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A new paper published in Current Biology describes how a sodium channel inherited from Neanderthals may be responsible for low pain tolerance in modern humans.
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While the in-depth study is compelling, this theory remains inconclusive.
If you have a low tolerance for pain new research suggests you should blame it on our Neanderthal cousins.
According to joint research from the Max Planck Institute for Evolutionary Anthropology in Germany and Sweden’s Karolinska Institutet, “people who inherited a special ion channel from Neanderthals experience more pain.”
In their paper, the researchers describe Nav1.7, a sodium channel “crucial for impulse generation and conduction in peripheral pain pathways,” which showed reduced inactivation in Neanderthals. Researchers deduced that because of this lowered level of activation, Neanderthals experienced heightened pain sensitivity in comparison to modern humans.
“In Neanderthals, the Nav1.7 protein carried three amino acid substitutions (M932L, V991L, and D1908G) relative to modern humans. We expressed Nav1.7 proteins carrying all combinations of these substitutions and studied their electrophysiological effects. Whereas the single amino acid substitutions do not affect the function of the ion channel, the full Neanderthal variant carrying all three substitutions, as well as the combination of V991L with D1908G, shows reduced inactivation, suggesting that peripheral nerves were more sensitive to painful stimuli in Neanderthals than in modern humans.”
The researchers also discovered that through passed down genes, “0.4 percent of present-day Britons” are carriers of the Neanderthal amino acid substitutions.
When Neanderthals and Denisovans—a group belonging to the Homo genus who were a species of early human and are also known as the Denisova hominins—mated with the earliest modern humans, several genetic variants from both groups (Neanderthals and Denisovans) emerged and have been passed down to us.
Additionally, the researchers also analyzed the SCN9A gene which acts as a guide for the production of the sodium channels and encodes the Nav1.7 protein. In their paper, the researchers share that humans who experience “loss-of-function mutations of SCN9A” tend to develop “insensitivity to pain” and anosmia (a lost sense of smell) whereas “gain-of-function mutations” cause people to present with “sensory symptoms and pain, with pain as the dominant symptom.”
“The Neanderthal variant of the ion channel carries three amino acid differences to the common, ‘modern’ variant,” says lead paper author and a researcher, Hugo Zeberg, in a news release.
“While single amino acid substitutions do not affect the function of the ion channel, the full Neanderthal variant carrying three amino acid substitutions leads to heightened pain sensitivity in present-day people,” Zeberg explains.
And it turns out that age is a factor in pain sensation, too. Zeberg says that those who carry the Neanderthal variant experience pain as if they “were eight years older.” In order to study the aforementioned genetic substitutions in real time, the researchers synthesized genes which included both the Neanderthal and modern human Nav1.7 sodium channel and transcribed them in vitro before injecting them into African clawed frog (Xenopus laevis) oocytes (ovarian cells.)
The researchers also used data from UK Biobank of 198,047 adult females and 164,897 adult males from the United Kingdom and found that those who were carriers of the variant ion channel had a lower tolerance for pain.
While compelling, the results are not definitive. The researchers conclude that while they cannot be absolutely certain that Neanderthals “necessarily experienced more pain that modern humans do,” there’s a strong case for this hypothesis being that Neanderthal peripheral nerve endings were extra sensitive to stimuli “as suggested by the observations in present-day people heterozygous for the Neanderthal Nav1.7 variant.”
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