Historical background on global cardiometabolic risk, epidemiological aspects of obesity and type 2 diabetes, ABCs of cardiovascular disease risk factors, visceral adiposity, metabolic syndrome and contribution to cardiometabolic risk.
Definition and History
The current definition of the metabolic syndrome encompasses a cluster of metabolic abnormalities linked to insulin resistance, which is often associated with a high-risk form of overweight/obesity: excess abdominal obesity. Because these abnormalities increase the risk of cardiovascular disease (CVD) and type 2 diabetes, numerous consensus groups have attempted to provide guidelines to identify patients in clinical practice with these atherogenic/diabetogenic metabolic abnormalities. Although the number of publications on the metabolic syndrome is soaring, the concept of a cluster of abnormalities including obesity, diabetes, dyslipidemia, and hypertension is not new and several physicians/investigators contributed to the development of this concept through astute clinical observations or epidemiological/metabolic studies. However, a clinical diagnosis of the metabolic syndrome is not sufficient to assess the risk of CVD. In order to properly evaluate and manage global CVD risk in clinical practice, it is important to take into account the risk associated with traditional risk factors as well as the potential additional contribution of abdominal obesity/insulin resistance and related complications. This global risk is referred to as global cardiometabolic risk.
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The Obesity and Type 2 Diabetes Epidemics
The number of people suffering from type 2 diabetes is skyrocketing worldwide. This phenomenon has been closely linked to soaring obesity, which has reached epidemic proportions in populations around the world. But just why are we facing this “two-pronged assault” by overweight/obesity and type 2 diabetes? The answer is rather simple. The machines we use and the environments in which we live and work are designed to spare us from physical exertion. Unfortunately, this sedentary environment worsens the effects of the energy-dense, refined, “fast food” diet that more and more people are adopting. Taken together, our environment and our diet lead to a positive energy balance, weight gain, and obesity. As obesity reaches epidemic proportions, so too does type 2 diabetes. Unless we make significant changes to both our diet and way of life, obesity and type 2 diabetes will continue to exact a heavy toll on societies worldwide.
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Epidemiological studies published over the last 50 years have shed light on the many factors that increase cardiovascular disease (CVD) risk. It is now widely accepted that an altered lipid profile including high cholesterol, LDL cholesterol (bad cholesterol), and triglyceride concentrations as well as low HDL cholesterol (good cholesterol), high blood pressure, smoking, and a sedentary lifestyle all increase one’s risk of CVD. Also considered a major CVD risk factor, type 2 diabetes is defined by high blood glucose levels. Though obesity is an acknowledged health hazard and a risk factor for CVD and type 2 diabetes, physicians have long been puzzled by the remarkable heterogeneity seen in clinical practice among individuals with similar excess body weight. Some obese patients have no clinical signs of CVD or type 2 diabetes, whereas other patients—who may be only slightly or moderately overweight—have a metabolic profile that predisposes them to CVD and/or type 2 diabetes. Studies have shown that the risk of CVD and type 2 diabetes does not depend on excess body weight per se, but rather on the location of this excess weight. Excess abdominal fat plays the greatest role in this regard.
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Visceral Adipose Tissue: the Culprit?
Visceral obesity (excess fat in the abdominal cavity) is closely linked to blood sugar and lipid problems that increase the risk of type 2 diabetes and coronary heart disease. Compared to normal weight individuals or obese subjects with low levels of visceral fat, obese patients with large amounts of visceral fat are characterized by high blood pressure, atherogenic dyslipidemia (elevated triglycerides and low levels of good HDL cholesterol), impaired glucose-insulin homeostasis (elevated blood glucose and a state of insulin resistance), and an inflammatory and pro-thrombotic (tendency to form clots in the blood, impeding blood flow) profile. Several studies have shown that a selective excess of visceral fat increases the risk of type 2 diabetes. The development of sophisticated imaging techniques has made it possible to accurately measure and distinguish visceral from subcutaneous fat (the fat located just under the skin). These non-invasive imaging techniques have also enabled researchers to conclude that, unlike visceral fat, subcutaneous fat is seldom associated with metabolic complications. It is unclear which factors influence whether dietary fat is stored under the skin or in the abdominal cavity. Variables such as age, sex, menopause, and ethnicity all influence where fat is stored.
It has been proposed that excess visceral fat may indicate that an individual’s subcutaneous adipose tissue is unable to serve as an “energy sink” for a calorie surplus resulting from excess energy intake and/or reduced energy expenditure. This inability may cause fat to accumulate at undesired locations, a phenomenon that has been described as ectopic fat deposition. Excess visceral fat may therefore be a “red light” or warning sign that excess energy is being stored as fat in unusual places, increasing the risk of diabetes and cardiovascular disease.
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