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. 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. 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.

Background. We examined the relationship between childhood sexual abuse (CSA), and interviewees' recollections of pathogenic parenting, testing for possible retrospective biases in the recollections of those who have experienced CSA.

Methods. Information about CSA, parental divorce and interviewees' recollections of parental rejection, parental overprotection and perceived autonomy (as assessed through a shortened version of the Parental Bonding Instrument) was obtained through telephone interviews with 3626 Australian twins who had also returned self-report questionnaires several years earlier. Recollections of parental behaviours were compared for individuals from pairs in which neither twin, at least one twin, or both twins reported CSA.

Results. Significant associations were noted between CSA and paternal alcoholism and between CSA and recollections of parental rejection. For women, individuals from CSA-discordant pairs reported levels of parental rejection that were significantly higher than those obtained from CSA-negative pairs. The levels of parental rejection observed for twins from CSA-discordant pairs did not differ significantly from those obtained from CSA-concordant pairs, regardless of respondent's abuse status. For men from CSA-discordant pairs, respondents reporting CSA displayed a tendency to report higher levels of parental rejection than did respondents not reporting CSA. Other measures of parenting behaviour (perceived autonomy and parental overprotection) failed to show a clear relationship with CSA.

Conclusions. The relationship between CSA and respondents' recollections of parental rejection is not due solely to retrospective bias on the part of abused individuals and, consistent with other studies, may reflect a pathological family environment with serious consequences for all siblings.

Background. Previous studies of parental discipline have identified little influence of heritability on parental control, and some influence of gene–environment correlations, shared environment and child temperament.

Method. Using interview data from 2003 female twins from a population-based twin registry and 1472 of their parents, we examined reports of parental discipline from four perspectives: (1) father and mother reporting separately on the type of discipline they provided for their offspring; (2) each twin reporting on the type of discipline they received from their parents; (3) each parent reporting on the discipline provided by their spouse; and, (4) each twin reporting on the discipline they provided for their own offspring. Using factor analysis and univariate structural equation modelling, we examined the structure of parental discipline, and the genetic and environmental influences thereon.

Results. The seven discipline items yielded two factors, physical discipline and limit setting, which were moderately positively correlated. Parents perceived discipline as largely a common environmental experience for the twins, whereas the twins indicated that discipline was influenced by unique environmental factors and the genotype of the child. Twins as parents indicated no influence of shared environment on discipline, with the majority of influence accounted for by non- shared environment and parental genotype.

Conclusions. Parents recall providing similar discipline to their children, whereas children emphasize the differences in parental discipline. Sources of individual variation in parental discipline vary according to which family member report is examined. In total, parental discipline is partially influenced by the genotype of both the parent and child, and by environmental factors shared by the twins and unique to the individual.

Background. There is conflicting evidence concerning the magnitude of genetic and shared environmental influences on juvenile antisocial behaviour (AB). The use of more than one assessment of AB may yield more accurate estimates of these influences.

Methods. Retrospective reports of antisocial behaviour prior to age 18 were obtained on two occasions from a population-based sample of 3522 adult males from male–male twin pairs: phone interviews (wave 1) and self-report questionnaires obtained 19 months later (wave 2). Structural equation modelling estimated the genetic and environmental influences on reliably-measured AB. Factors related to participation of co-twin at wave 1, attrition between waves 1 and 2, and reliability of wave 1 and wave 2 assessments were also investigated.

Results. Twin analyses revealed that genetic, shared environmental, and non-shared environmental influences accounted for approximately 33% (95% CI = 9–57%), 31% (95% CI = 10–51%) and 36% (95% CI = 29–44%) of the variance of reliably measured AB, respectively. We also found significant occasion-specific genetic influences on wave 1 AB. Wave 1 AB did not predict wave 1 participation of co-twin or attrition, but was related to reliability. Co-twins of MZ twins and younger twins were more likely to participate at wave 1; attrition was predicted by being a DZ twin, lack of initial participation of co-twin, fewer years of education, and fewer children. Being older, being unmarried, and having less psychopathology were associated with greater reliability.

Conclusions. When measurement error is taken into account, both genetic and shared environmental factors are significant influences on juvenile AB, accounting for approximately one- third of variation. The origin of the specific genetic influences on wave 1 AB is unclear, but may be due to factors related to measurement.

Background. Few studies have investigated independent associations of psychological, biological and social variables with repeated deliberate self-harm (DSH). Serotonin function has been linked to impulsive and suicidal behaviour and genetic polymorphisms have been identified within the serotonin system that could account for this link. This study tested hypotheses linking impulsiveness, genetic polymorphisms of tryptophan hydroxylase (TPH) and the 5-HT2c receptor and repeated DSH.

Methods. Individuals presenting after DSH were interviewed, completed personality questionnaires and gave venous blood samples. Genotypes were determined for TPH intron7 and 5-HT2c (cys-ser) polymorphisms. Follow-up to identify repetition of DSH was for 1 year.

Results. Males with the 5-HT2c serine variant were more impulsive than those with the cysteine variant (0·39 standardized units, P = 0·041, 95% CI 0·017 to 0·076). There was no association between impulsiveness and the TPH intron7 polymorphism overall but a weak association with the L allele in men (0·41 standardized units, P = 0·05, 95% CI 0·001 to 0·82). Impulsiveness, although high in the group as a whole, did not distinguish those who repeated DSH.

Conclusions. The personality trait of impulsiveness may in part be related to genotypes of the 5-HT2c receptor and TPH gene in men. Impulsiveness does not differ between those who do and do not repeat DSH.

Background. Epidemiological data on subtypes of social phobia are scarce and their defining features are debated. Hence, the present study explored the prevalence and descriptive characteristics of empirically derived social phobia subgroups in the general population.

Methods. To reveal subtypes, data on social distress, functional impairment, number of social fears and criteria fulfilled for avoidant personality disorder were extracted from a previously published epidemiological study of 188 social phobics and entered into an hierarchical cluster analysis. Criterion validity was evaluated by comparing clusters on the Social Phobia Scale (SPS) and the Social Interaction Anxiety Scale (SIAS). Finally, profile analyses were performed in which clusters were compared on a set of sociodemographic and descriptive characteristics.

Results. Three clusters emerged, consisting of phobics scoring either high (generalized subtype), intermediate (non-generalized subtype) or low (discrete subtype) on all variables. Point prevalence rates were 2·0%, 5·9% and 7·7% respectively. All subtypes were distinguished on both SPS and SIAS. Generalized or severe social phobia tended to be over-represented among individuals with low levels of educational attainment and social support. Overall, public-speaking was the most common fear.

Conclusions. Although categorical distinctions may be used, the present data suggest that social phobia subtypes in the general population mainly differ dimensionally along a mild–moderate–severe continuum, and that the number of cases declines with increasing severity.

Background. The present study used cluster analysis procedures to identify empirically subgroups of patients with social phobia in a large clinical sample.

Method. The Liebowitz Social Anxiety Scale (LSAS) was administered to 382 patients from several studies of the treatment of social phobia. LSAS fear ratings were summed into four subscale scores (social interaction, public speaking, observation by others, eating and drinking in public) based on a previous factor analytical study of the LSAS. In order to produce a stable and robust solution, these factor scores were submitted to a two-stage clustering procedure consisting of an agglomerative-hierarchical clustering method followed by an iterative non-hierarchical clustering method.

Results. Three patient subgroups were identified based on their pattern of feared social situations on the LSAS. These groups were labelled: (1) pervasive social anxiety; (2) moderate social interaction anxiety; and (3) dominant public speaking anxiety. Clusters differed significantly on age and age of social phobia onset, as well as on measures of social anxiety, general anxiety and depressive symptomatology. Clusters also differed in the percentage of assigned patients who met criteria for the generalized subtype of social phobia and avoidant personality disorder.

Conclusions. The results provide empirical support for the existence of three subgroups in a clinical sample of individuals with social phobia and contribute to the growing evidence for the heterogeneity of social phobia. Further study of the conceptual, clinical and aetiological significance of these subgroups is needed.

Background. In this paper we use data from the National Survey of Psychiatric Morbidity to examine how many people with neurotic disorders receive professional evaluation, and how this is affected by clinical and sociodemographic differences. We hypothesized that psychiatric symptoms and attendant dysfunctions would both have an effect on contacting, and that key demographic variables would not.

Method. The household component of the British National Surveys of Psychiatric Morbidity was based on a random sample of > 10000 subjects. Psychiatric symptoms and ICD-10 diagnosis were established by lay interviewers using the CIS-R. Social dysfunction was tapped by asking about difficulties in performing seven types of everyday activity. We examined symptom score, ADL deficit score and demographic variables in relation to contact with primary care physicians for psychiatric symptoms.

Results. The major determinant of contacting a primary care physician was severity, mainly due to the level of psychiatric symptoms, but with an independent contribution from social dysfunction. There were also significant contributions from sex, marital status, age, employment status and whether the subject had a physical condition as well.

Conclusions. The major influence on whether people seek the help of their family doctors for mental health problems is the severity of disorder. Although there are some social inequalities in access to family doctors, these are less important. The most salient finding from our study is that even people suffering from high levels of psychiatric symptoms very often do not have contact with professionals who might help them.

Background. Access to psychiatric treatment by people with neurotic disorders in the general population is likely to be affected both by the severity of disorder and by sociodemographic differences.

Method. In the household component of the National Surveys of Psychiatric Morbidity > 10000 subjects in Great Britain with psychiatric symptoms were interviewed using the CIS-R. They were also asked about difficulties experienced in performing seven types of everyday activity. All subjects classed as having an ICD-10 disorder were questioned about their experience of treatment with antidepressants, hypnotics, and counselling or psychotherapy.

Results. Less than 14% of people with current neurotic disorders were receiving treatment for them. Within the previous year, only a third had made contact with their primary care physician for their mental problem: of these < 30% were receiving treatment. Overall, 9% of people with disorders were given medication and 8% counselling or psychotherapy. A diagnosis of depressive episode was that most associated with antidepressant medication. Treatment access was affected by employment status, marital status, and age, but the major determinant was symptom severity. Neither sex nor social class influenced which people received treatment.

Conclusions. People with psychiatric disorders seldom receive treatment, even when they have consulted their primary care physician about them. In many cases, this must represent unmet needs with a strong claim on health resources. There are also inequalities in the receipt of treatment, although the major influence is the severity of disorder.

Background. Minor depression is a disabling condition commonly seen in primary care settings. Although considerable impairment is associated with minor depression, little is known about the course of the illness. Using a variety of clinical and functional measurements, this paper profiles the course of minor depression over a 1 year interval among a cohort of primary care patients.

Method. Patients at a university-based primary care facility were screened for potential cases of depression and selected into three diagnostic categories: an asymptomatic control group; patients with a diagnosis of major depression; and, a third category, defined as minor depression, consisting of patients who reported between two and four symptoms of depression, but who failed to qualify for a diagnosis of major depression. Functional status, service use, and physical, social and mental health were assessed at baseline and at 3-month intervals for the ensuing year.

Results. Respondents with a baseline diagnosis of minor depression exhibited marked impairment on most measures both at baseline and over the following four waves. Their responses in most respects were similar to, although not as severe as, those of respondents with a baseline diagnosis of major depression. Both groups were considerably more impaired than asymptomatic controls.

Conclusions. Minor depression is a persistently disabling condition often seen in primary care settings. Although quantitatively less severe than major depression, it is qualitatively similar and requires careful assessment and close monitoring over the course of the illness.

Background. Systematic and accurate depiction of a patient's course of illness is crucial for assessing the efficacy of maintenance treatments for bipolar disorder. This need to rate the long-term prospective course of illness led to the development of the National Institute of Mental Health prospective Life Chart Methodology (NIMH-LCMTM-p or LCM). The NIMH-LCMTM-p allows for the daily assessment of mood and episode severity based on the degree of mood associated functional impairment. We have previously presented preliminary evidence of the reliability and validity of the LCM, and its utility in clinical trials. This study is a further and more extensive validation of the clinician rated NIMH-LCMTM-p.

Methods. Subjects included 270 bipolar patients from the five sites participating in the Stanley Foundation Bipolar Network. Daily prospective LCM ratings on the clinician form were initiated upon entry, in addition to at least monthly ratings with the Inventory of Depressive Symptomatology-clinician rated (IDS-C), the Young Mania Rating Scale (YMRS) and the Global Assessment of Functioning (GAF). We correlated appropriate measures and time domains of the LCM with the IDS-C, YMRS and GAF.

Results. Severity of depression on the LCM and on the IDS-C were highly correlated in 270 patients (r = −0·785, P < 0·001). Similarly, a strong correlation was found between LCM mania and the YMRS (r = 0·656, P < 0·001) and between the LCM average severity of illness and the GAF (r = −0·732, P < 0·001).

Conclusions. These data further demonstrate the validity and potential utility of the NIMH- LCMTM-p for the detailed daily longitudinal assessment of manic and depressive severity and course, and response to treatment.

Background. A combined family study and recovered study design was utilized to examine several hypothesized relationships between personality and bulimia nervosa (BN).

Methods. We studied 47 women with a lifetime history of DSM-III-R BN (31 currently ill and 16 recovered), 44 matched control women (CW) with no history of an eating disorder (ED), and their first-degree female relatives (N = 89 and N = 100, respectively), some of whom had current or previous EDs.

Results. BN probands' relatives with no ED history had significantly elevated levels of perfectionism, ineffectiveness, and interpersonal distrust compared to CW probands' relatives with no ED history. In contrast, diminished interoceptive awareness, heightened stress reactivity and perfectionistic doubting of actions were found among the previously eating disordered relatives of bulimic probands compared to their never ill relatives. Finally, a sense of alienation and emotional responsivity to the environment were elevated among currently ill compared to recovered bulimic probands.

Conclusions. The fact that perfectionism, ineffectiveness and interpersonal distrust are transmitted independently of an ED in relatives suggests that they may be of potential aetiological relevance for BN. In contrast, diminished interoceptive awareness, heightened stress reactivity and perfectionistic doubting of actions are more likely consequent to, or exacerbated by, previously having experienced the illness. Finally, a sense of alienation and emotional responsivity to the environment are more likely to be associated with currently having BN.

Background. There is substantial evidence that the genetic liability to autism confers a risk for a range of more subtle social and communication impairments, as well as stereotyped and repetitive behaviours. Recent research suggests that increased expression of particular personality traits may be a manifestation of the liability to autism.

Methods. To investigate this we examined the personality traits of the adult relatives of 99 autistic and 36 Down's syndrome probands, using the informant version of the Modified Personality Assessment Schedule.

Results. There was significantly increased expression of the traits anxious, impulsive, aloof, shy, over-sensitive, irritable and eccentric among the autism relatives with evidence of different profiles for male and female relatives and for parents and adult children. Factor analysis revealed three broad groups of traits, two of which (‘withdrawn’ and ‘difficult’) appeared to reflect impairments in social functioning and a third group of anxiety related traits (‘tense’). Each of these factors differed in their pattern of associations with the factor we termed ‘withdrawn’ showing a similar pattern of association to that found for other autism related conditions. The ‘tense’ factor appeared in part to be related to the burden of caring for an autistic child.

Conclusions. This study confirms the finding that particular personality traits may aggregate in the family members of autistic individuals and furthermore that some of these traits may be a manifestation of the liability to autism.

Background. A high risk of schizophrenia has been found among Caribbean immigrants in the Netherlands and Great Britain. One hypothesis to explain these findings is that patients with a diagnosis of schizophrenia or patients with symptoms of psychosis not specifically diagnosed, emigrate more than the general population. Such selection might account for high rates of Surinamese patients with a diagnosis of schizophrenia in Netherlands psychiatric hospitals. We examined this hypothesis.

Methods. The files of patients with schizophrenia or patients suffering from unspecified psychosis were selected from the archives of the National Psychiatric Hospital in Surinam. These patients were traced to investigate patterns of emigration. Data from the Central Bureau for Statistics in the Netherlands and from the Central Population Bureau in Surinam provided the percentage of the general Surinamese population that emigrated to the Netherlands. The difference between the two percentages was evaluated using the chi-squared test. Using the same method the percentage of remigration from the Netherlands among Surinamese patients was compared with the percentage of remigration among the general Surinamese population.

Results. Surinamese patients with schizophrenia or unspecified psychosis did not emigrate more frequently to the Netherlands compared with the general Surinamese population. They did remigrate significantly more frequently.

Conclusion. High migration rates do not explain the high hospital admission rates for schizophrenia among Surinamese in the Netherlands.

Background. Although it is well recognized that individuals with schizophrenia display evidence of subtle neurological impairment, its aetiopathological and clinical significance continues to be unclear.

Methods. Patients presenting with a first episode of schizophrenia or schizophreniform psychosis (DSM-IV criteria) were examined using two previously validated neurological examinations. The majority (N = 35) were examined prior to their ‘first ever’ dose of neuroleptic while the remaining patients (N = 21) had been medicated for less than one month. The manner in which neurological functioning is influenced by symptomatology and handedness was ascertained.

Results. The majority of patients who were examined neuroleptic-naive displayed evidence of neurodysfunction. A combination of relative hand preference and symptomatology explained a significant proportion of the variance in neurological functioning. Mixed handedness among adults at the time of first presentation with schizophrenia was associated with more severe neurological impairment and a history of poorer scholastic attainment and pre-morbid social adjustment.

Conclusions. Neurological soft signs are an intrinsic part of schizophrenia rather than a direct consequence of treatment. Early developmental processes are associated with the level of subsequent neurological impairment in first episode schizophrenia. However, symptomatology appears to have an influence on the apparent severity of neurological impairment.

Background. While numerous studies have found disturbances in the Event-Related Potentials (ERPs) of patients with schizophrenia linked to task relevant target stimuli (most notably a reduction in P300 amplitude), few have examined ERPs to task irrelevant non-targets. We hypothesize, from current models of dysfunction in information processing in schizophrenia, that there will be less difference between ERPs to targets and non-targets in patients with schizophrenia than in controls.

Methods. EEGs were recorded for 40 subjects with schizophrenia and 40 age and sex matched controls during an auditory oddball reaction time task. ERPs to the targets and non-targets immediately preceding the targets were averaged separately.

Results. There was a disturbance in ERPs to targets but also to non-targets (reduced N100 amplitude and earlier P200 latency) and the difference between target and non-target ERP components (N100 and P200 amplitude and P200 latency), was significantly reduced in the schizophrenic group compared with controls.

Conclusions. These findings suggest a disturbance in processing task relevant and irrelevant stimuli, consistent with Gray's (1998) hypothesis of misattributions in the ‘match[ratio ]mismatch’ of novel (target) and familiar (non-target) sensory input compared with stored information.

Background. Memory deficits are commonly experienced by patients with schizophrenia, often persist even after effective psychotropic treatment of psychotic symptoms and have been demonstrated to interfere with many aspects of successful psychiatric rehabilitation. Because of significant impact on functional outcome, effective remediation of cognitive deficits has been increasingly cited as an essential component of comprehensive treatment. Efforts to remediate memory deficits have met with circumscribed success, leaving uncertain whether schizophrenia patients can be taught, without experimental induction, independently to employ semantic encoding or a range of other mnemonic techniques.

Method. We examined the feasibility of using memory and problem solving teaching techniques developed within educational psychology – techniques which promote intrinsic motivation and task engagement through contextualization and personalization of learning activities – to remediate memory deficits in a group of in-patients with chronic schizophrenia spectrum disorders.

Results. Although our memory remediation group significantly improved on the memory remediation task, they did not make greater gains on measures of immediate paragraph recall or list learning than the control groups.

Conclusions. Targeted remediation of memory appears to yield task specific improvement but the gains do not generalize to other memory tasks. Subjects receiving memory remediation failed to independently activate mnemonic encoding strategies learned and used successfully within training tasks to other general measures of verbal learning and memory.