This report prospectively examines the 4-year course, and predictors of course, of body dysmorphic disorder (BDD), a common and often severe disorder. No prior studies have prospectively examined the course of BDD in individuals ascertained for BDD.

The Longitudinal Interval Follow-Up Evaluation (LIFE) assessed weekly BDD symptoms and treatment received over 4 years for 166 broadly ascertained adults and adolescents with current BDD at intake. Kaplan–Meier life tables were constructed for time to remission and relapse. Full remission was defined as minimal or no BDD symptoms, and partial remission as less than full DSM-IV criteria, for at least 8 consecutive weeks. Full relapse and partial relapse were defined as meeting full BDD criteria for at least 2 consecutive weeks after attaining full or partial remission respectively. Cox proportional hazards regression examined predictors of remission and relapse.

Over 4 years, the cumulative probability was 0.20 for full remission and 0.55 for full or partial remission from BDD. A lower likelihood of full or partial remission was predicted by more severe BDD symptoms at intake, longer lifetime duration of BDD, and being an adult. Among partially or fully remitted subjects, the cumulative probability was 0.42 for subsequent full relapse and 0.63 for subsequent full or partial relapse. More severe BDD at intake and earlier age at BDD onset predicted full or partial relapse. Eighty-eight percent of subjects received mental health treatment during the follow-up period.

In this observational study, BDD tended to be chronic. Several intake variables predicted greater chronicity of BDD.

Criteria for mild cognitive impairment (MCI) consider impairment in instrumental activities of daily living (IADL) as exclusionary, but cross-sectional studies suggest that some high-level functional deficits are present in MCI. This longitudinal study examines informant-rated IADL in MCI, compared with cognitively normal (CN) older individuals, and explores whether functional abilities, particularly those with high cognitive demand, are predictors of MCI and dementia over a 2-year period in individuals who were CN at baseline.

A sample of 602 non-demented community dwelling individuals (375 CN and 227 with MCI) aged 70–90 years underwent baseline and 24-month assessments that included cognitive and medical assessments and an interview with a knowledgeable informant on functional abilities with the Bayer Activities of Daily Living Scale.

Significantly more deficits in informant-reported IADL with high cognitive demand were present in MCI compared with CN individuals at baseline and 2-year follow-up. Functional ability in CN individuals at baseline, particularly in activities with high cognitive demand, predicted MCI and dementia at follow-up. Difficulties with highly cognitively demanding activities specifically predicted amnestic MCI but not non-amnestic MCI whereas those with low cognitive demand did not predict MCI or dementia. Age, depressive symptoms, cardiovascular risk factors and the sex of the informant did not contribute to the prediction.

IADL are affected in individuals with MCI, and IADL with a high cognitive demand show impairment predating the diagnosis of MCI. Subtle cognitive impairment is therefore likely to be a major hidden burden in society.

Although basic research on neuroimmune interactions suggests that inflammatory processes may play a role in the development of fatigue, population-based evidence on this association is limited. This study examined whether plasma C-reactive protein (CRP) and interleukin-6 (IL-6), biomarkers of systemic inflammation, predict fatigue onset.

The Whitehall II study is a large-scale cohort study conducted in 20 civil service departments in London. Plasma CRP and IL-6 were measured in 4847 non-fatigued participants at phase 3 (1991–1993, aged 39–63 years). Fatigue was assessed using the Vitality subscale of the 36-item Short Form Health Survey (SF-36) at phase 3 and phase 4 (1995–1996).

During a mean follow-up of 3.1 years, 957 new fatigue cases (19.7%) were identified using the pre-established cut-off score of ⩽50 on the Vitality subscale. CRP values were dichotomized as low (<1.0 mg/l ) or high (⩾1.0 mg/l) using the Centers for Disease Control/American Heart Association recommendations. Similarly, IL-6 values were also dichotomized as low (<1.5 pg/ml) or high (⩾1.5 pg/ml). After full adjustment for sociodemographic and biobehavioral covariates, the odds ratios for new-onset fatigue were 1.28 [95% confidence interval (CI) 1.09–1.49, p = 0.003] for high CRP and 1.24 (95% CI 1.06–1.45, p = 0.008) for high IL-6. Similar results were found when CRP and IL-6 were treated as continuous variables.

Plasma CRP and IL-6 were prospectively associated with new-onset fatigue, supporting the hypothesis that low-grade inflammation has a role in the development of fatigue.

Being physically assaulted is known to increase the risk of the occurrence of post-traumatic stress disorder (PTSD) symptoms but it may also skew judgements about the intentions of other people. The objectives of the study were to assess paranoia and PTSD after an assault and to test whether theory-derived cognitive factors predicted the persistence of these problems.

At 4 weeks after hospital attendance due to an assault, 106 people were assessed on multiple symptom measures (including virtual reality) and cognitive factors from models of paranoia and PTSD. The symptom measures were repeated 3 and 6 months later.

Factor analysis indicated that paranoia and PTSD were distinct experiences, though positively correlated. At 4 weeks, 33% of participants met diagnostic criteria for PTSD, falling to 16% at follow-up. Of the group at the first assessment, 80% reported that since the assault they were excessively fearful of other people, which over time fell to 66%. Almost all the cognitive factors (including information-processing style during the trauma, mental defeat, qualities of unwanted memories, self-blame, negative thoughts about self, worry, safety behaviours, anomalous internal experiences and cognitive inflexibility) predicted later paranoia and PTSD, but there was little evidence of differential prediction.

Paranoia after an assault may be common and distinguishable from PTSD but predicted by a strikingly similar range of factors.

Increased reaction time variability (RTV) on cognitive tasks requiring a speeded response is characteristic of several psychiatric disorders. In attention deficit hyperactivity disorder (ADHD), the association with RTV is strong phenotypically and genetically, yet high RTV is not a stable impairment but shows ADHD-sensitive improvement under certain conditions, such as those with rewards. The state regulation theory proposed that the RTV difference score, which captures change from baseline to a rewarded or fast condition, specifically measures ‘state regulation’. By contrast, the interpretation of RTV baseline (slow, unrewarded) scores is debated. We aimed to investigate directly the degree of phenotypic and etiological overlap between RTV baseline and RTV difference scores.

We conducted genetic model fitting analyses on go/no-go and fast task RTV data, across task conditions manipulating rewards and event rate, from a population-based twin sample (n=1314) and an ADHD and control sibling-pair sample (n=1265).

Phenotypic and genetic/familial correlations were consistently high (0.72–0.98) between RTV baseline and difference scores, across tasks, manipulations and samples. By contrast, correlations were low between RTV in the manipulated condition and difference scores. A comparison across two different go/no-go task RTV difference scores (slow-fast/slow-incentive) showed high phenotypic and genetic/familial overlap (r = 0.75–0.83).

Our finding that RTV difference scores measure largely the same etiological process as RTV under baseline condition supports theories emphasizing the malleability of the observed high RTV. Given the statistical shortcomings of difference scores, we recommend the use of RTV baseline scores for most analyses, including genetic analyses.

Attention deficit hyperactivity disorder (ADHD) symptoms and autistic traits often occur together. The pattern and etiology of co-occurrence are largely unknown, particularly in adults. This study investigated the co-occurrence between both traits in detail, and subsequently examined the etiology of the co-occurrence, using two independent adult population samples.

Data on ADHD traits (Inattention and Hyperactivity/Impulsivity) were collected in a population sample (S1, n = 559) of unrelated individuals. Data on Attention Problems (AP) were collected in a population-based family sample of twins and siblings (S2, n = 560). In both samples five dimensions of autistic traits were assessed (social skills, routine, attentional switching, imagination, patterns).

Hyperactive traits (S1) did not correlate substantially with the autistic trait dimensions. For Inattention (S1) and AP (S2), the correlations with the autistic trait dimensions were low, apart from a prominent correlation with the attentional switching scale (0.47 and 0.32 respectively). Analyses in the genetically informative S2 revealed that this association could be explained by a shared genetic factor.

Our findings suggest that the co-occurrence of ADHD traits and autistic traits in adults is not determined by problems with hyperactivity, social skills, imagination or routine preferences. Instead, the association between those traits is due primarily to shared attention-related problems (inattention and attentional switching capacity). As the etiology of this association is purely genetic, biological pathways involving attentional control could be a promising focus of future studies aimed at unraveling the genetic causes of these disorders.

Undue influence of body shape or weight on self-evaluation – referred to as overvaluation – is considered a core feature across eating disorders, but is not a diagnostic requirement for binge eating disorder (BED). This study examined the concurrent and predictive significance of overvaluation of shape/weight in obese patients with BED participating in a randomized clinical trial testing cognitive behavioral therapy (CBT) and behavioral weight loss (BWL).

A total of 90 participants were randomly assigned to 6-month group treatments of CBT or BWL. Assessments were performed at baseline, throughout- and post-treatment, and at 6- and 12-month follow-ups after completing treatments with reliably administered semi-structured interviews and established measures.

Participants categorized with overvaluation (n = 52, 58%) versus without overvaluation (n = 38, 42%) did not differ significantly in demographic features (age, gender and ethnicity), psychiatric co-morbidity, body mass index or binge eating frequency. The overvaluation group had significantly greater levels of eating disorder psychopathology and poorer psychological functioning (higher depression and lower self-esteem) than the non-overvaluation group. Overvaluation of shape/weight significantly predicted non-remission from binge eating and higher frequency of binge eating at the 12-month follow-up, even after adjusting for group differences in depression and self-esteem levels.

Our findings suggest that overvaluation does not simply reflect concern commensurate with being obese or more frequent binge eating, but also is strongly associated with heightened eating-related psychopathology and psychological distress, and has negative prognostic significance for longer-term treatment outcomes. Overvaluation of shape/weight warrants consideration as a diagnostic specifier for BED as it provides important information about severity and treatment outcome.

The objective of the present study was to estimate the association between different leisure-time physical activity (LTPA) parameters from 11 to 50 years and cognitive functioning in late mid-adulthood.

The study used a prospective birth cohort study including participants in the UK National Child Development Study (NCDS) from age 11 to 50 years. Standardized z scores for cognitive, memory and executive functioning at age 50 represented the primary outcome measures. Exposures included self-reported LTPA at ages 11, 16, 33, 42, 46 and 50 years. Analyses were adjusted for important confounders including educational attainment and long-standing illness.

The adjusted difference in cognition score between women who reported LTPA for at least 4 days/week in five surveys or more and those who never reported LTPA for at least 4 days/week was 0.28 [95% confidence interval (CI) 0.20–0.35], 0.10 (95% CI 0.01–0.19) for memory score and 0.30 (95% CI 0.23–0.38) for executive functioning score. For men, the equivalent differences were: cognition 0.12 (95% CI 0.05–0.18), memory 0.06 (95% CI − 0.02 to 0.14) and executive functioning 0.16 (95% CI 0.10–0.23).

This study provides novel evidence about the lifelong association between LTPA and memory and executive functioning in mid-adult years. Participation in low-frequency and low-intensity LTPA was positively associated with cognitive functioning in late mid-adult years for men and women. The greatest benefit emerged from participating in lifelong intensive LTPA.

Patients with attention deficit-hyperactivity disorder (ADHD) exhibit difficulties in multiple attentional functions. Although high heritability rates suggest a strong genetic impact, aetiological pathways from genes and environmental factors to the ADHD phenotype are not well understood. Tracking the time course of deviant task processing using event-related electrophysiological brain activity should characterize the impact of familiality on the sequence of cognitive functions from preparation to response control in ADHD.

Preparation and response control were assessed using behavioural and electrophysiological parameters of two versions of a cued continuous performance test with varying attentional load in boys with ADHD combined type (n = 97), their non-affected siblings (n = 27) and control children without a family history of ADHD (n = 43).

Children with ADHD and non-affected siblings showed more variable performance and made more omission errors than controls. The preparatory Cue-P3 and contingent negative variation (CNV) following cues were reduced in both ADHD children and their non-affected siblings compared with controls. The NoGo-P3 was diminished in ADHD compared with controls whilst non-affected siblings were located intermediate but did not differ from both other groups. No clear familiality effects were found for the Go-P3. Better task performance was further associated with higher CNV and P3 amplitudes.

Impairments in performance and electrophysiological parameters reflecting preparatory processes and to some extend also for inhibitory response control, especially under high attentional load, appeared to be familially driven in ADHD and may thus constitute functionally relevant endophenotypes for the disorder.

Sleep loss produces abnormal increases in reward seeking but the mechanisms underlying this phenomenon are poorly understood. The present study examined the influence of one night of sleep deprivation on neural responses to a monetary reward task in a sample of late adolescents/young adults.

Using a within-subjects crossover design, 27 healthy, right-handed late adolescents/young adults (16 females, 11 males; mean age 23.1 years) underwent functional magnetic resonance imaging (fMRI) following a night of sleep deprivation and following a night of normal sleep. Participants' recent sleep history was monitored using actigraphy for 1 week prior to each sleep condition.

Following sleep deprivation, participants exhibited increased activity in the ventral striatum (VS) and reduced deactivation in the medial prefrontal cortex (mPFC) during the winning of monetary reward, relative to the same task following normal sleep conditions. Shorter total sleep time over the five nights before the sleep-deprived testing condition was associated with reduced deactivation in the mPFC during reward.

These findings support the hypothesis that sleep loss produces aberrant functioning in reward neural circuitry, increasing the salience of positively reinforcing stimuli. Aberrant reward functioning related to insufficient sleep may contribute to the development and maintenance of reward dysfunction-related disorders, such as compulsive gambling, eating, substance abuse and mood disorders.