For most of our lives, we have been told that we need at least 8 hours of sleep every night. However, now more than ever, it is difficult to even get 7 hours of sleep amidst all the procrastinated assignments, and not to mention, the Netflix shows that needed to be finished the day it was started. But, have you ever noticed that sometimes, the less you sleep, the less you feel tired? Well, that may potentially be the result of a mutated gene that leads to a natural short sleep trait in humans.
Now you may be thinking to yourself, “That’s great, it means that I can sleep for 5 hours every night and still be fine” but, this mutation is only present in roughly four out of every 100,000 people. Specifically, the mutation affects the ADRB1 gene, a gene that encodes a receptor for the common neural signaling molecule noradrenaline. To understand how this gene affects sleep, we first need to examine how the timing of sleep is determined. The timing of sleep in our bodies is primarily set by what is known as the circadian clock. The term itself originates from the Latin phrase, “circa diem” and is used to describe the body’s internal clock that, for example, signals alertness due to light exposure, or, initiates the production of melatonin, a hormone that promotes sleep, at night. For individuals who have a variation in their circadian rhythm and sleep on average 4-6 hours every night but still feel well-rested, the term, natural short sleep or NSS, is given.
In a recent study, analysis on SNP, or single nucleotide polymorphism, followed by WES, a process that sequences all of the protein-coding regions of genes in the genome, has allowed scientists to identify a very rare variant in the ADRB1 gene. This mutation causes the cytosine to switch to a guanine nucleotide in the coding sequence. This results in the alteration of the amino acid from alanine to valine.
To determine the effect this mutation has on sleep-related behaviors, scientists measured the sleeping as well as the waking behavior on mice that exhibited this mutation in comparison to mice that did not contain this mutation. The mice that contained the mutation exhibited an increased activity while they were awake in comparison to mice who did not contain the mutation. The phenotype for short sleep was also demonstrated by the significant decrease in the amount of NREM and REM sleep. To be exact, the non-REM sleep was approximately 53 minutes less, and the REM sleep was approximately 7 minutes less in mice who exhibited the mutation in the ADRB1 gene.
In humans who carried the mutation in the ADRB1 gene, it was discovered that they received approximately two hours less of sleep in comparison to the humans who did not carry the mutation. It is possible that due to the contrast in the physiology of mice and humans, the results from the mice study were only a fraction of the whole effect that would be demonstrated in humans. Additionally, because mice are nocturnal animals and they tend to be less dependent on consecutive hours of sleep, the results of the mice study may not have been as dependable to determine the impact on humans.
In conclusion, we should all aim for at least 8 hours of sleep, even if you are one of the 4 out of 100,000 that have a mutated gene; I mean, who could possibly say no to more sleep?