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Neuroticism is one of the major traits describing human personality, and a predictor of mental and physical disorders with profound public health significance. Individual differences in emotional variability are thought to reflect the core of neuroticism. However, the empirical relation between emotional variability and neuroticism may be partially the result of a measurement artifact reflecting neuroticism’s relation with higher mean levels— rather than greater variability—of negative emotion. When emotional intensity is measured using bounded scales, there is a dependency between variability and mean levels: at low (or high) intensity, it is impossible to demonstrate high variability. As neuroticism is positively associated with mean levels of negative emotion, this may account for the relation between neuroticism and emotional variability. In a metaanalysis of 11 studies (N = 1,205 participants; 83,411 observations), we tested whether the association between neuroticism and negative emotional variability was clouded by a dependency between variability and the mean. We found a medium-sized positive association between neuroticism and negative emotional variability, but, when using a relative variability index to correct for mean negative emotion, this association disappeared. This indicated that neuroticism was associated with experiencing more intense, but not more variable, negative emotions. Our findings call into question theory, measurement scales, and data suggesting that emotional variability is central to neuroticism. In doing so, they provide a revisionary perspective for understanding how this individual difference may predispose to mental and physical disorders.

Knowing yourself requires knowing not only what you are like in general (trait self-knowledge) but also how your personality fluctuates from moment to moment (state self-knowledge). We examined this latter form of self-knowledge. Participants (248 people; 2,938 observations) wore the Electronically Activated Recorder (EAR), an unobtrusive audio recorder, and completed experience-sampling self-reports of their personality states four times each day for 1 week. We estimated state self-knowledge by comparing self-reported personality states with consensual observer ratings of personality states coded from the EAR files, which formed the criterion for what participants were “actually” like in the moment. People had self-insight into their momentary extraversion, conscientiousness, and likely neuroticism, suggesting that people can accurately detect fluctuations in some aspects of their personality. However, the evidence for self-insight was weaker for agreeableness. This apparent self-ignorance may be partly responsible for interpersonal problems and for blind spots in trait self-knowledge.

•Neuroticism was unrelated to regional task-evoked brain activity.•Amygdala coupling with hippocampus increased with neuroticism.•Amygdala coupling with dIPFC increased with neuroticism.•Connectivity within the salience network increased with neuroticism.•Findings support a network-level basis of neuroticism in emotion processing. Neuroticism, a stable personality trait marked by heightened negative affect and emotional volatility, is a well-established transdiagnostic risk factor for internalizing psychopathology. While early research emphasized amygdala hyperreactivity as a core neural correlate, emerging evidence suggests that neuroticism may be more accurately characterized by dysfunctional connectivity between the amygdala and broader regulatory networks involved in emotion processing and cognitive control. In this cross-sectional fMRI study, 115 healthy adults completed a classification task involving negative emotional facial expressions. Neuroticism was assessed using a latent factor score derived from five validated self-report instruments. Brain activity and psychophysiological interaction analyses were conducted using both region-of-interest and whole-brain approaches. Associations between neural measures and neuroticism were tested using robust regression, controlling for age and sex. No evidence was found for an association between neuroticism and regional brain activity. However, higher neuroticism was associated with increased task-dependent functional connectivity between the amygdala and both the hippocampus and dorsolateral prefrontal cortex. Whole-brain analyses further revealed associations between neuroticism and amygdala coupling with regions implicated in emotion regulation and salience processing, including the anterior insula and dorsal cingulate cortex. These findings support the conceptualization of neuroticism as a network-level phenomenon, characterized by dysregulated interactions within fronto-limbic and salience circuits, rather than by localized changes in brain activity. Specifically, increased amygdala-hippocampal and amygdala-prefrontal connectivity may underlie the persistence and regulation difficulties of negative emotions that characterize the neurotic phenotype.

Trait neuroticism predicts an increased risk of mortality. However, high levels of both neuroticism and conscientiousness (i.e., healthy neuroticism) are associated with various positive health behaviors. Eating behavior is a modifiable risk factor for obesity and metabolic diseases. This study investigated the cross-sectional and longitudinal associations between healthy neuroticism and eating behaviors. The data from the Nathan Kline Institute for Psychiatric Research—Rockland Sample included 712 adults with complete assessments of personality, eating behaviors, and metabolic markers. Linear and mixed linear regression models were used to examine cross-sectional and longitudinal associations of eating behaviors and personality traits, adjusting for sociodemographics, sleep quality, and body mass index (BMI). Healthy neuroticism cross-sectionally predicted the disinhibition and hunger dimensions of eating behavior, a result that withstood the inclusion of disease burden, clinical metabolic markers, and other personality traits. Longitudinally, healthy neuroticism did not predict changes in eating behavior. Greater conscientiousness scores were associated with increased restraint. These findings provide the first evidence that neuroticism is associated with less maladaptive eating behavior when modulated by conscientiousness. The implications of these associations for the relationships between eating behavior, metabolic health, and personality are discussed.

Neuroticism is a personality trait of fundamental importance for psychological well-being and public health. It is strongly associated with major depressive disorder (MDD) and several other psychiatric conditions. Although neuroticism is heritable, attempts to identify the alleles involved in previous studies have been limited by relatively small sample sizes. Here we report a combined meta-analysis of genome-wide association study (GWAS) of neuroticism that includes 91 370 participants from the UK Biobank cohort, 6659 participants from the Generation Scotland: Scottish Family Health Study (GS:SFHS) and 8687 participants from a QIMR (Queensland Institute of Medical Research) Berghofer Medical Research Institute (QIMR) cohort. All participants were assessed using the same neuroticism instrument, the Eysenck Personality Questionnaire-Revised (EPQ-R-S) Short Form's Neuroticism scale. We found a single-nucleotide polymorphism-based heritability estimate for neuroticism of ~15% (s.e. = 0.7%). Meta-analysis identified nine novel loci associated with neuroticism. The strongest evidence for association was at a locus on chromosome 8 (P = 1.5 x [10.sup.-15]) spanning 4Mb and containing at least 36 genes. Other associated loci included interesting candidate genes on chromosome 1 (GRIK3 (glutamate receptor ionotropic kainate 3)), chromosome 4 (KLHL2 (Kelch-like protein 2)), chromosome 17 (CRHR1 (corticotropin-releasing hormone receptor 1) and MAPT (microtubule-associated protein Tau)) and on chromosome 18 (CELF4 (CUGBP elav-like family member 4)). We found no evidence for genetic differences in the common allelic architecture of neuroticism by sex. By comparing our findings with those of the Psychiatric Genetics Consortia, we identified a strong genetic correlation between neuroticism and MDD and a less strong but significant genetic correlation with schizophrenia, although not with bipolar disorder. Polygenic risk scores derived from the primary UK Biobank sample captured ~1% of the variance in neuroticism in the GS:SFHS and QIMR samples, although most of the genome-wide significant alleles identified within a UK Biobank-only GWAS of neuroticism were not independently replicated within these cohorts. The identification of nine novel neuroticism-associated loci will drive forward future work on the neurobiology of neuroticism and related phenotypes. Molecular Psychiatry (2016) 21, 749-757; doi: 10.1038/mp.2016.49; published online 12 April 2016

Individuals who encounter false information on social media may actively spread it further, by sharing or otherwise engaging with it. Much of the spread of disinformation can thus be attributed to human action. Four studies (total N = 2,634) explored the effect of message attributes (authoritativeness of source, consensus indicators), viewer characteristics (digital literacy, personality, and demographic variables) and their interaction (consistency between message and recipient beliefs) on self-reported likelihood of spreading examples of disinformation. Participants also reported whether they had shared real-world disinformation in the past. Reported likelihood of sharing was not influenced by authoritativeness of the source of the material, nor indicators of how many other people had previously engaged with it. Participants' level of digital literacy had little effect on their responses. The people reporting the greatest likelihood of sharing disinformation were those who thought it likely to be true, or who had pre-existing attitudes consistent with it. They were likely to have previous familiarity with the materials. Across the four studies, personality (lower Agreeableness and Conscientiousness, higher Extraversion and Neuroticism) and demographic variables (male gender, lower age and lower education) were weakly and inconsistently associated with self-reported likelihood of sharing. These findings have implications for strategies more or less likely to work in countering disinformation in social media.

Anxiety disorders are common, complex psychiatric disorders with twin heritabilities of 30–60%. We conducted a genome-wide association study of Lifetime Anxiety Disorder (ncase = 25 453, ncontrol = 58 113) and an additional analysis of Current Anxiety Symptoms (ncase = 19 012, ncontrol = 58 113). The liability scale common variant heritability estimate for Lifetime Anxiety Disorder was 26%, and for Current Anxiety Symptoms was 31%. Five novel genome-wide significant loci were identified including an intergenic region on chromosome 9 that has previously been associated with neuroticism, and a locus overlapping the BDNF receptor gene, NTRK2. Anxiety showed significant positive genetic correlations with depression and insomnia as well as coronary artery disease, mirroring findings from epidemiological studies. We conclude that common genetic variation accounts for a substantive proportion of the genetic architecture underlying anxiety.

Repetitive negative thinking (RNT) and neuroticism are risk factors for internalizing psychopathology. However, their interaction has only been investigated at the self-report level, and studies elucidating their interrelationship at the neural level are lacking. We therefore investigated the interaction of trait RNT and neuroticism with respect to the dynamics of neural networks during negative self-referential processing. A sample of 110 healthy subjects reported trait RNT and neuroticism, followed by an RNT induction paradigm during fMRI. Dynamic coactivation pattern (CAP) analysis was used to identify a set of recurring coactivation patterns and to quantify their persistence and count rates. Next, the effects of trait RNT, neuroticism, and their interaction on brain dynamics were tested using regression models. Negative interactions between RNT and neuroticism were found for persistence and counts of the canonical default mode network (DMN) as well as salience network (SAL) CAP. Simple slope analysis revealed that subjects scoring high on neuroticism exhibited a negative association between trait RNT and DMN as well as canonical SAL dynamics. Furthermore, trait RNT was positively associated with persistence and count rates of a hybrid FPN+DMN coactivation state. Our results suggest that individuals with high neuroticism who spend more time in SAL and DMN CAPs may be less vulnerable to RNT, potentially reflecting more adaptive network configurations. Furthermore, less segregated CAPs, evident by the concurrent activation of functionally antagonistic networks (FPN+DMN), emerge more often in individuals prone to RNT, likely reflecting disrupted network interactions.

Abstract Repetitive negative thinking (RNT) and neuroticism are two of the most prominent transdiagnostic risk factors for internalizing disorders. Previous research highlighted a complex relationship between neuroticism and RNT. However, no study has yet examined their interaction at the neural level. Trait RNT and neuroticism were assessed in a sample of 126 healthy participants, followed by a fMRI task designed to elicit RNT. Linear models were employed to examine the interaction between trait RNT and neuroticism and main effects of RNT on brain changes. No significant interaction between trait RNT and neuroticism in relation to DMN and AI recruitment was found. A positive association was observed between trait RNT and recruitment of the precuneus during negative self-referential processing compared to distraction; however, this result did not survive FDR correction for multiple comparisons. Exploratory analyses revealed that responses of the anterior insula during RNT compared to distraction were inversely related to self-reported trait RNT on the trend-level. Our results confirm the relevance of DMN recruitment for RNT and underscore a putative role of the anterior insula. The absence of a significant interaction between RNT and neuroticism may suggest that an alternative conceptualization of their relationship could better capture their underlying dynamics.