Overview of Epidemiology and Contribution of Obesity to Cardiovascular Disease
Section snippets
Epidemiology
The prevalence of obesity has increased dramatically worldwide over the last decades and has now reached epidemic proportions. For instance, the global prevalence of obesity has nearly doubled between 1980 and 2008. According to the World Health Organization, 35% of adults worldwide aged > 20 years were overweight (34% men and 35% women) in 2008 including 10% men and 14% women being considered as obese. Prevalence is particularly high in America with a high proportion of overweight and obesity
Obesity assessment
The most commonly used anthropometric tool to assess relative weight and classify obesity is the BMI, which is expressed as the ratio of total body weight over height squared (kg/m2). Individuals with a BMI < 18.5 kg/m2 are considered as being underweight, whereas those with a BMI between 18.5 and 24.9 kg/m2 are classified as having normal or acceptable weight. Individuals with a BMI ranging from 25 to 29.9 kg/m2 are classified as overweight while obesity is present when BMI reaches ≥ 30 kg/m2.
Obesity and CVD
Obesity has numerous consequences on the CV system. Chronic accumulation of excess body fat leads to a variety of metabolic changes, increasing the prevalence of CVD risk factors but also affecting systems modulating inflammation.40 In addition to its contribution as an independent CVD risk factor, obesity promotes alterations in other intermediate risk factors such as dyslipidemia, HTN, glucose intolerance, inflammatory state, obstructive sleep apnea/hypoventilation, and a prothrombotic state,
Abdominal obesity
In a state of a positive energy balance, excess FFAs should be preferentially stored in adipose tissue. Adipocytes expand in order to store energy and as the demand for lipid storage increases, pre-adipocytes located in the adipose tissue differentiate to become mature and participate to fat storage. When the adipose tissue has reached its maximal expansion capacity, a “spill over” of lipids from adipocytes occurs, resulting in an increase of circulating FFAs. Lipids then start to accumulate in
Conclusions
Basic, clinical and population studies have provided robust evidence supporting the notion that obesity is associated with numerous alterations increasing the risk of CVD (Fig 1, Fig 2). The pathophysiological processes linking obesity to atherosclerosis and CVD clearly involve a chronic inflammatory state. This inflammatory profile is usually the result of combined factors, such as visceral obesity and excess ectopic fat, insulin resistance, an atherogenic dyslipidemia and HTN. Such
Statement of Conflict of Interest
All authors declare that there are no conflicts of interest.
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Statement of Conflict of Interest: see page 377.