Body-Fat Distribution and Mortality Risk: Thinking Small

Updated:Jun 5,2014

Body-Fat Distribution and Mortality Risk: Thinking Small

Disclosure:Dr. Carr: Wyeth stock, modest; Dr. Tannock: None.
Pub Date: Thursday, April 9, 2009
Author: Molly C. Carr, MD and Lisa R. Tannock, PhD

Article Text

Significant data support the concept that abdominal adipose tissue is biologically and metabolically different than subcutaneous fat tissue and may play a causal role in the clustering of major cardiovascular risk factors such as dyslipidemia, elevated blood pressure, and diabetes. Body-fat distribution appears to be determined by a combination of aging, hormonal, environmental, perinatal, and genetic factors.[1] While abdominal adiposity and total body adipose levels are highly correlated, data are accumulating that support the idea that the distribution of adipose tissue may be of greater importance than the total burden of adiposity.

In this issue of Circulation, Zhang and colleagues [2] report 16-year follow-up data from the Nurses Health Study (n = 44,636 women and 3,507 deaths) and show that abdominal fat accumulation is associated with the increased risk of all-cause and cause-specific mortality [cardiovascular disease (CVD) and cancer]. They found that the women with increased waist circumference (WC) greater than 35 inches (88 cm) or waist-to-hip ratio (WHR) greater than 0.84 had a 60% to 70% greater risk of all-cause mortality, compared to individuals with low amounts of abdominal adiposity (less than 28 inches or less than 0.73, respectively). The association between abdominal fat and mortality risk remained after statistical adjustment for body weight (BMI), implying that the influence of abdominal adiposity on mortality risk was independent of total body adiposity. Abdominal girth remained an equally strong predictor of mortality risk across the subgroups of women stratified by tobacco use, menopause status, or age. Interestingly, increased WC appeared to be a better predictor of future risk in the normal-weight women (BMI < 25 kg/m2; RR = 2.35) compared to the overweight and obese women (BMI ≥ 25 kg/m2; RR = 1.78), although this may be because the normal weight reference group (with low levels of abdominal adiposity) had lower baseline risk than the obese (with low abdominal adiposity) reference group.

In the current study, body-fat distribution was assessed by several anthropomorphic measures (WC, WHR, and waist-to-height ratio), and they were all significantly correlated with BMI (r = 0.81 for BMI and WC). The women with the highest levels of abdominal adiposity were characterized by significantly higher BMI and lower levels of physical activity and were significantly less likely to use hormone replacement therapy and more likely to be hypertensive and hypercholesterolemic.

The current data support recent studies that have attempted to separate the contribution of abdominal and total body adiposity on CVD risk. The INTERHEART study, a worldwide case-control study (n = 29,972 in 52 countries) designed to evaluate the global applicability of risk factors for acute myocardial infarction, showed that abdominal obesity (measured by WHR) was more highly correlated with myocardial infarction than BMI and that abdominal obesity accounted for a greater proportion of CVD risk than smoking in Westernized countries.[3] Smaller clinical trials evaluating normal weight individuals who have adverse metabolic profiles (insulin resistance, dyslipidemia, hypertension) have consistently documented increased visceral adiposity in these individuals. Brochu et al. compared 'metabolically normal' to 'metabolically abnormal' (insulin resistant) obese women of similar age and BMI.[4] Using CT scans, they found that the 'metabolically abnormal' women had 50% more visceral adipose tissue but similar amounts of subcutaneous and total body fat, compared to the 'metabolically normal' women. Recent data compared body composition between participants of the Look AHEAD trial (an on-going, multicenter, randomized study investigating the effect of weight-loss interventions on cardiovascular events in type 2 diabetes patients; n = 1375) with overweight/obese but nondiabetic subjects (n = 254) using DEXA scan.[5] The authors found that the persons with diabetes had significantly less total body fat and leg fat (relative to their weight), but significantly more trunk fat (mean of 1.28 kg) compared to controls without diabetes, again implying that increased abdominal adiposity contributes to the development of metabolic abnormalities independent of total body adiposity.

The utility of the current epidemiologic data is in the identification of women (both normal weight and obese) with increased abdominal fat who have an increased risk of mortality. The vast majority of patients with increased abdominal obesity are also overweight or obese, but this study highlights the need to identify normal weight individuals, with abdominal adiposity and metabolic abnormalities, that may require treatment. An important finding from this study is the utility of using the simple WC measure in assessing health risk. There has been ongoing discussion as to what is the best marker of abdominal adiposity, with many studies using research tools (CT scan, DEXA) or attempting to adjust for total adiposity by measuring WHR. The use of CT scans or DEXA is neither practical nor feasible in routine clinical practice, and the requirement for two measurements (waist and hip) adds complexity and reduces accuracy compared to a single measure. Thus, the finding that increased WC was strongly associated with increase in all-cause and cause-specific mortality, in a graded fashion, supports the use of this simple clinical measurement. An important caveat, the study population was predominantly white so the findings require confirmation in other ethnic groups.

While it is becoming clear that abdominal adipose tissue and total-body adiposity may play diverse physiologic roles in influencing CVD risk factors, there are no interventions that preferentially reduce abdominal fat, except possibly exercise.[6] Individuals attempting weight loss often become discouraged with their perceived lack of success. Although it remains to be proven that losing WC reduces all-cause and cause-specific mortality, it is promising that even modest weight loss, with attendant reduction in WC can reduce risk factors. Current obesity treatment guidelines encourage clinicians to combine their focus by "thinking large," on a population level and "thinking small," on the individual patient level.

Aiming to impact obesity prevention at the population level, the American Heart Association recently published a scientific statement identifying potential targets of environmental and policy change, in a manner similar to CVD prevention and tobacco cessation policies.[7] The scientific statement provides an overview of public policy and environmental changes that may impact obesity prevention, such as encouraging the design of 'walkable' neighborhoods and workplace initiatives that increase physical activity, considering taxation of snack foods, changing school food and vending policies, and instituting restaurant certification programs. The authors promote the idea that obesity is driven by more than individual choice and encourages clinicians to step into the public policy arena and impact obesity prevention on the societal level.

On the individual patient level, weight-loss counseling by clinicians is considered the first line of obesity treatment, but overweight individuals are increasingly underrecognized and compliance with physician counseling is lacking. The obesity epidemic has raised the threshold at which people think of themselves as overweight, as recent data show that fewer overweight patients identify themselves as overweight [8], and there has been a reduction in physician weight-loss counseling.[9] Patients are more likely to attempt weight loss if they view themselves as overweight or obese and are counseled by their physicians. The current epidemiologic data should encourage us to consider body-fat distribution (especially WC) in identifying at-risk patients and target these patients for weight-loss counseling (even in subjects with normal BMI but increased WC). The key objective for clinicians is to first identify abdominal adiposity status, and then, to correct misconceptions and counsel on weight-loss strategies (caloric restriction, physical activity, behavioral therapy, pharmacotherapy, and surgery). To encourage "thinking small," shouldn't waist circumference be added to the patient's vital signs?


  1. Wajchenberg BL. Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome. Endocr Rev 2000;21(6):697-738.
  2. Zhang C, Rexrode KM, van Dam RM, et al. Abdominal obesity and the risk of all-cause, cardiovascular, and cancer mortality: sixteen years of follow-up in US women. Circulation 2008;117(13):1658-1667.
  3. Yusuf S, Hawken S, Ounpuu S, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 2004;364(9438):937-952.
  4. Brochu M, Tchernof A, Dionne IJ, et al. What are the physical characteristics associated with a normal metabolic profile despite a high level of obesity in postmenopausal women? J Clin Endocrinol Metab 2001;86(3):1020-1025.
  5. Heshka S, Ruggiero A, Bray GA, et al. Altered body composition in type 2 diabetes mellitus. Int J Obes (Lond). 2008;32(5):780-787.
  6. Ross R, Dagnone D, Jones PJ, et al. Reduction in obesity and related comorbid conditions after diet-induced weight loss or exercise-induced weight loss in men. A randomized, controlled trial. Ann Intern Med 2000;133(2):92-103.
  7. Kumanyika SK, Obarzanek E, Stettler N, et al. Population-based prevention of obesity: the need for comprehensive promotion of healthful eating, physical activity, and energy balance: a scientific statement from American Heart Association Council on Epidemiology and Prevention, Interdisciplinary Committee for Prevention (formerly the expert panel on population and prevention science). Circulation 2008;118(4):428-464.
  8. Johnson F, Cooke L, Croker H, et al. Changing perceptions of weight in Great Britain: comparison of two population surveys. BMJ 2008;337:a494.
  9. Abid A, Galuska D, Khan LK, et al. Are healthcare professionals advising obese patients to lose weight? A trend analysis. MedGenMed 2005;7(4):10.

-- The opinions expressed in this commentary are not necessarily those of the editors or of the American Heart Association --

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