My latest Mind and Matter column for the Wall Street Journal is on
gene-culture co-evolution:
Human beings, we tend to think, are at the mercy of their genes.
You either have blue eyes or you do not (barring contact lenses);
no amount of therapy can change it. But genes are at the mercy of
us, too. From minute to minute, they switch on and off (i.e., are
actively used as recipes to make proteins) in the brain, the immune
system or the skin in response to experience. Sunbathing, for
example, triggers the expression of genes for the pigment
melanin.
As a recent study confirms, on a much longer time
scale, genes are even at the mercy of culture. The paradigmatic
example is lactose tolerance. All mammals can digest lactose sugars
in milk as babies, but the lactase gene switches off at weaning
when no longer needed. In much of Europe and parts of Africa, by
contrast, most people can digest lactose even as adults, because
the lactase gene remains switched on. (About 90% of East Asians and
70% of South Indians are lactose-intolerant to some degree.)
This "lactase persistence" is caused by one of four genetic
mutations that occurred in different regions and at different
dates, one in Europe and three in Africa. Coincidentally, these
regions also saw the domestication of cattle and the adoption of
milk-drinking by adults around the same time. Of course, it's
plausible that the culture came first-drinking milk gave some
advantage to all, because milk has nutrition other than lactose in
it, but it especially benefited adults with mutations that allowed
lactose digestion. So such mutations spread.
The new study, of 5,000-year-old bones from the Basque region of
Spain, catches this evolutionary event in the act, finding that
just 27% of individuals were then lactose tolerant, much lower than
today. Concepción de la Rúa of Spain's University of the Basque
Country and her fellow authors conclude that the genetic change
most probably happened after cattle domestication, at a time "when
fresh milk consumption was already fully adopted as a consequence
of a cultural influence." Here we have genes at the mercy of
culture.
Could blue eyes be another example of the same
phenomenon-"culture-gene co-evolution"? Thanks to the work of the appropriately named (and blue-eyed)
Danish geneticist Hans Eiberg and his colleagues, we now know that
the chief mutation that causes blue eyes is a single letter change,
from A to G, at the 26,039,213rd position on chromosome 15, within
a gene called HERC2.
HERC2 has no effect on eye color, but it contains an unexpressed
segment of DNA that is needed for the switching on of a nearby gene
called OCA2, as demonstrated by newly published work by Robert-Jan Palstra and
others at Erasmus University in the Netherlands. The mutation that
causes blue eyes reduces the expression of OCA2 and hence reduces
pigment concentration. Paler eyes look bluer.
Why did this mutation become so common somewhere around the
shores of the Baltic sea around 6,000 years ago? The answer may lie
in the fact that the date coincides with the arrival of agriculture
in the area. When people began relying heavily on a diet of bread
at such a northern latitude, they probably became chronically
deficient in vitamin D, for bread is generally low in vitamin
D.
This wouldn't matter in a lower latitude, because the body can
synthesize vitamin D if exposed to ultraviolet sun rays. But in
northern Europe, diseases related to vitamin D deficiency, such as
rickets, would have become common. Any individual who had a genetic
mutation that lightened his or her skin (and eyes) would absorb
more sunlight, boosting health and the ability to survive and
breed. Paleness was selected.
When Nordic people started depending more on bread than on fish,
they got less vitamin D from their diet. As a result, they got
paler, improving the capacity of their skin to generate this
crucial nutrient just from scarce sunlight. How they lived changed,
in effect, how they looked.
