Evolution of Lactase Persistence and Non-Persistence
Introduction
Lactose intolerance is the inability to digest lactose and is the most common intestinal malabsorption disorder. Lactose is a sugar that is often found in dairy products, and most mammals lose the ability to digest this sugar post weaning. On the other hand, those with lactase persistence are able to continue digesting lactose into their adulthood through the production of an enzyme called lactase. The production of this enzyme is an inheritable trait most commonly found amongst European populations and pastoralist communities.
Genetics
Lactose intolerance is a genetic condition also referred to as ‘lactase non-persistence (LNP)’. This condition is the result of a decline in lactase production after weaning. Lactase is the enzyme that is responsible for the degradation of the sugar (lactose) found in milk and other dairy products into glucose and galactose. This decline is typically a normal trait in the developmental process of mammals into adulthood. Those with LNP will unfortunately suffer from side effects from incomplete digestion in the small intestine. These side effects include bloating, flatulence, diarrhea, and abdominal pain.
Those with lactase persistence (LP) have inherited the ability to produce lactase in adulthood through a T-mutation. The inheritable trait is then passed down as an autosomal dominant trait, noted as the lactase gene (LCT). Research shows that LP is heavily associated with single nucleotide polymorphisms (SNPs) that are located in the enhancer region which regulates lactase expression. This observation is most commonly found in European populations regarding the -13910T*-mutation. The LCT gene is found in the intron of the MCM6 gene, located upstream of the LCT gene. Among individuals of European descent, the A-allele of the SNP is associated with LP, while the G allele is associated with LNP. Since LP is observed to be a dominant trait, individuals with heterozygous alleles are observed to inherit the LP trait. Other than the -13910*T-mutation, other closely related mutations were also found to be associated with LP, however these were found commonly in populations in East Africa.
Studies have found that the -13910*T-mutation acts as a stimulus towards lactase production. Binding sites for intestinal transcription have also been found in the -13910 region, which further shows how this mutation is crucial to the regulation of lactase expression. In addition to this mutation, more recent studies have found that epigenetics have found a role in the regulation of lactase through DNA methylation. LNP haplotypes containing -13910*C alleles are found to store methylated cytosines with age. Overtime, this eventually silences the regulatory factors of LCT. This evidence explains that one’s genetic background allows for epigenetic changes that influence lactase production and expression overtime.
Lactose intolerance is heavily determined by genetic variations within the region of LCT. These variations ultimately control the production of lactase and whether or not the individual will develop LP or LNP into their adulthood.
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- ↑ 1.0 1.1 1.2 Zigli DD, Brew L, Obeng-Denteh W, Kwofie S. On the Application of Homeomorphism on Amoeba Proteus. Ghana Journal of Technology. 2021 Mar 31;5(2):43-7.
- ↑ Bartlett et al.: Oncolytic viruses as therapeutic cancer vaccines. Molecular Cancer 2013 12:103.
- ↑ Lee G, Low RI, Amsterdam EA, Demaria AN, Huber PW, Mason DT. Hemodynamic effects of morphine and nalbuphine in acute myocardial infarction. Clinical Pharmacology & Therapeutics. 1981 May;29(5):576-81.
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