Although risk for psychosis in velocardiofacial (22q11.2 deletion) syndrome (VCFS) is well established, the cognitive and familial factors that moderate that risk are poorly understood.

A total of 75 youth with VCFS were assessed at three time points, at 3-year intervals. Time 1 (T1) psychiatric risk was assessed with the Behavior Assessment System for Children (BASC). Data reduction of BASC scores yielded avoidance–anxiety and dysregulation factors. Time 2 (T2) neuropsychological and family function and time 3 (T3) prodromal/overt psychosis were assessed. Poisson regression models tested associations between T3 positive prodromal symptoms/overt psychosis and T1 psychiatric risk, T2 cognitive and familial factors, and their interactions.

T1 avoidance–anxiety ratings predicted T3 prodromal/overt psychosis. T2 verbal learning scores moderated this association, such that individuals with low avoidance–anxiety scores and stronger verbal learning skills were the least likely to demonstrate prodromal/overt psychosis at T3. Low scores on a T2 visual vigilance task also predicted T3 prodromal/overt psychosis, independently of the effect of T1 avoidance–anxiety scores. T1 dysregulation scores did not predict T3 prodromal/overt psychosis in a linear manner. Instead, the association between dysregulation and prodromal/overt psychosis was amplified by T2 levels of family organization, such that individuals with low dysregulation scores and low family organization scores were the most likely to exhibit T3 prodromal/overt psychosis.

Significant moderators of psychiatric risk in VCFS include verbal learning skills as well as levels of family organization, carrying implications for early identification and preventative treatment of youth with VCFS at highest risk for psychosis.

Early life stress has been associated with emotional dysregulations and altered architecture of limbic-prefrontal brain systems engaged in emotional processing. Serotonin regulates both, developmental and experience-dependent neuroplasticity in these circuits. Central serotonergic biosynthesis rates are regulated by Tryptophan hydroxylase 2 (TPH2) and transgenic animal models suggest that TPH2-gene associated differences in serotonergic signaling mediate the impact of aversive early life experiences on a phenotype characterized by anxious avoidance.

The present study employed an imaging genetics approach that capitalized on individual differences in a TPH2 polymorphism (703G/T; rs4570625) to determine whether differences in serotonergic signaling modulate the effects of early life stress on brain structure and function and punishment sensitivity in humans (n = 252).

Higher maltreatment exposure before the age of 16 was associated with increased gray matter volumes in a circuitry spanning thalamic-limbic-prefrontal regions and decreased intrinsic communication in limbic-prefrontal circuits selectively in TT carriers. In an independent replication sample, associations between higher early life stress and increased frontal volumes in TT carriers were confirmed. On the phenotype level, the genotype moderated the association between higher early life stress exposure and higher punishment sensitivity. In TT carriers, the association between higher early life stress exposure and punishment sensitivity was critically mediated by increased thalamic-limbic-prefrontal volumes.

The present findings suggest that early life stress shapes the neural organization of the limbic-prefrontal circuits in interaction with individual variations in the TPH2 gene to promote a phenotype characterized by facilitated threat avoidance, thus promoting early adaptation to an adverse environment.

Maternal smoking has consistently been associated with multiple adverse childhood outcomes including externalizing disorders. In contrast the association between maternal smoking during pregnancy (MSDP) and internalizing (anxiety and depressive) disorders in offspring has received less investigation.

We conducted a nationwide cohort study including 957635 individuals born in Denmark between 1991 and 2007. Data on MSDP and diagnoses of depression or anxiety disorders were derived from national registers and patients were followed up from the age of 5 years to the end of 2012. Hazard rate ratios (HRRs) were estimated using stratified Cox regression models. Sibling data were used to disentangle individual- and familial-level effects of MSDP and to control for unmeasured familial confounding.

At the population level, offspring exposed to MSDP were at increased risk for both severe depression [HRR 1.29, 95% confidence interval (CI) 1.22–1.36] and severe anxiety disorders (HRR 1.26, 95% CI 1.20–1.32) even when controlling for maternal and paternal traits. However, there was no association between MSDP and internalizing disorders when controlling for the mother's propensity for MSDP (depression: HRR 1.11, 95% CI 0.94–1.30; anxiety disorders: HRR 0.94, 95% CI 0.80–1.11) or comparing differentially exposed siblings (depression: HRR 1.18, 95% CI 0.75–1.89; anxiety disorders: HRR 0.87, 95% CI 0.55–1.36).

The results suggest that familial background factors account for the association between MSDP and severe internalizing disorders not the specific exposure to MSDP.

Few studies have examined the course of illness among severely depressed patients ascertained at first hospitalization. Using data from the Suffolk County Mental Health Project (SCMHP), we investigated the times to and predictors of the first full remission and the first relapse during a 4-year period in a first-admission cohort with major depressive disorder (MDD) with psychotic features.

The cohort included 87 county-wide, first-admission patients with a longitudinal consensus diagnosis of MDD with psychotic features who were systematically followed over a 4-year period. We examined the associations of background, clinical and treatment factors, and time-varying indices of antidepressant (AD) and antipsychotic (AP) medication use to time to remission and relapse using Cox regression.

By the 4-year follow-up, 60 respondents (69·0%) had achieved a period of full remission (median time of 22 weeks among remitters and 54 weeks in the full sample). In the multivariable analysis, longer time to remission was associated with longer latency between initial episode and hospitalization, lower pre-hospital Global Assessment of Functioning (GAF) score, and lack of insurance, but not use of medication. Twenty-six remitters (43·3%) relapsed (median time of 50 weeks among those who relapsed and 192 weeks among all remitters). None of the risk factors or time-varying medication variables was significantly associated with time to relapse.

Only two-thirds of the sample had at least one full remission by 4 years, and almost half of them subsequently relapsed. Poorer pre-hospital resources predicted remission but not relapse. Medication use over the follow-up was not associated with remission or relapse.

While the media may significantly influence public attitudes and government policies affecting the research agenda, how mental health research is reported in the media has been virtually unstudied. The aim of this study was to examine stories concerning mental health research published on the British Broadcasting Corporation (BBC) website between 1999 and 2008 and in New Scientist between 2008 and 2010.

Stories were retrieved from on-line archives. Story content was coded and assessed against: ‘disease burden’ of mental disorders; the general corpus of research papers in mental health and the countries from which they originated; the journals in which cited papers were published; and funding sources.

A total of 1015 BBC stories reporting mental health research and 133 New Scientist stories were found. The distribution of stories did not reflect ‘disease burden’; research on dementia was over-represented, while depression and alcohol were under-represented. There was an emphasis on biological research while stories on psychological interventions were rare. UK research was over-represented. Research funded by government and private non-profit sources was over-represented. Commentators from Alzheimer's Disease charities were prominent.

Consideration of reported stories may suggest approaches to working with the media to improve the public understanding of, and support for, mental health research. The role of commentators may be especially important.

Functional impairment is a defining feature of psychotic disorders. A range of factors has been shown to influence functioning, including negative symptoms, cognitive performance and cognitive reserve (CR). However, it is not clear how these variables may affect functioning in first-episode psychosis (FEP) patients. This 2-year follow-up study aimed to explore the possible mediating effects of CR on the relationship between cognitive performance or specific clinical symptoms and functional outcome.

A prospective study of non-affective FEP patients was performed (211 at baseline and 139 at follow-up). CR was entered in a path analysis model as potential mediators between cognitive domains or clinical symptoms and functioning.

At baseline, the relationship between clinical variables or cognitive performance and functioning was not mediated by CR. At follow-up, the effect of attention (p = 0.003) and negative symptoms (p = 0.012) assessed at baseline on functioning was partially mediated by CR (p = 0.032 and 0.016), whereas the relationship between verbal memory (p = 0.057) and functioning was mediated by CR (p = 0.014). Verbal memory and positive and total subscales of PANSS assessed at follow-up were partially mediated by CR and the effect of working memory on functioning was totally mediated by CR.

Our results showed the influence of CR in mediating the relationship between cognitive domains or clinical symptoms and functioning in FEP. In particular, CR partially mediated the relationship between some cognitive domains or clinical symptoms and functioning at follow-up. Therefore, CR could improve our understanding of the long-term functioning of patients with a non-affective FEP.

Depression and anxiety are prevalent in youth populations and typically emerge during adolescence. Repetitive negative thinking (RNT) is a putative transdiagnostic mechanism with consistent associations with depression and anxiety. Targeting transdiagnostic processes like RNT for youth depression and anxiety may offer more targeted, personalised and effective treatment.

A meta-analysis was conducted to examine the effect of psychological treatments on RNT, depression and anxiety symptoms in young people with depression or anxiety, and a meta-regression to examine relationships between outcomes.

Twenty-eight randomised controlled trials examining 17 different psychological interventions were included. Effect sizes were small to moderate across all outcomes (Hedge's g depression = −0.47, CI −0.77 to −0.17; anxiety = −0.42, CI −0.65 to −0.20; RNT = −0.45, CI −0.67 to −0.23). RNT-focused and non-RNT focused approaches had comparable effects; however, those focusing on modifying the process of RNT had significantly larger effects on RNT than those focusing on modifying negative thought content. Meta-regression revealed a significant relationship between RNT and depression outcomes only across all intervention types and with both depression and anxiety for RNT focused interventions only.

Consistent with findings in adults, this review provides evidence that reducing RNT with psychological treatment is associated with improvements in depression and anxiety in youth. Targeting RNT specifically may not lead to better outcomes compared to general approaches; however, focusing on modifying the process of RNT may be more effective than targeting content. Further research is needed to determine causal pathways.

Depression is a common and serious mental illness that begins early in life. An association between cardiovascular disease (CVD) and subsequent depression is clear in adults. We examined associations between individual CVD risk factors and depression in young people.

We searched MEDLINE, EMBASE, and PsycINFO databases from inception to 1 January 2020. We extracted data from cohort studies assessing the longitudinal association between CVD risk factors [body mass index (BMI), smoking, systolic blood pressure (SBP), total cholesterol, high-density lipoprotein] and depression, measured using a validated tool in individuals with mean age of 24 years or younger. Random effect meta-analysis was used to combine effect estimates from individual studies, including odds ratio (OR) for depression and standardised mean difference for depressive symptoms.

Based on meta-analysis of seven studies, comprising 15 753 participants, high BMI was associated with subsequent depression [pooled OR 1.61; 95% confidence interval (CI) 1.21–2.14; I2 = 31%]. Based on meta-analysis of eight studies, comprising 30 539 participants, smoking was associated with subsequent depression (pooled OR 1.73; 95% CI 1.36–2.20; I2 = 74%). Low, but not high, SBP was associated with an increased risk of depression (pooled OR 3.32; 95% CI 1.68–6.55; I2 = 0%), although this was based on a small pooled high-risk sample of 893 participants. Generalisability may be limited as most studies were based in North America or Europe.

Targeting childhood/adolescent smoking and obesity may be important for the prevention of both CVD and depression across the lifespan. Further research on other CVD risk factors including blood pressure and cholesterol in young people is required.

Both low intelligence and low emotional control have previously been linked to a higher risk of suicide, but it is unknown whether the associations apply consistently over the life course.

The study was based on data on intelligence and emotional control, collected from 48 738 Swedish men conscripted in 1969–1970, at ages 18–20 years. The data were linked to national registers giving information on subsequent suicidal behavior (completed and attempted suicide) up to the age of 59 years. The associations were investigated using logistic regression and Cox proportional hazards regression models, with adjustment for childhood socioeconomic status.

Intelligence and emotional control assessed in late adolescence both showed robust inverse associations with suicidal behavior over the 38-year follow-up. However, while the association between lower intelligence and higher rate of suicidal behavior remained the same throughout (~40% increased hazard per unit on a five-level scale), the association between lower emotional control and suicidal behavior was substantially stronger in early adulthood (~100% increased hazard per unit) than in late middle age (~30% increased hazard per unit).

The study adds to previous research by showing that the association between poor emotional control and subsequent suicide risk in men becomes weaker over the life course, while the association between low intelligence and suicide risk seems to be constant. The particularly high suicide risk of young men with poor emotional control may motivate targeted prevention efforts.

Alcohol use disorder (AUD) is associated with cognitive deficits but little is known to what degree this is caused by genetically influenced traits, i.e. endophenotypes, present before the onset of the disorder. The aim of the current study was to investigate to what degree family history (FH) of AUD is associated with cognitive functions.

Case-control cross-sectional study at an outpatient addiction research clinic. Treatment-seeking AUD patients (n = 106) were compared to healthy controls (HC; n = 90), matched for age and sex. The HC group was further subdivided into AUD FH positive (FH+; n = 47) or negative (FH−; n = 39) based on the Family Tree Questionnaire. Participants underwent psychiatric and substance use assessments, completed the Barratt Impulsiveness Scale and performed a comprehensive battery of neuropsychological tests assessing response inhibition, decision making, attention, working memory, and emotional recognition.

Compared to HC, AUD patients exhibited elevated self-rated impulsivity (p < 0.001; d = 0.62), as well as significantly poorer response inhibition (p = 0.001; d = 0.51), attention (p = 0.021; d = 0.38) and information gathering in decision making (p = 0.073; d = 0.34). Similar to AUD patients, FH+ individuals exhibited elevated self-rated impulsivity (p = 0.096; d = 0.46), and in addition significantly worse future planning capacity (p < 0.001; d = 0.76) and prolonged emotional recognition response time (p = 0.010; d = 0.60) compared to FH−, while no other significant differences were found between FH+ and FH−.

Elevated impulsivity, poor performance in future planning and emotional processing speed may be potential cognitive endophenotypes in AUD. These cognitive domains represent putative targets for prevention strategies and treatment of AUD.

Pre-menstrual dysphoric disorder (PMDD) is commonly studied in white women; consequently, it is unclear whether the prevalence of PMDD varies by race. Although a substantial proportion of black women report symptoms of PMDD, the Biocultural Model of Women's Health and research on other psychiatric disorders suggest that black women may be less likely than white women to experience PMDD in their lifetimes.

Multivariate multinomial logistic regression modeling was used with a sample of 2590 English-speaking, pre-menopausal American women (aged 18–40 years) who participated in the Collaborative Psychiatric Epidemiology Surveys in 2001–2003. The sample consisted of 1672 black women and 918 white women. The measure of PMDD yields a provisional diagnosis of PMDD consistent with DSM-IV criteria.

Black women were significantly less likely than white women to experience PMDD [odds ratio (OR) 0.44, 95% confidence interval (CI) 0.25–0.79] and pre-menstrual symptoms (OR 0.64, 95% CI 0.47–0.88) in their lifetimes, independently of marital status, employment status, educational attainment, smoking status, body mass index, history of oral contraceptive use, current age, income, history of past-month mood disorder, and a measure of social desirability. The prevalence of PMDD was 2.9% among black women and 4.4% among white women.

This study showed for the first time that black women were less likely than white women to experience PMDD and pre-menstrual symptoms, independently of relevant biological, social-contextual and psychological risk factors. This suggests that PMDD may be an exception to the usual direction of racial disparities in health. Further research is needed to determine the mechanisms that explain this health advantage.

The most common treatment for major depressive disorder (MDD) is antidepressant medication (ADM). Results are reported on frequency of ADM use, reasons for use, and perceived effectiveness of use in general population surveys across 20 countries.

Face-to-face interviews with community samples totaling n = 49 919 respondents in the World Health Organization (WHO) World Mental Health (WMH) Surveys asked about ADM use anytime in the prior 12 months in conjunction with validated fully structured diagnostic interviews. Treatment questions were administered independently of diagnoses and asked of all respondents.

3.1% of respondents reported ADM use within the past 12 months. In high-income countries (HICs), depression (49.2%) and anxiety (36.4%) were the most common reasons for use. In low- and middle-income countries (LMICs), depression (38.4%) and sleep problems (31.9%) were the most common reasons for use. Prevalence of use was 2–4 times as high in HICs as LMICs across all examined diagnoses. Newer ADMs were proportionally used more often in HICs than LMICs. Across all conditions, ADMs were reported as very effective by 58.8% of users and somewhat effective by an additional 28.3% of users, with both proportions higher in LMICs than HICs. Neither ADM class nor reason for use was a significant predictor of perceived effectiveness.

ADMs are in widespread use and for a variety of conditions including but going beyond depression and anxiety. In a general population sample from multiple LMICs and HICs, ADMs were widely perceived to be either very or somewhat effective by the people who use them.