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Background: Tea and coffee are the most consumed beverages worldwide and very often sweetened with sugar. However, the association between the use of sugar in tea or coffee and adverse events is currently unclear. Objectives: To investigate the association between the addition of sugar to coffee or tea, and the risk of all-cause mortality, cardiovascular mortality, cancer mortality and incident diabetes mellitus. Methods: Participants from the prospective Copenhagen Male Study, included from 1985 to 1986, without cardiovascular disease, cancer or diabetes mellitus at inclusion, who reported regular coffee or tea consumption were included. Self-reported number of cups of coffee and tea and use of sugar were derived from the study questionnaires. Quantity of sugar use was not reported. Primary outcome was all-cause mortality and secondary endpoints were cardiovascular mortality, cancer mortality and incident diabetes mellitus, all assessed through the Danish national registries. The association between adding sugar and all-cause mortality was analyzed by Cox regression analysis. Age, smoking status, daily alcohol intake, systolic blood pressure, body mass index, number of cups of coffee and/or tea consumed per day and socioeconomic status were included as covariates. Vital status of patients up and until 22.03.2017 was assessed. Sugar could be added to either coffee, tea or both. Results: In total, 2923 men (mean age at inclusion: 63±5 years) were included, of which 1007 (34.5%) added sugar. In 32 years of follow-up, 2581 participants (88.3%) died, 1677 in the non-sugar group (87.5%) versus 904 in the sugar group (89.9%). Hazard ratio of the sugar group compared to the non-sugar group was 1.06 (95% CI 0.98;1.16) for all-cause mortality. An interaction term between number of cups of coffee and/or tea per day and adding sugar was 0.99 (0.96;1.01). A subgroup analysis of coffee-only drinkers showed a hazard ratio of 1.11 (0.99;1.26). The interaction term was 0.98 (0.94;1.02). Hazard ratios for the sugar group compared to the non-sugar group were 1.11 (95% CI 0.97;1.26) for cardiovascular disease mortality, 1.01 (95% CI 0.87;1.17) for cancer mortality and 1.04 (95% CI 0.79;1.36) for incident diabetes mellitus. Conclusion: In the present population of Danish men, use of sugar in tea and/or coffee was not significantly associated with increased risk of mortality or incident diabetes. [ABSTRACT FROM AUTHOR]

Background: Studies indicate that physical activity during leisure and work have opposite associations with cardiovascular disease (CVD) risk factors, referred to as the physical activity health paradox. We investigated how sedentary behaviour and physical activity types during leisure and work are associated with systolic blood pressure (SBP), waist circumference (WC), and low-density lipoprotein cholesterol (LDL-C) in an adult general population sample using compositional data analysis. Methods: Participants wore accelerometers for 7 days (right thigh and iliac crest; 24 h/day) and had their SBP, WC, and LDL-C measured. Accelerometer data was analysed using the software Acti4 to derive daily time spent in sedentary behaviour and physical activity types. The measure of association was quantified by reallocating time between sedentary behaviour and 1) walking, and 2) high-intensity physical activity (HIPA; sum of climbing stairs, running, cycling, and rowing), during both domains. Results: In total, 652 participants were included in the analyses (median wear time: 6 days, 23.8 h/day). During leisure, the results indicated that less sedentary behaviour and more walking or more HIPA was associated with lower SBP, while during work, the findings indicated an association with higher SBP. During both domains, the findings indicated that less sedentary behaviour and more HIPA was associated with a smaller WC and lower LDL-C. However, the findings indicated less sedentary behaviour and more walking to be associated with a larger WC and higher LDL-C, regardless of domain. Conclusions: During leisure, less sedentary behaviour and more walking or HIPA seems to be associated with a lower SBP, but, during work, it seems to be associated with a higher SBP. No consistent differences between domains were observed for WC and LDL-C. These findings highlight the importance of considering the physical activity health paradox, at least for some risk factors for CVD. [ABSTRACT FROM AUTHOR]

Aims: Layer‐specific global longitudinal strain (GLS) has been demonstrated to predict outcome in various patient cohorts. However, little is known regarding the prognostic value of layer‐specific GLS in the general population and whether different layers entail differential prognostic information. The aim of the present study was to investigate the prognostic value of whole wall (GLSWW), endomyocardial (GLSEndo), and epimyocardial (GLSEpi) GLS in the general population. Methods and results: A total of 4013 citizens were included in the present study. All 4013 had two‐dimensional speckle tracking echocardiography performed and analysed. Outcome was a composite endpoint of incident heart failure and/or cardiovascular death. Mean age was 56 years and 57% were female. During a median follow‐up time of 3.5 years, 133 participants (3.3%) reached the composite outcome. Sex modified the relationship between all GLS parameters and outcome. In sex‐stratified analysis, no GLS parameter remained significant predictors of outcome in females. In contrast, GLSWW [hazard ratio (HR) 1.16, 95% confidence interval (CI) 1.02–1.31, per 1% decrease] and GLSEpi (HR 1.19, 95% CI 1.04–1.38, per 1% decrease) remained as significant predictors of outcome in males after multivariable adjustment (including demographic, clinical, biochemistry, and echocardiographic parameters). Lastly, only in males did GLS parameters provide incremental prognostic information to general population risk models. Conclusions: In the general population, sex modifies the prognostic value of GLS resulting in GLSEpi being the only layer‐specific prognosticator in males, while no GLS parameter provides independent prognostic information in females. [ABSTRACT FROM AUTHOR]

Military personnel may withhold information on mental health problems (MHPs) for fear of not being permitted to deploy. Past or current MHPs may, however, increase the risk of postdeployment MHPs. Using psychiatric diagnoses rather than self-report assessments in predeployment screening may be a more effective screening strategy for determining deployment fitness. This retrospective follow-up study investigated (a) the extent to which predeployment childhood and adult psychiatric diagnoses predicted postdeployment MHPs, measured as psychiatric diagnosis and the purchase of psychiatric drugs, and long-term sickness absence among formerly deployed Danish military personnel and (b) whether perceived combat exposure moderated or mediated the effect of predeployment psychiatric diagnoses. Complete data were available for 7,514 Danish military personnel who answered questions on perceived combat exposure between 6-8 months after returning from their first deployment to the Balkans, Iraq, or Afghanistan. Data on all psychiatric diagnoses given at Danish hospitals, all medicine purchases, and all sickness absences were retrieved from nationwide research registers. Personnel with predeployment psychiatric diagnoses had a statistically significant higher risk for both postdeployment long-term sickness absence, hazard ratio (HR) = 2.06, 95% CI [1.52, 2.80]; and postdeployment MHPs, HR = 2.38, 95% CI [1.73, 3.27], than personnel without a predeployment psychiatric diagnosis. Personnel with a predeployment psychiatric diagnosis demonstrated a higher risk of reporting high levels of perceived combat exposure. Perceived combat exposure was not found to moderate or mediate the effect of a predeployment psychiatric diagnosis on the two outcomes. Additional findings, limitations, and implications are discussed. [ABSTRACT FROM AUTHOR]

INTRODUCTION We examined changes in smoking habits in the general population according to prevalence and incidence of chronic diseases affected by smoking. METHODS We included 12283 individuals enrolled from 2003 in the Copenhagen General Population Study and re-examined from 2014. Participants were classified as either healthy or suffering from chronic obstructive pulmonary disease (COPD), asthma, diabetes mellitus, heart disease or stroke. RESULTS At entry, smoking prevalence was 15.4% in healthy participants, 29.8% with COPD, 15.8% with asthma, 21.7 % with diabetes mellitus, 17.2 % with ischemic heart disease/heart failure and 18.6% in participants with previous stroke. Smoking prevalence declined during the 10 years of observation. Among healthy subjects who developed one of the above mentioned diseases during follow-up, those who developed COPD had the highest initial smoking prevalence (51.5%). Quit rates were highest in those who developed asthma resulting in smoking prevalence of 8.2% versus 27.7% in COPD. After adjustment for age, smoking severity and genotype previously associated with heavy smoking (CHRNA3 rs1051730 AA), significant predictors of quitting were new diagnosis of ischemic heart disease/heart failure (OR=2.33, 95 % CI: 1.61–3.42), new diagnosis of asthma (OR=1.84, 95% CI: 1.18–2.90) and low number of pack-years. CONCLUSIONS Individuals with prevalent smoking related diseases continued to smoke more than healthy individuals. Incident heart disease and asthma, but not incident COPD, stroke or diabetes were associated with a higher chance of quitting. Special focus on smokers with COPD, asthma, diabetes, stroke and ischemic heart disease/heart failure is warranted to decrease smoking prevalence in these groups. Smokers with a new diagnosis of diabetes, stroke and COPD need special smoking cessation support. [ABSTRACT FROM AUTHOR]

Rationale: The diffusing capacity (DL) of the lung can be divided into two components: the diffusing capacity of the alveolar membrane (Dm) and the pulmonary capillary volume (Vc). DL is traditionally measured using a single-breath method, involving inhalation of carbon monoxide, and a breath hold of 8–10 seconds (DL,CO). This method does not easily allow calculation of Dm and Vc. An alternative single-breath method (DL,CO,NO), involving simultaneous inhalation of carbon monoxide and nitric oxide, and traditionally a shorter breath hold, allows calculation of Dm and Vc and the DL,NO/DL,CO ratio in a single respiratory maneuver. The clinical utility of Dm, Vc, and DL,NO/DL,CO in the pediatric age range is currently unknown but also restricted by lack of reference values. Objectives: The aim of this study was to establish reference ranges for the outcomes of DL,CO,NO with a 5 second breath hold, including the calculated outcomes Dm, Vc, and the DL,NO/DL,CO ratio, as well as to establish reference values for the outcomes of the traditional DL,CO method, with a 10 second breath hold in children. Methods: DL,CO,NO and DL,CO were measured in healthy children, of European descent, aged 5–17 years using a Jaeger Masterscreen PFT. The data were analyzed using the Generalized Additive Models for Location Scale and Shape (GAMLSS) statistical method. Measurements and Main Results: A total of 326 children were eligible for diffusing capacity measurements, resulting in 312 measurements of DL,CO,NO and 297 of DL,CO, respectively. Reference equations were established for the outcomes of DL,CO,NO and DL,CO, including the calculated values: Vc, Dm, and the DL,NO/DL,CO ratio. Conclusion: These reference values are based on the largest sample of children to date and may provide a basis for future studies of their clinical utility in differentiating between alterations in the pulmonary circulation and changes in the alveolar membrane in pediatric patients. [ABSTRACT FROM AUTHOR]

Background. Elevated resting heart rate (RHR) is associated with cardiovascular mortality and morbidity. Assessment of heart rate (HR) from Holter recording may afford a more precise estimate of the effect of RHR on cardiovascular risk, as compared to casual RHR. Comparative analysis was carried out in an age-stratified subsample of 131 subjects in the Copenhagen City Heart Study (CCHS). Methods. Casual RHR was assessed from electrocardiograms recorded during clinical assessment. Hourly daytime HRs were mapped by Holter recording. Holter RHR was defined as the average of the lowest 3 hourly HRs recorded and mean HR calculated from all daytime HRs. Follow-up was recorded from public registers. Outcome measure was hazard rate for the combined endpoint of cardiovascular mortality, non-fatal heart failure and non-fatal acute myocardial infarction. Comparison of casual RHR, Holter RHR and mean HR by Multivariate Cox regression was performed. Results. A total of 57 composite endpoints occurred during 17.1 years of follow-up. Regression analysis suggests correlation between Casual RHR and Holter RHR. Multivariate Cox regression analysis adjusted for gender and age demonstrated hazard rates of 1.02 ( p = 0.079) for casual RHR, 1.04 ( p = 0.036*) for Holter RHR, and 1.03 ( p = 0.093) for mean HR for each 10 beat increment in HR. Conclusions. In a comparative analysis on the correlation and significance of differing RHR measurement modalities RHR measured by 24-hour Holter recording was found to be marginally superior as a predictor of cardiovascular morbidity and mortality. The results presented here do not however warrant the abandonment of a tested epidemiological variable. [ABSTRACT FROM AUTHOR]

Abstract: Background: The inflammatory biomarkers soluble urokinase plasminogen activator receptor (suPAR) and C-reactive protein (CRP) independently predict cardiovascular disease (CVD). The prognostic implications of suPAR and CRP combined with Framingham Risk Score (FRS) have not been determined. Methods: From 1993 to 1994, baseline levels of suPAR and CRP were obtained from 2315 generally healthy Danish individuals (mean [SD] age: 53.9 [10.6] years) who were followed for the composite outcome of ischemic heart disease, stroke and CVD mortality. Results: During a median follow-up of 12.7years, 302 events were recorded. After adjusting for FRS, women with suPAR levels in the highest tertile had a 1.74-fold (95% confidence interval [CI]: 1.08–2.81, p=0.027) and men a 2.09-fold (95% CI: 1.37–3.18, p<0.001) increase in risk compared to the lowest tertile. Including suPAR and CRP together resulted in stronger risk prediction with a 3.30-fold (95% CI: 1.36–7.99, p<0.01) increase for women and a 3.53-fold (1.78–7.02, p<0.001) increase for men when both biomarkers were in the highest compared to the lowest tertile. The combined extreme tertiles of suPAR and CRP reallocated individuals predicted to an intermediate 10-year risk of CVD of 10–20% based on FRS, to low (<10%) or high (>20%) risk categories, respectively. This was reflected in a significant improvement of C statistics for men (p=0.034) and borderline significant for women (p=0.054), while the integrated discrimination improvement was highly significant (P≤0.001) for both genders. Conclusions: suPAR provides prognostic information of CVD risk beyond FRS and improves risk prediction substantially when combined with CRP in this setting. [Copyright &y& Elsevier]

Several animal studies indicate that mercury is a male reproductive toxicant, but human studies are few and contradictory. We examined semen characteristics and serum levels of reproductive hormones in relation to environmental exposure to mercury. Blood and semen samples were collected from 529 male partners of pregnant women living in Greenland, Poland and Ukraine between May 2002 and February 2004. The median concentration of the total content of mercury in whole blood was 9.2 ng ml−1 in Greenland (0.2-385.8 ng ml−1), 1.0 ng ml−1 in Poland (0.2-6.4 ng ml−1) and 1.0 ng ml−1 in Ukraine (0.2-4.9 ng ml−1). We found a significantly positive association between the blood levels of mercury and serum concentration of inhibin B in men from Greenland (β=0.074, 95% confidence interval (CI)=0.021 to 0.126) and in an analysis including men from all three regions (β=0.067, 95% CI=0.024 to 0.110). The association may be due to beneficial effects of polyunsaturated fatty acids (PUFAs), which are contained in seafood and fish. No significant association (P>0.05) was found between blood concentrations of mercury and any of the other measured semen characteristics (semen volume, total sperm count, sperm concentration, morphology and motility) and reproductive hormones (free androgen index (FAI), follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone and LH×testosterone) in any region. In conclusion, the findings do not provide evidence that environmental mercury exposure in Greenlandic and European men with median whole blood concentration up to 10 ng ml−1 has adverse effects on biomarkers of male reproductive health. [ABSTRACT FROM AUTHOR]

Objective. The mechanisms by which overweight and physical inactivity lead to hypertension are complex. Leptin, an adipocyte-derived hormone, has been linked with hypertension. We wanted to investigate the relationship between leptin, physical activity and new-onset hypertension. Methods. The study was a prospective cohort study of 744 women and 367 men, who were normotensive in the third Copenhagen City Heart Study (CCHS) examination, performed 1991-94. Based on questionnaire items, the participants were divided into two groups with low ( n == 674) and high ( n == 437) levels of leisure-time physical activity, respectively. Results. Between the third and the fourth CCHS examination, performed 2001-03, 304 had developed hypertension, defined as systolic blood pressure (SBP) ≥ 140 mmHg or diastolic blood pressure (DBP) ≥ 90 mmHg or use of antihypertensive medication. In a logistic regression model, including age, sex, body mass index, SBP, DBP, level of physical activity and leptin, we found a significant interaction between leptin and level of physical activity with new-onset hypertension as outcome variable ( p == 0.012). When we entered the interaction variables, effect of leptin with low level of physical activity and with high level of physical activity, respectively, in the original model, leptin predicted new-onset hypertension in participants with low level of physical activity [odds ratio (95% confidence interval): 1.16 (1.01-1.33) for one unit increase in log-transformed leptin levels, p == 0.038], but not in participants with high level of physical activity [0.88 (0.74-1.05), p == 0.15]. Conclusion. We found that leptin predicted new-onset hypertension but only in participants with low level of physical activity. [ABSTRACT FROM AUTHOR]

Background: In workplace respiratory disease prevention, a thorough understanding is needed of the relative contributions of lung function loss and respiratory symptoms in predicting adverse health outcomes. Methods: Copenhagen City Heart Study respiratory data collected at 4 examinations (1976--2003) and morbidity and mortality data were used to investigate these relationships. With 15 or more years of follow-up for a hospital diagnosis of chronic obstructive pulmonary disease (COPD) morbidity, COPD or coronary heart disease (CHD) mortality, and all-cause mortality, risks for these outcomes were estimated in relation to asthma, chronic bronchitis, shortness of breath, and lung function level at examination 2 (1981--1983) or lung function decline established from examinations 1 (1976--1978) to 2 using 4 measures (FEV1 slope, FEV1 relative slope, American College of Occupational and Environmental Medicine's Longitudinal Normal Limit [[LNL]], or a limit of 90 milliliters per year [[ml/yr]]). These risks were estimated by hazard ratios (HR) and 95%% confidence intervals (CI) adjusted for age, height-adjusted baseline forced expiratory volume in 1 second (FEV1/height2), and height. Results: For COPD morbidity, the increasing trend in the HR (95%% CI) by quartiles of the FEV1 slope reached a maximum of 3.77 (2.76--5.15) for males, 6.12 (4.63--8.10) for females, and 4.14 (1.57--10.90) for never-smokers. Significant increasing trends were also observed for mortality, with females at higher risk. Conclusion: Lung function decline was associated with increased risk of COPD morbidity and mortality emphasizing the need to monitor lung function change over time in at-risk occupational populations. [ABSTRACT FROM AUTHOR]

BackgroundLeptin and adiponectin are hormones secreted by adipose tissue, and both hormones are candidate intermediaries between adipose tissue and overweight-related diseases. So far, no prospective study has been published where the independent effects of these two hormones on the development of hypertension have been directly compared. The objective of this study was to investigate the relationships between plasma levels of leptin and adiponectin and new-onset hypertension in the Copenhagen City Heart Study (CCHS).MethodsIn a prospective study design, we examined new-onset hypertension in 620 women and 300 men who were normotensive in the third CCHS examination, which was performed in 1991–1994.ResultsBetween the third and the fourth CCHS examination, which was performed in 2001–2003, 254 had developed hypertension, defined as systolic blood pressure (SBP) ≥140 mm Hg, or diastolic blood pressure (DBP) ≥90 mm Hg, or use of antihypertensive medication. Using logistic regression analysis, adjusting for age, sex, estimated glomerular filtration rate, triglycerides, high-density lipoprotein cholesterol (HDL-C), fibrinogen, and glucose, and with leptin and adiponectin included in the same model, leptin was significantly associated with new-onset hypertension with an odds ratio (95% confidence interval) of 1.28 (1.08–1.53; P < 0.005) for 1 s.d. higher level of log-transformed leptin, whereas adiponectin was not significantly associated with new-onset hypertension having an odds ratio of 1.02 (0.84–1.24; P = 0.83) for 1 s.d. higher level of log-transformed adiponectin.ConclusionsIn the CCHS, leptin, but not adiponectin, was a significant independent predictor of new-onset hypertension.American Journal of Hypertension 2010; doi:10.1038/ajh.2009.244 [ABSTRACT FROM AUTHOR]

BackgroundLow-grade chronic inflammation has been proposed to play a major role in the pathogenesis of hypertension. Low-grade chronic inflammation is also closely associated with obesity, an established causative factor in the development of hypertension. The purpose of this study was to investigate the relationship between two markers of inflammation, C-reactive protein (CRP) and fibrinogen, and blood pressure (BP) and other hemodynamic variables in obese subjects.MethodsFrom a large cardiovascular study based in the general population, we selected subjects with a body mass index (BMI) ≥30 kg/m2, free of major cardiovascular diseases, not taking BP-lowering or lipid-lowering drugs (n = 487; women = 51.1%; median (5th to 95th percentile) age = 62 years (36–80)). The cardiovascular study included measurements of traditional and new risk factors, including ankle brachial BP index, a measure of subclinical atherosclerosis. CRP was determined by a high-sensitive assay.ResultsIn partial Spearman rank correlation analysis, adjusted for age and sex, we found no significant relationships between either CRP or fibrinogen and systolic BP, diastolic BP, pulse pressure, or ankle brachial index (ρ: −0.057 to 0.068; P > 0.13). However, fibrinogen and CRP were found to be significantly related to heart rate (ρ: 0.127–0.169; P < 0.01).ConclusionsIn this study of generally healthy obese subjects from the general population, we found no significant relationships between markers of inflammation and systolic BP or diastolic BP, showing that obese subjects with higher levels of inflammatory markers do not have higher BP levels than their obese counterparts with lower levels of inflammatory markers.American Journal of Hypertension 2009; doi:10.1038/ajh.2009.1American Journal of Hypertension (2009); 22, 4, 451–456. doi:10.1038/ajh.2009.1 [ABSTRACT FROM AUTHOR]

Background Risk prediction in elderly patients is increasingly relevant due to longer life expectancy. Objectives This study sought to examine whether electrocardiographic (ECG) changes provide prognostic information incremental to current risk models and to the conventional risk factors. Methods In all, 6,991 participants from the Copenhagen Heart Study attending an examination at age ≥65 years were included. ECG changes were defined as Q waves, ST-segment depression, T-wave changes, ventricular conduction defects, and left ventricular hypertrophy based on the Minnesota code. The primary endpoint was fatal cardiovascular disease (CVD) event and the secondary was fatal or nonfatal CVD event. In our study, 2,236 fatal CVD and 3,849 fatal or nonfatal CVD events occurred during a median of 11.9 and 9.8 years of follow-up. Results ECG changes were frequently present (30.6%) and associated with conventional risk factors. All ECG changes except 1 univariably predicted both endpoints. Event rates of ECG changes versus no ECG changes were respectively 41.4% versus 27.8% and 64.6% versus 50.8%. When added to existing risk scores, ECG changes independently increased the risk of both endpoints. Fatal CVD events: hazard ratio (HR): 1.33 (95% confidence interval [CI]: 1.29 to 1.36; p < 0.001) and fatal or nonfatal CVD events: HR: 1.21 (95% CI: 1.19 to 1.24; p < 0.001). When added to conventional risk factors, continuous net reclassification improvement was 42.3% (95% CI: 42.0 to 42.4; p < 0.001) for fatal and 29.2% (95% CI: 28.4 to 29.2; p < 0.001) for fatal or nonfatal events. Categorical net reclassification was 7.1% (95% CI: 6.7 to 9.0; p < 0.001) for fatal and 4.2% (95% CI: 3.5 to 5.6; p < 0.001) for fatal or nonfatal events. Conclusions Simple assessment of the existence of ECG changes improves risk prediction in the general population of persons age ≥65 years. [ABSTRACT FROM AUTHOR]

Abstract: Background: Low-grade inflammation is a marker for cardiovascular disease (CVD). The inflammatory biomarkers C-reactive protein (CRP) and soluble urokinase plasminogen activator receptor (suPAR) independently predict CVD. We tested the hypothesis that these biomarkers reflect different aspects of the inflammation associated with CVD. Methods: We studied 2273 subjects without CVD. Log-transformed CRP and suPAR were included in general linear and logistic regression models to compare associations with measures of anthropometry and subclinical organ damage (SOD). Owing to interactions on body mass index (BMI) (P<0.0001), the population was stratified by gender and smoking concerning anthropometry. Results: In both genders, independent of smoking, log-CRP was positively associated with BMI (β: 0.28 to 0.40, P<0.001) and waist circumference (WC) (β: 0.27 to 0.42, P<0.001). In contrast, in smoking women and men, log-suPAR was negatively associated with BMI and WC (β: −0.09 to −0.19, P<0.05). In non-smoking women, log-suPAR was positively associated with BMI and WC (β: 0.14 and 0.16, P<0.001), whereas no associations were found in non-smoking men. No interactions were found on SOD. Adjusted for age, sex, smoking, and physical activity, log-suPAR was associated with an increased urine albumin/creatinine ratio (standardized odds ratio (95% confidence interval (CI)) for highest vs. lower quartiles: 1.36 (1.21–1.52), whereas log-CRP was not (1.10 (0.99–1.22))), and extent of atherosclerosis (standardized proportional odds ratio (95% CI) for carotid plaques 0, 1≤ to ≤3, >3: 1.31 (1.16–1.47), whereas log-CRP was not (1.00 (0.89–1.11))). Conclusions: CRP is positively associated with anthropometric measures, whereas suPAR is linked to endothelial dysfunction and atherosclerosis. [Copyright &y& Elsevier]

Objective: To examine the assumption that postdeployment incidence of sickness and other absence from work are higher among Gulf War Veterans compared with nonveterans.Methods: A prospective registry study including a cohort of 721 Danish Gulf War Veterans and a control cohort of 3,629 nonveterans selected from the general Danish population. Outcome measures were up to 23 years postdeployment incidence of (1) long-term sickness absence and (2) long-term all types of absence from work. Long term with regard to sickness and other absence was defined as exceeding 8 weeks. The association between outcomes and information on deployment history was studied using time-to-event analysis. The index date was the return date from the last deployment to the Gulf. The follow-up period was the time from index date until April 27, 2014.Results: As the main finding, no difference was found between veterans and nonveterans in the incidence rate of long-term sickness absence. After an initial short period (3 months) with elevated incidence rate of long-term absence from work among veterans, there was no difference between the cohorts.Conclusion: Among Danish Gulf War Veterans, no postdeployment increased risk of long-term sickness absence or long-term absence from work was found as compared with nonveterans. [ABSTRACT FROM AUTHOR]

Background: A diagnosis of COPD is mainly considered in individuals with >10 pack-years of smoking. We tested the hypothesis that low smoking exposure, below the critical threshold of 10 pack-years, increases risk of COPD and leads to poor prognosis., Methods: We followed non-obstructed adult smokers from the Copenhagen City Heart Study for COPD, defined as a forced expiratory volume in 1 s (FEV 1 )/forced vital capacity <0.70 and FEV 1 <80% predicted, and for related clinical outcomes. First, we followed individuals for 5 years according to baseline smoking for risk of developing COPD, and thereafter for up to four decades for severe exacerbations and death., Results: In 6098 non-obstructed smokers, 1781 (29%) developed COPD after 5 years of follow-up: 23% of individuals with <10 pack-years of smoking at baseline, 26% of those with 10-19.9 pack-years, 30% of those with 20-39.9 pack-years and 39% of those with ≥40 pack-years. During four decades of follow-up, we recorded 620 exacerbations and 5573 deaths. Compared to individuals without COPD with <10 pack‑years of smoking, multivariable adjusted hazard ratios (HRs) for exacerbations were 1.94 (95% CI 1.36-2.76) in those without COPD and ≥10 pack-years, 2.83 (95% CI 1.72-4.66) in those with COPD and <10 pack-years, 4.34 (95% CI 2.93-6.43) in those with COPD and 10-19.9 pack-years, 4.39 (95% CI 2.98-6.46) in those with COPD and 20-39.9 pack-years and 4.98 (95% CI 3.11-7.97) in those with COPD and ≥40 pack-years. Corresponding HRs for all-cause mortality were 1.20 (95% CI 1.10-1.32), 1.31 (95% CI 1.13-1.53), 1.59 (95% CI 1.40-1.79), 1.81 (95% CI 1.62-2.03) and 1.81 (95% CI 1.55-2.10)., Conclusion: Low smoking exposure below the critical threshold of 10 pack-years increases risk of COPD in middle-aged adults within 5 years, and these individuals have increased risk of severe exacerbation and early death over four decades., Competing Interests: Conflict of interest: Y. Çolak reports grants from Sanofi; payment or honoraria for lectures, presentations, manuscript writing or educational events from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline and Sanofi; and support for attending meetings from Sanofi. A. Løkke reports grants from AstraZeneca, Boehringer Ingelheim, Chiesi and Sanofi; and payment or honoraria for lectures, presentations, manuscript writing or educational events from AstraZeneca, Boehringer Ingelheim, Chiesi, GlaxoSmithKline and Sanofi. P. Lange reports grants from AstraZeneca and Sanofi; consultancy fees from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline and Sanofi; and payment or honoraria for lectures, presentations, manuscript writing or educational events from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline and Sanofi. J. Vestbo reports consultancy fees from ALK, AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline and Teva; payment or honoraria for lectures, presentations, manuscript writing or educational events from AstraZeneca, Boehringer Ingelheim, Chiesi and GlaxoSmithKline; and participation on a data safety monitoring board or advisory board with AstraZeneca. J.L. Marott, B.G. Nordestgaard and S. Afzal have no potential conflicts of interest to disclose., (Copyright ©The authors 2024. For reproduction rights and permissions contact permissions@ersnet.org.)

Objective: The aim of this study was to estimate the association between self-reported perceived danger during deployment, measured as combat exposure or witnessing the consequences of war, and post-deployment suicide attempts among military personnel. Furthermore, the effect of post-deployment symptoms of posttraumatic stress disorder (PTSD) and/or depression on the risk of suicide attempts was also evaluated., Methods: This observational cohort study included Danish Army military personnel who returned from deployment in international missions from 1998 to 2016 and had completed a post-deployment questionnaire. Perceived exposure to danger was ascertained by self-report. Data on suicide attempt were retrieved from national registers. Adjusted Cox regression analyses were used to evaluate if military personnel indicating high level of combat exposure were more likely to have attempted suicides post-deployment than military personnel with lower levels of combat exposure., Results: Eighty-three suicide attempts were registered after homecoming among 12,218 military personnel. Perceived higher exposure to combat was associated with the risk of suicide attempt (hazard ratio = 1.08; 95% CI, 1.01-1.16). Furthermore, the association between combat exposure and suicide attempt was fully mediated by post-deployment symptoms of PTSD and/or depression. No association was found between witnessing consequences of war and the risk of post-deployment suicide attempt., Conclusions: This nationwide study found that combat exposure was associated with an increased risk of suicide attempt among military personnel. This association was, however, fully mediated by mental disorders (PTSD and/or depression). These findings suggest that better psychological follow-up of military personnel identified as having PTSD and/or depression may be warranted., (© Copyright 2021 Physicians Postgraduate Press, Inc.)