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A critical step in research on the epidemiology of post-traumatic stress disorder (PTSD) in low-resource settings is the validation of brief self-reported psychometric tools available in the public domain, such as the Impact Event Scale – Revised (IES-R).
We aimed to investigate the validity of the IES-R in a primary healthcare setting in Harare, Zimbabwe.
We analysed data from a survey of 264 consecutively sampled adults (mean age 38 years; 78% female). We estimated the area under the receiver operating characteristic curve and sensitivity, specificity and likelihood ratios for different cut-off points of the IES-R, against a diagnosis of PTSD made using the Structured Clinical Interview for DSM-IV. We performed factor analysis to evaluate construct validity of the IES-R.
The prevalence of PTSD was 23.9% (95% CI 18.9–29.5). The area under the curve for the IES-R was 0.90. At a cut-off of ≥47, the sensitivity of the IES-R to detect PTSD was 84.1 (95% CI 72.7–92.1) and specificity was 81.1 (95% CI 75.0–86.3). Positive and negative likelihood ratios were 4.45 and 0.20, respectively. Factor analysis revealed a two-factor solution, with both factors showing good internal consistency (Cronbach's factor-1 α = 0.95, factor-2 α = 0.76). In a post hoc analysis, we found the brief six-item IES-6 also performed well, with an area under the curve of 0.87 and optimal cut-off of 15.
The IES-R and IES-6 had good psychometric properties and performed well for indicating possible PTSD, but at higher cut-off points than those recommended in the Global North.
Exposure to adversity in childhood is associated with elevations in numerous physical and mental health outcomes across the life course. The biological embedding of early experience during periods of developmental plasticity is one pathway that contributes to these associations. Dimensional models specify mechanistic pathways linking different dimensions of adversity to health and well-being outcomes later in life. While findings from existing studies testing these dimensions have provided promising preliminary support for these models, less agreement exists about how to measure the experiences that comprise each dimension. Here, we review existing approaches to measuring two dimensions of adversity: threat and deprivation. We recommend specific measures for measuring these constructs and, when possible, document when the same measure can be used by different reporters and across the lifespan to maximize the utility with which these recommendations can be applied. Through this approach, we hope to stimulate progress in understanding how particular dimensions of early environmental experience contribute to lifelong health.
The present study examined patterns of stability and change in loneliness across adolescence. Data were drawn from the Environmental Risk (E-Risk) Longitudinal Twin Study, a UK population-representative cohort of 2,232 individuals born in 1994 and 1995. Loneliness was assessed when participants were aged 12 and 18. Loneliness showed modest stability across these ages (r = .25). Behavioral genetic modeling indicated that stability in loneliness was explained largely by genetic influences (66%), while change was explained by nonshared environmental effects (58%). Individuals who reported loneliness at both ages were broadly similar to individuals who only reported it at age 18, with both groups at elevated risk of mental health problems, physical health risk behaviors, and education and employment difficulties. Individuals who were lonely only at age 12 generally fared better; however, they were still more likely to finish school with lower qualifications. Positive family influences in childhood predicted reduced risk of loneliness at age 12, while negative peer experiences increased the risk. Together, the findings show that while early adolescent loneliness does not appear to exert a cumulative burden when it persists, it is nonetheless a risk for a range of concomitant impairments, some of which can endure.
Retrospective self-reports of childhood trauma are associated with a greater risk of psychopathology in adulthood than prospective measures of trauma. Heritable reporter characteristics are anticipated to account for part of this association, whereby genetic predisposition to certain traits influences both the likelihood of self-reporting trauma and of developing psychopathology. However, previous research has not considered how gene–environment correlation influences these associations.
To investigate reporter characteristics associated with retrospective self-reports of childhood trauma and whether these associations are accounted for by gene–environment correlation.
In 3963 unrelated individuals from the Twins Early Development Study, we tested whether polygenic scores for 21 psychiatric, cognitive, anthropometric and personality traits were associated with retrospectively self-reported childhood emotional and physical abuse. To assess the presence of gene–environment correlation, we investigated whether these associations remained after controlling for composite scores of environmental adversity across development.
Retrospectively self-reported childhood trauma was associated with polygenic scores for autism spectrum disorder (ASD), body mass index (BMI), post-traumatic stress disorder (PTSD) and risky behaviours. When composite scores of environmental adversity were controlled for, only associations with the polygenic scores for ASD and PTSD remained significant.
Genetic predisposition to ASD and PTSD may increase liability to experiencing or interpreting events as traumatic. Associations between genetic predisposition for risky behaviour and BMI with self-reported childhood trauma may reflect gene–environment correlation. Studies of the association between retrospectively self-reported childhood trauma and later-life outcomes should consider that genetically influenced reporter characteristics may confound associations, both directly and through gene–environment correlation.
Childhood adversities are major preventable risk factors for poor mental and physical health. Scientific advances in this area are not matched by clinical gains for affected individuals. We reflect on novel research directions that could accelerate clinical impact.
Complex traumas are traumatic experiences that involve multiple interpersonal threats during childhood or adolescence, such as repeated abuse. This type of trauma is hypothesized to lead to more severe psychopathology and poorer cognitive function than other non-complex traumas, such as road traffic accidents. However, empirical testing of this hypothesis has been limited to clinical or convenience samples and cross-sectional designs. To better understand this topic, we aimed to investigate psychopathology and cognitive function in young people exposed to complex, non-complex, or no trauma from a population-representative longitudinal cohort, and to consider the role of pre-existing vulnerabilities.
Participants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a population-representative birth-cohort of 2,232 children born in England and Wales in 1994-95. At age 18 years (93% participation), we assessed lifetime exposure to complex and non-complex trauma. We also assessed past-year psychopathology including general psychopathology ‘p’ and several psychiatric disorders, as well as current cognitive function including IQ, executive function, and processing speed. Additionally, we prospectively assessed early childhood vulnerabilities including internalizing and externalizing symptoms at age 5, IQ at age 5, family history of mental illness, family socioeconomic status, and sex.
We found that participants who had been exposed to complex trauma had more severe psychopathology and poorer cognitive function across wide-ranging measures at age 18, compared to both trauma-unexposed participants and those exposed to non-complex trauma. Early childhood vulnerabilities had an important role in these presentations, as they predicted risk of later complex trauma exposure, and largely explained associations of complex trauma with cognitive deficits, but not with psychopathology.
By conflating complex and non-complex traumas, current research and clinical practice under-estimate the severity of psychopathology and cognitive deficits linked with complex trauma, as well as the role of pre-existing vulnerabilities. A better understanding of the mental health needs of people exposed to complex trauma and underlying mechanisms could inform the development of new effective interventions.
Complex traumas are traumatic experiences that involve multiple interpersonal threats during childhood or adolescence, such as repeated abuse. These traumas are hypothesised to cause more severe psychopathology and poorer cognitive function than other non-complex traumas. However, empirical testing has been limited to clinical/convenience samples and cross-sectional designs.
To investigate psychopathology and cognitive function in young people exposed to complex, non-complex or no trauma, from a population-representative longitudinal cohort, and to consider the role of pre-existing vulnerabilities.
Participants were from the Environmental Risk Longitudinal Twin Study, a population-representative birth cohort of 2232 British children. At age 18 years (93% participation), we assessed lifetime exposure to complex and non-complex trauma, past-year psychopathology and current cognitive function. We also prospectively assessed early childhood vulnerabilities: internalising and externalising symptoms at 5 years of age, IQ at 5 years of age, family history of mental illness, family socioeconomic status and sex.
Participants exposed to complex trauma had more severe psychopathology and poorer cognitive function at 18 years of age, compared with both trauma-unexposed participants and those exposed to non-complex trauma. Early childhood vulnerabilities predicted risk of later complex trauma exposure, and largely explained associations of complex trauma with cognitive deficits, but not with psychopathology.
By conflating complex and non-complex traumas, current research and clinical practice underestimate the severity of psychopathology, cognitive deficits and pre-existing vulnerabilities linked with complex trauma. A better understanding of the mental health needs of people exposed to complex trauma could inform the development of new, more effective interventions.
Childhood trauma (CT) increases the risk of adult depression. Buffering effects require an understanding of the underlying persistent risk pathways. This study examined whether daily psychological stress processes – how an individual interprets and affectively responds to minor everyday events – mediate the effect of CT on adult depressive symptoms.
Middle-aged women (N = 183) reported CT at baseline and completed daily diaries of threat appraisals and negative evening affect for 7 days at baseline, 9, and 18 months. Depressive symptoms were measured across the 1.5-year period. Mediation was examined using multilevel structural equation modeling.
Reported CT predicted greater depressive symptoms over the 1.5-year time period (estimate = 0.27, s.e. = 0.07, 95% CI 0.15–0.38, p < 0.001). Daily threat appraisals and negative affect mediated the effect of reported CT on depressive symptoms (estimate = 0.34, s.e. = 0.08, 95% CI 0.22–0.46, p < 0.001). Daily threat appraisals explained more than half of this effect (estimate = 0.19, s.e. = 0.07, 95% CI 0.08–0.30, p = 0.004). Post hoc analyses in individuals who reported at least moderate severity of CT showed that lower threat appraisals buffered depressive symptoms. A similar pattern was found in individuals who reported no/low severity of CT.
A reported history of CT acts as a latent vulnerability, exaggerating threat appraisals of everyday events, which trigger greater negative evening affect – processes that have important mental health consequences and may provide malleable intervention targets.
Exposure to childhood adversity is a critical risk factor for the development of psychopathology. A growing field of research examines how exposure to childhood adversity is translated into biological risk for psychopathology through alterations in immune system functioning, most notably heightened levels of inflammation biomarkers. Though our knowledge about how childhood adversity can instantiate biological risk for psychopathology is growing, there remain many challenges and gaps in the field to understand how inflammation from childhood adversity contributes to psychopathology. This paper reviews research on the inflammatory outcomes arising from childhood adversity and presents four major challenges that future research must address: (a) the measurement of childhood adversity, (b) the measurement of inflammation, (c) the identification of mediators between childhood adversity and inflammation, and (d) the identification of moderators of inflammatory outcomes following childhood adversity. We discuss synergies and inconsistencies in the literature to summarize the current understanding of the association between childhood adversity, a proinflammatory phenotype, and the biological risk for psychopathology. We discuss the clinical implications of the inflammatory links between childhood adversity and psychopathology, including possibilities for intervention. Finally, this review conclude by delineates future directions for research, including issues of how best to detect, prevent, and understand these “hidden wounds” of childhood adversity.
A recent suicidal drive hypothesis posits that psychotic experiences (PEs) may serve to externalize internally generated and self-directed threat (i.e., self-injurious/suicidal behavior [SIB]) in order to optimize survival; however, it must first be demonstrated that such internal threat can both precede and inform PEs. The current study conducted the first known bidirectional analysis of SIB and PEs to test whether SIB could be considered as a plausible antecedent for PEs. Prospective data were utilized from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative birth cohort of 2232 twins, that captured SIB (any self-harm or suicidal attempt) and PEs at ages 12 and 18 years. Cross-lagged panel models demonstrated that the association between SIB at age 12 and PEs at age 18 was as strong as the association between PEs at age 12 and SIB at age 18. Indeed, the best representation of the data was a model where these paths were constrained to be equal (OR = 2.48, 95% CI = 1.63–3.79). Clinical interview case notes for those who reported both SIB and PEs at age 18, revealed that PEs were explicitly characterized by SIB/threat/death-related content for 39% of cases. These findings justify further investigation of the suicidal drive hypothesis.
The present study used a longitudinal and discordant twin design to explore in depth the developmental associations between victimization and loneliness from mid-childhood to young adulthood. The data were drawn from the Environmental Risk (E-Risk) Longitudinal Twin Study, a birth cohort of 2,232 individuals born in England and Wales during 1994–1995. Diverse forms of victimization were considered, differing across context, perpetrator, and timing of exposure. The results indicated that exposure to different forms of victimization was associated with loneliness in a dose–response manner. In childhood, bullying victimization was uniquely associated with loneliness, over and above concurrent psychopathology, social isolation, and genetic risk. Moreover, childhood bullying victimization continued to predict loneliness in young adulthood, even in the absence of ongoing victimization. Within-twin pair analyses further indicated that this longitudinal association was explained by genetic confounds. In adolescence, varied forms of victimization were correlated with young adult loneliness, with maltreatment, neglect, and cybervictimization remaining robust to controls for genetic confounds. These findings indicate that vulnerability to loneliness in victimized young people varies according to the specific form of victimization in question, and also to the developmental period in which it was experienced.
The mental health of children and young people can be disproportionally affected and easily overlooked in the context of emergencies and disasters. Child and adolescent mental health services can contribute greatly to emergency preparedness, resilience and response and, ultimately, mitigate harmful effects on the most vulnerable members of society.
Attention-deficit hyperactivity disorder (ADHD) is associated with poorer cognitive functioning. We used a developmental, genetically-sensitive approach to examine intelligence quotient (IQ) from early childhood to young adulthood among those with different ADHD courses to investigate whether changes in ADHD were reflected in differences in IQ. We also examined executive functioning in childhood and young adulthood among different ADHD courses.
Study participants were part of the Environmental Risk (E-Risk) Longitudinal Twin Study, a population-based birth cohort of 2232 twins. We assessed ADHD in childhood (ages 5, 7, 10 and 12) and young adulthood (age 18). We examined ADHD course as reflected by remission, persistence and late-onset. IQ was evaluated at ages 5, 12 and 18, and executive functioning at ages 5 and 18.
ADHD groups showed deficits in IQ across development compared to controls; those with persistent ADHD showed the greatest deficit, followed by remitted and late-onset. ADHD groups did not differ from controls in developmental trajectory of IQ, suggesting changes in ADHD were not reflected in IQ. All ADHD groups performed more poorly on executive functioning tasks at ages 5 and 18; persisters and remitters differed only on an inhibitory control task at age 18.
Differences in ADHD course – persistence, remission and late-onset – were not directly reflected in changes in IQ. Instead, having ADHD at any point across development was associated with lower average IQ and poorer executive functioning. Our finding that individuals with persistent ADHD have poorer response inhibition than those who remitted requires replication.
Social support has been shown to be associated with a reduced likelihood of developing psychotic experiences in the general population and even amongst those at high risk due to exposure to multiple forms of victimisation (poly-victimised). However, it is unclear whether this association is merely due to the confounding effects of shared environmental and genetic influences, or reverse causality. Therefore, we investigated whether social support has a unique environmentally mediated effect on adolescent psychotic experiences after accounting for familial factors, including genetic factors, and also prior psychopathology.
Participants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative cohort of 2232 UK-born twins. Adolescents were interviewed at age 18 about psychotic experiences and victimisation exposure since age 12, and their perceptions of social support. Prior childhood mental health problems and psychotic symptoms were assessed at age 12. The discordant twin method was used to disentangle the relative family-wide and unique-environmental effects of social support on psychotic experiences in the general population and among poly-victimised adolescents.
Perceived social support, particularly from friends, was found to have a unique environmentally mediated buffering effect on adolescent psychotic experiences in the whole sample and in the high-risk poly-victimised group.
The protective effects of social support on adolescent psychotic experiences cannot be accounted for by shared environmental or genetic factors, nor by earlier psychopathology. Our findings suggest that early intervention programmes focused on increasing perceptions of social support have the potential to prevent the emergence of psychotic experiences amongst adolescents.
In 785 mother–child (50% male) pairs from a longitudinal epidemiological birth cohort, we investigated associations between inflammation-related epigenetic polygenic risk scores (i-ePGS), environmental exposures, cognitive function, and child and adolescent internalizing and externalizing problems. We examined prenatal and postnatal effects. For externalizing problems, one prenatal effect was found: i-ePGS at birth associated with higher externalizing problems (ages 7–15) indirectly through lower cognitive function (age 7). For internalizing problems, we identified two effects. For a prenatal effect, i-ePGS at birth associated with higher internalizing symptoms via continuity in i-ePGS at age 7. For a postnatal effect, higher postnatal adversity exposure (birth through age 7) associated with higher internalizing problems (ages 7–15) via higher i-ePGS (age 7). Hence, externalizing problems were related mainly to prenatal effects involving lower cognitive function, whereas internalizing problems appeared related to both prenatal and postnatal effects. The present study supports a link between i-ePGS and child and adolescent mental health.
Attention-deficit hyperactivity disorder (ADHD) is associated with mental health problems and functional impairment across many domains. However, how the longitudinal course of ADHD affects later functioning remains unclear.
We aimed to disentangle how ADHD developmental patterns are associated with young adult functioning.
The Environmental Risk (E-Risk) Longitudinal Twin Study is a population-based cohort of 2232 twins born in England and Wales in 1994–1995. We assessed ADHD in childhood at ages 5, 7, 10 and 12 years and in young adulthood at age 18 years. We examined three developmental patterns of ADHD from childhood to young adulthood – remitted, persistent and late-onset ADHD – and compared these groups with one another and with non-ADHD controls on functioning at age 18 years. We additionally tested whether group differences were attributable to childhood IQ, childhood conduct disorder or familial factors shared between twins.
Compared with individuals without ADHD, those with remitted ADHD showed poorer physical health and socioeconomic outcomes in young adulthood. Individuals with persistent or late-onset ADHD showed poorer functioning across all domains, including mental health, substance misuse, psychosocial, physical health and socioeconomic outcomes. Overall, these associations were not explained by childhood IQ, childhood conduct disorder or shared familial factors.
Long-term associations of childhood ADHD with adverse physical health and socioeconomic outcomes underscore the need for early intervention. Young adult ADHD showed stronger associations with poorer mental health, substance misuse and psychosocial outcomes, emphasising the importance of identifying and treating adults with ADHD.
The aim of this study was to build a detailed, integrative profile of the correlates of young adults’ feelings of loneliness, in terms of their current health and functioning and their childhood experiences and circumstances.
Data were drawn from the Environmental Risk Longitudinal Twin Study, a birth cohort of 2232 individuals born in England and Wales in 1994 and 1995. Loneliness was measured when participants were aged 18. Regression analyses were used to test concurrent associations between loneliness and health and functioning in young adulthood. Longitudinal analyses were conducted to examine childhood factors associated with young adult loneliness.
Lonelier young adults were more likely to experience mental health problems, to engage in physical health risk behaviours, and to use more negative strategies to cope with stress. They were less confident in their employment prospects and were more likely to be out of work. Lonelier young adults were, as children, more likely to have had mental health difficulties and to have experienced bullying and social isolation. Loneliness was evenly distributed across genders and socioeconomic backgrounds.
Young adults’ experience of loneliness co-occurs with a diverse range of problems, with potential implications for health in later life. The findings underscore the importance of early intervention to prevent lonely young adults from being trapped in loneliness as they age.
This paper presents multilevel findings on adolescents' victimization exposure from a large longitudinal cohort of twins. Data were obtained from the Environmental Risk (E-Risk) Longitudinal Twin Study, an epidemiological study of 2,232 children (1,116 twin pairs) followed to 18 years of age (with 93% retention). To assess adolescent victimization, we combined best practices in survey research on victimization with optimal approaches to measuring life stress and traumatic experiences, and introduce a reliable system for coding severity of victimization. One in three children experienced at least one type of severe victimization during adolescence (crime victimization, peer/sibling victimization, Internet/mobile phone victimization, sexual victimization, family violence, maltreatment, or neglect), and most types of victimization were more prevalent among children from low socioeconomic backgrounds. Exposure to multiple victimization types was common, as was revictimization; over half of those physically maltreated in childhood were also exposed to severe physical violence in adolescence. Biometric twin analyses revealed that environmental factors had the greatest influence on most types of victimization, while severe physical maltreatment from caregivers during adolescence was predominantly influenced by heritable factors. The findings from this study showcase how distinct levels of victimization measurement can be harmonized in large-scale studies of health and development.
Background – Schizophrenia is a complex disease resulting from the interplay of genetic and environmental factors. However, psychiatric genetics and epidemiology have often worked as independent research fields. Aims – To review the evidence about the gene-environment interplay involved in the development of schizophrenia. Methods – Systematic review of medical and psychological databases. Results – On one hand, quantitative and molecular genetics showed high heritability for schizophrenia and identified genes likely to be involved in its pathophysiology. The strength of the association between candidate genes and schizophrenia is however modest, and the need for a more appropriate conceptualization of the genetic risk has been claimed. On the other hand, psychiatric epidemiology described several environmental factors liked with the onset or the course of schizophrenia. The observational nature of epidemiology, however, may hamper inference on causation. Gene-environment correlations and interactions influence the exposure and the vulnerability to the environment, respectively. Current findings suggest that gene-environment correlations and interactions may be common phenomena in the pathophysiology of schizophrenia. The consideration of gene-environment interplay may help to overcome many limitations of genetic and epidemiological studies in psychiatry and suggest innovative preventive and therapeutic strategies. Conclusions – Taking into account the complexity of schizophrenia pathophysiology, mental health genetics may provide a comprehensive and heuristic model of disease.
Aims – Genetics can offer new resources to epidemiology. This review will consider recent findings regarding the link between stress and depression as an example to illustrate the added value of employing genetics in epidemiological studies. Methods – Systematic review of medical and psychological databases. Results – Genetic and environmental factors may correlate. This suggests the potential for genetic mediation of the exposure to the environment. Gene-environment correlations can help epidemiologists to better understand causal pathways and suggest effective therapeutic strategies. Genetic and environmental factors may also interact. This suggests the potential for genetic modification of environmental effects on disease risk. Gene-environment interactions can help epidemiologists to identify vulnerable individuals and strata-specific environmental effects. Conclusions – New models of disease based on the interplay between genes and environments are providing epidemiology with a new set of testable hypotheses that will advance our understanding of mental health and illness.
Declaration of Interest: Dr. Danese is holder of the Wellcome Trust Research Training Fellowship in Clinical Science.