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Summary: 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 Val66Met polymorphism, anxiety, alcohol consumption, and cortisol stress response. Method: 98 healthy university students (54 females and 44 males), genotyped for the Val66Met 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 <0.001), drank more alcohol per week, (p <0.05), and showed significantly higher anticipatory cortisol response (p <0.05), but not in response to the CPT, than Val/Val homozygotes. The association of BDNF Val66Met polymorphism with HPA axis reactivity to stress was not modulated by gender. These results suggest that Met carriers are particularly sensitive in anticipating stressful events, which extends previous findings on the moderating role of the BDNF Val66Met polymorphism in the face of stressful life events. [Copyright &y& Elsevier]

Abstract: 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 paroxetine. 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. [ABSTRACT FROM AUTHOR]

Abstract: 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. [Copyright &y& Elsevier]

Abstract: Background: It has frequently been demonstrated that experimental lowering of serotonin (5-HT) neurotransmission by acute tryptophan depletion (ATD) induces a transient depressed mood in 50–60% of patients treated with a selective serotonin reuptake inhibitor (SSRI) who are in remission from depression. In unmedicated depressed patients, ATD has no immediate effect on symptoms. The effects in currently depressed medicated patients have not been investigated. Methods: Fourteen currently depressed patients (seven patients treated with a selective serotonin–noradrenalin reuptake inhibitor (SSNRI); seven other treatment, non-SSNRI) received ATD in a double-blind, crossover design. Different strengths of the ATD mixture (aimed at 50% and 90% reduction of tryptophan) were used on separate days. Psychiatric symptoms were assessed at both sessions prior to, at +6.5 h, and at +24 h after ATD. Results: The ATD mixtures induced the expected reductions of plasma tryptophan levels. Full but not partial depletion improved mood and other psychiatric symptoms at +24 h in patients who received SSNRI treatment, as indicated by clinical ratings and self-report. Subjective sleep quality also improved. Conclusions: The effects of ATD on psychiatric symptoms in currently depressed patients are remarkably different from the results in recently remitted SSRI-treated patients. ATD in currently depressed patients treated with serotonergic antidepressants possibly provides important information about the mechanism of action of SSRIs. [Copyright &y& Elsevier]

Investigates voluntary breath-holding (VBH) duration in patients with panic disorder, patients with a mood disorder and normal controls. Influence of motivational and cognitive factors on VBH; Depressive symptoms and fear of bodily sensation on breath holding duration; Suitability of VBH as a test to measure carbon dioxide sensitivity of suffocation alarm.

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. [Copyright &y& Elsevier]

Summary: 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 60min afterwards. Results: In adjusted analyses, high scores of hopelessness reactivity (β =.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. [Copyright &y& Elsevier]

Highlights: [•] We studied relations among attentional control and attentional bias in PTSD patients. [•] Attentional control moderated between PTSD symptoms and attentional bias. [•] High symptoms and low attentional control predicted attentional avoidance. [•] Low attentional control is a suggested risk factor for attentional bias in PTSD. [ABSTRACT FROM AUTHOR]

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. [Copyright &y& Elsevier]