The number of studies on electronic self-monitoring in affective disorder and other psychiatric disorders is increasing and indicates high patient acceptance and adherence. Nevertheless, the effect of electronic self-monitoring in patients with bipolar disorder has never been investigated in a randomized controlled trial (RCT). The objective of this trial was to investigate in a RCT whether the use of daily electronic self-monitoring using smartphones reduces depressive and manic symptoms in patients with bipolar disorder.

A total of 78 patients with bipolar disorder according to ICD-10 criteria, aged 18–60 years, and with 17-item Hamilton Depression Rating Scale (HAMD-17) and Young Mania Rating Scale (YMRS) scores ≤17 were randomized to the use of a smartphone for daily self-monitoring including a clinical feedback loop (the intervention group) or to the use of a smartphone for normal communicative purposes (the control group) for 6 months. The primary outcomes were differences in depressive and manic symptoms measured using HAMD-17 and YMRS, respectively, between the intervention and control groups.

Intention-to-treat analyses using linear mixed models showed no significant effects of daily self-monitoring using smartphones on depressive as well as manic symptoms. There was a tendency towards more sustained depressive symptoms in the intervention group (B = 2.02, 95% confidence interval −0.13 to 4.17, p = 0.066). Sub-group analysis among patients without mixed symptoms and patients with presence of depressive and manic symptoms showed significantly more depressive symptoms and fewer manic symptoms during the trial period in the intervention group.

These results highlight that electronic self-monitoring, although intuitive and appealing, needs critical consideration and further clarification before it is implemented as a clinical tool.

We aimed to test whether childhood bullying victimization increases risk for age-related disease at mid-life using biological markers including inflammation and adiposity, independent of other childhood risk factors and key adult variables.

The present study was a 50-year prospective longitudinal birth cohort study of all births in Britain in 1 week in 1958. Exposure to bullying was assessed prospectively when participants were aged 7 and 11 years (27.7% occasionally bullied; 14.6% frequently bullied). Blood inflammation biomarkers [C-reactive protein (CRP) and fibrinogen] and adiposity [body mass index (BMI) and waist:hip ratio] were measured at age 45 years.

Participants who had been frequently bullied in childhood showed increased levels of CRP at mid-life [β = 0.07, 95% confidence interval (CI) 0.04–0.10] and higher risk for clinically relevant inflammation cut-off [CRP > 3 mg/l: 20.4% v. 15.9%, odds ratio (OR) = 1.35, 95% CI 1.12–1.64]. Women who were bullied in childhood had higher BMI than non-bullied participants and were at increased risk of being obese (BMI ≥ 30 kg/m2: occasionally bullied: 26.0% v. 19.4%, OR = 1.45, 95% CI 1.18–1.77; frequently bullied: 26.2% v. 19.4%, OR = 1.41, 95% CI 1.09–1.83). Findings remained significant when controlling for childhood risk factors (e.g. parental social class; participants’ BMI and psychopathology in childhood) and key adult variables (e.g. adult social class, smoking, diet and exercise).

Bullied children show increases in risk factors for age-related disease in middle adulthood, independent of co-occurring childhood and adult risks. Given the high prevalence of bullying victimization in childhood, tackling this form of psychosocial stress early in life has the potential of reducing risk for age-related disease and its associated burden.

It is well known that web-based interventions can be effective treatments for depression. However, dropout rates in web-based interventions are typically high, especially in self-guided web-based interventions. Rigorous empirical evidence regarding factors influencing dropout in self-guided web-based interventions is lacking due to small study sample sizes. In this paper we examined predictors of dropout in an individual patient data meta-analysis to gain a better understanding of who may benefit from these interventions.

A comprehensive literature search for all randomized controlled trials (RCTs) of psychotherapy for adults with depression from 2006 to January 2013 was conducted. Next, we approached authors to collect the primary data of the selected studies. Predictors of dropout, such as socio-demographic, clinical, and intervention characteristics were examined.

Data from 2705 participants across ten RCTs of self-guided web-based interventions for depression were analysed. The multivariate analysis indicated that male gender [relative risk (RR) 1.08], lower educational level (primary education, RR 1.26) and co-morbid anxiety symptoms (RR 1.18) significantly increased the risk of dropping out, while for every additional 4 years of age, the risk of dropping out significantly decreased (RR 0.94).

Dropout can be predicted by several variables and is not randomly distributed. This knowledge may inform tailoring of online self-help interventions to prevent dropout in identified groups at risk.

Evidence suggests a relationship between exposure to trauma during childhood and functional impairments in psychotic patients. However, the impact of age at the time of exposure has been understudied in early psychosis (EP) patients.

Two hundred and twenty-five patients aged 18–35 years were assessed at baseline and after 2, 6, 18, 24, 30 and 36 months of treatment. Patients exposed to sexual and/or physical abuse (SPA) were classified according to age at the time of first exposure (Early SPA: before age 11 years; Late SPA: between ages 12 and 15 years) and then compared to patients who were not exposed to such trauma (Non-SPA). The functional level in the premorbid phase was measured with the Premorbid Adjustment Scale (PAS) and with the Global Assessment of Functioning (GAF) scale and the Social and Occupational Functioning Assessment Scale (SOFAS) during follow-up.

There were 24.8% of patients with a documented history of SPA. Late SPA patients were more likely to be female (p = 0.010). Comparison with non-SPA patients revealed that: (1) both Early and Late SPA groups showed poorer premorbid social functioning during early adolescence, and (2) while patients with Early SPA had poorer functional level at follow-up with lower GAF (p = 0.025) and lower SOFAS (p = 0.048) scores, Late SPA patients did not.

Our results suggest a link between exposure to SPA and the later impairment of social functioning before the onset of the disease. EP patients exposed to SPA before age 12 may present long-lasting functional impairment, while patients exposed at a later age may improve in this regard and have a better functional outcome.

Smaller hippocampal volume has often been observed in patients with post-traumatic stress disorder (PTSD). However, there is no consensus whether this is a result of stress/trauma exposure, or constitutes a vulnerability factor for the development of PTSD. Second, it is unclear whether hippocampal volume normalizes with successful treatment of PTSD, or whether a smaller hippocampus is a risk factor for the persistence of PTSD.

Magnetic resonance imaging (MRI) scans and clinical interviews were collected from 47 war veterans with PTSD, 25 healthy war veterans (combat controls) and 25 healthy non-military controls. All veterans were scanned a second time with a 6- to 8-month interval, during which PTSD patients received trauma-focused therapy. Based on post-treatment PTSD symptoms, patients were divided into a PTSD group who was in remission (n = 22) and a group in whom PTSD symptoms persisted (n = 22). MRI data were analysed with Freesurfer.

Smaller left hippocampal volume was observed in PTSD patients compared with both control groups. Hippocampal volume of the combat controls did not differ from healthy controls. Second, pre- and post-treatment analyses of the PTSD patients and combat controls revealed reduced (left) hippocampal volume only in the persistent patients at both time points. Importantly, hippocampal volume did not change with treatment.

Our findings suggest that a smaller (left) hippocampus is not the result of stress/trauma exposure. Furthermore, hippocampal volume does not increase with successful treatment. Instead, we demonstrate for the first time that a smaller (left) hippocampus constitutes a risk factor for the persistence of PTSD.

The treatment gap for serious mental disorders across low-income countries is estimated to be 89%. The model for Mental Health and Development (MHD) offers community-based care for people with mental disorders in 11 low- and middle-income countries.

In Kenya, using a pre-post design, 117 consecutively enrolled participants with schizophrenia-spectrum and bipolar disorders were followed-up at 10 and 20 months. Comparison outcomes were drawn from the literature. Costs were analysed from societal and health system perspectives.

From the societal perspective, MHD cost Int$ 594 per person in the first year and Int$ 876 over 2 years. The cost per healthy day gained was Int$ 7.96 in the first year and Int$ 1.03 over 2 years – less than the agricultural minimum wage. The cost per disability-adjusted life year averted over 2 years was Int$ 13.1 and Int$ 727 from the societal and health system perspectives, respectively, on par with antiretrovirals for HIV.

MHD achieved increasing returns over time. The model appears cost-effective and equitable, especially over 2 years. Its affordability relies on multi-sectoral participation nationally and internationally.

A lack of an aetiologically based nosology classification has contributed to instability in psychiatric diagnoses over time. This study aimed to examine the diagnostic stability of psychosis diagnoses using data from an incidence sample of psychosis cases, followed up after 10 years and to examine those baseline variables which were associated with diagnostic change.

Data were examined from the ÆSOP and ÆSOP-10 studies, an incidence and follow-up study, respectively, of a population-based cohort of first-episode psychosis cases from two sites. Diagnosis was assigned using ICD-10 and DSM-IV-TR. Diagnostic change was examined using prospective and retrospective consistency. Baseline variables associated with change were examined using logistic regression and likelihood ratio tests.

Slightly more (59.6%) cases had the same baseline and lifetime ICD-10 diagnosis compared with DSM-IV-TR (55.3%), but prospective and retrospective consistency was similar. Schizophrenia, psychotic bipolar disorder and drug-induced psychosis were more prospectively consistent than other diagnoses. A substantial number of cases with other diagnoses at baseline (ICD-10, n = 61; DSM-IV-TR, n = 76) were classified as having schizophrenia at 10 years. Many variables were associated with change to schizophrenia but few with overall change in diagnosis.

Diagnoses other than schizophrenia should to be regarded as potentially provisional.

Major depressive disorder and subthreshold depression have been associated with premature mortality. We investigated the association between depressive symptoms and mortality across the full continuum of severity.

We used Cox proportional hazards models to examine the association between depressive symptom severity, assessed using the eight-item Center for Epidemiological Studies Depression Scale (CES-D; range 0–8), and the risk of all-cause mortality over a 9-year follow-up, in 11 104 members of the English Longitudinal Study of Ageing.

During follow-up, one fifth of study members died (N = 2267). Depressive symptoms were associated with increased mortality across the full range of severity (ptrend < 0.001). Relative to study members with no symptoms, an increased risk of mortality was found in people with depressive symptoms of a low [hazard ratio (HR) for a score of 2 was 1.59, 95% confidence interval (CI) 1.40–1.82], moderate (score of 4: HR 1.80, 95% CI 1.52–2.13) and high (score of 8: HR 2.27, 95% CI 1.69–3.04) severity, suggesting risk emerges at low levels but plateaus thereafter. A third of participants (36.4%, 95% CI 35.5–37.3) reported depressive symptoms associated with an increased mortality risk. Adjustment for physical activity, physical illnesses, and impairments in physical and cognitive functioning attenuated this association (ptrend = 0.25).

Depressive symptoms are associated with an increased mortality risk even at low levels of symptom severity. This association is explained by physical activity, physical illnesses, and impairments in physical and cognitive functioning.

Depression is known to run in families, but the effects of parental history of other psychiatric diagnoses on depression rates are less well studied. Few studies have examined the impact of parental psychopathology on depression rates in older age groups.

We established a population-based cohort including all individuals born in Denmark after 1954 and alive on their 10th birthday (N = 29 76 264). Exposure variables were maternal and paternal history of schizophrenia, bipolar disorder, depression, anxiety or ‘other’ psychiatric diagnoses. Incidence rate ratios (IRRs) were estimated using Poisson regressions.

Parental history of any psychiatric diagnosis increased incidence rates of outpatient (maternal: IRR 1.88, p < 0.0001; paternal: IRR 1.68, p < 0.0001) and inpatient (maternal: IRR 1.99, p < 0.0001; paternal: IRR 1.83, p < 0.0001) depression relative to no parental history. IRRs for parental history of non-affective disorders remained relatively stable across age groups, while IRRs for parental affective disorders (unipolar or bipolar) decreased with age from 2.29–3.96 in the youngest age group to 1.53–1.90 in the oldest group. IRR estimates for all parental diagnoses were similar among individuals aged ⩾41 years (IRR range 1.51–1.90).

Parental history of any psychiatric diagnosis is associated with increased incidence rates of unipolar depression. In younger age groups, parental history of affective diagnoses is more strongly associated with rates of unipolar depression than non-affective diagnoses; however, this distinction disappears after age 40, suggesting that parental psychopathology in general, rather than any one disorder, confers risk for depression in middle life.

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by high rates of co-morbid psychopathology. Randomized controlled trials of multimodal interventions, combining pharmacological and psychological treatments, have shown a robust treatment effect for ADHD symptoms but outcomes for co-morbid symptoms have been mixed. This may be accounted for by the type of intervention selected and/or by methodological problems including lack of follow-up and low power. The current study addressed these limitations in a parallel-group randomized controlled trial conducted in Iceland.

A total of 95 adult ADHD patients who were already being treated with medication (MED) were randomly assigned to receive treatment as usual (TAU/MED) or 15 sessions of cognitive–behavioural therapy (CBT/MED) using the R&R2ADHD intervention which employs both group and individual modalities. Primary measures of ADHD symptoms and severity of illness, and secondary measures of anxiety, depression and quality of life were given at baseline, end of treatment and 3-month follow-up. Primary outcomes were rated by clinicians blind to treatment condition assignment.

CBT/MED showed overall (combined outcome at end of treatment and 3-month follow-up) significantly greater reduction in primary outcomes for clinician-rated and self-rated ADHD symptoms. Treatment effect of primary outcomes was maintained at follow-up, which suggests robust and lasting findings. In contrast to the primary outcomes, the secondary outcomes showed significant improvement over time.

The study provides evidence for the effectiveness of R&R2ADHD and demonstrates that there are differential effects over time for ADHD symptoms versus co-morbid problems, the latter taking longer to show positive effects.

There are currently no neuroanatomical biomarkers of anorexia nervosa (AN) available to make clinical inferences at an individual subject level. We present results of a multivariate machine learning (ML) approach utilizing structural neuroanatomical scan data to differentiate AN patients from matched healthy controls at an individual subject level.

Structural neuroimaging scans were acquired from 15 female patients with AN (age = 20, s.d. = 4 years) and 15 demographically matched female controls (age = 22, s.d. = 3 years). Neuroanatomical volumes were extracted using the FreeSurfer software and input into the Least Absolute Shrinkage and Selection Operator (LASSO) multivariate ML algorithm. LASSO was ‘trained’ to identify ‘novel’ individual subjects as either AN patients or healthy controls. Furthermore, the model estimated the probability that an individual subject belonged to the AN group based on an individual scan.

The model correctly predicted 25 out of 30 subjects, translating into 83.3% accuracy (sensitivity 86.7%, specificity 80.0%) (p < 0.001; χ2 test). Six neuroanatomical regions (cerebellum white matter, choroid plexus, putamen, accumbens, the diencephalon and the third ventricle) were found to be relevant in distinguishing individual AN patients from healthy controls. The predicted probabilities showed a linear relationship with drive for thinness clinical scores (r = 0.52, p < 0.005) and with body mass index (BMI) (r = −0.45, p = 0.01).

The model achieved a good predictive accuracy and drive for thinness showed a strong neuroanatomical signature. These results indicate that neuroimaging scans coupled with ML techniques have the potential to provide information at an individual subject level that might be relevant to clinical outcomes.

Stress and vulnerability likely interact to play a major role in psychosis. While much has been written about the neural diathesis-stress model in psychosis and its clinical risk states, little is known about HPA axis biomarkers in non-help-seeking individuals at familial high risk (FHR). We sought to prospectively measure pituitary volume (PV) in adolescents and young adults at FHR for schizophrenia and to follow their emerging sub-clinical psychotic symptoms and clinical trajectories.

Forty healthy controls and 38 relatives of patients with schizophrenia or schizoaffective disorder were identified in Pittsburgh, USA. PV was derived from baseline 1.5 T magnetic resonance imaging. Chapman's schizotypy scales were acquired at baseline, and structured clinical interviews for DSM-IV-TR Axis I diagnoses were attempted annually for up to 3 years.

Seven individuals converted to psychosis. PV did not differ between FHR and control groups overall. Within the FHR group, PV was positively correlated with Chapman's positive schizotypy (Magical Ideation and Perceptual Aberration) scores, and there was a significant group × PV interaction with schizotypy. PV was significantly higher in FHR subjects carrying any baseline Axis I diagnosis (p = 0.004), and higher still in individuals who went on to convert to psychosis (p = 0.0007).

Increased PV is a correlate of early positive schizotypy, and may predict trait vulnerability to subsequent psychosis in FHR relatives. These preliminary findings support a model of stress-vulnerability and HPA axis activation in the early phases of psychosis.

There is growing interest in the role of childhood adversities, including parental death and separation, in the etiology of psychotic disorders. However, few studies have used prospectively collected data to specifically investigate parental separation across development, or assessed the importance of duration of separation, and family characteristics.

We measured three types of separation not due to death: maternal, paternal, and from both parents, across the ages of 1–15 years among a cohort of 985 058 individuals born in Denmark 1971–1991 and followed to 2011. Associations with narrowly and broadly defined schizophrenia and bipolar disorder in the psychiatric register were assessed in terms of separation occurrence, age of separation, and number of years separated. Interactions with parental history of mental disorder were assessed.

Each type of separation was associated with all three outcomes, adjusting for age, sex, birth period, calendar year, family history of mental disorder, urbanicity at birth and parental age. Number of years of paternal separation was positively associated with both schizophrenia and bipolar disorder. Associations between separation from both parents and schizophrenia were stronger when separation occurred at later ages, while those with bipolar disorder remained stable across development. The first occurrence of paternal separation appeared to increase risk more when it occurred earlier in childhood. Associations differed according to parental history of mental disorder, although in no situation was separation protective.

Effects of parental separation may differ by type, developmental timing and family characteristics. These findings highlight the importance of considering such factors in studies of childhood adversity.

There is a clear need for effective interventions to reduce cannabis use in patients with first-episode psychosis. This follow-up of a randomized trial examined whether an intervention for parents, based on motivational interviewing and interaction skills (Family Motivational Intervention, FMI), was more effective than routine family support (RFS) in reducing cannabis use in patients with recent-onset schizophrenia.

In a single-blind trial with 75 patients in treatment for recent-onset schizophrenia, 97 parents were randomly assigned to either FMI or RFS. Assessments were conducted at baseline and at 3 and 15 months after the interventions had been ended. Analyses were performed on an intention-to-treat basis using mixed-effect regression models.

From baseline to the 15-month follow-up, there was a significantly greater reduction in FMI compared to RFS in patients’ quantity (p = 0.01) and frequency (p < 0.01) of cannabis use. Patients’ craving for cannabis use was also significantly lower in FMI at 15 months follow-up (p < 0.01). Both groups improved in parental distress and sense of burden; however, only FMI parents’ appraisal of patients’ symptoms showed further improvement at the 15-month follow-up (p < 0.05).

The results support the sustained effectiveness of FMI in reducing cannabis use in patients with recent-onset schizophrenia at 15 months follow-up. Findings were not consistent with regard to the long-term superiority of FMI over RFS in reducing parents’ distress and sense of burden.

Extensive evidence has shown that experiencing a traumatic event and post-traumatic stress disorder (PTSD) are associated with experiences of psychosis. However, less is known about specific PTSD symptoms and their relationship with psychotic experiences. This study aimed to examine the relationship between symptoms of PTSD with paranoia and auditory hallucinations in a large-scale sample.

The Adult Psychiatric Morbidity Survey (APMS) was utilized to examine the prevalence of lifetime trauma, symptoms of PTSD, and experiences of paranoia and auditory hallucinations (n = 7403).

There were significant bivariate associations between symptoms of PTSD and psychotic experiences. Multiple logistic regression analyses indicated that reliving and arousal symptoms were significant predictors for paranoia while reliving, but not arousal symptoms, also significantly predicted auditory hallucinations. A dose-response relationship was found, the greater the number of PTSD symptoms, the greater the odds were of experiencing both paranoia and hallucinations.

These findings illustrate that symptoms of PTSD are associated with increased odds of experiencing auditory hallucinations and paranoia. Overlaps appear to be present between the symptoms of PTSD and psychotic experiences. Increasing awareness of this association may advance work in clinical practice.

Cortical thickness measurement offers an index of brain development processes. In healthy individuals, cortical thickness is reduced with increasing age and is related to cognitive decline. Cortical thinning has been reported in schizophrenia. Whether cortical thickness changes differently over time in patients and its impact on outcome remain unanswered.

Data were examined from 109 patients and 76 healthy controls drawn from the Santander Longitudinal Study of first-episode schizophrenia for whom adequate structural magnetic resonance imaging (MRI) data were available (n = 555 scans). Clinical and cognitive assessments and MRIs were acquired at three regular time points during a 3-year follow-up period. We investigated likely progressive cortical thickness changes in schizophrenia during the first 3 years after initiating antipsychotic treatment. The effects of cortical thickness changes on cognitive and clinical variables were also examined along with the impact of potential confounding factors.

There were significant diagnoses × scan time interaction main effects for total cortical thickness (F1,309.1 = 4.60, p = 0.033) and frontal cortical thickness (F1,310.6 = 5.30, p = 0.022), reflecting a lesser thinning over time in patients. Clinical and cognitive outcome was not associated with progressive cortical changes during the early years of the illness.

Cortical thickness abnormalities do not unswervingly progress, at least throughout the first years of the illness. Previous studies have suggested that modifiable factors may partly account for cortical thickness abnormalities. Therefore, the importance of implementing practical actions that may modify those factors and improve them over the course of the illness should be highlighted.

Several questions remain unanswered regarding the magnitude and time course of cognitive improvement in response to antipsychotic treatment. The purpose of this study was to assess changes in cognitive performance in antipsychotic-naive or minimally medicated patients with first-episode schizophrenia during the first 12 months of treatment, in a case–control design. Patients were treated with flupenthixol decanoate depot injection, according to a standard algorithm. The primary outcome measure was change in MATRICS Cognitive Consensus Battery (MCCB) composite score over 12 months.

The sample comprised 92 patients and 100 healthy controls matched for age, sex, ethnicity and educational status. Cognitive function was assessed by means of the MCCB.

A mixed-effects model identified a significant group × time effect (p ≤ 0.0001) for the MCCB composite score, with patients showing a greater degree of change than the controls. For the other MCCB domains there were significant group × time effects at adjusted significance level for attention and vigilance (p ≤ 0.0001), visual learning (p ≤ 0.0001), verbal learning (p = 0.005) and working memory (p ≤ 0.0001), but not for reasoning and problem solving (p = 0.04), speed of processing (p = 0.03) and social cognition (p = 0.06). There were moderate correlations between change in MCCB composite score and change in symptomatology as assessed by Positive and Negative Syndrome Scale factor analysis-derived domains.

Substantial improvements in cognitive function were observed over and above a practice effect, and were significantly correlated with improvements in psychopathology and functionality.

This study examines the patterns and predictors of post-traumatic stress disorder (PTSD) symptom trajectories among adolescent survivors following the Wenchuan earthquake in China.

A total of 1573 adolescent survivors were followed up at 6, 12, 18 and 24 months post-earthquake. Participants completed the Posttraumatic Stress Disorder Self-Rating Scale (PTSD-SS), Adolescent Self-Rating Life Events Checklist, Social Support Rate Scale, and the Simplified Coping Style Questionnaire. Distinct patterns of PTSD symptom trajectories were established through grouping participants based on time-varying changes of developing PTSD (i.e. reaching the clinical cut-off on the PTSD-SS). Multivariate logistic regressions were used to examine predictors for trajectory membership.

PTSD prevalence rates at 6, 12, 18 and 24 months were 21.0, 23.3, 13.5 and 14.7%, respectively. Five PTSD symptom trajectories were observed: resistance (65.3% of the sample), recovery (20.0%), relapsing/remitting (3.3%), delayed dysfunction (4.2%) and chronic dysfunction (7.2%). Female gender and senior grade were related to higher risk of developing PTSD symptoms in at least one time point, whereas being an only child increased the possibility of recovery relative to chronic dysfunction. Family members’ injury/loss and witness of traumatic scenes could also cause PTSD chronicity. More negative life events, less social support, more negative coping and less positive coping were also common predictors for not developing resistance or recovery.

Adolescents’ PTSD symptoms showed an anniversary reaction. Although many adolescents remain euthymic or recover over time, some adolescents, especially those with the risk factors noted above, exhibit chronic, delayed or relapsing symptoms. Thus, the need for individualized intervention with these adolescents is indicated.

Prior meta-analytic work has highlighted important etiological distinctions between aggressive (AGG) and non-aggressive rule-breaking (RB) dimensions of antisocial behavior. Among these is the finding that RB is influenced by the environment more than is AGG. Relatively little research, however, has sought to identify the specific environmental experiences that contribute to this effect. The current study sought to do just this.

We examined whether unrelated adults residing in the same neighborhood (n = 1915 participants in 501 neighborhoods) were more similar in their AGG and RB than would be expected by chance. Analyses focused on simple multi-level models, with the participant as the lower-level unit and the neighborhood as the upper-level unit.

Results revealed little to no evidence of neighborhood-level variance in AGG. By contrast, 11+% of the variance in RB could be predicted from participant neighborhood, results that persisted even when considering the possibility of genetic relatedness across participants and neighborhood selection effects. Moreover, 17% of this neighborhood-level variance in RB was accounted for by neighborhood structural characteristics and social processes.

Findings bolster prior suggestions that broader contextual experiences, like the structural and social characteristics of one's neighborhood, contribute in a meaningful way to RB in particular. Our results also tentatively imply that this association may be environmental in origin. Future work should seek to develop additional, stronger designs capable of more clearly leveraging genetic un-relatedness to improve causal inferences regarding the environment.