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Schizophrenia (SCZ) is associated with an increased risk of violence compared to the general population. Previous studies have indicated smaller hippocampal and amygdala volumes in violent than non-violent psychotic patients. However, little is known about volumetric differences at the subdivision level of these structures. In the present study, hippocampal subfields and amygdala nuclei volumes were estimated with FreeSurfer from 3 T MRI of SCZ patients with (SCZ-V, n = 24) and without (SCZ-NV, n = 51) a history of severe violence and 90 healthy controls (HC). Volumetric differences between groups were explored with a general linear model covarying for confounders, in addition to follow-up analyses in patient groups controlling for clinical characteristics such as antipsychotic medication, duration of illness and illicit substance use. SCZ-V had smaller total hippocampal volume and smaller CA1, HATA, fimbria, and molecular layer of DG volumes compared to HC. Total amygdala volume together with basal nucleus, accessory basal nucleus, CTA, and paralaminar nucleus volumes were smaller in SCZ-V compared to HC. In SCZ-NV, compared to HC, the observed smaller volumes were limited to basal and paralaminar nucleus. There were no significant differences in hippocampal subfield and amygdala nuclei volumes between SCZ-V and SCZ-NV. Follow-up analyses showed that the results in patient groups were not affected by clinical characteristics. The results suggest that smaller hippocampal subfield and amygdala nuclei volumes may be relevant to violence risk in SCZ. However, the neurobiological signature of violence in SCZ should be further investigated in larger cohorts.

Some studies show that children with obesity are more likely to receive a diagnosis of depression, anxiety, or attention-deficit hyperactivity disorder (ADHD). But this does not necessarily mean obesity causes these conditions. Depression, anxiety, or ADHD could cause obesity. A child's environment, including family income or their parents' mental health, could also affect a child's weight and mental health. Understanding the nature of these relationships could help scientists develop better interventions for both obesity and mental health conditions. Genetic studies may help scientists better understand the role of the environment in these conditions, but it's important to consider both the child's and their parents’ genetics in these analyses. This is because parents and children share not only genes, but also environmental conditions. For example, families that carry genetic variants associated with higher body weight might also have lower incomes, if parents have been affected by biases against heavier people in society and the workplace. Children in these families could have worse mental health because of effects of their parent’s weight, rather than their own weight. Looking at both child and adult genetics can help disentangle these processes. Hughes et al. show that a child's own body mass index, a ratio of weight and height, is not strongly associated with the child’s mental health symptoms. They analysed genetic, weight, and health survey data from about 41,000 8-year-old children and their parents. The results suggest that a child's own BMI does not have a large effect on their anxiety symptoms. There was also no clear evidence that a child's BMI affected their symptoms of depression or ADHD. These results contradict previous studies, which did not account for parental genetics. Hughes et al. suggest that, at least for eight-year-olds, factors linked with adult weight and which differ between families may be more critical to a child's mental health than a child’s own weight. For older children and adolescents, this may not be the case, and the individual’s own weight may be more important. As a result, policies designed to reduce obesity in mid-childhood are unlikely to greatly improve the mental health of children. On the other hand, policies targeting the environmental or societal factors contributing to higher body weights, bias against people with higher weights, and poor child mental health directly may be more beneficial.

Background Mental health problems, and major depression in particular, are important public health issues. Following trends in the prevalence of major depression is difficult because of the costs and complications of diagnostic interviews and general population self-report health surveys. Scandinavian countries, however, have several central, population-based health registries. We aimed to investigate how well these registries capture the epidemiology of major depression in the population. Methods In two Norwegian regional surveys of general population health, each repeated after 10 years, responders were asked to report depressive symptoms using the Hopkins Symptom Checklist (HSCL) or the Hospital Anxiety and Depression Scale (HADS). Data were linked to three central health registries capturing contact with primary care, specialist care and prescriptions for antidepressants, to investigate how well these registries reflected self-reported depressive symptoms. Results Most responders scored low on Hopkins Symptom Checklist (HSCL) and the Hospital Anxiety and Depression Scale (HADS), but 10% and 13%, respectively, scored above cut-off, with only minor changes between the two survey times. Females scored higher than males. Older people scored lower than younger, and a social gradient was visible. Around 12% of those who scored above the cut-off on either scale were recorded in the central health registries during the following year. This correlation was highest in primary care data, followed by prescription data and lowest in specialist care. Females were more often recorded in registries ( p  < 0.001), as were younger people ( p  < 0.001). Conclusions There was a strong association between scores on screening for major depression in the general population surveys and being recorded in central health registries. There was a low sensitivity of these registries. and there was some variation in how sensitive the central health registries were in picking up depression, especially for males and older people. However, the stability of the measures over time suggests we may get an impression of the prevalence of major depression in the general population by using data from the central health registries. A combination of primary care data, prescription data and specialist care data have a higher sensitivity.

Epidemiological and clinical studies have found associations between depression and cardiovascular disease risk factors, and coronary artery disease patients with depression have worse prognosis. The genetic relationship between depression and these cardiovascular phenotypes is not known. We here investigated overlap at the genome-wide level and in individual loci between depression, coronary artery disease and cardiovascular risk factors. We used the bivariate causal mixture model (MiXeR) to quantify genome-wide polygenic overlap and the conditional/conjunctional false discovery rate (pleioFDR) method to identify shared loci, based on genome-wide association study summary statistics on depression (n = 450,619), coronary artery disease (n = 502,713) and nine cardiovascular risk factors (n = 204,402–776,078). Genetic loci were functionally annotated using FUnctional Mapping and Annotation (FUMA). Of 13.9K variants influencing depression, 9.5K (SD 1.0K) were shared with body-mass index. Of 4.4K variants influencing systolic blood pressure, 2K were shared with depression. ConjFDR identified 79 unique loci associated with depression and coronary artery disease or cardiovascular risk factors. Six genomic loci were associated jointly with depression and coronary artery disease, 69 with blood pressure, 49 with lipids, 9 with type 2 diabetes and 8 with c-reactive protein at conjFDR < 0.05. Loci associated with increased risk for depression were also associated with increased risk of coronary artery disease and higher total cholesterol, low-density lipoprotein and c-reactive protein levels, while there was a mixed pattern of effect direction for the other risk factors. Functional analyses of the shared loci implicated metabolism of alpha-linolenic acid pathway for type 2 diabetes. Our results showed polygenic overlap between depression, coronary artery disease and several cardiovascular risk factors and suggest molecular mechanisms underlying the association between depression and increased cardiovascular disease risk.

Patients in early phases of psychosis often struggle with depressive symptoms and low self-esteem. The main aims of the present study were to examine whether cognitive behavior therapy (CBT) compared to treatment as usual (TAU) would reduce depressive symptoms (primary outcome) and increase self-esteem (secondary outcome). Furthermore, we wanted to examine whether CBT reduces symptoms measured with the PANSS (positive, negative, cognitive, or excited symptoms) or increases general functioning compared to TAU. A total of 63 early psychosis patients were included and randomly assigned to receive either CBT (maximum 26 sessions) or TAU for a period of up to six months. A linear mixed model was used for longitudinal analysis, with a focus on whether patients in the CBT group or the TAU group changed differently to one another between the baseline and 15-month follow-up. There were no differences between the CBT group and TAU group regarding improvements in depressive symptoms measured with the Calgary Depression Scale for Schizophrenia (P = 0.188) or self-esteem measured with the Rosenberg Self-Esteem Scale (P = 0.580). However, patients in the CBT group improved significantly more on negative symptoms (P = 0.002) and social functioning (P = 0.001). We did not find CBT to be more effective than TAU in reducing depressive symptoms or increasing self-esteem in patients with early psychosis. However, CBT seems to improve negative symptoms and functioning. These results still need to be replicated in further studies as the present one was merely an exploratory analysis. ClinicalTrials.gov Identifier: NCT01511406. •CBT is no more effective than treatment as usual to reduce depressive symptoms.•CBT does not increase self-esteem compared to treatment as usual•Explorative findings shows that CBT improve negative symptoms/social functioning.

Background Despite many recent studies on burn-out and dissatisfaction among American medical doctors, less is known about doctors in the Scandinavian public health service. The aims of this study were to analyse long-term work-related predictors of life satisfaction among established doctors in Norway and to identify predictors in a subgroup of doctors who reported a decline in life satisfaction. Methods Two nationwide cohorts of doctors ( n  = 1052), who graduated medical school 6 years apart, were surveyed at graduation from medical school (T1, 1993/94 and 1999), and 4 (T2), 10 (T3), and 15 (T4) years later. Work-related predictors of life satisfaction (three items) obtained at T2 to T4 were analysed. Individual and lifestyle confounders were controlled for using mixed-models repeated-measures analyses, and logistic regression analyses were applied to identify predictors of the decrease in life satisfaction. Results Ninety per cent (947/1052) responded at least once, and 42% (450/1052) responded at all four times. Work-related predictors of higher life satisfaction in the adjusted model were work–home stress (β = − 0.20, 95% confidence interval [CI] = − 0.25 to − 0.16, p  < 0.001), perceived job demands (β = − 0.10, CI = − 0.15 to − 0.05, p  < 0.001), and colleague support (β = 0.05, CI = 0.04 to 0.07, p  < 0.001). The new adjusted individual predictors that we identified included female gender, reality weakness trait, and problematic drinking behaviour. Neuroticism trait and low colleague support predicted a decrease in life satisfaction. Conclusions Work–home stress, perceived job demands, and colleague support were the most important predictors of life satisfaction related to doctors’ work. When personality traits were controlled for, female doctors were more satisfied with their life than male doctors. These findings suggest that improving work-related factors with targeted interventions, including a supportive work environment, may increase life satisfaction among doctors.

Bipolar disorder (BD) is a highly heritable disorder with polygenic inheritance. Among the most consistent findings from functional magnetic imaging (fMRI) studies are limbic hyperactivation and dorsal hypoactivation. However, the relation between reported brain functional abnormalities and underlying genetic risk remains elusive. This is the first cross-sectional study applying a whole-brain explorative approach to investigate potential influence of BD case-control status and polygenic risk on brain activation. A BD polygenic risk score (PGRS) was estimated from the Psychiatric Genomics Consortium BD case-control study, and assigned to each individual in our independent sample (N=85 BD cases and 121 healthy controls (HC)), all of whom participated in an fMRI emotional faces matching paradigm. Potential differences in BOLD response across diagnostic groups were explored at whole-brain level in addition to amygdala as a region of interest. Putative effects of BD PGRS on brain activation were also investigated. At whole-brain level, BD cases presented with significantly lower cuneus/precuneus activation than HC during negative face processing (Z-threshold=2.3 as cluster-level correction). The PGRS was associated positively with increased right inferior frontal gyrus (rIFG) activation during negative face processing. For amygdala activation, there were no correlations with diagnostic status or PGRS. These findings are in line with previous reports of reduced precuneus and altered rIFG activation in BD. While these results demonstrate the ability of PGRS to reveal underlying genetic risk of altered brain activation in BD, the lack of convergence of effects at diagnostic and PGRS level suggests that this relation is a complex one.

Several genetic studies have implicated the CACNA1C SNP rs1006737 in bipolar disorder (BD) and schizophrenia (SZ) pathology. This polymorphism was recently found associated with increased amygdala activity in healthy controls and patients with BD. We performed a functional Magnetic Resonance Imaging (fMRI) study in a sample of BD and SZ cases and healthy controls to test for altered amygdala activity in carriers of the rs1006737 risk allele (AA/AG), and to investigate if there were differences across the diagnostic groups. Rs1006737 was genotyped in 250 individuals (N = 66 BD, 61 SZ and 123 healthy controls), all of Northern European origin, who underwent an fMRI negative faces matching task. Statistical tests were performed with a model correcting for sex, age, diagnostic category and medication status in the total sample, and then in each diagnostic group. In the total sample, carriers of the risk allele had increased activation in the left amygdala. Group-wise analyses showed that this effect was significant in the BD group, but not in the other diagnostic groups. However, there was no significant interaction effect for the risk allele between BD and the other groups. These results indicate that CACNA1C SNP rs1006737 affects amygdala activity during emotional processing across all diagnostic groups. The current findings add to the growing body of knowledge of the pleiotropic effect of this polymorphism, and further support that ion channel dysregulation is involved in the underlying mechanisms of BD and SZ.

Abstract Genetic liability for schizophrenia is associated with psychopathology in early life. It is not clear if these associations are time dependent during childhood, nor if they are specific across different forms of psychopathology. Using genotype and questionnaire data on children (N = 15 105) from the Norwegian Mother, Father and Child Cohort Study, we used schizophrenia polygenic risk scores to test developmental stability in associations with measures of emotional and behavioral problems between 18 months and 5 years, and domain specificity in associations with symptoms of depression, anxiety, conduct problems, oppositionality, inattention, and hyperactivity at 8 years. We then sought to identify symptom profiles—across development and domains—associated with schizophrenia polygenic liability. We found evidence for developmental stability in associations between schizophrenia polygenic risk scores and emotional and behavioral problems, with the latter being mediated specifically via the rate of change in symptoms (β slope = 0.032; 95% CI: 0.007–0.057). At age 8, associations were better explained by a model of symptom-specific polygenic effects rather than effects mediated via a general psychopathology factor or by domain-specific factors. Overall, individuals with higher schizophrenia polygenic risk scores were more likely (OR = 1.310 [95% CIs: 1.122–1.528]) to have a profile of increasing behavioral and emotional symptoms in early childhood, followed by elevated symptoms of conduct disorder, oppositionality, hyperactivity, and inattention by age 8. Schizophrenia-associated alleles are linked to specific patterns of early-life psychopathology. The associations are small, but findings of this nature can help us better understand the developmental emergence of schizophrenia.