Cognitive-behavioural therapy (CBT)-based guided self-help (GSH) has been suggested to be an effective intervention for mild to moderate anxiety and depression, yet the evidence seems inconclusive, with some studies reporting that GSH is effective and others finding that GSH is ineffective. GSH differs in important respects from other levels of self-help, yet the literature regarding exclusively guided self-help interventions for anxiety and depression has not been reviewed systematically.

A literature search for randomized controlled trials (RCTs) examining CBT-based GSH interventions for anxiety and depressive disorders was conducted. Multiple electronic databases were searched; several journals spanning key disciplines were hand-searched; reference lists of included review articles were scanned and relevant first authors were contacted.

Thirteen studies met the inclusion criteria. Meta-analysis indicated the effectiveness of GSH at post-treatment, although GSH was found to have limited effectiveness at follow-up or among more clinically representative samples. Studies that reported greater effectiveness of GSH tended to be of lower methodological quality and generally involved participants who were self-selected rather than recruited through clinical referrals.

Although there is support for the effectiveness of CBT-based GSH among media-recruited individuals, the finding that the reviewed RCTs had limited effectiveness within routine clinical practice demonstrates that the evidence is not conclusive. Further rigorous evidence based on clinical populations that examines longer-term outcomes is required before CBT-based GSH interventions can be deemed effective for adults accessing primary care services for treatment of anxiety and depression.

Depression has been associated with limbic hyperactivation and frontal hypoactivation in response to negative facial stimuli. Anxiety disorders have also been associated with increased activation of emotional structures such as the amygdala and insula. This study examined to what extent activation of brain regions involved in perception of emotional faces is specific to depression and anxiety disorders in a large community-based sample of out-patients.

An event-related functional magnetic resonance imaging (fMRI) paradigm was used including angry, fearful, sad, happy and neutral facial expressions. One hundred and eighty-two out-patients (59 depressed, 57 anxiety and 66 co-morbid depression-anxiety) and 56 healthy controls selected from the Netherlands Study of Depression and Anxiety (NESDA) were included in the present study. Whole-brain analyses were conducted. The temporal profile of amygdala activation was also investigated.

Facial expressions activated the amygdala and fusiform gyrus in depressed patients with or without anxiety and in healthy controls, relative to scrambled faces, but this was less evident in patients with anxiety disorders. The response shape of the amygdala did not differ between groups. Depressed patients showed dorsolateral prefrontal cortex (PFC) hyperactivation in response to happy faces compared to healthy controls.

We suggest that stronger frontal activation to happy faces in depressed patients may reflect increased demands on effortful emotion regulation processes triggered by mood-incongruent stimuli. The lack of strong differences in neural activation to negative emotional faces, relative to healthy controls, may be characteristic of the mild-to-moderate severity of illness in this sample and may be indicative of a certain cognitive-emotional processing reserve.

Previous research reported that childhood adversity predicts juvenile- onset but not adult-onset depression, but studies confounded potentially genuine differences in adversity with differences in the recency with which adversity was experienced. The current study paper took into account the recency of risk when testing for differences among child-, adolescent- and young adult-onset depressions.

Up to nine waves of data were used per subject from two cohorts of the Great Smoky Mountains Study (GSMS; n=1004), covering children in the community aged 9–16, 19 and 21 years. Youth and one of their parents were interviewed using the Child and Adolescent Psychiatric Assessment (CAPA) between ages 9 and 16; these same youth were interviewed using the Young Adult Psychiatric Assessment (YAPA) at ages 19 and 21. The most common psychosocial risk factors for depression were assessed: poverty, life events, parental psychopathology, maltreatment, and family dysfunction.

Consistent with previous research, most childhood psychosocial risk factors were more strongly associated with child-onset than with adolescent-/adult-onset depression. When potentially genuine risk differences among the depression-onset groups were disentangled from differences due to the recency of risk, child- and young adult-onset depression were no longer different from one another. Adolescent-onset depression was associated with few psychosocial risk factors.

There were no differences in putative risk factors between child- and young adult-onset depression when the recency of risk was taken into account. Adolescent-onset depression was associated with few psychosocial risk factors. It is possible that some adolescent-onset depression cases differ in terms of risk from child- and young adult-onset depression.

The suicide rate is higher in prisoners compared with the general population. The aim was to describe the characteristics of and longitudinal trends in prisoner suicides in England and Wales.

A case series was ascertained from the Safer Custody and Offender Policy Group at the Ministry of Justice and included a 9-year (1999–2007) national census of prisoner suicides. Questionnaires were completed by prison staff on sociodemographic, custodial, clinical and service-level characteristics of the suicides.

There was a fall in the number of prison suicides and a decline in the proportion of young prisoner (18–20 years) suicides over time. Females were over-represented. Upward trends were found in prisoners with a history of violence and with previous mental health service contact. A downward trend was found in those with a primary psychiatric diagnosis of drug dependence. Drug dependence was found to be significant in explaining suicides within the first week of custody.

The findings provide an important insight to aid a target set in the National Suicide Prevention Strategy in England to reduce suicides in the prisoner population by 20% and highlight an important area for policy development in mental health services. Examining trends identified subgroups that may require improved mental healthcare and recognized those that appeared to be having their treatment needs more adequately met. Evidence suggests that targeted suicide prevention strategies for subgroups of prisoners are required.

There is compelling evidence that children of mothers with postnatal depression (PD) experience poor developmental outcomes. However, no studies have specifically ascertained the risk of mortality for offspring during preschool years, the most catastrophic outcome in the vulnerable period. This nationwide population-based study aimed to investigate whether maternal depression in the first year after giving birth was associated with increased mortality risk among their preschool children aged up to 5 years.

Three nationwide population-based datasets [the National Health Insurance Research Database (NHIRD), birth certificate registry and death certificate registry] were linked in this study. A total of 10 236 offspring of mothers with PD were recruited, together with a comparison cohort of 81 888 births matched with the affected women in terms of maternal age and year of delivery. Each child was traced for 5 years from delivery between 2001 and 2003 until the end of 2008 to determine mortality during preschool years.

During preschool years, 98 (0.96%) deaths were identified among the offspring of mothers with PD and 470 (0.57%) children in the comparison cohort died. For children up to 5 years old, exposure to maternal PD was independently associated with a 1.47-fold [95% confidence interval (CI) 1.16–1.87] increased mortality risk, after adjusting for family income, urbanization level and the characteristics of mother, father and infant. The risk of death by unnatural causes was even higher (about 2.23 times the risk, 95% CI 1.34–3.70) among exposed offspring.

PD places preschool children at significantly increased risk of mortality, especially from unnatural causes of death.

Empathy is crucial for successful social relationships. Despite its importance for social interactions, little is known about empathy in schizophrenia. This study investigated the degree to which schizophrenia patients can accurately infer the affective state of another person (i.e. empathic accuracy).

A group of 30 schizophrenia patients and 22 healthy controls performed an empathic accuracy task on which they continuously rated the affective state of another person shown in a video (referred to as the ‘target’). These ratings were compared with the target's own continuous self-rating of affective state; empathic accuracy was defined as the correlation between participants' ratings and the targets' self-ratings. A separate line-tracking task was administered to measure motoric/attentional factors that could account for group differences in performance. Participants' self-rated empathy was measured using the Interpersonal Reactivity Index, and targets' self-rated emotional expressivity was measured using the Berkeley Expressivity Questionnaire.

Compared with controls, schizophrenia patients showed lower empathic accuracy although they performed the motoric tracking task at high accuracy. There was a significant group×target expressivity interaction such that patients showed a smaller increase in empathic accuracy with higher levels of emotional expressivity by the target, compared with controls. Patients' empathic accuracy was uncorrelated with self-reported empathy or clinical symptoms.

Schizophrenia patients showed lower empathic accuracy than controls, and their empathic accuracy was less influenced by the emotional expressivity of the target. These findings suggest that schizophrenia patients benefit less from social cues of another person when making an empathic judgement.

Hypothalamic-pituitary-adrenocortical (HPA) axis abnormalities have been found in patients with a psychotic disorder and first-degree relatives of patients with a psychotic disorder react with subtle increases in non-clinical psychotic experiences and negative emotions in the face of everyday stress. The current study investigated whether HPA axis functioning is altered in individuals at above average genetic risk for psychotic disorder, examining diurnal cortisol profiles, cortisol reactivity to daily stressors and the association between HPA axis activity and subclinical psychotic experiences.

Participants included siblings of patients with a psychotic disorder (n=60) and a healthy comparison group (n=63). The Experience Sampling Method (a structured diary technique) was employed to assess stress, psychotic experiences, negative affect and salivary cortisol repeatedly in the flow of daily life.

Multi-level analyses revealed higher diurnal cortisol levels and heightened cortisol reactivity to negative daily events in siblings compared with controls. Diurnal cortisol slope did not differ between the two groups, but momentary increases in psychotic experiences and negative affect were associated with increased cortisol in the sibling group.

Findings support altered HPA axis activity in individuals at above average genetic risk for psychotic disorder, as evidenced by higher diurnal cortisol levels and increased cortisol reactivity to daily stress. Results also suggest a dynamic association between cortisol secretion and the intensity of psychotic-like experiences and negative emotions in daily life, although the direction of this association remains to be elucidated.

Research suggests that subclinical psychotic experiences during adolescence represent the behavioral expression of liability for psychosis. Little is known, however, about the longitudinal trajectory of liability in general population samples.

Growth mixture modeling was used to examine longitudinal trajectories of self-reported positive psychotic experiences in the Youth Self Report (YSR), completed three times over a period of 6 years by a general population cohort of adolescents aged 10–11 years at baseline (n=2230).

Four groups with distinct developmental trajectories of low, decreasing, increasing and persistent levels of mild positive psychotic experiences were revealed. The persistent trajectory was associated strongly with cannabis use, childhood trauma, developmental problems and ethnic minority status, and consistently displayed strong associations with factors known to predict transition from subclinical psychotic experience to clinical psychotic disorder (severity of and secondary distress due to psychotic experiences, social and attentional problems and affective dysregulation) and also with high levels of parental-reported psychotic experiences and use of mental health care at the end of the follow-up period. Progressively weaker associations were found for the increasing, decreasing and low trajectories respectively.

The results suggest that the outcome of early developmental deviation associated with later expression of psychotic experiences is contingent on the degree of later interaction with environmental risks inducing, first, persistence of psychotic experiences and, second, progression to onset of need for care and service use. Insight into the longitudinal dynamics of risk states in representative samples may contribute to the development of targeted early intervention in psychosis.

Elevated striatal dopamine synthesis capacity is thought to be fundamental to the pathophysiology of schizophrenia and has also been reported in people at risk of psychosis. It is therefore unclear if striatal hyperdopaminergia is a vulnerability marker for schizophrenia, or a state feature related to the psychosis itself. Relatives of patients with schizophrenia are themselves at increased risk of developing the condition. In this study we examined striatal dopamine synthesis capacity in both members of twin pairs discordant for schizophrenia.

In vivo striatal dopamine synthesis capacity was examined using fluorine-18-l-dihydroxyphenylalanine (18F-DOPA) positron emission tomography (PET) scans in seven twin pairs discordant for schizophrenia and in a control sample of 10 healthy control twin pairs.

Striatal 18F-DOPA uptake was not elevated in the unaffected co-twins of patients with schizophrenia (p=0.65) or indeed in the twins with schizophrenia (p=0.89) compared to the control group. Levels of psychotic symptoms were low in the patients with schizophrenia who were in general stable [mean (s.d.) Positive and Negative Syndrome Scale (PANSS) total=56.8 (25.5)] whereas the unaffected co-twins were largely asymptomatic.

Striatal dopamine synthesis capacity is not elevated in symptom-free individuals at genetic risk of schizophrenia, or in well-treated stable patients with chronic schizophrenia. These findings suggest that striatal hyperdopaminergia is not a vulnerability marker for schizophrenia.

Cannabis consumption continues to be identified as a causal agent in the onset and development of psychosis. However, recent findings have shown that the effect of cannabis on psychosis may be moderated by childhood traumatic experiences.

Using hierarchical multivariate logistic analyses the current study examined both the independent effect of cannabis consumption on psychosis diagnosis and the combined effect of cannabis consumption and childhood sexual abuse on psychosis diagnosis using data from the Adult Psychiatric Morbidity Survey 2007 (n=7403).

Findings suggested that cannabis consumption was predictive of psychosis diagnosis in a bivariate model; however, when estimated within a multivariate model that included childhood sexual abuse, the effect of cannabis use was attenuated and was not statistically significant. The multivariate analysis revealed that those who had experienced non-consensual sex in childhood were over six times [odds ratio (OR) 6.10] more likely to have had a diagnosis of psychosis compared with those who had not experienced this trauma. There was also a significant interaction. Individuals with a history of non-consensual sexual experience and cannabis consumption were over seven times more likely (OR 7.84) to have been diagnosed with psychosis compared with those without these experiences; however, this finding must be interpreted with caution as it emerged within an overall analytical step which was non-significant.

Future studies examining the effect of cannabis consumption on psychosis should adjust analyses for childhood trauma. Childhood trauma may advance existing gene–environment conceptualisations of the cannabis–psychosis link.

The cerebellum is rich in cannabinoid receptors and implicated in the neuropathology of schizophrenia. Long-term cannabis use is associated with functional and structural brain changes similar to those evident in schizophrenia, yet its impact on cerebellar structure has not been determined. We examined cerebellar grey and white matter in cannabis users with and without schizophrenia.

Seventeen patients with schizophrenia and 31 healthy controls were recruited; 48% of the healthy group and 47% of the patients were long-term heavy cannabis users (mean 19.7 and 17.9 years near daily use respectively). Cerebellar measures were extracted from structural 3-T magnetic resonance imaging (MRI) scans using semi-automated methods, and examined using analysis of covariance (ANCOVA) and correlational analyses.

Cerebellar white-matter volume was reduced in cannabis users with and without schizophrenia compared to healthy non-users, by 29.7% and 23.9% respectively, and by 17.7% in patients without cannabis use. Healthy cannabis users did not differ in white-matter volume from either of the schizophrenia groups. There were no group differences in cerebellar grey matter or total volumes. Total cerebellar volume decreased as a function of duration of cannabis use in the healthy users. Psychotic symptoms and illness duration correlated with cerebellar measures differentially between patients with and without cannabis use.

Long-term heavy cannabis use in healthy individuals is associated with smaller cerebellar white-matter volume similar to that observed in schizophrenia. Reduced volumes were even more pronounced in patients with schizophrenia who use cannabis. Cannabis use may alter the course of brain maturational processes associated with schizophrenia.

Epidemiological investigations show that up to 30% of schizophrenic patients suffer from obsessive–compulsive symptoms (OCS) associated with negative impact on the general prognosis. It has been proposed that antiserotonergic second-generation antipsychotics (SGAs) might induce OCS, but investigations of large samples integrating psychopathology, neuropsychology and psychopharmacology are missing.

We stratified 70 patients with schizophrenia according to their mode of antipsychotic treatment: clozapine and olanzapine (group I) compared with aripiprazole and amisulpride (group II). The groups were matched according to age, sex, educational levels and severity of the psychotic disorder (Positive and Negative Syndrome Scale). As the primary endpoint, we evaluated OCS severity (Yale–Brown Obsessive–Compulsive Scale).

OCS were significantly more prevalent and severe in group I, in which OCS severity correlated with dosage of clozapine and duration of treatment. Pronounced cognitive deficits in group I were found in visuospatial perception and visual memory (Wechsler Adult Intelligence Scale-Revised block design, Rey–Osterrieth Complex Figure Test), impulse inhibition (go/no-go test), higher perseveration scores (Wisconsin Card Sorting Test) and reduced set-shift abilities (Trail Making Test Part B, Set-shift Task). These cognitive domains correlated with OCS severity.

OCS in schizophrenia are associated with antiserotonergic SGA treatment, but longitudinal studies have to prove causality. Before starting treatment with antiserotonergic SGAs, specific neurocognitive domains should be evaluated, as visuospatial learning and impulse inhibition performance might allow early detection of OCS secondary to antipsychotic treatment in schizophrenia.

Processing emotional facial expressions is of interest in eating disorders (EDs) as impairments in recognizing and understanding social cues might underlie the interpersonal difficulties experienced by these patients. Disgust and anger are of particular theoretical and clinical interest. The current study investigated the neural response to facial expressions of anger and disgust in bulimia nervosa (BN).

Participants were 12 medication-free women with BN in an acute episode (mean age 24 years), and 16 age-, gender- and IQ-matched healthy volunteers (HVs). Functional magnetic resonance imaging (fMRI) was used to examine neural responses to angry and disgusted facial expressions.

Compared with HVs, patients with BN had a decreased neural response in the precuneus to facial expressions of both anger and disgust and a decreased neural response to angry facial expressions in the right amygdala.

The neural response to emotional facial expressions in BN differs from that found in HVs. The precuneus response may be consistent with the application of mentalization theory to EDs, and the amygdala response with relevant ED theory. The findings are preliminary, but novel, and require replication in a larger sample.

Individuals with body dysmorphic disorder (BDD) may have perceptual distortions for their appearance. Previous studies suggest imbalances in detailed relative to configural/holistic visual processing when viewing faces. No study has investigated the neural correlates of processing non-symptom-related stimuli. The objective of this study was to determine whether individuals with BDD have abnormal patterns of brain activation when viewing non-face/non-body object stimuli.

Fourteen medication-free participants with DSM-IV BDD and 14 healthy controls participated. We performed functional magnetic resonance imaging (fMRI) while participants matched photographs of houses that were unaltered, contained only high spatial frequency (HSF, high detail) information or only low spatial frequency (LSF, low detail) information. The primary outcome was group differences in blood oxygen level-dependent (BOLD) signal changes.

The BDD group showed lower activity in the parahippocampal gyrus, lingual gyrus and precuneus for LSF images. There were greater activations in medial prefrontal regions for HSF images, although no significant differences when compared to a low-level baseline. Greater symptom severity was associated with lower activity in the dorsal occipital cortex and ventrolateral prefrontal cortex for normal spatial frequency (NSF) and HSF images.

Individuals with BDD have abnormal brain activation patterns when viewing objects. Hypoactivity in visual association areas for configural and holistic (low detail) elements and abnormal allocation of prefrontal systems for details are consistent with a model of imbalances in global versus local processing. This may occur not only for appearance but also for general stimuli unrelated to their symptoms.

Direct comparisons of brain function between obsessive compulsive disorder (OCD) and other anxiety or OCD spectrum disorders are rare. This study aimed to investigate the specificity of altered frontal-striatal and limbic activations during planning in OCD, a prototypical anxiety disorder (panic disorder) and a putative OCD spectrum disorder (hypochondriasis).

The Tower of London task, a ‘frontal-striatal’ task, was used during functional magnetic resonance imaging measurements in 50 unmedicated patients, diagnosed with OCD (n=22), panic disorder (n=14) or hypochondriasis (n=14), and in 22 healthy subjects. Blood oxygen level-dependent (BOLD) signal changes were calculated for contrasts of interest (planning versus baseline and task load effects). Moreover, correlations between BOLD responses and both task performance and state anxiety were analysed.

Overall, patients showed a decreased recruitment of the precuneus, caudate nucleus, globus pallidus and thalamus, compared with healthy controls. There were no statistically significant differences in brain activation between the three patient groups. State anxiety was negatively correlated with dorsal frontal-striatal activation. Task performance was positively correlated with dorsal frontal-striatal recruitment and negatively correlated with limbic and ventral frontal-striatal recruitment. Multiple regression models showed that adequate task performance was best explained by independent contributions from dorsolateral prefrontal cortex (positive correlation) and amygdala (negative correlation), even after controlling for state anxiety.

Patients with OCD, panic disorder and hypochondriasis share similar alterations in frontal-striatal brain regions during a planning task, presumably partly related to increased limbic activation.

Panic disorder (PD) is a heterogeneous syndrome that can present with a variety of symptom profiles that potentially reflect distinct etiologic pathways. The present study represents the most comprehensive examination of phenotypic variance in PD with and without agoraphobia for the purpose of identifying clinically relevant and etiologically meaningful subtypes.

Latent class (LC) and factor mixture analysis were used to examine panic symptom data ascertained from three national epidemiologic surveys [Epidemiological Catchment Area (ECA), National Comorbidity Study (NCS), National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), Wave 1], a twin study [Virginia Adult Twin Study of Psychiatric and Substance Use Disorders (VATSPSUD)] and a clinical trial (Cross-National Collaborative Panic Study [CNCPS]).

Factor mixture models (versus LC) generally provided better fit to panic symptom data and suggested two panic classes for the ECA, VATSPSUD and CNCPS, with one class typified by prominent respiratory symptoms. The NCS yielded two classes, but suggested both qualitative and quantitative differences. The more contemporary NESARC sample supported a two and three class model, with the three class model suggesting two variants of respiratory panic. The NESARC's three class model continued to provide the best fit when the model was restricted to a more severe form of PD/panic disorder with agoraphobia.

Results from epidemiologic and clinical samples suggest two panic subtypes, with one subtype characterized by a respiratory component and a second class typified by general somatic symptoms. Results are discussed in light of their relevance to the etiopathogenesis of PD.

Autistic-like traits (ALTs), that is restrictions in intuitive social interaction, communication and flexibility of interests and behaviors, were studied in two population-based Swedish twin studies, one in children and one in adults: (1) to examine whether the variability in ALTs is a meaningful risk factor for concomitant attention deficit hyperactivity disorder (ADHD), anxiety, conduct problems, depression and substance abuse, and (2) to assess whether common genetic and environmental susceptibilities can help to explain co-existence of ALTs and traits associated with such concomitant problems.

Two nationwide twin cohorts from Sweden (consisting of 11 222 children and 18 349 adults) were assessed by DSM-based symptom algorithms for autism. The twins were divided into six groups based on their degree of ALTs and the risk for concomitant mental health problems was calculated for each group. Genetic and environmental susceptibilities common to ALTs and the other problem types were examined using bivariate twin modeling.

In both cohorts, even the lowest degree of ALTs increased the risk for all other types of mental health problems, and these risk estimates increased monotonically with the number of ALTs. For all conditions, common genetic and environmental factors could be discerned. Overall, the phenotypic correlation between ALTs and the traits examined were less pronounced in adulthood than in childhood and less affected by genetic compared with environmental factors.

Even low-grade ALTs are relevant to clinical psychiatry as they increase the risk for several heterotypical mental health problems. The association is influenced partly by common genetic and environmental susceptibilities. Attention to co-existing ALTs is warranted in research on a wide range of mental disorders.

The DSM-V Working Group is currently re-evaluating distress as a primary diagnostic criterion for female sexual dysfunction (FSD). Here, for the first time, we explored the epidemiology of sexual distress and its putative aetiological relationship to FSD by estimating the influence of genetic and environmental risk factors.

Questionnaire data on a representative sample of 930 British female twins using validated scales of FSD and sexual distress were subject to variance components analyses to quantify latent genetic and environmental factors influencing phenotypic variation and covariation. Multiple regression analyses were used to identify other potential risk factors of sexual distress.

Of 319 women with any sexual problems, only 36.5% reported distress. Of women classified as functional, 16.5% felt sexual distress. Sexual distress had a heritability of 44% [95% confidence interval (CI) 0.33–0.54]. Bivariate analysis suggested that the majority (91% CI 86–99%) of the covariance between sexual distress and FSD was due to unique environmental effects common to both traits. Associations were found between sexual distress and other risk variables, including relationship dissatisfaction [odds ratio (OR) 1.6, p<0.001], anxiety sensitivity and obsessive–compulsive symptomatology (OR 1.2, p<0.01, for both).

There seems to be a weak phenotypic and genetic basis for including sexual distress as a diagnostic indicator of FSD. Instead, the data indicate that unrelated psychological factors play an important role in sexual distress and tentatively suggest that sexual distress is less a consequence of FSD and more related to general anxiety among women.

It is well known that the hypothalamic–pituitary–adrenal (HPA) axis is compromised in major depression and bipolar disorder. There is increasing evidence that subtle HPA abnormalities, such as elevated cortisol levels, precede the development of an affective disorder. Interpersonal stress is also associated with the development of affective disorders. The present study sought to determine whether interpersonal chronic and episodic stress moderated the relationship between cortisol levels in the natural environment and risk status, defined as having a parent with bipolar disorder.

Sixty-two offspring of parents with bipolar disorder (OBD) and 60 offspring with no family history of affective disorders (OFH−), aged 19.48 years (s.d.=3.38, range 14–28), completed interviews assessing mental disorders and chronic and episodic stress, and provided saliva samples over 3 days.

Regression analyses revealed that the OBD who experienced high interpersonal chronic stress displayed a larger cortisol rise following awakening than the OBD reporting low interpersonal chronic stress. The same relationship was also found for levels of non-interpersonal chronic stress. The OBD who reported experiencing severe interpersonal episodic stress exhibited higher levels of daytime cortisol than the OBD reporting interpersonal episodic stress of mild severity. Importantly, none of the above relationships were detected in the OFH−. Each of the interactions between family history of affective disorders and stress remained after controlling for age, gender and offspring lifetime affective disorders and current non-affective disorders.

A biological sensitivity to stress may underlie the susceptibility to affective disorders among the OBD.