The lead papers in this issue are two meta-analyses of controlled trials in a recently very active area: psychological treatments for schizophrenia. The findings of Pilling and colleagues are clear-cut. There is good evidence of worthwhile benefit from two forms of treatment. Family therapy delivered to people with schizophrenia who are in contact with carers, and particularly in single family rather than group approaches, lowers relapse rates and improves medication compliance. Cognitive therapy improves mental states and may be particularly useful for those with resistant symptoms. By contrast two other psychological treatments, social skills training and cognitive remediation, have failed to show evidence of benefit in controlled trials. The findings of these review articles have important implications for treatment.

The editorial in this issue reviews the orexins/hypocretins, a recently recognized group of neuropeptides, involved in sleep, arousal, narcolepsy and possibly other disorders.

Two articles concern epidemiology. Kessler and colleagues (pp. 959–976) report large scale development and validation of 10-item and 6-item versions of a scale with impressive performance in screening for DSM-IV psychiatric disorder in US and Australian general populations. Sacker & Wiggins (pp. 977–990) use two longitudinal cohort studies to examine gender and social class differences in psychological distress. Both narrowed over two decades with the higher rates in women and those in manual occupations falling, to become nearer males and non-manual occupations. Disadvantage is apparently lessening.

In another study of gender and disorder Fergusson and colleagues in New Zealand (pp. 991–996) find that the greater exposure of females to sexual violence explains some, but not all of their greater liability to internalizing disorders. In other aetiological studies, Enns et al. (pp. 997–1008) find associations of community disorder with lack of care on the Parental Bonding Instrument, while Reichborn-Kjennerud et al. (pp. 1009–1020) in a Norwegian twin sample find genetic links between back-neck pain and anxiety and depressive symptoms.

Four studies concern depression. In an important neuroendocrine study of chronic depression Watson et al. (pp. 1021–1028) find absence of the usual depressive HPA axis abnormalities, strongly suggesting that these normalize with time. Matsuo et al. (pp. 1029–1038) employ the little-used non-invasive technique of near infrared spectroscopy, to show a reduction in euthymic affective disorder patients compared with controls in the increase of oxyHb in the frontal region during a verbal fluency task and during hyperventilation, indicating persisting or antecedent abnormalities. In a controlled trial Chabrol et al. (pp. 1039–1047) find a brief cognitive-behavioural intervention reduces depression scores in postpartum mothers at risk for post-natal depression. Fava et al. (pp. 1049–1057) find personality disorder diagnoses to decline in frequency after treatment for depression, suggesting that depression contributes to and antidepressant ameliorates the behaviours and attitudes which comprise the personality disorders.

Two studies interface with psychoimmunology. In an important prospective study over up to 9 years, Leserman et al. (pp. 1059–1073) find progression of HIV accelerated by stressful life events, dysphoric mood and raised cortisol. Arnold et al. (pp. 1075–1089) report effects of inducing influenza-like symptoms in patients with chronic fatigue syndrome compared with normal controls. While somatic symptoms of CFS were exacerbated, cognitive and mood symptoms were not.

Three papers report findings in schizophrenia. Hooley & Campbell (pp. 1091–1099) find high expressed emotion relatives attribute more control to ill family members than do low EE relatives, but are actually themselves more controlling. Their high control predicts relapse in schizophrenia but not depression. Gooding & Tallent (pp. 1101–1107) find that schizophrenics show atypical perceptual biases in response to emotional chimeric faces. Malla et al. (pp. 1109–1119) report predictors of outcome at 1 year of first-episode psychosis, including some potential modifiable factors such as medication adherence and residual symptoms.

This issue features papers on consequences of trauma, psychiatric epidemiology, somatization and genetics.

In their editorial Breslau and colleagues (pp. 573–576) discuss two related issues: the linkage in PTSD between trauma and specific symptoms, and the place of the disorders that often occur co- morbidly with PTSD. They argue for the centrality of the first in the delineation of PTSD. The symptoms that follow trauma are the subject of several empirical papers later in the issue. Mayou & Bryant (pp. 671–675) report a range of symptoms 3 years after a road traffic accident, Altier et al. (pp. 677–685) report a variety of psychological disturbances 5 years after severe burns, and Simpson & Tate (pp. 687–697) report high rates of suicidal ideation and suicide attempts after traumatic brain injury. In a related paper Davidson and colleagues (pp. 661–670) examine in detail the effects of sertraline on PTSD.

This issue features groups of papers on genetics, the distributional nature of the milder disorder featuring most prominently in community surveys, diagnostic co-morbidity, neuropsychological and related aspects of schizophrenia.

The first group of papers come from genetic epidemiology, all from twin studies. Agrawal et al. (pp. 1155–1164) examine genetic and environmental origins of detailed aspects of social support. They find evidence for genetic elements in almost all aspects, with some smaller differences between males and females. Wichers et al. (pp. 1165–1174) report effects of pregnancy and birth complications and genetic elements on childhood behaviour problems. They find one specific complication, being of lower birth weight for gestational age, associated with problem behaviour, and an interaction with genetic effects, such that these are weaker in the presence of low birth weight. Johnson et al. (pp. 1175–1185) examine the heritability of depression measured on a symptom scale in Danish twins. They find genetic effects, which do not vary with age over a wide span from 45 to over 95. An accompanying editorial (pp. 1145–1148) looks at the future of genetic epidemiology in a time of accelerating molecular genetic research activity.

Epidemiological surveys frequently measure so-called common mental disorder, psychiatric symptoms in a milder range which may not necessarily fit defined criteria for specific disorders. Melzer et al. (pp. 1195–1201) using this kind of data from a community survey, find a continuous single distribution with no natural cut-off point. Brugha (pp. 1149–1154) in an accompanying editorial discusses the implications of such a dimensional approach and its relation to diagnosis.

Vanish 1. intr. To disappear from sight or become invisible, esp. in a rapid and mysterious way (Shorter Oxford English Dictionary, 1972).

There is a well-known view that hysteria has virtually disappeared in the Western world. There are two versions of this argument: one is that there was never a clinical disorder that coincided with the diagnosis, and hysteria has now been reconstructed as something else (e.g. Micale, 1993). The other is that hysteria did exist but has now become much rarer than it was (most famously, Veith, 1965). According to this view, hysteria is to be found in patients from developing countries, but in Western countries it is ‘virtually a historical curiosity’ (BMJ 1976). It is the latter view that is – in our experience – most commonly held by our colleagues in general psychiatry. Yet, this opinion is not shared by those who are involved in the clinical care of patients with neurological disorders: ‘to a psychiatrist who sees patients on the medical and surgical services of a general hospital, it appears that hysteria remains a rather common phenomenon’ (Brownsberger, 1966). A number of descriptions from liaison psychiatry services support this opinion (Akagi & House, 2001). There are good reasons why it might be difficult to judge just how common (or rare) hysteria really is. Epidemiology depends on reliable case definition, case ascertainment and selection of a suitable population to study (Neugebauer et al. 1980), and each of these poses problems in the study of hysterical disorders.

This issue features groups of papers on Gulf War syndrome, health service outcome assessment, somatization, personality disorders and depression.

Gulf War syndrome has been the subject of much scientific research and public controversy. Two research papers, both from the group at the Institute of Psychiatry in London report studies. David et al. (pp. 1357–1370) find cognitive abnormalities in Gulf War veterans compared with military controls, most attributable to mood disturbances, except for impairment of constructional ability. Everitt et al. (pp. 1371–1378) employ the statistical technique of cluster analysis to search for a unique syndrome in Gulf War veterans but fail to find it. In an accompanying editorial two authorities, from the USA and Canada, examine the issues.

Background. We aimed to determine if an association exists between uncomplicated hepatitis C virus (HCV) infection and depression or fatigue.

Method. A review of the literature was undertaken.

Results. There is an association between HCV infection and either depression or fatigue in certain circumstances – those who are aware they are HCV positive, those with advanced liver disease and those seen in specialist referral centres. All these studies are subject to important biases. There are only a few studies in which knowledge of HCV status and assessment of fatigue or depression is independent. These studies do not suggest an association. There is no association between conventional markers of liver disease and depression or fatigue.

Conclusions. Despite anecdotal evidence to the contrary, at the moment there is no evidence that HCV infection per se is associated with fatigue or depression, and there is a suggestion that it is not. The same risk factors that exist for fatigue in other physical illnesses, such as metabolic disorder, mood disorder, demographics and lack of exercise, certainly exist for HCV. Although there are elegant theoretical mechanisms, there is no compelling epidemiological evidence for an additional HCV specific fatigue or depression factor.

This issue features papers on community care, neuropsychological abnormalities in antisocial personality disorder, schizophrenia and other disorders, pharmacological aspects of affective disorders including effects of carbamazepine and lithium on inter-episode morbidity in bipolar disorder, and effects of tryptophan depletion in the relatives of bipolars.

Background. While there is a growing body of evidence on the efficacy of psychological interventions for schizophrenia, this meta-analysis improves upon previous systematic and meta-analytical reviews by including a wider range of randomized controlled trials and providing comparisons against both standard care and other active interventions.

Method. Literature searches identified randomized controlled trials of four types of psychological interventions: family intervention, cognitive behavioural therapy (CBT), social skills training and cognitive remediation. These were then subjected to meta-analysis on a variety of outcome measures. This paper presents results relating to the first two.

Results. Family therapy, in particular single family therapy, had clear preventative effects on the outcomes of psychotic relapse and readmission, in addition to benefits in medication compliance. CBT produced higher rates of ‘important improvement’ in mental state and demonstrated positive effects on continuous measures of mental state at follow-up. CBT also seems to be associated with low drop-out rates.

Conclusions. Family intervention should be offered to people with schizophrenia who are in contact with carers. CBT may be useful for those with treatment resistant symptoms. Both treatments, in particular CBT, should be further investigated in large trials across a variety of patients, in various settings. The factors mediating treatment success in these interventions should be researched.

Background. Previous studies that have examined genetic influences on suicidal behaviour were confounded by genetic vulnerability for psychiatric risk factors. The present study examines genetic influences on suicidality (i.e. suicidal ideation and/or suicide attempt) after controlling for the inheritance of psychiatric disorders.

Methods. Sociodemographics, combat exposure, lifetime DSM-III-R major depression, bipolar disorder, childhood conduct disorder, adult antisocial personality disorder, panic disorder, post-traumatic stress disorder, drug dependence, alcohol dependence and lifetime suicidal ideation and attempt were assessed in 3372 twin pairs from the Vietnam Era Twin Registry who were assessed in 1987 and 1992. Genetic risk factors for suicidality were examined in a multinomial logistic regression model. Additive genetic, shared environmental and non-shared environmental effects on suicidality were estimated using structural equation modelling, controlling for other risk factors.

Results. The prevalence of suicidal ideation and suicide attempt were 16·1% and 2·4% respectively. In a multinomial regression model, co-twin’s suicidality, being white, unemployment, being other than married, medium combat exposure and psychiatric disorders were significant predictors for suicidal ideation. Co-twin’s suicidality, unemployment, marital disruption, low education attainment and psychiatric disorders (except childhood conduct disorder) were significant predictors for suicide attempt. Model-fitting suggested that suicidal ideation was influenced by additive genetic (36%) and non-shared environmental (64%) effects, while suicide attempt was affected by additive genetic (17%), shared environmental (19%) and non-shared environmental (64%) effects.

Conclusions. There may be a genetic susceptibility specific to both suicidal ideation and suicide attempt in men, which is not explained by the inheritance of common psychiatric disorders.

The official definition of post-traumatic stress disorder (PTSD) in DSM-III and is subsequent DSM editions is based on a conceptual model that brackets traumatic or catastrophic events from less severe stressors and links them with a specific syndrome. The diagnosis of PTSD requires an identifiable stressor and the content of the defining symptoms refers to the stressor, for example, re-experiencing the stressor and avoidance of stimuli that symbolize the stressor. Temporal ordering is also required: when sleep problems and other symptoms of hyperarousal are part of the clinical picture, they must not have been present before the stressor occurred. The ICD-10 definition of PTSD follows the same model. The defining symptoms alone, without a connection to the stressor, are not regarded as PTSD (Green et al. 1995). Since the introduction of PTSD in DSM-III, the official definition has been adopted in most studies, although discussions about the validity of the definition has continued (Breslau & Davis, 1987; Davidson & Foa, 1993; Green et al. 1995). Although it is widely believed that other disorders (e.g. major depression) can be precipitated by external events, these disorders can occur independent of stressors and do not require a link with a traumatic event in their diagnostic criteria. Previous classifications that separated major depression into stress-related (reactive) or endogenous have been abandoned in newer versions of the DSM, because of lack of evidence of the validity of this distinction.

In this issue we publish three genetic epidemiology papers (Agrawal et al. 2002; Johnson et al. 2002; Wichers et al. 2002). Psychological Medicine in recent years has had genetic epidemiology as one of its major themes. We also publish some molecular genetic papers. This is a time when the development of molecular genetic technologies, which have already enabled the sequencing of the entire human genome, has been widely and appropriately hailed as a major advance, promising to generate a revolution in the understanding of causes of all human disease, including psychiatric, and in the discovery of new drugs. Psychological Medicine now has a distinguished American Editor from the world of genetic epidemiology in the person of Kenneth Kendler. This editorial, by his British editorial counterpart, is deliberately non-expert, and a view of the psychiatric future of genetic epidemiology from outside the field.

The basic findings for heritability of major psychiatric disorders have become well established and replicated in some decades of research. Family studies were followed by twin studies and adoption studies which established on a much firmer basis that a substantial element in the familiality was genetic. Disappointingly, the genes still remain to be identified with certainty. That is the task of molecular genetics. It is becoming increasingly clear that the task will not be an easy one, because for the most part we seem to have multi-gene disorders, with a number of or many genes of small effect, requiring large samples and quantitative trait methods to elucidate (Plomin et al. 1994).

The orexins/hypocretins are novel neuropeptides synthesized by neurons whose cell bodies are located in the lateral hypothalamus. Although these neurons are few in number, they send projections widely throughout the central nervous system (Kilduff & Peyron, 2000). There has been great excitement about the orexins/hypocretins from both the scientific and medical community. These peptides are remarkable in that they were discovered using state-of-the-art molecular techniques before their physiological actions were studied. Furthermore, there has been an exponential progress in our scientific knowledge of these peptides culminating in the orexins/hypocretins being linked to the sleep disorder, narcolepsy. With the importance of the orexins/hypocretins in sleep and arousal being increasingly recognized, it is likely that these peptides are altered by or contribute to several medical and psychiatric disorders.

Background. This paper examines genetic and environmental contributions to risk of cannabis dependence.

Method. Symptoms of cannabis dependence and measures of social, family and individual risk factors were assessed in a sample of 6265 young adult male and female Australian twins born 1964–1971.

Results. Symptoms of cannabis dependence were common: 11·0% of sample (15·1% of men and 7·8% of women) reported two or more symptoms of dependence. Correlates of cannabis dependence included educational attainment, exposure to parental conflict, sexual abuse, major depression, social anxiety and childhood conduct disorder. However, even after control for the effects of these factors, there was evidence of significant genetic effects on risk of cannabis dependence. Standard genetic modelling indicated that 44·7% (95% CI = 15–72·2) of the variance in liability to cannabis dependence could be accounted for by genetic factors, 20·1% (95% CI = 0–43·6) could be attributed to shared environment factors and 35·3% (95% CI = 26·4–45·7) could be attributed to non-shared environmental factors. However, while there was no evidence of significant gender differences in the magnitude of genetic and environmental influences, a model which assumed both genetic and shared environmental influences on risks of cannabis dependence among men and shared environmental but no genetic influences among women provided an equally good fit to the data.

Conclusions. There was consistent evidence that genetic risk factors are important determinants of risk of cannabis dependence among men. However, it remains uncertain whether there are genetic influences on liability to cannabis dependence among women.

In this edition of Psychological Medicine, research findings are reported from two studies of British Gulf War veterans (David et al. 2002; Everitt et al. 2002). Both studies were carried out at King's College ‘Gulf War Illness Research Unit’, which was established in 1996. The two studies were conducted to examine the causes of unexplained symptoms among Gulf War veterans. The results presented in these papers are important because they were derived from well-designed studies that employed a randomized sample of Gulf War veterans and two control populations of non-deployed ‘era’ veterans who served in the early 1990s and troops who participated in another hazardous deployment to Bosnia.

In one study, cognitive function and mood disturbances were evaluated using a comprehensive battery of neuropsychological tests and rating scales (David et al. 2002). A significant proportion of Gulf War veterans reporting ill health were found to have both lower cognitive function scores and depressed mood compared to well Gulf War veterans, era veterans and Bosnia troops. Importantly, a strong association was found between depressed mood and poor performance on cognitive function tests. It is noteworthy that among ill Gulf War veterans, most cognitive function measures were within the normal range, although they were significantly lower than those of controls.

Based on these and related research findings, the study investigators concluded that lower performance on cognitive function tests could be explained primarily by mood disturbances. However, they could not rule out the possibility that cognitive difficulties had led to depressed mood or that a neurotoxic environmental exposure had caused both health problems.

Background. Concerns have been raised about the scope and generalizability of much community mental health research. In particular, both experimental and control services are poorly characterized.

Methods. To review the effectiveness of ‘home treatment’ for mental health problems in terms of hospitalization, we conducted a systematic review, using Cochrane methodology but with a wider remit. Non-randomized studies were included in response to concerns about RCTs’ generalizability. All authors were followed up for data on service components. ‘Home treatment’ was defined broadly for the purposes of the literature search, but included studies were then assessed against service components specifically focused on delivering treatment at home. The study tested components and other features for associations with days in hospital, as well as conducting a conventional meta-analysis of data on days in hospital.

Results. We found 91 studies, 18 comparing home to in-patient treatment. Sixty per cent of authors responded to follow-up. The vast majority of the services studied had a ‘home treatment function’ and regularly visited patients at home. The heterogeneity of control services made meta-analysis problematical as did the limited availability of data. There was some evidence that ‘regular’ home visiting and combined responsibility for health and social care were associated with reduced hospitalization. The inclusion of non-randomized studies rarely affected the findings.

Conclusions. Evidence concerning the effectiveness of home treatment remains inconclusive. A centrally coordinated research strategy is recommended, with attention to study design. Experimental and control service components should be prospectively recorded and reported to enable meaningful analysis.

The well regarded Section of the World Psychiatric Association, on Epidemiology and Public Health, held its biennial meeting at Johns Hopkins University, Baltimore in June 2001. A new feature of the meeting was the ‘work group’, an opportunity to debate topical but unresolved issues. There was standing room only for a discussion on why the differences between self-report and clinician-rated measures of psychopathology matter (Brugha et al. 1999a). This is one of several topics increasingly debated in the context of the seemingly unremitting disparities between epidemiological estimates of the prevalence of psychiatric disorders (Regier et al. 1998). Recent comparisons of clinician and lay (self-report) measures suggest that dichotomous diagnostic categories cannot be measured reliably in large scale community surveys against a clinical standard measure (Brugha, et al. 1999b, 2001; Eaton et al. 2000).

Background. We aimed to explore the prevalence and factor structure of premenstrual symptoms in a sample of Australian twins; to investigate phenotypic associations between reported premenstrual symptoms, personality and reproductive dimensions; and to identify the relative contributions of genes and environment to premenstrual symptoms and the extent of genetic and environmental covariation with the personality trait Neuroticism and lifetime major depression.

Method. Seven hundred and twenty female twin pairs (454 monozygotic and 266 dizygotic) from the Australian National Health and Medical Research Council Twin Register reported on experience of 17 premenstrual symptoms during the previous 12 months. In the same questionnaire twins also responded to questions on symptom states, and personality dimensions including neuroticism. Interview data enabling diagnosis of lifetime history of DSM-IV major depression were also available. We fitted univariate and multivariate genetic models to the data.

Results. Most frequently reported symptoms were breast tenderness/pain and bloating/weight gain, followed by affective symptoms. Twelve-month prevalence was 2·4% for the combination of symptoms and functional interference meeting a very rough approximation of DSM-III-R criteria for late luteal dysphoric disorder. Principal factor analysis identified a single premenstrual (PMS) factor. Additive genetic influences (44% of total variance) were identified for PMS. Although we found genetic correlations of 0·62 between reported PMS and neuroticism, and 0·70 with lifetime major depression, 39% of the genetic variance of PMS was not explained by these factors.

Conclusions. Our findings support the existence of genetic influences on premenstrual symptoms, but we were unable to distinguish between liability to symptom experience and symptom reporting. Retrospective reporting may have contributed to our finding that PMS genes were shared in part with neuroticism and liability to lifetime major depression.

Background. For irrational fears and their associated phobias, epidemiological studies suggest sex differences in prevalence and twin studies report significant genetic effects. How does sex impact on the familial transmission of liability to fears and phobias?

Methods. In personal interviews with over 3000 complete pairs (of whom 1058 were opposite-sex dizygotic pairs), ascertained from a population-based registry, we assessed the lifetime prevalence of five phobias and their associated irrational fears analysed using a multiple threshold model. Twin resemblance was assessed by polychoric correlations and biometrical model-fitting incorporating sex-specific effects.

Results. For agoraphobia, situational and blood/injury fear/phobia, the best fit model suggested equal heritability in males and females and genetic correlations between the sexes of less than +0·50. For animal fear/phobias by contrast, the best fit model suggested equal heritability in males and females and a genetic correlation of unity. No evidence was found for an impact of family environment on liability to these fears or phobias. For social phobias, twin resemblance in males was explained by genetic factors and in females by familial–environmental factors.

Conclusion. The impact of sex on genetic risk may differ meaningfully across phobia subtypes. Sex-specific genetic risk factors may exist for agoraphobia, social, situational and blood-injury phobias but not for animal fear/phobia. These results should be interpreted in the context of the limited power of twin studies, even with large sample sizes, to resolve sex-specific genetic effects.

Background. Social skills training and cognitive remediation are psychological techniques with considerable face validity for the treatment of negative symptoms of schizophrenia and their consequences. This paper provides a meta-analytical review of these treatments. It includes an appreciable number of randomized controlled trials, using comparisons against both standard care and other active interventions. However, the assessment of particular outcomes sometimes had to be based on single studies.

Method. A detailed search strategy was used to identify randomized controlled trials of social skills training and cognitive remediation, primarily employing electronic databases. Randomized controlled trials (RCTs) that met predefined criteria were then subjected to meta-analysis on a variety of outcome measures.

Results. There was no clear evidence for any benefits of social skills training on relapse rate, global adjustment, social functioning, quality of life or treatment compliance. Cognitive remediation had no benefit on attention, verbal memory, visual memory, planning, cognitive flexibility or mental state.

Conclusions. Social skills training and cognitive remediation do not appear to confer reliable benefits for patients with schizophrenia and cannot be recommended for clinical practice.