Epigenetics may explain Lactose Intolerance better than Darwin


Epigenetics explains lactose intolerance better than genetic mutations.

Epigenetics is the study of changes in gene expression that do not involve changes in the DNA sequence. These changes can be caused by environmental factors, such as diet, stress, and exposure to toxins.

Lactose intolerance is caused by the body's inability to produce enough of the enzyme lactase, which is needed to digest lactose, the sugar found in milk. The LCT gene, which provides instructions for making lactase, is located on chromosome 2.

There are two main types of lactose intolerance: primary lactose intolerance and secondary lactose intolerance. Primary lactose intolerance is caused by a genetic mutation that reduces the production of lactase. This type of lactose intolerance is usually present from birth and is more common in people of African, Asian, and Native American descent.

Secondary lactose intolerance is caused by damage to the small intestine, such as from celiac disease or inflammatory bowel disease. This type of lactose intolerance can be temporary or permanent.

Epigenetic changes can also affect the expression of the LCT gene. For example, studies have shown that people with lactose intolerance have higher levels of DNA methylation in the LCT gene promoter region. DNA methylation is a process that adds a chemical tag to DNA, which can silence the gene.

So, while genetic mutations can play a role in lactose intolerance, epigenetic changes are thought to be a more important factor. This is because epigenetic changes can be influenced by environmental factors, such as diet and lifestyle.

For example, one study found that people who ate a high-fiber diet were less likely to be lactose intolerant. This is because fiber can help to protect the small intestine from damage, which can lead to secondary lactose intolerance.

Another study found that people who were breastfed for a longer period of time were less likely to be lactose intolerant. This is because breast milk contains lactase, which can help to keep the small intestine healthy and prevent lactose intolerance.

Overall, epigenetics is a complex field of study, and there is still much that we do not understand about how it affects lactose intolerance. However, the evidence suggests that epigenetic changes play a more important role than genetic mutations in this condition.

The article "Lactase nonpersistence is directed by DNA-variation-dependent epigenetic aging" by Labrie et al. (2016) investigates the genetic and epigenetic factors that contribute to the ability to digest lactose in adulthood. Lactose is a sugar found in milk and other dairy products. In most mammals, the ability to digest lactose declines after weaning, as the lactase gene is turned off. However, in some human populations, the lactase gene remains active in adulthood, allowing people to digest lactose throughout their lives.

The authors of the study focused on two genetic variants that are associated with lactase persistence. These variants are located in the promoter region of the lactase gene, which is the region of DNA that controls the gene's expression. The authors found that people who carry the lactase-persistence variants have lower levels of DNA methylation at the lactase promoter than people who do not carry these variants. DNA methylation is an epigenetic modification that can silence gene expression.

The authors also found that the level of DNA methylation at the lactase promoter increases with age in people who do not carry the lactase-persistence variants. This suggests that epigenetic changes play a role in the decline of lactase activity in adulthood.

The authors concluded that lactase nonpersistence is directed by DNA-variation-dependent epigenetic aging. The lactase-persistence variants protect the lactase gene from epigenetic inactivation, which allows the gene to remain active in adulthood.

The findings of this study have important implications for our understanding of lactose intolerance. They suggest that lactose intolerance is not simply a result of the lack of lactase activity, but is also influenced by epigenetic factors. This could lead to the development of new treatments for lactose intolerance that target the epigenetic mechanisms that control lactase expression.

In addition to the genetic and epigenetic factors discussed in the article, there are also environmental factors that can influence lactase persistence. These factors include diet, ethnicity, and geography. For example, people who consume a diet high in dairy products are more likely to be lactase persistent. Similarly, people of European descent are more likely to be lactase persistent than people of African or Asian descent.

The study by Labrie et al. (2016) provides important insights into the genetic and epigenetic factors that contribute to lactase persistence. These findings could lead to the development of new treatments for lactose intolerance and a better understanding of the evolution of this trait in humans.

Here are some additional questions that the study raises:

  • How do the lactase-persistence variants protect the lactase gene from epigenetic inactivation?

  • Can the epigenetic changes that lead to lactase nonpersistence be reversed?

  • How can we develop new treatments for lactose intolerance that target the epigenetic mechanisms involved?

These are just a few of the questions that need to be answered in order to fully understand the causes of lactase nonpersistence and lactose intolerance. The study by Labrie et al. (2016) is a significant step forward in our understanding of this complex trait, and it is likely to lead to new discoveries in the years to come.

Article snippets 

The inability to digest lactose, due to lactase nonpersistence, is a common trait in adult mammals, except in certain human populations that exhibit lactase persistence

Lactase nonpersistence is directed by DNA-variation-dependent epigenetic aging

It is not known how the lactase gene is dramatically downregulated with age in most individuals but remains active in some individuals

Epigenetically controlled regulatory elements accounted for the differences in lactase mRNA levels among individuals, intestinal cell types and species

lactase-persistence and lactase-nonpersistence DNA haplotypes demonstrated markedly different epigenetic aging.

accumulation of epigenetic changes with age, thereby influencing phenotypic outcome.

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