Let op het is Open Access maar met speciale Elsevier user rights, zie https://www.elsevier.com/about/policies/open-access-licenses/elsevier-user-license Background The presence of a comorbid borderline personality disorder (BPD) may be associated with an increase of suicidal behaviors in patients with depressive and anxiety disorders. The aim of this study is to examine the role of borderline personality traits on recurrent suicide attempts. Methods The Netherlands Study on Depression and Anxiety included 1838 respondents with lifetime depressive and/or anxiety disorders, of whom 309 reported at least one previous suicide attempt. A univariable negative binomial regression analysis was performed to examine the association between comorbid borderline personality traits and suicide attempts. Univariable and multivariable negative binomial regression analyses were performed to identify risk factors for the number of recurrent suicide attempts in four clusters (type and severity of axis-I disorders, BPD traits, determinants of suicide attempts and socio-demographics). Results In the total sample the suicide attempt rate ratio increased with 33% for every unit increase in BPD traits. A lifetime diagnosis of dysthymia and comorbid BPD traits, especially the symptoms anger and fights, were independently and significantly associated with recurrent suicide attempts in the final model (n=309). Limitations The screening of personality disorders was added to the NESDA assessments at the 4-year follow-up for the first time. Therefore we were not able to examine the influence of comorbid BPD traits on suicide attempts over time. Conclusions Persons with a lifetime diagnosis of dysthymia combined with borderline personality traits especially difficulties in coping with anger seemed to be at high risk for recurrent suicide attempts. For clinical practice, it is recommended to screen for comorbid borderline personality traits and to strengthen the patient's coping skills with regard to anger.
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Depression is a highly prevalent and seriously impairing disorder. Evidence suggests that music therapy can decrease depression, though the music therapy that is offered is often not clearly described in studies. The purpose of this study was to develop an improvisational music therapy intervention based on insights from theory, evidence and clinical practice for young adults with depressive symptoms. The Intervention Mapping method was used and resulted in (1) a model to explain how emotion dysregulation may affect depressive symptoms using the Component Process Model (CPM) as a theoretical framework; (2) a model to clarify as to how improvisational music therapy may change depressive symptoms using synchronisation and emotional resonance; (3) a prototype Emotion-regulating Improvisational Music Therapy for Preventing Depressive symptoms (EIMT-PD); (4) a ten-session improvisational music therapy manual aimed at improving emotion regulation and reducing depressive symptoms; (5) a program implementation plan; and (6) a summary of a multiple baseline study protocol to evaluate the effectiveness and principles of EIMT-PD. EIMT-PD, using synchronisation and emotional resonance may be a promising music therapy to improve emotion regulation and, in line with our expectations, reduce depressive symptoms. More research is needed to assess its effectiveness and principles.
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Hedonic (happiness) and eudaimonic (meaning in life) well-being are negatively related to depressive symptoms. Genetic variants play a role in this association, reflected in substantial genetic correlations. We investigated the overlap and differences between well-being and depressive symptoms, using results of Genome-Wide Association studies (GWAS) in UK Biobank. Subtracting GWAS summary statistics of depressive symptoms from those of happiness and meaning in life, we obtained GWASs of respectively “pure” happiness (neffective = 216,497) and “pure” meaning (neffective = 102,300). For both, we identified one genome-wide significant SNP (rs1078141 and rs79520962, respectively). After subtraction, SNP heritability reduced from 6.3% to 3.3% for pure happiness and from 6.2% to 4.2% for pure meaning. The genetic correlation between the well-being measures reduced from 0.78 to 0.65. Pure happiness and pure meaning became genetically unrelated to traits strongly associated with depressive symptoms, including loneliness, and psychiatric disorders. For other traits, including ADHD, educational attainment, and smoking, the genetic correlations of well-being versus pure well-being changed substantially. GWAS-by-subtraction allowed us to investigate the genetic variance of well-being unrelated to depressive symptoms. Genetic correlations with different traits led to new insights about this unique part of well-being. Our results can be used as a starting point to test causal relationships with other variables, and design future well-being interventions.
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