Obesity paradox in peripheral vascular disease

Abstract

To prevent cardiovascular diseases, it is essential to contro l risk factors, among which obesity is a world-wide issue that we are currently facing [1]. Obesity was found to be an independent cardiovascular risk factor by the FraminghamHeart study, inwhich the participants were followed up over 26 years; a higher risk was observed in both men and women whose body weights increased after the young adult years [2]. It has been shown that obesity, particularly visceral obesity, is closely related not only to classical cardiovascular risk factors such as dyslipidemia, diabetes, and hypertension, but also to insulin resistance, abnormal blood coagulation, chronic kidney disease, sleep apnea syndrome, and so on [1,3,4]. Endothelial dysfunction, a phenomenon recognized as an early stage of atherosclerosis, was also shown to be associated with obesity [5]. The mechanisms by which obesity has detrimental effects on the development or progression of atherosclerosis, have recently been studied vigorously. In obese patients, enlarged adipocytes were shown to secrete awide range of bioactive substances called adipokines, such as interleukin-6, tumor necrosis factor-a (TNF-a) and angiotensinogen, which act as pro-atherogenic factors [6]. Indeed, these adipokines levels in the adipose tissue and blood are reduced following reduction of body weight in obese patients [7]. Meanwhile, in a large-scale prospective cohort study, “J”or “U”-shaped curves were observed in the relationship between mortality and body mass index (BMI): not only higher but also lower BMIs were associated with higher mortality from cardiovascular diseases, cancer, or other causes of death [8]. Comparable