Although risk markers for depressive disorders (DD) are dynamic, especially during adolescence, few studies have examined how change in risk levels during adolescence predict DD onset during transition to adulthood. We compared two competing hypotheses of the dynamic effects of risk. The risk escalation hypothesis posits that worsening of risk predicts DD onset beyond risk level. The chronic risk hypothesis posits that persistently elevated risk level, rather than risk change, predicts DD onset.

Our sample included 393 girls (baseline age 13.5–15.5 years) from the adolescent development of emotions and personality traits project. Participants underwent five diagnostic interviews and assessments of risk markers for DD at 9-month intervals and were re-interviewed at a 6-year follow-up. We focused on 17 well-established risk markers. For each risk marker, we examined the prospective effects of risk level and change on first DD onset at wave six, estimated by growth curve modeling using data from the first five waves.

For 13 of the 17 depression risk markers, elevated levels of risk during adolescence, but not change in risk, predicted first DD onset during transition to adulthood, supporting the chronic risk hypothesis. Minimal evidence was found for the risk escalation hypothesis.

Participants who had a first DD onset during transition to adulthood have exhibited elevated levels of risk throughout adolescence. Researchers and practitioners should administer multiple assessments and focus on persistently elevated levels of risk to identify individuals who are most likely to develop DD and to provide targeted DD prevention.

The report examined reciprocal within-person associations among maternal depressive symptoms and offspring depressive, anxiety and irritability symptoms from early childhood to adolescence using a random intercept cross-lagged panel model (RI-CLPM).

Participants were 609 mother–child dyads participating in the Stony Brook Temperament Study. Child and maternal internalizing symptoms were assessed every 3 years from ages 3 to 15 using maternal report on the Child Behavior Checklist (CBCL) and Diagnostic Inventory for Depression, respectively.

At the between-person level, maternal depressive symptoms, and child depressive, anxiety, and irritability symptoms were all positively associated with one another. At the within-person level, greater within-person child anxiety symptoms at age 3 predicted both greater child anxiety and depressive symptoms at age 15 via greater child anxiety from ages 6 to 12, and greater within-person child irritability at age 3 predicted greater maternal depressive symptoms at age 15 via greater child irritability from ages 6 to 12.

Findings reveal novel within-person developmental pathways from early childhood internalizing problems to later internalizing problems in both the child and mother. Intervention and prevention efforts should thus focus on early identification and prevention of childhood internalizing symptoms to reduce negative effects on both child and parent symptoms.

This study leveraged machine learning to evaluate the contribution of information from multiple developmental stages to prospective prediction of depression and anxiety in mid-adolescence.

A community sample (N = 374; 53.5% male) of children and their families completed tri-annual assessments across ages 3–15. The feature set included several important risk factors spanning psychopathology, temperament/personality, family environment, life stress, interpersonal relationships, neurocognitive, hormonal, and neural functioning, and parental psychopathology and personality. We used canonical correlation analysis (CCA) to reduce the large feature set to a lower dimensional space while preserving the longitudinal structure of the data. Ablation analysis was conducted to evaluate the relative contributions to prediction of information gathered at different developmental periods and relative to previous disorder status (i.e. age 12 depression or anxiety) and demographics (sex, race, ethnicity).

CCA components from individual waves predicted age 15 disorder status better than chance across ages 3, 6, 9, and 12 for anxiety and 9 and 12 for depression. Only the components from age 12 for depression, and ages 9 and 12 for anxiety, improved prediction over prior disorder status and demographics.

These findings suggest that screening for risk of adolescent depression can be successful as early as age 9, while screening for risk of adolescent anxiety can be successful as early as age 3. Assessing additional risk factors at age 12 for depression, and going back to age 9 for anxiety, can improve screening for risk at age 15 beyond knowing standard demographics and disorder history.

Preschool psychiatric symptoms significantly increase the risk for long-term negative outcomes. Transdiagnostic hierarchical approaches that capture general (‘p’) and specific psychopathology dimensions are promising for understanding risk and predicting outcomes, but their predictive utility in young children is not well established. We delineated a hierarchical structure of preschool psychopathology dimensions and tested their ability to predict psychiatric disorders and functional impairment in preadolescence.

Data for 1253 preschool children (mean age = 4.17, s.d. = 0.81) were drawn from three longitudinal studies using a similar methodology (one community sample, two psychopathology-enriched samples) and followed up into preadolescence, yielding a large and diverse sample. Exploratory factor models derived a hierarchical structure of general and specific factors using symptoms from the Preschool Age Psychiatric Assessment interview. Longitudinal analyses examined the prospective associations of preschool p and specific factors with preadolescent psychiatric disorders and functional impairment.

A hierarchical dimensional structure with a p factor at the top and up to six specific factors (distress, fear, separation anxiety, social anxiety, inattention-hyperactivity, oppositionality) emerged at preschool age. The p factor predicted all preadolescent disorders (ΔR2 = 0.04–0.15) and functional impairment (ΔR2 = 0.01–0.07) to a significantly greater extent than preschool psychiatric diagnoses and functioning. Specific dimensions provided additional predictive power for the majority of preadolescent outcomes (disorders: ΔR2 = 0.06–0.15; functional impairment: ΔR2 = 0.05–0.12).

Both general and specific dimensions of preschool psychopathology are useful for predicting clinical and functional outcomes almost a decade later. These findings highlight the value of transdiagnostic dimensions for predicting prognosis and as potential targets for early intervention and prevention.

Adolescence is a key developmental period for the emergence of psychiatric disorders. However, there is still no consensus on the core mechanisms of dysfunction in youth. Neurobiological sensitivity to unpredictable threat has been associated with several psychiatric disorders in adults. The present study examined adolescent defensive motivation (startle reflex) and attention (event-related potentials) in anticipation of unpredictable threat in relation to both adolescent and maternal (i.e. familial risk) internalizing and externalizing spectra.

The sample included 395 15-year-old adolescents and their biological mothers. Adolescent startle potentiation and probe P300 suppression (indicating increased attention to threat) were measured in anticipation of predictable and unpredictable threat. Adolescent and maternal lifetime history of psychiatric disorders were assessed via semi-structured diagnostic interviews, and confirmatory factor analysis was used to model internalizing and externalizing spectra.

The adolescent internalizing spectrum was positively associated with adolescent startle potentiation and probe P300 suppression to unpredictable threat. Conversely, the adolescent externalizing spectrum was negatively associated with adolescent P300 suppression to unpredictable threat. The maternal internalizing spectrum was positively associated with adolescent startle potentiation to unpredictable threat and P300 suppression to both predictable and unpredictable threat. The maternal externalizing spectrum was negatively associated with adolescent startle potentiation to unpredictable threat and P300 suppression to both predictable and unpredictable threat. Adolescent and maternal internalizing and externalizing spectra were independently related to adolescent startle potentiation and P300 suppression.

Adolescent neurobiological sensitivity to unpredictable threat is associated with both personal history and familial risk for the internalizing and externalizing spectra.

Life stress and blunted reward processing each have been associated with the onset and maintenance of major depressive disorder. However, much of this work has been cross-sectional, conducted in separate lines of inquiry, and focused on recent life stressor exposure, despite the fact that theories of depression posit that stressors can have cumulative effects over the lifespan. To address these limitations, we investigated whether acute and chronic stressors occurring over the lifespan interacted with blunted reward processing to predict increases in depression over time in healthy youth.

Participants were 245 adolescent girls aged 8–14 years old (Mage = 12.4, s.d. = 1.8) who were evaluated at baseline and two years later. The reward positivity (RewP), an event-related potential measure of reward responsiveness, was assessed at baseline using the doors task. Cumulative lifetime exposure to acute and chronic stressors was assessed two years later using the Stress and Adversity Inventory for Adolescents (Adolescent STRAIN). Finally, depressive symptoms were assessed at both baseline and follow-up using the Children's Depression Inventory.

As hypothesized, greater lifetime acute stressor exposure predicted increases in depressive symptoms over two years, but only for youth exhibiting a blunted RewP. This interaction, however, was not found for chronic stressors.

Lifetime acute stressor exposure may be particularly depressogenic for youth exhibiting a blunted RewP. Conversely, a robust RewP may be protective in the presence of greater acute lifetime stressor exposure.

Awareness of adult separation anxiety (ASA) is growing, but there is a dearth of knowledge about how separation anxiety aggregates in families. We examined the intergenerational associations of separation anxiety and other forms of internalizing problems in an American community sample of 515 predominantly white children and their parents.

Children's separation anxiety (CSA), depression, and other anxiety disorders were modeled as latent factors using diagnoses from interviews and symptom scores from questionnaires completed by mothers, fathers, and children when children were 9 years old and again 3 years later. Parents' separation anxiety was assessed via a questionnaire and parents' other anxiety, depressive, and substance use disorders were assessed with a diagnostic interview when children were nine. Relationships between parents' and children's psychopathology were modeled using s.e.m.

Mothers' and fathers' ASA were related to all three psychopathology factors in offspring, over and above other parental disorders, in concurrent and prospective analyses. CSA was also related to maternal depression concurrently and prospectively and to maternal anxiety prospectively. Of all paternal psychopathology variables, only ASA was significantly related to children's psychopathology in either model.

Results indicate that parental separation anxiety is an important, but non-specific, risk factor for children's psychopathology. The pathway by which this risk is transmitted may be genetic or environmental, and the observed statistical associations likely also encompass child-to-parent effects.

This report examines between- and within-person associations between youth irritability and concurrent and prospective internalizing and externalizing symptoms from early childhood through adolescence. Distinguishing between- and within-person longitudinal associations may yield distinct, clinically relevant information about pathways to multifinality from childhood irritability.

Children’s irritability and co-occurring symptoms were assessed across five waves between ages 3 and 15 years using the mother-reported Child Behavior Checklist (N = 605, 46% female). Parental history of depressive disorders was assessed with a clinical interview.

Results demonstrated that between- and within-person irritability were uniquely associated with concurrent depressive, anxiety, and defiance symptoms, but not ADHD. Prior wave within-person irritability also predicted next wave depressive, anxiety, and defiance symptoms, controlling for prior symptoms; these prospective associations were bidirectional. Child sex and parental depressive disorders moderated associations.

Findings identify pathways from within- and between-person irritability to later internalizing and externalizing psychopathology. Results demonstrate the importance of parsing within- and between-person effects to understand nuanced relations among symptoms over childhood.

Risk factors for depressive disorders (DD) change substantially over time, but the prognostic value of these changes remains unclear. Two basic types of dynamic effects are possible. The ‘Risk Escalation hypothesis’ posits that worsening of risk levels predicts DD onset above average level of risk factors. Alternatively, the ‘Chronic Risk hypothesis’ posits that the average level rather than change predicts first-onset DD.

We utilized data from the ADEPT project, a cohort of 496 girls (baseline age 13.5–15.5 years) from the community followed for 3 years. Participants underwent five waves of assessments for risk factors and diagnostic interviews for DD. For illustration purposes, we selected 16 well-established dynamic risk factors for adolescent depression, such as depressive and anxiety symptoms, personality traits, clinical traits, and social risk factors. We conducted Cox regression analyses with time-varying covariates to predict first DD onset.

Consistently elevated risk factors (i.e. the mean of multiple waves), but not recent escalation, predicted first-onset DD, consistent with the Chronic Risk hypothesis. This hypothesis was supported across all 16 risk factors.

Across a range of risk factors, girls who had first-onset DD generally did not experience a sharp increase in risk level shortly before the onset of disorder; rather, for years before onset, they exhibited elevated levels of risk. Our findings suggest that chronicity of risk should be a particular focus in screening high-risk populations to prevent the onset of DDs. In particular, regular monitoring of risk factors in school settings is highly informative.

The coronavirus [coronavirus disease 2019 (COVID-19)] pandemic has introduced extraordinary life changes and stress, particularly in adolescents and young adults. Initial reports suggest that depression and anxiety are elevated during COVID-19, but no prior study has explored changes at the within-person level. The current study explored changes in depression and anxiety symptoms from before the pandemic to soon after it first peaked in Spring 2020 in a sample of adolescents and young adults (N = 451) living in Long Island, New York, an early epicenter of COVID-19 in the U.S.

Depression (Children's Depression Inventory) and anxiety symptoms (Screen for Child Anxiety Related Symptoms) were assessed between December 2014 and July 2019, and, along with COVID-19 experiences, symptoms were re-assessed between March 27th and May 15th, 2020.

Across participants and independent of age, there were increased generalized anxiety and social anxiety symptoms. In females, there were also increased depression and panic/somatic symptoms. Multivariable linear regression indicated that greater COVID-19 school concerns were uniquely associated with increased depression symptoms. Greater COVID-19 home confinement concerns were uniquely associated with increased generalized anxiety symptoms, and decreased social anxiety symptoms, respectively.

Adolescents and young adults at an early epicenter of the COVID-19 pandemic in the U.S. experienced increased depression and anxiety symptoms, particularly amongst females. School and home confinement concerns related to the pandemic were independently associated with changes in symptoms. Overall, this report suggests that the COVID-19 pandemic is having multifarious adverse effects on the mental health of youth.

Life events (LEs) are a risk factor for first onset and relapse of psychotic disorders. However, the impact of LEs on specific symptoms – namely reality distortion, disorganization, negative symptoms, depression, and mania – remains unclear. Moreover, the differential effects of negative v. positive LEs are poorly understood.

The present study utilizes an epidemiologic cohort of patients (N = 428) ascertained at first-admission for psychosis and followed for a decade thereafter. Symptoms were assessed at 6-, 24-, 48-, and 120-month follow-ups.

We examined symptom change within-person and found that negative events in the previous 6 months predicted an increase in reality distortion (β = 0.07), disorganized (β = 0.07), manic (β = 0.08), and depressive symptoms (β = 0.06), and a decrease in negative symptoms (β = −0.08). Conversely, positive LEs predicted fewer reality distortion (β = −0.04), disorganized (β = −0.04), and negative (β = −0.13) symptoms, and were unrelated to mood symptoms. A between-person approach to the same hypotheses confirmed that negative LEs predicted change in all symptoms, while positive LEs predicted change only in negative symptoms. In contrast, symptoms rarely predicted future LEs.

These findings confirm that LEs have an effect on symptoms, and thus contribute to the burden of psychotic disorders. That LEs increase positive symptoms and decrease negative symptoms suggest at least two different mechanisms underlying the relationship between LEs and symptoms. Our findings underscore the need for increased symptom monitoring following negative LEs, as symptoms may worsen during that time.

Early irritability predicts a broad spectrum of psychopathology spanning both internalizing and externalizing disorders, rather than any particular disorder or group of disorders (i.e. multifinality). Very few studies, however, have examined the developmental mechanisms by which it leads to such phenotypically diverse outcomes. We examined whether variation in the diurnal pattern of cortisol moderates developmental pathways between preschool irritability and the subsequent emergence of internalizing and externalizing symptoms 9 years later.

When children were 3 years old, mothers were interviewed about children's irritability and completed questionnaires about their children's psychopathology. Six years later, children collected saliva samples at wake-up and bedtime on three consecutive days. Diurnal cortisol patterns were modeled as latent difference scores between evening and morning samples. When children were approximately 12 years old, mothers again completed questionnaires about their children's psychopathology.

Among children with higher levels of irritability at age 3, a steeper diurnal cortisol slope at age 9 predicted greater internalizing symptoms and irritability at age 12, whereas a blunted slope at age 9 predicted greater externalizing symptoms at age 12, adjusting for baseline and concurrent symptoms.

Our results suggest that variation in stress system functioning can predict and differentiate developmental trajectories of early irritability that are relatively more internalizing v. those in which externalizing symptoms dominate in pre-adolescence.

There is an emerging consensus in developmental psychopathology that irritable youth are at risk for developing internalizing problems later in life. The current study explored if irritability in youth is multifactorial and the impact of irritability dimensions on psychopathology outcomes in adulthood.

We conducted exploratory factor analysis on irritability symptom items from a semi-structured diagnostic interview administered to a community sample of adolescents (ages 14–19; 42.7% male; 89.1% white). The analysis identified two factors corresponding to items from the mood disorders v. the oppositional defiant disorder (ODD) (Leibenluft and Stoddard) sections of the interview. These factors were then entered together into regression models predicting psychopathology assessed at age 24 (N = 941) and again at age 30 (N = 816). All models controlled for concurrent psychopathology in youth.

The two irritability dimensions demonstrated different patterns of prospective relationships, with items from the ODD section primarily predicting externalizing psychopathology, items from the mood disorder sections predicting depression at age 24 but not 30, and both dimensions predicting borderline personality disorder symptoms.

These results suggest that the current standard of extracting and compositing irritability symptom items from diagnostic interviews masks distinct dimensions of irritability with different psychopathological outcomes. Additionally, these findings add nuance to the prevailing notion that irritability in youth is specifically linked to later internalizing problems. Further investigation using more sensitive and multifaceted measures of irritability are needed to parse the meaning and clinical implications of these dimensions.