How we Adapted to the Diet and the Environment
(Published in the newspaper Amigoe on the 14th of January 2026)
In the last article, we learned about how certain mutations can shield some folks or groups from getting sick. Now, let’s dive into mutations in specific populations that made drinking milk possible. We’ll also explore how in Tibet, people can thrive on the high Tibetan plateau, with altitudes soaring up to 4,500 meters where the air is thin with less oxygen!
WHY MANY ADULTS CAN DRINK MILK TODAY
Back in the day, about ten thousand years ago, our ancestors were hunters and gatherers. But here’s the catch: adults couldn’t drink milk back then because their bodies couldn’t handle the lactose, the sugar in milk. You see, milk is packed with lactose, like 4.5 to 5 grams per 100 ml. When our ancestors sipped milk, the lactose made its way to their large intestines, where some friendly bacteria started breaking it down. And guess what? This fermentation process caused some not-so-fun side effects like flatulence, cramps, or diarrhea.
Back in the day, only babies could handle lactose. That’s because they had an enzyme called lactase, which helped them break down breast milk. The lactase enzyme is encoded by the LCT gene. But after childhood, the activity of the LCT gene decreased. Therefore, as we grow up, our bodies stop making lactase. So, lactose became a problem for us.
Lactase persistence in Europe
Lactase production usually drops after childhood. But when people in certain areas started raising livestock like cows, goats, and sheep, milk became a delicious new food source. And guess what? A genetic change happened in some folks that totally changed the game. This mutation happened in the MCM6 gene, which is right next to the LCT gene. The MCM6 gene decides if the LCT gene is “on” or “off.” People with this mutation in the MCM6 gene have the LCT gene turned on all the time, even as adults. So, they can make lactase for life and keep enjoying milk. We call this amazing ability lactase persistence.
The most common version of this mutation, −13910*T, likely started around 7,500 to 10,000 years ago in Europe. It’s believed to have happened among early farmers in the area that’s now Hungary or the Balkans. From there, it spread quickly across northern and western Europe.
Lactase persistence in Africa and the Middle East
But Europe was not the only place where this adjustment took place. In different parts of Africa and the Middle East, other, independent mutations emerged in the same control area of the MCM6 gene. These also caused lactase persistence. So this is another example of convergent evolution. This is similar to the independent formation of blonde hair in Europe and Oceania. So different populations developed similar adjustments, each in their own way.
In places where dairy farming was crucial for survival, like among the Maasai in East Africa or nomadic herders in the Middle East, this mutation gave them a huge evolutionary edge. Milk was like a lifesaver, offering water, fat, protein, and sugars, even in dry periods.. Those who could digest milk had a better shot at surviving and passing on their genes.
Milk-drinking Masai shepherd
Lactose intolerance
People with the mutated MCM6 gene can now digest lactose. But in East Asia, parts of South America, and some areas in Africa, most people still can’t handle lactose.
Milk products
By the way, folks without the mutated MCM6 gene that makes them lactose intolerant are more likely to handle certain milk products. For instance, yogurt is made by tiny bacteria called lactic acid bacteria (like Lactobacillus and Streptococcus) that break down some of the lactose into lactic acid. This means yogurt has way less lactose than milk. In fact, it can have as little as 30–50% of the original lactose! And guess what? These live yogurt cultures themselves have enzymes that help break down even more lactose in your gut. So, even many lactose-intolerant folks can enjoy yogurt, especially if it’s natural, unsweetened, and has live cultures.
Cheese is also low in lactose. During the cheese-making process, almost all the lactose goes away. Most of it is lost when the whey (the liquid that’s drained) is removed. The remaining lactose is turned into lactic acid during the ripening process. So, hard cheeses like Parmesan, Emmental, and Cheddar have almost no lactose. In fact, it’s usually less than 0.1%. Even people who don’t have the special enzyme lactase can usually eat these cheeses without any issues. Soft or fresh cheeses like mozzarella, cream cheese, and feta have a bit more lactose, but still way less than milk.
WHY DON'T TIBETANS SUFFER FROM ALTITUDE SICKNESS?
Tibetans call home the high mountains of Tibet, where the air is thin and there’s not much oxygen. Tibet is in Central Asia and is often called the “Roof of the World.” It’s a huge plateau that’s usually about 4,500 meters above sea level. Some parts, like the city of Lhasa, are a bit lower (around 3,650 meters), while other areas, especially near the Himalayas, go even higher. Because of this extreme altitude, the air pressure in Tibet is much lower than at sea level. The air pressure in Tibet is usually only 60 to 65 percent of the air pressure at sea level. This means there’s less oxygen in the air. It’s tough to get enough oxygen into your blood. For visitors, this can lead to altitude sickness.
The special variant of the EPAS1 gene
Fortunately, Tibetans have a special version of a gene called EPAS1. The EPAS1 gene is involved in the regulation of oxygen. The mutation of this gene has led to a special variant of this gene. The special variant of EPAS1 helps the body to handle oxygen better, even at high altitudes.
The Denisovanes and the special EPAS1 variant
Scientists have found out that this special EPAS1 variant comes from the Denisovanes. The Denisovanes were a group of people who lived a really long time ago, like 50,000 to 300,000 years back. They looked a bit like Neanderthals, but they were a different kind of people. They lived in Asia. Researchers figured out that this piece of DNA in Tibetans comes from when early modern humans and Denisovans crossed paths, probably tens of thousands of years ago. In short, thanks to ancient encounters between Denisovans and modern humans, Tibetans, and highland populations in Nepal, got a genetic advantage for living at high altitudes. Studies have shown that the EPAS1 variant also shows up in highland populations in Nepal. Nepal is also mostly on the Tibetan plateau and in the Himalayan region.
Reconstruction Denisovan woman
This is the final piece in this series about genetic mutations. We’ve learned a lot about how humans have changed over time because of mutations. They’ve given us some physical traits, like lighter skin in places with little sun and blonde hair and blue eyes. They’ve also helped us fight off diseases like malaria and HIV.
In addition, mutations allow us to exploit new food sources, such as milk, thanks to lactase persistence. The mutation of the EPAS1 gene allows us to cope with extreme living conditions, such as the low oxygen content on the Tibetan plateau.
Evolution isn’t just some abstract idea. It’s a real-life connection between our genes, the environment, and how we survive. Our DNA is like a living record of how we’ve changed and adapted over time. It shows that we’re constantly evolving and staying flexible as a species.
However, not all mutations are good for us! Many serious diseases are caused by mutations. An example is sickle cell disease. Sickle cell disease originates from Africa and is common in Curaçao. In the next series of three articles, this disease and its genetic origin will be discussed.