Journal of affective disorders最新文献

Objectives: This study aimed to examine the moderating effect of interoceptive sensibility on the relationship between depression and suicidal ideation. Specifically, this study aimed to explore which subdimensions of interoceptive sensibility moderate the relationship between depression and suicidal ideation by administering the K-MAIA to a Korean community sample.

Methods: A total of 1000 participants completed various questionnaires assessing depressive symptoms (Patient Health Questionnaire-9), multidimensional interoceptive awareness (Korean Multidimensional Assessment of Interoceptive Awareness), and suicidal ideation (Depressive Symptom Inventory-Suicidality Subscale). Moderating effect of each subdimension of interoceptive sensibility was examined through the PROCESS Macro v4.3.1 (Model 1) and latent moderated structural equations.

Results: Depressive symptoms (excluding suicidal ideation) and suicidal ideation were negatively correlated with four subdimensions of interoceptive sensibility (Attention Regulation, Mind-Body Connection Awareness, Return to Body, Trusting). The moderating effect of Trusting was only significant in the relationship between depressive symptoms and suicidal ideation. Specifically, higher Trusting significantly buffered the positive association between depressive symptoms and suicidal ideation.

Conclusions: This exploratory study suggests that Trusting subdimensions of interoceptive sensibility may reduce suicidal ideation in individuals experiencing depressive symptoms. By showing that interoceptive sensibility can buffer the relationship between depressive symptoms and suicidal ideation within a diverse community sample spanning a wide age range, these findings underscore the potential relevance of interoception-focused strategies for suicide prevention in various populations.

Background: Major depressive disorder (MDD) exhibits clinical neuroimaging heterogeneity, complicating efforts toward biologically informed stratification. In particular, heterogeneity in large-scale brain network function may reflect distinct patterns of dysfunction. This study aimed to identify data-driven functional heterogeneity within the default mode network (DMN) in MDD using resting-state functional MRI.

Methods: We employed the data-driven Subtype and Stage Inference (SuStaIn) model to analyze cross-sectional magnetic resonance imaging (MRI) data from 815 patients with MDD and 816 healthy controls. SuStaIn was used to identify subtype-specific patterns and their relative ordering in DMN functional alterations based on cross-sectional data.

Results: Two distinct fALFF-based patterns were identified. Subtype 1 showed early involvement of the right parahippocampal region, followed by ventrolateral prefrontal and temporal areas, consistent with a limbic-to-visuolinguistic functional gradient. Subtype 2 was characterized by predominant involvement of dorsolateral prefrontal, anterior cingulate, and insular regions, suggesting a dominant executive-control-related functional profile, as reflected by the model-inferred ordering. NeuroSynth-based cognitive decoding broadly supported these divergent functional associations.

Conclusions: This study identifies DMN-based functional subtypes of MDD with distinct model-inferred patterns of functional abnormality. By characterizing heterogeneity in large-scale brain network dysfunction, these findings provide a conceptual framework for future subtype-informed research and hypothesis generation in MDD.

Background: Treatment expectancy is a key mechanism underlying placebo. While well-documented in psychopharmacology and psychotherapy, its role in lifestyle-based interventions for mental disorders is uncertain. Given the emerging role of lifestyle based mental health care, a comprehensive evaluation of the role of treatment expectancy has not yet been explored, especially when compared to other more established therapies. The potential for genuine treatment efficacy to be masked by placebo response may bring into question the magnitude of effects of this treatment.

Methods: We sought to 1) investigate the role of treatment expectancy as a moderator of depression treatment outcomes in a completed randomised controlled trial of psychotherapy versus lifestyle therapy (the CALM trial) and 2) provide guidance on measuring and reporting expectancy effects in future trials. CALM was a two-arm, parallel-group, non-inferiority randomised controlled trial, comparing lifestyle therapy (delivered by accredited dietitians and exercise physiologists) and psychotherapy (facilitated by psychologists). A total of 182 participants (91 per arm) experiencing psychological distress (equivalent to 'indicative depression') during the COVID-19 pandemic were randomised. We assessed associations of expectancy (measured prior to randomisation using the Credibility-Expectancy Questionnaire) with reductions in depressive symptoms (as measured by the PHQ-9).

Results: Expectancy scores did not differ between treatment groups at baseline (β = 1.14; 95%CI = -1.93, 4.22). Both arms reduced PHQ-9 between baseline and 8-weeks (lifestyle mean difference = -30.25%, SD = 58.23%; psychotherapy mean difference = -22.46%, SD = 66.87%). However, higher expectancy was associated with a greater reduction in depression only in the psychotherapy arm: for every 1-unit increase in expectancy score depressive symptoms reduced by an additional 3.21% for psychotherapy compared to lifestyle therapy (95%CI = -5.77, -0.65).

Conclusions: In this study we showed that participants' expectations about treatment at enrolment were only associated with treatment response in psychotherapy. These findings highlight the need to account for modality-specific drivers of expectancy when evaluating all treatments for depression, and support the inclusion of expectancy in reporting guidelines for future trials.

Registration: The trial was registered with the Australian New Zealand Clinical Trials Registry (ACTRN12621000387820; https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=380897).

Background: Psoriasis is frequently accompanied by depression. However, the role of specific symptom domains, including cognitive-affective and somatic symptoms, as well as potential metabolic mediators between psoriasis and depression, remain unclear.

Methods: We analyzed data from the National Health and Nutrition Examination Survey (NHANES, n = 14,964) and the Health and Retirement Study (HRS, n = 4364). Depressive symptoms were classified into cognitive-affective and somatic domains. Cross-sectional associations were evaluated in NHANES, and longitudinal symptom trajectories were identified in HRS using group-based trajectory modeling. Based on genome-wide association study summary statistics, bidirectional and two-step Mendelian randomization (MR) were performed to assess causality and identify plasma metabolite mediators.

Results: In NHANES, total depressive symptoms (OR = 1.04, 95% CI: 1.01-1.06, P = 0.004) and somatic symptoms (OR = 1.08, 95% CI: 1.04-1.13, P < 0.001) showed positive associations with psoriasis, but not cognitive-affective symptoms. In HRS, persistently high trajectories of total (OR = 1.48, 95% CI: 1.08-2.03, P = 0.01) and somatic symptoms (OR = 1.64, 95% CI: 1.06-2.57, P = 0.03) were associated with psoriasis, with no significant association for the cognitive-affective domain. MR supported a causal relationship of psoriasis on depression and identified sphingomyelin (d17:2/16:0, d18:2/15:0) and urate as mediators, accounting for 10.2% and 6.8% of the total effect, respectively.

Conclusion: Depressive symptoms, especially somatic domains, were linked to psoriasis in both cross-sectional and longitudinal analyses. Lipid and antioxidant-related pathways involving sphingomyelin and urate may mediate the relationship between psoriasis and depression, offering potential targets for intervention.

People may experience cognitively dysfunctional processes during the posttraumatic phase, which can manifest as posttraumatic cognitive attributions reflected in their psychosocial lives. Challenges in meeting the need for belongingness are often linked to lower levels of life satisfaction. Therefore, this study adopts a dyadic perspective to explore whether belongingness mediates the association between posttraumatic cognitive attributions and life satisfaction within mother-daughter relationships as a distinct type of close bond. These relationships were examined using the Actor-Partner Interdependence Model (APIM) for the first time in the literature focusing on mother-daughter dyads. The study included 390 dyads, consisting of 780 adult participants in total. The results indicated that, for both mothers and daughters, life satisfaction and posttraumatic cognitive attributions were related to their own and each other's sense of belonging. This pattern was observed at both the actor and partner levels. Overall, the findings suggest that posttraumatic cognitive attributions are linked to dyadic processes that are relevant to both the individual's inner world and close relationships. Specifically, belongingness appears to be associated with higher life satisfaction following trauma, considering the experiences and interpersonal connections of both mothers and daughters. In addition to individual therapeutic work, it may be beneficial to address close emotional bonds such as mother-daughter relationships in an integrative manner. Interventions that strengthen belongingness may contribute to enhancing posttraumatic life satisfaction.

Background: Major depressive disorder (MDD) is a prevalent affective disorder with limited treatment efficacy. Transcranial alternating current stimulation (tACS) represents a promising non-invasive intervention for MDD; however, optimal stimulation parameters and the neural mechanism underlying tACS require further investigation.

Methods: The study used a randomized double-blind controlled design that included 72 outpatients with MDD, who were randomly divided into a low-administration (once daily) fixed (10 Hz) group, a low-administration (once daily) individual alpha frequency (IAF) group, a high-administration (twice daily) fixed (10 Hz) group, and a high-administration (twice daily) IAF group in a 1:1:1:1 randomization. The study period was 4 weeks, with an intervention period (2 weeks) and a follow-up period (2 weeks). During the intervention period, patients were required to complete 20 sessions of tACS and EEG were acquired pre- and post-treatment.

Results: No significant differences were observed between IAF and fixed groups or between high-and low-administration-frequency in clinical efficacy. However, high-administration-frequency and fixed groups showed a favorable trend in symptom improvement. EEG analysis revealed reduced alpha power spectral density (PSD) in the parietal lobe for high-administration-frequency stimulation and enhanced frontal functional connectivity in the two fixed groups.

Conclusions: The results suggested potential symptom improvement of tACS. However, in the absence of a sham control, the findings should be interpreted cautiously and regarded as preliminary evidence. EEG analyses revealed significant modulation of brain oscillatory patterns by tACS. Overall, this study provides the first comparison of antidepressant treatment effects under different stimulation frequencies or protocols and offers insights into the neural mechanisms underlying tACS.

Early childhood and family experience have profound effects on both emotional and neural development. The present study examined the unique associations between three early risk factors for depression-family history of depression, parenting style, and adverse childhood experiences (ACEs)-and neurophysiological reactivity to emotional stimuli, as indexed by the P300/Late Positive Potential (LPP) complex. Seventy-nine young adults (72.2% females; M = 21.7 years) completed the Family History Screen, Parental Bonding Instrument, and ACE questionnaire and performed an EEG task with pleasant, unpleasant, and neutral images. Linear mixed-effects models revealed that family history of depression and greater ACE scores were associated with reduced P300/LPP complex amplitude to pleasant images and greater P300/LPP complex amplitude to negative images, indicating a pattern of blunted sensitivity to positive stimuli and heightened sensitivity to negative stimuli. Conversely, greater parental care predicted lower LPP amplitude, particularly to negative images, indicative of a protective effect of supportive parenting. No significant associations were found with overprotection. These findings suggest that early experiences and family factors jointly contribute to modulate emotional neural processing, informing developmental pathways of vulnerability and resilience to affective disorders.

Background: Fluctuations in depressive symptoms across the menstrual cycle occur in some women, with a pronounced intensification during the luteal phase. Given that the GABAergic system is modulated by neurosteroids, alterations within this system may contribute to mood regulation in women with Major Depressive Disorder (MDD).

Methods: We investigated the association between gamma-aminobutyric acid (GABA) concentrations in the posterior and anterior cingulate cortex (PCC and ACC) and depressive symptoms in relation to menstrual cycle phase. Thirty-one unmedicated women diagnosed with MDD were evaluated. Clinical variables including depressive and anxiety symptomatology and prior depression history were assessed. GABA concentrations were quantified using proton magnetic resonance spectroscopy (¹H-MRS).

Results: PCC_GABA concentrations were significantly associated with the severity of the current depressive episode, with lower PCC_GABA concentrations in women with higher depression scores. When analyses were stratified by menstrual phase, this association was observed only among participants assessed during the premenstrual phase.

Conclusion: These findings suggest that PCC_GABA concentrations are associated with depressive symptom severity in unmedicated women during the premenstrual phase of the menstrual cycle. Further research is warranted to elucidate the neurosteroid-mediated modulation of GABAergic neurotransmission in the pathophysiology of mood disorders.