Exp Clin Endocrinol Diabetes 1997; 105: 54-60
DOI: 10.1055/s-0029-1211799
© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

The metabolic syndrome: from inherited survival trait to a health care problem

Stephen Colagiuri, Janette C. Brand Miller
  • Department of Endocrinology, Diabetes and Metabolism, Prince of Wales Hospital and Human Nutrition Unit, Department of Biochemistry, University of Sydney; Sydney, New South Wales, Australia
Further Information

Publication History

Publication Date:
14 July 2009 (online)

Summary

A critical role is proposed for the quantity and quality of dietary carbohydrate in the pathogenesis of the insulin resistance and hyperinsulinaemia which characterise the Metabolic Syndrome. We propose that an insulin-resistant genotype evolved to provide survival and reproductive advantages for the cold-climate, large game hunters of the last Ice Age who consumed a low carbohydrate, high protein diet with periodic starvation. Insulin resistance would have minimised glucose utilisation by muscles thereby facilitating the preferential utilisation of glucose by the brain, foetus and mammary gland. But beginning about 10,000 years ago following the end of the last Ice Age and the development of agriculture, dietary carbohydrate increased and the selection pressure for insulin resistance decreased in some groups. Agriculture began in the Middle East and spread throughout Europe long before it was developed elsewhere. Hence the prevalence of the insulin-resistant genotype decreased in Europeans and other groups exposed to a high carbohydrate intake for sufficiently long. Some geographically isolated groups such as the Pima Indians and Nauruans experienced conditions which further diminished the gene pool diversity and resulted in particularly insulin resistant populations. Traditional carbohydrate foods have a low glycaemic index and produce only modest increases in plasma insulin. However, the constant supply of highly refined high glycaemic index carbohydrate in modern diets, results in postprandial hyperinsulinaemia. The insulin-resistant genotype is now disadvantageous and predisposes to the development of the Metabolic Syndrome.

    >