You know those people who only need 4 hours of sleep a night, yet who are energetic to the point of making you feel exhausted just by seeing what they do in a day? Well, there’s an app for that. OK, not really, but there is a gene for that. It’s called DEC2 (also called BHLHE41), and the evidence for it is pretty convincing. The group that originally identified this gene even made mice with a mutation in the gene and the mice also became short sleepers, and at least one other group has identified mutations subsequently in the same gene in other families with short sleep phenomenon.
What does this gene do, can I have a copy of that mutation, you are asking yourself. Well the gene is a transcription regulator, which means that its role to control other genes. That usually means that the gene is quite important. What other gene does it regulate? Genes involved in sleep/circadian rhythm, immune function, and tumor progression, among other things.
Why immune function and tumor progression? Probably because sleep is very important in immune system regulation, and because clock genes (genes that are involved in circadian rhythm) are important in the growth of tumors.
So do these people with the mutation have health problems? Do they live shorter amount of time? It doesn’t appear that way. There are many famous people who are short sleepers, like Margaret Thatcher, and there doesn’t seem to be obvious health issues with them. A bit unfair, you say? Yes.
There are some important observations from this finding. First, it seems there is no absolute need for eight hours of sleep per night. The short sleepers are very alert and more energetic than other people. We haven’t evolve to minimize sleep length. Which makes sense, since for most of our evolutionary history, we didn’t have the artificial light.
Second, it seems that there is need for some sleep. There are no genes that allow you to go without any sleep. Well, there is–it’s called fatal insomnia–and as you can surmise from the name, you die if you have that mutation. It’s a prion disease, and the prion builds up until at middle age, you lose the ability to sleep properly. Namely, you lose the ability to dream. It turns out that the inability to dream leads to a host of problems, resulting in death. It’s a tragic disease, as chronicled here.
Now, another amyloid disease, Parkinson’s disease, shares something with fatal insomnia–namely that the first sign of Parkinson’s disease is loss of good quality sleep. It’s almost as if fatal insomnia is Parkinson’s disease in fast forward mode.
Why Do We Sleep?
It is still unclear why we sleep. We do know that:
For example, short periods of sleep loss at the time of vaccination reduce the vaccine’s effectiveness. Sleep loss is associated with increased obesity and with reduced levels of leptin and increased levels of ghrelin, the combination of which increases appetite. Sleep loss is also associated with diabetes and impaired glucose tolerance in a dose-related manner: individuals that report sleeping less than 6 h per night are ∼1.7 times as likely, and those that report sleeping less than 5 h per night are ∼2.5 times as likely, to have diabetes than individuals that obtain 7 h of sleep. Cardiovascular disease and hypertension are also associated with sleep loss: the risk of a fatal heart attack increases 45% in individuals who chronically sleep 5 h per night or less.
I will write a longer blog on sleep in the future.