First World Congress on the Insulin Resistance Syndrome
First World Congress on the Insulin Resistance Syndrome
Persons with insulin resistance can exhibit a number of clinical syndromes, including hypertension and polycystic ovary syndrome (PCOS), as well as metabolic abnormalities, including glucose intolerance, dyslipidemia, and a hypercoagulable state. Furthermore, insulin resistance is an important risk factor for the development of atherosclerosis and diabetes. At the First World Congress on the Insulin Resistance Syndrome (IRS), held November 21-22, 2003, in Los Angeles, California, conference organizer Yehuda Handlesman, MD, of the Metabolic Institute of America, Tarzana, California, noted that contributory causes of insulin resistance include obesity, sedentary lifestyle, and many other characteristics and conditions. The syndrome has been assigned international classification of disease (ICD-9) code 277.7 as the dysmetabolic syndrome.
Gerald M. Reaven, MD, Stanford University School of Medicine, Stanford, California, suggested that adiposity and physical fitness each account for approximately 25% of the variability in insulin sensitivity, with genetic factors responsible for an additional 50% of this variation. He illustrated the importance of genetic factors by citing the differences in insulin sensitivity between persons of European ancestry and those of South Asian or Mexican ancestry and the similarities in insulin sensitivity of related persons in a family.
Syndrome X, as Dr. Reaven originally termed it, included insulin resistance, hyperinsulinemia, dyslipidemia, hypertension, and increased risk of both diabetes and coronary heart disease (CHD). Those persons in the upper third of insulin resistance have increased risk of CHD and type 2 diabetes. When ascertaining a person's insulin sensitivity status, impaired fasting glucose (IFG) has a sensitivity of 0.10 and a specificity of 0.97, impaired glucose tolerance (IGT) has a sensitivity of 0.26 and a specificity of 0.95, fasting insulin in the highest tertile has a sensitivity of 0.66 and a specificity of 0.83, and insulin 2 hours following oral glucose in the highest tertile is associated with a sensitivity of 0.71 and a specificity of 0.86. Triglyceride levels and the triglyceride/HDL ratio are also useful measures, with triglyceride > 130 mg/dL and triglyceride/HDL > 3 and insulin > 15 mIU/mL reasonable cut-off points that have greater predictive power than the Adult Treatment Panel (ATP) III criteria for IRS. (Dr. Reaven pointed out that each laboratory must establish its own norms.)
Drs. Helke Fenster and Sun Kim, working with Dr. Reaven, showed that with a body mass index (BMI) cutoff of 25, 60% of subjects had insulin resistance, while with a waist circumference > 88 cm in women or > 102 cm in men, 68% had insulin resistance. In an analysis of data from 485 persons (208 with BMI ≤ 25 kg/m), the insulin area under the curve following oral glucose administration distinguished most precisely between insulin-sensitive and insulin-resistant persons, particularly when correlations were separately calculated for normal, overweight, and obese persons.
Persons with insulin resistance can exhibit a number of clinical syndromes, including hypertension and polycystic ovary syndrome (PCOS), as well as metabolic abnormalities, including glucose intolerance, dyslipidemia, and a hypercoagulable state. Furthermore, insulin resistance is an important risk factor for the development of atherosclerosis and diabetes. At the First World Congress on the Insulin Resistance Syndrome (IRS), held November 21-22, 2003, in Los Angeles, California, conference organizer Yehuda Handlesman, MD, of the Metabolic Institute of America, Tarzana, California, noted that contributory causes of insulin resistance include obesity, sedentary lifestyle, and many other characteristics and conditions. The syndrome has been assigned international classification of disease (ICD-9) code 277.7 as the dysmetabolic syndrome.
Gerald M. Reaven, MD, Stanford University School of Medicine, Stanford, California, suggested that adiposity and physical fitness each account for approximately 25% of the variability in insulin sensitivity, with genetic factors responsible for an additional 50% of this variation. He illustrated the importance of genetic factors by citing the differences in insulin sensitivity between persons of European ancestry and those of South Asian or Mexican ancestry and the similarities in insulin sensitivity of related persons in a family.
Syndrome X, as Dr. Reaven originally termed it, included insulin resistance, hyperinsulinemia, dyslipidemia, hypertension, and increased risk of both diabetes and coronary heart disease (CHD). Those persons in the upper third of insulin resistance have increased risk of CHD and type 2 diabetes. When ascertaining a person's insulin sensitivity status, impaired fasting glucose (IFG) has a sensitivity of 0.10 and a specificity of 0.97, impaired glucose tolerance (IGT) has a sensitivity of 0.26 and a specificity of 0.95, fasting insulin in the highest tertile has a sensitivity of 0.66 and a specificity of 0.83, and insulin 2 hours following oral glucose in the highest tertile is associated with a sensitivity of 0.71 and a specificity of 0.86. Triglyceride levels and the triglyceride/HDL ratio are also useful measures, with triglyceride > 130 mg/dL and triglyceride/HDL > 3 and insulin > 15 mIU/mL reasonable cut-off points that have greater predictive power than the Adult Treatment Panel (ATP) III criteria for IRS. (Dr. Reaven pointed out that each laboratory must establish its own norms.)
Drs. Helke Fenster and Sun Kim, working with Dr. Reaven, showed that with a body mass index (BMI) cutoff of 25, 60% of subjects had insulin resistance, while with a waist circumference > 88 cm in women or > 102 cm in men, 68% had insulin resistance. In an analysis of data from 485 persons (208 with BMI ≤ 25 kg/m), the insulin area under the curve following oral glucose administration distinguished most precisely between insulin-sensitive and insulin-resistant persons, particularly when correlations were separately calculated for normal, overweight, and obese persons.