In this population-based longitudinal study, we found that overweight and obesity manifested early in childhood. A majority of children who were obese by 3 years of age remained obese into adolescence. Among adolescents who were overweight or obese, the most excessive weight gain (i.e., the most rapid BMI acceleration) had occurred between 2 and 6 years of age. Even after this period of rapid weight gain, the BMI continued to increase at a lower but still positive rate, which led to a greater degree of obesity in this group, whereas in the group of adolescents with normal weight, the BMI standard-deviation score had been stable throughout childhood. Children who were large for gestational age at birth and children whose mothers were obese had an especially high risk of obesity, although the timing of the development of obesity did not differ from that among children whose mothers were of normal weight.

The mean BMI and the prevalence of obesity in our population were similar to those in recent representative national samples20,21 but are higher than those reported in earlier studies.22 A secular trend of increasing prevalence of obesity has been described previously,23,24 and the secular upward divergence of the 97th BMI percentile also occurs in early childhood,5 which is consistent with the age at which we observed the most rapid weight gain.

With our large sample size and a longitudinal study design that covered the entire age span from infancy to adolescence, we can discern that early childhood is the critical age for the development of sustained obesity. This period encompasses the “adiposity rebound,” the phase in early childhood during which the BMI starts to increase again, after having reached a nadir after infancy.25 Epidemiologic studies have shown that the risk of childhood obesity is far greater among children with an earlier or pronounced adiposity rebound.26 An upward deviation in BMI percentile may be an even more direct predictor of later adiposity.27 Therefore, the specific dynamics and patterns of BMI in this early childhood period, rather than the absolute BMI, appear to be important factors in identifying children at risk for obesity later in life.28

To date, most studies have not assessed an age span as comprehensive as that in our study, have had a limited sample size (fewer than 1000 children),16 or even if well-powered, have been restricted to an observational period that assessed only the first 2 years of life12 or that did not begin until 7 years of age and hence began after the most pronounced weight gain had occurred.10 Nevertheless, a considerable correlation exists between a high BMI during early childhood and prevalence of obesity later in life.4,9,12,29,30 The probability that young children who are obese will return to a normal weight in adolescence appears to be less than 20% and decreases further with age.

Children with normal weight showed much less variation in BMI standard-deviation score throughout childhood and adolescence than children who were obese. This finding may imply distinct dynamic BMI patterns in children with normal weight as compared with obese children. In studies that evaluated developmental trajectories of BMI, groups of children with “high rising BMI trajectory” diverged from those with fairly stable BMI trajectories beginning at approximately 3 years of age.31,32

Our data further showed that children who were large for gestational age at birth retained a higher BMI throughout childhood and adolescence, and almost half these children became overweight or obese in adolescence. This finding may seem to contradict the “Barker hypothesis” of low birth weight being associated with an increased likelihood of diabetes and cardiovascular complications, although not obesity per se, in adulthood.33 Rather, a rapid weight gain during childhood in children who had been small for gestational age at birth, even with the absolute BMI remaining within normal limits, was associated with later insulin resistance and coronary events.34 Hence, the association of cardiovascular disease and diabetes with low birth weight and rapid catch-up should be differentiated from the association of obesity with high birth weight.

The dynamic of increasing BMI does not end with adolescence but continues into adulthood.4 Obesity rates among adults are considerably higher than those among children, and most adults with obesity had had normal weight in childhood.35 However, if obesity does develop in childhood and continues through adolescence, it tends to persist; most obese adolescents become obese adults.4

With regard to prevention, the clinical manifestation of obesity is a late starting point. An excessive weight gain (an annual increase of ≥0.2 in the BMI standard-deviation score) during the preschool years was found to be even more relevant for adolescent overweight than excessive weight gain during late childhood and can be regarded as an early sign of ensuing obesity in adolescence that appears much earlier than the actual clinical manifestation of overweight.36 This same age interval of 2 to 6 years has been described as an important growth period for the prediction of adult overweight.16

A practical clinical implication of our study results would be surveillance for BMI acceleration, which should be recognized before 6 years of age, even in the absence of obesity. The tracking of growth and weight patterns, particularly in children with predisposing factors (e.g., maternal overweight or large-for-gestational-age status at birth), may help to identify children at increased risk and prompt early intervention even before overweight is evident. It is therefore important for health care professionals, educational staff, and parents to become more sensitive to this critical time period.

In addition to the mere expansion of fat mass, alterations in adipose tissue function occur in early childhood in parallel with the clinical increase in BMI.37 The early exposure to excess and dysfunctional fat triggers the development of preclinical metabolic and cardiovascular changes even in childhood.38 Epidemiologic evidence suggests that early childhood may be a sensitive period for arteriosclerosis on the basis of a positive association between childhood BMI at 4 years of age and high carotid intima media thickness in men at 60 to 64 years of age.39

The major strengths of the current study are the population-based design with a large, unselected cohort encompassing more than 51,000 children and 300,000 measurements across the entire age span from infancy to adolescence; the longitudinal design that allowed for childhood and adolescence data to be available for every child; and the specific evaluation of the rate of weight gain in 1-year intervals. In addition, selection bias was reduced because anthropometric data were obtained directly and uniformly at pediatric offices for all children who were seen by the participating pediatricians, regardless of the reasons for the visit, and were not dependent on active participation rates; hence they were less biased by socially patterned nonresponse. Finally, the analyses are based on real measurements rather than on the modeling of synthetic BMI trends from prediction models.

There are several limitations of the study. First, the number of visits ranged from 2 to 15, and there was some variation in the length of observation intervals because this was not a prospectively designed study but rather a patient registry study in which data were recorded at regularly planned and unplanned visits. Still, owing to the German system of well-child surveillance at defined ages, early childhood in particular is well represented with sequential data. Second, many of the children whose data were included in the CrescNet patient registry could not be included in our study owing to missing data points beyond 14 years of age; most of the children had simply not yet reached that age, and many were no longer being seen by pediatricians. Third, because we did not have access to the complete medical histories of the children, we cannot entirely exclude the possibility that chronically ill children were included in the data set, although this limitation is probably minimized by the large sample size. Finally, data on parental weight and on perinatal risk factors for obesity (e.g., maternal diabetes, maternal smoking history, and breast-feeding) would be desirable.20 Nevertheless, our objective was to determine, on the basis of BMI percentiles, the age at which obesity occurs and whether there is a critical period. Preliminary data from the LIFE Child study confirmed maternal BMI as a risk factor for childhood obesity, but the dynamics of BMI development in the children did not differ substantially according to the weight status of the mother. A child with known familial risk factors should be monitored closely for upward trends in BMI.

In our study, we categorized normal weight or obesity on the basis of BMI. Although BMI is not a direct reflection of body fat and may be affected by increasing muscle mass, BMI is the most widely applied criterion, with sex, age, and often ethnic-specific reference ranges available across the entire age span, and it is easily recordable without additional equipment.

In conclusion, in this current population-based longitudinal study, we found that obesity occurred early in life and once present, persisted into adolescence. The most excessive weight gain occurred early — between 2 and 6 years of age — and subsequently continued at a lower but still positive rate, which led to a greater degree of obesity.