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The present study examines whether neuroticism is predicted by genetic vulnerability, summarized as polygenic risk score for neuroticism (PRSN), in interaction with bullying, parental bonding, and childhood adversity. Data were derived from a general population adolescent and young adult twin cohort. The final sample consisted of 202 monozygotic and 436 dizygotic twins and 319 twin pairs. The Short Eysenck Personality questionnaire was used to measure neuroticism. PRSN was trained on the results from the Genetics of Personality Consortium (GPC) and United Kingdom Biobank (UKB) cohorts, yielding two different PRSN. Multilevel mixed-effects models were used to analyze the main and interacting associations of PRSN, childhood adversity, bullying, and parental bonding style with neuroticism. We found no evidence of gene–environment correlation. PRSN thresholds of .005 and .2 were chosen, based on GPC and UKB datasets, respectively. After correction for confounders, all the individual variables were associated with the expression of neuroticism: both PRSN from GPC and UKB, childhood adversity, maternal bonding, paternal bonding, and bullying in primary school and secondary school. However, the results indicated no evidence for gene–environment interaction in this cohort. These results suggest that genetic vulnerability on the one hand and negative life events (childhood adversity and bullying) and positive life events (optimal parental bonding) on the other represent noninteracting pathways to neuroticism.
The bidirectional relationship between poverty and poor physical and mental health is well-known. All physicians should have sufficient knowledge on poverty as a social determinant and its impact on (mental) health. The knowledge of poverty in physicians is seldom investigated. An online and paper survey was circulated in March/April 2022 in Belgium, to assess physician’s opinions about and attitudes toward patients in poverty. Not only was interest in the subject rather low, but there were also substantial contradictions in the responses. The lack of knowledge about poverty among physicians leads to reduced quality of medical care for this target group. This is an individual medical–ethical and societal problem. We suggest 10 point-action plan for policymakers, educational institutions, and physicians.
Research indicates that perinatal loss can cause profound psychological consequences in parents. However, a comprehensive summary of existing quantitative literature describing the association between perinatal loss and the development of depression/depressive symptoms or post-traumatic stress disorder (PTSD)/post-traumatic stress (PTS) symptoms in fathers has not been published.
A systematic literature search (from inception to December 2021), using the PubMed, EMBASE, and Web of Science databases to articles assessing depressive or PTS symptoms, was conducted following the Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines. Only studies investigating the period of intrauterine death from 20 weeks of gestation, stillbirth, or neonatal death within the first month after birth were included.
A final sample of 13 articles were eligible for inclusion. Some studies showed an increased risk of depressive and PTS symptoms in fathers after perinatal loss. However, many study results did not show significant differences, symptoms generally decreased over time, and the majority of studies showed higher levels of depressive and PTS symptoms in mothers, compared with fathers.
Although the majority of the included studies showed elevated levels of depressive and/or PTSD symptoms after perinatal loss in fathers, no clear firm conclusion can be drawn, as the included studies were very heterogeneous. More homogeneous research measuring depressive and PTS symptoms in fathers is needed at the time of the loss, as the current literature available shows several limitations and gaps.
Major depressive disorder (MDD) is closely related to obesity, inflammation, and insulin resistance, all together being etiologically linked to metabolic syndrome (MetS) development. The depressive disorder has a neuroendocrinological component, co-influencing the MetS, while MetS is characterised by increased cytokine levels, which are known to cause a depressed mood. This study aimed to establish biological subtypes of the depressive disorder based on researched clinical, laboratory, and anthropometric variables.
We performed a cross-sectional study on a sample of 293 subjects (145 suffering from a depressive disorder and 148 healthy controls). Results were analysed with multivariate statistical methods as well as with cluster and discriminant analysis. In order to classify depressive disorder on the grounds of laboratory, anthropometric, and clinical parameters, we performed cluster analysis, which resulted in three clusters.
The first cluster is characterised by low platelet serotonin, high cortisol levels, high blood glucose levels, high triglycerides levels, high Hamilton Depression Rating Scale score, high waist circumference, high C-Reactive Protein values, and a high number of previous depressive episodes, was named Combined (Metabolic) depression. The inflammatory depression cluster is defined with average platelet serotonin values, normal cortisol, and all other parameter levels, except for increased IL-6 levels. The serotoninergic depression cluster is characterised by markedly low platelet serotonin, and all other parameters are within the normal range.
From a biological point of view, depressive disorder is not uniform, and as such, these findings suggest potential clinically useful and generalisable biological subtypes of depressive disorder.
The aim of the current study was to explore the effect of gender, age at onset, and duration on the long-term course of schizophrenia.
Twenty-nine centers from 25 countries representing all continents participated in the study that included 2358 patients aged 37.21 ± 11.87 years with a DSM-IV or DSM-5 diagnosis of schizophrenia; the Positive and Negative Syndrome Scale as well as relevant clinicodemographic data were gathered. Analysis of variance and analysis of covariance were used, and the methodology corrected for the presence of potentially confounding effects.
There was a 3-year later age at onset for females (P < .001) and lower rates of negative symptoms (P < .01) and higher depression/anxiety measures (P < .05) at some stages. The age at onset manifested a distribution with a single peak for both genders with a tendency of patients with younger onset having slower advancement through illness stages (P = .001). No significant effects were found concerning duration of illness.
Our results confirmed a later onset and a possibly more benign course and outcome in females. Age at onset manifested a single peak in both genders, and surprisingly, earlier onset was related to a slower progression of the illness. No effect of duration has been detected. These results are partially in accord with the literature, but they also differ as a consequence of the different starting point of our methodology (a novel staging model), which in our opinion precluded the impact of confounding effects. Future research should focus on the therapeutic policy and implications of these results in more representative samples.
Patients with schizophrenia spectrum disorders (SSD) have worse physical health and reduced life expectancy compared to the general population. In 2009, the European Psychiatric Association, the European Society of Cardiology and the European Association for the Study of Diabetes published a position paper aimed to improve cardiovascular and diabetes care in patients with severe mental illnesses. However, the initiative did not produce the expected results. Experts in SSD or in cardiovascular and metabolic diseases convened to identify main issues relevant to management of cardiometabolic risk factors in schizophrenia patients and to seek consensus through the Delphi method.
The steering committee identified four topics: 1) cardiometabolic risk factors in schizophrenia patients; 2) cardiometabolic risk factors related to antipsychotic treatment; 3) differences in antipsychotic cardiometabolic profiles; 4) management of cardiometabolic risk. Twelve key statements were included in a Delphi questionnaire delivered to a panel of expert European psychiatrists.
Consensus was reached for all statements with positive agreement higher than 85% in the first round. European psychiatrists agreed on: 1) high cardiometabolic risk in patients with SSD, 2) importance of correct risk management of cardiometabolic diseases, from lifestyle modification to treatment of risk factors, including the choice of antipsychotic drugs with a favourable cardiometabolic profile. The expert panel identified the psychiatrist as the central coordinating figure of management, possibly assisted by other specialists and general practitioners.
This study demonstrates high level of agreement among European psychiatrists regarding the importance of cardiovascular risk assessment and management in subjects with SSD.
The present study aimed to (i) evaluate the association between insight and measures of executive functions and working memory in a sample of 132 patients with schizophrenia and (ii) to explore to what proportion neurocognitive dysfunction contributed to the variance in insight after controlling for symptomatology.
Subjects were evaluated with a standardized neurocognitive test battery and a semi-structured interview, the Psychosis Evaluation tool for Common use by Caregivers (PECC). PECC, apart from evaluating symptoms and side-effects, measures insight on a 4-point scale by two of its dimensions: awareness of having a mental illness (AMI) and awareness of having symptoms attributed to a mental illness (ASAMI). Executive functioning was measured by the Wisconsin Card Sort Test (WCST) and the Trail Making B (TMB). Working memory was measured by the Letter Number Sequencing (LNS) test from the Wechsler Adult Intelligence Scale (WAIS).
Only one significant association was found after correction for multiple testing, between WCST categories completed and AMI (r = −0.29, p = 0.0006). WCST categories completed explained only 7.9% of the variance in AMI, while symptomatology explained 20% of variance in AMI and 16.5% of variance in ASAMI.
The current results show a significant but subtle association with the WCST, which is in agreement with earlier literature. No other associations between cognitive functioning and insight were found. In general, these findings seem to suggest that factors other than cognition have a greater impact on insight in patients with schizophrenia.
A recent consensus conference has proposed guidelines for the monitoring for diabetes in patients with schizophrenia and also identifies the need of long-term prospective studies.
A large scale prospective study on metabolic risks of antipsychotic medication is currently ongoing. At baseline, patients get a full laboratory screening, ECG and an oral glucose tolerance test (OGTT). Baseline data on 100 non-diabetic patients at study inclusion and stable on medication for at least 6 months are presented.
Glucose abnormalities are found in 22% of patients at baseline. A monitoring protocol based only on fasting glucose would not have detected 63.6% of these patients with classifiable glucose abnormalities in our sample. Fasting insulin and measures for insulin resistance have a high predictive value for abnormalities late in the OGTT.
Already at baseline, metabolic problems are frequently present in patients with schizophrenia treated with antipsychotics. Adding assessment of fasting insulin in a monitoring protocol improves detection of glucose abnormalities late in an OGTT.
The aim of the current study was to explore the changing interrelationships among clinical variables through the stages of schizophrenia in order to assemble a comprehensive and meaningful disease model.
Twenty-nine centers from 25 countries participated and included 2358 patients aged 37.21 ± 11.87 years with schizophrenia. Multiple linear regression analysis and visual inspection of plots were performed.
The results suggest that with progression stages, there are changing correlations among Positive and Negative Syndrome Scale factors at each stage and each factor correlates with all the others in that particular stage, in which this factor is dominant. This internal structure further supports the validity of an already proposed four stages model, with positive symptoms dominating the first stage, excitement/hostility the second, depression the third, and neurocognitive decline the last stage.
The current study investigated the mental organization and functioning in patients with schizophrenia in relation to different stages of illness progression. It revealed two distinct “cores” of schizophrenia, the “Positive” and the “Negative,” while neurocognitive decline escalates during the later stages. Future research should focus on the therapeutic implications of such a model. Stopping the progress of the illness could demand to stop the succession of stages. This could be achieved not only by both halting the triggering effect of positive and negative symptoms, but also by stopping the sensitization effect on the neural pathways responsible for the development of hostility, excitement, anxiety, and depression as well as the deleterious effect on neural networks responsible for neurocognition.
Meta-analyses suggest that clinical psychopathology is preceded by dimensional behavioral and cognitive phenotypes such as psychotic experiences, executive functioning, working memory and affective dysregulation that are determined by the interplay between genetic and nongenetic factors contributing to the severity of psychopathology. The liability to mental ill health can be psychometrically measured using experimental paradigms that assess neurocognitive processes such as salience attribution, sensitivity to social defeat and reward sensitivity. Here, we describe the TwinssCan, a longitudinal general population twin cohort, which comprises 1202 individuals (796 adolescent/young adult twins, 43 siblings and 363 parents) at baseline. The TwinssCan is part of the European Network of National Networks studying Gene-Environment Interactions in Schizophrenia project and recruited from the East Flanders Prospective Twin Survey. The main objective of this project is to understand psychopathology by evaluating the contribution of genetic and nongenetic factors on subclinical expressions of dimensional phenotypes at a young age before the onset of disorder and their association with neurocognitive processes, such as salience attribution, sensitivity to social defeat and reward sensitivity.
Physical activity (PA) may be therapeutic for people with severe mental illness (SMI) who generally have low PA and experience numerous life style-related medical complications. We conducted a meta-review of PA interventions and their impact on health outcomes for people with SMI, including schizophrenia-spectrum disorders, major depressive disorder (MDD) and bipolar disorder. We searched major electronic databases until January 2018 for systematic reviews with/without meta-analysis that investigated PA for any SMI. We rated the quality of studies with the AMSTAR tool, grading the quality of evidence, and identifying gaps, future research needs and clinical practice recommendations. For MDD, consistent evidence indicated that PA can improve depressive symptoms versus control conditions, with effects comparable to those of antidepressants and psychotherapy. PA can also improve cardiorespiratory fitness and quality of life in people with MDD, although the impact on physical health outcomes was limited. There were no differences in adverse events versus control conditions. For MDD, larger effect sizes were seen when PA was delivered at moderate-vigorous intensity and supervised by an exercise specialist. For schizophrenia-spectrum disorders, evidence indicates that aerobic PA can reduce psychiatric symptoms, improves cognition and various subdomains, cardiorespiratory fitness, whilst evidence for the impact on anthropometric measures was inconsistent. There was a paucity of studies investigating PA in bipolar disorder, precluding any definitive recommendations. No cost effectiveness analyses in any SMI condition were identified. We make multiple recommendations to fill existing research gaps and increase the use of PA in routine clinical care aimed at improving psychiatric and medical outcomes.
Una conferencia de consenso reciente ha propuesto directrices para el control de la diabetes en pacientes con esquizofrenia e identifica también la necesidad de estudios prospectivos a largo plazo.
Un estudio prospectivo a gran escala sobre los riesgos metabólicos de la medicación antipsicótica está en curso en la actualidad. En la línea de base, los pacientes pasan por una detección selectiva completa de laboratorio, ECG y una prueba oral de tolerancia a la glucosa (POTG). Se presentan los datos de línea de base sobre 100 pacientes que no eran diabéticos al incorporarse al estudio y se mantuvieron estables con la medicación durante 6 meses al menos.
Se encuentran anomalías de la glucosa en 22% de los pacientes en la línea de base. Un protocolo de control basado únicamente en la glucosa en ayunas no habría detectado a 63,6% de estos pacientes con anomalías clasificables de la glucosa en nuestra muestra. La insulina en ayunas y las medidas para la resistencia a la insulina tienen un elevado valor predictivo de anomalías posteriores en la POTG.
Los problemas metabólicos están presentes con frecuencia ya en la línea de base en los pacientes con esquizofrenia tratados con antipsicóticos. Añadir la evaluación de la insulina en ayunas en un protocolo de control mejora la deteccíon de anomalías de la glucosa más tarde en una POTG.
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