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Letter to the Editor |
1 University of Alabama atBirmingham Birmingham, AL 35294 E-mail:weinsier{at}shrp.uab.edu
2 University of Lausanne Lausanne Switzerland
Dear Sir:
Several years ago Leibel et al (1) reported data suggesting that altered body weight produces changes in energy expenditure that favor a return to original body weight. Additional data from this group suggest that the compensatory changes in energy expenditure might be related to changes in thyroid or catecholamine status, or both (2). In this recent report, Rosenbaum et al (2) mentioned that "previous studies did not achieve the degree of weight stability and control of nutrient intake of this study and did not examine the same subjects during dynamic weight change as well as during static weight maintenance at altered body weights." In fact, we reported the metabolic responses of subjects during dynamic and energy balance phases of weight loss under tightly controlled metabolic ward conditions (3, 4). Our findings provide a potentially important contrast in results.
We measured resting metabolic rate (RMR), thyroid hormones, and plasma and urinary catecholamines in 24 overweight postmenopausal women (3). The metabolic variables were first assessed in the static phase of energy balance in the overweight state after 10 d in the General Clinical Research Center (GCRC). Subjects were then provided an energy-restricted diet containing 3347 kJ/d (800 kcal/d) while they were outpatients of the GCRC until they reached a normal body weight. They returned to the GCRC while still in the dynamic phase of weight loss and after 10 d underwent metabolic reassessment. After an additional 10 d in the GCRC, during which time energy balance was restored, a final assessment was made. Weight loss averaged 17% (12.7 kg; range: 74.0–61.3 kg) and mean body mass index (BMI; in kg/m2) fell from 28 to 23. Throughout the study, subjects received all meals from the GCRC so that we could control the macronutrient composition of the diet and provide a fixed content of sodium (174 mmol/d) and potassium (115 mmol/d) to avoid confounding effects on catecholamines.
Our findings during the dynamic phase of energy restriction are similar to those of Rosenbaum at el (2), showing significant reductions in RMR and triiodothyronine (T3) and an elevation in reverse T3 (rT3). Rosenbaum et al also found that urinary norepinephrine fell during energy restriction, whereas we observed no significant changes in 24-h urinary or fasting plasma concentrations of epinephrine or norepinephrine. During the static phase of weight-loss maintenance, Rosenbaum et al found that most of the metabolic responses to energy restriction persisted, including reduced RMR, reduced urinary norepinephrine, reduced T3, and elevated rT3. By contrast, in our subjects, during stabilization in the normal-weight state, all of the measured variables returned to levels that were statistically no different from those in the overweight state, including RMR adjusted for fat-free mass (FFM) (5) and fat mass, T3, and rT3 (3, 4) (Figure 1
).
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It is of more than academic interest to point out the similarities and differences between the results of our studies and those of Rosenbaum et al because both were conducted under tightly controlled metabolic ward conditions with use of identical energy restrictions (3347 kJ/d). Arguably, the outcomes should have been similar. Both studies suggest that during negative energy balance, RMR is reduced disproportionately to the decreases in FFM and fat mass and that thyroid hormones change in association with (and may possibly explain) the changes in energy requirements (5). However, our data suggest that on adaptation to a weight-reduced steady state, RMR and thermogenic hormones are appropriate for the subjects' new body composition and do not predispose the subjects to regain the lost weight.
Differences in the 2 studies might have contributed to the conflicting outcomes. The subjects studied by Rosenbaum et al were severely obese, with an average BMI of 
48, whereas our subjects were overweight, with a BMI of 28. This weight difference could account for the subjects' different metabolic responses. However, we believe that more plausible explanations exist. First, Rosenbaum et al's more obese subjects had an absolute RMR value 50% higher than that in our subjects. Thus, the fixed 3347-kJ/d energy-restricted diet would have produced an energy deficit almost twice that in our subjects. We confirmed in a subset of our subjects that 10 d of stabilization in the weight-reduced state was sufficient to produce a metabolic steady state (4). However, the considerably greater energy deficit in Rosenbaum et al's subjects could have necessitated a period longer than the 14 d they used to establish a steady state. Second, different statistical approaches were used to adjust RMR for changes in body composition after weight loss. We adjusted RMR for FFM and fat mass by using analysis of covariance (5, 7). Rosenbaum et al's findings in the earlier report of reduced RMR after weight loss (1) appear to have been based on the ratio of RMR to FFM, which may sometimes lead to spurious results (8, 9). When they adjusted RMR for changes in FFM and fat mass by using regression analysis, RMR values after weight loss were apparently not significantly different from baseline values (1).
In summary, both studies indicate that during the dynamic phase of energy restriction, thyroid hormones change in conjunction with reductions in RMR, placing subjects in an energy conservation mode. The findings of Rosenbaum et al suggest that on return to energy balance conditions, weight loss is associated with changes in thermogenic hormones which might, by virtue of effects on energy expenditure, favor a return to usual body weight. By contrast, our findings suggest that the energy-conserving metabolic changes persist only during the period of energy restriction. Once energy balance is restored, metabolic variables appear to normalize and become appropriate for the new reduced body mass and do not explain the weight-regain tendency of these subjects (7).
REFERENCES
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  K. D. Hall Computational model of in vivo human energy metabolism during semistarvation and refeeding Am J Physiol Endocrinol Metab, July 1, 2006; 291(1): E23 - E37. [Abstract] [Full Text] [PDF]
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 P. S. MacLean, J. A. Higgins, G. C. Johnson, B. K. Fleming-Elder, W. T. Donahoo, E. L. Melanson, and J. O. Hill Enhanced metabolic efficiency contributes to weight regain after weight loss in obesity-prone rats Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2004; 287(6): R1306 - R1315. [Abstract] [Full Text] [PDF]
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