There is a paucity of global data on cardiovascular disease (CVD) prevalence in people with type 2 diabetes (T2D). The primary objective of the CAPTURE study was to estimate the prevalence of ...established CVD and its management in adults with T2D across 13 countries from five continents. Additional objectives were to further characterize the study sample regarding demographics, clinical parameters and medication usage, with particular reference to blood glucose-lowering agents (GLAs: glucagon-like peptide-1 receptor agonists and sodium-glucose co-transporter-2 inhibitors) with demonstrated cardiovascular benefit in randomized intervention trials.
Data were collected from adults with T2D managed in primary or specialist care in Australia, China, Japan, Czech Republic, France, Hungary, Italy, Argentina, Brazil, Mexico, Israel, Kingdom of Saudi Arabia, and Turkey in 2019, using standardized methodology. CVD prevalence, weighted by diabetes prevalence in each country, was estimated for the overall CAPTURE sample and participating countries. Country-specific odds ratios for CVD prevalence were further adjusted for relevant demographic and clinical parameters.
The overall CAPTURE sample included 9823 adults with T2D (n = 4502 from primary care; n = 5321 from specialist care). The overall CAPTURE sample had median (interquartile range) diabetes duration 10.7 years (5.6-17.9 years) and glycated hemoglobin 7.3% (6.6-8.4%) 56 mmol/mol (49-68 mmol/mol). Overall weighted CVD and atherosclerotic CVD prevalence estimates were 34.8% (95% confidence interval CI 32.7-36.8) and 31.8% (95% CI 29.7-33.8%), respectively. Age, gender, and clinical parameters accounted for some of the between-country variation in CVD prevalence. GLAs with demonstrated cardiovascular benefit were used by 21.9% of participants, which was similar in participants with and without CVD: 21.5% and 22.2%, respectively.
In 2019, approximately one in three adults with T2D in CAPTURE had diagnosed CVD. The low use of GLAs with demonstrated cardiovascular benefit even in participants with established CVD suggested that most were not managed according to contemporary diabetes and cardiology guidelines. Study registration NCT03786406 (registered on December 20, 2018), NCT03811288 (registered on January 18, 2019).
Perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) are used in a variety of consumer products and have been detected worldwide in human blood. Recent studies mainly of highly exposed ...populations have indicated that PFOA and PFOS may affect serum cholesterol levels, but the magnitude of the effect may be inconsistent across exposure levels. The aim of the present cross-sectional study was to investigate the association between plasma PFOA and PFOS and total cholesterol in a general, middle-aged Danish population. The study population comprised 753 individuals (663 men and 90 women), 50-65 years of age, nested within a Danish cohort of 57,053 participants. Blood samples were taken from all cohort members at enrolment (1993-1997) and stored in a biobank at -150°C. Plasma levels of PFOA and PFOS and serum levels of total cholesterol were measured. The associations between plasma PFOA and PFOS levels and total cholesterol levels were analysed by generalized linear models, both crude and adjusted for potential confounders. We observed statistically significant positive associations between both perfluorinated compounds and total cholesterol, e.g. a 4.4 95% CI = 1.1-7.8 higher concentration of total cholesterol (mg/dL) per interquartile range of PFOA plasma level. Sex and prevalent diabetes appeared to modify the association between PFOA and PFOS, respectively, and cholesterol. In conclusion, this study indicated positive associations between plasma PFOA and PFOS levels and total cholesterol in a middle-aged Danish population, although whether the observed pattern of results reflects a causal association is unclear.
Cadmium is a human lung carcinogen and possesses estrogen-like activity. This combination of carcinogenic and estrogenic activity makes cadmium a contaminant of high concern for hormone-related ...cancers. Diet and smoking are the main sources of cadmium exposure. The aim of this study was to investigate the association between dietary cadmium intake and risk of breast, endometrial and ovarian cancer in Danish postmenopausal woman.
We estimated dietary cadmium intake in the Diet, Cancer and Health cohort at enrolment 1993-97. The estimates were based on food frequency questionnaires and cadmium contents in all foods. Among 23,815 postmenopausal women we identified 1390 breast, 192 endometrial, and 146 ovarian cancer cases from enrolment through December 31, 2010 using the Danish Cancer Registry. Cox regression was used to analyse the association between dietary cadmium intake and cancer risk.
Mean dietary cadmium intake was 14 µg/day. Cadmium was not associated with breast cancer, incidence rate ratio (IRR) = 0.99, 95% confidence interval (CI): 0.87-1.13 per 10 µg higher dietary cadmium intake/day; endometrial cancer, IRR = 1.08, 95% CI: 0.76-1.53; or ovarian cancer, IRR = 1.15, 95% CI: 0.78-1.70. We found a positive association between cadmium and endometrial cancer for the women with BMI<25 (IRR = 1.50, 95% CI: 0.94-2.39), whereas an inverse association was seen for the women with BMI≥25 (IRR = 0.69, 95% CI: 0.42-1.12); p value for interaction = 0.02.
Our study does not indicate that our estimated dietary cadmium intake is associated with hormone-related cancers in women.
Cadmium is a known carcinogen that can disrupt endocrine signalling. Cigarette smoking and food are the most common routes of non-occupational exposure to cadmium. Cadmium accumulates in the kidney ...and can be measured in urine, making urine cadmium (U-Cd) a biomarker of long-term exposure. However dietary-cadmium (D-Cd) intake estimates are often used as surrogate indicator of cadmium exposure in non-smoking subjects. It is therefore important to investigate the concordance between D-Cd estimates obtained with Food Frequency Questionnaires and U-Cd.
U-Cd levels were compared with estimated dietary-cadmium (D-Cd) intake in 1764 post-menopausal women from the Danish Diet, Cancer and Health cohort. For each participant, a food frequency questionnaire, and measures of cadmium content in standard recipes were used to judge the daily intake of cadmium, normalized by daily caloric intake. Cadmium was measured by ICP-MS in spot urine sampled at baseline and normalized by urinary creatinine. Information on diet, socio-demographics and smoking were self-reported at baseline.
Linear regressions between U-Cd and D-Cd alone revealed minimal but significant positive correlation in never smokers (R2 = 0.0076, β = 1.5% increase per 1 ng Cd kcal(-1), p = 0.0085, n = 782), and negative correlation in current smokers (R2 = 0.0184, β = 7.1% decrease per 1 ng Cd kcal(-1) change, p = 0.0006, n = 584). In the full study population, most of the variability in U-Cd was explained by smoking status (R2 = 0.2450, n = 1764). A forward selection model revealed that the strongest predictors of U-Cd were age in never smokers (Δ R2 = 0.04), smoking duration in former smokers (Δ R2 = 0.06) and pack-years in current smokers (Δ R2 = 0.07). Food items that contributed to U-Cd were leafy vegetables and soy-based products, but explained very little of the variance in U-Cd.
Dietary-Cd intake estimated from food frequency questionnaires correlates only minimally with U-Cd biomarker, and its use as a Cd exposure indicator may be of limited utility in epidemiologic studies.
Tobacco smoke exposure increases the risk of cancer in the liver, but little is known about the possible risk associated with exposure to ambient air pollution.
We evaluated the association between ...residential exposure to air pollution and primary liver cancer incidence.
We obtained data from four cohorts with enrolment during 1985–2005 in Denmark, Austria and Italy. Exposure to nitrogen oxides (NO2 and NOX), particulate matter (PM) with diameter of less than 10µm (PM10), less than 2.5µm (PM2.5), between 2.5 and 10µm (PM2.5–10) and PM2.5 absorbance (soot) at baseline home addresses were estimated using land-use regression models from the ESCAPE project. We also investigated traffic density on the nearest road. We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and random-effects meta-analyses to estimate summary hazard ratios (HRs) and 95% confidence intervals (CIs).
Out of 174,770 included participants, 279 liver cancer cases were diagnosed during a mean follow-up of 17 years. In each cohort, HRs above one were observed for all exposures with exception of PM2.5 absorbance and traffic density. In the meta-analysis, all exposures were associated with elevated HRs, but none of the associations reached statistical significance. The summary HR associated with a 10-μg/m3 increase in NO2 was 1.10 (95% confidence interval (CI): 0.93, 1.30) and 1.34 (95% CI: 0.76, 2.35) for a 5-μg/m3 increase in PM2.5.
The results provide suggestive evidence that ambient air pollution may increase the risk of liver cancer. Confidence intervals for associations with NO2 and NOX were narrower than for the other exposures.
•Tobacco smoke increases liver cancer risk but risk of air pollution is less studied.•Residential exposure to ambient air pollution for 4 European cohorts was assessed.•Exposure to ambient air pollution at residence may increase the risk of liver cancer.
Exposure to traffic noise and air pollution have both been associated with cardiovascular disease, though the mechanisms behind are not yet clear.
We aimed to investigate whether the two exposures ...were associated with levels of cholesterol in a cross-sectional design.
In 1993–1997, 39,863 participants aged 50–64year and living in the Greater Copenhagen area were enrolled in a population-based cohort study. For each participant, non-fasting total cholesterol was determined in whole blood samples on the day of enrolment. Residential addresses 5-years preceding enrolment were identified in a national register and road traffic noise (Lden) were modeled for all addresses. For air pollution, nitrogen dioxide (NO2) was modeled at all addresses using a dispersion model and PM2.5 was modeled at all enrolment addresses using a land-use regression model. Analyses were done using linear regression with adjustment for potential confounders as well as mutual adjustment for the three exposures.
Baseline residential exposure to the interquartile range of road traffic noise, NO2 and PM2.5 was associated with a 0.58mg/dl (95% confidence interval: −0.09; 1.25), a 0.68mg/dl (0.22; 1.16) and a 0.78mg/dl (0.22; 1.34) higher level of total cholesterol in single pollutant models, respectively. In two pollutant models with adjustment for noise in air pollution models and vice versa, the association between air pollution and cholesterol remained for both air pollution variables (NO2: 0.72 (0.11; 1.34); PM2.5: 0.70 (0.12; 1.28) mg/dl), whereas there was no association for noise (−0.08mg/dl). In three-pollutant models (NO2, PM2.5 and road traffic noise), estimates for NO2 and PM2.5 were slightly diminished (NO2: 0.58 (−0.05; 1.22); PM2.5: 0.57 (−0.02; 1.17) mg/dl).
Air pollution and possibly also road traffic noise may be associated with slightly higher levels of cholesterol, though associations for the two exposures were difficult to separate.
•Traffic noise and air pollution are both associated with cardiovascular disease.•A potential mechanism includes raised levels of blood lipids.•Air pollution was associated with total cholesterol in a study of 36,039 elderly.•Noise was weakly associated with cholesterol before adjustment for air pollution.•It was difficult to separate effects of air pollution and noise in relation to cholesterol.
Few modifiable risk factors for prostate cancer are known. Recently, disruption of the circadian system has been proposed to affect risk, as it entails an inhibited melatonin production, and ...melatonin has demonstrated beneficial effects on cancer inhibition. This suggests a potential role of traffic noise in prostate cancer.
Road traffic and railway noise was calculated for all present and historical addresses from 1987-2010 for a cohort of 24,473 middle-aged, Danish men. During follow-up, 1,457 prostate cancer cases were identified. We used Cox Proportional Hazards Models to calculate the association between noise exposure and incident prostate cancer. Incidence Rate Ratios (IRR) were calculated as crude and adjusted for smoking status, education, socioeconomic position, BMI, waist circumference, physical activity, calendar year, and traffic noise from other sources than the one investigated.
There was no association between residential road traffic noise and risk of prostate cancer for any of the three exposure windows: 1, 5 or 10-year mean noise exposure before prostate cancer diagnosis. This result persisted when stratifying cases by aggressiveness. For railway noise, there was no association with overall prostate cancer. There was no statistically significant effect modification by age, education, smoking status, waist circumference or railway noise, on the association between road traffic noise and prostate cancer, although there seemed to be a suggestion of an association among never smokers (IRR: 1.16; 95% CI: 1.00-1.36).
The present study does not support an overall association between either railway or road traffic noise and overall prostate cancer.
Introduction
Insulin degludec/insulin aspart (IDegAsp) provides effective glycaemic control with an acceptable safety profile in Japanese patients with diabetes in randomised clinical trials. This ...post-marketing surveillance study assessed long-term safety and clinical outcomes with IDegAsp in a Japanese real-world setting.
Methods
Multicentre, prospective, observational, open-label, single-arm study of Japanese patients with diabetes requiring insulin therapy, who had switched to IDegAsp at their treating physician’s discretion in clinical practice. One year after initiating IDegAsp, incidence of adverse events (AEs primary endpoint), serious AEs, adverse drug reactions (ADRs), and severe hypoglycaemia (secondary safety endpoints) were assessed in the safety analysis set (SAS). Secondary effectiveness endpoints were change from baseline in glycated haemoglobin (HbA
1c
) and fasting plasma glucose (FPG) in the effectiveness analysis set (EAS).
Results
Overall, 1321 patients were included (SAS,
n
= 1321; EAS,
n
= 1285); 4.2% with type 1 diabetes, 95.2% with type 2 diabetes, 0.7% with other/unknown diabetes type. In total, 204 AEs were reported in 132 patients (10.0% of the SAS), at a rate 95% confidence interval (CI) of 16.2 events/100 patient-years of exposure (PYE) 14.0; 18.4. By preferred term, ‘hypoglycaemia’ was the most frequent AE (45 events in 31 patients 2.3%; rate 95% CI 3.6 events/100 PYE 2.5; 4.6). Serious AEs occurred in 4.2% of patients (rate 95% CI 5.7 events/100 PYE 4.4; 7.0), and ADRs in 3.1% (rate 95% CI 4.6 reactions/100 PYE 3.4; 5.8). Six events of severe hypoglycaemia were reported in five patients (0.4%; rate 95% CI 0.5 events/100 PYE 0.1; 0.9). Change from baseline to 1 year was − 0.51% and − 32.1 mg/dL for HbA
1c
and FPG, respectively (
P
< 0.0001 for both).
Conclusion
In Japanese patients with diabetes, initiation of IDegAsp in real-world clinical practice was well tolerated, with no new safety signals, and associated with improved glycaemic control after 1 year.
Trial Registration
ClinicalTrials.gov identifier, NCT02821052.
Objective
Obesity rates in the United Kingdom are some of the highest in Western Europe, with considerable clinical and societal impacts. Obesity is associated with type 2 diabetes (T2D), ...osteoarthritis, cardiovascular disease, and increased mortality; however, relatively few studies have examined the occurrence of multiple obesity‐related outcomes in the same patient population. This study was designed to examine the associations between body mass index (BMI) and a broad range of obesity‐related conditions in the same large cohort from a UK‐representative primary care database.
Methods
Demographic data and diagnosis codes were extracted from the Clinical Practice Research Datalink GOLD database in January 2019. Adults registered for ≥ 3 years were grouped by BMI, with BMI 18.5–24.9 kg/m2 as reference group. Associations between BMI and 12 obesity‐related outcomes were estimated using Cox proportional hazard models, adjusted for age, sex, and smoking.
Results
More than 2.9 million individuals were included in the analyses and were followed up for occurrence of relevant outcomes for a median of 11.4 years during the study period. Generally, there was a stepwise increase in risk of all outcomes with higher BMI. Individuals with BMI 40.0–45.0 kg/m2 were at particularly high risk of sleep apnea (hazard ratio 95% confidence interval vs. reference group: 19.8 18.9–20.8), T2D (12.4 12.1–12.7), heart failure (3.46 3.35–3.57), and hypertension (3.21 3.15–3.26).
Conclusions
This study substantiates evidence linking higher BMI to higher risk of a range of serious health conditions, in a large, representative UK cohort. By focusing on obesity‐related conditions, this demonstrates the wider clinical impact and the healthcare burden of obesity, and highlights the vital importance of management, treatment approaches, and public health programs to mitigate the impact of this disease.
Oxidative potential (OP) has been suggested as a health-relevant measure of air pollution. Little information is available about OP spatial variation and the possibility to model its spatial ...variability. Our aim was to measure the spatial variation of OP within and between 10 European study areas. The second aim was to develop land use regression (LUR) models to explain the measured spatial variation.
OP was determined with the dithiothreitol (DTT) assay in ten European study areas. DTT of PM2.5 was measured at 16–40 sites per study area, divided over street, urban and regional background sites. Three two-week samples were taken per site in a one-year period in three different seasons. We developed study-area specific LUR models and a LUR model for all study areas combined to explain the spatial variation of OP.
Significant contrasts between study areas in OP were found. OP DTT levels were highest in southern Europe. DTT levels at street sites were on average 1.10 times higher than at urban background locations.
In 5 of the 10 study areas LUR models could be developed with a median R2 of 33%. A combined study area model explained 30% of the measured spatial variability. Overall, LUR models did not explain spatial variation well, possibly due to low levels of OP DTT and a lack of specific predictor variables.
•Oxidative potential (OP DTT) was measured in 10 European study areas.•OP DTT levels were the highest in southern and the lowest in northern Europe.•In 5 of the 10 study areas LUR models could be developed for OP DTT.
PDF
