Paleofantasy: What Evolution Really Tells Us about Sex, Diet, and How We Live (13 page)

A chicken-or-egg question, without chickens or eggs

The earliest remains of domesticated cattle date back about 8,000–9,000 years. Initially, before the controlled breeding mentioned in the previous section, and even now in some parts of Africa, the animals were used not as a source of fresh milk but for pulling plows or as sources of meat or blood. Fermented milk in the form of cheese or yogurt was sometimes consumed, but these dairy products usually have little lactose and hence cause fewer digestive problems than fresh milk does.

To understand the evolution of lactase persistence, it’s important to know which came first: milk drinking or the change in the lactase gene. In other words, did early humans somehow evolve the ability to tolerate lactose, via the random changes in genes that occur all the time, and then start to use dairy and fine-tune their domestication of cattle; or did the gene for lactase persistence evolve because of the evolutionary advantage of dairy consumption? Finding the answer has required some of the most sophisticated genetics, and archaeology, of our time.

When the relative proportion of a gene in a population changes through chance, the process is called genetic drift. Drift happens in most if not all populations, but it is most common in small groups, simply because a change that is neutral with respect to evolution—providing its bearer with neither benefit nor cost—is more likely to become fixed in a population if there are not a lot of other options.

The concept of genetic drift is relevant to our understanding of lactase persistence because it is a kind of default hypothesis: instead of selection producing the change in gene frequencies, the revised proportion of milk digesters could have arisen by chance alone. Many forms of many genes come and go, and it is certainly within the realm of possibility that lactase persistence genes arose in a few human populations by chance—the actual chemical alterations required are not that complicated. The genes would then have become established in the population slowly, with nearby genes on the same chromosome as the lactase persistence genes changing independently of the ones conferring lactase persistence. In this scenario, one wouldn’t expect to see big blocks of the same genes continuing to be associated with the lactase persistence genes.

Alternatively, if the gene rose in frequency not by chance, but because of selection favoring individuals who could digest milk, a different genetic pattern would be expected. In this case the genes surrounding the lactase persistence gene should be relatively more homogeneous than would be expected by chance, because strong selection would be carrying them along with the lactase persistence gene.

To picture this situation more clearly, imagine that the different forms of the genes are beads on a string, and then further picture the beads being able to slide on and off, with the probability of sliding increasing along with the amount of time that the beads stay together. If a string with the bead representing the lactase persistence gene keeps being plucked from the rest, it carries away, willy-nilly, the genes located next to it. The lactase persistence bead is propagated because it is advantageous, and the beads alongside are simply “hitchhikers,” to use the genetic terminology.

Comparing these predictions—similarity of the blocks of genes near the lactase persistence gene, versus random assortment—requires fairly complicated statistical analysis, but with the ability to determine genetic sequences at a fine scale, it was possible to perform the critical test during the first few years of the twenty-first century. The answer? Selection. The beads—genes—associated with lactase persistence were much more similar than you would expect under a leisurely drift hypothesis. People able to drink milk without gastrointestinal disturbance passed on their genes at a higher rate than did the lactose-intolerant, and the gene for lactase persistence spread quickly in Europe.

It may seem implausible that such a modest ability would produce such a large change in an entire population, but a gene doesn’t have to raise the reproductive success of its bearer all that much to become established. Anthropologists Rob Boyd and Joan Silk calculated that as little as a 3 percent increase in the reproductive fitness of those with lactase persistence would result in the widespread distribution of such a gene after only 300–350 generations.
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That’s about 7,000 years—a blink of the evolutionary eye. Other calculations have estimated that the forms of the gene allowing milk consumption are anywhere from about 2,200 to 20,000 years old—again, a shockingly brief interval in our history. But it seems to have been enough for at least some of us to take a step away from our early human ancestors.

What this means is that our own genome has evolved because of our cultural practices. Tolerating milk led us to keep more dairy cattle, which in turn continued to favor the genes for lactase persistence. This kind of coevolution, while not unknown before, is a beautiful example of what anthropologist Pascale Gerbault classifies as “niche construction.”
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All organisms inhabit what ecologists call a niche, a world defined by the requirements of the species; frogs need water, flies to eat, and weeds to hide in, while mosquitoes require hosts with blood and a refuge from swatters. The human niche is similarly constrained, and one of its proscriptions used to be milk. But once the early pastoralists evolved lactase persistence, we could shape our own destiny, in at least that one modest attribute. As anthropologist Alan Rogers put it, “We live in a radically changed environment, that we ourselves created.”
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Calcium, food, and water

What makes drinking milk so beneficial? Why did selection favor those few with the ability to digest dairy after weaning? The most obvious reason is that dairy provides a supplementary source of nutrition, something that may be scarce for pastoralists. But scientists have suggested at least two other possibilities.

First, according to the calcium assimilation hypothesis, lactose tolerance is advantageous at high latitudes, where sunlight can be scarce and hence vitamin D levels low, because it allows more efficient uptake of calcium, much the way the vitamin itself does. Milk drinkers would thus be more likely to avoid the debilitating bone disease of rickets.

Alternatively, perhaps alongside either supplemental nutrition or calcium assimilation or both, is the notion that milk, above all, is a source of uncontaminated fluid, something that can be in short supply in the deserts of northern Africa. Compounding the danger of dehydration that the scarcity of water poses, one of the effects of lactose intolerance is diarrhea, which dehydrates the body even more. Members of the Beja, a nomadic people who herd camels and goats in the arid lands between the Nile and the Red Sea, drink about 3 liters of fresh milk each day during the lengthy dry season. If they could not digest lactase, the lives of these pastoralists would be difficult, if not impossible.

Gerbault and colleagues examined the distribution of lactase persistence across Europe and the Middle East. How, they asked, does milk drinking correlate with the amount of dairy herding by a given group of people, the archaeological evidence of the start of cattle domestication, and the changes that have occurred in other variable genes besides the ones for lactase persistence? The scientists conducted computer simulations in which they entered a variety of starting conditions for all of these variables and then asked whether one or more of the hypotheses for the advantage of milk drinking—better calcium absorption or the coevolution of people and cattle—explained the patterns we now see. It was difficult to separate the ideas, since both are compatible with the northern expansion of milk drinking in prehistory, but Gerbault’s team concluded that the calcium hypothesis was a likely force in European, though not Middle Eastern or African, lactase persistence evolution.
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To test the idea more thoroughly, genetic samples from people in other parts of the world, including Asia, where lactase persistence is relatively rare, would be needed.

A final hypothesis about the adaptive significance of lactose tolerance—or more accurately, intolerance—was proposed in the late 1990s by B. Anderson and C. Vullo of the Division of Pediatrics at the Santa Anna Hospital in Italy. They noted that malaria is a common disease in places where people are less likely to have lactase persistence. What’s more, people who do not consume milk can suffer from low riboflavin levels, particularly if they are otherwise poorly nourished. The parasite that causes malaria doesn’t grow as quickly in cells that lack flavin, so Anderson and Vullo speculated that people without lactase would be protected from the disease.
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In this view, the trait that evolved in response to selection was the inability to digest milk, not the persistence of lactase. This seems an unlikely scenario, however, given that all other mammals lose the ability to digest lactose after weaning, making lactose intolerance a more likely ancestral state. Further research also revealed no connection between malaria and the genes for lactase persistence.

Africa, the milky continent

Africa is a funny place when it comes to milk. Lactose tolerance in northern Europe arose well after early humans had left Africa. If we accept the idea that selection on humans in Europe caused them to evolve a high degree of lactase persistence, then what are some groups of people in Africa, like the Beni-Amir pastoralists in Sudan, doing with a 64 percent frequency of lactase persistence? Isn’t it just too much of a coincidence to assume that such widely separated people evolved the same mutation at more or less the same time?

Geneticist Sarah Tishkoff of the University of Pennsylvania discovered the answer to this question by driving along the rutted—sometimes nonexistent—roads of East Africa, asking people from forty-three ethnic groups to participate in a study.
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She and her colleagues asked 470 volunteers to drink a solution of powdered lactose dissolved in water. The scientists then took blood samples at timed intervals to collect information about lactose digestion and a sample of the individual’s DNA at the same time. This test for lactose tolerance is not as accurate as the ones given in a Western medical facility, but it was far more feasible to administer in the field.

Tishkoff and her coworkers looked at their subjects’ DNA for genetic variations near the lactase gene itself, where the lactase persistence alterations had previously been discovered. They found a consistent pattern of a few of these variants in people who could tolerate lactose consumption, but the genes that had become altered were different from the ones previously discovered in northern Europeans. In other words, Africans had evolved lactase persistence independently of the Europeans, with the same trait—being able to digest milk—arising from different genes. In both places, however, the people who can tolerate lactose are, with a few exceptions, the ones whose ancestors kept cattle and other milk-yielding animals.

The African version of lactase persistence also arose more recently than the European version, given that people did not start keeping herd animals in southern Kenya and northern Tanzania until just over 3,000 years ago. Thus, lactose tolerance is one of the best examples not only of rapid evolution, but of convergent evolution, the independent evolution of a similar trait via different pathways. Other cases of convergent evolution include the wings of birds and bats, which have the same function but are anatomically quite distinct, and the sonar-like echolocation systems of some whales, bats, and shrews. The lactase example is more cryptic than these, since although no one would have suggested that wings arose in the common ancestor of birds and bats, the idea that humans evolved lactose tolerance only once seems on the surface to be more plausible than the reality of multiple occurrences.

Interestingly, about half of the Hadza people of Tanzania were found to have the lactase persistence gene—a hefty proportion, given that they are hunter-gatherers, not herders. Why did the Hadza evolve a trait they don’t use? Tishkoff and coworkers speculate that the gene might be useful in a different context. The same enzyme that enables the splitting of the lactose molecule is also used to break down phlorizin, a bitter compound in some of the native plants of Tanzania. Could the lactase persistence gene also help with digestion of other substances? No one knows for sure, but the idea certainly bears further investigation.

Microbes, milk, and what’s to come

Despite the strong evidence for recent evolution of lactase persistence in humans via natural selection, a number of questions remain. How exactly does the mutation in a gene associated with the lactase molecule manage to keep the ability to break up lactose in adults? And why does lactose tolerance stop at different times for different people? Finns generally have high levels of lactase persistence, but some of them lose the ability to digest lactose as teenagers, rather than either retaining it throughout life or losing it as small children. Addressing this problem means understanding how genes regulate each other at different times during the life span—a fundamental question in human biology.

At a more practical level, what does the evolution of lactase persistence mean for modern people who are concerned about dairy consumption? It certainly puts to rest the notion that because dairy “is not paleo,” it is not an appropriate part of the human diet. One’s ability to digest milk simply depends on one’s genes, and those genes have changed, at least in those of us whose heritage is rooted in pastoralists. (Note, as I mentioned earlier, that milk allergy, which is an immune reaction to the proteins found in milk, is distinct from lactose intolerance; both are genetic, but they arise from completely different genes.) Of course, people choose not to consume many foods they are capable of digesting, but the story of lactase persistence is an object lesson in escape from paleofantasy.

The science, of course, continues. A different way of trying to understand the question of variability in lactose tolerance might lie in another anomalous African population. At least some Somali people consume plenty of fresh milk but lack the genes identified by Tishkoff and others that should allow them to do so—rather a reversal of the Hadza. Catherine Ingram and others at University College London suggest that gut flora in the Somali may break down the lactose, making it easier to digest, in much the same manner that milk products such as yogurt and cheese are made digestible when their lactase is broken down in fermentation. Many people who are lactose-intolerant have an easier time digesting these products than they do fresh milk.
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It is tempting to speculate that a particular set of bacteria and other microbes were subject to selection among the Somali, which meant that they achieved the same end as the Europeans and other Africans with the lactase persistence gene, but through yet another means.