Neanderthals are an extinct species that lived about
40,000 years ago in which some modern humans mated with. From the mating, gene
transfer occurred where future descendants picked up some of the Neanderthal
genes. The difference between Neanderthals and modern-day humans is that
Neanderthals were known to be hunter-gathers while modern-day humans produced
and maintained a living through agriculture and domestication of animals. An
interesting gene that a group of humans currently obtain is a variant of a gene
that encodes an ion channel that initiates the sensation of pain. A group of
researchers in the UK studied the ion channel and found insightful information
that peoples with this variant of a gene experiences more pain than usual. The
ion channel of interest is the sodium channel called NAV1.7. This sodium
channel is important for impulse generation and peripheral pain pathways. This
variant gene is found in people from central and southern America as well as in
Europe. In the cell, an individual with Neanderthal variant genes that goes
through an action potential, which occurs in the ion channel, has two important
factors that occur during this process. One factor that occurs is that there is
an increase in the availability of sodium channels for activation. From this,
it results in an increase of sodium channels to remain open for a longer
period. This leads to a lower threshold of receiving pain. An interesting discovery was that individuals
that contained the ion channel, experienced pain as if they were eight years
older where pain sensitivity generally increases. When going into the genetics
of this variant gene, they figured out that there was a three amino acid
difference between the Neanderthals and modern-day humans. Due to these three
amino acid substitutions, individuals in present-day time have a higher pain
sensitivity. Now the true question is, do you think that your pain threshold is low?
Zeberg, H., Dannemann, M., Sahlholm, K., Tsuo, K., Maricic, T., Wiebe, V., . . . Pääbo, S. (2020). A Neanderthal Sodium Channel Increases Pain Sensitivity in Present-Day Humans. Current Biology, 30(17). doi:10.1016/j.cub.2020.06.045
Neanderthals may have had a lower threshold for pain. (2020, July 23). Retrieved October 05, 2020, from https://www.sciencedaily.com/releases/2020/07/200723115900.htm?fbclid=IwAR1Q_bk0x6uTEsd9u-xKPzykQT_bZnm86MwInWp8pCTi_ZAZoLqd9FOx6SI
This is so interesting! I have always wondered if there was a reason why some individuals claim to have a higher pain tolerance. Doing a little digging on the topic, I also found a study where laughing seemed to increase pain tolerance (Lapierre 2019). Subjects watched a comedy video that elicited laughter, and there was an increase in pain tolerance amongst the subjects (Lapierre 2019). It would be have been really interesting to reproduce this study on Neanderthals and present day humans. But who knows if Neanderthals even laughed. It would also be interesting to see of there were genetic variations in pain tolerance amongst different regions of the world based off the regions' "ancestors" and their migration patterns.
ReplyDeleteSources:
Lapierre SS, Baker BD, Tanaka H. Effects of mirthful laughter on pain tolerance: A randomized controlled investigation. J Bodyw Mov Ther. 2019 Oct;23(4):733-738. doi: 10.1016/j.jbmt.2019.04.005. Epub 2019 Apr 13. PMID: 31733755.
I have always wondered why each of us have different pain tolerances. I found a study that focused on the PX27 gene. Without going into too much detail, the researchers found more supporting evidence to suggest that PX27, and specifically SNP Rs7958311 was associated with pain modulation in humans. The researchers were able to find this by comparing two different cohorts by cold-press pain experiment and clinical pain meta-analysis between the two cohorts as well (Kambur, 2016).
ReplyDeleteGiven this, I wonder if humans 40,000 years ago may have had modulation with the PX27 gene as well with NAV1.7. It is interesting to think that our environment and lifestyle has really made an impact on how we perceive pain.
References:
Kambur, O., Cajanus, K., Kaunisto, M., Winsvold, B., Stubhaug, A., Zwartd, J. A., . . . Kalso, E. (2016). Genetic variation in P2RX7 and pain. Scandinavian Journal of Pain, 12(1), 127-127.
It is really interesting that it seems people who maintain this particular neanderthal gene actually experience a lower pain tolerance than individuals without this particular ancestry considering our more "comfortable" lifestyle. This almost points to further evidence of adaptation to make us more resilient to pain.
ReplyDeleteThis is especially interesting given the current opioid epidemic which often stems from increased perception of pain despite supposed increased resiliency. There are also so many other factors from our environment which contribute to pain sensations. I found an article which discusses how our social interactions and networks lead to increased pain tolerance due to increased beta-endorphins which binds to mu-opioid receptors in the CNS. The researchers found that this specific binding is used to promote social bonding in all primates, but this increased interaction among more social people also helps to increase pain tolerance (Johnson, K.V.A., Dunbar, R.I.M., 2016).
This would definitely be an interesting anthropological conversation to examine as well. Thanks for sharing!
Johnson, K. V., & Dunbar, R. I. (2016). Pain tolerance predicts human social network size. Scientific reports, 6, 25267. https://doi.org/10.1038/srep25267
I think that this was a very intriguing post. With this finding, I would imagine they would develop drugs to inhibit the NAV1.7 channel. I looked it up to see and found a drug called Goshajinkigan, a Japanese medicine that suppresses these channels to relieve pain (Imai et al., 2020). The article says that it is used clinically in Japan, and I wonder if it'll ever make its way to the United States.
ReplyDeleteRyota Imai, Shoichiro Horita, Yuko Ono, Keisuke Hagihara, Masaru Shimizu, Yuko Maejima, and Kenju Shimomura.BioResearch Open Access.Sep 2020.116-120.http://doi.org/10.1089/biores.2019.0034