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Meta-analyses show efficacy of mindfulness-based cognitive therapy (MBCT) in terms of relapse prevention and depressive symptom reduction in patients with major depressive disorder (MDD). However, most studies have been conducted in controlled research settings.
We aimed to investigate the effectiveness of MBCT in patients with MDD presenting in real-world clinical practice. Moreover, we assessed whether guideline recommendations for MBCT allocation in regard to recurrence and remission status of MDD hold in clinical practice.
This study assessed a naturalistic cohort of patients with (recurrent) MDD, either current or in remission (n = 765), who received MBCT in a university hospital out-patient clinic in The Netherlands. Outcome measures were self-reported depressive symptoms, worry, mindfulness skills and self-compassion. Predictors were MDD recurrence and remission status, and clinical and sociodemographic variables. Outcome and predictor analyses were conducted with linear regression.
MBCT adherence was high (94%). Patients with a lower level of education had a higher chance of non-adherence. Attending more sessions positively influenced improvement in depressive symptoms. Depressive symptoms significantly reduced from pre- to post-MBCT (Δ mean = 7.7, 95%CI = 7.0–8.5, Cohen's d = 0.75). Improvement of depressive symptoms was independent from MDD recurrence and remission status. Unemployed patients showed less favourable outcomes. Worry, mindfulness skills and self-compassion all significantly improved. These improvements were related to changes in depressive symptoms.
Previous efficacy results in controlled research settings are maintained in clinical practice. Results illustrate that MBCT is effective in routine clinical practice for patients suffering from MDD, irrespective of MDD recurrence and remission status.
Some people diagnosed with schizophrenia are more prone to committing acts of serious violence, especially in the presence of drug or alcohol misuse. The rarity of homicide has meant that no large controlled study has previously examined clinical risk factors.
To determine the risk factors for homicide by males diagnosed with schizophrenia.
A national nested case–control study of all previously admitted males diagnosed with schizophrenia, convicted of homicide between 1 January 1997 and 31 December 2012. Univariate and multivariable conditional logistic regression models were fitted to identify predictors of homicide in this population.
During the observation period 160 male patients with schizophrenia and a history of psychiatric admission were convicted of homicide, and they were matched with 542 male control patients who had not been convicted of homicide. Patients who committed homicide were more likely to have a history of violence and comorbid personality disorder or drug misuse. They were more likely to have missed their last contact with services prior to the offence and to have been non-adherent with their treatment plan. Almost all (94%) of homicides were committed by patients who had a history of alcohol or drug misuse and/or who were not in receipt of planned treatment.
In England and Wales, homicides by patients with schizophrenia without substance misuse and in receipt of planned care are exceptionally rare. To prevent serious violence, mental health services should focus on drug and alcohol misuse, treatment adherence and maintaining contact with services.
Comorbid physical conditions may be more common in people with autism spectrum disorder (ASD) than other people.
To identify what is and what is not known about comorbid physical conditions in people with ASD.
We undertook an umbrella systematic review of systematic reviews and meta-analyses on comorbid physical conditions in people with ASD. Five databases were searched. There were strict inclusion/exclusion criteria. We undertook double reviewing for eligibility, systematic data extraction and quality assessment. Prospective PROSPERO registration: CRD42015020896.
In total, 24 of 5552 retrieved articles were included, 15 on children, 1 on adults, and 8 both on children and adults. Although the quality of included reviews was good, most reported several limitations in the studies they included and considerable heterogeneity. Comorbid physical conditions are common, and some are more prevalent than in the general population: sleep problems, epilepsy, sensory impairments, atopy, autoimmune disorders and obesity. Asthma is not. However, there are substantial gaps in the evidence base. Fewer studies have been undertaken on other conditions and some findings are inconsistent.
Comorbid physical conditions occur more commonly in people with ASD, but the evidence base is slim and more research is needed. Some comorbidities compound care if clinicians are unaware, for example sensory impairments, given the communication needs of people with ASD. Others, such as obesity, can lead to an array of other conditions, disadvantages and early mortality. It is essential that potentially modifiable physical conditions are identified to ensure people with ASD achieve their best outcomes. Heightening clinicians’ awareness is important to aid in assessments and differential diagnoses, and to improve healthcare.
Psychotherapy research aims to investigate predictors and moderators of treatment outcome, but there are few consistent findings. This study aimed to investigate cytokines in patients undergoing treatment for anxiety disorders and whether the level of cytokines moderated the treatment outcome.
Thirty-seven patients with comorbid and treatment-resistant anxiety disorders were investigated using multilevel modelling. Serum cytokine levels were measured three times: pretreatment, in the middle of treatment, and at the end of treatment. Anxiety and metacognitions were measured weekly throughout treatment by self-report.
The levels of MCP1, TNF-α, and IL-1RA did not change during therapy or were not related to the level of anxiety. Metacognitive beliefs predicted anxiety, but the relationship between metacognitions and anxiety was not moderated by cytokines. Limitations of the study include that the patients were not fasting at blood sampling, and we did not assess body mass index, which may affect cytokine levels. The lack of significance for cytokines as a predictor or moderator may be due to a lack of power for testing moderation hypotheses, a problem associated with many psychotherapy studies.
Cytokines did not predict the outcome in the treatment of comorbid anxiety disorders in our sample. Furthermore, cytokines did not moderate the relationship between metacognitions and anxiety.
Physical health outcomes in severe mental illness are worse than in the general population. Routine physical health check completion in this group is poor.
To quantitatively and qualitatively evaluate the impact of point of care (POC) blood testing on physical health check completion in community mental health services.
In a prospective cohort design, we equipped an early intervention service (EIS) and a community mental health team (CMHT) with a POC blood testing device for 6 months. We compared rates of blood test and full physical health check completion in the intervention teams with a matched EIS and CMHT, historically and during the intervention. We explored attitudes to POC testing using thematic analysis of semi-structured interviews with patients and clinicians.
Although the CMHT scarcely used the POC device and saw no change in outcomes, direct comparison of testing rates in the intervention period showed increased physical health check completion in the EIS with the device (rate ratio RR = 5.18; 95% CI 2.54–12.44; P < 0.001) compared with usual care. The rate was consistent with the EIS's increasing rate of testing over time (RR = 0.45; 95% 0.09–2.08; P = 0.32). Similar trends were seen in blood test completion. POC testing was acceptable to patients but clinicians reported usability, provision and impact on the therapeutic relationship as barriers to uptake.
POC testing was beneficial and acceptable to patients and may increase physical health check uptake. Further research, accounting for clinician barriers, is needed to evaluate its clinical and cost-effectiveness.
To investigate if depression risk modifies the association between frailty and mortality in older adults.
Ongoing cohort study.
Albacete city, Spain
Eight hundred subjects, 58.8% women, over 70 years of age from the Frailty and Dependence in Albacete (FRADEA) study.
Frailty phenotype, Geriatric Depression Scale (GDS), comorbidity, disability, and drug use were collected at baseline. Six groups were categorized: (G1: non-frail/no depression risk; G2: non-frail/depression risk; G3: prefrail/no depression risk; G4: prefrail/depression risk; G5: frail/no depression risk; and G6: frail/depression risk). Mean follow-up was 2542 days (SD 1006). GDS was also analyzed as a continuous variable. The association between frailty and depression risk with 10-year mortality was analyzed.
Mean age was 78.5 years. Non-frail was 24.5%, prefrail 56.3%, frail 19.3%, and 33.5% at depression risk. Mean GDS score was 3.7 (SD 3.2), increasing with the number of frailty criteria (p < 0.001). Ten-year mortality rate was 44.9%. Mortality was 21.4% for the non-frail, 45.6% for the prefrail, and 72.7% for the frail participants, 56% for those with depression risk, and 39.3% for those without depression risk. Mean survival times for groups G1 to G6 were, respectively, 3390, 3437, 2897, 2554, 1887, and 1931 days. Adjusted mortality risk was higher for groups G3 (HR 2.1; 95% confidence interval (CI) 1.4–3.1), G4 (HR 2.5; 95% CI 1.7–3.8), G5 (HR 3.8; 95% CI 2.4–6.1), and G6 (HR 4.0; 95% CI 2.6–6.2), compared with G1 (p < 0.001). Interaction was found between frailty and depression risk, although they were independently associated with mortality.
Depression risk increases mortality risk in prefrail older adults but not in non-frail and frail ones. Depression should be monitored in these older adults to optimize health outcomes. Factors modulating the relationship between frailty and depression should be explored in future studies.
We propose that discussions of benzodiazepines in the current psychiatric literature have become negatively biased and have strayed from the scientific evidence base. We advocate returning to the evidence in discussing benzodiazepines and adhering to clear definitions and conceptual rigour in commentary about them.
Clinical intuition suggests that personality disorders hinder the treatment of depression, but research findings are mixed. One reason for this might be the way in which current assessment measures conflate general aspects of personality disorders, such as overall severity, with specific aspects, such as stylistic tendencies. The goal of this study was to clarify the unique contributions of the general and specific aspects of personality disorders to depression outcomes.
Patients admitted to the Menninger Clinic, Houston, between 2012 and 2015 (N = 2352) were followed over a 6–8-week course of multimodal inpatient treatment. Personality disorder symptoms were assessed with the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, 4th edition Axis II Personality Screening Questionnaire at admission, and depression severity was assessed using the Patient Health Questionnaire-9 every fortnight. General and specific personality disorder factors estimated with a confirmatory bifactor model were used to predict latent growth curves of depression scores in a structural equation model.
The general factor predicted higher initial depression scores but not different rates of change. By contrast, the specific borderline factor predicted slower rates of decline in depression scores, while the specific antisocial factor predicted a U shaped pattern of change.
Personality disorder symptoms are best represented by a general factor that reflects overall personality disorder severity, and specific factors that reflect unique personality styles. The general factor predicts overall depression severity while specific factors predict poorer prognosis which may be masked in prior studies that do not separate the two.
Although long-term outcomes of girls with attention-deficit hyperactivity disorder are understudied, high risk for adolescent and young-adult self-harm is salient. We present data on predictors and mediators of such risk, highlighting a recent dual-process model involving trait impulsivity plus family- and peer-related contributors. We conclude with recommendations for assessment and preventive intervention.
Atypical communication characteristics (ACCs), such as speech delay, odd pitch, and pragmatic difficulties, are common features of autism spectrum disorder (ASD) as are the symptoms of a wide range of psychiatric disorders. Using a simple retrospective method, this study aimed to better understand the relation and stability of ACCs with a broad range of psychiatric symptoms among large, well-characterized samples of clinic-referred children and adolescents with and without ASD. Youth with ASD had higher rates and a more variable pattern of developmental change in ACCs than the non-ASD diagnostic group. Latent class analysis yielded three ACC stability subgroups within ASD: Stable ACCs, Mostly Current-Only ACCs, and Little Professors. Subgroups exhibited differences in severity of ASD symptomatology, co-occurring psychiatric symptoms, and other correlates. Our findings provide support for the clinical utility of characterizing caregiver-perceived changes in ACCs in identifying children at risk for co-occurring psychopathology and other clinically relevant variables.
Research on sickness absence has typically focussed on single diagnoses, despite increasing recognition that long-term health conditions are highly multimorbid and clusters comprising coexisting mental and physical conditions are associated with poorer clinical and functional outcomes. The digitisation of sickness certification in the UK offers an opportunity to address sickness absence in a large primary care population.
Lambeth Datanet is a primary care database which collects individual-level data on general practitioner consultations, prescriptions, Quality and Outcomes Framework diagnostic data, sickness certification (fit note receipt) and demographic information (including age, gender, self-identified ethnicity, and truncated postcode). We analysed 326 415 people's records covering a 40-month period from January 2014 to April 2017.
We found significant variation in multimorbidity by demographic variables, most notably by self-defined ethnicity. Multimorbid health conditions were associated with increased fit note receipt. Comorbid depression had the largest impact on first fit note receipt, more than any other comorbid diagnoses. Highest rates of first fit note receipt after adjustment for demographics were for comorbid epilepsy and rheumatoid arthritis (HR 4.69; 95% CI 1.73–12.68), followed by epilepsy and depression (HR 4.19; 95% CI 3.60–4.87), chronic pain and depression (HR 4.14; 95% CI 3.69–4.65), cardiac condition and depression (HR 4.08; 95% CI 3.36–4.95).
Our results show striking variation in multimorbid conditions by gender, deprivation and ethnicity, and highlight the importance of multimorbidity, in particular comorbid depression, as a leading cause of disability among working-age adults.
Although attention-deficit hyperactivity disorder (ADHD) is classified as a neurodevelopmental disorder in the latest diagnostic manuals, it shows phenotypic and genetic associations of similar magnitudes across neurodevelopmental, externalising and internalising disorders.
To investigate if ADHD is aetiologically more closely related to neurodevelopmental than externalising or internalising disorder clusters, after accounting for a general psychopathology factor.
Full and maternal half-sibling pairs (N = 774 416), born between 1980 and 1995, were identified from the Swedish Medical Birth and Multi-Generation Registers, and ICD diagnoses were obtained from the Swedish National Patient Register. A higher-order confirmatory factor analytic model was fitted to examine associations between ADHD and a general psychopathology factor, as well as a neurodevelopmental, externalising and internalising subfactor. Quantitative genetic modelling was performed to estimate the extent to which genetic, shared and non-shared environmental effects influenced the associations with ADHD.
ADHD was significantly and strongly associated with all three factors (r = 0.67–0.75). However, after controlling for a general psychopathology factor, only the association between ADHD and the neurodevelopmental-specific factor remained moderately strong (r = 0.43, 95% CI = 0.42–0.45) and was almost entirely influenced by genetic effects. In contrast, the association between ADHD and the externalising-specific factor was smaller (r = 0.25, 95% CI = 0.24–0.27), and largely influenced by non-shared environmental effects. There remained no internalising-specific factor after accounting for a general factor.
Findings suggest that ADHD comorbidity is largely explained by genetically influenced general psychopathology, but the strong link between ADHD and other neurodevelopmental disorders is also substantially driven by unique genetic influences.
Health factors such as diabetes, severe obesity and chronic kidney disease are all associated with a more severe outcome following coronavirus disease 2019 (COVID-19) infection. However, there has been little exploration into the impact of mental and behavioural disorders on outcomes associated with COVID-19. We investigated outcomes for older people who used mental health services. Those who had a COVID-19-associated death had previously rated worse across a range of health and social problems, including mental health related problems. Our findings evidence the need to urgently explore whether mental and behavioural disorders should also be considered a health risk factor for a more severe outcome from COVID-19 infection in older people.
Light is the most important environmental influence (zeitgeber) on the synchronization of the circadian system in humans. Excess light exposure during the evening and night-time affects secretion of the hormone melatonin, which in turn modifies the temporal organization of circadian rhythms, including the sleep–wake cycle. As sleep disturbances are prominent in critically ill medical and psychiatric patients, researchers began to examine the impact of light exposure on clinical outcomes and length of hospitalization. In psychiatric inpatients, exposure to bright morning light or use of blue blocking glasses have proved useful interventions for mood disorders. Recently, knowledge about light and the circadian system has been applied to the design of inpatient facilities with dynamic lighting systems that change according to time of day. The installation of ‘circadian lighting’ alongside technologies for monitoring sleep–wake patterns could prove to be one of the most practical and beneficial innovations in inpatient psychiatric care for more than half a century.
The comorbidity of obsessive–compulsive symptoms (OCS) in the context of schizophrenia is often not recognised by clinicians, and patients may not report these symptoms until they become severe. However, there is a reported prevalence of 10–24% for obsessive–compulsive disorder (OCD) in schizophrenia and related disorders. The onset of OCS/OCD has been noted to occur both before and after the diagnosis of schizophrenia or schizoaffective disorder. It has also been known to occur following commencement of treatment with antipsychotic medications, especially clozapine. Current literature provides limited guidance for treatment. Review of the current evidence supports: addition of selective serotonin reuptake inhibitors (SSRIs) to antipsychotics; addition of aripiprazole, amisulpride or lamotrigine; or reduction in the dosage of clozapine. There is also evidence supporting the addition of cognitive–behavioural therapy and electroconvulsive therapy (ECT). The SSRIs that are evidenced to be useful are fluvoxamine, escitalopram, sertraline and paroxetine. More studies are needed to expand the evidence base. Early targeted interventions are recommended.
While taxonomy segregates anxiety symptoms into diagnoses, patients typically present with multiple diagnoses; this poses major challenges, particularly for youth, where mixed presentation is particularly common. Anxiety comorbidity could reflect multivariate, cross-domain interactions insufficiently emphasized in current taxonomy. We utilize network analytic approaches that model these interactions by characterizing pediatric anxiety as involving distinct, inter-connected, symptom domains. Quantifying this network structure could inform views of pediatric anxiety that shape clinical practice and research.
Participants were 4964 youths (ages 5–17 years) from seven international sites. Participants completed standard symptom inventory assessing severity along distinct domains that follow pediatric anxiety diagnostic categories. We first applied network analytic tools to quantify the anxiety domain network structure. We then examined whether variation in the network structure related to age (3-year longitudinal assessments) and sex, key moderators of pediatric anxiety expression.
The anxiety network featured a highly inter-connected structure; all domains correlated positively but to varying degrees. Anxiety patients and healthy youth differed in severity but demonstrated a comparable network structure. We noted specific sex differences in the network structure; longitudinal data indicated additional structural changes during childhood. Generalized-anxiety and panic symptoms consistently emerged as central domains.
Pediatric anxiety manifests along multiple, inter-connected symptom domains. By quantifying cross-domain associations and related moderation effects, the current study might shape views on the diagnosis, treatment, and study of pediatric anxiety.
Major depressive disorder (MDD) and alcohol use disorder (AUD) are highly comorbid, with greater clinical complexity and psychosocial impairment. Several antidepressants have been used in this population, with mixed results. This preliminary study aims to investigate the effects of the multimodal antidepressant vortioxetine in MDD + AUD subjects.
We retrospectively evaluated 57 MDD + AUD and 56 MDD outpatients, matched for baseline characteristics. Patients were assessed after 1, 3, and 6 months treatment with vortioxetine (10-20 mg/d, flexibly dosed) in combination with continuous psychosocial support. The primary outcome was improvement in depressive symptoms measured by the Montgomery-Åsberg Depression Rating Scale. We also investigated changes in anxiety, anhedonia, cognition, functioning, quality of life, and clinical global severity using the following instruments: Hamilton Anxiety Rating Scale, Snaith-Hamilton Pleasure Scale, Digit Symbol Substitution Test, Perceived Deficits Questionnaire-Depression, Functioning Assessment Short Test, Quality of Life Index, and Clinical Global Impression-Severity Scale.
Vortioxetine significantly improved mood in MDD + AUD patients (P < .001), with no differences when compared to MDD (P = .36). A substantial rate (45.6%) of comorbid subjects obtained clinical remission at endpoint (P = .36 vs MDD). We additionally observed baseline to endpoint improvements on all secondary outcomes (P < .001), with no significant difference between groups. Overall, vortioxetine was safe and well tolerated.
Given its effectiveness on mood, cognition, and functioning, its good safety and tolerability profile, and low potential for abuse, vortioxetine could represent a valid pharmacological intervention in MDD + AUD patients as part of an integrated therapeutic-rehabilitation program.
Substance use occurs at a high rate in persons with a psychiatric disorder. Genetically informative studies have the potential to elucidate the etiology of these phenomena. Recent developments in genome-wide association studies (GWAS) allow new avenues of investigation.
Using results of GWAS meta-analyses, we performed a factor analysis of the genetic correlation structure, a genome-wide search of shared loci, and causally informative tests for six substance use phenotypes (four smoking, one alcohol, and one cannabis use) and five psychiatric disorders (ADHD, anorexia, depression, bipolar disorder, and schizophrenia).
Two correlated externalizing and internalizing/psychosis factor were found, although model fit was beneath conventional standards. Of 458 loci reported in previous univariate GWAS of substance use and psychiatric disorders, about 50% (230 loci) were pleiotropic with additional 111 pleiotropic loci not reported from past GWAS. Of the 341 pleiotropic loci, 152 were associated with both substance use and psychiatric disorders, implicating neurodevelopment, cell morphogenesis, biological adhesion pathways, and enrichment in 13 different brain tissues. Seventy-five and 114 pleiotropic loci were specific to either psychiatric disorders or substance use phenotypes, implicating neuronal signaling pathway and clathrin-binding functions/structures, respectively. No consistent evidence for phenotypic causation was found across different Mendelian randomization methods.
Genetic etiology of substance use and psychiatric disorders is highly pleiotropic and involves shared neurodevelopmental path, neurotransmission, and intracellular trafficking. In aggregate, the patterns are not consistent with vertical pleiotropy, more likely reflecting horizontal pleiotropy or more complex forms of phenotypic causation.
Impulsivity and compulsivity are the defining features of various psychiatric disorders, including attention-deficit/hyperactivity disorder, obsessive–compulsive disorder, and behavioral and substance addictions. Once thought to be diametrically opposed, compulsivity and impulsivity are increasingly recognized as orthogonal symptom dimensions that are linked by shared neurobiological mechanisms. This chapter selectively reviews impulsivity and compulsivity from a transdiagnostic perspective. It begins by discussing the neurobiology of impulsivity and compulsivity and the relationship of these constructs to addictive disorders. The chapter then discusses the clinical features of specific compulsive and impulsive disorders (as well as gambling disorder, a putative behavioral addiction), with a focus on comorbidity and treatment. The complex interrelationships among compulsive, impulsive, and addictive disorders have implications for how these disorders are assessed and treated.
Compulsive buying disorder (CBD) is characterized by excessive shopping of unneeded or unwanted items that leads to distress or impairment. The classification of compulsive buying disorder remains elusive. Some researchers suggest that it should be grouped with behavioral addictions, while others have linked it to mood and to obsessive-compulsive disorders. CBD is relatively common, with prevalence rates in general population varying from 2 percent to 8 percent across different countries. Age of onset typically coincides with the age at which people first establish credit accounts and with emancipation from home. It shares similar clinical characteristics with classical addictive disorders including compulsive preoccupation, craving, loss of control and negative consequences of shopping. CBD tends to run in families and is associated with significant psychiatric comorbidity, particularly mood and anxiety disorders, substance use disorders, eating disorders, and other disorders of impulse control. Little is known about the neurobiological and genetic mechanisms underlying CBD, nor is there standard treatment. Cognitive-behavioral therapy is promising, while medication studies have been disappointing. Future research on CBD should target etiologic mechanisms and both psychological and pharmacological treatments. Beyond treatment, educational (i.e., learning new coping skills, media literacy instruction) and public policy efforts, as well as parental modeling of appropriate buying behavior, could be beneficial to those with CBD.