As far as we know, the Metabolic syndrome (MetS ) was first described in German in the 1920-ties. It was later redescribed by two groups in 1988. In 1998, the first uniform definition of the syndrome was given by WHO, but three years later the NECP/ATP III- committee suggested the definition that has been most commonly used in epidemiological research. By this definition, a subject with the MetS should show at least 3 out of maximal 5 disturbances in major cardiovascular risk factors, namely high blood pressure, diabetes/impaired glucose tolerance, hypertriglyceridemia, low HDL levels and abdominal obesity measured by waist circumference. According the NCEP criteria, 17% of middle-aged males in Sweden (the ULSAM study) showed the MetS in the early 70-ties. 20 years later, the prevalence of the MetS have rise to 22%. In another Swedish cohort, PIVUS, the prevalence at age 70 was 23%, a prevalence being higher in women then in men.
When incidence of cardiovascular (CV) mortality was followed for 28 years in the ULSAM cohort, the NCEP definition of the MetS was more powerful as a risk factor that the WHO definition. When later the incidence of the most common CV disorders myocardial infarction, stroke and heart failure were followed for 33 years, the MetS at age 50 was associated with a two-fold increased risk of myocardial infarction and heart failure, but a significant increased risk of stroke.
By MRI, abdominal obesity could the quantified subcutaneous and visceral fat mass.
Both the amount of subcutaneous and visceral fat were related to the MetS, but while visceral fat mainly was related to glucose and triglycerides, the subcutaneous fat was mainly related to HDL and blood pressure. Also insulin resistance was closely related to the MetS, both when evaluated by the HOMA insulin resistance index, a marker of hepatic insulin resistance in the fasting state, or by the gold standard euglycemic hyperinsulinemic clamp technique. Insulin resistance was, like the MetS, found to be a major risk factor for future myocardial infarction and heart failure, but less so for stroke.
An analysis of a number of environmental pollutants in the PIVUS study showed that many of those pollutants were increased in subjects with the MetS and in those who developed diabetes and abdominal obesity over the coming 5 years. Future animal studies are needed to confirm if environmental pollutants are drivers of the MetS.
