Second Gene Mutation that Lets People Survive on Less Sleep
A new gene that enables people to survive on much less sleep has been identified.
Most people require at least eight hours of sleep each night. Sleep deprivation can lead to multiple negative health impacts, including heart diseases and depression. However, some people have genetic variants which allow them to feel fully rested after only 4-5 hours, whilst avoiding any of the negative health impacts.
Back in 2009 the researchers led by Ying-Hui Fu, PhD, discovered that those with a mutation in their DEC2 gene averaged 6.25 hours sleep per night, compared to 8.06 hours in those without the mutation. 10 years on Fu and her team discovered another mutation in the ADRB1 gene that allows members of a family with the mutation to sleep for only 4.5 hours per night and not feel tired.
The same team have now uncovered another mutation in the NPSR1 gene after studying a family that required much less sleep than average. Two family members with the mutation averaged 5.5 and 4.3 hours of sleep a night respectively. NSPRI codes for a brain receptor that controls functions in sleep behaviour and arousal. When mice were engineered with the NPSR1 gene mutation, they were able to sleep less with no obvious impacts on health or memory. Although the family members did not appear to experience any of the negative effects of sleep deprivation, the researchers stress that longer term studies would be needed to confirm this.
Interestingly, another variation of the NPSR1 gene was found to correlate with people requiring 20 minutes less sleep on average in a population study of tens of thousands of people. The researchers suspect that NPSRI may have role in sleep related memory consolation.
The researchers were curious as to why gene mutations that promote shorter sleep requirements appear to be relatively uncommon in the population, as the gene would appear to be evolutionary advantageous. However, it is possible that many gene variants promote shorter sleep requirements in addition to the ones already identified. An alternative is that short sleep genes may have some negative health impacts that have not been identified yet.
It is possible that drugs could be developed to target either the NSPR1 or DEC2 genes, as a treatment for insomnia or other sleep disorders. However, further understanding of exactly how these genes function would be required before this stage. Both are involved in brain function, so targeting them could lead to negative neural side effects.