孩子长高 · 骨头怎么变长、什么真有用

参考文献 · 17

1. Baron, J., Sävendahl, L., De Luca, F., Dauber, A., Phillip, M., Wit, J. M., & Nilsson, O. (2015). Short and tall stature: a new paradigm emerges. Nature Reviews Endocrinology, 11(12), 735-746. Narrative review. Height gain is driven by chondrogenesis in the growth plate, which has resting, proliferative and hypertrophic zones; chondrocytes proliferate, hypertrophy and secrete matrix, and the new cartilage is remodelled into bone. The GH-IGF-1 axis is just one of many systems regulating the growth plate: GH acts through circulating IGF-I and locally, in part through local IGF-I production. Longitudinal growth is regulated by nutritional intake through leptin, IGF-I, sex steroids, thyroid hormone and glucocorticoids; undernourished children have impaired linear growth despite elevated GH levels, whereas obese children grow normally or slightly faster despite low GH. Estrogen accelerates loss of resting-zone progenitor cells and so the senescence of the growth plate. A GWAS meta-analysis identified 423 loci for adult height, mostly outside the GH-IGF-1 axis (full text, PMC5002943). 10.1038/nrendo.2015.165
2. Nilsson, O., & Baron, J. (2004). Fundamental limits on longitudinal bone growth: growth plate senescence and epiphyseal fusion. Trends in Endocrinology and Metabolism, 15(8), 370-374. Review. Longitudinal bone growth is rapid early in life, then slows and ceases; the decline is caused mainly by a falling rate of chondrocyte proliferation. This programmed senescence appears intrinsic to the growth plate rather than hormonal, possibly because stem-like resting-zone cells have a finite proliferative capacity that is gradually exhausted. In humans, proliferative exhaustion is followed by epiphyseal fusion, in which growth plate cartilage is replaced completely by bone. Much of the mechanistic evidence is from animals. 10.1016/j.tem.2004.08.004
3. Royal College of Paediatrics and Child Health. (2013). UK growth chart 2-18 years (girls and boys charts, issue 2). Further assessment is advised if height is below the 0.4th centile, if the height centile is more than 3 centile spaces below the mid-parental centile, or if height drops by more than 2 centile spaces once measurement error is excluded; a centile space is the distance between two centile lines. Most children's height centiles (nine out of ten) are within two centile spaces of the mid-parental centile, and only 1 percent are more than three spaces below. Four children out of five have an adult height within ±7 cm of the mid-parental target height. Puberty before 8 years in girls or 9 years in boys is likely to be precocious, and no signs of puberty by 13 years in girls or 14 years in boys is delayed; both need further assessment. Remove shoes and measure with a correctly installed stadiometer. www.rcpch.ac.uk/sites/default/files/Girls_2-18_years_growth_chart.pdf
4. Takahashi, Y., Kipnis, D. M., & Daughaday, W. H. (1968). Growth hormone secretion during sleep. The Journal of Clinical Investigation, 47(9), 2079-2090. Plasma GH was measured every 30 min with EEG on 38 nights in eight young adults. In seven, a GH peak lasting 1.5-3.5 h appeared with the onset of deep sleep; smaller peaks sometimes followed in later deep sleep. The peak was delayed when sleep onset was delayed, and subjects woken for 2-3 h who went back to sleep had another peak. The peak was unrelated to glucose, insulin or cortisol. Small physiological study in adults; it did not measure growth. 10.1172/JCI105893
5. Sassin, J. F., Parker, D. C., Mace, J. W., Gotlin, R. W., Johnson, L. C., & Rossman, L. G. (1969). Human growth hormone release: relation to slow-wave sleep and sleep-waking cycles. Science, 165(3892), 513-515. GH release during sleep is related to slow, synchronized (slow-wave) sleep; when the sleep-waking cycle was reversed by 12 hours, sleep-related GH release reversed with it, so the release does not follow a circadian rhythm independent of sleep. Small physiological study in adults. 10.1126/science.165.3892.513
6. Jelenkovic, A., Sund, R., Hur, Y.-M., Yokoyama, Y., Hjelmborg, J. v. B., Möller, S., et al., & Silventoinen, K. (2016). Genetic and environmental influences on height from infancy to early adulthood: An individual-based pooled analysis of 45 twin cohorts. Scientific Reports, 6, 28496. Pooled 45 twin cohorts from 20 countries, 180,520 paired measurements at ages 1-19 years. Shared environmental factors explained the largest share of height variation in early childhood, and their effect remained until early adulthood; the relative genetic contribution rose with age and was greatest in adolescence (up to 0.83 in boys and 0.76 in girls). Genetic variance was greatest in North America and Australia and lowest in East Asia, but the relative genetic proportion was roughly similar across regions. Heritability describes variation within these populations, not one child. 10.1038/srep28496
7. Brown, K. H., Peerson, J. M., Rivera, J., & Allen, L. H. (2002). Effect of supplemental zinc on the growth and serum zinc concentrations of prepubertal children: a meta-analysis of randomized controlled trials. The American Journal of Clinical Nutrition, 75(6), 1062-1071. Meta-analysis of 33 randomized trials. Zinc supplementation produced significant positive responses in height increments (effect size 0.350 SD, 95% CI 0.189-0.511) and weight increments (0.309), with no effect on weight-for-height. Growth responses were greater in children with low initial weight-for-age and, above age 6 months, low initial height-for-age. The authors conclude zinc programs should be considered in populations at risk of zinc deficiency, especially where underweight or stunting is common. 10.1093/ajcn/75.6.1062
8. Munns, C. F., Shaw, N., Kiely, M., Specker, B. L., Thacher, T. D., Ozono, K., et al. (2016). Global consensus recommendations on prevention and management of nutritional rickets. The Journal of Clinical Endocrinology & Metabolism, 101(2), 394-415. GRADE-based consensus of 33 experts from 11 organisations. Nutritional rickets is a disorder of defective chondrocyte differentiation and mineralization of the growth plate and defective osteoid mineralization, caused by vitamin D and/or calcium deficiency; it affects health, growth and development. Signs include swelling of wrists and ankles, leg deformity (bow legs or knock knees), rachitic rosary, delayed fontanelle closure, hypocalcemic seizures and failure to thrive. Low dietary calcium raises rickets risk independent of vitamin D status. 10.1210/jc.2015-2175
9. Lee, W. T., Leung, S. S., Wang, S. H., Xu, Y. C., Zeng, W. P., Lau, J., Oppenheimer, S. J., & Cheng, J. C. (1994). Double-blind, controlled calcium supplementation and bone mineral accretion in children accustomed to a low-calcium diet. The American Journal of Clinical Nutrition, 60(5), 744-750. Randomized, double-blind 18-month trial in 162 seven-year-old Chinese children with habitually low calcium intakes. The supplemented group gained significantly more radial bone mineral content (16.5% vs 13.97%) and BMC/bone width than controls, but there was no effect on height increment. Whether the higher bone mass is maintained was not known. 10.1093/ajcn/60.5.744
10. Hidayat, K., Zhang, L.-L., Rizzoli, R., Guo, Y.-X., Zhou, Y., Shi, Y.-J., Su, H.-W., Liu, B., & Qin, L.-Q. (2023). The effects of dairy product supplementation on bone health indices in children aged 3 to 18 years: a meta-analysis of randomized controlled trials. Advances in Nutrition, 14(5), 1187-1196. Meta-analysis of 21 publications of randomized trials. Dairy supplementation slightly increased whole-body and regional bone mineral content and density and height (0.21 cm, 95% CI 0.09-0.34; 15 trials), raised serum IGF-I and lowered parathyroid hormone. The authors note the magnitude of the bone improvement was very small, and read the IGF-I rise as consistent with the anabolic effect of protein. 10.1016/j.advnut.2023.06.010
11. Abbassi, V. (1998). Growth and normal puberty. Pediatrics, 102(2 Pt 3), 507-511. Review of published growth data in American children. Mean take-off age of the pubertal spurt is about 11 years in boys and 9 years in girls; peak height velocity comes at a mean 13.5 and 11.5 years, with whole-year peak velocity of 9.5 cm/y in boys and 8.3 cm/y in girls. Pubertal growth contributes about 30-31 cm in boys (17-18% of final height) and 27.5-29 cm in girls (17%). The size of pubertal growth correlates negatively with take-off age but not with final height. pubmed.ncbi.nlm.nih.gov/9685454
12. Smith, E. P., Boyd, J., Frank, G. R., Takahashi, H., Cohen, R. M., Specker, B., Williams, T. C., Lubahn, D. B., & Korach, K. S. (1994). Estrogen resistance caused by a mutation in the estrogen-receptor gene in a man. The New England Journal of Medicine, 331(16), 1056-1061. A 28-year-old man with a disruptive estrogen-receptor mutation was tall (204 cm) with incomplete epiphyseal closure and continued linear growth into adulthood despite otherwise normal puberty and normal testosterone; bone density was low and he did not respond to estrogen. Conclusion: estrogen is important for bone maturation and mineralization in men as well as women. Single case. 10.1056/NEJM199410203311604
13. Latronico, A. C., Brito, V. N., & Carel, J.-C. (2016). Causes, diagnosis, and treatment of central precocious puberty. The Lancet Diabetes & Endocrinology, 4(3), 265-274. Review. Central precocious puberty results from premature activation of the hypothalamic-pituitary-gonadal axis, mimicking normal puberty at an inappropriate age: before 8 years in girls and 9 years in boys. It can follow brain malformations or injuries, but in most girls the cause is unknown; MKRN3 defects occur in familial cases. GnRH agonists are the standard treatment. 10.1016/S2213-8587(15)00380-0
14. Carel, J.-C., Eugster, E. A., Rogol, A., Ghizzoni, L., Palmert, M. R., ESPE-LWPES GnRH Analogs Consensus Conference Group, et al. (2009). Consensus statement on the use of gonadotropin-releasing hormone analogs in children. Pediatrics, 123(4), e752-e762. Thirty experts from North America and Europe. The efficacy of GnRH analogs in increasing adult height is undisputed only in early-onset central precocious puberty (girls under 6 years). Few controlled prospective studies exist and many conclusions rely on expert opinion. Use of GnRH analogs for conditions other than central precocious puberty requires further investigation and cannot be suggested routinely. 10.1542/peds.2008-1783
15. Tyrrell, A. R., Reilly, T., & Troup, J. D. (1985). Circadian variation in stature and the effects of spinal loading. Spine, 10(2), 161-164. Stature measured to 1 mm in eight young adults: mean daily variation 19.3 mm (1.1% of stature); 54% of the daytime loss occurred in the first hour after rising and about 70% was regained in the first half of the night. Loading the spine increased shrinkage. Small physiological study in adults. 10.1097/00007632-198503000-00011
16. Malina, R. M. (2006). Weight training in youth — growth, maturation, and safety: an evidence-based review. Clinical Journal of Sport Medicine, 16(6), 478-487. Review of 22 experimental training studies in pre- and early-pubertal youth, mostly 8- and 12-week programmes: strength rose and was lost with detraining; the programmes did not influence growth in height and weight; only 10 studies monitored injuries (3 reported). Supervised programmes with low instructor-to-participant ratios were relatively safe. These are short trials, not long-term follow-up of stature or growth plates (abstract, PMID 17119361). 10.1097/01.jsm.0000248843.31874.be
17. British Society for Paediatric Endocrinology and Diabetes, Growth Disorders Special Interest Group. (2021). Clinical standards for growth assessment and referral criteria for children with a suspected growth disorder. UK guidance recommends referral for height below the 0.4th centile (-2.67 SDS). Additional criteria for growth assessment: height centile more than 3 centile spaces (>2.0 SDS) below the mid-parental centile and/or a drop in height of more than 1 centile space. Red flags: weight loss, constipation or diarrhoea, headaches, vomiting, abnormal fat stores, disproportion, dysmorphic features, anaemia, delayed puberty, clinical features of hypothyroidism or other chronic illness. Tall stature or accelerated growth (height >98th centile, or an increase of 1 centile space over more than a year before puberty) also merits assessment. Referral is recommended for girls with no signs of puberty by 13 and boys by 14. Heights should be measured accurately and plotted on growth charts (September 2021). www.bsped.org.uk/media/oo1hsxet/clinical-standards-for-growth-assessment-and-referral-criteria-for-children-with-a-suspected-growth-disorder.pdf