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Letter to the Editor |
Columbia Presbyterian Medical Center Columbia University College of Physicians and Surgeons Division of Molecular Genetics Russ Berrie Medical Pavilion, 6th Floor 1150 St Nicholas Avenue New York, NY 10032 E-mail: mr475{at}columbia.edu
Dear Sir:
Weinsier et al raise important issues regarding our studies of the effects of weight loss on systems of energy homeostasis, including carbohydrate metabolism, catecholamine excretion, and thyroid function (1). The nature and magnitude of the changes in energy metabolism that accompany weight reduction are critical issues from both physiologic and therapeutic perspectives. In their letter, Weinsier et al describe points of similarity and distinction between our respective studies of the effects on energy homeostasis of maintenance of a reduced body weight. We found that both the process of weight loss and the maintenance of a reduced body weight are associated with significant declines in total 24-h energy expenditure (TEE), resting energy expenditure (REE), and non–resting energy expenditure (NREE) beyond those expected from the changes in metabolic mass (1–3). In our recent article (1), we reported that both weight loss and the maintenance of a reduced body weight are associated with significant declines in urinary norepinephrine and dopamine excretion and circulating concentrations of triiodothyronine (T3). In earlier articles, we described decreases in REE in some subjects under these circumstances (2, 3). Weinsier et al (4, 5) noted similar decreases in REE, circulating T3 concentrations, and urinary catecholamine excretion during weight loss, but found that these decreases did not persist during sustained maintenance of a reduced body weight.
The differences in our results may have been due to differences in our subject populations and study designs. In our previous studies (2, 3), we found that maintenance of a reduced body weight (
10% below initial body weight) is associated with a significant decline in REE adjusted for fat-free mass (FFM) in obese premenopausal subjects but not in subjects who have never been obese. Weinsier et al point out that the obese subjects we studied were significantly fatter than the obese subjects they studied: the mean (±SEM) fat mass in our subjects was 67 ± 3 kg compared with 30–31 ± 1 kg in Weinsier et al's subjects (4, 5). Our obese subjects had significantly (
10%) higher REE (adjusted for FFM) at their usual body weights than did our never-obese subjects. We concluded that this relative increase in REE was due to increased cardiorespiratory work in the more obese subjects. After weight loss, the REE (adjusted for FFM) of our reduced-obese subjects was significantly lower than it had been in the same subjects before weight loss, but was similar to that of our never-obese subjects at their usual body weight. Thus, the adjusted REE of our reduced-obese subjects was not significantly lower than that of the never-obese subjects. The persistent decline in REE in our obese subjects during weight maintenance at a reduced body weight may reflect their higher REEs at usual body weight compared with Weinsier et al's "leaner" obese subjects.
The subjects in our inpatient studies were intentionally restricted to an amount of physical activity designed to maintain a degree of physical fitness equal to that on admission to the study (1–3). In contrast, Weinsier et al's subjects were not restricted with regard to physical activity (4, 5). The weight loss in Weinsier et al's subjects was apparently due to both a hypoenergetic diet and physical activity [which increased by 33% in the weight-reduced subjects (4)], whereas the weight loss in our subjects was intentionally achieved solely through a reduction in energy intake. Several studies showed that the addition of exercise to a weight-loss regimen will significantly blunt the decline in REE that occurs during and after weight loss (6–12). Thus, the lack of association of maintenance of a reduced body weight with lowered REE in Weinsier et al's subjects may also reflect effects of increased physical activity during their outpatient weight loss.
We showed previously that maintenance of a reduced body weight is associated with a significant decline in sympathetic nervous system tone as measured by effects on heart rate variability of sequential pharmacologic blockade of the sympathetic and parasympathetic branches of the autonomic nervous system (13). Schwartz et al (14) reported that weight loss induced by diet alone results in a 17% decline in urinary norepinephrine excretion (similar to the values in our studies), but that the addition of exercise to the weight-loss regimen abolishes this decline. Although we are aware of no studies that examined the effects of exercise training on the thyroid axis during maintenance of a reduced body weight, the observation that exercise increases sympathetic nervous system output (as reflected in blunting of the weight-loss-associated decline in urinary norepinephrine excretion) suggests that the decline in T3 might also be mitigated with exercise through sympathetic nervous system–mediated effects on the thyroid axis (1).
The observations by Weinsier et al (4, 5) indicate that the decreases in catecholamine excretion and in circulating concentrations of thyroid hormones that accompany weight loss by diet alone may be ameliorated by increased physical activity during weight loss or maintenance of a reduced body weight. However, despite the prevention of these endocrine adaptations to body weight reduction, the weight-reduced subjects studied by Weinsier et al still needed to increase their physical activity by 33% to maintain a reduced body weight without decreasing energy intake (4). Thus, Weinsier et al's subjects apparently experienced the same decreases in total energy expenditure experienced by our subjects and compensated for this decline by their increase in physical activity. Weinsier et al's observation that TEE does not change significantly after weight loss in weight-reduced subjects who significantly increase their physical activity agrees with our observation that TEE declines significantly in weight-reduced subjects who do not change their physical activity from baseline after losing weight. Furthermore, Weinsier et al's report of an increase in time spent in physical activity after weight loss, without a corresponding increase in NREE, agrees with our finding (2, 3) that the energy cost of NREE is significantly decreased after weight loss and that NREE is the component of energy expenditure most affected during maintenance of a reduced body weight.
A small, persistent excess of energy intake relative to expenditure will, over time, result in substantial weight gain. To avoid regain of lost weight, reduced-obese subjects must, as in our studies (1–3), significantly decrease their energy consumption or, as in Weinsier et al's studies (4), significantly increase their physical activity.
REFERENCES
This article has been cited by other articles:
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  M. Rosenbaum, J. Hirsch, D. A Gallagher, and R. L Leibel Long-term persistence of adaptive thermogenesis in subjects who have maintained a reduced body weight Am. J. Clinical Nutrition, October 1, 2008; 88(4): 906 - 912. [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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