SINCE THE TIME OF INTESTINAL BYPASS SURGERY AND more recently with the use of Roux-en-Y gastric bypass (RYGB) and laparoscopic gastric banding procedures, some patients who had been morbidly obese for many years seek operative interventions for treatment of obesity. Except for being obese, some of these patients are otherwise healthy without apparent diabetes, hypertension, sleep apnea, or osteoarthritis. When these patients are asked why they want to subject themselves to the considerable risks of an RYGB or other procedures, a typical response is because “I don’t want to die from obesity.” Why would such patients think they are going to die from being overweight when they have been obese for many years and, despite that, appear to be healthy? The United States and many areas of the developed world are in the midst of an obesity epidemic. One concern is that increasing rates of obesity will be associated with increased mortality that will undermine the considerable gains made in longevity because of better treatment for numerous diseases. But how lethal is obesity? On average, obese patients do have increased mortality, but not if patients are stratified based on the presence or absence of risk factors such as diabetes or hypertension. Life span is only minimally reduced when these risk factors are absent. There are plausible explanations for this. In response to overnutrition, some patients preferentially accumulate peripheral rather than central fat, preventing development of the metabolic syndrome. When the ability to accumulate subcutaneous fat is limited, overeating results in central obesity and ectopic fat deposition that causes insulin resistance, diabetes, and ultimately life-limiting cardiovascular disease. Thus, fat distribution, not overall fatness, is a critical determinate of the health risks of obesity. In this issue of JAMA, Bray et al explore another aspect of overeating that provides further insight into obesity. Healthy normal-weight volunteers who were given 1000 excess calories per day (40% above what was needed to maintain body weight) with differing amounts of protein all accumulated the same amount of fat; however, study participants who were given low protein diets gained less weight than those who received diets that had normal or elevated protein levels. Low protein diets also were associated with a net loss of lean body mass, whereas the other diets resulted in gains in lean body mass. These findings suggest that overnutrition with low protein diets causes fat accumulation without much weight gain, demonstrating how body weight may be a misleading indicator of fatness and, therefore, the risk of obesity. Similarly, body mass index (BMI), which is derived from body weight, is not a good measure of fatness or of the risks obesity pose to an individual patient. Even patients with very high BMI may not have substantial risk for cardiovascular disease if the large amounts of fat accumulated are in peripheral locations and, therefore, would reduce the deposition of ectopic fat that causes insulin resistance with subsequent development of diabetes. One of the most important risks of obesity is the development of cardiovascular disease. Obesity can cause diabetes, which in turn can contribute to cardiovascular disease. Controlling obesity should result in less cardiovascular disease. In another study in this issue of JAMA, Sjostrom et al evaluated the relationship between weight loss and cardiovascular disease, by examining long-term outcomes for cardiovascular events following bariatric surgery in the Swedish Obesity Surgery (SOS) study. In this large, matched cohort of obese Swedish patients who self-selected to undergo either bariatric surgery or pursue usual care, the authors show that patients in the bariatric surgery group compared with those in the control group had lower rates of cardiovascular deaths (28 deaths among 2010 patients vs 49 deaths among 2037 patients, respectively), and lower rates of the composite of first-time (fatal and nonfatal) cardiovascular events, which included myocardial infarction or stroke (199 cardiovascular events among 2010 patients vs 234 cardiovascular events among 2037 patients, respectively). Although the differences between groups were statistically significant, the absolute difference between groups was small, even with relatively long 14.7-year follow-up. Interpreting the clinical importance of these results is complicated by the authors’ findings that reduced cardiovascular events among the surgical patients were not related to either baseline weight or weight loss. In an earlier trial of
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Aug 29, 2024
Pedro Melendez + 2
Open Access
