In this new work, the UCSF researchers also created modified mice to understand how the mutation affects the need for sleep. Thus they discovered that ADRB1 is very expressed in the brainstem bridge, a key brain region in sleep regulation.
Then, with optogenetic techniques, which use light to activate certain cells, they stimulated the neurons in which they saw the gene expressed. This stimulus caused the sleeping mice to wake up, confirming that the ADRB1 mutation promotes alertness.
Although it is still necessary to know much better the mechanisms that regulate the cycles of sleep and wakefulness, it seems that the genes discovered in people who need less sleep provide more efficient rest management. DEC2 oscillates with day and night.
At dusk, it joins the MyoD1 gene, responsible for the production of orexin, a hormone that promotes wakefulness, blocking its activity, and before dawn, it is withdrawn allowing the MyoD1 to stimulate the production of orexin that awakens us.
The mutation in the DEC2 gene makes these brakes in orexin production weaker. And something similar happens with the ADRB1. In the mice with the mutation of this gene, the percentage of neurons that facilitate wakefulness was higher than those that made them sleep,
Fu tells Materia that neither the presence of these genetic variants nor the fact of sleeping less seems to have counterparts for mutants. In fact, he has observed that people who do not need so many hours of sleep naturally tend to be happier and have more energy.
On the contrary, other genetic analyzes, such as the one published in March this year in Nature Genomicsby a team led by Richa Saxena of the Massachusetts General Hospital, they have found correlations between the genes that favor insomnia and those that increase the propensity to suffer from psychiatric diseases such as depression or schizophrenia and even type 2 diabetes.
In many cases , the genes were the same. Signs like this suggest that the same mutations that allow you to sleep less may be a sign of a stronger nervous system and better overall health.
Despite having found these two genes related to greater ease for wakefulness, Fu believes that before starting to think about treatments for less and better sleep, “it is necessary to learn more about how sleep efficiency is regulated.” “We may one day be able to create tools that help people sleep better and be healthier.
But more efficient sleep can mean sleeping less for some, but not for others, ”he says. In addition, although there are genetic variants that explain how different people sleep, environmental conditions, such as electronic devices, the stress of work or family life or stimulants, have a great influence on how and how much we sleep. For most, controlling those factors remains the best option for healthy sleep.