Dianna J. Magliano

Television Viewing Time and Mortality The Australian Diabetes, Obesity and Lifestyle Study (AusDiab)

Background— Television viewing time, the predominant leisure-time sedentary behavior, is associated with biomarkers of cardiometabolic risk, but its relationship with mortality has not been studied. We examined the associations of prolonged television viewing time with all-cause, cardiovascular disease (CVD), cancer, and non-CVD/noncancer mortality in Australian adults. Methods and Results— Television viewing time in relation to subsequent all-cause, CVD, and cancer mortality (median follow-up, 6.6 years) was examined among 8800 adults ≥25 years of age in the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). During 58 087 person-years of follow-up, there were 284 deaths (87 CVD deaths, 125 cancer deaths). After adjustment for age, sex, waist circumference, and exercise, the hazard ratios for each 1-hour increment in television viewing time per day were 1.11 (95% confidence interval [CI], 1.03 to 1.20) for all-cause mortality, 1.18 (95% CI, 1.03 to 1.35) for CVD mortality, and 1.09 (95% CI, 0.96 to 1.23) for cancer mortality. Compared with a television viewing time of <2 h/d, the fully adjusted hazard ratios for all-cause mortality were 1.13 (95% CI, 0.87 to 1.36) for ≥2 to <4 h/d and 1.46 (95% CI, 1.04 to 2.05) for ≥4 h/d. For CVD mortality, corresponding hazard ratios were 1.19 (95% CI, 0.72 to 1.99) and 1.80 (95% CI, 1.00 to 3.25). The associations with both cancer mortality and non-CVD/noncancer mortality were not significant. Conclusions— Television viewing time was associated with increased risk of all-cause and CVD mortality. In addition to the promotion of exercise, chronic disease prevention strategies could focus on reducing sitting time, particularly prolonged television viewing.

Risk of Cardiovascular and All-Cause Mortality in Individuals With Diabetes Mellitus, Impaired Fasting Glucose, and Impaired Glucose Tolerance The Australian Diabetes, Obesity, and Lifestyle Study (AusDiab)

Background— Diabetes mellitus increases the risk of cardiovascular disease (CVD) and all-cause mortality. The relationship between milder elevations of blood glucose and mortality is less clear. This study investigated whether impaired fasting glucose and impaired glucose tolerance, as well as diabetes mellitus, increase the risk of all-cause and CVD mortality. Methods and Results— In 1999 to 2000, glucose tolerance status was determined in 10 428 participants of the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab). After a median follow-up of 5.2 years, 298 deaths occurred (88 CVD deaths). Compared with those with normal glucose tolerance, the adjusted all-cause mortality hazard ratios (HRs) and 95% confidence intervals (CIs) for known diabetes mellitus and newly diagnosed diabetes mellitus were 2.3 (1.6 to 3.2) and 1.3 (0.9 to 2.0), respectively. The risk of death was also increased in those with impaired fasting glucose (HR 1.6, 95% CI 1.0 to 2.4) and impaired glucose tolerance (HR 1.5, 95% CI 1.1 to 2.0). Sixty-five percent of all those who died of CVD had known diabetes mellitus, newly diagnosed diabetes mellitus, impaired fasting glucose, or impaired glucose tolerance at baseline. Known diabetes mellitus (HR 2.6, 95% CI 1.4 to 4.7) and impaired fasting glucose (HR 2.5, 95% CI 1.2 to 5.1) were independent predictors for CVD mortality after adjustment for age, sex, and other traditional CVD risk factors, but impaired glucose tolerance was not (HR 1.2, 95% CI 0.7 to 2.2). Conclusions— This study emphasizes the strong association between abnormal glucose metabolism and mortality, and it suggests that this condition contributes to a large number of CVD deaths in the general population. CVD prevention may be warranted in people with all categories of abnormal glucose metabolism.

Glucose indices, health behaviors, and incidence of diabetes in Australia: The Australian diabetes, obesity and lifestyle study

OBJECTIVE—This national, population-based study reports diabetes incidence based on oral glucose tolerance tests (OGTTs) and identifies risk factors for diabetes in Australians. RESEARCH DESIGN AND METHODS—The Australian Diabetes, Obesity and Lifestyle Study followed-up 5,842 participants over 5 years. Normal glycemia, impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and diabetes were defined using World Health Organization criteria. RESULTS—Age-standardized annual incidence of diabetes for men and women was 0.8% (95% CI 0.6–0.9) and 0.7% (0.5–0.8), respectively. The annual incidence was 0.2% (0.2–0.3), 2.6% (1.8–3.4), and 3.5% (2.9–4.2) among those with normal glycemia, IFG, and IGT, respectively, at baseline. Among those with IFG, the incidence was significantly higher in women (4.0 vs. 2.0%), while among those with IGT, it was significantly higher in men (4.4 vs. 2.9%). Using multivariate logistic regression, hypertension (odds ratio 1.64 [95% CI 1.17–2.28]), hypertriglyceridemia (1.46 [1.05–2.02]), log fasting plasma glucose (odds ratio per 1 SD 5.25 [95% CI 3.98–6.92]), waist circumference (1.26 [1.08–1.48]), smoking (1.70 [96% CI 1.11–2.63]), physical inactivity (1.56 [1.12–2.16]), family history of diabetes (1.82 [1.30–2.52]), and low education level (1.85 [1.04–3.31]) were associated with incident diabetes. In age- and sex-adjusted models, A1C was a predictor of diabetes in the whole population, in those with normal glycemia, and in those with IGT or IFG. CONCLUSIONS—Diabetes incidence is 10–20 times greater in those with IGT or IFG than those with normal glycemia. Measures of glycemia, A1C, metabolic syndrome components, education level, smoking, and physical inactivity are risk factors for diabetes.

Low serum 25-hydroxyvitamin D is associated with increased risk of the development of the metabolic syndrome at five years: results from a national, population-based prospective study (The Australian Diabetes, Obesity and Lifestyle Study: AusDiab).

CONTEXT Serum 25-hydroxyvitamin D [25(OH)D] concentration has been inversely associated with the prevalence of metabolic syndrome (MetS), but the relationship between 25(OH)D and incident MetS remains unclear. OBJECTIVE We evaluated the prospective association between 25(OH)D, MetS, and its components in a large population-based cohort of adults aged 25 yr or older. DESIGN We used baseline (1999-2000) and 5-yr follow-up data of the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab). PARTICIPANTS Of the 11,247 adults evaluated at baseline, 6,537 returned for follow-up. We studied those without MetS at baseline and with complete data (n = 4164; mean age 50 yr; 58% women; 92% Europids). OUTCOME MEASURES We report the associations between baseline 25(OH)D and 5-yr MetS incidence and its components, adjusted for age, sex, ethnicity, season, latitude, smoking, family history of type 2 diabetes, physical activity, education, kidney function, waist circumference (WC), and baseline MetS components. RESULTS A total of 528 incident cases (12.7%) of MetS developed over 5 yr. Compared with those in the highest quintile of 25(OH)D (≥34 ng/ml), MetS risk was significantly higher in people with 25(OH)D in the first (<18 ng/ml) and second (18-23 ng/ml) quintiles; odds ratio (95% confidence interval) = 1.41 (1.02-1.95) and 1.74 (1.28-2.37), respectively. Serum 25(OH)D was inversely associated with 5-yr WC (P < 0.001), triglycerides (P < 0.01), fasting glucose (P < 0.01), and homeostasis model assessment for insulin resistance (P < 0.001) but not with 2-h plasma glucose (P = 0.29), high-density lipoprotein cholesterol (P = 0.70), or blood pressure (P = 0.46). CONCLUSIONS In Australian adults, lower 25(OH)D concentrations were associated with increased MetS risk and higher WC, serum triglyceride, fasting glucose, and insulin resistance at 5 yr. Vitamin D supplementation studies are required to establish whether the link between vitamin D deficiency and MetS is causal.

Glucose indices, health behaviours and incidence of diabetes in Australia: the AusDiab study.

OBJECTIVE—This national, population-based study reports diabetes incidence based on oral glucose tolerance tests (OGTTs) and identifies risk factors for diabetes in Australians. RESEARCH DESIGN AND METHODS—The Australian Diabetes, Obesity and Lifestyle Study followed-up 5,842 participants over 5 years. Normal glycemia, impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and diabetes were defined using World Health Organization criteria. RESULTS—Age-standardized annual incidence of diabetes for men and women was 0.8% (95% CI 0.6–0.9) and 0.7% (0.5–0.8), respectively. The annual incidence was 0.2% (0.2–0.3), 2.6% (1.8–3.4), and 3.5% (2.9–4.2) among those with normal glycemia, IFG, and IGT, respectively, at baseline. Among those with IFG, the incidence was significantly higher in women (4.0 vs. 2.0%), while among those with IGT, it was significantly higher in men (4.4 vs. 2.9%). Using multivariate logistic regression, hypertension (odds ratio 1.64 [95% CI 1.17–2.28]), hypertriglyceridemia (1.46 [1.05–2.02]), log fasting plasma glucose (odds ratio per 1 SD 5.25 [95% CI 3.98–6.92]), waist circumference (1.26 [1.08–1.48]), smoking (1.70 [96% CI 1.11–2.63]), physical inactivity (1.56 [1.12–2.16]), family history of diabetes (1.82 [1.30–2.52]), and low education level (1.85 [1.04–3.31]) were associated with incident diabetes. In age- and sex-adjusted models, A1C was a predictor of diabetes in the whole population, in those with normal glycemia, and in those with IGT or IFG. CONCLUSIONS—Diabetes incidence is 10–20 times greater in those with IGT or IFG than those with normal glycemia. Measures of glycemia, A1C, metabolic syndrome components, education level, smoking, and physical inactivity are risk factors for diabetes.

Plasma Lipid Profiling Shows Similar Associations with Prediabetes and Type 2 Diabetes

The relationship between lipid metabolism with prediabetes (impaired fasting glucose and impaired glucose tolerance) and type 2 diabetes mellitus is poorly defined. We hypothesized that a lipidomic analysis of plasma lipids might improve the understanding of this relationship. We performed lipidomic analysis measuring 259 individual lipid species, including sphingolipids, phospholipids, glycerolipids and cholesterol esters, on fasting plasma from 117 type 2 diabetes, 64 prediabetes and 170 normal glucose tolerant participants in the Australian Diabetes, Obesity and Lifestyle Study (AusDiab) then validated our findings on 1076 individuals from the San Antonio Family Heart Study (SAFHS). Logistic regression analysis of identified associations with type 2 diabetes (135 lipids) and prediabetes (134 lipids), after adjusting for multiple covariates. In addition to the expected associations with diacylglycerol, triacylglycerol and cholesterol esters, type 2 diabetes and prediabetes were positively associated with ceramide, and its precursor dihydroceramide, along with phosphatidylethanolamine, phosphatidylglycerol and phosphatidylinositol. Significant negative associations were observed with the ether-linked phospholipids alkylphosphatidylcholine and alkenylphosphatidylcholine. Most of the significant associations in the AusDiab cohort (90%) were subsequently validated in the SAFHS cohort. The aberration of the plasma lipidome associated with type 2 diabetes is clearly present in prediabetes, prior to the onset of type 2 diabetes. Lipid classes and species associated with type 2 diabetes provide support for a number of existing paradigms of dyslipidemia and suggest new avenues of investigation.

Accuracy of the Australian National Death Index: comparison with adjudicated fatal outcomes among Australian participants in the Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID) study.

Objective: To assess the accuracy of the Australian National Death Index (NDI) in identifying deaths and recording cardiovascular and cancer causes of death.

How to best define the metabolic syndrome

The constellation of metabolic abnormalities including centrally distributed obesity, decreased high‐density lipoprotein cholesterol (HDL‐C), elevated triglycerides, elevated blood pressure (BP), and hyperglycaemia is known as the metabolic syndrome. Associated with increased risk of both type 2 diabetes and cardiovascular disease (CVD), the metabolic syndrome is thought to be a driver of the modern day epidemics of diabetes and CVD and has become a major public health challenge around the world 1. Since its initial description, several definitions of the syndrome have emerged. Each of these definitions used differing sets of criteria, the combination of which either reflected contrasting views on pathogenic mechanisms or clinical usefulness. The use of these definitions to conduct research into the metabolic syndrome in diverse populations resulted in wide ranging prevalence rates, inconsistencies and confusion, and spurred on the vigorous debate regarding how the metabolic syndrome should be defined. In response to this controversy, the International Diabetes Federation (IDF) has recently proposed a new definition, which is applicable to populations around the world 1, 2. It is envisaged that the development of the new definition for the metabolic syndrome will help resolve the confusion caused by the number of earlier attempts to define this important entity.

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.

The metabolic syndrome as a tool for predicting future diabetes: the AusDiab study

Objective.  To compare the ability of the metabolic syndrome (MetS), a diabetes prediction model (DPM), a noninvasive risk questionnaire and individual glucose measurements to predict future diabetes.