Originally, every human on Earth was lactose intolerant, like most mammals. That is, they lost the ability to digest lactose, the major sugar in milk, when their bodies stopped producing the necessary enzyme lactase after weaning. Then, some populations of humans domesticated milk-producing animals, and this seems to have generated strong natural selection [PDF] for a form of the lactase gene that remains active in adults.
In fact, milk-drinking populations in Europe and Africa have evolved "lactase persistence" independently [$-a]. This parallel evolution of a single trait motivates the new study by Gerbault et al. -- drinking milk might have different advantages for African pastoralists and Northern European farmers. Milk has two major dietary benefits:
Photo by bensonkua.
Photo by bensonkua.
- It's generally nutritious as a source of protein and calories, and
- Lactose can aid in calcium uptake in lieu of Vitamin D.
If the benefit of milk is calcium, not protein, then we would expect adult-active forms of the lactase-producing gene to be common in northern populations, and to decrease in frequency with decreasing latitude. This has been observed in a survey across Europe [$-a] -- but while the north-south pattern supports the calcium-benefit hypothesis, it is not conclusive evidence. This is because the same pattern could arise without any natural selection acting on the gene -- populations generally tend to be less genetically similar if they're farther away from each other, a phenomenon called isolation by distance, or IBD [PDF]. In fact, Gerbault et al. find that the north-south pattern of genetic similarity is replicated in genes that probably aren't under selection arising from life at high latitudes, suggesting that IBD, not selection, is responsible for the pattern in the lactase gene.
For a more conclusive test, Gerbault et al. developed computer simulations of the evolution of early European communities. By simulating populations' evolution with different strengths of selection acting on the lactase gene, they could estimate how probable a particular value of selection was given the present-day frequency of lactase persistence in the real population -- but also take into account the population genetic forces that create IBD. They found that in southern Europe, no natural selection was necessary to explain the present frequency of lactase persistence -- but in the north, selection coefficients as high as 1.8% were needed. That is, in northern Europe, lactase persistence is so common that the simulations only produced the observed frequency when people who could not drink milk as adults had, on average, 1.8% fewer children than those who could.
Photo by tricky.
Photo by tricky.
In contrast to Europe, African communities don't show the same gradual transition from frequent to rare lactase persistence, so IBD is less likely to explain the observed patterns. To explain the frequency of lactase persistence in African populations, the authors compared it to the frequency of pastoralism -- and, finding a strong positive correlation, they concluded that lactase persistence evolved in Africa because it allowed shepherds to derive more nutrition from the animals they kept.
In short, widespread lactase persistence evolved in Africa because milk is a good source of protein; but it seems to have evolved in Europe because milk is a good source of bone-building calcium. Human populations on separate continents arrived at the same evolutionary solution, but for slightly different reasons.
Update, 18 October 2009: I've submitted this post to the NESCent competition for a travel award for the ScienceOnline 2010 conference in Durham, NC, January 14‐17th, 2010.
Update, 15 December 2009: Ye gads. I won!
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Gerbault, P., Moret, C., Currat, M., & Sanchez-Mazas, A. (2009). Impact of selection and demography on the diffusion of lactase persistence PLoS ONE, 4 (7) DOI: 10.1371/journal.pone.0006369
Ingram, C., Mulcare, C., Itan, Y., Thomas, M., & Swallow, D. (2008). Lactose digestion and the evolutionary genetics of lactase persistence Human Genetics, 124 (6), 579-91 DOI: 10.1007/s00439-008-0593-6
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