Point: HOMA—Satisfactory for the Time Being
HOMA: The best bet for the simple determination of insulin sensitivity, until something better comes along
- Kirsten A. McAuley, MBCHB, PHD1,
- Jim I. Mann, FRACP1,
- J. Geoffrey Chase, PHD2,
- Thomas F. Lotz, DIP-ING2 and
- Geoffrey M. Shaw, FJFICM3
- 1Edgar National Centre for Diabetes Research, University of Otago, Dunedin, New Zealand
- 2Centre for Bioengineering, Department of Mechanical Engineering, University of Canterbury, Christchurch, New Zealand
- 3Department of Intensive Care, Christchurch Hospital and Christchurch School of Medicine and Health Sciences, University of Otago, Christchurch, New Zealand
- Address correspondence and reprint requests to Professor Jim I. Mann, Edgar National Centre for Diabetes Research, Department of Medical and Surgical Sciences, P.O. Box 913, Dunedin 9054, New Zealand. E-mail: jim.mann{at}otago.ac.nz
There is no doubt that the cluster of clinical and metabolic features associated with insulin resistance predicts risk of developing type 2 diabetes and cardiovascular disease (CVD) (1); however, whether there is merit in defining a syndrome is less clear (2). There is also a lack of agreement regarding the value of measuring insulin sensitivity in clinical practice (3). The widely used criteria for defining the metabolic syndrome (those recommended by the World Health Organization [4] and the Adult Treatment Panel III [5]) includes a measure of insulin resistance in the definition of the syndrome. A very recent approach suggested by a group representing the International Diabetes Federation involves identifying individuals with central obesity and a range of clinical and metabolic parameters associated with insulin resistance; however, it does not include a direct measure of insulin sensitivity (6). It is argued that measures of insulin resistance do not predict CVD when other more easily measured components of the metabolic syndrome cluster are present, and these measures based on fasting insulin are unreliable (3). However, measurement of insulin sensitivity has greatly enhanced the understanding of the pathophysiology of diabetes and relationships to cardiovascular outcomes (7). Dismissing the assessment of insulin sensitivity because its measurement is too variable or difficult (3) is understandable, but hardly desirable, as one major dimension of altered metabolism will be omitted from research and clinical assessments. It may prove to be much the same as assessing cardiovascular risk without serum cholesterol. A truly reliable simple measure may prove to be more appropriate than an aggregation of surrogates in predicting subsequent development of diabetes and CVD and in further explaining disease progression and response to treatment.
Several reviews (8,9) describe some of the numerous methods for measuring or estimating insulin sensitivity. The …
