scholarly journals Calcium Intake and Bone Mineral Acquisition during the Pubertal Growth Spurt: Three-Year Follow-Up of the Kitakata Kids Health Study in Japan

2020 ◽  
Vol 66 (2) ◽  
pp. 158-167 ◽  
Author(s):  
Katsuyasu KOUDA ◽  
Masayuki IKI ◽  
Yuki FUJITA ◽  
Harunobu NAKAMURA ◽  
Kazuhiro UENISHI ◽  
...  
Cancers ◽  
2021 ◽  
Vol 13 (24) ◽  
pp. 6238
Author(s):  
Jimmy Célind ◽  
Maria Bygdell ◽  
Jari Martikainen ◽  
Johan Styrke ◽  
Jan-Erik Damber ◽  
...  

Previous studies of pubertal timing and the risk of prostate cancer have used self-reported markers of pubertal development, recalled in mid-life, and the results have been inconclusive. Our aim was to evaluate the age at the pubertal growth spurt, an objective marker of pubertal timing, and the risk of prostate cancer and high-risk prostate cancer. This population-based cohort study included 31,971 men with sufficient height measurements to calculate age at peak height velocity (PHV). Outcomes were accessed through national registers. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated by Cox regressions with follow up starting at 20 years of age. In total, 1759 cases of prostate cancer including 449 high-risk were diagnosed during follow up. Mean follow up was 42 years (standard deviation 10.0). Compared to quintiles 2–4 (Q2–4), men in the highest age at PHV quintile (Q5) had lower risk of prostate cancer (HR 0.83, 95% CI 0.73–0.94), and of high-risk prostate cancer (0.73; 0.56–0.94). In an exploratory analysis with follow up starting at age at PHV, late pubertal timing was no longer associated with reduced risk of prostate cancer. Later pubertal timing was associated with reduced risk of prostate cancer and especially high-risk prostate cancer. We propose that the risk of prostate cancer might be influenced by the number of years with exposure to adult levels of sex steroids.


2020 ◽  
Vol 21 (1) ◽  
Author(s):  
V. Anusuya ◽  
Amit Nagar ◽  
Pradeep Tandon ◽  
G. K. Singh ◽  
Gyan Prakash Singh ◽  
...  

2010 ◽  
Vol 299 (6) ◽  
pp. E990-E997 ◽  
Author(s):  
Lijie Shi ◽  
Thomas Remer ◽  
Anette E. Buyken ◽  
Michaela F. Hartmann ◽  
Philipp Hoffmann ◽  
...  

Whether prepubertal estrogen production impacts on the timing of puberty is not clear. We aimed to investigate prepubertal 24-h estrogen excretion levels and their association with early and late pubertal markers. Daily urinary excretion rates of estrogens of 132 healthy children, who provided 24-h urine samples 1 and 2 yr before the start of the pubertal growth spurt [age at takeoff (ATO)], were quantified by stable isotope dilution/GC-MS. E-sum3 (estrone + estradiol + estriol) was used as a marker for potentially bioactive estrogen metabolites and E-sum5 (E-sum3 + 16-epiestriol + 16-ketoestradiol) for total estrogen production. Pubertal outcomes were ATO, age at peak height velocity (APHV), duration of pubertal growth acceleration (APHV-ATO), age at Tanner stage 2 for pubic hair (PH2), genital (G2, boys) and breast (B2, girls) development, and age at menarche. Prepubertal urinary estrogen excretions (E-sum3 and E-sum5) were not associated with ATO, APHV, and age at PH2 but with duration of pubertal growth acceleration ( P < 0.01) in both sexes. Girls with higher E-sum3 reached B2 0.9 yr ( P = 0.04) and menarche 0.3 yr earlier ( P = 0.04) than girls with lower E-sum3. E-sum3 was not associated with age at G2 in boys ( P = 0.6). For most pubertal variables, the associations with E-sum3 were stronger than with E-sum5. In conclusion, prepubertal estrogens may not be critical for the onset of the pubertal growth spurt but are correlated with its duration in both boys and girls. Prepubertal estrogen levels may already predict the timing of girls' menstruation and breast development but do not appear to affect sexual maturation in boys.


2014 ◽  
Vol 24 (6) ◽  
pp. 1168-1174 ◽  
Author(s):  
Weijun Wang ◽  
Zhiwei Wang ◽  
Zhen Liu ◽  
Zezhang Zhu ◽  
Feng Zhu ◽  
...  

PEDIATRICS ◽  
1980 ◽  
Vol 66 (3) ◽  
pp. 483-484
Author(s):  
Sonia Balsan ◽  
Robert Steendijk

From their observations in a boy with hypophosphatemic rickets Chan and Bartter1 conclude that administration of 1α,25-dihydroxyvitamin D3 (1,25-(OH)2D3) is the treatment of choice for this disease. Since this point of view is not shared by everybody, it demands careful scrutiny. The conclusion rests on the increased growth velocity, the radiologic healing of the rachitic lesions, and the increase in serum phosphorus which occurred when treatment was changed from vitamin D2 to 1,25-(OH)2D3. From the growth curve of this boy it appears that the increase in growth velocity could represent the pubertal growth spurt in a late maturer.


2020 ◽  
Vol 15 (5) ◽  
pp. 68-72
Author(s):  
V.L. Gritsinskaya ◽  
◽  
V.P. Novikova ◽  
A.I. Khavkin ◽  
◽  
...  

Objective. To identify specific features of pubertal growth spurt in adolescents depending on their nutritional status in prepuberty. Patients and methods. We analyzed the dynamics of height and weight in 645 children (331 boys and 314 girls) aged between 8 and 16 years. All study participants were divided into three groups depending on whether their weight and height at the age of 8 years were within the normal limits given in the ‘WHO Growth Reference 2007’: children with physical development; underweight children; and overweight children. Results. The dynamics of somatometric parameters during pubertal growth spurt varied between children with different nutritional status. Underweight boys demonstrated prolonged and low-amplitude pubertal growth pattern; in boys with normal physical development, the growth spurt was usually shorter and had high amplitude. In overweight boys, the pubertal growth spurt started with higher annual increase in height, had a more pronounced amplitude, and was shorter than in peers (р < 0.001 ÷ р < 0.05). Both underweight girls and girls with normal physical development demonstrated low-amplitude pubertal growth spurt lasting for two years. Overweight girls had two peaks of pubertal growth spurt, which usually started earlier than in other girls (р < 0.001 ÷ р < 0.01). Conclusion. Our findings can be used as a guide for predicting pubertal spurt in children during medical examinations, determining adequate physical activity in physical education classes at school and in sports sections. Key words: children, nutritional status, pubertal growth spurt


1993 ◽  
Vol 14 (9) ◽  
pp. 336-367

Puberty is a transitional stage associated with many changes, both physical and emotional. The endocrinologic changes, consisting of two processes, gonadarche and adrenarche, result in the development of secondary sexual characteristics and the pubertal growth spurt. Gonadarche, the maturation of the gonads, is initiated by the episodic pulsatile secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus. Adrenarche refers to the increase in adrenal androgen secretion (the mechanism responsible for this is unknown). Both of these processes cause an increase in sex steroid secretion, which results in the physical changes of puberty. In the United States, normal puberty occurs between 8 to 13 years in girls and 9 to 14 years in boys.


1993 ◽  
Vol 265 (2) ◽  
pp. E236-E242 ◽  
Author(s):  
Z. Hu ◽  
R. D. Friberg ◽  
A. L. Barkan

Growth hormone-releasing hormone (GHRH) has been shown in vitro to increase proliferation of pituitary somatotrophs, to increase transcription of the GH gene, to promote accumulation of GH mRNA, and to stimulate GH release. The in vivo involvement of hypothalamic GHRH in regulating GH mRNA content had never been clearly documented. We studied pituitary GH mRNA and GH contents and serum concentrations of GH and insulin-like growth factor I (IGF-I) in rats of both sexes during pubertal growth spurt and investigated the effects of GHRH deficiency (brought about by neonatal administration of monosodium glutamate, MSG) and exogenous GHRH administration on these parameters. In both sexes, GH mRNA content increased three- to fourfold between 4 and 12 wk of life and declined thereafter toward 33 wk of life. This was accompanied by virtually parallel changes in pituitary GH content and in serum IGF-I. Neonatal MSG abolished the pubertal increases in GH mRNA, pituitary GH, and serum IGF-I and severely impaired growth rate. Exogenous GHRH (25 micrograms/kg sc every 8 h for 7 days) given to intact animals between 6 and 7 wk of life significantly augmented pituitary GH mRNA content but was less effective in MSG-treated rats. We conclude that 1) pubertal growth spurt in both sexes is associated with rising pituitary GH mRNA content; 2) GHRH deficiency abolishes the puberty-associated increase in GH synthesis and secretion and attenuates somatic growth rate; and 3) exogenous GHRH augments GH mRNA content. Thus puberty-associated augmentation of GHRH secretion is an important mechanism of somatic growth.


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