Central Obesity in Older Adults: What Should Be the Priority?

A growing body of literature shows that visceral fat, but not subcutaneous fat, is associated with development of cardiovascular disease (CVD), and there are disparate functions and implications of fat stored in these 2 different depots. Although the overall relationship between visceral fat and CVD is rarely contested, the relationship in older adults has been heterogeneous. For example, pooled analyses from large, well-characterized, epidemiologic cohorts have shown that the magnitude of association between obesity (measured by body mass index) and atherosclerosis does not differ across the age spectrum. This is in contrast to a body of literature showing that the relationship between obesity and CVD is weaker with increasing age. As such, questions remain about the role of central obesity in predicting atherosclerotic CVD (ASCVD) in older adults. This is an important issue given the global obesity epidemic and an increasingly aging population. In this issue of the Journal of the American Heart Association (JAHA), Schousboe et al examine associations of central adiposity and incident ASCVD in the study of MrOS Sleep (Outcomes of Sleep Disorders in Older Men), an ancillary to the study of MrOS (Osteoporotic Fractures in Men). MrOS Sleep is a large, epidemiologic cohort of older white men with comprehensively measured and adjudicated ASCVD outcomes. The ability to comprehensively assess and evaluate central obesity as a predictor of ASCVD outcomes in a large study of older adults is uncommon, and to our knowledge, this is only the second study to do so. Schousboe et al found no significant associations between visceral adipose tissue or android-gynoid fat mass ratio and ASCVD; and this finding persisted in the subset of their cohort who did not have comorbid conditions and the subset who were overweight or normal weight. The null and paradoxical findings of this study leave us grappling with the clinical and public health implications of developing and/or maintaining higher levels of central adiposity over the life course. Although the MrOS Sleep study data set is a rich resource within which to examine the relationship between central obesity and incident ASCVD, as with all epidemiologic cohorts with data for older adults, there are complexities and potential biases that may be exacerbated in this context. Schousboe et al acknowledged concerns, such as their inability to use computed tomography or magnetic resonance imaging to measure visceral adipose tissue and the unavailability of medical records to confirm the self-reported health conditions of participants at study baseline. Additional biases that influence these types of analyses include measurement error, collider stratification bias (the “obesity paradox”), and reverse causality. With regard to measurement error, the increasing use of direct measurements of central obesity, as done by Schousboe et al with dual-energy x-ray absorptiometry for visceral adipose tissue, helps to minimize the concerns that emerge when proxy measures, such as body mass index, are used in obesity research (Figure). A contemporary approach is the concordant measurement and analysis of subcutaneous fat and lean mass, which allows for better understanding of the underlying cause of CVD in older adults. Widespread utility of concordant measures in observational epidemiologic studies is limited by cost and the participant burden associated with multiple in-clinic visits and imaging. Collider stratification bias (Figure) is a distinctive form of selection bias that may account for the paradoxical findings that were observed. This bias emerges from the fact that to participate in a study of central adiposity at ≥70 years, it is necessary to have survived to older age and to have preserved physical and cognitive function. Few Americans are truly free of cardiometabolic disease at the age of 70 years, and this The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From the University of California San Diego School of Medicine, La Jolla, CA (C.A.M.A); and Wake Forest School of Medicine, Winston-Salem, NC (M.M.-C.). Correspondence to: Cheryl A. M. Anderson, PhD, MPH, MS, Division of Preventive Medicine, Department of Family Medicine and Public Health, University of California San Diego School of Medicine; Division of Hypertension and Nephrology, Department of Medicine, 9500 Gilman Dr, MC 0628, La Jolla, CA 92093-0628. E-mail: c1anderson@ucsd.edu J Am Heart Assoc. 2018;7:e010119. DOI: 10.1161/JAHA.118. 010119. a 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.