<unk>  is a consequence of<unk>  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<unk>  in the lining of the duodenum.<unk> , 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<unk> , passes intact into the colon. Bacteria in the colon can metabolise<unk> , 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).<unk>  in infants (congenital<unk>  deficiency) is caused by mutations in the LCT gene. The LCT gene provides the instructions for making<unk> . Mutations are believed to interfere with the function of<unk> , causing affected infants to have a severely impaired ability to digest<unk>  in breast milk or formula.<unk>  in adulthood is result from 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. 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. Populations that are<unk>  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. The<unk>  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<unk>  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,<unk>  is more common in Asian Americans, African Americans, Mexican Americans, and Native Americans. Analysis of the DNA of 94 ancient skeletons in Europe and Russia concluded that the mutation for<unk>  tolerance appeared about 4,300 years ago and spread throughout the European population. Some human populations have developed<unk>  persistence, in which<unk>  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<unk> -persistent individuals, but it is also consistent with a physiological response to decrease<unk>  production when it is not needed in cultures in which dairy products are not an available food source. Although populations in Europe, India, Arabia, and Africa were first thought to have high rates of<unk>  persistence because of a single mutation,<unk>  persistence has been traced to a number of mutations that occurred independently. Different alleles for<unk>  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. 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<unk>  in adults. Age-dependent expression of LCT in mice intestinal epithelium has been DNA methylation in the gene enhancer.<unk>  is classified according to its causes as: Primary hypolactasia Primary hypolactasia, or primary<unk>  deficiency, is genetic, only affects adults, and is caused by the absence of a<unk>  persistence allele. In individuals without the<unk>  persistence allele, less<unk>  is produced by the body over time, leading to hypolactasia in adulthood. The frequency of<unk>  persistence, which allows<unk>  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. Secondary hypolactasia Secondary hypolactasia or secondary<unk>  deficiency, also called acquired hypolactasia or acquired<unk>  deficiency, is caused by an injury to the small intestine. This form of<unk>  can occur in both infants and<unk>  persistent adults and is generally reversible. It may be caused by acute gastroenteritis, coeliac disease, Crohn's disease, ulcerative colitis, chemotherapy, intestinal parasites (such as giardia), or other environmental causes. Primary congenital alactasia Primary congenital alactasia, also called congenital<unk>  deficiency, is an extremely rare, autosomal recessive enzyme defect that prevents<unk>  expression from birth. People with congenital<unk>  deficiency cannot digest<unk>  from birth, so cannot digest breast milk. This genetic defect is characterized by a complete lack of<unk>  (alactasia). About 40 cases have been reported worldwide, mainly limited to Finland. Before the 20th century, babies born with congenital<unk>  deficiency often did not survive, but death rates decreased with soybean-derived infant formulas and manufactured<unk> -free dairy products.
Lactose intolerance
Appendix cancer
Sucrose intolerance
Gastroenteritis
Fructose malabsorption
Microscopic colitis
Glucose-galactose malabsorption
Saccharopinuria