This issue features substantial groups of papers on anxiety disorders and on depression. A review article (pp. 589–599) provides a meta-analysis of antidepressant treatment trials in people with schizophrenia. The authors find suggestive evidence of benefit but this depends on small studies. No evidence is found of psychotic worsening.

Since the mid-1980s Ian Goodyer and his colleagues have been engaged in trying to understand the dynamics of the relationship between acute and chronic life stresses and depression in adolescents (Goodyer et al. 1985, 1986). One of the great strengths of their work has been their attention to an array of potential risk factors ranging from the apparently exogenous (such as life events, e.g. Goodyer et al. 1988; Goodyer & Altham, 1991; Goodyer, 1999), through those of uncertain origin (e.g. peer and family relationships and problems, Goodyer et al. 1990), to those that can be regarded as being endogenous to the child (e.g. measures of temperament or endocrine function, Goodyer et al. 1993, 1996, 1998; Herbert et al. 1996). They have then typically attempted to determine how subsets of these factors interact in the generation of disorder (see Goodyer, 2002 for a speculative presentation of his current thinking about the relationships between social adversity and depression). A second characteristic of their research lies in its frequent attention to outcomes over time, as opposed to cross-sectional relationships (e.g. Goodyer et al. 1997a,b). Thirdly, in line with growing evidence that the relationships between environmental stress (and perhaps neuro-anatomical correlates) and depression change as repeated episodes occur (Lewinsohn et al. 1999; Daley et al. 2000), they have distinguished among first, recurrent, remitting and chronic depressive episodes. The group's latest work, presented in this issue (Goodyer et al. 2003), nicely illustrates these characteristics, and their extension to consideration of potential dynamic relations among endocrine parameters in relation to psychopathology.

I have been asked to comment on the three articles on social phobia in this issue of Psychological Medicine. The three papers in one way or another concern themselves with important issues in the assessment and diagnosis of social phobia (also known as social anxiety disorder; Liebowitz et al. 2000). I do so with the caveat that I am an author on one of the papers and do not claim the same degree of objectivity in examining my own work as I do in examining the work of others. The three papers concern the psychometric evaluation of a modified version of the Clinical Global Impression (CGI) (Guy, 1976) in a sample of persons with social phobia (Zaider et al. 2003), the development of a self-report screening questionnaire for social phobia (Newman et al. 2003) and the characteristics of social phobia in the Australian National Survey of Mental Health and Wellbeing (NSMHWB) (Lampe et al. 2003).

Background. Depression is common in people with schizophrenia and is associated with substantial morbidity and an increased risk of suicide. Our aim was to review systematically all the randomized controlled trials that have investigated the clinical effectiveness of antidepressant medication in the treatment of depression in people who also suffer with schizophrenia.

Method. Electronic searches of ClinPsych, the Cochrane Library, the Cochrane Schizophrenia Group's Register of Trials, EMBASE and Medline were completed. Reference lists from identified articles were hand searched.

Results. Eleven small studies were identified and all randomized fewer than 30 subjects to each group. We could only perform analyses on a subset of the trials. For five trials (aggregate N=209) the proportion improved in the antidepressant group was 26% (95% CI 10% to 42%) higher than in the placebo group. In six studies (aggregate N=267) the standardized mean difference on the Hamilton Rating Scale for Depression at the end of the trial was −0·27 (95% CI −0·7 to 0·2). There was no evidence that antidepressant treatment given during the stable phase of illness led to a deterioration of psychotic symptoms in the included trials.

Conclusions. The literature reviewed was, overall, of poor quality and only a small number of trials could contribute towards the meta-analysis. The results provide weak evidence for the effectiveness of antidepressants in those with schizophrenia and depression and could be explained by publication bias. We need further research to determine the best approach towards treating depression in people with schizophrenia.

Background. This longitudinal study investigated whether patterns of cortisol and DHEA that precede the onset of an episode of major depression influence time to recovery in a community ascertained sample of adolescents meeting DSM-IV criteria for major depression.

Method. Sixty adolescents aged 12 to 16 at high risk for psychiatric disorders were followed for 24 months. At 12 months, 30 had experienced an episode of major depression and 30 had not. The second follow-up repeated the psychiatric evaluations with all participants completing the Kiddie-SADS Schedule for Schizophrenia and Affective Disorders. Hormone characteristics and self-reports completed at entry (the Mood and Feelings questionnaire and the Ruminations scale) together with intervening undesirable life events in the 12 months prior to onset, were used to determine the best pattern of psychosocial and endocrine features to predict persistent major depression.

Results. Compared to the never depressed (N=30) and remitted adolescents (N=19), persistently depressed cases (N=11) had a raised morning cortisol/DHEA ratio at entry. Only persistent cases had higher levels of self-reported depressive symptoms and ruminations at entry compared to never depressed. There was no difference in exposure to undesirable life events before onset of disorder between remitted and persistent groups. Logistic regression techniques showed that only the cortisol/DHEA ratio predicted persistence.

Conclusions. In community adolescents at high risk for psychiatric disorder persistent major depression may be distinguished from sporadic forms by the 08.00 h salivary cortisol/DHEA ratio prior to onset.

Background. The clinical Global Impression Scale (CGI) is commonly used as a primary outcome measure in studies evaluating the efficacy of treatments for anxiety disorders. The current study evaluated the psychometric properties and predictors of clinicians' ratings on an adapted version of the CGI among individuals with social anxiety disorders.

Method. An independent assessor administered the CGI Severity of Illness and Improvement ratings to 123 patients at baseline and the subset of treated patients again mid- and post-treatment.

Results. Improvement ratings were strongly related to both concurrent Severity of Illness and changes in Severity of Illness ratings from baseline. Additionally, both CGI ratings were positively correlated with both self-report and clinician-administered measures of social anxiety, depression, impairment and quality of life. Measures of social anxiety symptoms accounted for a large portion of the variance in Severity of Illness ratings, with significant additional variance accounted for by measures of impairment and depression. Changes in social anxiety symptoms from baseline accounted for significant variance in Improvement ratings, but no significant additional variance was accounted for by changes in impairment and depressive symptoms.

Conclusions. Our findings support the utility of the CGI as an index of global severity and symptom-specific improvement among individuals with social anxiety disorder.

Background. The development and validation of the Social Phobia Diagnostic Questionnaire (SPDQ), a new self-report diagnostic instrument for social phobia is described in three separate studies.

Study 1. The participants were 125 undergraduates seeking help for an anxiety disorder of whom 60 had social phobia. Receiver operating characteristics (ROC) analysis was conducted comparing SPDQ diagnoses and clinician-based Anxiety Disorder Interview Schedule-IV (ADIS-IV) diagnoses of social phobia. Diagnoses made by the SPDQ showed an 85% specificity, an 82% sensitivity and kappa agreement with the ADIS-IV of 0·66.

Study 2. The participants were 462 undergraduates who completed the SPDQ and a battery of additional questionnaires. The SPDQ had good internal consistency (α=0·95), good split-half reliability (r=0·90) and strong convergent and discriminant validity.

Study 3. The participants were 145 undergraduates who completed the SPDQ at two time points separated by 2 weeks as well as several additional questionnaires. Scores on the SAD, FNE and SISST of SPDQ categorized undergraduates were also compared to scores on these measures from 35 clinical community participants to determine the clinical validity of the SPDQ. The SPDQ had strong 2-week test–retest reliability and good convergent and discriminant validity. Undergraduates diagnosed with social phobia by the SPDQ were not significantly different on the SAD, FNE and SISST from the socially phobic community sample, but both groups had significantly higher scores than undergraduates identified by the SPDQ as not meeting criteria for social phobia, demonstrating clinical validity of the SPDQ.

Conclusions. These three studies provide preliminary evidence of the strong psychometric properties of the SPDQ as a measure to identify socially phobic participants.

Background. This article reports data on social phobia from the first large scale Australian epidemiological study. Prevalence rates, demographic correlates and co-morbidity in the sample that met criteria for social phobia are reported and gender differences examined.

Method. Data were obtained from a stratified sample of 10641 participants as part of the Australian National Survey of Mental Health and Well-Being (NSMHWB). A modified version of the Composite International Diagnostic Interview (CIDI) was used to determine the presence of social phobia, as well as other DSM-IV anxiety, affective and substance use disorders. The interview also screened for the presence of nine ICD-10 personality disorders, including anxious personality disorder, the equivalent of DSM-IV avoidant personality disorder (APD).

Results. The estimated 12 month prevalence of social phobia was 2·3%, lower than rates reported in several recent nationally representative epidemiological surveys and closer to those reported in the Epidemiological Catchment Area study (ECA) and other DSM-III studies. Considerable co-morbidity was identified. Data indicated that the co-morbidity with depression and alcohol abuse and dependence were generally subsequent to onset of social phobia and that the additional diagnosis of APD was associated with a greater burden of affective disorder. Social phobia most often preceded major depression, alcohol abuse and generalized anxiety disorder.

Conclusions. Social phobia is a highly prevalent, highly co-morbid disorder in the Australian community. Individuals with social phobia who also screen positively for APD appear to be at greater risk of co-morbidity with all surveyed disorders except alcohol abuse or dependence.

Background. Natural disasters such as earthquakes affect large numbers of people. Given the extent of the mental health problem following earthquakes, brief, effective and cost-effective treatment interventions are urgently needed. The present study examined whether cognitive-behavioural treatment could be shortened to a minimum number of sessions without undermining its effectiveness in post-traumatic stress disorder (PTSD).

Method. The study participants (N=231) were consecutive referrals to five project sites in the earthquake region in Turkey a mean of 13 months after the disaster. A modified behavioural treatment (BT) was used, which involved self-exposure instructions based on an enhancement of ‘sense of control’ rather than a habituation rationale and minimal cognitive interventions. The duration of treatment was variable, involving as many sessions as required for clinical improvement. Survival analysis was used to explore the minimum number of sessions required for clinical improvement, and multiple regression analysis to examine the predictors of outcome.

Results. The survivors received a mean of 4·3 sessions. Significant treatment effects and clinically meaningful effect sizes were noted on all measures. The treatment improved all PTSD and depression symptoms. The cumulative proportion of improved cases was 76% after one session and 88% after two sessions. No baseline variable predicted treatment outcome.

Conclusions. The modified BT appears to be promising as an effective one- or two-session intervention for earthquake survivors. It may be particularly useful in large-scale disasters as a cost-effective treatment that can be relatively easily disseminated to mass populations. Further research is needed to clarify the possible role of a treatment focus on sense of control in rapid recovery from traumatic stress.

Background. Considerable endocrine and non-endocrine evidence supports the hypothesis of increased cholinergic activity relative to noradrenergic activity in major depression. We previously reported functional sex differences (sexual diergism) in hypothalamo–pituitary–adrenal cortical (HPA) hormone responses to the administration of low-dose physostigmine (PHYSO), a cholinesterase inhibitor, in 12 female and eight male unipolar major depressives and 12 female and eight male individually matched control subjects. Because growth hormone (GH) secretion also is influenced by cholinergic mechanisms, we measured GH in the samples from this study.

Method. Subjects underwent four test sessions 5–7 days apart: PHYSO (8 μg/kg i.v.), arginine vasopressin (AVP) (0·08 U/kg i.m.), PHYSO+AVP and saline control. The AVP was administered as a second stimulus to HPA axis hormone secretion. PHYSO and AVP produced no side-effects in about half the subjects and predominantly mild side-effects in the other half, with no significant patient–control differences. Point biserial correlations between side-effects (absent or present) after PHYSO and the corresponding GH responses were non-significant in all groups.

Results. Afternoon baseline GH was significantly higher in the women than in the men, but it was not significantly different between the female or the male patients and their respective matched controls. AVP administration had no effect on GH. PHYSO administration acutely stimulated GH secretion, to a similar degree in the women and men. The depressed patients as a group had a significantly greater average post-PHYSO GH response than did their controls, with a trend toward a significant sex×diagnosis interaction: The female depressives had a significantly greater GH response than their female controls, whereas the male depressives had a similar GH response as their male controls.

Conclusions. These findings suggest sexual diergism (functional sex differences) in baseline and cholinergically stimulated plasma GH measures between major depressives and matched normal controls.

Background. Disturbed immune activity and vascular inflammation are associated both with clinical depression and coronary atherogenesis, and may constitute a mechanism through which depression contributes to coronary heart disease. If this is the case, then non-clinical depressive symptoms and psychological distress should be associated with immune activation and vascular inflammation. We tested this hypothesis in a healthy middle-aged sample.

Method. Measures of depressive symptoms and hopelessness were obtained from 226 volunteers (122 men, 104 women) aged 47–59 years, drawn from the Whitehall II epidemiological cohort. C-reactive protein, fibrinogen, plasma interleukin-6, tumour necrosis factor alpha, interleukin-1 receptor antagonist, and T- and B-lymphocyte, and natural killer cells numbers and percentages were assessed.

Results. There were no associations between measures of depressive symptoms or hopelessness and markers of immune activation or inflammatory response.

Conclusions. Factors such as the measures of depressive symptoms, the choice of inflammatory and immune indices, and sample size, are unlikely to be responsible for these null effects. Associations may be confined to clinically depressed or older age populations, but there are problems of confounding by co-morbidity and health compromising behaviours in this literature. We conclude that disturbances of immune function and inflammatory processes are unlikely to be primarily responsible for the associations between depressive symptoms and coronary heart disease described in the literature, and that other pathways are involved.

Background. The objective of this study was to determine whether older adults with first-ever onset of depression after age 60 years (late onset depression, LOD) have smaller frontal lobes than elderly patients with early-onset depression (EOD) and aged controls.

Method. Twenty-seven subjects with LOD, 24 with EOD and 37 controls underwent volumetric MRI to determine right and left frontal lobe volumes and total brain volume.

Results. The right frontal volume of subjects with LOD was 8·0% and 5·6% smaller than that of patients with EOD (P<0·01) and controls (NS) respectively. Volume of the left frontal lobe was not significantly different from EOD or controls. All analyses were adjusted for age, gender and total brain volume. Unlike controls and those with EOD, patients with LOD did not display a significant positive correlation between cognitive scores and total brain, left frontal or right frontal volumes.

Conclusion. LOD is associated with right frontal lobe atrophy and loss of the correlation between cognitive performance and brain volume. This adds support to the fronto-striatal hypothesis of depression and suggests that structural brain changes have a particular role in cases of LOD.

Background. The rate of binocular rivalry has been reported to be slower in subjects with bipolar disorder than in controls when tested with drifting, vertical and horizontal gratings of high spatial frequency.

Method. Here we assess the rate of binocular rivalry with stationary, vertical and horizontal gratings of low spatial frequency in 30 subjects with bipolar disorder, 30 age- and sex-matched controls, 18 subjects with schizophrenia and 18 subjects with major depression. Along with rivalry rate, the predominance of each of the rivaling images was assessed, as was the distribution of normalized rivalry intervals.

Results. The bipolar group demonstrated significantly slower rivalry than the control, schizophrenia and major depression groups. The schizophrenia and major depression groups did not differ significantly from the control group. Predominance values did not differ according to diagnosis and the distribution of normalized rivalry intervals was well described by a gamma function in all groups.

Conclusions. The results provide further evidence that binocular rivalry is slow in bipolar disorder and demonstrate that rivalry predominance and the distribution of normalized rivalry intervals are not abnormal in bipolar disorder. It is also shown by comparison with previous work, that high strength stimuli more effectively distinguish bipolar from control subjects than low strength stimuli. The data on schizophrenia and major depression suggest the need for large-scale specificity trials. Further study is also required to assess genetic and pathophysiological factors as well as the potential effects of state, medication, and clinical and biological subtypes.

Background. We tested the hypotheses that the addition of medication to psychotherapy enhances participation in the latter by: (1) speeding the acquisition of the psychotherapy's targeted skill; and (2) facilitating higher skill level acquisition.

Method. Participants were 431 chronically depressed patients who received Cognitive Behavioral Analysis System of Psychotherapy (CBASP), alone (N=214) or in combination with nefazodone (N=217), as part of a randomized chronic depression study (Keller et al. 2000). CBASP, developed specifically to treat chronic depression, uses a specific procedure, ‘situational analysis’ to help patients engage in more effective goal-oriented interpersonal behaviours. At the end of each session, therapists rated patients on their performance of situational analysis. Outcome on depressive symptoms was assessed with the 24-item Hamilton Rating Scale for Depression.

Results. Although reductions in depression were significantly greater in combined treatment compared to CBASP alone, there were no between-group differences in either the rate of skill acquisition or overall skill level at the end of treatment. Proficiency in the use of the main skill taught in psychotherapy at treatment midpoint predicted outcome independently of medication status and of baseline depressive severity.

Conclusions. Effective participation in CBASP, as reflected by proficiency in the compensatory skill taught in psychotherapy, is not enhanced by the addition of medication and does not mediate the between-group difference in depression outcome.

Background. Numerous studies have documented high rates of co-morbidity between major depressive disorder (MDD) and the anxiety disorders (ANX). However, the reason for this is unclear. Family studies provide one potentially useful approach for addressing this issue.

Method. We explored six explanations of the co-morbidity between MDD and ANX using a family study of a large community sample of young adults and their first-degree relatives. Participants included 112 probands with a lifetime history of both MDD and one or more ANX, 290 probands with a history of MDD but no ANX, 43 probands with a history of one or more ANX but no MDD, 352 probands with no lifetime history of either MDD or ANX, and the probands' 2608 first-degree relatives. Probands were assessed using semi-structured diagnostic interviews on two occasions in adolescence and a third time at age 24. Diagnostic data on relatives were collected using both direct and family history interviews.

Results. Compared with controls, MDD aggregated in the families of probands with MDD, whether or not they had co-morbid ANX; ANX aggregated in the families of probands with ANX, regardless of whether they had co-morbid MDD; and co-morbid MDD/ANX aggregated only in the families of probands with both MDD and ANX. The relatives of probands with ANX alone had a significantly higher rate of ANX than the relatives of probands with MDD alone, although none of the other comparisons between the depressed and anxious groups were significant.

Conclusions. This pattern of findings is largely, although not completely, consistent with the view that MDD and ANX are transmitted independently within families, and suggests that the co-morbidity between MDD and ANX is caused by non-familial aetiological factors.

Background. In this paper, data from the British National Survey of Psychiatric Morbidity are used to assess depressive disorders and markers of social disadvantage in women bringing up children on their own.

Method. The household component of the British National Surveys of Psychiatric Morbidity was based on a stratified random sample of >10000 subjects. This paper reports on 5281 women interviewed in person. Psychiatric symptoms and ICD-10 diagnoses were established by lay interviewers using the CIS-R. Results are presented in terms of depressive episode and mixed anxiety/depressive disorder. Housing tenure and access to a car were used as proxy measures of material status. The life event rate in the 6 months before interview was used to indicate overall exposure to stress, and subjects were asked in detail about perceived social support. Information was collected about various other sociodemographic attributes. Lone mothers were compared with supported mothers and with women not involved in care of children under 16.

Results. Lone mothers had prevalence rates of depressive episode of 7%, about three times higher than any other group. The milder condition, mixed anxiety/depression, was also increased in frequency. These increased rates of depressive conditions were no longer apparent after controlling for measures of social disadvantage, stress and isolation.

Conclusions. Lone mothers are increasing in numbers as marital stability declines. Their high rates of material disadvantage and of depressive disorder may have considerable implications for psychiatric and social policy.

Background. Although urban place of birth has been identified as a risk factor for schizophrenia, the extent to which this association is mediated by socially patterned risk factors such as obstetric complications and childhood socio-economic position is unclear. The diagnostic specificity of the association within the clinical psychotic syndromes is also unclear.

Method. A population cohort of 696025 males and females, born in Sweden between 1973 and 1980 and with linked birth and socio-economic data was followed up from age 16 for up to 9·8 years. Hospitalized cases of schizophrenia and other non-affective psychosis were identified from the Swedish Inpatient Discharge Register. We examined associations of these disorders with a three-level measure of urbanicity of birthplace before and after controlling for measures of foetal nutrition, obstetric complications and level of maternal education.

Results. Urban compared to rural birthplace was associated both with increased risk of adult onset schizophrenia (hazard ratio 1·34, CI 0·91–1·96) and other non-affective psychoses (hazard ratio 1·63, CI 1·18–2·26). None of these associations was greatly affected by adjustment for obstetric complications or maternal educational level. In the group of other non-affective psychoses urban–rural differences in disease risk were strongest among those born in the winter months.

Conclusion. Urbanization of birthplace is associated with increased risk of non-affective psychosis but this is not confined to narrowly defined cases. The magnitude of the association in Sweden is lower than that reported in other studies. Causal factors underlying this association appear to operate independently of risks associated with obstetric complications and parental educational status.

Background. The purpose of this study was to evaluate the clinical correlates of agoraphobic fear and avoidance and panic disorder in a non-clinical sample of adolescents.

Method. In a sample of 2365 high school students, combined data from a questionnaire and a structured clinical interview were used to classify subjects with agoraphobic fear and avoidance. Panic symptoms, major depression, childhood separation anxiety disorder, anxiety sensitivity and negative affectivity were also assessed.

Results. Fifteen subjects met study criteria for agoraphobic fear and avoidance in the past year. Only three (20%) of those with agoraphobia symptoms reported histories of panic attacks and there was no overlap between those with agoraphobic fear and avoidance and the 12 subjects who met DSM-III-R criteria for panic disorder. However, subjects with agoraphobia symptoms and those with panic disorder reported similar levels of anxiety sensitivity and negative affectivity. Childhood separation anxiety disorder was more common among those with agoraphobic fear and avoidance compared to those without.

Conclusion. Agoraphobic avoidance is rare in non-clinical samples of adolescents and usually not associated with panic attacks. However, adolescents with agoraphobia symptoms and those with panic disorder have similar clinical correlates consistent with a panic/agoraphobia spectrum model.

Background. Judgements made on chimeric faces elicit reliably a perceptual bias to the left hemispace, presumed to be due to right hemisphere dominance for emotional processes. Major depressive illness has been shown to attenuate this bias. The aim of this work was to examine lateral perceptual bias in bipolar I and II patients in a hypomanic state and unipolar depressed patients and those with unilateral hemisphere damage following stroke.

Method. Sixty patients with DSM-IV affective disorder (30 bipolar I or II, currently hypomanic, 30 unipolar depressives), 30 right brain-damaged patients, 30 left brain-damaged patients and 30 healthy controls were given the Happy–Sad Chimeric Faces Test.

Results. Right hemisphere damaged and unipolar depressed patients both showed a significantly reduced left hemispatial bias (LHB) compared to controls, bipolars and left brain-damaged patients. No significant difference in mean LHB between controls and both hypomanics and left brain-damaged patients was found. There was no significant association between LHB and clinical variables.

Conclusions. The results suggest a physiological distinction between bipolar and unipolar depression. The significantly diminished left hemifacial bias in depressed patients suggests right hemisphere dysfunction.