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As the word itself says, a syndrome is not a disease in its own right, but a set of various diseases that coexist in the same individual. Metabolic Syndrome (MS) was first described many years ago, but it came back to the fore again in 1998 by Alberti and Zimmet who tried to give it a more modern definition. It was then in 2001 that Grundy defined simpler and easily determinable criteria in an outpatient setting. When compared with other diagnostic criteria, such as those of the International Diabetes Federation, it was seen that the 2001 criteria had a higher specificity, even if a lower sensitivity, and therefore were those to be preferred in identifying the truly affected patients by SM. The MS criteria actually represent the most important modifiable cardiovascular risk factors, as they are related to Visceral Obesity and Insulin Resistance (IR), which proceed in parallel in individuals. Visceral adipose tissue is a true endocrine organ that produces many hormone-acting substances called Adipokines. These are the main responsible for the establishment and maintenance of the IR, as well as for hypertension, hypertriglyceridemia and blood coagulation alterations. In fact, in patients with MS, excess adipose tissue is almost always accompanied by a decrease in muscle tissue, i.e. a state of sarcopenia. Muscle tissue also produces cytokines and hormonal substances with protective function against the cardiovascular risk factors present in the MS criteria, the lack of muscle mass reduces the production of these molecules and therefore the presence of sarcopenia further worsens the entity of the cardiovascular risk. There are other additional factors, other than those present in the classifications, which can play an important role in MS. Current scientific evidence shows a correlation between vitamin D and risk, incidence, number and severity of the components of the Metabolic Syndrome and its complications (DM2 and cardiovascular diseases). About 90% of obese and diabetic patients have a more or less serious deficiency of vitamin D, and this condition has been directly correlated with the dysfunctional adiposity index (LAP index). The other condition that is frequently observed in MS patients is hyperuricemia and this seems mainly due to the high consumption of fructose in the diet. The consequences of fructose metabolism can lead to a decrease in intracellular ATP, an increase in uric acid production, oxidative stress, inflammation, and an increase in lipid synthesis, which are associated with endothelial dysfunction. The latter represents an early manifestation of vascular disease and a stimulus for the development of Metabolic Cardiorenal Syndrome.