Resting energy expenditure and adiposity accretion among children with Down syndrome: a 3-year prospective study.

Down syndrome (DS), or trisomy 21, is associated with intellectual disability, and many medical conditions1–3. Up to 30% of children with DS are obese (BMI-for-age ≥95th percentile)4, 5, representing a higher prevalence than children without DS (17%)6 and children with other intellectual disabilities (12 – 30%)4, 7. One recent population based study in the Netherlands found that children with DS were twice as likely to be obese as children who did not have DS (4.2% vs 1.8% for boys; 5.1% vs 2.2% for girls)8. Anecdotal studies provide estimates of obesity among children with DS ranging from 18.8 to 31%9, 10. As life expectancy has increased for individuals with DS over the past decades, the health complications associated with excess adiposity such as type 2 diabetes and cardiovascular disease are becoming more significant concerns11, 12. Furthermore, individuals with disabilities, in general, suffer from significant disparities in obesity burden and medical management, and there is less research conducted with this population13. Therefore, it is important to understand the factors that lead to obesity among people with DS. Lower resting energy expenditure (REE) relative to body size and composition is one mechanism that may predispose individuals to excessive weight gain. Small differences in REE could potentially accumulate over time and contribute to significant excessive weight gain, but previous studies of REE and weight gain for children have yielded mixed results9, 14–22. Previous studies suggesting lower REE in children with DS23–25 had some limitations, such as small sample size, lack of a control group, not controlling for other family factors related to obesity, possible recruitment bias of control families without DS (control families with no children with DS may participate for different reasons than families of a child with DS), and technical difficulties in REE measurements (excess movement during measurement procedure). Furthermore, with the exception of one study with a one year follow-up24, these studies were cross-sectional and did not investigate whether lower REE was predictive of weight and adiposity gain over time. The primary aim of this study was to examine whether children with DS showed differences in baseline REE that contributed to changes in fat mass (FM) over a three-year follow up. We hypothesized that: 1) REE, adjusted for FFM, would be lower in children with DS than in sibling controls, 2) changes in FM over the three year period would be associated with baseline REE, adjusted for baseline FFM, baseline FM, sex, and age. A secondary aim was to explore potential mechanisms that could explain why children with DS have a lower REE such as higher FM and lower thyroid function that are typical of children with DS compared with children without DS1, 2, 4, 7, 26. While FFM is the primary contributor to REE, FM does explain some additional variance in REE, especially in obese subjects27–29.