The role of estrogen in bone growth and maturation during childhood and adolescence

Twenty years ago it was believed that pubertal growth was stimulated by testicular androgen in boys and by adrenal androgen in girls. Estrogen, which was used to inhibit growth in excessively tall girls, was not thought to have growth-promoting effects. We hypothesized that estrogen has a biphasic effect on epiphyseal growth, with maximal stimulation at low levels. We showed that the administration of low doses of estrogen, corresponding to a serum estradiol level of about 4 pg/ml (15 pmol/l) caused more than a 60% increase over the prepubertal growth rate in both boys and girls. To test the hypothesis that estrogen is the principal mediator of the pubertal growth spurt in boys, we administered the aromatase inhibitor, testolactone, to boys with familial male-limited precocious puberty. Testolactone produced near normalization of both growth velocity and bone maturation, despite levels of serum testosterone that remained within the adult male range. The observation that low levels of estrogen stimulate growth and bone maturation suggested that estrogen might explain the more rapid epiphyseal maturation of prepubertal girls compared to boys. To determine whether prepubertal girls have higher estrogen levels than prepubertal boys, we developed an ultrasensitive recombinant cell bioassay for estrogen with a sensitivity of 0.02 pg/ml (0.07 pmol/l) estradiol equivalents. Prepubertal girls had approximately eight-fold higher levels of serum estradiol than did prepubertal boys (0.6 +/- 0.6 pg/ml (SD) (2.2 +/- 2.2 pmol/l) vs 0.08 +/- 0.2 pg/ml (0.29 +/- 0.73 pmol/l), P < 0.05). We concluded that the pubertal growth spurt of both sexes is driven primarily by estrogen, and that the more rapid epiphyseal maturation of prepubertal girls (vs boys) may be explained by their higher estradiol levels.     

A longitudinal cephalometric study of the soft tissue profile of short- and long-face syndromes from 7 to 17 years

The longitudinal growth and development of the soft tissue drape for boys and girls with long and short vertical patterns was examined from age 7 to 17 years. The sample was taken from the Denver Growth Study and consisted of 32 subjects who were selected on the basis of their percentage of lower anterior vertical face height. All subjects were of northern European ancestry, and none had undergone orthodontic treatment. The sexual dimorphism was evident as anticipated for several soft tissue measurements. The boys showed continued growth through age 16 years in contrast to the girls who attained the adult size of the soft tissue integument around 14 years. A significant difference between vertical facial patterns was reported for all soft tissue variables with the exception of the soft tissue thickness at A point and the upper lip height. The boys and girls with long vertical patterns exhibited a thicker and longer soft tissue drape for the most variables when compared with those with short facial patterns. These soft tissue differences are believed to be compensatory mechanisms in long-face subjects, which may attempt to mask the vertical dysplasia, thereby producing a more normal facial profile. Individual growth assessments revealed that the perioral soft tissues follow a pattern similar to that of the mean group patterns. The subjects with long vertical facial patterns experienced their pubertal growth spurt earlier than the short-face subjects. This may have clinical implications in the timing of orthodontic intervention and treatment.     

Determinants of growth in diabetic pubertal subjects

OBJECTIVE: To analyze the relationship among metabolic control, IGF-I, and growth in pubertal diabetic subjects. RESEARCH DESIGN AND METHODS: In 72 diabetic children, we have studied the pattern of change of IGF-I, IGF-I SD score, IGF binding protein (BP)-1, and growth rate in different pubertal stages and have analyzed their relation to age sex, weight/length index, HbA1c, insulin concentration, insulin dose, and dehydroepiandrosteronesulfate (DHEAS). RESULTS: The serum IGF-I values increased up to Tanner stage 4 and thereafter decreased, whereas IGFBP-1 showed the inverse pattern. When transforming the IGF-I values into SD scores, correcting for age, sex, and pubertal stage, it was shown that the deviation from normal values increased with increasing pubertal stage in boys, but was equal in stages 3-5 in girls. Using multiple regression analysis, HbA1c, insulin dose, and DHEAS were significantly correlated to IGF-I SD score (R2 = 0.253, P = 0.001). IGFBP-I levels in the afternoon were within normal range. LogIGFBP-1 showed an inverse correlation, to insulin concentration in single correlation (r = -0.26, P = 0.02). In single correlation, growth rate correlated significantly to insulin dose (r = 0.25, P = 0.03). In a multiple regression analysis, only DHEAS and IGF-I SD score were found to be significantly correlated to growth rate (R2 = 0.370, P < 0.001). The 18 adolescents who had reached their final height did not deviate from their target final height, according to their recorded growth since birth. CONCLUSIONS: In a group of fairly well-controlled diabetic children, the normal increase in IGF-I during puberty is blunted. Despite decreased IGF-I levels, target final height was attained, probably because of adequate insulin compensation leading to normal IGFBP-l, thus adequate bioavailability of IGF-I. Our results point out the importance of sufficient exogenous insulin in the period of rapid linear growth.     

Reference values for height and weight in Prader-Willi syndrome based on 315 patients

The spontaneous growth of 315 patients (109 girls and 208 boys) with Prader-Willi syndrome (PWS) was analysed in a mixed longitudinal and cross-sectional manner. 33 patients were seen in the department between 1970 and 1994; height and weight of 76 patients from Germany were evaluated by means of a questionnaire with detailed measuring instructions, and 206 definite cases were added from the literature. Mean ( SD) length of newborn babies with PWS was 50.2+/-2.8 cm (145 boys) and 48.9 3.3 cm (79 girls). Mean weight at birth was 2945 570 g in boys and 2782+/-594 g in girls. During the 1st year, the children's growth was nearly normal, thereafter short stature was present in approximately 50% of PWS patients. Between 3 and 13 years of age, the 50th percentile for height in PWS is roughly identical with the 3rd percentile in healthy controls. Body weight was normal for all boys and girls during the first 2 years. Thereafter, a rapid weight gain occurred; after an age of 10 years weight-for-height index in nearly all patients exceeded the normal range. The extent of pubertal growth was reduced for the group. Mean adult height was 161.6+/-8.1 cm (23 males) and 150.2+/-5.5 cm (21 females). Head circumference for age was normal for boys and girls. CONCLUSION: Reference data on spontaneous development of growth and weight gain of children with Prader-Willi syndrome are described allowing a better counselling of patients and parents.     

Tumor-related arthrodesis. Reconstruction of the shoulder contour using a free TRAM (Transverse Rectus Abdominis Musculocutaneous) flap]

We evaluated growth hormone binding protein (GHBP) activity in a group of obese children (12 boys and 12 girls, age 3.1-14.7 years, BMI 21.1-33.3, 11 prepubertal and 13 early pubertal) and in 26 age-matched normal weight children (14 boys and 12 girls, age 2.1-16.0 years, BMI 14.2-21.4, 18 prepubertal and 8 early pubertal). All children were of normal stature. GHBP activity was significantly higher in the obese (39.1 +/- 1.1%) than in the control children (28.3 +/- 1.0%, p < 0.0001). Mean serum GHBP was not different between boys and girls or between prepubertal and pubertal subjects. A positive correlation was found between BMI and GHBP levels only in the normal weight children (r = 0.425, p < 0.05). Baseline insulin concentrations in the obese children were 97.6 +/- 7.9 pmol/l (normal values, 45.0 +/- 18.6 pmol/l), and the mean insulin AUC following OGTT in the obese was 811.3 +/- 160.7 pmol/l (normal values, 373.1 +/- 150.1 pmol/l). Serum GHBP activity in the obese was not correlated with baseline serum insulin concentrations or with the insulin AUC following OGTT. In conclusion, we found that obese children have elevated GHBP activity, and speculate that this phenomenon may serve to compensate for their reduced GH secretion and accelerated GH clearance.     

Growth charts, growth velocity and bone development in childhood obesity

OBJECTIVE: To compare the growth charts of obese subjects (4-18 years) with the Tanner's growth curves and to analyze the growth velocities and bone age of obese children in prepuberty and adolescence. Moreover to compare the relationship between the serum insulinemic and glycemic levels and height standard deviation score (HSDS). DESIGN: Growth charts: this study included 1250 obese subjects (669 males, 581 females) observed between 1981 and 1993 and divided into seven age categories (4-6, 7-8, 9-10, 11-12, 13-14, 15-16, 17-18 years). Growth velocities: yearly growth velocities of 579 obese subjects (325 males, 254 females) were compared to growth velocities of 473 controlled children of the same sex, chronological age and pubertal stage. Bone age (BA) of 846 obese subjects (470 males, 376 females) was estimated. Blood analysis: insulin secretion of 70 obese children was considered and compared to 70 lean controls of equal chronological age and sex. MEASUREMENTS: Growth rate, standardized height and other physical characteristics of the children were measured by trained examiners. All subjects were evaluated singularly for at least 4 years with a follow-up every 6 months. BA was estimated by radiograph of the left hand and wrist using the Tanner-Whitehouse II system by a single observer. For the insulin secretion study and glycemic levels oral glucose tolerance test (OGTT) was performed using a glucose load of 1.75 g/kg per body weight. Plasma insulin was assessed by a double antibody radioimmunoassay. RESULTS: In adipose children the growth charts, referred to 97th centile, 50th centile and 3rd centile, were superior to those of the normal population up to the age of 13 and 12.5 years for male and for female respectively; growth decreases at the above age in both sexes. The obese subjects were equal in height to the non obese subjects as they reached their 18th birthday. The growth velocity (cm/yr) of the obese child, in the age range considered here, does not show differences when compared with the lean child in the prepubertal status (P not significant) but decreases during Tanner's stage II, III IV in boys and girls (P < 0.0001). BA is more advanced over chronological age (delta BA-CA) in both sexes. The increase of BA over CA does not show a remarkable difference during pubertal maturation in boys (P not significant); whereas in girls the delta BA-CA decreases with advancing sexual maturation (P < 0.0001). Our obese subjects have significantly higher plasma insulinemic levels compared with the lean controls (P < 0.0001). Moreover there is a positive correlation between plasma insulinemic levels and HSDS (r = 0.881, P < 0.0001). We did not observe a correlation between serum glycemic levels and HSDS. CONCLUSION: Our data demonstrate that the growth increase in an obese child starts in the first years of life. The statural advantage acquired in the first years of life would be exploited and maintained up to the beginning of puberty and with a growth velocity equal to that of the lean subject. Skeletal maturation is strongly increased in both sexes. Bone age remained advanced during the entire period of pubertal development. During puberty obese subjects demonstrate a less notable growth spurt when compared with lean subjects. The growth advantage gradually decreases and final adult height of obese and normal subjects is equal.     

Impact of puberty on family relations: Effects of pubertal status and pubertal timing.

This investigation examines the impact of pubertal status and pubertal timing, independent of each other and of chronological age, on the family relationships of adolescent boys and girls. The sample is composed of 204 families with a firstborn child between the ages of 10 and 15. Measures included adolescent and parental reports of closeness, conflict, and autonomy as well as assessments of each adolescent's pubertal status and pubertal timing (early, on time, or late maturing). Findings indicate that (a) pubertal maturation is associated with increased emotional distance between youngsters and their parents; (b) pubertal maturation (among girls) and early pubertal maturation (among boys) increase conflict between adolescents and their mothers, but not necessarily fathers; and (c) pubertal maturation, and especially late maturation, may be accompanied by increased behavioral autonomy for the adolescent. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Individual and familial influences on the onset of sexual intercourse among urban African American adolescents.

A sample of 198 African American families, living in urban poverty, participated in a longitudinal study of adolescent sexual development beginning when children were in the 4th or 5th grade. Self-reports of family conflict and pubertal development and videotaped family interaction data were collected at 2 time points approximately 2 years apart. Youths reported on sexual debut at each time point. More boys than girls reached sexual debut early. Greater levels of family conflict predicted early sexual debut. Observational data indicated more developed preadolescents with greater family conflict and less positive affect were least likely to delay debut. Changes in pubertal development and observed family conflict were associated with early debut. Possible mediating mechanisms and implications for preventive interventions are discussed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

It's about timing and change: Pubertal transition effects on symptoms of major depression among African American youths.

Effects of early physical maturation and accelerated pubertal changes on symptoms of major depression were examined in 639 African American children. Three rival hypotheses, early timing, off-time, and stressful change, were tested using 2 waves of data (mean ages = 11 and 13 years). The pubertal effect operates differently according to children's gender and age. For girls, early maturation was consistently associated with elevated levels of depressive symptoms. For boys, early maturers manifested elevated levels of depression only at age 11, but these symptoms subsided by age 13. Boys who experienced accelerated pubertal growth over time displayed elevated symptom levels. Results support the early timing hypothesis for girls and the stressful change hypothesis for boys. Time at assessment is critical when examining boys' pubertal transition. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Development's tortoise and hare: Pubertal timing, pubertal tempo, and depressive symptoms in boys and girls.

Although the sequence of pubertal maturation remains consistent across most individuals, the timing and tempo of development fluctuate widely. While past research has largely focused on the sequelae of pubertal timing, a faster tempo of maturation might also present special challenges to children for acclimating to new biological and social milestones. Using latent growth curve modeling, the present study investigated how pubertal tempo and pubertal timing predicted depressive symptoms over a 4-year period in a sample of children recruited from New York City area public schools. Rate of intraindividual change in parent-reported Tanner stages was used as an index of pubertal tempo, and more advanced Tanner development at an earlier chronological age was used as an index of pubertal timing. For girls (N = 138, M = 8.86 years old at Time 1), pubertal timing emerged as the most salient factor, and the tempo at which girls progressed through puberty was not significant. In boys (N = 128, M = 9.61 years old at Time 1), both timing and tempo of development were significant; notably, however, the effects of pubertal tempo were stronger than those of timing. These findings highlight the need to consider multiple sources of individual variability in pubertal development and suggest different pubertal challenges for boys and girls. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

GH and GnRH analog treatment in children who enter puberty at short stature

It is well known that height at the onset of puberty is closely related to final height. To improve final height of short children who enter puberty at short stature, twenty-one short boys and six short girls were treated with a combination of GH and GnRH analog. The boys started the combination treatment at a mean age of 12.0 years when their mean height was 128.5 cm (-2.74 SD) and the girls at a mean age of 10.68 years when their mean height was 126.4 cm (-2.23 SD). The boys discontinued GnRH at a mean age of 16.88 years after a mean treatment period of 4.89 years when their height was 153.7 cm (-2.75 SD), and the girls at a mean age of 13.89 years after a mean treatment period of 3.20 years when their height was 143.3 cm (-1.94 SD). Bone age maturation significantly decelerated during the combination treatment. Bone age rarely exceeded 14 years in boys and did not exceed 13 years in girls. Bone age maturation during combination treatment decelerated after bone age 12 years in boys and 10.5 years in girls. On average, bone age matured at a mean rate of 0.48 years a year in boys and 0.56 years a year in girls during the combination treatment. During the combination treatment, height velocity did not decelerate rapidly and remained at 3-5 cm/year for a longer duration because of the bone age deceleration, although a definite pubertal growth spurt was not observed. As a consequence, the mean projected height SDS for bone age increased 1.50 (+/- 0.76) SD in boys and 1.24 (+/- 0.49) SD during the combination treatment. Although most of the patients have not yet reached their final height, combined GnRH analog and GH treatment should increase the pubertal height gain and the adult height in short children who enter puberty early for height, when the post-GST growth is taken into account. The combination treatment seems more effective in boys than in girls. This improvement is attributed to the lengthening of the treatment period by slower bone maturation and maintained growth velocity.     

Growth changes in children and adolescents with short-term diabetes

OBJECTIVE: Height and weight changes during the first 3 years of diabetes were prospectively followed in 152 diabetic children and adolescents. RESEARCH DESIGN AND METHODS: The study sample consisted of 152 Caucasian diabetic patients (84 boys; 68 girls) followed from diabetes onset in the Paediatric Diabetes Unit and 80 Caucasian normal subjects (49 boys; 31 girls) assessed in the Outpatient General Paediatric Clinic of the same hospital for routine examination and not affected by problems that might influence growth. Diabetic patients and control subjects were consecutively enrolled in the study between 1989 and 1992; diabetic patients with positive markers for celiac disease (positive antiendomysial antibodies) and thyroid disease (positive antimicrosomial antibodies) or any other chronic disease were not considered in the study. Mean age of diabetic patients (8.9 +/- 4.1 years) and control subjects (8.5 +/- 4.2 years) at recruitment in the study was similar. RESULTS: At onset of diabetes, the mean height expressed as the height standard deviation score (HSDS) was significantly greater than the expected values (P < 0.0001) and was independent of sex and pubertal stage. During the first 3 years of diabetes, HSDS decreased significantly (F = 6.9; P < 0.001). Meanwhile, growth velocity as standard deviation score (SDS) decreased significantly between the 1st and 2nd year (-0.12 +/- 2.1; -0.76 +/- 2.6, respectively; P < 0.05), but it was similar between the 2nd and 3rd year of diabetes. Weight expressed as SDS increased significantly during the first 2 years of diabetes but not thereafter. Height changes during the study period were independent from pubertal stage and sex. Metabolic control and insulin requirement, in our series, were not clearly related to height and weight changes. CONCLUSIONS: Diabetic patients at onset of diabetes are taller than age- and sex-matched nondiabetic subjects. During the first years of the disease, linear growth decreases independently of metabolic control and weight changes.     

Calcium and magnesium balance in 9-14-y-old children

Few data are available regarding calcium and magnesium absorption and endogenous fecal excretion in children. We used a multitracer stable isotope technique to assess calcium and magnesium balance in 12 boys and 13 girls aged 9-14 y (mean weight: 42 kg) maintained on relatively high calcium intakes (mean: 1310 +/- 82 mg/d). There were no significant differences in absorption of calcium or magnesium from milk between boys and girls. Calcium retention (balance) correlated positively with calcidiol (25-hydroxyvitamin D) concentration (r = 0.48, P = 0.02) and serum alkaline phosphatase activity (r = 0.44, P = 0.03). There was no significant relation between magnesium balance and concentration. When data from this study were combined with our previously reported data, an increase in total calcium absorption was seen for pubertal (Tanner stages 2-4) but not prepubertal (Tanner stage 1) white children over the range of intakes from approximately 750 to 1350 mg/d. Despite intakes similar to the 1989 recommended dietary allowance for magnesium (mean intake: 6.4 +/- 1.2 mg.kg-1.d-1), 11 of the 25 subjects (6 girls and 5 boys) were in negative magnesium balance. We conclude that benefits from higher calcium intakes, < or = 1350 mg/d, were most apparent in pubertal children. In addiction, higher magnesium intakes should be considered for children.     

Twenty-four-hour concentration profiles of gonadotropin and estradiol (E2) in prepubertal and early pubertal girls: the diurnal rise of E2 is opposite the nocturnal rise of gonadotropin

To investigate the detailed pattern of circulating gonadotropin and estradiol (E2) concentrations around the onset of puberty, plasma gonadotropin and E2 were measured at 20-min intervals for 24 h in seven prepubertal and six early pubertal normal short girls. The hormone concentrations obtained were analyzed by Cluster pulse detection algorithm, cosinor analysis, and cross-correlation analysis. All subjects showed spontaneous LH and FSH pulses, and six early pubertal girls showed spontaneous E2 pulses. Cosinor analysis revealed 24-h LH rhythms in all subjects except two early pubertal girls and 24-h FSH rhythms in all subjects except one early pubertal girl. The acrophases (clocktime for maximal value) in the 24-h rhythm of LH and FSH were both found in the late hours of sleep. All subjects except three prepubertal girls showed significant 24-h E2 rhythms. In contrast to the 24-h LH and FSH rhythms, the acrophase of the 24-h E2 rhythm was found in the daytime waking period. Cross-correlation analysis demonstrated significant positive cross-correlations between LH and E2 that were maximum at an E2 lag of 5.7-9.3 h in three of the six early pubertal girls. In conclusion, the E2 concentration profiles in girls around the onset of puberty show marked 24-h rhythm, with acrophase during the daytime waking period. There exists a 5.7- to 9.3-h time lag between LH and E2 time series, and this long time lag might correspond to the time required for aromatization for E2 synthesis.     

Leptin levels in children with central precocious puberty

Several studies have suggested that sufficient serum leptin levels may be involved in the initiation of puberty. To assess further the relationship between leptin and the onset of puberty in humans, we measured the serum leptin concentration in children with central precocious puberty (CPP). We studied 65 children with either idiopathic (IPP; n = 50 girls and 3 boys) or neurogenic central precocious puberty (NPP; n = 5 girls and 7 boys). The serum leptin levels in these patients were compared with normative data from healthy children and adolescents using SD scores that adjust for body mass index (BMI) and Tanner stage. The mean SD scores of IPP and NPP girls were +0.4 +/- 0.1 and +1.0 +/- 0.5, respectively, compared with that of age-matched prepubertal girls and +0.7 +/- 0.2 and +1.6 +/- 0.6 compared with that of girls matched for pubertal stage. The CPP girls with lower BMIs contributed larger SD scores, such that the leptin SD score was negatively correlated with BMI. A similar, modest increase in leptin levels in the CPP girls was evident when additional normative data were considered. The mean leptin SD scores of IPP and NPP boys were -0.9 +/- 0.5 and +0.7 +/- 0.3, respectively, compared with that of normal boys at Tanner stage 3-4. Serum leptin levels in the boys with CPP were not different from those in healthy boys in any of the normative studies. These data should be interpreted cautiously, but they suggest that girls with CPP have modestly elevated serum leptin concentrations compared with those in healthy children and adolescents. In addition, the negative correlation between the leptin SD score and BMI suggests that sufficient leptin levels may be associated with initiation of puberty in girls.     

Serum leptin levels in normal children: relationship to age, gender, body mass index, pituitary-gonadal hormones, and pubertal stage

It is commonly accepted that at least in girls puberty starts when a minimum level of body mass or a certain amount of body fat are present. However the precise signal by which adipose stores inform the hypothalamus of the degree of energetic reserves is unknown. Leptin is a hormone produced by the adipocytes to regulate food intake and energy expenditure at the hypothalamic level. To understand whether leptin is the adipose tissue signal that allows puberty, 789 normal children of both sexes, age 5-15 yr, were transversally studied. Leptin levels, as well as gonadal and gonadotropins, levels, were analyzed in addition to the determination of auxological parameters. In an age-related analysis, leptin levels in girls rose from 5-15 yr (from 4.3 +/- 0.4 to 8.5 +/- 0.9 micrograms/L) in parallel with body weight. Boys always had lower leptin levels than girls (3.3 +/- 0.3 micrograms/L at 5 yr), but they rose in parallel with weight until 10 yr (5.3 +/- 0.7 micrograms/L), when a striking decrease was observed until 15 yr (3.0 +/- 0.3 micrograms/L). In girls, leptin was the first hormone to rise followed by FSH and later by LH and estradiol. A similar pattern occurred in boys, despite the fact that leptin dropped after 10 yr when testosterone rises. Divided into three pubertal stages, i.e. P1 = prepuberty, P2 = early puberty, and P3 = overt puberty, in girls the four hormones rose progressively from P1 to P3, but from P2 to P3 the present increment was greater for LH and estradiol. In boys, leptin decreased from P1 to P3, whereas FSH, LH, and testosterone rose. The age-related changes were not caused by adiposity variations, because data did not change when subtracting values of children over 97% of standard deviation score of body mass index. In conclusion: 1) leptin appears to increase in both boys and girls before the appearance of other reproductive hormones related to puberty; 2) leptin levels in boys are always lower than in girls, although they increase with age until the age 10 yr; 3) leptin in boys declines about the time testosterone increases. Leptin may well be a permissive factor for the initiation of pubertal events.     

Genetic and Environmental Influences on Pubertal Development: Longitudinal Data From Finnish Twins at Ages 11 and 14.

To study sources of individual differences in pubertal development, the authors fit a sex-limitation common factor model to data reported, at ages 11 and 14 years, by 1,891 twin pairs on items that comprise the Pubertal Development Scale (PDS; A. C. Petersen, L. Crockett, M. Richards, & A. Boxer, 1988). The model divides variation into a general pubertal factor and item-specific variation and, in addition, decomposes it into constituent sources. In both boys and girls, genetic influences made the largest contribution to variance common to PDS items. Genetic and nonshared environmental factors accounted for variation specific to PDS items in boys, whereas for girls, common environmental influences were added for growth spurt and menarcheal status. For both common and item-specific variation, genetic effects were partially sex specific. Subsidiary analyses found accelerated maturation in both boys and girls who at age 14 were reared in father-absent homes. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Parental autonomy granting during adolescence: Exploring gender differences in context.

This study investigated the ways in which 2 indicators of parental autonomy granting, adolescents' decision-making input and parental knowledge of adolescents' daily experiences, differed as a function of contextual factors (i.e., parents' gender role attitudes or sibling dyad sex composition) and boys' and girls' personal qualities (i.e., gender, pubertal status, developmental status, or birth order) in a sample of 194 families with firstborn (M?=?15.0 years) and second-born (M?=?12.5 years) adolescents. Firstborns were granted more autonomy than second-borns, especially in families with firstborn girls and second-born boys. Girls in families marked by traditional maternal gender role attitudes were granted fewer autonomy opportunities. Postmenarcheal second-born girls were granted more opportunities for autonomy than were premenarcheal second-born girls, but only in families with less traditional maternal gender role attitudes. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Individual differences in boys' and girls' timing and tempo of puberty: Modeling development with nonlinear growth models.

Pubertal development is a nonlinear process progressing from prepubescent beginnings through biological, physical, and psychological changes to full sexual maturity. To tether theoretical concepts of puberty with sophisticated longitudinal, analytical models capable of articulating pubertal development more accurately, we used nonlinear mixed-effects models to describe both the timing and tempo of pubertal development in the sample of 364 White boys and 373 White girls measured across 6 years as part of the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development. Individual differences in timing and tempo were extracted with models of logistic growth. Differential relations emerged for how boys' and girls' timing and tempo of development were related to physical characteristics (body mass index, height, and weight) and psychological outcomes (internalizing problems, externalizing problems, and risky sexual behavior). Timing and tempo are associated in boys but not girls. Pubertal timing and tempo are particularly important for predicting psychological outcomes in girls but only sparsely related to boys' psychological outcomes. Results highlight the importance of considering the nonlinear nature of puberty and expand the repertoire of possibilities for examining important aspects of how and when pubertal processes contribute to development. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Serum concentrations of type I and III procollagen propeptides in healthy children and girls with central precocious puberty during treatment with gonadotropin-releasing hormone analog and cyproterone acetate

Serum levels of type I and III procollagen propeptides (s-PICP and s-PIIINP) were measured in 466 healthy school children and in 23 girls with central precocious puberty (CPP) during GnRH analog and cyproterone acetate therapy, using two commercially available RIAs. In normal children, s-PICP and s-PIIINP changed significantly with age and pubertal development stages. For s-PIIINP, a peak was seen at 12 yr for girls and 13 yr for boys; no peak could be discerned for s-PICP. The prepubertal (Tanner stage 1) s-PICP value (mean +/- SD) for girls was 374 +/- 132 micrograms/L, the midpubertal value (stage 3) was 442 +/- 135 micrograms/L, and the postpubertal value (stage 5) was 203 +/- 103 micrograms/L. The mean s-PIIINP levels for girls were 9.1 +/- 2.4, 15.0 +/- 4.3, and 6.8 +/- 3.1 micrograms/L, respectively. For boys, levels were 362 +/- 119, 544 +/- 138, and 359 +/- 256 micrograms/L for s-PICP and 8.5 +/- 2.2, 14.5 +/- 5.0, and 8.6 +/- 3.8 micrograms/L for s-PIIINP (P < 0.001 for both propeptides in both boys and girls). There was, however, a large variation in normal values for both propeptides within the age groups and pubertal stages. There was a significant correlation of s-PICP and s-PIIINP levels to height velocity in girls (r = 0.35; P < 0.001 and r = 0.33; P < 0.001, respectively), while in boys, only s-PIIINP showed significant correlation to height velocity (r = 0.40; P < 0.001). In untreated girls with CPP, serum levels of s-PIIINP were elevated [PIIINP SD score (SDS), 2.13]. Levels of s-PICP were normal (PICP SDS, 0.39). Levels of both propeptides decreased within 2 months after initiation of therapy and remained below initial values (P < 0.01). The decrease in s-PIIINP after 2 months of therapy showed a significant correlation with the fall in height velocity SDS for chronological age after 6 months of therapy (r = 0.64; P < 0.01). We conclude that s-PIIINP and, to a lesser degree, s-PICP reflect growth in normal children, but due to the large variation, both propeptides seem unsuitable as markers for screening of growth disorders in children.