Although quality of life (QoL) is receiving increasing attention in bipolar disorder (BD) research and practice, little is known about its naturalistic trajectory. The dual aims of this study were to prospectively investigate: (a) the trajectory of QoL under guideline-driven treatment and (b) the dynamic relationship between mood symptoms and QoL.

In total, 362 patients with BD receiving guideline-driven treatment were prospectively followed at 3-month intervals for up to 5 years. Mental (Mental Component Score – MCS) and physical (Physical Component Score – PCS) QoL were measured using the self-report SF-36. Clinician-rated symptom data were recorded for mania and depression. Multilevel modelling was used to analyse MCS and PCS over time, QoL trajectories predicted by time-lagged symptoms, and symptom trajectories predicted by time-lagged QoL.

MCS exhibited a positive trajectory, while PCS worsened over time. Investigation of temporal relationships between QoL and symptoms suggested bidirectional effects: earlier depressive symptoms were negatively associated with mental QoL, and earlier manic symptoms were negatively associated with physical QoL. Importantly, earlier MCS and PCS were both negatively associated with downstream symptoms of mania and depression.

The present investigation illustrates real-world outcomes for QoL under guideline-driven BD treatment: improvements in mental QoL and decrements in physical QoL were observed. The data permitted investigation of dynamic interactions between QoL and symptoms, generating novel evidence for bidirectional effects and encouraging further research into this important interplay. Investigation of relevant time-varying covariates (e.g. medications) was beyond scope. Future research should investigate possible determinants of QoL and the interplay between symptoms and wellbeing/satisfaction-centric measures of QoL.

Maternal exposures to fever and infections in pregnancy have been linked to subsequent psychiatric morbidity in the child. This study examined whether fever and common infections in pregnancy were associated with psychosis-like experiences (PLEs) in the child.

A longitudinal study of 46 184 children who participated in the 11-year follow-up of the Danish National Birth Cohort was conducted. Pregnant women were enrolled between 1996 and 2002 and information on fever, genitourinary infections, respiratory tract infection, and influenza-like illness during pregnancy was prospectively collected in two interviews during pregnancy. PLEs were assessed using the seven-item Adolescent Psychotic-Like Symptom Screener in a web-based questionnaire completed by the children themselves at age 11.

PLEs were reported among 11% of the children. Multinomial logistic regression models with probability weights to adjust for potential selection bias due to attrition suggested that maternal fever, genitourinary infections and influenza-like illness were associated with a weak to moderate increased risk of subclinical psychosis-like symptoms in the offspring, whereas respiratory tract infections were not. No clear pattern was observed between the strengths of the associations and the timing of exposure, or the type of psychosis-like symptom.

In this study, maternal exposures to fevers and common infections in pregnancy were generally associated with a subtle excess risk of PLEs in the child. A more pronounced association was found for influenza-like illness under an a priori definition, leaving open the possibility that certain kinds of infections may constitute important risk factors.

Reports of changes in patients’ social behavior during deep brain stimulation (DBS) raised the question whether DBS induces changes in personality. This study explored if (1) DBS is associated with changes in personality in patients suffering from treatment-resistant depression (TRD), (2) how personality dimensions and depression are associated, and (3) if TRD patients’ self-ratings of personality are valid.

TRD patients were assessed before DBS (n = 30), 6 months (t2, n = 21), 2 (t3, n = 17) and 5 years (t4, n = 11) after the initiation of DBS of the supero-lateral branch of the medial forebrain bundle (slMFB-DBS). Personality was measured with the NEO-Five-Factor Inventory (NEO-FFI), depression severity with Hamilton (HDRS), and Montgomery–Åsberg Depression Rating Scale (MADRS).

Personality dimensions did not change with slMFB-DBS compared with baseline. Extraversion was negatively correlated with HDRS28 (r = −0.48, p < 0.05) and MADRS (r = −0.45, p < 0.05) at t2. Inter-rater reliability was high for the NEO-FFI at baseline (Cronbach's α = 0.74) and at t4 (α = 0.65). Extraversion [t(29) = −5.20; p < 0.001] and openness to experience [t(29) = −6.96; p < 0.001] differed statistically significant from the normative sample, and did not predict the antidepressant response.

slMFB-DBS was not associated with a change in personality. The severity of depression was associated with extraversion. Personality of TRD patients differed from the healthy population and did not change with response, indicating a possible scar effect. Self-ratings of personality seem valid to assess personality during TRD.

Associations between parenting and child outcomes are often interpreted as reflecting causal, social influences. However, such associations may be confounded by genes common to children and their biological parents. To the extent that these shared genes influence behaviours in both generations, a passive genetic mechanism may explain links between them. Here we aim to quantify the relative importance of passive genetic v. social mechanisms in the intergenerational association between parent–offspring relationship quality and offspring internalizing problems in adolescence.

We used a Children-of-Twins (CoT) design with data from the parent-based Twin and Offspring Study of Sweden (TOSS) sample [909 adult twin pairs and their offspring; offspring mean age 15.75 (2.42) years], and the child-based Swedish Twin Study of CHild and Adolescent Development (TCHAD) sample [1120 adolescent twin pairs; mean age 13.67 (0.47) years]. A composite of parent-report measures (closeness, conflict, disagreements, expressions of affection) indexed parent–offspring relationship quality in TOSS, and offspring self-reported internalizing symptoms were assessed using the Child Behavior Checklist (CBCL) in both samples.

A social transmission mechanism explained the intergenerational association [r = 0.21 (0.16–0.25)] in our best-fitting model. A passive genetic transmission pathway was not found to be significant, indicating that parental genetic influences on parent–offspring relationship quality and offspring genetic influences on their internalizing problems were non-overlapping.

These results indicate that this intergenerational association is a product of social interactions between children and parents, within which bidirectional effects are highly plausible. Results from genetically informative studies of parenting-related effects should be used to help refine early parenting interventions aimed at reducing risk for psychopathology.

Many preschool-age children meet criteria for psychiatric disorders, and rates approach those observed in later childhood and adolescence. However, there is a paucity of longitudinal research examining the outcomes of preschool diagnoses.

Families with a 3-year-old child (N = 559) were recruited from the community. Primary caregivers were interviewed using the Preschool Age Psychiatric Assessment when children were 3 years old (n = 541), and, along with children, using the Schedule for Affective Disorders and Schizophrenia for School-Age Children Present and Lifetime Version when children were 9 and 12 years old.

Rates of disruptive behavior disorders (DBD) decreased from preschool to middle childhood and early adolescence, whereas rates of attention-deficit/hyperactivity disorder (ADHD) increased. Rates of any psychiatric disorder and depression increased from preschool to early adolescence only. Preschoolers with a diagnosis were over twice as likely to have a diagnosis during later periods. Homotypic continuity was present for anxiety disorders from preschool to middle childhood, for ADHD from preschool to early adolescence, and for DBD through both later time points. There was heterotypic continuity between preschool anxiety and early adolescent depression, and between preschool ADHD and early adolescent DBD. Dimensional symptom scores showed homotypic continuity for all diagnostic categories and showed a number of heterotypic associations as well.

Results provide moderate support for the predictive validity of psychiatric disorders in preschoolers. Psychopathology in preschool is a significant risk factor for future psychiatric disorders during middle childhood and early adolescence.

Using a longitudinal twin design and a latent growth curve/autoregressive approach, this study examined the genetic–environmental architecture of substance use across adolescence.

Self-reports of substance use (i.e. alcohol, marijuana) were collected at ages 13, 14, 15, and 17 years from 476 twin pairs (475 boys, 477 girls) living in the Province of Quebec, Canada. Substance use increased linearly across the adolescent years.

ACE modeling revealed that genetic, as well as shared and non-shared environmental factors explained the overall level of substance use and that these same factors also partly accounted for growth in substance use from age 13 to 17. Additional genetic factors predicted the growth in substance use. Finally, autoregressive effects revealed age-specific non-shared environmental influences and, to a lesser degree, age-specific genetic influences, which together accounted for the stability of substance use across adolescence.

The results support and expand the notion that genetic and environmental influences on substance use during adolescence are both developmentally stable and developmentally dynamic.

Being breastfed in infancy has been shown to benefit neurodevelopment. However, whether the benefits persist to old age remains unclear.

We examined the associations between breastfeeding and its duration on cognitive ability in young adulthood and old age, and on aging-related cognitive change over five decades. In total, 931 men from the Helsinki Birth Cohort Study born in 1934–1944 in Finland took the Finnish Defence Forces Basic Intellectual Ability Test (total and verbal, arithmetic and visuospatial subtest scores) twice, at ages 20.2 and 67.9 years, and had data on breastfeeding (yes v. no) and its duration (‘never breastfed’, ‘up to 3’, ‘3 to 6’ and ‘6 or more months’). Linear and mixed model regressions tested the associations.

At 20.2 years, breastfed men had higher cognitive ability total and visuospatial subtest scores [mean differences (MDs) ranged between 3.0–3.9, p values < 0.013], and its longer duration predicted higher cognitive ability total and arithmetic and visuospatial subtest scores (MDs ranged between 3.0 and 4.8, p values < 0.039). At 67.9 years, breastfed men had higher total cognitive ability and all subtest scores (MDs ranged between 2.6 and 3.4, p values < 0.044) and its longer duration predicted all cognitive ability scores (MDs ranged between 3.1 and 4.7, p values < 0.050). Verbal subtest scores decreased over five decades in men who were never breastfed or were breastfed for 3 months or less, and increased in those breastfed for longer than 3 months.

Neurodevelopmental advantages of breastfeeding and its longer duration persist into old age, and longer duration of breastfeeding may benefit aging-related change, particularly in verbal reasoning ability.

The prevalence and severity of neurocognitive dysfunctioning of patients with somatic symptom and related disorders (SSRD) is unknown. Furthermore, the influence of comorbid depression and anxiety has not been evaluated. This study examines neurocognitive dysfunctioning of patients with SSRD and explores if comorbid depression and anxiety is associated with specific neurocognitive dysfunctioning.

Cross-sectional study with consecutive patients suffering from SSRD visiting an outpatient specialty mental health care Centre of Excellence for SSRD. Extensive neuropsychological assessment and assessment of depression and anxiety symptom levels using the Patient-Health-Questionnaire-9 and General Anxiety Disorder questionnaire-7 were performed at intake. Multivariate analysis was performed.

The study sample consisted of 201 SSRD patients, with a mean age of 43 years (Standard deviation = 13) years; 37.8% were male. Neurocognitive dysfunction in the domains information processing speed, sustained and divided attention, working memory, verbal and visual memory were reported, compared with normative data. Comorbid depression and anxiety occurred frequently within the sample (75.1% and 65.7%, respectively). Neurocognitive dysfunctioning was worse in patients suffering from comorbid depression [multivariate F (7,161) = 2.839, p = 0.008] but not in patients with comorbid anxiety.

Poor neurocognitive performance of patients with SSRD is common and worsens in case of comorbid depression. This may explain treatment dropout of patients with SSRD from neurocognitive behavioral therapy. Research on novel interventions is needed targeting neurocognitive functioning of patients with SSRD, particularly those with comorbid depression.

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.

Access to transition-related medical interventions (TRMIs) for transgender veterans has been the subject of substantial public interest and debate. To better inform these important conversations, the current study investigated whether undergoing hormone or surgical transition intervention(s) relates to the frequency of recent suicidal ideation (SI) and symptoms of depression in transgender veterans.

This study included a cross-sectional, national sample of 206 self-identified transgender veterans. They self-reported basic demographics, TRMI history, recent SI, and symptoms of depression through an online survey.

Significantly lower levels of SI experienced in the past year and 2-weeks were seen in veterans with a history of both hormone intervention and surgery on both the chest and genitals in comparison with those who endorsed a history of no medical intervention, history of hormone therapy but no surgical intervention, and those with a history of hormone therapy and surgery on either (but not both) the chest or genitals when controlling for sample demographics (e.g., gender identity and annual income). Indirect effect analyses indicated that lower depressive symptoms experienced in the last 2-weeks mediated the relationship between the history of surgery on both chest and genitals and SI in the last 2-weeks.

Results indicate the potential protective effect that TRMI may have on symptoms of depression and SI in transgender veterans, particularly when both genitals and chest are affirmed with one's gender identity. Implications for policymakers, providers, and researchers are discussed.

Research has long noted higher prevalence rates of suicidal thoughts and behaviors among individuals with psychotic symptoms. Major theories have proposed several explanations to account for this association. Given the differences in the literature regarding the operationalization of psychosis and sample characteristics, a quantitative review is needed to determine to what extent and how psychosis confers risk for suicidality.

We searched PsycInfo, PubMed, and GoogleScholar for studies published before 1 January 2016. To be included in the analysis, studies must have used at least one psychosis-related factor to longitudinally predict suicide ideation, attempt, or death. The initial search yielded 2541 studies. Fifty studies were retained for analysis, yielding 128 statistical tests.

Suicide death was the most commonly studied outcome (43.0%), followed by attempt (39.1%) and ideation (18.0%). The median follow-up length was 7.5 years. Overall, psychosis significantly conferred risk across three outcomes, with weighted mean ORs of 1.70 (1.39–2.08) for ideation, 1.36 (1.25–1.48) for attempt, and 1.40 (1.14–1.72) for death. Detailed analyses indicated that positive symptoms consistently conferred risk across outcomes; negative symptoms were not significantly associated with ideation, and were protective against death. Some small moderator effects were detected for sample characteristics.

Psychosis is a significant risk factor for suicide ideation, attempt, and death. The finding that positive symptoms increased suicide risk and negative symptoms seemed to decrease risk sheds light on the potential mechanisms for the association between psychosis and suicidality. We note several limitations of the literature and offer suggestions for future directions.

Individual differences in neuroticism, extraversion, and conscientiousness are associated with, and may predict onset of, internalizing disorders. These general traits can be parsed into facets, but there is a surprising paucity of research on facet risk for internalizing disorders. We examined general traits and facets of neuroticism, extraversion, and conscientiousness in predicting first onsets of depressive and anxiety disorders.

A community sample of 550 adolescent females completed general and facet-level personality measures and diagnostic interviews. Interviews were re-administered 18 months later.

First onsets of depressive disorders were predicted by neuroticism, extraversion, and conscientiousness. Facets predicting first onset of depression included depressivity (neuroticism facet) and lower positive emotionality and sociability (extraversion facets). First onsets of generalized anxiety disorder (GAD) were predicted by neuroticism, and particularly the facet of anxiousness. First onsets of social phobia were predicted at the facet level by anxiousness. First onsets of specific phobia were predicted by neuroticism, low conscientiousness, and all neuroticism facets. In multivariate analyses, first onsets of depression were uniquely predicted by depressivity, and onsets of GAD and social phobia were uniquely predicted by anxiousness over and above the general trait of neuroticism.

General traits predict first onsets of depressive and anxiety disorders. In addition, more specific associations are evident at the facet level. Facets can refine our understanding of the links between personality and psychopathology risk, and provide finer-grained targets for personality-informed interventions.

Guidelines about post-traumatic stress disorder (PTSD) recommend broad categories of drugs, but uncertainty remains about what pharmacological treatment to select among all available compounds.

Cochrane Central Register of Controlled Trials register, MEDLINE, PsycINFO, National PTSD Center Pilots database, PubMed, trial registries, and databases of pharmaceutical companies were searched until February 2016 for double-blind randomised trials comparing any pharmacological intervention or placebo as oral therapy in adults with PTSD. Initially, we performed standard pairwise meta-analyses using a random effects model. We then carried out a network meta-analysis. The main outcome measures were mean change on a standardised scale and all-cause dropout rate. Acute treatment was defined as 8-week follow up.

Desipramine, fluoxetine, paroxetine, phenelzine, risperidone, sertraline, and venlafaxine were more effective than placebo; phenelzine was better than many other active treatments and was the only drug, which was significantly better than placebo in terms of dropouts (odds ratio 7.50, 95% CI 1.72–32.80). Mirtazapine yielded a relatively high rank for efficacy, but the respective value for acceptability was not among the best treatments. Divalproex had overall the worst ranking.

The efficacy and acceptability hierarchies generated by our study were robust against many sources of bias. The differences between drugs and placebo were small, with the only exception of phenelzine. Considering the small amount of available data, these results are probably not robust enough to suggest phenelzine as a drug of choice. However, findings from this review reinforce the idea that phenelzine should be prioritised in future trials in PTSD.

Prior research has typically found a negative relationship between chronic pain and memory, and we examined whether cognitive control processes (e.g. reflection and rumination) moderated this relationship in individuals with Chiari malformation Type I (CM). CM is a neurological condition in which the cerebellar tonsils descend into the medullary and upper cervical spine regions potentially resulting in severe headaches and neck pain.

CM patients who had (n = 341) and had not (n = 297) undergone decompression surgery completed the McGill Pain Questionnaire-Short Form-Revised (SF-MPQ-2), the Rey Auditory Verbal Learning Test (RAVLT), and the Rumination-Reflection Questionnaire (RRQ). Immediate recall scores were compared to those of 102 healthy controls, and delayed recall performance was compared across other variables within the CM group.

CM patients performed more poorly on immediate recall than did controls. Within CM patients, we observed main effects for reflection and age, and a pain x reflection x surgical status (surgery v. no surgery) interaction in which non-decompressed individuals with low levels of pain and high levels of reflection showed superior delayed recall relative to non-decompressed individuals with higher pain and all decompressed individuals.

CM patients show an immediate recall deficit relative to controls, regardless of surgical status. High levels of reflection were associated with better delayed recall performance in non-decompressed CM patients with lower pain levels. High levels of chronic pain may overwhelm increased focused attention abilities, but higher levels of reflection partially overcome the distracting effects of pain and this may represent a type of resilience.

Accumulating evidence links blood pressure variability (BPV) with white matter hyperintensities (WMH) and stroke. The longitudinal association between BPV with late onset depression (LOD) and cognitive decline remains unexplored.

Prospective cohort study of 2812 participant's age ⩾65 years (median age 72 years, 63.6% female) without dementia or stroke. Serial clinic visits assessed blood pressure, cognitive function, depression disorder, and depressive symptoms. A brain magnetic resonance imaging (MRI) substudy was performed in 1275 persons to examine possible associations with WMH.

The interaction between symptomatic LOD and systolic BPV was associated with cognitive decline on the Isaac Set Test [slope −4.45; 95% confidence interval (CI) −8.92 to −0.16, p = 0.04], Benton Visual Retention Test (slope −0.89; 95% CI −1.77 to −0.01, p = 0.049), Mini Mental State Examination (slope −1.08; 95% CI −1.86 to −0.30, p = 0.007) and Finger Tapping Test (slope −7.53; 95% CI −13.71 to −1.34, p = 0.017) but not Trail Making Test-A or -B/A. The MRI substudy demonstrated that systolic BPV was associated with cognitive decline via interactions with depression and total WMH volume, but this was not dependent on either deep or periventricular WMH volumes.

The findings show that the interaction between systolic BPV with symptomatic depression and WMH increases cognitive decline in persons ⩾65 years of age. Future work could extend these findings by examining systolic BPV in relation to cognitive decline and WMH in older populations with depression.

Childhood trauma is a non specific risk factor for adult eating disorders (ED), and the hypothalamic-pituitary-adrenal (HPA) axis seems to mediate such a risk. Here we explored the impact of different types of childhood trauma and of traumatic load on the cortisol awakening response (CAR) of women with anorexia nervosa (AN) or bulimia nervosa (BN).

Saliva samples were collected at awakening and after 15, 30, 60 min to measure cortisol levels by 121 women (44 AN patients, 36 BN patients and 41 healthy women). Participants filled in the Childhood Trauma Questionnaire.

AN and BN patients with childhood maltreatment exhibited an attenuated CAR compared with non-maltreated ones. In the whole ED patient group, the CAR showed a progressive impairment with the increasing number of reported trauma types. Although significant negative correlations emerged between the type or the number of traumas and the CAR, only the number of traumas remained significantly associated with the CAR in a stepwise multiple regression analysis.

Present findings confirm that childhood trauma is associated with an impaired CAR in adult AN and BN patients and demonstrate for the first time a negative dose-dependent effect of the traumatic load on HPA axis activity.

Sleep disturbances are prominent correlates of acute mood episodes and inadequate recovery in bipolar disorder (BD), yet the mechanistic relationship between sleep physiology and mood remains poorly understood. Using a series of pre-sleep mood inductions and overnight sleep recording, this study examined the relationship between overnight mood regulation and a marker of sleep intensity (non-rapid eye movement sleep slow wave activity; NREM SWA) during the interepisode phase of BD.

Adults with interepisode BD type 1 (BD; n = 20) and healthy adult controls (CTL; n = 23) slept in the laboratory for a screening night, a neutral mood induction night (baseline), a happy mood induction night, and a sad mood induction night. NREM SWA (0.75–4.75 Hz) was derived from overnight sleep EEG recordings. Overnight mood regulation was evaluated using an affect grid pleasantness rating post-mood induction (pre-sleep) and the next morning.

Overnight mood regulation did not differ between groups following the sad or happy inductions. SWA did not significantly change for either group on the sad induction night compared with baseline. In BD only, SWA on the sad night was related to impaired overnight negative mood regulation. On the happy induction night, SWA increased relative to baseline in both groups, though SWA was not related to overnight mood regulation for either group.

These findings indicate that SWA disruption may play a role in sustaining negative mood state from the previous night in interepisode BD. However, positive mood state could enhance SWA in bipolar patients and healthy adults.

Identifying genetic relationships between complex traits in emerging adulthood can provide useful etiological insights into risk for psychopathology. College-age individuals are under-represented in genomic analyses thus far, and the majority of work has focused on the clinical disorder or cognitive abilities rather than normal-range behavioral outcomes.

This study examined a sample of emerging adults 18–22 years of age (N = 5947) to construct an atlas of polygenic risk for 33 traits predicting relevant phenotypic outcomes. Twenty-eight hypotheses were tested based on the previous literature on samples of European ancestry, and the availability of rich assessment data allowed for polygenic predictions across 55 psychological and medical phenotypes.

Polygenic risk for schizophrenia (SZ) in emerging adults predicted anxiety, depression, nicotine use, trauma, and family history of psychological disorders. Polygenic risk for neuroticism predicted anxiety, depression, phobia, panic, neuroticism, and was correlated with polygenic risk for cardiovascular disease.

These results demonstrate the extensive impact of genetic risk for SZ, neuroticism, and major depression on a range of health outcomes in early adulthood. Minimal cross-ancestry replication of these phenomic patterns of polygenic influence underscores the need for more genome-wide association studies of non-European populations.

Prior studies using self-report questionnaires and laboratory-based methods suggest that schizophrenia is characterized by abnormalities in emotion regulation (i.e. using strategies to increase or decrease the frequency, duration, or intensity of negative emotion). However, it is unclear whether these abnormalities reflect poor emotion regulation effort or adequate effort, but limited effectiveness. It is also unclear whether dysfunction results primarily from one of the three stages of the emotion regulation process: identification, selection, or implementation.

The current study used ecological momentary assessment (EMA) to address these questions in the context of everyday activities. Participants included 28 outpatients diagnosed with schizophrenia (SZ) and 28 demographically matched healthy controls (CN) who completed 6 days of EMA reports of in-the-moment emotional experience, emotion regulation strategy use, and context.

Results indicated that SZ demonstrated adequate emotion regulation effort, but poor effectiveness. Abnormalities were observed at each of the three stages of the emotion regulation process. At the identification stage, SZ initiated emotion regulation efforts at a lower threshold of negative emotion intensity. At the selection stage, SZ selected more strategies than CN and strategies attempted were less contextually appropriate. At the implementation stage, moderate to high levels of effort were ineffective at decreasing negative emotion.

Findings suggest that although SZ attempt to control their emotions using various strategies, often applying more effort than CN, these efforts are unsuccessful; emotion regulation abnormalities may result from difficulties at the identification, selection, and implementation stages.