OBJECTIVE: Social transitions are increasingly common for transgender children. A social transition involves a child presenting to other people as a member of the "opposite" gender in all contexts (e.g., wearing clothes and using pronouns of that gender). Little is known about the well-being of socially transitioned transgender children. This study examined self-reported depression, anxiety, and self-worth in socially transitioned transgender children compared with 2 control groups: age- and gender-matched controls and siblings of transgender children. METHOD: As part of a longitudinal study (TransYouth Project), children (9-14 years old) and their parents completed measurements of depression and anxiety (n = 63 transgender children, n = 63 controls, n = 38 siblings). Children (6-14 years old; n = 116 transgender children, n = 122 controls, n = 72 siblings) also reported on their self-worth. Mental health and self-worth were compared across groups. RESULTS: Transgender children reported depression and self-worth that did not differ from their matched-control or sibling peers (p = .311), and they reported marginally higher anxiety (p = .076). Compared with national averages, transgender children showed typical rates of depression (p = .290) and marginally higher rates of anxiety (p = .096). Parents similarly reported that their transgender children experienced more anxiety than children in the control groups (p = .002) and rated their transgender children as having equivalent levels of depression (p = .728). CONCLUSION: These findings are in striking contrast to previous work with gender-nonconforming children who had not socially transitioned, which found very high rates of depression and anxiety. These findings lessen concerns from previous work that parents of socially transitioned children could be systematically underreporting mental health problems.
The human brain requires a wide variety of experiences and environmental inputs in order to develop normally. Children who are neglected by caregivers or raised in institutional environments are deprived of numerous types of species-expectant environmental experiences. In this review, we articulate a model of how the absence of cognitive stimulation and sensory, motor, linguistic, and social experiences common among children raised in deprived early environments constrains early forms of learning, producing long-term deficits in complex cognitive function and associative learning. Building on evidence from animal models, we propose that deprivation accelerates the neurodevelopmental process of synaptic pruning and limits myelination, resulting in age-specific reductions in cortical thickness and white matter integrity among children raised in deprived early environments. We review evidence linking early experiences of psychosocial deprivation to reductions in cognitive ability, associative and implicit learning, language skills, and executive functions as well as atypical patterns of cortical and white matter development-domains that should be profoundly influenced by deprivation through the learning and neural mechanisms we propose. These patterns of atypical development are difficult to explain with existing models that emphasize stress pathways and accelerated limbic system development. A learning account of how deprived early environments influence cognitive and neural development provides a complementary perspective to stress models and highlights novel pathways through which deprivation might confer risk for internalizing and externalizing psychopathology. We end by reviewing evidence for plasticity in cognitive and neural development among children raised in deprived environments following interventions that improve caregiving quality.
BackgroundAlthough childhood adversity is a strong determinant of psychopathology, it remains unclear whether there are 'sensitive periods' when a first episode of adversity is most harmful.AimsTo examine whether variation in the developmental timing of a first episode of interpersonal violence (up to age 18) associates with risk for psychopathology.MethodUsing cross-sectional data, we examined the association between age at first exposure to four types of interpersonal violence (physical abuse by parents, physical abuse by others, rape, and sexual assault/molestation) and onset of four classes of DSM-IV disorders (distress, fear, behaviour, substance use) (n = 9984). Age at exposure was defined as: early childhood (ages 0-5), middle childhood (ages 6-10) and adolescence (ages 11-18).ResultsExposure to interpersonal violence at any age period about doubled the risk of a psychiatric disorder (odds ratios (ORs) = 1.51-2.52). However, few differences in risk were observed based on the timing of first exposure. After conducting 20 tests of association, only three significant differences in risk were observed based on the timing of exposure; these results suggested an elevated risk of behaviour disorder among youth first exposed to any type of interpersonal violence during adolescence (OR = 2.37, 95% CI 1.69-3.34), especially being beaten by another person (OR = 2.44; 95% CI 1.57-3.79), and an elevated risk of substance use disorder among youth beaten by someone during adolescence (OR = 2.77, 95% CI 1.94-3.96).ConclusionsChildren exposed to interpersonal violence had an elevated risk of psychiatric disorder. However, age at first episode of exposure was largely unassociated with psychopathology risk.
BackgroundTraumatic events are associated with increased risk of psychotic experiences, but it is unclear whether this association is explained by mental disorders prior to psychotic experience onset.AimsTo investigate the associations between traumatic events and subsequent psychotic experience onset after adjusting for post-traumatic stress disorder and other mental disorders.MethodWe assessed 29 traumatic event types and psychotic experiences from the World Mental Health surveys and examined the associations of traumatic events with subsequent psychotic experience onset with and without adjustments for mental disorders.ResultsRespondents with any traumatic events had three times the odds of other respondents of subsequently developing psychotic experiences (OR = 3.1, 95% CI 2.7-3.7), with variability in strength of association across traumatic event types. These associations persisted after adjustment for mental disorders.ConclusionsExposure to traumatic events predicts subsequent onset of psychotic experiences even after adjusting for comorbid mental disorders.
Exposure to trauma is pervasive in societies worldwide and is associated with substantial costs to the individual and society, making it a significant global public health concern. We present evidence for trauma as a public health issue by highlighting the role of characteristics operating at multiple levels of influence - individual, relationship, community, and society - as explanatory factors in both the occurrence of trauma and its sequelae. Within the context of this multi-level framework, we highlight targets for prevention of trauma and its downstream consequences and provide examples of where public health approaches to prevention have met with success. Finally, we describe the essential role of public health policies in addressing trauma as a global public health issue, including key challenges for global mental health and next steps for developing and implementing a trauma-informed public health policy agenda. A public health framework is critical for understanding risk and protective factors for trauma and its aftermath operating at multiple levels of influence and generating opportunities for prevention.
BACKGROUND: Although there is robust evidence linking childhood adversities (CAs) and an increased risk for psychotic experiences (PEs), little is known about whether these associations vary across the life-course and whether mental disorders that emerge prior to PEs explain these associations. METHOD: We assessed CAs, PEs and DSM-IV mental disorders in 23 998 adults in the WHO World Mental Health Surveys. Discrete-time survival analysis was used to investigate the associations between CAs and PEs, and the influence of mental disorders on these associations using multivariate logistic models. RESULTS: Exposure to CAs was common, and those who experienced any CAs had increased odds of later PEs [odds ratio (OR) 2.3, 95% confidence interval (CI) 1.9-2.6]. CAs reflecting maladaptive family functioning (MFF), including abuse, neglect, and parent maladjustment, exhibited the strongest associations with PE onset in all life-course stages. Sexual abuse exhibited a strong association with PE onset during childhood (OR 8.5, 95% CI 3.6-20.2), whereas Other CA types were associated with PE onset in adolescence. Associations of other CAs with PEs disappeared in adolescence after adjustment for prior-onset mental disorders. The population attributable risk proportion (PARP) for PEs associated with all CAs was 31% (24% for MFF). CONCLUSIONS: Exposure to CAs is associated with PE onset throughout the life-course, although sexual abuse is most strongly associated with childhood-onset PEs. The presence of mental disorders prior to the onset of PEs does not fully explain these associations. The large PARPs suggest that preventing CAs could lead to a meaningful reduction in PEs in the population.
\textlessh3\textgreaterImportance\textless/h3\textgreater\textlessp\textgreaterDespite long-standing interest in the association of psychiatric disorders with intelligence, few population-based studies of psychiatric disorders have assessed intelligence.\textless/p\textgreater\textlessh3\textgreaterObjective\textless/h3\textgreater\textlessp\textgreaterTo investigate the association of fluid intelligence with past-year and lifetime psychiatric disorders, disorder age at onset, and disorder severity in a nationally representative sample of US adolescents.\textless/p\textgreater\textlessh3\textgreaterDesign, Setting, and Participants\textless/h3\textgreater\textlessp\textgreaterNational sample of adolescents ascertained from schools and households from the National Comorbidity Survey Replication–Adolescent Supplement, collected 2001 through 2004. Face-to-face household interviews with adolescents and questionnaires from parents were obtained. The data were analyzed from February to December 2016.\textitDSM-IVmental disorders were assessed with the World Health Organization Composite International Diagnostic Interview, and included a broad range of fear, distress, behavior, substance use, and other disorders. Disorder severity was measured with the Sheehan Disability Scale.\textless/p\textgreater\textlessh3\textgreaterMain Outcomes and Measures\textless/h3\textgreater\textlessp\textgreaterFluid IQ measured with the Kaufman Brief Intelligence Test, normed within the sample by 6-month age groups.\textless/p\textgreater\textlessh3\textgreaterResults\textless/h3\textgreater\textlessp\textgreaterThe sample included 10 073 adolescents (mean [SD] age, 15.2 [1.50] years; 49.0% female) with valid data on fluid intelligence. Lower mean (SE) IQ was observed among adolescents with past-year bipolar disorder (94.2 [1.69];\textitP = .004), attention-deficit/hyperactivity disorder (96.3 [0.91];\textitP = .002), oppositional defiant disorder (97.3 [0.66];\textitP = .007), conduct disorder (97.1 [0.82];\textitP = .02), substance use disorders (alcohol abuse, 96.5 [0.67];\textitP < .001; drug abuse, 97.6 [0.64];\textitP = .02), and specific phobia (97.1 [0.39];\textitP = .001) after adjustment for a wide range of potential confounders. Intelligence was not associated with posttraumatic stress disorder, eating disorders, and anxiety disorders other than specific phobia, and was positively associated with past-year major depression (mean [SE], 100 [0.5];\textitP = .01). Associations of fluid intelligence with lifetime disorders that had remitted were attenuated compared with past-year disorders, with the exception of separation anxiety disorder. Multiple past-year disorders had a larger proportion of adolescents less than 1 SD below the mean IQ range than those without a disorder. Across disorders, higher disorder severity was associated with lower fluid intelligence. For example, among adolescents with specific phobia, those with severe disorder had a mean (SE) of 4.4 (0.72) points lower IQ than those without severe disorder (\textitP < .001), and those with alcohol abuse had a mean (SE) of 5.6 (1.2) points lower IQ than those without severe disorder (\textitP < .001).\textless/p\textgreater\textlessh3\textgreaterConclusions and Relevance\textless/h3\textgreater\textlessp\textgreaterNumerous psychiatric disorders were associated with reductions in fluid intelligence; associations were generally small in magnitude. Stronger associations of current than past disorders with intelligence suggest that active symptoms of psychiatric disorders interfere with cognitive functioning. Early identification and treatment of children with mental disorders in school settings is critical to promote academic achievement and long-term success.\textless/p\textgreater
Nonfatal injury is common among adolescents in the U.S., but little is known about the bi-directional associations between injury and mental health. Utilizing a nationally representative sample of U.S. adolescents, we examined 1) associations between lifetime mental health history and subsequent injury; 2) concurrent associations between injury and mental health; and 3) associations between injury and subsequent mental disorders. Data were drawn from the National Comorbidity Survey Replication-Adolescent Supplement (NCS-A), a national survey of adolescents aged 13 through 17 years (N = 10,123). Twelve-month prevalence of nonfatal injury requiring medical attention was assessed along with lifetime, 12-month, and 30-day prevalence of DSM-IV depressive, anxiety, behavior, substance use, and bipolar disorders. We used Poisson regression to examine associations between 1) lifetime history of mental disorders and 12-month exposure to injury; 2) concurrent associations between 12-month exposure to injury and 12-month prevalence of mental disorders; and 3) 12-month exposure to injury and 30-day prevalence of mental disorders. A total of 11.6% of adolescents experienced an injury requiring medical attention in the year before the survey. Lifetime history of mental disorders was not associated with past-year injury. Behavior and bipolar disorders were concurrently associated with past-year injury. Past-year injury occurrence predicted increased risk for past-month anxiety disorders and decreased risk of past-month depressive disorders. Our findings reveal reciprocal associations between injury and mental disorders and highlight the need for systematic assessment, prevention, and treatment of mental disorders among injured youth.
OBJECTIVE: Child abuse exerts a deleterious impact on a broad array of mental health outcomes. However, the neurobiological mechanisms that mediate this association remain poorly characterized. Here, we use a longitudinal design to prospectively identify neural mediators of the association between child abuse and psychiatric disorders in a community sample of adolescents. METHOD: Structural magnetic resonance imaging (MRI) data and assessments of mental health were acquired for 51 adolescents (aged 13-20; M=16.96; SD=1.51), 19 of whom were exposed to physical or sexual abuse. Participants were assessed for abuse exposure (time 1), participated in MRI scanning and a diagnostic structured interview (time 2), and 2 years later were followed-up to assess psychopathology (time 3). We examined associations between child abuse and neural structure, and identified whether abuse-related differences in neural structure prospectively predicted psychiatric symptoms. RESULTS: Abuse was associated with reduced cortical thickness in medial and lateral prefrontal and temporal lobe regions. Thickness of the left and right parahippocampal gyrus predicted antisocial behavior symptoms, and thickness of the middle temporal gyrus predicted symptoms of generalized anxiety disorder. Thickness of the left parahippocampal gyrus mediated the longitudinal association of abuse with antisocial behavior. CONCLUSION: Child abuse is associated with widespread disruptions in cortical structure, and these disruptions are selectively associated with increased vulnerability to internalizing and externalizing psychopathology. Identifying predictive biomarkers of vulnerability following childhood maltreatment may uncover neurodevelopmental mechanisms linking environmental experience with the onset of psychopathology.
Background Although childhood adversities are known to predict increased risk of post-traumatic stress disorder (PTSD) after traumatic experiences, it is unclear whether this association varies by childhood adversity or traumatic experience types or by age. Aims To examine variation in associations of childhood adversities with PTSD according to childhood adversity types, traumatic experience types and life-course stage. Method Epidemiological data were analysed from the World Mental Health Surveys (n = 27 017). Results Four childhood adversities (physical and sexual abuse, neglect, parent psychopathology) were associated with similarly increased odds of PTSD following traumatic experiences (odds ratio (OR) = 1.8), whereas the other eight childhood adversities assessed did not predict PTSD. Childhood adversity–PTSD associations did not vary across traumatic experience types, but were stronger in childhood–adolescence and early-middle adulthood than later adulthood. Conclusions Childhood adversities are differentially associated with PTSD, with the strongest associations in childhood–adolescence and early-middle adulthood. Consistency of associations across traumatic experience types suggests that childhood adversities are associated with generalised vulnerability to PTSD following traumatic experiences.
Child maltreatment is associated with increased risk of an array of mental and physical health problems. We reviewed studies examining associations of child maltreatment, assessed either alone or in combination with other adversities, with cardiovascular disease (CVD) and type 2 diabetes. A search was conducted in PubMed for relevant studies until December 2015. Forty publications met inclusion criteria. Consistent positive associations were noted across a range of childhood adversities. Child maltreatment was associated with CVD (myocardial infarction, stroke, ischemic heart disease, coronary heart disease) in 91.7% of studies, with diabetes in 88.2% of studies, and with blood pressure/hypertension in 61.5% of studies. Inclusion of mental disorders tended to attenuate associations. Sex-related differences were under-examined. Implications for future research and intervention efforts are discussed.
When providing mental health services to adults, we are often treating individuals who, among their other roles, are also parents. The goal of this article was to provide practitioners with the state of the science about both the impact of parental psychopathology on children and the role that children's well-being has in parental psychopathology. We discuss the benefits of integrated care for adult clients who are parents, as well as the barriers to providing integrated care for both parents and children in psychotherapy, and provide recommendations for practice. With this information, practitioners will gain greater awareness of their opportunities to treat adults in their parenting roles as well as to contribute to prevention of mental disorders in children.
The human brain is remarkably plastic. The brain changes dramatically across development, with ongoing functional development continuing well into the third decade of life and substantial changes occurring again in older age. Dynamic changes in brain function are thought to underlie the innumerable changes in cognition, emotion, and behavior that occur across development. The brain also changes in response to experience, which raises important questions about how the environment influences the developing brain. Longitudinal functional magnetic resonance imaging (fMRI) studies are an essential means of understanding these developmental changes and their cognitive, emotional, and behavioral correlates. This paper provides an overview of common statistical models of longitudinal change applicable to developmental cognitive neuroscience, and a review of the functionality provided by major software packages for longitudinal fMRI analysis. We demonstrate that there are important developmental questions that cannot be answered using available software. We propose alternative approaches for addressing problems that are commonly faced in modeling developmental change with fMRI data.
Research on childhood adversity has traditionally focused on single types of adversity, which is limited because of high co-occurrence, or on the total number of adverse experiences, which assumes that diverse experiences influence development similarly. Identifying dimensions of environmental experience that are common to multiple types of adversity may be a more effective strategy. We examined the unique associations of two such dimensions (threat and cognitive deprivation) with automatic emotion regulation and cognitive control using a multivariate approach that simultaneously examined both dimensions of adversity. Data were drawn from a community sample of adolescents (N = 287) with variability in exposure to violence, an indicator of threat, and poverty, which is associated with cognitive deprivation. Adolescents completed tasks measuring automatic emotion regulation and cognitive control in neutral and emotional contexts. Violence was associated with automatic emotion regulation deficits, but not cognitive control; poverty was associated with poor cognitive control, but not automatic emotion regulation. Both violence and poverty predicted poor inhibition in an emotional context. Utilizing an approach focused on either single types of adversity or cumulative risk obscured specificity in the associations of violence and poverty with emotional and cognitive outcomes. These findings suggest that different dimensions of childhood adversity have distinct influences on development and highlight the utility of a differentiated multivariate approach.
Social anxiety and depression are common mental health problems among adolescents and are frequently comorbid. Primary aims of this study were to (1) elucidate the nature of individual differences in specific emotion regulation deficits among adolescents with symptoms of social anxiety and depression, and (2) determine whether repetitive negative thinking (RNT) functions as a transdiagnostic factor. A diverse sample of adolescents (N = 1065) completed measures assessing emotion regulation and symptoms of social anxiety and depression. Results indicated that adolescents with high levels of social anxiety and depression symptoms reported decreased emotional awareness, dysregulated emotion expression, and reduced use of emotion management strategies. The hypothesized structural model in which RNT functions as a transdiagnostic factor exhibited a better fit than an alternative model in which worry and rumination function as separate predictors of symptomatology. Findings implicate emotion regulation deficits and RNT in the developmental psychopathology of youth anxiety and mood disorders.
\textlessp\textgreaterNook et al. show that emotion concept representations develop from a monodimensional focus on positive versus negative valence in childhood to multidimensional organization in adulthood. This expansion is facilitated by increasing verbal knowledge.\textless/p\textgreater
Environmental contributions are thought to play a primary role in the familial aggregation of anxiety, but parenting influences remain poorly understood. We examined dynamic relations between maternal anxiety, maternal emotion regulation (ER) during child distress, maternal accommodation of child distress, and child anxiety. Mothers (N=45) of youth ages 3–8 years (M=4.8) participated in an experimental task during which they listened to a standardized audio recording of a child in anxious distress pleading for parental intervention. Measures of maternal and child anxiety, mothers’ affective states, mothers’ ER strategies during the child distress, and maternal accommodation of child anxiety were collected. Mothers’ resting respiratory sinus arrhythmia (RSA) reactivity during the recording was also acquired. Higher maternal negative affect and greater maternal ER switching (i.e., using multiple ER strategies in a short time without positive regulatory results) during child distress were associated with child anxiety. Sequential mediation modeling showed that maternal anxiety predicted ineffective maternal ER during child distress exposure, which in turn predicted greater maternal accommodation, which in turn predicted higher child anxiety. Findings support the mediating roles of maternal ER and accommodation in linking maternal and child anxiety, and suggest that ineffective maternal ER and subsequent attempts to accommodate child distress may act as mechanisms underlying the familial aggregation of anxiety.
Parasympathetic nervous system influences on cardiac functions-commonly indexed via respiratory sinus arrhythmia (RSA)-are central to self-regulation. RSA suppression during challenging emotional and cognitive tasks is often associated with better emotional and behavioral functioning in preschoolers. However, the links between RSA suppression and child behavior across various challenging interpersonal contexts remains unclear. The present study experimentally evaluated the relationship between child RSA reactivity to adult (mother vs. study staff) direction and disruptive behavior problems in children ages 3-8 with varying levels of disruptive behavior problems (N = 43). Reduced RSA suppression in the context of mothers' play-based direction was associated with more severe child behavior problems. In contrast, RSA suppression in the context of staff play-based direction was not associated with behavior problems. Findings suggest that the association between RSA suppression and child behavior problems may vary by social context (i.e., mother vs. other adult direction-givers). Findings are discussed in regard to RSA as an indicator of autonomic self-regulation that has relevance to child disruptive behavior problems.
Despite calls to incorporate population science into neuroimaging research, most studies recruit small, non-representative samples. Here, we examine whether sample composition influences age-related variation in global measurements of gray matter volume, thickness, and surface area. We apply sample weights to structural brain imaging data from a community-based sample of children aged 3-18 (N = 1162) to create a "weighted sample" that approximates the distribution of socioeconomic status, race/ethnicity, and sex in the U.S. Census. We compare associations between age and brain structure in this weighted sample to estimates from the original sample with no sample weights applied (i.e., unweighted). Compared to the unweighted sample, we observe earlier maturation of cortical and sub-cortical structures, and patterns of brain maturation that better reflect known developmental trajectories in the weighted sample. Our empirical demonstration of bias introduced by non-representative sampling in this neuroimaging cohort suggests that sample composition may influence understanding of fundamental neural processes.The influence of sample composition on human neuroimaging results is unknown. Here, the authors weight a large, community-based sample to better reflect the US population and describe how applying these sample weights changes conclusions about age-related variation in brain structure.