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EDITORIAL |
1 From the Department of Medicine, Obesity Research Center, St Luke's–Roosevelt Hospital, New York, NY
2 Reprints not available. Address correspondence to D Gallagher, Body Composition Unit, Obesity Research Center, 1090 Amsterdam Avenue, New York, NY 10025. E-mail: dg108{at}columbia.edu.
See corresponding article on page 1193
Two parallel trends exist in the developed world: an increasing percentage of the population is obese and older. Moreover, debilitating illnesses such as cardiovascular disease and diabetes are common to both obesity and aging (1). Many of these older persons seek weight-loss treatment for their obesity. According to the 2001–2002 National Health and Nutrition Examination Survey, 69.1% of women older than 60 y were overweight or obese (2) and 49.8% of this age group reported trying to lose weight (3).
It has been postulated that older persons function optimally at a higher body weight, which raises a concern about the efficacy of weight loss in these persons. It is well established that, during the latter adult years, skeletal muscle mass decreases and body fat becomes centralized (4, 5). Characterization of the aging process in skeletal muscle mass has identified losses in muscle mass, force, and strength, which collectively are defined as sarcopenia. In the elderly, the loss of skeletal muscle mass is correlated with physical impairment and disability. Persons who are obese and sarcopenic are reported to have worse outcomes, including functional impairment, disabilities, and falls (6).
Adipose tissue infiltration of skeletal muscle mass increases with age (7), and computerized tomography–derived midthigh low-density lean tissue, also referred to as reduced muscle attenuation, is directly related to age and adiposity in women (8). Accordingly, reduced muscle attenuation is considered to reflect a greater intermuscular adipose tissue (IMAT) content, and greater thigh IMAT is associated with poorer leg function in the elderly.
In this issue of the Journal, Mazzali et al (9) present the results of a cross-sectional study involving 35 healthy, obese, postmenopausal women, 15 of whom [body mass index (BMI; in kg/m2) >29] consumed a hypocaloric diet to produce a weight loss of 5.4% of body weight. Measurements included a whole-body dual-energy X-ray absorptiometry scan for fat mass; computerized tomography scan of the midthigh to determine skeletal muscle area, including normal- and low-density areas; and biochemical analyses for the measurement of insulin, cholesterol, triacylglycerol, HDL, LDL, leptin, adiponectin, and C-reactive protein concentrations. In the cross-sectional study, BMI, sagittal abdominal diameter (SAD), and leg subcutaneous adipose tissue (single slice) were independent predictors of insulin resistance measured by homeostasis model assessment (HOMA) in addition to triacylglycerol, HDL-cholesterol, adiponectin, leptin, and C-reactive protein concentrations. This finding is consistent with our knowledge that the anatomic distribution of adipose tissue is an important determinant of metabolic and cardiovascular disease risk. Significant reductions in the anthropometric measures body weight, BMI, and SAD were observed with weight loss. More advanced measurement techniques showed a reduction in total body fat (8.4%), which reflected decreases in SAT (6.6%), IMAT (23.1%), and low-density lean tissue (8.0%), all of which were determined from a single midthigh slice. Fat mass accounted for 
69% of the observed weight loss. No direct measure was acquired for visceral adipose tissue; however, the changes observed in waist circumference (–3.3%) and SAD (–6.2%) suggest that both visceral adipose tissue and abdominal subcutaneous adipose tissue were lost. Interestingly, a simple measure of fat distribution, SAD, was the best predictor of insulin resistance with weight loss, which likely reflects visceral adipose tissue loss. Previous studies involving 10% weight loss in obese postmenopausal women have shown a 25% reduction in total visceral adipose tissue mass (10).
Within the fat-free mass compartment, appendicular lean tissue also decreased (2.9%) and reflected 38% of the loss of fat-free body mass. No significant change was noted for muscle cross-sectional area. Corresponding significant reductions occurred in HOMA-derived insulin resistance, HDL cholesterol, and leptin, but no significant change in adiponectin was observed. Low-density lean tissue is derived from muscle attenuation, reflects both IMAT and intramyocellular lipid, decreases as a function of overall muscle adiposity, and is strongly associated with insulin sensitivity (11). Overall, the prescribed weight loss in these obese postmenopausal women consisted of a small and appropriate amount of lean tissue loss relative to that reported in younger persons. The observed changes in fat tissue and its distribution were associated with improvements in insulin resistance.
The current study provides important information on the effects of modest weight loss on fat distribution and corresponding metabolic and cardiovascular disease risk factors in older Italian women. These data provide no evidence that age should be considered a risk factor for modest weight loss in obese older persons.
ACKNOWLEDGMENTS
The author had no conflict of interest.
REFERENCES
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