What this means

Most mammals stop producing the lactase enzyme after weaning, and so did most humans for most of history. Around 8–10,000 years ago a regulatory variant arose in an MCM6 enhancer (just upstream of the LCT lactase gene) that kept lactase production going into adulthood. It spread quickly in dairying populations — northern Europeans are now near-fixed for the A persistence allele. Independent persistence variants arose in parts of East and West Africa and the Middle East, so rs4988235 alone doesn't fully predict tolerance outside Europe.

Most mammals stop making the milk-digesting enzyme (lactase) after weaning, and so did most humans for most of history. Around 8–10,000 years ago, a tiny DNA change appeared that kept lactase production going into adulthood — and it spread fast in populations that herded cattle. Northern Europeans now almost all carry it. Different DNA changes that do the same job arose independently in East Africa, West Africa, and the Middle East, so this one test doesn't fully cover everyone's ability to digest milk outside Europe.

Caveats

• This variant is the European persistence allele — different variants drive persistence in African and Arabian populations.
• The gut microbiome also matters; some non-persistent people tolerate small amounts of dairy fine.
• Lactose intolerance and dairy allergy are different things.
• Self-reported tolerance often differs from formal hydrogen breath testing.

References

• Enattah et al. — Identification of a variant associated with adult-type hypolactasia (Nature Genetics, 2002)
• Tishkoff et al. — Convergent adaptation of human lactase persistence in Africa and Europe (Nature Genetics, 2007)