Abstract
To the Editor: We are grateful to Beattie and Wiskin for taking an interest in our work. We agree that the area of energy requirements in paediatric inflammatory bowel disease (IBD) is controversial and that further work is necessary to determine the best nutritional management of children with IBD. We still believe that our data support the argument against the simple division of resting energy expenditure (REE) by fat-free mass (FFM) to adjust for differences in body composition in any population, and that raising the denominator to the power of 0.5 was a valid way of achieving this aim in the IBD cohort we studied. Our conclusion differs from that of Azcue et al (1), but it is nonetheless appropriate because their conclusion was drawn from inappropriate data expression. We clearly demonstrated that when REE is divided by FFM a negative relation is produced whereby those individuals with higher FFM display lower REE and those with lower FFM display higher REE. Following this model, it would be expected that the Crohn group would display higher REE per kilogram of FFM due to having lower FFM than controls, as we state in our original article. Azcue et al compared children with Crohn disease and anorexia nervosa and their findings do not necessarily fit our model. However, they also stated that this comparison is potentially confounded by the older age and exclusive female sex of the children with anorexia. Beattie and Wiskin also interpret the findings of Varille et al (2) as suggesting the reduction in REE between pre- and postsurgical adolescents with Crohn disease is indicative of increased inflammation presurgery preventing the physiological downregulation of REE associated with poor nutrition. Although a valid interpretation, it is contrary to Varille and colleagues own conclusion, being that the decrease in REE postsurgery is related to the actual removal of gut rather than the impact of inflammation. Also, as suggested by Beattie and Wiskin, our work indicates the raised REE per kilogram of FFM reported in the Crohn disease group is possibly due to inappropriate expression of the raw data because the disease group had a lower FFM than did the controls. Therefore, we agree that expression of data in an appropriate manner is necessary to answer the important question of how REE changes in individuals with IBD, and we hope that our original study has contributed to this literature.
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