2 ± 7 7 45 4 ± 7 4 0 002 91 0 ± 4 9

2 ± 7.7 45.4 ± 7.4 0.002 91.0 ± 4.9 LY2606368 89.6 ± 6.6 0.231 5.1 ± 2.8 3.5 ± 3.1 0.009 n = 45 n = 47 n = 45 n = 47 n = 45 n = 47 1 to 20.4 53.0 ± 9.1 50.0 ± 10.1 0.136 91.0 ± 5.3 91.3 ± 6.6 0.842 6.1 ± 3.7 4.7 ± 3.8 0.067 n = 47 n = 49 n = 47 n = 49 n = 47 n = 49 All values are mean ± SD BMI body mass index Figure 2 illustrates the gains in BMI as expressed in Z-score from 1.0 to 7.9 years on, in EARLIER as compared to LATER subgroup. Under the histogram, the distribution of the pubertal stages from P1

to P5 documents the difference in the age-related progression of sexual maturation between the two MENA subgroups. Fig. 2 Changes in BMI from 1.0 to 20.4 years in healthy subjects segregated by the median of menarcheal age. The diagram I-BET151 chemical structure illustrates that the change in BMI Z-score from 1.0 year of age on between subjects with menarcheal age below (EARLIER) and above (LATER) the median is statistically significant at 7.9 and 8.9 years, an age at which all girls were still prepubertal (Tanner stage P1) as indicated below the diagram. The difference culminates at 12.4 years, and then declines afterwards. Note that the progression of BMI from birth to 1.0 year of age was very similar in the EARLIER (from 13.0 to 16.7 kg/m2) and LATER (from 13.1 to 17.0 kg/m2) subgroups (see Table 3). The number of subjects

for each age is presented in Table 3. See text for further details. P values between EARLIER and LATER group at each age are indicated above the diagram Discussion The recently published report from Javaid et al. [30] showed that change in BMI during childhood, from 1 to 12 years, was inversely associated with hip ZD1839 chemical structure fracture risk in later life. As potential selleck explanations, the authors suggested either a direct effect of low fat mass on bone mineralization or altered timing of pubertal maturation [30]. Our study carried out in a cohort

of healthy females whose BMI remained within the normal range complements this report by demonstrating that femoral neck aBMD measured by the end of skeletal development is also linked to gain in BMI during a very similar time interval, precisely from 1 to 12.4 years. Furthermore, our study documents that BMI gain during this time frame is inversely correlated with pubertal timing as prospectively assessed by recording the age of menarche. We previously reported that in healthy adult females, a relatively later menarcheal age by 1.9 year is associated with a deficit in FN aBMD by nearly 0.4 T-score [12]. Taking into account that FN aBMD tracks from early to late adulthood [15, 16], our observation should pertain to the risk of hip fracture in relation with childhood growth [30]. In the study by Javaid et al., BW and BMI measured at birth and 1 year of age were not related to hip fracture [30].

Comments are closed.