Pubertal Tempo Research Articles

Attenuated hypothalamic-pituitary-adrenal axis functioning predicts accelerated pubertal development in girls 1 year later.

Accelerated pubertal development has been linked to adverse early environments and may heighten subsequent mental and physical health risks. Hypothalamic-pituitary-adrenal axis functioning has been posited as a mechanism whereby stress may affect pubertal development, but the literature lacks prospective tests of this mechanism. The current study assessed 277 youth (M = 10.84 years, SD = 1.14), 138 boys and 139 girls, who reported on their pubertal development and underwent the Trier Social Stress Test for Children at baseline and returned to the laboratory approximately 1 year later (M = 1.12 years, range = 0.59-1.98 years). For girls, lower cortisol area under the curve (with respect to ground) at Time 1 predicted more advanced pubertal development at Time 2, controlling for Time 1 pubertal development. This association persisted after additional covariates including age, body mass index, race, and maltreatment history were introduced, and was driven by adrenal rather than gonadal development. Cortisol was not linked to boys' subsequent pubertal development, and no interaction by gender or by maltreatment appeared. These results suggest that attenuated cortisol, reported in other studies of children exposed to early adversity, may contribute to accelerated pubertal tempo in girls.

Modeling pubertal timing and tempo and examining links to behavior problems.

Research on the role of puberty in adolescent psychological development requires attention to the meaning and measurement of pubertal development. Particular questions concern the utility of self-report, the need for complex models to describe pubertal development, the psychological significance of pubertal timing vs. tempo, and sex differences in the nature and psychological significance of pubertal development. We used longitudinal self-report data to model linear and logistic trajectories of pubertal development, and used timing and tempo estimates from these models, and from traditional approaches (age at menarche and time from onset of breast development to menarche), to predict psychological outcomes of internalizing and externalizing behavior problems, and early sexual activity. Participants (738 girls, 781 boys) reported annually from ages 9 through 15 on their pubertal development, and they and their parents reported on their behavior in mid-to-late adolescence and early adulthood. Self-reports of pubertal development provided meaningful data for both boys and girls, producing good trajectories, and estimates of individuals' pubertal timing and tempo. A logistic model best fit the group data. Pubertal timing was estimated to be earlier in the logistic compared to linear model, but linear, logistic, and traditional estimates of pubertal timing correlated highly with each other and similarly with psychological outcomes. Pubertal tempo was not consistently estimated, and associations of tempo with timing and with behavior were model dependent. Advances in modeling facilitate the study of some questions about pubertal development, but assumptions of the models affect their utility in psychological studies.

Longterm endocrine effects of cancer

Survival after childhood cancer has increased over the last 25 years with around 80% overall survival but outlook is not trouble free. Within 25 years of diagnosis, 4% will have a second tumour. Cardiotoxicity from anthracyclines, radiation related health problems and endocrine deficiencies all contribute to increased mortality, with 18% reported to have died 30 years after diagnosis. Memory processing deficits after childhood cranial radiation result in additional burdens of intellectual, psychosocial and emotional disability. Endocrine late effects of radiation and chemotherapy can be direct, resulting in hypofunction of endocrine glands or indirect resulting in metaplasia, cancer and altered bone growth. Deficiencies of hypothalamic pituitary hormones can be expected in 60-100% of patients by 8-10 years after radiation exposure. Pubertal timing and tempo is altered by cranial radiation, with combinations of early puberty and growth hormone deficiency causing diagnostic and management confusion. Evolution of hormonal losses need be recognized. Gonadal dysfunction occurs after both radiation and chemotherapy at any age.The prepubertal testis is not protected from effects of chemotherapy. Age at treatment, type and dose all predict outcome. Loss of function in germinal epithelium and Leydig cells is not reflected in gonadotrophin alterations until age 9-10 years. Abnormal timing of menarche in survivors of central nervous system tumours is common. Follicular reserve in young females after cancer treatment is reduced with high risk for premature menopause and little evidence that the ovary can be protected from insult, although 50% of children exposed to early radiation or chemotherapy retain sufficient gonadal function to initiate or complete puberty. Preservation of gonadal tissue prior to cancer treatment is now a priority, with semen storage, or gonadal biopsy being offered or considered in both sexes before exposure to gonadotoxins. However, fertility recovery can occur and appropriate contraceptive needs must be met. Cerebral arteritis occurs after brain radiation, with early cerebrovascular accident. HRT may need to be tailored to reduce this risk. Solid organ radiation exposure is hazardous. Thyroid cancer after radiation exposure occurs at 20 times population risk, with regular thyroid ultrasound every 2 years now recommended and FNA as required. Pelvic radiation results in poor pregnancy outcomes with increased foetal loss and small for dates infants. Bladder risks for cancer after cyclophosphamide, abdominal and pelvic radiation are worsened by smoking and alcohol. Bowel risks are currently unknown. 1 in 700 adults is now a survivor of childhood cancer and 60% have at least one chronic health problem. Ongoing surveillance is required to improve outcomes for this group of young people.

Pubertal development, personality, and substance use: a 10-year longitudinal study from childhood to adolescence.

Most research linking early pubertal development to substance use has focused on the effects of pubertal timing (age at which a certain stage of pubertal development is reached or pubertal status at a particular age--related to the maturation disparity hypothesis), but little research has focused on pubertal tempo (rate of growth through pubertal stages--related to the maturation compression hypothesis). However, both timing and tempo have not only been identified as important components of pubertal development, with different predictors, but have also been shown to be independently associated with other adolescent psychopathologies. Using latent growth-curve modeling, this study examined how pubertal status at age 12 and pubertal tempo (between 11 and 13 years) related to substance use from 15 to 16 years in boys from low socioeconomic backgrounds (N = 871). Results showed that both pubertal status at age 12 and tempo were significant predictors of increased levels of substance use and problems in mid to late adolescence. In an attempt to identify mechanisms that may explain the association between pubertal development and substance use it was found that sensation seeking partially mediated the association between pubertal status at age 12 and substance use behaviors. Impulse control was found to moderate the association sensation seeking had with marijuana use frequency, with high sensation-seeking scores predicting higher marijuana use frequency only at low levels of impulse control. These findings highlight the importance of considering multiple sources of individual variability in the pubertal development of boys and provide support for both the maturational disparity and compression hypotheses.

Body fat in children does not adversely influence bone development: a 7‐year longitudinal study (EarlyBird 18)

Both negative and positive associations have been reported between body fat and bone density. Extra mechanical loading from excess fat may lead to greater bone mass. Excess ectopic fat may lead to bone demineralisation through inflammatory pathways. Longitudinally collected data from narrow-angle beam densitometry gives a novel insight into bone growth through adolescence. There is no evidence of a deleterious effect of body fat on children's growing bones after adjustment for height and age. Body fat, mediated by puberty, is associated with larger bones in boys and bones that are both denser and larger in girls. Bone growth is an important determinant of peak bone mass and fracture risk, but there is limited data on the impact of fat-on-bone development at a time when childhood obesity is reaching epidemic proportions. Accordingly, we explored the effect of body fat (BF) on bone growth over time in the context of age, pubertal tempo and gender. A cohort of 307 children was measured biannually from 9-16 years for height and weight, and every 12 months for percent BF, bone area (BA), bone mineral content and areal bone mineral density (aBMD) by dual-energy X-ray absorptiometry. Pubertal tempo was determined quantitatively by age at peak height velocity. Percent BF increased and then fell in the boys, but increased throughout in the girls. aBMD and BA increased in both genders (P < 0.001). Greater BF was associated with higher aBMD and BA in girls (P < 0.001), but only BA in boys (P < 0.001). The extra aBMD associated with increased BF was greater in older girls. The rise in aBMD and BA was associated with earlier puberty in both genders (P < 0.001). The impact of BF on aBMD was greater in later puberty in girls (0.0025 g cm(-2) per 10% BF at 10 years versus 0.016 g cm(-2) per 10% BF at 14 years, P < 0.001). Greater BF is associated with larger bones, but also denser bones in girls. The effects of fat and puberty are complex and gender specific, but BF of contemporary UK children does not appear to be deleterious to bone quality.

Peer relationships and depressive symptomatology in boys at puberty.

The physical changes of puberty coincide with an increase in the salience of peer relationships and a growing risk for depression and other forms of psychopathology. Previously, we reported that pubertal tempo, defined as a child's rate of intraindividual change in pubertal status (measured using parent-reported Tanner stages; Marshall & Tanner, 1970), was associated with changes in boys'--but not girls'--depressive symptoms over and above effects explained by pubertal timing (Mendle, Harden, Brooks-Gunn, & Graber, 2010). The present study extends this previous research by examining changes in the quality of peer relationships in the association between individual differences in pubertal development and change in boys' depressive symptoms. Boys (N = 128, M = 9.61 years, SD = 0.70, at Time 1) were recruited from public schools and assessed annually for 4 years. Results from latent growth curve models indicated that earlier pubertal timing and more rapid pubertal tempo were associated with greater decrements in the quality of boys' peer relationships. After accounting for the association between change in peer relationships and depressive symptoms, the direct effects of pubertal timing and tempo on depressive symptoms were no longer significant. These results highlight a multifaceted approach to studying puberty and emphasize how social mechanisms may intersect with biological risk to produce psychological distress.

Quality of early family relationships and the timing and tempo of puberty: effects depend on biological sensitivity to context.

Guided by evolutionary-developmental theories of biological sensitivity to context and reproductive development, the current research examined the interactive effects of early family environments and psychobiologic reactivity to stress on the subsequent timing and tempo of puberty. As predicted by the theory, among children displaying heightened biological sensitivity to context (i.e., higher stress reactivity), higher quality parent-child relationships forecast slower initial pubertal tempo and later pubertal timing, whereas lower quality parent-child relationships forecast the opposite pattern. No such effects emerged among less context-sensitive children. Whereas sympathetic nervous system reactivity moderated the effects of parent-child relationships on both breast/genital and pubic hair development, adrenocortical activation only moderated the effect on pubic hair development. The current results build on previous research documenting what family contexts predict variation in pubertal timing by demonstrating for whom those contexts matter. In addition, the authors advance a new methodological approach for assessing pubertal tempo using piecewise growth curve analysis.

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.

A Randomised Study of Two Doses of Biosynthetic Human Growth Hormone on Final Height of Pubertal Children with Growth Hormone Deficiency

Aims: To determine the effectiveness of different doses of r-hGH therapy during puberty in children with growth hormone deficiency (GHD). Methods: Randomized controlled trial of different doses of r-hGH therapy administered during puberty in 49 children with GHD. The patients were allocated randomly using a random number table to one of two groups: group 1 (15 IU/m²/week) or group 2 (30 IU/m²/week). Patients were included if they had received r-hGH daily at a dose of 15 IU/m²/week (0.7 mg/m²/day) for at least 1 year before randomization. Results: Height increase standard deviation scores (SDS) were similar between the two groups (group 1: 1.1; group 2: 1.2; p = 0.81). Conclusion: A higher dose of r-hGH administered during puberty does not appear to have a significant effect on final height of children with GH deficiency. Altering pubertal tempo or intensifying prepubertal r-hGH therapy may be a more promising approach to improving final height in children with GH deficiency.

Metformin Therapy during Puberty Delays Menarche, Prolongs Pubertal Growth, and Augments Adult Height: A Randomized Study in Low-Birth-Weight Girls with Early-Normal Onset of Puberty

Low-birth-weight (LBW) girls who enter puberty earlier (around 8-9 yr) tend to have earlier menarche, earlier growth arrest, and a shorter adult stature. At present, there is no therapy for most of these girls. In LBW girls with early puberty, hyperinsulinemic insulin resistance could underpin their rapid transit through puberty and their loss of adult stature. We explored the effects of insulin sensitization with metformin during puberty. In an open-labeled, prospective study, 22 LBW girls (birth weight < -1.5 sd score for gestational age) with early-normal puberty (stage 2 breast development at age 8-9 yr) were randomized to remain untreated (n = 12) or to receive metformin (850 mg/d; n = 10) for 36 months (mean age at start, 9.0 yr). All girls remained untreated between 36 and 42 months. Pubertal growth, body composition by absorptiometry, uterine-ovarian size by ultrasound, fasting insulin, glucose, lipids, leptin, IGF-I, and IGF-binding protein-1 were assessed. Metformin treatment resulted in a longer duration from stage 2 breast development to menarche (P < 0.01; median difference, +1.0 yr), taller near-adult height (P < 0.01), and leaner body composition (P < 0.001). Metformin was also associated with lower insulin resistance and leptin and IGF-I levels and higher SHBG and IGF-binding protein-1 levels and with a more favorable lipid profile. Bone mineral density and uterine-ovarian growth were unaffected. Metformin treatment for 36 months in LBW girls with early-normal puberty normalized their pubertal progression to menarche and increased height gains up to adult stature. These data support the concept that insulin is a major codeterminant of the pubertal tempo and pubertal height gain in girls.