Mindfulness meditation has become a common method for reducing stress, stress-related psychopathology and some physical symptoms. As mindfulness programs become ubiquitous, concerns have been raised about their unknown potential for harm. We estimate multiple indices of harm following Mindfulness-Based Stress Reduction (MBSR) on two primary outcomes: global psychological and physical symptoms. In secondary analyses, we estimate multiple indices of harm on anxiety and depressive symptoms, discomfort in interpersonal relations, paranoid ideation and psychoticism.

Intent-to-treat analyses with multiple imputations for missing data were used on pre- and post-test data from a large, observational dataset (n = 2155) of community health clinic MBSR classes and from MBSR (n = 156) and waitlist control (n = 118) participants from three randomized controlled trials conducted contemporaneous to community classes in the same city by the same health clinic MBSR teachers. We estimate the change in symptoms, proportion of participants with increased symptoms, proportion of participants reporting greater than a 35% increase in symptoms, and for global psychological symptoms, clinically significant harm.

We find no evidence that MBSR leads to higher rates of harm relative to waitlist control on any primary or secondary outcome. On many indices of harm across multiple outcomes, community MBSR was significantly preventative of harm.

Engagement in MBSR is not predictive of increased rates of harm relative to no treatment. Rather, MBSR may be protective against multiple indices of harm. Research characterizing the relatively small proportion of MBSR participants that experience harm remains important.

Mismatch negativity (MMN) is an event-related potential (ERP) component reflecting auditory predictive coding. Repeated standard tones evoke increasing positivity (‘repetition positivity’; RP), reflecting strengthening of the standard's memory trace and the prediction it will recur. Likewise, deviant tones preceded by more standard repetitions evoke greater negativity (‘deviant negativity’; DN), reflecting stronger prediction error signaling. These memory trace effects are also evident in MMN difference wave. Here, we assess group differences and test-retest reliability of these indices in schizophrenia patients (SZ) and healthy controls (HC).

Electroencephalography was recorded twice, 2 weeks apart, from 43 SZ and 30 HC, during a roving standard paradigm. We examined ERPs to the third, eighth, and 33rd standards (RP), immediately subsequent deviants (DN), and the corresponding MMN. Memory trace effects were assessed by comparing amplitudes associated with the three standard repetition trains.

Compared with controls, SZ showed reduced MMNs and DNs, but normal RPs. Both groups showed memory trace effects for RP, MMN, and DN, with a trend for attenuated DNs in SZ. Intraclass correlations obtained via this paradigm indicated good-to-moderate reliabilities for overall MMN, DN and RP, but moderate to poor reliabilities for components associated with short, intermediate, and long standard trains, and poor reliability of their memory trace effects.

MMN deficits in SZ reflected attenuated prediction error signaling (DN), with relatively intact predictive code formation (RP) and memory trace effects. This roving standard MMN paradigm requires additional development/validation to obtain suitable levels of reliability for use in clinical trials.

The GluN2B subunit of N-methyl-d-aspartate receptors is crucially involved in the physiology of the prefrontal cortex during working memory (WM). Consistently, genetic variants in the GluN2B coding gene (GRIN2B) have been associated with cognitive phenotypes. However, it is unclear how GRIN2B genetic variation affects gene expression and prefrontal cognitive processing. Using a composite score, we tested the combined effect of GRIN2B variants on prefrontal activity during WM performance in healthy subjects.

We computed a composite score to combine the effects of single nucleotide polymorphisms on post-mortem prefrontal GRIN2B mRNA expression. We then computed the composite score in independent samples of healthy participants in a peripheral blood expression study (n = 46), in a WM behavioural study (n = 116) and in a WM functional magnetic resonance imaging study (n = 122).

Five polymorphisms were associated with GRIN2B expression: rs2160517, rs219931, rs11055792, rs17833967 and rs12814951 (all corrected p < 0.05). The score computed to account for their combined effect reliably indexed gene expression. GRIN2B composite score correlated negatively with intelligence quotient, WM behavioural efficiency and dorsolateral prefrontal cortex activity. Moreover, there was a non-linear association between GRIN2B genetic score and prefrontal activity, i.e. both high and low putative genetic score levels were associated with high blood oxygen level-dependent signals in the prefrontal cortex.

Multiple genetic variants in GRIN2B are jointly associated with gene expression, prefrontal function and behaviour during WM. These results support the role of GRIN2B genetic variants in WM prefrontal activity in human adults.

Common mental disorders (CMD) cause large suffering and high societal costs. Cognitive behavioural therapy (CBT) can effectively treat CMD, but access to treatment is insufficient. Guided self-help (GSH) CBT, has shown effects comparable with face-to-face CBT. However, not all patients respond to GSH, and stepping up non-responders to face-to-face CBT, could yield larger response rates. The aim was to test a stepped care model for CMD in primary care by first evaluating the effects of GSH-CBT and secondly, for non-responders, evaluating the additional effect of face-to-face CBT.

Consecutive patients (N = 396) with a principal disorder of depression, anxiety, insomnia, adjustment or exhaustion disorder were included. In Step I, all patients received GSH-CBT. In Step II, non-responders were randomized to face-to-face CBT or continued GSH. The primary outcome was remission status, defined as a score below a pre-established cutoff on a validated disorder-specific scale.

After GSH-CBT in Step I, 40% of patients were in remission. After Step II, 39% of patients following face-to-face CBT were in remission compared with 19% of patients after continued GSH (p = 0.004). Using this stepped care model required less than six therapy sessions per patient and led to an overall remission rate of 63%.

Stepped care can be effective and resource-efficient to treat CMD in primary care, leading to high remission rates with limited therapist resources. Face-to-face CBT speeded up recovery compared with continued GSH. At follow-ups after 6 and 12 months, remission rates were similar in the two groups.

The cognitive and academic outcomes of infants exposed to radiation after the meltdown at Chornobyl have been intensely debated. Western-based investigations indicate that no adverse effects occurred, but local studies reported increased cognitive impairments in exposed compared with non-exposed children. Our initial study found that at age 11 years, school grades and neuropsychological performance were similar in 300 children evacuated to Kiev as infants or in utero compared with 300 classmate controls, yet more evacuee mothers believed that their children had memory problems. This study re-examined the children's performance and academic achievement at age 19 years.

In 2005–2006, we conducted an 8-year follow-up of the evacuees (n=265) and classmate controls (n=261) assessed in Kiev in 1997. Outcomes included university attendance, tests of intelligence, attention, and memory, and subjective appraisals of memory problems. Scores were standardized using a local population-based control group (n=327). Analyses were stratified by parental education.

Evacuees and classmates performed similarly and in the normal range on all tests, and no differential temporal changes were found. The results were comparable for the in utero subsample. The rates of university attendance and self-reported memory problems were also similar. Nevertheless, the evacuee mothers were almost three times as likely to report that their children had memory problems compared with controls.

Chornobyl did not influence the cognitive functioning of exposed infants although more evacuee mothers still believed that their offspring had memory problems. These lingering worries reflect a wider picture of persistent health concerns as a consequence of the accident.

Neurocognitive deficits are important aspects of the schizophrenic disorders because they have a strong impact on social and vocational outcomes. We expanded on previous research by focusing on the neurocognitive profiles of persons at high risk (HR) or ultra-high risk (UHR) for schizophrenic and affective psychoses. Our main aim was to determine whether neurocognitive measures are sufficiently sensitive to predict a group affiliation based on deficits in functional domains.

This study included 207 help-seeking individuals identified as HR (n = 75), UHR (n = 102) or at high risk for bipolar disorder (HRBip; n = 30), who were compared with persons comprising a matched, healthy control group (CG; n = 50). Neuropsychological variables were sorted according to their load in a factor analysis and were compared among groups. In addition, the likelihood of group membership was estimated using logistic regression analyses.

The performance of HR and HRBip participants was comparable, and intermediate between the controls and UHR. The domain of processing speed was most sensitive in discriminating HR and UHR [odds ratio (OR) 0.48, 95% confidence interval (CI) 0.28–0.78, p = 0.004] whereas learning and memory deficits predicted a conversion to schizophrenic psychosis (OR 0.47, 95% CI 0.25–0.87, p = 0.01).

Performances on neurocognitive tests differed among our three at-risk groups and may therefore be useful in predicting psychosis. Overall, cognition had a profound effect on the extent of general functioning and satisfaction with life for subjects at risk of psychosis. Thus, this factor should become a treatment target in itself.

The dopamine transporter gene (DAT1) and visual memory deficits have been consistently reported to be associated with attention-deficit/hyperactivity disorder (ADHD). This study aimed to examine whether a DAT1 haplotype affected functional and structural brain alterations in children with ADHD and whether those alterations were associated with visual memory.

We recruited a total of 37 drug-naïve children with ADHD (17 with the DAT1 rs27048 (C)/rs429699 (T) haplotype and 20 without the CT haplotype) and 37 typically developing children (17 with the CT haplotype and 20 without the CT haplotype). Visual memory was assessed by the pattern recognition memory (PRM) and spatial recognition memory (SRM) tasks. We analyzed functional and structural brain architecture with regional homogeneity (ReHo) and gray matter volume (GMV).

The CT haplotype was associated with decreased ReHo in the left superior occipital gyrus, cuneus, and precuneus; and decreased GMV in the left superior occipital gyrus, cuneus, and precuneus, and in the right angular gyrus. Significant interactions of ADHD and the CT haplotype were found in the right postcentral gyrus for ReHo and in the right supplementary motor area for GMV. For the ADHD-CT group, we found negative correlations of total correct responses in PRM and SRM and positive correlations of mean latency of correct responses in PRM with the GMV in the left superior occipital gyrus, cuneus, and precuneus.

Our findings suggest that the DAT1-related GMV alterations in the posterior cortical regions may contribute to visual memory performance in children with ADHD.

The impact of underlying parental psychological vulnerability on the future mental health of offspring is not fully understood. Using a prospective cohort design, we investigated the association between dysfunctional parental personality traits and risks of offspring self-harm, depression and anxiety.

The association between dysfunctional parental personality traits (monotony avoidance, impulsivity, anger, suspicion, and detachment), measured in both mothers and fathers when offspring were age 9 years, and risk of offspring depression, anxiety and self-harm at age 18 years, was investigated in a population-based cohort (ALSPAC) from over 8000 parents and children.

Higher levels of dysfunctional maternal, but not paternal, personality traits were associated with an increased risk of self-harm, depression, and anxiety in offspring. Maternal associations were best explained by the accumulation of dysfunctional traits. Associations were strongest for offspring depression: Offspring of mothers with three or more dysfunctional personality traits were 2.27 (1.45–3.54, p < 0.001) times as likely to be depressed, compared with offspring of mothers with no dysfunctional personality traits, independently of maternal depression and other variables.

The accumulation of dysfunctional maternal personality traits is associated with the risk of self-harm, depression, anxiety in offspring independently of maternal depression and other confounding variables. The absence of associations for equivalent paternal traits makes a genetic explanation for the findings unlikely. Further research is required to elucidate the underlying mechanism. Mothers with high levels of dysfunctional personality traits may benefit from additional support to reduce the risk of adverse psychological outcomes occurring in their offspring.

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.

Disturbances in emotion regulation (ER) are characteristic of both patients with bipolar disorder (BD) and schizophrenia (SZ). We investigated the temporal dynamics of brain activation during cognitive ER in BD and SZ to understand the contribution of temporal characteristics of disturbed ER to their unique and shared symptomatology.

Forty-six participants performed an ER-task (BD, n = 15; SZ, n = 16; controls, n = 15) during functional magnetic resonance imaging, in which they were instructed to use cognitive reappraisal techniques to regulate their emotional responses. Finite impulse response modeling was applied to estimate the temporal dynamics of brain responses during cognitive reappraisal (v. passive attending) of negative pictures. Group, time, and group × time effects were tested using multivariate modeling.

We observed a group × time interaction during ER in the ventrolateral prefrontal cortex (VLPFC), supplementary motor area (SMA) and inferior occipital gyrus. Patients with SZ demonstrated initial hyper-activation of the VLPFC and SMA activation that was not sustained in later regulatory phases. Response profiles in the inferior occipital gyrus in SZ showed abnormal activation in the later phases of regulation. BD-patients showed general blunted responsivity in these regions.

These results suggest that ER-disturbances in SZ are characterized by an inefficient initialization and failure to sustain regulatory control, whereas in BD, a failure to recruit regulatory resources may represent initial deficits in formulating adequate representations of the regulatory needs. This may help to further understand how ER-disturbances give rise to symptomatology of BD and SZ.

Early pubertal timing in girls is associated with elevated risk for dieting and eating pathology. The relative importance of biological versus socio-environmental mechanisms in explaining this association remains unclear. Moreover, these mechanisms may differ between objective measures of pubertal development and girls' subjective perceptions of their own maturation.

The sample comprised 924 sister pairs from the National Longitudinal Study of Adolescent Health. Objective pubertal timing (menarcheal age), girls' perceptions of pubertal status and timing relative to peers, dieting and disordered eating behaviors were assessed during a series of confidential in-home interviews.

Behavioral genetic models indicated that common genetic influences accounted for the association between early menarcheal age and increased risk for dieting in adolescence. In contrast, girls' subjective perceptions of their timing relative to peers were associated with dieting through an environmental pathway. Overall, subjective and objective measures of pubertal timing accounted for 12% of the variance in dieting.

Genetic differences in menarcheal age increase risk for dieting among adolescent girls, while girls' perceptions of their maturation represent an environmentally mediated risk.

Epidemiological studies show a dose–response association between cannabis use and the risk of psychosis. This review aimed to determine whether there are identifiable risk-thresholds between the frequency of cannabis use and psychosis development.

Systematic search of Embase, MEDLINE, PsycINFO, CINAHL, and Web of Science for relevant studies (1 January 2010–26 April 2021). Case–control or cohort studies that investigated the relationship between cannabis use and the risk of psychosis development that reported effect estimates [odds ratios (OR), hazard ratios (HR), risk ratios (RR)] or the raw data to calculate them, with information on the frequency of cannabis consumption were included. Effect estimates were extracted from individual studies and converted to RR. Two-stage dose–response multivariable meta-analytic models were utilized and sensitivity analyses conducted. The Newcastle Ottawa Scale was used to assess the risk of bias of included studies.

Ten original (three cohorts, seven case–control) studies were included, including 7390 participants with an age range of 12–65 years. Random-effect model meta-analyses showed a significant log-linear dose–response association between cannabis use frequency and psychosis development. A restricted cubic-splines model provided the best fit for the data, with the risk of psychosis significantly increasing for weekly or more frequent cannabis use [RR = 1.01, 95% confidence interval (CI) 0.93–1.11 yearly; RR = 1.10, 95% CI 0.97–1.25 monthly; RR = 1.35, 95% CI 1.19–1.52 weekly; RR = 1.76, 95% CI 1.47–2.12 daily]

Individuals using cannabis frequently are at increased risk of psychosis, with no significant risk associated with less frequent use. Public health prevention messages should convey these risk-thresholds, which should be refined through further work.