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==Overview==
==Overview==
[[Disaccharide]]s cannot be absorbed through the wall of the small intestine into the bloodstream, so in the absence of [[lactase]], [[lactose]] present in ingested dairy products remains uncleaved and passes intact into the [[Colon (anatomy)|colon]]. The [[operon]]s of [[Gut flora|enteric bacteria]] quickly switch over to lactose [[metabolism]], and the resulting in-vivo [[fermentation (biochemistry)|fermentation]] produces copious amounts of gas (a mixture of [[hydrogen]], [[carbon dioxide]], and [[methane]]). This, in turn, may cause a range of abdominal symptoms, including stomach [[cramp]]s, [[nausea]], [[bloating]], [[acid reflux]] and [[flatulence]]. In addition, as with other unabsorbed sugars (such as [[sorbitol]], [[mannitol]], and [[xylitol]]), the presence of lactose and its fermentation products raises the [[osmotic pressure]] of the [[colon (anatomy)|colon]] contents. you fart alot. =-{
[[Disaccharide]]s cannot be absorbed through the wall of the small intestine into the bloodstream, so in the absence of [[lactase]], [[lactose]] present in ingested dairy products remains uncleaved and passes intact into the [[Colon (anatomy)|colon]]. The [[operon]]s of [[Gut flora|enteric bacteria]] quickly switch over to lactose [[metabolism]], and the resulting in-vivo [[fermentation (biochemistry)|fermentation]] produces copious amounts of gas (a mixture of [[hydrogen]], [[carbon dioxide]], and [[methane]]). This, in turn, may cause a range of abdominal symptoms, including stomach [[cramp]]s, [[nausea]], [[bloating]], [[acid reflux]] and [[flatulence]]. In addition, as with other unabsorbed sugars (such as [[sorbitol]], [[mannitol]], and [[xylitol]]), the presence of lactose and its fermentation products raises the [[osmotic pressure]] of the [[colon (anatomy)|colon]] contents.


== Lactase biology ==
== Lactase biology ==

Revision as of 16:41, 21 October 2010

Lactose intolerance
SpecialtyEndocrinology Edit this on Wikidata
Frequency65%, 10%

Lactose intolerance is the inability to metabolize lactose, because of a lack of the required enzyme lactase in the digestive system. It is estimated that 75% of adults worldwide show some decrease in lactase activity during adulthood.[1] The frequency of decreased lactase activity ranges from as little as 5% in northern Europe, up to 71% for Sicily, to more than 90% in some African and Asian countries.[2]

Overview

Disaccharides cannot be absorbed through the wall of the small intestine into the bloodstream, so in the absence of lactase, lactose present in ingested dairy products remains uncleaved and passes intact into the colon. The operons of enteric bacteria quickly switch over to lactose metabolism, and the resulting in-vivo fermentation produces copious amounts of gas (a mixture of hydrogen, carbon dioxide, and methane). This, in turn, may cause a range of abdominal symptoms, including stomach cramps, nausea, bloating, acid reflux and flatulence. In addition, as with other unabsorbed sugars (such as sorbitol, mannitol, and xylitol), the presence of lactose and its fermentation products raises the osmotic pressure of the colon contents.

Lactase biology

The normal mammalian condition is for the young of a species to experience reduced lactase production at the end of the weaning period (a species-specific length of time). In humans, in non-dairy consuming societies, lactase production usually drops about 90% during the first four years of life, although the exact drop over time varies widely.[3]

However, certain human populations have a mutation on chromosome 2 which eliminates the shutdown in lactase production, making it possible for members of these populations to continue consumption of fresh milk and other dairy products throughout their lives without difficulty. This appears to be an evolutionarily recent adaptation to dairy consumption, and has occurred independently in both northern Europe and east Africa in populations with a historically pastoral lifestyle.[4] Lactase persistence, allowing lactose digestion to continue into adulthood, is a dominant allele, making lactose intolerance a recessive genetic trait. A noncoding variation in the MCM6 gene has been strongly associated with adult type hypolactasia (lactose intolerance).[5]

Some cultures, such as that of Japan, where dairy consumption has been on the increase compared with traditional dietary patterns, demonstrate a lower prevalence of lactose intolerance in spite of a genetic predisposition.[6]

Pathological lactose intolerance can be caused by coeliac disease, which damages the villi in the small intestine that produce lactase. This lactose intolerance is temporary. Lactose intolerance associated with coeliac disease ceases after the patient has been on a gluten-free diet long enough for the villi to recover (BMJ Textbook of Gastroenterology, Chapter 11, Celiac Disease, Dr.Jamie Gregor & Dr. Diamond Sherin Alidina).

Certain people who report problems with consuming lactose are not actually lactose intolerant. In a study of 323 Sicilian adults, Carroccio et al. (1998) found only 4% were both lactose intolerant and lactose maldigesters, while 32.2% were lactose maldigesters but did not test as lactose intolerant. However, Burgio et al. (1984) found that 72% of 100 Sicilians were lactose intolerant in their study and 106 of 208 northern Italians (i.e., 51%) were lactose intolerant.

Lactose intolerance by group

Global map of lactose intolerance frequencies.

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Human group Individuals examined Intolerance (%) Reference Allele frequency
Basques 85 0.3 [7] N/A
Dutch N/A 1 [8] N/A
Swedes N/A 2 [9] 0.14
Europeans in Australia 160 4 [9] 0.20
Northern Europeans and Scandinavians N/A 5 [5][10] N/A
British N/A 5–15 [12] 0.184-0.302[13]
Swiss N/A 10 [9] 0.316
European Americans 245 12 [9] 0.346
Tuareg N/A 13 [12] N/A
Germans N/A 15 [12] N/A
Eastern Slavs (Russians, Belarusians, Ukrainians) N/A 15 [14] N/A
Austrians N/A 15–20 [12] N/A
Spaniards (non-Basque) N/A 15 [15] N/A
Northern French N/A 17 [12] N/A
Finns 134 18 [9] 0.424
Central Italians 65 19 [16] N/A
Indians N/A 20 [5][10] N/A
African Tutsi N/A 20 [9] 0.447
African Fulani N/A 23 [9] 0.48
Bedouins N/A 25 [12] N/A
Portuguese adults 102 35 [17] N/A
Southern Italians 51 41 [16] N/A
African American Children N/A 45 [5] N/A
Saami (in Russia and Finland) N/A 25–60 [18] N/A
Northern Italians 89 52 [16] N/A
North American Hispanics N/A 53 [12] N/A
Balkans N/A 55 [12] N/A
Mexican American Males N/A 55 [5][10] N/A
Cretans N/A 56 [5] N/A
African Maasai 21 62 [19] N/A
Southern French N/A 65 [12] N/A
Greek Cypriots N/A 66 [5][10] N/A
Jews, Mizrahi (Iraq, Iran, etc) N/A 85 [20] N/A
Jews, North American N/A 68.8 [5][10] N/A
Jews, Sephardic N/A 62 [20] N/A
Jews, Yemenite N/A 44 [20] N/A
Sicilians 100 71 [21][22] N/A
South Americans N/A 65–75 [12] N/A
Rural Mexicans N/A 73.8 [5][10] N/A
African Americans 20 75 [9] 0.87
Kazakhs from northwest Xinjiang 195 76.4% [23]
Lebanese 75 78 [24] N/A
Central Asians N/A 80 [12] N/A
Alaskan Eskimo N/A 80 [5][10] N/A
Australian Aborigines 44 85 [9] 0.922
Inner Mongolians 198 87.9 [23]
African Bantu 59 89 [9] 0.943
Asian Americans N/A 90 [5][10] N/A
Northeastern Han Chinese 248 92.3 [23]
Chinese 71 95 [9] 0.964
Southeast Asians N/A 98 [5][10] N/A
Thais 134 98 [9] 0.99
Native Americans 24 100 [9] 1.00

The statistical significance varies greatly depending on number of people sampled.

Lactose intolerance levels also increase with age. At ages 2 – 3 yrs., 6 yrs., and 9 - 10 yrs., the amount of lactose intolerance is, respectively:

Chinese and Japanese populations typically lose between 20 and 30 percent of their ability to digest lactose within three to four years of weaning. Some studies have found that most Japanese can consume 200 ml (8 fl oz) of milk without severe symptoms (Swagerty et al., 2002).[6]

Ashkenazi Jews can keep 20 - 30 percent of their ability to digest lactose for many years.[8][25][27] Of the 10% of the Northern European population that develops lactose intolerance, the development of lactose intolerance is a gradual process spread out over as many as 20 years.[28]

Diagnosis

To assess lactose intolerance, the intestinal function is challenged by ingesting more dairy than can be readily digested. Clinical symptoms typically appear within 30 minutes but may take up to 2 hours, depending on other foods and activities.[29] Substantial variability of the clinical response (symptoms of nausea, cramping, bloating, diarrhea, and flatulence) is to be expected, as the extent and severity of lactose intolerance varies between individuals.

When considering the need for confirmation, it is important to distinguish lactose intolerance from a milk allergy, which is an abnormal immune response (usually) to milk proteins. This may be done by giving lactose-free milk to a person displaying a reaction to milk. If the condition is purely lactose intolerance, the sufferer's symptoms will vanish, but if it is a milk allergy, the person will have the same reaction to the lactose-free milk as to normal milk. (An intermediate result might suggest that the person has both conditions.) Since lactose intolerance is the normal state for most adults on a worldwide scale and is not considered a disease condition, a medical diagnosis is not normally required. However, if confirmation is necessary, three tests are available.

Hydrogen breath test

In a hydrogen breath test, after an overnight fast, 50 grams of lactose (in a solution with water) is swallowed. If the lactose cannot be digested, enteric bacteria metabolize it and produce hydrogen. This, along with methane, can be detected in the patient's breath by a clinical gas chromatograph or a compact solid state detector. The test takes about 2 to 3 hours. A medical condition with similar symptoms is fructose malabsorption.

In conjunction, measuring the blood glucose level every 10 – 15 minutes after ingestion will show a "flat curve" in individuals with lactose malabsorption, while the lactase persistent will have a significant "top", with an elevation of typically 50 to 100% within 1 – 2 hours. However, given the need for frequent blood draws, this approach has been largely supplanted by breath testing.

Stool acidity test

This test can be used to diagnose lactose intolerance in infants, for whom other forms of testing are risky or impractical.[30]

Intestinal biopsy

An intestinal biopsy can confirm lactose intolerance following discovery of elevated hydrogen in the hydrogen breath test.[31] However, given the invasive nature of this test, and the need for a highly specialized laboratory to measure lactase enzymes or mRNA in the biopsy tissue, this approach is used almost exclusively in clinical research.

History of diagnosis

The ancient Greek physician Hippocrates (460-370 B.C.) first noted gastrointestinal upset and skin problems in some who consumed milk;[32] patients experiencing the former symptom may likely have been suffering from lactose intolerance. However, it was only in the 20th century that the syndrome was more widely described by modern medical science.

The condition was first recognized in the 1950s and 1960s when various organizations like the United Nations began to engage in systematic famine-relief efforts in countries outside Europe for the first time. Holzel et al. (1959) and Durand (1959) produced two of the earliest studies of lactose intolerance. As anecdotes of embarrassing dairy-induced discomfort increased, the First World donor countries could no longer ascribe the reports to spoilage in transit or inappropriate food preparation by the Third World recipients.

Because the first nations to industrialize and develop modern scientific medicine were dominated by people of European descent, adult dairy consumption was long taken for granted. Westerners for some time did not recognize that the majority of the human ethno-genetic groups could not consume dairy products during adulthood. The term Milk drinking syndrome stands for a phenomenon when European experience is extrapolated to the other populations of the world.[33]

Since then, the relationship between lactase and lactose has been thoroughly investigated in food science due to the growing market for dairy products among non-Europeans.

Originally it was hypothesised that gut bacteria such as E. coli produced the lactase enzyme needed to cleave lactose into its constituent monosaccharides, and thus become metabolisable and digestible by humans. Some form of human-bacteria symbiosis was proposed as a means of producing lactase in the human digestive tract.

Nomenclature

According to Heyman (2006), approximately 70% of the global population cannot tolerate lactose in adulthood. Thus, some argue that the terminology should be reversed — lactose intolerance should be seen as the norm, and the minority groups should be labeled as having lactase persistence. A counter-argument to this is that the cultures that don't generally consume unmodified milk products have little need to discuss their intolerance to it, leaving the cultures for which lactose intolerance is a significant dietary issue to define its terminology.

History of genetic prevalence

The ability to digest lactose into adulthood (lactase persistence) would have only been useful to humans after the invention of animal husbandry and the domestication of animal species that could provide a consistent source of milk. Hunter-gatherer populations before the Neolithic revolution were overwhelmingly lactose intolerant,[34][35] as are modern hunter-gatherers. Genetic studies suggest that the oldest mutations associated with lactase persistence only reached appreciable levels in human populations in the last ten thousand years.[36][37] Therefore lactase persistence is often cited as an example of both recent human evolution[38][39] and, as lactase persistence is a genetic trait but animal husbandry a cultural trait, gene-culture coevolution.[40]

Several genetic markers for lactase persistence have been identified, and these show that the allele has multiple origins in different parts of the world (i.e. it is an example of convergent evolution).[41] The version of the allele most common amongst Europeans is estimated to have risen to significant frequencies about 7,500 years ago in Central Europe, a place and time approximately corresponding to the archaeological Linearbandkeramik culture.[42] Since North Africans also possess this version of the allele it is probable that it actually originated earlier, in the Near East, but that the earliest farmers did not have high levels of lactase persistence and, subsequently, did not consume significant amounts of unprocessed milk.[43] Lactase persistence in Sub-Saharan Africa almost certainly had a separate origin, probably more than one,[44] and it is also likely that there was a separate origin associated with the domestication of the Arabian camel.[45] None of the mutations so far identified have been shown to be causal for the lactase persistence allele, and it is thought that there are several more yet to be discovered.[46]

The evolutionary processes driving the rapid spread of lactase persistence in some populations are not known.[41] In some East African ethnic groups lactase persistence has gone from negligible to near-ubiquitous frequencies in just three thousand years, suggesting a very strong selective pressure.[38][39] But some models for the spread of lactase persistence in Europe attribute it primarily to a form of genetic drift.[47] Competing theories on why the ability to digest lactose might be selected for include nutritional benefits, milk as a water source in times of drought, and increased calcium absorption helping to prevent rickets and osteomalacia in low-light regions.[41]

Roman authors recorded that the people of northern Europe, particularly Britain and Germany, drank unprocessed milk. This corresponds very closely with modern European distributions of lactose intolerance, where the people of Britain, Germany and Scandinavia have a good tolerance, and those of southern Europe, especially Italy, have a poorer tolerance.[48]

In east Asia, historical sources also attest that the Chinese did not consume milk, whereas the nomads that lived on the borders did. Again, this reflects modern distributions of intolerance. China is particularly notable as a place of poor tolerance, whereas in Mongolia and the Asian steppes horse milk is drunk regularly. This tolerance is thought to be advantageous, as the nomads do not settle down long enough to process mature cheese. Given that their prime source of income is generated through horses, to ignore their milk as a source of calories would be greatly detrimental. The nomads also make an alcoholic beverage, called Kumis, from horse milk, although the fermentation process reduces the amount of lactose present.

Managing lactose intolerance

For persons living in societies where the diet contains relatively little dairy, lactose intolerance is not considered a condition that requires treatment. However, those living among societies that are largely lactose-tolerant may find lactose intolerance troublesome. Although there are still no methodologies to reinstate lactase production, some individuals have reported their intolerance to vary over time (depending on health status and pregnancy[49]).

Lactose intolerance is not usually an all-or-nothing condition: the reduction in lactase production—and hence, the amount of lactose that can be tolerated—varies from person to person. Since lactose intolerance poses no further threat to a person's health, managing the condition consists of minimizing the occurrence and severity of symptoms. Berdanier and Hargrove recognise four general principles: avoidance of dietary lactose, substitution to maintain nutrient intake, regulation of calcium intake, and use of enzyme substitute.[31]

Avoiding lactose-containing products

Since each individual's tolerance to lactose varies, according to the US National Institute of Health, "Dietary control of lactose intolerance depends on people learning through trial and error how much lactose they can handle."[50] Label reading is essential, as commercial terminology varies according to language and region.[31]

Lactose is present in two large food categories: conventional dairy products, and as a food additive (in dairy and non dairy products).

Dairy products

Lactose is a water-soluble molecule. Therefore fat percentage and the curdling process have an impact on which foods may be tolerated. After the curdling process, lactose is found in the water portion (along with whey and casein) but is not found in the fat portion. Dairy products which are "fat reduced" or "fat free" generally have a slightly higher lactose percentage. Additionally, low fat dairy foods also often have various dairy derivatives such as milk solids added to them to enhance sweetness, increasing the lactose content.

Milk. Human milk has the highest lactose percentage at around 9%. Unprocessed cow milk has 4.7% lactose. Unprocessed milk from other bovids contains similar lactose percentages (goat milk 4.1%,[51] buffalo 4.86%,[52] yak 4.93%,[53] sheep milk 4.6%)

Butter. The butter-making process separates the majority of milk's water components from the fat components. Lactose, being a water soluble molecule, will still be present in small quantities in the butter unless it is also fermented to produce cultured butter.

Yogurt, Frozen Yogurt and kefir. People can be more tolerant of traditionally made yogurt than milk, because it contains lactase enzyme produced by the bacterial cultures used to make the yogurt. Frozen yogurt, if cultured similarly to its unfrozen counterpart, will contain similarly reduced lactose levels. However, many commercial brands contain milk solids, increasing the lactose content.[54]

Cheeses. Traditionally made hard cheese (such as Emmental) and soft ripened cheeses may create less reaction than the equivalent amount of milk because of the processes involved. Fermentation and higher fat content contribute to lesser amounts of lactose. Traditionally made Emmental or Cheddar might contain 10% of the lactose found in whole milk. In addition, the traditional aging methods of cheese (over 2 years) reduces their lactose content to practically nothing. [55] Commercial cheese brands, however, are generally manufactured by modern processes that do not have the same lactose reducing properties, and as no regulations mandate what qualifies as an "aged" cheese, this description does not provide any indication of whether the process used significantly reduced lactose.

Sour cream if made in the traditional way, may be tolerable, but most modern brands add milk solids. Consult labels.[56]

Examples of lactose levels in foods. As scientific consensus has not been reached concerning lactose percentage analysis methods [57] (non-hydrated form or the mono-hydrated form), and considering that dairy content varies greatly according to labeling practices, geography and manufacturing processes, lactose numbers may not be very reliable. The following are examples of lactose levels in foods which commonly set off symptoms. These quantities are to be treated as guidelines only.

Dairy product Serving size Lactose content
Milk, regular 250 mL 12 g
Milk, reduced fat 250 mL 13 g
Yogurt, plain, regular 200 g 9 g
Yogurt, plain, low-fat 200 g 12 g
Cheddar cheese 30 g .02 g
Cottage cheese 30 g .1 g
Butter 1 tsp .03 g
Ice cream 50 g 3 g

[58]

Lactose in non-dairy products

Lactose (also present when labels state lactoserum, whey, milk solids, modified milk ingredients, etc.) is a commercial food additive used for its texture, flavour and adhesive qualities, and is found in foods such as processed meats[59] (sausages/hot dogs, sliced meats, pâtés), gravy stock powder, margarines[60] sliced breads,[61][62] breakfast cereals, potato chips,[63] processed foods, medications, pre-prepared meals, meal replacement (powders and bars), and protein supplements (powders and bars).

Kosher products labeled pareve are free of milk. However, if a "D" (for "Dairy") is present next to the circled "K", "U", or other hechsher, the food likely contains milk solids[59] (although it may also simply indicate that the product was produced on equipment shared with other products containing milk derivatives).

Alternative products

Plant-based milks and derivatives are inherently lactose free: soy milk, rice milk, almond milk, hazelnut milk, oat milk, hemp milk, peanut milk, horchata.

The dairy industry has created low-lactose or lactose-free products to replace regular dairy. Lactose-free milk can be produced by passing milk over lactase enzyme bound to an inert carrier; once the molecule is cleaved, there are no lactose ill-effects. Forms are available with reduced amounts of lactose (typically 30% of normal), and alternatively with nearly 0%. The only noticeable difference from regular milk is a slightly sweeter taste due to the adding of the lactase enzyme. It does not however contain more sugar, and is nutritionally identical to regular milk.

Finland, where approximately 17% of the Finnish-speaking population has hypolactasia,[64] has had "HYLA" (acronym for hydrolysed lactose) products available for many years. Lactoce of low-lactose level cow's milk products, ranging from ice cream to cheese is enzymatically hydrolysed into glucose and galactose. The ultra-pasteurization process, combined with aseptic packaging, ensures a long shelf-life. In 2001, Valio launched a lactose-free milk drink which is not sweet like HYLA milk but has the fresh taste of ordinary milk. Valio patented chromatographic separation method to remove lactose. Valio also markets these products in Sweden, Estonia, Belgium and the US.

In the UK, where an estimated 15% of the population are affected by lactose intolerance, Lactofree produces milk, cheese, and yogurt products which contain only 0.03% lactose.

Alternatively, a bacterium such as L. acidophilus may be added, which affects the lactose in milk the same way it affects the lactose in yogurt (see above).

Lactase supplementation

When lactose avoidance is not possible, or on occasions when a person chooses to consume such items, then enzymatic lactase supplements may be used.[65][66]

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,[67] and it therefore 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.

Enzymatic lactase supplementation may have an advantage over avoiding dairy products, in that alternative provision does not need to be made to provide sufficient calcium intake, especially in children.[68]

Rehabituation to dairy products

For healthy individuals with secondary lactose intolerance, it may be possible in some cases for the bacteria in the large intestine to adapt to an altered diet and break down small quantities of lactose more effectively[69] by habitually consuming small amounts of dairy products several times a day over a period of time. Reintroducing dairy in this way to people who have an underlying or chronic illness, however, is not recommended, as certain illnesses damage the intestinal tract in a way which prevents the lactase enzyme from being expressed.

Some studies indicate that environmental factors (more specifically, the consumption of lactose) may "play a more important role than genetic factors in the etio-pathogenesis of milk intolerance",[6] but some other publications suggest that lactase production does not seem to be induced by dairy/lactose consumption.[70]

Nutritional concerns

Primary lactose intolerance

Populations where primary lactose intolerance is the norm have demonstrated similar health levels to westerners (outside of malnutrition issues; see the History of genetic prevalence subsection above), or better health.

Secondary lactose intolerance

Dairy products are relatively good and accessible sources of calcium and potassium and many countries mandate that milk be fortified with vitamin A and vitamin D. Consequently, in dairy-consuming societies, dairy is often a main source of these nutrients and, for lacto-vegetarians, a main source of vitamin B12. Individuals who reduce or eliminate consumption of dairy must obtain these nutrients elsewhere. However, Asian populations for whom dairy is not part of their food culture do not present decreased health and sometimes present above average health, as in Japan.

Plant based milk substitutes are not naturally rich in calcium, potassium, or vitamins A or D (and, like most non-animal products, contain no vitamin B12). However, prominent brands are often voluntarily fortified with many of these nutrients.

An increasing number of calcium-fortified breakfast foods — such as orange juice, bread, and dry cereal — have been appearing on supermarket shelves. Many fruits and vegetables are rich in potassium and vitamin A; animal products like meat and eggs are rich in vitamin B12, and the human body itself produces some vitamin D from exposure to direct sunlight. Finally, a dietitian or physician may recommend a vitamin or mineral supplement to make up for any remaining nutritional shortfall.

Lactose-reduced dairy products have the same nutritional content as their full-lactose counterparts, but their taste and appearance may differ slightly.

Most infants with gastroenteritis due to rotavirus do not develop lactose intolerance,[71] so these infants do not benefit from being put on a lactose-free diet unless symptoms of lactose intolerance are severe and persistent.

Congenital lactase deficiency

Congenital lactase deficiency, or CLD, is an autosomal recessive disorder which prevents the expression of lactase.[72] Before the 20th century, infants with this disease rarely survived. As substitute and lactose-free infant formulas later became available, nursing infants affected with CLD could now have their normal nutritional needs met. Beyond infancy, individuals with CLD usually have the same nutritional concerns as those affected by secondary lactose intolerance.

See also

References

  • Durand, P. (1959). "Lactosurie et saccharosurie". In Ed. E. Rossi, E. Gautier, and J. W. Weber (ed.). Paediat. IV. Carbohydrate Metabolism in Children. Basel. pp. 496–502.{{cite book}}: CS1 maint: multiple names: editors list (link)
  • Holzel A, Schwarz V, Sutcliffe KW (1959). "Defective lactose absorption causing malnutrition in infancy". Lancet. 1 (7083): 1126–8. doi:10.1016/S0140-6736(59)90710-X. PMID 13665980.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  • Carroccio A, Montalto G, Cavera G, Notarbatolo A (1998). "Lactose intolerance and self-reported milk intolerance: relationship with lactose maldigestion and nutrient intake. Lactase Deficiency Study Group". J Am Coll Nutr. 17 (6): 631–6. PMID 9853544.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  • McGee, Harold (2004). "Milk after infancy: dealing with lactose". On food and cooking: the science and lore of the kitchen. New York: Scribner. pp. 14–15. ISBN 0-684-80001-2.
  • Rusynyk RA, Still CD (2001). "Lactose intolerance" (PDF). J Am Osteopath Assoc. 101 (4 Suppl Pt 1): S10–2. PMID 11392211.

Notes

  1. ^ "Improved lactose digestion and intolerance among African-American adolescent girls fed a dairy-rich diet". Journal of the American Dietetic Association. 2000. Retrieved 2009-02-03. Approximately 75% of the world's population loses the ability to completely digest a physiological dose of lactose after infancy
  2. ^ Bulhoes, A. C.; et al. (2007-11). "Correlation between lactose absorption and the C/T-13910 and G/A-22018 mutations of the lactase-phlorizin hydrolase (LCT) gene in adult-type hypolactasia". Brazilian Journal of Medical and Biological Research. Retrieved 2008-07-19. {{cite web}}: Check date values in: |date= (help); Explicit use of et al. in: |author= (help)
  3. ^ Soy and Lactose Intolerance Wayback: Soy Nutrition
  4. ^ Coles Harriet (2007-01-20). "The lactase gene in Africa: Do you take milk?". The Human Genome, Wellcome Trust. Retrieved 2008-07-18.
  5. ^ a b c d e f g h i j k l Enattah NS, Sahi T, Savilahti E, Terwilliger JD, Peltonen L, Järvelä I (2002). "Identification of a variant associated with adult-type hypolactasia". Nat. Genet. 30 (2): 233–7. doi:10.1038/ng826. PMID 11788828.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ a b c Yoshida Y, Sasaki G, Goto S, Yanagiya S, Takashina K (1975). "Studies on the etiology of milk intolerance in Japanese adults". Gastroenterol. Jpn. 10 (1): 29–34. PMID 1234085.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ^ N.S. Enattah; et al. (1, September 2007). "Evidence of Still-Ongoing Convergence Evolution of the Lactase Persistence T-13910 Alleles in Humans". American Journal of Human Genetics. {{cite web}}: Check date values in: |date= (help); Explicit use of et al. in: |author= (help)
  8. ^ a b Flatz G (1987). "Genetics of lactose digestion in humans". Adv. Hum. Genet. 16: 1–77. PMID 3105269.
  9. ^ a b c d e f g h i j k l m Kretchmer N (1972). "Lactose and lactase". Sci. Am. 227 (4): 71–8. PMID 4672311.
  10. ^ a b c d e f g h i "Lactose Intolerance: The Molecular Explanation". UC Davis Nutritional Genomics.
  11. ^ Anne Charlotte Jäger (1, February 2006). "Laktose-intolerans: Gentest for laktose-intolerans - hurtig og billig diagnostik". DSKB-NYT. {{cite web}}: Check date values in: |date= (help)
  12. ^ a b c d e f g h i j k de Vrese M, Stegelmann A, Richter B, Fenselau S, Laue C, Schrezenmeir J (2001). "Probiotics--compensation for lactase insufficiency". Am. J. Clin. Nutr. 73 (2 Suppl): 421S–429S. PMID 11157352.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ G.D. Smith et al., Lactase persistence-related genetic variant: population substructure and health outcomes. European Journal of Human Genetics, 2008.
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