Social anxiety disorder (SAD) is surprisingly prevalent among people with psychosis and exerts significant impact on social disability. The processes that underlie its development remain unclear. The aim of this study was to investigate the relationship between shame cognitions arising from a stigmatizing psychosis illness and perceived loss of social status in co-morbid SAD in psychosis.

This was a cross-sectional study. A sample of individuals with SAD (with or without psychosis) was compared with a sample with psychosis only and healthy controls on shame proneness, shame cognitions linked to psychosis and perceived social status.

Shame proneness (p < 0.01) and loss of social status (p < 0.01) were significantly elevated in those with SAD (with or without psychosis) compared to those with psychosis only and healthy controls. Individuals with psychosis and social anxiety expressed significantly greater levels of shame (p < 0.05), rejection (p < 0.01) and appraisals of entrapment (p < 0.01) linked to their diagnosis and associated stigma, compared to those without social anxiety.

These findings suggest that shame cognitions arising from a stigmatizing illness play a significant role in social anxiety in psychosis. Psychological interventions could be enhanced by taking into consideration these idiosyncratic shame appraisals when addressing symptoms of social anxiety and associated distress in psychosis. Further investigation into the content of shame cognitions and their role in motivating concealment of the stigmatized identity of being ‘ill’ is needed.

In previous studies an association between deployment to Iraq or Afghanistan and an overall increased risk for post-traumatic stress disorder (PTSD) in UK armed forces has not been found. The lack of a deployment effect might be explained by including, in the comparison group, personnel deployed on other operations or who have experienced traumatic stressors unrelated to deployment.

The sample comprised 8261 regular UK armed forces personnel who deployed to Iraq, Afghanistan or other operational areas or were not deployed. Participants completed the PTSD CheckList – Civilian Version (PCL-C) and provided information about deployment history, demographic and service factors, serious accidents and childhood experiences.

Deployment to Iraq or Afghanistan [odds ratio (OR) 1.2, 95% confidence interval (CI) 0.6–2.2] or elsewhere (OR 1.1, 95% CI 0.6–2.0) was unrelated to PTSD although holding a combat role was associated with PTSD if deployed to Iraq or Afghanistan (OR 2.7, 95% CI 1.9–3.9). Childhood adversity (OR 3.3, 95% CI 2.1–5.0), having left service (OR 2.7, 95% CI 1.9–4.0) and serious accident (OR 2.1, 95% CI 1.4–3.0) were associated with PTSD whereas higher rank was protective (OR 0.3, 95% CI 0.12–0.76).

For the majority of UK armed forces personnel, deployment whether to Iraq, Afghanistan or elsewhere confers no greater risk for PTSD than service in the armed forces per se but holding a combat role in those deployed to Iraq or Afghanistan is associated with PTSD. Vulnerability factors such as lower rank, childhood adversity and leaving service, and having had a serious accident, may be at least as important as holding a combat role in predicting PTSD in UK armed forces personnel.

Herpes virus infections can cause cognitive impairment during and after acute encephalitis. Although chronic, latent/persistent infection is considered to be relatively benign, some studies have documented cognitive impairment in exposed persons that is untraceable to encephalitis. These studies were conducted among schizophrenia (SZ) patients or older community dwellers, among whom it is difficult to control for the effects of co-morbid illness and medications. To determine whether the associations can be generalized to other groups, we examined a large sample of younger control individuals, SZ patients and their non-psychotic relatives (n=1852).

Using multivariate models, cognitive performance was evaluated in relation to exposures to herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2) and cytomegalovirus (CMV), controlling for familial and diagnostic status and sociodemographic variables, including occupation and educational status. Composite cognitive measures were derived from nine cognitive domains using principal components of heritability (PCH). Exposure was indexed by antibodies to viral antigens.

PCH1, the most heritable component of cognitive performance, declines with exposure to CMV or HSV-1 regardless of case/relative/control group status (p = 1.09 × 10−5 and 0.01 respectively), with stronger association with exposure to multiple herpes viruses (β = −0.25, p = 7.28 × 10−10). There were no significant interactions between exposure and group status.

Latent/persistent herpes virus infections can be associated with cognitive impairments regardless of other health status.

Much is still unclear about the role of personality in the structure of common psychiatric disorders such as depressive/anxiety disorders and alcohol dependence. This study will therefore examine whether various traits of negative emotionality and impulsivity showed shared or specific associations with these disorders.

Cross-sectional data were used from the Netherlands Study of Depression and Anxiety (NESDA), including individuals with no DSM-IV psychiatric disorder (n = 460), depressive/anxiety disorder only (i.e. depressive and/or anxiety disorder; n = 1398), alcohol dependence only (n = 32) and co-morbid depressive/anxiety disorder plus alcohol dependence (n = 358). Aspects of negative emotionality were neuroticism, hopelessness, rumination, worry and anxiety sensitivity, whereas aspects of impulsivity included disinhibition, thrill/adventure seeking, experience seeking and boredom susceptibility.

Aspects of negative emotionality formed a homogeneous dimension, which was unrelated to the more heterogeneous construct of impulsivity. Although all aspects of negative emotionality were associated with alcohol dependence only, associations were much stronger for depressive/anxiety disorder only and co-morbid depressive/anxiety disorder with alcohol dependence. The results for impulsivity traits were less profound and more variable, with disinhibition and boredom susceptibility showing modest associations with both depressive/anxiety disorder and alcohol dependence, whereas low thrill/adventure seeking and high disinhibition were more strongly related with the first and the latter, respectively.

Our results suggest that depressive/anxiety disorder and alcohol dependence result from shared as well as specific aetiological pathways as they showed the same associations with all aspects of negative emotionality, disinhibition and boredom susceptibility as well as specific associations with thrill/adventure seeking and disinhibition.

Various studies support the inclusion of cannabis withdrawal in the diagnosis of cannabis use disorder (CUD) in the upcoming DSM-5. The aims of the current study were to (1) estimate the prevalence of DSM-5 cannabis withdrawal (criterion B), (2) estimate the role of genetic and environmental influences on individual differences in cannabis withdrawal and (3) determine the extent to which genetic and environmental influences on cannabis withdrawal overlap with those on DSM-IV-defined abuse/dependence.

The sample included 2276 lifetime cannabis-using adult Australian twins. Cannabis withdrawal was defined in accordance with criterion B of the proposed DSM-5 revisions. Cannabis abuse/dependence was defined as endorsing one or more DSM-IV criteria of abuse or three or more dependence criteria. The classical twin model was used to estimate the genetic and environmental influences on variation in cannabis withdrawal, along with its covariation with abuse/dependence.

Of all the cannabis users, 11.9% met criteria for cannabis withdrawal. Around 50% of between-individual variation in withdrawal could be attributed to additive genetic variation, and the rest of the variation was mostly due to non-shared environmental influences. Importantly, the genetic influences on cannabis withdrawal almost completely (99%) overlapped with those on abuse/dependence.

We have shown that cannabis withdrawal symptoms exist among cannabis users, and that cannabis withdrawal is moderately heritable. Genetic influences on cannabis withdrawal are the same as those affecting abuse/dependence. These results add to the wealth of literature that recommends the addition of cannabis withdrawal to the diagnosis of DSM-5 CUD.

Using longitudinal and prospective measures of psychotic experiences during adolescence, we assessed the risk of developing psychosis in three groups showing low, increasing and elevated psychotic experiences associated with bullying by peers and cannabis use in a UK sample of adolescents.

Data were collected by self-report from 1098 adolescents (mean age 13.6 years; 60.9% boys) at five separate time points, equally separated by 6 months, across a 24-month period. General growth mixture modelling identified three distinct trajectories of adolescents reporting psychotic experiences: elevated, increasing and low.

Controlling for cannabis use, bullying by peers significantly predicted change in psychotic experiences between Time 2 and Time 5 in adolescents belonging to the increasing group. No effect was found for the elevated or low groups. Controlling for bullying, an earlier age of cannabis use and cannabis use more than twice significantly predicted change in psychotic experiences in adolescents belonging to the increasing group. Cannabis use at any age was significantly associated with subsequent change in psychotic experiences in the low group. Reverse causal associations were examined and there was no evidence for psychotic experiences at Time 1 predicting a subsequent change in cannabis use between Times 2 and 5 in any trajectory group.

Bullying by peers and cannabis use are associated with adolescents' reports of increasing psychotic experiences over time. Further research into the longitudinal development of psychosis in adolescence and the associated risk factors would allow for early intervention programmes to be targeted more precisely.

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of elevated alanine aminotransferase (ALT). NAFLD is associated with insulin resistance and hepatic inflammation. Similarly, patients with depression exhibit insulin resistance and increased inflammatory markers. However, no study has shown a clear association between elevated ALT and the development of depression. The aim of the study was to test whether elevated ALT, a surrogate marker for NAFLD, predicts the development of depression.

The present prospective cohort study investigated 12 180 employed adults referred for health examinations that included fasting blood tests and anthropometric measurements between 2003 and 2010. Exclusion criteria were: baseline minor/major depression, excessive alcohol consumption and other causes for ALT elevation. Depression was evaluated by the eight-item Patient Health Questionnaire (PHQ-8) score.

The final cohort included 5984 subjects [69.4% men, aged 45.0 (s.d. = 10.24) years]. The incidence rate of minor and major depression was 3.8% and 1.4%, respectively. Elevated ALT was a significant independent predictor for the occurrence of minor [odds ratio (OR) 2.02, 95% confidence interval (CI) 1.40–2.92] and major (OR 3.132, 95% CI 1.81–5.40) depression after adjusting for age, gender, body mass index, education level, serum levels of lipids, glucose, smoking and physical activity. Adding subjective health and affective state parameters (sleep disturbances, self-rated health, anxiety and burnout) as potential mediators only slightly ameliorated the association. Persistently elevated ALT was associated with the greatest risk for minor or major depression as compared with elevation only at baseline or follow-up (p for trend < 0.001).

Elevated ALT was associated with developing depressive symptoms, thus suggesting that NAFLD may represent an independent modifiable risk factor for depression.

Specific cognitions and behaviours are hypothesized to be important in maintaining chronic fatigue syndrome (CFS). Previous research has shown that a substantial proportion of CFS patients have co-morbid anxiety and/or depression. This study aims to measure the prevalence of specific cognitions and behaviours in patients with CFS and to determine their association with co-morbid anxiety or depression disorders.

A total of 640 patients meeting Oxford criteria for CFS were recruited into a treatment trial (i.e. the PACE trial). Measures analysed were: the Cognitive Behavioural Response Questionnaire, the Chalder Fatigue Scale and the Work and Social Adjustment Scale. Anxiety and depression diagnoses were from the Structured Clinical Interview for DSM-IV. Multivariate analysis of variance was used to explore the associations between cognitive-behavioural factors in patients with and without co-morbid anxiety and/or depression.

Of the total sample, 54% had a diagnosis of CFS and no depression or anxiety disorder, 14% had CFS and one anxiety disorder, 14% had CFS and depressive disorder and 18% had CFS and both depression and anxiety disorders. Cognitive and behavioural factors were associated with co-morbid diagnoses; however, some of the mean differences between groups were small. Beliefs about damage and symptom focussing were more frequent in patients with anxiety disorders while embarrassment and behavioural avoidance were more common in patients with depressive disorder.

Cognitions and behaviours hypothesized to perpetuate CFS differed in patients with concomitant depression and anxiety. Cognitive behavioural treatments should be tailored appropriately.

Schizo-affective disorder has not been studied to any significant extent using functional imaging. The aim of this study was to examine patterns of brain activation and deactivation in patients meeting strict diagnostic criteria for the disorder.

Thirty-two patients meeting Research Diagnostic Criteria (RDC) for schizo-affective disorder (16 schizomanic and 16 schizodepressive) and 32 matched healthy controls underwent functional magnetic resonance imaging (fMRI) during performance of the n-back task. Linear models were used to obtain maps of activations and deactivations in the groups.

Controls showed activation in a network of frontal and other areas and also deactivation in the medial frontal cortex, the precuneus and the parietal cortex. Schizo-affective patients activated significantly less in prefrontal, parietal and temporal regions than the controls, and also showed failure of deactivation in the medial frontal cortex. When task performance was controlled for, the reduced activation in the dorsolateral prefrontal cortex (DLPFC) and the failure of deactivation of the medial frontal cortex remained significant.

Schizo-affective disorder shows a similar pattern of reduced frontal activation to schizophrenia. The disorder is also characterized by failure of deactivation suggestive of default mode network dysfunction.

Although transient psychotic disorders are currently classified as a category separate from schizophrenia (SZ) and affective disorders, their distinctive features remain uncertain. This study examines the family psychiatric morbidity of the ICD-10 category of ‘acute and transient psychotic disorders’ (ATPDs), pointing out differences from SZ and bipolar disorder (BD).

From a cohort of 2.5 million persons, we identified all patients enrolled in the Danish Psychiatric Register who were ever admitted with ATPDs (n=2537), SZ (n = 10639) and BD disorder (n=5292) between 1996 and 2008. The relative risk (RR) of ATPDs, SZ and BD associated with psychiatric morbidity in first-degree relatives (FDRs) was calculated as the incidence rate ratio using Poisson regression.

The RR of ATPDs [1.93, 95% confidence interval (CI) 1.76–2.11] was higher if patients with ATPDs had at least one FDR admitted with any mental disorder than patients without family psychiatric antecedents. An additional risk arose if they had FDRs admitted not only with ATPDs (RR 1.60, 95% CI 1.33–1.92) but also with SZ (RR 2.06, 95% CI 1.70–2.50) and/or BD (RR 1.55, 95% CI 1.23–1.96). Despite some overlap, the risk of SZ (RR 2.80, 95% CI 2.58–3.04) and BD (RR 3.68, 95% CI 3.29–4.12) was markedly higher if patients with SZ and BD had FDRs admitted with the same condition.

These findings suggest that family psychiatric predisposition has a relatively modest impact on ATPDs and argue against a sharp differentiation of ATPDs from SZ and BD.

The mechanisms that contribute to emotion dysregulation in anxiety disorders are not well understood. Two common disorders, generalized anxiety disorder (GAD) and panic disorder (PD), were examined to test the hypothesis that both disorders are characterized by hypo-activation in prefrontal cortex (PFC) during emotion regulation. A competing hypothesis that GAD in particular is characterized by PFC hyper-activation during emotion regulation (reflecting overactive top-down control) was also evaluated.

Twenty-two medication-free healthy control (HC), 23 GAD, and 18 PD participants underwent functional magnetic resonance imaging (fMRI) during a task that required them to reappraise (i.e. reduce) or maintain emotional responses to negative images.

GAD participants reported the least reappraisal use in daily life, and reappraisal use was inversely associated with anxiety severity and functional impairment in these participants. During fMRI, HCs demonstrated greater activation during both reappraisal and maintenance than either GAD or PD participants (who did not differ) in brain areas important for emotion regulation (e.g. dorsolateral and dorsomedial PFC). Furthermore, across all anxious participants, activation during reappraisal in dorsolateral and dorsomedial PFC was inversely associated with anxiety severity and functional impairment.

Emotion dysregulation in GAD and PD may be the consequence of PFC hypo-activation during emotion regulation, consistent with insufficient top-down control. The relationship between PFC hypo-activation and functional impairment suggests that the failure to engage PFC during emotion regulation may be part of the critical transition from dispositionally high anxiety to an anxiety disorder.

Overweight/obesity and depression are both major public health problems among adolescents. However, the question of a link between overweight/obesity and depression remains unresolved in this age group. We examined whether obesity increases risk of depression, or depression increases risk of obesity, or whether there is a reciprocal effect.

A two-wave prospective cohort study of adolescents aged 11–17 years at baseline (n = 4175) followed up a year later (n = 3134) sampled from the Houston metropolitan area. Overweight was defined as 95th percentile >body mass index (BMI) ⩽85th percentile and obese as BMI >95th percentile. Three indicators of depression were examined: any DSM-IV mood disorder, major depression, and symptoms of depression.

Data for the two-wave cohort indicated no evidence of reciprocal effects between weight and depression. Weight status predicted neither major depression nor depressive symptoms. However, mood disorders generally and major depression in particular increased risk of future obesity more than twofold. Depressed males had a sixfold increased risk of obesity. Females with depressive symptoms had a marginally increased risk of being overweight but not obese.

Our findings, combined with those of recent meta-analyses, suggest that obese youths are not more likely to become depressed but that depressed youths are more likely to become obese.

Initiation of cannabis use typically follows alcohol use, but the reverse order does occur and is more common for African-Americans (AAs) than European-Americans (EAs). The aim of this study was to test for differences in the order of initiation of cannabis and alcohol use between AA and EA women and to determine whether order and ethnicity contribute independently to risk for rapid progression to cannabis-related problems.

Data were drawn from structured psychiatric interviews of 4102 women (mean age = 21.6 years), 3787 from an all-female twin study and 315 from a high-risk family study; 18.1% self-identified as AA, 81.9% as EA. Ethnicity and order of initiation of cannabis and alcohol use were modeled as predictors of transition time from first use to onset of cannabis use disorder symptom(s) using Cox proportional hazards regression analyses.

AA women were nearly three times as likely as EA women to initiate cannabis use before alcohol use. Using cannabis before alcohol [hazard ratio (HR) 1.44, 95% confidence interval (CI) 1.08–1.93] and AA ethnicity (HR 1.59, 95% CI 1.13–2.24) were both associated with rapid progression from first use to cannabis symptom onset even after accounting for age at initiation and psychiatric risk factors.

The findings indicate that AA women are at greater risk for rapid development of cannabis-related problems than EA women and that this risk is even higher when cannabis use is initiated before alcohol use. Prevention programs should be tailored to the various patterns of cannabis use and relative contributions of risk factors to the development of cannabis-related problems in different ethnic groups.

Schizophrenia is characterized by deficits in emotional prosody (EP) perception. However, it is not clear which stages of processing prosody are abnormal and whether the presence of semantic content contributes to the abnormality. This study aimed to examine event-related potential (ERP) correlates of EP processing in 15 chronic schizophrenia individuals and 15 healthy controls.

A total of 114 sentences with neutral semantic content [sentences with semantic content (SSC) condition] were generated by a female speaker (38 with happy, 38 with angry, and 38 with neutral intonation). The same sentences were synthesized and presented in the ‘pure prosody’ sentences (PPS) condition where semantic content was unintelligible.

Group differences were observed for N100 and P200 amplitude: patients were characterized by more negative N100 for SSC, and more positive P200 for angry and happy SSC and happy PPS. Correlations were found between delusions and P200 amplitude for happy SSC and PPS. Higher error rates in the recognition of EP were also observed in schizophrenia: higher error rates in neutral SSC were associated with reduced N100, and higher error rates in angry SSC were associated with reduced P200.

These results indicate that abnormalities in prosody processing occur at the three stages of EP processing, and are enhanced in SSC. Correlations between P200 amplitude for happy prosody and delusions suggest a role that abnormalities in the processing of emotionally salient acoustic cues may play in schizophrenia symptomatology. Correlations between ERP and behavioral data point to a relationship between early sensory abnormalities and prosody recognition in schizophrenia.

Cannabis can induce transient psychotic symptoms, but not all users experience these adverse effects. We compared the neural response to Δ9-tetrahydrocannabinol (THC) in healthy volunteers in whom the drug did or did not induce acute psychotic symptoms.

In a double-blind, placebo-controlled, pseudorandomized design, 21 healthy men with minimal experience of cannabis were given either 10 mg THC or placebo, orally. Behavioural and functional magnetic resonance imaging measures were then recorded whilst they performed a go/no-go task.

The sample was subdivided on the basis of the Positive and Negative Syndrome Scale positive score following administration of THC into transiently psychotic (TP; n = 11) and non-psychotic (NP; n = 10) groups. During the THC condition, TP subjects made more frequent inhibition errors than the NP group and showed differential activation relative to the NP group in the left parahippocampal gyrus, the left and right middle temporal gyri and in the right cerebellum. In these regions, THC had opposite effects on activation relative to placebo in the two groups. The TP group also showed less activation than the NP group in the right middle temporal gyrus and cerebellum, independent of the effects of THC.

In this first demonstration of inter-subject variability in sensitivity to the psychotogenic effects of THC, we found that the presence of acute psychotic symptoms was associated with a differential effect of THC on activation in the ventral and medial temporal cortex and cerebellum, suggesting that these regions mediate the effects of the drug on psychotic symptoms.

Convergent studies provide support for abnormalities in the structure and functioning of the prefrontal cortex (PFC) and the amygdala, the key components of the neural system that subserves emotional processing in major depressive disorder (MDD). We used resting-state functional magnetic resonance imaging (fMRI) to examine potential amygdala–PFC functional connectivity abnormalities in treatment-naive subjects with MDD.

Resting-state fMRI data were acquired from 28 individuals with MDD and 30 healthy control (HC) subjects. Amygdala–PFC functional connectivity was compared between the MDD and HC groups.

Decreased functional connectivity to the left ventral PFC (VPFC) from the left and right amygdala was observed in the MDD group, compared with the HC group (p < 0.05, corrected).

The treatment-naive subjects with MDD showed decreased functional connectivity from the amygdala to the VPFC, especially to the left VPFC. This suggests that these connections may play an important role in the neuropathophysiology of MDD at its onset.

Psychopathy and antisocial personality disorder (ASPD) are both characterized by impulsive, externalizing behaviors. Researchers have argued, however, that psychopathy is distinguished from ASPD by the presence of interpersonal–affective features that reflect an underlying deficit in emotional sensitivity. No study to date has tested for differential relations of these disorders with the brain's natural orienting response to sudden aversive events.

Electroencephalography was used to assess cortical reactivity to abrupt noise probes presented during the viewing of pleasant, neutral and unpleasant pictures in 140 incarcerated males diagnosed using the Psychopathy Checklist – Revised and DSM-IV criteria for ASPD. The primary dependent measure was the P3 event-related potential response to the noise probes.

Psychopaths showed significantly smaller amplitude of P3 response to noise probes across trials of all types compared with non-psychopaths. Follow-up analyses revealed that this overall reduction was attributable specifically to the affective–interpersonal features of psychopathy. By contrast, no group difference in general amplitude of probe P3 was evident for ASPD versus non-ASPD participants.

The findings demonstrate a reduced cortical orienting response to abrupt aversive stimuli in participants exhibiting features of psychopathy that are distinct from ASPD. The specificity of the observed effect fits with the idea that these distinctive features of psychopathy reflect a deficit in defensive reactivity, or mobilization of the brain's defensive system, in the context of threat cues.

A family history (FH) of alcohol dependence (AD) not only increases the risk for AD, but is also associated with an increased risk for mood and anxiety disorders. However, it is unknown how a FH of AD affects neural substrates in patients with mood and anxiety disorders. In this study we examined the effects of an alcoholic FH on cognitive and emotional functions in these patients using functional magnetic resonance imaging (fMRI).

In a sample of non-alcoholic patients with depressive and/or anxiety disorders from the Netherlands Study of Depression and Anxiety (NESDA) neuroimaging study, patients with a first-degree FH of AD (FH + ; n = 31) were compared with patients without a FH (FH–; n = 77) on performance and brain activation during visuospatial planning and emotional word encoding. Results were compared with those of healthy controls (HCs) without a FH of AD (n = 31).

FH+ patients performed slower during planning with increasing task load, coupled with stronger blood oxygen level-dependent responses in dorsal prefrontal areas compared with FH− patients and HCs. FH was not associated with performance differences during word encoding, but right insula activation during positive word encoding was present in FH+ patients, comparable with HCs, but absent in FH− patients.

This study demonstrates subtle impairments during planning in FH+ compared with FH− patients and HCs, whereas activation during mood-incongruent stimuli in FH+ patients was similar to HCs but not FH− patients, suggesting that the presence of a FH of AD is a useful marker for the neurophysiological profile in mood/anxiety disorders and possible predictor for treatment success.

Most studies reporting the gender difference in age at onset of schizophrenia show an earlier onset in males, but vary considerably in their estimates of the difference. This may be due to variations in study design, setting and diagnostic criteria. In particular, several studies conducted in developing countries have found no difference or a reversed effect whereby females have an earlier onset. The aim of the study was to investigate gender differences in age of onset, and the impact of study design and setting on estimates thereof.

Study methods were a systematic literature search, meta-analysis and meta-regression.

A total of 46 studies with 29218 males and 19402 females fulfilled the inclusion criteria and were entered into a meta-analysis. A random-effects model gave a pooled estimate of the gender difference of 1.07 years (95% confidence interval 0.21–1.93) for age at first admission of schizophrenia, with males having earlier onset. The gender difference in age at onset was not significantly different between developed and developing countries. Studies using Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria showed a significantly greater gender difference in age at onset than studies using International Classification of Diseases (ICD) criteria, the latter showing no difference.

The gender difference in age of onset in schizophrenia is smaller than previously thought, and appears absent in studies using ICD. There is no evidence that the gender difference differs between developed and developing countries.

Only a minority of trauma victims (<10%) develops post-traumatic stress disorder (PTSD), suggesting that victims vary in predispositions to the PTSD response to traumas. It is assumed that the influence of predispositions is inversely related to trauma severity: when trauma is extreme predispositions are assumed to play a secondary role. This assumption has not been tested. We estimate the influence of key predispositions on PTSD induced by an extreme trauma – associated with a high percentage of PTSD – (sexual assault), relative to events of lower magnitude (accidents, disaster, and unexpected death of someone close).

The National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) is representative of the adult population of the USA. A total of 34 653 respondents completed the second wave in which lifetime PTSD was assessed. We conducted three series of multinomial logistic regressions, comparing the influence of six predispositions on the PTSD effect of sexual assault with each comparison event. Three pre-existing disorders and three parental history variables were examined.

Predispositions predicted elevated PTSD risk among victims of sexual assault as they did among victims of comparison events. We detected no evidence that the influence of predispositions on PTSD risk was significantly lower when the event was sexual assault, relative to accidents, disasters and unexpected death of someone close.

Important predispositions increase the risk of PTSD following sexual assault as much as they do following accidents, disaster, and unexpected death of someone close. Research on other predispositions and alternative classifications of event severity would be illuminating.