Evolution is often sold as a species/population converging on a single ideal solution for a population. This is incorrect. For one, the ideal solution in 2013 is not necessarily the ideal for 2014. Peter and Rosemary Grant demonstrated that ground finch weight and beak size varied from year to year, that this corresponded to shifts in food availability due to weather, and that the change was driven by genetics, not starvation. Beyond that, there is often more than one good strategy at a time. Wal-Mart and Rodeo Drive both technically sell clothes, but they’re not in competition. When you combine temporal variation with the existence of multiple viable strategies, you get population diversity.
What this means is that even if a gene is very, very bad, it’s probably there for a reason. At worst, it was a local optimum for a problem that no longer exists. See: sickle cell anemia. Sickle cell is a very nasty disease caused by a single gene. But being heterozygnous for the sickle-cell allele gives you some resistance to malaria. Which is useless if you live in the USA in the 2000s, but highly relevant if you’re in Africa now, and even more so Africa in the past. That is why the allele stuck around.
Moreover, the returns to a particular strategy depend on other people’s strategies. You’ll make more money selling cheap, mass-market clothes if there’s no Wal-Mart in your city. This is known as frequency dependent selection.
The moral of this story is: any time you see a genetic trait that looks negative but is widespread, look around. It’s almost certainly either linked to an advantage you aren’t seeing, or is advantageous under a different set of circumstances.
As we talked about previously, this appears to be the case for the trait known as sensory processing sensitivity . Belsky et al have an exhaustive synthesis of various ways high sensitivity has been shown to correlative with both unusually positive and unusually negative outcomes, depending on environment. You remember the DRD4 7R mutation, that was associated with ADHD and susceptibility to the individual’s mother’s trauma? More prevalent in nomadic and nomadic-descended populations than sedentary. And carriers do better than non-carriers when nomadic but worse when sedentary.
I tripped a little bit reading this, because something associated with ADHD and nomadicism seems like a novelty seeking gene, which is associated with extroversion. High sensitivity is highly correlated with introversion, and even the extroverts among them have very different brain patterns than low sensitivity extroverts. I got this from Quiet, which the library has unfortunately taken back so I can’t look up the specifics. I wonder if the extraverts were the ones who had good childhood environment. And it turns out this isn’t the only allele linked with both high sensitivity and ADHD. 5-HTTLPR short is too.
Quantifying the advantages of high sensitivity in humans is hard. Luckily, there’s a number of very good animal models. That’s a severe understatement. A more accurate statement would be “you can’t throw a rock without hitting a member of a species that demonstrates a shy-bold continuum.” This may mean we haven’t defined our terms well enough, but it could also mean that almost all species demonstrate frequency dependent selection in sensory sensitivity. The theme seems to be that higher sensitivity animals are more cautious, and thus get eaten less, but every once in a while a low sensitivity animal blunders its way into something amazing, like a new source of food, or founding a start up.