Cannabis use and hypomania in young people: a prospective analysis

Background: Cannabis use in young people is common and associated with psychiatric disorders. However, the prospective link between cannabis use and bipolar disorder symptoms has rarely been investigated. The study hypothesis was that adolescent cannabis use is associated with hypomania in early adulthood via several potential etiological pathways. Methods: Data were used from the Avon Longitudinal Study of Parents and Children, a UK birth cohort study. The prospective link between cannabis use at age 17 and hypomania at age 22–23 years was tested using regression analysis, adjusted for gender, early environmental risk factors, alcohol and drug use, and depression and psychotic symptoms at age 18 years. Path analysis examined direct and indirect effects of the link and whether gender, childhood family adversity, or childhood abuse are associated with hypomania via an increased risk of cannabis use. Results: Data were available on 3370 participants. Cannabis use at least 2–3 times weekly was associated with later hypomania (OR = 2.21, 95% CI = 1.49–3.28) after adjustment. There was a dose–response relationship (any use vs weekly). Cannabis use mediated the association of both childhood sexual abuse and hypomania, and male gender and hypomania. The cannabis use-hypomania link was not mediated by depression or psychotic symptoms. Conclusions: Adolescent cannabis use may be an independent risk factor for future hypomania, and the nature of the association suggests a potential causal link. Cannabis use mediates the link between childhood abuse and future hypomania. As such it might be a useful target for indicated prevention of hypomania

Epidemiology and risk factors for bipolar disorder

Bipolar disorder is a multifactorial illness with uncertain aetiology. Knowledge of potential risk factors enables clinicians to identify patients who are more likely to develop bipolar disorder, which directs further investigation, follow up and caution when prescribing. Ideally, identifying directly causative factors for bipolar disorder would enable intervention on an individual or population level to prevent the development of the illness, and improve outcomes through earlier treatment. This article reviews the epidemiology of bipolar disorder, along with putative demographic, genetic and environmental risk factors, while assessing the strength of these associations and to what extent they might be said to be ‘causative’. While numerous genetic and environmental risk factors have been identified, the attributable risk of individual factors is often small, and most are not specific to bipolar disorder but are associated with several mental illnesses. Therefore, while some genetic and environmental factors have strong evidence supporting their association with bipolar disorder, fewer have sufficient evidence to establish causality. There is increasing interest in the role of specific gene–environment interactions, as well as the mechanisms by which risk factors interact to lead to bipolar disorder

Chapter 9 Bipolar disorder

The Adult Psychiatric Morbidity Survey (APMS) series provides data on the prevalence of both treated and untreated psychiatric disorder in the English adult population (aged 16 and over). This survey is the fourth in a series and was conducted by NatCen Social Research, in collaboration with the University of Leicester, for NHS Digital. The previous surveys were conducted in 1993 (16-64 year olds) and 2000 (16-74 year olds) by the Office for National Statistics, which covered England, Scotland and Wales. The 2007 Survey included people aged over 16 and covered England only. The survey used a robust stratified, multi-stage probability sample of households and assesses psychiatric disorder to actual diagnostic criteria for several disorders. The report features chapters on: common mental disorders, mental health treatment and service use, post-traumatic stress disorder, psychotic disorder, autism, personality disorder, attention-deficit/hyperactivity disorder, bipolar disorder, alcohol, drugs, suicidal thoughts, suicide attempts and self-harm, and comorbidity. All the APMS surveys have used largely consistent methods. They have been designed so that the survey samples can be combined. This is particularly useful for examination of low prevalence population groups and disorders. For example, in the APMS 2014 survey report, analyses of psychotic disorder (Chapter 5) and autism (Chapter 6) have been run using the 2007 and 2014 samples combined. Due to the larger sample size, we consider estimates based on the combined sample to be the more robust. Further notes on the Autism chapter can be found with that chapter and in the ‘Additional notes on autism’ document below

Is treatment for bipolar disorder more effective earlier in illness course?:A comprehensive literature review

Background: We aimed to investigate a key element of the early intervention approach whether treatment at an earlier stage of bipolar disorder is more effective than later in its course. Methods: A comprehensive literature review using Medline, Embase, Psychinfo, PsycArticle, and Web of Science, as data sources, with a subsequent narrative synthesis. Study quality was assessed using the Cochrane risk of bias method. Results: Our search strategy yielded eight primary papers and two meta-analyses (of psychological therapies and Olanzapine) in total representing 8942 patients. Five studies focused on comparisons between first and multiple episodes, and the others on fewer vs more episode categories. There was a consistent finding, suggesting treatment in earlier illness stage resulted in better outcomes in terms of response, relapse rate, time to recurrence, symptomatic recovery, remission, psychosocial functioning, and employment. This effect was found for pharmacological (Lithium, Olanzapine, Divalproex) and psychological treatments. Limitations: There was high risk of selection, performance, and attrition bias in most studies. First admission or presentation is unlikely to equate to first episode, because of the duration of untreated illness. Some patients having experienced multiple episodes could be “treatment resistant”. Study heterogeneity precluded meta-analysis. Conclusions: Psychological and pharmacological treatments in the early stages of illness are more effective than in the later stages of bipolar disorder across multiple domains. There is a first episode and the early phase effect. Consistent with the staging model of illness, findings provide evidence for the clinical utility of an early intervention approach in bipolar disorder to improve patient outcomes

Personality traits and change in depression status at 18 months:Findings from a British Psychiatric Morbidity Survey

BACKGROUND: Depression is a common mental disorder, yet it shows low remission rates. The available evidence on personality traits as factors associated with the course of depression has common methodological limitations. Identifying personality traits linked with depression can improve understanding of the course of illness. Therefore, we aimed to investigate personality traits that are associated with the course of depression over 18 months.METHODS: longitudinal data of 2366 Adult Psychiatric Morbidity Survey respondents were analysed. Assessments were applied at two-time points (baseline) and follow-up (about 18 months later). We assessed the total score on the screening questionnaire from the Structured Clinical Interview (SCID-II) for the dependent, obsessive-compulsive, and borderline personalities. Depression was measured using the revised Clinical Interview Schedule (CIS-R) version.RESULTS: An increase of one score on the borderline personality scale at baseline increased the odds of experiencing persistent depression by 1.50 times (OR = 1.50, 95 % CI [1.22-1.86]), depression onset by 1.30 times (OR = 1.30, 95 % CI [1.14-1.50]), and recovery by 1.52 times (OR = 1.52, 95 % CI [1.35-1.70]), comparing to no depression group. Elevated scores of dependent personality traits significantly predicted depression persistence (OR = 1.95, 95 % CI [1.52-2.49]). An increase of one score on the obsessive-compulsive personality scale increases the odds of depression onset by 1.21 times (OR = 1.21, 95 % CI [1.04-1.39]).LIMITATIONS: The APMS survey defined depression statuses in a limited sense, which may affect the generalisability of these results.CONCLUSION: The present study confirms previous findings and contributes evidence suggesting that personality dysfunctions worsen depression outcomes.</p

Depression and schizophrenia : cause, consequence or trans-diagnostic issue?

The presence of depression in schizophrenia has been a challenge to the Kraepelinian dichotomy, with various attempts to save the fundamental distinction including evoking and refining diagnoses such as schizoaffective disorder. But the tectonic plates are shifting. Here we put forward a summary of recent evidence regarding the prevalence, importance, possible aetiological pathways and treatment challenges that recognising depression in schizophrenia bring. Taken together we propose that depression is more than co-morbidity and that increased effective therapeutic attention to mood symptoms will be needed to improve outcomes and to support prevention

At-risk mental state for psychosis : identification and current treatment approaches

© The Royal College of Psychiatrists 2016. The concept of an ‘at-risk mental state’ for psychosis arose from previous work attempting to identify a putative psychosis prodrome. In this article we summarise the current criteria used to identify ‘at-risk’ individuals, such as the ultra-highrisk (UHR) criteria, and the further identification of important clinical risk factors or biomarkers to improve prediction of who might develop a psychotic disorder. We also discuss important ethical issues in classifying and treating at-risk individuals, current treatment trials in this area and what treatment current services can offer

Bullying victimization and psychosis : the inter-dependence and independence of risk trajectories

In the last several years a number of studies have noted an association between bullying and psychotic symptoms. Our aim here is to offer an overview on the topic, focusing especially on a developmental perspective. First, we highlight the latest studies to date regarding psychosis across the continuum and its relationship with bullying. In the second section, we summarize the three main explanatory models investigated: developmental, biological and cognitive models. In the discussion section we affirm that the sharing of numerous risk factors put people at risk of both psychosis and of being bullied, and bullying itself may further enhance the development of psychosis. Moreover, bullying is a risk factor for several mental disorders and is non-specific for psychosis, but there is some particularity in the trajectory involved between victimization and the onset of psychosis. In conclusion we recommend that the study of bullying in psychosis requires careful study of the developmental trajectories involved and research should now focus on how personal, social and biological factors interact between them