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Background Some, but not all, observational studies have suggested that taller stature is associated with a significant increased risk of glioma. In a pooled analysis of observational studies, we investigated the strength and consistency of this association, overall and for major sub-types, and investigated effect modification by genetic susceptibility to the disease.
Methods We standardized and combined individual-level data on 1354 cases and 4734 control subjects from 13 prospective and 2 case–control studies. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) for glioma and glioma sub-types were estimated using logistic regression models stratified by sex and adjusted for birth cohort and study. Pooled ORs were additionally estimated after stratifying the models according to seven recently identified glioma-related genetic variants.
Results Among men, we found a positive association between height and glioma risk (≥190 vs 170–174 cm, pooled OR = 1.70, 95% CI: 1.11–2.61; P-trend = 0.01), which was slightly stronger after restricting to cases with glioblastoma (pooled OR = 1.99, 95% CI: 1.17–3.38; P-trend = 0.02). Among women, these associations were less clear (≥175 vs 160–164 cm, pooled OR for glioma = 1.06, 95% CI: 0.70–1.62; P-trend = 0.22; pooled OR for glioblastoma = 1.36, 95% CI: 0.77–2.39; P-trend = 0.04). In general, we did not observe evidence of effect modification by glioma-related genotypes on the association between height and glioma risk.
Conclusion An association of taller adult stature with glioma, particularly for men and stronger for glioblastoma, should be investigated further to clarify the role of environmental and genetic determinants of height in the etiology of this disease.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/4/1075?rss=1
Background Refugee immigrants have poorer health than other immigrant groups but little is known about their mortality. A comparison of mortality among refugees and non-refugee immigrants is liable to exaggerate the former if the latter includes labour migrants, whose mortality risk may be lower than that of the general population. To avoid bias, labour migrants are not included in this study. The aim was to investigate mortality risks among refugees compared with non-labour non-refugee immigrants in Sweden.
Methods Population-based cohort design, starting 1 January 1998 and ending with death or censoring 31 December 2006. Persons included in the study were those aged 18–64 years, had received a residence permit in Sweden 1992–98 and were defined by the Swedish Board of Migration as either a refugee or a non-labour non-refugee immigrant. The outcomes were all-cause and cause-specific mortalities and the main exposure was being a refugee. Cox-regression models estimated hazard ratios (HRs) of mortality.
Results The study population totalled 86 395 persons, 49.3% women, 24.2 % refugees. Adjusted for age and origin, refugee men had an over-risk of cardiovascular mortality (HR = 1.58, 95% CI = 1.08–2.33). With socio-economic factors added to the model, refugee men still had an over-risk mortality in cardiovascular disease (HR = 1.53, 95% CI = 1.04–2.24) and external causes (HR = 1.59, 95% CI = 1.01–2.50).
Conclusion Refugee men in Sweden have a higher mortality risk in cardiovascular and external causes compared with male non-labour non-refugee immigrants. This study suggests that the refugee experience resembles other stressors in terms of the association with cardiovascular mortality.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/4/1153?rss=1
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Background Regular alcohol drinking contributes both favourably and adversely to health in the Western populations, but its effects on overall and cause-specific mortality in China are still poorly understood.
Methods A nationally representative prospective cohort study included 220 000 men aged 40–79 years from 45 areas in China in 1990–91, and >40 000 deaths occurred during 15 years of follow-up. Cox regression was used to relate alcohol drinking to overall and cause-specific mortality, adjusting for age, area, smoking and education.
Results Overall, 33% of the participants reported drinking alcohol regularly at baseline, consuming mainly distilled spirits, with an estimated mean amount consumed of 372 g/week (46.5 units per week). After excluding all men with prior disease at baseline and the first 3 years of follow-up, there was a 5% [95% confidence interval (CI) 2–8] excess risk of overall mortality among regular drinkers. Compared with non-drinkers, the adjusted hazard ratios among men who drank <140, 140–279, 280–419, 420–699 and ≥700 g/week were 0.97, 1.00, 1.02, 1.12 and 1.27, respectively (P < 0.0001 for trend). The strength of the relationship appeared to be greater in smokers than in non-smokers. There was a strong positive association of alcohol drinking with mortality from stroke, oesophageal cancer, liver cirrhosis or accidental causes, a weak J-shaped association with mortality from ischaemic heart disease, stomach cancer and lung cancer and no apparent relationship with respiratory disease mortality.
Conclusion Among Chinese men aged 40–79 years, regular alcohol drinking was associated with a small but definite excess risk of overall mortality, especially among smokers.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/4/1101?rss=1
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Background The extent to which adult height, a biomarker of the interplay of genetic endowment and early-life experiences, is related to risk of chronic diseases in adulthood is uncertain.
Methods We calculated hazard ratios (HRs) for height, assessed in increments of 6.5 cm, using individual–participant data on 174 374 deaths or major non-fatal vascular outcomes recorded among 1 085 949 people in 121 prospective studies.
Results For people born between 1900 and 1960, mean adult height increased 0.5–1 cm with each successive decade of birth. After adjustment for age, sex, smoking and year of birth, HRs per 6.5 cm greater height were 0.97 (95% confidence interval: 0.96–0.99) for death from any cause, 0.94 (0.93–0.96) for death from vascular causes, 1.04 (1.03–1.06) for death from cancer and 0.92 (0.90–0.94) for death from other causes. Height was negatively associated with death from coronary disease, stroke subtypes, heart failure, stomach and oral cancers, chronic obstructive pulmonary disease, mental disorders, liver disease and external causes. In contrast, height was positively associated with death from ruptured aortic aneurysm, pulmonary embolism, melanoma and cancers of the pancreas, endocrine and nervous systems, ovary, breast, prostate, colorectum, blood and lung. HRs per 6.5 cm greater height ranged from 1.26 (1.12–1.42) for risk of melanoma death to 0.84 (0.80–0.89) for risk of death from chronic obstructive pulmonary disease. HRs were not appreciably altered after further adjustment for adiposity, blood pressure, lipids, inflammation biomarkers, diabetes mellitus, alcohol consumption or socio-economic indicators.
Conclusion Adult height has directionally opposing relationships with risk of death from several different major causes of chronic diseases.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/5/1419?rss=1
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Background We examined associations between socio-economic status (SES) indicators and cardiovascular disease (CVD) risk factors among urban and rural South Indians.
Methods Data from a population-based birth cohort of 2218 men and women aged 26–32 years from Vellore, Tamilnadu were used. SES indicators included a household possessions score, attained education and paternal education. CVD risk factors included obesity, hypertension, impaired glucose tolerance or diabetes, plasma total cholesterol to high density lipoprotein (HDL) ratio and triglyceride levels and consumption of tobacco and alcohol. Multiple logistic regression analysis was used to assess associations between SES indicators and risk factors.
Results Most risk factors were positively associated with possessions score in urban and rural men and women, except for tobacco use, which was negatively associated. Trends were similar with the participants’ own education and paternal education, though weaker and less consistent. In a concurrent analysis of all the three SES indicators, adjusted for gender and urban/rural residence, independent associations were observed only for the possessions score. Compared with those in the lowest fifth of the score, participants in the highest fifth had a higher risk of abdominal obesity [odds ratio (OR) = 6.4, 95% CI 3.4–11.6], high total cholesterol to HDL ratio (OR = 2.4, 95% CI 1.6–3.5) and glucose intolerance (OR = 2.8, 95% CI 1.9–4.1). Their tobacco use (OR = 0.4, 95% CI 0.2–0.6) was lower. Except for hypertension and glucose intolerance, risk factors were higher in urban than rural participants independently of SES.
Conclusion In this young cohort of rural and urban south Indians, higher SES was associated with a more adverse CVD risk factor profile but lower tobacco use.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/5/1315?rss=1
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The Nanoro Health and Demographic Surveillance System (HDSS), located in the rural centre of Burkina Faso, was established in 2009 by the Clinical Research Unit of Nanoro with the aim of providing a core framework for clinical trials and also to support the Burkina Faso health authorities in generating epidemiological data that can contribute to the setup and assessment of health interventions. In the baseline of initial census, 54 781 individuals were recorded of whom 56.1% are female. After the initial census, vital events such as pregnancies, births, migrations and deaths have been monitored, and data on individuals and household characteristics are updated during regular 4-monthly household visits. The available data are categorized into demographic, cultural, socio-economic and health information, and are used for monitoring and evaluation of population development issues. As a young site, our objective has been to strengthen our skills and knowledge and share new scientific experiences with INDEPTH and HDSS sites in Burkina Faso. In addition, all data produced by the Nanoro HDSS will be made publicly available through the INDEPTH data sharing system.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/5/1293?rss=1
Background The South-East Asia region (SEAR) accounts for one-quarter of the world's population, 40% of the global poor and ~30% of the global disease burden, with a disproportionately large share of tuberculosis (35%), injuries (30%), maternal (33%) and <5-year-old mortality (30%). In this article, we describe the disease burden and status of epidemiological research and capacity in the SEAR to understand, analyse and develop capacity in response to the diverse burdens of diseases in the region.
Methods Data on morbidity, mortality, risk factors, social determinants, research capacity, health education, workforce and systems in the SEAR were obtained using global data on burden of disease, peer-reviewed journals, World Health Organization (WHO) technical and advisory reports, and where available, validated country reports and key informants from the region.
Results SEAR countries are afflicted with a triple burden of disease—infectious diseases, non-communicable diseases and injuries. Of the seven WHO regions, SEAR countries account for the highest proportion of global mortality (26%) and due to relatively younger ages at death, the second highest percentage of total years of life lost (30%). The SEAR exceeds the global average annual mortality rate for all three broad cause groupings—communicable, maternal, perinatal and nutritional conditions (334 vs 230 per 100 000); non-communicable diseases (676 vs 573 per 100 000); and injuries (101 vs 78 per 100 000). Poverty, education and other social determinants of health are strongly linked to inequities in health among SEAR countries and within socio-economic subgroups. India, Thailand and Bangladesh produce two-thirds of epidemiology publications in the region. Significant efforts to increase health workforce capacity, research and training have been undertaken in the region, yet considerable heterogeneity in resources and capacity remains.
Conclusions Health systems, statistics and surveillance programmes must respond to the demographic, economic and epidemiological transitions that define the current disease burden and risk profile of SEAR populations. Inequities in health must be critically analysed, documented and addressed through multi-sectoral approaches. There is a critical need to improve public health intelligence by building epidemiological capacity in the region.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/3/847?rss=1
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The KEMRI/Centers for Disease Control and Prevention (CDC) Health and Demographic Surveillance System (HDSS) is located in Rarieda, Siaya and Gem Districts (Siaya County), lying northeast of Lake Victoria in Nyanza Province, western Kenya. The KEMRI/CDC HDSS, with approximately 220 000 inhabitants, has been the foundation for a variety of studies, including evaluations of insecticide-treated bed nets, burden of diarrhoeal disease and tuberculosis, malaria parasitaemia and anaemia, treatment strategies and immunological correlates of malaria infection, and numerous HIV, tuberculosis, malaria and diarrhoeal disease treatment and vaccine efficacy and effectiveness trials for more than a decade. Current studies include operations research to measure the uptake and effectiveness of the programmatic implementation of integrated malaria control strategies, HIV services, newly introduced vaccines and clinical trials. The HDSS provides general demographic and health information (such as population age structure and density, fertility rates, birth and death rates, in- and out-migrations, patterns of health care access and utilization and the local economics of health care) as well as disease- or intervention-specific information. The HDSS also collects verbal autopsy information on all deaths. Studies take advantage of the sampling frame inherent in the HDSS, whether at individual, household/compound or neighbourhood level.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/4/977?rss=1
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Source: http://www.nejm.org/doi/full/10.1056/NEJMc1212355?ai=rv&af=R&rss=currentIssue
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Background In studies of all-cause mortality, the fundamental epidemiological concepts of rate and risk are connected through a well-defined one-to-one relation. An important consequence of this relation is that regression models such as the proportional hazards model that are defined through the hazard (the rate) immediately dictate how the covariates relate to the survival function (the risk).
Methods This introductory paper reviews the concepts of rate and risk and their one-to-one relation in all-cause mortality studies and introduces the analogous concepts of rate and risk in the context of competing risks, the cause-specific hazard and the cause-specific cumulative incidence function.
Results The key feature of competing risks is that the one-to-one correspondence between cause-specific hazard and cumulative incidence, between rate and risk, is lost. This fact has two important implications. First, the naïve Kaplan–Meier that takes the competing events as censored observations, is biased. Secondly, the way in which covariates are associated with the cause-specific hazards may not coincide with the way these covariates are associated with the cumulative incidence. An example with relapse and non-relapse mortality as competing risks in a stem cell transplantation study is used for illustration.
Conclusion The two implications of the loss of one-to-one correspondence between cause-specific hazard and cumulative incidence should be kept in mind when deciding on how to make inference in a competing risks situation.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/3/861?rss=1
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Background Current physical activity guidelines imply that, by comparison with moderate physical activity (MPA), the benefits of engaging in vigorous physical activity (VPA) are attributed to the greater energy expenditure dose per unit of time and do not relate to intensity per se. The purpose of this study was to determine whether VPA influences the metabolic syndrome (MetS) independent of its influence on the energy expenditure dose of moderate-to-vigorous physical activity (MVPA).
Methods Participants consisted of 1841 adults from the 2003–06 National Health and Nutrition Examination Survey, a representative cross-sectional study. MPA and VPA were measured objectively over 7 days using Actigraph accelerometers. MetS was determined using an established clinical definition. Associations between physical activity and the MetS were determined using logistic regression and controlled for relevant covariates.
Results Analyses revealed that VPA remained a meaningful predictor of the MetS after controlling for the total energy expenditure dose of MVPA such that the relative odds of the MetS was 0.28 (95% confidence interval 0.17–0.46) in the group with the highest VPA compared with the group with no VPA. VPA had a greater influence on the MetS than an equivalent energy expenditure dose of MPA. For instance, between 0 and 500 MET min/week of MPA the adjusted prevalence of the MetS decreased by 15.5%, whereas between 0 and 500 MET min/week of VPA the prevalence decreased by 37.1%.
Conclusion These cross-sectional findings suggest that VPA per se has an important role in cardiometabolic disease prevention.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/4/1132?rss=1
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Background Previous studies on the association between childhood infections and childhood leukaemia have produced inconsistent results, likely due to the recall error/bias of infection data reported by the parents. The current study used a population-based and record-based case–control design to evaluate the association between childhood leukaemia and infections using the National Health Insurance Research Database of Taiwan.
Methods In all, 846 childhood acute lymphoblastic leukaemia (ALL) and 193 acute myeloid leukaemia (AML) patients newly diagnosed between 2000 and 2008, aged >1 and <10 years, were included. Up to four controls (3374 for ALL and 766 for AML) individually matched to each case on sex, birth date and time of diagnosis (reference date for the controls) were identified. Conditional logistic regression was performed to assess the association between childhood leukaemia and infections.
Results Having any infection before 1 year of age was associated with an increased risk for both childhood ALL (odds ratio = 3.2, 95% confidence interval 2.2–4.7) and AML (odds ratio = 6.0, 95% confidence interval 2.0–17.8), with a stronger risk associated with more episodes of infections. Similar results were observed for infections occurring >1 year before the cases’ diagnosis of childhood leukaemia.
Conclusions Children with leukaemia may have a dysregulated immune function present at an early age, resulting in more episodes of symptomatic infections compared with healthy controls. However, confounding by other infectious measures such as birth order and day care attendance could not be ruled out. Finally, the results are only relevant to the medically diagnosed infections.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/4/1050?rss=1
Background Both genetic and environmental factors contribute to triglyceride, low-density lipoprotein-cholesterol (LDL-C), and high-density lipoprotein-cholesterol (HDL-C) levels. Although genome-wide association studies are currently testing the genetic factors systematically, testing and reporting one or a few factors at a time can lead to fragmented literature for environmental chemical factors. We screened for correlation between environmental factors and lipid levels, utilizing four independent surveys with information on 188 environmental factors from the Centers of Disease Control, National Health and Nutrition Examination Survey, collected between 1999 and 2006.
Methods We used linear regression to correlate each environmental chemical factor to triglycerides, LDL-C and HDL-C adjusting for age, age2, sex, ethnicity, socio-economic status and body mass index. Final estimates were adjusted for waist circumference, diabetes status, blood pressure and survey. Multiple comparisons were controlled for by estimating the false discovery rate and significant findings were tentatively validated in an independent survey.
Results We identified and validated 29, 9 and 17 environmental factors correlated with triglycerides, LDL-C and HDL-C levels, respectively. Findings include hydrocarbons and nicotine associated with lower HDL-C and vitamin E (-tocopherol) associated with unfavourable lipid levels. Higher triglycerides and lower HDL-C were correlated with higher levels of fat-soluble contaminants (e.g. polychlorinated biphenyls and dibenzofurans). Nutrients and vitamin markers (e.g. vitamins B, D and carotenes), were associated with favourable triglyceride and HDL-C levels.
Conclusions Our systematic association study has enabled us to postulate about broad environmental correlation to lipid levels. Although subject to confounding and reverse causality bias, these findings merit evaluation in additional cohorts.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/3/828?rss=1
Proteases play a decisive role in health and disease. They fulfil diverse functions and have been associated with the pathology of gastrointestinal disorders such as inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). The current knowledge focuses on host-derived proteases including matrix metalloproteinases, various serine proteases and cathepsins. The possible contribution of bacterial proteases has been largely ignored in the pathogenesis of IBD and IBS, although there is increasing evidence, especially demonstrated for proteases from pathogenic bacteria. The underlying mechanisms extend to proteases from commensal bacteria which may be relevant for disease susceptibility. The intestinal microbiota and its proteolytic capacity exhibit the potential to contribute to the pathogenesis of IBD and IBS. This review highlights the relevance of host- and bacteria-derived proteases and their signalling mechanisms.
Source: http://pmj.bmj.com/cgi/content/short/89/1047/25?rss=1
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Background The South-East Asia region (SEAR) accounts for one-quarter of the world's population, 40% of the global poor and ~30% of the global disease burden, with a disproportionately large share of tuberculosis (35%), injuries (30%), maternal (33%) and <5-year-old mortality (30%). In this article, we describe the disease burden and status of epidemiological research and capacity in the SEAR to understand, analyse and develop capacity in response to the diverse burdens of diseases in the region.
Methods Data on morbidity, mortality, risk factors, social determinants, research capacity, health education, workforce and systems in the SEAR were obtained using global data on burden of disease, peer-reviewed journals, World Health Organization (WHO) technical and advisory reports, and where available, validated country reports and key informants from the region.
Results SEAR countries are afflicted with a triple burden of disease—infectious diseases, non-communicable diseases and injuries. Of the seven WHO regions, SEAR countries account for the highest proportion of global mortality (26%) and due to relatively younger ages at death, the second highest percentage of total years of life lost (30%). The SEAR exceeds the global average annual mortality rate for all three broad cause groupings—communicable, maternal, perinatal and nutritional conditions (334 vs 230 per 100 000); non-communicable diseases (676 vs 573 per 100 000); and injuries (101 vs 78 per 100 000). Poverty, education and other social determinants of health are strongly linked to inequities in health among SEAR countries and within socio-economic subgroups. India, Thailand and Bangladesh produce two-thirds of epidemiology publications in the region. Significant efforts to increase health workforce capacity, research and training have been undertaken in the region, yet considerable heterogeneity in resources and capacity remains.
Conclusions Health systems, statistics and surveillance programmes must respond to the demographic, economic and epidemiological transitions that define the current disease burden and risk profile of SEAR populations. Inequities in health must be critically analysed, documented and addressed through multi-sectoral approaches. There is a critical need to improve public health intelligence by building epidemiological capacity in the region.
Source: http://ije.oxfordjournals.org/cgi/content/short/41/3/847?rss=1
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Source: http://www.nejm.org/doi/full/10.1056/NEJMp1212347?ai=rv&af=R&rss=currentIssue
