Talk:Lactase persistence
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Text and/or other creative content from this version of Lactose intolerance was copied or moved into Lactase persistence with this edit on 7 September 2011. The former page's history now serves to provide attribution for that content in the latter page, and it must not be deleted as long as the latter page exists. |
Text and/or other creative content from this version of Developmental regulation of lactase expression in mammals was copied or moved into Lactase persistence with this edit on 7 September 2011. The former page's history now serves to provide attribution for that content in the latter page, and it must not be deleted as long as the latter page exists. |
Map doesn't make sense
editThe map on the article is entirely unscientific. Among other things, why are continents arbitrarily divided at points that do not have any significant correlation to demographics. For example, what does the lines dividing South America or France in half even mean? The data itself is also very dubious. The populations of Argentina and Uruguay for instance are around 90% of European origin. It would make a lot more sense for their lactose intolerance to be lower than that of, say, Haiti or Guatemala. --132.183.15.120 (talk) 18:37, 5 January 2012 (UTC)
Agreed, the map seems to be completely random. Even with the numbers posted right beside it, to does not seem to reflect them, assuming the sources in the table and the table itself is reliable. Kniwor (talk) 06:00, 3 April 2012 (UTC)
Genetic nomenclature
editThe nomenclature used for the genetic changes in this article are nothing like standard and confusing and very difficult to understand.
eg "It was found that C−13910 (C at position -13910 upstream of the gene LCT)"
Something like "LCT: c.-13910C" is closer to the appropriate nomenclature. The nucleotide should come after the number. But, while this is correct in form, it is probably wrong in fact because I don't know where the numbering starts. The "c." at the start says that number counts from translation start; this is not necessarily the same as "upstream from the gene" — Preceding unsigned comment added by 121.44.8.29 (talk) 07:18, 28 April 2013 (UTC)
Please fix table
editWould somebody with the know-how please fix the Distribution table such that the Intolerance% figures are correctly sortable. At present they are sorting in an alpha string sequence instead of a numeric one. — Preceding unsigned comment added by 124.149.45.241 (talk) 14:50, 20 January 2014 (UTC)
Table
editI don't know about people from other regions, but Balkans doesn't have 55% of population intolerant, the number is just too high. The amount of dairy eaten in this part of the world just makes it impossible. I don't know where did the author of reference 27 find this data, but I can't find any other that corroborate it. — Preceding unsigned comment added by 93.87.247.84 (talk) 21:14, 19 May 2014 (UTC)
Persistence or intolerance?
editI'm confused by this article, which I've read after reading the one on Lactose intolerance of which it is evidently a spinoff article; because the table in the Distribution section claims to record not Lactase persistence but Lactose intolerance (with no comment). I'm not an expert, but a quick glance at the literature says that these are not the same thing. Indeed some recent papers suggest that lactose intolerance is so badly defined a concept as to make statistics almost meaningless. Lactase persistence/deficiency on the other hand is more readily measured both by pathological tests and genetic markers.
If there were more figures in the Allele frequency column, it would make more sense. But without these, it suggests that this section should be moved to the other article and that it should contain some health warnings. Chris55 (talk) 13:58, 18 July 2014 (UTC)
Room for Expansion
editAdditional information about the allelic mutation distribution amongst different geographic populations: this would help to illustrate that not all human lactase persistence is derived from a common ancestor.
The Global Spread section: There is great room for expansion in this section. For example discussing the fact that lactase persistence is a convergent evolution amongst populations.
Evolutionary Advantage section: clarification could be more specifically made about the more ancestral advantages of lactase persistence which may have led to it gaining genetic traction. In addition, there is evidence of two different evolutionary processes which affect European population’s vs Middle Eastern/African populations. I would like to explore these a little more within this or the Global Spread section.
In addition, more graphics displaying ancestral distribution of LP alleles may be helpful to include. Thomas.2553 (talk) 17:58, 30 September 2014 (UTC)thomas.2553
Possible Suggestions for expanding:
1. Perhaps adding a section about the difference between drinking fresh milk (requires lactase persistence) and fermented products like cheese lessening the need for lactase persistence? 2. Adding that milk usage was likely in the population before the lactase persistence gene arose. 3. Talking about populations that were pastoral and yet have very low lactase persistence rates.
This could be an interesting area to expand on. I will look in to more data regarding these types of facts. I will look further into recommendation 2. It would be interesting to explore whether or not the lactase persistence gene has been seen in any other organisms which may or may not be closely related to humans.Thomas.2553 (talk) 18:07, 3 October 2014 (UTC)
Note of Revisions
editThank you to those who helped revise my edits. I appreciate the use of the AWB to help edit some of the changes made by the other OSU student (London.34.osu.edu) and myself. While I had not looked in to the vitamin D deficiency angle, I fact checked this portion of the other student's addition and found the research to be quite interesting. I will continue to research and make minor edits to the page's format. I think there is some overlapping information within the sections, so I will go in to the page and try to remove repetitive information.Thomas.2553 (talk) 21:47, 2 December 2014 (UTC)
Section on nonhumans unclear
editThe first paragraph of the section concerns how most mammals can't absorb lactose in adulthood and that lactase persistence might be unique to humans, and then the following paragraph remarks how domestic cats can be lactose intolerant in adulthood.
This is confusing because based on the first part, the reader would assume domestic cats to be unable to absorb lactose in adulthood, but the second part puts that into question by implying that lactose intolerance is the exception among domestic cats. Maybe this is another issue with the difference between nonpersistence and intolerance?
Maybe it assumes the reader has an expectation that cats often drink milk and is trying to clarify that cats are no exception to the rule in the first part of the section, counter to popular belief. That seems to be roughly the goal of the cited article. However, the WebMD article also states that some cats are lactose tolerant in adulthood, which apparently conflicts with the rest of the section. — Preceding unsigned comment added by Adrusi (talk • contribs) 02:31, 30 August 2015 (UTC)
External links modified
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Imprecise terminology
editThis statement is problematic: "Today, this haplotype can be found in 80% of Europeans and those of European ancestry (e.g. Oceanians and Americans)..." Both of those classifications (Oceanians and Americans) are vague geographical terms that provide little insight into ancestry, and both regions were entirely occupied until relatively recently by people who were not of European ancestry. Perhaps the parenthetical phrase can simply be dropped as unnecessary and confusing. 850 C (talk) 18:24, 14 April 2016 (UTC)
LP frequencies
editThe frequency tables were apparently deemed inappropriate in a lactase persistence afd [1]. I've therefore replaced them with external links to the LP genotype and phenotype frequencies, and moved the lactase persistence phenotype frequencies here since they are raw percentages like the lactase persistence genotype frequencies:
Lactase persistence frequencies
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Lactase persistence phenotype frequencieseditDistributionedit
The precision of these figures varies greatly depending on number of people sampled. Lactose intolerance levels also increase with age. At ages 2–3 yr, 6 yr, and 9–10 yr, the amount of lactose intolerance is, respectively:
Chinese and Japanese populations typically lose between 20 and 30% of their ability to digest lactose within three to four years of weaning. Some studies have found that most Japanese can consume 200 ml (8 fl oz) of milk without severe symptoms.[31] Milk tolerance is about 81% in Japanese adults.[31] Of the 10% of the Northern European population who develop lactose intolerance, it is a gradual process spread out over as many as 20 years.[32] The allele frequencies associated with lactase persistence (T-13910) were 10.9% in ancient groups of Hungary, 35.9% in modern-day Hungarians and 40% in Hungarian Szeklers of Transylvania, respectively.[33] Lactase persistence genotype frequencieseditGenetic analysis of lactase persistence has identified five main causal variants associated with the LP trait: T-13910, C-14010, G-13907, G-14009 and G-13915. The T-13910 mutation primarily occurs among lactose tolerant populations in Europe, from where it is believed to have arisen and dispersed. G-13915 is centered in the Middle East, the allele's presumed area of origin. The G-13907 variant is concentrated among Afroasiatic speakers in Northeast Africa.[34] The G-14009 mutation is based in Ethiopia.[35] C-14010 is today most common among pastoralist groups inhabiting eastern Africa, having likely arrived from parts of the Sahara that were previously inhabited by Afroasiatic-speaking populations. This was deduced from the existence of animal husbandry- and milking-related loanwords of Afroasiatic origin in various Nilo-Saharan and Niger-Congo languages, as well as from the earliest appearance of processed milk lipids on ceramics which were found at the Tadrart Acacus archaeological site in Libya (radiocarbon-dated to ~7,500 BP, close to the estimated age of the C-14010 allele).[36] Below are frequencies of lactase persistence associated alleles in global populations:
Referencesedit
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Alternatively, the LP genotype frequencies can simply be noted alongside the LP phenotype frequencies. Soupforone (talk) 05:02, 30 September 2017 (UTC)
Evolutionary History
editThe Evolutionary History section is out of date, in particular the first paragraph, where it suggests that lactase persistence emerged 10,000 years ago. They now have ancient DNA from fossil skeletons showing that people who raised dairy cows and consumed dairy products since 8000 BP were all lactose intolerant. For example, LBK, Yamna, some people in the Middle East. The studies cited here were using DNA from people alive today, analyzing things like microsatellite variation, then estimating divergence times. That kind of analysis is, at best, good to within a close order or magnitude. All this has been widely reported in the press and popular science magazines, as the new data has been flooding in from one study after another. Lactase persistence is actually half as old as previously thought. Zyxwv99 (talk) 23:27, 8 December 2017 (UTC)
What about cats?
editIn the section "In nonhumans" it is stated this is "a uniquely human phenomenon." As the statement was unsourced, I've marked it as such. AFAIK it's wrong because cats have lactase persistence too (and BTW, while editing the above mentioned section I've seen a commented reference linking to something about cats and lactose intolerance.) If someone knows a good reference to quote, it would be nice. --Arny (talk) 10:37, 9 September 2019 (UTC)
- "As the statement was unsourced, I've marked it as such", I agree this is a big claim and requires some sources. "(...) cats have lactase persistence too", do they? My very brief Googling seems to confirm they mostly don't as by this piece. Ideally, we would get a book chapter or scientific article quantitatively stating how little (if any) lactase the "average adult cat" has or something similar. BernardoSulzbach (talk) 01:40, 10 September 2019 (UTC)
Lactase persistence evolved from a milk consuming community of lactose intolerants; lactese persistence evolved after the usage of milk, not beforehand
editIt's a myth that many individuals were lactase persistent before the lifelong usage of milk.
Even if one person in three thousand was lactase persistent, it's a lie that the whole community changed customs for that individual.
The truth is that all individuals - absolutely all - of milk consuming societirs initially were lactose intolerant.
Most people had issues with milk, so initially they would mostly eat other food, use it mixed, drink small quantities or let it ferment not necessarily in a conscious manner about the craft of fermentation, but simply allow it to get a little bit older in a shadowy place, covered with leaves and inside it should had herbs to inhibit the bacterial growth.
Many individuals of the first milk-consuming societies would have bowel issues; mainly gasses. But consumption in small quantities mixed with food, herbs and some fermentation and cooking, would constitute the milk less burdensome for the bowel. That initial processing would give time, for gene deactivation with histones and DNA methylation. If histones and methyl groups are beneficial for a specific DNA gene suppression; they usually occupy the same DNA section for many generations. Initially we thought that histones and methyl groups are neutral, or protective for the DNA code, but actually under some conditions of their necessary presence, they increase the rate of mutations versus the other regions (this doesn't mean that histones and methyl groups are hamful, but when combined and are forced to dwell for many generations in the same place). Some people claim that even when the DNA labeling is removed for meiosis (meiosis because we care about what is carried to the next generation), some bends and defects might remain, or the damage might be cause during the preparation for meiosis; the last one is considered the case, because some de-labeling might be relatively violent if repeated in the same DNA place for many generations; that certainly increases the rate of mutations (the rate of mutations in a region which has to get labeled and de-labeled for many generations is higher, and then the resulting mutant region doesn't require labeling or it might require only in some conditions; thus a mutation in this region is beneficial because then less cell functions will be occupied needlessly. — Preceding unsigned comment added by 2A02:2149:8484:1700:916C:77A9:F6B9:2583 (talk) 10:56, 30 September 2019 (UTC)
milk contains proteins as well ...
editThe text says: "The consumption of lactose has been shown to benefit humans with lactase persistence through adulthood. For example, the 2009 British Women's Heart and Health Study[42] investigated the effects on women's health of the alleles that coded for lactase persistence. Where the C allele indicated lactase nonpersistence and the T allele indicated lactase persistence, the study found that women who were homozygous for the C allele exhibited worse health than women with a C and a T allele and women with two T alleles." Whhhhelll... DOES this show the effect is one of CONSUMING LACTOSE ? Or rather one of consunming MILK, whichever component(s) of that milk may cause the positive health effects, as long as consumption is made possible at all by being able to digest lactose ? Just curious, being a rather intolerant being myself, as far as lactose goes. No marginal question by the way, having all those products present in supermarkets nowadays that contain everything dairy products usually contain, minus the lactose. So, is the argument quoted above consistent at all ? --MistaPPPP (talk) — Preceding undated comment added 19:51, 2 January 2022 (UTC)