The Biology of Stature

Jee, Youn Hee; Baron, Jeffrey

doi:10.1016/j.jpeds.2016.02.068

Cited by 30 publications

(25 citation statements)

References 76 publications

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“…1C, dashed line) (29). Androgens also mediate growth spurt in part through their conversion to estrogen and also through their own action in the growth plate (5). Normal pubertal timing seems to be changing, but it is still defined as above 8 years in girls and 9 years in boys (13).…”

Section: Precocious Exposure To Sex Steroidsmentioning

confidence: 99%

“…Growth rate is slow but, as the epiphyseal plate fusion is delayed, these patients keep growing into adulthood, developing tall stature with eunuchoid proportions (increased arm span and upper-tolower segment ratio) only later in life ( Fig. 1D) (5).…”

Section: Prolonged Growth Due To Delayed Fusion Of Growth Platementioning

confidence: 99%

“…The main endocrine factors that regulate growth are GH/IGF-1 axis and sex steroids, each one of them having more importance in a specific period of life (5). During pregnancy, fetal growth is influenced by nutritional status, insulin and IGF system.…”

Section: Introductionmentioning

confidence: 99%

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MANAGEMENT OF ENDOCRINE DISEASE: Diagnostic and therapeutic approach of tall stature

Albuquerque

Scalco

Jorge

2017

European Journal of Endocrinology

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Tall stature is defined as a height of more than 2 standard deviations (s.d.) above average for same sex and age. Tall individuals are usually referred to endocrinologists so that hormonal disorders leading to abnormal growth are excluded. However, the majority of these patients have familial tall stature or constitutional advance of growth (generally associated with obesity), both of which are diagnoses of exclusion. It is necessary to have familiarity with a large number of rarer overgrowth syndromes, especially because some of them may have severe complications such as aortic aneurysm, thromboembolism and tumor predisposition and demand-specific follow-up approaches. Additionally, endocrine disorders associated with tall stature have specific treatments and for this reason their recognition is mandatory. With this review, we intend to provide an up-to-date summary of the genetic conditions associated with overgrowth to emphasize a practical diagnostic approach of patients with tall stature and to discuss the limitations of current growth interruption treatment options.

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Section: Precocious Exposure To Sex Steroidsmentioning

confidence: 99%

Section: Prolonged Growth Due To Delayed Fusion Of Growth Platementioning

confidence: 99%

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MANAGEMENT OF ENDOCRINE DISEASE: Diagnostic and therapeutic approach of tall stature

Albuquerque

Scalco

Jorge

2017

European Journal of Endocrinology

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“…Short stature is a common medical concern that pediatricians and pediatric endocrinologists often evaluate in their daily practice since poor growth may be a symptom of an underlying, treatable medical condition [1]. Linear growth is the result of chondrogenesis at the growth plate and all forms of short stature are therefore due to decreased chondrogenesis at the growth plates [2].…”

Section: Introductionmentioning

confidence: 99%

“…Using this approach, an increasing number of monogenic causes of growth disorders are being identified, thereby gradually diminishing the number of children who receive the unhelpful diagnosis of “idiopathic” short stature. The GWA studies on height variation as well as the expanding genetic diagnoses of growth disorders indicate that childhood growth disorders are highly genetically heterogeneous [1–2] and that a large fraction of the genes important for growth are involved in cellular processes previously not implicated in regulation of growth. These findings will likely affect the way we diagnose childhood growth disorders.…”

Section: Introductionmentioning

confidence: 99%

Genetics of Short Stature

Jee¹,

Andrade

Baron³

et al. 2017

Endocrinology and Metabolism Clinics of North America

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Synopsis Short stature is a common and heterogeneous condition which is often genetic in etiology. For most children with genetic short stature, the specific molecular causes remain unknown, but with advances in exome/genome sequencing and bioinformatics approaches, new genetic causes of growth disorders have been identified, contributing to the understanding of the underlying molecular mechanisms of longitudinal bone growth and growth failure. These genetic causes can involve not only hormonal deficiencies, including the growth hormone-IGF-1 axis, thyroid hormone or glucocorticoid and defects in hormonal receptors or subsequent signaling, but also defects in fundamental cellular processes (intracellular signaling pathways, transcriptional regulation, and DNA repair), extracellular matrix, or paracrine signaling. Especially, heterozygous and/or mild mutations in SHOX, NPR2, ACAN, IGF1, IGF1R, or FGFR3 have been associated with isolated short stature without other prominent or noticeable phenotype while homozygous and/or severe mutations in these genes cause severe short stature with bone malformation, that is, a chondrodysplasia. Identifying new genetic causes of growth disorders has the potential to improve diagnosis, prognostic accuracy, individualized management, and help avoid unnecessary testing for endocrine and other disorders.

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Early maturity, shortened stature, and hardship: Can life‐history trade‐offs indicate social stratification and income inequality in the United States?

Rivara

Madrigal

2019

American J Hum Biol

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ObjectiveLife‐history strategies promote reproductive fitness and survival. Limited energy availability and competing energetic demands between life‐history decisions may result in organismal trade‐offs leading to selection for “optimal” traits that facilitate fitness and survival in present environmental conditions. Few life‐history analyses have been conducted in food abundant/high resource human populations. Here, we use a life‐history theory framework integrated with a biocultural approach to assess whether trade‐offs between growth (height) and the onset of reproductive maturation (ages at menarche) were observed in a sample of adult women living in the United States.MethodsAdult women (18 years and older) from the National Health and Nutrition Examination Survey (NHANES) 2005 to 2006 were analyzed using complex survey regression to evaluate associations between ages at menarche, height, and biological, socio‐economic, demographic, and anthropometric variables.Associations between stature, ages at menarche, and socio‐economic status (household income and education level) suggest life‐history trade‐offs in this populations may be mitigated by access to resources and marginalization.ConclusionsThese study results have applied public health implications. We demonstrate that females who experience early menarche in the US population achieve short stature. Our study also demonstrates the need for implementing life‐history analyses in Western affluent populations, where marginalization may result in life‐history trade‐offs.

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The Biology of Stature

Cited by 30 publications

References 76 publications

MANAGEMENT OF ENDOCRINE DISEASE: Diagnostic and therapeutic approach of tall stature

MANAGEMENT OF ENDOCRINE DISEASE: Diagnostic and therapeutic approach of tall stature

Genetics of Short Stature

Early maturity, shortened stature, and hardship: Can life‐history trade‐offs indicate social stratification and income inequality in the United States?

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