Unravelling risks for child psychopathologies – general lessons from eating disorder researchMaughan, Barbara
doi: 10.1111/jcpp.12472pmid: 26463417
Clarifying risks for childhood disorders is one of the core aims of research in developmental psychopathology; disseminating findings from the most robust and clinically relevant of that risk research is a core aim of JCPP. This issue exemplifies that tradition, including articles that use a range of research designs and strategies to confirm – or in some instances disconfirm – the roles of hypothesized risks. It begins with one of our occasional series of reviews of risk research: Culbert, Racine and Klump's lucid synthesis of recent findings on the causes of eating disorders, and the accompanying Commentary by Smith and Davis. These will, of course, be of special interest to those who work in the eating disorders field, but – like all good reviews – their underlying messages have a wider resonance and relevance for the field. We highlight just three issues of particular interest in this Editorial.
Research Review: What we have learned about the causes of eating disorders – a synthesis of sociocultural, psychological, and biological researchCulbert, Kristen M.; Racine, Sarah E.; Klump, Kelly L.
doi: 10.1111/jcpp.12441pmid: 26095891
Background Eating disorders are severe psychiatric disorders with a complex etiology involving transactions among sociocultural, psychological, and biological influences. Most research and reviews, however, focus on only one level of analysis. To address this gap, we provide a qualitative review and summary using an integrative biopsychosocial approach. Methods We selected variables for which there were available data using integrative methodologies (e.g., twin studies, gene‐environment interactions) and/or data at the biological and behavioral level (e.g., neuroimaging). Factors that met these inclusion criteria were idealization of thinness, negative emotionality, perfectionism, negative urgency, inhibitory control, cognitive inflexibility, serotonin, dopamine, ovarian hormones. Literature searches were conducted using PubMed. Variables were classified as risk factors or correlates of eating disorder diagnoses and disordered eating symptoms using Kraemer et al.'s (1997) criteria. Findings Sociocultural idealization of thinness variables (media exposure, pressures for thinness, thin‐ideal internalization, thinness expectancies) and personality traits (negative emotionality, perfectionism, negative urgency) attained ‘risk status’ for eating disorders and/or disordered eating symptoms. Other factors were identified as correlates of eating pathology or were not classified given limited data. Effect sizes for risk factors and correlates were generally small‐to‐moderate in magnitude. Conclusions Multiple biopsychosocial influences are implicated in eating disorders and/or disordered eating symptoms and several can now be considered established risk factors. Data suggest that psychological and environmental factors interact with and influence the expression of genetic risk to cause eating pathology. Additional studies that examine risk variables across multiple levels of analysis and that consider specific transactional processes amongst variables are needed to further elucidate the intersection of sociocultural, psychological, and biological influences on eating disorders.
Commentary: An exemplar of progress in understanding complex disorders – reflections on what we have learned about eating disorders (Culbert et al., 2015)Smith, Gregory T.; Davis, Heather A.
doi: 10.1111/jcpp.12455pmid: 26463418
A number of recent advances in eating disorders research have helped clarify the nature of risk for the development of such disorders. Culbert et al. () provide an empirical and thoughtful review of these recent advances. The authors identified empirically established risk factors in each of several categories of risk for eating disorders: genetic influences, neurotransmitter activity, hormones, personality, and sociocultural influences. We highlight three implications of their review. First, the review can serve as an important asset to eating disorder researchers, both substantively, by providing a comprehensive account of empirically supported risk processes; and methodologically, by highlighting good standards of evidence for acceptance of a candidate risk factor. Second, eating disorder risk is increased by both transdiagnostic and eating disorder‐specific factors; there is a need to understand how these types of factors transact with each other. Third and most important, we highlight the importance of Culbert et al.'s advocacy for the development of theoretical models, and empirical tests of those models that specify transactions among different types of risk factors, such as those based on genetic, neurobiological, personality, and social processes.
Implicit sequence learning in juvenile anorexia nervosa: neural mechanisms and the impact of starvationFirk, Christine; Mainz, Verena; Schulte‐Ruether, Martin; Fink, Gereon; Herpertz‐Dahlmann, Beate; Konrad, Kerstin
doi: 10.1111/jcpp.12384pmid: 25623396
Background Previous studies have reported that cognitive deficits occur in patients with anorexia nervosa (AN) and that these deficits may represent a predisposition towards developing AN or perpetuate the disorder. Specifically, dysfunctional implicit learning may contribute to the development of highly resistant dieting behaviours that are fundamental to the persistence of the disorder. Thus, the aims of this study were (a) to investigate implicit sequence learning in adolescent patients with AN before and after weight recovery and (b) to elucidate the associated neural mechanisms in acute AN relative to healthy controls. Methods In a behavioural study, implicit sequence learning was assessed using a serial reaction time task in 27 adolescents with AN before (T1) and after weight recovery (T2) compared with age‐matched healthy controls (HC) who were assessed at similar time intervals. The neural correlates of implicit sequence learning were subsequently investigated in 19 AN patients shortly after they were admitted to the hospital and 20 HC using functional magnetic resonance imaging (fMRI). Results At T1, AN patients showed reduced sequence learning compared with HC. However, no behavioural differences between HC and AN patients were found at T2. At the neural level, acute AN patients showed reduced thalamic activation during sequence learning compared with HC subjects. Conclusions Our data suggest that the impaired implicit learning observed in adolescent AN patients before weight gain is a state‐related dysfunction that normalises with weight gain. Thus, implicit learning deficits do not appear to represent a predisposition towards developing AN; rather, these deficits should be considered when planning psychotherapeutic interventions for acute AN. Reduced thalamic activation during the acute stage of AN may indicate a starvation‐induced dysfunction of the neural circuitry that is involved in behavioural flexibility.
Adolescent girls’ neural response to reward mediates the relation between childhood financial disadvantage and depressionRomens, Sarah E.; Casement, Melynda D.; McAloon, Rose; Keenan, Kate; Hipwell, Alison E.; Guyer, Amanda E.; Forbes, Erika E.
doi: 10.1111/jcpp.12410pmid: 25846746
Background Children who experience socioeconomic disadvantage are at heightened risk for developing depression; however, little is known about neurobiological mechanisms underlying this association. Low socioeconomic status (SES) during childhood may confer risk for depression through its stress‐related effects on the neural circuitry associated with processing monetary rewards. Methods In a prospective study, we examined the relationships among the number of years of household receipt of public assistance from age 5–16 years, neural activation during monetary reward anticipation and receipt at age 16, and depression symptoms at age 16 in 123 girls. Results Number of years of household receipt of public assistance was positively associated with heightened response in the medial prefrontal cortex during reward anticipation, and this heightened neural response mediated the relationship between socioeconomic disadvantage and current depression symptoms, controlling for past depression. Conclusions Chronic exposure to socioeconomic disadvantage in childhood may alter neural circuitry involved in reward anticipation in adolescence, which in turn may confer risk for depression.
Effect of housing relocation and neighborhood environment on adolescent mental and behavioral healthByck, Gayle R.; Bolland, John; Dick, Danielle; Swann, Gregory; Henry, David; Mustanski, Brian
doi: 10.1111/jcpp.12386pmid: 25656159
Background This study examined whether relocating from a high‐poverty neighborhood to a lower poverty neighborhood as part of a federal housing relocation program (HOPE VI; Housing Opportunities for People Everywhere) had effects on adolescent mental and behavioral health compared to adolescents consistently living in lower poverty neighborhoods. Methods Sociodemographic, risk behavior, and neighborhood data were collected from 592 low‐income, primarily African‐American adolescents and their primary caregivers. Structured psychiatric interviews were conducted with adolescents. Prerelocation neighborhood, demographic, and risk behavior data were also included. Hierarchical Linear Modeling (HLM) was used to test associations between neighborhood variables and risk outcomes. HLM was used to test whether the effect of neighborhood relocation and neighborhood characteristics might explain differences in sexual risk taking, substance use, and mental health outcomes. Results Adolescents who relocated of HOPE VI neighborhoods (n = 158) fared worse than control group participants (n = 429) on most self‐reported mental health outcomes. The addition of subjective neighborhood measures generally did not substantively change these results. Conclusions Our findings suggest that moving from a high‐poverty neighborhood to a somewhat lower poverty neighborhood is not associated with better mental health and risk behavior outcomes in adolescents. The continued effects of having grown up in a high‐poverty neighborhood, the small improvements in their new neighborhoods, the comparatively short length of time they lived in their new neighborhood, and/or the stress of moving appears to worsen most of the mental health outcomes of HOPE VI compared to control group participants who consistently lived in the lower poverty neighborhoods.
Attention bias and anxiety in young children exposed to family violenceBriggs‐Gowan, Margaret J.; Pollak, Seth D.; Grasso, Damion; Voss, Joel; Mian, Nicholas D.; Zobel, Elvira; McCarthy, Kimberly J.; Wakschlag, Lauren S.; Pine, Daniel S.
doi: 10.1111/jcpp.12397pmid: 26716142
Background Attention bias toward threat is associated with anxiety in older youth and adults and has been linked with violence exposure. Attention bias may moderate the relationship between violence exposure and anxiety in young children. Capitalizing on measurement advances, this study examines these relationships at a younger age than previously possible. Methods Young children (mean age 4.7, ±0.8) from a cross‐sectional sample oversampled for violence exposure (N = 218) completed the dot‐probe task to assess their attention biases. Observed fear/anxiety was characterized with a novel observational paradigm, the Anxiety Dimensional Observation Scale. Mother‐reported symptoms were assessed with the Preschool Age Psychiatric Assessment and Trauma Symptom Checklist for Young Children. Violence exposure was characterized with dimensional scores reflecting probability of membership in two classes derived via latent class analysis from the Conflict Tactics Scales: Abuse and Harsh Parenting. Results Family violence predicted greater child anxiety and trauma symptoms. Attention bias moderated the relationship between violence and anxiety. Conclusions Attention bias toward threat may strengthen the effects of family violence on the development of anxiety, with potentially cascading effects across childhood. Such associations may be most readily detected when using observational measures of childhood anxiety.
Early life stress is associated with default system integrity and emotionality during infancyGraham, Alice M.; Pfeifer, Jennifer H.; Fisher, Philip A.; Carpenter, Samuel; Fair, Damien A.
doi: 10.1111/jcpp.12409pmid: 25809052
Background Extensive animal research has demonstrated the vulnerability of the brain to early life stress (ELS) with consequences for emotional development and mental health. However, the influence of moderate and common forms of stress on early human brain development is less well‐understood and precisely characterized. To date, most work has focused on severe forms of stress, and/or on brain functioning years after stress exposure. Methods In this report we focused on conflict between parents (interparental conflict), a common and relatively moderate form of ELS that is highly relevant for children's mental health outcomes. We used resting state functional connectivity MRI to examine the coordinated functioning of the infant brain (N = 23; 6–12‐months‐of‐age) in the context of interparental conflict. We focused on the default mode network (DMN) due to its well‐characterized developmental trajectory and implications for mental health. We further examined DMN strength as a mediator between conflict and infants’ negative emotionality. Results Higher interparental conflict since birth was associated with infants showing stronger connectivity between two core DMN regions, the posterior cingulate cortex (PCC) and the anterior medial prefrontal cortex (aMPFC). PCC to amygdala connectivity was also increased. Stronger PCC‐aMPFC connectivity mediated between higher conflict and higher negative infant emotionality. Conclusions The developing DMN may be an important marker for effects of ELS with relevance for emotional development and subsequent mental health. Increasing understanding of the associations between common forms of family stress and emerging functional brain networks has potential to inform intervention efforts to improve mental health outcomes.
Internalising symptoms and body dissatisfaction: untangling temporal precedence using cross‐lagged models in two cohortsPatalay, Praveetha; Sharpe, Helen; Wolpert, Miranda
doi: 10.1111/jcpp.12415pmid: 25902846
Background Cross‐sectional studies demonstrate that body dissatisfaction and internalising symptoms are correlated and are both overrepresented in girls compared to boys. However, it is not clear whether body dissatisfaction typically precedes internalising symptoms or vice versa. Existing literature provides theoretical and empirical support for both possibilities, but is limited in two ways: (a) no study has simultaneously tested the two temporal hypotheses within the same model, and (b) the studies focus almost exclusively on early adolescents resulting in little being known about development from preadolescence and across puberty. Methods This study used data from 5485 primary school students (49.1% girls, aged 8–9 years at baseline) and 5981 secondary school students (53.9% girls, aged 11–12 years at baseline). Self‐reports of internalising symptoms and body dissatisfaction were collected over three consecutive years at 1‐year intervals. Cross‐lagged models were estimated in the two cohorts, for boys and girls separately, to examine the temporal associations between these two domains across the three measurement points. Results In the younger cohort, internalising symptoms predicted body dissatisfaction 1‐year later for both boys and girls, whereas there was no evidence for the reverse being true. In the older cohort, internalising symptoms predicted later body dissatisfaction for boys. However, in girls, body dissatisfaction predicted later internalising symptoms. Conclusions In preadolescents, internalising symptoms drive later body dissatisfaction regardless of gender, suggesting body dissatisfaction is a specific manifestation of a tendency towards negative affect. From age 11, girls develop a distinct risk profile whereby body dissatisfaction drives later internalising symptoms. Preventative interventions in this field would benefit from adopting a developmentally sensitive approach that takes into account gender differences in risk pathways.