Human evolution
Darwin's children
Dec 13th 2007
From The Economist print edition
Human evolution has speeded up over the past 80,000 years. That raises awkward questions about the concept of race
Stone
PROBABLY, more bad science has been conducted on the concept of human race than on any other field of biology. The reason is that an awful lot of research into race has been motivated by preconceived ideas that one lot of people are somehow better than another lot, rather than being a disinterested investigation of regional variations in a single species and the evolutionary pressures that have created them.
Contrariwise, even well constructed studies, if they do find racial differences, risk opposition from those who deny that people from different parts of the world could ever differ genetically from one another in important ways. As a result, only the foolish or the daring rush in to add to the carnage. It remains to be seen which category the authors of two papers in this week's Proceedings of the National Academy of Sciences fall into.
One of the papers, written by Andrea Migliano and her colleagues at Cambridge University, looks at a local outcome of human evolutionthe short stature often known as pygmyismand tries to explain the evolutionary circumstances that cause it. The other, by Robert Moyzis of the University of California, Irvine, and his colleagues, asks a broader question: how much evolutionary change has happened since Homo sapiens climbed out of his African cradle and began to colonise the world? The answer is, quite a lotand the rate of change seems to have speeded up.
Breed early and breed often
The best known pygmies are the Aka, Efe and Mbuti of central Africa. However, by the standard definitionwhich is that a group's men have an average height below 1.55 metresthere are also pygmies in the Andaman Islands, Malaysia, Thailand, Indonesia, the Philippines, Papua New Guinea, Brazil and Bolivia.
African pygmies usually live in forests, and the conventional explanation for their stature has been that it makes it easier for them to move through dense vegetation. There are also two competing explanations: that small bodies keep cool more readily than large ones (pygmyism tends to be a tropical phenomenon) or that pygmies live in places with unreliable food supplies, and their size means they can make do with smaller meals.
Dr Migliano and her team reject all these explanations. Some non-African pygmies live outside forests and many live in cool, dry areas. Moreover, some of the world's tallest people, such as the Turkana and Maasai of East Africa, suffer periodic interruptions to their food supply. Instead, the researchers suggest that short stature is not a desirable feature in itself, but is rather a consequence of something else, namely a need to reproduce early.
By adding pre-existing data for African pygmies to new information they have collected about the Aeta and the Batak of the Philippines, they show that at the beginnings of their lives all these pygmy populations follow the same growth curves as taller people, including Turkana and Americans. This demonstrates that pygmyism is not a result of early malnutrition, as another hypothesis has it. At the age of about 12, however, pygmies stop growing. That is also the age at which they become sexually matureabout three years earlier than taller people.
The other part of the argument is that all observed pygmy populations have a short life expectancy. Indeed, this, according to Dr Migliano's hypothesis, is the crucial evolutionary pressure. Of the six groups of pygmies for whom data exist, two have a life expectancy of 24 years and the other four about 16 years.
Exactly why that is so probably varies from place to place (in the case of the Filipino groups, Dr Migliano cites tuberculosis, measles and malaria as the most likely causes), but the actual reasons do not affect the evolutionary argument. This is that a short life exerts pressure to mature early, and thus switch resources from growth to reproduction. A mathematical model used by the team confirms that, given pygmy life expectancies, their growth and reproduction patterns have indeed been optimised by natural selection. The various pygmy groups are thus the products of harsh circumstances.
Local heroes
Such alteration of stature is a particularly clear example of what Dr Moyzis's paper suggests is a wider phenomenonthat Homo sapiens is continuing to undergo local evolution. He and his colleagues reckon they can both estimate the rate of evolution and identify many of the evolving genes, by using a trick with the clumsy name of linkage disequilibrium.
Genes are linked together in cell nuclei on structures called chromosomes. These come in pairs, one from each parent. However, when sperm and egg cells are formed, the maternal and paternal chromosomes swap bits of DNA to create a new mixture. The pieces of DNA swapped are complementarythat is, they contain the same types of gene. But they may contain different versions of the genes in question, and these different versions can have different biological effects.
Over the generations this process of swapping mixes the genes up thoroughly, and an equilibrium emerges. If a new mutation appears, however, it will take quite a while for that thorough mixing to happen. This means recent mutations can be spotted because they are still linked to the same neighbouring bits of DNA as they were when they first appeared. Moreover, the size of these neighbouring blocks gives an indication of how long ago the mutation in question emerged; long blocks suggest a recent mutation because the mixing process has not had time to break them up.
All this has been known for decades, but it is only recently that enough human DNA sequences have become available for the technique to be used to compare people from different parts of the world. And this is what Dr Moyzis and his colleagues have now done.
What they have found is that about 1,800 protein-coding genes, some 7% of the total known, show signs of having been subject to recent natural selection. By recent, they mean within the past 80,000 years. Moreover, as the chart shows, the rate of change has speeded up over the course of that period. (The sudden fall-off at the end is caused because the linkage-disequilibrium method cannot easily detect very recent mutations, rather than by a sudden reduction in the rate of evolution.) The researchers put this acceleration down to two things. First, the human population has expanded rapidly during that period, which increases the size of the gene pool in which mutations can occur. Second, the environment in which people find themselves has also changed rapidly, creating new contexts in which those mutations might have beneficial effects.
That environmental change itself has two causes. The past 80,000 years is the period in which humanity has spread out of Africa to the rest of the world, and each new place brings its own challenges. It has also been a period of enormous cultural change, and that, too, creates evolutionary pressures. In acknowledgment of these diverse circumstances, the researchers looked in detail at the DNA of four groups of people from around the planet: Yoruba from Africa, Han Chinese and Japanese from Asia, and Europeans.
Various themes emerged. An important one was protection from disease, suspected to be a consequence of the increased risk of infection that living in settlements brings. In this context, for example, various mutations of a gene called G6PD that are thought to offer protection from malaria sprang up independently in different places.
A second theme is response to changes in diet caused by the domestication of plants and animals. One example of this is variation in LCT, a gene involved in the metabolism of lactose, a sugar found in milk. All human babies can metabolise lactose, but only some adults can manage the trick. That fact, and the gene involved, have been known for some time. But Dr Moyzis's team have worked out the details of the evolution of LCT. They suspect that it was responsible for the sudden spread of the Indo-European group of humanity about 4,000 years ago, and also for the more recent spread of the Tutsis in Africa, whose ancestors independently evolved a tolerant version of the gene.
The pressures behind other changes are less obvious. In the past 2,000-3,000 years, for example, Europeans have undergone changes in the gene for a protein that moves potassium ions in and out of nerve cells and taste buds. There have also been European changes in genes linked to cancer and Alzheimer's disease. Chinese, Japanese and Europeans, meanwhile, have all seen changes in a serotonin transporter. Serotonin is one of the brain's messenger molecules, and is particularly involved in establishing mood.
The finding that may cause most controversy, however, is that in the Asian groups there has been strong selection for one variant of a gene that, in a different form, is responsible for Gaucher's disease. A few years ago two of the paper's other authors, Gregory Cochran and Henry Harpending, suggested that the Gaucher's form of the gene might be connected with the higher than average intelligence notable among Ashkenazi Jews. The unstated inference is that something similar might be true in Asians, too.
The Ashkenazim paper caused quite a stir at the time. It was merely a hypothesis, but it did suggest a programme of research that could be conducted to test the hypothesis. So far, no onedaring or foolishhas tried. Eventually, however, such questions will have to be faced. The paper Dr Moyzis and his colleagues have just published is a ranging shot, but the amount of recent human evolution it has exposed is surprising. Others will no doubt follow, and the genetic meaning of the term race, if it has one, will be exposed for all to see.
Artificial selection can indeed be a lot faster.
