Response to: Szabó T et al. (2008) Differentiating between body fat and lean mass—how should we measure obesity? Nat Clin Pract Endocrinol Metab doi:10.1038/ncpendmet0999

Original article: Romero-Corral A et al. (2008) Differentiating between body fat and lean mass–how should we measure obesity? Nat Clin Pract Endocrinol Metab 4: 322–323 doi:10.1038/ncpendmet0809

We read with interest the comments by Szabó and colleagues. We agree that merely differentiating between body fat mass and lean mass to assess the risk for total and cardiovascular mortality related to bodyweight might be too simplistic, and a complex interaction between these two components in maintaining cardiometabolic homeostasis is a more likely biological scenario.1

As pointed out by Szabó and colleagues, in certain pathologies, such as congestive heart failure and chronic kidney disease that are known for their catabolic features, an excess in adiposity and/or bodyweight might be associated with improved survival.2,3 However, whether the adipose tissue is itself protective, or is a marker of better prognosis, remains unclear. Our Viewpoint discussed the obesity paradox in patients with and without coronary disease from the general population, where the majority of patients do not suffer from cachexia. Therefore, the obesity paradox cannot be explained simply by the wasting state hypothesis.

Furthermore, in large epidemiological studies conducted in the general population, differentiating adiposity from lean mass seems to assess risk better than other widely used measures of obesity.4,5 Moreover, in the elderly, where most of the mortality occurs, studies such as the one conducted by Wannamethee and colleagues,6 have shown that by discriminating between an excess in adiposity and taking into account its distribution along with the amount of lean mass or even the combination of low lean mass and high fat mass (sarcopenic obesity) confers a significant increased risk for mortality than does preserved lean mass and low adiposity. By taking into account measures of bodyweight that reflect these two components, we might be able to develop better ways to assess mortality related to bodyweight.

Finally, we have recently shown that even in subjects with a normal weight and body mass index but with an excess in adiposity, labeled as “normal weight obesity,” there is a greater risk for cardiometabolic dysregulation, including metabolic syndrome, dyslipidemia and coronary artery disease.7 So it would appear that simply differentiating between adiposity and lean mass, and also taking into account its distribution, improves cardiovascular risk prediction in the general population, although we acknowledge this might not be true for certain conditions.

We again appreciate the interest of Szabó et al., and are pleased that this Viewpoint accomplished its purpose, namely to elicit a healthy discussion on whether and how we should rethink the way we measure obesity and its relationship with health outcomes.