Obesity Epidemiology

OBESITY AND CARDIOVASCULAR DISEASE 183intolerance. 40 Weight loss induced by bariatric surgery in morbidly obese patients hasalso produced significant improvement or resolution of type 2 diabetes, hyperlipidemia,hypertension, and obstructive sleep apnea. 41 In the general population, however, confoundingby unintentional weight loss from existing diseases and aging makes it moredifficult to evaluate the effects of weight loss on CHD. So far, most epidemiologic studiesdo not distinguish between intentional and unintentional weight loss.In the Iowa Women’s Health Study, 42 unintentional weight loss was associated withincreased CVD mortality, but only among women with existing chronic diseases. Thisfinding reflects a well-known phenomenon called “reverse causation” (weight loss causedby existing diseases rather than the reverse; discussed in Chapter 4). Eilat-Adar et al. 43reported that intentional weight loss after 6 months of dietary counseling was associatedwith lower incidence of CHD over 4 years of follow-up, but there may have beenconfounding from other health-related behaviors associated with attempted weight loss.Other studies that did not distinguish intentional from unintentional weight loss foundthat weight loss since young adulthood was, in general, not significantly associated withrisk of CHD. 29,38 However, more recent weight loss in older individuals has been associatedwith increased CHD risk. 39 More often than not, weight loss in older individualsreflects loss in lean body mass due to aging and existing chronic diseases, a conditiontermed fragility. In Chapter 11, we will discuss the relationship between intentional andunintentional weight loss and total mortality.Fatness versus Fitness in Predicting CHDAs discussed in Chapter 8, the fat and fi t hypothesis suggests that higher levels ofphysical fitness reduce the adverse impact of overweight and obesity on health, makingobesity a less important determinant of morbidity and mortality than fitness. In thatmost people find it difficult to sustain weight loss, the hypothesis has appeal; even withoutweight loss, physical fitness can be improved by increasing physical activity levels.So far, evidence to support this hypothesis has been limited largely to data from theAerobics Center Longitudinal Study (ACLS). 44 The ACLS measured physical fitnessusing a maximal treadmill exercise test and found that low fitness conferred greatertotal and CVD mortality risk compared with fatness, and that fitness eliminated excessrisk associated with fatness in men. Data also showed that lean men with lower cardiorespiratoryfitness had a higher risk of all-cause and CVD mortality than did morephysically fit men with higher overall or abdominal fat mass. This study, however,included only 428 deaths, and was unable to investigate the effects of adiposity amongnever-smokers. In an examination of the joint effects of fitness and fatness on mortalityin 2506 women and 2860 men followed for more than 22 years in the Lipid ResearchClinics Study, Stevens et al. 45 found that both fitness and fatness predicted total andCVD mortality, and that physical fitness did not eliminate the association between obesityand excess mortality.Three additional studies examined the relative importance of physical activity andobesity on CHD risk without testing physical fitness (Table 9.2). Physical activity is themain nongenetic determinant of physical fitness as well as the primary focus of publichealth recommendations. It is useful, therefore, to evaluate the fat and fi t hypothesisby studying the role of physical activity in modifying the relationship between obesityand mortality. Wessel et al. 46 found a significant association between self-reported physicalfunction score (rather than BMI) and lower incidence of coronary artery diseaseamong 906 women undergoing coronary angiography for suspected ischemia. However,