To follow and predict the evolution of adiposity during growth, individual adiposity curves, assessed by the weight/height2 index, were drawn for 151 children from the age of 1 month to 16 yr. Adiposity increases during the 1st yr and then decreases. A renewed rise, termed here the adiposity rebound, occurs at about 6 yr. Individual weight/height2 curves may differ regarding their percentile range level and age at adiposity rebound. The present study shows a relationship between the age at adiposity rebound and final adiposity. An early rebound (before 5.5 yr) is followed by a significantly higher adiposity level than a later rebound (after 7 yr). This phenomenon is observed whatever the subject's adiposity at 1 yr. The present observations might be connected with the cellularity of adipose tissue.

On the basis of a longitudinal study of growth in French children, we attempted to find a valid index for estimating adiposity, and to specify the optimal conditions for its use. The Quetelet index was found suitable for application to children, but as with all methods, a certain lack of precision proved unavoidable because of the different stages of growth observed at a given age. For use by clinicians, we provide charts, based on the Quetelet index and on age, permitting estimation of adiposity in any child on the basis of longitudinal study measurements. For use by epidemiologists, we give standard values for studying groups of subjects, even when a reference population is not available. Body adiposity may be expressed independently of age and sex.

The development of adiposity was followed in 164 subjects from the age of one month to adulthood. The 25th and 75th centiles of the weight/height2 (W/H2) index were chosen as cut-off points to define the lean, medium and fat subjects at both one and 21 years of age. Only 42% of the children remained in their original category, that is 41% of the lean infants at one year stayed lean, 42% of the medium infants stayed medium and 41% of the fat infants stayed fat. Accordingly, most fat infants did not stay fat, but twice as many fat as non-fat infants became fat adults (41 and 20% respectively). The relative risk of being fat adults was 1 for the lean, 1 for the medium and 2 for the fat infants at one year. Several paths of development emerged: they were related to age at the second rise in adiposity, termed adiposity rebound, which usually occurs at about six years, as observed on skinfold thickness and W/H2 charts. The earlier the rebound, the higher the adiposity at adult age, whether this was measured by W/H2 index or subscapular skinfold. The cohorts of children who left the channel they had been following included fat infants with a late rebound who subsequently returned to normal, and lean infants with an early rebound who grew fatter. Other cohorts remained in their original groups, for example, fat infants with an early rebound who stayed fat and lean infants with a late one who stayed lean. Age at rebound provided two indications: the existence of a regulartory process among the transiently fat or lean infants who returned to average after a late or early rebound respectively, and pathological development among the children who became fat or lean after an early or late rebound. Age at rebound is an indicator of the subsequent development of fatness.

Plasma free dehydroepiandrosterone (DHA), androstenedione (delta), testosterone (T), dihydrotestosterone (DHT), estrone (E1), and estradiol (E2) were measured by radioimmunoassay in 55 boys and 54 girls 3.5 to 16.3 years of age. Plasma DHA increased significantly between 6 and 8 years of age in girls and between 8 and 10 years of age in boys. A further significant increase was noted between 10 and 12 years of age in both sexes. Delta rose significantly between 8 and 10 years of age in girls and between 10 and 12 years in boys. In contrast, no significant increase in T, DHT, or E1, was noted prior to 12 years of age in both sexes. However, E2 showed a significant increase between 10 and 12 years of age in girls. This early rise in the course of pubertal development of the two sex steroids predominantly of adrenal origin, DHA and delta, and its occurence 1 to 2 years earlier in girls than in boys, as does puberty itself, suggest a possible role for these steroids in the mechanisms involved in triggering the hypothalamic-pituitary-gonadal axis at puberty.