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RESEARCH DESIGN AND METHODS -Insulin-treated diabetic subjects (n = 1,008) on the Canterbury Diabetes Registry were tracked over 9 years, and their vital status was determined. Death rates were standardized using direct and indirect methods. Cox proportional hazard regression was used to model the effects of demographic and clinical covariates on survival time.RESULTS -At study entry, age ranged from 2.9 to 92.7 years, with mean 48.7 ± 20.4 years; age at diagnosis was 0.2-88.9 years, mean 34.5 ± 20.0 years; and duration of diabetes was 0.1-58.5 years, mean 14.0 ± 10.6 years. There were 303 deaths in 7,372 person-years of follow-up with a standardized mortality ratio (SMR) of 2.6 (95% CI 2.4-3.0). Relative mortality was greatest for those aged 30-39 years .2]). The death rate for the diabetic cohort standardized against the Segi world standard population was 16.2 per 1,000. Attained age, sex, and clinical subtype were significant predictors of mortality. The SMR for subjects with type 1 diabetes and age at onset Ͻ30 years was 3.7 (CI 2.7-5.0), 2.2 (1.8-2.6) for those with onset Ն30 years, and 3.1 (2.5-3.7) for subjects suspected of having latent autoimmune diabetes in adulthood or insulin-treated type 2 diabetes. Life expectancy was reduced for both sexes at all ages.CONCLUSIONS -Mortality rates for insulin-treated diabetic individuals remain high, resulting in shortened life spans relative to the general population. Marked differences in mortality exist between clinical groups of subjects. Further research is needed to improve diabetes classification and to clarify differences in health outcomes.

A cohort of 447 subjects with Type 2 diabetes mellitus (208 male, 239 female; age range 30-82, median 62 years; and of predominantly European origin) was characterized in a clinic survey in 1989. Individual status (dead or alive) at 1 June 1995 was ascertained. Mortality rates were compared with the general New Zealand population by calculating standardized mortality ratios (SMR) and the hazard ratio (HR) of prognostic factors evaluated with Cox's proportional hazards model. At 6 years, 289 subjects were confirmed as alive and 133 as dead; only 25 were untraceable. Six-year survival for the cohort was 70% (95% CI 66-74). SMR was 2.53 (95% CI 1.99-2.68) for the female cohort and 2.03 (95% CI 1.60-2.59) for the male cohort. Factors assessed at baseline (1989) that were independently prognostic of total mortality included age, male sex, pre-existing coronary artery disease (CAD) (HR 2.2, 95% CI 1.5-3.3) and plasma cholesterol (HR for 1.4 mmol l(-1) change: 1.49, 95% CI 1.2-1.9). HDL-cholesterol was protective in women (HR for 0.4 mmol l(-1) change: 0.72, 95% CI 0.51-1.00) but not men. Glycated haemoglobin was not a significant predictor of total mortality. Predictors of CAD mortality (in those subjects free of CAD in 1989) included plasma cholesterol (HR for 1.4 mmol l(-1) change: 1.86 95% CI 1.20-2.89), glycated haemoglobin (HR for 1.8% change: 1.9 95% CI 1.04-3.47), male sex, peripheral vascular disease, and smoking. There is therefore increased mortality in Type 2 diabetic subjects in Canterbury, New Zealand. HDL-cholesterol is protective against total mortality in females.

Mortality rates are high for insulin-treated diabetic individuals relative to the general population.