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In 2010, it was estimated that among all industrialized Western countries, between one in three to one in five people had the metabolic syndrome. In the United States alone that amounted to approximately 50 million to 75 million people. This population seems to be expanding at an alarming rate. It is estimated that by 2020, nearly one half of people in the United States will have the metabolic syndrome. The metabolic syndrome plays an important role in cardiac, vascular, and kidney disease.
Experts disagree on the precise definition of the metabolic syndrome. According to the National Cholesterol Education Program Adult Treatment Panel (ATP III), any three of the following criteria meet the definition: abdominal obesity (waist circumference), elevated serum triglycerides, lower high-density lipoprotein (HDL) cholesterol, high blood pressure, and elevated fasting blood glucose. The World Health Organization has slightly different criteria: abdominal obesity, cholesterol derangements, high blood pressure, and high insulin levels.
Many experts now agree that visceral, but not necessarily subcutaneous, obesity leads to the development of the metabolic syndrome. It may be surprising to note that subcutaneous fat accumulation is actually protective rather than harmful. Subcutaneous adiposity is a normal physiologic response to caloric excess, serving protective functions during times of starvation or stress. However, problems begin to arise when these adipocytes begin to accumulate too much fat. At first, subcutaneous adipocytes disseminate warning signals involving hormones that regulate the hypothalamus’s appetite center and also stimulate non-adipocytes to begin oxidizing free fatty acids.
If caloric surplus continues despite compensatory warning signals, subcutaneous adipocytes eventually become resistant to insulin. The body is forced to store fatty acids in the viscera rather than subcutaneously. A cascade of inflammatory events rooted in dysfunctional hormonal signaling results in an inflammatory syndrome known as lipotoxicity. This leads to mineralocorticoid abnormalities with salt and water retention, oxidative stress damage, atherosclerosis, and hepatic lipid dysregulation. Chronic caloric surplus that continues unabated after the body’s compensatory mechanisms have reached their saturation point has been proposed to be the sine qua non of the metabolic syndrome. The mechanisms behind this require further discussion.
Modern societies have revolutionized the food supply by producing a plethora of inexpensive, readily available calorie-rich foods. In the United States this began in the 1960s. It is termed the gastronomic revolution, a phrase that characterizes the preparation of food at home as a chore and commercially produced food, available at reasonable prices, as the more attractive alternative. Further exacerbating the revolution, the composition of food was also dramatically changed to heighten sales by encouraging consumption of larger portions. In addition, commercially available food and beverages were made rich in salt, fat, glucose, and simple sugars. They were also low in protective antiinflammatory antioxidants. This gastronomic experiment, though profitable for some, became a general recipe for poor public health several decades later. Approximately two thirds of all Americans are now at least overweight, and nearly one third of them carry the diagnosis of metabolic syndrome. This profound abundance of high-calorie foods will continue to encourage overindulgence.
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