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| ==Overview== | | ==Overview== |
| | Lactose intolerance was first discovered by Hippocrate, the ancient Greek physician 2500 years ago. In 1906, Pimmer discovered lactase enzyme in the [[intestine]] of infant dogs, pigs, and rats. The association between the ethnicity and lactose intolerance was discovered in 1966 by Bayless and Rosensweig. In 1978, breath hydrogen test was used by Levitt to diagnose lactose intolerance. |
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| ==Historical Perspective== | | ==Historical Perspective== |
| doi:[https://doi.org/10.1053%2Fj.nainr.2005.08.004 10.1053/j.nainr.2005.08.004]
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| ===Discovery=== | | ===Discovery=== |
| *Lactose intolerance was first discovered by Hippocrate, ancient Greek physician 2500 years ago <ref>Wilson J. Milk intolerance: Lactose intolerance and cow's milk protein allergy. Newborn and infant nursing reviews. 2005 Dec 31;5(4):203-7</ref> | | *Lactose intolerance was first discovered by Hippocrate, the ancient Greek physician 2500 years ago.<ref name="pmid4718561" /> |
| *In 1906, Pimmer was the first scientist that discovered lactase enzyme in the intestine of infant dogs, pigs, and rats; also he found that this enzyme decreases in the adult intestine of these animals.<ref name="pmid4718561">{{cite journal |vauthors=Neale G |title=The geographical incidence of lactase deficiency |journal=Pathol Microbiol (Basel) |volume=39 |issue=3 |pages=238–47 |year=1973 |pmid=4718561 |doi= |url=}}</ref> | | *In 1906, Pimmer was the first scientist to discover lactase enzyme in the [[intestine]] of infant dogs, pigs, and rats. He also found that this enzyme decreased in the adult intestine of these animals.<ref name="pmid4718561">{{cite journal |vauthors=Neale G |title=The geographical incidence of lactase deficiency |journal=Pathol Microbiol (Basel) |volume=39 |issue=3 |pages=238–47 |year=1973 |pmid=4718561 |doi= |url=}}</ref> |
| *In 1959, Durand and Holzei et al decribed congenital lactase deficiency<ref name="pmid4718561" /> | | *In 1959, Durand and Holzei et al decribed [[Congenital disorder|congenital]] [[lactase]] deficiency<ref name="pmid4718561" /> |
| *In 1962, Doell and Kretchmer
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| * Holzel et al (1959) and Durand (1959) produced two of the earliest studies of lactose intolerance.
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| *The association between [important risk factor/cause] and [disease name] was made in/during [year/event].
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| *In [year], [scientist] was the first to discover the association between [risk factor] and the development of [disease name].
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| *In [year], [gene] mutations were first implicated in the pathogenesis of [disease name].<ref name="pmid11788828">{{cite journal |vauthors=Enattah NS, Sahi T, Savilahti E, Terwilliger JD, Peltonen L, Järvelä I |title=Identification of a variant associated with adult-type hypolactasia |journal=Nat. Genet. |volume=30 |issue=2 |pages=233–7 |year=2002 |pmid=11788828 |doi=10.1038/ng826 |url=}}</ref>
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| *Now Leena Peltonen’s team at the University of California, Los Angeles, has discovered the genetic basis for lactose intolerance. The discovery supports the theory that retaining the ability to digest milk evolved only in some peoples in the past ten thousand years, as an adaptation to dairy farming.
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| *Originally it was [[Hypothesis|hypothesised]] that gut bacteria such as [[E. coli]] produced the [[lactase]] enzyme needed to cleave lactose into its constituent [[Monosaccharide|monosaccharides]] and thus become metabolisable and digestible by humans. Some form of human-bacteria symbiosis was proposed as a means of producing lactase in the human digestive tract. Genetics and protein analysis techniques by the early 1970s revealed this to be untrue; humans produce their own lactase enzyme natively in intestine cells.
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| *Most humans normally cease to produce lactase after weaning and as a result become lactose intolerant. It is, therefore, not surprising that as adults, as much as 75% of the world’s human population is intolerant to ingested dietary lactose
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| ==Outbreaks==
| | *The association between the ethnicity and lactose intolerance was discovered in 1966 by Bayless and Rosensweig and in 1968 by Neale. |
| *There have been several outbreaks of [disease name], which are summarized below: | |
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| ==Landmark Events in the Development of Treatment Strategies== | | *In the early 1970s, lactase-phlorizin hydrolase (LPH) gene [[Mutation|mutations]] were first implicated in the pathogenesis of lactose intolerance.<ref name="pmid11788828">{{cite journal |vauthors=Enattah NS, Sahi T, Savilahti E, Terwilliger JD, Peltonen L, Järvelä I |title=Identification of a variant associated with adult-type hypolactasia |journal=Nat. Genet. |volume=30 |issue=2 |pages=233–7 |year=2002 |pmid=11788828 |doi=10.1038/ng826 |url=}}</ref> |
| *In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name]. | | *In 1978, breath hydrogen test was used by Levitt to diagnose lactose intolerance<ref name="pmid25298621">{{cite journal |vauthors=Rana SV, Malik A |title=Hydrogen breath tests in gastrointestinal diseases |journal=Indian J Clin Biochem |volume=29 |issue=4 |pages=398–405 |year=2014 |pmid=25298621 |pmc=4175689 |doi=10.1007/s12291-014-0426-4 |url=}}</ref> |
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| ==Impact on Cultural History==
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| ==Famous Cases==
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| *The following are a few famous cases of [[disease name]]:
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| ==References== | | ==References== |
| {{Reflist|2}} | | {{Reflist|2}} |
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| {{WH}}
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| {{WS}}
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| [[Category: (name of the system)]]
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| __NOTOC__
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| {{Lactose intolerance}}
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| {{CMG}}
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| ==Overview==
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| The ancient Greek physician [[Hippocrates]] (460-370 B.C.) first noted gastrointestinal upset and skin problems in some who consumed milk. The condition was first recognized in the 1950s and 1960s when various organizations like the United Nations began to engage in systematic famine-relief efforts in countries outside Europe for the first time. Holzel et al (1959) and Durand (1959) produced two of the earliest studies of lactose intolerance.
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| == Historical Perspective ==
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| The ancient Greek physician [[Hippocrates]] (460-370 B.C.) first noted gastrointestinal upset and skin problems in some who consumed milk;<ref>[http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B758X-4HMW41X-B&_coverDate=12%2F31%2F2005&_alid=508637183&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=12938&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=409a42b93cb26955160d265431eec835 ''Milk Intolerance: Lactose Intolerance and Cow's Milk Protein Allergy'', J. Wilson, Newborn and Infant Nursing Reviews, Volume 5, Issue 4, Pages 203-207, Dec. 2005]</ref> patients experiencing the former symptom may likely have been suffering from lactose intolerance. However, it was only in the last few decades that the syndrome was more widely described by modern medical science.
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| The condition was first recognized in the 1950s and 1960s when various organizations like the United Nations began to engage in systematic famine-relief efforts in countries outside Europe for the first time. Holzel et al (1959) and Durand (1959) produced two of the earliest studies of lactose intolerance. As anecdotes of embarrassing dairy-induced discomfort piled up, the First World donor countries could no longer ascribe the reports to spoilage in transit or inappropriate food preparation at the recipient end in the Third World.
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| Since the first nations to industrialize and develop modern scientific [[medicine]] were dominated by people of Western and Northern European descent, adult dairy consumption was long taken for granted. Westerners for some time did not recognize that the majority of the human ethno-genetic groups could not consume dairy products during adulthood. Although there had been regular contact between Europeans and non-Europeans throughout history, the notion that large-scale medical studies should be representative of the ethnic diversity of the human populations (as well as all genders and ages) did not become well-established until after the American Civil Rights Movement.
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| Since then, the relationship between lactase and lactose has been thoroughly investigated in food science due to the growing market for dairy products among non-Europeans.
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| Originally it was [[hypothesis]]ed that gut bacteria such as [[E. coli]] produced the [[lactase]] enzyme needed to cleave lactose into its constituent [[monosaccharide]]s and thus become metabolisable and digestible by humans. Some form of human-bacteria symbiosis was proposed as a means of producing lactase in the human digestive tract. Genetics and protein analysis techniques by the early 1970s revealed this to be untrue; humans produce their own lactase enzyme natively in intestine cells.
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| According to Heyman (2006), approximately 70% of the global population cannot tolerate lactose in adulthood. Thus, some argue that the terminology should be reversed — lactose intolerance should be seen as the norm, and the minority groups should be labeled as having ''lactase persistence''. A counter argument to this is that the cultures that don't generally consume unmodified milk products have little need to discuss their intolerance to it, leaving the cultures for which lactose intolerance is a significant dietary issue to define its terminology.
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| === History of Genetic Prevalence ===
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| Lactose intolerance has been studied as an aid in understanding ancient diets and population movement in prehistoric societies. Milking an animal vastly increases the efficiency of raising it in regards to the calories that can be extracted compared to consumption of its meat alone. It is not surprising then, that consuming milk products became an important part of the agricultural way of life in the Neolithic.
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| Given that at this time the majority of the population of all areas was lactose intolerant, it is believed that most of the milk was used to make mature cheeses (mostly lactose free). This also corresponds to the amount of lactose in the milk; horse milk has a great deal of lactose, and goat's milk has very little. Roman authors also remark that the people of northern Europe, particularly Britain and Germany drank unprocessed milk (as opposed to the Romans who made cheese). This corresponds very closely with modern European distributions of lactose intolerance, where the people of Britain, Germany and Scandinavia have a good tolerance, and those of southern Europe, especially Italy, have a poorer tolerance.<ref>http://www.gnxp.com/MT2/archives/001681.html</ref>
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| In east Asia, historical sources also attest that the Chinese did not consume milk, whereas the nomads that lived on the borders did. Again, this reflects modern distributions of intolerance. China is particularly notable as a place of poor tolerance, whereas in Mongolia and the Asian steppes horse milk is drunk regularly. Here they even make an alcoholic beverage, called Kumis, from horse milk (although the fermentation process reduces the amount of lactose present). This tolerance is thought to be advantageous as the nomads do not settle down long enough to process mature cheese or may find themselves regularly going through brief periods of starvation; and given that their prime source of income is generated through horses, to ignore their milk as a source of calories would be greatly detrimental.
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| The African Fulani have a nomadic origin and their culture once completely revolved around cow, goat, and sheep herding. Dairy products were once a large source of nutrition for them. As might be expected if lactase persistence evolved in response to dairy product consumption, they are particularly tolerant to lactose (about 77% of the population). Many Fulani still live in Guinea-Conakry, Burkina Faso, Mali, Nigeria, Niger, Cameroon, and Chad.
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| There is some debate on exactly where and when the mutation(s) occurred. Some argue for separate mutation events in Sweden (which has one of the lowest levels of lactose intolerance in the world) and the Arabian Peninsula around 4000 BC. However, others argue for a single mutation event in the Middle East at about 4500 BC which then subsequently radiated. Some sources suggest a third and more recent mutation in the East African Tutsi. Whatever the precise origin in time and place, most modern Western Europeans and people of European ancestry show the effects of this mutation (that is, they are able to safely consume milk products all their lives) while most modern East Asians, sub-Saharan Africans and native peoples of the Americas and Pacific Islands do not (making them lactose intolerant as adults).<ref>http://us.cambridge.org/Books/kiple/lactose.htm</ref>
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| The Maasai ability to consume dairy without exhibiting symptoms may be due to a different genetic mutation than westeners.<ref>Swaminathan, Nikhil. ''[http://www.sciam.com/article.cfm?articleID=727EA883-E7F2-99DF-36D89AB12E930315&sc=I100322|African Adaptation to Digesting Milk Is "Strongest Signal of Selection Ever]December 11, 2006, Scientific American.com''.</ref>
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| A thorough scientific overview of genetic polymorphisms of intestinal lactase activity in adult hypolactasia, is in chapter 76 of OMMBID.<ref>[[Charles Scriver]], Beaudet, A.L., Valle, D., Sly, W.S., Vogelstein, B., Childs, B., Kinzler, K.W. (Accessed 2007). [http://www.ommbid.com The Online Metabolic and Molecular Bases of Inherited Disease]. New York: McGraw-Hill. -
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| Summaries of 255 chapters, full text through many universities. There is also the [http://books.mcgraw-hill.com/medical/ommbid/blog/ OMMBID blog].
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| </ref> A noncoding variation in the MCM6 gene has been strongly associated with adult type hypolactasia.<ref>{{cite journal |author=Enattah N, Sahi T, Savilahti E, Terwilliger J, Peltonen L, Järvelä I |title=Identification of a variant associated with adult-type hypolactasia |journal=Nat Genet |volume=30 |issue=2 |pages=233-7 |year=2002 |id=PMID 11788828}}</ref>
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| ==References==
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| {{Reflist|2}}
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| {{WS}}
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| {{WH}} | | {{WH}} |
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| [[Category:Gastroenterology]] | | [[Category:Gastroenterology]] |
| [[Category:Endocrinology]] | | [[Category:Medicine]] |
| | [[Category:Up-To-Date]] |