To identify sources of race/ethnic differences related to post-traumatic stress disorder (PTSD), we compared trauma exposure, risk for PTSD among those exposed to trauma, and treatment-seeking among Whites, Blacks, Hispanics and Asians in the US general population.

Data from structured diagnostic interviews with 34 653 adult respondents to the 2004–2005 wave of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) were analysed.

The lifetime prevalence of PTSD was highest among Blacks (8.7%), intermediate among Hispanics and Whites (7.0% and 7.4%) and lowest among Asians (4.0%). Differences in risk for trauma varied by type of event. Whites were more likely than the other groups to have any trauma, to learn of a trauma to someone close, and to learn of an unexpected death, but Blacks and Hispanics had higher risk of child maltreatment, chiefly witnessing domestic violence, and Asians, Black men, and Hispanic women had higher risk of war-related events than Whites. Among those exposed to trauma, PTSD risk was slightly higher among Blacks [adjusted odds ratio (aOR) 1.22] and lower among Asians (aOR 0.67) compared with Whites, after adjustment for characteristics of trauma exposure. All minority groups were less likely to seek treatment for PTSD than Whites (aOR range: 0.39–0.61), and fewer than half of minorities with PTSD sought treatment (range: 32.7–42.0%).

When PTSD affects US race/ethnic minorities, it is usually untreated. Large disparities in treatment indicate a need for investment in accessible and culturally sensitive treatment options.

The present study aimed to (a) characterize 10-year trajectory patterns of depressive symptoms and (b) investigate the association between depressive trajectory and subsequent obesity, metabolic function and cortisol level.

In a prospective study of Taiwanese adults aged ⩾60 years (n=3922) between 1989 and 1999, depression was assessed using a 10-item short-form of the Center for Epidemiologic Studies Depression Scale and information on body mass index (BMI) was collected by self-report. A subsample (n=445) of the original cohort in 1989 was drawn to assess metabolic variables and cortisol levels in a 2000 follow-up. After trajectory analyses were performed, multinomial logistic regression analyses were used to estimate the association estimates.

We identified four distinctive trajectories of depressive symptoms: class 1 (persistent low, 41.8%); class 2 (persistent mild, 46.8%); class 3 (late peak, 4.2%); and class 4 (high-chronic, 7.2%). The results from both complete cases and multiple imputation analyses indicated that the odds of obesity were lower in the class 2, 3 or 4 elderly, as compared with those in class 1, while the odds of underweight were higher. The classes of older adults with more and persistent depressive symptoms showed a trend toward having both a lower BMI (p=0.01) and a higher cortisol level (p=0.04) compared with those with low depressive symptoms.

Incremental increases in depressive symptoms over time were associated with reduced risk of obesity and higher cortisol levels.

As a behavioral addiction with clinical and phenomenological similarities to substance addiction, recreational and pathological gambling represent models for studying the neurobiology of addiction, without the confounding deleterious brain effects which may occur from chronic substance abuse.

A community sample of individuals aged 18–65 years who gamble was solicited through newspaper advertising. Subjects were grouped a priori into three groups (no-risk, at-risk, and pathological gamblers) based on a diagnostic interview. All subjects underwent a psychiatric clinical interview and neurocognitive tests assessing motor impulsivity and cognitive flexibility. Subjects with a current axis I disorder, history of brain injury/trauma, or implementation or dose changes of psychoactive medication within 6 weeks of study enrollment were excluded.

A total of 135 no-risk, 69 at-risk and 46 pathological gambling subjects were assessed. Pathological gamblers were significantly older, and exhibited significant deficiencies in motor impulse control (stop-signal reaction times), response speed (median ‘go’ trial response latency) and cognitive flexibility [total intra-dimensional/extra-dimensional (IDED) errors] versus controls. The finding of impaired impulse control and cognitive flexibility was robust in an age-matched subgroup analysis of pathological gamblers. The no-risk and at-risk gambling groups did not significantly differ from each other on task performance.

Impaired response inhibition and cognitive flexibility exist in people with pathological gambling compared with no-risk and at-risk gamblers. The early identification of such illness in adolescence or young adulthood may aid in the prevention of addiction onset of such disabling disorders.

Prevention of relapse and recurrence represents an important task in the successful treatment of major depressive disorder (MDD). The aim of this meta-analysis was to examine the efficacy of the sequential integration of psychotherapy and pharmacotherapy in reducing the risk of relapse and recurrence in MDD.

Keyword searches were conducted in Medline, EMBASE, PsycINFO and the Cochrane Library from inception of each database to December 2008. Randomized controlled trials examining the efficacy of the administration of psychotherapy after successful response to acute-phase pharmacotherapy in the treatment of adults with MDD were considered for inclusion in the meta-analysis.

Eight high-quality studies with 442 patients in a sequential treatment arm and 433 in a control treatment arm were included. The pooled risk ratio (RR) for relapse/recurrence was 0.797 [95% confidence interval (CI) 0.659–0.964] according to the random-effects model, suggesting a relative advantage in preventing relapse/recurrence for the sequential administration of treatments compared with control conditions. Performing subgroup analyses, we found a trend favoring psychotherapy during continuation of antidepressant drugs compared to antidepressants or treatment as usual (RR 0.842, 95% CI 0.674–1.051). Patients randomized to psychotherapy while antidepressants were discontinued were significantly less likely to experience relapse/recurrence compared to controls (RR 0.650, 95% CI 0.463–0.912).

We found evidence that the sequential integration of psychotherapy and pharmacotherapy is a viable strategy for preventing relapse and recurrence in MDD. In addition, our findings suggest that discontinuation of antidepressant drugs may be feasible when psychotherapy is provided.

Depression increases the risk of subsequent vascular events in both cardiac and non-cardiac patients. Atherosclerosis, the underlying process leading to vascular events, has been associated with depression. This association, however, may be confounded by the somatic-affective symptoms being a consequence of cardiovascular disease. While taking into account the differentiation between somatic-affective and cognitive-affective symptoms of depression, we examined the association between depression and atherosclerosis in a community-based sample.

In 1261 participants of the Nijmegen Biomedical Study (NBS), aged 50–70 years and free of stroke and dementia, we measured the intima–media thickness (IMT) of the carotid artery as a measure of atherosclerosis and we assessed depressive symptoms using the Beck Depression Inventory (BDI). Principal components analysis (PCA) of the BDI items yielded two factors, representing a cognitive-affective and a somatic-affective symptom cluster. While correcting for confounders, we used separate multiple regression analyses to test the BDI sum score and both depression symptom clusters.

We found a significant correlation between the BDI sum score and the IMT. Cognitive-affective, but not somatic-affective, symptoms were also associated with the IMT. When we stratified for coronary artery disease (CAD), the somatic-affective symptom cluster correlated significantly with depression in both patients with and patients without CAD.

The association between depressive symptoms and atherosclerosis is explained by the somatic-affective symptom cluster of depression. Subclinical vascular disease thus may inflate depressive symptom scores and may explain why treatment of depression in cardiac patients hardly affects vascular outcome.

Longitudinal research supports that suicidal thoughts and behaviors in adolescence predict maladjustment in young adulthood. Prior research supports links between suicide attempt and aggression, perhaps because of a propensity for impulsive behavior in states of high negative affect that underlies both problems. Such vulnerability may increase risk for intimate partner violence and generally poor young adulthood relational adjustment.

A total of 153 men participated in annual assessments from ages 10–32 years and with a romantic partner at three assessments from ages 18–25 years. Multi-method/multi-informant constructs were formed for parent/family risk factors, adolescent psychopathology (e.g. suicide-attempt history, mother-, father-, teacher- and self-reported physical aggression) and young adulthood relational distress (jealousy and low relationship satisfaction) and maladaptive relationship behavior (observed, self- and partner-reported physical and psychological aggression toward a partner, partner-reported injury, official domestic violence arrest records and relationship instability).

Across informants, adolescent aggression was correlated with suicide-attempt history. With few exceptions, aggression and a suicide attempt in adolescence each predicted negative romantic relationship outcomes after controlling for measured confounds. Adolescent aggression predicted young adulthood aggression toward a partner, in part, via relationship dissatisfaction.

Boys' aggression and suicide-attempt history in adolescence each predict poor relationship outcomes, including partner violence, in young adulthood. Findings are consistent with the theory of a trait-like vulnerability, such as impulsive aggression, that undermines adaptation across multiple domains in adolescence and young adulthood. Prevention and intervention approaches can target common causes of diverse public health problems.

Many patients with schizophrenia exhibit neurocognitive impairments, namely, in attentional, mnestic and executive functions. While these deficits limit psychosocial rehabilitation, their effect on psychoeducation is unknown. Within the framework of the longitudinal Munich Cognitive Determinants of Psychoeducation and Information in Schizophrenic Psychoses (COGPIP) study, we examined: (a) whether illness knowledge after psychoeducation could be predicted more precisely from the neurocognitive than from the psychopathological status of the patients; (b) which neurocognitive domains are best predictors.

A total of 116 in-patients with schizophrenic or schizoaffective disorders were randomized to a neurocognitive training or control condition (2 weeks) followed by a manualized psychoeducational group programme (4 weeks) and then observed over a 9-month follow-up. Repeated measurements included – among others – the Positive and Negative Syndrome Scale and a comprehensive neuropsychological test battery from which normative T scores were used to calculate one global and five domain-specific neurocognitive composite scores. Illness knowledge was measured by a questionnaire (WFB-52) tailored to the psychoeducational programme.

Multiple linear regression analyses showed that, apart from baseline illness knowledge, neurocognition significantly predicted knowledge outcome as well as knowledge gain (measured by reliable change indices) after psychoeducation. This was not true for psychopathology. Among the domain-specific neurocognitive composite scores, only memory acquisition was a significant predictor of knowledge outcome and gain.

Neurocognition, not psychopathology, is a significant predictor of illness knowledge after psychoeducation in schizophrenia. This finding should guide efforts to tailor psychoeducational interventions more closely to the patient's needs and resources.

Elevated striatal dopamine synthesis capacity is thought to be fundamental to the pathophysiology of schizophrenia and has also been reported in people at risk of psychosis. It is therefore unclear if striatal hyperdopaminergia is a vulnerability marker for schizophrenia, or a state feature related to the psychosis itself. Relatives of patients with schizophrenia are themselves at increased risk of developing the condition. In this study we examined striatal dopamine synthesis capacity in both members of twin pairs discordant for schizophrenia.

In vivo striatal dopamine synthesis capacity was examined using fluorine-18-l-dihydroxyphenylalanine (18F-DOPA) positron emission tomography (PET) scans in seven twin pairs discordant for schizophrenia and in a control sample of 10 healthy control twin pairs.

Striatal 18F-DOPA uptake was not elevated in the unaffected co-twins of patients with schizophrenia (p=0.65) or indeed in the twins with schizophrenia (p=0.89) compared to the control group. Levels of psychotic symptoms were low in the patients with schizophrenia who were in general stable [mean (s.d.) Positive and Negative Syndrome Scale (PANSS) total=56.8 (25.5)] whereas the unaffected co-twins were largely asymptomatic.

Striatal dopamine synthesis capacity is not elevated in symptom-free individuals at genetic risk of schizophrenia, or in well-treated stable patients with chronic schizophrenia. These findings suggest that striatal hyperdopaminergia is not a vulnerability marker for schizophrenia.

The cross-sectional association between impaired glucose/diabetes and depression is inconsistent. We examined the longitudinal associations between diabetes, indicators of glucose metabolism and depressive symptoms over 2 years of follow-up.

Participants were 4338 men and women from the English Longitudinal Study of Ageing, a prospective study of community-dwelling older adults [aged 62.9 (s.d.=9.0) years, 45.2% men]. Depressive symptoms were assessed at baseline and after 2 years of follow-up using the eight-item Centre of Epidemiological Studies – Depression (CES-D) scale. Glycated haemoglobin (HbA1c) levels, fasting glucose and other biological and behavioural risk factors were also assessed at baseline.

Approximately 11.5% of the sample were categorized with elevated depressive symptoms at follow-up (a score ⩾4 on the CES-D). There was an association between HbA1c and depressive symptoms at follow-up [per unit increase, odds ratio (OR) 1.17, 95% confidence interval (CI) 1.03–1.33] after adjustment for age and baseline CES-D. Cross-sectionally, the probability of depressive symptoms increased with increasing HbA1c levels until the value of 8.0% after which there was a plateau [p(curve)=0.03]. Compared with those with normal fasting glucose, participants with diabetes (confirmed through self-report or elevated fasting blood glucose) at baseline had an elevated risk of depressive symptoms at follow-up (OR 1.52, 95% CI 1.01–2.30) after adjusting for depressive symptoms at baseline, behavioural and sociodemographic variables, adiposity and inflammation.

These data suggest that poor glucose metabolism and diabetes are risk factors for future depression in older adults. There was no evidence of a U-shaped association.

Suicide rates vary widely across nations and ethnic groups. This study aims to explore potential factors contributing to inter-ethnic differences in suicide rates.

Study subjects came from a case-control psychological autopsy study conducted in Taiwan, including 116 consecutive suicides from two aboriginal groups and Taiwanese Han; 113 of them each matched with two living controls. Gender-, age- and method-specific suicide rates, population attributable fraction (PAF) of suicide for five major risk factors, help-seeking before suicide and emergency medical aid after suicide were compared between the three ethnic groups.

One aboriginal group (the Atayal) had significantly higher adjusted rate ratios (RR) of suicide than the other aboriginal group (the Ami) [RR 0.20, 95% confidence intervals (CI) 0.12–0.34] and the Han (RR 0.26, 95% CI 0.16–0.40). Such differences can be explained by higher PAFs of suicide for three major risk factors (substance dependence, PAF 47.6%, 95% CI 25.5–64.2; emotionally unstable personality disorder, PAF 52.7%, 95% CI 32.8–69.0; family history of suicidal behaviour, PAF 43.5%, 95% CI 23.2–60.2) in this group than in the other two groups. This higher suicide rate was substantially reduced from 68.2/100 000 per year to 9.1/100 000 per year, comparable with the other two groups, after stepwise removal of the effects of these three risk factors. Suicide rates by self-poisoning were also significantly higher in this group than in the other two groups.

Higher rates of specific risk factors and use of highly lethal pesticides for suicide contributed to the higher suicide rate in one ethnic group in Taiwan. These findings have implications for developing ethnicity-relevant suicide prevention strategies.

Cannabis consumption continues to be identified as a causal agent in the onset and development of psychosis. However, recent findings have shown that the effect of cannabis on psychosis may be moderated by childhood traumatic experiences.

Using hierarchical multivariate logistic analyses the current study examined both the independent effect of cannabis consumption on psychosis diagnosis and the combined effect of cannabis consumption and childhood sexual abuse on psychosis diagnosis using data from the Adult Psychiatric Morbidity Survey 2007 (n=7403).

Findings suggested that cannabis consumption was predictive of psychosis diagnosis in a bivariate model; however, when estimated within a multivariate model that included childhood sexual abuse, the effect of cannabis use was attenuated and was not statistically significant. The multivariate analysis revealed that those who had experienced non-consensual sex in childhood were over six times [odds ratio (OR) 6.10] more likely to have had a diagnosis of psychosis compared with those who had not experienced this trauma. There was also a significant interaction. Individuals with a history of non-consensual sexual experience and cannabis consumption were over seven times more likely (OR 7.84) to have been diagnosed with psychosis compared with those without these experiences; however, this finding must be interpreted with caution as it emerged within an overall analytical step which was non-significant.

Future studies examining the effect of cannabis consumption on psychosis should adjust analyses for childhood trauma. Childhood trauma may advance existing gene–environment conceptualisations of the cannabis–psychosis link.

Generalized anxiety disorder (GAD) is under-researched despite its high prevalence and large impact on the healthcare system. There is a paucity of functional magnetic resonance imaging (fMRI) studies that explore the neural correlates of emotional processing in GAD. The present study investigated the blood oxygen level dependent (BOLD) response to processing positive and negative facial emotions in patients with GAD.

A total of 15 female GAD patients and 16 female controls undertook an implicit face emotion task during fMRI scanning. They also performed a face emotion recognition task outside the scanner.

The only behavioural difference observed in GAD patients was less accurate detection of sad facial expressions compared with control participants. However, GAD patients showed an attenuated BOLD signal in the prefrontal cortex to fearful, sad, angry and happy facial expressions and an attenuated signal in the anterior cingulate cortex to happy and fearful facial expressions. No differences were found in amygdala response.

In contrast with previous research, this study found BOLD signal attenuation in the ventrolateral and medial prefrontal cortex and the anterior cingulate cortex during face emotion processing, consistent with a hypothesis of hypo-responsivity to external emotional stimuli in GAD. These decreases were in areas that have been implicated in emotion and cognition and may reflect an altered balance between internally and externally directed attentional processes.

The prevalence of family childhood adversities (FCAs) and their joint effects on the first onset of subsequent mental disorders throughout the life course are rarely examined, especially in Asian communities.

Face-to-face household interviews of 5201 people aged 18–70 years in Beijing and Shanghai were conducted by a multi-stage household probability sampling method. The first onsets of four broad groups of mental disorders and six categories of FCAs were assessed using The World Mental Health Composite International Diagnostic Interview (WMH-CIDI). Joint effects of FCAs were analyzed by the best fitting of several competitive multivariate models.

FCAs were highly prevalent and inter-correlated. Half of them were in a family-dysfunction cluster. The best-fitting model included each of six types of FCA (with family-dysfunction FCAs being the strongest predictors), number of family-dysfunction FCAs, and number of other FCAs. Family-dysfunction FCAs had a significant subadditive association with subsequent disorders. Little specificity was found for the effects of particular FCAs with particular disorders. Predictive effects of FCAs reached the highest in ages 13–24 compared to ages 4–12 and ⩾25. Estimates of population-attributable risk proportions indicated that all FCAs together explained 38.5% of all first-onset disorders.

Chinese children were exposed to a broad spectrum of inter-related FCAs, as found in Western countries. FCAs related to family dysfunction were especially associated with subsequent mental disorders. Biological and/or environmental factors that mediate these long-term effects should be studied in prospective research on broad groups of FCAs.

Depression and anxiety are common after diagnosis of breast cancer. We examined to what extent these are recurrences of previous disorder and, controlling for this, whether shame, self-blame and low social support after diagnosis predicted onset of depression and anxiety subsequently.

Women with primary breast cancer who had been treated surgically self-reported shame, self-blame, social support and emotional distress post-operatively. Psychiatric interview 12 months later identified those with adult lifetime episodes of major depression (MD) or generalized anxiety disorder (GAD) before diagnosis and onset over the subsequent year. Statistical analysis examined predictors of each disorder in that year.

Of the patients, two-thirds with episodes of MD and 40% with episodes of GAD during the year after diagnosis were experiencing recurrence of previous disorder. Although low social support, self-blame and shame were each associated with both MD and GAD after diagnosis, they did not mediate the relationship of disorder after diagnosis with previous disorder. Low social support, but not shame or self-blame, predicted recurrence after controlling for previous disorder.

Anxiety and depression during the first year after diagnosis of breast cancer are often the recurrence of previous disorder. In predicting disorder following diagnosis, self-blame and shame are merely markers of previous disorder. Low social support is an independent predictor and therefore may have a causal role.

Some neuroimaging studies have supported the hypothesis of progressive brain changes after a first episode of psychosis. We aimed to determine whether (i) first-episode psychosis patients would exhibit more pronounced brain volumetric changes than controls over time and (ii) illness course/treatment would relate to those changes.

Longitudinal regional grey matter volume and ventricle:brain ratio differences between 39 patients with first-episode psychosis (including schizophrenia and schizophreniform disorder) and 52 non-psychotic controls enrolled in a population-based case-control study.

While there was no longitudinal difference in ventricle:brain ratios between first-episode psychosis subjects and controls, patients exhibited grey matter volume changes, indicating a reversible course in the superior temporal cortex and hippocampus compared with controls. A remitting course was related to reversal of baseline temporal grey matter deficits.

Our findings do not support the hypothesis of brain changes indicating a progressive course in the initial phase of psychosis. Rather, some brain volume abnormalities may be reversible, possibly associated with a better illness course.

Cannabis use is considered a component cause of psychotic illness, interacting with genetic and other environmental risk factors. Little is known, however, about these putative interactions. The present study investigated whether an urban environment plays a role in moderating the effects of adolescent cannabis use on psychosis risk.

Prospective data (n=1923, aged 14–24 years at baseline) from the longitudinal population-based German Early Developmental Stages of Psychopathology cohort study were analysed. Urbanicity was assessed at baseline and defined as living in the city of Munich (1562 persons per km2; 4061 individuals per square mile) or in the rural surroundings (213 persons per km2; 553 individuals per square mile). Cannabis use and psychotic symptoms were assessed three times over a 10-year follow-up period using the Munich version of the Composite International Diagnostic Interview.

Analyses revealed a significant interaction between cannabis and urbanicity [10.9% adjusted difference in risk, 95% confidence interval (CI) 3.2–18.6, p=0.005]. The effect of cannabis use on follow-up incident psychotic symptoms was much stronger in individuals who grew up in an urban environment (adjusted risk difference 6.8%, 95% CI 1.0–12.5, p=0.021) compared with individuals from rural surroundings (adjusted risk difference −4.1%, 95% CI −9.8 to 1.6, p=0.159). The statistical interaction was compatible with substantial underlying biological synergism.

Exposure to environmental influences associated with urban upbringing may increase vulnerability to the psychotomimetic effects of cannabis use later in life.

Personal debt is one of many factors associated with anxiety, depression and suicidality. The aim of this study was to examine the relationship between personal debt and suicidal ideation in the context of sociodemographic factors, employment and income, lifestyle behaviours, and recently experienced traumatic events.

Interviews were conducted with a random probability sample comprising 7461 respondents for the third national survey of psychiatric morbidity of adults in England. Fieldwork was carried out throughout 2007. The prevalence of suicidal thoughts in the past week, past year and lifetime was assessed and current sources of debt were recorded.

In 2007, 4.3% of adults in England had thought about taking their own life in the past 12 months, ranging from 1.8% of men aged ⩾55 years to 7.0% of women aged 35–54 years. Those in debt were twice as likely to think about suicide after controlling for sociodemographic, economic, social and lifestyle factors. Difficulty in making hire purchase or mail order repayments and paying off credit card debt, in addition to housing-related debt (rent and mortgage arrears), was strongly associated with suicidal thoughts. Feelings of hopelessness partially mediated the relationship between debt and suicidal ideation.

The number of debts, source of the debt and reasons for debt are key correlates of suicidal ideation. Individuals experiencing difficulties in repaying their debts because they are unemployed or have had a relationship breakdown or have heavy caring responsibilities may require psychiatric evaluation in addition to debt counselling.

Interpersonal functioning is central to social anxiety disorder (SAD). Empirical examinations of interpersonal behaviors in individuals with SAD have frequently relied on analogue samples, global retrospective reports and laboratory observation. Moreover, research has focused on avoidance and safety behaviors, neglecting potential links between SAD and affiliative behaviors.

The influence of situational anxiety and emotional security on interpersonal behaviors was examined for individuals with SAD (n=40) and matched normal controls (n=40). Participants monitored their behavior and affect in naturally occurring social interactions using an event-contingent recording procedure.

Individuals with SAD reported higher levels of submissive behavior and lower levels of dominant behavior relative to controls. Consistent with cognitive–behavioral and evolutionary theories, elevated anxiety in specific events predicted increased submissiveness among individuals with SAD. Consistent with attachment theory, elevations in event-level emotional security were associated with increased affiliative behaviors (increased agreeable behavior and decreased quarrelsome behavior) among members of the SAD group. Results were not accounted for by concurrent elevations in sadness or between-group differences in the distribution of social partners.

These findings are consistent with predictions based on several theoretical perspectives. Further, the present research documents naturally occurring interpersonal patterns of individuals with SAD and identifies conditions under which these individuals may view social interactions as opportunities for interpersonal connectedness.

Lower cognitive functioning in early childhood has been proposed as a risk factor for depression in later life but its association with depressive symptoms during adolescence has rarely been investigated. Our study examines the relationship between total intelligence quotient (IQ) score at age 8 years, and depressive symptoms at 11, 13, 14 and 17 years.

Study participants were 5250 children and adolescents from the Avon Longitudinal Study of Parents and their Children (ALSPAC), UK, for whom longitudinal data on depressive symptoms were available. IQ was assessed with the Wechsler Intelligence Scale for Children III, and self-reported depressive symptoms were measured with the Short Mood and Feelings Questionnaire (SMFQ).

Multi-level analysis on continuous SMFQ scores showed that IQ at age 8 years was inversely associated with depressive symptoms at age 11 years, but the association changed direction by age 13 and 14 years (age–IQ interaction, p<0.0001; age squared–IQ interaction, p<0.0001) when a higher IQ score was associated with a higher risk of depressive symptoms. This change in IQ effect was also found in relation to pubertal stage (pubertal stage–IQ interaction, 0.00049<p⩽0.038). At age 17 years, however, sex-specific differences emerged (sex–age squared–IQ interaction, p=0.0075). Whilst the risk effect of higher childhood IQ scores for depressive symptoms declined in females, and some analyses even supported an inverse association by age 17 years, it persisted in males.

Our results suggest that the association between cognitive ability in childhood and depressive symptoms in adolescence varies according to age and/or pubertal stage.