Lactose intolerance

[1][6] People are typically able to drink at least one cup of milk without developing symptoms, with greater amounts tolerated if drunk with a meal or throughout the day.[5] The ability to digest lactose is most common in people of Northern European descent, and to a lesser extent in some parts of the Middle East and Africa.[12] The medicalization of lactose intolerance as a disorder has been attributed to biases in research history, since most early studies were conducted amongst populations which are normally tolerant,[9] as well as the cultural and economic importance and impact of milk in countries such as the United States.Lactose, a disaccharide molecule found in milk and dairy products, cannot be directly absorbed through the wall of the small intestine into the bloodstream, so, in the absence of lactase, passes intact into the colon.[citation needed] Bacteria in the colon can metabolise lactose, and the resulting fermentation produces copious amounts of gas (a mixture of hydrogen, carbon dioxide, and methane) that causes the various abdominal symptoms.The unabsorbed sugars and fermentation products also raise the osmotic pressure of the colon, causing an increased flow of water into the bowels (diarrhea).Mutations are believed to interfere with the function of lactase, causing affected infants to have a severely impaired ability to digest lactose in breast milk or formula.[19] Lactose intolerance in adulthood is a result of gradually decreasing activity (expression) of the LCT gene after infancy, which occurs in most humans.[22] Analysis of the DNA of 94 ancient skeletons in Europe and Russia concluded that the mutation for lactose tolerance appeared about 4,300 years ago and spread throughout the European population.[35] Substantial variability in response (symptoms of nausea, cramping, bloating, diarrhea, and flatulence) is to be expected, as the extent and severity of lactose intolerance varies among individuals.[38] In conjunction, measuring blood glucose level every 10 to 15 minutes after ingestion will show a "flat curve" in individuals with lactose malabsorption, while the lactase persistent will have a significant "top", with a typical elevation of 50% to 100%, within one to two hours.[43] Modern techniques have enabled a bedside test, identifying presence of lactase enzyme on upper gastrointestinal endoscopy instruments.[28] These polymorphisms may be detected by molecular biology techniques at the DNA extracted from blood or saliva samples; genetic kits specific for this diagnosis are available.[43] Regular consumption of dairy food by lactase deficient individuals may also reduce symptoms of intolerance by promoting colonic bacteria adaptation.When dining out, carrying lactose intolerance cards that explain dietary restrictions in the local language can help communicate needs to restaurant staff.[66] Lactose is often used as the primary filler (main ingredient) in most prescription and non-prescription solid pill form medications, though product labeling seldom mentions the presence of 'lactose' or 'milk', and neither do product monograms provided to pharmacists, and most pharmacists are unaware of the very wide scale yet common use of lactose in such medications until they contact the supplier or manufacturer for verification.While essentially the same process as normal intestinal lactose digestion, direct treatment of milk employs a different variety of industrially produced lactase.This enzyme, produced by yeast from the genus Kluyveromyces, takes much longer to act, must be thoroughly mixed throughout the product, and is destroyed by even mildly acidic environments.[46][49][72] The way to induce tolerance is based on progressive exposure, consuming smaller amounts frequently, distributed throughout the day.[74] Worldwide, about 65% of people experience some form of lactose intolerance as they age past infancy, but there are significant differences between populations and regions.[76] In northern European countries, early adoption of dairy farming conferred a selective evolutionary advantage to individuals that could tolerate lactose.[77] Conversely, regions of the south, such as Africa, did not adopt dairy farming as early and tolerance from milk consumption did not occur the same way as in northern Europe.[46] Lactose intolerance is common among people of Jewish descent, as well as from West Africa, the Arab countries, Greece, and Italy.[83] Genetic analysis shows lactase persistence has developed several times in different places independently in an example of convergent evolution.One was that early research was conducted solely on European-descended populations, which have an unusually low incidence of lactose intolerance[87] and an extensive cultural history of dairying.[88][89][90] Subsequent research revealed that lactose intolerance was more common globally than tolerance,[91][92][93][94][95] and that the variation was due to genetic differences, not an adaptation to cultural practices.
An estimate of the percentage of adults that can digest lactose in the indigenous population of the Old World [ 75 ]
Milk allergytwo simple sugarsSpecialtyGastroenterologySymptomsbloatingdiarrheaflatulencenauseaComplicationslactoseDifferential diagnosisIrritable bowel syndromeceliac diseaseinflammatory bowel diseaselactase supplementsMedicationdairy productsabdominal paingastrointestinal tractenzymelactasesmall intestinesglucosegalactosepremature babiesgenetic disorderhydrogen breath teststool acidity testmammalsweaningancestral staterecent evolutionlactase persistencedomesticationdairy animalsAfrican countriesArab countriesTraditional foodmedicalizationlactose sugarsmall intestinelactase enzymeallergycrampsborborygmivomitingadolescentsanaphylaxisduodenumdisaccharideBacteriafermentationhydrogencarbon dioxidemethaneosmotic pressurenatural selectionTanzaniaepigeneticDNA methylationenhancerpastoralistgastroenteritiscoeliac diseaseCrohn's diseaseulcerative colitischemotherapyintestinal parasitesgiardiaautosomal recessiveFinlandsoybeaninfant formulasenteropathiespolymorphismsmolecular biologygluten-free dietgoat's milksheep's milkbuffalo milkyak milklactobacilliyogurtcurdlingcottage cheeselactic acidhard cheesesKosherparevefleishighechsherfood additivecaseincaseinatelactoserummilk solidsmodified milk ingredientssausageshot dogspâtésmargarinesbreadspotato chipsprocessed foodsmedicationsmilk stoutMilk substitutePlant-based milkssoy milkrice milkalmond milkcoconut milkhazelnutoat milkhemp milkpeanut milkAspergillusβ-galactosidaseKluyveromycesIrish peopleanthropologyhuman geneticsarchaeologyconvergent evolutionmedicineHippocratespsychosomaticFermented dairy productsFood intoleranceGlucose-galactose malabsorptionGluten intoleranceLactagenRecent human evolutionSoy cheeseplant milkSucrose intoleranceeMedicineBibcodeWayback MachineProQuestDiseasesDBMedlinePlusPatient UKhuman digestive systemEsophagusEsophagitisCandidalEosinophilicHerpetiformBoerhaave syndromeMallory–Weiss syndromeZenker's diverticulumBarrett's esophagusEsophageal motility disorderNutcracker esophagusAchalasiaEsophagogastric junction outflow obstructionDiffuse esophageal spasmGastroesophageal reflux diseaseLaryngopharyngeal refluxEsophageal strictureInlet patchMegaesophagusEsophageal intramural pseudodiverticulosisAcute esophageal necrosisStomachGastritisAtrophicMénétrier's diseasePeptic (gastric) ulcerCushing ulcerDieulafoy's lesionDyspepsiaFunctional dyspepsiaPyloric stenosisAchlorhydriaGastroparesisGastroptosisPortal hypertensive gastropathyGastric antral vascular ectasiaGastric dumping syndromeGastric volvulusBuried bumper syndromeGastrinomaZollinger–Ellison syndromeEnteropathyJejunumEnteritisDuodenitisJejunitisIleitisPeptic (duodenal) ulcerCurling's ulcerMalabsorptionCoeliacTropical sprueBlind loop syndromeSmall intestinal bacterial overgrowthWhipple'sShort bowel syndromeSteatorrheaMilroy diseaseBile acid malabsorptionLarge intestineAppendixAppendicitisColitisPseudomembranousUlcerativeIschemicMicroscopicCollagenousLymphocyticDysenteryFunctional colonic diseaseIntestinal pseudoobstructionOgilvie syndromeMegacolonToxic megacolonDiverticulitisDiverticulosisEnterocolitisNecrotizingGastroenterocolitisVascularAbdominal anginaMesenteric ischemiaAngiodysplasiaBowel obstructionIntussusceptionVolvulusFecal impactionConstipationFunctionalInfectiousIntestinal adhesionsRectumProctitisRadiation proctitisProctalgia fugaxRectal prolapseAnismusSolitary rectal ulcer syndromeRectal strictureAnal canalAnal fissureAnal fistulaAnal abscessHemorrhoidAnal dysplasiaPruritus aniAnal strictureGI bleedingBlood in stoolHematemesisMelenaHematocheziaAccessoryHepatitisViral hepatitisAutoimmune hepatitisAlcoholic hepatitisCirrhosisFatty liverBudd–Chiari syndromeHepatic veno-occlusive diseasePortal hypertensionNutmeg liverAlcoholic liver diseaseLiver failureHepatic encephalopathyAcute liver failureLiver abscessPyogenicAmoebicHepatorenal syndromePeliosis hepatisMetabolic disordersWilson's diseaseHemochromatosisGallbladderCholecystitisGallstone / CholelithiasisCholesterolosisAdenomyomatosisPostcholecystectomy syndromePorcelain gallbladderBile ductbiliary treeCholangitisPrimary sclerosing cholangitisSecondary sclerosing cholangitisAscendingCholestasisMirizzi's syndromeBiliary fistulaHaemobiliaCommon bile ductCholedocholithiasisBiliary dyskinesiaSphincter of Oddi dysfunctionPancreaticPancreatitisChronicHereditaryPancreatic abscessPancreatic pseudocystExocrine pancreatic insufficiencyPancreatic fistulaHerniaDiaphragmaticCongenitalHiatusInguinalIndirectDirectUmbilicalFemoralObturatorSpigelianLumbarPetit'sGrynfeltt–LesshaftIncisionalInternal herniaRichter'sPeritonealPeritonitisSpontaneous bacterial peritonitisHemoperitoneumPneumoperitoneumInborn errorcarbohydrate metabolismmonosaccharideglycogen storage diseasesSucroseInborn errors of renal tubular transportRenal glycosuriaFructose malabsorptionDe Vivo DiseaseFanconi-Bickel syndromeHexoseFructoseEssential fructosuriaFructose intolerancegalactosemiaGALK deficiencyGALT deficiencyGALE deficiencyglycogenGlycogenesisGSD type 0GSD type IVAdult polyglucosan body diseaseLafora diseaseGlycogenolysisGSD type IIIGSD type VIGSD type VGSD type IXLysosomalGlycogen storage disease type IIDanon diseaseGlycolysisMODY 2GSD type VIITriosephosphate isomerase deficiencyPyruvate kinase deficiencyAldolase A deficiencyMitochondrial pyruvate carrier deficiencyGluconeogenesisPyruvate carboxylase deficiencyFructose bisphosphatase deficiencyGSD type IPentose phosphate pathwayGlucose-6-phosphate dehydrogenase deficiencyTransaldolase deficiency6-phosphogluconate dehydrogenase deficiencyHyperoxaluriaPrimary hyperoxaluriaPentosuriaAMP-activated protein kinasePRKAG2