Asia-Oceania and the global epidemic of diabetes.
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Biomedical subjects
Publications and source records attributed to T A Welborn.
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Serum insulin 1 h post-glucose load is examined in this prospective study of 2971 Caucasoid subjects aged > 20 years in 1966 and followed to 1989. The serum insulin levels as a continuous variable show no significant linear association with coronary heart disease (CHD) deaths in either sex after accounting for age by Cox proportional hazards analysis. In males the quintile classes of serum insulin show a striking U-shaped pattern with both the highest and lowest quintiles having significant associations with CHD deaths. In females the insulin quintiles show no direct association. Analysis for interactions of risk variables indicate that in females the relative protection of low cholesterol levels is abolished by hyperinsulinaemia after 12 years. Thus, serum insulin is not a direct aetiological risk factor for CHD. The findings suggest that the associations are likely to be due to confounding effects of unmeasured variables including lipid subfractions.
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The community of Busselton in Western Australia has participated in repeated cross-sectional health surveys and other health interventions since 1966. Health surveys of adults were conducted every three years from 1966 to 1981. Health interventions, including programs for high blood pressure, smoking, high blood cholesterol levels and obesity, were implemented in the community. Mortality rates for the Busselton area are compared with rates for the remainder of the southwest region of Western Australia in an attempt to determine if the surveys and associated interventions have had any impact on survival. Statistical comparisons via Poisson regression analysis showed that mortality rates for males over the period 1965 to 1989 in Busselton declined at a similar rate to the southwest. However, for females, especially those aged 45 to 74 years, mortality rates declined significantly faster in Busselton than in the southwest, suggesting a beneficial impact on survival of the surveys and associated interventions.
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A cohort of 888 rural, nonaboriginal persons with non-insulin-dependent diabetes mellitus identified in Western Australia through surveys in 1978-1982 were followed for death until the end of 1986. A total of 257 deaths were observed. Excess mortality in this cohort as compared with the general Australian population was investigated by calculating standardized mortality ratios and using the Cox proportional hazards regression model with hazard rates for the general population as the baseline. The overall standardized mortality ratio was 1.83 (95% confidence interval 1.51-2.16) for women and 1.43 (95% confidence interval 1.18-1.67) for men. Cause-specific comparisons with the general population showed that the majority of excess deaths could be attributed to diseases of the circulatory system. Factors assessed at the baseline survey that were independently prognostic of shorter survival were early onset of diabetes (for females only), high plasma glucose level, retinopathy, macrovascular disease, albuminuria (for females only), and elevated plasma creatinine level. Reductions in life expectancy at 60 years of age as compared with the general population averaged about 5 years but could be as much as 16 years for female diabetics with early onset of diabetes, high plasma glucose levels, and several complications.
OBJECTIVE: To investigate duration of the period between diabetes onset and its clinical diagnosis. RESEARCH DESIGN AND METHODS: Two population-based groups of white patients with non-insulin-dependent diabetes (NIDDM) in the United States and Australia were studied. Prevalence of retinopathy and duration of diabetes subsequent to clinical diagnosis were determined for all subjects. Weighted linear regression was used to examine the relationship between diabetes duration and prevalence of retinopathy. RESULTS: Prevalence of retinopathy at clinical diagnosis of diabetes was estimated to be 20.8% in the U.S. and 9.9% in Australia and increased linearly with longer duration of diabetes. By extrapolating this linear relationship to the time when retinopathy prevalence was estimated to be zero, onset of detectable retinopathy was calculated to have occurred approximately 4-7 yr before diagnosis of NIDDM. Because other data indicate that diabetes may be present for 5 yr before retinopathy becomes evident, onset of NIDDM may occur 9-12 yr before its clinical diagnosis. CONCLUSIONS: These findings suggest that undiagnosed NIDDM is not a benign condition. Clinically significant morbidity is present at diagnosis and for years before diagnosis. During this preclinical period, treatment is not being offered for diabetes or its specific complications, despite the fact that reduction in hyperglycemia, hypertension, and cardiovascular risk factors is believed to benefit patients. Imprecise dating of diabetes onset also obscures investigations of the etiology of NIDDM and studies of the nature and importance of risk factors for diabetes complications.
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Subjects with diabetes who attended rural surveys in Western Australia from 1978 to 1982 were followed up to ascertain death rates and the causes of death recorded on death certificates. Cardiovascular disease was assigned as the direct cause of death in 63% of deaths, with equal rates in male and female subjects, and renal disease in 8% of deaths with the proportion in women (12%) being greater than that in men (4%). The diagnosis of diabetes was stated on only 65% of the death certificates, and in only 24% was diabetes recorded as a direct or antecedent cause. In the same cohort the Australian Bureau of Statistics coded diabetes as the underlying cause of death in 24%, while attributing deaths to cardiovascular disease in 50% of the cases. This study suggests that diabetes is considerably underreported both on doctors' death certificates and in the mortality figures of the Australian Bureau of Statistics.
We report the prevalence of diabetes in a population sample of 10,083 persons who were aged 25 to 64 years in eight city centres. One hundred and sixty-nine persons were known to have diabetes and 48 persons were newly-discovered to have diabetes on the basis of fasting hyperglycaemia (plasma glucose level, equal to or greater than 7.8 mmol/L). Type-1 diabetes was identified by clinical criteria and accounted for 19% of cases of known diabetes, but this proportion ranged from 67% of persons with known diabetes in the age-group of 25-29 years, to between 9% and 15% in the age-groups of persons who were 50 years of age and over. For both known and newly-discovered cases, persons with type-2 diabetes showed a significant male preponderance, which suggests that an environmental factor is operating preferentially on male subjects to cause this form of diabetes. The results of the present study, when taken with those of other recent prevalence studies, enable an approximate estimate of numbers of persons with diabetes in Australia. Approximately 250,000 persons have diagnosed diabetes, of whom 40,000 persons have type-1 diabetes, including 7000 persons who are less than 25 years of age. The number of persons with undiagnosed diabetes who could be identified on the basis of fasting hyperglycaemia is estimated to be 75,000; an additional 150,000 persons would be diagnosed to have diabetes if they were to undergo glucose tolerance tests. This study gave prevalence rates for known diabetes in Australia in 1984 of 1.6% at all ages and 2.4% for adults who were 21 years of age and older; additionally, the estimated prevalence rates for undiagnosed diabetes were 1.4% for all ages and 2.2% for adults.
The prevalence and incidence of diabetes mellitus in the age group zero to 14 years in Western Australia were determined from a survey by means of Schools Health Services. Additional information from the State's computer-linked hospital records system, the State's only children's hospital, diabetic clinics and physicians enabled virtually complete ascertainment of cases of childhood diabetes. Only 60% of school-age diabetic children were known to school nurses before the survey, but the nurses were able to identify two-thirds of the remainder during the survey. Among non-Aboriginal children, the prevalence of diabetes in the age group zero to 14 years was 0.59 per 1000 children and the incidence was 12.3 per 100,000 children per year. These rates are somewhat lower than those that have been reported from the United Kingdom and North America, and substantially lower than the rates that were reported from Scandinavia. All but one of the diabetic children who were identified required insulin and were assumed to be insulin-dependent. An excess of boys was found. None of 8715 Aboriginal or part-Aboriginal children had insulin-dependent diabetes mellitus, which indicates that this racial group has a low prevalence of this condition. In case--control studies, which used questionnaires for parents, no significant trends were found in relation to the history of immunizations or of specific viral illnesses except for a past history of varicella which was less frequent in diabetic children. A past history of established breast-feeding (of more than one week) was less frequent in diabetic children, as was the ingestion of vitamin C supplements before the onset of diabetes. Some evidence for a seasonality of onset was obtained. The diabetic children were absent from school for more days and had more admissions to hospital than did non-diabetic children. The majority of diabetic children were prescribed insulin twice a day or more often (84%); performed home blood-glucose monitoring (74%); and attended hospital diabetic clinics (91%).
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The prevalence of diabetic complications is reported from a cross-sectional study of rural diabetic subjects in Western Australia. Logistic-regression analysis has been used to discover potential risk factors associated with each complication. A distinction has been made between time-related variables (age, age at diagnosis, duration of diabetes) and other risk variables. We have attempted to identify the major time-related risk variables for each complication and then examined the effect of other risk variables after accounting for the major time-related variables. The important time-related variables were found to be duration of diabetes for retinopathy, age for macrovascular disease, duration and age at diagnosis of diabetes for sensory neuropathy, and age for renal impairment. When matched on these important time-related variables, the overall prevalences of complications for insulin-dependent (IDDM) compared with non-insulin-dependent (NIDDM) diabetic patients were essentially the same. An exception is renal impairment, for which IDDM patients had a higher prevalence than did NIDDM patients of the same age. After allowing for time-related variables, the analysis also demonstrates positive independent associations between diabetic control (glycosylated hemoglobin) and retinopathy and between diabetic control and macrovascular disease. Plasma cholesterol (positively) and high-density lipoprotein cholesterol (negatively) were related independently to both macrovascular disease and renal impairment. Very few differences in the risk-factor profiles for complications were found for IDDM compared with NIDDM patients after allowing for time-related variables.
We have estimated the prevalence of diabetes and impaired glucose tolerance from the Busselton 1981 Population Survey using the 1980 World Health Organization (WHO) criteria. Standardized to the Australian non-Aboriginal population aged 25 years and over, the prevalence rates in this white community were 2.5% for known diabetes; 0.9% for newly discovered diabetes; 2.9% for impaired glucose tolerance; and 6.3% for all categories of abnormal glucose tolerance. There appears to have been a real increase in the frequency of diabetes since 1966. Using fasting serum C-peptide values and clinical criteria, 14% of all diabetic subjects were insulin-dependent. The male:female ratio for all categories of abnormal glucose tolerance was 1.4:1. Data from the United States indicate spectacularly higher rates for diabetes and impaired glucose tolerance in the white population. A national study of the prevalence of diabetes and impaired glucose tolerance in Australia is recommended. For epidemiological purposes, a single blood glucose value two hours after a 75 g oral glucose tolerance test is sufficient to categorize glucose tolerance as defined by WHO.
A cross-sectional study of 1084 Caucasoid diabetic subjects in rural Western Australia revealed a high rate of clinical macrovascular disease (46%), including coronary heart disease (13%), stroke (8%), and peripheral vascular disease (38%). Age was the major time-related variable for total macrovascular disease and for peripheral vascular disease, with identical prevalence rates in Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes when age was taken into account. In 179 Type 1 diabetic subjects, logistic regression analysis showed no associated risk factors other than age. In 905 Type 2 diabetic subjects the independent risk factors for total macrovascular disease, identified by a forward step-wise selection procedure, were age as the major contributor, with plasma creatinine levels and plasma glucose levels (all p less than 0.001), high-density lipoprotein cholesterol levels, serum total cholesterol levels, and the (supine-erect) systolic blood pressure difference (all p less than 0.05). There were no direct associations with percentage desirable weight, cigarette smoking or male sex. Type 2 diabetic subjects demonstrated a very strong negative association between high-density lipoprotein cholesterol levels and coronary heart disease, and significant associations were found also between plasma glucose levels and coronary heart disease (p less than 0.01), and glycosylated haemoglobin levels and peripheral vascular disease (p less than 0.001).