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European archives of psychiatry and clinical neuroscience (2022). doi:10.1007/s00406-022-01440-6, Published by Steinkopff, Darmstadt

Background 5-HTTLPR/rs25531 is suspected to be involved in the pathogenesis of both coronary heart disease (CHD)1 and depression. We aimed to investigate the role of 5-HTTLPR/rs25531 in the development of depressive symptoms among CHD patients in a longitudinal design. Methods N = 265 participants with CHD diagnosis were included while hospitalized in a department of cardiology and genotyped for the 5-HTTLPR/rs25531. Depressive symptoms were measured using the Patient Health Questionnaire (PHQ-9)7 at baseline and after 6 and 12 months. Binary logistic regression models were used to analyze the association of 5-HTTLPR/rs25531 with the prevalence of depressive symptoms at each time point as well as with the incidence and persistence of depressive symptoms at follow-up. Results “LALA” genotype was associated with a higher prevalence of depressive symptoms 12 months after study inclusion. “LALA” genotype was associated with a higher incidence of depressive symptoms 6 and 12 months after study inclusion. There was no association of 5-HTTLPR/rs25531 with the persistence of depressive symptoms. Limitations Inclusion criteria did not demand a particular cardiac event at baseline, which aggravated the interpretation of the time-specific results. The majority of the participants was of male gender which could cause bias. The present study only vaguely differentiated between ethnical groups which might cause bias regarding nationality-dependent allele distributions. Conclusion The present study suggests a time-dependent association of the “LALA” genotype with depressive symptoms in CHD patients. 5-HTTLPR/rs25531 might be an important marker to detect risk groups for later onset depressive symptoms among CHD patients.

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.

Depression and coronary heart disease (CHD) are prevalent and often co-occurring disorders. Both have been associated with a dysregulated stress system. As a central element of the stress system, the FKBP5 gene has been shown to be associated with depression. In a prospective design, this study aims to investigate the association of FKBP5 with depressive symptoms in CHD patients. N = 268 hospitalized CHD patients were included. Depressive symptoms were measured using the Hospital Anxiety and Depression Scale (HADS-D) at four time points (baseline, and after 1 month, 6 months, and 12 months). The functional FKBP5 single-nucleotide polymorphism (SNP) rs1360780 was selected for genotyping. Linear regression models showed that a higher number of FKBP5 C alleles was associated with more depressive symptoms in CHD patients both at baseline (p = 0.015) and at 12-months follow-up (p = 0.025) after adjustment for confounders. Further analyses revealed that this effect was driven by an interaction of FKBP5 genotype with patients’ prior CHD course. Specifically, only in patients with a prior myocardial infarction or coronary revascularization, more depressive symptoms were associated with a higher number of C alleles (baseline: p = 0.046; 1-month: p = 0.026; 6-months: p = 0.028). Moreover, a higher number of C alleles was significantly related to a greater risk for dyslipidemia (p = .016). Our results point to a relevance of FKBP5 in the association of the two stress-related diseases depression and CHD.

Alcohol misuse during adolescence (AAM) has been associated with disruptive development of adolescent brains. In this longitudinal machine learning (ML) study, we could predict AAM significantly from brain structure (T1-weighted imaging and DTI) with accuracies of 73 -78% in the IMAGEN dataset (n∼1182). Our results not only show that structural differences in brain can predict AAM, but also suggests that such differences might precede AAM behavior in the data. We predicted 10 phenotypes of AAM at age 22 using brain MRI features at ages 14, 19, and 22. Binge drinking was found to be the most predictable phenotype. The most informative brain features were located in the ventricular CSF, and in white matter tracts of the corpus callosum, internal capsule, and brain stem. In the cortex, they were spread across the occipital, frontal, and temporal lobes and in the cingulate cortex. We also experimented with four different ML models and several confound control techniques. Support Vector Machine (SVM) with rbf kernel and Gradient Boosting consistently performed better than the linear models, linear SVM and Logistic Regression. Our study also demonstrates how the choice of the predicted phenotype, ML model, and confound correction technique are all crucial decisions in an explorative ML study analyzing psychiatric disorders with small effect sizes such as AAM.

The lancet / Regional health. Europe 19, 100413 (2022). doi:10.1016/j.lanepe.2022.100413, Published by Elsevier, [Amsterdam]

Background: Anxiety and post-traumatic stress disorder (PTSD) are known etiologic and prognostic risk factors in patients with coronary heart disease (CHD). However, few studies have assessed the prevalence of a comprehensive set of anxiety and stress related disorders in CHD. Moreover, it is unclear whether these disorders are associated with CHD symptoms, severity and cardiovascular events and procedures. Methods: We determined the 12-month prevalence of anxiety disorders and PTSD in N = 1024 hospitalized patients with CHD and examined associations with cardiac disease characteristics, cardiovascular events and procedures. Anxiety and PTSD diagnoses were determined with the Composite International Diagnostic Interview. Socio-demographic variables were assessed with a questionnaire and cardiovascular variables were extracted from medical charts. Results: 12-month prevalence for any anxiety disorder was 11.2% for men and 24.8% for women; 12-month PTSD prevalence was 1.1% and 5.2%, respectively. The most common anxiety disorders were specific phobia (men: 8.2%, women: 18.8%) and agoraphobia and/or panic disorder (combined prevalence men: 2.9%, women: 9.9%). Anxiety disorders were not associated with any cardiovascular variables. Limitations: Due to lack of follow-up data no conclusions regarding stability of diagnoses are possible. Associations of PTSD and medical variables could not be determined because of low PTSD prevalence. Conclusions: Compared to the general population, anxiety disorders were more frequent in younger (

Background: From birth to young adulthood, health and development of young people are strongly linked to their living situation, including their family’s socioeconomic position (SEP) and living environment. The impact of regional characteristics on development in early childhood beyond family SEP has been rarely investigated. This study aimed to identify regional predictors of global developmental delay at school entry taking family SEP into consideration. Method: We used representative, population-based data from mandatory school entry examinations of the German federal state of Brandenburg in 2018/2019 with n=22,801 preschool children. By applying binary multilevel models, we hierarchically analyzed the effect of regional deprivation defined by the German Index of Socioeconomic Deprivation (GISD) and rurality operationalized as inverted population density of the children’s school district on global developmental delay (GDD) while adjusting for family SEP (low, medium and high). Results: Family SEP was significantly and strongly linked to GDD. Children with the highest family SEP showed a lower odds for GDD compared to a medium SEP (female: OR=4.26, male: OR=3.46) and low SEP (female: OR=16.58, male: OR=12.79). Furthermore, we discovered a smaller, but additional and independent effect of regional socioeconomic deprivation on GDD, with a higher odds for children from a more deprived school district (female: OR=1.35, male: OR=1.20). However, rurality did not show a significant link to GDD in preschool children beyond family SEP and regional deprivation. Conclusion: Family SEP and regional deprivation are risk factors for child development and of particular interest to promote health of children in early childhood and over the life course.

Zusammenfassung 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.

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.

To compare the diagnostic accuracy of German depression screening instruments in patients with coronary heart disease (CHD).1019 CHD patients completed the Patient Health Questionnaire (PHQ-9 and PHQ-2) and the Hospital Anxiety and Depression Scale (HADS-D). The Composite International Diagnostic Interview served as reference standard for "any depressive disorder" and "major depression".The accuracy of the PHQ-9 and the HADS-D was comparable according to the area under the curve, and both were superior to the PHQ-2. The optimal cut-off according to the Youden index (maximum sum of sensitivity and specificity) was 7 for both instruments. At this optimal cut-off, the PHQ-9 had a higher sensitivity compared to the HADS-D, but a lower specificity (below 68). Results remained similar when patients who reported that they currently underwent treatment for depression were excluded.The PHQ-9 and the HADS-D have comparable overall diagnostic accuracy in CHD patients. In line with previous screening studies with CHD patients, the optimal cut-offs were below the cut-offs that are recommended in the literature.ZIEL: Vergleich der Erkennungsgüte von drei Depressions-Screeninginstrumenten bei Patienten mit koronarer Herzerkrankung (KHK).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.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).PHQ-9 und HADS-D haben eine vergleichbare Diskriminationsfähigkeit für depressive Störungen bei KHK-Patienten.

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.