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Background and Objectives: Depression has been associated with alterations in social functioning. Decoding and understanding others' mental states and adaptive reasoning are important for social functioning. This study examined theory of mind (ToM) and socio-moral reasoning (SMR) in adolescent girls with and without depression. Within the depression group, we examined associations between relevant clinical features (depression severity, anxiety symptoms and borderline personality traits) and ToM and SMR.Methods: A cross-sectional study was conducted, whereby 43 adolescent girls (mean age = 16.19, SD = 1.24) meeting full or subthreshold criteria for depression and 40 adolescent girls (mean age = 15.44, SD = 1.24) with no psychiatric diagnosis were recruited. ToM was assessed using the Movie for the Assessment of Social Cognition; SMR was evaluated via the Socio-Moral Reasoning Aptitude Level task.Results: Analyses of covariance indicated that adolescents with depression did not differ from controls in ToM abilities but showed lower socio-maturity scores on the SMR task. This difference disappeared after controlling for the number of words used to justify responses. Amongst adolescents with depression, multiple linear regression analyses revealed that higher levels of borderline personality traits were associated with lower levels of mentalization (ToM task), and more severe depressive symptoms were associated with lower socio-moral maturity stages (SMR task) LIMITATIONS: Directional associations were not studied, and the sample included only girls.Conclusions: Findings may help to explain clinical heterogeneity in social cognitive functioning observed in individuals with depression. [ABSTRACT FROM AUTHOR]

Abstract: Acute tryptophan depletion (ATD) in currently depressed patients has no immediate effect on symptoms, but leads to transient symptom improvement or worsening the next day. In view of recent findings concerning the cognitive effects of serotonin manipulations, we used ATD in fourteen depressed patients to investigate whether cognitive effects following ATD predict symptom changes. We found that symptom improvement 24h after ATD was associated with an improved recall of positive words and with less attentional bias and recall of negative words, 5h after ATD. These results indicate that serotonergic alterations affect emotional processing which may subsequently lead to symptom changes. [Copyright &y& Elsevier]

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]

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]

• Adolescents with depression were marginally faster than those in the comparison group to recognise sadness, although this trend disappeared once covarying for age and use of antidepressant medication. • Within the depression group, severity of depression symptoms and borderline personality features were associated with poorer emotional facial expression recognition (EFER) performance. • Discrepancies between group and within-group differences may explain some of the clinical heterogeneity observed in studies of EFER amongst adolescents with depression. • Studying clinical features in relation to EFER in adolescents with depression allows for a more nuanced understanding of social difficulties that may be experienced in depression. Studies have reported that emotional facial expression recognition (EFER) may be altered in individuals with depression. This study examined EFER in adolescent girls with and without depression and further examined associations between relevant clinical features of depression and EFER. Fifty adolescent girls aged 12 to 19 years old meeting criteria for depression or subthreshold levels of symptomatology and 55 adolescent girls with no psychiatric diagnosis completed EFER tasks. Reaction time and accuracy for recognising expressions at high and low intensities, and sensitivity in recognising happiness, sadness, anger and fear were assessed. Data were analysed using linear mixed models. Adolescents with depression were marginally faster than those in the comparison group to recognize sadness, although this trend disappeared once covarying for age and antidepressant use. Amongst adolescents with depression, clinical features were associated with poorer EFER performance. In contrast, anxiety symptoms were linked to better accuracy and heightened sensitivity towards happiness. A better understanding of EFER in adolescent girls with and without depression, and how clinical features might be associated with altered patterns of EFER could help to explain clinical heterogeneity observed in such studies of adolescents with depression. Knowledge of socio-cognitive alterations associated with depression will help to better develop and tailor interventions. [ABSTRACT FROM AUTHOR]

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]

Screening is done to improve health outcomes by identifying and effectively treating individuals with unrecognized conditions. Depression screening has been proposed to identify previously unrecognized depression cases. Including individuals already diagnosed or treated for depression in screening test accuracy studies could exaggerate accuracy and the yield of new cases from screening. The present study investigated (1) the proportion of depression screening tool accuracy primary studies published in 2018–2021 that excluded individuals with a confirmed depression diagnosis or who were already undergoing treatment; and (2) whether this has improved since the last review of studies published in 2013–2015, which found that five of 89 (5.6%) primary studies appropriately excluded such individuals. MEDLINE was searched from January 1, 2018 through May 21, 2021 for primary studies on depression screening tool accuracy. Eighteen of 106 (17.0%; 95% Confidence Interval [CI], 11.0% to 25.3%) primary studies excluded currently diagnosed or treated individuals. This was 11.4% (95% CI, 2.8% to 20.0%) greater than in similar studies published in 2013–2015. There has been an improvement since 2015, but the proportion of studies that exclude individuals already known to have depression remains low. This may bias research findings intended to inform clinical practice. [ABSTRACT FROM AUTHOR]

Tryptophan hydroxylase 2 (TPH2) is the rate-limiting enzyme in brain serotonin synthesis. The TPH2 gene has frequently been investigated in relation to psychiatric morbidity. The aim of the present review is to integrate results from association studies between TPH2 single nucleotide polymorphisms (SNPs) and various psychiatric disorders, which we furthermore quantified with meta-analysis. We reviewed 166 studies investigating 69 TPH2 SNPs in a broad range of psychiatric disorders, including over 30,000 patients. According to our meta-analysis, TPH2 polymorphisms show strongest associations with mood disorders, suicide (attempt) and schizophrenia. Despite small effect sizes, we conclude that TPH2 SNPs in the coding and non-coding areas (rs4570625, rs11178997, rs11178998, rs10748185, rs1843809, rs4290270, rs17110747) are each associated with one or more psychopathological conditions. Our findings highlight the possible common serotonergic mechanisms of the investigated psychiatric disorders. Yet, the functional relevance of most TPH2 polymorphisms is unclear. Characterizing how exactly the different TPH2 variants influence the serotonergic neurotransmission is a next necessary step in understanding the psychiatric disorders where serotonin is implicated. [ABSTRACT FROM AUTHOR]

Depression is associated with alterations in hypothalamic–pituitary–adrenal (HPA) axis activity. A proposed mechanism to explain these alterations are changes in DNA methylation levels, secondary to early life adversity (ELA), at stress-related genes. Two gene regions that have been implicated in the literature, the glucocorticoid receptor gene ( NR3C1 ) exon 1F and the FKBP5 gene intron 7 were examined in 67 individuals (33 depressed patients and 34 controls). We investigated whether cortisol concentrations, evaluated in 25 depressed patients and 20 controls, and measures of ELA were associated with the degree of methylation at these candidate gene regions. Mean NR3C1 exon 1F DNA methylation levels were significantly increased in the depressed cohort and the degree of methylation was found to be positively associated with morning cortisol concentrations. DNA methylation levels at specific CG sites within the NR3C1 exon 1F were related to childhood emotional abuse severity. DNA methylation at CG38 was related to both HPA axis and childhood emotional abuse measures in the depressed group. No FKBP5 differences were revealed. Our findings suggest that hypermethylation at the NR3C1 exon 1F may occur in depression. This locus-specific epigenetic change is associated with higher basal HPA axis activity, possibly reflecting acquired glucocorticoid receptor resistance. [ABSTRACT FROM AUTHOR]