In this study, we examined the relationship between polygenic liability for depression and number of stressful life events (SLEs) as risk factors for early-onset depression treated in inpatient, outpatient or emergency room settings at psychiatric hospitals in Denmark.

Data were drawn from the iPSYCH2012 case-cohort sample, a population-based sample of individuals born in Denmark between 1981 and 2005. The sample included 18 532 individuals who were diagnosed with depression by a psychiatrist by age 31 years, and a comparison group of 20 184 individuals. Information on SLEs was obtained from nationwide registers and operationalized as a time-varying count variable. Hazard ratios and cumulative incidence rates were estimated using Cox regressions.

Risk for depression increased by 35% with each standard deviation increase in polygenic liability (p < 0.0001), and 36% (p < 0.0001) with each additional SLE. There was a small interaction between polygenic liability and SLEs (β = −0.04, p = 0.0009). The probability of being diagnosed with depression in a hospital-based setting between ages 15 and 31 years ranged from 1.5% among males in the lowest quartile of polygenic liability with 0 events by age 15, to 18.8% among females in the highest quartile of polygenic liability with 4+ events by age 15.

These findings suggest that although there is minimal interaction between polygenic liability and SLEs as risk factors for hospital-treated depression, combining information on these two important risk factors could potentially be useful for identifying high-risk individuals.

In a perinatal cohort of women in urban and rural Turkey, we investigated associations between antenatal depressive symptoms and subsequent changes in perceived quality of key family relationships.

Of 730 women recruited in their third trimester (94.6% participation), 578 (79.2%) were reassessed at a mean of 4.1 (s.d. = 3.3) months after childbirth, 488 (66.8%) were reassessed at 13.7 (s.d. = 2.9) months, and 448 (61.4%) at 20.8 (s.d. = 2.7) months. At all four examinations, self-reported quality of relationship with the husband, mother and mother-in-law was ascertained using the Close Persons Questionnaire with respect to emotional support, practical support and negative aspects of the relationship. Antenatal depressive symptoms were defined using the Edinburgh Postnatal Depression Scale. A range of covariates in mixed models was considered including age, education, number of children, family structure, physical health, past emotional problems and stressful life events.

Key findings were as follows: (i) reported emotional and practical support from all three relationships declined over time in the cohort overall; (ii) reported emotional support from the husband, and emotional and practical support from the mother-in-law, declined more strongly in women with antenatal depressive symptoms; (iii) associations between depressive symptoms and worsening spouse relationship were more pronounced in traditional compared with nuclear families.

Antenatal depressive symptoms predicted marked decline in the quality of key relationships over the postnatal period. This may account for some of the contemporaneous associations between depression and worse social support, and may compound the risk of perinatal depression in subsequent pregnancies.

The psychological risk factors of premenstrual dysphoric disorder (PMDD) are not fully understood, but initial evidence points to a potential role of unfavorable cognitive emotion regulation (ER-) strategies. Given the symptom cyclicity of PMDD, ambulatory assessment is ideally suited to capture psychological and physiological processes across the menstrual cycle. Our study examines habitual ER-strategies in women with PMDD and their predictive value for the course of mood and basal cortisol across the cycle in affected women.

Women with and without PMDD (n = 61 each) were compared regarding habitual mindfulness, reappraisal, and repetitive negative thinking (RNT). Momentary affect and cortisol output were assessed over two consecutive days per cycle phase (menstrual, follicular, ovulatory, late luteal).

Women with PMDD reported lower mindfulness, less use of reappraisal and stronger RNT than controls (ps < 0.035). In women with PMDD, higher mindfulness and reappraisal and lower RNT predicted decreased negative and increased positive affect across the menstrual cycle (ps < 0.027). However, women using more favorable ER-strategies displayed stronger mood cyclicity, resulting in stronger mood deterioration in the late luteal phase, thereby resembling women with more unfavorable ER-strategies toward the end of the cycle. Lower mindfulness predicted lower cortisol in the menstrual phase.

Protective ER-strategies seem to be generally linked to better momentary mood in women with PMDD, but do not appear to protect affected women from premenstrual mood deterioration. Habitual mindfulness, in turn, seems to buffer blunted cortisol activity in women with PMDD, especially in the menstrual phase.

Maternal smoking has known adverse effects on fetal development. However, research on the association between maternal smoking during pregnancy and offspring intellectual disability (ID) is limited, and whether any associations are due to a causal effect or residual confounding is unknown.

Cohort study of all Danish births between 1995 and 2012 (1 066 989 persons from 658 335 families after exclusions), with prospectively recorded data for cohort members, parents and siblings. We assessed the association between maternal smoking during pregnancy (18.6% exposed, collected during prenatal visits) and offspring ID (8051 cases, measured using ICD-10 diagnosis codes F70–F79) using logistic generalised estimating equation regression models. Models were adjusted for confounders including measures of socio-economic status and parental psychiatric diagnoses and were adjusted for family averaged exposure between full siblings. Adjustment for a family averaged exposure allows calculation of the within-family effect of smoking on child outcomes which is robust against confounders that are shared between siblings.

We found increased odds of ID among those exposed to maternal smoking in pregnancy after confounder adjustment (OR 1.35, 95% CI 1.28–1.42) which attenuated to a null effect following adjustment for family averaged exposure (OR 0.91, 95% CI 0.78–1.06).

Our findings are inconsistent with a causal effect of maternal smoking during pregnancy on offspring ID risk. By estimating a within-family effect, our results suggest that prior associations were the result of unmeasured genetic or environmental characteristics of families in which the mother smokes during pregnancy.

Multiple predictors have been associated with persistent somatic symptoms. However, previous studies problematically defined the persistence of symptoms, conflated participants' sex and gender, and focused on patient populations. Therefore, we studied associations between predictors, especially sex and gender, and longitudinal patterns of somatic symptoms in the general adult population. We also assessed whether predictors for persisting symptoms differ between sexes.

To identify developmental trajectories of somatic symptoms, assessed by the SCL-90 SOM, we used latent class trajectory modeling in the Dutch Lifelines Cohort Study [N = 150 494; 58.6% female; median time to follow-up: 46.0 (min–max: 22.0–123.0) months]. To identify predictors of trajectories, we applied multiple logistic regression analyses. Predictors were measured by surveys at baseline and a composite gender index was previously developed.

A five-class linear LCGA model fitted the data best: 93.7% of the population had a stable symptom trajectory, whereas 1.5% and 4.8% of the population had a consistently increasing or decreasing symptom trajectory, respectively. Female sex predicted severe, stable symptom severity (OR 1.74, 95% CI 1.36–2.22), but not increasing symptom severity (OR 1.15, 95% CI 0.99–1.40). Femininity was protective hereof (OR 0.60, 95% CI 0.44–0.82 and OR 0.66, 95% CI 0.51–0.85, respectively). Merely a few predictors of symptom severity, for instance hours of paid employment and physical functioning, differed in strength between sexes. Yet, effect sizes were small.

Female sex and femininity predict symptom trajectories. No large sex differences in the strength of additional predictors were found, thus it may not be clinically useful to distinguish between predictors specific to male or female patients of persistent somatic symptoms.

Individuals with depression often experience widespread and persistent cognitive deficits, which might be due to brain atrophy and cerebral small vessel disease (CSVD). We therefore studied the associations between depression, markers of brain atrophy and CSVD, and cognitive functioning.

We used cross-sectional data from the population-based Maastricht study (n = 4734; mean age 59.1 ± 8.6 years, 50.2% women), which focuses on type 2 diabetes. A current episode of major depressive disorder (MDD, n = 151) was assessed by the Mini-International Neuropsychiatric Interview. Volumes of cerebral spinal fluid, white matter, gray matter and white matter hyperintensities, presence of lacunar infarcts and cerebral microbleeds, and total CSVD burden were assessed by 3 T magnetic resonance imaging. Multiple linear and logistic regression analyses tested the associations between MDD, brain markers and cognitive functioning in memory, information processing speed, and executive functioning & attention, and presence of cognitive impairment. Structural equation modeling was used to test mediation.

In fully adjusted models, MDD was associated with lower scores in information processing speed [mean difference = −0.18(−0.28;−0.08)], executive functioning & attention [mean difference = −0.13(−0.25;−0.02)], and with higher odds of cognitive impairment [odds ratio (OR) = 1.60(1.06;2.40)]. MDD was associated with CSVD in participants without type 2 diabetes [OR = 1.65(1.06;2.56)], but CSVD or other markers of brain atrophy or CSVD did not mediate the association with cognitive functioning.

MDD is associated with more impaired information processing speed and executive functioning & attention, and overall cognitive impairment. Furthermore, MDD was associated with CSVD in participants without type 2 diabetes, but this association did not explain an impaired cognitive profile.

There is now a well-established link between childhood adversity (CA) and schizophrenia. Similar structural abnormalities to those found in schizophrenia including alterations in grey-matter volume have also been shown in those who experience CA.

We examined whether global estimates of cortical thickness or surface area were altered in those familial high-risk subjects who had been referred to a social worker or the Children's Panel compared to those who had not.

We found that the cortical surface area of those who were referred to the Children's Panel was significantly smaller than those who had not been referred, but cortical thickness was not significantly altered. There was also an effect of social work referral on cortical surface area but not on thickness.

Cortical surface area increases post-natally more than cortical thickness. Our findings suggest that CA can influence structural changes in the brain and it is likely to have a greater impact on cortical surface area than on cortical thickness.

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder which frequently persists into adulthood. The primary goal of the current study was to (a) investigate attentional functions of stimulant medication-naïve adults with ADHD, and (b) investigate the effects of 6 weeks of methylphenidate treatment on these functions.

The study was a prospective, non-randomized, non-blinded, 6-week follow-up design with 42 stimulant medication-naïve adult patients with ADHD, and 42 age and parental education-matched healthy controls. Assessments included measures of visual attention, based on Bundesen's Theory of Visual Attention (TVA), which yields five precise measures of aspects of visual attention; general psychopathology; ADHD symptoms; dyslexia screening; and estimates of IQ.

At baseline, significant differences were found between patients and controls on three attentional parameters: visual short-term memory capacity, threshold of conscious perception, and to a lesser extent visual processing speed. Secondary analyses revealed no significant correlations between TVA parameter estimates and severity of ADHD symptomatology. At follow-up, significant improvements were found specifically for visual processing speed; this improvement had a large effect size, and remained when controlling for re-test effects, IQ, and dyslexia screen performance. There were no significant correlations between changes in visual processing speed and changes in ADHD symptomatology.

ADHD in adults may be associated with deficits in three distinct aspects of visual attention. Improvements after 6 weeks of medication are seen specifically in visual processing speed, which could represent an improvement in alertness. Clinical symptoms and visual attentional deficits may represent separate aspects of ADHD in adults.

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.