Height
- Lafyva
- Jun 1, 2019
- 3 min read
Updated: May 26
CMH method predicts the target height by adding 6.5 cm to the mid parental height in boys or subtracting 6.5 cm from the mid parental height in girls.
"Running economy, which has traditionally been measured as the oxygen cost of running at a given velocity, has been accepted as the physiological criterion for ‘efficient’ performance and has been identified as a critical element of overall distance running performance."
"A variety of anthropometric dimensions could influence biomechanical effectiveness. These include: average or slightly smaller than average height for men and slightly greater than average height for women"
"Can taking vitamins make you grow taller?" "In brief: No Your stature is inherited and growth retardation is a specialty question for an endocrinologist."
Genomic analysis of ancient human remains identifies specific genes that changed during and after the transition in Europe from hunting and gathering to farming about 8,500 years ago. Many of the genes are associated with height, immunity, lactose digestion, light skin pigmentation, blue eye color and celiac disease risk.
Other variants were located on immune-associated genes, which made sense because "the Neolithic period involved an increase in population density, with people living close to one another and to domesticated animals,"
We hypothesized that a shift toward gender equality in 19th century Sweden increased mate selection freedom for women and amplified sexual selection for height. A mathematical model supported environmental factors as the main force driving population height change, and suggested a limited role for sexual selection. More generally, the model provides a framework for studying interactions between cultural change and evolutionary selection mechanisms.
GROWTH RETARDATION
Impaired linear growth or growth retardation is characterized by a deceleration of growth velocity, or a fall in the percentile channels for height and weight. Growth failure is seen in a variety of gastrointestinal disorders and is usually associated with a delay in skeletal or bone age. Disease-associated growth delay should be distinguished from genetic short stature and constitutional delay in growth. Children with genetic short stature are low in height percentiles but grow at a normal velocity, with a bone age that is commensurate with chronological age. In contrast, children with constitutional delay in growth have short stature and normal growth velocity, but delayed skeletal age leading to a normal growth potential. Children with constitutional delay in growth may continue to grow into their 20s.
There is increasing evidence from preclinical and human studies that nutrition in the late foetal and early neonatal period has a significant impact on neurodevelopment across the lifespan.
Conclusion: Optimizing nutrition during foetal and early postnatal life is a golden opportunity to impact neurodevelopment and brain function across the lifespan.
Stunted growth is a reduced growth rate in human development. It is a primary manifestation of malnutrition (or more precisely undernutrition) and recurrent infections, such as diarrhea and helminthiasis, in early childhood and even before birth, due to malnutrition during fetal development brought on by a malnourished mother. The definition of stunting according to the World Health Organization (WHO) is for the "height for age" value to be less than two standard deviations of the WHO Child Growth Standards median.
Diagnosis
Growth stunting is identified by comparing measurements of children's heights to the World Health Organization 2006 growth reference population: children who fall below the fifth percentile of the reference population in height for age are defined as stunted, regardless of the reason. https://en.wikipedia.org/wiki/Stunted_growth#Diagnosis
Also:
A decrease in absolute endocranial size has occurred between fossil specimens and recent populations in H. sapiens. This variation is also associated with noticeable nonallometric variations in the relative size and shape of the different areas of the brain of fossil and extant AMH, which may be described and summarised as follows. The overall shape of the endocasts does not exhibit noticeable changes in width, but it does show substantial vertical and anteroposterior variations. The frontal lobes have become relatively shorter anteroposteriorly and their surface has decreased. Parietal lobes are longer while the surface of the parietotemporal lobes has not changed. Occipital lobes have become shorter vertically and their surface has decreased. This is related to an anteroposterior
“compression” of the endocast and to a vertical “compression” of its upper part where its width does not differ between fossil and extant AMH.
