Personality traits (e.g. neuroticism) and the social environment predict risk for internalizing disorders and suicidal behavior. Studying these characteristics together and prospectively within a population confronted with high stressor exposure (e.g. U.S. Army soldiers) has not been done, yet could uncover unique and interactive predictive effects that may inform prevention and early intervention efforts.

Five broad personality traits and social network size were assessed via self-administered questionnaires among experienced soldiers preparing for deployment (N = 4645) and new soldiers reporting for basic training (N = 6216). Predictive models examined associations of baseline personality and social network variables with recent distress disorders or suicidal behaviors assessed 3- and 9-months post-deployment and approximately 5 years following enlistment.

Among the personality traits, elevated neuroticism was consistently associated with increased mental health risk following deployment. Small social networks were also associated with increased mental health risk following deployment, beyond the variance accounted for by personality. Limited support was found for social network size moderating the association between personality and mental health outcomes. Small social networks also predicted distress disorders and suicidal behavior 5 years following enlistment, whereas unique effects of personality traits on these more distal outcomes were rare.

Heightened neuroticism and small social networks predict a greater risk for negative mental health sequelae, especially following deployment. Social ties may mitigate adverse impacts of personality traits on psychopathology in some contexts. Early identification and targeted intervention for these distinct, modifiable factors may decrease the risk of distress disorders and suicidal behavior.

Most epidemiological studies show a decrease of internalizing disorders at older ages, but it is unclear how the prevalence exactly changes with age, and whether there are different patterns for internalizing symptoms and traits, and for men and women. This study investigates the impact of age and sex on the point prevalence across different mood and anxiety disorders, internalizing symptoms, and neuroticism.

We used cross-sectional data on 146 315 subjects, aged 18–80 years, from the Lifelines Cohort Study, a Dutch general population sample. Between 2012 and 2016, five current internalizing disorders – major depression, dysthymia, generalized anxiety disorder, social phobia, and panic disorder – were assessed according to DSM-IV criteria. Depressive symptoms, anxiety symptoms, neuroticism, and negative affect (NA) were also measured. Generalized additive models were used to identify nonlinear patterns across age, and to investigate sex differences.

The point prevalence of internalizing disorders generally increased between the ages of 18 and 30 years, stabilized between 30 and 50, and decreased after age 50. The patterns of internalizing symptoms and traits were different. NA and neuroticism gradually decreased after age 18. Women reported more internalizing disorders than men, but the relative difference remained stable across age (relative risk ~1.7).

The point prevalence of internalizing disorders was typically highest between age 30 and 50, but there were differences between the disorders, which could indicate differences in etiology. The relative gap between the sexes remained similar across age, suggesting that changes in sex hormones around the menopause do not significantly influence women's risk of internalizing disorders.

Depressive and anxiety disorders are highly comorbid, which has been theorized to be due to an underlying internalizing vulnerability. We aimed to identify groups of participants with differing vulnerabilities by examining the course of internalizing psychopathology up to age 45.

We used data from 24158 participants (aged 45+) in 23 population-based cross-sectional World Mental Health Surveys. Internalizing disorders were assessed with the Composite International Diagnostic Interview (CIDI). We applied latent class growth analysis (LCGA) and investigated the characteristics of identified classes using logistic or linear regression.

The best-fitting LCGA solution identified eight classes: a healthy class (81.9%), three childhood-onset classes with mild (3.7%), moderate (2.0%), or severe (1.1%) internalizing comorbidity, two puberty-onset classes with mild (4.0%) or moderate (1.4%) comorbidity, and two adult-onset classes with mild comorbidity (2.7% and 3.2%). The childhood-onset severe class had particularly unfavorable sociodemographic outcomes compared to the healthy class, with increased risks of being never or previously married (OR = 2.2 and 2.0, p < 0.001), not being employed (OR = 3.5, p < 0.001), and having a low/low-average income (OR = 2.2, p < 0.001). Moderate or severe (v. mild) comorbidity was associated with 12-month internalizing disorders (OR = 1.9 and 4.8, p < 0.001), disability (B = 1.1–2.3, p < 0.001), and suicidal ideation (OR = 4.2, p < 0.001 for severe comorbidity only). Adult (v. childhood) onset was associated with lower rates of 12-month internalizing disorders (OR = 0.2, p < 0.001).

We identified eight transdiagnostic trajectories of internalizing psychopathology. Unfavorable outcomes were concentrated in the 1% of participants with childhood onset and severe comorbidity. Early identification of this group may offer opportunities for preventive interventions.

Resting pulse is robustly and inversely associated with the risk for externalizing disorders and may be positively associated with internalizing disorders. We know little about the causal nature of these associations.

We examined resting pulse at conscription examination in 369 301 males born 1960–80 with a mean (s.d.) follow-up of 29.1 (7.7) years. From pulse rates, we predicted, using Cox models, the risk for criminal behavior (CB), drug abuse (DA), alcohol use disorder (AUD), major depression (MD), and anxiety disorders (AD), assessed from medical, criminal, and pharmacy registries. Co-relative analyses were conducted on the general population, cousin, half-sibling, full-sibling, and monozygotic pairs discordant for the outcome. Twin/sibling modeling for pulse was performed using OpenMX.

Familial resemblance for pulse resulted entirely from genetic factors. In the general population, the risk for externalizing disorders (CB, DA, and AUD) and internalizing disorders (MD and AD) were, respectively, significantly associated with low and high resting pulse rate. For CB, DA, and AUD, co-relative analyses showed that the inverse association with pulse resulted entirely from familial common causes (aka ‘confounders’). By contrast, co-relative analyses found that the association between higher pulse and MD and AD resulted from direct causal effects.

Resting pulse has a negative and positive association with, respectively, the risk for externalizing and for internalizing disorders. Co-relative analyses indicate that the nature of these associations differ, suggesting that elevated pulse appears to directly increase the risk for internalizing disorders while the reduced pulse is a risk index for underlying traits that predispose to externalizing disorders.

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.

Attention-deficit hyperactivity disorder (ADHD) and anxiety disorders have been proposed as precursors of bipolar disorder, but their joint and relative roles in the development of bipolar disorder are unknown.

To test the prospective relationship of ADHD and anxiety with onset of bipolar disorder.

We examined the relationship between ADHD, anxiety disorders and bipolar disorder in a birth cohort of 2 409 236 individuals born in Denmark between 1955 and 1991. Individuals were followed from their sixteenth birthday or from January 1995 to their first clinical contact for bipolar disorder or until December 2012. We calculated incidence rates per 10 000 person-years and tested the effects of prior diagnoses on the risk of bipolar disorder in survival models.

Over 37 394 865 person-years follow-up, 9250 onsets of bipolar disorder occurred. The incidence rate of bipolar disorder was 2.17 (95% CI 2.12–2.19) in individuals with no prior diagnosis of ADHD or anxiety, 23.86 (95% CI 19.98–27.75) in individuals with a prior diagnosis of ADHD only, 26.05 (95% CI 24.47–27.62) in individuals with a prior diagnosis of anxiety only and 66.16 (95% CI 44.83–87.47) in those with prior diagnoses of both ADHD and anxiety. The combination of ADHD and anxiety increased the risk of bipolar disorder 30-fold (95% CI 21.66–41.40) compared with those with no prior ADHD or anxiety.

Early manifestations of both internalising and externalising psychopathology indicate liability to bipolar disorder. The combination of ADHD and anxiety is associated with a very high risk of bipolar disorder.

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Research suggests that personality traits have both direct and indirect effects on the development of psychological symptoms, with indirect effects mediated by stressful or traumatic events. This study models the direct influence of personality traits on residualized changes in internalizing and externalizing symptoms following a stressful and potentially traumatic deployment, as well as the indirect influence of personality on symptom levels mediated by combat exposure.

We utilized structural equation modeling with a longitudinal prospective study of 522 US National Guard soldiers deployed to Iraq. Analyses were based on self-report measures of personality, combat exposure, and internalizing and externalizing symptoms.

Both pre-deployment Disconstraint and externalizing symptoms predicted combat exposure, which in turn predicted internalizing and externalizing symptoms. There was a significant indirect effect for pre-deployment externalizing symptoms on post-deployment externalizing via combat exposure (p < 0.01). Negative Emotionality and pre-deployment internalizing symptoms directly predicted post-deployment internalizing symptoms, but both were unrelated to combat exposure. No direct effects of personality on residualized changes in externalizing symptoms were found.

Baseline symptom dimensions had significant direct and indirect effects on post-deployment symptoms. Controlling for both pre-exposure personality and symptoms, combat experiences remained positively related to both internalizing and externalizing symptoms. Implications for diagnostic classification are discussed.

Individuals with borderline personality disorder (BPD) frequently display co-morbid mental disorders. These disorders include ‘internalizing’ disorders (such as major depressive disorder and anxiety disorders) and ‘externalizing’ disorders (such as substance use disorders and antisocial personality disorder). It is hypothesized that these disorders may arise from latent ‘internalizing’ and ‘externalizing’ liability factors. Factor analytic studies suggest that internalizing and externalizing factors both contribute to BPD, but the extent to which such contributions are familial is unknown.

Participants were 368 probands (132 with BPD; 134 without BPD; and 102 with major depressive disorder) and 885 siblings and parents of probands. Participants were administered the Diagnostic Interview for DSM-IV Personality Disorders, the Revised Diagnostic Interview for Borderlines, and the Structured Clinical Interview for DSM-IV.

On confirmatory factor analysis of within-person associations of disorders, BPD loaded moderately on internalizing (factor loading 0.53, s.e. = 0.10, p < 0.001) and externalizing latent variables (0.48, s.e. = 0.10, p < 0.001). Within-family associations were assessed using structural equation models of familial and non-familial factors for BPD, internalizing disorders, and externalizing disorders. In a Cholesky decomposition model, 84% (s.e. = 17%, p < 0.001) of the association of BPD with internalizing and externalizing factors was accounted for by familial contributions.

Familial internalizing and externalizing liability factors are both associated with, and therefore may mutually contribute to, BPD. These familial contributions account largely for the pattern of co-morbidity between BPD and internalizing and externalizing disorders.

Numerous studies have supported an association between maternal depression and child psychiatric outcomes, but few have controlled for the confounding effects of both maternal and offspring co-morbidity. Thus, it remains unclear whether the correspondence between maternal and offspring depressive and anxiety disorders is better explained by associations between shared features of maternal and offspring internalizing disorders or by specific effects exerted by unique aspects of individual disorders.

Pairs of mothers and offspring overselected for maternal depression (n = 815) were assessed at offspring age 15 years for anxiety and depressive disorders; 705 completed a follow-up at offspring age 20 years. For both mothers and offspring, structural equation modeling was used to distinguish transdiagnostic internalizing pathology – representing the overlap among all depressive and anxiety disorders – from diagnosis-specific forms of pathology. To discriminate between general versus specific pathways of intergenerational transmission of psychopathology, we examined (a) the general association between the maternal and offspring internalizing factors and (b) the correlations between maternal and offspring diagnosis-specific pathology for each disorder.

For mothers and offspring, a unidimensional latent variable model provided the best fit to the correlations among depressive and anxiety disorders. The maternal transdiagnostic internalizing factor strongly predicted the corresponding factor among offspring. In addition, the unique component of post-traumatic stress disorder among offspring was significantly related to the analogous unique component among mothers, but specific components of other maternal disorders, including depression, did not predict corresponding offspring pathology.

Results suggest that intergenerational transmission of internalizing disorders is largely non-specific.

The distribution and co-morbidity of common psychiatric disorders can be largely explained as manifestations of two broad psychopathological spectra of internalizing and externalizing disorders. Twin studies suggest that these spectra arise from genetic factors.

Structural equation twin modeling was applied to interview and questionnaire data on personality traits and lifetime psychiatric disorders on more than 5300 members of male–male (MM) and female–female (FF) twin pairs.

The best-fitting models for both the externalizing and internalizing spectra differed significantly in males and females. In males, the externalizing genetic common factor was best indexed by four disorders in the following order: antisocial personality disorder (ASPD), drug abuse/dependence (DAD), alcohol abuse dependence (AAD) and conduct disorder (CD). In females, the four disorders most closely related to the externalizing common factor were, in order: DAD, AAD, nicotine dependence (ND) and ASPD. Personality traits of novelty seeking (NS) and extraversion (E) better indexed the genetic externalizing spectrum in females than in males. In both males and females, major depression (MD) and generalized anxiety disorder (GAD) best indexed the genetic internalizing common factor. Panic disorder (PD) and agoraphobia (AgP) better reflected the internalizing genetic common factor in women, and neuroticism (N) in men. Genetic correlations between the two spectra were estimated at + 0.53 in males and + 0.52 in females.

The disorders that optimally index the genetic liability to externalizing and internalizing disorders in the general population differ meaningfully in men and women. In both sexes, these genetic spectra are better assessed by psychiatric disorders than by personality traits.

We examined the relationship between the onset and pattern of childhood mental health disorders and subsequent current smoking status at age 17 years.

Data were from a prospective cohort study of 2868 births of which 1064 supplied information about their current smoking at 17 years of age. The association between the onset and pattern of clinically significant mental health disorders in the child and subsequent smoking at age 17 years was estimated via multivariable logistic regression.

Relative to 17 year olds who never had an externalizing disorder, 17-year-olds who had an externalizing disorder at age 5, 8 or 14 years were, respectively, 2.0 times [95% confidence interval (CI) 1.24–3.25], 1.9 (95% CI 1.00–3.65) or 3.9 times (95% CI 1.73–8.72) more likely to be a current smoker. Children with an ongoing pattern of externalizing disorder were 3.0 times (95% CI 1.89–4.84) more likely to be smokers at the age of 17 years and those whose mothers reported daily consumption of 6–10 cigarettes at 18 weeks' gestation were 2.5 times (OR 2.46, 95% CI 1.26–4.83) more likely to report smoking at 17 years of age. Associations with early anxiety and depression in the child were not found.

Current smoking in 17-year-olds may be underpinned by early emergent, and then, ongoing, externalizing disorder that commenced as young as age 5 years as well as exposure to early prenatal maternal smoking. The associations documented in adults and adolescents that link tobacco smoking and mental health are likely to be in play at these early points in development.