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Human height
Human height
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Height measurement using a stadiometer

Human height or stature is the distance from the bottom of the feet to the top of the head in a human body, standing erect. It is measured using a stadiometer,[1] in centimetres when using the metric system or SI system,[2][3] or feet and inches when using United States customary units or the imperial system.[4][5]

In the early phase of anthropometric research history, questions about height measuring techniques for measuring nutritional status often concerned genetic differences.[6]

Height is also important because it is closely correlated with other health components, such as life expectancy.[6] Studies show that there is a correlation between small stature and a longer life expectancy. Individuals of small stature are also more likely to have lower blood pressure and are less likely to acquire cancer. The University of Hawaii has found that the "longevity gene" FOXO3 that reduces the effects of aging is more commonly found in individuals of small body size.[7] Short stature decreases the risk of venous insufficiency.[8]

When populations share genetic backgrounds and environmental factors, average height is frequently characteristic within the group. Exceptional height variation (around 20% deviation from average) within such a population is sometimes due to gigantism or dwarfism, which are medical conditions caused by specific genes or endocrine abnormalities.[9]

The development of human height can serve as an indicator of two key welfare components, namely nutritional quality and health.[10] In regions of poverty or warfare, environmental factors like chronic malnutrition during childhood or adolescence may result in delayed growth and/or marked reductions in adult stature even without the presence of any of these medical conditions.

Determinants of growth

[edit]
The median (50th percentile) growth curves for males and females 0−20 years in the United States

The study of height is known as auxology.[11]

Growth has long been recognized as a measure of the health of individuals, hence part of the reasoning for the use of growth charts. For individuals, as indicators of health problems, growth trends are tracked for significant deviations, and growth is also monitored for significant deficiency from genetic expectations. Genetics is a major factor in determining the height of individuals, though it is far less influential regarding differences among populations. Average height is relevant to the measurement of the health and wellness standard of living and quality of life of populations.[12]

Humans grow fastest (other than in the womb) as infants and toddlers, rapidly declining from a maximum at birth to roughly age 2, tapering to a slowly declining rate, and then, during the pubertal growth spurt (with an average girl starting her puberty and pubertal growth spurt at 10 years[13] and an average boy starting his puberty and pubertal growth spurt at 12 years[14][15]), a rapid rise to a second maximum (at around 11−12 years for an average female, and 13−14 years for an average male), followed by a steady decline to zero. The average female growth speed trails off to zero at about 15 or 16 years, whereas the average male curve continues for approximately 3 more years, going to zero at about 18−19, although there is limited research to suggest minor height growth after the age of 19 in males.[16] These are also critical periods where stressors such as malnutrition (or even severe child neglect) have the greatest effect.

Moreover, the health of a mother throughout her life, especially during her critical period and pregnancy, has a role. A healthier child and adult develops a body that is better able to provide optimal prenatal conditions.[17] The pregnant mother's health is essential for herself but also the fetus as gestation is itself a critical period for an embryo/fetus, though some problems affecting height during this period are resolved by catch-up growth assuming childhood conditions are good. Thus, there is a cumulative generation effect such that nutrition and health over generations influence the height of descendants to varying degrees.

The age of the mother also has some influence on her child's height. Studies in modern times have observed a gradual increase in height with maternal age, though these early studies suggest that trend is due to various socio-economic situations that select certain demographics as being more likely to have a first birth early in the mother's life.[18][19][20] These same studies show that children born to a young mother are more likely to have below-average educational and behavioural development, again suggesting an ultimate cause of resources and family status rather than a purely biological explanation.[19][20]

In 1988, it was observed that first-born males were shorter than later-born males.[21] However, in 2013, the reverse observation was made.[22] The study authors suggest that the cause may be socioeconomic in nature.

Genetics

[edit]

The precise relationship between genetics and environment is complex and uncertain. Differences in human height is 60−80% heritable, according to several twin studies[23] and has been considered polygenic since the Mendelian–biometrician debate a hundred years ago. A genome-wide association (GWA) study of more than 180,000 individuals has identified hundreds of genetic variants in at least 180 loci associated with adult human height.[24] The number of individuals has since been expanded to 253,288 individuals and the number of genetic variants identified is 697 in 423 genetic loci.[25] In a separate study of body proportion using sitting-height ratio, it reports that these 697 variants can be partitioned into three specific classes: (1) variants that primarily determine leg length, (2) variants that primarily determine spine and head length, or (3) variants that affect overall body size. This gives insights into the biological mechanisms underlying how these 697 genetic variants affect overall height.[26] These loci do not only determine height, but other features or characteristics. As an example, 4 of the 7 loci identified for intracranial volume had previously been discovered for human height.[27] Height, like other phenotypic traits, is determined by a combination of genetics and environmental factor. A child's height based on parental heights is subject to regression toward the mean, therefore extremely tall or short parents will likely have correspondingly taller or shorter offspring, but their offspring will also likely be closer to average height than the parents themselves. Genetic potential and several hormones, minus illness, is a basic determinant for height. Other factors include the genetic response to external factors such as diet, exercise, environment, and life circumstances.[citation needed]

Environmental and epigenetic effects

[edit]

The effect of environment on height is illustrated by studies performed by anthropologist Barry Bogin and coworkers of Guatemala Mayan children living in the United States. In the early 1970s, when Bogin first visited Guatemala, he observed that Mayan Indian men averaged 157 cm (5 ft 2 in) in height and the women averaged 142 cm (4 ft 8 in). Bogin took another series of measurements after the Guatemalan Civil War, during which up to a million Guatemalans fled to the United States. He discovered that Maya refugees, who ranged from six to twelve years old, were significantly taller than their Guatemalan counterparts.[28] By 2000, the American Maya were 10.24 centimetres (4.0 in) taller than the Guatemalan Maya of the same age, largely due to better nutrition and health care.[29] Bogin also noted that American Maya children had relatively longer legs, averaging 7.02 centimetres (2.8 in) longer than the Guatemalan Maya (a significantly lower sitting height ratio).[29][30]

The Nilotic peoples of Sudan such as the Shilluk and Dinka have been described as some of the tallest in the world. Dinka Ruweng males investigated by Roberts in 1953−1954 were on average 181 cm (5 ft 11 in) tall, and Shilluk males averaged 182 cm (6 ft 0 in).[31] The Nilotic people are characterized as having long legs, narrow bodies and short trunks, an adaptation to hot weather.[32] However, male Dinka and Shilluk refugees measured in 1995 in Southwestern Ethiopia were on average only 176 cm (5 ft 9 in) and 172 cm (5 ft 8 in) tall, respectively. As the study points out, Nilotic people "may attain greater height if privileged with favourable environmental conditions during early childhood and adolescence, allowing full expression of the genetic material."[33] Before fleeing, these refugees were subject to privation as a consequence of the succession of civil wars in their country from 1955 to the present.

Attributed as a significant reason for the trend of increasing height in parts of Europe are the egalitarian populations where proper medical care and adequate nutrition had been relatively equally distributed as of 2004.[34] The uneven distribution of nutritional resources makes it more plausible for individuals with better access to resources to grow taller, while individuals with worse access to resources have a lessened chance of growing taller.[35]

Changes in diet (nutrition) and a general rise in quality of health care and standard of living are the cited factors in Asian populations. Malnutrition including chronic undernutrition and acute malnutrition is known to have caused stunted growth in various populations.[36] This has been seen in North Korea, parts of Africa, certain historical Europe, and other populations.[17] Developing countries such as Guatemala have rates of stunting in children under 5 living as high as 82.2% in Totonicapán, and 49.8% nationwide.[37]

Average height in a nation is correlated with protein quality. Nations that consume more protein in the form of meat, dairy, eggs, and fish tend to be taller, while those that obtain more protein from cereals tend to be shorter.[citation needed] Therefore, populations with high cattle per capita and high consumption of dairy live longer and are taller. Historically, this can be seen in the cases of the United States, Argentina, New Zealand and Australia in the beginning of the 19th century.[38] Moreover, when the production and consumption of milk and beef is taken to consideration, it can be seen why the Germanic people who lived outside of the Roman Empire were taller than those who lived at its heart.[39]

Role for an individual

[edit]
Male Stature vs Age (US CDC)
Female Stature vs Age (US CDC)

Connection to health

[edit]

Studies show that there is a correlation between small stature and a longer life expectancy. Individuals of small stature are also more likely to have lower blood pressure and are less likely to acquire cancer. The University of Hawaii has found that the "longevity gene" FOXO3 that reduces the effects of aging is more commonly found in individuals of a small body size.[7] Short stature decreases the risk of venous insufficiency.[8] Certain studies have shown that height is a factor in overall health while some suggest tallness is associated with better cardiovascular health and shortness with longevity.[40] Cancer risk has also been found to grow with height.[41] Moreover, scientists have also observed a protective effect of height on risk for Alzheimer's disease, although this fact could be a result of the genetic overlap between height and intracranial volume and there are also genetic variants influencing height that could affect biological mechanisms involved in Alzheimer's disease etiology, such as insulin-like growth factor 1 (IGF-1).[42]

Nonetheless, modern westernized interpretations of the relationship between height and health fail to account for the observed height variations worldwide.[43] Cavalli-Sforza, L.L., and Cavalli-Sforza, F., note that variations in height worldwide can be partly attributed to evolutionary pressures resulting from differing environments. These evolutionary pressures result in height-related health implications. While tallness is an adaptive benefit in colder climates such as those found in Europe, shortness helps dissipate body heat in warmer climatic regions.[43] Consequently, the relationships between health and height cannot be easily generalized since tallness and shortness can both provide health benefits in different environmental settings.

In the end, being excessively tall can cause various medical problems, including cardiovascular problems, because of the increased load on the heart to supply the body with blood, and problems resulting from the increased time it takes the brain to communicate with the extremities. For example, Robert Wadlow, the tallest human known to verifiable history, developed difficulty in walking as his height increased throughout his life. In many of the pictures of the latter portion of his life, Wadlow can be seen gripping something for support. Late in his life, although he died at age 22, he had to wear braces on his legs and walk with a cane; and he died after developing an infection in his legs because he was unable to feel the irritation and cutting caused by his leg braces.

Sources are in disagreement about the overall relationship between height and longevity. Samaras and Elrick, in the Western Journal of Medicine, demonstrate an inverse correlation between height and longevity in several mammals including humans.[40]

Women whose height is under 150 cm (4 ft 11 in) may have a small pelvis, resulting in such complications during childbirth as shoulder dystocia.[44]

A study done in Sweden in 2005 has shown that there is a strong inverse correlation between height and suicide among Swedish men.[45]

A large body of human and animal evidence indicates that shorter, smaller bodies age more slowly, and have fewer chronic diseases and greater longevity. For example, a study found eight areas of support for the "smaller lives longer" thesis. These areas of evidence include studies involving longevity, life expectancy, centenarians, male vs. female longevity differences, mortality advantages of shorter people, survival findings, smaller body size due to calorie restriction, and within-species body size differences. They all support the conclusion that smaller individuals live longer in healthy environments and with good nutrition. However, the difference in longevity is modest. Several human studies have found a loss of 0.5 years/centimeter of increased height (1.2 yr/inch). But these findings do not mean that all tall people die young. Many live to advanced ages and some become centenarians.[46][dubiousdiscuss]

In medicine, height is measured to monitor child development, this is a better indicator of growth than weight in the long term.[47] For older people, excessive height loss is a symptom of osteoporosis.[48] Height is also used to compute indicators like body surface area or body mass index.

Occupational success

[edit]

There is a large body of research in psychology, economics, and human biology that has assessed the relationship between several physical features (e.g. body height) and occupational success.[49] The correlation between height and success was explored decades ago.[50][51] Shorter people are considered to have an advantage in certain sports (e.g. gymnastics, race car driving, etc.), whereas in many other sports taller people have a major advantage. In most occupational fields, body height is not relevant to how well people are able to perform; nonetheless several studies found that success was positively correlated with body height, although there may be other factors such as sex or socioeconomic status that are correlated with height which may account for the difference in success.[49][50][52][53]

A demonstration of the height-success association can be found in the realm of politics. In the United States presidential elections, the taller candidate won 22 out of 25 times in the 20th century.[54] Nevertheless, Ignatius Loyola, founder of the Jesuits, was 150 cm (4 ft 11 in) and several prominent world leaders of the 20th century, such as Vladimir Lenin, Benito Mussolini, Nicolae Ceaușescu, and Joseph Stalin were of below-average height. These examples, however, were all before modern forms of multimedia (i.e., television), which may further height discrimination in modern society. Further, growing evidence suggests that height may be a proxy for confidence, which is likewise strongly correlated with occupational success.[55]

Extremes

[edit]

The tallest living man is Sultan Kösen of Turkey at 251 cm (8 ft 3 in),[56] and the tallest living woman is Rumeysa Gelgi, also of Turkey, at 215 cm (7 ft 1 in).[57] The tallest man in modern history was Robert Wadlow (1918−1940), from Illinois, United States, who was 272 cm (8 ft 11 in) at the time of his death.[58] The tallest woman in modern history was Zeng Jinlian (1964−1982) of China, who measured 246 cm (8 ft 1 in) at the time of her death.[59] The shortest adult human on record was Chandra Bahadur Dangi (1939−2015) of Nepal at 55 cm (1 ft 10 in).[60]

Until the wedding of former Chinese professional basketball player Sun Mingming on 4 August 2013,[61] the tallest living married couple were ex-basketball players Yao Ming and Ye Li (both of China), standing at 229 cm (7 ft 6 in) and 190 cm (6 ft 3 in) respectively, giving a combined height of 419 cm (13 ft 9 in). They married in Shanghai, China, on 6 August 2007.[62]

Pre-modern period

[edit]
Average human height in the Eastern Mediterranean from the Upper Paleolithic (before 16,000 BC) period, through to 1996
Average adult height by year of birth, World
Annual change in average female height by year of birth
Annual change in average male height by year of birth

In general, modern humans living in developed countries are taller than their ancient counterparts, but this was not always the case.

Pre-modern times

[edit]

Certain ancient human populations were quite tall, even surpassing the average height of the tallest of modern countries. For instance, certain hunter-gatherer populations living in Europe during the Paleolithic Era and India during the Mesolithic Period averaged heights of around 183 cm (6 ft 0 in) for males, and 172 cm (5 ft 8 in) for females.[63]

Human height worldwide sharply declined with the advent of the Neolithic Revolution, likely due to significantly less protein consumption by agriculturalists as compared with hunter-gatherers.

During the Bronze Age, height varied significantly by region. The people of the Indus Valley Civilization were among the tallest in the world, with an average height of 176 cm (5 ft 9 in) for males and 166 cm (5 ft 5 in) for females.[64] The people of Ancient Egypt stood around 167 cm (5 ft 6 in) for males and 157 cm (5 ft 2 in) for females.[65] The Ancient Greeks averaged 166 cm (5 ft 5 in) for males and 154 cm (5 ft 1 in) for females. The Romans were slightly taller, with an average height of 169 cm (5 ft 7 in) for males and 158 cm (5 ft 2 in) for females.[66]

18th century

[edit]

In the first half of the eighteenth century, the average height of an English male was 165 cm (5 ft 5 in), and the average height of an Irish male was 168 cm (5 ft 6 in), according to a study by economist John Komlos and Francesco Cinnirella. The estimated mean height of English, German, and Scottish soldiers was 163 cm (5 ft 4 in) − 165 cm (5 ft 5 in) for the period as a whole, while that of Irish was 167 cm (5 ft 6 in). The average height of male slaves and convicts in North America was 171 cm (5 ft 7 in).[67]

Before the mid-nineteenth century, there were cycles in height, with periods of increase and decrease;[68] however, apart from the decline associated with the transition to agriculture, examinations of skeletons show no significant differences in height from the Neolithic Revolution through the early 1800s.[69][70]

19th century

[edit]

In the eighteenth and nineteenth centuries, people of European descent in North America were far taller than those in Europe and were one of the tallest in the world.[34] The original indigenous population of Plains Native Americans was also among the tallest populations of the world at the time.[71] Some studies also suggest that there existed the correlation between the height and the real wage, moreover, the correlation was higher among the less developed countries. The difference in height between children from different social classes was already observed by the age of two.[72]

The average height of Americans and Europeans decreased during periods of rapid industrialization, possibly due to rapid population growth and broad decreases in economic status.[73] This has become known as the early-industrial growth puzzle (in the U.S. context, the Antebellum Puzzle). In England, during the early nineteenth century, the difference between the average height of English upper-class youth (students of Sandhurst Military Academy) and English working-class youth (Marine Society boys) reached 22 cm (8.7 in), the highest that has been observed.[74]

In general, there were no significant differences in regional height levels throughout the nineteenth century.[75] The only exceptions to this rather uniform height distribution were people in the Anglo-Saxon settlement regions who were taller than the average and people from Southeast Asia with below-average heights. However, at the end of the nineteenth century and in the middle of the first globalization period, heights between rich and poor countries began to diverge.[76] These differences did not disappear in the deglobalization period of the two World wars. In 2014, Baten and Blum found that in the nineteenth century, important determinants of height were the local availability of cattle, meat and milk as well as the local disease environment. In the late twentieth century, however, technologies and trade became more important, decreasing the impact of local availability of agricultural products.[77]

Netherlands

[edit]

Data derived from burials show that before 1850, the mean stature of males and females in Leiden, Netherlands, was respectively 167 cm (5 ft 6 in) and 156 cm (5 ft 1 in). The average height of 19-year-old Dutch orphans in 1865 was 160 cm (5 ft 3 in).[78]

From 1830 to 1857, the average height of a Dutch person decreased, even while Dutch real GNP per capita was growing at an average rate of more than 0.5% per year. The worst decline was in urban areas that in 1847, the urban height penalty was 2.5 cm (1.0 in). Urban mortality was also much higher than in rural regions. In 1829, the average urban and rural Dutchman was 164 cm (5 ft 5 in). By 1856, the average rural Dutchman was 162 cm (5 ft 4 in) and urban Dutchman was 158 cm (5 ft 2 in).[79]

In the late nineteenth century, the Netherlands was a land renowned for its short population, but as of 2012, Dutch people were among the world's tallest, with young men averaging 183 cm (6 ft 0 in) tall.[80]

Modern period

[edit]

In the 150 years since the mid-nineteenth century, the average human height in industrialised countries has increased by up to 10 cm (3.9 in).[81] However, these increases appear to have largely levelled off.[81][82]

A 2004 report citing a 2003 UNICEF study on the effects of malnutrition in North Korea, due to "successive famines," found young adult males to be significantly shorter.[specify] In contrast South Koreans "feasting on an increasingly Western-influenced diet," without famine, were growing taller. The height difference is minimal for Koreans over forty years old, who grew up at a time when economic conditions in the North were roughly comparable to those in the South, while height disparities are most acute for Koreans who grew up in the mid-1990s a demographic in which South Koreans are about 12 cm (4.7 in) taller than their North Korean counterparts as this was a period during which the North was affected by a harsh famine where hundreds of thousands, if not millions, died of hunger.[83] A study by South Korean anthropologists of North Korean children who had defected to China found that eighteen-year-old males were 12.7 cm (5 in) shorter than South Koreans their age due to malnutrition.[84]

The height of British children growing up during the years of austerity has decreased: as of 2019, the average five-year-old boy measured 112.5 cm (3 ft 8.3 in) and the average girl 111.7 cm (3 ft 8.0 in). They were shorter and more obese than many of their European peers.[85]

Adult height between populations often differs significantly. For example, the average height of women from the Czech Republic is greater than that of men from Malawi. This may be caused by genetic differences, childhood lifestyle differences (nutrition, sleep patterns, physical labor), or both.

Depending on sex, genetic, and environmental factors, shrinkage of stature may begin in middle age in some individuals but tends to be universal in the extremely aged. This decrease in height is due to such factors as decreased height of inter-vertebral discs because of desiccation, atrophy of soft tissues, and postural changes secondary to degenerative disease.

Working on data of Indonesia, the study by Baten, Stegl and van der Eng suggests a positive relationship of economic development and average height. In Indonesia, human height has decreased coincidentally with natural or political shocks.[86]

Average around the world

[edit]
A textile label showing the difference in average height around the world as shown on this polo shirt. What is a medium size in the United States and Europe is large size for Asia.

As with any statistical data, the accuracy of the findings may be challenged. In this case, for the following reasons:

  • Some studies may allow subjects to self-report values.[87] Generally speaking, self-reported height tends to be taller than measured height, although the overestimation of height depends on the reporting subject's height, age, gender and region.[88][89][90][91]
  • Test subjects may have been invited instead of random sampling, resulting in sampling bias.
  • Some countries may have significant height gaps between different regions. For instance, one survey shows there is 10.8 centimetres (4.3 in) difference in mean height between the tallest state and the shortest state in Germany.[92] Under such circumstances, the mean height may not represent the total population unless sample subjects are appropriately taken from all regions with using weighted average of the different regional groups.
  • Different social groups can show different mean height. According to a study in France, executives and professionals are 2.6 centimetres (1.0 in) taller, and university students are 2.55 centimetres (1.0 in) taller than the national average.[93] As this case shows, data taken from a particular social group may not represent a total population in some countries.
  • Height measurement can vary over the course of a day, due to factors such as a decrease from exercise done directly before measurement (i.e., inversely correlated), or an increase after lying down for a significant period of time (i.e., positively correlated). For example, one study revealed a mean decrease of 1.54 centimetres (0.6 in) in the heights of 100 children from getting out of bed in the morning to between 4 and 5 p.m. that same day.[94]

In 2017, men from Bosnia and Herzegovina, the Netherlands, Montenegro, and Serbia have the tallest average height.[95][96]

In 2024, the world's three tallest populations were in the Netherlands, Montenegro, and Estonia.[97][98]

A 2005 study found teenagers from the Dinaric Alps to be the tallest people in the world.[99]

Dinka people are sometimes noted for their height, with the Tutsi of Rwanda believed to be the tallest people in Africa.[100] In a sample of 52 Dinka Agaar, Roberts and Bainbridge reported a mean height of 182 cm (6 ft 0 in). In 227 Dinka Ruweng, they reported 181 cm (5 ft 11 in). Both figures derived from 1953 to 1954.[101] In Tibet, the Khampas are known for their tall height. Mean height of male Khampas is 180 cm (5 ft 11 in).[102][103]

Measurement

[edit]

Height measurements are by nature subject to statistical sampling errors even for a single individual. In a clinical situation, height measurements are seldom taken more often than once per office visit, which may mean sampling taking place a week to several months apart. The smooth 50th percentile male and female growth curves illustrated above are aggregate values from thousands of individuals sampled at ages from birth to age 20. In reality, a single individual's growth curve shows large upward and downward spikes, partly due to actual differences in growth velocity, and partly due to small measurement errors.

For example, a typical measurement error of plus or minus 0.5 cm (0.2 in) may completely nullify 0.5 cm of actual growth resulting in either a "negative" 0.5 cm growth (due to overestimation in the previous visit combined with underestimation in the latter), up to a 1.5 cm (0.6 in) growth (the first visit underestimating and the second visit overestimating) in the same elapsed period between measurements. Note there is a discontinuity in the growth curves at age 2, which reflects the difference in recumbent length (with the child on his or her back), used in measuring infants and toddlers, and standing height typically measured from age 2 onwards.

Crown-rump length is the measurement of the length of human embryos and fetuses from the top of the head (crown) to the bottom of the buttocks (rump). It is typically determined from ultrasound imagery and can be used to estimate gestational age.

Until two years old, recumbent length is used to measure infants.[104] Length measures the same dimension as height, but height is measured standing up while the length is measured lying down. In developed nations, the average total body length of a newborn is about 50 cm (20 in), although premature newborns may be much smaller.

Standing height is used to measure children over two years old[105] and adults who can stand without assistance. Measure is done with a stadiometer. In general, standing height is about 0.7 cm (0.3 in) less than recumbent length.[106]

Surrogate height measurements are used when standing height and recumbent length are impractical. For example, the Chumlea equation, which uses knee height, can be used to estimate the height of hospitalized patients when standard methods are impractical.[107] Some other techniques include arm span, sitting height, and ulna length.

See also

[edit]

Citations

[edit]
  1. ^ "Stadiometers and Height Measurement Devices". stadiometer.com. Archived from the original on 10 October 2018. Retrieved 6 June 2014.
  2. ^ "Using the BMI-for-Age Growth Charts". cdc.gov. Centers for Disease Control. Archived from the original on 30 January 2014. Retrieved 5 July 2014.
  3. ^ Price, Beth; et al. (2009). MathsWorld Year 8 VELS Edition. Australia: MacMillan. p. 626. ISBN 978-0-7329-9251-4.
  4. ^ Lapham, Robert; Agar, Heather (2009). Drug Calculations for Nurses. USA: Taylor & Francis. p. 223. ISBN 978-0-340-98733-9.
  5. ^ Carter, Pamela J. (2008). Lippincott's Textbook for Nursing Assistants: A Humanistic Approach to Caregiving. USA: Lippincott, Williams & Wilkins. p. 306. ISBN 978-0-7817-6685-2.
  6. ^ a b Baten, Joerg; Matthias, Blum (2012). "Growing Tall: Anthropometric Welfare of World Regions and its Determinants, 1810-1989". Economic History of Developing Regions. 27. doi:10.1080/20780389.2012.657489. S2CID 154506540 – via ResearchGate.
  7. ^ a b "Shorter men live longer, study shows".
  8. ^ a b "Tall height".
  9. ^ Ganong, William F. (2001) Review of Medical Physiology, Lange Medical, pp. 392-397, ISBN 0071605673.
  10. ^ Baten, Jörg (2016). A History of the Global Economy. From 1500 to the Present. Cambridge University Press. ISBN 978-1-107-50718-0.
  11. ^ Hermanussen, Michael (ed) (2013) Auxology – Studying Human Growth and Development, Schweizerbart, ISBN 9783510652785.
  12. ^ Bolton-Smith, C. (2000). "Accuracy of the estimated prevalence of obesity from self reported height and weight in an adult Scottish population". Journal of Epidemiology & Community Health. 54 (2): 143–148. doi:10.1136/jech.54.2.143. PMC 1731630. PMID 10715748.
  13. ^ "Early Puberty in Girls". Nationwide Children's. Retrieved 5 June 2020.
  14. ^ "Early Puberty in Boys". Nationwide Children's. Retrieved 5 June 2020.
  15. ^ "Is Your Child Growing Normally?". THE MAGIC FOUNDATION. Retrieved 20 June 2020.
  16. ^ Hulanicka, B.; Kotlarz, K. (1983). "The final phase of growth in height". Annals of Human Biology. 10 (5): 429–433. doi:10.1080/03014468300006621. ISSN 0301-4460. PMID 6638938.
  17. ^ a b Grantham-Mcgregor, S.; Cheung, Y. B.; Cueto, S.; Glewwe, P.; Richter, L.; Strupp, B. (2007). "Developmental potential in the first 5 years for children in developing countries". The Lancet. 369 (9555): 60–70. doi:10.1016/S0140-6736(07)60032-4. PMC 2270351. PMID 17208643.
  18. ^ Table 1. Association of 'biological' and demographic variables and height. Figures are coefficients (95% confidence intervals) adjusted for each of the variables shown in Rona RJ, Mahabir D, Rocke B, Chinn S, Gulliford MC (2003). "Social inequalities and children's height in Trinidad and Tobago". European Journal of Clinical Nutrition. 57 (1): 143–50. doi:10.1038/SJ.ejcn.1601508. PMID 12548309.
  19. ^ a b Miller, Jane E. (1993). "Birth Outcomes by Mother's Age At First Birth in the Philippines". International Family Planning Perspectives. 19 (3): 98–102. doi:10.2307/2133243. JSTOR 2133243.
  20. ^ a b Pevalin, David J. (2003). "Outcomes in Childhood and Adulthood by Mother's Age at Birth: evidence from the 1970 British Cohort Study". ISER Working Papers.
  21. ^ Hermanussen, M.; Hermanussen, B.; Burmeister, J. (1988). "The association between birth order and adult stature". Annals of Human Biology. 15 (2): 161–165. doi:10.1080/03014468800009581. PMID 3355105.
  22. ^ Myrskyla, M (July 2013). "The association between height and birth order: evidence from 652,518 Swedish men". Journal of Epidemiology and Community Health. 67 (7): 571–7. doi:10.1136/jech-2012-202296. hdl:10810/64275. PMID 23645856. S2CID 19510422.
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General and cited bibliography

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Further reading

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Revisions and contributorsEdit on WikipediaRead on Wikipedia
from Grokipedia
Human height, or stature, measures the vertical distance from the bottom of the feet to the top of the head in an erect bipedal posture. It is a complex polygenic trait with estimates ranging from 60% to 80%, where genetic variants at hundreds of loci contribute additively to variation, though environmental factors like during growth critically influence final attained height by modulating and skeletal development. Males exhibit greater average stature than females, with a of approximately 12 cm in recent birth cohorts, arising from differences in growth trajectories, particularly during where testosterone promotes longer linear growth in males relative to estrogen's effects in females. Average adult heights vary markedly across populations, reflecting genetic ancestry and historical environmental conditions; for instance, men born in 1996 in northern European countries exceed 180 cm, while those in parts of average under 165 cm. Over the past century, mean heights in numerous populations have risen substantially—up to 20 cm in cases like South Korean women and Iranian men—primarily attributable to enhanced childhood , reduced , and socioeconomic improvements that mitigate stunting from caloric or protein deficits. This secular trend underscores as a of , with stagnation or reversal in some developed nations potentially signaling nutritional shifts or other causal factors like altered protein intake. correlates with and cardiovascular health in adulthood, though extremes—such as the tallest verified individual, at 272 cm due to pituitary , or verified shortest adults around 55 cm from primordial dwarfism—often involve pathological disruptions to endocrine or skeletal rather than adaptive variation.

Definition and Measurement

Anthropometric Standards

Anthropometric standards for human height define protocols for precise measurement and reference norms derived from population data, enabling consistent assessment across health, , and design applications. Stature, or standing height, is standardized as the vertical distance from the floor to the vertex (highest point) of the head, with the subject positioned erect, heels together and touching a vertical backboard, knees straight, shoulders relaxed, and arms hanging naturally at the sides, while gazing straight ahead in the Frankfurt horizontal plane (a line passing through the inferior margins of the left and right orbits and the upper margin of the external auditory meatus). Measurements are taken using a stadiometer or wall-mounted device, with readings repeated at least twice to achieve agreement within 0.2 cm (or 0.25 inches), and the average of the closest values recorded to minimize error. International Organization for Standardization (ISO) 7250-1 establishes a core set of body measurements, including stature, to facilitate cross-population comparisons and applications in , with landmarks precisely defined to account for postural variations and reduce inter-observer discrepancies. For infants and children under 2 years, supine length replaces standing height due to limited , measured on a recumbent board with the head aligned against a fixed headpiece and feet extended against a footboard. These protocols ensure reliability, as evidenced by national surveys like the U.S. National Health and Nutrition Examination Survey (NHANES), which report measurement precision errors below 0.5 cm through trained examiners and calibrated equipment. Reference standards provide percentile distributions or z-scores for interpreting height relative to age, sex, and population norms. The (WHO) Child Growth Standards, based on longitudinal data from healthy, breastfed children in diverse global sites (2006-2008), define height-for-age curves from birth to 5 years, flagging deviations below -2 standard deviations as stunting indicative of chronic . For older children and adolescents, WHO and Centers for Disease Control and Prevention (CDC) growth charts extend norms to 20 years, incorporating cross-sectional U.S. data from 1963-1994 updated with recent cohorts; for example, WHO height-for-age standards indicate a normal range for 13-year-old girls from -2 to +2 standard deviations (approximately the 3rd to 97th percentiles) of 144–169 cm, with heights below approximately 144 cm classified as short stature. Adult reference data, such as CDC's NHANES-derived percentiles (e.g., mean U.S. adult male height of 175.3 cm in 2015-2018), stratify by demographics to reflect secular trends and ethnic variations. In , anthropometric standards emphasize accommodation limits, using the 5th female (smallest stature) for minimum clearances and 95th male (largest) for overhead reaches, as outlined in design guidelines to cover 90% of users without over-specification. These percentiles derive from large-scale surveys like the U.S. Army's ANSUR II (1988-2001), which measured over 4,000 personnel to update equipment sizing, highlighting reductions in average height (e.g., 2-3 cm decline in young adults) due to demographic shifts. Adherence to such standards mitigates risks in fields like and vehicle , where non-compliance has led to documented injuries from inadequate fit.

Methods and Accuracy

Standing height, the primary measure of human stature, is obtained by positioning the subject barefoot on a flat surface with heels together and against a vertical stadiometer, ensuring the head, shoulders, and buttocks contact the backrest while the subject gazes horizontally. The measurement is taken from the floor to the highest point of the head, typically read to the nearest 0.1 cm after two readings within 0.2 cm of each other to verify consistency. Standard protocols, such as those from the U.S. Centers for Disease Control and Prevention (CDC), emphasize calibration of equipment and trained observers to minimize systematic errors from posture or misalignment. Stadiometers, often wall-mounted or freestanding devices with a horizontal headpiece, provide higher accuracy than flexible tape measures, which can introduce errors from sagging or inconsistent tension, with technical measurement errors as low as 0.1-0.2 cm for stadiometers versus higher variability for tapes. For adults and older children capable of standing unaided, this direct vertical measurement is preferred; infants and those with mobility limitations require recumbent length using an infantometer, which overestimates standing height by about 0.7-1 cm due to spinal differences. Observer reduces inter-observer variability to under 0.5 cm, though reliability assessments show anthropometric height measurements remain susceptible to procedural deviations. Diurnal variation poses a key accuracy challenge, as spinal disc compression causes an average height loss of 0.5-1.5 cm from morning to evening, with studies reporting a decrease of 0.98 cm over a day. This fluctuation, driven by gravitational loading and hydration cycles, necessitates consistent timing—ideally morning after rest—to standardize data, as uncorrected evening measures can underestimate true stature by up to 1 cm. Age, obesity, and occupational loading exacerbate this variation, with older adults showing greater amplitude due to reduced disc elasticity. Self-reported heights, often used in surveys, exhibit lower reliability with systematic overestimation by 1-2 cm in adults, particularly among those with higher , underscoring the superiority of direct .

Biological Determinants

Genetic Factors

Human height is a highly heritable trait, with genetic factors accounting for approximately 80% of variation in adult height among individuals in well-nourished populations, as estimated from twin and studies. estimates derived from such studies range from 80% to 90%, reflecting the strong influence of in environments where nutritional and health constraints are minimized. These figures indicate that while environmental factors like explain the remaining variance, genetic predispositions set the primary potential for stature. Height is a classic polygenic trait, influenced by thousands of genetic variants across the genome rather than a few major genes. Genome-wide association studies (GWAS) have identified over 12,000 independent single-nucleotide polymorphisms (SNPs) associated with height, primarily common variants that collectively explain 40-50% of the phenotypic variance. These SNPs cluster in genomic regions involved in skeletal growth regulation, such as those affecting proliferation in growth plates and signaling pathways like (IGF1). Polygenic risk scores (PRS) constructed from these variants can predict adult height with accuracies capturing up to 54% of variance when combined with family data, though predictions are less precise across diverse ancestries due to differences in and allele frequencies. The gap between explained variance (40-50%) and total (80%) suggests contributions from rare variants, structural variants, and epistatic interactions not yet fully captured by current GWAS. Notable examples include variants in the HMGA2 gene, where a common SNP (rs1042725) is associated with height differences of about 0.4 cm per , influencing body size through regulation of and validated in both human and animal models. Other loci, such as those near GDF5 and NPR2, affect height via impacts on bone morphogenesis and natriuretic peptide signaling, respectively, but no single variant accounts for more than a small fraction of . Parental height provides a practical proxy for genetic potential, with mid-parental height ( of parents' heights, adjusted for ) predicting offspring stature within 8-10 cm in 95% of cases, underscoring the cumulative polygenic architecture. Epigenetic modifications and gene-environment interactions may modulate expression, but core genetic effects remain dominant in determining baseline height trajectories.

Environmental and Nutritional Influences

Environmental factors, particularly and exposure to during childhood, exert significant influence on attained adult height beyond genetic predispositions. High protein and calorie intake during growth periods supports achieving maximal genetic height potential by providing essential energy and building blocks for tissue elongation. A balanced diet providing adequate proteins, calcium, vitamin D, and zinc during childhood and puberty supports individuals in reaching their genetic height potential by promoting proper skeletal growth and development. Inadequate in early life leads to stunting, characterized by impaired linear growth that often persists into adulthood, with deficits accumulating from fetal development through . Protein-energy malnutrition, especially deficiencies in essential from sources like and , restricts skeletal growth by limiting the availability of building blocks for bone and tissue elongation. shortages, including (e.g., from oysters and beef), magnesium (e.g., from almonds and leafy greens), calcium (e.g., from dairy and greens), vitamin D (e.g., from fatty fish), vitamin K2 (e.g., from fermented foods and animal products), iron, and , further compromise height potential by disrupting cellular proliferation, hormonal signaling, and bone mineralization in growth plates. Once these growth plates close, typically after puberty, diet supports overall health but cannot increase bone length or height. Adequate sleep is also critical, as growth hormone is primarily released during deep sleep stages, supporting linear growth and height attainment. Transient disruptions like short-term sleep loss, moderate undereating, and irregular stimulant use during puberty (ages ~14–17) are unlikely to cause permanent growth stunting; any effect is minimal or none, with strong catch-up potential before growth plates close, as genetics, overall nutrition, and health dominate height outcomes. Intense exercise, without overtraining and paired with sufficient nutrition, stimulates growth hormone release and supports skeletal development without impairing attained height. Chronic infections and poor amplify nutritional deficits through mechanisms like enteric pathogens that impair absorption and trigger inflammatory responses diverting energy from growth to immune defense, alongside avoidance of diseases and growth-suppressing medications. Populations with high burdens of diarrheal diseases and helminth infections exhibit reduced average heights, as repeated illness episodes cumulatively shorten growth trajectories. coverage, such as access to toilets reducing , has been associated with height gains equivalent to 0.3 standard deviations in child populations once coverage exceeds 50-75% in communities. Historical secular trends demonstrate these effects: average adult heights in increased by approximately 10-12 cm over the 20th century, attributable primarily to enhanced , reduced childhood morbidity, and better measures rather than genetic shifts. In modern contexts, technology-related behaviors such as excessive screen time contribute to sedentarism, obesity, and sleep disruption via blue light suppression of melatonin, potentially advancing puberty onset—particularly in girls—which may lead to shorter adult height by hastening epiphyseal closure despite an initial growth acceleration. Conversely, later maturation under favorable environmental conditions extends the pre-pubertal growth phase, often enabling individuals to exceed mid-parental height predictions and experience upward shifts in height percentiles. Catch-up growth following nutritional recovery is possible but limited; children stunted before age two rarely fully compensate, retaining 5-10 cm shortfalls in adulthood due to irreversible alterations in growth plate function. Cross-national data confirm that per capita protein intake from animal sources correlates strongly with male height averages, with countries like the benefiting from high dairy consumption yielding mean male heights of 183 cm as of birth cohorts from the . Conversely, persistent in low-income regions sustains height gaps, where environmental insults compound to explain up to 54% of international variation in child stature. These patterns underscore height as a of cumulative environmental quality, with interventions targeting early-life and yielding measurable gains in population-level stature.

Hormonal and Developmental Mechanisms

Human height is primarily determined through longitudinal bone growth at the epiphyseal growth plates, where chondrocytes proliferate, hypertrophy, and undergo to elongate long bones such as the and . This process is tightly regulated by hormonal signals that integrate nutritional status, genetic factors, and developmental timing. Growth occurs in distinct phases: rapid fetal and infantile growth driven largely by nutrition and insulin-like factors, steady childhood growth mediated by the (GH)- (IGF-1) axis, and an accelerated pubertal spurt influenced by sex steroids, followed by epiphyseal fusion that halts further elongation. The GH-IGF-1 axis forms the core endocrine pathway for childhood linear growth. GH, secreted pulsatile by the under hypothalamic growth hormone-releasing hormone (GHRH) stimulation, acts directly on growth plate chondrocytes to promote proliferation and indirectly via hepatic IGF-1 production, which circulates systemically and amplifies local effects at the growth plate. IGF-1 binds to receptors on chondrocytes, stimulating their division, hypertrophy, and matrix synthesis, thereby driving bone elongation; deficiencies in either GH or IGF-1, as seen in isolated GH deficiency or , result in proportionate with reduced growth velocity. Local IGF-1 production in the growth plate, induced by GH, accounts for much of the axis's anabolic effects independent of systemic levels. Thyroid hormones, primarily thyroxine (T4) and (T3), are essential for normal skeletal maturation and growth plate function, exerting both direct effects on differentiation and indirect modulation via enhancement of GH-IGF-1 responsiveness. in juveniles impairs bone growth by delaying and reducing height velocity, often leading to delayed skeletal age and potential permanent stature deficits if untreated beyond ; treatment with restores growth potential through catch-up mechanisms but underscores thyroid hormones' permissive role in GH action. Sex steroids orchestrate the pubertal growth spurt and subsequent termination of growth. Testosterone in males sustains prolonged pre-pubertal growth plate activity and contributes to the spurt via signaling, while —derived from gonadal sources in females and of androgens in males—accelerates of the growth plate by promoting vascular invasion, , and fusion of epiphyses, typically around ages 14-16 in females and 16-18 in males. Higher levels explain earlier epiphyseal closure and shorter average adult stature in females; inhibitors, which block estrogen synthesis, have been shown to delay fusion and increase final height in boys with or conditions like . Disruptions, such as , advance these processes and curtail height potential.

Patterns of Variation

Adult males are, on average, taller than females worldwide, with a global mean difference of approximately 13 cm for adults born in recent decades. This equates to a male-to-female height ratio of about 1.08, meaning males are roughly 8% taller. The disparity arises primarily during , when males undergo a later onset (around age 12-14) and more extended growth spurt compared to females (onset around age 10-12), leading to greater post-pubertal linear growth in males. Biologically, the difference stems from sex chromosome effects and gonadal hormones. Males' XY complement results in gene dosage imbalances—particularly from Y-chromosome genes and incomplete X-chromosome inactivation in females—that favor taller stature in males, accounting for a substantial portion of the gap. in females accelerates bone maturation and epiphyseal closure earlier, truncating growth potential, whereas testosterone in males sustains skeletal elongation longer. Sex-biased contributes further, with studies estimating it explains 12-23% of the average difference through autosomal loci showing divergent activity between sexes. The degree of dimorphism shows limited variation across human populations, typically ranging from 7-10% taller males, though environmental factors like can modulate absolute heights without greatly altering the ratio. Latitude correlates weakly with dimorphism levels, with marginally greater differences in higher-latitude societies, potentially linked to resource availability or selection pressures, but genetic underpinnings remain dominant globally. In resource-scarce contexts, such as historical or developing populations, nutritional constraints may compress overall stature more in males, slightly reducing dimorphism.

These growth trajectories illustrate how pubertal divergence amplifies dimorphism, with males overtaking and surpassing females in height by .

Global and Regional Averages

The adult height for individuals born in 1996, corresponding to current young adults as of 2025, stands at 171 cm for males and 159 cm for females globally, yielding an overall average of approximately 165 cm assuming equal sex ratios, based on pooled anthropometric data from the NCD (NCD-RisC). This represents an analysis of measurements from over 18.6 million adults across more than 200 countries, emphasizing standardized, measured heights rather than self-reports to minimize bias. The global male-female height difference averages 12 cm, or a ratio of approximately 1.07, with regional variations in this dimorphism influenced by both genetic and environmental factors. Regional disparities in average heights are pronounced, driven primarily by differences in childhood , , and socioeconomic conditions rather than genetic divergence alone, as evidenced by historical increases within populations. These regional patterns reflect continental ancestry differences in average adult male stature and build: European-descent populations are typically tallest (~178–182 cm in northern groups), heavier (~80–90 kg), with higher fat-free mass variability; East Asian-descent shorter (~170–175 cm), leaner (~65–75 kg), with shorter limbs relative to torso; Sub-Saharan African-descent variable—Nilotic peoples like the Dinka averaging 185+ cm with long slender limbs, while West/Central groups ~165–170 cm, exhibiting higher muscle and bone density and lower body fat at equivalent BMI; Native American-descent intermediate (~170–175 cm), stockier builds. Substantial overlap exists due to dietary and environmental factors. exhibits the highest regional averages, with males in Northern and Western countries often exceeding 180 cm; for instance, Dutch males born in 1996 average 182.5 cm (95% credible interval: 180.6–184.5 cm), and similar figures apply in neighboring nations like Denmark and Latvia. Female averages in Europe cluster around 162–170 cm, with Lithuanian women averaging approximately 167.8 cm for 19-year-olds in 2019. In , U.S. males average around 175-177 cm and females 163 cm, per national health surveys, though these lag behind European peaks due to rising and nutritional shifts. For example, in the United States, a height of 187 cm for adult men (aged 20 and over) is approximately at the 93rd percentile according to CDC/NHANES 2015–2018 anthropometric data, with the 90th percentile around 185 cm and the 95th percentile around 188 cm. This demonstrates that percentiles are population-specific, varying significantly by region due to differences in average heights, and no single global percentile exists for a given height. In contrast, records the lowest regional averages, with males around 165 cm and females near 152 cm for recent cohorts, meaning that 4 feet 11 inches (150 cm) is short for adult women in many countries (e.g., approximately the 5th percentile in the US versus an average of 163 cm) but near average in regions like South Asia (e.g., India ~152 cm), attributable to persistent challenges in protein intake and despite economic growth. Asia exhibits greater inter-population height variation among women compared to Europe, with averages spanning approximately 152–163 cm across countries, due to vast geographic, ethnic, economic, nutritional, and genetic/environmental disparities (e.g., malnutrition in South and Southeast Asia versus improved nutrition in East Asia); Europe shows more homogeneity, with female averages clustering around 162–170 cm, reflecting consistent living standards, nutrition, and healthcare in the post-20th century. This pattern holds in NCD-RisC aggregates and other datasets. East and show intermediate figures, such as Japanese males at approximately 172 cm, reflecting rapid post-war gains from improved diets but plateauing in recent decades. Sub-Saharan African averages vary widely by nation but generally fall between 165–170 cm for males, hampered by high rates of infectious disease and undernutrition, though select ethnic groups like the Dinka of exhibit exceptional statures exceeding 185 cm due to genetic selection. averages hover around 172 cm for males, with gains in countries like (averaging 173-175 cm) outpacing others amid urbanization. These patterns underscore environmental causation over innate regional genetic inferiority, as height gaps have widened since 1896—from 8 cm to 12 cm for males—correlating with divergent improvements in living standards rather than fixed biological limits. Data from NCD-RisC highlight that while high-income regions sustain tall statures, many developing areas continue secular increases, though at diminishing rates where obesity now offsets nutritional benefits. Heights significantly above regional means, such as 192 cm, illustrate variation: placing individuals near the 99th percentile in lower-average countries like Brazil, but in the 90-95th percentile in taller nations like the Netherlands. Self-reported surveys often inflate figures by 1–2 cm, underscoring the value of measured datasets for accuracy. Average human height exhibited marked secular increases during the 19th and 20th centuries, particularly in and , driven by enhancements in , , and socioeconomic conditions. In European men, average stature rose by approximately 11 cm from the to the , reflecting a consistent gain of over 1 cm per . Similar patterns emerged in , where male heights reached 177 cm by 1970, up substantially from early 19th-century levels around 170 cm. These trends aligned with broader improvements following the , though pre-industrial fluctuations showed medieval Englishmen averaging closer to modern heights than their 18th-century counterparts, indicating episodic rather than unidirectional change prior to sustained modern gains. Skeletal evidence from the ancient Middle East around 1000 BC indicates average male heights of approximately 1.65–1.70 m. Globally, the saw the most pronounced secular accelerations in regions transitioning from undernutrition, with the NCD Risk Factor Collaboration documenting height gains for cohorts born between 1896 and 1996. South Korean women experienced the largest increase at 20.2 cm (: 17.5–22.7 cm), while Iranian men gained similarly, surpassing many European increments. In developing Asia and , post-World War II correlated with rapid stature improvements, often exceeding 10 cm per century, as evidenced by data from over 200 countries. These shifts underscore environmental influences outweighing genetic stability, as estimates remain consistent across eras yet population averages diverged sharply with living standards. In high-income nations, secular gains plateaued by the late , with minimal further increases or slight reversals linked to rising and dietary shifts. For instance, U.S. adult heights stabilized after mid-century peaks, contrasting continued modest rises in until the 2000s. In , rapid height escalation slowed post-2005 in urban areas, reflecting nutritional transitions. Recent analyses indicate annual changes near zero in many developed cohorts born after , suggesting limits to environmental optimization amid emerging health trade-offs like increased BMI. Rural populations in places like showed persistent positive trends into the 2010s, albeit diminishing, highlighting uneven global convergence.

Extremes and Pathologies

Record Heights

The tallest person in , verified by multiple medical measurements, is (United States, 1918–1940), who reached 272 cm (8 ft 11.1 in) on 27 June 1940 in . His height resulted from pituitary gigantism, with growth continuing unabated due to excessive production; he required leg braces from age 9 and died at 22 from an infected blister exacerbated by his size. The tallest woman ever verified is (China, 1964–1982), measured at 246.3 cm (8 ft 1 in) on 13 February 1982 in Yujiang. Like Wadlow, her extreme stature stemmed from endocrine disorders, though records note challenges in precise measurement due to ; she died at 17 from osteoporosis-related complications. The shortest adult man ever confirmed is (Nepal, 1939–2015), at 54.6 cm (21.5 in), verified by medical examination at CIWEC Clinic Travel Medicine Center in on 29 October 2012. His limited growth from birth, yet he lived to 75, outliving many with similar conditions. The shortest woman ever recorded is (Netherlands, 1876–1895), who measured 61 cm (24 in) at maturity. Born with , she toured as a performer and died at 19 from and ; recognizes her record based on historical medical attestations, though pre-20th-century verifications lack modern imaging standards. Guinness World Records maintains these as benchmarks requiring irrefutable evidence, such as physician-certified , radiographic confirmation where applicable, and exclusion of temporary conditions like malnutrition-induced stunting without genetic basis. Claims exceeding these, such as unverified historical figures like (alleged 236 cm in Roman records), lack contemporary documentation and are dismissed.
CategoryNameHeightVerification DateNationality
Tallest man ever272 cm27 June 1940American
Tallest woman ever246.3 cm13 February 1982Chinese
Shortest man ever54.6 cm29 October 2012Nepali
Shortest woman ever61 cmHistoricalDutch

Conditions Causing Gigantism and Dwarfism

Gigantism arises from excessive secretion of growth hormone (GH) during childhood, before the closure of epiphyseal growth plates, resulting in accelerated linear growth and excessive adult height. The condition is predominantly caused by benign pituitary adenomas that overproduce GH and insulin-like growth factor 1 (IGF-1), stimulating unchecked skeletal growth. In rare instances, other etiologies include McCune-Albright syndrome, characterized by activating mutations in the GNAS gene leading to mosaic GH hypersecretion, or familial cases linked to genetic alterations such as aryl hydrocarbon receptor-interacting protein (AIP) mutations or X-linked acrogigantism (X-LAG) due to GPR101 gene duplications on the X chromosome. Pituitary gigantism accounts for approximately 0.6% of pituitary adenomas in children and adolescents, with a genetic etiology identified in about 46% of cases in international reviews, though no cause is found in over 50% despite testing. Dwarfism refers to severe short stature, typically defined as an adult height below 147 cm (4 feet 10 inches), and is classified into proportionate forms, where body parts are proportionally small, and disproportionate forms, involving abnormal limb-trunk ratios. Proportionate dwarfism often stems from endocrine deficiencies, such as (GHD) due to , where the fails to produce adequate GH, leading to reduced IGF-1 levels and impaired longitudinal bone growth; this is a treatable cause affecting up to 1 in 3,500 to 10,000 children. Other proportionate causes include or chronic conditions like renal disease impairing GH responsiveness. Disproportionate dwarfism is primarily driven by genetic skeletal dysplasias affecting . , the most common form, results from a gain-of-function in the FGFR3 (most frequently G380R), inhibiting proliferation in growth plates and yielding rhizomelic shortening (proximal limbs disproportionately short); it has an incidence of 1 in 15,000 to 40,000 births and follows autosomal dominant inheritance, with 80% of cases sporadic from de novo . Hypochondroplasia, a milder allelic variant of , involves different FGFR3 mutations, while , a lethal form, shares FGFR3 alterations but causes severe in infancy. Additional disproportionate causes encompass (COMP mutations) and diastrophic dysplasia (SLC26A2 mutations), both impairing cartilage matrix formation. Over 400 skeletal dysplasias exist, but predominates, comprising about 70% of disproportionate cases.

Genetic and Syndromic Disorders

Genetic and syndromic disorders encompass a range of inherited conditions that disrupt normal growth processes, leading to either pronounced or excessive height, often alongside multisystem manifestations such as skeletal anomalies, cardiac defects, or endocrine imbalances. These syndromes typically arise from mutations in genes involved in skeletal development, hormone signaling, or chromosomal abnormalities, distinguishing them from isolated deficiencies or environmental factors. Diagnosis often requires , with defined as height below the 3rd for age and sex, while tall stature exceeds the 97th , though syndromic features guide clinical evaluation.

Disorders Associated with Short Stature

, the most common form of disproportionate , results from a gain-of-function in the FGFR3 on 4p16.3, inhibiting proliferation in growth plates and yielding rhizomelic shortening of limbs, , and frontal bossing; adult height averages 131 cm in males and 123 cm in females, with an incidence of approximately 1 in 15,000-40,000 live births. , caused by heterozygous mutations in genes of the RAS/MAPK pathway (e.g., in 50% of cases), features (often 20-30% below mean), , , and pectus deformities; final adult height is reduced by about 20-30 cm without intervention, affecting 1 in 1,000-2,500 individuals. , a chromosomal disorder involving partial or complete X (45,X in 50% of cases), leads to averaging 143 cm in untreated females due to SHOX , alongside , cardiac anomalies, and ; prevalence is 1 in 2,000-2,500 female births. Prader-Willi syndrome stems from paternal deletion or imprinting defects at 15q11.2-q13, producing (final height 10-15 cm below mean), , hyperphagia-induced , and mild ; growth failure links to hypothalamic dysfunction mimicking GH resistance, with incidence around 1 in 10,000-30,000. Silver-Russell syndrome involves hypomethylation of 11p15 (60% of cases) or maternal 7, manifesting as severe pre- and postnatal growth restriction ( height often < -3 SD), body asymmetry, and clinodactyly; it affects roughly 1 in 100,000.

Disorders Associated with Tall Stature

Marfan syndrome, an autosomal dominant connective tissue disorder from mutations in FBN1 on chromosome 15q21.1, causes tall stature with disproportionately long limbs (arm span exceeding height by >5 cm), , and , alongside aortic root dilation; average adult height exceeds population norms by 10-20 cm, with prevalence of 1 in 5,000. (47,XXY karyotype, incidence 1 in 500-1,000 males) results in tall stature (eunuchoid proportions, leg length > trunk), , small testes, and infertility due to ; final height averages 10-15 cm above male norms from delayed epiphyseal closure. Sotos syndrome, driven by NSD1 haploinsufficiency (90% of cases), presents early overgrowth (birth weight >90th percentile), advanced , and tall stature persisting into adulthood, with and developmental delay; it occurs in about 1 in 14,000. Other syndromic overgrowth includes Beckwith-Wiedemann syndrome, featuring prenatal macrosomia, , and elevated cancer risk from 11p15.5 imprinting defects (e.g., CDKN1C mutations), with childhood height often >97th percentile though stabilizing later; prevalence is 1 in 10,340. due to gene variants mimics Marfan-like tall habitus with lens dislocation and thrombosis risk, but differs in downward lens subluxation and intellectual involvement. While pituitary from AIP mutations can yield extreme heights (>2 m prepubertally), it represents a rarer genetic subset often requiring surgical intervention, comprising ~29% of familial cases. Management across these disorders may involve for short stature syndromes (e.g., approved for Turner and Noonan) or surveillance for complications in tall stature conditions, guided by genetic confirmation.

Health Correlations

Positive Associations

Taller adult height is associated with a reduced risk of coronary heart disease and other cardiovascular conditions in multiple epidemiological studies. For instance, analyses of large cohorts have shown that individuals in the tallest height quartiles experience approximately 20-30% lower rates of ischemic heart disease mortality compared to those in the shortest quartiles, potentially due to factors like larger coronary artery size or better childhood nutrition reflected in stature. Similarly, taller stature correlates with lower incidence of respiratory diseases, including chronic obstructive pulmonary disease, with population data indicating a 15-25% decreased risk for taller men and women. In terms of cognitive , taller individuals demonstrate lower prevalence of ; one of over 500 participants found that men approximately 5 feet 11 inches or taller had nearly 60% reduced odds of developing the condition relative to shorter men under 5 feet 7 inches, possibly linked to height as a marker of early-life neurodevelopmental advantages. Taller height also serves as a proxy for improved overall childhood and , which independently predicts better cognitive performance in adulthood, with taller adults scoring higher on average in tests of and executive function across diverse populations. Regarding and pain perception, taller men and women report higher levels of and positive emotions, alongside lower frequencies of reported and sadness; survey data from representative samples reveal effect sizes equivalent to several years of additional in terms of hedonic outcomes. These associations persist after adjusting for socioeconomic factors, suggesting a partial direct link between stature and perceptual metrics. For reproductive health, taller women experience fewer adverse pregnancy outcomes, such as or preterm delivery, with meta-analyses estimating a 10-15% risk reduction per standard deviation increase in maternal height.

Negative Risks and Trade-offs

Taller adult height correlates with elevated risks of multiple cancers, independent of other factors like or . Prospective cohort studies and meta-analyses indicate that each 10 cm increase in height is associated with a 10-18% higher overall cancer incidence, with risks extending to site-specific types such as colorectal (14% per 10 cm), postmenopausal , (particularly high-grade), , esophageal, and cervical cancers. This pattern holds across diverse populations, including East Asians, and is attributed to mechanistic factors including a larger number of divisible cells prone to oncogenic mutations, prolonged exposure to growth-promoting hormones during development, and higher circulating levels of (IGF-1), which accelerates but also tumor initiation. In cardiovascular domains, taller stature reduces odds of coronary heart disease by approximately 14% per standard deviation increase but heightens risks of (AF) and venous thromboembolism (VTE). Genetically predicted height via elevates AF odds, potentially due to greater atrial stretch from expanded body size, increased cardiac demands, and longer vascular pathways facilitating clot formation. Similarly, VTE and thrombosis risks rise with height, linked to elevated hydrostatic in extended lower extremities and proportionally larger blood volumes straining venous return. Additional trade-offs include , , and heightened susceptibility to skin and bone infections, as identified in large-scale phenome-wide analyses associating taller height with over 700 non-cardiovascular conditions. These burdens reflect biomechanical and physiological costs: greater leverage amplifies loading, predisposing to arthropathies, while expanded tissue demands higher metabolic rates and throughput, straining systems like circulation and increasing vulnerability to proliferative disorders. In extreme tallness, as in untreated or from excess, complications compound to include , , , , colon polyps, and excess mortality from cardiovascular and neoplastic causes, often manifesting by the third or fourth decade. Such patterns underscore height as a proxy for developmental trade-offs, where gains in stature—favoring in resource-variable ancestral environments—incur modern morbidity from unchecked growth signaling. Numerous epidemiological studies have documented an inverse association between adult and , with taller individuals exhibiting higher all-cause mortality rates. A 2023 analysis of Polish national data found a statistically significant negative between height and lifespan in both sexes, persisting after controlling for birth cohort effects, suggesting that taller stature may confer a disadvantage. Similarly, a 2021 reported a U-shaped dose-response relationship between height and all-cause mortality, with the lowest risk at approximately 174 cm for men and 158 cm for women, and elevated risks at both extremes. This pattern aligns with earlier findings from a 2017 review, which attributed shorter lifespans in taller populations to factors like increased cellular proliferation and metabolic demands, though genetic and environmental confounders, such as early-life influencing both height and health, complicate . Regarding morbidity, height displays opposing associations with (CVD) and cancer risks, reflecting potential trade-offs. Shorter stature correlates with elevated CVD incidence and mortality, including coronary heart disease and ; for instance, a 2012 prospective study of over 1 million adults linked each 6.5 cm decrease in height to a 15-20% higher of fatal CVD events, possibly due to shared risk factors like or lower childhood socioeconomic conditions. Conversely, taller height increases cancer susceptibility across multiple sites, with a 2022 Mendelian randomization analysis estimating that each standard deviation increase in height (about 10 cm) raises overall cancer odds by 18%, attributed to greater organ size and cell numbers elevating oncogenic exposure. These divergent risks may explain the net longevity penalty for extreme height, as cancer's higher lethality in taller cohorts offsets CVD advantages. Height loss in older age further ties to morbidity and reduced , independent of baseline stature. A 2023 Japanese observed that height reductions of 0.5 cm or more over five years predicted a 20-30% increase in all-cause mortality, linked to frailty, , and vertebral fractures. This underscores height as a dynamic of aging-related morbidity, where accelerated shrinkage signals underlying or nutritional deficits.

Societal and Evolutionary Impacts

Economic and Occupational Outcomes

Taller individuals consistently exhibit higher across numerous studies, a phenomenon known as the height premium. A and of 42 empirical studies confirmed this association in 33 cases, estimating an average wage increase of approximately 1-2% per additional centimeter of height, though the effect diminishes after controlling for factors like and . The premium is stronger for men than women and varies regionally, being smaller in high-income countries like the and (around 0.5-1% per cm) and larger in and (up to 2-3% per cm), potentially due to differences in labor market , nutritional signaling of ability, or cultural preferences for physical stature. In quantitative terms, a 10 cm height increase correlates with roughly 15% higher lifetime wages for men and 10% for women, based on aggregated findings from labor market data across multiple countries. For example, in U.S. samples, a man 6 feet (183 cm) tall earns an estimated $166,000 more over a 30-year career than one 5 feet 5 inches (165 cm) tall, even after adjusting for age and qualifications. This premium arises not solely from bias but also from height's correlation with cognitive ability and early-life health, which influence productivity and human capital formation; twin studies and Mendelian randomization analyses support a causal link beyond mere appearance. Occupationally, height advantages extend to promotions and attainment. Taller workers are more likely to secure supervisory roles, with Swedish registry data showing each additional standard deviation in height (about 7 cm) raising leadership probability by 2-3 percentage points among men. Among CEOs, 58% exceed 6 feet, compared to 14.5% of U.S. men, and the average CEO height is 3 inches above the population mean of 5 feet 9 inches, suggesting selection for perceived dominance or confidence in executive tracks. Height's role surpasses in some income models, persisting into later career stages without decline. While beneficial in most sectors, extreme heights can limit opportunities in specialized fields with physical constraints, such as aviation cockpits (typically requiring 5'2" to 6'3") or certain military roles with uniform fit standards, though these affect few and do not offset the broader premium. Overall, the height premium reflects intertwined biological, developmental, and social mechanisms rather than arbitrary prejudice alone.

Reproductive and Mate Selection Dynamics

In mate selection, women consistently express a preference for men taller than themselves, with studies indicating an ideal male approximately 21 cm greater than the female's own , compared to men's more modest preference for partners about 8 cm shorter. This asymmetry reflects greater selectivity by women regarding male , often associating taller stature with perceived attractiveness, dominance, and genetic quality. Men, in contrast, show weaker preferences overall, though taller men are rated higher in across short- and long-term contexts. These preferences partially manifest in actual pairings, where taller men pair with relatively taller women, but the remains modest, suggesting height influences but does not dominate . Positive for height occurs across populations, with a meta-analytic of r = 0.23, indicating individuals tend to select partners of similar stature, yet men are typically taller than their partners by an of 10-15 cm due to sex-specific preferences. In short-term relationships, taller men exhibit stronger preferences for shorter women relative to long-term contexts, potentially prioritizing physical dimorphism for reproductive signaling. Height correlates with reproductive success, particularly for men, where taller individuals have more offspring in contemporary and historical populations, as evidenced by analyses of large cohorts showing a positive linear relationship between male height and number of children fathered. This pattern holds after controlling for socioeconomic factors, implying selection pressure favoring male height via mate choice and possibly direct fitness benefits like health indicators. For women, the association is weaker or curvilinear, with moderately tall women sometimes showing higher fertility, though extreme shortness can enhance reproductive output in resource-limited settings by reducing energetic costs of gestation and lactation. Overall, sexual selection appears to drive male height evolution more strongly, contributing to observed sexual dimorphism, while female height optima balance fertility and viability trade-offs.

Discrimination and Cultural Biases

, often termed heightism, manifests in employment contexts where taller individuals receive preferential treatment in hiring, promotions, and compensation. Empirical studies indicate a consistent "height premium" in labor markets, with taller workers earning higher ; for instance, a of global data found that a 10 cm increase in correlates with approximately a 2-4% wage increase for men, varying by region and attenuated for women. In the United States, longitudinal analyses show that men 6 feet tall earn about $166,000 more over a 30-year compared to those 5 feet 5 inches tall, independent of and , suggesting implicit biases favoring perceived and competence in taller candidates. These patterns persist across countries, including , where nationwide surveys from 1989 onward reveal employer preferences for height in job selection, particularly for roles signaling authority. Cultural biases reinforce these outcomes through stereotypes associating height with dominance, intelligence, and , while shorter stature evokes perceptions of inferiority or weakness, especially for men. documents implicit biases where short individuals are granted less personal and viewed as less capable leaders, contributing to workplace exclusion without overt intent. Such prejudices extend beyond professional spheres; in Western societies, media and social norms amplify height as a proxy for and success, leading to stigmatization of short men, though legal protections remain minimal, as height is rarely classified as an immutable trait warranting anti-discrimination laws akin to those for race or . In reproductive and , height biases influence mate selection, with women exhibiting strong preferences for taller male partners, reflecting evolutionary signals of genetic fitness, resource access, and protection. Studies of preferences confirm that taller men receive more interest in both short-term and long-term contexts, with patterns showing couples where men exceed women in height by an average of 12-15 cm, though actual pairings modestly align with stated ideals due to availability constraints. These preferences, observed consistently in data, disadvantage shorter men in competitive mating markets, exacerbating without equivalent penalties for short women, who face less stringent height expectations from partners. Overall, height-related arises from intertwined biological signaling and societal reinforcement, rather than isolated malice, yet yields measurable disparities in opportunity and well-being.

References

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