LCT gene and lactose intolerance

As it happens, not long ago I was yet again in a conversation about diary products, lactose intolerance, and evolution. It is very popular these days to repeat the mantra “cow’s milk is for cows, not for humans”. More and more people are buying into these “veganistic” idea that we were never meant to drink milk, but we “forced ourselves into evolving in drinking it, but it hasn’t worked very well, and that’s why it’s harmful for us”.

When I hear stuff like that, I shake my head, and think “would they believe they if they started ingesting mercury, they would eventually evolve to be able to live off mercury rather than just dying for its poisonous characteristics”?

That said, one colleague made the acute objection that the cows we drink the milk of are those we selectively bred for the very reason they produced milk we could drink. Of course, he also made the blind-faith leap that “this is how evolution works” (no, it isn’t — in fact, human aided selective breading only goes to show that evolution could never work unaidedly; plus, selective adaptation manipulates existing information, but never adds new information).

Back to lactose intolerance

So, on the train home I went back to the lactose intolerance issue, as I remembered things to be different to what they had said in the office. I had objected, but I could not remember all the facts, so…

Human genome posses a gene called LCT. This gene is responsible for producing the enzyme lactase, which is necessary for breaking down lactose (a sugare). If you don’t have lactase, you are lactose intolerant. Easy peasy.

All humans possess and have always possessed the LCT gene, to knowledge. All babies are normally born with functional LCT, as they must produce lactase in order to assimilate the mother’s milk (which contains lactose, just like cow milk). According to genetic information, the lactase-production should switch off after weaning. Humans, however, have lost the ability to rapidly switch off lactase production, hence they continue to be able to drink lactose-containing milk (like cow and human milk), but the older you get the less lactase you produce, and it happens to everybody; it can happens faster for some, meaning that you can become lactose intolerant when you’re still young. This is called primary lactose intolerance and would actually be “normality” for humans.

Humans, therefore, haven’t gained the ability to break down lactose, they have instead lost the function that switches that ability off right after weaning. So, it’s technically a loss of function. That makes sense when you think there is no record of beneficial mutations to date.

There are however various mutations that interest the area. For example there are mutations that enable permanent lactase production; these seems to be very common in African populations. You can also be born lactose intolerant, only for the LCT gene to wake up later and start producing lactase when you’re already weaned off. This happened to me, for example. Up to the age of one I was unable to digest milk (even human milk), but to this day I no longer have that problem.

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