Towards an interdisciplinary formalization of soundscapes.

Soundscapes have been studied by researchers from various disciplines, each with different perspectives, approaches, and terminologies. Consequently, the research field determines the actual concept of a specific soundscape with the associated components and also affects the definition itself. This complicates interdisciplinary communication and comparison of results, especially when research areas are involved which are not directly focused on soundscapes. For this reason, we present a formalization that aims to be independent of the concepts from the various disciplines, with the goal of being able to capture the heterogeneous data structure in one layered model. Our model consists of time-dependent sound sources and geodata that influence the acoustic composition of a soundscape represented by our sensor function. Using a case study, we present the application of our formalization by classifying land use types. For this we analyze soundscapes in the form of recordings from different devices at 23 different locations using three-dimensional convolutional neural networks and frequency correlation matrices. In our results, we present that soundscapes can be grouped into classes, but the given land use categories do not have to correspond to them.

Association of regional white matter hyperintensities with hypertension and cognition in the population-based 1000BRAINS study.

BACKGROUND: White matter hyperintensities of presumed vascular origin (WMH) are frequent in cerebral magnetic resonance imaging of older people. They are promoted by vascular risk factors, especially hypertension, and are associated with cognitive deficits at the group level. It has been suggested that not only the severity, but also the location, of lesions might critically influence cognitive deficits and represent different pathologies. METHODS: In 560 participants (65.2 ± 7.5 years, 51.4% males) of the population-based 1000BRAINS study, we analyzed the association of regional WMH using Fazekas scoring separately for cerebral lobes, with hypertension and cognition. RESULTS: WMH most often affected the frontal lobe (83.7% score >0), followed by the parietal (75.8%), temporal (32.7%), and occipital lobe (7.3%). Higher Fazekas scores in the frontal, parietal, and temporal lobe were associated with higher blood pressure and antihypertensive treatment in unadjusted ordinal regression models and in models adjusted for age, sex, and vascular risk factors (e.g., age- and sex-adjusted odds ratio = 1.14, 95% confidence interval = 1.03-1.25 for the association of frontal lobe WMH Fazekas score with systolic blood pressure [SBP] [per 10 mm Hg]; 1.13 [1.02-1.23] for the association of parietal lobe score with SBP; 1.72 [1.19-2.48] for the association of temporal lobe score with antihypertensive medications). In linear regressions, higher frontal lobe scores were associated with lower performance in executive function and non-verbal memory, and higher parietal lobe scores were associated with lower performance in executive function, verbal-, and non-verbal memory. CONCLUSIONS: Hypertension promotes WMH in the frontal, parietal, and temporal lobe. WMH in the frontal and parietal lobe are associated with reduced executive function and memory.

Associations Between Built Environment Factors and SARS-CoV-2 Infections at the Neighbourhood Level in a Metropolitan Area in Germany.

COVID-19-related health outcomes displayed distinct geographical patterns within countries. The transmission of SARS-CoV-2 requires close spatial proximity of people, which can be influenced by the built environment. Only few studies have analysed SARS-CoV-2 infections related to the built environment within urban areas at a high spatial resolution. This study examined the association between built environment factors and SARS-CoV-2 infections in a metropolitan area in Germany. Polymerase chain reaction (PCR)-confirmed SARS-CoV-2 infections of 7866 citizens of Essen between March 2020 and May 2021 were analysed, aggregated at the neighbourhood level. We performed spatial regression analyses to investigate associations between the cumulative number of SARS-CoV-2 infections per 1000 inhabitants (cum. SARS-CoV-2 infections) up to 31.05.2021 and built environment factors. The cum. SARS-CoV-2 infections in neighbourhoods (median: 11.5, IQR: 8.1-16.9) followed a marked socially determined north-south gradient. The effect estimates of the adjusted spatial regression models showed negative associations with urban greenness, i.e. normalized difference vegetation index (NDVI) (adjusted ß = - 35.36, 95% CI: - 57.68; - 13.04), rooms per person (- 10.40, - 13.79; - 7.01), living space per person (- 0.51, - 0.66; - 0.36), and residential (- 0.07, 0.16; 0.01) and commercial areas (- 0.15, - 0.25; - 0.05). Residential areas with multi-storey buildings (- 0.03, - 0.12; 0.06) and green space (0.03, - 0.05; 0.11) did not show a substantial association. Our results suggest that the built environment matters for the spread of SARS-CoV-2 infections, such as more spacious apartments or higher levels of urban greenness are associated with lower infection rates at the neighbourhood level. The unequal intra-urban distribution of these factors emphasizes prevailing environmental health inequalities regarding the COVID-19 pandemic.

[Urban Epidemiology as an Integrative Approach to Sustainable and Healthy Urban Development]. / Stadtepidemiologie als integrativer Ansatz für eine nachhaltige, gesundheitsfördernde Stadtentwicklung.

Understanding the complex relationships between the physical and social environment and health in urban areas is essential for the development of appropriate measures of health promotion, disease prevention, and health protection. This article aims to characterize the comparatively new approach of urban epidemiology with its relevance for research and practice of urban health. Research in urban epidemiology provides important data and methodological foundations for integrated reporting, health impact assessments, and evaluation of interventions. Current challenges and solutions are outlined and initial recommendations for research, practice, and education and training are presented for discussion. Methods and findings of urban epidemiology can contribute in many ways to health-promoting, sustainable urban development.

[Primary Care Inequalities to the Disadvantage of the Population of Socially Deprived Urban Areas: A Case Study of Essen, Germany]. / Primärärztliche Versorgungsungleichheiten zu Ungunsten der Bevölkerung sozial benachteiligter Stadtgebiete ­ eine Fallanalyse am Beispiel der Stadt Essen.

Background As a large city in the middle of a metropolitan area, the city of Essen is characterized by strong social segregation and a north-south divide in the social status of its population. The conventional demand planning does not take such strong disparities within a planning unit into account. The present study aims to analyze the distribution of primary care structures using the example of two large urban areas within the city of Essen and to identify perspectives for strengthening primary care in disadvantaged urban areas. Methods First, a secondary data analysis was carried out at the district level and the study area Essen North (258,790 residents), consisting of 19 districts, was defined on the basis of two inclusion criteria - 1. location of the district north of the A40 freeway and 2. a mean subsistence rate>17.20 percent (average value of the city of Essen). Subsequently the study area was compared with the rest of the city (332,242 residents) with regard to the indicators a) social status, and b) available general practioners and pediatricians. The data of the selected indicators is based on the social reporting of the city of Essen and the "Online Practice Search" (Online-Praxissuche) of the Association of Statutory Health Insurance Physicians North Rhine. The resulting database (last update: 10/20212) was then evaluated at the district level and the primary care situation of the two urban areas was compared. Results The results revealed a significantly lower primary care coverage in the socially disadvantaged study area Essen North by about 25 percent for general practioners and by almost half for pediatricians. Thus, higher social disadvantage was associated with poorer access to primary care close to home, especially for children and adolescents. Conclusion The distribution of primary care providers in the city of Essen increases the risk of contributing to the manifestation of geographic disparities and health inequalities. The existing planning system in particular is not suitable for addressing the threatening or already existing undersupply of primary health care to the population in disadvantaged urban districts.

Genome-wide association study of panic disorder reveals genetic overlap with neuroticism and depression.

Panic disorder (PD) has a lifetime prevalence of 2-4% and heritability estimates of 40%. The contributory genetic variants remain largely unknown, with few and inconsistent loci having been reported. The present report describes the largest genome-wide association study (GWAS) of PD to date comprising genome-wide genotype data of 2248 clinically well-characterized PD patients and 7992 ethnically matched controls. The samples originated from four European countries (Denmark, Estonia, Germany, and Sweden). Standard GWAS quality control procedures were conducted on each individual dataset, and imputation was performed using the 1000 Genomes Project reference panel. A meta-analysis was then performed using the Ricopili pipeline. No genome-wide significant locus was identified. Leave-one-out analyses generated highly significant polygenic risk scores (PRS) (explained variance of up to 2.6%). Linkage disequilibrium (LD) score regression analysis of the GWAS data showed that the estimated heritability for PD was 28.0-34.2%. After correction for multiple testing, a significant genetic correlation was found between PD and major depressive disorder, depressive symptoms, and neuroticism. A total of 255 single-nucleotide polymorphisms (SNPs) with p < 1 × 10-4 were followed up in an independent sample of 2408 PD patients and 228,470 controls from Denmark, Iceland and the Netherlands. In the combined analysis, SNP rs144783209 showed the strongest association with PD (pcomb = 3.10 × 10-7). Sign tests revealed a significant enrichment of SNPs with a discovery p-value of <0.0001 in the combined follow up cohort (p = 0.048). The present integrative analysis represents a major step towards the elucidation of the genetic susceptibility to PD.

Neighbourhood socio-economic status and positive affectivity among older residents in Germany: a cross-sectional analysis with data from the Heinz Nixdorf Recall Study.

BACKGROUND: Physical and social neighbourhood characteristics can vary according to the neighbourhood socio-economic status (SES) and influence residents' perceptions, behaviours and health outcomes both positively and negatively. Neighbourhood SES has been shown to be predictive of mental health, which is relevant for healthy ageing and prevention of dementia or depression. Positive affectivity (PA) is an established indicator of mental health and might indicate a positive emotional response to neighbourhood characteristics. In this study, we focussed on the association of neighbourhood SES with PA among older residents in Germany and considered social integration and environmental perceptions in this association. METHODS: We used questionnaire-based data of the ongoing population-based Heinz Nixdorf Recall Study for our cross-sectional analysis, complemented by secondary data on social welfare rates in the neighbourhood of residents' address. PA was assessed using the Positive and Negative Affect Schedule (PANAS) in 2016. Linear regression models were performed to estimate the associations and adjusted for socio-demographic variables. RESULTS: Higher social welfare rates were associated with lower PA scores. The strongest negative association from the crude model (b = -1.916, 95%-CI [-2.997, -0.835]) was reduced after controlling for socio-demographic variables (b = -1.429, 95%-CI [-2.511, -0.346]). Social integration factors (b = -1.199, 95%-CI [-2.276, -0.121]) and perceived environmental factors (b = -0.875, 95%-CI [-1.971, 0.221]) additionally diminished the association of social welfare rates with PA in the full model (b = -0.945, 95%-CI [-2.037, 0.147]). CONCLUSION: Our results suggest that neighbourhoods have an influence on the occurrence and the extent of PA. Public health interventions that address socio-economic disadvantage in the neighbourhood environment could be an effective and far-reaching way to reduce the risk of depression and depressive symptoms due to low PA in older residents.

Smoking intensity and urinary nicotine metabolites by socioeconomic status in the Heinz Nixdorf Recall study.

BACKGROUND: Smoking intensity, which is generally based on self-reported average cigarettes per day (CPD), is a major behavioural risk factor and strongly related to socioeconomic status (SES). To assess the validity of the CPD measure, correlations with objective markers of tobacco smoke exposure - such as urinary nicotine metabolites - were examined. Yet, it remains unclear, whether this correlation is affected by SES, which may indicate imprecise or biased self-reports of smoking intensity. METHODS: We investigated the role of SES in the association between CPD and nicotine metabolites in current smokers among the participants of the population-based, prospective Heinz Nixdorf Recall Study. We determined urinary cotinine and additionally trans-3'-hydroxy-cotinine. SES was assessed by the International Socio-Economic Index of occupational status, and education. We calculated correlations (Pearson's r) between logarithmised CPD and cotinine in subgroups of SES and analysed SES and further predictors of cotinine in multiple linear regression models separately by gender. RESULTS: Median reported smoking intensity was 20 CPD in male and 19 CPD in female smokers. Men showed higher cotinine concentrations (median 3652 µg/L, interquartile range (IQR) 2279-5422 µg/L) than women (3127 µg/L, IQR 1692-4920 µg/L). Logarithmised CPD correlated moderately with cotinine in both, men and women (Pearson's r 0.4), but correlations were weaker in smokers with lower SES: Pearson's r for low, intermediate, and high occupational SES was 0.35, 0.39, and 0.48 in men, and 0.28, 0.43, and 0.47 in women, respectively. Logarithmised CPD and urinary creatinine were main predictors of cotinine in multiple regression models, whereas SES showed a weak negative association in women. Results were similar for trans-3'-hydroxy-cotinine. CONCLUSIONS: Decreasing precision of self-reported CPD was indicated for low SES in men and women. We found no strong evidence for biased self-reports of smoking intensity by SES.

Germline variation in the insulin-like growth factor pathway and risk of Barrett's esophagus and esophageal adenocarcinoma.

Genome-wide association studies (GWAS) of esophageal adenocarcinoma (EAC) and its precursor, Barrett's esophagus (BE), have uncovered significant genetic components of risk, but most heritability remains unexplained. Targeted assessment of genetic variation in biologically relevant pathways using novel analytical approaches may identify missed susceptibility signals. Central obesity, a key BE/EAC risk factor, is linked to systemic inflammation, altered hormonal signaling and insulin-like growth factor (IGF) axis dysfunction. Here, we assessed IGF-related genetic variation and risk of BE and EAC. Principal component analysis was employed to evaluate pathway-level and gene-level associations with BE/EAC, using genotypes for 270 single-nucleotide polymorphisms (SNPs) in or near 12 IGF-related genes, ascertained from 3295 BE cases, 2515 EAC cases and 3207 controls in the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON) GWAS. Gene-level signals were assessed using Multi-marker Analysis of GenoMic Annotation (MAGMA) and SNP summary statistics from BEACON and an expanded GWAS meta-analysis (6167 BE cases, 4112 EAC cases, 17 159 controls). Global variation in the IGF pathway was associated with risk of BE (P = 0.0015). Gene-level associations with BE were observed for GHR (growth hormone receptor; P = 0.00046, false discovery rate q = 0.0056) and IGF1R (IGF1 receptor; P = 0.0090, q = 0.0542). These gene-level signals remained significant at q < 0.1 when assessed using data from the largest available BE/EAC GWAS meta-analysis. No significant associations were observed for EAC. This study represents the most comprehensive evaluation to date of inherited genetic variation in the IGF pathway and BE/EAC risk, providing novel evidence that variation in two genes encoding cell-surface receptors, GHR and IGF1R, may influence risk of BE.

Prevalence and risk factors of migraine and non-migraine headache in older people - results of the Heinz Nixdorf Recall study.

BACKGROUND: The prevalence of migraine and non-migraine headache declines with age. METHODS: Data from the third visit (2011-2015) of the population-based Heinz Nixdorf Recall study were analysed (n = 2038, 51% women, 65-86 years). Possible risk factors for headache activity (obesity, education, smoking, sports, alcohol, partnership status, living alone, having children, sleep quality, depression, hypertension, diabetes mellitus, stroke, coronary heart disease, medication), and headache symptoms were assessed. We estimated the lifetime prevalence and the prevalence of current active headache of migraine with and without aura, and non-migraine headache. The associations between possible risk factors and headache activity (active vs. inactive) were estimated by age and sex-adjusted odds ratios and 95% confidence intervals (OR [95% CI]) using multiple logistic regression. RESULTS: The lifetime prevalence of migraine was 28.6% (n = 584). One hundred and ninety-two (9.4%) had still-active migraine, 168 (3.5%) had migraine with aura, and 416 (5.9%) had migraine without aura. One hundred and sixty-eight (8.2%) had "episodic infrequent migraine, 0-8 headache days/month", 10 (0.5%) had "episodic frequent migraine, 9-14 headache days/month", and five (0.2%) had "chronic migraine, ≥15 headache days/month". Overall, 10 (0.5%) had "chronic headache, any headache on ≥15 days/month". Female gender and younger age were the most important associated migraine risk factors. Depression (1.62 [1.06; 2.47]) and poor sleep (1.06 [1.00; 1.12]) were associated with migraine and headache activity in general. Antihypertensives were associated with headache remission (0.80 [0.64; 1.00]). Additionally, undertaking less sports (0.72 [0.51; 1.03]) was associated with higher migraine activity. CONCLUSIONS: Headaches and migraines are not rare in the older population. They are related to mood and sleep disturbance, and migraine even to less physical activity. Antihypertensives are related to headache remission.

Vitamin D and white matter hyperintensities: results of the population-based Heinz Nixdorf Recall Study and 1000BRAINS.

BACKGROUND AND PURPOSE: Cross-sectional studies showed an inverse association between serum 25-hydroxyvitamin D (25OHD) and white matter hyperintensities (WMHs) whereas the few longitudinal studies did not. The association between baseline 25OHD and WMHs at 10-year follow-up in the Heinz Nixdorf Recall Study plus 1000BRAINS was investigated. METHODS: Data of 505 participants (49% women, 56.2 ± 6.6 years) with 25OHD at baseline (2000-2003) and WMH volume and grade of WMHs using the Fazekas classification at 10-year follow-up were analysed. The association between deseasonalized 25OHD and the base-10 logarithm of WMH volume was evaluated by multiple linear regression, adjusted for age, sex, education, smoking, alcohol consumption, sports, diabetes mellitus, systolic blood pressure and total cholesterol. ß-estimators were transformed back (10ß ). Using multiple logistic regression, odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated to evaluate the association between deseasonalized 25OHD and Fazekas grades (0, absence and 1, punctate foci vs. 2, beginning and 3, large confluence). RESULTS: Mean 25OHD was 17.0 ± 8.2 ng/ml, and mean deseasonalized 25OHD was 16.9 ± 7.5 ng/ml. Mean WMH volume was 16.6 ± 17.4 ml, range 1-132 ml. Most grade 2-3 WMHs were found to be periventricular (39% of the participants), parietal (32%) and frontal (31%) (temporal 6%, occipital 3%). The linear regression showed an inverse association between 25OHD and WMH volume. On average, a 25OHD increase of 1 ng/ml was associated with a reduced WMH volume by a factor of 0.99 (95% CI 0.98; 1.00) (fully adjusted). There was also some indication for an inverse association between 25OHD and extent of periventricular (OR 0.98 [95% CI 0.96; 1.01]), frontal (0.99 [0.97; 1.02]) and parietal (0.98 [0.95; 1.00]) WMHs according to the Fazekas classification. CONCLUSIONS: Lower 25OHD may be a risk factor for the occurrence of WMHs.

Pathway-Specific Genetic Risk for Alzheimer's Disease Differentiates Regional Patterns of Cortical Atrophy in Older Adults.

Brain aging is highly variable and represents a challenge to delimit aging from disease processes. Moreover, genetic factors may influence both aging and disease. Here we focused on this issue and investigated effects of multiple genetic loci previously identified to be associated with late-onset Alzheimer's disease (AD) on brain structure of older adults from a population sample. We calculated a genetic risk score (GRS) using genome-wide significant single-nucleotide polymorphisms from genome-wide association studies of AD and tested its effect on cortical thickness (CT). We observed a common pattern of cortical thinning (right inferior frontal, left posterior temporal, medial occipital cortex). To identify CT changes by specific biological processes, we subdivided the GRS effect according to AD-associated pathways and performed follow-up analyses. The common pattern from the main analysis was further differentiated by pathway-specific effects yielding a more bilateral pattern. Further findings were located in the superior parietal and mid/anterior cingulate regions representing 2 unique pathway-specific patterns. All patterns, except the superior parietal pattern, were influenced by apolipoprotein E. Our step-wise approach revealed atrophy patterns that partially resembled imaging findings in early stages of AD. Our study provides evidence that genetic burden for AD contributes to structural brain variability in normal aging.

[Effects of Noise Protection Measures on Annoyance, Sleep Disorders, and Cardiovascular Diseases: A Model Calculation]. / Auswirkungen lärmmindernder Maßnahmen auf die Häufigkeit von Lärmbelästigung, Schlafstörungen und Herz-Kreislauf-Erkrankungen ­ eine Modellrechnung.

AIM: In Germany, traffic noise-related threshold values are currently set at 70 decibels (dB) during the day and 60 dB at night. According to recent study results, these threshold values might not sufficiently protect against disease risks. The model calculation presented here aimed to estimate the effects of 3 specific noise-protection measures on annoyance, sleep disorders, and cardiovascular diseases. METHODS: For road traffic noise and railway noise, 3 noise reduction approaches were modeled: (1) weighted 24 hours noise levels (LDEN) of at most 65 dB, and nightly sound pressure levels (LNight) of 55 dB; (2) LDEN of at most 60 dB and LNight of 50 dB; and (3) a general reduction of road and railway noise pressure levels by 3 dB. As an example, the effects of approaches (1) to (3) were determined for the study population of the NORAH study on disease risks (Rhine-Main area). The health consequences were estimated based on the results of the WHO Noise Guidelines (2018) and the NORAH study on disease risks. RESULTS: The model calculations showed that noise protection approach (1) could reduce the number of people suffering from sleep disturbances as a result of nightly traffic noise and of those highly annoyed as well as the number of people suffering from traffic-related cardiovascular disease by 5 to 10%. Noise protection approach (2) could reduce traffic-related cardiovascular diseases by at least about 10%; according to the WHO Noise Guidelines, it would even be possible to reduce road traffic noise-related ischemic heart disease by more than 30%. All of these measures would be of particular benefit to the highly exposed population - an already vulnerable group due to their limited socio-economic resources. With the general reduction of traffic noise pressure levels by 3 dB, the incidence of annoyance, sleep disturbances and cardiovascular diseases could be reduced particularly among those exposed to low to medium noise pressure levels. CONCLUSIONS: Considering the different objectives and target groups of the investigated noise protection measures, the introduction and implementation of specific threshold values should be supplemented by general noise reduction measures in the range below the threshold values.

Risk prediction for coronary heart disease by a genetic risk score - results from the Heinz Nixdorf Recall study.

BACKGROUND: A Genetic risk score for coronary artery disease (CAD) improves the ability of predicting coronary heart disease (CHD). It is unclear whether i) the use of a CAD genetic risk score is superior to the measurement of coronary artery calcification (CAC) for CHD risk assessment and ii) the CHD risk assessment using a CAD genetic risk score differs between men and women. METHODS: We included 4041 participants (age-range: 45-76 years, 1919 men) of the Heinz Nixdorf Recall study without CHD or stroke at baseline. A standardized weighted CAD genetic risk score was constructed using 70 known genetic variants. The risk score was divided into quintiles (Q1-Q5). We specified low (Q1), intermediate (Q2-Q4) and high (Q5) genetic risk groups. Incident CHD was defined as fatal and non-fatal myocardial infarction, stroke and coronary death. The association between the genetic risk score and genetic risk groups with incident CHD was assessed using Cox models to estimate hazard ratios (HR) and 95%-confidence intervals (CI). The models were adjusted by age and sex (Model1), as well as by established CHD risk factors (RF) and CAC (Model2). The analyses were further stratified by sex and controlled for multiple testing. RESULTS: During a median follow-up time of 11.6 ± 3.7 years, 343 participants experienced CHD events (219 men). Per-standard deviation (SD) increase in the genetic risk score was associated with 18% increased risk for incident CHD (Model1: p = 0.002) which did not change after full adjustment (Model2: HR = 1.18 per-SD (p = 0.003)). In Model2 we observed a 60% increased CHD risk in the high (p = 0.009) compared to the low genetic risk group. Stratifying by sex, only men showed statistically significantly higher risk for CHD (Model2: HR = 1.23 per-SD (p = 0.004); intermediate: HR = 1.52 (p = 0.04) and high: HR = 1.88 (p = 0.008)) with no statistically significant risk observed in women. CONCLUSION: Our results suggest that the CAD genetic risk score could be useful for CHD risk prediction, at least in men belonging to the higher genetic risk group, but it does not outbalance the value of CT-based quantification of CAC which works independently on both men and women and allows better risk stratification in both the genders.

Association between lipoprotein(a) (Lp(a)) levels and Lp(a) genetic variants with coronary artery calcification.

BACKGROUND: To examine the association between lipoprotein(a) (Lp(a)) levels, LPA (rs10455872 and rs3798220) and IL1F9 (rs13415097) single nucleotide polymorphisms (SNPs) with coronary artery calcification (CAC), an important predictor for coronary artery disease (CAD). METHODS: We used data from 3799 (mean age ± SD: 59.0 ± 7.7 years, 47.1% men) Heinz Nixdorf Recall study participants. We applied linear regression models to explore the relation between the log-transformed Lp(a) levels and LPA and IL1F9 SNPs with loge (CAC + 1). The association between the SNPs and log-transformed Lp(a) levels was further assessed using linear regression. The models were adjusted for age and sex (Model 1) and additionally for Lp(a) levels (Model 2). RESULTS: We observed a statistically significant association between log-transformed Lp(a) levels and CAC (Model 1: beta per log-unit increase in Lp(a) levels = 0.11; 95% confidence interval [95% CI] [0.04; 0.18], p = 0.002). Furthermore, the LPA SNP rs10455872 showed a statistically significant association with CAC (Model 1: beta per allele = 0.37 [0.14; 0.61], p = 0.002). The association between rs10455872 and CAC was attenuated after adjustment for Lp(a) levels (Model 2: beta per allele = 0.26 [- 0.01; 0.53], p = 0.06). Both LPA SNPs also showed a statistically significant association with Lp(a) levels (Model 1: betars10455872 per allele: 1.56 [1.46; 1.65], p < 0.0001 and betars3798220 per allele: 1.51 [1.33; 1.69], p < 0.0001)). The Mendelian randomization analysis showed that Lp(a) is a causal risk factor for CAC (estimate per log-unit increase in Lp(a) levels (95% CI), p: 0.27 [0.11; 0.44], p = 0.001). The IL1F9 SNP did not show any statistically significant association with Lp(a) levels or with CAC. CONCLUSIONS: We provide evidence for the association of LPA rs10455872 with higher levels of Lp(a) and CAC in our study. The results of our study suggest that rs10455872, mediated by Lp(a) levels, might play a role in promoting the development of atherosclerosis leading to cardiovascular disease events.

Prevalence and psychosocial correlates of subjectively perceived decline in five cognitive domains: Results from a population-based cohort study in Germany.

OBJECTIVE: Subjective cognitive decline (SCD) was frequently investigated for memory in healthy aging or in relation to diseases like dementia. It was found to be related to sociodemographic and psychological variables as well as cognitive abilities. The prevalence of SCD in other cognitive domains and their relation to these variables is largely unknown to date. The present study aimed to fill this gap. METHODS: A total of 807 subjects (18-85 years of age, M = 57.8 years, female: 43%) completed the Juelich Questionnaire on Subjective Cognitive Decline, to investigate SCD in memory, attention, language, motor, and executive functions. Logistic regression analyses were used to estimate association of depressive symptomatology, emotionality, and general cognitive performance as well as age, gender, and educational attainment with domain-specific SCD. RESULTS: The highest prevalence rate was obtained for the memory domain (65.9%), followed by the attention (54.6%), motor (52.9%), executive (39.7%), and language domain (31.5%). Of the psychosocial factors, only age, depressive symptomatology and emotionality were consistently and strongly associated with domain-specific SCD prevalence. CONCLUSIONS: SCD is prevalent not only in the memory domain, but also in other major cognitive domains. Our results also suggest that the suspicion from previous research, that subjective memory decline might be more strongly associated with depressive symptomatology and emotionality than with actual decline of cognitive performance, might also apply to the attention, motor, executive, and language domain. Further investigations using neuropsychological testing for specific cognitive functions and employing longitudinal designs are required for substantiating this suspicion.

Walkability and its association with prevalent and incident diabetes among adults in different regions of Germany: results of pooled data from five German cohorts.

BACKGROUND: Highly walkable neighbourhoods may increase transport-related and leisure-time physical activity and thus decrease the risk for obesity and obesity-related diseases, such as type 2 diabetes (T2D). METHODS: We investigated the association between walkability and prevalent/incident T2D in a pooled sample from five German cohorts. Three walkability measures were assigned to participant's addresses: number of transit stations, points of interest, and impedance (restrictions to walking due to absence of intersections and physical barriers) within 640 m. We estimated associations between walkability and prevalent/incident T2D with modified Poisson regressions and adjusted for education, sex, age at baseline, and cohort. RESULTS: Of the baseline 16,008 participants, 1256 participants had prevalent T2D. Participants free from T2D at baseline were followed over a mean of 9.2 years (SD: 3.5, minimum: 1.6, maximum: 14.8 years). Of these, 1032 participants developed T2D. The three walkability measures were not associated with T2D. The estimates pointed toward a zero effect or were within 7% relative risk increase per 1 standard deviation with 95% confidence intervals including 1. CONCLUSION: In the studied German settings, walkability differences might not explain differences in T2D.

[Expenditures of The German Statutory Health Insurance for Health Promotion and Disease Prevention 2012-2017: Positive Effects Due To The Disease Prevention Law?] / Ausgaben der gesetzlichen Krankenversicherung für Gesundheitsförderung und Prävention 2012­2017: Positive Effekte durch das Präventionsgesetz?

BACKGROUND: The German Prevention Act aims to strengthen health promotion and disease prevention. The law makes changes to the so-called "§20 measures". Target values were newly given for the expenditures of the health insurance funds in this area. The objective here was to examine how the prevention expenditures of the statutory health insurance developed in the period from 2012 to 2017, and whether the requirements of the Prevention Act were met. METHODS: The accounting results of the statutory health insurance funds were evaluated for the period 2012-2017. The expenditures per insured person were calculated and the changes in expenditures were analysed. The effect of the prevention law was highlighted by differentiation of the time periods 2012-2014 and 2014-2017. RESULTS: In 2017, about 2.5% of the total expenditure of the German statutory health insurance, around 5 billion euros, was accounted for in the reported prevention areas. Nearly 60% of these prevention expenditures were on early detection and vaccinations. Expenditure on "§20 measures" amounted to € 7.17 per insured person and thus reached the statutory guideline but accounted for less than 10% of all prevention expenditure. Although prevention expenditure per insured person increased over the period, the proportion of money spent on prevention measures as a whole had decreased since 2015. Expenditure on prevention measures that were directly aimed at the insured (individual approach, bonus programmes) and the setting approach (non-occupational settings, worksite health promotion) had hardly increased overall since the Prevention Act came into force. This effect is due to the equally strong decrease in bonuses for health-conscious behaviour among insured persons, despite the sharp increase in expenditure on company and noncompany settings. CONCLUSION: The proportion of money spent on disease prevention in total expenditure is still decreasing. The targets set by the Prevention Act, however, have been reached. Thus, target values have apparently proved to be an effective instrument for regulating prevention expenditure and have led to an increase in expenditure in the setting approach. Overall, there has been no expenditure effect in the area of disease prevention since the Prevention Act was enacted, as compensation was made at the expense of the non-setting measures without target values.

[Study Designs for Effect Evaluation in Disease Prevention and Health Promotion - Meaning of Internal and External Validity in Intervention Studies]. / Studiendesigns zur Wirkungsevaluation in Prävention und Gesundheitsförderung ­ Die Bedeutung interner und externer Validität für die Evidenzbasierung in Lebenswelten.

BACKGROUND: Health promotion and disease prevention in Germany have become more important as a result of the Prevention Act that gives special attention to the setting. So far, however, there is neither a common understanding of the terms of this approach, nor are its potentials empirically derived. Therefore, a discussion about suitable evaluation and study concepts is required. AIMS AND METHODS: The aims of this study were to address the meaning of internal and external validity of intervention studies in health promotion and disease prevention. We provide an overview of the achievable bias control for different study designs and provide examples for the evaluation of setting-based approaches. RESULTS: Interventions in settings are often characterized by a multitude of measures, actors and intervention contexts. Methods of analysis from evidence-based medicine are viewed critically for health promotion and disease prevention in Germany. Such studies are considered to provide a high degree of internal validity, but the extrapolation of the results to "reality" is viewed as low. In contrast, the extrapolation of study results is not more of a challenge for setting projects than for any other research area. It is not limited by different contexts, but rather by different causal relationships. Impact assessment aims at causally attributing an observed outcome to the intervention. Thus, the epistemological requirements do not differ between studies that are designed for internal or external validity. The international discussion focuses on the refinement of (quasi)-experimental study designs. Examples for the evaluation of setting projects, mainly from Germany, illustrate that those alternative methods have already been used in evaluation practice. CONCLUSION: A challenge for health promotion and disease prevention in settings is to systematically assess the different needs for evidence-basing. At present, there is a wealth of findings in a large number of intervention fields. These findings must be compiled and analyzed to determine whether and to what extent further evaluations need to be initiated and by which methods.

[Acoustic quality and urban health-more than just noise and silence]. / Akustische Qualität und Stadtgesundheit ­ Mehr als nur Lärm und Stille.

New approaches in urban development are required to transform cities into sustainable places. This demands a higher degree of urban density, which is hardly conceivable without an increase in sound - mostly in the form of noise. To achieve a high level of acceptance for densification, high-quality and acoustically pleasant urban spaces are essential. Noise reduction measures are necessary, but not sufficient. What is needed is a broadening of the perspective of noise. For urban public health we propose the soundscape approach from two different scientific disciplines. Here, sounds are qualities that can be designed in urban spaces and are an important resource for a healthy city. Linking knowledge about the acoustic environment with human perception will significantly improve our understanding of the relationships between urban acoustic environments, urban spatial contexts, and their effects on human health, both qualitatively and quantitatively. However, a systematic application of these approaches to urban soundscapes is still missing, as is the joint implementation of soundscape approaches in noise impact and urban public health research. This paper aims to introduce the terms sound and noise as well as two soundscape approaches. Subsequently, the aims and methods of the acoustic quality and health in urban environments (SALVE) pilot project are presented. The paper provides early insight into the new field of urban sound quality and soundscapes in the context of urban public health.