Obesity Research Center, St. Lukes-Roosevelt Hospital, and Columbia University Institute of Human Nutrition New York, New York, 10025
Address correspondence to: Dympna Gallagher, Ed.D., St. Lukes Roosevelt Hospital, Obesity Research Center, Columbia University, 1090 Amsterdam Avenue, 14th Floor, New York, New York 10025. E-mail: dg108{at}columbia.edu.
To the editor:
An article (1) with accompanying editorial (2) published recently in this journal provides new data and a comprehensive discussion of energy expenditure in dietary-restricted (DR) animals. The aim was to provide evidence bearing on the hypothesis that reduced oxygen consumption may lower the formation of reactive oxygen species (1), thereby reducing oxidative damage and extending lifespan. This hypothesis implies that oxygen consumption in DR animals is reduced beyond that expected on the basis of reduced body size or altered body composition. The resulting analysis found that after adjusting for the amount of fat-free mass (FFM), resting energy expenditure (REE) was 13% lower (-250 kJ/d) in DR animals. These findings were interpreted to mean that DR lowers REE independent of DR-induced changes in body composition. The editorial (2) recommends regression-based approaches to adjusting metabolic data when concomitant changes in body composition occur.
It is quite certain that adjusting changes in energy expenditure for changes in FFM can provide no evidence of rate of oxygen flux at the cellular level, which is the level at which oxygen flux must decrease if exposure to free radicals is to be lessened. Although normalizing for FFM may be preferable to using body weight or body surface area, FFM is a construct that lumps together diverse fluids, organs, and tissues with different cellular oxidative requirements. Heterogeneity in heat-producing tissues that make up body mass and FFM has long been recognized (3, 4, 5, 6), and the existence of large between-organ differences in the rates of energy flux is well established (3, 4, 5, 6). Brain and visceral organs such as liver, heart, and kidney have high metabolic rates in the postabsorptive state, whereas adipose and skeletal muscle tissues have relatively low metabolic rates. Specifically, organs such as liver, brain, kidney, and heart account for only approximately 5% of total body weight (67% of FFM); in reference male and female, they collectively account for 5859% of whole body REE (7). If the mass of one or more high-metabolic-rate organs were to decrease in greater proportion than the mass of low-metabolic-rate organs, REE normalized for FFM would be lower, although the energy flux (kilocalories per kilogram per day) of each organ remained unchanged. Therefore, in order for FFM-adjusted REE to provide evidence for reduced oxygen flux, data must be presented showing that that the proportion of FFM represented by each organ/tissue/fluid is identical in DR and control animals.
The authors do not present or cite such evidence, and the proposition that all organs comprising FFM are changed in a constant proportion after DR is unlikely to be true. A number of animal studies (8, 9, 10, 11, 12) have reported that weight change is accompanied by disproportionate changes in the size of various organs. More recently, Mayer et al. (13) reported preliminary data that organs are reduced disproportionately in patients with anorexia nervosa compared with controls.
It is unfortunate that in this otherwise excellent study and discussion that the heterogeneity of FFM and its bearing on the oxidative flux hypothesis of DR and aging was ignored. Future investigations should consider the in vivo measurements of individual organs and tissues (14, 15) and, where possible, the measurement of tissue specific metabolic rates.
Received February 28, 2003.
References
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