When a single genetic mutation first let ancient Europeans drink milk, it set the stage for a continental upheaval. During the most recent ice age, milk was essentially a toxin to adults because — unlike children — they could not produce the lactase enzyme required to break down lactose, the main sugar in milk. But as farming started to replace hunting and gathering in the Middle East around 11,000 years ago, cattle herders learned how to reduce lactose in dairy products to tolerable levels by fermenting milk to make cheese or yogurt. Several thousand years later, a genetic mutation spread through Europe that gave people the ability to produce lactase — and drink milk — throughout their lives.
Young children almost universally produce lactase and can digest the lactose in their mother's milk. But as they mature, most switch off the lactase gene. Only 35% of the human population can digest lactose beyond the age of about seven or eight (2). “If you're lactose intolerant and you drink half a pint of milk, you're going to be really ill.
Most people who retain the ability to digest milk can trace their ancestry to Europe, where the trait seems to be linked to a single nucleotide in which the DNA base cytosine changed to thymine in a genomic region not far from the lactase gene. There are other pockets of lactase persistence in West Africa (see Nature 444, 994–996; 2006), the Middle East and south Asia that seem to be linked to separate mutations3 (so called 'Lactase hotspots').
The single-nucleotide switch in Europe happened relatively recently. Thomas and his colleagues estimated the timing by looking at genetic variations in modern populations and running computer simulations of how the related genetic mutation might have spread through ancient populations4. They proposed that the trait of lactase persistence, dubbed the LP allele, emerged about 7,500 years ago in the broad, fertile plains of Hungary.