Distribution of the Lactase Persistence Gene
Mammalian babies drink milk. Almost all non-human adult mammals do not drink milk. Some human adult mammals drink milk (northern Europeans, East Africans, West Africans), while many adult human mammals (East Asian, Bantu, Basque) cannot drink milk without suffering lactose intolerance symptoms (lactose, a milk sugar, cannot be metabolized).
Here's the story: mammalian infants have an enzyme, lactase that enables lactose to be metabolized. This enzyme is normally lost after infants are weaned. However in certain groups where dairy farming has been carried out, a gene, "lactase persistence gene", enables the enzyme to continue to be present. This gene was not present in these groups (Northern Europeans/East Africans) 8000 to 10,000 years ago, but is now (77% or higher in Northern Europeans). Therefore it must have appeared as a mutation and by enhancing survivability, spread.
This was the story I heard in John Hawkes' audiobook, "The Rise of Humans", (see also the article linked in the picture caption), and it seemed plausible, but as physicist I wanted numbers. The best science according to Fr. Stanley Jaki is quantitative, so that predictions or retrodictions can be assessed quantitatively. And I have found such a mathematical test in an article by Todd Bersagiliari and many others, Genetic Signatures of Strong Recent Positive Selection at the Lactase Gene.
MATHEMATICS IN EVOLUTIONDancing on a tightrope of very involved statistical and Markov chain calculations (I have to confess I don't fully understand all the math, but accept it) the authors find that this mutated gene, which allowed persistence of the lactase enzyme action, enhanced survivability by between .09 and 0.19 for the Scandinavian population and between 0.014 and 0.15 for the East African. I take this "coefficient of selection" to mean that those Scandinavians carrying this dominant gene produced between 1.09 to 1.19 more children per generation than those who did not have the gene. Their retrodictive frequencies are in accord with the relative frequencies of the gene: orange to red, high; blue to indigo, low.
COMMENTARYHere are some of the features of this problem that I don't understand. The lactose intolerance symptoms described in the linked article (and others) cause discomfort but are not altogether debilitating. In many cases, yogurt and other dairy products in which lactose has been degraded can be eaten by lactose intolerant individuals. If dairy farming started out with products such as those, whence the 10 to 20 % increase in progeny from lactase persistent gene, which enabled less refined dairy products to be eaten?
When this article was posted as a short commentary in the Biologos Forum, I put a question to one of the authors of the linked paper: how did the mathematical analysis distinguish between a single mutation that spread and multiple mutations? He answered that the analysis was predicated on just a single mutation, and that was all that was necessary for the spread of the desirable trait.
If one looks at the map of incidence of high proportion of this gene, it appears in multiple regions: Northern Europe, East Africa and the Arabian peninsula, West Africa, such that migration of peoples with the gene would not have been a likely mechanism for its spread. (I've read various accounts of where the mutation originated--Hungary, Iranian plateau--but a single geographic origin doesn't seem to be compatible with the present distribution.)
My point then is (and it's altogether speculative) what about God directing such a mutation (or more) to occur where dairy farming was prevalent? There's no way of proving it (or disproving it), but it's consistent with the facts.
And we'll leave it there for critical comments (be nice, please). Finally, let me say that I'm happy to not throw brickbats at the Neo-Darwinians who argue for survival of the fittest as a mechanism for evolution (provided God lends a helping hand).