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Little is known about the effect of ethnicity on the response to antipsychotic medication in patients with schizophrenia.
To determine whether ethnicity moderates the response to antipsychotic medication in patients with schizophrenia, and whether this moderation is independent of confounders.
We analysed 18 short-term, placebo-controlled registration trials of atypical antipsychotic medications in patients with schizophrenia (N = 3880). A two-step, random-effects, individual patient data meta-analysis was applied to establish the moderating effect of ethnicity (White versus Black) on symptom improvement according to the Brief Psychiatric Rating Scale (BPRS) and on response, defined as >30% BPRS reduction. These analyses were corrected for baseline severity, baseline negative symptoms, age and gender. A conventional meta-analysis was performed to determine the effect size of antipsychotic treatment for each ethnic group separately.
In the complete data-set, 61% of patients were White, 25.6% of patients were Black and 13.4% of patients were of other ethnicities. Ethnicity did not moderate the efficacy of antipsychotic treatment: pooled β-coefficient for the interaction between treatment and ethnic group was −0.582 (95% CI −2.567 to 1.412) for mean BPRS change, with an odds ratio of 0.875 (95% CI 0.510–1.499) for response. These results were not modified by confounders.
Atypical antipsychotic medication is equally effective in both Black and White patients with schizophrenia. In registration trials, White and Black patients were overrepresented relative to other ethnic groups, limiting the generalisability of our findings.
Cognitive deficits may be characteristic for only a subgroup of first-episode psychosis (FEP) and the link with clinical and functional outcomes is less profound than previously thought. This study aimed to identify cognitive subgroups in a large sample of FEP using a clustering approach with healthy controls as a reference group, subsequently linking cognitive subgroups to clinical and functional outcomes.
204 FEP patients were included. Hierarchical cluster analysis was performed using baseline brief assessment of cognition in schizophrenia (BACS). Cognitive subgroups were compared to 40 controls and linked to longitudinal clinical and functional outcomes (PANSS, GAF, self-reported WHODAS 2.0) up to 12-month follow-up.
Three distinct cognitive clusters emerged: relative to controls, we found one cluster with preserved cognition (n = 76), one moderately impaired cluster (n = 74) and one severely impaired cluster (n = 54). Patients with severely impaired cognition had more severe clinical symptoms at baseline, 6- and 12-month follow-up as compared to patients with preserved cognition. General functioning (GAF) in the severely impaired cluster was significantly lower than in those with preserved cognition at baseline and showed trend-level effects at 6- and 12-month follow-up. No significant differences in self-reported functional outcome (WHODAS 2.0) were present.
Current results demonstrate the existence of three distinct cognitive subgroups, corresponding with clinical outcome at baseline, 6- and 12-month follow-up. Importantly, the cognitively preserved subgroup was larger than the severely impaired group. Early identification of discrete cognitive profiles can offer valuable information about the clinical outcome but may not be relevant in predicting self-reported functional outcomes.
Given the ongoing opioid crisis in the United States (US), we investigated the opioid situation in Europe. The aims of the study are to provide an overview of trends in prescription opioid (PO) use and opioid-related adversities between 2010 and 2018 for different opioids in 19 European countries and to present a comparison with similar data from the US.
A multisource database study with national data from 19 European countries evaluating trends between 2010 and 2018 in (a) PO consumption, (b) high-risk (HR) opioid users, (c) opioid-related hospital admissions, (d) opioid-related overdose deaths, (e) opioid use disorder treatment entries, and (f) patients in opioid substitution therapy (OST). Within and between-country comparisons and comparisons with data from the US were made.
There was considerable variation between European countries. Most countries showed increased PO consumption with the largest increase and the highest consumption in the United Kingdom (UK) compared to the rest of Europe and the US in 2018 (UK: 58,088 defined daily doses for statistical purposes/1000 population/day). In 2018, Scotland had the highest rates (per 100,000 population) of HR opioid users (16·2), opioid-related hospital admissions (118), opioid-related deaths (22·7), opioid use disorder treatment admissions (190), and OST patients (555) of all included European countries. These rates were similar or even higher than those in the US in 2018. Other countries with high rates of opioid-related adversities were Northern Ireland (synthetic and “other” opioids), Ireland (heroin and methadone), and England (all opioids). All other countries had no or little increase in opioid-related adversities.
Apart from the British Isles and especially Scotland, there is no indication of an opioid crisis comparable to that in the US in the 19 European countries that were part of this study. More research is needed to identify drivers and develop interventions to stop the emerging opioid crisis in the UK and Ireland.
There is increasing evidence that smoking is a risk factor for severe mental illness, including bipolar disorder. Conversely, patients with bipolar disorder might smoke more (often) as a result of the psychiatric disorder.
We conducted a bidirectional Mendelian randomisation (MR) study to investigate the direction and evidence for a causal nature of the relationship between smoking and bipolar disorder.
We used publicly available summary statistics from genome-wide association studies on bipolar disorder, smoking initiation, smoking heaviness, smoking cessation and lifetime smoking (i.e. a compound measure of heaviness, duration and cessation). We applied analytical methods with different, orthogonal assumptions to triangulate results, including inverse-variance weighted (IVW), MR-Egger, MR-Egger SIMEX, weighted-median, weighted-mode and Steiger-filtered analyses.
Across different methods of MR, consistent evidence was found for a positive effect of smoking on the odds of bipolar disorder (smoking initiation ORIVW = 1.46, 95% CI 1.28–1.66, P = 1.44 × 10−8, lifetime smoking ORIVW = 1.72, 95% CI 1.29–2.28, P = 1.8 × 10−4). The MR analyses of the effect of liability to bipolar disorder on smoking provided no clear evidence of a strong causal effect (smoking heaviness betaIVW = 0.028, 95% CI 0.003–0.053, P = 2.9 × 10−2).
These findings suggest that smoking initiation and lifetime smoking are likely to be a causal risk factor for developing bipolar disorder. We found some evidence that liability to bipolar disorder increased smoking heaviness. Given that smoking is a modifiable risk factor, these findings further support investment into smoking prevention and treatment in order to reduce mental health problems in future generations.
Background. Frequency and quantity of alcohol consumption are metrics commonly used to measure alcohol consumption behaviors. Epidemiological studies indicate that these alcohol consumption measures are differentially associated with (mental) health outcomes and socioeconomic status (SES). The current study aims to elucidate to what extent genetic risk factors are shared between frequency and quantity of alcohol consumption, and how these alcohol consumption measures are genetically associated with four broad phenotypic categories: (i) SES; (ii) substance use disorders; (iii) other psychiatric disorders; and (iv) psychological/personality traits.
Methods. Genome-Wide Association analyses were conducted to test genetic associations with alcohol consumption frequency (N = 438 308) and alcohol consumption quantity (N = 307 098 regular alcohol drinkers) within UK Biobank. For the other phenotypes, we used genome-wide association studies summary statistics. Genetic correlations (rg) between the alcohol measures and other phenotypes were estimated using LD score regression.
Results. We found a substantial genetic correlation between the frequency and quantity of alcohol consumption (rg = 0.52). Nevertheless, both measures consistently showed opposite genetic correlations with SES traits, and many substance use, psychiatric, and psychological/personality traits. High alcohol consumption frequency was genetically associated with high SES and low risk of substance use disorders and other psychiatric disorders, whereas the opposite applies for high alcohol consumption quantity.
Conclusions. Although the frequency and quantity of alcohol consumption show substantial genetic overlap, they consistently show opposite patterns of genetic associations with SES-related phenotypes. Future studies should carefully consider the potential influence of SES on the shared genetic etiology between alcohol and adverse (mental) health outcomes.
Supervised injectable heroin (SIH) treatment has emerged over the past 15 years as an intensive treatment for entrenched heroin users who have not responded to standard treatments such as oral methadone maintenance treatment (MMT) or residential rehabilitation.
To synthesise published findings for treatment with SIH for refractory heroin-dependence through systematic review and meta-analysis, and to examine the political and scientific response to these findings.
Randomised controlled trials (RCTs) of SIH treatment were identified through database searching, and random effects pooled efficacy was estimated for SIH treatment. Methodological quality was assessed according to criteria set out by the Cochrane Collaboration.
Six RCTs met the inclusion criteria for analysis. Across the trials, SIH treatment improved treatment outcome, i.e. greater reduction in the use of illicit ‘street’ heroin in patients receiving SIH treatment compared with control groups (most often receiving MMT).
SIH is found to be an effective way of treating heroin dependence refractory to standard treatment. SIH may be less safe than MMT and therefore requires more clinical attention to manage greater safety issues. This intensive intervention is for a patient population previously considered unresponsive to treatment. Inclusion of this low-volume, high-intensity treatment can now improve the impact of comprehensive healthcare provision.
Impulsivity is a multidimensional construct, including impulsive decision-making and impulsive action, representing relatively independent neurocircuitries. ADHD is treated with methylphenidate, a drug that binds to dopamine transporters. This study in 24 adult male patients with ADHD shows that dopamine transporter occupancy by methylphenidate in the putamen correlates with improvements in cognitive but not in motor impulsivity.
This chapter reviews the evidence for first-line treatment of major depressive disorder (MDD), and strategies for patients with treatment-resistant depression. Many trials have investigated the efficacy of selective serotonin reuptake inhibitors (SSRIs) compared with other antidepressants. Patients with MDD are at higher risk of suicide, and guidelines indicate that patients should be assessed for suicide at the start of treatment and regularly over the course of treatment. As augmenting agents, atypical antipsychotics, lithium, and triiodothyronine (T3) have been studied the most extensively, and shown to have benefit. However, their risks and side-effect profiles may make them less attractive to patients, and patient preference and safety should determine treatment decisions for refractory or chronic MDD. The use of biomarkers, including pharmacogenetic testing, may one day provide more accurate predictors of response or adverse outcomes, allowing targeted treatments and the promise of personalized medicine.
This chapter emphasizes the importance of adequate care of pharmacological evidence on treating panic disorder. It focuses on the optimal first-line pharmacotherapy of panic disorder. The chapter discusses the optimal duration of maintenance therapy, and describes the optimal approach to pharmacotherapy in the treatment-refractory patient. It reviews the antidepressants and benzodiazepines with regard to efficacy in acute and long-term treatment, the side-effects and risks involved, drop-out rates, onset of action and efficacy in comorbid conditions. Given the comparable efficacy of the pharmacological classes described in acute phase treatment and the efficacy in long-term treatment, other considerations determine which agent should be considered the first-line pharmacotherapy of panic disorder. The first-line pharmacotherapy for panic disorder has been selective serotonin reuptake inhibitor (SSRIs) for some time, and there is now sufficient evidence to indicate that the SNRI venlafaxine should also be considered as a first-line agent.
Inconsistent findings have been reported on the role of comorbid alcohol
use disorders as risk factors for a persistent course of depressive and
To determine whether the course of depressive and/or anxiety disorders is
conditional on the type (abuse or dependence) or severity of comorbid
alcohol use disorders.
In a large sample of participants with current depression and/or anxiety
(n = 1369) we examined whether the presence and
severity of DSM-IV alcohol abuse or alcohol dependence predicted the
2-year course of depressive and/or anxiety disorders.
The persistence of depressive and/or anxiety disorders at the 2-year
follow-up was significantly higher in those with remitted or current
alcohol dependence (persistence 62% and 67% respectively), but not in
those with remitted or current alcohol abuse (persistence 51% and 46%
respectively), compared with no lifetime alcohol use disorder
(persistence 53%). Severe (meeting six or seven diagnostic criteria) but
not moderate (meeting three to five criteria) current dependence was a
significant predictor as 95% of those in the former group still had a
depressive and/or anxiety disorder at follow-up. This association
remained significant after adjustment for severity of depression and
anxiety, psychosocial factors and treatment factors.
Alcohol dependence, especially severe current dependence, is a risk
factor for an unfavourable course of depressive and/or anxiety disorders,
whereas alcohol abuse is not.
Neurotoxic effects of ecstasy have been reported, although it remains
unclear whether effects can be attributed to ecstasy, other recreational
drugs or a combination of these.
To assess specific/independent neurotoxic effects of heavy ecstasy use
and contributions of amphetamine, cocaine and cannabis as part of The
Netherlands XTC Toxicity (NeXT) study.
Effects of ecstasy and other substances were assessed with
1H-magnetic resonance spectroscopy, diffusion tensor imaging,
perfusion weighted imaging and
([123I]β-CIT) single photon emission computed tomography
(serotonin transporters) in a sample (n=71) with broad
variation in drug use, using multiple regression analyses.
Ecstasy showed specific effects in the thalamus with decreased
[123I]β-CIT binding, suggesting serotonergic axonal damage;
decreased fractional anisotropy, suggesting axonal loss; and increased
cerebral blood volume probably caused by serotonin depletion. Ecstasy had
no effect on brain metabolites and apparent diffusion coefficients.
Converging evidence was found for a specific toxic effect of ecstasy on
serotonergic axons in the thalamus.
Wim Groot, Professor of Health Economics Maastricht University; Coordinator ‘NWO Prioriteitprogramma’ SCHOLAR on ‘Schooling, Labour Market and Economic Development’ University of Amsterdam,
Henriëtte Maassen van den Brink, Professor of Economics Department of Economics and Econometrics University of Amsterdam
Education and health are the two most important investments in human capital individuals make. Their economic value lies in the effects they have on productivity: both education and health make individuals more productive. Education and health have a considerable impact on individual well being as well. The wealth of nations is to a large extent determined by the educational attainment and the health status of their population. Compared to the abundance of empirical studies that document the individual rate of return to education (see previous chapters), we know little about the returns to investments in health.
There is evidence to support the claim that there is a positive relation between education and health. Some of this evidence is surveyed in Grossman and Kaestner (1997). This survey concludes that ‘A number of studies in the United States suggest that years of formal schooling completed is the most important correlate of good health’ (Grossman and Kaestner, 1997: 73). Not only in the United States, but also elsewhere – and in particular in developing countries – the positive association between education and health is well documented.
According to the 2003 Human Development Report, ‘Education, health, nutrition and water and sanitation complement each other, with investments in any one contributing to better outcomes in the others’ (UN, 2003: 85). The positive association between education and health can be partly attributed to differences in income between countries.
Education affects health, but investments in health and education have some common attributes as well.
One of the most important social developments of the past decades in western countries has been the increase in the educational level of the population. The increase in the education level of the workforce has been accompanied by higher than average growth rates for jobs for better-educated workers. Also, for a number of jobs there has been an upgrade in the skills needed to perform adequately. Despite this increase, we may ask whether the increase in the demand for better-educated labour has kept pace with the increase in the supply of skilled workers. If the growth in the supply of better-educated people outpaces the growth in demand, overeducation of the workforce is the likely result. Overeducation is defined as a job–worker match where the worker actually has more education than is required for the job (and conversely for undereducation). It is commonly measured in years. In 1981 Duncan and Hoffman started the overeducation literature by distinguishing education required for the job and actual education. In the 1980s Hartog (see Hartog and Oosterbeek, 1988) introduced the concept of overeducation in the Netherlands, and later continued to contribute (Hartog, 1993, 1997, 2000). At the end of the 1990s he concluded that the ORU specifications (based on over-, required, and undereducation) are useful extensions of the standard Mincer specification (see also chapter 1) but only if these specifications are embedded in structural labour models.
Surveying the literature of the past twenty-five years several explanations can be given for overeducation.
Dialectical behaviour therapy (DBT) is widely considered to be a promising treatment for borderline personality disorder (BPD). However, the evidence for its efficacy published thus far should be regarded as preliminary.
To compare the effectiveness of DBT with treatment as usual for patients with BPD and to examine the impact of baseline severity on effectiveness.
Fifty-eight women with BPD were randomly assigned to either 12 months of DBT or usual treatment in a randomised controlled study. Participants were recruited through clinical referrals from both addiction treatment and psychiatric services. Outcome measures included treatment retention and the course of suicidal, self-mutilating and self-damaging impulsive behaviours.
Dialectical behaviour therapy resulted in better retention rates and greater reductions of self-mutilating and self-damaging impulsive behaviours compared with usual treatment, especially among those with a history of frequent self-mutilation.
Dialectical behaviour therapy is superior to usual treatment in reducing high-risk behaviours in patients with BPD.
The extent of social dysfunctioning and its relationship to psychological disorders among Dutch primary care patients was examined. Social dysfunctioning in these patients was rather limited, but was more pronounced in patients with a psychological disorder than in those without. Disabilities were largely restricted to the occupational and social roles, with family role functioning and self-care relatively intact. Social dysfunctioning was moderately related to psychopathology, with higher levels of dysfunctioning in more severe and depressed cases. The extent of social dysfunctioning among patients with both anxiety and depression was similar to that of patients with a single diagnosis of depression. Depressed patients had a similar level of dysfunctioning to non-psychotic psychiatric out-patients. Analyses regarding the effects of diagnosis and severity on social dysfunctioning revealed considerable overlap between these two aspects of psychopathology. This study supports the need for a simultaneous but separate assessment of psychopathology and social dysfunctioning. However, future research should incorporate additional predictors of social dysfunctioning (e.g. personality, life events, long-term difficulties, physical disorders), and prospective studies should be conducted to clarify the temporal sequences of symptom severity, diagnosis, and comorbidity on the one hand, and social dysfunctioning on the other.
The question of the relationship between anxiety and depression remains to be solved. The fact that clinical pictures show substantial overlap makes it difficult, using conventional instruments, to distinguish between the co-occurrence of anxiety and depression and overlap in definitions and measurement of the two syndromes. This calls for the construction of scales which exclude symptoms common to both syndromes and incorporate symptoms specific only to anxiety or only to depression; i.e. scales with maximum discriminant validity. This article describes the construction of two such scales based on PSE symptoms; a prototypical anxiety scale and a prototypical depression scale. In a sample of 134 non-psychotic psychiatric out-patients these scales show good reliability and validity, both as a measure of severity and as a screening device. Compared to the Hamilton anxiety and depression scales (HARS and HRSD), the correlation between the prototypical anxiety and depression scales is low.
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