Elsevier

Progress in Cardiovascular Diseases

Volume 56, Issue 4, January–February 2014, Pages 369-381
Progress in Cardiovascular Diseases

Overview of Epidemiology and Contribution of Obesity to Cardiovascular Disease

https://doi.org/10.1016/j.pcad.2013.10.016Get rights and content

Abstract

The prevalence of obesity has increased worldwide and is a source of concern since the negative consequences of obesity start as early as in childhood. The most commonly used anthropometric tool to assess relative weight and classify obesity is the body mass index (BMI); BMI alone shows a U- or a J-shaped association with clinical outcomes and mortality. Such an inverse relationship fuels a controversy in the literature, named the ‘obesity paradox', which associates better survival and fewer cardiovascular (CV) events in patients with elevated BMI afflicted with chronic diseases compared to non-obese patients. However, BMI cannot make the distinction between an elevated body weight due to high levels of lean vs. fat body mass. Generally, an excess of body fat (BF) is more frequently associated with metabolic abnormalities than a high level of lean body mass. Another explanation for the paradox is the absence of control for major individual differences in regional BF distribution. Adipose tissue is now considered as a key organ regarding the fate of excess dietary lipids, which may determine whether or not body homeostasis will be maintained (metabolically healthy obesity) or a state of inflammation/insulin resistance will be produced, with deleterious CV consequences. Obesity, particularly visceral obesity, also induces a variety of structural adaptations/alterations in CV structure/function. Adipose tissue can now be considered as an endocrine organ orchestrating crucial interactions with vital organs and tissues such as the brain, the liver, the skeletal muscle, the heart and blood vessels themselves. Thus, the evidence reviewed in this paper suggests that adipose tissue quality/function is as important, if not more so, than its amount in determining the overall health and CV risks of overweight/obesity.

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.

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