The Framingham Study showed in 2005 men and 2521 women that the 28-year age-adjusted rates (per 100) of CHD was 26.3 for a mean BMI of 21.6kg/m2 and 42.2 for a mean BMI of 31 in men, and 19.5 for a BMI of 20.4 and 28.8 for a BMI of 32.3 in women, respectively (82). The 28-year age-adjusted relative risks and their 95% confidence intervals for the highest quintile compared to the lowest were 1.9 (1.4-2.5) for CHD and 1.8 (1.4-2.4) for CHD excluding angina pectoris for men and 1.7 (1.3-2.3) and 1.6 (1.2-2.3) for women, respectively. The Gothenburg study, in a 12-year incidence period, showed in a multivariate analysis, that the WHR was the strongest predictor (84) of myocardial infarction in 1462 women. In 1990, the Nurses Health Study, during an 8-year observation, clearly showed in a population of 121700 females that obesity is a determinant of CHD; after control for cigarette smoking, which is essential to assess the true effect of obesity, even mild-to-moderate overweight increased the risk of CHD (Figure 25.4) (85). This study showed a relative risk of 3.3 for a BMI of > 29 kg/m2 when compared to BMI < 21; a negative effect of obesity remained appreciable after a multivariate correction for hypertension, diabetes and high cholesterol levels. Similarly, the Honolulu Heart Program demonstrated over a 20-year observation period that a mean subscapular skinfold thickness of 27.2 mm increased the risk of developing CHD in Japanese American men aged 45-65 years by 1.5 when compared to a thickness of 8.1 mm (86). The Rochester Coronary Heart Disease project suggested that both weight and BMI are mildly associated with angina but not clearly with myocardial infarction or sudden unexpected death (87). This last event appears related to morbid obesity rather than to modest overweight. Duflou et al. showed in 22 patients with morbid obesity that dilated cardiomyopathy was the most frequent cause of sudden cardiac death followed by severe coronary atherosclerosis, left ventricular hypertrophy, pulmonary embolism and hypoplastic coronary arteries (Figure 25.5) (7). Recently the Paris Prospective Study has shown that increased BMI, along with resting heart rate, systolic or diastolic blood pressure, tobacco consumption, diabetes
status, serum cholesterol, and parental history of sudden death, was an independent predictor of sudden death during follow-up (23 years on average) (88,89).
The interaction betwen CHD and obesity has recently been confirmed by the PROCAM study, in which 16 288 men aged 40.6 + 11.3 years and 7328 women aged 36.0 + 12.3 years were enrolled between 1979 and 1991 (90). Among the 10 856 men aged 36-65 years at study entry, 313 deaths occurred within a follow-up period of 7.1 + 2.4 years. Among these men, increased mortality was seen at high BMI in both smokers and non-smokers and was caused by coronary heart disease (CHD).
Increased mortality at low BMI was seen in smokers but not in non-smokers and was due to an increase in cancer deaths. However, in this study the BMI-associated increase in CHD death was completely accounted for by the factors contained in the risk algorithm, indicating that the effect of overweight and obesity on CHD is mediated via other risk factors.
The relationship between obesity per se and CHD therefore appears doubtful when the measure of adiposity is expressed with a classical anthropo-metric variable such as weight and BMI, which may be inadequate surrogates for adiposity itself. As previously mentioned, the association between obesity and CHD becomes more robust when the distribution of fat is considered. Although Gillum et al. (34) and Hodgson et al. (91) found that the increased risk for ACVD present in abdominal adiposity is indirectly mediated by the presence of the other classical risk factors, several subsequent papers confirmed that the abdominal distribution of fat is an independent risk for CHD. Clark et al. found that, at least in black women, the strongest predictor for CHD is WHR > 0.85 followed by a family history of CHD and cigarette smoking (92). From forensic autopsy evaluations, Kortelainen and Sarkioja found that abdominal accumulation of fat is associated with the severity of coronary atherosclerosis and myocardial hypertrophy in women with no clinical evidence of cardiovascular disease (93,94). They also found that coronary lesions and myocardial hypertrophy are more advanced as WHR increases. Recently Gaudet et al. found that abdominal obesity is a powerful predictor of CHD in men, even in a group of patients with raised LDL cholesterol levels due to familial hypercholesterolaemia (95).
The relationship between obesity and CHD is operative not only in the elderly population but also in children and adolescents. Excessive body weight between 5 and 18 years is an independent predictor of future mortality in > 13 000 person (96). Similarly, in the Harvard Growth Study, BMI between 13 and 18 years predicted CHD mortality: adolescents with a BMI above the 75th percentile have a relative risk of 2.3 as compared to those in the 25th percentile (97). These impressive data justify the notion that atherosclerosis may be considered a nutritional disease of childhood (98). The relationship between weight gain and CHD has been emphasized in a recent paper which demonstrated in 6874 men aged 47 to 55 years at baseline and free of a history of myocardial infarction, followed for an average period of 19.7 years, that high BMI predicted death from CHD only at levels above 27.5 kg/m2 and that men with stable weight (defined as + 4% change from age 20) had the lowest death rate from CHD (99). The authors conclude that weight gain from age 20, even a very moderate increase, is strongly associated with an increased risk of CHD.
Obesity has been shown to be a risk factor also for cerebrovascular disease (CVD), although its negative role appears more clearly in women than in men. In the Framingham Study the 28-year age-adjusted relative risk for CVD was reported to be 1.4 (0.9-2.2) for men and 1.6 (1.1-2.4) for women in the upper quintile of BMI as compared to those in the lowest (83). Fatal stroke was also predicted by WHR in women in the Gothenburg Study and in US male army veterans (100). The relationship between obesity and stroke has not been confirmed in the Honolulu Heart Study where neither BMI nor central obesity was a predictor for such events (86). However, more recently publications from this group showed that elevated body mass was associated with an increased risk of thromboembolic stroke in non-smoking men in older middle age who were free from commonly observed conditions related to cardiovascular disease (101). In 1997 Rexrode et al. demonstrated in a prospective study that, during a 16-year follow-up, a BMI of > 27 kg/m2 significantly increased the risk of ischaemic stroke, with relative risk of 2.37 (95% CI 1.60-3.50) for a BMI of 32kg/m2 or more (102). No relationship was observed for haemorrhagic stroke. This study also showed that a weight gain of 20 kg or more was associated with a relative risk for ischaemic stroke of 2.52 (95% CI 1.80-3.52).
Folsom et al. for the ARIC (Atherosclerosis Risk In Communities Study) recently found that, in diabetic patients, the relative risk for ischaemic stroke was 1.74 (1.4-2.2) for a 0.11 increment of WHR, whereas the risk was not statistically related to BMI (103). This study further emphasizes the role of regional fat distribution, rather than total fat mass, as an important risk factor for CVD.
Literature data on the effects of obesity on lower limb circulation are more contrasting than those regarding the coronary and cerebral circulaions. While the Framingham Study showed that the relative risk for intermittent claudication was 0.9 (0.5-1.4) for men and 1.1 (0.6-1.8) for women in the fifth quintile compared to the first quintile, a retrospective study in a small group of female patients (52-82 years) showed that obesity was a predictive risk factor for peripheral vascular disease (PVD) (83). This latter finding is supported by the data of the Swedish Obese Subjects Study which showed, in 1006 male and female subjects, that obesity was significantly associated with intermittent claudication (104).
While obesity per se does not appear to confer a significant risk for the development of PVD, the association of obesity and diabetes mellitus does contribute to an enhanced risk of lower limb problems. As thoroughly demonstrated in epidemiologi-cal studies, severe complications of PVD are very frequent in people with non-insulin-dependent diabetes, who have a 10- to 15-fold increased risk for lower extremity amputation and a 3.4- to 5.7-fold increased risk for caudication (80,105). This increased risk appears to be consistent in diabetics independently of total fat mass or fat distribution.
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