Working memory (WM) deficits in schizophrenia (SCZ) have been linked to impairments in the encoding phase that are associated with aberrant neuronal functioning. Similar abnormalities have been observed in unaffected first-degree relatives (REL) and are thus discussed as candidate endophenotypes. The process of WM consolidation – i.e. the formation of durable WM representations – is assumed to be impaired in SCZ, but no study has investigated WM consolidation and neuronal correlates of visual WM encoding in REL before.

We examined whole-brain activation during the encoding phase with an event-related functional magnetic resonance imaging study design in 25 SCZ subjects, 22 REL subjects, and 25 healthy controls. Subjects performed a visual masked change detection task that assessed WM performance and consolidation.

SCZ showed deficient WM performance indicating an impairment consolidation process, accompanied by broad neuronal hypoactivation, most prominently in frontal brain regions, as well as increased activity of the anterior cingulate during the encoding phase. REL showed decreased neuronal activity in the middle and medial frontal gyrus and increased activity in the precentral gyrus and insula during encoding, but no significant behavioral deficits were observed. In respect of given consolidation times, REL showed a shift from decreased frontal activity at short time intervals to increased frontal activity at longer time intervals.

Findings suggest WM consolidation may be slowed in REL so that the deployment of compensatory neuronal resources during encoding is needed to assure proper WM performance. This supports the view of WM-related neuronal dysfunctions as a potential endophenotypic marker.

Larger grey matter volume of the inferior frontal gyrus (IFG) is among the most replicated biomarkers of genetic risk for bipolar disorders (BD). However, the IFG is a heterogeneous prefrontal region, and volumetric findings can be attributable to changes in cortical thickness (CT), surface area (SA) or gyrification. Here, we investigated the morphometry of IFG in participants at genetic risk for BD.

We quantified the IFG cortical grey matter volume in 29 affected, 32 unaffected relatives of BD probands, and 42 controls. We then examined SA, CT, and cortical folding in subregions of the IFG.

We found volumetric group differences in the right IFG, with the largest volumes in unaffected high-risk and smallest in control participants (F2,192 = 3.07, p = 0.01). The volume alterations were localized to the pars triangularis of the IFG (F2,97 = 4.05, p = 0.02), with no differences in pars opercularis or pars orbitalis. Pars triangularis volume was highly correlated with its SA [Pearson r(101) = 0.88, p < 0.001], which significantly differed between the groups (F2,97 = 4.45, p = 0.01). As with volume, the mean SA of the pars triangularis was greater in unaffected (corrected p = 0.02) and affected relatives (corrected p = 0.05) compared with controls. We did not find group differences in pars triangularis CT or gyrification.

These findings strengthen prior knowledge about the volumetric findings in this region and provide a new insight into the localization and topology of IFG alterations. The unique nature of rIFG morphology in BD, with larger volume and SA early in the course of illness, could have practical implications for detection of participants at risk for BD.

A stepped care approach involves patients first receiving low-intensity treatment followed by higher intensity treatment. This two-step randomized controlled trial investigated the efficacy of a sequential stepped care approach for the psychological treatment of binge-eating disorder (BED).

In the first step, all participants with BED (n = 135) received unguided self-help (USH) based on a cognitive-behavioral therapy model. In the second step, participants who remained in the trial were randomized either to 16 weeks of group psychodynamic-interpersonal psychotherapy (GPIP) (n = 39) or to a no-treatment control condition (n = 46). Outcomes were assessed for USH in step 1, and then for step 2 up to 6-months post-treatment using multilevel regression slope discontinuity models.

In the first step, USH resulted in large and statistically significant reductions in the frequency of binge eating. Statistically significant moderate to large reductions in eating disorder cognitions were also noted. In the second step, there was no difference in change in frequency of binge eating between GPIP and the control condition. Compared with controls, GPIP resulted in significant and large improvement in attachment avoidance and interpersonal problems.

The findings indicated that a second step of a stepped care approach did not significantly reduce binge-eating symptoms beyond the effects of USH alone. The study provided some evidence for the second step potentially to reduce factors known to maintain binge eating in the long run, such as attachment avoidance and interpersonal problems.

Approximately seven million people in the UK are engaged in informal caregiving. Informal caregivers are at risk of poorer mental and physical health. However, less is known about how the relationship between the informal caregiving and psychological distress changes over time. The aim of this study was to investigate longitudinal associations between the informal caregiving and psychological distress amongst UK men and women aged 16+.

Data were analysed from the UK Household Longitudinal Study (UKHLS, n = 9368), a nationally representative study of UK households. Longitudinal linear mixed modelling was used to estimate associations between the longitudinal patterns of informal caregiving (non-caregiver/one episode of 1–2 years/intermittent caregiving/3+ years caregiving) and trajectories of psychological distress across seven waves of UKHLS data.

Informal caregiving was not associated with psychological distress for men. Women engaged in long-term (⩾3 years) or intermittent caregiving had higher levels of psychological distress at the point of initiation, compared with women who were not caregivers throughout the study period (3+ years caregiver: regression coefficient 0.48, 95% confidence interval (CI) 0.07–0.89; intermittent caregiver: regression coefficient 0.47, 95% CI 0.02–0.92). Trajectories of psychological distress changed little over time, suggesting a plateau effect for these caregiving women.

Women engaged in long-term or repeated shorter episodes of informal caregiving reported more symptoms of psychological distress than non-caregiving women. Given the increased risk of reporting psychological distress and the increasing importance of the informal care sector, the risk of poorer mental health of informal caregivers should be a priority for public health.

Psychosis is characterized by problems in social functioning that exist well before illness onset, and in individuals at clinical high risk (CHR) for psychosis. Trust is an essential element for social interactions that is impaired in psychosis. In the trust game, chronic patients showed reduced baseline trust, impaired response to positive social feedback, and attenuated brain activation in reward and mentalizing areas. We investigated whether first-episode psychosis patients (FEP) and CHR show similar abnormalities in the neural and behavioral mechanisms underlying trust.

Twenty-two FEP, 17 CHR, and 43 healthy controls performed two trust games, with a cooperative and an unfair partner in the fMRI scanner. Region of interest analyses were performed on mentalizing and reward processing areas, during the investment and outcome phases of the games.

Compared with healthy controls, FEP and CHR showed reduced baseline trust, but like controls, learned to trust in response to cooperative and unfair feedback. Symptom severity was not associated with baseline trust, however in FEP associated with reduced response to feedback. The only group differences in brain activation were that CHR recruited the temporo-parietal junction (TPJ) more than FEP and controls during investment in the unfair condition. This hyper-activation in CHR was associated with greater symptom severity.

Reduced baseline trust may be associated with risk for psychotic illness, or generally with poor mental health. Feedback learning is still intact in CHR and FEP, as opposed to chronic patients. CHR however show distinct neural activation patterns of hyper-activation of the TPJ.

Most research on the prevalence, distribution, and psychiatric comorbidity of intellectual disability (ID) relies on clinical samples, limiting the generalizability and utility of ID assessment in a legal context. This study assessed ID prevalence in a population-representative sample of US adolescents and examined associations of ID with socio-demographic factors and mental disorders.

Data were drawn from the National Comorbidity Survey Adolescent Supplement (N = 6256). ID was defined as: (1) IQ ⩽ 76, measured using the Kaufman Brief Intelligence Test; (2) an adaptive behavior score ⩽76, and (3) age of onset ⩽18 measured using a validated scale. The Composite International Diagnostic Interview assessed 15 lifetime mental disorders. The Sheehan disability scale assessed disorder severity. We used logistic regression models to estimate differences in lifetime disorders for adolescents with and without ID.

ID prevalence was 3.2%. Among adolescents with ID, 65.1% met lifetime criteria for a mental disorder. ID status was associated with specific phobia, agoraphobia, and bipolar disorder, but not behavior disorders after adjustment for socio-demographics. Adolescents with ID and mental disorders were significantly more likely to exhibit severe impairment than those without ID.

These findings highlight how sample selection and overlap between ID and psychopathology symptoms might bias understanding of the mental health consequences of ID. For example, associations between ID and behavior disorders widely reported in clinical samples were not observed in a population-representative sample after adjustment for socio-demographic confounders. Valid assessment and understanding of these constructs may prove influential in the legal system by influencing treatment referrals and capital punishment decisions.

Current definitions of intellectual disability (ID) are based on three criteria: formal designation of low intelligence through artificial problem-solving tasks, impairment in one's ability to function in his/her social environment, and early age of onset. In a national population sample of adolescents, the majority of those with ID met criteria for a lifetime mental disorder. Phobias and bipolar disorder, but not behavior disorders, were elevated in adolescents with ID. Findings highlight the need to consider how behavioral problems are conceptualized and classified in people with ID.

Identifying characteristics of individuals at greatest risk for prolonged grief disorder (PGD) can improve its detection and elucidate the etiology of the disorder. The Safe Passage Study, a study of women at high risk for sudden infant death syndrome (SIDS), prospectively examined the psychosocial functioning of women while monitoring their healthy pregnancies. Mothers whose infants died of SIDS were followed in bereavement.

Pre-loss data were collected from 12 000 pregnant mothers and analyzed for their associations with grief symptoms and PGD in 50 mothers whose infants died from SIDS, from 2 to 48 months after their infant's death, focusing on pre-loss risk factors of anxiety, depression, alcohol use, maternal age, the presence of other living children in the home, and previous child loss.

The presence of any four risk factors significantly predicted PGD for 24 months post-loss (p < 0.003); 2–3 risk factors predicted PGD for 12 months (p = 0.02). PGD rates increased in the second post-loss year, converging in all groups to approximately 40% by 3 years. Pre-loss depressive symptoms were significantly associated with PGD. Higher alcohol intake and older maternal age were consistently positively associated with PGD. Predicted risk scores showed good discrimination between PGD and no PGD 6–24 months after loss (C-statistic = 0.83).

A combination of personal risk factors predicted PGD in 2 years of bereavement. There is a convergence of risk groups to high rates at 2–3 years, marked by increased PGD rates in mothers at low risk. The risk factors showed different effects on PGD.

There is an established relationship between depression and sexual functioning in women. However, there is limited research examining the relationship between perinatal depression and sexual functioning.

This study draws on the Mercy Pregnancy and Emotional Wellbeing Study and reports on 211 women recruited in early pregnancy and followed to 12 months postpartum. Women were assessed for depression using the Structured Clinical Interview for the DSM-IV, repeated measurement of depressive symptoms using the Edinburgh Postnatal Depression Scale and sexual functioning using the Female Sexual Functioning Inventory. Data were also collected on antidepressant use, mode of delivery, history of childhood trauma, breastfeeding and partner support.

Women showed a decline in sexual functioning over pregnancy and the first 6 months postpartum, which recovered by 12 months. For women with depression, sexual functioning was lower throughout pregnancy and continued to be lower at 6 months postpartum than those without depression. Ongoing depressive symptoms at 12 months were also associated with lower sexual functioning. Sexual functioning was not predicted by mode of delivery, antidepressant use or childhood trauma. Breastfeeding predicted lower sexual functioning only at 6 months. Higher partner support predicted higher female sexual functioning.

Pregnancy and the postpartum are a time of reduced sexual functioning for women; however, women with depression are more likely to have lower levels of sexual functioning and this was not predicted by antidepressant use. In women with perinatal depression, consideration of the impact on sexual functioning should be an integral part of care.

The independent effects of depressive symptoms and sleep problems for future physical illness risk have yet to be studied systematically across a variety of disease endpoints.

We analysed data from 7395 participants (65.81 ± 9.39 years; 54.8% female) from the English Longitudinal Study of Ageing (ELSA). Baseline was wave 4 and participants were followed up for 6 years until wave 7. Sleep was measured using an adapted version of the Jenkins Sleep Problems questionnaire and depressive symptoms using the Centre for Epidemiological Studies Depression scale. Participants with the illness of interest at baseline [coronary heart disease (CHD), cancer, diabetes/high blood glucose, arthritis] were excluded from models predicting the onset of that illness at follow-up. Logistic regression was used, entering depressive symptoms and sleep problems simultaneously into models controlling for a wide range of covariates.

In fully adjusted models depressive symptoms predicted incident CHD (OR 1.11, 95% CI 1.04–1.20, p = 0.004) and diabetes/high blood glucose (OR 1.13, 95% CI 1.04–1.22, p = 0.002) independent of sleep problems; both depressive symptoms (OR 1.10, 95% CI 1.04–1.16, p = 0.002) and sleep problems (OR 1.14, 95% CI 1.02–1.26, p = 0.019) predicted incident arthritis.

Sleep problems and depressive symptoms, and a combination of both, were differentially associated with physical illness onset 6 years later. Our findings highlight the importance of taking into account somatic and affective experiences when looking across a variety of different physical illnesses.

Data on the relationship between intelligence quotient (IQ) and violence perpetration are scarce and nationally representative data from the UK adult population is lacking. Therefore, our goal was to examine the relationship between IQ and violence perpetration using nationally representative community-based data from the UK.

We analyzed cross-sectional data from the 2007 Adult Psychiatric Morbidity Survey. IQ was estimated using the National Adult Reading Test (NART). Violence perpetration referred to being in a physical fight or having deliberately hit anyone in the past 5 years. We conducted logistic regression analysis to assess the association between IQ (exposure variable) and violence perpetration (outcome variable).

There were 6872 participants aged ⩾16 years included in this study. The prevalence of violence perpetration decreased linearly with increasing IQ [16.3% (IQ 70–79) v. 2.9% (IQ 120–129)]. After adjusting for demographic and behavioral factors, childhood adversity, and psychiatric morbidity, compared with those with IQ 120–129, IQ scores of 110–119, 100–109, 90–99, 80–89, and 70–79 were associated with 1.07 [95% confidence interval (CI) 0.63–1.84], 1.90 (95% CI 1.12–3.22), 1.80 (95% CI 1.05–3.13), 2.36 (95% CI 1.32–4.22), and 2.25 (95% CI 1.26–4.01) times higher odds for violence perpetration, respectively.

Lower IQ was associated with violence perpetration in the UK general population. Further studies are warranted to assess how low IQ can lead to violence perpetration, and whether interventions are possible for this high-risk group.

The Triarchic Psychopathy Measure (TriPM) provides Disinhibition, Boldness, and Meanness scales for assessing the three trait domains of the triarchic model. Here we examined the genetic and environmental etiology of these three domains, including evaluation of potential sex differences.

A total of 1016 men and women ages 19–20 years were drawn from the University of Southern California Risk Factors for Antisocial Behavior twin study.

Scores for the three TriPM scales were correlated to differing degrees, with the strongest phenotypic correlation between Disinhibition and Meanness. No sex differences were found in the genetic and environmental influences underlying these three domains, suggesting that the same genes and life experiences contribute to these traits in young men and women. For TriPM Disinhibition and Boldness, genetic factors explained about half or less of the variance, with the rest of the variance being explained by non-shared environmental factors. For TriPM Meanness, on the other hand, genetic, shared environmental, and non-shared environmental factors accounted for the variance. The phenotypic correlation between Disinhibition and Meanness was explained in part by common genes (26%), with the remainder attributable about equally to common shared (39%), and non-shared environmental influences (35%).

These findings contribute to our understanding of psychopathic personality traits by demonstrating the importance of heritable factors for disinhibition and boldness facets of psychopathy, and the importance of shared environmental influences for the meanness facet.

Depression is a common and significant health problem. Hearing loss is the third most common chronic physical condition in the USA and might be a factor in depression. To determine whether hearing loss is associated with depressive symptoms in US adults ages 20–69 years.

National Health and Nutrition Examination Survey (NHANES) data (2011–2012) were used to assess the potential relationship between hearing loss and depression, in adults (20–69 years) who answered the Patient Health Questionnaire (PHQ-9) depression screening module, with pure tone audiometry measurements, and complete information on the co-variates data (n = 3316). The degree of speech-frequency hearing loss (SFHL) and high-frequency hearing loss (HFHL) were defined as slight/mild hearing loss ⩾26–40 dB; moderate/worse hearing loss ⩾41 dB by pure tone audiometry examination.

Moderate/worse HFHL was statistically significantly associated with depressive symptoms (OR 1.54, 95% CL 1.04–2.27) when the analyses were conducted among all participants. Further stratification by gender and age groups found that moderate/worse HFHL (OR 3.85, 95% CL 1.39–10.65) and moderate/worse SFHL (OR 5.75, 95% CL 1.46–22.71) were associated with depressive symptoms in women ages 52–69 years.

Moderate/worse speech frequency and HFHL are associated with depression in women ages 52–69 years, independent of other risk factors. Hearing screenings are likely to reduce delays in diagnosis and provide early opportunities for noise prevention counseling and access to hearing aids. Health professionals should be aware of depressive signs and symptoms in patients with hearing loss.

Based on the vulnerability–stress model, we aimed to (1) determine new onset of depression in individuals who had not shown evidence of depression at baseline (5 years earlier) and (2) identify social, psychological, behavioral, and somatic predictors.

Longitudinal data of N = 10 036 participants (40–79 years) were evaluated who had no evidence of depression at baseline based on Patient Health Questionnaire (PHQ-9), no history of depression, or intake of antidepressants. Multivariate logistic regression models were used to predict the onset of depression.

Prevalence of new cases of depression was 4.4%. Higher rates of women (5.1%) than men (3.8%) were due to their excess incidence <60 years of age. Regression analyses revealed significant social, psychological, behavioral, and somatic predictors: loneliness [odds ratio (OR) 2.01; 95% confidence interval (CI) 1.48–2.71], generalized anxiety (OR 2.65; 1.79–3.85), social phobia (OR 1.87; 1.34–2.57), panic (OR 1.67; 1.01–2.64), type D personality (OR 1.85; 1.47–2.32), smoking (OR 1.35; 1.05–1.71), and comorbid cancer (OR 1.58; 1.09–2.24). Protective factors were age (OR 0.88; 0.83–0.93) and social support (OR 0.93; 0.90–0.95). Stratified by sex, cancer was predictive for women; for men smoking and life events. Entered additionally, the PHQ-9 baseline score was strongly predictive (OR 1.40; 1.34–1.47), generalized anxiety became only marginally, and panic was no longer predictive. Other predictors remained significant, albeit weaker.

Psychobiological vulnerability, stress, and illness-related factors were predictive of new onset of depression, whereas social support was protective. Baseline subclinical depression was an additional risk weakening the relationship between anxiety and depression by taking their overlap into account. Vulnerability factors differed between men and women.

Exercise has mood-enhancing effects and can improve cognitive functioning, but the effects in first-episode psychosis (FEP) remain understudied. We examined the feasibility and cognitive effects of exercise in FEP.

Multi-center, open-label intervention study. Ninety-one outpatients with FEP (mean age = 30 years, 65% male) received usual care plus a 12-week supervised circuit-training program, consisting of high-volume resistance exercises, aerobic training, and stretching. Primary study outcome was cognitive functioning assessed by Cogstate Brief Battery (processing speed, attention, visual learning, working memory) and Trailmaking A and B tasks (visual attention and task shifting). Within-group changes in cognition were assessed using paired sample t tests with effect sizes (Hedges’ g) reported for significant values. Relationships between exercise frequency and cognitive improvement were assessed using analysis of covariance. Moderating effects of gender were explored with stratified analyses.

Participants exercised on average 13.5 (s.d. = 11.7) times. Forty-eight percent completed 12 or more sessions. Significant post-intervention improvements were seen for processing speed, visual learning, and visual attention; all with moderate effect sizes (g = 0.47–0.49, p < 0.05). Exercise participation was also associated with a positive non-significant trend for working memory (p < 0.07). Stratified analyses indicated a moderating effect of gender. Positive changes were seen among females only for processing speed, visual learning, working memory, and visual attention (g = 0.43–0.69). A significant bivariate correlation was found between total training frequency and improvements in visual attention among males (r = 0.40, p < 0.05).

Supported physical exercise is a feasible and safe adjunct treatment for FEP with potential cognitive benefits, especially among females.

Psychosocial and health-related risk factors for depressive symptoms are known. It is unclear if these are associated with depressive symptom patterns over time. We identified trajectories of depressive symptoms and their risk factors among midlife women followed over 15 years.

Participants were 3300 multiracial/ethnic women enrolled in a multisite longitudinal menopause and aging study, Study of Women's Health Across the Nation. Biological, psychosocial, and depressive symptom data were collected approximately annually. Group-based trajectory modeling identified women with similar longitudinal patterns of depressive symptoms. Trajectory groups were compared on time-invariant and varying characteristics using multivariable multinomial analyses and pairwise comparisons.

Five symptom trajectories were compared (50% very low; 29% low; 5% increasing; 11% decreasing; 5% high). Relative to whites, blacks were less likely to be in the increasing trajectory and more likely to be in the decreasing symptom trajectory and Hispanics were more likely to have a high symptom trajectory than an increasing trajectory. Psychosocial/health factors varied between groups. A rise in sleep problems was associated with higher odds of having an increasing trajectory and a rise in social support was associated with lower odds. Women with low role functioning for 50% or more visits had three times the odds of being in the increasing symptom group.

Changes in psychosocial and health characteristics were related to changing depressive symptom trajectories. Health care providers need to evaluate women's sleep quality, social support, life events, and role functioning repeatedly during midlife to monitor changes in these and depressive symptoms.

Studies suggest that 10–15% of perinatal women experience depressive symptoms. Due to the risks, problems with detection, and barriers to treatment, effective universal preventive interventions are needed. The aim of this study was to assess the effectiveness of an automated internet intervention (‘Mamma Mia’) on perinatal depressive symptoms. Mamma Mia is tailored specifically to the perinatal phase and targets risk and protective factors for perinatal depressive symptoms.

A total of 1342 pregnant women were randomized to an intervention (‘Mamma Mia’) and control group. Data were collected at gestational week (gw) 21–25, gw37, 6 weeks after birth, and 3 and 6 months after birth. We investigated whether (1) the intervention group displayed lower levels of depressive symptoms compared with the control group, (2) the effect of Mamma Mia changed over time, (3) the effect on depressive symptoms was moderated by baseline depressive symptoms, previous depression, and parity, and (4) this moderation changed by time. Finally, we examined if the prevalence of mothers with possible depression [i.e. Edinburgh Postnatal Depression Scale (EPDS)-score ⩾10] differed between the intervention and control group.

Participants in the Mamma Mia group displayed less depressive symptoms than participants in the control group during follow-up [F(1) = 7.03, p = 0.008]. There were indications that the effect of Mamma Mia was moderated by EPDS score at baseline. The prevalence of women with EPDS-score ⩾10 was lower in the Mamma Mia group at all follow-up measurements.

The study demonstrated the effects of the automated web-based universal intervention Mamma Mia on perinatal depressive symptoms.

The mental health and social functioning of millions of forcibly displaced individuals worldwide represents a key public health priority for host governments. This is the first longitudinal study with a representative sample to examine the impact of interpersonal trust and psychological symptoms on community engagement in refugees.

Participants were 1894 resettled refugees, assessed within 6 months of receiving a permanent visa in Australia, and again 2–3 years later. Variables measured included post-traumatic stress disorder symptoms, depression/anxiety symptoms, interpersonal trust and engagement with refugees’ own and other communities.

A multilevel path analysis was conducted, with the final model evidencing good fit (Comparative Fit Index = 0.97, Tucker–Lewis Index = 0.89, Root Mean Square Error of Approximation = 0.05, Standardized Root-Mean-Square-Residual = 0.05). Findings revealed that high levels of depression symptoms were associated with lower subsequent engagement with refugees’ own communities. In contrast, low levels of interpersonal trust were associated with lower engagement with the host community over the same timeframe.

Findings point to differential pathways to social engagement in the medium-term post-resettlement. Results indicate that depression symptoms are linked to reduced engagement with one's own community, while interpersonal trust is implicated in engagement with the broader community in the host country. These findings have potentially important implications for policy and clinical practice, suggesting that clinical and support services should target psychological symptoms and interpersonal processes when fostering positive adaptation in resettled refugees.

Probands with attention-deficit/hyperactivity disorder (ADHD) are at increased risk for several psychiatric and neurodevelopmental disorders. The risk of these disorders among the siblings of probands has not been thoroughly assessed in a population-based cohort.

Every child born in Finland in 1991–2005 and diagnosed with ADHD in 1995–2011 were identified from national registers. Each case was matched with four controls on sex, place, and date of birth. The full siblings of the cases and controls were born in 1981–2007 and diagnosed in 1981–2013. In total, 7369 cases with 12 565 siblings and 23 181 controls with 42 753 siblings were included in the analyses conducted using generalized estimating equations.

44.2% of the cases and 22.2% of the controls had at least one sibling diagnosed with any psychiatric or neurodevelopmental disorder (risk ratio, RR = 2.1; 95% CI 2.0–2.2). The strongest associations were demonstrated for childhood-onset disorders including ADHD (RR = 5.7; 95% CI 5.1–6.3), conduct and oppositional disorders (RR = 4.0; 95% CI 3.5–4.5), autism spectrum disorders (RR = 3.9; 95% CI 3.3–4.6), other emotional and social interaction disorders (RR = 2.7; 95% CI 2.4–3.1), learning and coordination disorders (RR = 2.6; 95% CI 2.4–2.8), and intellectual disability (RR = 2.4; 95% CI 2.0–2.8). Also, bipolar disorder, unipolar mood disorders, schizophrenia spectrum disorders, other neurotic and personality disorders, substance abuse disorders, and anxiety disorders occurred at increased frequency among the siblings of cases.

The results offer potential utility for early identification of neurodevelopmental and psychiatric disorders in at-risk siblings of ADHD probands and also argue for more studies on common etiologies.

Posttraumatic stress disorder (PTSD) and stress/trauma exposure are cross-sectionally associated with advanced DNA methylation age relative to chronological age. However, longitudinal inquiry and examination of associations between advanced DNA methylation age and a broader range of psychiatric disorders is lacking. The aim of this study was to examine if PTSD, depression, generalized anxiety, and alcohol-use disorders predicted acceleration of DNA methylation age over time (i.e. an increasing pace, or rate of advancement, of the epigenetic clock).

Genome-wide DNA methylation and a comprehensive set of psychiatric symptoms and diagnoses were assessed in 179 Iraq/Afghanistan war veterans who completed two assessments over the course of approximately 2 years. Two DNA methylation age indices (Horvath and Hannum), each a weighted index of an array of genome-wide DNA methylation probes, were quantified. The pace of the epigenetic clock was operationalized as change in DNA methylation age as a function of time between assessments.

Analyses revealed that alcohol-use disorders (p = 0.001) and PTSD avoidance and numbing symptoms (p = 0.02) at Time 1 were associated with an increasing pace of the epigenetic clock over time, per the Horvath (but not the Hannum) index of cellular aging.

This is the first study to suggest that posttraumatic psychopathology is longitudinally associated with a quickened pace of the epigenetic clock. Results raise the possibility that accelerated cellular aging is a common biological consequence of stress-related psychopathology, which carries implications for identifying mechanisms of stress-related cellular aging and developing interventions to slow its pace.

Previous research has shown prospectively that religiosity/spirituality protects against depression, but these findings are commonly critiqued on two grounds, namely: (1) apparent religiosity/spirituality reflects merely an original absence of depression or elevated mood and (2) religiosity/spirituality too often is measured as a global construct. The current study investigates the relationship between depression and religiosity/spirituality by examining its multidimensional structural integrity.

Confirmatory factor analyses with a previously observed cross-cultural factor structure of religiosity/spirituality variables were conducted on an independent sample, diagnostic and familial risk subgroups from this sample, and a subsample of the original cross-cultural sample. Linear regressions onto a previous diagnosis of major depressive disorder (MDD) 5 years prior to assess the potential attenuating impact of a previous depression was explored.

Across familial risk groups and clinical subgroups, each of the previously validated religiosity/spirituality domains was confirmed, namely: religious/spiritual commitment, contemplative practice, sense of interconnectedness, the experience of love, and altruistic engagement. Previous MDD diagnosis was associated with a lower religious/spiritual commitment among high-risk individuals, higher contemplation among low-risk individuals, and lower importance of religion or spirituality regardless of risk group.

Structural integrity was found across familial risk groups and diagnostic history for a multidimensional structure of religiosity/spirituality. Differential associations between a previous diagnosis of MDD and level of religiosity/spirituality across domains suggest a complex and interactive relation between depression, familial risk, and religiosity/spirituality. Accounting for an empirically valid, multidimensional understanding of religiosity/spirituality may advance research on mechanisms underlying the relationship between religiosity/spirituality and mental health.