ABSTRACT
Childhood maltreatment and intimate partner violence (IPV) victimization are major psychiatric risk factors. Maltreatment substantially increases the likelihood of subsequent IPV victimization, but what drives this association is poorly understood. We analyzed retrospective self-reports of maltreatment and IPV in 12794 participants (58% women, 42% men) from the Twins Early Development Study at ages 21 and 26 using quantitative genetic methods. We estimated the etiological influences common to maltreatment and IPV, and the direct causal effect of maltreatment on IPV beyond such common influences. Participants exposed to maltreatment (~7% of the sample) were 3 times more likely to experience IPV victimization than their peers at age 21, 4 times more likely at 26. The association between maltreatment and IPV was mostly due to environmental influences shared by co-twins (42-43%) and genetic influences (30-33%). The association between maltreatment and IPV was similar for women and men, but its etiology partly differed by sex. Maltreatment had a moderate-to-large effect on IPV in phenotypic models (ß = 0.23-0.34), decreasing to a small-to-moderate range in causal models accounting for their common etiology (ß = 0.15-0.21). Risk factors common to maltreatment and IPV victimization are largely familial in origin, environmental and genetic. Even considering common risk factors, experiencing maltreatment is causally related to subsequent IPV victimization. Interventions promoting safe intimate relationships among young adults exposed to maltreatment are warranted and should address family-level environmental risk and individual-level risk shaped by genetics.
ABSTRACT
In many everyday decisions, individuals choose between trialling something novel or something they know well. Deciding when to try a new option or stick with an option that is already known to you, known as the "explore/exploit" dilemma, is an important feature of cognition that characterises a range of decision-making contexts encountered by humans. Recent evidence has suggested preferences in explore/exploit biases are associated with psychopathology, although this has typically been examined within individual disorders. The current review examined whether explore/exploit decision-making represents a promising transdiagnostic target for psychosis, depression, and anxiety. A systematic search of academic databases was conducted, yielding a total of 29 studies. Studies examining psychosis were mostly consistent in showing that individuals with psychosis explored more compared with individuals without psychosis. The literature on anxiety and depression was more heterogenous; some studies found that anxiety and depression were associated with more exploration, whereas other studies demonstrated reduced exploration in anxiety and depression. However, examining a subset of studies that employed case-control methods, there was some evidence that both anxiety and depression also were associated with increased exploration. Due to the heterogeneity across the literature, we suggest that there is insufficient evidence to conclude whether explore/exploit decision-making is a transdiagnostic target for psychosis, depression, and anxiety. However, alongside our advisory groups of lived experience advisors, we suggest that this context of decision-making is a promising candidate that merits further investigation using well-powered, longitudinal designs. Such work also should examine whether biases in explore/exploit choices are amenable to intervention.
ABSTRACT
BACKGROUND: The Sensitivity to Threat and Affiliative Reward (STAR) model proposes low threat sensitivity and low affiliation as risk factors for callous-unemotional (CU) traits. Preliminary evidence for the STAR model comes from work in early childhood. However, studies are needed that explore the STAR dimensions in late childhood and adolescence when severe conduct problems (CP) emerge. Moreover, it is unclear how variability across the full spectrum of threat sensitivity and affiliation gives rise to different forms of psychopathology beyond CU traits. METHODS: The current study addressed these gaps using parent- and child-reported data from three waves and a sub-study of the Adolescent Brain Cognitive Development Study® of 11,878 youth (48% female; ages 9-12). RESULTS: Consistent with the STAR model, low threat sensitivity and low affiliation were independently related to CU traits across informants and time. Moreover, there was significant interaction between the STAR dimensions, such that children with lower sensitivity to threat and lower affiliation had higher parent-reported CU traits. Unlike CU traits, children with higher threat sensitivity had higher parent-reported CP and anxiety. Finally, children with lower affiliation had higher parent-reported CP, anxiety, and depression. Results largely replicated across informants and time, and sensitivity analysis revealed similar findings in children with and without DSM-5 defined CP. CONCLUSIONS: Results support the STAR model hypotheses as they pertain to CU traits and delineate threat sensitivity and affiliation as independent transdiagnostic risk factors for different types of psychopathology. Future research is needed to develop fuller and more reliable and valid measures of affiliation and threat sensitivity across multiple assessment modalities.
ABSTRACT
OBJECTIVE: The role of negative parenting in the development of callous-unemotional (CU) traits remains unclear. Both negative parenting and CU traits are influenced by genetic and environmental factors. The authors used genetically informed longitudinal cross-lagged models to examine the extent to which reciprocal effects between negative parenting and children's CU traits in mid-to-late childhood are genetic versus environmental in origin. METHODS: In 9,260 twin pairs from the Twins Early Development Study, the authors estimated cross-lagged effects between negative parenting (discipline and feelings) and children's CU traits in mid (ages 7-9) and late (ages 9-12) childhood. RESULTS: CU traits were strongly heritable and stable. Stability was explained largely by genetic factors. The influence of negative parenting on the development of CU traits was small and driven mostly by genetic and shared environmental factors. In mid childhood, the influence of children's CU traits on subsequent negative parenting (i.e., evoked by children's CU traits) was also small and mostly genetic in origin. In late childhood, CU traits showed no effects on negative parental discipline and small effects on negative parental feelings, which reflected mostly shared environmental factors. CONCLUSIONS: In mid-to-late childhood, genetic factors strongly influenced the development of CU traits, whereas environmental effects of negative parenting were small. Negative parenting was also relatively unaffected by CU traits. The small reciprocal effects originated mostly from genetic and shared environmental factors. Therefore, repeated intensive interventions addressing multiple risk factors rather than negative parenting alone may be best positioned to support families of children with CU traits across development.
Subject(s)
Conduct Disorder , Humans , Child , Conduct Disorder/genetics , Conduct Disorder/psychology , Parenting/psychology , Antisocial Personality Disorder/etiology , Emotions/physiology , Parents , EmpathyABSTRACT
BACKGROUND: Adolescence is a period of heightened vulnerability to developing mental health problems, and rates of mental health disorder in this age group have increased in the last decade. Preventing mental health problems developing before they become entrenched, particularly in adolescents who are at high risk, is an important research and clinical target. Here, we report the protocol for the trial of the 'Building Resilience through Socioemotional Training' (ReSET) intervention. ReSET is a new, preventative intervention that incorporates individual-based emotional training techniques and group-based social and communication skills training. We take a transdiagnostic approach, focusing on emotion processing and social mechanisms implicated in the onset and maintenance of various forms of psychopathology. METHODS: A cluster randomised allocation design is adopted with randomisation at the school year level. Five-hundred and forty adolescents (aged 12-14) will be randomised to either receive the intervention or not (passive control). The intervention is comprised of weekly sessions over an 8-week period, supplemented by two individual sessions. The primary outcomes, psychopathology symptoms and mental wellbeing, will be assessed pre- and post-intervention, and at a 1-year follow-up. Secondary outcomes are task-based assessments of emotion processing, social network data based on peer nominations, and subjective ratings of social relationships. These measures will be taken at baseline, post-intervention and 1-year follow-up. A subgroup of participants and stakeholders will be invited to take part in focus groups to assess the acceptability of the intervention. DISCUSSION: This project adopts a theory-based approach to the development of a new intervention designed to target the close connections between young people's emotions and their interpersonal relationships. By embedding the intervention within a school setting and using a cluster-randomised design, we aim to develop and test a feasible, scalable intervention to prevent the onset of psychopathology in adolescence. TRIAL REGISTRATION: ISRCTN88585916. Trial registration date: 20/04/2023.
Subject(s)
Mental Disorders , Resilience, Psychological , Humans , Adolescent , Emotions , Schools , Randomized Controlled Trials as TopicABSTRACT
Background: Childhood maltreatment profoundly influences social and emotional development, increasing psychiatric risk. Alterations in the implicit processing of threat-related cues following early abuse and neglect represent a marker of mental health vulnerability. Less is known about how early adversity influences the perception of positive social cues, despite their central role in establishing and maintaining social interactions and their association with better mental health outcomes.Methods: The sample consisted of 42 children and adolescents with substantiated childhood maltreatment experiences and 32 peers (mean age 13.3), matched on age, pubertal status, gender, socioeconomic status, ethnicity, and cognitive ability. A computerised experimental task assessed the perceived emotional intensity of positive (happy) and negative (fearful) facial expressions. Mental health symptoms were measured via self- and parental reports, and perceived social support was self-reported.Results: The experience of abuse and neglect was associated with heightened perceived intensity of positive facial cues. Cross-sectional post-hoc moderation and mediation analyses, employing a model-building approach, revealed that in maltreatment-exposed participants: (i) their increased response to positive facial cues was associated with lower symptoms; (ii) the presence of social support accounted for their heightened perceived intensity of positive facial cues; (iii) the presence of social support putatively contributed to lower symptoms by increasing the perceived intensity of positive facial cues. No group differences in perceived intensity of negative expressions were observed.Conclusions: These findings provide fresh insight into how positive faces are processed following maltreatment experience in childhood. Maltreatment experience was found to be associated with heightened perceived intensity of happy faces, which in turn was associated with better mental health and greater levels of social support. This suggests that heightened saliency of positive emotions acts protectively in children with maltreatment experience.
The impact of childhood maltreatment on perceiving positive social cues, especially explicit emotional intensity appraisal, is less understood compared to the extensive focus on its role in processing threat-related cues and psychiatric risk.In this study, we found that maltreatment experience was associated with heightened perceived intensity of happy faces, which in turn was associated with better mental health and greater levels of social support.These findings suggest that heightened saliency of positive emotions may act protectively in children with maltreatment experience.
Subject(s)
Adverse Childhood Experiences , Resilience, Psychological , Adolescent , Humans , Child , Cues , Cross-Sectional Studies , Emotions/physiologyABSTRACT
Externalizing behavioral problems in young children are associated with later delinquency and crime,1 which can cause burdens at both personal and socialeconomic levels. The heterogeneity of externalizing problems emphasizes the importance of examining the etiological mechanisms that underlie externalizing problems and related behaviors. The present study focuses on 2 risk factors for externalizing behavioral problems in early childhood: callous-unemotional traits (CU), characterized as a lack of guilt and empathy,2 and irritability, a tendency to show anger and frustration.3 Behavioral genetic studies find that externalizing problems, CU, and irritability are heritable,4,5 raising the possibility of common genetic effects linking the 3 behaviors, but this has not been previously explored. Neurological evidence suggests distinct pathways from CU and irritability to externalizing problems,6 implying that the genetic and environmental factors linking externalizing problems and CU may differ from those linking externalizing problems and irritability. We predict that there will be common genetic influences operating across externalizing problems, CU, and irritability; but we also predict unique genetic and environmental influences representing distinctive risks shared between externalizing problems and CU, and between externalizing problems and irritability, respectively.
Subject(s)
Conduct Disorder , Problem Behavior , Child , Humans , Child, Preschool , Conduct Disorder/genetics , Conduct Disorder/psychology , Irritable Mood , Empathy , Risk Factors , EmotionsSubject(s)
Language Development Disorders , Humans , Language Development Disorders/etiology , ChildABSTRACT
Neurodevelopment is not merely a process of brain maturation, but an adaptation to constraints unique to each individual and to the environments we co-create. However, our theoretical and methodological toolkits often ignore this reality. There is growing awareness that a shift is needed that allows us to study divergence of brain and behaviour across conventional categorical boundaries. However, we argue that in future our study of divergence must also incorporate the developmental dynamics that capture the emergence of those neurodevelopmental differences. This crucial step will require adjustments in study design and methodology. If our ultimate aim is to incorporate the developmental dynamics that capture how, and ultimately when, divergence takes place then we will need an analytic toolkit equal to these ambitions. We argue that the over reliance on group averages has been a conceptual dead-end with regard to the neurodevelopmental differences. This is in part because any individual differences and developmental dynamics are inevitably lost within the group average. Instead, analytic approaches which are themselves new, or simply newly applied within this context, may allow us to shift our theoretical and methodological frameworks from groups to individuals. Likewise, methods capable of modelling complex dynamic systems may allow us to understand the emergent dynamics only possible at the level of an interacting neural system.
Subject(s)
Brain , Research Design , HumansABSTRACT
BACKGROUND: Prosocial behaviours - acts that benefit others - are of crucial importance for many species including humans. However, adolescents with conduct problems (CP), unlike their typically developing (TD) peers, demonstrate markedly reduced engagement in prosocial behaviours. This pattern is particularly pronounced in adolescents with CP and high levels of callous-unemotional traits (CP/HCU) who are at increased risk of developing psychopathy in adulthood. While a substantial amount of research has investigated the cognitive-affective mechanisms thought to underlie antisocial behaviour, much less is known about the mechanisms that could explain reduced prosocial behaviours in adolescents with CP. METHODS: Here we examined the willingness to exert effort to benefit oneself (self) and another person (other, prosocial condition) in children with CP/HCU, CP and lower levels of CU traits (CP/LCU) and their TD peers. The task captured both prosocial choices, and actual effort exerted following prosocial choices, in adolescent boys aged 11-16 (27 CP/HCU; 34 CP/LCU; 33 TD). We used computational modelling to reveal the mechanistic processes involved when choosing prosocial acts. RESULTS: We found that both CP/HCU and CP/LCU groups were more averse to initiating effortful prosocial acts than TD adolescents - both at a cognitive and at a behavioural level. Strikingly, even if they chose to initiate a prosocial act, the CP/HCU group exerted less effort following this prosocial choice than other groups. CONCLUSIONS: Our findings indicate that reduced exertion of effort to benefit others may be an important factor that differentiates adolescents with CP/HCU from their peers with CP/LCU. They offer new insights into what might drive low prosocial behaviour in adolescents with CP, including vulnerabilities that may particularly characterise those with high levels of CU traits.
Subject(s)
Adolescent Behavior , Conduct Disorder , Motivation , Social Behavior , Humans , Adolescent , Male , Conduct Disorder/physiopathology , Conduct Disorder/psychology , Child , Motivation/physiology , Adolescent Behavior/physiology , Emotions/physiology , Empathy/physiology , Antisocial Personality Disorder/physiopathology , Antisocial Personality Disorder/psychology , Peer GroupABSTRACT
Antisocial behaviour (ASB) incurs substantial costs to the individual and society. Cognitive neuroscience has the potential to shed light on developmental risk for ASB, but it cannot achieve this potential in an 'essentialist' framework that focuses on the brain and cognition isolated from the environment. Here, we present the case for studying the social transactional and iterative unfolding of brain and cognitive development in a relational context. This approach, which we call the study of the 'embedded brain', is needed to fully understand how risk for ASB arises during development. Concentrated efforts are required to develop and unify methods to achieve this approach and reap the benefits for improved prevention and intervention of ASB.
Subject(s)
Antisocial Personality Disorder , Conduct Disorder , Humans , Conduct Disorder/psychology , Brain , Behavior Therapy , EmotionsABSTRACT
BACKGROUND: Childhood maltreatment is associated with altered neurocognitive functioning, which is thought to reflect, in part, adaptation to early adverse environmental experiences. However, we continue to lack a precise mechanistic understanding linking atypical neurocognitive processing with social functioning and psychiatric outcomes following early adversity. OBJECTIVE: The present work investigated interpersonal problem-solving, resting-state functional connectivity (rsFC), and mental health symptoms in adolescents with documented maltreatment experience and explored whether altered neural function contributes in part to poorer social functioning. METHODS: Forty adolescents (aged 12-17) with documented experiences of abuse or neglect and a carefully matched group of 42 non-maltreated peers participated in this study that measured task-based interpersonal problem-solving skills and rsFC. RESULTS: Adolescents with maltreatment experience showed poorer interpersonal problem-solving performance, which partly accounted for their elevated mental health symptoms. Resting-state seed-based analyses revealed that adolescents with maltreatment experience showed a significant increase in rsFC between medial Default Mode Network (DMN) hubs, the medial prefrontal cortex (mPFC), with a posterior cluster, including the posterior cingulate cortex (PCC), precuneus (PCu), retrosplenial cortex (RSC), and lingual gyrus (LG). Moderation analyses revealed that maltreatment-related increased DMN rsFC partly accounted for poorer performance in interpersonal problem-solving. CONCLUSION: Poorer interpersonal problem-solving, partly accounted for by atypical coupling between DMN medial hubs, was associated with maltreatment exposure. Interventions tailored to enhance interpersonal problem-solving represents a promising avenue to promote resilience and reduce the likelihood of mental health disorder following maltreatment experience.
Subject(s)
Mental Disorders , Humans , Adolescent , Child , Gyrus Cinguli , Magnetic Resonance Imaging , Neural Pathways/diagnostic imaging , Mental Health , BrainABSTRACT
People readily and automatically process facial emotion and identity, and it has been reported that these cues are processed both dependently and independently. However, this question of identity independent encoding of emotions has only been examined using posed, often exaggerated expressions of emotion, that do not account for the substantial individual differences in emotion recognition. In this study, we ask whether people's unique beliefs of how emotions should be reflected in facial expressions depend on the identity of the face. To do this, we employed a genetic algorithm where participants created facial expressions to represent different emotions. Participants generated facial expressions of anger, fear, happiness, and sadness, on two different identities. Facial features were controlled by manipulating a set of weights, allowing us to probe the exact positions of faces in high-dimensional expression space. We found that participants created facial expressions belonging to each identity in a similar space that was unique to the participant, for angry, fearful, and happy expressions, but not sad. However, using a machine learning algorithm that examined the positions of faces in expression space, we also found systematic differences between the two identities' expressions across participants. This suggests that participants' beliefs of how an emotion should be reflected in a facial expression are unique to them and identity independent, although there are also some systematic differences in the facial expressions between two identities that are common across all individuals. (PsycInfo Database Record (c) 2024 APA, all rights reserved).
Subject(s)
Emotions , Facial Recognition , Humans , Anger , Happiness , Fear , Sadness , Facial ExpressionABSTRACT
Studies report that the microstructural integrity of the uncinate fasciculus (UF; connecting the anterior temporal lobe to the orbitofrontal cortex) is abnormal in adults with psychopathy and children with conduct problems (CP), especially those with high callous-unemotional (CU) traits. However, it is unknown if these abnormalities are 'fixed' or 'reversible'. Therefore, we tested the hypothesis that a reduction in CP symptoms, following a parenting intervention, would be associated with altered microstructural integrity in the UF. Using diffusion tensor imaging tractography we studied microstructural differences (mean diffusivity (MD) and radial diffusivity (RD)) in the UF of 43 typically developing (TD) and 67 boys with CP before and after a 14-week parenting intervention. We also assessed whether clinical response in CP symptoms or CU traits explained changes in microstructure following the intervention. Prior to intervention, measures of MD and RD in the UF were increased in CP compared to TD boys. Following intervention, we found that the CP group had a significant reduction in RD and MD. Further, these microstructural changes were driven by the group of children whose CU traits improved (but not CP symptoms as hypothesized). No significant microstructural changes were observed in the TD group. Our findings suggest, for the first time, that microstructural abnormalities in the brains of children with CP may be reversible following parenting intervention.
Subject(s)
Conduct Disorder , White Matter , Male , Adult , Humans , Child , Diffusion Tensor Imaging/methods , White Matter/diagnostic imaging , Parenting , Conduct Disorder/diagnostic imaging , Conduct Disorder/therapy , Antisocial Personality Disorder/psychologyABSTRACT
Resting-state functional connectivity (rsFC) has the potential to shed light on how childhood abuse and neglect relates to negative psychiatric outcomes. However, a comprehensive review of the impact of childhood maltreatment on the brain's resting state functional organization has not yet been undertaken. We systematically searched rsFC studies in children and youth exposed to maltreatment. Nineteen studies (total n = 3079) met our inclusion criteria. Two consistent findings were observed. Childhood maltreatment was linked to reduced connectivity between the anterior insula and dorsal anterior cingulate cortex, and with widespread heightened amygdala connectivity with key structures in the salience, default mode, and prefrontal regulatory networks. Other brain regions showing altered connectivity included the ventral anterior cingulate cortex, dorsolateral prefrontal cortex, and hippocampus. These patterns of altered functional connectivity associated with maltreatment exposure were independent of symptoms, yet comparable to those seen in individuals with overt clinical disorder. Summative findings indicate that rsFC alterations associated with maltreatment experience are related to poor cognitive and social functioning and are prognostic of future symptoms. In conclusion, maltreatment is associated with altered rsFC in emotional reactivity, regulation, learning, and salience detection brain circuits. This indicates patterns of recalibration of putative mechanisms implicated in maladaptive developmental outcomes.
Subject(s)
Brain , Child Abuse , Adolescent , Humans , Child , Amygdala , Brain Mapping , Gyrus Cinguli , Child Abuse/psychology , Magnetic Resonance ImagingABSTRACT
When building causal knowledge in behavioural genetics, the natural randomisation of genotypes at conception (approximately analogous to the artificial randomisation occurring in randomised controlled trials) facilitates the discovery of genetic causes. More importantly, the randomisation of genetic material within families also enables a better identification of (environmental) risk factors and aetiological pathways to diseases and behaviours.
Subject(s)
Genetics, Behavioral , Genotype , Humans , Random AllocationABSTRACT
BACKGROUND/AIM: Cannabis use is highly prevalent in adolescents; however, little is known about its effects on adolescent brain function. METHOD: Resting-state functional magnetic resonance imaging was used in matched groups of regular cannabis users (N = 70, 35 adolescents: 16-17 years old, 35 adults: 26-29 years old) and non-regular-using controls (N = 70, 35 adolescents/35 adults). Pre-registered analyses examined the connectivity of seven major cortical and sub-cortical brain networks (default mode network, executive control network (ECN), salience network, hippocampal network and three striatal networks) using seed-based analysis methods with cross-sectional comparisons between user groups and age groups. RESULTS: The regular cannabis use group (across both age groups), relative to controls, showed localised increases in connectivity only in the ECN analysis. All networks showed localised connectivity differences based on age group, with the adolescents generally showing weaker connectivity than adults, consistent with the developmental effects. Mean connectivity across entire network regions of interest (ROIs) was also significantly decreased in the ECN in adolescents. However, there were no significant interactions found between age group and user group in any of the seed-based or ROI analyses. There were also no associations found between cannabis use frequency and any of the derived connectivity measures. CONCLUSION: Regular cannabis use is associated with changes in connectivity of the ECN, which may reflect allostatic or compensatory changes in response to regular cannabis intoxication. However, these associations were not significantly different in adolescents compared to adults.
Subject(s)
Cannabis , Hallucinogens , Adult , Adolescent , Humans , Cross-Sectional Studies , Magnetic Resonance Imaging , Brain/diagnostic imaging , Brain Mapping , Cannabinoid Receptor Agonists , Neural Pathways/diagnostic imagingABSTRACT
Patch foraging is a near-ubiquitous behaviour across the animal kingdom and characterises many decision-making domains encountered by humans. We review how a disposition to explore in adolescence may reflect the evolutionary conditions under which hunter-gatherers foraged for resources. We propose that neurocomputational mechanisms responsible for reward processing, learning, and cognitive control facilitate the transition from exploratory strategies in adolescence to exploitative strategies in adulthood - where individuals capitalise on known resources. This developmental transition may be disrupted by psychopathology, as there is emerging evidence of biases in explore/exploit choices in mental health problems. Explore/exploit choices may be an informative marker for mental health across development and future research should consider this feature of decision-making as a target for clinical intervention.
ABSTRACT
Observational studies frequently report phenotypic associations between low resting heart rate (RHR) and higher levels of antisocial behaviour (ASB), although it remains unclear whether this relationship reflects causality. To triangulate evidence, we conducted two-sample univariable Mendelian randomisation (MR), multivariable MR and linkage disequilibrium score regression (LDSC) analyses. Genetic data were accessed from published genome-wide association studies (GWAS) for RHR (n = 458,835) and ASB (n = 85,359) for the univariable analyses, along with a third GWAS for heart rate variability (HRV; n = 53,174) for all other analyses. Genome-wide significant (p < 5 × 10-8) single-nucleotide polymorphisms associated with RHR (n = 278) were selected as instrumental variables and the outcome was a composite measure of ASB. No causal association was observed between RHR and ASB (BIVW = - 0.0004, p = 0.841). The multivariable MR analyses including RHR and HRV also suggested no causal associations (BIVW = 0.016, p = 0.914) and no genetic correlations between the heart rate measures and ASB were observed using LDSC (rg = 0.057, p = 0.169). Sensitivity analyses suggested that our results are not likely to be affected by heterogeneity, pleiotropic effects, or reverse causation. These findings suggest that individual differences in autonomic nervous system functioning indexed by RHR are not likely to directly contribute to the development of ASB. Therefore, previously observed associations between RHR and ASB may arise from confounding, reverse causation, and/or additional study characteristics. Further causally informative longitudinal research is required to confirm our findings, and caution should be applied when using measures of RHR in interventions targeting ASB.