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Updated: Jul 4, 2025

Author Spotlight: Implementation of BIVA for Analyzing Disease Risk Factors in Patients with Low Body Cell Mass
Published on: July 14, 2023
Interaction effect of systemic inflammation and modifiable rheumatoid cachexia risk factors on resting energy
Beatriz Y Hanaoka1, Jing Zhao1, Kristen Heitman1
1Division of Rheumatology-Immunology, McCampbell Hall, 1581 Dodd Drive, Room 505, Columbus, OH, 43210.
Background:
In rheumatoid cachexia (RC), high resting energy expenditure (REE) is associated with loss of muscle mass driven by proinflammatory cytokines. The objectives of this study were to investigate parameters associated with RC, and the interaction between systemic inflammation and modifiable risk factors for RC on REE.
Methods:
Thirty-five rheumatoid arthritis (RA) and nineteen non-RA controls comparable in age, sex, race and BMI underwent measures of REE by indirect calorimetry. Clinical, dietary, body composition and physical function data were collected. Homeostasis model assessment for insulin resistance (HOMA-IR) and serum interleukin-6 (IL-6) were used as parameters of IR and systemic inflammation, respectively. Regression models tested association between REE and dependent variables, including pre-specified interaction tests involving HOMA-IR and IL-6 and dietary intake of protein per weight (PPW) and IL-6.
Results:
RA subjects were mostly women (94%) and had a median age of 54 years (50.5, 70) and BMI of 30.5 kg/m2 (26.1, 36.9). We observed a significant interaction effect between PPW and serum IL-6 on REE among RA subjects in the multiple regression model among RA. The upper tertile of PPW demonstrated a significant negative correlation between REE and IL-6 (β=-19.97, 95% CI [-35.41, -4.54], p=0.01). The lower tertile of PPW demonstrated a significant positive correlation between REE and IL-6 (β=42.24, 95% CI [4.25, 80.23], p=0.03).
Conclusions:
While IR can lead to muscle catabolism, IR was not significantly associated with REE in RA individuals. Higher dietary protein intake could attenuate the effect of systemic inflammation on REE in RA patients.

