In this study we found that the incidence of diabetes in Aboriginal people was high, comparable to those in other high risk populations such as Pima Indians [10
] and people in Mauritius [11
]. The observed diabetes incidence rate among participating Aboriginal adults was higher than those reported in the general Australian population [12
] and in European [13
] and American black and white populations [15
]. For example, diabetes incidence rates in Aboriginal women were 4-8 times as high as those in the general Australian women for different age groups, while the corresponding values in Aboriginal men were 2-4 times of their general Australian counterparts [12
Given the life expectancy of around 60 years for Australian Aboriginal peoples, the cumulative incidence of diabetes at age of 60 years calculated in this study provides an approximate estimate of lifetime risk of developing diabetes in this population. That is, the lifetime risk of diabetes among these Aboriginal men is one in two, and among these Aboriginal women is two in three. A previous study reported that lifetime risk of diabetes was 33% for males and 39% for females in the US [16
]. The high lifetime probability of diabetes among Aboriginal Australians calls for implementation of effective primary prevention strategies at the population level. It also calls for a more sophisticated understanding of the nature of diabetes susceptibility in this population.
Results from several longitudinal studies have shown that the presence of IGT/IFG is a significant predictor of the development of diabetes [11
]. This study adopted the new American Diabetes Associate threshold for IFG. Studies in other populations have shown that those with new threshold of IFG are at increased risk of diabetes [7
]. In our study, IFG and IGT identified distinct groups with 36 participants with IFG only and 58 with IGT only. Their contributions to the prediction of incident diabetes are independent of each other, suggesting that the causes and physiological bases of IFG and IGT may be somewhat different. Raised hepatic glucose output and a defect in early insulin secretion are characteristics of IFG, while peripheral insulin resistance is often characteristic of IGT [21
]. The presence of either IFG alone or IGT alone doubled the risk of diabetes compared to the normal glucose group. Even after adjusting for the presence of either IFG or IGT, the other remained to be a significant predictor of diabetes. This supports investigation of both IFG and IGT to capture high risk individuals in Aboriginal populations.
Baseline BMI value is an import predictor of diabetes. Overweight individuals have over twofold risk and obese individuals have over fourfold risk of diabetes relative to those with normal baseline BMI values. This finding is consistent with that from a previous study in Aboriginal populations [4
]. BMI has been found to be a significant predictor of diabetes in the US general population [22
] and in other high risk populations such as South African Indians [23
], Pima Indians [24
] and Nauruans [25
The dose-response relationship between BMI and risk of diabetes exists regardless the presence of IFG/IGT. This is comparable with the results from a study of American Indians which have shown that BMI is a significant predictor of diabetes in both normal glucose tolerance group and IGT group [17
]. We found the association between IFG/IGT and diabetes was independent of obesity status. The IFG/IGT group had a higher risk of diabetes in all normal weight, overweight and obese groups. Our findings stress the importance of reducing obesity and managing IFG and IGT on diabetes prevention. However, it should be pointed out that a considerable proportion of diabetes cases were from those with a normal baseline BMI (< 25 kg/m2
) and normoglycemia, suggesting that other factors might have been important for the development of diabetes in this population. We previously reported that albuminuria was an important predictor of diabetes [26
]. Hematocrit [27
], inflammatory markers [28
] and gamma-glutamyltransferase [32
] are some potential useful predictors. Assessing novel risk factors in this population is currently in progress.
Some limitations of this study should be pointed out. First, the diabetes cases were identified through reviews of hospital and outpatient records. Ninety two percent of the participants had at least one occasion of hospitalisations during the follow up period. We could miss some diagnoses when diabetes was not severe enough for hospital care. This may underestimate the true incidence. Second, we relied on routinely documented diagnosis information in hospital records for identification of diabetes cases during follow-ups, and misdiagnosis might occur at routine practice. Furthermore, the true date of diagnosis of diabetes was probably earlier than that documented in hospital records. Third, there was potential for loss to follow-up of participants' hospital care due to out-migration to other communities. In reality, the hospital in our study setting is the only hospital serving the entire region, so that most people who had out-migrated to communities within several hundred kilometres, the usual pattern, would still have their hospital care recorded in the centralised hospital data system. Permanent out-migration is very uncommon. Fourth, because the sample size was relatively small for old age groups in this study, the incidence estimates may not be precise, as reflected in the wide 95% confidence intervals. Fifth, the data were collected in a remote community, it remains to be verified if the findings apply to other Aboriginal groups. Caution should be exercised in generalising the findings to the broader Aboriginal population in Australia. Sixth, cumulative incidence rates were estimated based on incidence data collected over one decade rather than over life time. If incidence rates change over time, so does an individual's life time risk of diabetes. Finally, the presence of IGT among some participants was determined according to the postprandial glucose values due to the absence of oral glucose tolerance tests. Some IGT individuals might have been misclassified as normal.