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Do I Have IBS?
Published in Melissa G. Hunt, Aaron T. Beck, Reclaim Your Life From IBS, 2022
Melissa G. Hunt, Aaron T. Beck
In many other human populations, however, primarily people from pastoral cultures that developed cow, sheep, and goat herding early on (including many African, most Indian, and most European and Middle Eastern peoples), several different genetic mutations occurred that kept the lactase production gene switched on (a trait called lactase persistence). You may have heard that humans shouldn’t drink milk because we didn’t “evolve” to, but in fact this is incorrect. The extended lactase production mutation occurred independently in different human populations at different times. It was a tremendous advantage under certain environmental circumstances, allowing the introduction of cow, goat, sheep, and even reindeer and yak milk products as major forms of dietary protein. Animal milk is a fantastic way to turn otherwise totally indigestible grass into a high-quality, complete, tasty, and versatile protein, so the ability to digest it was strongly selected for in those populations where it arose. This is actually exactly how evolution works – a spontaneous genetic mutation arises that confers survival and reproductive advantage and is therefore selected for and passed on to the next generation. So, in fact, lots of humans did evolve to drink milk. But not all people did, so there are indeed many people who are lactose-intolerant. Because cow’s milk has become such a major part of the Western diet, actually being lactose-intolerant in America or Europe can be quite problematic.
Dairy Milk
Published in Robert E.C. Wildman, Richard S. Bruno, Handbook of Nutraceuticals and Functional Foods, 2019
Joshua D. McDonald, Richard S. Bruno
Age-dependent declines in lactose digestion are attributed to the down-regulation of the gene that encodes lactase. Nearly two-thirds of the global population experience age-associated decreases in lactase expression, but rates of lactase persistence vary considerably by geographic region (Table 17.3).98, 102 Descendants from societies that raise cattle (e.g., Scandinavia, Netherlands) appear to maintain functional lactase into adulthood.98 Lactase persistence is typically greatest (>90%) in northern Europe, and relatively high (∼50%) in central and southern Europe and parts of the Middle East and West Africa where cattle farming is prevalent.103 However, low rates occur in the rest of Africa (∼5%–20%) and Asia (<5%).103
Irritable Bowel Syndrome
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
In North-Western Europe, adult lactase persistence, caused by a mutation in the gene MCM6 (minichromosome maintenance 6) that controls down-regulation of lactase production in enterocytes, co-evolved with dairy-based farming, and today the vast majority of people in Ireland, the UK, the Netherlands, Germany and Scandinavia retain as adults the ability to digest lactose to glucose and galactose. Lactase activity can be directly measured in biopsies from small bowel mucosa, but for clinical purposes the most accurate indirect test for lactase activity is genotyping for LCT-13910 C/T. Only those with ‘wild-type’, i.e. CC, have lactose malabsorption. Several other mutations, like LCT-22019 G/A, have been found to cause lactase persistence in other parts of the world.
The influence of Scandinavian presence on Greenlandic lactase persistence
Published in Scandinavian Journal of Gastroenterology, 2023
Símun Niclasen, Stig Andersen, Nadja Albertsen, Henrik Bygum Krarup
Lactose is the primary saccharide in milk and constitutes 4–5 g/L. It requires enzymatic hydrolysis in the mucosa in the small intestine by lactase into d-glucose and d-galactose before it can be absorbed. In most populations, lactase levels decline after weaning, although at different rates among different people [1]. The ability to produce lactase throughout life is called lactase persistence, as opposed to lactase non-persistence (LNP), and is inherited as an autosomal dominant trait [2]. Differences in lactase activity between lactase persistence and non-persistence can occur by 3 years old or earlier [3]. The inability to effectively digest lactose can be due to adult LNP, to primary (congenital) lactase deficiency caused by coding sequence mutations in the lactase gene, or secondary lactase deficiency, caused by disease in the intestinal mucosa [2,4].
Very low frequency of the lactase persistence allele LCT-13910T in the Armenian population
Published in Annals of Human Biology, 2022
Stefan Németh, Gernot Kriegshäuser, Kristine Hovhannesyan, Hasmik Hayrapetyan, Christian Oberkanins, Tamara Sarkisian
Lactase is encoded by the LCT gene (OMIM 603202), and the sustained activity of lactase in adult-life is associated with at least five independent single nucleotide variants in a regulatory region upstream of the LCT locus, which serves as a transcriptional enhancer (Ingram et al. 2007; Jensen et al. 2011; Fang et al. 2012; Liebert et al. 2016). There are clear geographic distribution differences for each of the causative variants for lactase persistence (LP), even though some of them co-occur in East Africa (Itan et al. 2010; Liebert et al. 2017). In Europe, variant rs4988235, which is characterised by a C > T exchange at position −13910 upstream of the LCT gene (LCT-13910T) is highly prevalent (Enattah et al. 2002). Other variants such as −13907 G (rs41525747), −13915 G (rs41380347), −14009 G (rs869051967) and −14010 C (rs145946881) are found at variable frequencies in the Middle East and Africa (Liebert et al. 2017). The advantageous consequence of LP is the possibility of dietary consumption of animal milk by adults without symptoms ascribed to lactose intolerance. Positive selection for LP (Gerbault et al. 2009; Itan et al. 2009; Ingram et al. 2009; Allentoft et al. 2015), but also other factors including population expansion and migration have been proposed as underlying mechanisms for currently observed allele frequencies (Gerbault et al. 2011).
Use of genetic testing for hypolactasia trait in the North Denmark Region
Published in Scandinavian Journal of Gastroenterology, 2020
Morten Mørk, Stine Linding Andersen, Inge Søkilde Pedersen, Anja Ernst, Simon Lykkeboe, Henrik Bygum Krarup
Lactose intolerance (LI) is one among a range of possible diagnoses in patients with unspecific gastrointestinal symptoms [1]. Such patient complaints are common, and there is no clear consensus on when and how to diagnose LI [2,3]. LI is per definition present in individuals who experience gastrointestinal symptoms, such as abdominal pain, diarrhea, nausea, flatulence and bloating, because of lactose malabsorption [2–5]. Lactose malabsorption results from lactose maldigestion caused by lactase deficiency [4,6], i.e., markedly reduced intestinal brush-border lactase activity relative to the activity observed in infants [6,7]. Lactase deficiency can be primary (genetically programmed) or secondary (resulting from intestinal disease or abdominal surgery) [7]. Globally, about two-thirds of adults have acquired primary lactase deficiency, also termed adult-type hypolactasia (ATH), which is caused by a downregulation of the intestinal lactase expression during childhood or adolescence [8–10]. The low lactase activity causes lactose malabsorption, which in many of these individuals results in gastrointestinal symptoms and thus primary LI. In contrast, individuals with the genetic trait of lactase persistence (LP) typically retain sufficient lactase activity to avoid lactose malabsorption and remain lactose tolerant into adulthood [11] and throughout life unless they contract intestinal disease-causing secondary lactose malabsorption and thus secondary LI. The prevalence of LP varies between populations and is high in Northern Europe, particularly in Scandinavia [12].