Morbid obesity is linked to a higher mortality rate but the association between more modest overweight and mortality appears less clear (Figure 25.1) (1,2). Although data from more than four million subjects initially suggested a direct positive association between body weight and overall mortality, subsequent studies showed an increased mortality only above a certain threshold, but described J- or even U-shaped associations between weight and mortality (3,4). The relationship of indicators of obesity to all-cause mortality has been extensively analysed: univariate analysis concerning the body mass index (BMI) for various age groups, the two sexes, and variable periods of follow-up has almost invariably shown minimum levels of risk for BMI values of 27-29 (5,6).
However, the quantification of the excess mortality from all causes associated with obesity remains controversial. It has been recently shown in a large cohort of obese persons that morbid obesity (BMI > 40 kg/m2) was a strong predictor of premature death while moderate degrees of obesity (BMI 25-32 kg/m2) were not significantly associated with excess mortality (7).
Much of the obesity-associated mortality is linked to the negative effect of excessive fat distribution on myocardial function and perfusion. As we will outline later in the chapter, much of the information on the relationship between obesity and heart disease derives from autopsy studies of massively obese patients dying of congestive heart failure without clinical evidence of hypertension or cardiac disease. In obesity major haemodynamic changes take place affecting cardiac output, cardiac index and left ventricular stroke work; this increased cardiac output is determined by a major increase in total body fat mass which requires increased blood flow to support metabolism (Table 25.1). It has been estimated that 2-3 mL of blood is necessary to perfuse every 100 g of adipose tissue at rest: in a patient with 100 kg of fat this would require up to a 3 L/min increase in blood flow. This increased workload leads to an increased ventricular mass and hypertrophy which predispose to an important imbalance between perfusion and metabolic demand (8). In the light of these observations obesity determines, at heart levels, structural alterations which make the myocardium and coronary vessels more prone to the atherosclerotic damage independently from the classic risk factors which are usually present in overweight people.
Undoubtedly, the negative effects of obesity appear closely linked to fat distribution. Central fat distribution is closely linked with a state of insulin resistance and the metabolic abnormalities associated with this syndrome; they all represent powerful risk factors for atherosclerotic cardiovascular disease (ACVD) (9). Nonetheless obesity irrespectively from fat distribution is associated with diabetes mellitus, hypertension and dyslipidaemia, which all predispose to ACVD (10).
ACVD is closely associated with adiposity as measured by either weight, BMI, or measures of central fat accumulation. This relationship is in part mediated by the other risk factors which co-segregate with obesity, in part by obesity itself. The rela-
International Textbook of Obesity. Edited by Per Bjorntorp. © 2001 John Wiley & Sons, Ltd.
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