Australian Death Research Articles

How many Australian deaths from heart disease and stroke could be avoided by a small reduction in population cholesterol levels?

AbstractAim: To quantify the number of premature deaths from coronary heart disease and ischaemic stroke that potentially could be avoided annually among the Australian population if a sustained 10% reduction in the mean population level of low‐density lipoprotein cholesterol were to be achieved.Methods: Data were obtained on the number of deaths from coronary heart disease and stroke in the Australian population, subdivided into age and sex strata, and on the mean population level of low‐density lipoprotein cholesterol. Published relative risks (95% CI) from a meta‐analysis of lipid‐lowering therapy were used to calculate the reduction in the relative risk for coronary heart disease and stroke associated with a 5%, 10% and 15% reduction in low‐density lipoprotein cholesterol. The expected number of deaths from coronary heart disease and ischaemic stroke avoidable with a 10% reduction in low‐density lipoprotein cholesterol was modelled. Secondary analyses were performed assuming reductions in low‐density lipoprotein cholesterol of 5% and 15%.Results: A 10% reduction in low‐density lipoprotein cholesterol would prevent 2279 deaths from coronary heart disease (95% CI: 2025–2531 deaths) and 641 deaths from ischaemic stroke (95% CI: 440–881 deaths). The projected benefits are greatest among the elderly, although some benefit would be expected in all age and sex groups and among individuals with a broad range of baseline levels of low‐density lipoprotein cholesterol.Conclusions: A small leftward shift in the low‐density lipoprotein cholesterol distribution of the adult Australian population has the potential to save about 3000 lives from coronary heart disease and stroke annually. Achieving this goal will require the active participation of key public health, food industry and government stakeholders.

Smoking questions on the Australian death notification form: adopting international best practice?

Australia's achievement in tobacco control has been remarkable, but relies on indirect estimates of tobacco-attributed mortality, and on using relative risks from Western countries to calculate tobacco's impact. To accelerate the decline in smoking, more precise measures of tobacco's relative importance among different population subgroups are required. We propose that more direct and accurate measures of tobacco-attributed mortality are needed, which could be achieved by adding a small set of voluntary questions about the smoking status of the deceased to a revised death notification form. Ideally, this form should also record the smoking status of the next-of-kin or family informant, as this would help establish a living control group. Such information will provide data on tobacco-attributed deaths with incomparable precision, allowing accurate monitoring of the current state of the smoking epidemic, and its evolution over time. This is particularly pertinent for sections of the population in which tobacco control measures have been less successful. A number of practical concerns have been raised, but we do not believe these are insurmountable.

Coronary heart disease events in Aboriginal Australians: incidence in an urban population

To determine the incidence of coronary heart disease (CHD) events in an urban Aboriginal population. Cohort study of 906 Aboriginal people without CHD from 998 who had undergone risk-factor assessment in the Perth Aboriginal Atherosclerosis Risk Study (PAARS) in 1998-1999. PAARS cohort data were electronically linked to a range of databases that included Western Australian hospital morbidity data and death registry data. We analysed data from January 1980 to December 2006 to identify previous admissions for CHD from 1980 to baseline (1998-1999) and new events from baseline to 2006. First CHD event (hospital admission or death). There were 891 linked records for the 906 participants without previous CHD. The event rate was 12.6/1000 person-years (95% CI, 10.2-15.6/1000 person-years). Annual CHD event rates ranged from 8 to 18/1000 person-years. After adjustment for age (sex was not associated with the risk factors assessed), factors associated with risk of a CHD event in the PAARS cohort were a history of diabetes, overweight or obesity (indicated by body mass index), smoking, and hypertension, but not waist circumference. People with these risk factors were 1.9-2.7 times more likely to experience a CHD event. Compared with previously published information from a remote Aboriginal community in the Northern Territory, the incidence of CHD events among urban-dwelling Aboriginal people was not significantly different (P > 0.05 overall and for subgroups defined by age and sex). City-dwelling Aboriginal Australians have an incidence of CHD events comparable to that of Aboriginal people living in remote northern Australia.

Maternal mortality: What can we learn from stories of postpartum haemorrhage?

Death from pregnancy is rare in developed countries such as Australia but is still common in third world and developing countries. The investigation of each maternal death yields valuable information and lessons that all health care providers involved with the care of women can learn from. The aim of these investigations is to prevent future maternal morbidity and mortality. Obstetric haemorrhage remains a leading cause of maternal death internationally. It is the most common cause of death in developing countries. In Australia and the United Kingdom, obstetric haemorrhage is ranked as the 4th and 3rd most common cause of direct maternal death respectively. In a number of cases there are readily identifiable factors associated with the care that the women received that may have contributed to their death. It is from these identifiable factors that both midwives and doctors can learn to help prevent similar episodes from occurring. This article will identify some of the lessons that can be learnt from the recent Australian and UK maternal death reports. This paper presents an overview of the process and systems for the reporting of maternal death in Australia. It will then specifically focus on obstetric haemorrhage, with a focus on postpartum haemorrhage, for the 12-year period, 1994-2005. Vignettes from the maternal mortality reports in Australia and the United Kingdom are used to highlight the important lessons for providers of maternity care.

Risk Prediction Scores for Postoperative Mortality After Esophagectomy: Validation of Different Models

BackgroundDifferent prediction models for operative mortality after esophagectomy have been developed. The aim of this study is to independently validate prediction models from Philadelphia, Rotterdam, Munich, and the ASA. MethodsThe scores were validated using logistic regression models in two cohorts of patients undergoing esophagectomy for cancer from Switzerland (n = 170) and Australia (n = 176). ResultsAll scores except ASA were significantly higher in the Australian cohort. There was no significant difference in 30-day mortality or in-hospital death between groups. The Philadelphia and Rotterdam scores had a significant predictive value for 30-day mortality (p = 0.001) and in-hospital death (p = 0.003) in the pooled cohort, but only the Philadelphia score had a significant prediction value for 30-day mortality in both cohorts. Neither score showed any predictive value for in-hospital death in Australians but were highly significant in the Swiss cohort. ASA showed only a significant predictive value for 30-day mortality in the Swiss. For in-hospital death, ASA was a significant predictor in the pooled and Swiss cohorts. The Munich score did not have any significant predictive value whatsoever. ConclusionNone of the scores can be applied generally. A better overall predictive score or specific prediction scores for each country should be developed.

Linkage of Hospital and Death Records Increased Identification of Dementia Cases and Death Rate Estimates

Background/Aim: To use health record data linkage to improve case ascertainment and death rate estimates of deaths with dementia. Methods: Retrospective population study. Western Australians older than 20 years who died between 1990 and 2005 with a dementia diagnosis in Western Australian hospitals and/or death records using the Western Australian Data Linkage System were classed as having a lifetime history of dementia. Cases with dementia documented on death certificates were classified as having dementia as a contributory cause of death (COD). Age-standardized death rates (ASDR) were estimated. Results: 29,884 decedents were identified with a lifetime history of dementia. 88.2% had hospital records and 55.9% had death records indicating dementia. The ASDRs for dementia as a contributory COD increased from 50 to 81 per 100,000 person-years from 1990 to 2005. ASDR for lifetime history of dementia increased from 80 to 140 per 100,000 person-years over the same time period. In 2005, 50.1% (95% confidence interval: 47.2–53.1) of all females and 39.2% (35.8–42.7) of all males aged 85+ years died with dementia. Conclusion: Data linkage nearly doubled case ascertainment of deaths with dementia because people hospitalized with dementia often lacked dementia documentation at death. These results have important implications for strategic healthcare planning. Data linkage methodology could improve studies of hospitalisation trends in dementia.

Sleep Apnea as an Independent Risk Factor for All-Cause Mortality: The Busselton Health Study

Previously published cohort studies in clinical populations have suggested that obstructive sleep apnea (OSA) is a risk factor for mortality associated with cardiovascular disease. However, it is unknown whether sleep apnea is an independent risk factor for all-cause mortality in a community-based sample free from clinical referral bias. Residents of the Western Australian town of Busselton underwent investigation with a home sleep apnea monitoring device (MESAM IV). OSA was quantified via the respiratory disturbance index (RDI). Mortality status was determined in 397/400 participants (99.3%) after up to 14 years (mean follow-up 13.4 years) by data matching with the Australian National Death Index and the Western Australian Death Register. Univariate analyses and multivariate Cox proportional hazards modelling were used to ascertain the association between sleep apnea and mortality after adjustment for age, gender, body mass index, mean arterial pressure, total cholesterol, high-density lipoprotein cholesterol, diabetes, and medically diagnosed angina in those free from heart attack or stroke at baseline (n = 380). Among the 380 participants, 18 had moderate-severe OSA (RDI > or = 15/hr, 6 deaths) and 77 had mild OSA(RDI 5 to < 15/hr, 5 deaths). Moderate-to-severe OSA was independently associated with greater risk of all-cause mortality (fully adjusted hazard ratio [HR] = 6.24, 95% CL 2.01, 19.39) than non-OSA (n = 285, 22 deaths). Mild OSA (RDI 5 to < 15/hr) was not an independent risk factor for higher mortality (HR = 0.47, 95% CL 0.17, 1.29). Moderate-to-severe sleep apnea is independently associated with a large increased risk of all-cause mortality in this community-based sample.

Causes of death in young Australians with type 1 diabetes: a review of coronial postmortem examinations

To determine the causes of death in Australians with type 1 diabetes mellitus who died aged 40 years or younger. Retrospective review of autopsy reports at the Department of Forensic Medicine, Sydney, New South Wales, 1 January 1994-31 December 2006. Causes of mortality in people with type 1 diabetes aged <40 years. Of the 26 682 autopsy reports, 1914 were for individuals with diabetes (type 1, 400; type 2, 1514). Cardiovascular disease accounted for 51% of deaths (169/333) in people with type 1 diabetes aged >40 years, versus 13% among those aged <or= 40 years (9/67; P=0.001). Acute complications of diabetes (27%; 18/67), unnatural deaths (28%; 19/67), and sudden unexpected deaths (22%; 15/67) were the predominant causes of death in young individuals with diabetes. Sudden unexpected death was more common in those with type 1 diabetes compared with a sex-matched control population in the same age range (22% v 5%; Xi(2) P<0.001). Of the sudden unexpected deaths, 10 people were found dead in an undisturbed bed with no cause of death found at autopsy ("dead-in-bed" syndrome; mean age [SD], 30.2 [9.4] years; males : females=4 :1). In deceased young people with type 1 diabetes examined by the Coroner, acute diabetic complications, unnatural causes, and sudden unexpected deaths were the predominant causes of death. The relatively high frequency of sudden unexpected deaths, such as dead-in-bed syndrome, requires further investigation.

Making pregnancy safer in Australia: The importance of maternal death review

Australia is one of the safest countries in the world to birth. Because maternal deaths are rare, often the focus during pregnancy is on the well-being of the fetus. The relative safety of birth has fostered a shift in the focus of maternal health, from survival, to the model of care or the birth experience. Yet women still die in Australia as a result of child bearing and many of these deaths are associated with avoidable factors. The purpose of this paper is to outline the maternal death monitoring and review process in Australia and to present to clinicians the salient features of the most recently published Australian maternal death report. The notion of preventability and the potential for practice to have an effect on reducing maternal mortality are also discussed.

Influenza-related hospitalisation and death in Australians aged 50 years and older

SummaryEstimating the true burden of influenza is problematic because relatively few hospitalisations or deaths are specifically coded as influenza related. Statistical regression techniques using influenza and respiratory syncytial virus surveillance data were used to estimate the number of excess hospitalisations and deaths attributable to influenza. Several International Classification of Diseases 10th Revision (ICD-10) groupings were used for both hospitalisation and mortality estimates, including influenza and pneumonia, other respiratory disorders, and circulatory disorders. For Australians aged 50–64 years, the annual excess hospitalisations attributable to influenza were 33.3 (95%CI: 23.2–43.4) per 100,000 for influenza and pneumonia and 57.6 (95%CI: 32.5–82.8) per 100,000 for other respiratory disorders. For Australians aged ≥65 years, the annual excess hospitalisations attributable to influenza were 157.4 (95%CI: 108.4–206.5) per 100,000 for influenza and pneumonia and 282.0 (95%CI: 183.7–380.3) per 100,000 for other respiratory disorders. The annual excess all-cause mortality attributable to influenza was 6.4 (95%CI: 2.6–10.2) per 100,000 and 116.4 (95%CI: 71.3–161.5) per 100,000, for Australians aged 50–64 years and those aged ≥65 years, respectively. In the age-group ≥65 years, a significant association was found between influenza activity and circulatory mortality. We conclude that influenza is responsible for a substantial amount of mortality and morbidity, over and above that which is directly diagnosed as influenza in Australians aged ≥50 years.

Sudden Unexplained Death in Young Australians with Type 1 Diabetes Mellitus: Clinical and Genetic Analysis of dead in bed Cases

Sudden Unexplained Death in Young Australians with Type 1 Diabetes Mellitus: Clinical and Genetic Analysis of dead in bed Cases

Characteristics and outcomes of patients who “did not wait” after attending Perth public hospital emergency departments, 2000–2003

To determine characteristics and outcomes of patients who did not wait to see a doctor in emergency departments (EDs). Population-based outcome study using probabilistically linked ED and Western Australian death records, with ED records from all seven Perth public hospitals that have EDs from 1 July 2000 to 30 June 2003. Rates of "did not wait" (DNW) presentations, overall and for individual hospitals; characteristics of DNW patients; mortality rates among DNW patients at 2, 7 and 30 days. DNW rates varied from 2.6% to 6.3% (average, 4.1%) and were generally lower in tertiary teaching hospitals. DNW patients had conditions of lower urgency, predominantly Australasian Triage Scale category 4 (67.1%) and 5 (23.4%). The DNW rates in these categories were 5.8% and 10.6%, respectively (P < 0.001). Patients referred by health care providers had lower DNW rates (0.5%; P < 0.001). DNW patients were more frequently male (4.4% v 3.8%; P < 0.001), and young to middle-aged adults (15-44 years; 5.8%; P < 0.001). Patients with a higher than average DNW rate were more likely to arrive by private transport (5.0%; P < 0.001) or with police (5.8%; P < 0.001), re-present for review (8.6%; P < 0.001) or have social or behavioural problems (7.7%; P < 0.001). Most patients (91.9%) did not wait on only one occasion. The 30-day mortality rate among DNW patients was significantly lower than for patients seen by a doctor and discharged (0.14 v 0.20%; P = 0.026), and for all patients seen in the ED (1.28%; P < 0.001). Patients who did not wait for medical assessment in Perth EDs had conditions of lower acuity and had lower mortality rates than those who waited for assessment.

Australian firearms legislation and unintentional firearm deaths: a theoretical explanation for the absence of decline following the 1996 gun laws

Worldwide, the development of successful interventions aimed at lowering the incidence of firearm-related death presents a notable challenge for public health and safety practitioners. Relatively little research has addressed the impacts of significant epochs of regulatory reform upon firearm-related deaths in countries like Australia, where strict firearms regulations were introduced in 1996. Australia’s gun controls are considered to be amongst the most stringent in the developed world. Briefly, the National Firearms Agreement (NFA), ratified by Federal Parliament in 1996 and implemented across all states and territories by the end of 1997, prohibited certain types of firearms, particularly semi-automatic rifles and semi-automatic and pump-action shotguns. To facilitate the removal of these firearms, a government-funded ‘buyback’ scheme was implemented, where owners were compensated for handing in their firearms.

The Diversity of Bioactive Proteins in Australian Snake Venoms

Australian elapid snakes are among the most venomous in the world. Their venoms contain multiple components that target blood hemostasis, neuromuscular signaling, and the cardiovascular system. We describe here a comprehensive approach to separation and identification of the venom proteins from 18 of these snake species, representing nine genera. The venom protein components were separated by two-dimensional PAGE and identified using mass spectrometry and de novo peptide sequencing. The venoms are complex mixtures showing up to 200 protein spots varying in size from <7 to over 150 kDa and in pI from 3 to >10. These include many proteins identified previously in Australian snake venoms, homologs identified in other snake species, and some novel proteins. In many cases multiple trains of spots were typically observed in the higher molecular mass range (>20 kDa) (indicative of post-translational modification). Venom proteins and their post-translational modifications were characterized using specific antibodies, phosphoprotein- and glycoprotein-specific stains, enzymatic digestion, lectin binding, and antivenom reactivity. In the lower molecular weight range, several proteins were identified, but the predominant species were phospholipase A2 and alpha-neurotoxins, both represented by different sequence variants. The higher molecular weight range contained proteases, nucleotidases, oxidases, and homologs of mammalian coagulation factors. This information together with the identification of several novel proteins (metalloproteinases, vespryns, phospholipase A2 inhibitors, protein-disulfide isomerase, 5'-nucleotidases, cysteine-rich secreted proteins, C-type lectins, and acetylcholinesterases) aids in understanding the lethal mechanisms of elapid snake venoms and represents a valuable resource for future development of novel human therapeutics.

Effect of the medical emergency team on long-term mortality following major surgery

IntroductionIntroducing an intensive care unit (ICU)-based medical emergency team (MET) into our hospital was associated with decreased postoperative in-hospital mortality after major surgery. The purpose of the present study was to assess the effect of the MET and other variables on long-term mortality in this patient population.MethodsWe conducted a prospective, controlled, before-and-after trial in a University-affiliated hospital. Participants included consecutive patients admitted for major surgery (surgery requiring hospital stay > 48 hours) during a four month control phase and a four month MET phase. The intervention involved the introduction of a hospital-wide ICU-based MET service to evaluate and treat ward patients with acutely deranged vital signs. Information on long-term mortality was obtained from the Australian death registry. The main outcome measure was patient mortality at 1500 days. Data on patient demographics, surgery undertaken and whether the surgery was scheduled or unscheduled was obtained from the hospital electronic database. Multivariable analysis was conducted to determine independent predictors of 1500-day mortality.ResultsThere were 1,369 major operations in 1,116 patients during the control period and 1,313 operations in 1,067 patients during the MET (intervention) period. Overall survival at 1500 days was 65.8% in the control period and 71.6% during the MET period (P = 0.001). Patients in the control phase were statistically less likely to be admitted under orthopaedic surgery, urology and faciomaxillary surgery units, but more likely to be admitted under cardiac surgery or neurosurgery units. Patients in the MET period were less likely to undergo unscheduled surgery. Multivariable analysis revealed that age, unscheduled surgery and admission under thoracic surgery, neurosurgery, oncology and general medicine were independent predictors of increased 1500-day mortality. Admission during the MET period was also an independent predictor of decreased 1500-day mortality (odds ratio 0.74; P = 0.005).ConclusionIntroduction of a MET service in a teaching hospital was associated with increased long-term survival even after adjusting for other factors that contribute to long-term surgical mortality.

CANADIAN HEROIN SUPPLY AND THE AUSTRALIAN ‘HEROIN SHORTAGE’

We wish to comment on the recent article by Wood et al. [1], which questioned whether law enforcement contributed to the Australian heroin shortage in 2001. We agree with Wood et al. that reductions in international heroin supply may have played a larger role than we supposed in the Australian heroin shortage. We stress, however, that we acknowledged in our paper that changes in source countries probably did play a role (p. 466) [2]. We have never claimed, as some of our critics have assumed, that law enforcement activity was the sole, or even the major explanation of the Australian heroin shortage. None the less, for the following reasons we doubt that Australian heroin shortage can be wholly or largely explained by a reduction in heroin production in source countries. First, the timing of the onset of the Australian shortage can be specified to within a month. There was a simultaneous reduction in heroin availability reported by heroin users throughout the whole of Australia that began in late December and early January 2001. Time-series analysis of a wealth of monthly data reflecting the size of the heroin market pointed strongly to the occurrence of an external ‘shock’ to the heroin supply system on that date (e.g. [3–8]). This was clearest in the most direct indicators of heroin use, namely, fatal and non-fatal drug overdoses [9,10]. It was echoed in data on heroin price, purity and availability [11,12]. All analyses pointed to January 2001 as the time when there was a substantial change in the heroin market. This was consistent with the reports of heroin users, treatment providers, police [13,14] and the researchers who conducted research on the ground to investigate this unique event [15,16]. There was no comparable event in Vancouver that was reported at the time by key informants whom we contacted when undertaking our analyses of the reasons for Australian heroin shortage [14]. Secondly, the size of the decrease in fatal and non-fatal overdose in Australia was much larger (as well as more immediate) than the smaller (and more gradual) decline in overdoses observed in Vancouver. This reduction also occurred in the much larger heroin market of Sydney and Melbourne (the capital cities of States where it has been estimated there were possibly 70 000 regular heroin users in 2000 [17]) than the much smaller Vancouver market (where it might be estimated that there were 2000 such users, estimated from the number of overdose deaths) where fewer than half of the injectors surveyed reported daily heroin use. Thirdly, if the decline in overdose mortality in Vancouver data can be used to estimate the contribution that declining supply may have made in Australia, then it would explain about half the observed decline in Australian overdose deaths. This still leaves open the possibility that high-level law enforcement contributed to the Australian shortage. Fourthly, we did not argue that heroin seizures directly affected heroin supply in Australia. Rather, we argued that large seizures deterred large-scale centralized heroin importation syndicates from importing heroin in large quantities into Australia. This is supported by the fact that the amount of heroin seized in Australia was much larger than that in Vancouver in terms of both the absolute size (total kg) and in terms of probable market share [18]. Such large seizures might be expected to have a larger deterrent effect on heroin importers when supply in source countries was declining. Fifthly, the hypothesis that source country supply wholly explains the Australian shortage does not explain why there was a much larger reduction in heroin supply in Australia than in Vancouver, when Australian cities have a much larger heroin market, and are geographically much closer to source countries in the Golden Triangle than Vancouver. We agree with Wood et al. that we should avoid premature acceptance of the hypothesis that law enforcement activities played a major role in the Australian heroin shortage, given the paucity of data in the literature indicating that law enforcement activities have large effects on the size of heroin or other drug markets. We also believe that scepticism should be responsive to evidence when something unusual happened, as our data indicate that it clearly did in Australia in January 2001. It would be unwise to rule out on a priori grounds the possibility that the Australian heroin shortage may have been one of those rare occasions in which law enforcement activities contributed to reduced drug supply.

Factors predictive of preferred place of death in the general population of South Australia

In a population survey, 2652 respondents aged 15+years reported their preferred place of death, if dying of ‘a terminal illness such as cancer or emphysema’, to be home (70%), a hospital (19%), hospice (10%), or nursing home (< 1%). The majority of respondents in all socio-demographic categories reported a preference for dying at home, with the greatest majorities occurring in younger age groups. After weighting to the age-sex distribution of all South Australian cancer deaths, 58% in our survey declared a preference to die at home, which is much higher than the 14% of cancer deaths that actually occurred at home in South Australia in 2000-2002. Multivariable analyses indicate that predictors of preferred home death include younger age, male, born in the UK/Ireland or Italy/Greece, better physical health, poorer mental health, and fewer concerns about dying at home. Predictors of preference for death in a hospice rather than hospital include older age, female, single, metropolitan residence, having higher educational and income levels, paid employment, awareness of advanced directives, and interpreting ‘dying with dignity’ as death without pain or suffering. Investigating the differences between preferred and actual places of death may assist service providers to meet end-of-life wishes.

Better wine for better health: Fact or fiction?

In the first decade of the twenty-first century, the potential therapeutic effects of regular moderate wine consumption are being increasingly acknowledged. They include a reduction in the risk of, and death from, cardiovascular disease, which accounted for 40% of all Australian deaths in 2000. The reduction in risk for wine consumers is similar to that of consumers of fruits, grains and vegetables, which, together with wine, are the core components of a 'Mediterranean-style diet'. The chemical components of wine considered primarily responsible for this therapeutic effect are ethanol, and the phenolic compounds and their polyphenolic forms. Indeed, moderate wine consumption has been observed to supplement the cardioprotective effects of an already high phenolic diet, and more importantly, to counter the harmful effects of a high fat diet on blood clotting, endothelial function and lipid oxidation, which contribute to the development of cardiovascular disease. This paper explores both the viticultural and vinification factors that influence phenolic concentration in grapes and wine. The synthesis and accumulation of phenolic compounds in grapes is primarily dependent upon varietal factors, the expression of which is influenced by a combination of climatic and viticultural factors such as sunlight and temperature during ripening, as well as ripeness at harvest. While the maximum possible concentration of phenolic compounds in a wine will be determined by the content in the constituent grapes, factors which influence the extraction of the phenolic compounds from the skins and seeds primarily influence their concentration in the juice, must and wine. Once harvested, the concentration of phenolic compounds in grapes is invariate, but extraction efficiency can vary during vinification. Accordingly, this paper also explores innovative techniques and technologies that can increase the phenolic content of the resultant wine. At best, winemaking can only extract at 50% of the total phenolic compounds accumulated in the grapes. Therefore, the phenolic content of the resultant wine can only be increased by supplementation of the must during fermentation with additional sources of phenolic compounds. Alternatively, a grape seed extract could be added to wine post fermentation to supplement its phenolic content, although this same grape seed extract may also be added to other foods such as yoghurt, from which the phenolic compounds are readily absorbed. Regular and moderate consumption of wine by consumers should, however, be placed in context with the other constituents and characteristics of a healthy diet and lifestyle. Indeed, wine consumers generally have fewer risk factors for cardiovascular disease compared with beer and spirits consumers, which is reflected in an approximately 25% to 35% lower risk of cardiovascular disease for wine consumers compared to consumers of beer and spirits, respectively.

Kava use, dyslipidaemia and biomarkers of dietary quality in Aboriginal people in Arnhem Land in the Northern Territory (NT), Australia.

Heavy kava use has been associated with sudden death in Aboriginal Australians in Arnhem Land (Northern Territory, Australia) where poor diets and a high incidence of premature coronary heart disease are known. Heavy kava users may suffer additional risk if further malnourished. Among 98 people (62 males, 36 females) in one community, 36 never used kava, 26 were past users, and 36 were continuing users. Across kava-using groups skinfold thickness, body mass index and body fat decreased. Total- and LDL-cholesterol were elevated in kava users compared to both former users and never users. HDL-cholesterol was higher in current users vs never users. Across kava-using groups, triglycerides, homocysteine and diet-derived antioxidant vitamins alpha-tocopherol and retinol, did not vary. Plasma carotenoid levels (indicative of vegetable and fruit intake) were very low, but when adjusted for plasma cholesterol, did not vary between kava-using groups. An obsession for kava drinking may mediate kava's direct effects on nutritional status.

Causes of sudden cardiac death in young Australians.

To determine the causes of sudden cardiac death in people aged 35 years or younger. A review of all autopsies performed between 1 January 1994 and 31 December 2002 at a major Sydney forensic medicine department serving an area with over 2 million people. Incidence of various types of cardiac disease causing sudden death in those aged <or= 35 years; proportion of deaths in which no cause was found at autopsy. There were 10 199 autopsies performed during the study period. Of these, 2986 (29.2%) deaths occurred in people aged <or= 35 years; 193 were classified as sudden cardiac deaths. The cause of sudden death in this group was not established in 60 (31%), and was presumed to be due to primary arrhythmogenic disorders. Coronary artery disease occurred in 46 (24%), hypertrophic cardiomyopathy/unexplained left ventricular hypertrophy in 29 (15%), and myocarditis in 23 (12%). Unexplained deaths, presumed to result from sudden primary arrhythmogenic causes, occur in young Australians with structurally normal hearts. That underlying disease-causing genetic defects may be involved has clinical implications for family members.