Why do some people get diarrhea after drinking milk? It turns out that this is the "trouble"

Many people have had this experience: bloating or diarrhea right after drinking milk, and they always suspect that it is the milk, but other people are fine after drinking the same milk? In fact, it is the lactose in the milk that is causing the problem! Your bloating or diarrhea is actually a sign of lactose intolerance .

Why are some people lactose intolerant? Obviously, it starts with lactose.

Bloating when lactose intolerance occurs. Copyright image. Reproduction without permission.

01

How does the human body digest and metabolize lactose?

To understand lactose, we must first talk about sugars that provide energy to the human body, that is, carbohydrates.

Monosaccharides are the simplest sugars. Common monosaccharides include glucose, fructose and galactose . Humans mainly obtain energy by consuming carbohydrates. Among them, glucose is equivalent to gasoline in a car, providing a constant source of power for our bodies. We also usually consume fructose and galactose, and these two monosaccharides will eventually be digested and metabolized to provide energy for the human body.

Many carbohydrates are usually ingested into the human body in the form of "disaccharides" , and one of them is a disaccharide that can easily cause gastrointestinal discomfort - lactose. It is composed of a glucose molecule and a galactose molecule and is widely found in milk and other dairy products.

Milk contains a lot of lactose. This is a copyrighted image and is not authorized for reproduction.

In order to better use lactose as an energy source, the human body needs to break it down into two monosaccharides when digesting it. At this time, a scissor-like tool, lactase , comes into play. Lactase is generally only found in our small intestine and is expressed by the lactase gene in the small intestinal cells.

When we drink milk, lactose passes through the stomach and reaches the small intestine. The lactose in the milk is broken down into glucose and galactose under the action of lactase. The folds on the villi of the small intestine increase the surface area of ​​the small intestine, which helps the human body absorb glucose and galactose.

02

When you are lactose intolerant

What happens to lactose in the body?

Some people feel nauseous or have bloating, flatulence, diarrhea, etc. after drinking milk. These are symptoms of lactose intolerance. Lactose intolerant people lack or have no lactase in their small intestines , and the digestion pathway of lactose in these people is changed. Lactose intolerant people will even protest every time they think of milk!

Due to the lack of lactase, when the lactose in the milk reaches the villi of the small intestine, more than 75% of the lactose will not be broken down and absorbed. The lactose will move along the small intestine to the large intestine, where there are many intestinal microorganisms that can ferment the lactose into hydrogen, methane, and carbon dioxide to form a mixed gas that will cause flatulence or bloating.

At the same time, lactose will also produce some short-chain fatty acids, such as acetate, butyrate and propionate, under the action of microorganisms. These short-chain fatty acids cannot be digested by the human body, which means they will stay in our intestines for a period of time. These undigested lactose and fermentation products will increase the osmotic pressure of the intestine, causing the intestine to absorb more water, which will eventually lead to diarrhea .

Microorganisms in the large intestine convert lactose into gas and fatty acids, causing bloating and diarrhea. Copyright image, unauthorized reproduction

03

What are the symptoms of lactase deficiency?

There are 4 types of lactase deficiency:

1. Primary lactase deficiency

Most adults who are lactose intolerant are not born with this condition. As mammals, human small intestinal cells express and secrete lactase during infancy, so infants are able to digest the lactose in breast milk. Once weaned, the expression capacity of the lactase gene in most mammals will decrease, so the production of lactase will also decrease . Humans also follow this rule. From about 2-5 years old, the expression of lactase will begin to gradually decrease, although the symptoms of lactose intolerance may not become obvious until adulthood.

Mammals can digest lactose during infancy.

This condition is called primary lactase deficiency , the most common cause of lactose intolerance worldwide, and is caused by a genetic defect that runs in families. Primary lactase deficiency occurs when humans grow up with less reliance on milk and dairy products, which reduces the production of lactase.

2. Secondary lactase deficiency

Secondary lactase deficiency is caused by a disease in the small intestine or other parts of the body . This condition can occur at any age and may be caused by small intestine surgery or taking certain medications. Possible causes of secondary lactase deficiency include:

Gastroenteritis – infection of the stomach and intestines

Celiac disease – an intestinal disorder caused by a reaction to a protein called gluten (found in wheat)

Crohn's disease - a long-term condition that causes inflammation of the lining of the digestive system

Ulcerative colitis – a long-term disease that affects the large intestine

Chemotherapy - a cancer treatment Acute illness can lead to insufficient lactase production, causing lactose intolerance, but once the small intestine disease is cured in a short period of time, lactase can be re-produced. However, if it is caused by a long-term illness, it may lead to permanent lactase deficiency.

3. Congenital lactase deficiency

In rare cases, lactase deficiency may also be congenital, that is, when the baby is born, it lacks lactase and cannot break down lactose into glucose and galactose. This is an autosomal recessive genetic disease. Babies who cannot break down lactose find it difficult to feed through breast milk and will have diarrhea from birth. At this time, the baby can be fed sugar-free milk or milk with added lactase.

4. Developmental lactase deficiency

Some premature babies (born before the 37th week of pregnancy) have temporary lactose intolerance because their small intestine is not fully developed at birth and cannot digest lactose. This is called developmental lactase deficiency, but it usually improves as the baby grows older.

04

The evolution of lactose tolerance in humans

Around 65% of people worldwide experience some form of lactose intolerance after infancy, but there are significant differences between regions: the lactose intolerance rate in Northern Europeans is only 5%, while the prevalence in some parts of Asia is over 90%.

From an evolutionary perspective, some populations have better lactose tolerance genes than others. For example, most Caucasians from northern Europe have high lactase activity until they reach adulthood, so they exhibit the characteristics of "lactase persistence."

Why Caucasians? It is generally believed that this group began to domesticate cattle and other milk-producing animals very early, and they continued to consume dairy products from childhood to adulthood. It is generally believed that they "cultivated" more autosomes that are conducive to increasing lactase persistence through natural selection.

Similar "lactase persistence" phenomena have been observed in other human groups that rely on dairy products. However, humans distributed in the grasslands of the earth, such as modern Kazakhstan, Russia, and Mongolia, also continue to drink large amounts of milk from childhood to adulthood, but many of them do not have lactase persistence. If drinking large amounts of milk continuously can lead to the mutation of lactase persistence, then the grassland residents must have evolved this lactose tolerance trait long ago, just like the Nordic people. This is not the case. Why is this?

Ethnic groups living in the Caucasus region, Image source: Wikipedia

In a study published in Nature some time ago, researchers compared archaeological evidence of milk use in Europe as early as 9,000 years ago with genetics and found that lactose tolerance evolved unusually quickly after Europeans began drinking milk. So what caused the huge genetic shift that led to lactose tolerance in so many Europeans so quickly?

Richard Evershed, director of the Biogeochemical Research Centre at the University of Bristol, said: "In order for genetic mutations to occur and evolve rapidly, there must be some factor that kills people who do not carry the gene!" Evershed found a lot of evidence that humans began drinking milk widely throughout Europe about 9,000 years ago. From a huge database from 554 archaeological sites in Europe, it was speculated that special "stressors" such as famine and pathogens would aggravate the gastrointestinal effects of milk on lactose-intolerant patients, leading to fatal diarrhea and dehydration.

If malnutrition is accompanied by diarrhea and dehydration, it will be fatal! Therefore , during that period, lactose intolerance was gradually eliminated and the ability to digest milk became more valuable.

The team also tested this using modelling, which showed that genetic variation in lactase persistence does increase when populations are exposed to famine or pathogens .

Nature magazine reveals that Europeans were the first to evolve into lactose tolerance. Image source: Nature

Do you still think that lactose tolerance can be achieved by drinking more milk? You know, evolution takes a very long time to complete, and human life is very short. It is unrealistic to want to acquire the trait of lactose tolerance by drinking more milk !

Does lactose intolerance mean that you have to say goodbye to milk and other dairy products? Not necessarily. In fact, you can drink some low-lactose milk or eat "aged" cheese , such as cheddar cheese and Parmesan cheese, which have much less lactose than regular milk.

References:

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[8] Mobassaleh M, Montgomery RK, Biller JA, Grand RJ. Development of carbohydrate absorption in the fetus and neonate. Pediatrics. 1985 Jan;75(1 Pt 2):160-6.

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