Lactose intolerance

Short description: Inability to digest lactose

Not to be confused with Milk allergy.

Lactose intolerance

Other names| Lactase deficiency, hypolactasia, alactasia
Lactose is made up of two simple sugars
Specialty| Gastroenterology
Symptoms| Abdominal pain, bloating, diarrhea, flatulence, nausea[1]
Complications| Does not cause damage to the GI tract[2]
Usual onset| 30–120 minutes after consuming dairy products[1]
Duration| Lifelong
Causes| Non-increased ability to digest lactose (genetic, small intestine injury)[1]
Differential diagnosis| Irritable bowel syndrome, celiac disease, inflammatory bowel disease, milk allergy[1]
Treatment| Decreasing lactose in the diet, lactase supplements, treat the underlying cause[1]
Medication| Lactase
Frequency| ~65% of people worldwide (less common in Northern Europeans and East Africans)[3]
Deaths| 0

Lactose intolerance is a lessened ability or a complete inability to digest lactose, a sugar found in dairy products.[1] Humans vary in the amount of lactose they can tolerate before symptoms develop.[1] Symptoms may include abdominal pain, bloating, diarrhea, flatulence, and nausea.[1] These symptoms typically start thirty minutes to two hours after eating or drinking something containing lactose,[1] with the severity typically depending on the amount consumed.[1] Lactose intolerance does not cause damage to the gastrointestinal tract.[2]

Lactose intolerance is due to the lack of the enzyme lactase in the small intestines to break lactose down into glucose and galactose.[3] There are four types: primary, secondary, developmental, and congenital.[1] Primary lactose intolerance occurs as the amount of lactase declines as people grow up.[1] Secondary lactose intolerance is due to injury to the small intestine. Such injury could be the result of infection, celiac disease, inflammatory bowel disease, or other diseases.[1][4] Developmental lactose intolerance may occur in premature babies and usually improves over a short period of time.[1] Congenital lactose intolerance is an extremely rare genetic disorder in which little or no lactase is made from birth.[1] The reduction of lactase production starts typically in late childhood or early adulthood,[1] and prevalence increases with age.

Diagnosis may be confirmed if symptoms resolve following eliminating lactose from the diet.[1] Other supporting tests include a hydrogen breath test and a stool acidity test.[1] Other conditions that may produce similar symptoms include irritable bowel syndrome, celiac disease, and inflammatory bowel disease.[1] Lactose intolerance is different from a milk allergy.[1] Management is typically by decreasing the amount of lactose in the diet, taking lactase supplements (the amount of supplements should be based on the amount of lactose consumed), or treating the underlying disease.[1][5] 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.[1][6]

Worldwide, around 65% of adults are affected by lactose malabsorption.[7] Other mammals usually lose the ability to digest lactose after weaning. Lactose intolerance is the ancestral state of all humans before the recent evolution of lactase persistence in some populations, which extends lactose tolerance into adulthood.[8] Lactase persistence evolved in several populations independently, probably as an adaptation to the domestication of dairy animals around 10,000 years ago.[9][10] Today the prevalence of lactose tolerance varies widely between regions and ethnic groups. The ability to digest lactose is most common in people of Northern European descent, and to a lesser extent in some parts of Central Asia, West Asia, and Africa.[7]

Lactose intolerance is most common among people of East Asian descent (with 90% lactose intolerance), people of Jewish descent, people in African and Arab countries, and among some people of Southern European descent. Traditional food cultures reflect local variations in tolerance and historically many societies have adapted to low levels of tolerance by making dairy products that contain less lactose than fresh milk.[11] One ethnographic example of this is kumis, a fermented milk product that contains little to no lactose, which is the main source of dairy nutrition in Mongolia.[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,[8] as well as the cultural and economic importance and impact of milk in countries such as the United States.[13]

## Contents

* 1 Terminology
* 2 Signs and symptoms
* 3 Causes
* 4 Diagnosis
* 4.1 Hydrogen breath test
* 4.2 Lactose tolerance test
* 4.3 Stool acidity test
* 4.4 Intestinal biopsy
* 4.5 Stool sugar chromatography
* 4.6 Genetic diagnostic
* 5 Management
* 5.1 Dietary avoidance
* 5.2 Milk substitutes
* 5.3 Lactase supplements
* 5.4 Rehabituation to dairy products
* 6 Epidemiology
* 7 History
* 7.1 History of research
* 8 Other animals
* 9 See also
* 10 References
* 11 External links

## Terminology

Lactose intolerance primarily refers to a syndrome with one or more symptoms upon the consumption of food substances containing lactose sugar. Individuals may be lactose intolerant to varying degrees, depending on the severity of these symptoms.

Hypolactasia is the term specifically for the small intestine producing little or no lactase enzyme.[14] If a person with hypolactasia consumes lactose sugar, it results in lactose malabsorption.[2] The digestive system is unable to process the lactose sugar, and the unprocessed sugars in the gut produce the symptoms of lactose intolerance.

Lactose intolerance is not an allergy, because it is not an immune response, but rather a sensitivity to dairy caused by a deficiency of lactase enzyme. Milk allergy, occurring in about 2% of the population, is a separate condition, with distinct symptoms that occur when the presence of milk protein, whey, triggers an immune reaction.[15] A milk allergy most often appears in the first year of life, while lactose intolerance typically appears later in life.[16]

Lauren Ornelas, the founder of Food Empowerment Project, has coined[17][18] the term lactose normal[19] to replace lactose intolerance, as the latter term suggests that there is something abnormal[20] or medically pathological about it, and originated in a context of cultural bias and failure to recognize the fact that most weaned humans are unable to digest lactose. Some have expressed preference for the term lactose normal.[21][22]

## Signs and symptoms

The principal manifestation of lactose intolerance is an adverse reaction to products containing lactose (primarily milk), including abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi, and vomiting (particularly in adolescents). These appear thirty minutes to two hours after consumption.[1] The severity of these signs and symptoms typically increases with the amount of lactose consumed; most lactose-intolerant people can tolerate a certain level of lactose in their diets without ill effects.[23][24]

Because lactose intolerance is not an allergy, it does not produce allergy symptoms (such as itching, hives, or anaphylaxis).

## Causes

Lactose intolerance is a consequence of lactase deficiency, which may be genetic (primary hypolactasia and primary congenital alactasia) or environmentally induced (secondary or acquired hypolactasia). In either case, symptoms are caused by insufficient levels of lactase in the lining of the duodenum. 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. 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).[25][8]

Lactose intolerance in infants (congenital lactase deficiency) is caused by mutations in the LCT gene. The LCT gene provides the instructions for making lactase. 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.[26] Lactose intolerance in adulthood is a result of gradually decreasing activity (expression) of the LCT gene after infancy, which occurs in most humans. The specific DNA sequence in the MCM6 gene helps control whether the LCT gene is turned on or off.[27] At least several thousand years ago, some humans developed a mutation in the MCM6 gene that keeps the LCT gene turned on even after breast feeding is stopped.[28] 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 be expressed as 2q21.[28] The lactase deficiency also could be linked to certain heritages and varies widely. A 2016 study of over 60,000 participants from 89 countries found 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 18–57) in Latin America, 70% (57–83) in the Middle East, 66% (45–88) in northern Africa, 42% (13–71) in northern America, 45% (19–71) in Oceania, 63% (54–72) in sub-Saharan Africa, and 28% (19–37) in northern, southern and western Europe." According to Johns Hopkins Medicine, in the United States lactose intolerance is more common in Asian Americans, African Americans, Mexican Americans, and Native Americans.[29] 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.[30]

Some human populations have developed lactase persistence, in which lactase production continues into adulthood probably as a response to the benefits of being able to digest milk from farm animals. Some have argued that this links intolerance to natural selection favoring lactase-persistent individuals, but it is also consistent with a physiological response to decrease lactase production when it is not needed in cultures in which dairy products are not an available food source.[31] Although populations in Europe, India, Arabia, and Africa were first thought to have high rates of lactase persistence because of a single mutation, lactase persistence has been traced to a number of mutations that occurred independently.[10] Different alleles for lactase persistence have developed at least three times in East African populations, with persistence extending from 26% in Tanzania to 88% in the Beja pastoralist population in Sudan.[32]

The accumulation of epigenetic factors, primarily DNA methylation, in the extended LCT region, including the gene enhancer located in the MCM6 gene near C/T-13910 SNP, may also contribute to the onset of lactose intolerance in adults.[33][34] Age-dependent expression of LCT in mice intestinal epithelium has been linked to DNA methylation in the gene enhancer.[34]

Lactose intolerance is classified according to its causes as:

Primary hypolactasia
Primary hypolactasia, or primary lactase deficiency, is genetic, develops in childhood at various ages, and is caused by the absence of a lactase persistence allele. In individuals without the lactase persistence allele, less lactase is produced by the body over time, leading to hypolactasia in adulthood.[2][35] The frequency of lactase persistence, which allows lactose tolerance, varies enormously worldwide, with the highest prevalence in Northwestern Europe, declines across southern Europe and the Middle East and is low in Asia and most of Africa, although it is common in pastoralist populations from Africa.[8]
Secondary hypolactasia
Secondary hypolactasia or secondary lactase deficiency, also called acquired 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.[36] It may be caused by acute gastroenteritis, coeliac disease, Crohn's disease, ulcerative colitis,[37] chemotherapy, intestinal parasites (such as giardia), or other environmental causes.[2][38][39][40]
Primary congenital alactasia
Primary 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 birth, so cannot digest breast milk. This genetic defect is characterized by a complete lack of lactase (alactasia). About 40 cases have been reported worldwide, mainly limited to Finland. Before the 20th century, babies born with congenital lactase deficiency often did not survive,[2] but death rates decreased with soybean-derived infant formulas and manufactured lactose-free dairy products.[41]

## Diagnosis

In order to assess lactose intolerance, intestinal function is challenged by ingesting more dairy products than can be readily digested. Clinical symptoms typically appear within 30 minutes, but may take up to two hours, depending on other foods and activities.[42] 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.[43]

The next step is to determine whether it is due to primary lactase deficiency or an underlying disease that causes secondary lactase deficiency.[2] Physicians should investigate the presence of undiagnosed coeliac disease, Crohn's 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 cow's milk proteins. They may be distinguished in diagnosis by giving lactose-free milk, producing no symptoms in the case of lactose intolerance, but the same reaction as to normal milk in the presence of a milk allergy. A person can have both conditions. If positive confirmation is necessary, four tests are available.[44]

### Hydrogen breath test

In a hydrogen breath test, the most accurate lactose intolerance test, after an overnight fast, 25 grams of lactose (in a solution with water) are swallowed. If the lactose cannot be digested, enteric bacteria metabolize it and produce hydrogen, which, along with methane, if produced, can be detected on the patient's breath by a clinical gas chromatograph or compact solid-state detector. The test takes about 2.5 hours to complete. If the hydrogen levels in the patient's breath are high, they may have lactose intolerance. This test is not usually done on babies and very young children, because it can cause severe diarrhea.[45]

### Lactose tolerance test

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. However, due to the need for frequent blood sampling, this approach has been largely replaced by breath testing.[46]

After an overnight fast, blood is drawn and then 50 grams of lactose (in aqueous solution) are swallowed. Blood is then drawn again at the 30-minute, 1-hour, 2-hour, and 3-hour marks. If the lactose cannot be digested, blood glucose levels will rise by less than 20 mg/dl.[47]

### Stool acidity test

This test can be used to diagnose lactose intolerance in infants, for whom other forms of testing are risky or impractical.[48] The infant is given lactose to drink. If the individual is tolerant, the lactose is digested and absorbed in the small intestine; otherwise, it is not digested and absorbed, and it reaches the colon. The bacteria in the colon, mixed with the lactose, cause acidity in stools. Stools passed after the ingestion of the lactose are tested for level of acidity. If the stools are acidic, the infant is intolerant to lactose.[49] Stool pH in lactose intolerance is less than 5.5.

### Intestinal biopsy

An intestinal biopsy must confirm lactase deficiency following discovery of elevated hydrogen in the hydrogen breath test.[50] Modern techniques have enabled a bedside test, identifying presence of lactase enzyme on upper gastrointestinal endoscopy instruments.[51] However, for research applications such as mRNA measurements, a specialist laboratory is required.

### Stool sugar chromatography

### Genetic diagnostic

## Management

When lactose intolerance is due to secondary lactase deficiency, treatment of the underlying disease may allow lactase activity to return to normal levels.[5] In people with celiac disease, lactose intolerance normally reverts or improves several months after starting a gluten-free diet, but temporary dietary restriction of lactose may be needed.[4][52]

People with primary lactase deficiency cannot modify their body's ability to produce lactase.[1] In societies where lactose intolerance is the norm, it is not considered a condition that requires treatment. However, where dairy is a larger component of the normal diet, a number of efforts may be useful. There are four general principles in dealing with lactose intolerance: avoidance of dietary lactose, substitution to maintain nutrient intake, regulation of calcium intake, and use of enzyme substitute.[50] Regular consumption of dairy food by lactase deficient individuals may also reduce symptoms of intolerance by promoting colonic bacteria adaptation.[11]

### Dietary avoidance

The primary way of managing the symptoms of lactose intolerance is to limit the intake of lactose to a level that can be tolerated.[53] Lactase deficient individuals vary in the amount of lactose they can tolerate,[1] and some report that their tolerance varies over time, depending on health status and pregnancy.[54][55] 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 only mild symptoms, with greater amounts tolerated if consumed with a meal or throughout the day.[1][55][11]

Typical lactose levels in dairy products[56] Dairy product | Serving
size | Lactose
content | Fraction

|
|
|

Milk, regular  | 250 ml(g)  | 12 g  | 4.8%0
Milk, reduced fat  | 250 ml(g)  | 13 g  | 5.2%0
Yogurt, plain, regular  | 200 g  | 9 g  | 4.5%0
Yogurt, plain, low-fat  | 200 g  | 12 g  | 6.0%0
Cheddar cheese  | 30 g  | 0.02 g  | 0.07%
Cottage cheese  | 30 g  | 0.1 g  | 0.33%
Butter  | 5 g  | 0.03 g  | 0.6%0
Ice cream  | 50 g  | 3 g  | 6.0%0

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

* Milk – unprocessed cow's milk is about 4.7% lactose; goat's milk 4.7%;[57] sheep's milk 4.7%;[58] buffalo milk 4.86%;[59] and yak milk 4.93%.[60]
* Sour cream and buttermilk – if made in the traditional way, this may be tolerable, but most modern brands add milk solids.[61]
* Yogurt – lactobacilli used in the production of yogurt metabolize lactose to varying degrees, depending on the type of yogurt.[62] Some bacteria found in yogurt also produce their own lactase, which facilitates digestion in the intestines of lactose intolerant individuals.[11]
* Cheese – The curdling of cheese concentrates most of the lactose from milk into the whey: fresh cottage cheese contains 7% of the lactose found in an equivalent mass of milk.[56] Further fermentation and aging converts the remaining lactose into lactic acid; traditionally made hard cheeses, which have a long ripening period, contain virtually no lactose:[63] cheddar contains less than 1.5% of the lactose found in an equivalent mass of milk.[56] However, manufactured cheeses may be produced using processes that do not have the same lactose-reducing properties.[64]

There used to be[65] a lack of standardization on how lactose is measured and reported in food. The different molecular weights of anhydrous lactose or lactose monohydrate result in up to 5% difference.[66] One source recommends using the "carbohydrates" or "sugars" part of the nutritional label as surrogate for lactose content,[63] but such "lactose by difference" values are not assured to correspond to real lactose content.[65] The stated dairy content of a product also varies according to manufacturing processes and labelling practices, and commercial terminology varies between languages and regions.[50] As a result, absolute figures for the amount of lactose consumed (by 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 product likely contains milk solids,[67] although it may also simply indicate the product was produced on equipment shared with other products containing milk derivatives.

Lactose is also a commercial food additive 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. As such, lactose is found in foods such as processed meats (sausages/hot dogs, sliced meats, pâtés),[67] gravy stock powder, margarines,[68] sliced breads,[69][70] breakfast cereals, potato chips,[71] processed foods, medications, prepared meals, meal replacements (powders and bars), protein supplements (powders and bars), and even beers in the milk stout style. Some barbecue sauces and liquid cheeses used in fast-food restaurants may also contain lactose. When dining out, carrying lactose intolerance cards that explain dietary restrictions in the local language can help communicate needs to restaurant staff.[72] 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.[citation needed]

### Milk substitutes

Plant-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 replace dairy-based foods for those with lactose intolerance.[73]

### Lactase supplements

When lactose avoidance is not possible, or on occasions when a person chooses to consume such items, then enzymatic lactase supplements may be used.[74][75]

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 available in tablet form in a variety of doses, in many countries without a prescription. It functions well only in high-acid environments, such as that found in the human gut due to the addition of gastric juices from the stomach. Unfortunately, too much acid can denature it,[76] so it should not be taken on an empty stomach. Also, the enzyme is ineffective if it does not reach the small intestine by 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 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. Its main use is in producing the lactose-free or lactose-reduced dairy products sold in supermarkets.[77]

### Rehabituation to dairy products

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 dairy foods.[11][55][78] The way to induce tolerance is based on progressive exposure, consuming smaller amounts frequently, distributed throughout the day.[79] Lactose intolerance can also be managed by ingesting live yogurt cultures containing lactobacilli that are able to digest the lactose in other dairy products.[80]

## Epidemiology

An estimate of the percentage of adults that can digest lactose in the indigenous population of the Old World and Oceania[81]

Worldwide, about 80% of people experience some form of lactose intolerance as they age past infancy, but there are significant differences between populations and regions. As few as 5% of northern Europeans are lactose intolerant, while as many as 90% of adults in parts of Asia are lactose intolerant.[82]

In northern European countries, early adoption of dairy farming conferred a selective evolutionary advantage to individuals that could tolerate lactose. This led to higher frequencies of lactose tolerance in these countries. For example, almost 100% of Irish people are predicted to be lactose tolerant.[81] 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.[11] Lactose intolerance is common among people of Jewish descent, as well as from West Africa, the Arab countries, Greece, and Italy.[82] Different populations will present certain gene constructs depending on the evolutionary and cultural pre-settings of the geographical region.[11]

## History

Main article: Biology:Lactase persistence

Greater lactose tolerance has come about in two ways.[83] Some populations have developed genetic changes to allow the digestion of lactose: lactase persistence.[83] Other populations developed cooking methods like milk fermentation.[83]

Lactase persistence in humans evolved relatively recently (in the last 10,000 years) among some populations. Around 8,000 years ago in modern-day Turkey, humans became reliant on newly-domesticated animals that could be milked; such as cows, sheep, and goats. This resulted in higher frequency of lactase persistence.[84] Lactase persistence became high in regions such as Europe, Scandinavia, the Middle East and Northwestern India. However, most people worldwide remain lactase non-persistent.[8] Populations that raised animals not used for milk tend to have 90–100 percent of a lactose intolerant rate.[85] For this reason, lactase persistence is of some interest to the fields of anthropology, human genetics, and archaeology, which typically use the genetically derived persistence/non-persistence terminology.[86]

The rise of dairy and producing dairy related products from cow milk alone, varies across different regions of the world, aside from genetic predisposition.[11] The process of turning milk into cheese dates back earlier than 5200 BC.[87]

DNA analysis in February 2012 revealed that Ötzi was lactose intolerant, supporting the theory that lactose intolerance was still common at that time, despite the increasing spread of agriculture and dairying.[88]

Genetic analysis shows lactase persistence has developed several times in different places independently in an example of convergent evolution.[32]

### History of research

It was not until relatively recently that medicine recognised the worldwide prevalence of lactose intolerance and its genetic causes. Its symptoms were described as early as Hippocrates (460–370 BC),[89] but until the 1960s, the prevailing assumption in Western medicine was that tolerance was the norm. Intolerance was explained as the result of a milk allergy, intestinal pathogens, or as being psychosomatic – it being recognised that some cultures did not practice dairying, and people from those cultures often reacted badly to consuming milk.[90][91] Two reasons have been given for this misconception. One was that early research was conducted solely on European-descended populations, which have an unusually low incidence of lactose intolerance[81] and an extensive cultural history of dairying. As a result, researchers wrongly concluded that tolerance was the global norm. Another reason is that lactose intolerance tends to be under-reported: most lactose-intolerant individuals can tolerate at least some lactose before they show symptoms, and their symptoms differ in severity. The large majority of people are able to digest a small quantity of milk (e.g., the amount used in a cup of tea or coffee) without developing any adverse effects.[23] 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 amounts of dairy, or have only mild symptoms, may be unaware that they cannot digest lactose.

Eventually, in the 1960s, it was recognised that lactose intolerance was correlated with race in the United States.[92][93][94] Subsequent research revealed that lactose intolerance was more common globally than tolerance,[95][96][97][98][99] and that the variation was due to genetic differences, not an adaptation to cultural practices.[91][100]

## Other animals

Most mammals normally cease to produce lactase and become lactose intolerant after weaning.[8] The downregulation of lactase expression in mice could be attributed to the accumulation of DNA methylation in the Lct gene and the adjacent Mcm6 gene.[34]

## See also

* Food intolerance
* Gastroenterology
* Glucose-galactose malabsorption
* Gluten intolerance
* Lactase persistence
* Lactagen
* Recent human evolution
* Soy cheese
* Soy milk and plant milk
* Sucrose intolerance

## References

1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 "Lactose Intolerance". June 2014. https://www.niddk.nih.gov/health-information/digestive-diseases/lactose-intolerance?dkrd=hispt0264.
2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 "Lactose intolerance in infants, children, and adolescents". Pediatrics 118 (3): 1279–86. September 2006. doi:10.1542/peds.2006-1721. PMID 16951027. Bibcode: 2006Pedia.118.1279H.
3. ↑ 3.0 3.1 Malik, TF; Panuganti, KK (January 2020). "Lactose Intolerance". (StatPearls [Internet]). StatPearls. NBK532285.
4. ↑ 4.0 4.1 "Diagnosing and Treating Intolerance to Carbohydrates in Children". Nutrients 8 (3): 157. March 2016. doi:10.3390/nu8030157. PMID 26978392.
5. ↑ 5.0 5.1 "Lactose intolerance". Asia Pacific Journal of Clinical Nutrition 24 (Suppl 1): S9–13. 2015. doi:10.6133/apjcn.2015.24.s1.02. PMID 26715083.
6. ↑ "NIH consensus development conference statement: Lactose intolerance and health". NIH Consensus and State-Of-The-Science Statements 27 (2): 1–27. February 2010. PMID 20186234. https://consensus.nih.gov/2010/lactosestatement.htm.
7. ↑ 7.0 7.1 "Lactase Non-persistence and Lactose Intolerance". Current Gastroenterology Reports 19 (5). May 2017. doi:10.1007/s11894-017-0558-9. PMID 28421381.
8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 "Genetics of lactase persistence and lactose intolerance". Annual Review of Genetics 37: 197–219. 2003. doi:10.1146/annurev.genet.37.110801.143820. PMID 14616060.
9. ↑ "On the Evolution of Lactase Persistence in Humans". Annual Review of Genomics and Human Genetics 18 (1): 297–319. August 2017. doi:10.1146/annurev-genom-091416-035340. PMID 28426286.
10. ↑ 10.0 10.1 "Lactose digestion and the evolutionary genetics of lactase persistence". Human Genetics 124 (6): 579–91. January 2009. doi:10.1007/s00439-008-0593-6. PMID 19034520.
11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 "The Interrelationships between Lactose Intolerance and the Modern Dairy Industry: Global Perspectives in Evolutional and Historical Backgrounds". Nutrients 7 (9): 7312–31. August 2015. doi:10.3390/nu7095340. PMID 26404364.
12. ↑ Abdel-Salam, Ahmed M.; Al-Dekheil, Ali; Babkr, Ali; Farahna, Mohammed; Mousa, Hassan M. (December 2010). "High fiber probiotic fermented mare's milk reduces the toxic effects of mercury in rats". North American Journal of Medical Sciences 2 (12): 569–575. doi:10.4297/najms.2010.2569. PMID 22558569. ""Fermentation destroys lactose in milk, converting it into lactic acid, ethanol, and carbon dioxide. This makes kumis acceptable for lactose intolerant people. Traditional kumis is prepared by mixing fermented milk with fresh raw mares' milk."".
13. ↑ Wiley, Andrea S. (2004). ""Drink Milk for Fitness": The Cultural Politics of Human Biological Variation and Milk Consumption in the United States". American Anthropologist 106 (3): 506–517. doi:10.1525/aa.2004.106.3.506.
14. ↑ "Hypolactasia: a common enzymes deficiency leading to lactose malabsorption and intolerance". Polskie Archiwum Medycyny Wewnetrznej 122 (Suppl 1): 60–4. 2012. doi:10.20452/pamw.1519. PMID 23222197.
15. ↑ "Cow's milk allergy versus cow milk intolerance". Annals of Allergy, Asthma & Immunology 89 (6 Suppl 1): 56–60. December 2002. doi:10.1016/S1081-1206(10)62124-2. PMID 12487206.
16. ↑ "Symptoms & Causes of Lactose Intolerance - NIDDK" (in en-US). https://www.niddk.nih.gov/health-information/digestive-diseases/lactose-intolerance/symptoms-causes.
17. ↑ "Citations". Greener by Default. https://www.greenerbydefault.com/citations. Retrieved June 8, 2026. "lauren Ornelas coined the term"
18. ↑ Eisen, Jessica (January 2019). "Milked: Nature, Necessity, and American Law". p. 88. https://lawcat.berkeley.edu/nanna/record/1128892/files/fulltext.pdf. Retrieved June 8, 2026. "Food justice advocate lauren Ornelas, for example, emphasizes her preference for the term lactose normal over the term lactose intolerant, given that lactase impersistence is in fact the global norm, and in light of the colonial origins of milk-drinking in the Americas."
This related URL may also be of interest: https://lawcat.berkeley.edu/record/1128892?v=pdf
19. ↑ "Lactose Intolerance". Food Empowerment Project. https://foodispower.org/access-health/lactose-intolerance/. Retrieved June 8, 2026. "we refer to those who do not digest lactose as 'lactose normal'"
20. ↑ "Understanding Lactose Intolerance Fact Sheet" (PDF). Physicians Committee for Responsible Medicine (PCRM). August 20, 2024. p. 1. https://pcrm.widen.net/s/ll7l5msrmn. Retrieved June 11, 2026. "This has resulted in an important change in terminology: Those who could not digest milk were once called 'lactose intolerant' or 'lactase deficient.' They are now regarded as the norm"
21. ↑ "Native Food for Life: Lesson 4". Grand Traverse Band of Ottawa and Chippewa Indians. July 30, 2021. p. 2. https://www.gtbindians.org/downloads/lesson_4_class_handout.pdf. Retrieved June 8, 2026. "The term lactose intolerant is not an accurate name. A better term would be lactose normal. ... being lactose normal is not a problem that needs to be fixed!"
22. ↑ Kraus-Polk, Julian; Hamerschlag, Kari (March 2021). "The State of School Lunch in California". Friends of the Earth. p. 13. https://foe.org/wp-content/uploads/2021/03/SchoolFoodReport_No-Execsummary.pdf. Retrieved June 8, 2026.
23. ↑ 23.0 23.1 "Milk intolerance and microbe-containing dairy foods". Journal of Dairy Science 70 (2): 397–406. February 1987. doi:10.3168/jds.S0022-0302(87)80023-1. PMID 3553256. https://www.journalofdairyscience.org/article/S0022-0302(87)80023-1/abstract.
24. ↑ "Tolerance of different dairy products in subjects with symptomatic lactose malabsorption due to adult type hypolactasia". Gastroenterology Review 5: 310–315. 2011. doi:10.5114/pg.2011.25381.
25. ↑ Lactose intolerance~overview at eMedicine
26. ↑ "Lactose intolerance: MedlinePlus Genetics" (in en). https://medlineplus.gov/genetics/condition/lactose-intolerance/.
27. ↑ Genetics Home Reference. "MCM6". https://medlineplus.gov/genetics/gene/mcm6/.
28. ↑ 28.0 28.1 Benjamin Phelan (23 October 2012). "Evolution of lactose tolerance: Why do humans keep drinking milk?". http://www.slate.com/articles/health_and_science/human_evolution/2012/10/evolution_of_lactose_tolerance_why_do_humans_keep_drinking_milk.html.
29. ↑ "Lactose Intolerance". Johns Hopkins Health Library. http://www.hopkinsmedicine.org/healthlibrary/conditions/digestive_disorders/lactose_intolerance_85,P00388/.
30. ↑ Gibbons, Ann (2 April 2015). "How Europeans evolved white skin". Science. doi:10.1126/science.aab2435. https://www.science.org/content/article/how-europeans-evolved-white-skin.
31. ↑ "Gene-culture coevolution between cattle milk protein genes and human lactase genes". Nature Genetics 35 (4): 311–3. December 2003. doi:10.1038/ng1263. PMID 14634648. Bibcode: 2003NaGen..35..311B.
32. ↑ 32.0 32.1 "Convergent adaptation of human lactase persistence in Africa and Europe". Nature Genetics 39 (1): 31–40. January 2007. doi:10.1038/ng1946. PMID 17159977.
33. ↑ "Lactase nonpersistence is directed by DNA-variation-dependent epigenetic aging". Nature Structural & Molecular Biology 23 (6): 566–73. June 2016. doi:10.1038/nsmb.3227. PMID 27159559.
34. ↑ 34.0 34.1 34.2 Oh, Edward; Jeremian, Richie; Oh, Gabriel; Groot, Daniel; Susic, Miki; Lee, KwangHo; Foy, Kelly; Laird, Peter W. et al. (2017-01-31). "Transcriptional heterogeneity in the lactase gene within cell-type is linked to the epigenome". Scientific Reports 7 (1). doi:10.1038/srep41843. PMID 28139744. Bibcode: 2017NatSR...741843O.
35. ↑ "Identification of a variant associated with adult-type hypolactasia". Nature Genetics 30 (2): 233–7. February 2002. doi:10.1038/ng826. PMID 11788828. Bibcode: 2002NaGen..30..233E.
36. ↑ "Lactose intolerance". http://www.milk.co.uk/page.aspx?intPageID=59.
37. ↑ Secondary lactase deficiency causes
38. ↑ Lawson, Margaret; Bentley, Donald; Lifschitz, Carlos (2002). Pediatric gastroenterology and clinical nutrition. London: Remedica. p. 109. ISBN 978-1-901346-43-5. https://books.google.com/books?id=dLLgzcMsbo0C&pg=PA109.
39. ↑ Pediatric Lactose Intolerance at eMedicine
40. ↑ "Lactose intolerance". American Family Physician 65 (9): 1845–50. May 2002. PMID 12018807. http://www.aafp.org/link_out?pmid=12018807.
41. ↑ "Dietary treatment of lactose intolerance in infants and children". Journal of the American Dietetic Association 91 (12): 1567–71. December 1991. doi:10.1016/S0002-8223(21)01435-8. PMID 1960350.
42. ↑ R. Bowen (December 28, 2006). "Lactose Intolerance (Lactase Non-Persistence)". Colorado State University. http://www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/lactose_intol.html.
43. ↑ Malik, Talia F.; Panuganti, Kiran K. (2023-04-17). Lactose Intolerance. PMID 30335318. https://www.ncbi.nlm.nih.gov/books/NBK532285/. Retrieved 2024-05-27.
44. ↑ "Is it just lactose intolerance?". Allergy and Asthma Proceedings 33 (5): 432–6. 2012. doi:10.2500/aap.2012.33.3584. PMID 23026186.
45. ↑ "Lactose Intolerance Tests and Results". http://www.webmd.com/digestive-disorders/tc/lactose-intolerance-exams-and-tests.
46. ↑ "Hydrogen Breath Test and Lactose Intolerance". WebMD. http://www.webmd.com/digestive-disorders/hydrogen-breath-test.
47. ↑ "Lactose tolerance tests". 3 May 2011. https://www.medlineplus.gov/ency/article/003500.htm.
48. ↑ National Digestive Diseases Information Clearinghouse (March 2006). "Lactose Intolerance — How is lactose intolerance diagnosed?". National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health. http://digestive.niddk.nih.gov/ddiseases/pubs/lactoseintolerance/#diagnosed.
49. ↑ "Stool Acidity Test". Jay W. Marks, M.D.. http://www.medicinenet.com/stool_acidity_test/article.htm#stool.
50. ↑ 50.0 50.1 50.2 Hargrove, James L.; Berdanier, Carolyn D. (1993). Nutrition and gene expression. Boca Raton: CRC Press. ISBN 978-0-8493-6961-2.
51. ↑ "A biopsy-based quick test in the diagnosis of duodenal hypolactasia in upper gastrointestinal endoscopy". Endoscopy 38 (7): 708–12. July 2006. doi:10.1055/s-2006-925354. PMID 16761211.
52. ↑ "Celiac disease: an immune dysregulation syndrome". Current Problems in Pediatric and Adolescent Health Care 44 (11): 324–7. December 2014. doi:10.1016/j.cppeds.2014.10.002. PMID 25499458. "Initially, reduced levels of lactase and sucrase activities might necessitate further dietary restrictions until the villi have healed and those sugars are better tolerated.".
53. ↑ "Lactose intolerance - Treatment". http://www.nhs.uk/Conditions/lactose-intolerance/Pages/Treatment.aspx.
54. ↑ Lactose Intolerance at eMedicine Roy, Barakat, Nwakakwa, Shojamanesh, Khurana, July 5, 2006
55. ↑ 55.0 55.1 55.2 "Adaptation to Lactose in Lactase Non Persistent People: Effects on Intolerance and the Relationship between Dairy Food Consumption and Evalution [sic] of Diseases". Nutrients 7 (8): 6751–79. August 2015. doi:10.3390/nu7085309. PMID 26287234.
56. ↑ 56.0 56.1 56.2 "Diet for Lactose Intolerance". http://www.gastro.net.au/diets/lactose.html.
57. ↑ Eddleman, Harold (25 December 2003). "Composition of Human, Cow, and Goat Milks". GoatWorld.com. http://www.goatworld.com/articles/goatmilk/colostrum.shtml.
58. ↑ "Amount of Lactose in Milk Products". Food Intolerance Network. 21 November 2013. https://www.food-intolerance-network.com/food-intolerances/lactose-intolerance/tables-of-lactose-content.html.
59. ↑ Peeva (2001). "Composition of buffalo milk. Sources of specific effects on the separate components". Bulgarian Journal of Agricultural Science 7: 329–35. http://bjas.hit.bg/07/693A.htm.
60. ↑ "Milk trait heritability and correlation with heterozygosity in yak". Journal of Applied Genetics 45 (2): 215–24. 2004. PMID 15131352. http://jag.igr.poznan.pl/2004-Volume-45/2/pdf/2004_Volume_45_2-215-224.pdf.
61. ↑ "A Comparison of Dry Sweet Cream Buttermilk and Non-Fat Dry Milk Solids in Breadmaking". Journal of Dairy Science 34 (2): 136–44. February 1, 1951. doi:10.3168/jds.S0022-0302(51)91682-7. https://www.journalofdairyscience.org/article/S0022-0302(51)91682-7/abstract.
62. ↑ Perkins, Sharon (19 November 2018). "Can a Lactose Intolerant Eat Some Yogurt & Aged Cheese?". SFGATE. http://healthyeating.sfgate.com/can-lactose-intolerant-eat-yogurt-aged-cheese-6130.html.
63. ↑ 63.0 63.1 "Dairy Good: Home". http://www.ilovecheese.com/lactose_intolerant_faqs.asp.
64. ↑ Muthukummarappan, K; Biswas, A.C.; Metzger, L.E.; Kapoor, R (2007). "Effect of Natural Cheese Characteristics on Process Cheese Properties". Journal of Dairy Science (Plum X Metrics) 90 (4): 1625–1634. doi:10.3168/jds.2006-746. PMID 17369202. https://www.journalofdairyscience.org/article/S0022-0302(07)71648-X/fulltext. Retrieved April 19, 2022.
65. ↑ 65.0 65.1 Portnoy, Matilde; Barbano, David M. (July 2021). "Lactose: Use, measurement, and expression of results". Journal of Dairy Science 104 (7): 8314–8325. doi:10.3168/jds.2020-18706. PMID 33814136.
66. ↑ "Goat Dairy Foods". http://drinc.ucdavis.edu/goat1.htm.
67. ↑ 67.0 67.1 "General guidelines for milk allergy". Oregon Health & Science University. http://www.ohsu.edu/xd/health/health-information/topic-by-id.cfm?ContentTypeId=90&ContentId=P01696.
68. ↑ "Margarine Regulations". http://www.gov.ns.ca/JUST/REGULATIONS/regs/marge.htm.
69. ↑ "Enriched White Bread in Canada". The Canadian Celiac Association. http://www.celiac.ca/Articles/PAB Enriching GF Foods.html.
70. ↑ Riggs, Lloyd K; Beaty, Annabel; Johnson, Arnold H (December 1946). "Influence of Nonfat Dry Milk Solids on the Nutritive Value of Bread". Journal of Dairy Science 29 (12): 821–9. doi:10.3168/jds.S0022-0302(46)92546-5.
71. ↑ "Bartek, food additive company". http://www.bartek.ca/pdfs/Applications/SavouryProducts/SavourySnackFoods/Savoury Snack Foods Alphabetical List of Product Names.pdf.
72. ↑ "Allergen Card - Milk/Dairy". https://allergyfacts.org.au/shop/food-preparation-tools/allergen-cards/allergen-card-milk-dairy.
73. ↑ Trotta, Teresa; Posa, Francesca; Mori, Giorgio; Porro, Chiara (2017). "Dairy Products and Their Role in Human Health". Advances in Dairy Products. pp. 248–61. doi:10.1002/9781118906460.ch2f. ISBN 978-1-118-90646-0. https://books.google.com/books?id=z100DwAAQBAJ&pg=PA248.
74. ↑ "Management and treatment of lactose malabsorption". World Journal of Gastroenterology 12 (2): 187–91. January 2006. doi:10.3748/wjg.v12.i2.187. PMID 16482616.
75. ↑ "[Effect of exogenous lactase on the absorption of lactose and its intolerance symptoms]" (in zh). Wei Sheng Yan Jiu = Journal of Hygiene Research 28 (5): 309–11. September 1999. PMID 12712706.
76. ↑ "Physicochemical characteristics of commercial lactases relevant to their application in the alleviation of lactose intolerance". Applied Biochemistry and Biotechnology 134 (2): 179–91. August 2006. doi:10.1385/ABAB:134:2:179. PMID 16943638.
77. ↑ Belloch, C.; Querol, A.; Barrio, E. (2011-01-01), Fuquay, John W., ed., Yeasts and Molds | Kluyveromyces spp. (2nd ed.), San Diego: Academic Press, pp. 754–764, ISBN 978-0-12-374407-4, https://www.sciencedirect.com/science/article/pii/B9780123744074004994, retrieved 2022-01-14
78. ↑ Tally, Steve (1998). "Lactose intolerant? Drink more milk". Agricultures Magazine 1 (2): 2. http://www.agriculture.purdue.edu/agricultures/past/Spring1998/1998-Spring-Spotlights.pdf. Steve Tally
79. ↑ "Undernourished Children and Milk Lactose". Food and Nutrition Bulletin 37 (1): 85–99. March 2016. doi:10.1177/0379572116629024. PMID 26893059.
80. ↑ "Scientific Opinion on the substantiation of health claims related to live yoghurt cultures and improved lactose digestion (ID 1143, 2976) pursuant to Article 13(1) of Regulation (EC) No 1924/2006". EFSA Journal 8 (10). 2010. doi:10.2903/j.efsa.2010.1763.
81. ↑ 81.0 81.1 81.2 "A worldwide correlation of lactase persistence phenotype and genotypes". BMC Evolutionary Biology 10 (1): 36. February 2010. doi:10.1186/1471-2148-10-36. PMID 20144208. Bibcode: 2010BMCEE..10...36I.
82. ↑ 82.0 82.1 "Lactose intolerance". https://medlineplus.gov/genetics/condition/lactose-intolerance/.
83. ↑ 83.0 83.1 83.2 "Insights into human evolution from ancient and contemporary microbiome studies". Current Opinion in Genetics & Development 41: 14–26. December 2016. doi:10.1016/j.gde.2016.07.003. PMID 27507098.
84. ↑ Thompson, Helen (28 December 2012). "An Evolutionary Whodunit: How Did Humans Develop Lactose Tolerance?". https://www.npr.org/sections/thesalt/2012/12/27/168144785/an-evolutionary-whodunit-how-did-humans-develop-lactose-tolerance.
85. ↑ Pray, W. Steven (2000). "Lactose Intolerance: The Norm Among the World's Peoples". American Journal of Pharmaceutical Education 64 (2): 205–207. ProQuest 211177586. http://archive.ajpe.org/legacy/pdfs/aj640216.pdf. Retrieved 2019-11-20.
86. ↑ "Archaeology: The milk revolution". Nature 500 (7460): 20–2. August 2013. doi:10.1038/500020a. PMID 23903732. Bibcode: 2013Natur.500...20C.
87. ↑ "Fatty acid specific δ13C values reveal earliest Mediterranean cheese production 7,200 years ago". PLOS ONE 13 (9). 2018. doi:10.1371/journal.pone.0202807. PMID 30183735. Bibcode: 2018PLoSO..1302807M.
88. ↑ "New insights into the Tyrolean Iceman's origin and phenotype as inferred by whole-genome sequencing". Nat Commun 3. 2012. doi:10.1038/ncomms1701. PMID 22426219. Bibcode: 2012NatCo...3..698K.
89. ↑ Wilson J (December 2005). "Milk Intolerance: Lactose Intolerance and Cow's Milk Protein Allergy". Newborn and Infant Nursing Reviews 5 (4): 203–7. doi:10.1053/j.nainr.2005.08.004.
90. ↑ "Isolated Intestinal Lactase Deficiency in the Adult". Lancet 2 (7303): 324–6. August 1963. doi:10.1016/s0140-6736(63)92991-x. PMID 14044269.
91. ↑ 91.0 91.1 "Primary adult lactose intolerance and the milking habit: a problem in biological and cultural interrelations. I. Review of the medical research". The American Journal of Digestive Diseases 14 (12): 819–36. December 1969. doi:10.1007/bf02233204. PMID 4902756.
92. ↑ "A racial difference in incidence of lactase deficiency. A survey of milk intolerance and lactase deficiency in healthy adult males". JAMA 197 (12): 968–72. September 1966. doi:10.1001/jama.1966.03110120074017. PMID 5953213.
93. ↑ "Isolated Lactase Deficiency: Correlation of Laboratory Studies and Clinical Data". Archives of Internal Medicine 120 (3): 261–269. 1967. doi:10.1001/archinte.1967.00300030003003.
94. ↑ "Milk and lactose intolerance in healthy Orientals". Science 160 (3823): 83–4. April 1968. doi:10.1126/science.160.3823.83-a. PMID 5694356. Bibcode: 1968Sci...160...83H.
95. ↑ "Tribal incidence of lactase deficiency in Uganda". Lancet 1 (7440): 725–9. April 1966. doi:10.1016/s0140-6736(66)90888-9. PMID 4159716.
96. ↑ "Lactase Deficiency in the South African Bantu". South African Medical Journal 41 (46): 1194–6. 1967. PMID 6080167.
97. ↑ "Lactose intolerance in various ethnic groups in South-East Asia". Australasian Annals of Medicine 17 (4): 300–6. November 1968. doi:10.1111/imj.1968.17.4.300. PMID 5701921.
98. ↑ "Lactose intolerance in Thailand". Nature 221 (5182): 758–9. February 1969. doi:10.1038/221758b0. PMID 5818369. Bibcode: 1969Natur.221..758F.
99. ↑ "Lactose maldigestion in Australian Aboriginal children". The Medical Journal of Australia 1 (2): 46–9. January 1967. doi:10.5694/j.1326-5377.1967.tb21011.x. PMID 6016903.
100. ↑ "Evidence against nutritional adaption of tolerance to lactose". Humangenetik 13 (2): 118–25. 1971. doi:10.1007/bf00295793. PMID 5114667.

## External links

Classification|

* ICD-10: E73
* ICD-9-CM: 271.3
* OMIM: 223100
* MeSH: D007787
* DiseasesDB: 7238

|

External resources|

* MedlinePlus: 000276
* eMedicine: med/3429 ped/1270

* Wade, Nicholas (1 March 2010). "Human Culture, an Evolutionary Force". New York Times. https://www.nytimes.com/2010/03/02/science/02evo.html.

Lactose intolerance Global Network https://lactosa.org/en/

* v
* t
* e

Diseases of the digestive system (primarily K20–K93, 530–579)

Upper GI tract|

| Esophagus|

* Esophagitis
* Candidal
* Eosinophilic
* Herpetiform
* Rupture
* Boerhaave syndrome
* Mallory–Weiss syndrome
* UES
* Zenker's diverticulum
* LES
* Barrett's esophagus
* Esophageal motility disorder
* Nutcracker esophagus
* Achalasia
* Diffuse esophageal spasm
* Gastroesophageal reflux disease (GERD)
* Laryngopharyngeal reflux (LPR)
* Esophageal stricture
* Megaesophagus

|

Stomach|

* Gastritis
* Atrophic
* Ménétrier's disease
* Gastroenteritis
* Peptic (gastric) ulcer
* Cushing ulcer
* Dieulafoy's lesion
* Dyspepsia
* Pyloric stenosis
* Achlorhydria
* Gastroparesis
* Gastroptosis
* Portal hypertensive gastropathy
* Gastric antral vascular ectasia
* Gastric dumping syndrome
* Gastric volvulus
* Buried bumper syndrome

Lower GI tract:
Intestinal/
Enteropathy|

| Small intestine
(Duodenum/Jejunum/Ileum)|

* Enteritis
* Duodenitis
* Jejunitis
* Ileitis
* Peptic (duodenal) ulcer
* Curling's ulcer
* Malabsorption: Coeliac
* Tropical sprue
* Blind loop syndrome
* Small bowel bacterial overgrowth syndrome
* Whipple's
* Short bowel syndrome
* Steatorrhea
* Milroy disease
* Bile acid malabsorption

|

Large intestine
(Appendix/Colon)|

* Appendicitis
* Colitis
* Pseudomembranous
* Ulcerative
* Ischemic
* Microscopic
* Collagenous
* Lymphocytic
* Functional colonic disease
* IBS
* Intestinal pseudoobstruction / Ogilvie syndrome
* Megacolon / Toxic megacolon
* Diverticulitis/Diverticulosis

Large and/or small|

* Enterocolitis
* Necrotizing
* Gastroenterocolitis
* IBD
* Crohn's disease
* Vascular: Abdominal angina
* Mesenteric ischemia
* Angiodysplasia
* Bowel obstruction: Ileus
* Intussusception
* Volvulus
* Fecal impaction
* Constipation
* Diarrhea
* Infectious
* Intestinal adhesions

Rectum|

* Proctitis
* Radiation proctitis
* Proctalgia fugax
* Rectal prolapse
* Anismus

Anal canal|

* Anal fissure/Anal fistula
* Anal abscess
* Hemorrhoid
* Anal dysplasia
* Pruritus ani

GI bleeding/BIS|

* Upper
* Hematemesis
* Melena
* Lower
* Hematochezia

Accessory|

| Liver|

* Hepatitis
* Viral hepatitis
* Autoimmune hepatitis
* Alcoholic hepatitis
* Cirrhosis
* PBC
* Fatty liver
* NASH
* Vascular
* Budd–Chiari syndrome
* Hepatic veno-occlusive disease
* Portal hypertension
* Nutmeg liver
* Alcoholic liver disease
* Liver failure
* Hepatic encephalopathy
* Acute liver failure
* Liver abscess
* Pyogenic
* Amoebic
* Hepatorenal syndrome
* Peliosis hepatis
* Metabolic disorders
* Wilson's disease
* Hemochromatosis

|

Gallbladder|

* Cholecystitis
* Gallstones/Cholecystolithiasis
* Cholesterolosis
* Adenomyomatosis
* Postcholecystectomy syndrome
* Porcelain gallbladder

Bile duct/
Other biliary tree|

* Cholangitis
* Primary sclerosing cholangitis
* Secondary sclerosing cholangitis
* Ascending
* Cholestasis/Mirizzi's syndrome
* Biliary fistula
* Haemobilia
* Gallstones/Cholelithiasis

* Common bile duct
* Choledocholithiasis
* Biliary dyskinesia
* Sphincter of Oddi dysfunction

Pancreatic|

* Pancreatitis
* Acute
* Chronic
* Hereditary
* Pancreatic abscess
* Pancreatic pseudocyst
* Exocrine pancreatic insufficiency
* Pancreatic fistula

Abdominopelvic|

| Hernia|

* Diaphragmatic
* Congenital
* Hiatus

* Inguinal
* Indirect
* Direct
* Umbilical
* Femoral
* Obturator
* Spigelian

* Lumbar
* Petit's
* Grynfeltt-Lesshaft

* Undefined location
* Incisional
* Internal hernia
* Richter's

|

Peritoneal|

* Peritonitis
* Spontaneous bacterial peritonitis
* Hemoperitoneum
* Pneumoperitoneum

* v
* t
* e

Inborn error of carbohydrate metabolism: monosaccharide metabolism disorders (E73–E74, 271)
Including glycogen storage diseases (GSD)

Sucrose, transport
(extracellular)|

| Disaccharide catabolism|

* Congenital alactasia
* Sucrose intolerance

|

Monosaccharide transport|

* Glucose-galactose malabsorption
* Inborn errors of renal tubular transport (Renal glycosuria)
* Fructose malabsorption

Hexose → glucose|

| Monosaccharide catabolism|

| Fructose:|

* Essential fructosuria
* Fructose intolerance

|

Galactose / galactosemia:|

* GALK deficiency
* GALT deficiency/GALE deficiency

Glucose ⇄ glycogen]]|

| Glycogenesis|

* GSD type 0 (glycogen synthase deficiency)
* GSD type IV (Andersen's disease, branching enzyme deficiency)
* Adult polyglucosan body disease (APBD)

|

Glycogenolysis|

| Extralysosomal:|

* GSD type III (Cori's disease, debranching enzyme deficiency)
* GSD type VI (Hers' disease, liver glycogen phosphorylase deficiency)
* GSD type V (McArdle's disease, myophosphorylase deficiency)
* GSD type IX (phosphorylase kinase deficiency)

|

Lysosomal (LSD):|

* GSD type II (Pompe's disease, glucosidase deficiency)

Glucose ⇄ CAC]]|

| Glycolysis|

* MODY 2/HHF3
* GSD type VII (Tarui's disease, phosphofructokinase deficiency)
* Triosephosphate isomerase deficiency
* Pyruvate kinase deficiency

|

Gluconeogenesis|

* PCD
* Fructose bisphosphatase deficiency
* GSD type I (von Gierke's disease, glucose 6-phosphatase deficiency)

Pentose phosphate pathway|

* Glucose-6-phosphate dehydrogenase deficiency
* Transaldolase deficiency
* 6-phosphogluconate dehydrogenase deficiency

Other|

* Hyperoxaluria
* Primary hyperoxaluria
* Pentosuria
* Aldolase A deficiency

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