In an important paper in this issue Murphy et al. (pp. 503–512) report on incidence rates for depression over 40 years in the Stirling County Study. Incidence rates remained stable, contrary to most evidence that is principally based on prevalence or retrospective lifetime prevalence. Incidence rates were only a little higher in women than in men.

Incidence rates are assuming increasing importance in psychiatry as they do in other areas of epidemiology. Prevalence rates are complex, depending not only on incidence of new cases of the disorder, but its persistence, and in a recurrent disorder, recurrence. Incidence rates are unbiased by these factors, a particularly valuable attribute when considering risk factors. In depression, development and widespread use of antidepressants, newer patterns of care, and in the opposite direction, increased urbanization with its accompanying social pressures, could have produced considerable changes in outcome in the last 40 years. Changes in enumerated prevalences alone could reflect changed length of episodes and rates of recurrence, so giving a misleading picture as to what has happened to the disorder.

The Stirling County Study is one of the classics of epidemiology. Its originator, Alexander Leighton, is an author of the present paper with his wife, Jane Murphy, who has directed the study since the mid-1970s. Representative community samples were studied cross-sectionally in 1952, 1969 and 1992, and the previously studied samples restudied on follow-up at the later points. The design enables a separation of period effects, involving all subjects at one time point, from cohort effects. In this study similar temporal stability of prevalence has been found (Murphy et al. 2000b) to that now reported for incidence.

The last decade has seen a renewed interest and research effort focused on the broad areas of personality and personality disorder. Issues preoccupying researchers include problems of classification (especially categorical versus dimensional models), the absence of theoretical models, and implications of the suggested continuity between ‘normal’ personality dimensions and personality disorder.

Vascular dementia (VaD) is the second most common subtype of dementia in Western countries (Desmond, 1996) and, overall, may be the most common subtype of dementia in the world (Henderson, 1994). Furthermore, the recognition of some major risk factors of cerebrovascular disease makes VaD a form of ‘preventable senility’ (Hachinski, 1992). The last decade has seen a major re-evaluation of the concept of VaD (Erkinjuntti & Hachinski, 1993; Hachinski, 1994), with new diagnostic criteria having been proposed (World Health Organization, 1993; American Psychiatric Association, 1994) but without any consensus (Wetterling et al. 1996). Indeed, some investigators have called for the abandonment of the diagnosis of VaD and the adoption of alternative nosology (Hachinski, 1994). It is therefore time to re-examine the concept of VaD and evaluate its distinctive features.

There is now a considerable body of epidemiological evidence from developing countries and multilateral agencies that so called common mental disorders are common and disabling (e.g. Murray & Lopez, 1996; Patel et al. 1998). The logical next step is to identify efficacious and cost-effective health services interventions that can tackle the all-important ‘so-what’ question that is posed by doctors and policy makers in developing countries when confronted with startling prevalence statistics. The rise of evidence-based medicine has highlighted the need for quality trials that can inform and guide clinical practice. This editorial poses the question of whether we need treatment evidence from developing countries. The key issue is whether we can assume that psychiatric treatment evidence can be applied from one culture, or region, to another. If, for example, this was possible, then clinical practice in developing countries could be fairly well informed by trials conducted in the West. However, there are several factors that limit the cross-cultural applicability of treatment research in psychiatry.

The cornerstone of evidence-based medicine is the belief that good quality research should form the basis of clinical practice and decision-making (Muir Gray, 1997). Psychiatry has kept abreast of this movement (Geddes et al. 1997) and claims have been made that randomized-controlled trials (the highest quality primary evaluative research) can be used to justify 65% of routine clinical decisions (Geddes et al. 1996). However, it is largely published research that forms the ‘knowledge base’ of the evidence movement. A fundamental difficulty arises when published research results are a biased sample of all research results – published and unpublished. Publication bias presents one such threat and has been much discussed in wider healthcare (Easterbrook et al. 1991; Dickersin & Min, 1993; Dickersin, 1997), but has been little discussed or researched in psychiatry, despite the fact that psychiatry is likely to be at least as prone to publication bias as other specialities.

Background. Over the past two decades, scores of articles and several books have been published calling for more attention to the prevention of eating disorders, but less than two dozen prevention intervention studies have been conducted to date.

Methods. This paper reports the results of a systematic review of 20 empirical intervention studies on eating disorders prevention, discussing the data accumulated on what has and has not been effective. Beyond a description of study design and findings, this paper devotes special attention to the theoretical orientations of the studies and their implied assumptions about preventive strategies.

Results. Though there has been a compelling interest in social, political and economic factors influencing the incidence of disordered eating, little of this interest has been carried over into the prevention end of eating disorders research. Most studies reported thus far have been designed to target and measure change principally on the individual level, to the exclusion of considering leverage points for intervention in the larger social environment.

Conclusions. This paper concludes with a recommendation for new attention to a model of proactive primary prevention targeted at environmental change and cross-disciplinary collaboration to achieve a reduction in the incidence of eating disorders.

Background. Although there have been many follow-up studies of severe puerperal psychiatric illness, few have been very long-term.

Methods. Sixty-four subjects from 85 (75·3%) in an unselected sample of women admitted to a psychiatric hospital within 6 months of childbirth were successfully followed up a mean of 23 years (range 17–28) later. Most subjects were interviewed in detail, with further information obtained from general practice and hospital records. Data included subsequent illnesses and diagnoses, subsequent childbirth, longitudinal social function, current symptoms and social function.

Results. Seventy-five per cent of subjects had further psychiatric illnesses, most of them unrelated to childbirth, and 37% had at least three subsequent episodes. The risk of puerperal psychiatric illness was 29% in subsequent pregnancies. At outcome interview the majority of subjects were well, with satisfactory social adjustment. Diagnoses in subsequent psychiatric illnesses showed considerable consistency with index diagnoses, with some shift to bipolar disorder. Further illnesses were less likely to occur where the index illness occurred with first child, onset was within 1 month of delivery, and where the index diagnosis was unipolar depression.

Conclusions. There is a high risk of subsequent non-puerperal recurrences following severe puerperal psychotic illness, showing considerable diagnostic consistency with the index episode, but with good functional outcome. Puerperal illnesses showed strong continuities with non-puerperal illnesses in these women.

Background. There is considerable disagreement about what happens to the risk of anxiety and depression disorders and symptoms as people get older.

Methods. A search was made for studies that examine the occurrence of anxiety, depression or general distress across the adult life span. To be included, a study had to involve a general population sample ranging in age from at least the 30s to 65 and over and use the same assessment method at each age.

Results. There was no consistent pattern across studies for age differences in the occurrence of anxiety, depression or distress. The most common trend found was for an initial rise across age groups, followed by a drop. Two major factors producing this variability in results were age biases in assessment of anxiety and depression and the masking effect of other risk factors that vary with age. When other risk factors were statistically controlled, a more consistent pattern emerged, with most studies finding a decrease in anxiety, depression and distress across age groups. This decrease cannot be accounted for by exclusion of elderly people in institutional care from epidemiological surveys or by selective mortality of people with anxiety or depression.

Conclusion. There is some evidence that ageing is associated with an intrinsic reduction in susceptibility to anxiety and depression. However, longitudinal studies covering the adult life span are needed to distinguish ageing from cohort effects. More attention needs to be given to understanding the mechanism behind any ageing-related reduction in risk for anxiety and depression with age. Possible factors are decreased emotional responsiveness with age, increased emotional control and psychological immunization to stressful experiences.

Background. Research on the management and the outcome of treatment of medically unexplained symptoms is very limited. Development of simple but effective techniques for treatment and demonstration of their effectiveness when applied in primary health care are needed.

Methods. A randomized controlled trial was carried out with follow-up assessments at 3 months after baseline assessments using the Short Explanatory Model Interview (SEMI), General Health Questionnaire (GHQ-30), Bradford Somatic Inventory (BSI) and patient satisfaction on a visual analogue scale. The study was carried out in a general out-patient clinic in Sri Lanka.

The intervention group received six, 30 min sessions based on the principles of cognitive behavioural therapy over a period of 3 months. The control group received standard clinical care.

Results. Eighty patients out of the 110 patients referred, were eligible. Sixty-eight were randomly allocated equally to the control and treatment groups. All 34 in the treatment group accepted the treatment offer and 22 completed between three and six sessions. At 3 months, 24 in the treatment and 21 in the control group completed follow-up assessments. Intention-to-treat analysis revealed significant differences in mean scores of outcome measures (adjusted for baseline scores) between control and intervention groups respectively – complaints 6·1 and 3·8 (P = 0·001), GHQ 10·4 and 6·3 (P = 0·04), BSI score 15·6 and 13·2 (P [les ] 0·01), visits 7·9 and 3·1 (P = 0·004).

Conclusions. Intervention based on cognitive behavioural therapy is feasible and acceptable to patients with medically unexplained symptoms from a general out-patients clinic in Sri Lanka. It had a significant effective in reducing symptoms, visits and distress, and in increasing patient satisfaction.

Background. Several empirical studies have found temporal lobe impairments in many patients with schizophrenia. The strength and consistency of this evidence, however, has not been evaluated and synthesized quantitatively. Hence, we ask to what extent are temporal cortices really defective in schizophrenia?

Methods. Meta-analytical methods were used to determine the magnitude of evidence in support of structural and physiological temporal–hippocampal system deficits in schizophrenia. We report effect sizes from studies since 1980 that used structural (CT, MRI) and functional (SPECT, PET) neuroimaging methods.

Results. Both structural and functional imaging literatures are distinguished by heterogeneity whereby most patients show normative temporal function and structure, a minority shows diminished values and some patients demonstrate augmented function and structure rather than a deficit.

Conclusions. The findings are hard to incorporate within single disease models that propose major involvement of the temporal system in schizophrenia, at least at the degree of resolution obtained with current imaging technology.

Background. An association between social rhythm disruption (SRD) and onset of manic episodes has recently been observed. Whether other types of bipolar (depressive and cycling) or unipolar depressive episodes are similarly related to SRD is unclear, as is the association between severely threatening life events and onset of bipolar manic, depressed and cycling episodes.

Methods. Bipolar patients with purely manic (N = 21), purely depressed (N = 21) and cycling (N = 24) episodes, and 44 patients with recurrent unipolar depression, were interviewed with the Bedford College Life Events and Difficulties Schedule. The presence of severe and SRD events during the year prior to index episode onset was then determined.

Results. More manic than cycling and unipolar subjects experienced SRD events during 8- and 20-week pre-onset periods, and severe events during 20-week pre-onset periods. Controlling for age and prior number of episodes left most findings unchanged. An earlier finding of more manic subjects with SRD events in an 8-week pre-onset versus control period was also replicated.

Conclusions. It appears that manic onsets are influenced by stressful life events, especially those involving SRD, in a unique manner compared to onsets of other types of bipolar and unipolar episodes. Onset of bipolar cycling episodes, in contrast, seems to be relatively unaffected by SRD or severe life events. These findings refine the hypothesis that SRD may precipitate onset of affective episodes to be specific to manic onsets.

Background. Interferons are a class of cytokines profoundly affecting immune function. Several interferons are now synthesized and used clinically, notably for viral diseases and cancer. In addition to their desired immune effects, interferons cause a number of toxicities, including prominent effects on the nervous system.

Methods. This literature review focused on the incidence of depression associated with interferon treatment. Possible neurochemical mechanisms and remedial strategies were also considered.

Results. Interferon treatment, particularly with the alpha subtype, is unquestionably linked with depression, but the strength of association is uncertain because of erratic ascertainment and pre- treatment co-morbidity. A likely pathogenic mechanism has been described, involving interferon suppression of serotonin synthesis. Controlled treatment trials of interferon-induced depression are not yet available.

Conclusions. Neurotoxicity substantially limits the use of interferons. At least some of the risk of depression appears to derive from their anti-serotonergic effects, consistent with the large body of evidence pointing to a general link between serotonin and affective illness. Vigilant detection and aggressive treatment of depression is necessary to optimize interferon treatment of many patients.

Background. The Stirling County Study provides a 40-year perspective on the epidemiology of psychiatric disorders in an adult population in Atlantic Canada. Across samples selected in 1952, 1970 and 1992 current prevalence of depression was stable. This paper concerns time trends in annual incidence as assessed through cohorts selected from the first two samples.

Methods. Consistent interview data were analysed by a computerized diagnostic algorithm. The cohorts consisted of subjects at risk for a first depression: Cohort-1 (N = 575) was followed 1952–1970; Cohort-2 (N = 639) was followed 1970–1992. Life-table methods were used to calculate incidence rates and proportional hazards procedures were used for statistical assessment.

Results. Average annual incidence of depression was 4·5 per 1000 for Cohort-1 and 3·7 for Cohort- 2. Differences by gender, age and time were not statistically significant. The stability of incidence and the similarity of distribution by gender and age in these two cohorts corresponds to findings about the two early samples. In contrast, current prevalence in the recent sample was distributed differently and showed an increase among women under 45 years.

Conclusions. The stability of the incidence of depression emphasizes the distinctive characteristics of current prevalence in the recent sample and suggests that the dominance of women in rates of depression may have occurred among those born after the Second World War. The results offer partial support for the interpretation of an increase in depression based on retrospective data in other recent studies but they indicate that the increase is specific to women.

Background. Studies of urban–rural differences in prevalence of non-psychotic mental disorder have not given consistent findings. Such differences have received relatively little study in Great Britain.

Methods. Data from 9777 subjects in the Household Survey of the National Morbidity Survey of Great Britain were analysed for differences between urban, semi-rural and rural areas. Psychiatric morbidity was assessed by scores on the Revised Clinical Interview Schedule (CIS-R), together with alcohol dependence, drug dependence, receipt of treatment from general practitioners. Associations with other characteristics were examined by logistic regression.

Results. Urban subjects had higher rates than rural of CIS-R morbidity, alcohol dependence and drug dependence, with semi-rural subjects intermediate. Urban subjects also tended to be members of more deprived social groups, with more adverse living circumstances and greater life stress, factors themselves associated with disorder. Urban–rural differences in alcohol and drug dependence were no longer significant after adjustment for these factors by logistic regression, and differences on CIS-R morbidity were considerably reduced. There were no differences in treatment.

Conclusions. There are considerable British urban–rural differences in mental health, which may largely be attributable to more adverse urban social environments.

Background. There is extensive evidence of statistical associations between family discord/maladaptation and antisocial behaviour in the children, but questions remain on the extent to which the psychopathological risks are genetically or environmentally mediated.

Methods. Twin pairs (N = 1350), aged 8 to 16 years, in the general population-based Virginia Twin Study of Adolescent Behavioral Development were assessed using the Child and Adolescent Psychiatric Assessment interview administered separately to both twins and both parents. Structured interviews for parental lifetime psychiatric disorders were also administered to the mothers and fathers. Maternal reports on Olsson's Family Adaptability and Cohesiveness questionnaire and the Dyadic Adjustment Scale were used as indices of the family environment. A path analytical model based on an extended twin-family design was used to test hypotheses about parent–offspring similarity for conduct disorder symptomatology.

Results. Family discord and maladaptation, which intercorrelated at 0·63, were associated with a roughly two-fold increase in risk for conduct disorder symptomatology. When parental conduct disorder was included in the model the environmental mediation effect for family maladaptation remained, but that for family discord was lost.

Conclusion. It is concluded that there is true environmental mediation from family maladaptation, operating as a shared effect, which accounts for 3·5% of the phenotypic variance. The assumptions underlying this genetic research strategy are made explicit, together with its strengths and limitations.

Background. Social support theory and observational risk factor studies suggest that increased antenatal psychosocial support could prevent post-natal depression. We used empirical knowledge of risk and protective factors for post-natal depression not employed previously in order to develop and evaluate an antenatal preventive intervention.

Methods. We conducted a pragmatic randomized controlled trial in antenatal clinics. We screened 1300 primiparous women and 400 screened positive, 69 screen-positive women were untraceable or not eligible. Of 292 women who completed baseline assessment, 209 consented to randomization, of these 190 provided outcome data 3 months post-natally. ‘Preparing for Parenthood’, a structured antenatal risk factor reducing intervention designed to increase social support and problem-solving skills, was compared with routine antenatal care only. We compared the percentage depressed at 3 months after childbirth using the self-completion General Health Questionnaire Depression scale and Edinburgh Post-natal Depression Scale (EPDS), and the Schedules for Clinical Assessment in Neuropsychiatry a systematic clinical interview.

Results. Assignment to the intervention group did not significantly impact on post-natal depression (odds ratio for GHQ-Depression 1·22 (95% CI 0·63–2·39), P = 0·55) or on risk factors for depression. Forty-five per cent of the intervention group women attended sufficient sessions to be likely to benefit from intervention if effective. Attenders benefited no more than non-attenders.

Conclusions. Prevention services targeting post-natal depression should not implement antenatal support programmes on these lines until further research has demonstrated the feasibility and effectiveness of such methods. The development of novel, low cost interventions effective in reducing risk factors should be completed before further trial evaluation.

Background. Previous longitudinal studies of the association between depression and cognitive dysfunction have had relatively short follow-up periods. This report presents a long-term study of the association between baseline syndromal depression and cognitive outcome measured 9 to 12 years later.

Methods. Self-CARE (D) depression, cognitive function and pre-morbid intelligence were recorded on 1083 subjects on entry to the Medical Research Council trial of treatment of hypertension in older adults in 1983–5. In 1994–5, we aimed to re-interview all survivors to assess cognitive function using the MMSE. We used multivariate analysis to explore whether baseline depression predicted cognitive outcome after this long follow-up period.

Results. Baseline depression was crudely associated with poorer cognitive outcome at time 2. However, this long-term prospective association was no longer apparent after adjusting for baseline cognitive performance, which was associated with baseline depression and robustly predicted cognitive outcome at time 2. We found that gender modified the association between depression and poorer cognitive outcome, so that the association was statistically significant only among men.

Conclusion. Propensity for depression and failing cognition may have common determinants that still need to be established by future neurobiological investigations in conjunction with further long-term prospective epidemiological research.

Background. This study examined associations between childhood circumstances, adolescent mental health and life events, and the development of suicidal behaviour in young people aged between 15 and 21 years.

Method. Data were gathered over the course of a 21-year longitudinal study of a birth cohort of 1265 children born in New Zealand. The measures collected included: (1) patterns of suicidal behaviour (ideation, attempt) (15–21 years); (2) social background, family functioning, parental and individual adjustment during childhood (0–16 years); and (3) time dynamics of mental health and stressful life events during adolescence and early adulthood (15–21 years).

Results. By the age of 21 years, 28·8% of the sample reported having thought about killing themselves and 7·5% reported having made a suicide attempt. The childhood profile of those at greatest risk of suicidal behaviour was that of a young person reared in a family environment characterized by socio-economic adversity, marital disruption, poor parent–child attachment and exposure to sexual abuse, and who as a young adolescent showed high rates of neuroticism and novelty seeking. With the exception of the socio-economic and personality measures, the effects of childhood factors were largely mediated by mental health problems and exposure to stressful life events during adolescence and early adulthood. Mental health problems including depression, anxiety disorders, substance use disorder, and to some extent conduct disorder, in addition to exposure to adverse life events, were significantly associated with the onset of suicidal behaviours.

Conclusions. Findings support a life course model of the aetiology of suicidal behaviour in which risk of developing suicidal behaviour depends on accumulative exposure to a series of social, family, personality and mental health factors.

Background. Rates of child and adolescent conduct disorder (CD) have increased steadily over the past several decades. What is not known is whether the underlying genetic and environmental influences on individual differences in CD have also changed.

Methods. Retrospective reports of antisocial behaviour prior to age 18 were obtained from a population-based sample of 2769 adult males from male–male twin pairs born between 1940 and 1974. Using a summary score of number of CD symptoms, structural equation modelling was used to investigate whether mean level and variation in CD increased with more recent cohorts, and whether any increase in variance could be explained by familial or non-familial factors.

Results. Both mean level CD symptoms and variation were increased in more recent cohorts. Model fitting indicated that the primary increase in variance was due to familial factors, most notably, an increase in the shared environmental influences on CD, from 0·01 (95% CI = 0·00; 0·27) to 0·30 (95% CI = 0·01; 0·44). Heritability estimates remained largely unchanged, although an increase in genetic factors could not be ruled out.

Conclusions. Secular changes in sociodemographic factors responsible for increasing rates of CD may also account for the greater magnitude of shared environmental influences on variation in CD found among more recent cohorts.

Background. Child sexual abuse (CSA) is associated, after controlling for other adversities, with a range of non-psychotic disorders in adult life. There is a need to clarify whether CSA contributes to risk of disorder in the absence of such adversities, and given that associations may be accounted for by genetic mechanisms, whether they are seen where the perpetrator of CSA is not a biological relative, and where there has been only one incident.

Methods. A questionnaire-based study of a socio-economically representative sample of women age 25–36 (N = 862) was carried out. Parental care and control were assessed using the Parental Bonding Instrument, and CSA using a previously validated questionnaire. Current affective symptoms were assessed from the depression scale of the GHQ-28.

Results. Low maternal and paternal care were associated with risk of abuse by a biologically unrelated perpetrator before the age of 11, but not during early adolescence. Low maternal care and CSA each made independent contributions to the prediction of affective symptoms. CSA by a non- relative was strongly associated with GHQ depression, as was CSA by a non-relative that had occurred only once.

Conclusions. Quality of parental care probably influences risk of CSA by unrelated abusers in younger children, while there may be a combination of genetic and parental influences on the risk of abuse by a relative. The strong association of affective symptoms in adult life with CSA by a non- relative suggests an environmental effect. Studies, utilizing genetic designs, of the role of childhood trauma in relation to adult affective symptoms are needed.