The metabolic syndrome is a multiplex risk factor that consists of several risk correlates of metabolic origin. In addition, to dyslipidemia, hypertension, and hyperglycermia, the syndrome carries a prothrombotic state and a proinflammatory state. Persons with the metabolic syndrome are at essentially twice the risk for cardiovascular disease compared with those without the syndrome. It further raises the risk for type 2 diabetes by about 5-fold. Although some investigators favor keeping risk factors separate for purposes of clinical management, others believe that identifying individuals with an aggregation of risk factors provides additional useful information to guide clinical management. In particular it focuses attention on obesity and sedentary life habits that are the root of the syndrome. This review addresses the prevalence of this clustering phenomenon throughout the world. Such seems appropriate because of the increasing prevalence of obesity in almost all countries. The available evidence indicates that in most countries between 20% and 30% of the adult population can be characterized as having the metabolic syndrome. In some populations or segments of the population, the prevalence is even higher. On the other hand, in parts of developing world in which young adults predominate, the prevalence is lower; but with increasing affluence and aging of the population, the prevalence undoubtedly with rise.

The metabolic syndrome (MetS) is a multiplex risk factor for atherosclerotic cardiovascular disease (ASCVD).^1,2 It consists of atherogenic dyslipidemia (ie, elevated triglycerides and apolipoprotein B-containing lipoproteins and low high-density lipoproteins [HDL]), elevations of blood pressure (BP) and glucose, and prothrombotic and proinflammatory states. Many persons with the MetS have insulin resistance that predisposes them to either prediabetes or type 2 diabetes. Obesity and physical inactivity are the driving force behind the syndrome³; but a second set of factors, metabolic susceptibility, usually is required for the MetS to become evident.² Susceptibility factors include adipose tissue disorders (typically manifest as abdominal obesity), genetic and racial factors, aging, and endocrine disorders. Genetic aberrations affecting specific metabolic risk factors can further modify expression of the syndrome. The MetS is often associated with other medical conditions, notably, fatty liver, cholesterol gallstones, obstructive sleep apnea, gout, depression, musculosketal disease, and polycystic ovarian syndrome.

The risk for ASCVD accompanying the MetS is approximately doubled compared with an absence of the syndrome.¹ For example, a recent meta-analysis including 43 cohorts (172 573 individuals) reported that metabolic syndrome conveyed a relative risk (RR) for CVD events and death of 1.78.⁴ In women the risk was highest (RR 2.63). In addition, risk was still associated with the syndrome after adjusting for traditional CVD risk factors (RR 1.54); this finding indicates that risk accompanying the syndrome cannot be explained entirely by the latter. Other reports support this conclusion.⁵ In those without type 2 diabetes, the likelihood of developing diabetes is increased approximately 5-fold. The MetS appears to promote the development of ASCVD at multiple levels.

• Elevations of apo B-containing lipoproteins initiate atherogenesis and drive lesion development.⁶
•  Atherosclerotic plaque development is accelerated by low levels of HDL, by elevated BP, by inflammatory cytokines, and likely by elevated plasma glucose.⁷ 
• More advanced plaques tend to become unstable, which in turn predisposes to plaque rupture.⁸ When rupture occurs, a prothrombotic state promotes propagation of thrombi that can worsen cardiovascular syndromes.