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Lactose can not be absorbed directly into the intestinal tract and must be broken down into two smaller sugars consisting of sugars by an enzyme called lactase. Normally, the activity of the lactase-producing gene, LCT, declines after infancy. New evidence suggests that this decline is due not to the modification of the genetic code, but to the chemical modification of the DNA, so that the lactase gene is deactivated. These changes that affect gene activity while leaving the DNA sequence intact are called epigenetics. Epigenetic modification that disables the lactase gene does not occur in lactose tolerant individuals. This new discovery provides an important insight into how lactose intolerance develops with age or after trauma to the intestinal tract.
I am a microbiologist and I have been interested in the causes of lactose intolerance because it afflicts a close friend. He is of Norwegian origin and, like most Norwegians, is genetically tolerant to lactose. However, he became definitely lactose intolerant at the age of 45 after a long diet of antibiotics.
There are other cases of people who should be able to digest lactose because of their genetics, but lose it late, either spontaneously or when the small intestine is damaged by disease or other trauma. In most cases, lactose intolerance disappears when the underlying cause is treated, but some people become definitely lactose intolerant.
It seems possible, even likely, that such a digestive tract trauma could trigger the same epigenetic change as the normally deactivated lactase gene in childhood. Scientists have discovered other cases of such epigenetic changes induced by the environment, although further research is needed to establish the persistence and consequences of these changes.
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Lactose intolerance is mainly due to your genes
While the ability to produce the lactase enzyme persists until adulthood in only about 35% of adults worldwide, this proportion varies considerably between ethnic groups. In the United States, the proportion of lactose-tolerant people is about 64%, reflecting the mix of ethnic groups that populate the country.
The ability of adults to digest lactose has appeared in humans relatively recently. Specific genetic modifications – known as single-nucleotide polymorphisms (SNPs) – reflecting the persistence of lactase have occurred independently in various populations at about the same time as their domestication of dairy animals. None of these SNPs are found in the lactase gene, but rather in a region close to the DNA that controls its activity. Scientists are trying to understand how these changes affect the behavior of this gene.
Researchers have recently shown that one of the SNPs altered the level of epigenetic modification of DNA in the lactase gene control regions. Specifically, the SNP prevents small chemical units, called methyl groups (which consist of one carbon atom and three hydrogen atoms), from being attached to the DNA. Methyl groups play a particularly important role in the regulation of gene activity because, when they are added to the DNA, they deactivate the gene.
These studies imply that after early childhood, the lactase gene is usually cleaved by methylation of DNA. SNPs that modify the DNA sequence in the control region, however, prevent this methylation from occurring. This, in turn, leads to the production of lactase because the gene is conserved.
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To date, five different SNPs have been strongly associated with the persistence of lactase and a dozen others have been found in isolated populations. The durations of these SNPs in different cultures range from 3,000 (Tanzania) to 12,000 (Finland) years. The fact that the trait persists and spreads in these populations indicates that the ability to digest milk beyond infancy has a significant selective advantage.
Your microbiome and lactose intolerance
Symptoms of lactose intolerance include diarrhea, stomach pain, cramps, bloating, and flatulence, all of which result from an inability to break down lactose in the body. small intestine. As undigested lactose enters the large intestine, water penetrates to reduce the lactose concentration, thereby producing diarrhea. Lactose is ultimately consumed by the microorganisms of the large intestine, producing, as by-products, various gases that cause bloating, cramps and flatulence.
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Recent studies have shown that some people can relieve the symptoms of lactose intolerance by altering the population of their intestinal microbes, called microbiome, to encourage bacteria that digest lactose. More specifically, the bacteria, called "lactic acid bacteria", eat lactose but produce lactic acid by-product in place of the gas. Although lactic acid has no nutritional value, it does not cause the unpleasant symptoms of lactose intolerance. This adaptation of the intestinal microbiome may explain how some former pastoral populations lacking genetic evidence of lactase persistence have tolerated a diet rich in dairy products.
Ingesting lactic acid bacteria as probiotics can lessen the symptoms of lactose intolerance, but these bacteria may not persist in the colon. A promising new strategy is to "feed" the lactic acid bacteria with a complex sugar that they can digest but that humans can not digest. In the first clinical trials, subjects using this "prebiotic" reported an improvement in lactose tolerance and a corresponding change in their intestinal microbiome. More important clinical trials are underway.
So there is hope for people with lactose intolerance that real ice cream is back on the menu.
Patricia L. Foster is Professor Emeritus of Biology at the University of Indiana. She receives funding from the US Army Research Office. She is a member of the Union of Concerned Scientists and Concerned Scientists of Indiana University.
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