Scattered through the genomes of humans around the world we can find remnants of a Neanderthal ancestry. In some, this bestows resilience to illness, or even a unique head shape. A rare few, it seems, have inherited the Neanderthals’ sensitive side.
Evolutionary geneticists have taken a close look at a genetic variation in Neanderthal DNA known to play a role in generating impulses in some nerves, concluding this particular form of the gene made them prone to feeling more pain.
A search through a database of half a million modern British genomes revealed around 0.4 percent of people happen to still be carrying a copy of this mutated version.
Sure enough, individuals who carried the gene also tended to experience more pain symptoms than the average Brit.
It’s the kind of work we’ve only been able to conduct in recent years as improved sequencing technology has revealed unprecedented details of DNA scavenged from Neanderthal remains.
Among the sequences deciphered by the team was a gene responsible for making a protein called Nav1.7; the work was led by Svante Pääbo at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany along with Hugo Zeberg from the Karolinska Institute in Stockholm.
Nestled within a nerve cell’s membrane, Nav1.7 functions as a gateway for sodium, ultimately playing a key role in determining the trigger point for impulses we interpret as painful.
Without this channel, we wouldn’t feel discomfort at all. But some variations of Nav1.7 tip sensitivity in the other direction, unlocking far more easily and giving rise to chronic pain.
“People have described it as a volume knob, setting the gain of the pain in nerve fibres,” Zeberg explained to Ewen Callaway at Nature news.
A version of this gene found in Neanderthal genomes, the researchers discovered, has mutations that would change three amino acids in the protein. To determine whether these changes would make much of a difference to Nav1.7’s function, they inserted the sequence into frog eggs and human kidney tissue.
It was apparent that having any one of the amino acids swapped out wouldn’t be a big deal.
But those three changes together turned Nav1.7 into a trigger-happy channel capable of kicking off painful impulses far sooner than unmutated forms.
In spite of the hints that the Neanderthal form of Nav1.7 is associated with increased pain in modern humans, the results can’t tell us what Neanderthals might have felt, let alone why this sequence evolved in the first place.
Pain is a complex phenomenon that involves a whole suite of genes responsible for a variety of processes, with subtle differences enhancing sensations in some people, and all but eliminating any form of discomfort in others.
We’re pretty sure Neanderthals felt discomfort, given evidence of painkillers found embedded in their plaque. Signs of injury were also common among Neanderthals, along with clear indications of great care taken to nurse the infirm back to health.
So if we were to take the liberty to speculate a little, it’s not hard to imagine that turning up that pain volume knob might have come in handy for our stocky hominin cousins, faced with dealing with trauma in some pretty brutal environments.
Rather than deal with the consequences of antagonising an injured limb by walking on it or further inflaming an infected tooth, Neanderthals might have taken to rest sooner, perhaps relying on a solid network of family to help them heal quickly.
Looking for clues in the rest of their genome could tell us more about how they lived their lives.
Given how often the two branches of our family tree procreated, insight into their genes also provides us with a clearer understanding of our own history.
It’s a shame Neanderthals vanished when they did. They could have taught modern humans a thing or two about getting along with sensitivity.
This research was published in Current Biology.
