In its pure form, lactose cannot be transported across the mucosa of the small intestine. To be absorbed, it must be hydrolyzed by lactase to free glucose and galactose. These two simple sugars are rapidly and completely absorbed in the normal small intestine. The rate of lactase synthesis is high from birth until ages 3-5 years. Between ages 5 and 14 years, many people undergo a genetically programmed reduction in lactase synthesis that results in a lactase activity level only 5-10% of that of infancy. This reduction, known as lactase nonpersis-tence or primary lactase deficiency, is not related to the continued intake of milk or lactose. As noted, less than one-third of the world's adult population is genetically predisposed to maintaining a high degree of lactase activity or lactase persistence throughout adulthood.
Lactase persistence in the human population is inherited as a dominant genetic trait. It has been observed that lactose intolerance is 'ancient and globally distributed,' predating the appearance of a persistent lactase variant that was naturally selected in dairying regions. Hollox et al. report, ''the continued adult production of lactase results from the persistent expression of the protein lac-tose-phlorizin hydrolase which is encoded by the lactase gene (LCT) on chromosome 2.'' Swallow notes, ''the distribution of different lactase pheno-types in human populations is highly variable and is controlled by a polymorphic element cis- acting to the lactase gene. A putative causal nucleotide change has been identified and occurs on the background of a very extended haplotype that is frequent in Northern Europeans, where lactase persistence is frequent.''
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