, Volume 44, Issue 5, pp 537-543

Genetic versus environmental aetiology of the metabolic syndrome among male and female twins


Aims/hypothesis. The aetiology of the metabolic syndrome including hyperinsulinaemia, glucose intolerance, dyslipidaemia, hypertension and obesity is not known. We studied the relative impact of genetic versus environmental factors for the development of the components in the syndrome among male and female twins. Methods. A total of 303 elderly twin pairs participated in the study. We report concordances and heritability estimates of the components by classic twin analysis to assess the proportion of variation attributed to genetic factors. Results. All components correlated significantly. The concordance rates for glucose intolerance, overall obesity and low HDL-cholesterol were significantly higher among monozygotic than dizygotic twins indicating a genetic influence on the development of these phenotypes. The heritability estimates for glucose concentration, BMI and HDL-cholesterol among monozygotic twins confirmed these findings. The heritability estimates for waist-to-hip ratio, fasting insulin and triglycerides, however, were low, indicating a major environmental influence. We found a higher genetic influence on glucose intolerance and systolic blood pressure and a lower genetic influence on low HDL-cholesterol and diastolic blood pressure among male twins compared to female twins. Conclusion/interpretation. Based on the correlations between the components in the syndrome, we propose a core complex including hyperinsulinaemia, obesity, hypertriglyceridaemia and low HDL-cholesterol with only weak associations to glucose concentrations and blood pressure levels. The study confirms the notion of a multifactorial aetiology of the components including genetic and non-genetic factors. The differences in aetiology between male and female twins indicate an influence of sex on several of the components in the metabolic syndrome. [Diabetologia (2001) 44: 537–543]
Received: 2 October 2000 and in revised form: 2 January 2001