It has long been acknowledged that hearing impairment may increase the risk for psychotic experiences. Recent work suggests that young people in particular may be at risk, indicating a possible developmental mechanism.

The hypothesis that individuals exposed to hearing impairment in early adolescence would display the highest risk for psychotic symptoms was examined in a prospective cohort study of a population sample of originally 3021 adolescents and young adults aged 14–24 years at baseline, in Munich, Germany (Early Developmental Stages of Psychopathology Study). The expression of psychosis was assessed at multiple time points over a period of up to 10 years, using a diagnostic interview (Munich Composite International Diagnostic Interview; CIDI) administered by clinical psychologists.

Hearing impairment was associated with CIDI psychotic symptoms [odds ratio (OR) 2.04, 95% confidence interval (CI) 1.10–3.81], particularly more severe psychotic symptoms (OR 5.66, 95% CI 1.64–19.49). The association between hearing impairment and CIDI psychotic symptoms was much stronger in the youngest group aged 14–17 years at baseline (OR 3.28, 95% CI 1.54–7.01) than in the older group aged 18–24 years at baseline (OR 0.82, 95% CI 0.24–2.84).

The finding of an age-specific association between hearing impairment and psychotic experiences suggests that disruption of development at a critical adolescent phase, in interaction with other personal and social vulnerabilities, may increase the risk for psychotic symptoms.

The prevalence of psychological distress and common mental disorders has been shown to peak in midlife but analyses have ignored the association of poor material circumstances with prevalence. This study aimed to test the hypothesis that the midlife prevalence peak occurs only in lower-income households.

Pooled data were used from the annual Health Survey for England, a nationally representative cross-sectional study, on community-dwelling individuals aged ⩾16 years from years 1997 to 2006 (n=100 457). 12-item General Health Questionnaire scores, reported mental illness diagnoses and receipt of relevant medication were assessed in relation to household income and age. Analyses were separated by gender and adjusted for age, ethnicity, smoking, social class, education and co-morbidities.

Prevalence of psychological distress, diagnoses and treatments rose with age until early middle age and declined subsequently. In analyses conducted separately by income categories, this pattern was marked in low-income groups but absent in high-income groups. Income-related inequalities in the prevalence of psychological distress were greatest in midlife; for example, in men aged 45–54 years the odds ratio of receiving psychiatric medication in the lowest income group compared with the highest was 7.50 [95% confidence interval (CI) 4.24–13.27] and in women aged 45–54 years the odds ratio of reporting mental illness was 10.25 (95% CI 6.16–17.05).

An increased prevalence of psychological distress, common mental disorder diagnoses and treatment in midlife is not a universal phenomenon but is found only in those in low-income households. This implies the phenomenon is not inevitable but is potentially manageable or preventable.

Auditory P50 sensory gating deficits correlate with genetic risk for schizophrenia and constitute a plausible endophenotype for the disease. The well-supported role of catechol-O-methyltransferase (COMT), brain-derived neurotrophic factor (BDNF) and neuregulin 1 (NRG1) genes in neurodevelopment and cognition make a strong theoretical case for their influence on the P50 endophenotype.

The possible role of NRG1, COMT Val158Met and BDNF Val66Met gene polymorphisms on the P50 endophenotype was examined in a large sample consisting of psychotic patients, their unaffected relatives and unrelated healthy controls using linear regression analyses.

Although P50 deficits were present in patients and their unaffected relatives, there was no evidence for an association between NRG1, COMT Val158Met or BDNF Val66Met genotypes and the P50 endophenotype.

The evidence from our large study suggests that any such association between P50 indices and NRG1, COMT Val158Met or BDNF Val66Met genotypes, if present, must be very subtle.

Very few longitudinal studies have evaluated prospective neurodevelopmental and psychosocial risk factors for obsessive–compulsive disorder (OCD). Furthermore, despite the heterogeneous nature of OCD, no research has examined risk factors for its primary symptom dimensions, such as contamination/washing.

Potential risk factors for symptoms or diagnosis of OCD in adulthood and for specific adult obsessive–compulsive (OC) symptom dimensions were examined in the Dunedin Study birth cohort. The presence of obsessions and compulsions and psychological disorders was assessed using the Diagnostic Interview Schedule (DIS) at ages 26 and 32 years. Individuals with a diagnosis of OCD at either age (n=36) were compared to both a healthy control group (n=613) and an anxious control group (n=310) to determine whether associations between a risk factor and an OCD diagnosis were specific.

Childhood neurodevelopmental, behavioral, personality and environmental risk factors were associated with a diagnosis of OCD and with OC symptoms at ages 26 and 32. Social isolation, retrospectively reported physical abuse and negative emotionality were specific predictors of an adult OCD diagnosis. Of note, most risk factors were associated with OC symptoms in adulthood and several risk factors predicted specific OCD dimensions. Perinatal insults were linked to increased risk for symmetry/ordering and shameful thoughts dimensions, whereas poor childhood motor skills predicted the harm/checking dimension. Difficult temperament, internalizing symptoms and conduct problems in childhood also predicted specific symptom dimensions and lower IQ non-specifically predicted increased risk for most dimensions.

The current findings underscore the need for a dimensional approach in evaluating childhood risk factors for obsessions and compulsions.

Evidence is accumulating that child sexual abuse (CSA) is associated with many psychiatric disorders in adulthood. This paper uses the detailed information available from the 2007 Adult Psychiatric Morbidity Survey of England (APMS 2007) to quantify links between CSA and a range of psychiatric conditions.

The prevalence of psychiatric disorder was established in a random sample of the English household population (n=7403), which also provided sociodemographic and experiential information.

We analyzed six types of common mental disorder, alcohol abuse and drug abuse, and people who screened positively for post-traumatic stress disorder (PTSD) and eating disorders. All were strongly and highly significantly associated with CSA, particularly if non-consensual sexual intercourse was involved, for which odds ratios (ORs) ranged from 3.7 to 12.1. These disorders were also related to adult sexual abuse (ASA), although the likelihood of reverse causality is then increased. Revictimization in adulthood was common, and increased the association of CSA with disorder. For several disorders, the relative odds were higher in females but formal tests for moderation by gender were significant only for common mental disorders and only in relation to non-consensual sexual intercourse. The population attributable fraction (PAF) was higher in females in all cases.

The detailed and high-quality data in APMS 2007 provided important confirmation both of the strength of association of CSA with psychiatric disorder and of its relative non-specificity. Our results have major implications at the public health level and the individual level, in particular the need for better recognition and treatment of the sequelae of CSA.

Although antipsychotic medication still represents the treatment of choice for schizophrenia, its objective impact on symptoms is only in the medium-effect size range and at least 50% of patients discontinue medication in the course of treatment. Hence, clinical researchers are intensively looking for complementary therapeutic options. Metacognitive training for schizophrenia patients (MCT) is a group intervention that seeks to sharpen the awareness of schizophrenia patients on cognitive biases (e.g. jumping to conclusions) that seem to underlie delusion formation and maintenance. The present trial combined group MCT with an individualized cognitive-behavioural therapy-oriented approach entitled individualized metacognitive therapy for psychosis (MCT+) and compared it against an active control.

A total of 48 patients fulfilling criteria of schizophrenia were randomly allocated to either MCT+ or cognitive remediation (clinical trial NCT01029067). Blind to intervention, both groups were assessed at baseline and 4 weeks later. Psychopathology was assessed using the Positive and Negative Syndrome Scale (PANSS) and the Psychotic Symptom Rating Scales (PSYRATS). Jumping to conclusions was measured using a variant of the beads task.

PANSS delusion severity declined significantly in the combined MCT treatment compared with the control condition. PSYRATS delusion conviction as well as jumping to conclusions showed significantly greater improvement in the MCT group. In line with prior studies, treatment adherence and subjective efficacy was excellent for the MCT.

The results suggest that the combination of a cognition-oriented and a symptom-oriented approach ameliorate psychotic symptoms and cognitive biases and represents a promising complementary treatment for schizophrenia.

There is relative little information about the prevalence and risk factors of co-morbid anxiety and depression in later life. These disorders are often associated with worse response to treatment than either condition alone, and researching their epidemiology in diverse settings is vital to policy makers. We therefore investigated the co-occurrence of anxiety and depressive syndromes amongst older adults living in developing countries and measured the separate and joint effect of these two disorders on levels of associated disability.

The 10/66 study carried out cross-cultural surveys of all residents aged 65 years or over (n=15021) in 11 sites in seven countries (People's Republic of China, India, Cuba, Dominican Republic, Venezuela, Mexico and Peru). Anxiety was measured by using the Geriatric Mental State Examination and the Automated Geriatric Examination for Computer Assisted Taxonomy diagnostic system. Depression was assessed according to International Classification of Diseases 10th revision (ICD-10) and EURO-D criteria. Disability was measured by using the World Health Organization's Disablement Assessment Scale Version II. Zero-inflated negative binomial regression models were used to investigate the association of common mental disorders and disability.

The prevalence of co-occurring anxiety and depression (with the exclusion of subthreshold disorders) ranged between 0.9% and 4.2% across sites. Gender, socio-economic status, urbanicity and physical co-morbidities were associated with the different co-morbid states. Having both disorders was linked to higher disability scores than having anxiety or depression alone.

Given the close association of co-morbid anxiety and depression with disability, new policies to improve prevention, recognition and treatment will be needed to adapt to ageing populations and their mental health needs.

For many years, the prevailing paradigm has stated that in each individual with schizophrenia (SZ) the genetic risk is due to a combination of many genetic variants, individually of small effect. Recent empirical data are prompting a re-evaluation of this polygenic, common disease–common variant (CDCV) model. Evidence includes a lack of the expected strong positive findings from genome-wide association studies and the concurrent discovery of many different mutations that individually strongly predispose to SZ and other psychiatric disorders. This has led some to adopt a mixed model wherein some cases are caused by polygenic mechanisms and some by single mutations. This model runs counter to a substantial body of theoretical literature that had supposedly conclusively rejected Mendelian inheritance with genetic heterogeneity. Here we ask how this discrepancy between theory and data arose and propose a rationalization of the recent evidence base.

In light of recent empirical findings, we reconsider the methods and conclusions of early theoretical analyses and the explicit assumptions underlying them.

We show that many of these assumptions can now be seen to be false and that the model of genetic heterogeneity is consistent with observed familial recurrence risks, endophenotype studies and other population-wide parameters.

We argue for a more biologically consilient mixed model that involves interactions between disease-causing and disease-modifying variants in each individual. We consider the implications of this model for moving SZ research beyond statistical associations to pathogenic mechanisms.

Symptoms of anxiety and depression are common in older people, but the relative importance of factors operating in early and later life in influencing risk is unclear, particularly in the case of anxiety.

We used data from five cohorts in the Healthy Ageing across the Life Course (HALCyon) collaborative research programme: the Aberdeen Birth Cohort 1936, the Caerphilly Prospective Study, the Hertfordshire Ageing Study, the Hertfordshire Cohort Study and the Lothian Birth Cohort 1921. We used logistic regression to examine the relationship between factors from early and later life and risk of anxiety or depression, defined as scores of 8 or more on the subscales of the Hospital Anxiety and Depression Scale, and meta-analysis to obtain an overall estimate of the effect of each.

Greater neuroticism, poorer cognitive or physical function, greater disability and taking more medications were associated in cross-sectional analyses with an increased overall likelihood of anxiety or depression. Associations between lower social class, either in childhood or currently, history of heart disease, stroke or diabetes and increased risk of anxiety or depression were attenuated and no longer statistically significant after adjustment for potential confounding or mediating variables. There was no association between birth weight and anxiety or depression in later life.

Anxiety and depression in later life are both strongly linked to personality, cognitive and physical function, disability and state of health, measured concurrently. Possible mechanisms that might underlie these associations are discussed.

The clinical benefit for depression of an interactive computer-assisted cognitive-behavioral program on CD-ROM, the Wellness Workshop (WW), was evaluated in a randomized controlled trial.

A total of 191 individuals referred by primary-care physicians were randomly assigned to a control group, where physician-directed treatment as usual (TAU) was provided, or to a treatment group, where TAU was supplemented with the WW CD-ROM, delivered by mail (WW+TAU). Data were collected at baseline, at 6 weeks' post-intervention, and at a 6-month follow-up assessment. Participants were given a strong incentive by a reimbursement of $75 for completion of each assessment. Measures included symptom ratings obtained via structured clinical diagnostic interviews, as well as a battery of self-report questionnaires on symptoms specifically targeted by the intervention.

Analysis of results demonstrated evidence for skill acquisition for improving dysfunctional thinking and reducing anxiety. Among those who met diagnostic criteria for depression, WW+TAU participants were three times more likely to remit at 6 weeks' post-test than TAU participants.

The evidence supports the conclusion that the WW intervention added benefit to traditional care for depression. No placebo comparison group was included and the WW+TAU participants received slightly more attention (a supportive telephone contact, ⩽5 min from a psychologist 2 weeks after receiving the program). Overall, the findings add support to the accumulating evidence for the potential clinical benefit of computer-assisted behavioral health interventions.

There is a general consensus in the literature that schizophrenia causes difficulties with facial emotion perception and discrimination. Functional brain imaging studies have observed reduced limbic activity during facial emotion perception but few studies have examined the relation to flat affect severity.

A total of 26 people with schizophrenia and 26 healthy controls took part in this event-related functional magnetic resonance imaging study. Sad, happy and neutral faces were presented in a pseudo-random order and participants indicated the gender of the face presented. Manual segmentation of the amygdala was performed on a structural T1 image.

Both the schizophrenia group and the healthy control group rated the emotional valence of facial expressions similarly. Both groups exhibited increased brain activity during the perception of emotional faces relative to neutral ones in multiple brain regions, including multiple prefrontal regions bilaterally, the right amygdala, right cingulate cortex and cuneus. Group comparisons, however, revealed increased activity in the healthy group in the anterior cingulate, right parahippocampal gyrus and multiple visual areas. In schizophrenia, the severity of flat affect correlated significantly with neural activity in several brain areas including the amygdala and parahippocampal region bilaterally.

These results suggest that many of the brain regions involved in emotional face perception, including the amygdala, are equally recruited in both schizophrenia and controls, but flat affect can also moderate activity in some other brain regions, notably in the left amygdala and parahippocampal gyrus bilaterally. There were no significant group differences in the volume of the amygdala.

It has been suggested that childhood obsessive-compulsive disorder (OCD) may be a risk factor for the development of an eating disorder (ED) later in life, but prospective studies are lacking. We aimed to determine the prevalence of ED at follow-up and clinical predictors in a longitudinal clinical sample of adolescents/young adults diagnosed with OCD in childhood.

All contactable (n=231) young people with OCD assessed over 9 years at a national and specialist paediatric OCD clinic were included in this study. At follow-up, 126 (57%) young people and parents completed the ED section of the Developmental and Well-being Assessment. Predictors for ED were investigated using logistic regression.

In total, 16 participants (12.7%) had a diagnosis of ED at follow-up. Having an ED was associated with female gender and persistent OCD at follow-up. There was a trend for family history of ED being predictive of ED diagnosis. Five (30%) of those who developed an ED at follow-up had ED symptoms or food-related obsessions/compulsions at baseline. A difference in predictors for an ED versus other anxiety disorders at follow-up was identified.

This study provides initial evidence that baseline clinical predictors such as female gender and family history of ED might be specific to the later development of ED in the context of childhood OCD. Clinicians should be alert to ED subthreshold symptoms in young girls presenting with OCD. Future longitudinal studies are needed to clarify the relationship between childhood OCD and later ED.

DSM-5 may mark the shift from a categorical classification of personality pathology to a dimensional system. Although dimensional and categorical conceptualizations of personality pathology are often viewed as competing, it is possible to develop categories (prototypes) from combinations of dimensions. Robust prototypes could bridge dimensions and categories within a single classification system.

To explore prototype structure and robustness, we used finite mixture modeling to identify empirically derived personality pathology prototypes within a large sample (n=8690) of individuals from four settings (clinical, college, community, and military), assessed using a dimensional measure of normal and abnormal personality traits, the Schedule for Nonadaptive and Adaptive Personality (SNAP). We then examined patterns of convergent and discriminant external validity for prototypes. Finally, we investigated the robustness of the dimensional structure of personality pathology.

The resulting prototypes were meaningful (externally valid) but non-robust (sample dependent). By contrast, factor analysis revealed that the dimensional structures underlying specific traits were highly robust across samples.

We interpret these results as further evidence of the fundamentally dimensional nature of an empirically based classification of personality pathology.

According to cognitive theories of depression, negative biases affect most cognitive processes including perception. Such depressive perception may result not only from biased cognitive appraisal but also from automatic processing biases that influence the access of sensory information to awareness.

Twenty patients with major depressive disorder (MDD) and 20 healthy control participants underwent behavioural testing with a variant of binocular rivalry, continuous flash suppression (CFS), to investigate the potency of emotional visual stimuli to gain access to awareness. While a neutral, fearful, happy or sad emotional face was presented to one eye, high-contrast dynamic patterns were presented to the other eye, resulting in initial suppression of the face from awareness. Participants indicated the location of the face with a key press as soon as it became visible. The modulation of suppression time by emotional expression was taken as an index of unconscious emotion processing.

We found a significant difference in the emotional modulation of suppression time between MDD patients and controls. This difference was due to relatively shorter suppression of sad faces and, to a lesser degree, to longer suppression of happy faces in MDD. Suppression time modulation by sad expression correlated with change in self-reported severity of depression after 4 weeks.

Our finding of preferential access to awareness for mood-congruent stimuli supports the notion that depressive perception may be related to altered sensory information processing even at automatic processing stages. Such perceptual biases towards mood-congruent information may reinforce depressed mood and contribute to negative cognitive biases.

Early Intervention in Psychosis Services (EIS) for young people in England experiencing first-episode psychosis (FEP) were commissioned in 2002, based on an expected incidence of 15 cases per 100 000 person-years, as reported by schizophrenia epidemiology in highly urban settings. Unconfirmed reports from EIS thereafter have suggested higher than anticipated rates. The aim of this study was to compare the observed with the expected incidence and delineate the clinical epidemiology of FEP using epidemiologically complete data from the CAMEO EIS, over a 6-year period in Cambridgeshire, for a mixed rural–urban population.

A population-based study of FEP (ICD-10, F10–39) in people aged 17–35 years referred between 2002 and 2007; the denominator was estimated from mid-year census statistics. Sociodemographic variation was explored by Poisson regression. Crude and directly standardized rates (for age, sex and ethnicity) were compared with pre-EIS rates from two major epidemiological FEP studies conducted in urban English settings.

A total of 285 cases met FEP diagnoses in CAMEO, yielding a crude incidence of 50 per 100 000 person-years [95% confidence interval (CI) 44.5–56.2]. Age- and sex-adjusted rates were raised for people from black ethnic groups compared with the white British [incidence rate ratio (IRR) 2.1, 95% CI 1.1–3.8]. Rates in our EIS were comparable with pre-EIS rates observed in more urban areas after age, sex and ethnicity standardization.

Our findings suggest that the incidence observed in EIS is far higher than originally anticipated and is comparable to rates observed in more urban settings prior to the advent of EIS. Sociodemographic variation due to ethnicity and other factors extend beyond urban populations. Our results have implications for psychosis aetiology and service planning.

Prior work has suggested that genetic influences on major depressive disorder (MDD) may be activated by the experience of negative life events. However, it is unclear whether these results persist when controlling for the possibility of confounding active gene–environment correlations (rGE).

We examined a sample of 1230 adopted and biological siblings between the ages of 10 and 20 years from the Sibling Interaction and Behavior Study. MDD was measured via a lifetime DSM-IV symptom count. Number of deaths experienced served as our environmental risk experience. Because this variable is largely independent of the individual's choices/behaviors, we were able to examine gene–environment interactions while circumventing possible rGE confounds.

Biometric analyses revealed pronounced linear increases in the magnitude of genetic influences on symptoms of MDD with the number of deaths experienced, such that genetic influences were estimated to be near-zero for those who had experienced no deaths but were quite large in those who had experienced two or more deaths (i.e. accounting for roughly two-thirds of the phenotypic variance). By contrast, shared and non-shared environmental influences on symptoms of MDD were not meaningfully moderated by the number of deaths experienced.

Such results constructively replicate prior findings of genetic moderation of depressive symptoms by negative life events, thereby suggesting that this effect is not a function of active rGE confounds. Our findings are thus consistent with the notion that exposure to specific negative life events may serve to activate genetic risk for depression during adolescence.

There is compelling evidence that children of mothers with postnatal depression (PD) experience poor developmental outcomes. However, no studies have specifically ascertained the risk of mortality for offspring during preschool years, the most catastrophic outcome in the vulnerable period. This nationwide population-based study aimed to investigate whether maternal depression in the first year after giving birth was associated with increased mortality risk among their preschool children aged up to 5 years.

Three nationwide population-based datasets [the National Health Insurance Research Database (NHIRD), birth certificate registry and death certificate registry] were linked in this study. A total of 10 236 offspring of mothers with PD were recruited, together with a comparison cohort of 81 888 births matched with the affected women in terms of maternal age and year of delivery. Each child was traced for 5 years from delivery between 2001 and 2003 until the end of 2008 to determine mortality during preschool years.

During preschool years, 98 (0.96%) deaths were identified among the offspring of mothers with PD and 470 (0.57%) children in the comparison cohort died. For children up to 5 years old, exposure to maternal PD was independently associated with a 1.47-fold [95% confidence interval (CI) 1.16–1.87] increased mortality risk, after adjusting for family income, urbanization level and the characteristics of mother, father and infant. The risk of death by unnatural causes was even higher (about 2.23 times the risk, 95% CI 1.34–3.70) among exposed offspring.

PD places preschool children at significantly increased risk of mortality, especially from unnatural causes of death.

Patient-reported outcomes (PROs) are widely used for evaluating the care of patients with psychosis. Previous studies have reported a considerable overlap in the information captured by measures designed to assess different outcomes. This may impair the validity of PROs and makes an a priori choice of the most appropriate measure difficult when assessing treatment benefits for patients. We aimed to investigate the extent to which four widely established PROs [subjective quality of life (SQOL), needs for care, treatment satisfaction and the therapeutic relationship] provide distinct information independent from this overlap.

Analyses, based on item response modelling, were conducted on measures of SQOL, needs for care, treatment satisfaction and the therapeutic relationship in two large samples of patients with psychosis.

In both samples, a bifactor model matched the data best, suggesting sufficiently strong concept factors to allow for four distinct PRO scales. These were independent from overlap across measures due to a general appraisal tendency of patients for positive or negative ratings and shared domain content. The overlap partially impaired the ability of items to discriminate precisely between patients from lower and higher PRO levels. We found that widely used sum scores were strongly affected by the general appraisal tendency.

Four widely established PROs can provide distinct information independent from overlap across measures. The findings may inform the use and further development of PROs in the evaluation of treatments for psychosis.

Early visual processing deficits are reliably detected in schizophrenia and show relationships to poor real-world functioning. However, the nature of this relationship is complex. Theoretical models and recent studies using statistical modeling approaches suggest that multiple intervening factors are involved. We previously reported that a direct and significant association between visual processing and functional status was mediated by a measure of social perception. The present study examined the contribution of negative symptoms to this model.

We employed structural equation modeling (sem) to test several models of outcome, using data from 174 schizophrenia out-patients. Specifically, we examined the direct and indirect relative contributions of early visual processing, social perception and negative symptoms to functional outcome.

First, we found that, similar to social perception, a measure of negative symptoms mediated the association between visual information processing and functional status. Second, we found that the inclusion of negative symptoms substantially enhanced the explanatory power of the model. Notably, it was the experiential aspect of negative symptoms (avolition and anhedonia) more than the expressive aspect (affective flattening and alogia) that accounted for significant variance in functional outcome, especially in the social component of the construct of functional outcome.

Social perception and negative symptoms play relevant roles in functional impairment in schizophrenia. Both social perception and negative symptoms statistically mediate the connection between visual processing and functional outcome. However, given the lack of association between social perception and negative symptoms, these constructs appear to have an impact on functioning through separate pathways.

Psychiatric conditions in which symptoms arise involuntarily (‘diseases’) might be assumed to be more heritable than those in which choices are essential (behavioral disorders). We sought to determine whether psychiatric ‘diseases’ (Alzheimer's disease, schizophrenia, and mood and anxiety disorders) are more heritable than behavioral disorders (substance use disorders and anorexia nervosa).

We reviewed the literature for recent quantitative summaries of heritabilities. When these were unavailable, we calculated weighted mean heritabilities from twin studies meeting modern methological standards.

Heritability summary estimates were as follows: bipolar disorder (85%), schizophrenia (81%), Alzheimer's disease (75%), cocaine use disorder (72%), anorexia nervosa (60%), alcohol dependence (56%), sedative use disorder (51%), cannabis use disorder (48%), panic disorder (43%), stimulant use disorder (40%), major depressive disorder (37%), and generalized anxiety disorder (28%).

No systematic relationship exists between the disease-like character of a psychiatric disorder and its heritability; many behavioral disorders seem to be more heritable than conditions commonly construed as diseases. These results suggest an error in ‘common-sense’ assumptions about the etiology of psychiatric disorders. That is, among psychiatric disorders, there is no close relationship between the strength of genetic influences and the etiologic importance of volitional processes.