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Mother and father depression symptoms often co-occur, and together can have a substantial impact on child emotional well-being. Little is understood about symptom-level mechanisms underlying the co-occurrence of depression symptoms within families.
The objective was to use network analysis to examine depression symptoms in mothers and fathers after having a baby, and emotional symptoms in children in early adolescence.
We examined data from 4492 mother–father–child trios taken from a prospective, population-based cohort in the UK. Symptoms were examined using two unregularised partial correlation network models. The initial model was used to examine the pattern of associations, i.e. the overall network structure, for mother and father depression symptoms, and then to identify bridge symptoms that reinforce depression symptoms between parents during offspring infancy. The second model examined associations between the parent symptom network, including bridge symptoms, with later child emotional difficulties.
The study included 4492 mother–father–child trios; 2204 (49.1%) children were female. Bridge symptoms reinforcing mother and father depression symptoms were feeling guilty and self-harm ideation. For mothers, the bridge symptom of feeling guilty, and symptoms of anhedonia, panic and sadness were highly connected with child emotional difficulties. For fathers, the symptom of feeling overwhelmed associated with child emotional difficulties. Guilt and anhedonia in fathers appeared to indirectly associate with child emotional difficulties through the same symptom in mothers.
Our findings suggest that specific symptom cascades are central for co-occurring depression in parents and increased vulnerability in children, providing potential therapeutic targets.
Sipping, an early form of alcohol initiation, is associated with aspects of psychopathology and personality that reflect long-term risk for harmful alcohol use. In the Adolescent Brain and Cognitive Development cohort (N = 11,872), sipping by age 9–10 was concurrently associated with impulsivity, other aspects of externalizing, and prodromal schizophrenia symptoms. Still, these associations were cross-sectional in nature, leaving open the possibility that these features of psychopathology and personality might not reflect long-term risk for alcohol consumption and related harm across development. Here, we attempted to replicate baseline concurrent associations across three waves of data to extend concurrent associations to prospective ones. Most cross-sectional associations replicated across waves, such that impulsivity, other aspects of externalizing, reward sensitivity (e.g., surgency, sensation seeking), and prodromal schizophrenia symptoms were associated with increased odds of having sipped alcohol by the age of 12. Nevertheless, not all concurrent associations replicated prospectively; impulsigenic features did not reflect long-term risk for sipping. Thus, some psychopathology features appeared to reflect stable risk factors, whereas others appeared to reflect state-dependent risk factors. All told, sipping might not reflect long-term risk for harmful alcohol use, and the nature of sipping may change across development.
The network paradigm for psychiatric disorder nosology was proposed based on the hypothesis that mental disorders are caused by networks of symptoms that are themselves causally related. Researchers have widely applied and integrated this paradigm to examine a variety of mental disorders, particularly depression. Existing studies generally focus on the correlation structure of symptoms, inferring causal relationships. Thus, presumption of causality may not be justified. The goal of this review was to examine the assumptions necessary for causal inference in network studies of depression. Specifically, we examined whether and how network studies address common violations of causal assumptions (i.e. no measurement error, exchangeability, and positivity). Of the 41 studies reviewed, five (12%) studies discussed sources of confounding unrelated to measurement error; none discussed positivity; and five conducted post-hoc analysis for measurement error. Depression network studies, in principle, are conducted under the assumption that symptom relationships are causal. Yet, in practice, studies seldomly discussed or adequately tested assumptions required to infer causality. Researchers continue to design studies that are unable to support the credibility of the network paradigm for the study of depression. There is a critical need to ensure scientific efforts cease to perpetuate problematic designs and findings to a potentially unsubstantiated paradigm.
Prevalence of smoking in schizophrenia (SCZ) is larger than in general population. Genetic studies provided some evidence of a causal effect of smoking on SCZ. We aim to characterize the genetic susceptibility to SCZ affected by genetic susceptibility to smoking.
Multi-trait-based conditional and joint analysis was applied to the largest European SCZ genome-wide association studies (GWAS) to remove genetic effects on SCZ driven by smoking, estimated by generalized summary data-based Mendelian randomization. Enrichment analysis was performed to compare original v. conditional GWAS. Change in genetic correlation between SCZ and relevant traits after conditioning was assessed. Colocalization analysis was performed to identify specific loci confirming general findings.
Conditional analysis identified 19 new risk loci for SCZ and 42 lost loci whose association with SCZ may be partially driven by smoking. These results were strengthened by colocalization analysis. Enrichment analysis indicated a higher association of differentially expressed genes at prenatal brain stages after conditioning. Genetic correlation of SCZ with substance use and dependence, attention deficit-hyperactivity disorder, and several externalizing traits significantly changed after conditioning. Colocalization of association signal between SCZ and these traits was identified for some of the lost loci, such as CHRNA2, CUL3, and PCDH7.
Our approach led to identification of potential new SCZ loci, loci partially associated to SCZ through smoking, and a shared genetic susceptibility between SCZ and smoking behavior related to externalizing phenotypes. Application of this approach to other psychiatric disorders and substances may lead to a better understanding of the role of substances on mental health.
Psychotic disorders exhibit a complex aetiology that combines genetic and environmental factors. Among the latter, obstetric complications (OCs) have been widely studied as risk factors, but it is not yet well understood how OCs relate to the heterogeneous presentations of psychotic disorders. We assessed the clinical phenotypes of individuals with a first episode of psychosis (FEP) in relation to the presence of OCs.
Two-hundred seventy-seven patients with an FEP were assessed for OCs using the Lewis–Murray scale, with data stratified into three subscales depending on the timing and the characteristics of the obstetric event, namely: complications of pregnancy, abnormal foetal growth and development and difficulties in delivery. We also considered other two groups: any complications during the pregnancy period and all OCs taken altogether. Patients were clinically evaluated with the Positive and Negative Syndrome Scale for schizophrenia.
Total OCs and difficulties in delivery were related to more severe psychopathology, and this remained significant after co-varying for age, sex, traumatic experiences, antipsychotic dosage and cannabis use.
Our results highlight the relevance of OCs for the clinical presentation of psychosis. Describing the timing of the OCs is essential in understanding the heterogeneity of the clinical presentation.
Increased reactivity to minor stressors is considered a risk factor for psychosis, especially in vulnerable individuals. In the present study, we investigated affective and psychotic stress reactivity as well as its link with psychotic symptoms and psychopathology in youths with 22q11.2 deletion syndrome (22q11DS), a neurogenetic condition associated with a high risk for psychosis.
A 6-day ecological momentary assessment protocol was used to assess perceived daily-life stress as well as affective and psychotic reactivity to stress in participants with 22q11DS (n = 38, age = 18.4) and healthy controls (HC; n = 53, age = 19.1). Psychotic symptoms, general psychopathology, and coping strategies were also assessed through clinical interviews and questionnaires.
Participants with 22q11DS reported higher levels of perceived social stress (b = 0.21, p = 0.036) but lower levels of activity-related stress (b = −0.31, p = 0.003) in their daily lives compared to HC. The groups did not differ in affective or psychotic reactivity to stress, but individuals with 22q11DS who reported increased affective reactivity to social stressors showed more severe positive psychotic symptoms (rs = 0.505, p = 0.008). Finally, avoidance coping strategies moderated the association between stress and negative affects.
Our results suggest an increased vulnerability for daily social stress in youths with 22q11DS, and link elevated social stress reactivity to heightened psychotic symptom severity. Given the high risk for psychosis in 22q11DS, interventions should focus on reducing social stress and developing adaptive coping strategies.
The present study examined high-risk personality traits and associations with psychopathology across multiple levels of a hierarchical-dimensional model of psychopathology in a large adolescent, general population sample. Confirmatory factor analyses were run using data from two randomized controlled trials of Australian adolescents (N = 8,654, mean age = 13.01 years, 52% female). A higher-order model – comprised of general psychopathology, fear, distress, alcohol use/harms, and conduct/inattention dimensions – was selected based on model fit, reliability, and replicability. Indirect-effects models were estimated to examine the unique associations between high-risk personality traits (anxiety sensitivity, negative thinking, impulsivity, and sensation seeking) and general and specific dimensions and symptoms of psychopathology. All personality traits were positively associated with general psychopathology. After accounting for general psychopathology, anxiety sensitivity was positively associated with fear; negative thinking was positively associated with distress; impulsivity was positively associated with conduct/inattention; and sensation seeking was positively associated with alcohol use/harms and conduct/inattention, and negatively associated with fear. Several significant associations between personality traits and individual symptoms remained after accounting for general and specific psychopathology. These findings contribute to our understanding of the underlying structure of psychopathology among adolescents and have implications for the development of personality-based prevention and early intervention programs.
This editorial reflects on current methodological trends in translational research in mental health. It aims to build a bridge between two fields that are frequently siloed off from each other: interventional research and phenomenologically informed research. Recent years have witnessed a revival of phenomenological approaches in mental health, often – but not only – as a means of connecting the subjective character of experience with neurobiological explanatory accounts of illness. Rich phenomenological knowledge accrued in schizophrenia, and wider psychosis research, has opened up new opportunities for improving prediction, early detection, diagnosis, prognostic stratification, treatment and ethics of care. Novel qualitative studies of delusions and hallucinations have challenged longstanding assumptions about their nature and meaning, uncovering highly complex subjective dimensions that are not adequately captured by quantitative methodologies. Interdisciplinary and participatory research efforts, informed by phenomenological insights, have prompted revisions of pre-established narratives of mental disorder dominated by a dysfunction framework and by researcher-centric outcome measures. Despite these recent advances, there has been relatively little effort to integrate and translate phenomenological insights across applied clinical research, with the goal of producing more meaningful, patient-valued results. It is our contention that phenomenological psychopathology – as the basic science of psychiatry – represents an important methodology for advancing evidence-based practices in mental health, and ultimately improving real-world outcomes. Setting this project into motion requires a greater emphasis on subjectivity and the structures of experience, more attention to the quality and patient-centredness of outcome measures, and the identification of treatment targets that matter most to patients.
The causal impacts of recreational cannabis legalization are not well understood due to the number of potential confounds. We sought to quantify possible causal effects of recreational cannabis legalization on substance use, substance use disorder, and psychosocial functioning, and whether vulnerable individuals are more susceptible to the effects of cannabis legalization than others.
We used a longitudinal, co-twin control design in 4043 twins (N = 240 pairs discordant on residence), first assessed in adolescence and now age 24–49, currently residing in states with different cannabis policies (40% resided in a recreationally legal state). We tested the effect of legalization on outcomes of interest and whether legalization interacts with established vulnerability factors (age, sex, or externalizing psychopathology).
In the co-twin control design accounting for earlier cannabis frequency and alcohol use disorder (AUD) symptoms respectively, the twin living in a recreational state used cannabis on average more often (βw = 0.11, p = 1.3 × 10−3), and had fewer AUD symptoms (βw = −0.11, p = 6.7 × 10−3) than their co-twin living in an non-recreational state. Cannabis legalization was associated with no other adverse outcome in the co-twin design, including cannabis use disorder. No risk factor significantly interacted with legalization status to predict any outcome.
Recreational legalization was associated with increased cannabis use and decreased AUD symptoms but was not associated with other maladaptations. These effects were maintained within twin pairs discordant for residence. Moreover, vulnerabilities to cannabis use were not exacerbated by the legal cannabis environment. Future research may investigate causal links between cannabis consumption and outcomes.
Carter's Psychopathology is an accessible, engaging, and well-organized text covering the study, understanding, diagnosis, treatment, and prevention of psychological disorders. Fully integrating gender and culture in the presentation of mental disorders, and using a sensitive and inclusive language to encourage an empathic approach to psychopathology, this introductory textbook offers students a strong foundation of the socio-cultural factors influencing how we treat mental disorders. Featuring: boxes such as 'the power of words', promoting the use of respectful, empathic language, and 'the power of evidence', demonstrating that scientific evidence can answer questions about psychopathology treatments; real-world case studies and examples; 'concept checks' questions to test the student's mastery of the material covered in each section; chapter summaries listing the 'take-home' points discussed; and key terms and glossary highlighting terms that students will need to understand and become familiar with, this textbook provides a hands-on approach to the study of psychopathology.
Both maternal and, separately, paternal mental illness are associated with diminished academic attainment among children. However, the differential impacts of diagnostic type and degree of parental burden (e.g. one v. both parents affected) on these functional outcomes are unknown.
Using the Swedish national patient (NPR) and multi-generation (MGR) registers, 2 226 451 children (1 290 157 parental pairs), born 1 January 1973–31 December 1997, were followed through 31 December 2013. Diagnostic status of all cohort members was defined for eleven psychiatric disorders, and families classed by exposure: (1) parents affected with any disorder, (2) parents affected with a disorder group (e.g. neuropsychiatric disorders), and (3) parents affected with a specific disorder (e.g. ADHD). Pairs were further defined as ‘unaffected,’ ‘single-affected,’, or ‘dual-affected.’ Among offspring, the study evaluated fulfillment of four academic milestones, from compulsory (primary) school through University (college). Sensitivity analyses considered the impact of child's own mental health, as well as parental education, on main effects.
Marked reductions in the odds of achievement were observed, emerging at the earliest levels of schooling for both single-affected [adjusted odds ratio (aOR), 0.50; 95% CI 0.49–0.51] and dual-affected (aOR 0.29, 95% CI 0.28–0.30) pairs and persisting thereafter [aOR range (single), 0.52–0.65; aOR range (dual), 0.30–0.40]. This pattern was repeated for analyses within diagnosis/diagnostic group. Main results were robust to adjustment for offspring mental health and parent education level.
Parental mental illness is associated with profound reductions in educational attainment in the subsequent generation, with children from dual-affected families at uniquely high risk.
Summarizes how psychologists define psychopathology. Discusses ways in which abnormality was viewed historically, and modern mental health care. Identifies the research methods that psychologists utilize.
The s100b inflammatory protein is involved in schizophrenia pathophysiology. We aim at studying the evolution of the s100b serum levels in acutely relapsed paranoid schizophrenia patients at three different time points (admission, discharge and 3 months after hospital discharge 3MAHD).
Twenty-three paranoid schizophrenia inpatients meeting DSM-IV criteria participated in the research. Twenty-three healthy subjects matched by age, gender and season acted as the control group. Psychopathology was measured with the Positive and Negative Syndrome Scale (PANSS). Serum s100b levels were determined at 12:00 and 24:00 h with an enzyme-linked immunoassay kit.
Patients had significant higher serum s100b levels at admission and discharge (12:00 h) than the group of healthy subjects. At admission and discharge, s100b serum levels at 24 h had decreased compared to the 24:00 h s100b levels of the healthy subjects. At 3MAHD patients and healthy subjects had similar levels of serum s100b protein. Positive and negative PANSS scores decreased significantly between admission and discharge. Positive and negative PANSS scores decreased between discharge and 3MAHD, but these changes had no statistical significance.
Our study confirms that the acute inflammatory response produced in acutely relapsed patients is reversed after 3 month of hospital discharge. The variations of serum s100b concentrations when the patients suffer from an acute relapse may be a useful predictor of disease evolution.
Studies reporting that highly intelligent individuals have more mental health disorders often have sampling bias, no or inadequate control groups, or insufficient sample size. We addressed these caveats by examining the difference in the prevalence of mental health disorders between individuals with high and average general intelligence (g-factor) in the UK Biobank.
Participants with g-factor scores standardized relative to the same-age UK population, were divided into two groups: a high g-factor group (g-factor 2 SD above the UK mean; N = 16,137) and an average g-factor group (g-factor within 2 SD of the UK mean; N = 236,273). Using self-report questionnaires and medical diagnoses, we examined group differences in the prevalence of 32 phenotypes, including mental health disorders, trauma, allergies, and other traits.
High and average g-factor groups differed across 15/32 phenotypes and did not depend on sex and/or age. Individuals with high g-factors had less general anxiety (odds ratio [OR] = 0.69, 95% CI [0.64;0.74]) and post-traumatic stress disorder (PTSD; OR = 0.67, 95 %CI [0.61;0.74]), were less neurotic (β = −0.12, 95% CI [−0.15;−0.10]), less socially isolated (OR = 0.85, 95% CI [0.80;0.90]), and were less likely to have experienced childhood stressors and abuse, adulthood stressors, or catastrophic trauma (OR = 0.69–0.90). However, they generally had more allergies (e.g., eczema; OR = 1.13–1.33).
The present study provides robust evidence that highly intelligent individuals do not have more mental health disorders than the average population. High intelligence even appears as a protective factor for general anxiety and PTSD.
Recent technological advances enable the collection of intensive longitudinal data. This scoping review aimed to provide an overview of methods for collecting intensive time series data in mental health research as well as basic principles, current applications, target constructs, and statistical methods for this type of data.
In January 2021, the database MEDLINE was searched. Original articles were identified that (1) used active or passive data collection methods to gather intensive longitudinal data in daily life, (2) had a minimum sample size of N ⩾ 100 participants, and (3) included individuals with subclinical or clinical mental health problems.
In total, 3799 original articles were identified, of which 174 met inclusion criteria. The most widely used methods were diary techniques (e.g. Experience Sampling Methodology), various types of sensors (e.g. accelerometer), and app usage data. Target constructs included affect, various symptom domains, cognitive processes, sleep, dysfunctional behaviour, physical activity, and social media use. There was strong evidence on feasibility of, and high compliance with, active and passive data collection methods in diverse clinical settings and groups. Study designs, sampling schedules, and measures varied considerably across studies, limiting the generalisability of findings.
Gathering intensive longitudinal data has significant potential to advance mental health research. However, more methodological research is required to establish and meet critical quality standards in this rapidly evolving field. Advanced approaches such as digital phenotyping, ecological momentary interventions, and machine-learning methods will be required to efficiently use intensive longitudinal data and deliver personalised digital interventions and services for improving public mental health.
Understanding deviations from typical brain development is a promising approach to comprehend pathophysiology in childhood and adolescence. We investigated if cerebellar volumes different than expected for age and sex could predict psychopathology, executive functions and academic achievement.
Children and adolescents aged 6–17 years from the Brazilian High-Risk Cohort Study for Mental Conditions had their cerebellar volume estimated using Multiple Automatically Generated Templates from T1-weighted images at baseline (n = 677) and at 3-year follow-up (n = 447). Outcomes were assessed using the Child Behavior Checklist and standardized measures of executive functions and school achievement. Models of typically developing cerebellum were based on a subsample not exposed to risk factors and without mental-health conditions (n = 216). Deviations from this model were constructed for the remaining individuals (n = 461) and standardized variation from age and sex trajectory model was used to predict outcomes in cross-sectional, longitudinal and mediation analyses.
Cerebellar volumes higher than expected for age and sex were associated with lower externalizing specific factor and higher executive functions. In a longitudinal analysis, deviations from typical development at baseline predicted inhibitory control at follow-up, and cerebellar deviation changes from baseline to follow-up predicted changes in reading and writing abilities. The association between deviations in cerebellar volume and academic achievement was mediated by inhibitory control.
Deviations in the cerebellar typical development are associated with outcomes in youth that have long-lasting consequences. This study highlights both the potential of typical developing models and the important role of the cerebellum in mental health, cognition and education.
The multifactorial nature of psychopathology, whereby both genetic and environmental factors contribute risk, has long been established. In this paper, we provide an update on genetically informative designs that are utilized to disentangle genetic and environmental contributions to psychopathology. We provide a brief reminder of quantitative behavioral genetic research designs that have been used to identify potentially causal environmental processes, accounting for genetic contributions. We also provide an overview of recent molecular genetic approaches that utilize genome-wide association study data which are increasingly being applied to questions relevant to psychopathology research. While genetically informative designs typically have been applied to investigate the origins of psychopathology, we highlight how these approaches can also be used to elucidate potential causal environmental processes that contribute to developmental course and outcomes. We highlight the need to use genetically sensitive designs that align with intervention and prevention science efforts, by considering strengths-based environments to investigate how positive environments can mitigate risk and promote children’s strengths.
The most fundamental emotional systems that show trait control are evolutionarily old and extensively conserved. Psychology in general has benefited from non-human neuroscience and from the analytical simplicity of behaviour in those with simpler nervous systems. It has been argued that integration between personality, psychopathology, and neuroscience is particularly promising if we are to understand the neurobiology of human experience. Here, we provide some general arguments for a non-human approach being at least as productive in relation to personality, psychopathology, and their interface. Some early personality theories were directly linked to psychopathology (e.g., Eysenck, Panksepp, and Cloninger). They shared a common interest in brain systems that naturally led to the use of non-human data; behavioural, neural, and pharmacological. In Eysenck’s case, this also led to the selective breeding, at the Maudsley Institute, of emotionally reactive and non-reactive strains of rat as models of trait neuroticism or trait emotionality. Dimensional personality research and categorical approaches to clinical disorder then drifted apart from each other, from neuropsychology, and from non-human data. Recently, the conceptualizations of both healthy personality and psychopathology have moved towards a common hierarchical trait perspective. Indeed, the proposed two sets of trait dimensions appear similar and may even be eventually the same. We provide, here, an introduction to this special issue of Personality Neuroscience, where the authors provide overviews of detailed areas where non-human data inform human personality and its psychopathology or provide explicit models for translation to human neuroscience. Once all the papers in the issue have appeared, we will also provide a concluding summary of them.
Perceived loneliness and objective social network size are related but distinct factors, which negatively affect mental health and are prevalent in patients who have experienced childhood maltreatment (CM), for example, patients with persistent depressive disorder (PDD) and borderline personality disorder (BPD). This cross-diagnostic study investigated whether loneliness, social network size, or both are associated with self-reported CM.
Loneliness and social network size were assessed in a population-based sample at two time points (Study 1, N = 509), and a clinical group of patients with PDD or BPD (Study 2, N = 190) using the UCLA Loneliness Scale and the Social Network Index. Further measures were the Childhood Trauma Questionnaire, and standard depression rating scales. Linear regression analyses were applied to compare associations of loneliness or social network size with CM. Multiple mediation analyses were used to test the relative importance of loneliness and social network size in the relationship between CM and depressive symptoms.
In both studies, loneliness showed a stronger association than social network size with CM. This was particularly marked for emotional neglect and emotional abuse. Loneliness but not social network size mediated the relationship between CM and depressive symptoms.
Loneliness is particularly associated with self-reported CM, and in this respect distinct from the social network size. Our results underline the importance of differentiating both psychosocial constructs and suggest focusing on perceived loneliness and its etiological underpinnings by mechanism-based psychosocial interventions.
The capacity for lying is a common human phenomenon with evolutionary explanations, in which one seeks to deceive usually to avoid harmful or undesired consequences. The spectrum of lies is vast and varies from the content to the motivation. Pathological lying has the potential to affect mental evaluations thus motivating an important discussion regarding this behaviour.
The authors aim to explore the psychopathological concept and spectrum of pathological lies, from their underlying motives to their implications and challenges in psychiatric diagnosis with recourse to a clinical case example.
A review of pertinent literature on the topic with focus on that which is most relevant to the theme was included. The authors present the clinical case of a middle-aged female who presented with mythomania which included the fabrication of having attempted murder.
The literature demonstrates a relationship between compulsive lying and personality disorders. Head trauma and other central nervous system issues may also play a role. Some traits may facilitate the detection of deception, such as dramatic and unmotivated constructs with a positive self-portrayal. The clinical case description correlates the personality factors associated with mythomania, namely antisocial personality disorder, differing from the typical presentation as her fabrications portrayed her negatively.
The implication of pathological lying is that it may interfere with mental assessment thus altering, by way of deception, the psychiatric evaluation as lies may be difficult to detect upon a first evaluation. The psychiatrist should be alerted to the possibility of fabrication when dealing with a patient with predisposing factors.