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From a public health standpoint, it is equally important to link to other data sources to enrich cohort databases with high quality data stored within the healthcare system, from public authorities and from other databases with relevance for health. [...]an endorsement on a broad societal and institutional level is needed. [...]large-scale cohort studies with the Swiss Cohort & Biobank as a prime example are ideal tools to derive public health interventions and to evaluate policies considering individual and population heterogeneities. Conflict of Interest The author declares that they do not have any conflicts of interest. 1.GBD 2019 Diseases and Injuries Collaborators.Global burden of 369 Diseases and Injuries in 204 Countries and Territories, 1990-2019: a Systematic Analysis for the Global Burden of Disease Study 2019.Lancet(2020)396(10258):1204–22.10.1016/S0140-6736(20)30925-9 2.GBD 2019 Demographics Collaborators.Global Age-sex-specific Fertility, Mortality, Healthy Life Expectancy (HALE), and Population Estimates in 204 Countries and Territories, 1950-2019: a Comprehensive Demographic Analysis for the Global Burden of Disease Study 2019.Lancet(2020)396(10258):1160–203.10.1016/S0140-6736(20)30977-6 3.Probst-HenschNBochudMChioleroACrivelliLDratvaJFlahaultASwiss Cohort & Biobank - the White Paper.Public Health Rev(2022)43:1605660.10.3389/phrs.2022.1605660 4.SudlowCGallacherJAllenNBeralVBurtonPDaneshJUK Biobank: an Open Access Resource for Identifying the Causes of a Wide Range of Complex Diseases of Middle and Old Age.Plos Med(2015)12(3):e1001779.10.1371/journal.pmed.1001779 5.StolkRPRosmalenJGPostmaDSde BoerRANavisGSlaetsJPUniversal Risk Factors for Multifactorial Diseases: LifeLines: a Three-Generation Population-Based Study.Eur J Epidemiol(2008)23(1):67–74.10.1007/s10654-007-9204-4 6.ZinsMBonenfantSCartonMCoeuret-PellicerMGueguenAGourmelenJThe CONSTANCES Cohort: an Open Epidemiological Laboratory.BMC Public Health(2010)10:479.10.1186/1471-2458-10-479 7.PetersAGerman National CohortCPetersAGreiserKHGottlicherSAhrensWFramework and Baseline Examination of the German National Cohort (NAKO).Eur J Epidemiol(2022)37(10):1107–24.10.1007/s10654-022-00890-5 8.VlaanderenJde HooghKHoekGPetersAProbst-HenschNScalbertADeveloping the Building Blocks to Elucidate the Impact of the Urban Exposome on Cardiometabolic-Pulmonary Disease: The EU EXPANSE Project.Environ Epidemiol(2021)5(4):e162.10.1097/EE9.0000000000000162 9.PetersANawrotTSBaccarelliAA.Hallmarks of Environmental Insults.Cell(2021)184(6):1455–68.10.1016/j.cell.2021.01.043 10.FagherazziG.Towards a European \"Cohort Moonshot\": Revisiting the Long-Term Strategy to Support Health Research of Tomorrow.Eur J Epidemiol(2023)38(1):121–2.10.1007/s10654-022-00939-5

In the recent years, short-term heart rate variability (HRV) describing complex variations of beat-to-beat interval series that are mainly controlled by the autonomic nervous system (ANS) has been increasingly analyzed to assess the ANS activity in different diseases and under various conditions. In contrast to long-term HRV analysis, short-term investigations (<30 min) provide a test result almost immediately. Thus, short-term HRV analysis is suitable for ambulatory care, patient monitoring and all those applications where the result is urgently needed. In a previous study, we could show significant variations of 5-min HRV indices according to age in almost all domains (linear and nonlinear) in 1906 healthy subjects from the KORA S4 cohort. Based on the same group of subjects, general gender-related influences on HRV indices are to be determined in this study. Short-term 5-min HRV indices from linear time and frequency domain and from nonlinear methods (compression entropy, detrended fluctuation analysis, traditional and segmented Poincaré plot analysis, irreversibility analysis, symbolic dynamics, correlation and mutual information analysis) were determined from 782 females and 1124 males. First, we examined the gender differences in two age clusters (25-49 years and 50-74 years). Secondly, we investigated the gender-specific development of HRV indices in five age decade categories, namely for ages 25-34, 35-44, 45-54, 55-64 and 65-74 years. In this study, significant modifications of the indices according to gender could be obtained, especially in the frequency domain and correlation analyses. Furthermore, there were significant modifications according to age in nearly all of the domains. The gender differences disappeared within the last two age decades and the age dependencies disappeared in the last decade. To summarize gender and age influences need to be considered when performing HRV studies even if these influences only partly differ.

Obesity is a major health problem that is determined by interactions between lifestyle and environmental and genetic factors. Although associations between several genetic variants and body-mass index (BMI) have been identified, little is known about epigenetic changes related to BMI. We undertook a genome-wide analysis of methylation at CpG sites in relation to BMI. 479 individuals of European origin recruited by the Cardiogenics Consortium formed our discovery cohort. We typed their whole-blood DNA with the Infinium HumanMethylation450 array. After quality control, methylation levels were tested for association with BMI. Methylation sites showing an association with BMI at a false discovery rate q value of 0·05 or less were taken forward for replication in a cohort of 339 unrelated white patients of northern European origin from the MARTHA cohort. Sites that remained significant in this primary replication cohort were tested in a second replication cohort of 1789 white patients of European origin from the KORA cohort. We examined whether methylation levels at identified sites also showed an association with BMI in DNA from adipose tissue (n=635) and skin (n=395) obtained from white female individuals participating in the MuTHER study. Finally, we examined the association of methylation at BMI-associated sites with genetic variants and with gene expression. 20 individuals from the discovery cohort were excluded from analyses after quality-control checks, leaving 459 participants. After adjustment for covariates, we identified an association (q value ≤0·05) between methylation at five probes across three different genes and BMI. The associations with three of these probes—cg22891070, cg27146050, and cg16672562, all of which are in intron 1 of HIF3A—were confirmed in both the primary and second replication cohorts. For every 0·1 increase in methylation β value at cg22891070, BMI was 3·6% (95% CI 2·4–4·9) higher in the discovery cohort, 2·7% (1·2–4·2) higher in the primary replication cohort, and 0·8% (0·2–1·4) higher in the second replication cohort. For the MuTHER cohort, methylation at cg22891070 was associated with BMI in adipose tissue (p=1·72 × 10−5) but not in skin (p=0·882). We observed a significant inverse correlation (p=0·005) between methylation at cg22891070 and expression of one HIF3A gene-expression probe in adipose tissue. Two single nucleotide polymorphisms—rs8102595 and rs3826795—had independent associations with methylation at cg22891070 in all cohorts. However, these single nucleotide polymorphisms were not significantly associated with BMI. Increased BMI in adults of European origin is associated with increased methylation at the HIF3A locus in blood cells and in adipose tissue. Our findings suggest that perturbation of hypoxia inducible transcription factor pathways could have an important role in the response to increased weight in people. The European Commission, National Institute for Health Research, British Heart Foundation, and Wellcome Trust.

The present study evaluated the ability of the visceral adiposity index (VAI), the lipid accumulation product (LAP), and product of triglycerides and glucose (TyG), three novel, insulin resistance-related markers, to discriminate prediabetes/diabetes in the general German population. Altogether 2,045 Germans (31–72 years, 53.3% women) without known diabetes and a history of Myocardial Infarction (MI)/stroke from the Cooperative Health Research in the Region of Augsburg (KORA) F4 Study were eligible. The discriminatory accuracy of the markers for oral glucose tolerance test (OGTT)-defined prediabetes/diabetes according to the American Diabetes Association (ADA) criteria was assessed by the area under the receiver operating characteristic (ROC) curve (AUC). The Youden Index (YI) was used to determine optimal cut-off values, and a non-parametric ROC regression was used to examine whether the discriminatory accuracy varied by sex and age. 365 men (38.2%) and 257 women (23.6%) were newly diagnosed with prediabetes/diabetes. AUCs for TyG, LAP and VAI were 0.762 (95% CI 0.740–0.784), 0.743 (95% CI 0.720–0.765), and 0.687 (95% CI 0.662–0.712), respectively. The optimal cut-off values for the LAP and TyG were 56.70 and 8.75 in men, and 30.40 and 8.53 in women. In conclusion, TyG and LAP provide good discrimination of persons with prediabetes/diabetes.

The association between short-term exposure to extreme weather events and health has been well established. In addition, there is a large body of epidemiological literature on the short and long-term effects of ambient exposure to PM2.5. We hypothesize that the health impact associated with exposure to air pollution and weather is larger than the risk estimated based on the health effects of air pollution and weather alone. Not much work has been done to estimate the acute and chronic effects associated with simultaneous exposure to multiple environmental agents such as weather and particulate matter. In this editorial we highlight challenges in addressing these interactions. Around the globe, exposure to weather parameters, composition of gaseous and particulate air pollution, and the ventilation rates vary by season. Furthermore, weather and pollution mixtures exhibit different exposure-response function and act through different pathophysiological mechanisms. The synergistic analysis of ambient air pollution and weather require studies collecting appropriate data and advancing methodological approaches. Due to large variation in space and time, carefully designed multi-center studies will be important to address these challenges and provide novel stimuli for promoting measures to slow climate change and improve air pollution in urban areas and in cities around the world.

DNA methylation (DNAm) has been revealed to play a role in various diseases. Here we performed epigenome-wide screening and validation to identify mortality-related DNAm signatures in a general population-based cohort with up to 14 years follow-up. In the discovery panel in a case-cohort approach, 11,063 CpGs reach genome-wide significance (FDR<0.05). 58 CpGs, mapping to 38 well-known disease-related genes and 14 intergenic regions, are confirmed in a validation panel. A mortality risk score based on ten selected CpGs exhibits strong association with all-cause mortality, showing hazard ratios (95% CI) of 2.16 (1.10–4.24), 3.42 (1.81–6.46) and 7.36 (3.69–14.68), respectively, for participants with scores of 1, 2–5 and 5+ compared with a score of 0. These associations are confirmed in an independent cohort and are independent from the ‘epigenetic clock’. In conclusion, DNAm of multiple disease-related genes are strongly linked to mortality outcomes. The DNAm-based risk score might be informative for risk assessment and stratification. DNA methylation is modulated by environmental factors and has a role in many complex diseases. Here, the authors find that methylation at specific DNA sites is associated with all-cause mortality, and a methylation-based risk score may be informative for risk assessment and stratification.

Current day concentrations of ambient air pollution have been associated with a range of adverse health effects, particularly mortality and morbidity due to cardiovascular and respiratory diseases. In this review, we summarize the evidence from epidemiological studies on long-term exposure to fine and coarse particles, nitrogen dioxide (NO 2 ) and elemental carbon on mortality from all-causes, cardiovascular disease and respiratory disease. We also summarize the findings on potentially susceptible subgroups across studies. We identified studies through a search in the databases Medline and Scopus and previous reviews until January 2013 and performed a meta-analysis if more than five studies were available for the same exposure metric. There is a significant number of new studies on long-term air pollution exposure, covering a wider geographic area, including Asia. These recent studies support associations found in previous cohort studies on PM 2.5 . The pooled effect estimate expressed as excess risk per 10 μg/m 3 increase in PM 2.5 exposure was 6% (95% CI 4, 8%) for all-cause and 11% (95% CI 5, 16%) for cardiovascular mortality. Long-term exposure to PM 2.5 was more associated with mortality from cardiovascular disease (particularly ischemic heart disease) than from non-malignant respiratory diseases (pooled estimate 3% (95% CI −6, 13%)). Significant heterogeneity in PM 2.5 effect estimates was found across studies, likely related to differences in particle composition, infiltration of particles indoors, population characteristics and methodological differences in exposure assessment and confounder control. All-cause mortality was significantly associated with elemental carbon (pooled estimate per 1 μg/m 3 6% (95% CI 5, 7%)) and NO 2 (pooled estimate per 10 μg/m 3 5% (95% CI 3, 8%)), both markers of combustion sources. There was little evidence for an association between long term coarse particulate matter exposure and mortality, possibly due to the small number of studies and limitations in exposure assessment. Across studies, there was little evidence for a stronger association among women compared to men. In subjects with lower education and obese subjects a larger effect estimate for mortality related to fine PM was found, though the evidence for differences related to education has been weakened in more recent studies.

AbstractObjectiveTo investigate the associations between air pollution and mortality, focusing on associations below current European Union, United States, and World Health Organization standards and guidelines.DesignPooled analysis of eight cohorts.SettingMulticentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) in six European countries.Participants325 367 adults from the general population recruited mostly in the 1990s or 2000s with detailed lifestyle data. Stratified Cox proportional hazard models were used to analyse the associations between air pollution and mortality. Western Europe-wide land use regression models were used to characterise residential air pollution concentrations of ambient fine particulate matter (PM2.5), nitrogen dioxide, ozone, and black carbon.Main outcome measuresDeaths due to natural causes and cause specific mortality.ResultsOf 325 367 adults followed-up for an average of 19.5 years, 47 131 deaths were observed. Higher exposure to PM2.5, nitrogen dioxide, and black carbon was associated with significantly increased risk of almost all outcomes. An increase of 5 µg/m3 in PM2.5 was associated with 13% (95% confidence interval 10.6% to 15.5%) increase in natural deaths; the corresponding figure for a 10 µg/m3 increase in nitrogen dioxide was 8.6% (7% to 10.2%). Associations with PM2.5, nitrogen dioxide, and black carbon remained significant at low concentrations. For participants with exposures below the US standard of 12 µg/m3 an increase of 5 µg/m3 in PM2.5 was associated with 29.6% (14% to 47.4%) increase in natural deaths.ConclusionsOur study contributes to the evidence that outdoor air pollution is associated with mortality even at low pollution levels below the current European and North American standards and WHO guideline values. These findings are therefore an important contribution to the debate about revision of air quality limits, guidelines, and standards, and future assessments by the Global Burden of Disease.

Environmental factors such as tobacco smoking may have long-lasting effects on DNA methylation patterns, which might lead to changes in gene expression and in a broader context to the development or progression of various diseases. We conducted an epigenome-wide association study (EWAs) comparing current, former and never smokers from 1793 participants of the population-based KORA F4 panel, with replication in 479 participants from the KORA F3 panel, carried out by the 450K BeadChip with genomic DNA obtained from whole blood. We observed wide-spread differences in the degree of site-specific methylation (with p-values ranging from 9.31E-08 to 2.54E-182) as a function of tobacco smoking in each of the 22 autosomes, with the percent of variance explained by smoking ranging from 1.31 to 41.02. Depending on cessation time and pack-years, methylation levels in former smokers were found to be close to the ones seen in never smokers. In addition, methylation-specific protein binding patterns were observed for cg05575921 within AHRR, which had the highest level of detectable changes in DNA methylation associated with tobacco smoking (-24.40% methylation; p = 2.54E-182), suggesting a regulatory role for gene expression. The results of our study confirm the broad effect of tobacco smoking on the human organism, but also show that quitting tobacco smoking presumably allows regaining the DNA methylation state of never smokers.