Although gender differences in rates of internalizing disorders, particularly depression, are well documented, the causes of these differences are not well understood. One influential hypothesis [Cutler & Nolen-Hoeksema, Sex Roles (1991), 24, 425–438] proposes that higher rates of depression in females compared to males may be partially attributable to gender differences in the effects of childhood sexual abuse. The present study has evaluated this possibility by reviewing evidence for gender moderating the effects of childhood victimization on psychiatric outcomes.

Literature search using PsycINFO and Medline, applying the following inclusion criteria: publication from 1996 to 2006, community-based sampling, adequate male-to-female sample ratio, use of clearly defined psychiatric outcomes, and a statistical test of gender differences in the effects of childhood victimization on psychiatric outcomes.

Thirty studies met inclusion criteria. Overall, the results were mixed. Nearly half of all studies find no gender differences. In studies that do observe gender differences, victimization tends to be associated with higher psychiatric risk in females in studies with adult samples, whereas in samples of youth, victimization tends to be associated with higher psychiatric risk in males. With respect to outcome, when gender differences were observed, outcomes were distributed across both internalizing and externalizing categories for both genders.

The gender differences in prevalence rates of internalizing disorders, such as depression, do not appear to be attributable to differential effects of childhood victimization.

This review systematically appraised the research evidence for local versus global information processing to test the hypothesis that people with eating disorders (ED) had weak central coherence.

Searches on Medline, EMBASE, PsycINFO and ISI Web of Science databases were conducted in November 2006 and subsequently updated in September 2007. Each search was conducted in two steps: (1) neuropsychological tasks measuring central coherence and (2) words related to cognitive functioning in eating disorders. Data were summarized in a meta-analysis if the number of studies for a given test was >5.

Data were extracted from 16 studies. Meta-analyses were conducted for four tasks obtaining moderate effect sizes. The majority of studies found global processing difficulties across the ED spectrum. The results are less clear regarding local processing.

People with ED have difficulties in global processing. It is less certain as to whether they have superior local processing. Currently, there is insufficient evidence to refute the weak central coherence hypothesis.

Cognitive models suggest that distress associated with auditory hallucinations is best understood in terms of beliefs about voices. What is less clear is what factors govern such beliefs. This study aimed to explore the way in which traumatic life events contribute towards beliefs about voices and any associated distress.

The difference in the nature and prevalence of traumatic life events and associated psychological sequelae was compared in two groups of voice hearers: psychiatric voice hearers with predominantly negative beliefs about voices (PVH) and non-psychiatric voice hearers with predominantly positive beliefs about voices (NPVH). The data from the two groups were then combined in order to examine which factors could significantly account for the variance in beliefs about voices and therefore levels of distress.

Both groups reported a high prevalence of traumatic life events although significantly more PVH reported trauma symptoms sufficient for a diagnosis of post-traumatic stress disorder (PTSD). Furthermore, significantly more PVH reported experiencing childhood sexual abuse. Current trauma symptoms (re-experiencing, avoidance and hyperarousal) were found to be a significant predictor of beliefs about voices. Trauma variables accounted for a significant proportion of the variance in anxiety and depression.

The results suggest that beliefs about voices may be at least partially understood in the context of traumatic life events.

Chemical weapons exercise an enduring and often powerful psychological effect. This had been recognized during the First World War when it was shown that the symptoms of stress mimicked those of mild exposure to gas. Debate about long-term effects followed the suggestion that gassing triggered latent tuberculosis.

A random sample of 103 First World War servicemen awarded a war pension for the effects of gas, but without evidence of chronic respiratory pathology, were subjected to cluster analysis using 25 common symptoms. The consistency of symptom reporting was also investigated across repeated follow-ups.

Cluster analysis identified four groups: one (n=56) with a range of somatic symptoms, a second (n=30) with a focus on the respiratory system, a third (n=12) with a predominance of neuropsychiatric symptoms, and a fourth (n=5) with a narrow band of symptoms related to the throat and breathing difficulties. Veterans from the neuropsychiatric cluster had multiple diagnoses including neurasthenia and disordered action of the heart, and reported many more symptoms than those in the three somatic clusters.

Mild or intermittent respiratory disorders in the post-war period supported beliefs about the damaging effects of gas in the three somatic clusters. By contrast, the neuropsychiatric group did not report new respiratory illnesses. For this cluster, the experience of gassing in a context of extreme danger may have been responsible for the intensity of their symptoms, which showed no sign of diminution over the 12-year follow-up.

Victims of war captivity sometimes suffer from complex post-traumatic stress disorder (PTSD), a unique form of PTSD that entails various alterations in personality. These alterations may involve changes in attachment orientation.

The sample comprised two groups of veterans from the 1973 Yom Kippur War: 103 ex-prisoners of war (ex-POWs) and 106 comparable control veterans. They were assessed at two points in time, 18 years and 30 years after the war.

Ex-POWs suffered from more post-traumatic symptoms than controls at both measurements points and these symptoms increased only among ex-POWs from Time 1 to Time 2. In addition, both attachment anxiety and attachment avoidance increased with time among ex-POWs, whereas they decreased slightly or remained stable among controls. Finally, the increases in attachment anxiety and avoidance were positively associated with the increase in post-traumatic symptoms among both study groups. Further analyses indicated that early PTSD symptoms predicted later attachment better than early attachment predicted later PTSD symptoms.

The results suggest that: (1) complex traumas are implicated in attachment orientations and PTSD symptoms even many years after captivity; (2) there is an increase in attachment insecurities (anxiety, avoidance) and an increase in PTSD symptoms decades after the captivity; (3) and post-traumatic stress symptoms predict attachment orientations better than attachment orientations predict an increase in PTSD symptoms.

Recent studies suggest that purging disorder (PD) may be a common eating disorder that is associated with clinically significant levels of distress and high levels of psychiatric co-morbidity. However, no study has established evidence of disorder-related impairment or whether distress is specifically related to PD rather than to co-morbid disorders.

Three groups of normal-weight women [non-eating disorder controls (n=38), with PD (n=24), and with bulimia nervosa (BN)-purging subtype (n=57)] completed structured clinical interviews and self-report assessments.

Both PD and BN were associated with significant co-morbidity and elevations on indicators of distress and impairment compared to controls. Compared to BN, PD was associated with lower rates of current and lifetime mood disorders but higher rates of current anxiety disorders. Elevated distress and impairment were maintained in PD and BN after controlling for Axis I and Axis II disorders.

PD is associated with elevated distress and impairment and should be considered for inclusion as a provisional disorder in nosological schemes such as the Diagnostic and Statistical Manual to facilitate much-needed research on this clinically significant syndrome.

Prospective, longitudinal studies of risk factors for anorexia nervosa (AN) are lacking and existing cross-sectional studies are generally narrow in focus and lack methodological rigor. Building on two studies that used the Oxford Risk Factor Interview (RFI) to establish time precedence and comprehensively assess potential risk correlates for AN, the present study advances this line of research and represents the first case-control study of risk factors for AN in the USA.

The RFI was used for retrospective assessment of a broad range of risk factors, while establishing time precedence. Using a case-control design, 50 women who met DSM-IV criteria for AN were compared to those with non-eating disorder DSM-IV psychiatric disorders (n=50) and those with no psychiatric disorder (n=50).

Women with psychiatric disorders reported higher rates of negative affectivity, maternal and paternal parenting problems, family discord, parental mood and substance disorder, and physical and sexual abuse than women with no psychiatric disorder. Women with AN specifically reported greater severity and significantly higher rates of negative affectivity, perfectionism and family discord, and higher parental demands than women with other psychiatric disorders. The role of weight and shape concerns was most salient in the year preceding onset of AN.

Convergent data identifying common risk factors as well as those more severe in the development of AN are emerging to inform longitudinal risk factor and prevention studies for this disorder.

Objective binge eating (OBE) and self-induced vomiting (SIV) occur and co-occur across a range of eating disorders but the extent to which the risk factors for these two behaviours overlap is unclear. Examination of this overlap was the focus of the current report.

A population of female Australian twins (n=1002), mean age 35 years (s.d.=2.11, range 28–40), participated in three waves of data collection and were assessed for lifetime disordered eating with a semi-structured interview at wave 3 and a self-report questionnaire at wave 1; risk factors were assessed via self-report at waves 1 and 3.

Non-shared environmental influences were the largest contributor to the variance of both OBE and SIV, with a more modest contribution of genetic influences. Between 5% and 14% of the environmental risk factors for OBE and SIV were shared and 27–100% of genetic risk factors were shared. SIV initiation was predicted by higher neuroticism and novelty seeking and lower maternal and paternal care, whilst lower levels of perceived paternal care, higher lifetime BMI, and a wider BMI range predicted OBE initiation. Retrospective correlates associated with both SIV and OBE onset were parental comments about weight, whilst higher levels of parental conflict, expectations and criticism was associated with OBE onset only.

The substantial extent of non-overlap between risk factors for SIV and OBE suggests that each of these behavioural disturbances warrants future investigation in its own right, not only when they occur in conjunction with each other.

This study examined healthcare services used by adults diagnosed with an eating disorder (ED) in a large health maintenance organization in the Pacific Northwest.

Electronic medical records were used to collect information on all out-patient and in-patient visits and medication dispenses, from 2002 to 2004, for adults aged 18–55 years who received an ED diagnosis during 2003. Healthcare services received the year prior to, and following, the receipt of an ED diagnosis were examined. Cases were matched to five comparison health plan members who had a health plan visit close to the date of the matched case's ED diagnosis.

Incidence of EDs (0.32% of the 104 130 females, and 0.02% of the 93 628 males) was consistent with prior research employing treatment-based databases, though less than community-based samples. Most cases (50%) were first identified during a primary-care visit and psychiatric co-morbidity was high. Health services use was significantly elevated in all service sectors among those with an ED when compared with matched controls both in the year preceding and that following the receipt of the incident ED diagnosis. Contrary to expectations, healthcare utilization was found to be similarly high across the spectrum of EDs (anorexia nervosa, bulimia nervosa, and eating disorders not otherwise specified).

The elevation in health service use among women both before and after diagnosis suggests that EDs merit identification and treatment efforts commensurate with other mental health disorders (e.g. depression) which have similar healthcare impact.

While the role of genetic factors in self-report measures of emotion has been frequently studied, we know little about the degree to which genetic factors influence emotional facial expressions.

Twenty-eight pairs of monozygotic (MZ) and dizygotic (DZ) twins from the Minnesota Study of Twins Reared Apart were shown three emotion-inducing films and their facial responses recorded. These recordings were blindly scored by trained raters. Ranked correlations between twins were calculated controlling for age and sex.

Twin pairs were significantly correlated for facial expressions of general positive emotions, happiness, surprise and anger, but not for general negative emotions, sadness, or disgust or average emotional intensity. MZ pairs (n=18) were more correlated than DZ pairs (n=10) for most but not all emotional expressions.

Since these twin pairs had minimal contact with each other prior to testing, these results support significant genetic effects on the facial display of at least some human emotions in response to standardized stimuli. The small sample size resulted in estimated twin correlations with very wide confidence intervals.

The association between poor mental health and poverty is well known but its mechanism is not fully understood. This study tests the hypothesis that the association between low income and mental disorder is mediated by debt and its attendant financial hardship.

The study is a cross-sectional nationally representative survey of private households in England, Scotland and Wales, which assessed 8580 participants aged 16–74 years living in general households. Psychosis, neurosis, alcohol abuse and drug abuse were identified by the Clinical Interview Schedule – Revised, the Schedule for Assessment in Neuropsychiatry (SCAN), the Alcohol Use Disorder Identification Test (AUDIT) and other measures. Detailed questions were asked about income, debt and financial hardship.

Those with low income were more likely to have mental disorder [odds ratio (OR) 2.09, 95% confidence interval (CI) 1.68–2.59] but this relationship was attenuated after adjustment for debt (OR 1.58, 95% CI 1.25–1.97) and vanished when other sociodemographic variables were also controlled (OR 1.07, 95% CI 0.77–1.48). Of those with mental disorder, 23% were in debt (compared with 8% of those without disorder), and 10% had had a utility disconnected (compared with 3%). The more debts people had, the more likely they were to have some form of mental disorder, even after adjustment for income and other sociodemographic variables. People with six or more separate debts had a six-fold increase in mental disorder after adjustment for income (OR 6.0, 95% CI 3.5–10.3).

Both low income and debt are associated with mental illness, but the effect of income appears to be mediated largely by debt.

Few large studies describe links between maternal mental illness and risk of major birth defect in offspring. Evidence is sparser still for how effects vary between maternal diagnoses and no previous study has assessed risk with paternal illnesses.

A population-based birth cohort was created by linking Danish national registers. We identified all singleton live births during 1973–1998 (n=1.45 m), all parental psychiatric admissions from 1969 onwards, and all fatal birth defects until 1 January 1999. Linkage and case ascertainment were almost complete. Relative risks were estimated using Poisson regression.

Risk of fatal birth defect was elevated in relation to history of any maternal admission and also with affective disorders specifically, although the strongest effect found was with maternal schizophrenia. The rate was more than doubled in this group compared to the general population [relative risk (RR) 2.34, 95% confidence interval (CI) 1.45–3.77], which also represented a significant excess risk compared with all other admitted maternal disorders (p=0.018). Risk of death from causes other than birth defect was no higher with schizophrenia than with other maternal conditions. There was no elevation in risk of fatal birth defect if the father was admitted with schizophrenia or any other psychiatric diagnosis.

There are many possible explanations for a higher risk of fatal birth defect with maternal schizophrenia and affective disorder. These include genetic effects directly linked with maternal illness, lifestyle factors (diet, smoking, alcohol and drugs), poor antenatal care, psychotropic medication toxicity, and gene–environment interactions. Further research is needed to elucidate the causal mechanisms.

Psychotic illness is strongly associated with the maternal uniparental disomy (mUPD) genetic subtype of Prader–Willi syndrome (PWS), but not the deletion subtype (delPWS). This study investigates the clinical features of psychiatric illness associated with PWS. We consider possible genetic and other mechanisms that may be responsible for the development of psychotic illness, predominantly in those with mUPD.

The study sample comprised 119 individuals with genetically confirmed PWS, of whom 46 had a history of psychiatric illness. A detailed clinical and family psychiatric history was obtained from these 46 using the PAS-ADD, OPCRIT, Family History and Life Events Questionnaires.

Individuals with mUPD had a higher rate of psychiatric illness than those with delPWS (22/34 v. 24/85, p<0.001). The profile of psychiatric illness in both genetic subtypes resembled an atypical affective disorder with or without psychotic symptoms. Those with delPWS were more likely to have developed a non-psychotic depressive illness (p=0.005) and those with mUPD a bipolar disorder with psychotic symptoms (p=0.00005). Individuals with delPWS and psychotic illness had an increased family history of affective disorder. This was confined exclusively to their mothers.

Psychiatric illness in PWS is predominately affective with atypical features. The prevalence and possibly the severity of illness are greater in those with mUPD. We present a ‘two-hit’ hypothesis, involving imprinted genes on chromosome 15, for the development of affective psychosis in people with PWS, regardless of genetic subtype.