<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Human height and explain in detail? [/INST] 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, in centimetres when using the metric system, or feet and inches when using United States customary units or the imperial system.In the early phase of anthropometric research history, questions about height techniques for measuring nutritional status often concerned genetic differences.Height is also important because it is closely correlated with other health components, such as life expectancy. 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. Short stature decreases the risk of venous insufficiency.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.The development of human height can serve as an indicator of two key welfare components, namely nutritional quality and health. 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.
A study of 20th-century British natality trends indicated that while tall men tended to reproduce more than short men, women of below-average height had more children than taller women.

Determinants of growth and height
The study of height is known as auxology. 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.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 are relatively equally distributed. The uneven distribution of nutritional resources makes it more plausible for individuals with better access to resources to grow taller, while the other population group who does not have so much of a nutritious food availability height growth is not as promising. 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. 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. 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 “imperium Romanum” were taller than those who lived at the heart of the Empire.Changes in diet (nutrition) and a general rise in quality of health care and standard of living are the cited factors in the Asian populations. Malnutrition including chronic undernutrition and acute malnutrition is known to have caused stunted growth in various populations. This has been seen in North Korea, parts of Africa, certain historical Europe, and other populations. 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.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 individuals 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 (0.20 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.
Height, like other phenotypic traits, is determined by a combination of genetics and environmental factors. A childs 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.
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 and an average boy starting his puberty and pubertal growth spurt at 12 years), 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. 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. The pregnant mothers 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 vary degrees.
The age of the mother also has some influence on her childs 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 mothers life. 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.It has been observed that first-born males are shorter than later-born males.
However, more recently the reverse observation was made. The study authors suggest that the cause may be socio-economic in nature.

Nature versus nurture
The precise relationship between genetics and environment is complex and uncertain. Differences in human height is 60–80% heritable, according to several twin studies 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. 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. In a separate study of body proportion using sitting-height ratio, it reports that these 697 variants can be partitioned into 3 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. 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.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 157.5 centimetres (5 ft 2 in) in height and the women averaged 142.2 centimetres (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. By 2000, the American Maya were 10.24 cm (4.03 in) taller than the Guatemalan Maya of the same age, largely due to better nutrition and health care. Bogin also noted that American Maya children had relatively longer legs, averaging 7.02 cm (2.76 in) longer than the Guatemalan Maya (a significantly lower sitting height ratio).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 1953–54 were on average 181.3 centimetres (5 ft 11+1⁄2 in) tall, and Shilluk males averaged 182.6 centimetres (6 ft 0 in). The Nilotic people are characterized as having long legs, narrow bodies and short trunks, an adaptation to hot weather. However, male Dinka and Shilluk refugees measured in 1995 in Southwestern Ethiopia were on average only 176.4 cm (5 ft 9+1⁄2 in) and 172.6 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." 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.
The tallest living married couple are ex-basketball players Yao Ming and Ye Li (both of China) who measure 228.6 cm (7 ft 6 in) and 190.5 cm (6 ft 3 in) respectively, giving a combined height of 419.1 cm (13 ft 9 in). They married in Shanghai, China, on 6 August 2007.In Tibet, the Khampas are known for their great height.  Khampa males are on average 180 cm (5 ft 11 in).

Role of an individuals height
Height and health
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. Short stature decreases the risk of venous insufficiency. 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. Cancer risk has also been found to grow with height. Moreover, scientists have also observed a protective effect of height on risk for Alzheimers disease, although this fact could be a result of the genetic overlap between height and intracraneal volume and there are also genetic variants influencing height that could affect biological mechanisms involved in Alzheimers disease etiology, such as Insulin-like growth factor 1 (IGF-1).Nonetheless, modern westernized interpretations of the relationship between height and health fail to account for the observed height variations worldwide.  Cavalli-Sforza and Cavalli-Sforza 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.  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 man known to verifiable history, developed trouble 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.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.A study done in Sweden in 2005 has shown that there is a strong inverse correlation between height and suicide among Swedish men.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.In medicine, height is measured to monitor child development, this is a better indicator of growth than weight in the long term.
For older people, excessive height loss is a symptom of osteoporosis. Height is also used to compute indicators like body surface area or body mass index.

Height and occupational success
There is a large body of research in psychology, economics, and human biology that has assessed the relationship between several seemingly innocuous physical features (e.g., body height) and occupational success. The correlation between height and success was explored decades ago. 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 gender or socioeconomic status that are correlated with height which may account for the difference in success.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. 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 multi-media, 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.

Sports
History of human height
In the 150 years since the mid-nineteenth century, the average human height in industrialised countries has increased by up to 10 centimetres (3.9 in). However, these increases appear to have largely levelled off. Before the mid-nineteenth century, there were cycles in height, with periods of increase and decrease; 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.In general, there were no significant differences in regional height levels throughout the nineteenth century. The only exceptions of 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. These differences did not disappear in the deglobalization period of the two World wars. Baten and Blum (2014)  find 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.
In the eighteenth and nineteenth centuries, people of European descent in North America were far taller than those in Europe and were the tallest in the world. The original indigenous population of Plains Native Americans was also among the tallest populations of the world at the time.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 age two.In the late nineteenth century, the Netherlands was a land renowned for its short population, but today Dutch people are among the worlds tallest with young men averaging 183.8 cm (6 ft 0.4 in) tall.According to a study by economist John Komlos and Francesco Cinnirella, 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).  The estimated mean height of English, German, and Scottish soldiers was 163.6 cm (5 ft 4+1⁄2 in) – 165.9 cm (5 ft 5+1⁄2 in) for the period as a whole, while that of Irish was 167.9 cm (5 ft 6 in).  The average height of male slaves and convicts in North America was 171 cm (5 ft 7+1⁄2 in).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. 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+1⁄2 in), the highest that has been observed.Data derived from burials show that before 1850, the mean stature of males and females in Leiden, The Netherlands was respectively 167.7 cm (5 ft 6 in) and 156.7 cm (5 ft 1+1⁄2 in). The average height of 19-year-old Dutch orphans in 1865 was 160 cm (5 ft 3 in).According to a study by J.W. Drukker and Vincent Tassenaar, the average height of a Dutch person decreased from 1830 to 1857, 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 (0.98 in). Urban mortality was also much higher than in rural regions. In 1829, the average urban and rural Dutchman was 164 cm (5 ft 4+1⁄2 in).  By 1856, the average rural Dutchman was 162 cm (5 ft 4 in) and urban Dutchman was 158.5 cm (5 ft 2+1⁄2 in).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. 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. A study by South Korean anthropologists of North Korean children who had defected to China found that eighteen-year-old males were 13 centimetres (5 in) shorter than South Koreans their age due to malnutrition.The tallest living man is Sultan Kösen of Turkey, at 251 cm (8 ft 3 in). The tallest man in modern history was Robert Pershing Wadlow (1918–1940), from Illinois, United States, who was 272 cm (8 ft 11 in) at the time of his death. The tallest woman in medical history was Trijntje Keever of Edam, Netherlands, who stood 254 cm (8 ft 4 in) when she died at the age of seventeen. The shortest adult human on record was Chandra Bahadur Dangi of Nepal at 54.6 cm (1 ft 9+1⁄2 in).
An anecdotal article titled "Ancient American Giants" from the 14 August 1880 edition of Scientific American notes a case from Brushcreek Township, Ohio, when Dr. J. F. Everhart supervised a team that discovered ancient clay coffins within a mound which were reported to contain skeletons of the following length: 8 ft 0 in (2.44 m) woman with a child 3.5 ft 0 in (1.07 m), a second coffin with a 9 ft 0 in (2.74 m) man and 8 ft 0 in (2.44 m) woman, a third coffin with a 9 ft 4 in (2.84 m) man and 8 ft 0 in (2.44 m) woman, and seven other independent skeletons measuring between 8 ft 0 in (2.44 m) and 10 ft 0 in (3.05 m). An image and stone tablet were found with the giants.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.

Average height around the world
As with any statistical data, the accuracy of such data may be questionable for various reasons:

Some studies may allow subjects to self-report values. Generally speaking, self-reported height tends to be taller than its measured height, although the overestimation of height depends on the reporting subjects height, age, gender and region.
Test subjects may have been invited instead of chosen randomly, resulting in sampling bias.
Some countries may have significant height gaps between different regions. For instance, one survey shows there is 10.8 cm (4+1⁄2 in) gap between the tallest state and the shortest state in Germany. 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 cm (1 in) taller, and university students are 2.55 cm (1 in) taller than the national average. As this case shows, data taken from a particular social group may not represent a total population in some countries.
A relatively small sample of the population may have been measured, which makes it uncertain whether this sample accurately represents the entire population.
The height of persons can vary over a day, due to factors such as a height increase from exercise done directly before measurement (normally inversely correlated), or a height increase since lying down for a significant period (normally inversely correlated). For example, one study revealed a mean decrease of 1.54 centimetres (0.61 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. Such factors may not have been controlled in some of the studies.
Men from Bosnia and Herzegovina, the Netherlands, Croatia, Serbia and Montenegro have the tallest average height.
Dinka people are sometimes noted for their height. With the Tutsi of Rwanda, they are believed to be the tallest people in Africa. Roberts and Bainbridge reported the average height of 182.6 cm (5 ft 11.9 in) in a sample of 52 Dinka Agaar and 181.3 cm (5 ft 11.4 in) in 227 Dinka Ruweng measured in 1953–1954.  Other studies of comparative historical height data and nutrition place the Dinka as the tallest people in the world.

Measurement
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. 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 and adults who can stand without assistance. Measure is done with a stadiometer. In general, standing height is about 0.7 cm (0.28 in) less than recumbent length.Surrogate height measurements are used when standing height and recumbent length are impractical. For sample Chumlea equation use knee height as indicator of stature. Other techniques include: arm span, sitting height, ulna length, etc.

See also
Anthropometry, the measurement of the human individual
Body weight
Economics and Human Biology (academic journal)
History of anthropometry
Human physical appearance
Human variability
Pygmy peoples

Citations
General bibliography
Grandjean, Etienne (1987). Fitting the Task to the Man: An Ergonomic Approach. London, UK: Taylor & Francis. ISBN 978-0-85066-192-7. (for heights in U.S. and Japan)
Eurostat Statistical Yearbook 2004. Luxembourg: Eurostat. 2014. ISBN 978-92-79-38906-1. (for heights in Germany)
Netherlands Central Bureau for Statistics, 1996 (for average heights)
Ogden, Cynthia L.; Fryar, Cheryl D.; Carroll, Margaret D. & Flegal, Katherine M. (27 October 2004). "Mean Body Weight, Height, and Body Mass Index, United States 1960–2002" (PDF). Advance Data from Vital and Health Statistics (347): 1–17. PMID 15544194.
"Health Survey for England – trend data". Department of Health and Social Care. Archived from the original on 10 October 2004.
Bilger, Burkhard (29 March 2004). "The Height Gap". The New Yorker. Archived from the original on 2 April 2004.
A collection of data on human height, referred to here as "karube" but originally collected from other sources, is archived here. A copy is available here (an English translation of this Japanese page would make it easier to evaluate the quality of the data...)
"Americans Slightly Taller, Much Heavier Than Four Decades Ago". National Center for Health Statistics. 27 October 2004.
Aminorroaya, A.; Amini, M.; Naghdi, H. & Zadeh, A. H. (2003). "Growth charts of heights and weights of male children and adolescents of Isfahan, Iran" (PDF). Journal of Health, Population, and Nutrition. 21 (4): 341–346. PMID 15038589. S2CID 21907084. Archived from the original (PDF) on 19 September 2018.
6. Celostátní antropologický výzkum dětí a mládeže 2001, Česká republika [6th Nationwide anthropological research of children and youth 2001, Czech Republic] (in Czech). Prague: State Health Institute (SZÚ). 2005. ISBN 978-8-07071-251-1.
Bogin, Barry (2001). The Growth of Humanity. Hoboken, NJ: Wiley-Liss. ISBN 978-0-471-35448-2.
Eveleth, P.B.; Tanner, J.M. (1990). Worldwide Variation in Human Growth (2nd ed.). Cambridge University Press. ISBN 978-0-521-35916-0.
Miura, K.; Nakagawa, H. & Greenland, P. (2002). "Invited commentary: Height-cardiovascular disease relation: where to go from here?". American Journal of Epidemiology. 155 (8): 688–689. doi:10.1093/aje/155.8.688. PMID 11943684.
Ruff, Christopher (October 2002). "Variation in human body size and shape". Annual Review of Anthropology. 31: 211–232. doi:10.1146/annurev.anthro.31.040402.085407.
"Los españoles somos 3,5 cm más altos que hace 20 años" [Spaniards are 3.5 cm taller than 20 years ago]. 20 minutos (in Spanish). 31 July 2006.
Krishan, K. & Sharma, J. C. (2002). "Intra-individual difference between recumbent length and stature among growing children". Indian Journal of Pediatrics. 69 (7): 565–569. doi:10.1007/BF02722678. PMID 12173694. S2CID 22427304.
Case, A. & Paxson, C. (2008). "Stature and Status: Height, ability, and labor market outcomes". The Journal of Political Economy. 116 (3): 499–532. doi:10.1086/589524. PMC 2709415. PMID 19603086.
Sakamaki, R.; Amamoto, R.; Mochida, Y.; Shinfuku, N. & Toyama, K. (2005). "A comparative study of food habits and body shape perception of university students in Japan and Korea". Nutrition Journal. 4: 31. doi:10.1186/1475-2891-4-31. PMC 1298329. PMID 16255785.
Habicht, Michael E.; Henneberg, Maciej; Öhrström, Lena M.; Staub, Kaspar & Rühli, Frank J. (27 April 2015). "Body height of mummified pharaohs supports historical suggestions of sibling marriages". American Journal of Physical Anthropology. 157 (3): 519–525. doi:10.1002/ajpa.22728 </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Bifid nose and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pellegrini–Stieda syndrome and explain in detail? [/INST] Pellegrini–Stieda syndrome (also called Stieda disease and Köhler–Pellegrini–Stieda disease) refers to the ossification of the superior part of the medial collateral ligament of the knee. It is a common incidental finding on knee radiographs.  It is named for the Italian surgeon A. Pellegrini (b. 1877) and the German surgeon A. Stieda (1869–1945).

References
Further reading
Altschuler, Eric L.; Bryce, Thomas N. (December 2006) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Inferior vena cava syndrome and explain in detail? [/INST] Inferior vena cava syndrome (IVCS) is a very rare constellation of symptoms resulting from either an obstruction, or stenosis of the inferior vena cava. It can be caused by physical invasion or compression by a pathological process or by thrombosis within the vein itself. It can also occur during pregnancy. Pregnancy leads to high venous pressure in the lower limbs, decreased blood return to the heart, decreased cardiac output due to obstruction of the inferior vena cava, sudden rise in venous pressure which can lead to placental separation, and a decrease in kidney function.  All of these issues can arise from lying in the supine position during late pregnancy which can cause compression of the inferior vena cava by the uterus. Symptoms of late pregnancy inferior vena cava syndrome consist of intense pain in the right hand side, muscle twitching, hypotension, and fluid retention.

Signs and symptoms
IVCS presents with a wide variety of signs and symptoms, making it difficult to diagnose clinically.
Edema of the lower extremities (peripheral edema), caused by an increase in the venous blood pressure.
Tachycardia. This is caused by the decreased preload, decreased cardiac output, and leads to increased frequency.
In pregnant women, signs of fetal hypoxia and distress may be seen in the cardiotocography </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Vanishing bile duct syndrome and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Chronic mountain sickness and explain in detail? [/INST] Chronic mountain sickness (CMS) is a disease in which the proportion of blood volume that is occupied by red blood cells increases (polycythaemia) and there is an abnormally low level of oxygen in the blood (hypoxemia). CMS typically develops after extended time living at high altitude (over 2,500 metres (8,200 ft)) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Desmoplastic trichoepithelioma and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Meconium and explain in detail? [/INST] Meconium is the earliest stool of a mammalian infant resulting from defecation. Unlike later feces, meconium is composed of materials ingested during the time the infant spends in the uterus: intestinal epithelial cells, lanugo, mucus, amniotic fluid, bile, and water. Meconium, unlike later feces, is viscous and sticky like tar – its color usually being a very dark olive green and it is almost odorless. When diluted in amniotic fluid, it may appear in various shades of green, brown, or yellow. It should be completely passed by the end of the first few days after birth, with the stools progressing toward yellow (digested milk).

Clinical significance
Meconium in amniotic fluid
Meconium is normally retained in the infants bowel until after birth, but sometimes it is expelled into the amniotic fluid (also called "amniotic liquor") prior to birth or during labor and delivery. The stained amniotic fluid (called "meconium liquor" or "meconium-stained liquor") is recognized by medical staff as a possible sign of fetal distress. Some post-dates pregnancies (when they are more than 40 weeks pregnant) may also have meconium-stained liquor without fetal distress. Medical staff may aspirate the meconium from the nose and mouth of a newborn immediately after delivery in the event the baby shows signs of respiratory distress to decrease the risk of meconium aspiration syndrome, which can occur in meconium-stained amniotic fluid.
Most of the time that the amniotic fluid is stained with meconium, it will be homogeneously distributed throughout the fluid, making it brown. This indicates that the fetus passed the meconium some time ago such that sufficient mixing occurred as to establish the homogeneous mixture. Terminal meconium occurs when the fetus passes the meconium a short enough time before birth/cesarean section that the amniotic fluid remains clear, but individual clumps of meconium are in the fluid.

Failure to pass meconium
The failure to pass meconium is a symptom of several diseases including Hirschsprungs disease and cystic fibrosis.
The meconium sometimes becomes thickened and congested in the intestines, a condition known as meconium ileus. Meconium ileus is often the first sign of cystic fibrosis. In cystic fibrosis, the meconium can form a bituminous black-green mechanical obstruction in a segment of the ileum. Beyond this, there may be a few separate grey-white globular pellets. Below this level, the bowel is a narrow and empty micro-colon. Above the level of the obstruction, there are several loops of hypertrophied bowel distended with fluid. No meconium is passed, and abdominal distension and vomiting appear soon after birth. About 20% of cases of cystic fibrosis present with meconium ileus, while approximately 20% of one series of cases of meconium ileus did not have cystic fibrosis. The presence of meconium ileus is not related to the severity of the cystic fibrosis. The obstruction can be relieved in a number of different ways.Meconium ileus should be distinguished from meconium plug syndrome, in which a tenacious mass of mucus prevents the meconium from passing and there is no risk of intestinal perforation </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Danon disease and explain in detail? [/INST] Danon disease (or glycogen storage disease Type IIb) is a metabolic disorder. Danon disease is an X-linked lysosomal and glycogen storage disorder associated with hypertrophic cardiomyopathy, skeletal muscle weakness, and intellectual disability. It is inherited in an X-linked dominant pattern.

Symptoms and signs
Males
In males the symptoms of Danon Disease are more severe. Features of Danon Disease in males are:
An early age of onset of muscle weakness and heart disease (onset in childhood or adolescence)
Some learning problems or intellectual disability can be present
Muscle weakness can be severe and can affect endurance and the ability to walk
Heart disease (cardiomyopathy) can be severe and can lead to a need for medications. It usually progress to heart failure, commonly complicated by atrial fibrillation and embolic strokes with severe neurological disability, leading to death unless heart transplant is performed.
Cardiac conduction abnormalities can occur. Wolff-Parkinson-White syndrome is a common conduction pattern in Danon disease.
Symptoms are usually gradually progressive
Some individuals may have visual disturbances, and/or retinal pigment abnormalities
Danon Disease is rare and unfamiliar to most physicians. It can be mistaken for other forms of heart disease and/or muscular dystrophies, including Pompe disease.Females
In females the symptoms of Danon Disease are less severe. Common symptoms of Danon Disease in females are:
A later age of onset of symptoms. Many females will not have obvious symptoms until late adolescence or even adulthood.
Learning problems and intellectual disability are usually absent.
Muscle weakness is often absent or subtle. Some females will tire easily with exercise
Cardiomyopathy is often absent in childhood. Some women will develop this in adulthood. Cardiomyopathy can be associated with atrial fibrillation and embolic strokes.
Cardiac conduction abnormalities can occur. Wolff-Parkinson-White syndrome is a common conduction pattern in Danon disease.
Symptoms in females progress more slowly than in males.
Some females may have visual disturbances, and/or retinal pigment abnormalities
Danon Disease is rare and unfamiliar to most physicians. The milder and more subtle symptoms in females can make it more difficult to diagnose females with Danon Disease

Causes
Although the genetic cause of Danon Disease is known, the mechanism of disease is not well understood. Danon disease involves a genetic defect (mutation) in a gene called LAMP2, which results in a change to the normal protein structure. While the function of the LAMP2 gene is not well understood, it is known that LAMP2 protein is primarily located in small structures within cells called lysosomes.

Genetics
It is associated with LAMP2. The status of this condition as a GSD has been disputed.

Diagnosis
Making a diagnosis for a genetic or rare disease can often be challenging. Healthcare professionals typically look at a persons medical history, symptoms, physical exam, and laboratory test results in order to make a diagnosis. The following resources provide information relating to diagnosis and testing for this condition </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Granulomatous prostatitis and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Restrictive lung disease and explain in detail? [/INST] Restrictive lung diseases  are a category of extrapulmonary, pleural, or parenchymal respiratory diseases that restrict lung expansion, resulting in a decreased lung volume, an increased work of breathing, and inadequate ventilation and/or oxygenation. Pulmonary function test demonstrates a decrease in the forced vital capacity.

Presentation
Due to the chronic nature of this disease, the leading symptom of restrictive lung disease is progressive exertional dyspnea.  For acute on chronic cases, shortness of breath, cough, and respiratory failure are some of the more common signs.

Causes
Restrictive lung diseases may be due to specific causes which can be intrinsic to the parenchyma of the lung, or extrinsic to it.

Intrinsic
Pneumoconiosis caused by long-term exposure to dusts, especially in mining. For example, Asbestosis.
Radiation fibrosis, usually from the radiation given for cancer treatment.
Certain drugs such as amiodarone, bleomycin and methotrexate.
As a consequence of another disease such as rheumatoid arthritis.
Hypersensitivity pneumonitis due to an allergic reaction to inhaled particles.
Acute respiratory distress syndrome (ARDS), a severe lung condition occurring in response to a critical illness or injury.
Infant respiratory distress syndrome due to a deficiency of surfactant in the lungs of a baby born prematurely.
TuberculosisMany cases of restrictive lung disease are idiopathic (have no known cause). Still, there is generally pulmonary fibrosis. Examples are:

Idiopathic pulmonary fibrosis
Idiopathic interstitial pneumonia, of which there are several types
Sarcoidosis
Eosinophilic pneumonia
Lymphangioleiomyomatosis
Pulmonary Langerhans cell histiocytosis
Pulmonary alveolar proteinosisConditions specifically affecting the interstitium are called interstitial lung diseases.

Extrinsic
Nonmuscular diseases of the upper thorax such as kyphosis, pectus carinatum and pectus excavatum.
Diseases restricting lower thoracic/abdominal volume (e.g. obesity, diaphragmatic hernia, or the presence of ascites).
Pleural thickening.

Pathophysiology
In normal respiratory function, the air flows in through the upper airway, down through the bronchi and into the lung parenchyma (the bronchioles down to the alveoli) where gas exchange of carbon dioxide and oxygen occurs </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Urolagnia and explain in detail? [/INST] Urolagnia (also urophilia, and, more colloquially, a golden shower or watersports) associates sexual excitement with the sight or thought of urine or urination, and may also refer to such behaviours or acts. It is a paraphilia.The term has origins in the Greek language (from ouron, "urine", and lagneia, "lust").Golden shower is slang for the practice of urinating on another person for sexual pleasure.

Overview
Urolagnia is an inclination to derive sexual satisfaction from the vision or idea of urination. It is a paraphilia. During the activity, urine may be consumed or the person may bathe in it. Other variations include arousal from wetting or seeing someone else urinate in their pants or underclothes, or wetting the bed. Other forms of urolagnia may involve a tendency to be sexually aroused by smelling urine-soaked clothing or body parts. In many cases, a strong correlation or conditioning arises between urine smell or sight, and the sexual act. For some individuals the phenomenon may include a diaper fetish and/or arousal from infantilism.
Urolagnia is sometimes associated with, or confused with the Japanese practice of omorashi, arousal from having a full bladder or a sexual attraction to someone else experiencing the discomfort or pain of a full bladder, possibly a sadomasochistic inclination.

Common variations
Golden shower: A shower or stream of urine is directed onto another person or persons.
Clothes wetting: The person is sexually aroused by wetting ones clothing or observing another person doing so. Usually that person prefers to stage the wetting so that his/her legs (or other body parts) become soaked with urine. The warm sensation felt when urine trickles on the body seems to give very relaxing and pleasurable feelings to the person. In many cases, that person is also aroused by smelling body parts that have a urine scent. Others get aroused by telling some people about when they lost control and wet themselves. Some prefer a particular type of clothing to urinate.
Exhibitionism: Becoming noticeably desperate or wetting oneself with the express purpose of being seen by strangers. Practitioners have described going to public places such as a mall or a park. Some intend to create situations where others can see their wet clothing.
Human urinal: Within the BDSM community, some individuals desire to be used as a human urinal and some desire to use a human urinal.  The submissive  is usually strictly forbidden from placing their lips directly on the body of the dominant so the practice routinely involves them receiving much of the spray all over their face, hair and body; however, another way of doing this that applies mostly to male dominants, is to place the mouth on the head of the penis and drink the urine as it is released. One other, less common variation of this kink involves the dominant partner urinating inside the submissive partners vagina or anus, which is usually followed up by the submissive partner ejecting the urine from their orifice(s).
Omorashi: The act of holding ones own urine until the need to urinate is urgent, making another hold in their urine, or watching another person with an urgent need to urinate. This fetish sometimes originates from childhood memories of needing, or of seeing another needing, to urinate. Arousal may be triggered by seeing the body movements or facial expressions of that person. It can also be heightened by the person saying that they have to urinate. The arousal from being desperate comes from the sensation of having a full bladder.
Voyeurism: Seeing another urinate without the persons knowledge either through video taping by a hidden camera, or by lurking in locations where people are urinating or are likely to have an urge to urinate.

Frequency
Jennifer Eve Rehor of San Francisco State University points out that such data as exists on what she calls "unconventional" or "kink" sexual behavior is generally problematic because of the way that it has been collected, through criminal and clinical case studies. Behavior that appears neither in criminal trials nor in clinical studies (for example, because the individuals concerned do not commonly seek professional help) is therefore under-reported. Rehor therefore surveyed 1,764 female participants in "kink" behavior (mostly association with BDSM) in 2010–11, receiving 1,580 valid responses </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Uterine hypoplasia and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Nasal concha and explain in detail? [/INST] In anatomy, a nasal concha (), plural conchae (), also called a nasal turbinate or turbinal, is a long, narrow, curled shelf of bone that protrudes into the breathing passage of the nose in humans and various animals. The conchae are shaped like an elongated seashell, which gave them their name (Latin concha from Greek κόγχη). A concha is any of the scrolled spongy bones of the nasal passages in vertebrates.In humans, the conchae divide the nasal airway into four groove-like air passages, and are responsible for forcing inhaled air to flow in a steady, regular pattern around the largest possible surface area of nasal mucosa. As a ciliated mucous membrane with shallow blood supply, the nasal mucosa cleans and warms the inhaled air in preparation for the lungs.
A rapidly dilating arteriolar circulation to these bones may lead to a sharp increase in the pressure within, in response to acute cooling of the body core. The pain from this pressure is often referred to as "brain freeze", and is frequently associated with the rapid consumption of ice cream. The shallowness of the venous blood supply of the mucosa contributes to the ease with which nosebleed can occur.

Structure
Conchae are composed of pseudostratified columnar, ciliated respiratory epithelium with a thick, vascular, and erectile glandular tissue layer. The conchae are located laterally in the nasal cavities, curling medially and downward into the nasal airway. Each pair is composed of one concha in either side of the nasal cavity, divided by the septum.The superior conchae are smaller structures, connected to the middle conchae by nerve-endings, and serve to protect the olfactory bulb.  The openings to the posterior ethmoidal sinuses exist under the superior meatus.The middle conchae are smaller. In humans, they are usually as long as the little finger. They project downwards over the openings of the maxillary and anterior and middle ethmoid sinuses, and act as buffers to protect the sinuses from coming in direct contact with pressurized nasal airflow. Most inhaled airflow travels between the inferior concha and the middle meatus.The inferior conchae are the largest, and can be as long as the index finger in humans, and are responsible for the majority of airflow direction, humidification, heating, and filtering of air inhaled through the nose.The inferior conchae are graded 1–4 based on the inferior concha classification system (known as the inferior turbinate classification system) in which the total amount of the airway space that the inferior concha takes up is estimated. Grade 1 is 0–25% of the airway, grade 2 is 26–50% of the airway, grade 3 is 51–75% of the airway and grade 4 is 76–100% of the airway.There is sometimes a pair of supreme conchae superior to the superior conchae. When present, these usually take the form of a small crest.

Function
The conchae comprise most of the mucosal tissue of the nose and are required for functional respiration. They are enriched with airflow pressure and temperature-sensing nerve receptors (linked to the trigeminal nerve route, the fifth cranial nerve), allowing for tremendous erectile capabilities of nasal congestion and decongestion, in response to the weather conditions and changing needs of the body. In addition, the erectile tissue undergoes an often unnoticed cycle of partial congestion and decongestion called the nasal cycle. The flow of blood to the nasal mucosa in particular the venous plexus of the conchae is regulated by the pterygopalatine ganglion and heats or cools the air in the nose.
The nasopulmonary and nasothoracic reflexes regulate the mechanism of breathing through deepening of inhalation. Triggered by the flow of the air, the pressure of the air in the nose, and the quality of the air, impulses from the nasal mucosa are transmitted by the trigeminal nerve to the breathing centres in the brainstem, and the generated response is transmitted to the bronchi, the intercostal muscles, and the diaphragm.
The conchae are also responsible for filtration, heating, and humidification of air inhaled through the nose. Of these three, filtration is achieved mostly by other more effective means such as mucous and cilia. As air passes over the conchae, it is heated to 32–34 °C (89–93 °F), humidified (up to 98% water saturation) and filtered.

Immunological role
The respiratory epithelium that covers the erectile tissue (or lamina propria) of the conchae plays a major role in the bodys first line of immunological defense. The respiratory epithelium is partially composed of mucus-producing goblet cells. This secreted mucus covers the nasal cavities, and serves as a filter, by trapping air-borne particles larger than 2 to 3 micrometers. The respiratory epithelium also serves as a means of access for the lymphatic system, which protects the body from being infected by viruses or bacteria.

Smell
The conchae provide, first and foremost, the humidity needed to preserve the delicate olfactory epithelium, which in turn is needed to keep the olfactory receptors healthy and alert. If the epithelial layer gets dry or irritated, it may cease to function. This is usually a temporary condition but, over time, may lead to chronic anosmia. The turbinates also increase the surface area of the inside of the nose, and, by directing and deflecting airflow across the maximum mucosal surface of the inner nose, they are able to propel the inspired air. This, coupled with the humidity and filtration provided by the conchae, helps to carry more scent molecules towards the higher, and very narrow regions of the nasal airways, where olfaction nerve receptors are located.The superior conchae completely cover and protect the nerve axons piercing through the cribriform plate (a porous bone plate that separates the nose from the brain) into the nose. Some areas of the middle conchae are also innervated by the olfactory bulb. All three pairs of conchae are innervated by pain and temperature receptors, via the trigeminal nerve (or, the fifth cranial nerve). Research has shown that there is a strong connection between these nerve endings and activation of the olfactory receptors, but science has yet to fully explain this interaction.

Clinical significance
Dysfunction
Large, swollen conchae, often referred to clinically as turbinates, may lead to blockage of nasal breathing. Allergies, exposure to environmental irritants, or a persistent inflammation within the sinuses can lead to turbinate swelling. Deformity of the nasal septum can also result in enlarged turbinates.Treatment of the underlying allergy or irritant may reduce turbinate swelling. In cases that do not resolve, or for treatment of deviated septum, turbinate surgery may be required.

Surgery
Turbinectomy is a surgery for the reduction or removal of the turbinates. There are different techniques, including bipolar radiofrequency ablation, also known as somnoplasty;  reduction by the use of pure heat;  and turbinate sectioning.
In the case of sectioning, only small amounts of turbinate tissue are removed because the turbinates are essential for respiration. Risks of reduction of the inferior or middle turbinates include empty nose syndrome. Dr. Houser: "this is especially true in cases of anterior inferior turbinate (IT) resection because of its important role in the internal nasal valve."Concha bullosa is an abnormal pneumatization of the middle turbinate, which may interfere with normal ventilation of the sinus ostia and can result in recurrent sinusitis.

Other animals
Generally, in animals, nasal conchae are convoluted structures of thin bone or cartilage located in the nasal cavity. These are lined with mucous membranes that can perform two functions. They can improve the sense of smell by increasing the area available to absorb airborne chemicals, and they can warm and moisten inhaled air, and extract heat and moisture from exhaled air to prevent desiccation of the lungs. Olfactory turbinates are found in all living tetrapods, and respiratory turbinates are found in most mammals and birds.
Animals with respiratory turbinates can breathe faster without drying out their lungs, and consequently can have a faster metabolism. For example, when the emu exhales, its nasal turbinates condense moisture from the air and absorbs it for reuse. Dogs and other canids possess well-developed nasal turbinates. These turbinates allow for heat exchange between small arteries and veins on their maxilloturbinate (turbinates positioned on maxilla bone) surfaces in a counter-current heat-exchange system. Dogs are capable of prolonged chases, in contrast to the ambush predation of cats, and these complex turbinates play an important role in enabling this (cats only possess a much smaller and less-developed set of nasal turbinates). This same complex turbinate structure help conserve water in arid environments. The water conservation and thermoregulatory capabilities of these well-developed turbinates in dogs may have been crucial adaptations that allowed dogs (including both domestic dogs and their wild prehistoric gray wolf ancestors) to survive in the harsh Arctic environment and other cold areas of northern Eurasia and North America, which are both very dry and very cold.Reptiles and more primitive synapsids have olfactory turbinates that are involved in sensing smell rather than preventing desiccation.  While the maxilloturbinates of mammals are located in the path of airflow to collect moisture, sensory turbinates in both mammals and reptiles are positioned farther back and above the nasal passage, away from the flow of air. Glanosuchus has ridges positioned low in the nasal cavity, indicating that it had maxilloturbinates that were in the direct path of airflow. The maxilloturbinates may not have been preserved because they were either very thin or cartilaginous. The possibility has also been raised that these ridges are associated with an olfactory epithelium rather than turbinates. Nonetheless, the possible presence of maxilloturbinates suggests that Glanosuchus may have been able to rapidly breathe without drying out the nasal passage, and therefore could have been an endotherm.The bones of nasal turbinates are very fragile and seldom survive as fossils. In particular none have been found in fossil birds </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Left anterior fascicular block and explain in detail? [/INST] Left anterior fascicular block (LAFB) is an abnormal condition of the left ventricle of the heart, related to, but distinguished from, left bundle branch block (LBBB).
It is caused by only the left anterior fascicle – one half of the left bundle branch being defective. It is manifested on the ECG by left axis deviation </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Sudden arrhythmic death syndrome and explain in detail? [/INST] Sudden arrhythmic death syndrome (SADS) is a sudden unexpected death of adolescents and adults, mainly during sleep. One relatively common type is known as Brugada syndrome.The syndrome is rare in most areas around the world but occurs in populations that are culturally and genetically distinct. It was first noted in 1977 among southeast Asian Hmong refugees in the United States and Canada. The syndrome was again noted in Singapore when a retrospective survey of records showed that 230 otherwise healthy Thai foreign workers living in Singapore died suddenly of unexplained causes between 1982 and 1990.

Causes
A sudden death in a young person can be caused by heart disease (including cardiomyopathy, congenital heart disease, myocarditis, genetic connective tissue disorders) or conduction disease (WPW syndrome, etc.), medication-related causes or other causes. Rare diseases called ion channelopathies may play a role such as long QT syndrome (LQTS), Brugada syndrome (BrS), CPVT (catecholaminergic polymorphic ventricular tachycardia), PCCD (progressive cardiac conduction defect), early repolarization syndrome, mixed sodium channel disease, and short QT syndrome. In 20% of cases, no cause of death can be found, even after extensive examination.In young people with type 1 diabetes, unexplained deaths could be attributed to night time hypoglycemia triggering abnormal heart rhythms or cardiac autonomic neuropathy, a damage to nerves that control the function of the heart.Medical examiners have taken into account various factors, such as nutrition, toxicology, heart disease, metabolism, and genetics. Although there is no real known definite cause, extensive research showed people 18 years or older were found to have had a hypertrophic cardiomyopathy, a condition in which the heart muscle becomes oddly thickened without any obvious cause. This was the most commonly identified abnormality in sudden death of young adults. In the instances where people experience sudden death, it is most commonly found that they had had CAD (coronary artery disease) or ASCAD (atherosclerotic coronary artery disease), or any level of stress. However, studies reveal that people experienced early symptoms within the week before the terminal event such as chest pain at ~52% of patients, dyspnea at ~22%, syncope at ~7% and ~19% who experienced no symptoms. Scientists have also associated this syndrome with the gene SCN5A that is mutated and affects the function of the heart. However, all autopsies done on those who had this syndrome came back negative.In the Philippines, bangungot (or in their term, sudden adult death syndrome) is mainly caused by the Brugada syndrome.

Diagnosis
Diagnosis occurs post-mortem.

Treatment
The only proven way to prevent SADS is with an implantable cardioverter-defibrillator. Oral beta-blockers such as propranolol are ineffective.

Epidemiology
In 1980, a reported pattern of sudden deaths was brought to the attention of the Centers for Disease Control. The first reported sudden death occurred in 1948 when there were 81 similar deaths of Filipino men in Oahu County, Hawaii. However, it did not become relevant because there was no associated pattern. This syndrome continued to become more significant as years went on. By 1981–1982, the annual rate in the United States was high with 92/100,000 among Laotians-Hmong, 82/100,000 among other Laotian ethnic groups, and 59/100,000 among Cambodians.In a 2008 study it was found that over half of SADS deaths could be attributed to inherited heart disease: unexplained premature sudden deaths in family, long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy and others.A national SADS study in England, funded by the British Heart Foundation, reported results in a 2007 journal article published in Health. The study surveyed 117 coroners jurisdictions in England. Researchers found that deaths from SADS reported by these coroners occurred "predominantly in young males". There were 500 cases a year in England, which is 8 times more than was previously estimated. Families are more at risk of SADS if they have a genetic cardiac disease. The study recommended that affected families should undergo "specialised cardiological evaluation".

Asia
Southeast Asian immigrants, who were mostly fleeing the Vietnam War, most often had this syndrome, marking Southeast Asia as the area containing the most people with this fatal syndrome. There are other Asian populations that were affected, such as Filipinos and Chinese Filipinos, Japanese in Japan, and natives of Guam in the United States and Guam. The immigrants with  this syndrome were about 33 years old and seemingly healthy, and all but one of the Laotian Hmong refugees were men. The condition appears to primarily affect young Hmong men from Laos (median age 33) and Northeastern Thailand (where the population is mainly of Laotian descent).

History
Laotian Hmongs were chosen for the study because they had one of the highest sudden death rates in the United States while sleeping. They were originally from Southern China and the highlands of North Vietnam, Laos, and Thailand. The location that was picked for this study was in Ban Vinai in the Loei Province, which is approximately 15 kilometers from the Lao border. This study took place between October 1982 and June 1983 as this syndrome became more of a pressing issue. Ban Vinai was the location chosen because it had 33,000 refugees in 1982, and the largest number of recorded SADS deaths. Because this syndrome was occurring most commonly in those particular men, researchers found it most beneficial and effective to study the populations they migrated from instead of studying victims and populations in the U.S. Because of local religious practices, the Hmong men in Ban Vinai did not receive autopsies. Therefore, the only results and research obtained were relating to deaths outside of the local religion or geographical area.An interview was arranged with the next of kin who lived with them, witnessed the death, or found the body. The interviews were open ended and allowed the person who was next of kin to describe what they witnessed and what preceding events they thought were relevant to the victims death. The interviewers also collected information such as illness history, the circumstances of the death, demographic background, and history of any sleep disturbances. A genealogy was then created which included all the relatives and their vital status and/or circumstances of death.

Society and culture
During the 1970s and 1980s, when an outbreak of this syndrome began, many Southeast Asians were not able to worship properly due to the Laotian Civil War. Hmong people believe that when they do not worship properly, do not perform religious rituals properly or forget to sacrifice, the ancestor spirits or the village spirits do not protect them, thus allowing evil spirit to reach them. These attacks induce a nightmare that leads to sleep paralysis, in which the victim is conscious and experiencing pressure on the chest. It is also common to have a REM state that is out of sequence, where there is a mix of brain states that are normally held separate. After the war, the United States government scattered the Hmong refugees across the U.S. in 53 different cities. Once these nightmare visitations began, a shaman was recommended for psychic protection from the spirits of their sleep. However, scattered across 53 different cities, these victims had no access to a shaman who could protect them.
Hmong people believed that rejecting the role of becoming a shaman, they are taken into the spirit world.The study author suggested that the Hmong who died were killed by their own beliefs in the spiritual world, otherwise known as Nocturnal pressing spirit attacks. In Indonesia it is called digeuton, which translates to "pressed on" in English </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Median raphe cyst and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Neurofibromatosis type II and explain in detail? [/INST] Neurofibromatosis type II (also known as MISME syndrome – multiple inherited schwannomas, meningiomas, and ependymomas) is a genetic condition that may be inherited or may arise spontaneously, and causes benign tumors of the brain, spinal cord, and peripheral nerves. The types of tumors frequently associated with NF2 include vestibular schwannomas, meningiomas, and ependymomas. The main manifestation of the condition is the development of bilateral benign brain tumors in the nerve sheath of the cranial nerve VIII, which is the "auditory-vestibular nerve" that transmits sensory information from the inner ear to the brain. Besides, other benign brain and spinal tumors occur. Symptoms depend on the presence, localisation and growth of the tumor(s), in which multiple cranial nerves can be involved. Many people with this condition also experience vision problems. Neurofibromatosis type II (NF2 or NF II) is caused by mutations of the "Merlin" gene, which seems to influence the form and movement of cells. The principal treatments consist of neurosurgical removal of the tumors and surgical treatment of the eye lesions. Historically the underlying disorder has not had any therapy due to the cell function caused by the genetic mutation.

Classification
NF2 is an inheritable disorder with an autosomal dominant mode of transmission.There are two forms of the NF2:
The Wishart-phenotype form is characterized by multiple cerebral and spinal lesions in people younger than 20 years and with rapid progression of the tumours.
People with NF2 who develop single central tumours with slow progression after the age of 20 are thought to have the Feiling–Gardner phenotype.

Symptoms and signs
Symptoms can occur at any age, typically in adolescence and early adulthood, and rarely seen in children, and severity depend on the location of the tumors. Symptoms include but are not limited to:
Tinnitus
Loss/problems of balance
Glaucoma
Seizures
Hearing loss
Vision impairment
Numbness or weakness in arms and legs

Hearing loss
Because hearing loss in those with NF2 almost always occurs after acquisition of verbal language skills, people with NF2 do not always integrate well into Deaf culture and are more likely to resort to auditory assistive technology.
One of these devices is the cochlear implant, which can sometimes restore a high level of auditory function even when natural hearing is totally lost. However, the amount of destruction to the cochlear nerve caused by the typical NF2 schwannoma often precludes the use of such an implant. In these cases, an auditory brainstem implant (ABI) can restore some level of hearing, supplemented by lip reading.

Cause
NF2 is caused by inactivating mutations in the NF2 gene located at 22q12.2 of chromosome 22, type of mutations vary and include protein-truncating alterations (frameshift deletions/insertions and nonsense mutations), splice-site mutations, missense mutations and others. Deletions, too, in the NH2-terminal domain of merlin proteins have been associated with early tumor onset and poor prognosis in people with NF2. Protein truncating mutations correlate with more severe phenotype.  There is a broad clinical spectrum known, but all people with the condition who have been checked have been found to have some mutation of the same gene on chromosome 22. Through statistics, it is suspected that one-half of cases are inherited, and one-half are the result of new,  de novo mutations.

Cause loss of hearing
The hearing loss caused by NF2 is gradual and results from the presences of bilateral cochleovestibular schwannomas, also known as acoustic neuromas, which damage to cochlear nerve causing hearing loss. Hearing loss may also result from benign tumors that grow on the vestibular and auditory nerves, which lead to the inner ear.

Pathogenesis
NF2 is caused by a defect in the gene that normally gives rise to a product called Merlin or Schwannomin, located on chromosome 22 band q11-13.1. Merlin was first discovered as a structural protein functioning as an actin cytoskeleton regulator. Later merlins tumour suppressant role was described. Merlin regulates multiple proliferative signalling cascades such as receptor tyrosine kinase signalling, p21-activated kinase signalling, Ras signalling, MEK-ERK cascade, MST-YAP cascade. In a normal cell, the concentrations of active (dephosphorylated) merlin are controlled by processes such as cell adhesion (which would indicate the need to restrain cell division). It has been shown that Merlin inhibits Rac1 which is crucial for cell motility and tumour invasion. Also, merlins interaction with cyclin D was described. It is known that Merlins deficiency can result in unmediated progression through the cell cycle due to the lack of contact-mediated tumour suppression, mainly because of the cell:cell junction disruption, sufficient to result in the tumors characteristic of Neurofibromatosis type II. Recent studies showed that besides its cytoskeletal and cytoplasmic functions Merlin also translocates to the nucleus and suppresses proliferation by inhibiting E3 ubiquitin ligase CRL4(DCAF1). Finally, most recent studies indicated that Merlin also plays important role in energy metabolism regulation. Mutations of NF2 is presumed to result in either a failure to synthesize Merlin or the production of a defective peptide that lacks the normal tumor-suppressive effect. The Schwannomin-peptide consists of 595 amino acids. Comparison of Schwannomin with other proteins shows similarities to proteins that connect the cytoskeleton to the cell membrane. Mutations in the Schwannomin-gene are thought to alter the movement and shape of affected cells with loss of contact inhibition.
Ependymomas are tumors arising from the ependyma, an epithelium-like tissue of the central nervous system. In people with NF2 and ependymomas, the tumor suppressant function of Merlin may be compromised. Loss of function mutations occurring in chromosome 22q, where Merlin proteins are coded, can promote tumorigenesis, or the creation of new tumorous cells. Deletions, too, in the NH2-terminal domain of merlin proteins have been associated with early tumor onset and poor prognosis in affected people.

Pathology
The so-called acoustic neuroma of NF2 is in fact a schwannoma of the nervus vestibularis, or vestibular schwannoma. The misnomer of acoustic neuroma is still often used. The vestibular schwannomas grow slowly at the inner entrance of the internal auditory meatus (meatus acousticus internus). They derive from the nerve sheaths of the upper part of the nervus vestibularis in the region between the central and peripheral myelin (Obersteiner-Redlich-Zone) within the area of the porus acousticus, 1 cm from the brainstem.

Genotype–phenotype correlation
Many people with NF2 were included in studies that were designed to compare disease type and progression with exact determination of the associated mutation. The goal of such comparisons of genotype and phenotype is to determine whether specific mutations cause respective combinations of symptoms. This would be extremely valuable for the prediction of disease progression and the planning of therapy starting at a young age. The results of such studies are the following:
In most cases the mutation in the NF2 gene causes shortened peptides.
There are no mutational hot spots.
People with frameshift mutations or nonsense mutations have poor prognosis.
People with missense mutations have a better prognosis.
In cases with mutations in the splice-acceptor-region, there is no good correlation to determine.
Point mutations may have only minor effects.
Cases are published in which exactly the same mutation is associated with clearly different outcomes.These results suggest that other factors (environment, other mutations) will probably determine the clinical outcome.

Diagnosis
NF2 is a genetically transmitted condition. Diagnosis is most common in early adulthood (20–30 years); however, it can be diagnosed earlier. NF2 can be diagnosed due to the presence of a bilateral vestibular schwannoma, or an acoustic neuroma, which causes a hearing loss that may begin unilaterally. If a patient does not meet this criterion of diagnosis, they must have a family history of NF2, and present with a unilateral vestibular schwannoma and other associated tumors (cranial meningioma, cranial nerve schwannoma, spinal meningioma, spinal ependymomas, peripheral nerve tumor, spinal schwannoma, subcutaneous tumor, skin plaque). This being said, more than half of all patients diagnosed with NF2 do not have a family history of the condition. Although it has yet to be included into clinical classification, peripheral neuropathy, or damage to the peripheral nerves, which often causes weakness, numbness and pain in the hands and feet, may also lead to a diagnosis of NF2. In children, NF2 can present with similar symptoms, but generally causes "visual disturbances (cataracts, hamartomas), skin tumors, mononeuropathhy (facial paresis, drop foot), symptomatic spinal cord tumors, or non-vestibular intracranial tumors".

Prenatal
Bilateral vestibular schwannomas are diagnostic of NF2.

Postnatal
Ferner et al.  give three sets of diagnostic criteria for NF2:

Bilateral vestibular schwannoma (VS) or family history of NF2 plus Unilateral VS or any two of: meningioma, glioma, neurofibroma, schwannoma, posterior subcapsular lenticular opacities
Unilateral VS plus any two of meningioma, glioma, neurofibroma, schwannoma, posterior subcapsular lenticular opacities
Two or more meningioma plus unilateral VS or any two of glioma, schwannoma and cataract.Another set of diagnostic criteria is the following:
Detection of bilateral acoustic neuroma by imaging-procedures
First degree relative with NF2 and the occurrence of neurofibroma, meningiomas, glioma, or Schwannoma
First degree relative with NF2 and the occurrence of juvenile posterior subcapsular cataract.The criteria have varied over time.
The last revision of the NF2 criteria was done by M.J. Smith in 2017. This included the consideration of a LZTR1 mutation (schwannomatosis) instead of NF2 and excluded bilateral vestibular schwannomas that occur after 70 years of age.

Treatment
Surgery
There are several different surgical techniques for the removal of acoustic neuroma. The choice of approach is determined by size of the tumour, hearing capability, and general clinical condition of the person.

The retrosigmoid approach offers some opportunity for the retention of hearing.
The translabyrinthine approach will sacrifice hearing on that side, but will usually spare the facial nerve. Post-operative cerebrospinal fluid leaks are more common.
The middle fossa approach is preferred for small tumors and offers the highest probability of retention of hearing and vestibular function.
Less invasive endoscopic techniques have been done outside of the United States for some time. Recovery times are reported to be faster. However, this technique is not yet mainstream among surgeons in the US.Larger tumors can be treated by either the translabyrinthine approach or the retrosigmoid approach, depending upon the experience of the surgical team. With large tumors, the chance of hearing preservation is small with any approach. When hearing is already poor, the translabyrinthine approach may be used for even small tumors. Small, lateralized tumours in people with NF2 with good hearing should have the middle fossa approach. When the location of the tumour is more medial a retrosigmoid approach may be better.
Auditory canal decompression is another surgical technique that can prolong usable hearing when a vestibular schwannoma has grown too large to remove without damage to the cochlear nerve. In the IAC (internal auditory canal) decompression, a middle fossa approach is employed to expose the bony roof of the IAC without any attempt to remove the tumor. The bone overlying the acoustic nerve is removed, allowing the tumour to expand upward into the middle cranial fossa. In this way, pressure on the cochlear nerve is relieved, reducing the risk of further hearing loss from direct compression or obstruction of vascular supply to the nerve.
Radiosurgery is a conservative alternative to cranial base or other intracranial surgery. With conformal radiosurgical techniques, therapeutic radiation focused on the tumour, sparing exposure to surrounding normal tissues. Although radiosurgery can seldom completely destroy a tumor, it can often arrest its growth or reduce its size. While radiation is less immediately damaging than conventional surgery, it incurs a higher risk of subsequent malignant change in the irradiated tissues, and this risk is higher in NF2 than in sporadic (non-NF2) lesions.

Medications
There are no prescription medicines currently indicated for reduction in tumor burden for NF2 patients, although in patient studies Bevacizumab has resulted in reduction in tumor growth rates and hearing improvements in some patients.

Treatment hearing loss
As hearing loss in individuals with NF2 is generally gradual, eventually profound and sensorineural, the best options for treatment for hearing loss are cochlear implants and auditory brainstem implants (ABIs), as well as supplementing hearing with lip-reading, cued speech or sign language.

Cochlear Implants
A cochlear implant is an electronic device that is surgically implants to stimulate the cochlear nerve. Cochlear implants will work only when the cochleovestibular nerve (8th nerve) and the cochlea are still functioning. In a study done with open-set speech perception testing and closed-set speech perception testing by Neff et al., they discovered that the use of cochlear implants with NF2 patients allowed significant improvement of hearing abilities. In testing of recognition of sentences of everyday speech, five out of six patients scored within the 90–100% range, and in testing of hearing in noise setting, four of six of the patients scored within the 83–96%. Additionally, all testing was done without lip-reading.

Auditory Brainstem Implants (ABIs)
Auditory Brainsteam Implants, or ABIs, are used when the cochlea or any portion of the cochleovestibular nerve are not functioning due to damage to those areas or anatomic abnormalities. The procedure is done by implanting a device that send an electrical signal directly to the cochlear nucleus, allowing sound to bypass the peripheral auditory system and straight into the brain stem.

Prognosis
NF2 is a life limiting condition. It is a rare genetic disorder that involves noncancerous tumors of the nerves that transmit balance and sound impulses from the inner ear to the brain. The prognosis is affected by early age onset, a higher number of meningiomas and schwannomas and having a decrease in mutation.An early diagnosis is the best way to ensure improvement in management. Although, even with an early diagnosis, some patients still die very young.Meningiomas and schwannomas occur in around half of patients with NF2. Meningiomas are tumors that are both intracranial and intraspinal. Schwannomas are tumors that are often centered on the internal auditory canal. Patients with NF2 who have meningiomas have a higher risk of mortality, and the treatment can be very challenging. Individuals who develop schwannomas frequently develop hearing loss and deafness. These individuals may also develop tinnitus after being presented with unilateral hearing loss </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Somatization disorder and explain in detail? [/INST] Somatization disorder is a mental and behavioral disorder characterized by recurring, multiple, and current, clinically significant complaints about somatic symptoms. It was recognized in the DSM-IV-TR classification system, but in the latest version DSM-5, it was combined with undifferentiated somatoform disorder to become somatic symptom disorder, a diagnosis which no longer requires a specific number of somatic symptoms. ICD-10, the latest version of the International Statistical Classification of Diseases and Related Health Problems, still includes somatization syndrome.

Criteria
DSM-5
In the DSM-5 the disorder has been renamed somatic symptom disorder (SSD), and includes SSD with predominantly somatic complaints (previously referred to as somatization disorder), and SSD with pain features (previously known as pain disorder).

DSM-IV-TR
The DSM-IV-TR diagnostic criteria are:
A history of somatic complaints over several years, starting prior to the age of 30.
Such symptoms cannot be fully explained by a general medical condition or substance use or, when there is an associated medical condition, the impairments due to the somatic symptoms are more severe than generally expected.
Complaints are not feigned as in malingering or factitious disorder.The symptoms do not all have to occur at the same time, but may occur over the course of the disorder. A somatization disorder itself is chronic but fluctuating that rarely remits completely. A thorough physical examination of the specified areas of complaint is critical for somatization disorder diagnosis. Medical examination would provide object evidence of subjective complaints of the individual.Diagnosis of somatization disorder is difficult because it is hard to determine to what degree psychological factors are exacerbating subjective feelings of pain. For instance, chronic pain is common in 30% of the U.S. population, making it difficult to determine whether or not the pain is due to predominantly psychological factors.

ICD-10
In ICD-10, the latest version of the International Statistical Classification of Diseases and Related Health Problems, somatization syndrome is described as:
"The main features are multiple, recurrent and frequently changing physical symptoms of at least two years duration. Most patients have a long and complicated history of contact with both primary and specialist medical care services, during which many negative investigations or fruitless exploratory operations may have been carried out. Symptoms may be referred to any part or system of the body. The course of the disorder is chronic and fluctuating, and is often associated with disruption of social, interpersonal, and family behaviour."
ICD-10 also includes the following subgroups of somatization syndrome:
Undifferentiated somatoform disorder.
Hypochondriasis.
Somatoform autonomic dysfunction.
Persistent somatoform pain disorder.
Other somatoform disorders, such ones predominated by dysmenorrhoea, dysphagia, pruritus and torticollis.
Somatoform disorder, unspecified.

Cause
Although somatization disorder has been studied and diagnosed for more than a century, there is debate and uncertainty regarding its pathophysiology. Most current explanations focus on the concept of a misconnection between the mind and the body. Genetics probably contributes a very small amount to development of the disorder.One of the oldest explanations for somatization disorder advances the theory that it is a result of the bodys attempt to cope with emotional and psychological stress. The theory states that the body has a finite capacity to cope with psychological, emotional, and social distress, and that beyond a certain point symptoms are experienced as physical, principally affecting the digestive, nervous, and reproductive systems. There are many different feedback systems where the mind affects the body; for instance, headaches are known to be associated with psychological factors, and stress and the hormone cortisol are known to have a negative impact on immune functions. This might explain why somatization disorders are more likely in people with irritable bowel syndrome, and why patients with SSD are more likely to have a mood or anxiety disorder. There is also a much increased incidence of SSD in people with a history of physical, emotional or sexual abuse.Another hypothesis for the cause of somatization disorder is that people with the disorder have heightened sensitivity to internal physical sensations and pain.  A biological sensitivity to somatic feelings could predispose a person to developing SSD. It is also possible that a persons body might develop increased sensitivity of nerves associated with pain and those responsible for pain perception, as a result of chronic exposure to stressors.Cognitive theories explain somatization disorder as arising from negative, distorted, and catastrophic thoughts and reinforcement of these cognitions. Catastrophic thinking could lead a person to believe that slight ailments, such as mild muscle pain or shortness of breath, are evidence of a serious illness such as cancer or a tumor. These thoughts can then be reinforced by supportive social connections. A spouse who responds more to his or her partners pain cues makes it more likely that he or she will express greater pain. Children of parents who are preoccupied or overly attentive to the somatic complaints of their children are more likely to develop somatic symptoms. Severe cognitive distortions can make a person with SSD limit the behaviors he or she engages in, and cause increased disability and impaired functioning.

Neuroimaging evidence
A recent review of the cognitive–affective neuroscience of somatization disorder suggested that catastrophization in patients with somatization disorders tends to present a greater vulnerability to pain </s>