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Background Patients with various psychiatric disorders may suffer from feelings of anger, sometimes leading to maladaptive (e.g., aggressive) behaviors. We examined to what extent depressive and anxiety disorders, relevant clinical correlates, and sociodemographics determined the level of trait anger and the prevalence of recent anger attacks. Methods In the Netherlands Study of Depression and Anxiety (NESDA), the Spielberger Trait Anger Subscale and the Anger Attacks Questionnaire were analyzed in patients with depressive (n = 204), anxiety (n = 288), comorbid (n = 222), and remitted disorders (n = 1,107), as well as in healthy controls (n = 470) based on DSM-IV criteria. Results On average, participants were 46.2 years old (SD = 13.1) and 66.3% were female. Trait anger and anger attacks were most prevalent in the comorbid group (M = 18.5, SD = 5.9, and prevalence 22.1%), followed by anxiety disorder, depressive disorder, remitted disorder, and controls (M = 12.7; SD = 2.9, and prevalence 1.3%). Major depressive disorder, social phobia, panic disorder, and generalized anxiety disorder were most strongly associated to trait anger and anger attacks. Limitations Due to a cross-sectional design, it was not possible to provide evidence for temporal or causal relationships between anger and depressive and anxiety disorders. Conclusions Trait anger and anger attacks are linked to depressive and anxiety disorders, although the strength of the relationship differed among both anger constructs.

Introduction: Feelings of anger and irritability are prominent symptoms of bipolar disorder (BD) that may occur during hypomanic, depressive and, especially, during mixed mood states. We aimed to determine whether such constructs are associated with the conversion to BD in subjects with a history of unipolar depression. Methods: Data were derived from the depressed participants of Netherlands Study of Depression and Anxiety with 9 years of follow-up. Hypomania was ascertained using the Composite International Diagnostic Interview at 2, 4, 6, and 9 years follow-up. Cross-sectionally, we studied the association between prevalent hypomania and anger related constructs with the “Spielberger Trait Anger subscale,” the “Anger Attacks” questionnaire, the cluster B personality traits part of the “Personality Disorder Questionnaire,” and “aggression reactivity.” Prospectively, we studied whether aggression reactivity predicted incident hypomania using Cox regression analyses. Results: Cross-sectionally, the bipolar conversion group (n = 77) had significantly higher scores of trait anger and aggression reactivity, as well as a higher prevalence on “anger attacks,” “antisocial traits,” and “borderline traits” compared to current (n = 349) as well as remitted (n = 1159) depressive patients. In prospective analyses in 1744 participants, aggression reactivity predicted incident hypomania (n = 28), with a multivariate-adjusted hazard ratio of 1.4 (95% confidence interval: 1.02–1.93; p =.037). Conclusion: Anger is a risk factor for conversion from unipolar depression to BD. In addition, patients who converted to BD showed on average more anger, agitation and irritability than people with a history of unipolar depression who had not converted.

Background Research has shown that sad mood inductions (SMIs) have effects on cognition in depression-vulnerable samples (e.g., recovered depressed patients), but not in never-depressed individuals. A recent study however, found that an SMI followed by a brief period of suppressing negative thoughts affects subsequent information processing in never-depressed individuals, even while the sad mood had already dissipated. We investigated the relevance of this finding for depression, and also whether this effect would be robust against minor procedural variations. Method 32 recovered depressed and 32 never-depressed individuals underwent an SMI followed by a writing task during which either instructions to suppress negative thoughts or no instructions were given. Finally, participants completed a scrambled sentences task (SST). Results Recovered depressed participants unscrambled significantly more negative sentences on the SST than the control group. Thought suppression did not affect performance in either group. SST performance correlated with various aspects of cognitive reactivity. Conclusion A brief period of thought suppression during sadness does not have an effect on cognition in never-depressed nor in recovered depressed individuals.

Background: Previous research has indicated a strong association of smoking with depression and anxiety disorders, but the direction of the relationship is uncertain. Most research has been done in general population samples. We investigated the effect of smoking and nicotine dependence on the severity and course of depressive and anxiety symptoms in psychiatric patients.Methods: Data came from the Netherlands Study of Depression and Anxiety (NESDA) including participants with a current diagnosis of depression and/or an anxiety disorder (N = 1725). The course of smoking status and symptoms of depression, general anxiety, social anxiety, and agoraphobia were measured at baseline and after one and two years. Age, gender, education, alcohol use, physical activity, and negative life events were treated as covariates.Results: At baseline, the symptoms of depression, general anxiety, and agoraphobia were more severe in nicotine-dependent smokers than in never-smokers, former smokers, and non-dependent smokers. These differences remained after adjusting for covariates. Smaller differences were observed for severity of social anxiety which were no longer significant after controlling for covariates. Over a two-year follow-up, the improvement of depressive and anxiety symptoms was slower in nicotine-dependent smokers than in the other groups even after controlling for covariates. There were no differences between the groups in the course of symptoms of social anxiety and agoraphobia over time.Conclusions: In psychiatric patients, smoking is associated with higher severity of depressive and anxiety symptoms, and with slower recovery, but only when smokers are nicotine-dependent. (C) 2012 Elsevier Ireland Ltd. All rights reserved.

Background: Hypothalamus-Pituitary-Adrenal (HPA) axis dysregulation is often seen in major depression, and is thought to represent a trait vulnerability - rather than merely an illness marker - for depressive disorder and possibly anxiety disorder. Vulnerability traits associated with stress-related disorders might reflect increased sensitivity for the development of psychopathology through an association with HPA axis activity. Few studies have examined the association between psychological trait factors and the cortisol awakening response, with inconsistent results. The present study examined the relationship between multiple psychological trait factors and the cortisol awakening curve, including both the dynamic of the CAR and overall cortisol awakening levels, in a sample of persons without psychopathology, hypothesizing that persons scoring high on vulnerability traits demonstrate an elevated cortisol awakening curve.Methods: From 2981 participants of the Netherlands Study of Depression and Anxiety (NESDA), baseline data from 381 controls (aged 18-65) without previous, current and parental depression and anxiety disorders were analyzed. Psychological measures included the Big Five personality traits (neuroticism, extraversion, openness to experience, conscientiousness, and agreeableness) measured using the NEO-FFI, anxiety sensitivity assessed by the Anxiety Sensitivity Index, cognitive reactivity to sadness (hopelessness, acceptance/coping, aggression, control/perfectionism, risk aversion, and rumination) as measured by the LEIDS-R questionnaire, and mastery, assessed using the Pearlin and Schooler Mastery scale. Salivary cortisol levels were measured at awakening, and 30, 45, and 60 min afterwards.Results: In adjusted analyses, high scores of hopelessness reactivity (beta = .13, p = .02) were consistently associated with a higher cortisol awakening response. In addition, although inconsistent across analyses, persons scoring higher on extraversion, control/perfectionism reactivity, and mastery tended to show a slightly flatter CAR. No significant associations were found for neuroticism, openness to experience, agreeableness, conscientiousness, anxiety sensitivity, and acceptance/coping, aggression, or risk aversion reactivity.Conclusion: Of various psychological traits, only hopelessness reactivity, a trait that has been associated with depression and suicidality, is consistently associated with HPA axis dysregulation. Hopelessness reactivity may represent a predisposing vulnerability for the development of a depressive or anxiety disorder, possibly in part mediated by HPA axis activity. (C) 2010 Elsevier Ltd. All rights reserved.

Depressive symptoms are common during pregnancy and the post-partum period. Although essential n-3 PUFA may have beneficial effects on depression, it remains unclear whether they are also effective for perinatal depression. The purpose of the present study was to assess the efficacy of n-3 supplementation for perinatal depression, by performing a meta-analysis on currently available data. After a thorough literature search, we included seven randomised controlled trials in the meta-analysis, all with EPA and/or DHA supplementation. Most studies were judged to be of low-to-moderate quality, mainly due to small sample sizes and failure to adhere to Consolidated Standards of Reporting Trials guidelines. Some studies were not primarily designed to address perinatal depression. A total of 309 women on n-3 fatty acid supplementation were compared with 303 women on placebo treatment. n-3 Supplementation was not found to be significantly more effective than placebo at post-treatment with a pooled effect size (Hedges's g) of − 0·03 (95 % CI − 0·18, 0·13; P = 0·76) using a fixed-effects model. Heterogeneity was low-to-moderate (I2 = 30 %). In a subgroup analysis of three small studies of pregnant women with major depression, there was some indication of effectiveness (effect size 0·17; 95 % CI − 0·21, 0·55). In conclusion, the question of whether EPA and DHA administration is effective in the prevention or treatment of perinatal depression cannot be answered yet. Future research should focus on women who are clinically depressed (or at risk). The quality of research in this area needs to improve.

Objective: We compared the efficacy of cognitive behavior therapy (CBT), paroxetine and placebo in the treatment of noncardiac chest pain (NCCP). We also investigated whether pre- to mid-treatment reduction of (heart-focused) anxiety mediated mid- to post-treatment pain reduction. Methods: Sixty-nine adults with NCCP were randomly assigned to 16 weeks of outpatient treatment with CBT, paroxetine or placebo. The comparison between placebo and paroxetine was carried out in a double-blind fashion. The main outcome measure was a chest pain index (duration*intensity) as derived from daily pain diaries. Putative mediator measures were general anxiety (HADS:A) and heart-focused anxiety (Cardiac Anxiety Questionnaire). Results: Eleven patients treated with paroxetine or placebo dropped out prematurely. Intent-to-treat analysis showed that CBT was significantly superior to placebo and to paroxetine in reducing NCCP at posttreatment. Only CBT significantly reduced heart-focused anxiety compared to placebo at mid- and post-treatment. Pre- to mid-treatment reduction of heart-focused anxiety predicted mid- to post-treatment NCCP reduction. The indirect effect of CBT on pain reduction by reducing heart-focused anxiety was significant compared to placebo but not to paroxctine. Conclusion: CBT is an effective treatment option for patients with NCCP. Paroxetine is not more effective than placebo on the short term. Reduction of heart-focused anxiety by CBT seems to mediate subsequent reduction of NCCP compared to placebo. The results provide further support for cognitive behavioral models of NCCP and point to the potential benefits of, in particular, cognitive-behavioral interventions to modify heart-focused anxiety. (C) 2010 Elsevier Inc. All rights reserved.

Depressive disorders are associated with various cognitive impairments. Studies on whether or not these impairments persist into the euthymic phase have shown conflicting results, due to differences in test versions and in study samples. In this paper, we aimed to compare the cognitive performance of remitted depressed patients with that of age- and gender-matched healthy volunteers across a wide range of cognitive domains. In two studies, we found few differences on neutral as well as emotional information processing tests. The findings indicate that remitted depressed patients who use antidepressant medication still show an increased recognition of facial expression of fear compared to healthy controls. Patients also performed worse on a test of recognition of abstract visual information from long-term memory. No other residual cognitive impairments were found. These results indicate that most of the cognitive impairments associated with depression resolve with recovery through medication, even when recovery is incomplete. Considering the finding that remitted depressed patients have higher levels of cognitive reactivity, future studies may investigate the possibility that these cognitive impairments have not resolved but have become latent, and may therefore easily be triggered by small changes in mood state.

Cognitive reactivity (CR) is a psychological vulnerability marker of depression, whereas response to acute tryptophan depletion (ATD; a serotonergic challenge procedure) is a biological vulnerability marker. The aim of this study was to investigate the relationship between these markers. Thirty-nine remitted depressed patients participated in 2 ATD sessions in a double-blind crossover design. CR, assessed prior to the ATD sessions, predicted depressive response to high-dose ATD. CR also diminished the effects of 2 known predictors of ATD response: gender and residual symptoms. Neuroticism and behavioral inhibition were unrelated to ATD response. CR is associated with an increased sensitivity to reductions of serotonin concentrations. These findings present a small step toward unifying cognitive and neurobiological theories of depression.

Background Depression is a major risk factor for cardiovascular disease. An important risk factor for cardiovascular disease, low heart rate variability, often has been found in depressed patients and has been associated with impulsivity. The present study investigated whether experimental lowering of serotonin would decrease heart rate variability and increase impulsivity in remitted depressed patients, in particular in those patients with disturbed impulse control. Methods Nineteen patients in remission from depression received high-dose and low-dose acute tryptophan depletion in a randomized, counterbalanced, double-blind crossover design. Heart rate variability and impulsivity were assessed during each acute tryptophan depletion session and during a baseline session. Suicidal ideation during past depression was used as an index for individual differences in impulse control. Results High-dose acute tryptophan depletion led to a larger increase in depressive symptoms than did low-dose acute tryptophan depletion. High-dose acute tryptophan depletion decreased heart rate variability and increased impulsivity and anxiety, but only in patients with a history of suicidal ideation. Symptom effects of high-dose acute tryptophan depletion correlated with low heart rate variability at baseline. Conclusions Depressed patients who have problems with controlling impulsivity might be more at risk for developing cardiovascular disease, possibly related to increased vulnerability to impaired 5-hydroxytryptamine function.

The present study investigated whether scores on the Autobiographical Memory Test (AMT) in 55 patients with borderline personality disorder (BPD) were modified after long-term psychotherapy and whether the pretreatment AMT scores would predict improvement in depression severity or BPD symptom severity at the end of treatment. In addition, it was analysed whether changes in ratings of mood, thought suppression, dissociation, and BPD symptom severity following treatment were associated with changes in AMT scores. Only patients with BPD and a comorbid diagnosis of depression at time 1, generated significantly more specific memories and fewer categoric memories after 15 months of therapy. Moreover, these changes were unrelated to type of therapy and changes in depression severity, borderline symptom severity, dissociation, or thought suppression. The AMT scores at initial assessment did not predict depression severity at 15 months. The percentage of negative specific memories tended to predict BPD symptom severity.

Depression is associated with reduced brain serotonin (5-hydroxytryptamine; 5-HT) function and with cognitive dysfunctions. A diet rich in α-lactalbumin protein has been found to increase the ratio tryptophan /large neutral amino acids (Trp/σLNAA), and to improve cognitive functioning in individuals with high neuroticism scores. Since cognitive dysfunctions sometimes persist after remission of depression, the present study investigated the effects of α-lactalbumin-enriched diet on cognition in recovered depressed patients. Twenty-three recovered depressed patients and 20 healthy matched controls without a history of depression consumed meals rich in α-lactalbumin or casein protein in a double-blind crossover design. Mood, cognitive function and plasma amino acids were assessed at both sessions before and after dietary intake. Alpha-lactalbumin protein had no effect on mood, but improved abstract visual memory and impaired simple motor performance. These effects were independent of history of depression. Supplements of lactalbumin may be useful for nutrition research in relation to age- or disease-related memory decline. The present findings should be further examined in different (e.g. medicated) samples. The long-term effects of α-lactalbumin should also be investigated.

BackgroundAcute tryptophan depletion transiently induces symptoms in those with remitted depression. The behavioural specificity is uncertain, however. Recently, symptom provocation studies have become controversial, particularly in the USA.AimsTo assess the specificity of acute tryptophan depletion. To investigate systematically the subjective experiences of those taking part in a symptom provocation study.MethodTwenty individuals with remitted depression underwent acute tryptophan depletion in a double-blind, crossover trial. Psychiatric symptoms and self-schemata relevant to depression were assessed. The quality of the informed consent procedure and subjective experiences were also evaluated.ResultsAcute tryptophan depletion induced a specific depressive response. The effects were more pronounced in females than in males. Participants were quite satisfied with the informed consent procedure. They had understood that this was a fundamental research project and personal benefits were not expected. However, some participants still found it a positive experience.ConclusionsAcute tryptophan depletion is a suitable model of vulnerability to depression, from both a scientific and an ethical perspective.

Alpha-lactalbumin is a tryptophan-rich protein fraction. A diet enriched with alpha-lactalbumin increases the ratio of tryptophan to the other large neutral amino acids, which may in turn increase brain serotonin content. In stress-vulnerable individuals, alpha-lactalbumin improved mood and attenuated the cortisol response after experimental stress. The aim of the present study was to investigate the effects of an alpha-lactalbumin-enriched diet on mood and stress response in recovered depressed subjects and healthy controls. Forty-three subjects (twenty-three recovered depressed and twenty healthy subjects) received alpha-lactalbumin and casein (placebo) on separate days, in a double-blind randomised crossover design. On both occasions, subjects underwent a stress test (an unsolvable mental arithmetic task with loud noise). The stress test affected mood in both conditions. Although the alpha-lactalbumin diet led to the expected rises in tryptophan and tryptophan:large neutral amino acids ratio, only minimal effects were found on mood and cortisol response to experimental stress. The results were the same for recovered depressed patients and controls. A 1 d diet enriched with alpha-lactalbumin is not sufficient to prevent a stress-induced mood deterioration or a cortisol response in unmedicated, recovered depressed subjects. Future studies may investigate the effects of longer-term diets or may investigate different samples (e.g. medicated patients).

It has frequently been demonstrated that acute tryptophan depletion (ATD) induces a transient depressed mood in some patients who are in remission from depression. However, the effects of ATD on cognitive processes in remitted depressed patients have not been investigated. The aim of the present study was to investigate the effects of different extents of depletion on mood and cognitive tasks involving neutral and emotional stimuli. Twenty patients in remission or in partial remission from depression received ATD in a double-blind, crossover design. Mood was assessed at both sessions before, at +6.5 h and +24 h afterdepletion. Cognitive assessment in both sessions started at +4.75 h, and also before and after the whole procedure. The ATD mixtures induced the expected reductions of plasma tryptophan levels. High-dose ATD induced a depressive response in a subsample of patients and impaired theprocessing of positive information independent of mood change. Attention for neutral stimuli (Stroop interference) improved in a dose-dependent manner. ATD may affect mood and cognition via different pathways: one implicated in mood regulation and the processing ofemotional information, and one for the processing of neutral information. The first pathway may be more important for discriminating vulnerability to impaired serotonin function. The comparison of the effects of high-dose and low-dose ATD is useful for those studies aiming to investigate the relationships among 5-HT, mood and cognition.

Extensive evidence exists for an association between attentional bias (AB; attentional vigilance or avoidance) and anxiety. Recent studies in healthy participants suggest that attentional control (AC) may facilitate inhibition of automatic attentional processes associated with anxiety. To investigate relationships among AC, trauma-related AB, symptom severity and trait anxiety in patients with Posttraumatic Stress Disorder (PTSD), participants (N = 91) completed self-report measures of AC, posttraumatic stress symptoms (PTSS) and trait anxiety. AB was measured with a pictorial version of the Dot Probe Test. AC moderated the relationship between PTSS and AB (threat avoidance). Patients high in PTSS and low in AC showed attentional avoidance. No association between PTSS and AB in patients with medium or high levels of AC was found. A similar pattern of results was observed for the relationship between trait anxiety, AC and AB. These results suggest that a low ability to control attention is a risk factor for AB in PTSD. This first clinical study corroborates the accumulating evidence from analog studies that individual differences in top-down attentional control are of considerable importance in the expression of AB in anxious psychopathology.

Public health strategies have been successful in preventing morbidity and death during the prime years of our lives but there is too little knowledge on how to address the consequences of our success, the fate of the overwhelming majority of people now enjoying higher longevity. We assert that striving for just healthy longevity is too limited an approach as for most people a satisfactory life is not dependent on an optimal level of physical and mental functioning. Here we present a conceptual framework, introducing vitality as a key competence that combines the narrow, functional definition of health and the broader perception of self-rated life satisfaction. Vitality is the ability of a person to set ambitions which are appropriate for one's life situation and to realize these goals despite functional limitations. A focus on vitality presents a striking opportunity to experience a satisfactory life in keeping with longevity from which society as a whole could strongly benefit. It necessitates a paradigm shift in our thinking that should lead to a new type of health strategy that appropriately integrates the needs and desires of the older generation.

The White Bear Suppression Inventory (WBSI) aims to measure the general tendency to suppress unwanted negative thoughts. The aims of the present study were: (a) to assess the psychometric properties of the WBSI in a clinical population; (b) to evaluate the association of the WBSI with dimensional and categorical measures of psychopathology; and (c) to explore the relationship of the WBSI with measures for dissociation while controlling for level of psychopathology. In a sample of 254 consecutive psychiatric outpatients the factor structure and internal consistency of the WBSI were found to be good. Moreover, WBSI scores were significantly and positively related to all of the dimensional measures for psychopathology of the Symptom Checklist-90 and did not differ between patients with a DSM-IV anxiety disorder, affective disorder or no psychiatric diagnosis. Finally, WBSI scores were unrelated to measures for proneness to dissociation (Dissociation Questionnaire and Somatic Dissociation Questionnaire) while controlling for level of psychopathology. It is concluded that: (a) thought suppression is a common phenomenon among psychiatric patients with various complaints; and (b) that dissociation is not related to thought suppression.

The aim of this study was to assess to what extent patients with unexplained chest pain (UCP) are interested in a medical psychological treatment, and to find biographical or medical status variables predictive of that need. A total of 1053 patients with a discharge diagnosis of UCP from two cardiac out-patient clinics were approached by mail. Of these, 77.2% returned the questionnaire, which inquired about duration, frequency, and intensity of UCP; limitations in activities; and whether they would like medical psychological treatment for their UCP. Results showed little spontaneous recovery, and indicated no association between duration of UCP and interest in treatment. Younger patients and males were more interested in treatment. Furthermore, limitations in activities rather than frequency or intensity of pain was the most important predictor of interest in treatment. A three-step plan is proposed to enhance care for patients with UCP.

The aim of this study was to develop and evaluate the feasibility of a cognitive behavioural treatment for unexplained chest pain (UCP), based on the cognitive model of UCP. Ten patients were treated. The diagnosis had been made by a cardiologist two years before the start of treatment. The treatment incorporated breathing and relaxation training, identifying and challenging beliefs about the cause of UCP, behavioural experiments and problem solving for social problems. Patients improved significantly with regard to intensity and duration of chest pain, anxiety and functional limitations. Moreover, the reduction of scores for fear of bodily sensations and of credibility ratings of idiosyncratic disease related negative automatic thoughts was significant. The changes in scores for the inclination to interpret bodily sensations catastrophically almost reached the level of significance. These results suggests that therapy results may be cognitively mediated.

The hypothesis was investigated that more accurate perception of heartbeats by patients with panic disorder is an artefact of arousal. Twenty-three patients with panic disorder, 16 patients with a mood disorder and 21 normal controls were tested. There were more panic patients who accurately perceived their heart rates ( N =7) than depressed patients ( N =0) or normals ( N =2). The nine accurate perceivers had higher scores on questionnaires measuring the cognitions associated with panic. For non-accurate perceivers, perceived heart rates were unrelated to actual heart rates, unrelated to cognitive factors, but significantly related to arousal. It is concluded that the accurate perception of heartbeats by patients with panic disorder is both fact and artefact: some patients are accurate perceivers, but the majority are not.

The aim of the present study was to assess the contribution of somatosensory amplification to somatization. Two questions were addressed: (1) whether somatization is associated with somatosensory amplification independent of level of anxiety or depression, and (2) whether any differences in somatization between patients with panic disorder or depressive disorder and controls can be attributed to differences in somatosensory amplification. The subjects were 673 consecutive psychiatric outpatients. In this sample, 124 patients received a V-code or no psychiatric diagnosis (controls), 82 a single diagnosis of panic disorder, and 68 a single diagnosis of major depression. The following measures were used: the Somatosensory Amplification Scale (SSAS), Symptom Checklist-90 (SCL-90), and Hospital Anxiety and Depression Scale (HADS). SCL-90 somatization scores were significantly associated with anxiety scores and to a lesser extent with SSAS scores for somatosensory amplification, independent of gender, presence of physical illness, and depression scores. Moreover, after statistically controlling for differences in somatosensory amplification, panic disorder patients still obtained significantly higher somatization scores than depressive disorder patients, who manifested significantly higher levels of somatization than controls. It is concluded that somatization primarily reflects somatized anxiety and not somatosensory amplification. Somatization associated with panic attacks may result from other mechanisms, such as the psychophysiology of anxiety and cognitive misappraisal of benign bodily symptoms. Further studies into the concurrent validity of the SSAS as a measure of interoceptive acuity are needed.

BACKGROUND The Beck Depression Inventory-II (BDI-II), the Inventory of Depressive Symptoms (self-report) (IDS-SR) and the Montgomery-Äsberg Depression Rating Scale (MADRS) are questionnaires that assess symptom severity in patients with a depressive disorder, often part of Routine Outcome Monitoring (ROM). We aimed to generate reference values for both "healthy" and "clinically depressed" populations. METHODS We included 1295 subjects from the general population (ROM reference-group) recruited through general practitioners, and 4627 psychiatric outpatients diagnosed with Major Depressive Disorder (MDD) or dysthymia (ROM patient-group). The outermost 5% of observations were used to define limits for one-sided reference intervals (95th percentiles; P95). Receiver Operating Characteristics (ROC) analyses were used to yield alternative cut-off values. Internal consistency was assessed. RESULTS The mean age was 40.3yr (SD=12.6) and 39.3 (SD=12.3) for the ROM reference and patient-groups, respectively, and 62.8% versus 61.0% were female. Cut-off (P95) values differed for women and men, being respectively 15 and 12 for the BDI-II, 23 and 18 for the IDS-SR, and 12.5 and 9 for the MADRS. ROC analyses yielded almost equal reference values. The discriminative power of the BDI-II, IDS-SR and MADRS scores was very high. Internal consistency was excellent for total scores and satisfactory for all subscales, except for the IDS-SR subscale Atypical Characteristics. LIMITATIONS Substantial non-response and limited generalizability. CONCLUSIONS For the BDI-II, IDS-SR and MADRS a comprehensive set of reference values were provided. Reference values were higher in women than in men, implying the use of sex-specific cut-off values. Either instrument can be offered to every patient with MAS disorders to make responsible decisions about continuing, changing or terminating therapy.

Negative affect in healthy populations regulates the appraisal of demanding situations, which tunes subsequent effort mobilization and adjustments in cognitive control. In the present study, we hypothesized that dysphoria in depressed individuals similarly modulates this adaptation, possibly through a neural mechanism involving serotonergic regulation. We tested the effect of dysphoria induced by acute tryptophan depletion (ATD) in remitted depressed patients on conflict adaptation in a Simon task. ATD temporarily lowers the availability of the serotonin precursor L-Tryptophan and is known to increase depressive symptoms in approximately half of remitted depressed participants. We found that depressive symptoms induced by ATD were associated with increased conflict adaptation. Our finding extends recent observations implying an important role of affect in regulating conflict-driven cognitive control.

Objective. Irritable and nonirritable depressed patients differ on demographic and clinical characteristics. We investigated whether this extends to psychological and physiological measures.Method. We compared irritable and nonirritable unipolar depressed patients on symptomatology, personality, and (psycho)physiological measures (cortisol, cholesterol, and heart rate variability). Symptomatology was reassessed after one year, and we also compared depressed patients who were irritable or non-irritable at both time points (Irr++ versus Irr−−).Results. Almost half (46%;N=420) of the sample was classified as irritable. These patients scored higher on depression severity, anxiety, hypomanic symptoms, and psychological variables. No differences were observed on physiological markers after correction for depression severity. The same pattern was found when comparing Irr++ and Irr−− groups.Conclusion. Irritable and non-irritable depressed patients differ on clinical and psychological variables, but not on the currently investigated physiological markers. The clinical relevance of the distinction and the significance of the hypomanic symptoms remain to be demonstrated.

BACKGROUND The brain-derived neurotrophic factor (BDNF) is a key protein in maintaining neuronal integrity. The BDNF gene is thought to play an important role in the pathophysiology of mood and anxiety disorders. The aim of this study was to investigate, for the first time in a single study, the association between BDNF Val(66)Met polymorphism, anxiety, alcohol consumption, and cortisol stress response. METHOD 98 healthy university students (54 females and 44 males), genotyped for the Val(66)Met polymorphism, participated in a physical-stress procedure (cold pressure test, CPT) after having been informed that they would undergo a painful experience. Indices of anxiety and of stress were collected from repeated measurement of salivary cortisol, blood pressure, and heart rate. RESULTS BDNF Met carriers, were more anxious during the CPT (p

Beneficial effects of omega-3 fatty acids have been reported for several psychiatric disorders, particularly for depression. Association studies show a relationship between omega-3 intake and depression risk. Meta-analyses of clinical trials have shown a moderate effect of supplementation on depressive symptoms, but not on normal mood states. Few studies have investigated effects on cognition. The purpose of this study was to examine effects of omega-3 supplements on cognition and mood of recovered depressed individuals. Seventy-one participants were randomized to receive either omega-3 or placebo for four weeks in a randomized double-blind design. Results showed small effects of omega-3 supplementation on aspects of emotional decision-making and on self-reported states of depression and tension. Some of the effects were confounded by learning effects. No significant effects were observed on memory, attention, cognitive reactivity and depressive symptoms. While inconclusive, the present findings may indicate that omega-3 supplementation has selective effects on emotional cognition and mood in recovered depressed participants.

Background: Few studies have investigated the importance of psychological characteristics for chronicity of depression. Knowledge about psychological differences between chronically depressed persons and nonchronically depressed persons may help to improve treatment of chronic depression. This is the first study to simultaneously compare in large samples various psychological characteristics between chronically depressed and nonchronically depressed adults.Method: Baseline data were drawn from the Netherlands Study of Depression and Anxiety (NESDA), an ongoing longitudinal cohort study aimed at examining the long-term course of depressive and anxiety disorders in different health care settings and phases of illness. Participants were aged 18 to 65 years at the baseline assessment in 2004-2007 and had a current diagnosis of DSM-IV major depressive disorder (N = 1,002). Chronicity of depression was defined as being depressed for 24 months or more in the past 4 to 5 years. The chronicity criterion was fulfilled by 31% (n = 312). The NEO Five-Factor Inventory measured the 5 personality domains, the Leiden Index of Depression Sensitivity-Revised was used to measure cognitive reactivity (eg, hopelessness, rumination), and the Mastery Scale measured external locus of control.Results: Compared to the nonchronically depressed persons, the chronically depressed persons reported significantly higher levels of neuroticism (OR = 1.81; 95% CI, 1.55-2.12; P Conclusions: Our findings suggest that extraversion, rumination, and external locus of control, but not neuroticism, are differentiating psychological characteristics for chronicity of depression. These findings provide suggestions for more specific interventions, focused on extraversion, rumination, and external locus of control, in the treatment of chronic depression. J Clin Psychiatry 2011;72(3):288-294 (C) Copyright 2011 Physicians Postgraduate Press

BackgroundPast episodes of depressive or anxiety disorders and subthreshold symptoms have both been reported to predict the occurrence of depressive or anxiety disorders. It is unclear to what extent the two factors interact or predict these disorders independently.AimsTo examine the extent to which history, subthreshold symptoms and their combination predict the occurrence of depressive (major depressive disorder, dysthymia) or anxiety disorders (social phobia, panic disorder, agoraphobia, generalised anxiety disorder) over a 2-year period.MethodThis was a prospective cohort study with 1167 participants: the Netherlands Study of Depression and Anxiety. Anxiety and depressive disorders were determined with the Composite International Diagnostic Interview, subthreshold symptoms were determined with the Inventory of Depressive Symptomatology–Self Report and the Beck Anxiety Inventory.ResultsOccurrence of depressive disorder was best predicted by a combination of a history of depression and subthreshold symptoms, followed by either one alone. Occurrence of anxiety disorder was best predicted by both a combination of a history of anxiety disorder and subthreshold symptoms and a combination of a history of depression and subthreshold symptoms, followed by any subthreshold symptoms or a history of any disorder alone.ConclusionsA history and subthreshold symptoms independently predicted the subsequent occurrence of depressive or anxiety disorder. Together these two characteristics provide reasonable discriminative value. Whereas anxiety predicted the occurrence of an anxiety disorder only, depression predicted the occurrence of both depressive and anxiety disorders.

Introduction: Smoking is a known risk indicator for depression and some of the anxiety disorders. No data are available on the role of age at smoking onset in the development of depression and anxiety disorders. We examined the association of smoking onset age on the onset age of depression and anxiety disorders. Methods: Participants of the Netherlands Study of Depression and Anxiety Disorders who developed psychopathology after starting smoking were selected (N = 1,055). The dependent variable was the time to onset of psychopathology after starting smoking, and the independent variable was age at smoking onset. Results: The time period between smoking onset and the onset of depression and/or anxiety disorders was 5 years shorter for early-onset smokers than for late-onset smokers. Moreover, a greater percentage of early-onset smokers than late-onset smokers had the first onset of psychopathology within the first 5 years after starting smoking. Age at smoking onset predicted age at psychopathology onset after controlling for the effects of gender, education, and childhood trauma. When separate analyses were done for depression and anxiety disorders, this pattern of results was found only for anxiety disorders. Conclusions: A young age at smoking onset is associated with a shorter time to first onset of an anxiety disorder. This study with psychiatric patients extends previous findings in general population samples that smoking and depression and anxiety disorders are associated. © The Author 2011. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved.

Background: Suicidal ideation is the most stable symptom of depression across episodes. This relative stability may be brought about by increased cognitive reactivity to sad mood (CR) during periods of remission. The idea is that a network of depressive cognitions, which include suicidal ideation, becomes strengthened with each episode of depression. Consequently, the whole network may be more easily re-activated, for instance by an episode of low mood. We examined the association between reactivity of suicidal cognitions during recovery and the presence of suicidal ideation and behavior during the previous depressive episode. Methods: In a case-control design, the CR profiles of recovered depressed participants with (N = 355) and without (N = 250) a history of suicidal ideation were compared. Structured clinical interviews were used to determine diagnoses and prior symptoms. Cognitive reactivity profile was measured with the Leiden Index of Depression Sensitivity-Revised (LEIDS-R). Results: Suicidal ideation during a depressive episode was associated with a distinct CR profile during remission: elevated hopelessness reactivity scores. This relationship between prior suicidality and current CR was independent of anxiety disorder comorbidity. Moreover, a history of suicide attempt(s) was also associated with a distinct CR profile. These individuals had both higher hopelessness reactivity and higher aggression reactivity than the non-suicidal and suicidal ideation groups. Limitations: Symptoms during the previous depressive episode were assessed retrospectively. Conclusions: This is the first study to show that CR may underlie the relative stability of suicidal symptoms independent of anxiety comorbidity and that suicidal ideation and suicidal behavior are associated with distinct patterns of CR. Since CR is a potentially treatable vulnerability marker of depression recurrence, this has important clinical implications. (C) 2009 Elsevier B.V. All rights reserved.

Background Serotonin is implicated in both mood and cognition. It has recently been shown that antidepressant treatment has immediate effects on emotional information processing, which is much faster than any clinically significant effects. This review aims to investigate whether the effects on emotional information processing are reliable, and whether these effects are related to eventual clinical outcome. Treatment-efficiency may be greatly improved if early changes in emotional information processing are found to predict clinical outcome following antidepressant treatment. Methods Review of studies investigating the short-term effects of serotonin manipulations (including medication) on the processing of emotional information, using PubMed and PsycInfo databases. Results Twenty-five studies were identified. Serotonin manipulations were found to affect attentional bias, facial emotion recognition, emotional memory, dysfunctional attitudes and decision making. The sequential link between changes in emotional processing and mood remains to be further investigated. Limitations The number of studies on serotonin manipulations and emotional information processing in currently depressed subjects is small. No studies yet have directly tested the link between emotional information processing and clinical outcome during the course of antidepressant treatment. Conclusions Serotonin function is related to several aspects of emotional information processing, but it is unknown whether these changes predict or have any relationship with clinical outcome. Suggestions for future research are provided.

Objective: This study, to the authors' knowledge, is the first randomized controlled trial comparing the efficacy of cognitive behavior therapy (CBT), paroxetine, and a placebo (administered in a double blind fashion) in the treatment of hypochondriasis. Method: The authors randomly assigned 112 subjects with hypochondriasis according to DSM-IV criteria to 16 weeks of outpatient treatment with CBT, paroxetine, or a placebo. The main outcome measure was the Whiteley Index. The authors made pretest and posttest assessments and analyzed all outcome measures using a General Linear Model 3"2 repeated measures analysis of variance with Helmert contrasts. The authors considered subjects who scored at least one standard deviation below the mean pretest score on the Whiteley Index as responders. All analyses were conducted on intent-to-treat and completer bases. Results: On the Whiteley Index, Helmert contrasts on the intent-to-treat and completer cohorts revealed that pooled CBT and paroxetine were significantly superior to placebo, but did not differ significantly from each other. The responder analysis on the intent-to-treat cohort and completer cohort, respectively, revealed the following percentages of responders per group: CBT group, 45% and 54%; paroxetine group, 30% and 38%; and placebo group, 14% and 12%. In the intent-to-treat analysis, only CBT differed significantly from the placebo. In the completer analysis, both paroxetine and CBT differed significantly from the placebo. Conclusions: CBT or paroxetine are effective short-term treatment options for subjects with hypochondriasis.

The current study tested whether "suffocation sensations" (respiratory loads) are automatically evaluated in a negative way by people fearing these sensations. It was found that, after having been primed with a slight respiratory load, participants with high suffocation fear (n=15) reacted more quickly to suffocation words and more slowly to positive words than participants with low suffocation fear (n=21). However, the effect was present only in participants who had noticed the primes. The findings are relevant to the cognitive model of panic disorder because automatic negative appraisal of sensations may play a role in initiating a panic attack.

Background Acute tryptophan depletion (ATD) induces depressive symptoms in remitted depressed patients treated with serotonergic medications, but not in patients treated with noradrenergic medications or electroconvulsive therapy. A recent study suggests that cognitive therapy (CT) protects against the effects of ATD, but the evidence is questionable. The present study compared the effect of ATD in patients who were treated with antidepressant medication and CT ( n = 17) versus antidepressant medication alone ( n = 23) during their latest episode. Methods Forty remitted depressed patients underwent high-dose and low-dose ATD in a randomized double-blind crossover design. Results There were no differences in response to ATD between treatment groups. This applied to groups defined by lifetime and by recent CT experience. Conclusions Cognitive therapy does not protect against the effects of rapidly lowered plasma tryptophan levels in remitted depressed patients who are also treated with antidepressant medication.

Background: In this study the effects of treatment with cognitive therapy, antidepressants or pill-placebo on the locus of control orientation in panic disorder patients were analysed, as well as the relation of this panic locus of control with panic frequency and cognitive measures of panic. Methods: A Multidimensional Anxiety Locus of Control scale (MALC) was developed and completed with other measures (ACQ and BSQ) before and after treatment. Patients also kept a panic diary. Results: Four subscales were derived from the MALC: one Internal, and three external (a Chance, a Medication, and a Therapist) locus of anxiety control orientation scales. Cognitive therapy was superior over pill-placebo on most outcome measures whereas antidepressants were only superior in reducing the number of panic attacks. Treatment with cognitive therapy resulted in an increase of ‘internal’ anxiety control orientation and a decrease of ‘chance’ and ‘medication’ orientation, in comparison with antidepressant therapy. The residualized gain scores on the MALC subscales correlated with clinical improvement in subjects treated with cognitive therapy only. Conclusions: Results suggest that the locus of control orientation is important in evaluating the differential effects of treatments in panic disorder. A differential effect on panic locus of control in favor of cognitive therapy in comparison to medication was found.

This article describes a reanalysis of seven studies on heart beat perception (HBP) in panic disorder. The pooled sample had 709 participants from eight diagnostic categories. Accurate HBP was uncommon, but more prevalent among panic disorder patients than among healthy controls, depressed patients, patients with palpitations and individuals with infrequent panic attacks. No differences were found between panic disorder patients and patients with other anxiety disorders. Accurate perceivers had higher anxiety sensitivity scores than inaccurate perceivers. The data remain inconclusive as to whether perceived heart rate is correlated with anxiety in inaccurate perceivers. Physical exercise, distraction, variations in instructions and treatment each influenced HBP. However, the influence was different than previously thought. Finally, it is suggested that HBP may be understood in terms of schema-guided information processing.

Background: Seventeen to 43% of patients with non-cardiac chest pain suffer from anxiety/panic disorders. Cognitive behavioural therapy (CBT) is effective in reducing non-cardiac chest pain. However, no data are available indicating that pain reduction following CBT may be cognitively mediated or whether success of CBT is dependent on the presence of panic. The aim of the study was threefold: (1) does CBT have a differential effect on cognitive measures; (2) does a relationship exist between improvement in non-cardiac chest pain and changes in cognitive measures, and (3) can panic be established as a moderator of the effect of treatment? Methods: Sixty-five patients with non-cardiac chest pain completed a randomised trial comparing study CBT with ‘care as usual’. Dependent measures were: frequency of chest pain, anxiety, the fear of bodily sensations, attributions and catastrophic cognitions. Results: CBT had a differential effect on most of the cognitive measures. Pain reduction was associated with the development of more adequate cognitions with respect to chest pain, independent of anxiety reduction. Although panic patients reported higher baseline scores on the cognitive measures, no differences in treatment results were found between panic and no-panic patients. Conclusions: Pain reduction following CBT may be cognitively mediated. The presence of panic did not affect the outcome of treatment, implying a broad applicability of the cognitive model for treatment of patients with non-cardiac chest pain.

Voluntary breath-holding duration was investigated in patients with panic disorder, patients with a mood disorder, and normal controls. There were no differences in mean breath-holding durations, but the pattern of scores was different among groups. Furthermore, the scores were influenced by motivational and cognitive factors. It is argued that voluntary breath-holding is not a suitable test to measure carbon dioxide sensitivity or suffocation alarm threshold in panic disorder.

A sample of young patients with schizophrenia was studied in a longitudinal design to investigate the stability of an earlier reported four-dimensional symptom model (positive symptoms, negative symptoms, disorganization, and depression). Symptoms were measured in an acute phase soon after hospitalization, in a remitted stage 3 months later, and in a "mixed" phase 1 year after the second assessment. A different factor structure was found at each measurement, but a stable four-dimensional structure could be defined that closely resembled the factor structure of the first assessment. The symptom dimensions were uncorrelated, except disorganization and depression. Whether meaningful subtypes could be defined using statistical criteria also was investigated. With cluster analysis, four subtypes were defined that could be characterized as follows: rapid treatment responders, slower responders, and two relapse groups. Although some indication of the validity of these subtypes was found, it is concluded that there is a high risk of creating artificial boundaries with this approach.

Point prevalence and lifetime prevalence of respiratory disorders were assessed in 100 panic disorder (PD), 100 major depressive disorder (DD) and 100 V-code (VC) patients. Both current and past frequency of respiratory diseases were significantly higher in PD patients in comparison to VC patients, while no significant differences in point and lifetime prevalence between PD and DD or DD and VC patients were observed. It is hypothesized that a disturbed respiratory physiology may have differential effects depending upon the nature of the disorder and the appraisal by the patient.