IMPORTANCE Adverse childhood experiences (ACEs) are well-established risk factors for health problems in a population. However, it is not known whether screening for ACEs can accurately identify individuals who develop later health problems.OBJECTIVE To test the predictive accuracy of ACE screening for later health problems.

Recent years have seen the rapid proliferation of clinical prediction models aiming to support risk stratification and individualized care within psychiatry. Despite growing interest, attempts to synthesize current evidence in the nascent field of precision psychiatry have remained scarce. This systematic review therefore sought to summarize progress towards clinical implementation of prediction modeling for psychiatric outcomes. We searched MEDLINE, PubMed, Embase, and PsychINFO databases from inception to September 30, 2020, for English-language articles that developed and/or validated multivariable models to predict (at an individual level) onset, course, or treatment response for non-organic psychiatric disorders (PROSPERO: CRD42020216530). Individual prediction models were evaluated based on three key criteria: (i) mitigation of bias and overfitting; (ii) generalizability, and (iii) clinical utility. The Prediction model Risk Of Bias ASsessment Tool (PROBAST) was used to formally appraise each study’s risk of bias. 228 studies detailing 308 prediction models were ultimately eligible for inclusion. 94.5% of developed prediction models were deemed to be at high risk of bias, largely due to inadequate or inappropriate analytic decisions. Insufficient internal validation efforts (within the development sample) were also observed, while only one-fifth of models underwent external validation in an independent sample. Finally, our search identified just one published model whose potential utility in clinical practice was formally assessed. Our findings illustrated significant growth in precision psychiatry with promising progress towards real-world application. Nevertheless, these efforts have been inhibited by a preponderance of bias and overfitting, while the generalizability and clinical utility of many published models has yet to be formally established. Through improved methodological rigor during initial development, robust evaluations of reproducibility via independent validation, and evidence-based implementation frameworks, future research has the potential to generate risk prediction tools capable of enhancing clinical decision-making in psychiatric care.

Growing evidence suggests heterogeneity within interpersonal-callous (IC) youth based on co-occurring anxiety. The developmental validity of this proposed taxonomy remains unclear however, as most previous research is cross-sectional and/or limited to adolescence. We aimed to identify low-anxiety (IC/ANX−) and high-anxiety (IC/ANX+) IC variants, and compare these groups on (a) early risk exposures, (b) psychiatric symptoms from mid-childhood to early adolescence, and (c) school-based functioning. Using the Avon Longitudinal Study of Parents and Children (ALSPAC), a prospective epidemiological birth cohort, model-based cluster analysis was performed on children with complete age-13 IC and anxiety scores (n=6791). Analysis of variance was used to compare resulting clusters on: (a) prenatal and postnatal family adversity and maternal psychopathology, and harsh parenting; (b) developmental differences in attention-deficit/hyperactivity disorder (ADHD), conduct disorder (CD), oppositional defiant disorder (ODD), emotional difficulties, and low prosocial behavior at 7, 10, and 13 years; and (c) teacher-reported discipline problems, along with standardized test performance. We identified a four-cluster solution: ‘typical’, ‘low’, ‘IC/ANX−’, and ‘IC/ANX+’. IC/ANX+ youth showed the highest prenatal and postnatal levels of family adversity and maternal psychopathology, highest levels of ADHD, CD, ODD and emotional difficulties, greatest discipline problems, and lowest national test scores (all p<.001). IC/ANX+ also showed a distinct pattern of increasing psychopathology from age 7 to 13 years. Adolescent IC subtypes were successfully validated in ALSPAC across multiple raters using prenatal and early postnatal risk, repeated measures of psychopathology, and school-based outcomes. Greater prenatal environmental risk among IC/ANX+ youth suggests an important target for early intervention.

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The tendency to select threatening over benign interpretations of ambiguous bodily sensations and cues characterises young people with chronic pain. However, previous studies disagree over whether these biases extend to nonbodily harm situations such as social evaluation. Understanding the content of these biases is crucial to the development of pain management strategies seeking to modify such biases. Two hundred forty-three young people aged 16 to 19 years completed an expanded version of the Adolescent Interpretation of Bodily Threat task. Using a factor-analytic approach, we removed items that did not consistently associate with bodily harm or social evaluation. Next, we examined whether the variance underlying negative and benign interpretations of bodily harm and social evaluation situations were best represented as a common factor (ie, one-factor model), 2 distinct factors (ie, 2-factor model), or one common and 2 distinct factors (ie, 2-factor bifactor model) in all adolescents. We then compared youth with and without persistent and impairing pain on factor scores derived from the best-fitting model. Although negative interpretations of bodily harm and social evaluation situations emerged as distinct factors, benign interpretations across situations were best captured by a common factor and 2 situation-specific factors (ie, bifactor model). Group comparisons showed that young people with moderate-to-high pain interference were more likely to endorse negative interpretations across all situations, and less likely to manifest a general benign interpretational style, than youth without interfering pain, although some of these group differences were explained by co-occurring anxiety and depressive symptoms. Replication of these findings is needed.

BackgroundChildhood victimization elevates the average risk of developing functional impairment in adulthood. However, not all victimized children demonstrate poor outcomes. Although research has described factors that confer vulnerability or resilience, it is unknown if this knowledge can be translated to accurately identify the most vulnerable victimized children.ObjectiveTo build and internally validate a risk calculator to identify those victimized children who are most at risk of functional impairment at age 18 years.ParticipantsWe utilized data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative birth cohort of 2232 UK children born in 1994–95.MethodsVictimization exposure was assessed repeatedly between ages 5 and 12 years along with a range of individual-, family- and community-level predictors. Functional outcomes were assessed at age 18 years. We developed and evaluated a prediction model for psychosocial disadvantage and economic disadvantage using the Least Absolute Shrinkage and Selection Operator (LASSO) regularized regression with nested 10-fold cross-validation.ResultsThe model predicting psychosocial disadvantage following childhood victimization retained 12 of 22 predictors, had an area under the curve (AUC) of 0.65, and was well-calibrated within the range of 40–70% predicted risk. The model predicting economic disadvantage retained 10 of 22 predictors, achieved excellent discrimination (AUC = 0.80), and a high degree of calibration.ConclusionsPrediction modelling techniques can be applied to estimate individual risk for poor functional outcomes in young adulthood following childhood victimization. Such risk prediction tools could potentially assist practitioners to target interventions, which is particularly useful in a context of scarce resources.

Previous factor-analytic studies identify significant comorbidity between interpersonal-callous (IC) traits and low prosocial behavior (LPB), which, in turn, is associated with high levels of childhood risk exposure and psychopathology. Longitudinal associations between IC, LPB, or their combination, and early-adult health and social functioning have not been investigated, however. Extending a previously-identified bifactor model within a prospective birth cohort, this study applied latent path analysis to test direct and indirect pathways (via adolescent delinquency, substance use, and physical activity) between these general and specific factors (age 13) and (i) emotional problems (age 18), (ii) physical health problems (age 18), and (iii) classification as 'not in education, employment, or training' (NEET; age 20). All models controlled for childhood adversity and IQ. Bifactor-specific estimates indicated that the residual IC factor did not reliably denote unique variance over and above a general factor (IC/LPB). IC/LPB itself was directly associated with NEET classification, while the residual LPB factor was associated with better emotional and physical health. IC/LPB also indirectly associated with emotional problems via greater adolescent delinquency, and with physical health problems via lower physical activity. In contrast, residual LPB variance was either non-significantly or negatively related to these adolescent domains. Findings indicate that the shared variance underlying IC and LPB confers an increased risk for poor health and functional outcomes in emerging adulthood, and highlight delinquency and physical inactivity as potential adolescent treatment targets that may mitigate the risk for health difficulties at high levels of this IC/LPB construct.

In 671 mother–child (49% male) pairs from an epidemiological birth cohort, we investigated (a) prospective associations between DNA methylation (at birth) and trajectories (ages 7–13) of oppositional defiant disorder (ODD), and the ODD subdimensions of irritable and headstrong; (b) common biological pathways, indexed by DNA methylation, between ODD trajectories and attention deficit hyperactivity disorder (ADHD); (c) genetic influence on DNA methylation; and (d) prenatal risk exposure associations. Methylome‐wide significant associations were identified for the ODD and headstrong, but not for irritable. Overlap analysis indicated biological correlates between ODD, headstrong, and ADHD. DNA methylation in ODD and headstrong was (to a degree) genetically influenced. DNA methylation associated with prenatal risk exposures of maternal anxiety (headstrong) and cigarette smoking (ODD and headstrong).