 Home > Active Ingredient News > Study of Nervous System > How can I sleep only 4 hours a night and be energetic?

How can I sleep only 4 hours a night and be energetic?

 Last Update: 2021-04-27
 Source: Internet
 Author: User

Tags

what tamiflu body

what function astrocytes

Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com

News from March 24, 2021 //--What time do you usually go to bed at night? Do you like to take a nap?

Although most experts recommend that adults sleep 7-9 hours a day, the best time to fall asleep is 10 o'clock in the evening to 12 o'clock, and 2-4 o'clock in the afternoon is suitable for nap, but you may have your own best sleep mode.

No matter how much you sleep or how you sleep, these habits may be "factory settings" already written in your genes.
Today, let's take a look at the sleep-related genes that scientists have identified!

1.
Short sleep gene

Adequate and effective sleep is essential to our health.
However, some people are born short sleepers.
They sleep much shorter than the average person.
They neither want to sleep more, nor do they have any obvious negative health effects in the case of short sleep.

In October 2020, the team of Fu Huihui and Louis J Ptáček from the University of California, San Francisco, published a research paper entitled Mutations in Metabotropic Glutamate Receptor 1 Contribute to Natural Short Sleep Trait in the Current Biology magazine, a sub-Journal of Cell.
They found that two independent mutations in the GRM1 gene cause familial natural short sleep, and mice carrying both mutations exhibit short sleep behavior.
And its brain slices all showed changes in electrical characteristics and increased excitatory synaptic transmission.
These results fully demonstrate the important role of GRM1 in regulating sleep time.

In fact, this is not the first time the team has discovered the short sleep gene.
Prior to this, they had reported genes such as DEC2, ADRB1 and NPSR1, and their effects were even stronger than GRM1.

The first short-sleep gene was reported in 2009, when the team discovered a specific mutation in the DEC2 gene in a mother and daughter.
They felt well rested after about 6 hours of sleep each night.
Up.
A protein encoded by DEC2 helps shut down the expression of other genes, including genes that encode orexin, which is known to regulate wakefulness.
Although this discovery provides the first conclusive evidence that natural short sleep can be inherited.
But this mutation is very rare and does not apply to all short sleepers.
This study was published in the Science Journal in 2009 under the title The transcriptional repressor DEC2 regulates sleep length in mammals.

In 2019, after ten years of painstaking research, the team once again reported a short sleep gene-ADRB1.
By studying another family that contained natural short sleepers, the researchers identified this mutation.
This mutation is also extremely rare, and they estimate its incidence to be approximately 0.
004%.
On average, mice with this mutation sleep 1 hour less per day than control mice.
The research was published in the Neuron journal on August 28, 2019 under the title A Rare Mutation of β1-Adrenergic Receptor Affects Sleep/Wake Behaviors.

Soon after, Fu Huihui's team issued another article, reporting the short sleep gene NPSR1.
They found that mutations in this gene are related to the natural short sleep phenotype of humans.
People with NPSR1 mutations often sleep 2-4 hours less than average, while experimental mice sleep 71 minutes less than average.
In addition, these mice are also resistant to memory deficits related to lack of sleep.
This study was published in the journal Science Translational Medicine in October 2019 under the title Mutant neuropeptide S receptor reduces sleep duration with preserved memory consolidation.

If the above gene mutations are extremely rare, then the following gene seems to be much more common.
Studies have shown that on average one in five people in Europe contains this gene.

Researchers from the University of Edinburgh in the UK and the University of Munich in Germany conducted a high-density whole-genome association study on 4,251 people in 7 European populations and found that a gene called ABCC9 has a certain effect on people's sleep.

This study showed that an intron mutation of this gene affects approximately 5% of sleep time changes.
People with this mutation get an average of 30 minutes more sleep per night than people without the gene.
In Drosophila, individuals with RNA interference knockout of their conserved ABCC9 homologue suffer from insomnia in the first 3 hours of night compared with normal Drosophila.
The research was published in the Journal of Molecular Psychiatry in January 2013 under the title AK(ATP) channel gene effect on sleep duration: from genome-wide association studies to function in Drosophila.

2.
Long sleep gene

Some people can get energetic for a little sleep, but others are not so lucky and need to sleep longer than most people.

The team of Professor Masashi Yanagisawa from the University of Tsukuba, Japan, used EEG/EMG-based random mutant mouse screening studies and found that splicing mutations in the Sik3 protein kinase gene can significantly reduce the total awake time.
The research was published in the journal Nature in November 2016 under the title Forward-genetics analysis of sleep in randomly mutagenized mice.

The researchers used forward genetics methods.
First, they screened out a family of lethargic mice.
The mice in this family were awake for only 8.
7 hours a day, which was far less than the waking time of normal mice (about 13 hour).
Further analysis of the data reveals that the sleepiness of the mice is mainly non-rapid eye movement sleep (NREMS) time increase.

So, what is the gene for lethargy? The researchers found that a mutation in an intron of a kinase gene called Sik3 in the sleepy family of mice was the cause of the phenotype.
The intron itself does not participate in the coding of the protein, but this mutation of Sik3 at the site recognized by the spliceosome in the intron results in the wrong splicing of the mRNA of Sik3, and ultimately results in a deletion of the Sik3 protein.
In order to verify that the lack of this segment of the Sik3 protein is the main cause of sleepiness in mice, the researchers used gene editing to create the deletion of the Sik3 gene in normal mice, and found that the phenotype is the same as that of sleepy mice, thus proving that Their assumptions.

3.
Early sleep gene

Fu Huihui's team at the University of California, San Francisco also reported an "early bed gene" in 2007.
They found that a mutated "clock" gene allows some people to go to bed early and get up early, leading to a condition called familial advanced sleep phase syndrome (FASPS).
This research was published in Cell on January 12, 2007 under the title Modeling of a Human Circadian Mutation Yields Insights into Clock Regulation by PER2.

Researchers studied mice carrying the human FASPS gene and found that the mutated Period 2 (Per2) clock gene (which is essential for resetting the central clock of the body according to light) cannot be modified by another enzyme that controls it.
This loss of control leads to a reduction in the number of copies of the Per2 signal and a change in sleep patterns.
These evidences may help reveal how these people’s natural body clocks are set to such an early awakening schedule.

4.
The nap gene

Some people are accustomed to nap during the day, and some people can't sleep at all during the day.
Recently, a study led by researchers from Massachusetts General Hospital (MGH) showed that how long a person sleeps during the day is controlled to a certain extent by his genes.

The team has previously identified genes related to sleep time, insomnia, and the tendency to get up early or "night owl".
In order to understand the genetic mechanism of daytime nap, the researchers conducted a genome-wide association study (GWAS),

In this largest study to date, the MGH team worked with institutions such as the University of Murcia in Spain to identify dozens of genetic regions that control the tendency to nap during the day.
They also found preliminary evidence that the siesta habit is related to cardiometabolic health.

After studying the data in depth, the research team discovered at least three potential mechanisms that promote nap: sleep tendency, that is, some people need more sleep than others; sleep interruption, that is, nap during the day can help make up for the poor quality of sleep the night before ; Early risers, those who rise early may take a nap to make up for their sleep.

This study was published in the journal Nature Communications in February 2021 under the title Genetic determinants of daytime napping and effects on cardiometabolic health.

People often like to use words like "self-discipline" and "laziness" to evaluate people with different sleep habits.
Now, more and more scientific researches tell us that different sleep patterns may be determined by genes, so this evaluation Maybe it's not fair.
In any case, we should respect differences and needs.
No matter how you sleep, getting adequate and efficient sleep and letting your body and brain rest is the kingly way! ()

references:

Guangsen Shi, Chen Yin, Zenghua Fan.
Et al.
Mutations in Metabotropic Glutamate Receptor 1 Contribute to Natural Short Sleep Trait.
Current biology,VOLUME 31, ISSUE 1, P13-24.
E4, JANUARY 11, 2021.
https://doi .
org/10.
1016/j.
cub.
2020.
09.
071

Ying He, Christopher R.
Jones, Nobuhiro Fujiki.
et al.
The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals.
Science 14 Aug 2009: Vol.
325, Issue 5942, pp.
866-870.
DOI: 10.
1126/science.
1174443

Shi G, Xing L, Wu D, et al.
A Rare Mutation of β1-Adrenergic Receptor Affects Sleep/Wake Behaviors.
Neuron.
2019;103(6):1044-1055.
e7.
doi:10.
1016/j.
neuron.
2019.
07.
026

Lijuan Xing, Guangsen Shi, Yulia Mostovoy.
et al.
Mutant neuropeptide S receptor reduces sleep duration with preserved memory consolidation.
Science Translational Medicine 16 Oct 2019: Vol.
11, Issue 514, eaax2014 DOI: 10.
1126/scitranslmed.
aax2014

Allebrandt KV, Amin N, Müller-Myhsok B, et al.
A K(ATP) channel gene effect on sleep duration: from genome-wide association studies to function in Drosophila.
Mol Psychiatry.
2013;18(1):122-132.
doi:10.
1038/mp.
2011.
142

Y.
Xu,K.
L.
Toh,C.
R.
Jones.
et al.
Modeling of a Human Circadian Mutation Yields Insights into Clock Regulation by PER2.
Cell 128, 59–70, January 12, 2007.
https://doi.
org/10.
1016/j.
cell.
2006.
11.
043

Funato, H.
, Miyoshi, C.
, Fujiyama, T.
et al.
Forward-genetics analysis of sleep in randomly mutagenized mice.
Nature 539, 378–383 (2016).
https://doi.
org/10.
1038/nature20142

Dashti, H.
S.
, Daghlas, I.
, Lane, J.
M.
et al.
Genetic determinants of daytime napping and effects on cardiometabolic health.
Nat Commun 12, 900 (2021).
https://doi.
org/10.
1038/s41467-020-20585-3

This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.