Low physical activity reduces total energy expenditure in women with rheumatoid arthritis: implications for dietary intake recommendations12345

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ABSTRACT

Background:

Rheumatoid arthritis (RA) causes cachexia, a metabolic response characterized by loss of muscle mass and elevated resting energy expenditure (REE). However, energy expenditure in physical activity in subjects with RA is lower than that in healthy subjects. It is not known which effect predominates in regulating total energy expenditure (TEE), and thus whether the dietary energy requirements of subjects with RA are higher or lower than those of healthy subjects.

Objective:

Our objective was to determine TEE in women with RA by using the reference method of doubly labeled water (2H218O).

Design:

In this case-control study, we examined 20 women with RA and 20 healthy women who were matched for age and body mass index.

Results:

The patients with RA were cachectic (their body cell mass was 14% lower than that of the controls, P < 0.001), but REE was not elevated, reflecting good disease control. Mean (± SD) TEE was 1344 kJ/d lower in the patients than in the controls (9133 ± 1335 compared with 10 477 ± 1992 kJ/d; P < 0.02). The energy expenditure in physical activity of the patients was 1034 kJ/d lower than that of the controls (P < 0.04), which accounted for 77% of the difference in TEE between the 2 groups. The physical activity level (TEE/REE) of the patients also tended to be lower than that of the controls (1.70 ± 0.24 compared with 1.89 ± 0.36; P < 0.07).

Conclusion:

A low physical activity level is the main determinant of lower-than-normal TEE, and thus energy requirements, in women with RA.

KEY WORDS

Rheumatoid arthritis
energy metabolism
doubly labeled water
physical activity
total energy expenditure
women

Cited by (0)

1

From the Nutrition, Exercise Physiology, and Sarcopenia Laboratory (RR, JW, NL, and LS), Mass Spectrometry Laboratory (GJD), and Energy Metabolism Laboratory (SR), Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, and the Division of Rheumatology/Immunology, Department of Medicine, New England Medical Center and Tufts University School of Medicine, Boston (RR).

2

Nancy Lundgren is deceased.

3

The contents of this article do not necessarily reflect the views or policies of the USDA, and mention of trade names, commercial products, or organizations does not imply endorsement by the US government.

4

Supported by a Clinical Science Grant from the Arthritis Foundation, USDA Cooperative Agreement 58-1950-9-001, and National Research Service Award T32 AG00209-09.

5

Reprints not available. Address correspondence to R Roubenoff, Nutrition, Exercise Physiology, and Sarcopenia Laboratory, Jean Mayer USDA HNRCA, Tufts University, 711 Washington Street, Boston, MA 02111. E-mail: [email protected].