Dolphins, Race, and Aspm—Here We Go Again?
A gene linked—notoriously—to IQ and race has been linked to big dolphin brains
Posted Sep 20, 2012
Aspm is back. The gene first came to prominence in 2005, in a paper in Science (a magazine I write for). One version of the gene seemed to show strong positive selection in humans—meaning it had spread through our ancestors at about Mach 10, presumably because it gave humans who had it a big advantage over those who lacked it. For reasons I explain below, the researchers guessed that this advantage was an intelligence boost. And in a tantalizing parallel, a different team of geneticists has now linked changes in aspm to bigger brains in dolphins. That’s intriguing, but as I explain in my new book (The Violinist’s Thumb, a quirky history of genetics and DNA), the gene has an ugly back story.
For background, aspm seems to help stem cells divide evenly. When stem cells begin dividing in the fetal brain, they can either produce two more stem cells each round, or they can settle down, get a job, and become regular neurons. Neurons are good, clearly, but whenever a neuron forms, the population of stem cells (which will make more neurons in the future) necessarily goes down. So building a big brain requires first building up a base population of stem cells.
One key to that buildup is symmetric division. If stem cells divide equally, so both daughter cells look more or less the same, each one becomes another stem cell. If the split is unequal, neurons form prematurely. Aspm seems to promotes symmetry and thereby help pack the brain with neurons. We know this because if aspm malfunctions, you get a birth defect called microcephaly, a tragically small brain that leads to profound disabilities. To be sure, aspm isn’t the gene responsible for building big brains—there’s no such single gene. But it’s critical to the process, and the primate line has almost certainly benefited from distinct changes in aspm.
None of that is controversial. But the authors of a now-notorious Science paper did three things. First, they determined that a unique version of aspm started spreading, quite quickly, in human beings around 6,000 years ago. Second, they made a modest leap, and suggested that that new version spread because it boosted brain power. Third—and here’s where things got hairy—they said they found the gene far more often in people of European and Asian descent than in people of African descent.
(Adding fuel to the fire, in a separate but related paper, they found similar discrepancies for a version of the microcephalin gene, which also leads to microcephaly and which started spreading in humans around 37,000 years ago.)
Some scientists jumped all over the results, denouncing them nasty and just plain wrong. Aspm gets busy in many cells besides neurons (as does microcephalin), and certain versions of it have been linked to everything from sperm production to speaking tonal languages, so it could have spread for any number of reasons unrelated to smarts. Perhaps more damningly, follow-up work showed no difference in IQ scores between people who had the supposed brain-boosting versions, which seemed to kill the theory. Afterward, the lead author of the original aspm paper, Bruce Lahn—who, for what it’s worth, is of Chinese ancestry—acknowledged, “On the scientific level, I am a little bit disappointed. But in the context of the social and political controversy, I am a little bit relieved.”
The hubbub over aspm had mostly died down, but a brand new paper has found evidence of positive selection among dolphins and their ilk—which means the gene presumably provided a big boost for some reason. And given that dolphins are generally considered the one mammal species whose brain power rivals that of primates, it’s tempting to conclude that aspm boosted the cognitive power of dolphins.
Tempting, but true? Again, aspm probably gave primates generally a brain boost. But the collapse of the human-centric results from 2005 provides reason to be cautious. I expect that some of the old debates about aspm will flare up again. (See, for example, the comments here.) As for whether the debates will lead to firm answers about the genetic origins of our hypertrophied brains, I’m far less sure...