What follows is a piece I wrote (quite a while ago now) for students planning on sitting Scholarship Biology. It was intended to start them thinking :) I’ve just been asked to contribute to a panel discussion on RNZ around this subject, so thought it might be timely to re-post this article (I think time has been kind to it!).

Here’s a question to consider: are humans still evolving? What sort of evidence could we use to answer this question?

We do tend to view evolution as something that happened in the past, and see the study of evolution as a ‘historical’ science. But nothing could be further from the truth. Evolution is an ongoing process, and we can detect its influence on the present-day human gene pool just as easily as we can view the development of our species’ family tree.

Remember that evolution is essentially a change in a population’s gene pool, as the result of ‘drivers’ such as natural selection and genetic drift. And studies of present-day human evolution look just there, at our genes. Some of these studies are summarised in a [relatively] recent paper in Science (Michael Balter (2005) “Are humans still evolving?” Science 309: 234-237), which is the basis for this posting.

To some degree the answer to this question depends on whether we are talking about ‘western’ populations. In the developed world, the combination of modern medicine, new agricultural and technological techniques, and cultural changes have significantly reduced the effects of natural selection: individuals who in the ‘old days’ would have been removed from the population (by famine, warfare, or disease) without contributing to the gene pool, now survive and have children. But in the developing countries, people are still subject to these selection pressures, so it’s probably here that we should be looking for evidence of evolutionary change: the spread of alleles that give resistance to diseases such as malaria, for example.

In those parts of the world where malaria is endemic, anyone with a genotype giving resistance to malaria would be at a selective advantage: they’d be more likely to survive and reproduce, passing their advantageous combination of genes on to at least some of their children. The overlap between the geographic spread of malaria in Africa with the presence of the sickle-cell allele is an example: individuals heterozygous for this allele are at a selective advantage over unaffected individuals (and those homozygous for the allele) where malaria is present. And other gene loci also seem to be involved in resistance to malaria. Variants of the glucose-6-phosphate dehydrogenase gene (which is involved in cellular respiration), one of the Duffy blood group alleles, and one haemoglobin C allele are all more common where malaria is endemic.

Another example is that of the “CCR5” gene. This gene codes for CCR5, a surface protein on white blood cells that is also the docking site for the HIV virus. People homozygous for a mutation (‘delta 32’) in this gene are resistant to attack by HIV, and are thus at a selective advantage in areas where HIV, and AIDS, are common. Yet the mutation is most common in white Europeans, and very rare in other ethnic groups – including Africans. AIDS is far more common in Africa than in Europe, so these differences in allele frequency are difficult to explain – unless they are the result of some other selective pressure that predates the AIDS epidemic. Scientists have dated the origins of the delta 32 mutation to around 700 years ago, and the current hypothesis is that it provided protection against an epidemic disease of that time, perhaps plague or smallpox. Can you make a prediction about the future prevalence of this particular allele, given the relative frequency of AIDS in different parts of the world, and the availability of medical care for patients?