Revista Espanola De Cardiologia
The relative control of transmissible infectious or parasitic diseases witnessed during the epidemiologic transition in the 20th century as a result of the great progress in prevention and treatment (antibiotics, antiparasitic agents) has enabled the progressive eclosion of other, nontransmissible diseases. The 4 most representative of these are cardiovascular disease, cancer, obesity, and diabetes mellitus (DM). Obesity and DM share, in part, the same genetic “soil,” and their expression has been hastened by the spectacular changes in lifestyle during the second half of the 20th century, and which are still taking place. In essence, these changes concern the forsaking of healthy dietary habits (diets rich in fiber, low in saturated fats and soluble sugars, and with abundant fruit and vegetables), the cessation of regular physical exercise, and the adoption of unhealthy habits, such as smoking or excessive consumption of alcohol. Obesity and type 2 DM are now so common that they warrant the descriptive designation of “diabesity.” These diseases condition or facilitate the possible accumulation in susceptible persons of other metabolic diseases (dyslipidemia, hyperuricemia) and non-metabolic disorders (high blood pressure, nonalcoholic fatty liver disease, or steatohepatitis), and even the appearance of low grade inflammatory markers (C-reactive protein, interleukin 6) or stigmas of an antifibrinolytic, prothrombotic state. This accumulation, which may or may not be sequential, of such a variety of inter-related, pathophysiological changes, often due to the common link of insulin resistance, promotes and accelerates the development of (macro) vascular atherogenesis (a chronic, inflammatory process with its own features), and it may provoke the clinical onset of serious consequences, including ischemic heart disease, stroke, and obliterating arteritis of peripheral vessels of the limbs, especially the legs. Historically, the concept of the metabolic syndrome (MS) is quite recent. The syndrome was characterized in clinical practice by M. Hanefeld 1 during the 1970s as the coexistence of truncal obesity, dyslipoproteinemia, glucose intolerance or type 2 DM, hypertension, hyperuricemia, hypercoagulation and fibrinolysis defects, hyperandrogenism, fatty liver, bile stones, osteoporosis, and a high incidence of cardiovascular disease. In 1987, the association of some of these components (but not obesity!) and their link with the main pathophysiologic feature of insulin resistance was named syndrome X by Reaven. 2 This seminal study triggered basic and clinical research in the field and led to the wider and more complex concept of the MS.