Syndrome X also known as metabolic syndrome is a condition that has at its center insulin resistance and at least 3 of the other 5 diagnostic criteria. These other criteria according to Steinbaum (2004) are:
- Abdominal obesity, waist circumference of 40 inches or more for men, 35 inches or more for women.
- Elevated triglycerides, >150mg/dL
- Lowered HDL cholesterol, <40mg/dL men, <50mg/gL women)
- Hypertension, >130/85mmHg
- And elevated fasting glucose levels. >110mg/dl (but this number was lowered to
100mg/dL since Steinbaum wrote her paper)
Insulin resistance happens when target tissue are unable to respond adequately to proper insulin level. Because these cells are unresponsive, B-cells of Langerhans secrete more insulin, starting a viscous cycle because as resistance worsens, secretion increases.
Steinbaum (2004) calls the overproduction of glucose by the liver, the impaired peripheral glucose utilization, and the increased production of fatty acids the “hallmarks of metabolic syndrome.”
Once the beta cells can no longer maintain the high rate of insulin production, we find an increase in hepatic glucose production in both, the fasting state and after a meal, with decreased glucose absorption, eventually leading to type II diabetes.
The abnormal fatty acid metabolism and increased abdominal obesity also lead to an increase in glucose production. The intra-abdominal adipose tissue does not react to insulin. Because of that, it undergoes lipolysis creating free fatty acids. Once in the liver, these free fatty acids churn up glucose production and for triglycerides. Everything I just described, impaired glucose tolerance, hyperinsulinemia, hypertriglyceridemia, and visceral body fat are found in syndrome X. Moreover, this mechanism is ultimately responsible for coronary disease.
One theory connects hyperinsulinemia with cardiovascular disease because of an increase in the hypercoagulable state and because insulin affects thrombosis. Impaired glucose tolerance and hyperinsulinemia contribute to impaired fibrinilysis. This can be observed by increased levels of plasminogen activation inhibitor-1 antigen (PAI-1) and tissue plasminogen activator antigen (t-PA). PAI-1 prevents clot dissolution by inhibiting t-PA and research shows that these factors contribute to coronary artery disease.
According to Garvey and Hermayer, (1998) the clinical implications are the following:
There is not one single standardized test for the metabolic syndrome.
Metabolic syndrome should lead to careful screening and monitoring of other co-conditions.
Patients with metabolic syndrome require more aggressive treatment for the cardiovascular risk profile.
Drug therapy to avoid worsening of metabolic syndrome
Primary goal of treatment is to normalize all abnormalities that are associated with metabolic syndrome.
Steinbaum S. (2004). The Metabolic Syndrome: An Emerging Health Epidemic in Women. Progress in Cardiovascular Diseases, Vol. 46, No. 4, (January/February)pp 321-336
Garvey W., Hermayer K. (1998). Clinical implications of the insulin resistance syndrome, Clinical Cornerstone, Volume 1, Issue 3, Pages 13-28, ISSN 1098-3597, DOI: 10.1016/S1098-3597(98)90015-1.