Estimating the burden of disease attributable to high cholesterol in South Africa in 2000

Objectives To estimate the burden of disease attributable to high cholesterol in adults aged 30 years and older in South Africa in 2000. Design World Health Organization comparative risk assessment (CRA) methodology was followed. Small community studies were used to derive the prevalence by population group. Population-attributable fractions were calculated and applied to revised burden of disease estimates for the relevant disease categories for each population group. The total attributable burden for South Africa in 2000 was obtained by adding the burden attributed to high cholesterol for the four population groups. Monte Carlo simulation-modelling techniques were used for uncertainty analysis. Setting South Africa. Subjects Black African, coloured, white and Indian adults aged 30 years and older. Outcome measures Mortality and disability-adjusted life years (DALYs) from ischaemic heart disease (IHD) and ischaemic stroke. Results Overall, about 59% of IHD and 29% of ischaemic stroke burden in adult males and females (30+ years) were attributable to high cholesterol (≥ 3.8 mmol/l), with marked variation by population group. High cholesterol was estimated to have caused 24 144 deaths (95% uncertainty interval 22 404 - 25 286) or 4.6% (95% uncertainty interval 4.3 - 4.9%) of all deaths in South Africa in 2000. Since most cholesterol-related cardiovascular disease events occurred in middle or old age, the loss of life years comprised a smaller proportion of the total: 222 923 DALYs (95% uncertainty interval 206 712 - 233 460) or 1.4% of all DALYs (95% uncertainty interval 1.3 - 1.4%) in South Africa in 2000. Conclusions High cholesterol is an important cardiovascular risk factor in all population groups in South Africa.

Estimating the burden of disease attributable to urban outdoor air pollution in South Africa in 2000

Objectives To quantify the mortality burden attributed to urban outdoor air pollution in South Africa in 2000. Design The study followed comparative risk assessment (CRA) methodology developed by the World Heath Organization (WHO). In most urban areas, annual mean concentrations of particulate matter (PM) with diameters less than 10 μum (PM10) from monitoring network data and PM with diameters less than 2.5 μm (PM2.5) derived using a ratio method were weighted according to population size. PM10 and PM2.5 data from air-quality assessment studies in areas not covered by the network were also included. Population-attributable fractions calculated using risk coefficients presented in the WHO study were weighted by the proportion of the total population (33%) in urban environments, and applied to revised estimates of deaths and years of life lost (YLLs) for South Africa in 2000. Setting South Africa. Subjects Children under 5 years and adults 30 years and older. Outcome measures Mortality and YLLs from lung cancer and cardiopulmonary disease in adults (30 years and older), and from acute respiratory infections (ARIs) in children aged 0 - 4 years. Results Outdoor air pollution in urban areas in South Africa was estimated to cause 3.7% of the national mortality from cardiopulmonary disease and 5.1% of mortality attributable to cancers of the trachea, bronchus and lung in adults aged 30 years and older, and 1.1% of mortality from ARIs in children under 5 years of age. This amounts to 4 637 or 0.9% (95% uncertainty interval 0.3 - 1.5%) of all deaths and about 42 000 YLLs, or 0.4% (95% uncertainty interval 0.1 - 0.7%) of all YLLs in persons in South Africa in 2000. Conclusion Urban air pollution has under-recognised public health impacts in South Africa. Fossil fuel combustion emissions and traffic-related air pollution remain key targets for public health in South Africa.

Estimating the burden of disease attributable to high blood pressure in South Africa in 2000

Objectives To estimate the burden of disease attributable to high blood pressure (BP) in adults aged 30 years and older in South Africa in 2000. Design World Health Organization comparative risk assessment (CRA) methodology was followed. Mean systolic BP (SBP) estimates by age and sex were obtained from the 1998 South African Demographic and Health Survey adult data. Population-attributable fractions were calculated and applied to revised burden of disease estimates for the relevant disease categories for South Africa in 2000. Monte Carlo simulation modelling techniques were used for uncertainty analysis. Setting South Africa Subjects Adults aged 30 years and older. Outcome measures Mortality and disability-adjusted life years (DALYs) from ischaemic heart disease (IHD), stroke, hypertensive disease and other cardiovascular disease (CVD). Results High BP was estimated to have caused 46 888 deaths (95% uncertainty interval 44 878 - 48 566) or 9% (95% uncertainty interval 8.6 - 9.3%) of all deaths in South Africa in 2000, and 390 860 DALYs (95% uncertainty interval 377 955 - 402 256) or 2.4% of all DALYs (95% uncertainty interval 2.3 - 2.5%) in South Africa in 2000. Overall, 50% of stroke, 42% of IHD, 72% of hypertensive disease and 22% of other CVD burden in adult males and females (30+ years) were attributable to high BP (systolic BP ≥ 115 mmHg). Conclusions High BP contributes to a considerable burden of CVD in South Africa and results indicate that there is considerable potential for health gain from implementing BP-lowering interventions that are known to be highly costeffective.

Estimating the burden of disease attributable to lead exposure in South Africa in 2000

Objectives To estimate the burden of disease attributable to lead exposure in South Africa in 2000. Design World Health Organization comparative risk assessment (CRA) methodology was followed. Recent community studies were used to derive mean blood lead concentrations in adults and children in urban and rural areas. Population-attributable fractions were calculated and applied to revised burden of disease estimates for the relevant disease categories for South Africa in the year 2000. Monte Carlo simulation-modelling techniques were used for the uncertainty analysis. Setting South Africa. Subjects Children under 5 and adults 30 years and older. Outcome measures Cardiovascular mortality and disability-adjusted life years (DALYs) in adults 30 years and older and mild mental disability DALYs in children under 5 years. Results Lead exposure was estimated to cause 1 428 deaths (95% uncertainty interval 1 086-1 772) or 0.27% (95% uncertainty interval: 0.21 - 0.34%) of all deaths in South Africa in 2000. Burden of disease attributed to lead exposure was dominated by mild mental disability in young children, accounting for 75% of the total 58 939 (95% uncertainty interval 55 413 - 62 500) attributable DALYs. Cardiovascular disease in adults accounted for the remainder of the burden. Conclusions Even with the phasing out of leaded petrol, exposure to lead from its ongoing addition to paint, paraoccupational exposure and its use in backyard 'cottage industries' will continue to be an important public health hazard in South Africa for decades. Young children, especially those from disadvantaged communities, remain particularly vulnerable to lead exposure and poisoning.

Interpersonal violence : an important risk factor for disease and injury in South Africa

Background Burden of disease estimates for South Africa have highlighted the particularly high rates of injuries related to interpersonal violence compared with other regions of the world, but these figures tell only part of the story. In addition to direct physical injury, violence survivors are at an increased risk of a wide range of psychological and behavioral problems. This study aimed to comprehensively quantify the excess disease burden attributable to exposure to interpersonal violence as a risk factor for disease and injury in South Africa. Methods The World Health Organization framework of interpersonal violence was adapted. Physical injury mortality and disability were categorically attributed to interpersonal violence. In addition, exposure to child sexual abuse and intimate partner violence, subcategories of interpersonal violence, were treated as risk factors for disease and injury using counterfactual estimation and comparative risk assessment methods. Adjustments were made to account for the combined exposure state of having experienced both child sexual abuse and intimate partner violence. Results Of the 17 risk factors included in the South African Comparative Risk Assessment study, interpersonal violence was the second leading cause of healthy years of life lost, after unsafe sex, accounting for 1.7 million disability-adjusted life years (DALYs) or 10.5% of all DALYs (95% uncertainty interval: 8.5%-12.5%) in 2000. In women, intimate partner violence accounted for 50% and child sexual abuse for 32% of the total attributable DALYs. Conclusions The implications of our findings are that estimates that include only the direct injury burden seriously underrepresent the full health impact of interpersonal violence. Violence is an important direct and indirect cause of health loss and should be recognized as a priority health problem as well as a human rights and social issue. This study highlights the difficulties in measuring the disease burden from interpersonal violence as a risk factor and the need to improve the epidemiological data on the prevalence and risks for the different forms of interpersonal violence to complete the picture. Given the extent of the burden, it is essential that innovative research be supported to identify social policy and other interventions that address both the individual and societal aspects of violence.

Mortality attributable to smoking in Vietnamese men in 2008

Objective Smoking prevalence among Vietnamese men is among the highest in the world. Our aim was to provide estimates of tobacco attributable mortality to support tobacco control policies. Method We used the Peto–Lopez method using lung cancer mortality to derive a Smoking Impact Ratio (SIR) as a marker of cumulative exposure to smoking. SIRs were applied to relative risks from the Cancer Prevention Study, Phase II. Prevalence-based and hybrid methods, using the SIR for cancers and chronic obstructive pulmonary disease and smoking prevalence for all other outcomes, were used in sensitivity analyses. Results When lung cancer was used to measure cumulative smoking exposure, 28% (95% uncertainty interval 24–31%) of all adult male deaths (> 35 years) in Vietnam in 2008 were attributable to smoking. Lower estimates resulted from prevalence-based methods [24% (95% uncertainty interval 21–26%)] with the hybrid method yielding intermediate estimates [26% (95% uncertainty interval 23–28%)]. Conclusion Despite uncertainty in these estimates of attributable mortality, tobacco smoking is already a major risk factor for death in Vietnamese men. Given the high current prevalence of smoking, this has important implications not only for preventing the uptake of tobacco but also for immediate action to adopt and enforce stronger tobacco control measures.

Global, regional, and national age–sex specifi c all-cause and cause-specifi c mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013

Background Up-to-date evidence on levels and trends for age-sex-specific all-cause and cause-specific mortality is essential for the formation of global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013) we estimated yearly deaths for 188 countries between 1990, and 2013. We used the results to assess whether there is epidemiological convergence across countries. Methods We estimated age-sex-specific all-cause mortality using the GBD 2010 methods with some refinements to improve accuracy applied to an updated database of vital registration, survey, and census data. We generally estimated cause of death as in the GBD 2010. Key improvements included the addition of more recent vital registration data for 72 countries, an updated verbal autopsy literature review, two new and detailed data systems for China, and more detail for Mexico, UK, Turkey, and Russia. We improved statistical models for garbage code redistribution. We used six different modelling strategies across the 240 causes; cause of death ensemble modelling (CODEm) was the dominant strategy for causes with sufficient information. Trends for Alzheimer's disease and other dementias were informed by meta-regression of prevalence studies. For pathogen-specific causes of diarrhoea and lower respiratory infections we used a counterfactual approach. We computed two measures of convergence (inequality) across countries: the average relative difference across all pairs of countries (Gini coefficient) and the average absolute difference across countries. To summarise broad findings, we used multiple decrement life-tables to decompose probabilities of death from birth to exact age 15 years, from exact age 15 years to exact age 50 years, and from exact age 50 years to exact age 75 years, and life expectancy at birth into major causes. For all quantities reported, we computed 95% uncertainty intervals (UIs). We constrained cause-specific fractions within each age-sex-country-year group to sum to all-cause mortality based on draws from the uncertainty distributions. Findings Global life expectancy for both sexes increased from 65·3 years (UI 65·0–65·6) in 1990, to 71·5 years (UI 71·0–71·9) in 2013, while the number of deaths increased from 47·5 million (UI 46·8–48·2) to 54·9 million (UI 53·6–56·3) over the same interval. Global progress masked variation by age and sex: for children, average absolute differences between countries decreased but relative differences increased. For women aged 25–39 years and older than 75 years and for men aged 20–49 years and 65 years and older, both absolute and relative differences increased. Decomposition of global and regional life expectancy showed the prominent role of reductions in age-standardised death rates for cardiovascular diseases and cancers in high-income regions, and reductions in child deaths from diarrhoea, lower respiratory infections, and neonatal causes in low-income regions. HIV/AIDS reduced life expectancy in southern sub-Saharan Africa. For most communicable causes of death both numbers of deaths and age-standardised death rates fell whereas for most non-communicable causes, demographic shifts have increased numbers of deaths but decreased age-standardised death rates. Global deaths from injury increased by 10·7%, from 4·3 million deaths in 1990 to 4·8 million in 2013; but age-standardised rates declined over the same period by 21%. For some causes of more than 100 000 deaths per year in 2013, age-standardised death rates increased between 1990 and 2013, including HIV/AIDS, pancreatic cancer, atrial fibrillation and flutter, drug use disorders, diabetes, chronic kidney disease, and sickle-cell anaemias. Diarrhoeal diseases, lower respiratory infections, neonatal causes, and malaria are still in the top five causes of death in children younger than 5 years. The most important pathogens are rotavirus for diarrhoea and pneumococcus for lower respiratory infections. Country-specific probabilities of death over three phases of life were substantially varied between and within regions. Interpretation For most countries, the general pattern of reductions in age-sex specific mortality has been associated with a progressive shift towards a larger share of the remaining deaths caused by non-communicable disease and injuries. Assessing epidemiological convergence across countries depends on whether an absolute or relative measure of inequality is used. Nevertheless, age-standardised death rates for seven substantial causes are increasing, suggesting the potential for reversals in some countries. Important gaps exist in the empirical data for cause of death estimates for some countries; for example, no national data for India are available for the past decade.

Class participation as a learning and assessment strategy in law : facilitating students’ engagement, skills development and deep learning

Assessment has widely been described as being ‘at the centre of the student experience’. It would be difficult to conceive of the modern teaching university without it. Assessment is accepted as one of the most important tools that an educator can deploy to influence both what and how students learn. Evidence suggests that how students allocate time and effort to tasks and to developing an understanding of the syllabus is affected by the method of assessment utilised and the weighting it is given. This is particularly significant in law schools where law students may be more preoccupied with achieving high grades in all courses than their counterparts from other disciplines. However, well-designed assessment can be seen as more than this. It can be a vehicle for encouraging students to learn and engage more broadly than with the minimums required to complete the assessment activity. In that sense assessment need not merely ‘drive’ learning, but can instead act as a catalyst for further learning beyond what a student had anticipated. In this article we reconsider the potential roles and benefits in legal education of a form of interactive classroom learning we term assessable class participation (‘ACP’), both as part of a pedagogy grounded in assessment and learning theory, and as a platform for developing broader autonomous approaches to learning amongst students. We also consider some of the barriers students can face in ACP and the ways in which teacher approaches to ACP can positively affect the socio-emotional climates in classrooms and thus reduce those barriers. We argue that the way in which a teacher facilitates ACP is critical to the ability to develop positive emotional and learning outcomes for law students, and for teachers themselves.

Latent class analysis reveals distinct subgroups of patients based on symptom occurrence and demographic and clinical characteristics

Context Cancer patients experience a broad range of physical and psychological symptoms as a result of their disease and its treatment. On average, these patients report ten unrelieved and co-occurring symptoms. Objectives To determine if subgroups of oncology outpatients receiving active treatment (n=582) could be identified based on their distinct experience with thirteen commonly occurring symptoms; to determine whether these subgroups differed on select demographic, and clinical characteristics; and to determine if these subgroups differed on quality of life (QOL) outcomes. Methods Demographic, clinical, and symptom data from one Australian and two U.S. studies were combined. Latent class analysis (LCA) was used to identify patient subgroups with distinct symptom experiences based on self-report data on symptom occurrence using the Memorial Symptom Assessment Scale (MSAS). Results Four distinct latent classes were identified (i.e., All Low (28.0%), Moderate Physical and Lower Psych (26.3%), Moderate Physical and Higher Psych (25.4%), All High (20.3%)). Age, gender, education, cancer diagnosis, and presence of metastatic disease differentiated among the latent classes. Patients in the All High class had the worst QOL scores. Conclusion Findings from this study confirm the large amount of interindividual variability in the symptom experience of oncology patients. The identification of demographic and clinical characteristics that place patients are risk for a higher symptom burden can be used to guide more aggressive and individualized symptom management interventions.

Tracking control of a class of Hamiltonian mechanical systems with disturbances

This paper presents a trajectory-tracking control strategy for a class of mechanical systems in Hamiltonian form. The class is characterised by a simplectic interconnection arising from the use of generalised coordinates and full actuation. The tracking error dynamic is modelled as a port-Hamiltonian Systems (PHS). The control action is designed to take the error dynamics into a desired closed-loop PHS characterised by a constant mass matrix and a potential energy with a minimum at the origin. A transformation of the momentum and a feedback control is exploited to obtain a constant generalised mass matrix in closed loop. The stability of the close-loop system is shown using the close-loop Hamiltonian as a Lyapunov function. The paper also considers the addition of integral action to design a robust controller that ensures tracking in spite of disturbances. As a case study, the proposed control design methodology is applied to a fully actuated robotic manipulator.

The effect of HLA-DR genes on susceptibility to and severity of ankylosing spondylitis

Objective. To analyze the effect of HLA-DR genes on susceptibility to and severity of ankylosing spondylitis (AS). Methods. Three hundred sixty- three white British AS patients were studied; 149 were carefully assessed for a range of clinical manifestations, and disease severity was assessed using a structured questionnaire. Limited HLA class I typing and complete HLA-DR typing were performed using DNA-based methods. HLA data from 13,634 healthy white British bone marrow donors were used for comparison. Results. A significant association between DR1 and AS was found, independent of HLA-B27 (overall odds ratio [OR] 1.4, 95% confidence interval [95% CI] 1.1-1.8, P = 0.02; relative risk [RR] 2.7, 95% CI 1.5-4.8, P = 6 x 10-4 among homozygotes; RR 2.1, 95% CI 1.5-2.8, P = 5 x 10-6 among heterozygotes). A large but weakly significant association between DR8 and AS was noted, particularly among DR8 homozygotes (RR 6.8, 95% CI 1.6-29.2, P = 0.01 among homozygotes; RR 1.6, 95% CI 1.0-2.7, P = 0.07 among heterozygotes). A negative association with DR12 (OR 0.22, 95% CI 0.09-0.5, P = 0.001) was noted. HLA-DR7 was associated with younger age at onset of disease (mean age at onset 18 years for DR7-positive patients and 23 years for DR7-negative patients; Z score 3.21, P = 0.001). No other HLA class I or class H associations with disease severity or with different clinical manifestations of AS were found. Conclusion. The results of this study suggest that HLA-DR genes may have a weak effect on susceptibility to AS independent of HLA-B27, but do not support suggestions that they affect disease severity or different clinical manifestations.

Dissection of class III major histocompatibility complex haplotypes associated with rheumatoid arthritis

Objective. We have previously identified a single-nucleotide polymorphism (SNP) haplotype involving the lymphotoxin α (LTA) and tumor necrosis factor (TNF) loci (termed haplotype LTA-TNF2) on chromosome 6 that shows differential association with rheumatoid arthritis (RA) on HLA-DRB1*0404 and *0401 haplotypes, suggesting the presence of additional non-HLA-DRB1 RA susceptibility genes on these haplotypes. To refine this association, we performed a case-control association study using both SNPs and microsatellite markers in haplotypes matched either for HLA-DRB1*0404 or for HLA-DRB1*0401. Methods. Fourteen SNPs lying between HLA-DRB1 and LTA were genotyped in 87 DRB1*04-positive families. High-density microsatellite typing was performed using 24 markers spanning 2,500 kb centered around the TNF gene in 305 DRB1*0401 or *0404 cases and 400 DRB1*0401 or *0404 controls. Single-marker, 2-marker, and 3-marker minihaplotypes were constructed and their frequencies compared between the DRB1*0401 and DRB1*0404 matched case and control haplotypes. Results. Marked preservation of major histocompatibility complex haplotypes was seen, with chromosomes carrying LTA-TNF2 and either DRB1*0401 or DRB1*0404 both carrying an identical SNP haplotype across the 1-Mb region between TNF and HLA-DRB1. Using microsatellite markers, we observed two 3-marker minihaplotypes that were significantly overrepresented in the DRB1*0404 case haplotypes (P = 0.00024 and P = 0.00097). Conclusion. The presence of a single extended SNP haplotype between LTA-TNF2 and both DRB1*0401 and DRB1*0404 is evidence against this region harboring the genetic effects in linkage disequillbrium with LTA-TNF2. Two RA-associated haplotypes on the background of DRB1*0404 were identified in a 126-kb region surrounding and centromeric to the TNF locus.

Burden attributable to child maltreatment in Australia

Child maltreatment is a complex phenomenon, with four main types (childhood sexual abuse, physical abuse, emotional abuse, and neglect) highly interrelated. All types of maltreatment have been linked to adverse health consequences and exposure to multiple forms of maltreatment increases risk. In Australia to date, only burden attributable to childhood sexual abuse has been estimated. This study synthesized the national evidence and quantified the burden attributable to the four main types of child maltreatment. Meta-analyses, based on quality-effects models, generated pooled prevalence estimates for each maltreatment type. Exposure to child maltreatment was examined as a risk factor for depressive disorders, anxiety disorders and intentional self-harm using counterfactual estimation and comparative risk assessment methods. Adjustments were made for co-occurrence of multiple forms of child maltreatment. Overall, an estimated 23.5% of self-harm, 20.9% of anxiety disorders and 15.7% of depressive disorders burden in males; and 33.0% of self-harm, 30.6% of anxiety disorders and 22.8% of depressive disorders burden in females was attributable to child maltreatment. Child maltreatment was estimated to cause 1.4% (95% uncertainty interval 0.4–2.3%) of all disability-adjusted life years (DALYs) in males, and 2.4% (0.7–4.1%) of all DALYs in females in Australia in 2010. Child maltreatment contributes to a substantial proportion of burden from depressive and anxiety disorders and intentional self-harm in Australia. This study demonstrates the importance of including all forms of child maltreatment as risk factors in future burden of disease studies.

Interval training intensity affects energy intake compensation in obese men

Abstract PURPOSE: Compensatory responses may attenuate the effectiveness of exercise training in weight management. The aim of this study was to compare the effect of moderate- and high-intensity interval training on eating behavior compensation. METHODS: Using a crossover design, 10 overweight and obese men participated in 4-week moderate (MIIT) and high (HIIT) intensity interval training. MIIT consisted of 5-min cycling stages at ± 20% of mechanical work at 45%VO(2)peak, and HIIT consisted of alternate 30-s work at 90%VO(2)peak and 30-s rests, for 30 to 45 min. Assessments included a constant-load exercise test at 45%VO(2)peak for 45 min followed by 60-min recovery. Appetite sensations were measured during the exercise test using a Visual Analog Scale. Food preferences (liking and wanting) were assessed using a computer-based paradigm, and this paradigm uses 20 photographic food stimuli varying along two dimensions, fat (high or low) and taste (sweet or nonsweet). An ad libitum test meal was provided after the constant-load exercise test. RESULTS: Exercise-induced hunger and desire to eat decreased after HIIT, and the difference between MIIT and HIIT in desire to eat approached significance (p = .07). Exercise-induced liking for high-fat nonsweet food tended to increase after MIIT and decreased after HIIT (p = .09). Fat intake decreased by 16% after HIIT, and increased by 38% after MIIT, with the difference between MIIT and HIIT approaching significance (p = .07). CONCLUSIONS: This study provides evidence that energy intake compensation differs between MIIT and HIIT.