%) reported having undergone cosmetic surgery, of whom 71 were operated on during the course of the study and seven before the first data collection. Symptoms of depression and anxiety [odds ratio (OR) 1.66, 95% confidence interval (CI) 1.07–2.57] and a history of deliberate self-harm (OR 2.88, 95% CI 1.46–5.68), parasuicide (OR 3.29, 95% CI 1.53–7.08) and illicit drug use (OR 2.46, 95% CI 1.07–5.82) predicted prospective cosmetic surgery. Moreover, those who underwent surgery during the course of the study experienced a greater increase than other females in symptoms of depression and anxiety (t=2.07, p=0.04) and eating problems (t=2.71, p<0.01). Patients' use of alcohol also increased more than among non-patients (t=2.47, p=0.01).

A series of mental health symptoms predict cosmetic surgery. Cosmetic surgery does not in turn seem to alleviate such mental health problems.

We aim to (1) determine whether a behavioural sleep intervention for children with attention-deficit/hyperactivity disorder (ADHD) leads to sustained benefits; and (2) examine the factors associated with treatment response.

This study was a randomised controlled trial of 244 children (5–13 years) with ADHD from Victoria, Australia. All participants had a moderate/severe sleep problem that met American Academy of Sleep Medicine criteria for an eligible sleep disorder by parent report. The two-session intervention covered sleep hygiene and standardised behavioural strategies. The control group received usual care. Parent- and teacher-reported outcomes at 12 months included sleep, ADHD severity, quality of life, daily functioning, behaviour, and parent mental health. Adjusted mixed effects regression analyses examined 12 month outcomes. Interaction analyses were used to determine moderators of intervention outcomes over time. The trial was registered with ISRCTN, http://www.controlled-trials.com (ISRCTN68819261).

Intervention children were less likely to have a moderate/severe sleep problem by parent report at 12 months compared to usual care children (28.4% v. 46.5%, p = 0.03). Children in the intervention group fared better than the usual care group in terms of parent-reported ADHD symptoms (Cohen's d: −0.3, p < 0.001), quality of life (d: 0.4, p < 0.001), daily functioning (d: −0.5, p < 0.001), and behaviour (d: −0.3, p = 0.005) 12 months later. The benefits of the intervention over time in terms of sleep were less for children not taking ADHD medication and children with parents experiencing depression.

A behavioural sleep intervention for ADHD is associated with small sustained improvements in child wellbeing. Children who are not taking ADHD medication or have parents with depression may require follow-up booster sleep sessions.

Major depressive disorder (MDD), represent a major source of risk for suicidality. However, knowledge about risk factors for future suicide attempts (SAs) within MDD is limited. The present longitudinal study examined a wide range of putative non-clinical risk factors (demographic, social, lifestyle, personality) and clinical risk factors (depressive and suicidal indicators) for future SAs among persons with MDD. Furthermore, we examined the relationship between a number of significant predictors and the incidence of a future SA.

Data are from 1713 persons (18–65 years) with a lifetime MDD at the baseline measurement of the Netherlands Study of Depression and Anxiety who were subsequently followed up 2, 4 and 6 years. SAs were assessed in the face-to-face measurements. Cox proportional hazard regression analyses were used to examine a wide range of possible non-clinical and clinical predictors for subsequent SAs during 6-year follow-up.

Over a period of 6 years, 3.4% of the respondents attempted suicide. Younger age, lower education, unemployment, insomnia, antidepressant use, a previous SA and current suicidal thoughts independently predicted a future SA. The number of significant risk factors (ranging from 0 to 7) linearly predicted the incidence of future SAs: in those with 0 predictors the SA incidence was 0%, which increased to 32% incidence in those with 6+ predictors.

Of the non-clinical factors, particularly socio-economic factors predicted a SA independently. Furthermore, preexisting suicidal ideation and insomnia appear to be important clinical risk factors for subsequent SA that are open to preventative intervention.

Thought disorder has been proposed as an indicator of schizotypy, which is considered to be necessary but not sufficient for the development of schizophrenia. It is unclear whether thought disorder is an indicator of susceptibility (i.e. an endophenotype) for schizophrenia. The goal of the present study was to elucidate the role of thought disorder in relation to schizotypy by examining its presence in high-risk individuals during mid-childhood.

The sample consisted of 265 subjects drawn from the New York High-Risk Project. Individuals at high risk for schizophrenia (i.e. offspring of parents with schizophrenia) were compared with individuals at low risk for schizophrenia (i.e. offspring of parents with affective disorder or offspring of psychiatrically normal parents). Videotaped interviews were rated for thought disorder using the Scale for the Assessment of Thought, Language, and Communication (TLC). The same subjects were administered diagnostic interviews in late adolescence/early adulthood.

Although positive thought disorder was equally present in subjects with affective and non-affective psychoses, negative thought disorder (namely, poverty of speech and poverty of content of speech) was elevated only in subjects with schizophrenia-related psychosis. Logistic regression analyses revealed that negative thought disorder added to the prediction of schizophrenia-related psychosis outcomes over and above positive thought disorder.

These findings suggest that negative thought disorder may have a specific association with schizotypy, rather than a more general association with psychosis. The findings also support consideration of negative thought disorder as an endophenotypic indicator of a schizophrenia diathesis.

Associations between early life maltreatment, social information processing (SIP) and aggression in childhood and adolescence have been widely documented. Few studies have examined the importance of childhood maltreatment independent of SIP in the etiology of adult aggression. Furthermore, moderating effects of childhood maltreatment on the SIP–aggression links have not been explored.

Hierarchical, multi-level models were fitted to data from n=2752 twins aged 20–55 years from the PennTwins Cohort. Adult aggression was assessed with the Life History of Aggression questionnaire. Childhood maltreatment was measured using the Childhood Trauma Questionnaire. Two aspects of SIP were examined: hostile attribution biases (HAB); negative emotional responses (NER).

Childhood maltreatment was positively correlated with adult aggression, independently of HAB and NER. In addition, childhood maltreatment moderated the relationships between both aspects of SIP and adult aggression. Specifically, the relationship between NER and aggression was stronger among individuals with higher levels of childhood maltreatment and NER was not associated with aggression for adults who experienced low levels of childhood maltreatment. Moderating effects of childhood maltreatment on the NER–aggression link were supported for total childhood maltreatment, emotional neglect and emotional abuse. In contrast, HAB was more strongly associated with adult aggression at lower levels of emotional abuse and physical neglect.

The current study provides insight into the mechanisms by which early life experiences influence adult aggression. Our findings suggest that childhood maltreatment may not only lead to increased levels of aggression in adulthood but may also modify the associations between SIP and adult aggression.

Chronic early trauma alters children's stress reactivity and increases the prevalence of anxiety disorders; yet the neuroendocrine and immune mechanisms underpinning this effect are not fully clear. Animal studies indicate that the mother's physiology and behavior mediate offspring stress in a system-specific manner, but few studies tested this external-regulatory maternal role in human children exposed to chronic stress.

We followed a unique cohort of children exposed to continuous wartime trauma (N = 177; exposed; N = 101, controls; N = 76). At 10 years, maternal and child's salivary immunoglobulin A (s-IgA) and oxytocin (OT), biomarkers of the immune and affiliation systems, were assayed, maternal and child relational behaviors observed, mother and child underwent psychiatric diagnosis, and child anxiety symptoms assessed.

War-exposed mothers had higher s-IgA, lower OT, more anxiety symptoms, and their parenting was characterized by reduced sensitivity. Exposed children showed higher s-IgA, more anxiety disorders and post traumatic stress disorder, and more anxiety symptoms. Path analysis model defined three pathways by which maternal physiology and behavior impacted child anxiety; (a) increasing maternal s-IgA, which led to increased child s-IgA, augmenting child anxiety; (b) reducing maternal OT, which linked with diminished child OT and social repertoire; and (c) increasing maternal anxiety, which directly impacted child anxiety.

Our findings, the first to measure immune and affiliation biomarkers in mothers and children, detail their unique and joint effects on children's anxiety in response to stress; highlight the relations between chronic stress, immune activation, and anxiety in children; and describe how processes of biobehavioral synchrony shape children's long-term adaptation.

Oppositional defiant disorder (ODD) is frequently co-occurring with attention deficit hyperactivity disorder (ADHD) in children and adolescents. Because ODD is a precursor of later conduct disorder (CD) and affective disorders, early diagnostic identification is warranted. Furthermore, the predictability of three recently confirmed ODD dimensions (ODD-irritable, ODD-headstrong and ODD-hurtful) may assist clinical decision making.

Receiver-operating characteristic (ROC) analysis was used in order to test the diagnostic accuracy of the Conners' Parent Rating Scale revised (CPRS-R) and the parent version of the Strength and Difficulties Questionnaire (PSDQ) in the prediction of ODD in a transnational sample of 1093 subjects aged 5–17 years from the International Multicentre ADHD Genetics study. In a second step, the prediction of three ODD dimensions by the same parent rating scales was assessed by backward linear regression analyses.

ROC analyses showed adequate diagnostic accuracy of the CPRS-R and the PSDQ in predicting ODD in this ADHD sample. Furthermore, the three-dimensional structure of ODD was confirmed by confirmatory factor analysis and the CPRS-R emotional lability scale significantly predicted the ODD irritable dimension.

The PSDQ and the CPRS-R are both suitable screening instruments in the identification of ODD. The emotional lability scale of the CPRS-R is an adequate predictor of irritability in youth referred for ADHD.

Scientific interest in the therapeutic effects of classical psychedelics has increased in the past two decades. The psychological effects of these substances outside the period of acute intoxication have not been fully characterized. This study aimed to: (1) quantify the effects of psilocybin, ayahuasca, and lysergic acid diethylamide (LSD) on psychological outcomes in the post-acute period; (2) test moderators of these effects; and (3) evaluate adverse effects and risk of bias.

We conducted a systematic review and meta-analysis of experimental studies (single-group pre-post or randomized controlled trials) that involved administration of psilocybin, ayahuasca, or LSD to clinical or non-clinical samples and assessed psychological outcomes ⩾24 h post-administration. Effects were summarized by study design, timepoint, and outcome domain.

A total of 34 studies (24 unique samples, n = 549, mean longest follow-up = 55.34 weeks) were included. Classical psychedelics showed significant within-group pre-post and between-group placebo-controlled effects on a range of outcomes including targeted symptoms within psychiatric samples, negative and positive affect-related measures, social outcomes, and existential/spiritual outcomes, with large between-group effect in these domains (Hedges' gs = 0.84 to 1.08). Moderator tests suggest some effects may be larger in clinical samples. Evidence of effects on big five personality traits and mindfulness was weak. There was no evidence of post-acute adverse effects.

High risk of bias in several domains, heterogeneity across studies, and indications of publication bias for some models highlight the need for careful, large-scale, placebo-controlled randomized trials.