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How Do You Know if Your Lactose Intolerant Yahoo Answers

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Medical status

Lactose intolerance
Other names Lactase deficiency, hypolactasia, alactasia, lactose challenged
Lactose Haworth.svg
Lactose is made upward of two unproblematic sugars
Specialty Gastroenterology
Symptoms Abdominal pain, bloating, diarrhea, flatulence, nausea[one]
Complications Does not cause damage to the GI tract[two]
Usual onset 30–120 min later dairy products[1]
Causes Decreased power to digest lactose (genetic, small intestine injury)[ane]
Diagnostic method Symptoms resolve post-obit eliminating lactose[1]
Differential diagnosis Irritable bowel syndrome, celiac disease, inflammatory bowel disease, milk allergy[one]
Treatment Decreasing lactose in the diet, lactase supplements, treat the underlying crusade[one]
Frequency ~65% of people (less common in Northern Europeans)[three]

Lactose intolerance is a mutual condition caused by a decreased power to digest lactose, a sugar found in dairy products.[1] Those afflicted vary in the corporeality of lactose they can tolerate before symptoms develop.[1] Symptoms may include abdominal pain, bloating, diarrhea, gas, and nausea.[ane] These symptoms typically kickoff thirty minutes to two hours after eating or drinking milk-based nutrient.[1] Their severity typically depends on the amount a person eats or drinks.[ane] Lactose intolerance does not cause damage to the alimentary canal.[two]

Lactose intolerance is due to the lack of the enzyme lactase in the modest intestines to suspension lactose downwards into glucose and galactose.[3] At that place are four types: primary, secondary, developmental, and congenital.[i] Primary lactose intolerance occurs as the amount of lactase declines every bit people age.[1] Secondary lactose intolerance is due to injury to the pocket-size intestine. Such injury could be the result of infection, celiac affliction, inflammatory bowel disease, or other diseases.[1] [4] Developmental lactose intolerance may occur in premature babies and usually improves over a short period of fourth dimension.[1] Built lactose intolerance is an extremely rare genetic disorder in which footling or no lactase is fabricated from nascency.[i] The onset of primary lactose intolerance, the most mutual type, is typically in late childhood or early on machismo,[i] but prevalence increases with historic period.[5]

Diagnosis may exist confirmed if symptoms resolve post-obit eliminating lactose from the diet.[1] Other supporting tests include a hydrogen jiff examination and a stool acerbity exam.[1] Other conditions that may produce similar symptoms include irritable bowel syndrome, celiac illness, and inflammatory bowel disease.[1] Lactose intolerance is unlike from a milk allergy.[1] Management is typically by decreasing the corporeality of lactose in the nutrition, taking lactase supplements, or treating the underlying illness.[1] [vi] People are usually able to drink at least one cup of milk per sitting without developing significant symptoms, with greater amounts tolerated if drunk with a repast or throughout the day.[1] [vii]

Well-nigh adults (around 65–70% of the globe's population) are afflicted by lactose malabsorption.[5] [8] Other mammals normally lose the ability to digest lactose after weaning and this was the bequeathed state of all humans before the recent evolution of lactase persistence, which extends lactose tolerance into adulthood.[ix] Lactase persistence evolved in several populations independently, probably equally an adaptation to the domestication of dairy animals around 10,000 years agone.[x] [eleven] Today the prevalence of lactose tolerance varies widely between regions and ethnic groups.[5] The power to digest lactose is most common in people of European descent, and to a bottom extent in parts of the Middle East and Africa.[5] [viii] Traditional food cultures reflect local variations in tolerance[5] and historically many societies have adjusted to low levels of tolerance past making dairy products that incorporate less lactose than fresh milk.[12] The medicalization of lactose intolerance equally a disorder has been attributed to biases in inquiry history (since virtually early on studies were conducted amongst populations where tolerance is the norm)[9] too equally the cultural and economical importance of milk in countries such every bit the United States.[xiii]

Terminology [edit]

Lactose intolerance primarily refers to a syndrome having 1 or more than symptoms upon the consumption of food substances containing lactose. Individuals may be lactose intolerant to varying degrees, depending on the severity of these symptoms. "Lactose malabsorption" refers to the physiological concomitant of lactase deficiency (i.eastward., the body does not have sufficient lactase capacity to digest the amount of lactose ingested).[2] Hypolactasia (lactase deficiency) is distinguished from defect.[xiv]

Lactose intolerance is not an allergy, because it is not an immune response, but rather a sensitivity to dairy acquired by lactase deficiency. Milk allergy, occurring in about 2% of the population, is a split condition, with distinct symptoms that occur when the presence of milk proteins trigger an immune reaction.[15]

Signs and symptoms [edit]

The primary manifestation of lactose intolerance is an adverse reaction to products containing lactose (primarily milk), including abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi, and airsickness (particularly in adolescents). These appear one-half to two hours after consumption.[i] The severity of these signs and symptoms typically increases with the corporeality of lactose consumed; most lactose-intolerant people tin can tolerate a sure level of lactose in their diets without sick furnishings.[xvi] [17]

Causes [edit]

Lactose intolerance is a consequence of lactase deficiency, which may exist genetic (primary hypolactasia and primary built alactasia) or environmentally induced (secondary or acquired hypolactasia). In either example, symptoms are acquired past insufficient levels of lactase in the lining of the duodenum. Lactose, a disaccharide molecule constitute in milk and dairy products, cannot be direct captivated through the wall of the pocket-size intestine into the bloodstream, so, in the absence of lactase, passes intact into the colon.[ commendation needed ] Leaner in the colon can metabolise lactose, and the resulting fermentation produces copious amounts of gas (a mixture of hydrogen, carbon dioxide, and methyl hydride) that causes the various abdominal symptoms. The unabsorbed sugars and fermentation products also raise the osmotic pressure of the colon, causing an increased period of water into the bowels (diarrhea).[18] [9]

The LCT cistron provides the instructions for making lactase. The specific DNA sequence in the MCM6 gene helps control whether the LCT gene is turned on or off.[19] At least several thousand years agone, some humans developed a mutation in the MCM6 gene that keeps the LCT gene turned on even after chest feeding is stopped.[20] Populations that are lactose intolerant lack this mutation. The LCT and MCM6 genes are both located on the long arm (q) of chromosome 2 in region 21. The locus can exist expressed as 2q21.[xx] The lactase deficiency besides could exist linked to certain heritages and varies widely. A 2016 study of over 60,000 participants from 89 countries constitute regional prevalence of lactose malabsorption was "64% (54–74) in Asia (except Middle East), 47% (33–61) in eastern Europe, Russia, and former Soviet Republics, 38% (CI xviii–57) in Latin America, lxx% (57–83) in the Middle E, 66% (45–88) in northern Africa, 42% (13–71) in northern America, 45% (nineteen–71) in Oceania, 63% (54–72) in sub-Saharan Africa, and 28% (nineteen–37) in northern, southern and western Europe."[five] Co-ordinate to Johns Hopkins Medicine, lactose intolerance is more than mutual in Asian Americans, African Americans, Mexican Americans, and Native Americans.[21] Analysis of the DNA of 94 aboriginal skeletons in Europe and Russia ended that the mutation for lactose tolerance appeared about 4,300 years ago and spread throughout the European population.[22]

Some man populations take developed lactase persistence, in which lactase production continues into adulthood probably as a response to the benefits of being able to digest milk from subcontract animals. Some accept argued that this links intolerance to natural pick favoring lactase-persistent individuals, but it is also consistent with a physiological response to subtract lactase product when it is not needed in cultures in which dairy products are non an available food source.[23] Although populations in Europe, India, Arabia, and Africa were outset idea to have high rates of lactase persistence considering of a single mutation, lactase persistence has been traced to a number of mutations that occurred independently.[11] Different alleles for lactase persistence have developed at to the lowest degree 3 times in East African populations, with persistence extending from 26% in Tanzania to 88% in the Beja pastoralist population in Sudan.[24]

The accumulation of epigenetic factors, primarily DNA methylation, in the extended LCT region, including the factor enhancer located in the MCM6 gene near C/T-13910 SNP, may also contribute to the onset of lactose intolerance in adults.[25] [26] Age-dependent expression of LCT in mice intestinal epithelium has been Dna methylation in the cistron enhancer.[26]

Lactose intolerance is classified according to its causes as:

Primary hypolactasia [edit]

Primary hypolactasia, or master lactase deficiency, is genetic, only affects adults, and is acquired past the absence of a lactase persistence allele. In individuals without the lactase persistence allele, less lactase is produced by the trunk over time, leading to hypolactasia in adulthood.[two] [27] The frequency of lactase persistence, which allows lactose tolerance, varies enormously worldwide, with the highest prevalence in Northwestern Europe, declines beyond southern Europe and the Middle E and is depression in Asia and well-nigh of Africa, although it is mutual in pastoralist populations from Africa.[9]

Secondary hypolactasia [edit]

Secondary hypolactasia or secondary lactase deficiency, too called caused hypolactasia or acquired lactase deficiency, is caused by an injury to the small intestine. This form of lactose intolerance can occur in both infants and lactase persistent adults and is generally reversible.[28] It may be acquired past acute gastroenteritis, coeliac disease, Crohn's disease, ulcerative colitis,[29] chemotherapy, intestinal parasites (such as giardia), or other environmental causes.[2] [thirty] [31] [32]

Principal congenital alactasia [edit]

Chief congenital alactasia, also called congenital lactase deficiency, is an extremely rare, autosomal recessive enzyme defect that prevents lactase expression from birth.[2] People with congenital lactase deficiency cannot digest lactose from nativity, and then cannot assimilate breast milk. This genetic defect is characterized by a complete lack of lactase (alactasia). About forty cases accept been reported worldwide, mainly limited to Finland. Before the 20th century, babies born with congenital lactase deficiency oftentimes did non survive,[2] but death rates decreased with soybean-derived babe formulas and manufactured lactose-free dairy products.[33]

Diagnosis [edit]

In order to assess lactose intolerance, intestinal function is challenged by ingesting more dairy products than tin can be readily digested. Clinical symptoms typically announced inside 30 minutes, merely may take up to two hours, depending on other foods and activities.[34] Substantial variability in response (symptoms of nausea, cramping, bloating, diarrhea, and flatulence) is to be expected, equally the extent and severity of lactose intolerance varies among individuals.

The next pace is to determine whether it is due to main lactase deficiency or an underlying disease that causes secondary lactase deficiency.[2] Physicians should investigate the presence of undiagnosed coeliac disease, Crohn disease, or other enteropathies when secondary lactase deficiency is suspected and infectious gastroenteritis has been ruled out.[2]

Lactose intolerance is distinct from milk allergy, an immune response to moo-cow'south milk proteins. They may be distinguished in diagnosis past giving lactose-free milk, producing no symptoms in the example of lactose intolerance, but the aforementioned reaction every bit to normal milk in the presence of a milk allergy. A person can take both weather. If positive confirmation is necessary, 4 tests are available.[35]

Hydrogen breath test [edit]

In a hydrogen jiff test, the most accurate lactose intolerance test, later on an overnight fast, 25 grams of lactose (in a solution with h2o) are swallowed. If the lactose cannot be digested, enteric bacteria metabolize information technology and produce hydrogen, which, along with methyl hydride, if produced, can exist detected on the patient'due south breath past a clinical gas chromatograph or compact solid-country detector. The exam takes about 2.five hours to consummate. If the hydrogen levels in the patient'due south jiff are loftier, they may have lactose intolerance. This test is not usually washed on babies and very young children, because it tin cause severe diarrhea.[36]

Lactose tolerance test [edit]

In conjunction, measuring blood glucose level every 10 to 15 minutes after ingestion will show a "apartment curve" in individuals with lactose malabsorption, while the lactase persistent will have a significant "height", with a typical height of l% to 100%, within one to two hours. Yet, due to the need for frequent claret sampling, this approach has been largely replaced past jiff testing.[37]

Later an overnight fast, blood is drawn and then 50 grams of lactose (in aqueous solution) are swallowed. Blood is then fatigued once more at the 30-minute, 1-hour, 2-hour, and three-hr marks. If the lactose cannot exist digested, blood glucose levels will rising by less than 20 mg/dl.[38]

Stool acidity test [edit]

This exam tin can be used to diagnose lactose intolerance in infants, for whom other forms of testing are risky or impractical.[39] The baby is given lactose to drink. If the individual is tolerant, the lactose is digested and absorbed in the small-scale intestine; otherwise, it is not digested and absorbed, and information technology reaches the colon. The leaner in the colon, mixed with the lactose, cause acidity in stools. Stools passed later the ingestion of the lactose are tested for level of acidity. If the stools are acidic, the babe is intolerant to lactose.[40] Stool pH in lactose intolerance is less than 5.v.

Intestinal biopsy [edit]

An intestinal biopsy must confirm lactase deficiency following discovery of elevated hydrogen in the hydrogen breath test.[41] Modern techniques have enabled a bedside exam, identifying presence of lactase enzyme on upper gastrointestinal endoscopy instruments.[42] All the same, for research applications such as mRNA measurements, a specialist laboratory is required.

Stool sugar chromatography [edit]

Chromatography can be used to split and place undigested sugars present in faeces. Although lactose may be detected in the faeces of people with lactose intolerance, this test is non considered reliable enough to conclusively diagnose or exclude lactose intolerance.[ citation needed ]

Genetic diagnostic [edit]

Genetic tests may be useful in assessing whether a person has primary lactose intolerance. Lactase activity persistence in adults is associated with ii polymorphisms: C/T 13910 and G/A 22018 located in the MCM6 gene.[27] 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. The process consists of extracting and amplifying DNA from the sample, following with a hybridation protocol in a strip. Colored bands are obtained as final outcome, and depending on the different combinations, information technology would be possible to determine whether the patient is lactose intolerant. This test allows a noninvasive definitive diagnostic.

Management [edit]

When lactose intolerance is due to secondary lactase deficiency, handling of the underlying disease may allow lactase activity to render to normal levels.[half-dozen] In people with celiac disease, lactose intolerance unremarkably reverts or improves several months subsequently starting a gluten-costless diet, but temporary dietary brake of lactose may be needed.[4] [43]

People with main lactase deficiency cannot change their body's power to produce lactase.[i] In societies where lactose intolerance is the norm, it is non considered a condition that requires treatment. Withal, where dairy is a larger component of the normal nutrition, a number of efforts may be useful. There are four full general principles in dealing with lactose intolerance: avoidance of dietary lactose, commutation to maintain nutrient intake, regulation of calcium intake, and utilize of enzyme substitute.[41] Regular consumption of dairy food by lactase deficient individuals may also reduce symptoms of intolerance by promoting colonic bacteria adaptation.[44]

Dietary avoidance [edit]

The primary way of managing the symptoms of lactose intolerance is to limit the intake of lactose to a level that can be tolerated.[45] Lactase deficient individuals vary in the amount of lactose they can tolerate,[i] and some written report that their tolerance varies over time, depending on health condition and pregnancy.[46] [47] However, as a rule of thumb, people with primary lactase deficiency and no small intestine injury are usually able to consume at least 12 grams of lactose per sitting without symptoms, or with but mild symptoms, with greater amounts tolerated if consumed with a meal or throughout the day.[1] [47] [44]

Typical lactose levels in dairy products[48]
Dairy product Serving size Lactose content Percentage
Milk, regular 250 ml/k 12 g 4.lxxx%
Milk, reduced fat 250 ml/g thirteen g 5.20%
Yogurt, plain, regular 200 g 9 g 4.l%
Yogurt, patently, low-fat 200 one thousand 12 g 6.00%
Cheddar cheese xxx g 0.02 g 0.07%
Cottage cheese 30 chiliad 0.1 g 0.33%
Butter 5 g 0.03 g 0.6%
Ice cream 50 g 3 g vi.00%

Lactose is found primarily in dairy products, which vary in the corporeality of lactose they contain:

  • Milk – unprocessed cow's milk is about four.7% lactose; goat'southward milk 4.7%;[49] sheep's milk 4.7%;[50] buffalo milk iv.86%;[51] and yak milk 4.93%.[52]
  • Sour foam and buttermilk – if fabricated in the traditional fashion, this may exist tolerable, but most modernistic brands add milk solids.[53]
  • Butter – the process of making butter largely removes lactose, only it is still present in pocket-sized quantities; clarified butter contains a negligible amount of lactose.[54]
  • Yogurt – lactobacilli used in the product of yogurt metabolize lactose to varying degrees, depending on the blazon of yogurt.[55] Some bacteria found in yogurt also produce their own lactase, which facilitates digestion in the intestines of lactose intolerant individuals.[44]
  • Cheese – fermentation also reduces the lactose content of cheeses and aging reduces it further; traditionally made hard cheeses might contain simply 10% of the lactose found in an equivalent volume of milk.[56] Nevertheless, manufactured cheeses may be produced using processes that do not accept the same lactose-reducing properties.[ citation needed ]

There is no standardized method for measuring the lactose content of food.[57] The stated dairy content of a product also varies according to manufacturing processes and labelling practices, and commercial terminology varies between languages and regions.[41] As a result, absolute figures for the amount of lactose consumed (past weight) may not be very reliable. Kosher products labeled pareve or fleishig are free of milk. However, if a "D" (for "dairy") is present next to the circled "K", "U", or other hechsher, the food production likely contains milk solids,[58] although it may as well simply indicate the product was produced on equipment shared with other products containing milk derivatives.

Lactose is also a commercial food condiment used for its texture, flavor, and adhesive qualities. It is found in additives labelled as casein, caseinate, whey, lactoserum, milk solids, modified milk ingredients, etc.[ citation needed ] As such lactose is found in foods such equally processed meats (sausages/hot dogs, sliced meats, pâtés),[58] gravy stock powder, margarines,[59] sliced breads,[60] [61] breakfast cereals, tater fries,[62] candy foods, medications, prepared meals, meal replacements (powders and bars), poly peptide supplements (powders and bars), and fifty-fifty beers in the milk stout manner. Some barbecue sauces and liquid cheeses used in fast-nutrient restaurants may also contain lactose. Lactose is often used as the chief filler (main ingredient) in most prescription and not-prescription solid pill form medications, though production labeling seldom mentions the presence of 'lactose' or 'milk', and neither do product monograms provided to pharmacists, and about pharmacists are unaware of the very wide calibration yet mutual use of lactose in such medications until they contact the supplier or manufacturer for verification.[ citation needed ]

Milk substitutes [edit]

Institute-based milks and derivatives such as soy milk, rice milk, almond milk, coconut milk, hazelnut milk, oat milk, hemp milk, macadamia nut milk, and peanut milk are inherently lactose-free. Low-lactose and lactose-free versions of foods are often available to supersede dairy-based foods for those with lactose intolerance.[63]

Lactase supplements [edit]

When lactose avoidance is not possible, or on occasions when a person chooses to consume such items, so enzymatic lactase supplements may exist used.[64] [65]

Lactase enzymes similar to those produced in the small intestines of humans are produced industrially by fungi of the genus Aspergillus. The enzyme, β-galactosidase, is bachelor in tablet course in a variety of doses, in many countries without a prescription. It functions well merely in loftier-acid environments, such equally that constitute in the human gut due to the addition of gastric juices from the breadbasket. Unfortunately, also much acrid can denature it,[66] so it should not exist taken on an empty stomach. Likewise, the enzyme is ineffective if it does non attain the small intestine past the time the problematic food does. Lactose-sensitive individuals can experiment with both timing and dosage to fit their particular needs.

While essentially the same process equally normal intestinal lactose digestion, directly 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. Its main use is in producing the lactose-gratis or lactose-reduced dairy products sold in supermarkets.[67]

Rehabituation to dairy products [edit]

Regular consumption of dairy foods containing lactose can promote a colonic bacteria adaptation, enhancing a favorable microbiome, which allows people with primary lactase deficiency to diminish their intolerance and to consume more than dairy foods.[44] [47] [68] The way to induce tolerance is based on progressive exposure, consuming smaller amounts frequently, distributed throughout the day.[69] Lactose intolerance can also exist managed by ingesting live yogurt cultures containing lactobacilli that are able to digest the lactose in other dairy products.[70]

Epidemiology [edit]

Rough rates of lactose intolerance in dissimilar regions of the globe

An estimate of the percentage of adults that can assimilate lactose in the indigenous population of the Quondam World[71]

Overall, about 65% of people experience some form of lactose intolerance equally they age past infancy, but in that location are significant differences between populations and regions; rates are equally low every bit 5% among northern Europeans and as high as over 90% of adults in some communities of Asia.[72]

Some populations, from an evolutionary perspective, have a better genetic makeup for tolerating lactose than others. In northern European countries, early adoption of dairy farming conferred a selective evolutionary advantage to individuals that could ameliorate tolerate lactose. This led to higher frequencies of these countries' people having a tolerance to lactose. Conversely, regions of the south, such as Africa, did not prefer dairy farming as early on historically and therefore tolerance from milk consumption did not develop the aforementioned way as in northern European countries.[44] Lactose intolerance is common among people of Jewish descent, as well every bit from West Africa, the Arab countries, Greece, and Italy.[72] Different populations will present certain gene constructs depending on the evolutionary and cultural pre-settings of the geographical region.[44]

History [edit]

Greater lactose tolerance has come well-nigh in two means.[73] Some populations have developed genetic changes that resulted in ongoing production of lactase.[73] Other populations adult cooking methods like milk fermentation.[73]

Lactase persistence is the phenotype associated with diverse autosomal dominant alleles prolonging the activeness of lactase beyond infancy; conversely, lactase nonpersistence is the phenotype associated with chief lactase deficiency. Amidst mammals, lactase persistence is unique to humans—information technology evolved relatively recently (in the last 10,000 years) among some populations, and the majority of people worldwide remain lactase nonpersistent.[9] Effectually 8,000 years agone in modern-day Turkey, humans became reliant on newly domesticated animals such equally cows, sheep, and goats. This newfound reliance resulted in higher frequency near the gene responsible for producing the lactase enzyme.[74] Populations that domesticated animals that could be milked continued to be lactase persistent in areas such as North and North western Europe, Scandinavia, the modern Middle East and Northwestern India. Populations that raised animals not used for milk made up the balance of the earth's populations. These populations tend to have 90-100 percent of a lactose intolerant charge per unit.[75] For this reason, lactase persistence is of some interest to the fields of anthropology, human genetics, and archeology, which typically use the genetically derived persistence/non-persistence terminology.[76]

The rising of dairy and producing dairy related products from moo-cow milk solitary, varies across different regions of the world, aside from genetic predisposition.[44] The process of turning milk into cheese dates dorsum earlier than 5200 BC.[77]

Deoxyribonucleic acid analysis in Feb 2012 revealed that Ötzi was lactose intolerant, supporting the theory that lactose intolerance was even so common at that fourth dimension, despite the increasing spread of agriculture and dairying.[78]

Genetic assay shows lactase persistence has adult several times in dissimilar places independently in an example of convergent development.[24]

History of research [edit]

It is not until relatively recently that medicine recognised the worldwide prevalence of lactose intolerance and its genetic causes. Its symptoms were described as early every bit Hippocrates (460–370 BC),[79] simply until the 1960s, the prevailing assumption was that tolerance was the norm. Intolerance was explained as the issue of a milk allergy, abdominal pathogens, or every bit being psychosomatic – it being recognised that some cultures did non practice dairying, and people from those cultures oftentimes reacted desperately to consuming milk.[80] [81] Two reasons have been given for this misconception. One was that near European-descended populations have a low incidence of lactose intolerance[82] and an extensive cultural history of dairying. Therefore, tolerance actually was the norm in nearly of the societies investigated by early medical researchers. Some other reason is that lactose intolerance tends to be nether-reported: lactose intolerant individuals tin tolerate at least some lactose before they prove symptoms, and their symptoms differ in severity. Nearly people are able to digest a small quantity of milk, for example in tea or java, without suffering whatever adverse effects.[xvi] Fermented dairy products, such as cheese, also contain significantly less lactose than plain milk. Therefore, in societies where tolerance is the norm, many lactose intolerant people who consume only small-scale amounts of dairy, or have only mild symptoms, may be unaware that they cannot digest lactose.

Eventually, in the 1960s, information technology was recognised that lactose intolerance was correlated with race in the United States.[83] [84] [85] Subsequent research revealed that lactose intolerance was more common globally than tolerance,[86] [87] [88] [89] [90] and that the variation was due to genetic differences, non an accommodation to cultural practices.[81] [91]

Other animals [edit]

About mammals normally cease to produce lactase and get lactose intolerant later weaning.[9] The downregulation of lactase expression in mice could be attributed to the accumulation of DNA methylation in the Lct gene and the next Mcm6 gene.[92]

See also [edit]

  • Nutrient intolerance
  • Gastroenterology
  • Glucose-galactose malabsorption
  • Gluten intolerance
  • Lactase persistence
  • Soy cheese
  • Soy milk and found milk
  • Sucrose intolerance

References [edit]

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External links [edit]

  • Lactose intolerance at Curlie
  • Wade, Nicholas (one March 2010). "Human Culture, an Evolutionary Force". New York Times.

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Source: https://en.wikipedia.org/wiki/Lactose_intolerance

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