This study was intended to establish the pathogenic significance of sport and exercise in the development of eating disorders. Hospitalized eating disordered patients and an age-matched control group were assessed. Historical and current physical activity data were collected. An in-depth interview was also conducted to ascertain the age of onset of the diagnostic symptoms for eating disorders, and to determine whether: (i) exercising predated dieting; (ii) patients had been involved in competitive athletics; (iii) exercise was excessive; and (iv) weight loss was inversely related to level of exercise. The results indicated that patients were more physically active than controls from adolescence onwards, and prior to the onset of the primary diagnostic criteria for anorexia nervosa. A content analysis of the interview data indicated that 78% of patients engaged in excessive exercise, 60% were competitive athletes prior to the onset of their disorder, 60% reported that sport or exercise pre-dated dieting, and 75% claimed that physical activity levels steadily increased during the period when food intake and weight loss decreased the most. Together our results suggest that overactivity should not be routinely viewed as a secondary symptom in anorexia nervosa, equivalent to other behaviours. For a number of anorexic women, sport/exercise is an integral part of the pathogenesis and progression of self-starvation.

Background. The close association between generalized anxiety disorder (GAD) and major depressive disorder (MDD) prompts questions about how to characterize them in future diagnostic systems. We tested whether risk factors for MDD and GAD are similar or different.

Method. The representative 1972–73 Dunedin birth cohort of 1037 males and females was followed to age 32 with 96% retention. Adult GAD and MDD were diagnosed at ages 18, 21, 26, and 32 years, and juvenile anxiety/depression were also taken into account. Thirteen prospective risk measures indexed domains of family history, adverse family environment, childhood behavior, and adolescent self-esteem and personality traits.

Results. Co-morbid MDD+GAD was antedated by highly elevated risk factors broadly across all domains. MDD+GAD was further characterized by the earliest onset, most recurrence, and greatest use of mental health services and medication. Pure GAD had levels of risk factors similar to the elevated levels for co-morbid MDD+GAD; generally, pure MDD did not. Pure GAD had risks during childhood not shared by pure MDD, in domains of adverse family environment (low SES, somewhat more maltreatment) and childhood behavior (internalizing problems, conduct problems, somewhat more inhibited temperament). Pure MDD had risks not shared by pure GAD, in domains of family history (of depression) and personality (low positive emotionality).

Conclusions. Specific antecedent risk factors for pure adult MDD versus GAD may suggest partly different etiological pathways. That GAD and co-morbid MDD+GAD share many risk markers suggests that the presence of GAD may signal a pathway toward relatively more severe internalizing disorder.

A series of in-patients, a series of out-patients and a series of women from a general population sample, all aged under 65, and all living in the same area of south-east London, were examined using the ninth edition of the Present State Examination (PSE). An ‘index of definition’ (ID), based on number, type and severity of PSE symptoms, was constructed in order to define a threshold point above which sufficient information was available to allow classification into one of the functional psychoses or neuroses. The index specified 8 levels of definition of disorder; the threshold point for a ‘case’ lying between levels 4 and 5. The identification of ‘cases’ by this means in the general population series was highly concordant with global clinical judgement.

When the 3 series were compared, the in-patient series contained the most definite cases, the out-patient series was intermediate, and the general population series was characterized mainly by below-threshold conditions.

Disorders above the threshold point were classified using the CATEGO program. The clinical severity of the depressive disorders and anxiety states identified in this way in the 3 series was compared on the basis of symptom and syndrome profiles and PSE scores. As expected, the inpatients had the most severe, and the general population ‘cases’ the least severe disorders.

It is suggested that the PSE-ID-CATEGO techniques can be used to help standardize certain aspects of case-finding and case-description in both referred and non-referred populations and thereby make the results of surveys more comparable.

Background. Although the traditional view of bipolar affective disorder is that the majority of patients have full remission between episodes, recent evidence suggests that residual cognitive deficits are present. The aim of this study was to determine whether memory and executive deficits were present in a well-defined clinically remitted group of patients.

Methods. This was a case–control study of bipolar patients in remission (N = 18). Subjects had to fulfil stringent clinical criteria for inclusion into the study and had to have been in remission for at least 4 months. Subjects also had no history of substance dependence. The cognitive battery examined memory and executive function.

Results. Patients in excellent clinical remission and who reported good social adaptation showed impairment on tests of visuospatial recognition memory. Accuracy on four tests of executive function was not impaired in patients in remission compared with controls, although response latency on these executive tests was still impaired.

Conclusions. As our group and others have shown, patients with mania and unipolar depression show generalized impairment on tests of memory and executive function. In comparison, this study has demonstrated that patients in remission show a relatively specific impairment in memory with recovery of accuracy measures on executive function task. The increased response latency on the executive tasks suggests a possible small residual impairment. These findings suggest that in neuroanatomical terms, more posterior cortical function (temporal lobe) has not improved but there is at least some recovery of frontal lobe function in remission.

There is a commonly held perception in psychology that enquiring about suicidality, either in research or clinical settings, can increase suicidal tendencies. While the potential vulnerability of participants involved in psychological research must be addressed, apprehensions about conducting studies of suicidality create a Catch-22 situation for researchers. Ethics committees require evidence that proposed studies will not cause distress or suicidal ideation, yet a lack of published research can mean allaying these fears is difficult. Concerns also exist in psychiatric settings where risk assessments are important for ensuring patient safety. But are these concerns based on evidence? We conducted a review of the published literature examining whether enquiring about suicide induces suicidal ideation in adults and adolescents, and general and at-risk populations. None found a statistically significant increase in suicidal ideation among participants asked about suicidal thoughts. Our findings suggest acknowledging and talking about suicide may in fact reduce, rather than increase suicidal ideation, and may lead to improvements in mental health in treatment-seeking populations. Recurring ethical concerns about asking about suicidality could be relaxed to encourage and improve research into suicidal ideation and related behaviours without negatively affecting the well-being of participants.

Background. Little research has examined genetic and environmental contributions to psychopathic personality traits. Additionally, no studies have examined etiological connections between psychopathic traits and the broad psychopathological domains of internalizing (mood and anxiety) and externalizing (antisocial behavior, substance abuse). The current study was designed to fill these gaps in the literature.

Method. Participants were 626 pairs of 17-year-old male and female twins from the community. Psychopathic traits were indexed using scores on the Multidimensional Personality Questionnaire (MPQ). Symptoms of internalizing and externalizing psychopathology were obtained via structured clinical interviews. Structural equation modeling was used to estimate genetic and environmental influences on psychopathic personality traits as well as the degree of genetic overlap between these traits and composites of internalizing and externalizing.

Results. Twin analyses revealed significant genetic influence on distinct psychopathic traits (Fearless Dominance and Impulsive Antisociality). Moreover, Fearless Dominance was associated with reduced genetic risk for internalizing psychopathology, and Impulsive Antisociality was associated with increased genetic risk for externalizing psychopathology.

Conclusions. These results indicate that different psychopathic traits as measured by the MPQ show distinct genetically based relations with broad dimensions of DSM psychopathology.

The concept of schizophrenia only covers the 30% poor outcome fraction of a much broader multidimensional psychotic syndrome, yet paradoxically has become the dominant prism through which everything ‘psychotic’ is observed, even affective states with mild psychosis labelled ‘ultra-high risk’ (for schizophrenia). The inability of psychiatry to frame psychosis as multidimensional syndromal variation of largely unpredictable course and outcome – within and between individuals – hampers research and recovery-oriented practice. ‘Psychosis’ remains firmly associated with ‘schizophrenia’, as evidenced by a vigorous stream of high-impact but non-replicable attempts to ‘reverse-engineer’ the hypothesized biological disease entity, using case–control paradigms that cannot distinguish between risk for illness onset and risk for poor outcome. In this paper, the main issues surrounding the concept of schizophrenia are described. We tentatively conclude that with the advent of broad spectrum phenotypes covering autism and addiction in DSM5, the prospect for introducing a psychosis spectrum disorder – and modernizing psychiatry – appears to be within reach.

Background. Although depressed patients demonstrate impaired performance on a range of neuropsychological tests, there is little research that examines either frontal cognitive deficits or possible differences in test performance between melancholic and non-melancholic subtypes.

Methods. Depressed subjects were administered a broad neuropsychological battery. In an overall analysis, 77 depressed subjects were compared with 28 controls. In a second set of analyses, the depressed sample was divided into melancholic and non-melancholic subsets according to DSM-III-R, the CORE system and the Newcastle scale. These depressed subsets were contrasted to controls and with each other using ANCOVA controlling for age, IQ, simple reaction time and Hamilton Depression scores where appropriate.

Results. The total depressed sample was impaired on most mnemonic tasks, simple reaction time and Trails B. Similar findings applied to DSM-III-R melancholic and non-melancholic subjects. When defined by the CORE and Newcastle (narrower definitions of melancholia), melancholic patients were additionally impaired on WCST (perseverative response) and (for Newcastle) digit symbol substitution. In contrast, the cognitive performance of the CORE and Newcastle-defined non-melancholic patients was largely unimpaired.

Conclusions. Using narrower definitions of melancholia, i.e. CORE and (in particular) Newcastle, melancholic patients were impaired on mnemonic tasks and tasks of selective attention, and set-shifting while non-melancholic subjects were largely unimpaired in their cognitive performance. These differences may be due to impairment of specific neuroanatomical regions in narrowly defined melancholic patients, in particular the anterior cingulate.

Background. Serotonin is a good candidate for major depression. We attempted to replicate the study by Caspi and colleagues [Science (2003) 301, 386–389] which reported a significant interaction between serotonin transporter (5-HTTLPR) genotype and stressful life events when predicting major depression.

Method. We typed the serotonin promoter 5-HTTLPR gene in 1206 male and female twins aged 19–78 years (mean=39, S.D.=11). A DSM-IV diagnosis of major depression was available for 1199 twins. Most of these twins had participated in a 1988–1990 study which included a stressful life events inventory and self-report measure of depression based on the SCL-90 and DSSI/sAD. Complete 5-HTT genotype and life events data, self-report symptoms and major depression diagnoses were available for 1091 subjects. We regressed categorical and ordinal measures of depression onto stressful life events and genotype.

Results. There were significant main effects for stressful life events but there was no evidence for any effect of 5-HTT genotype, nor a genotype×stressful life event interaction.

Conclusions. Regardless of whether our results were based on binary logistic or ordinal regression analyses we found no evidence to support a main effect of 5-HTTLPR, or an interaction between the 5-HTTLPR genotype and stressful life events on major depression. Only 20% of our subjects were aged below 30 years. It is possible that the effect reported by Caspi and colleagues is specific to young people, in which case our study has much less power in this age group.

The strategies used by 40 chronic schizophrenic out-patients with persistent auditory hallucinations to cope with the intrusive phenomena were explored. Frequent coping mechanisms included changes in activity, interpersonal contact, manipulations of physiological arousal, and attentional control. A high risk of suicide was noted.

Coping behaviour appeared somewhat independent of clinical and sociodemographic variables. Successful coping appeared to result from systematic application of widely used coping strategies. The implications for the clinical management of patients with persistent auditory hallucinations are discussed.

Background. The long-term use of methamphetamine (MAMP) can result in psychosis but it is not clear why some individuals develop psychotic symptoms, while others use MAMP regularly over long periods and remain unscathed. We set out to characterize MAMP users and to examine the relationship of pre-morbid personality, pre-morbid social function and other psychiatric disorders to MAMP psychosis.

Method. Four hundred and forty-five amphetamine users were recruited from a psychiatric hospital and a detention centre in Taipei, and were assessed with the Diagnostic Interview for Genetic Studies (DIGS). Their parents were interviewed with the Premorbid Schizoid and Schizotypal Traits (PSST) and the Premorbid Social Adjustment (PSA) schedules. Pre-morbid characteristics and psychiatric co-morbidity were compared between the MAMP users with a lifetime diagnosis of MAMP psychosis and those without.

Results. The MAMP users with psychosis presented a clinical picture which mimicked the positive symptoms of schizophrenia: 85% had auditory hallucinations; 71% persecutory delusions; 63% delusions of reference. Compared with their non-psychotic counterparts, these MAMP users were younger at first MAMP use, used larger amounts of MAMP, had a significantly higher mean PSST score, and higher rates of major depressive disorder, alcohol dependence and antisocial personality disorder.

Conclusions. Earlier and larger use of MAMP was associated with increased risk of psychosis. Our data are also compatible with the view that pre-morbid schizoid/schizotypal personality predisposes MAMP users to develop psychosis, and that the greater the personality vulnerability, the longer the psychosis will persist.

We aimed to establish the treatment effect of physical activity for depression in young people through meta-analysis. Four databases were searched to September 2016 for randomised controlled trials of physical activity interventions for adolescents and young adults, 12–25 years, experiencing a diagnosis or threshold symptoms of depression. Random-effects meta-analysis was used to estimate the standardised mean difference (SMD) between physical activity and control conditions. Subgroup analysis and meta-regression investigated potential treatment effect modifiers. Acceptability was estimated using dropout. Trials were assessed against risk of bias domains and overall quality of evidence was assessed using GRADE criteria. Seventeen trials were eligible and 16 provided data from 771 participants showing a large effect of physical activity on depression symptoms compared to controls (SMD = −0.82, 95% CI = −1.02 to −0.61, p < 0.05, I2 = 38%). The effect remained robust in trials with clinical samples (k = 5, SMD = −0.72, 95% CI = −1.15 to −0.30), and in trials using attention/activity placebo controls (k = 7, SMD = −0.82, 95% CI = −1.05 to −0.59). Dropout was 11% across physical activity arms and equivalent in controls (k = 12, RD = −0.01, 95% CI = −0.04 to 0.03, p = 0.70). However, the quality of RCT-level evidence contributing to the primary analysis was downgraded two levels to LOW (trial-level risk of bias, suspected publication bias), suggesting uncertainty in the size of effect and caution in its interpretation. While physical activity appears to be a promising and acceptable intervention for adolescents and young adults experiencing depression, robust clinical effectiveness trials that minimise risk of bias are required to increase confidence in the current finding. The specific intervention characteristics required to improve depression remain unclear, however best candidates given current evidence may include, but are not limited to, supervised, aerobic-based activity of moderate-to-vigorous intensity, engaged in multiple times per week over eight or more weeks. Further research is needed. (Registration: PROSPERO-CRD 42015024388).