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Nature Reviews. Endocrinology Dec 2015In the past, the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis was often considered to be the main system that regulated childhood growth and, therefore,... (Review)
Review
In the past, the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis was often considered to be the main system that regulated childhood growth and, therefore, determined short stature and tall stature. However, findings have now revealed that the GH-IGF-1 axis is just one of many regulatory systems that control chondrogenesis in the growth plate, which is the biological process that drives height gain. Consequently, normal growth in children depends not only on GH and IGF-1 but also on multiple hormones, paracrine factors, extracellular matrix molecules and intracellular proteins that regulate the activity of growth plate chondrocytes. Mutations in the genes that encode many of these local proteins cause short stature or tall stature. Similarly, genome-wide association studies have revealed that the normal variation in height seems to be largely due to genes outside the GH-IGF-1 axis that affect growth at the growth plate through a wide variety of mechanisms. These findings point to a new conceptual framework for understanding short and tall stature that is centred not on two particular hormones but rather on the growth plate, which is the structure responsible for height gain.
Topics: Animals; Body Height; Gene Dosage; Growth Disorders; Growth Plate; Human Growth Hormone; Humans; Insulin-Like Growth Factor I
PubMed: 26437621
DOI: 10.1038/nrendo.2015.165 -
Growth Hormone & IGF Research :... Feb 2018Adult height and growth patterns are largely genetically programmed. Studies in twins have indicated that the heritability of height is high (>80%), suggesting that... (Review)
Review
Adult height and growth patterns are largely genetically programmed. Studies in twins have indicated that the heritability of height is high (>80%), suggesting that genetic variation is the main determinant of stature. Height exhibits a normal (Gaussian) distribution according to sex, age, and ancestry. Short stature is usually defined as a height which is 2 standard deviations (S.D.) less than the mean height of a specific population. This definition includes 2.3% of the population and usually includes healthy individuals. In this group of short stature non-syndromic conditions, the genetic influence occurs polygenically or oligogenically. As a rule, each common genetic variant accounts for a small effect (1mm) on individual height variation. Recently, several studies demonstrated that some rare variants can cause greater effect on height, without causing a syndromic condition. In more extreme cases, height SDS below 2.5 or 3 (which would comprise approximately 0.6 and 0.1% of the population, respectively) is frequently associated with syndromic conditions and are usually caused by a monogenic defect. More than 1,000 inherited/genetic diseases have growth disorder as an important phenotype. These conditions are usually responsible for syndromic short stature. In the coming years, we expect to discover several genetic causes of short stature, thereby explaining the phenotype of what we currently classify as short stature of unknown cause. These discoveries will have a profound impact on the follow-up and treatment of these children.
Topics: Body Height; Dwarfism; Genetic Variation; Growth Disorders; Humans; Phenotype
PubMed: 29249624
DOI: 10.1016/j.ghir.2017.12.003 -
Hypertension Research : Official... Feb 2022
Topics: Body Height; Cardiovascular Physiological Phenomena; Humans
PubMed: 34876696
DOI: 10.1038/s41440-021-00812-0 -
Hormone Research in Paediatrics 2017Increasing agreement exists about the use of length-for-age as the indicator of choice in monitoring the long-term impact of chronic nutritional deficiency. Yet, already... (Review)
Review
BACKGROUND/AIMS
Increasing agreement exists about the use of length-for-age as the indicator of choice in monitoring the long-term impact of chronic nutritional deficiency. Yet, already shortly after World War I, a causal link between nutrition and growth was questioned. Also, modern meta-analyses of controlled nutrition intervention studies show that the net effect of nutrition on body height is small. Broad evidence obtained from historic observations on human starvation made since the 19th century questions an obligatory association between nutrition and growth. Many additional explanations for the apparent shortness of people from developing countries have been published since, focusing on genetic factors, environment, economy, epigenetics, and, recently, psychosocial factors, such as strategic growth adjustments suggesting stature to be a social signal.
CONCLUSION
The marked variability in average population height of up to 20 cm within a few generations complicates the use of normative growth charts, even though they have been widely propagated. We support the concept of local growth references, for example using the "Synthetic Growth References" methodology. These references combine local growth information obtained from a given population of interest and common features of human population growth, with LMS values for height, weight, and BMI from birth to maturity. .
Topics: Body Height; Body Mass Index; Body Weight; Female; Growth Charts; Growth Disorders; Humans; Male; Malnutrition; Nutritional Status
PubMed: 27992861
DOI: 10.1159/000454832 -
Frontiers in Endocrinology 2020Humans show marked variation in body size around the world, both within and among populations. At present, the tallest people in the world are from the Netherlands and... (Review)
Review
Humans show marked variation in body size around the world, both within and among populations. At present, the tallest people in the world are from the Netherlands and the Balkan countries, while the shortest populations are central African Pygmies. There are genetic, genetic plasticity, developmental, and environmental bases for size variation in from the recent past and the present. Early populations of species also have shown considerable size variation. Populations from the present and the past are also marked by sexual dimorphism, which, itself, shows group variation. There is abundant evidence for the effects of limited food and disease on human growth and resultant adult body size. This environmental influence has been reflected in "secular trends" (over a span of years) in growth and adult size from socioeconomic prosperity or poverty (availability of resources). Selective and evolutionary advantages of small or large body size also have been documented. Heritability for human height is relatively great with current genome-wide association studies (GWAS) identifying hundreds of genes leading to causes of growth and adult size variation. There are also endocrinological pathways limiting growth. An example is the reduced tissue sensitivity to human growth hormone (HGH) and insulin-like growth factor (IGF-1) in Philippine and African hunter-gatherer populations. In several short-statured hunter-gatherer populations (Asian, African, and South American), it has been hypothesized that short life expectancy has selected for early maturity and truncated growth to enhance fertility. Some island populations of humans and other mammals are thought to have been selected for small size because of limited resources, especially protein. The high-protein content of milk as a staple food may contribute to tall stature in East African pastoral peoples. These and other evolutionary questions linked to life history, male competition, reproduction, and mobility are explored in this paper.
Topics: Adult; Animals; Biological Evolution; Body Height; Body Size; Ethnicity; Genetic Variation; Genome-Wide Association Study; Growth Disorders; Growth and Development; Humans; Mammals; Phenotype
PubMed: 32210916
DOI: 10.3389/fendo.2020.00107 -
Pediatric Dentistry Oct 2018
Topics: Body Height; Child Development; Growth Charts; Humans; Reference Values
PubMed: 32074918
DOI: No ID Found -
Journal of Paediatrics and Child Health Sep 2019
Topics: Body Dysmorphic Disorders; Body Height; Humans; Social Class
PubMed: 31524979
DOI: 10.1111/jpc.14438 -
Canadian Family Physician Medecin de... Apr 2021
Topics: Body Height; Body Weight; Humans
PubMed: 33853917
DOI: 10.46747/cfp.6704279 -
Hypertension Research : Official... Jul 2022
Topics: Body Height; Brachial Artery; Endothelium, Vascular; Humans; Regional Blood Flow; Vasodilation
PubMed: 35444291
DOI: 10.1038/s41440-022-00909-0 -
Annals of Human Biology Feb 2021Children with achondroplasia (ACH) appear to lack a pubertal growth spurt in height. To explore the growth spurt in height and its segments sitting height and leg...
Children with achondroplasia (ACH) appear to lack a pubertal growth spurt in height. To explore the growth spurt in height and its segments sitting height and leg length, in a large sample of ACH cases using growth curve modelling. Height and sitting height were measured longitudinally in ACH children, and the data were analysed using the SITAR (SuperImposition by Translation and Rotation) growth model, which estimates a mean growth curve and random effects for individuals defining differences in size, pubertal timing and intensity. Out of 402 ACH children, 85 boys and 75 girls aged 7-20 years had respectively 529 and 454 measurements of height and sitting height, with leg length calculated by difference. SITAR analysis identified peaks in mean height velocity at 13.3 and 11.3 years in boys and girls, with peak velocities of 4.3 and 4.4 cm/year. Mean peak velocity for sitting height was 3.0 cm/year, but leg length showed no peak. The SITAR models explained 92% to 99% of the cross-sectional variance. ACH children do experience a growth spurt in puberty, but only half that of control children. The spurt is due entirely to sitting height, with no leg length spurt.
Topics: Achondroplasia; Adolescent; Argentina; Body Height; Child; Female; Growth; Humans; Leg; Male; Puberty; Sitting Position
PubMed: 33533281
DOI: 10.1080/03014460.2021.1883109