Mortality in Type 2 Diabetes Mellitus
Background: Type 2 diabetes is associated with an increase in age-related mortality. A systematic review and meta-analysis were performed to define the relative risks (RR) of all-cause or cause-specific mortality in type 2 diabetes and to determine gaps in current research.
Methods: A comprehensive literature search was undertaken for studies (published 1990–2010) on mortality in type 2 diabetes. The study reports on the measure of mortality as defined by RR for all-cause and cause-specific mortality, heterogeneity, sensitivity analyses and biases.
Results: In total 35 studies (220,689 patients; mean follow-up of 10.7 years) were eligible for inclusion: 33 studies reported increased mortality risks; 24 had full data on 95% confidence intervals (CIs), one study reported no excess mortality in men diagnosed after 65 years whereas three reported increased mortality in similar age groups in both sexes. Meta-analysis showed RR = 1.85 (95% CI 1.79–1.92) for all-cause mortality [men RR=1.57 (95% CI 1.46–1.68); women RR=2.0 (95% CI 1.89–2.12)], RR=1.76 (95% CI 1.66–1.88) for cardiovascular mortality and RR=2.26 (95% CI: 1.7–3.02) for stroke. There was no statistically significant evidence of publication bias.
Conclusion: Type 2 diabetes increases mortality approximately two-fold increase and macrovascular disease is the principal cause of death.
Type 2 diabetes remains one of the most challenging global health problems of our time and with increasing prevalence the burden will escalate. The disease is associated with an increase in mortality rate. In 1983, this rate was quoted as four to five times that in the general population; more recent studies have suggested that the rate is twice that seen in the population without diabetes. The degree of diabetes-related mortality is age-related however, so tends to be less in patients diagnosed in their late 70s (47–51% are diagnosed aged 65 years or more), when compared with those in their mid-40s. Given these differential mortality rates associated with differential diagnostic rates, and that 50% also have evidence of complications at diagnosis, the fact that type 2 diabetes reduces life expectancy does not translate directly (linearly) to an ability to predict death rates in these patients. However, what is known is that 89% of people diagnosed with type 2 diabetes have one or more modifiable risk factors so that the proportion of preventable deaths should not be underestimated.
In type 2 diabetes, macrovascular disease is the predominant cause of mortality, with CVD accounting for 52–80% of deaths, followed by renal disease (heralded by albuminuria) 10–20% of mortality, and cerebrovascular disease 15%, which is approximately twice that seen in the population without diabetes in the first five years following diagnosis. Various researchers have also documented increased relative mortality risk in type 2 diabetes associated with cancers, and more recently there has been inconclusive and contradictory evidence of the effects of various insulin therapies or secretagogues associated with increased malignancy risks.
Tight glycaemic regulation has been shown to be difficult to maintain in type 2 diabetes. Evidence suggests that in itself it has little effect on mortality from cardiovascular disease. Efforts are therefore aimed at continual optimisation of treatments for the atherogenic risk factors in CVD including hypertension, cholesterol/hyperlipidaemia, obesity, smoking, and alcohol consumption; alongside satisfactory glycaemic control. However, past studies have used the hazard ratio (which measures the rate at which events have occurred rather than how many events have occurred) to estimate mortality risks in type 2 diabetes, as well as there being issues around small sample size. Given the conflicting evidence concerning all-cause or cause-specific mortality in type 2 diabetes when compared with the population without diabetes, the purpose of this systematic review and meta-analysis was to explore, review, and summarise the evidence to clarify current knowledge and research gaps, and to identify possible future strategies for improvement.
Abstract and Introduction
Abstract
Background: Type 2 diabetes is associated with an increase in age-related mortality. A systematic review and meta-analysis were performed to define the relative risks (RR) of all-cause or cause-specific mortality in type 2 diabetes and to determine gaps in current research.
Methods: A comprehensive literature search was undertaken for studies (published 1990–2010) on mortality in type 2 diabetes. The study reports on the measure of mortality as defined by RR for all-cause and cause-specific mortality, heterogeneity, sensitivity analyses and biases.
Results: In total 35 studies (220,689 patients; mean follow-up of 10.7 years) were eligible for inclusion: 33 studies reported increased mortality risks; 24 had full data on 95% confidence intervals (CIs), one study reported no excess mortality in men diagnosed after 65 years whereas three reported increased mortality in similar age groups in both sexes. Meta-analysis showed RR = 1.85 (95% CI 1.79–1.92) for all-cause mortality [men RR=1.57 (95% CI 1.46–1.68); women RR=2.0 (95% CI 1.89–2.12)], RR=1.76 (95% CI 1.66–1.88) for cardiovascular mortality and RR=2.26 (95% CI: 1.7–3.02) for stroke. There was no statistically significant evidence of publication bias.
Conclusion: Type 2 diabetes increases mortality approximately two-fold increase and macrovascular disease is the principal cause of death.
Introduction
Type 2 diabetes remains one of the most challenging global health problems of our time and with increasing prevalence the burden will escalate. The disease is associated with an increase in mortality rate. In 1983, this rate was quoted as four to five times that in the general population; more recent studies have suggested that the rate is twice that seen in the population without diabetes. The degree of diabetes-related mortality is age-related however, so tends to be less in patients diagnosed in their late 70s (47–51% are diagnosed aged 65 years or more), when compared with those in their mid-40s. Given these differential mortality rates associated with differential diagnostic rates, and that 50% also have evidence of complications at diagnosis, the fact that type 2 diabetes reduces life expectancy does not translate directly (linearly) to an ability to predict death rates in these patients. However, what is known is that 89% of people diagnosed with type 2 diabetes have one or more modifiable risk factors so that the proportion of preventable deaths should not be underestimated.
In type 2 diabetes, macrovascular disease is the predominant cause of mortality, with CVD accounting for 52–80% of deaths, followed by renal disease (heralded by albuminuria) 10–20% of mortality, and cerebrovascular disease 15%, which is approximately twice that seen in the population without diabetes in the first five years following diagnosis. Various researchers have also documented increased relative mortality risk in type 2 diabetes associated with cancers, and more recently there has been inconclusive and contradictory evidence of the effects of various insulin therapies or secretagogues associated with increased malignancy risks.
Tight glycaemic regulation has been shown to be difficult to maintain in type 2 diabetes. Evidence suggests that in itself it has little effect on mortality from cardiovascular disease. Efforts are therefore aimed at continual optimisation of treatments for the atherogenic risk factors in CVD including hypertension, cholesterol/hyperlipidaemia, obesity, smoking, and alcohol consumption; alongside satisfactory glycaemic control. However, past studies have used the hazard ratio (which measures the rate at which events have occurred rather than how many events have occurred) to estimate mortality risks in type 2 diabetes, as well as there being issues around small sample size. Given the conflicting evidence concerning all-cause or cause-specific mortality in type 2 diabetes when compared with the population without diabetes, the purpose of this systematic review and meta-analysis was to explore, review, and summarise the evidence to clarify current knowledge and research gaps, and to identify possible future strategies for improvement.