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Die Sportpsychiatrie und -psychotherapie ist ein relativ junges Arbeitsgebiet, das sich insbesondere mit zwei Schwerpunkten befasst: zum einen mit den Besonderheiten in Diagnostik und Therapie psychischer Erkrankungen bei Leistungssportler:innen sowie Bewegung und Sport in der Entstehung und Behandlung psychischer Erkrankungen. Während alle psychischen Erkrankungen prinzipiell auch bei (Leistungs‑)Sportler:innen auftreten können, gibt es darüber hinaus sport(art)spezifische psychische Erkrankungen, wie z. B. die Anorexia athletica und andere Essstörungen, die chronisch traumatische Enzephalopathie, Missbrauch und Abhängigkeit von leistungssteigernden Substanzen (Doping) oder die Muskeldysmorphie. In qualitativ hochwertigen klinischen Studien konnte die therapeutische Wirksamkeit von Bewegung und Sport bei verschiedenen psychischen Erkrankungen belegt werden. Ein sportpsychiatrisches Basiswissen sollten alle in Psychiatrie und Psychotherapie klinisch Tätigen besitzen.
Objective:
Brain-derived neurotrophic factor (BDNF) supports neurogenesis, angiogenesis, and promotes the survival of various cell types in the brain and the coronary system. Moreover, BDNF is associated with both coronary heart disease (CHD) and depression. The current study aims to investigate whether serum BDNF levels are associated with the course of depressive symptoms in CHD patients.
Methods:
At baseline, N = 225 CHD patients were enrolled while hospitalized. Of these, N = 190 (84%) could be followed up 6 months later. Depressive symptoms were assessed both at baseline and at the 6-months follow-up using the Patient Health Questionnaire (PHQ-9). Serum BDNF concentrations were measured using fluorometric Enzyme-linked immunosorbent assays (ELISA).
Results:
Logistic regression models showed that lower BDNF levels were associated with persistent depressive symptoms, even after adjustment for age, sex, smoking and potential medical confounders. The incidence of depressive symptoms was not related to lower BDNF levels. However, somatic comorbidity (as measured by the Charlson Comorbidity Index) was significantly associated with the incidence of depressive symptoms.
Conclusions:
Our findings suggest a role of BDNF in the link between CHD and depressive symptoms. Particularly, low serum BDNF levels could be considered as a valuable biomarker for the persistence of depressive symptoms among depressed CHD patients.
Physiological mechanisms of an anti-depressive effect of physical exercise in major depressive disorder (MDD) seem to involve alterations in brain-derived neurotrophic factor (BDNF) level. However, previous studies which investigated this effect in a single bout of exercise, did not control for confounding peripheral factors that contribute to BDNF-alterations. Therefore, the underlying cause of exercise-induced BDNF-changes remains unclear. The current study aims to investigate serum BDNF (sBDNF)-changes due to a single-bout of graded aerobic exercise in a group of 30 outpatients with MDD, suggesting a more precise analysis method by taking plasma volume shift and number of platelets into account. Results show that exercise-induced increases in sBDNF remain significant (p<.001) when adjusting for plasma volume shift and controlling for number of platelets. The interaction of sBDNF change and number of platelets was also significant (p=.001) indicating larger sBDNF-increase in participants with smaller number of platelets. Thus, findings of this study suggest an involvement of peripheral as well as additional possibly brain-derived mechanisms explaining exercise-related BDNF release in MDD. For future studies in the field of exercise-related BDNF research, the importance of controlling for peripheral parameters is emphasized.
Physical activity (PA) can play an important role in improving the mental and physical health in patients with mental disorders but is not well studied in this population. The aim of this study was to assess the status of PA in outpatients with mental disorders, compare the convergence of self-rating and accelerometer measurement and examine the influence of social cognitive variables from the Motivation-Volition (MoVo) model and clinical measures on PA. Eighty-four patients were recruited from three psychiatric outpatient clinics and local psychiatrists (Distribution of ICD-10-Diagnoses: F3.x = 59.5%, F4.x = 20.2%, F2.x = 17.9%, F1.x = 2.4%). PA, Self-efficacy, Outcome-expectancies, Intention, Self-concordance, Action- and Coping-planning, Health-related Quality of Life (SF-12) and Psychiatric Symptoms (SCL-27) were assessed through questionnaires. PA was assessed objectively by accelerometers. Most of the participants did not reach PA recommendations. Subjective and objective measurement of PA showed good accordance for total PA on group level but lower accordance on individual level. Motivational and volitional determinants of health behavior change showed a similar pattern of correlations with PA as in populations without mental disorders. Outpatients with mental disorders have the ability and are willing to perform PA but a large proportion of our sample did not meet PA recommendations. To assess group levels of PA, subjective and objective measurement seem equally apt, for individual diagnostics, a combination of both should be considered. Social cognitive determinants of health behavior change seem to be as helpful for the design of PA interventions for patients with mental disorders as they are in other populations.
Ziel Vergleich der Erkennungsgüte von drei Depressions-Screeninginstrumenten bei Patienten mit koronarer Herzerkrankung (KHK).
Methodik 1019 KHK-Patienten erhielten den Patient Health Questionnaire (PHQ-9 und PHQ-2) und die Hospital Anxiety and Depression Scale (HADS-D) sowie ein klinisches Interview (Composite International Diagnostic Interview) als Referenzstandard.
Ergebnisse Bezüglich der Erkennungsgüte waren PHQ-9 und HADS-D dem PHQ-2 überlegen. Optimale Cut-off-Werte waren 7 (PHQ-9 und HADS-D) und 2 (PHQ-2).
Schlussfolgerung PHQ-9 und HADS-D haben eine vergleichbare Diskriminationsfähigkeit für depressive Störungen bei KHK-Patienten.
Objective:
Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF).
Methods:
The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment.
Results:
Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS.
Conclusion:
Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.