BMI compared with central obesity indicators as a predictor of diabetes incidence in Mauritius.

The aim of the study was to compare BMI with waist circumference (WC), waist-to-hip ratio (WHR), and waist-to-stature ratio (WSR) as a predictor of diabetes incidence. A total of 1,841 men and 2,104 women of Mauritian Indian and Mauritian Creole ethnicity, aged 25-74 years, free of diabetes, hypertension, cardiovascular disease, and gout were seen at baseline in 1987 or 1992, and follow-up in 1992 and/or 1998. At all time points, participants underwent a 2 h 75 g oral glucose tolerance test. Hazard ratios for diabetes incidence were estimated applying an interval-censored survival analysis using age as timescale. Six hundred and twenty-eight individuals developed diabetes during the follow-up period. Multivariable adjusted hazard ratios for diabetes incidence corresponding to a 1 s.d. increase in baseline BMI, WC, WHR, and WSR for Mauritian Indians were 1.49 (1.31-1.71), 1.58 (1.38-1.81), 1.54 (1.37-1.72), and 1.61 (1.41-1.84) in men and 1.33 (1.17-1.51), 1.35 (1.19-1.53), 1.39 (1.24-1.55), and 1.38 (1.21-1.57) in women, respectively; and for Mauritian Creoles they were 1.86 (1.51-2.30), 2.07 (1.68-2.56), 1.92 (1.62-2.26), and 2.17 (1.76-2.69) in men and 1.29 (1.06-1.55), 1.27 (1.04-1.55), 1.24 (1.04-1.48), and 1.27 (1.04-1.55) in women. Paired homogeneity tests showed that there was no difference between BMI and each of the central obesity indicators (all P > 0.05). The relation of BMI with the development of diabetes was as strong as that for indicators of central obesity in this study population.

Comparison of body mass index with waist circumference, waist-to-hip ratio, and waist-to-stature ratio as a predictor of hypertension incidence in Mauritius.

OBJECTIVE: Comparison of BMI with waist circumference, waist-to-hip ratio (WHR), and waist-to-stature ratio (WSR) as a predictor of hypertension incidence. METHODS: A total of 1658 men and 1976 women of Mauritian Indian and Mauritian Creole ethnicity, aged 25-74 years, free of hypertension, diabetes, cardiovascular disease, and gout at baseline in 1987 or 1992, were re-examined in 1992 and/or 1998 using the same survey methodology. Hazard ratios (HRs) for hypertension incidence were estimated applying an interval censored survival analysis (R program) using age as timescale based on baseline obesity indicators. RESULTS: A total of 787 incident hypertension cases were identified during the follow-up. HRs for hypertension incidence adjusting for baseline systolic blood pressure and cohort corresponding to a 1 SD increase in BMI, waist circumference, WHR, and WSR were 1.20 (1.24), 1.19 (1.21), 1.14 (1.10), and 1.20 (1.26) in Mauritian Indian men (women) and 1.23 (1.32), 1.34 (1.23), 1.41 (1.13), and 1.43 (1.33) in Mauritian Creoles, respectively, indicating that all obesity indicators significantly predicted hypertension incidence except for WHR in Mauritian Creole women. Paired homogeneity tests showed that there was no difference between BMI and the other three indicators for most of the comparisons with two exceptions: WSR was stronger than BMI (P = 0.002) in Mauritian Creole men but BMI was stronger than WHR (P = 0.047) in Mauritian Indian women in predicting the incident cases of hypertension. CONCLUSION: The relation of the development of hypertension with BMI was as strong as that with central obesity indicators in the population studied.

Metabolic syndrome and cardiovascular disease.

The clustering of metabolic and pathophysiological cardiovascular risk factors has long been recognized but it was Reaven who popularized the syndrome in the Banting lecture of 1988. Since 1999, several major international or national organizations proposed their own definitions for the syndrome, named the metabolic syndrome. The prevalence of the metabolic syndrome varies according to definition, ethnicity and gender. The prevalence is under 20% among Chinese and Korean people but over 50% among Maori and Pacific Islanders in New Zealand. People with the metabolic syndrome have 50-60% higher cardiovascular risk than those without. The absolute cardiovascular risk of the metabolic syndrome, however, is not necessarily higher than those of its individual components. The pathogenesis underlying the clustering of cardiovascular risk factors remains unclear. Factors including genetic disposition, obesity, insulin resistance and inflammation have been suggested as being involved. Since the metabolic syndrome is multifactorial in origin, strategies for reducing cardiovascular risk in individuals with the metabolic syndrome involve the management of multiple risks. Lifestyle changes are an effective first-line management; pharmacological interventions for hypertension, diabetes and dyslipidaemia are in accordance with established guidelines. Pharmacological and surgical therapies for obesity are effective in selected patients. In this article we discuss the definitions, prevalence, pathogenesis and management of the metabolic syndrome in relation to cardiovascular risk.