TO THE EDITOR: We read with much interest the recent report entitled “Patterns of growth associated with the timing of adiposity rebound” in Obesity by Williams and Goulding (1), who examined the patterns of growth for 458 children born in 1972–1973, with early, medium, and late adiposity rebound (AR). Authors showed that early AR was associated with increased depositions of fat in middle childhood. These findings confirm the importance of AR for the prediction of later fatness (2). Consistently, in a study conducted in 76 obese adolescents (3), we showed that 97% of them had early AR (before 6 years) and that median age at AR was 2 years (Figure 1).
Because there are significant positive correlations between BMI in infancy/adolescence and adulthood, it is commonly believed that most obese adults were also fat in childhood. However, although fat children are more likely to become fat adults, most obese adults were not fat as children (4). Williams and Goulding showed that children with early AR were not overweight before the rebound (1). Similarly, in our study, most obese adolescents were normal weight at the time of AR, with a mean BMI close to the median reference percentile (Figure 1). Some studies even showed that children with early AR had lower fatness in early childhood (1,2). In our sample of obese adolescents, we observed that while most of them had very early AR (65% before 2 years), only 8% had actually been obese at the time of AR, according to Cole et al.'s International Obesity Task Force cutoffs. In average, obesity started at the age of 5 years, while AR started 3 years earlier (Figure 1). The very early AR recorded in obese subjects suggests that determinants of future risks have operated early in life.
In conclusion, BMI growth trajectories of obese individuals do not generally follow an elevated percentile throughout childhood but rather indicate normal or even low BMI values at young age followed by high values later on. This particular trajectory and early AR should be looked at because of their association with later metabolic risk (2,5).