Jessica L. Harding

Diabetes and risk of physical disability in adults: a systematic review and meta-analysis

BACKGROUND According to previous reports, the risk of disability as a result of diabetes varies from none to double. Disability is an important measure of health and an estimate of the risk of disability as a result of diabetes is crucial in view of the global diabetes epidemic. We did a systematic review and meta-analysis to estimate this risk. METHODS We searched Ovid, Medline, Embase, Cochrane Library, and Cumulative Index to Nursing and Allied Health Literature up to Aug 8, 2012. We included studies of adults that compared the risk of disability-as measured by activities of daily living (ADL), instrumental activities of daily living (IADL), or mobility-in people with and without any type of diabetes. We excluded studies of subpopulations with specific illnesses or of people in nursing homes. From the studies, we recorded population characteristics, how diabetes was diagnosed (by doctor or self-reported), domain and definition of disability, and risk estimates for disability. We calculated pooled estimates by disability type and type of risk estimate (odds ratio [OR] or risk ratio [RR]). RESULTS Our systematic review returned 3224 results, from which 26 studies were included in our meta-analyses. Diabetes increased the risk of mobility disability (15 studies; OR 1.71, 95% CI 1.53-1.91; RR 1.51, 95% CI 1.38-1.64), of IADL disability (ten studies; OR 1.65, 95% CI 1.55-1.74), and of ADL disability (16 studies; OR 1.82, 95% CI 1.63-2.04; RR 1.82, 95% CI 1.40-2.36). INTERPRETATION Diabetes is associated with a strong increase in the risk of physical disability. Efforts to promote healthy ageing should account for this risk through prevention and management of diabetes. FUNDING Monash University, Baker IDI Bright Sparks Foundation, Australian Postgraduate Award, VicHealth, National Health and Medical Research Council, Australian Research Council, Victorian Government.

Cancer Risk Among People With Type 1 and Type 2 Diabetes: Disentangling True Associations, Detection Bias, and Reverse Causation

OBJECTIVE Evidence indicates an increased risk of certain cancers among people with type 2 diabetes. Evidence for rarer cancers and for type 1 diabetes is limited. We explored the excess risk of site-specific cancer incidence and mortality among people with type 1 and type 2 diabetes, compared with the general Australian population. RESEARCH DESIGN AND METHODS Registrants of a national diabetes registry (953,382) between 1997 and 2008 were linked to national death and cancer registries. Standardized incidence and mortality ratios (SIRs/SMRs) are reported. RESULTS For type 1 diabetes, significant elevated SIRs were observed for pancreas, liver, esophagus, colon and rectum (females only [F]), stomach (F), thyroid (F), brain (F), lung (F), endometrium, and ovary, and decreased SIRs were observed for prostate in males. Significantly increased SMRs were observed for pancreas, liver, and kidney (males only), non-Hodgkin’s lymphoma, brain (F), and endometrium. For type 2 diabetes, significant SIRs were observed for almost all site-specific cancers, with highest SIRs observed for liver and pancreas, and decreased risks for prostate and melanoma. Significant SMRs were observed for liver, pancreas, kidney, Hodgkin’s lymphoma, gallbladder (F), stomach (F), and non-Hodgkin’s lymphoma (F). Cancer risk was significantly elevated throughout follow-up time but was higher in the first 3 months postregistration, suggesting the presence of detection bias and/or reverse causation. CONCLUSIONS Type 1 and type 2 diabetes are associated with an excess risk of incidence and mortality for overall and a number of site-specific cancers, and this is only partially explained by bias. We suggest that screening for cancers in diabetic patients is important.

Mortality trends among people with type 1 and type 2 diabetes in Australia: 1997-2010

OBJECTIVE With improvements in cardiovascular disease (CVD) rates among people with diabetes, mortality rates may also be changing. However, these trends may be influenced by coding practices of CVD-related deaths on death certificates. We analyzed trends of mortality over 13 years in people with diabetes and quantified the potential misclassification of CVD mortality according to current coding methods. RESEARCH DESIGN AND METHODS A total of 1,136,617 Australians with diabetes registered on the National Diabetes Services Scheme between 1997 and 2010 were linked to the National Death Index. Excess mortality relative to the Australian population was reported as standardized mortality ratios (SMRs). Potential misclassification of CVD mortality was determined by coding CVD according to underlying cause of death (COD) and then after consideration of both the underlying and other causes listed in part I of the death certificate. RESULTS For type 1 diabetes, the SMR decreased in males from 4.20 in 1997 to 3.08 in 2010 (Ptrend < 0.001) and from 3.92 to 3.46 in females (Ptrend < 0.01). For type 2 diabetes, the SMR decreased in males from 1.40 to 1.21 (Ptrend < 0.001) and from 1.56 to 1.22 in females (Ptrend < 0.001). CVD deaths decreased from 35.6 to 31.2% and from 31.5 to 27.2% in males and females with type 1 diabetes, respectively (Ptrend < 0.001 for both sexes). For type 2 diabetes, CVD decreased from 44.5 to 29.2% in males and from 45.5 to 31.6% in females (Ptrend < 0.001 for both sexes). Using traditional coding methods, ∼38 and 26% of CVD deaths are underestimated in type 1 diabetes and type 2 diabetes, respectively. CONCLUSIONS All-cause and CVD mortality has decreased in diabetes. However, the total CVD mortality burden is underestimated when only underlying COD is considered. This has important ramifications for understanding mortality patterns in diabetes.

Persistent organic pollutants and diabetes: a review of the epidemiological evidence.

The prevalence of diabetes and obesity has increased rapidly over the last few decades in both developed and developing countries. While it is intuitively appealing to suggest that lifestyle risk factors such as decreased physical activity and adoption of poor diets can explain much of the increase, the evidence to support this is poor. Given this, there has been an impetus to look more widely than traditional lifestyle and biomedical risk factors, especially those risk factors, which arise from the environment. Since the industrial revolution, there has been an introduction of many chemicals into our environment, which have now become environmental pollutants. There has been growing interest in one key class of environmental pollutants known as persistent organic pollutants (POPs) and their potential role in the development of diabetes. This review will summarise and appraise the current epidemiological evidence relating POPs to diabetes and highlight gaps and flaws in this evidence.

Psychosocial stress is positively associated with body mass index gain over 5 years: Evidence from the longitudinal AusDiab study

Emerging evidence suggests that psychosocial stress may influence weight gain. The relationship between stress and weight change and whether this was influenced by demographic and behavioral factors was explored.

Age-specific trends from 2000-2011 in all-cause and cause-specific mortality in type 1 and type 2 Diabetes: A cohort study of more than one million people

OBJECTIVE To analyze changes by age-group in all-cause and cause-specific mortality rates from 2000–2011 in people with diabetes. RESEARCH DESIGN AND METHODS A total of 1,189,079 (7.3% with type 1 diabetes) Australians with diabetes registered on the National Diabetes Service Scheme between 2000 and 2011 were linked to the National Death Index. Mortality rates in the total population were age standardized to the 2001 Australian population. Mortality rates were calculated for the following age-groups: 0 to <40 years, ≥ 40 to <60 years, and ≥60 to ≤85 years. Annual mortality rates were fitted using a Poisson regression model including calendar year as a covariate and age and sex where appropriate, with Ptrend reported. RESULTS For type 1 diabetes, all-cause, cardiovascular disease (CVD), and diabetes age-standardized mortality rates (ASMRs) decreased each year by 0.61, 0.35, and 0.14 per 1,000 person-years (PY), respectively, between 2000 and 2011, Ptrend < 0.05, while cancer mortality remained unchanged. By age, significant decreases in all-cause, CVD, and diabetes mortality rates were observed in all age-groups, excluding diabetes mortality in age-group 0–40 years. For type 2 diabetes, all-cause, CVD, and diabetes ASMRs decreased per year by 0.18, 0.15, and 0.03 per 1,000 PY, respectively, Ptrend < 0.001, while cancer remained unchanged. By age, these decreases were observed in all age-groups, excluding 0–40 years, where significant increases in all-cause and cancer mortality were noted and no change was seen for CVD and diabetes mortality. CONCLUSIONS All-cause, CVD, and diabetes ASMRs in type 1 and type 2 diabetes decreased between 2000 and 2011, while cancer ASMRs remained unchanged. However, younger populations are not benefiting from the same improvements as older populations. In addition, the absence of a decline in cancer mortality warrants urgent attention.

Excess risk of dying from infectious causes in those with type 1 and type 2 diabetes

OBJECTIVE To investigate infection-related mortality in individuals with type 1 and type 2 diabetes. RESEARCH DESIGN AND METHODS A total of 1,108,982 individuals with diabetes who were registered with the Australian Diabetes register between 2000 and 2010 were linked to the National Death Index. Mortality outcomes were defined as infection-relatedA-B death (ICD codes A99–B99), pneumonia (J12–J189), septicemia (A40 and A41), and osteomyelitis (M86). RESULTS During a median follow-up of 6.7 years, there were 2,891, 2,158, 1,248, and 147 deaths from infection-relatedA-B causes, pneumonia, septicemia, or osteomyelitis, respectively. Crude mortality rates from infectionsA-B were 0.147 and 0.431 per 1,000 person-years in type 1 and type 2 diabetes, respectively. Standardized mortality ratios (SMRs) were higher in type 1 and type 2 diabetes for all outcomes after adjustment for age and sex. For infection-relatedA-B mortality, SMRs were 4.42 (95% CI 3.68–5.34) and 1.47 (1.42–1.53) for type 1 and type 2 diabetes (P < 0.001), respectively. For pneumonia in type 1 diabetes, SMRs were approximately 5 and 6 in males and females, respectively, while the excess risk was ∼20% for type 2 (both sexes). For septicemia, SMRs were approximately 10 and 2 for type 1 and type 2 diabetes, respectively, and similar by sex. For osteomyelitis in type 1 diabetes, SMRs were 16 and 58 in males and females, respectively, and ∼3 for type 2 diabetes (both sexes). CONCLUSIONS Although death owing to infection is rare, we confirm that patients with diabetes have an increased mortality from a range of infections, compared with the general population, and that the increased risk appears to be greater for type 1 than type 2 diabetes.

Cancer Risk Among People With Type 1 and Type 2 Diabetes: Disentangling True Associations, Detection Bias, and Reverse Causation. Diabetes Care 2015;38:264–270

The authors of the article cited above noticed an error in the way they had described their definitions of type 1 and type 2 diabetes in the research design and methods section. The description as published is as follows:Diabetes type is classified by the health practitioner completing registration. However, for the current study, type 1 diabetes status was assigned to registrants who were classified as type 1 on the NDSS and were diagnosed before the age of 30 years, and the time between diagnosis date and date of first insulin use was <1 year. For those missing data on date of diagnosis (59.1% type 1 diabetes and 36.1% type 2 diabetes) or insulin initiation date (many of whom registered in the early years of the operation of the NDSS and …

The validity of self-reported cancer in an Australian population study.

Objective: The aim of this study is to determine the validity of self‐reported cancer data by comparing it to the Australian Cancer Database (ACD).

Hypertension, antihypertensive treatment and cancer incidence and mortality: a pooled collaborative analysis of 12 Australian and New Zealand cohorts

Background: Observational studies examining associations between hypertension and cancer are inconsistent. We explored the association of hypertension, graded hypertension and antihypertensive treatment with cancer incidence and mortality. Method: Eighty-six thousand five hundred and ninety-three participants from the Australian and New Zealand Diabetes and Cancer Collaboration were linked to the National Death Index and Australian Cancer Database. Cox proportional hazards models estimated hazard ratios and 95% confidence intervals (95% CI) for the association of treated and untreated hypertension with cancer incidence and mortality. Results: Over a median follow-up of 15.1 years, 12 070 incident and 4350 fatal cancers were identified. Untreated and treated hypertension, compared with normotension, were associated with an increased risk for cancer incidence [hazard ratio 1.06, 95% CI (1.00–1.11) and 1.09 (1.02–1.16) respectively], and cancer mortality (1.07, 0.98–1.18) and (1.15, 1.03–1.28), respectively. When compared with untreated hypertension, treated hypertension did not have a significantly greater risk for cancer incidence (1.03, 0.97–1.10) or mortality (1.07, 0.97–1.19). A significant dose–response relationship was observed between graded hypertension and cancer incidence and mortality; Ptrend = 0.053 and Ptrend = 0.001, respectively. When stratified by treatment status, these relationships remained significant in untreated, but not in treated, hypertension. Conclusion: Hypertension, both treated and untreated, is associated with a modest increased risk for cancer incidence and mortality. Similar risks in treated and untreated hypertension suggest that the increased cancer risk is not explained by the use of antihypertensive treatment.