Kidney and related chronic disease profiles and risk factors in three remote Australian Aboriginal communities

Morbidities and deaths from noncommunicable chronic diseases are greatly increased in remote Australian Aboriginal communities, but little is known of the underlying community-based health profiles. We describe chronic-disease profiles and their risk factors in 3 remote communities in the Northern Territory. Consenting adults (18+ years of age) in 3 communities participated in a brief history and examination between 2000 and mid-2003 as part of a systematic program to improve chronic-disease awareness and management. Participation was 67%,128%, and 62% in communities A, B, and C, respectively with a total of 1070 people examined. Current smokers included 41% of females and 72% of males. Most men were current drinkers, but most women were not. Parameters of body weight differed markedly by community, with mean body mass index (BMC) varying from 21.4 to 27.9 kg/m(2). Rates of chronic diseases were excessive but differed markedly; an almost threefold difference in the likelihood of any morbidity existed between communities A and C. Rates increased with age, but the greatest numbers of people with morbidities were in the middle-aged group. Most people had multiple morbidities with tremendous overlap. Hypertension and kidney disease appear to be early manifestations of the integrated chronic-disease syndrome, while diabetes is a late manifestation or complication. Substantial numbers of new cases of disease were identified by testing, and blood pressure improved in treated people with hypertension. Wide variations occur in body habitus, risk factors, and chronic-disease rates among communities, but an overwhelming need for effective smoking interventions exists in all. Systematic screening is useful in identifying high-risk individuals, most at early treatable stages there. Findings are very important for estimating current treatment needs, future burdens of disease, and for needs-based health services planning. Resources required will vary according to the burden of disease. (C) 2005 by the National Kidney Foundation, Inc.

Contribution of changes in risk factors to the decline of coronary heart disease mortality in Australia over three decades

BACKGROUND: Coronary heart disease has been a major cause of mortality in Australian adults, but the rate has declined by 83% from the 1968 peak by the year 2000. The study objective is to determine the contribution of changes in population risk factors - mean serum cholesterol and diastolic blood pressure and tobacco smoking prevalence - to the decline in coronary heart disease mortality in Australia over three decades. METHODS: Coronary heart disease deaths (International Classification of Disease-9, 410-414) and population by year, age group and sex were obtained from the Australian Bureau of Statistics. Risk factor levels were obtained from population surveys and estimated average annual changes by period were used to calculate average annual 'attributable' proportional declines in CHD mortality by period (age 35-64 years). RESULTS: Over the period 1968-2000, 74% of male decline and 81% of the female decline in coronary heart disease mortality rate was accounted for by the combined effect of reductions in the three risk factors. In males 36% of the decline was contributed by reductions in diastolic blood pressure, 22% by cholesterol and 16% by smoking. For females 56% was from diastolic blood pressure reduction, 20% from cholesterol and 5% from smoking. Effects of reductions in serum cholesterol on coronary heart disease mortality occurred mainly in the 1970s. Declines in diastolic blood pressure had effects on coronary heart disease mortality over the three decades, and declines in tobacco smoking had a significant effect in males in the 1980s. CONCLUSION: Most of the spectacular decline in coronary heart disease mortality over the last three decades in Australia can be ascribed to reductions in population risk factors from primary and secondary prevention.

Environmental Risk Factors for Parkinson's Disease

Parkinson’s disease (PD) is a progressive, degenerative, neurological disease. The progressive disability associated with PD results in substantial burdens for those with the condition, their families and society in terms of increased health resource use, earnings loss of affected individuals and family caregivers, poorer quality of life, caregiver burden, disrupted family relationships, decreased social and leisure activities, and deteriorating emotional well-being. Currently, no cure is available and the efficacy of available treatments, such as medication and surgical interventions, decreases with longer duration of the disease. Whilst the cause of PD is unknown, genetic and environmental factors are believed to contribute to its aetiology. Descriptive and analytical epidemiological studies have been conducted in a number of countries in an effort to elucidate the cause, or causes, of PD. Rural residency, farming, well water consumption, pesticide exposure, metals and solvents have been implicated as potential risk factors for PD in some previous epidemiological studies. However, there is substantial disagreement between the results of existing studies. Therefore, the role of environmental exposures in the aetiology of PD remains unclear. The main component of this thesis consists of a case-control study that assessed the contribution of environmental exposures to the risk of developing PD. An existing, previously unanalysed, dataset from a local case-control study was analysed to inform the design of the new case-control study. The analysis results suggested that regular exposure to pesticides and head injury were important risk factors for PD. However, due to the substantial limitations of this existing study, further confirmation of these results was desirable with a more robustly designed epidemiological study. A new exposure measurement instrument (a structured interviewer-delivered questionnaire) was developed for the new case-control study to obtain data on demographic, lifestyle, environmental and medical factors. Prior to its use in the case-control study, the questionnaire was assessed for test-retest repeatability in a series of 32 PD cases and 29 healthy sex-, age- and residential suburb-matched electoral roll controls. High repeatability was demonstrated for lifestyle exposures, such as smoking and coffee/tea consumption (kappas 0.70-1.00). The majority of environmental exposures, including use of pesticides, solvents and exposure to metal dusts and fumes, also showed high repeatability (kappas >0.78). A consecutive series of 163 PD case participants was recruited from a neurology clinic in Brisbane. One hundred and fifty-one (151) control participants were randomly selected from the Australian Commonwealth Electoral Roll and individually matched to the PD cases on age (± 2 years), sex and current residential suburb. Participants ranged in age from 40-89 years (mean age 67 years). Exposure data were collected in face-to-face interviews. Odds ratios and 95% confidence intervals were calculated using conditional logistic regression for matched sets in SAS version 9.1. Consistent with previous studies, ever having been a regular smoker or coffee drinker was inversely associated with PD with dose-response relationships evident for packyears smoked and number of cups of coffee drunk per day. Passive smoking from ever having lived with a smoker or worked in a smoky workplace was also inversely related to PD. Ever having been a regular tea drinker was associated with decreased odds of PD. Hobby gardening was inversely associated with PD. However, use of fungicides in the home garden or occupationally was associated with increased odds of PD. Exposure to welding fumes, cleaning solvents, or thinners occupationally was associated with increased odds of PD. Ever having resided in a rural or remote area was inversely associated with PD. Ever having resided on a farm was only associated with moderately increased odds of PD. Whilst the current study’s results suggest that environmental exposures on their own are only modest contributors to overall PD risk, the possibility that interaction with genetic factors may additively or synergistically increase risk should be considered. The results of this research support the theory that PD has a multifactorial aetiology and that environmental exposures are some of a number of factors to contribute to PD risk. There was also evidence of interaction between some factors (eg smoking and welding) to moderate PD risk.

Estimation of contribution of changes in classic risk factors to trends in coronary-event rates across the WHO MONICA Project populations

Background From the mid-1980s to mid-1990s, the WHO MONICA Project monitored coronary events and classic risk factors for coronary heart disease (CHD) in 38 populations from 21 countries. We assessed the extent to which changes in these risk factors explain the variation in the trends in coronary-event rates across the populations. Methods In men and women aged 35-64 years, non-fatal myocardial infarction and coronary deaths were registered continuously to assess trends in rates of coronary events. We carried out population surveys to estimate trends in risk factors. Trends in event rates were regressed on trends in risk score and in individual risk factors. Findings Smoking rates decreased in most male populations but trends were mixed in women; mean blood pressures and cholesterol concentrations decreased, body-mass index increased, and overall risk scores and coronary-event rates decreased. The model of trends in 10-year coronary-event rates against risk scores and single risk factors showed a poor fit, but this was improved with a 4-year time lag for coronary events. The explanatory power of the analyses was limited by imprecision of the estimates and homogeneity of trends in the study populations. Interpretation Changes in the classic risk factors seem to partly explain the variation in population trends in CHD. Residual variance is attributable to difficulties in measurement and analysis, including time lag, and to factors that were not included, such as medical interventions. The results support prevention policies based on the classic risk factors but suggest potential for prevention beyond these.

The Australian Burden of Disease Study: measuring the loss of health from diseases, injuries and risk factors

This is an overview of the first burden of disease and injury studies carried out in Australia. Methods developed for the World Bank and World Health Organization Global Burden of Disease Study were adapted and applied to Australian population health data. Depression was found to be the top-ranking cause of non-fatal disease burden in Australia, causing 8% of the total years lost due to disability in 1996. Mental disorders overall were responsible for nearly 30% of the non-fatal disease burden. The leading causes of total disease burden (disability-adjusted life years [DALYs]) were ischaemic heart disease and stroke, together causing nearly 18% of the total disease burden. Depression was the fourth leading cause of disease burden, accounting for 3.7% of the total burden. Of the 10 major risk factors to which the disease burden can be attributed, tobacco smoking causes an estimated 10% of the total disease burden in Australia, followed by physical inactivity (7%).

Genetic and environmental risk factors and their interactions for Parkinson's disease in a Chinese population

The interaction between genetic and environmental factors for PD was examined in a Chinese population. It was found that although the intron 2 MAOB (GT)(n) repeat polymorphism was not associated with PID in the population, a relationship might have been masked by the protective effect of tea drinking. In individuals who did not drink tea (<1 cup/day), the possession of short length less than or equal to 178 bp (GT), alleles conferred a borderline significant increased risk for PD (adjusted OR = 1.47; C.l. = 1.03-2. 1). As the extent of tea consumption increased, the association between the less than or equal to178 bp allele and PD disappeared. This result suggests that the MAOB gene may be associated with PD in Chinese if the putative protective effect of tea drinking is taken into account. The significance of this finding is unclear as the study may be limited because of its marginal significance and limited numbers. However, it does demonstrate the importance of considering putative positive and negative environmental risk factors in any examination of genetic risk factors for PD. (C) 2003 Elsevier Science Ltd. All rights reserved.

Ross River virus disease in Australia, 1886-1998, with analysis of risk factors associated with outbreaks

Ross River virus (RE) is a mosquito-borne arbovirus responsible for outbreaks of polyarthritic disease throughout Australia. To better understand human and environmental factors driving such events, 57 historical reports oil RR Outbreaks between 1896 and 1998 were examined collectively. The magnitude, regularity, seasonality, and locality of outbreaks were found to be wide ranging; however, analysis of climatic and tidal data highlighted that environmental conditions let differently ill tropical, arid, and temperate regions. Overall, rainfall seems to be the single most important risk factor, with over 90% of major outbreak locations receiving higher than average rainfall in preceding mouths. Many temperatures were close to average, particularly in tropical populations; however, in arid regions, below average maximum temperatures predominated, and ill southeast temperate regions, above average minimum temperatures predominated. High spring tides preceded coastal Outbreaks, both in the presence and absence of rainfall, and the relationship between rainfall and the Southern Oscillation Index and Lit Nina episodes suggest they may be useful predictive tools, but only ill southeast temperate regions. Such heterogeneity predisposing outbreaks supports the notion that there are different RE epidemiologies throughout Australia but also Suggests that generic parameters for the prediction and control of outbreaks are of limited use at a local level.

Smoking and elevated blood pressure are the most important risk factors for subarachnoid hemorrhage in the Asia-Pacific region - An overview of 26 cohorts involving 306,620 participants

Background and Purpose - The cause of subarachnoid hemorrhage ( SAH) is poorly understood and there are few large cohort studies of risk factors for SAH. We investigated the risk of SAH mortality and morbidity associated with common cardiovascular risk factors in the Asia-Pacific region and examined whether the strengths of these associations were different in Asian and Australasian ( predominantly white) populations. Methods - Cohort studies were identified from Internet electronic databases, searches of proceedings of meetings, and personal communication. Hazard ratios (HRs) for systolic blood pressure (SBP), current smoking, total serum cholesterol, body mass index (BMI), and alcohol drinking were calculated from Cox models that were stratified by sex and cohort and adjusted for age at risk. Results - Individual participant data from 26 prospective cohort studies ( total number of participants 306 620) that reported incident cases of SAH ( fatal and/or nonfatal) were available for analysis. During the median follow-up period of 8.2 years, a total of 236 incident cases of SAH were observed. Current smoking (HR, 2.4; 95% CI, 1.8 to 3.4) and SBP > 140 mm Hg ( HR, 2.0; 95% CI, 1.5 to 2.7) were significant and independent risk factors for SAH. Attributable risks of SAH associated with current smoking and elevated SBP ( similar to 140 mm Hg) were 29% and 19%, respectively. There were no significant associations between the risk of SAH and cholesterol, BMI, or drinking alcohol. The strength of the associations of the common cardiovascular risk factors with the risk of SAH did not differ much between Asian and Australasian regions. Conclusions - Cigarette smoking and SBP are the most important risk factors for SAH in the Asia-Pacific region.

Interfaces between cardiovascular and kidney disease among Aboriginal Australians

Rates of kidney disease among several indigenous groups have been shown to be substantially higher than corresponding non-indigenous groups. This excess has been clearly shown among Aboriginal Australians with respect to both end-stage kidney disease and early kidney disease. Rates of cardiovascular disease among Aboriginal Australians are also very high, as are rates of diabetes, smoking, and possibly overweight and obesity. These factors have been traditionally linked with cardiovascular and renal disease as part of a broader metabolic syndrome. However, the links and interfaces between cardiovascular and kidney disease in this environment extend beyond these traditional factors. The factors associated with atherosclerosis have expanded in recent years to include markers of inflammation, some infection, antioxidants, and other non-traditional risk factors. Given the high rates of acute infection and poor living conditions endured by many indigenous people, one might expect these non-traditional risk factors to be highly prevalent. In this review, we explore the relationships between markers of inflammation, some serological markers of infection, and other selected markers and both cardiovascular and renal disease. In doing so, we demonstrate links between kidney and cardiovascular disease at a number of levels, beyond the traditional cardiovascular/renal risk factors. Many of these factors are beyond the control of the individual or even community; addressing these issues a broader focus and biopsychosocial model. (C) 2005 by the National Kidney Foundation, Inc.