A recent neuroscience paper investigates the link between sleep deprivation and the gut.
Words By Sereena Kang
One of the many mysteries in the field of neuroscience is understanding why we need sleep. Intuitively we all understand having a good night’s sleep refreshes us both physically and mentally, whilst a lack of sleep is linked to a decline in cognition and general wellbeing. At the extreme level, given enough sleep deprivation can be fatal.
A recent paper published in June has investigated this lethality that comes from extreme sleep deprivation. With results reported in Cell, Alexandra Vaccaro and colleagues from Harvard Medical School sought to understand the exact biological processes which led to death from sleep deprivation. What the researchers unexpectedly found was significant damage in the gut. Oxidative stress, the damage created by unstable molecules attacking DNA leading to cell death, was observed in the guts of mice and flies. This was due to a build up in reactive oxygen species (ROS). ROS are generally helpful for cells and support them – we would not be able to function without them – however, when ROS levels are higher than their counterpart, antioxidants, this leads to damage in the form of oxidative stress.
To further investigate this potential link, the researchers also cleared the reactive oxygen species from the gut by giving the flies oral antioxidants, whilst continuing to sleep deprive them. What they found was that these flies lived as long as a normal fly. So in other words, preventing oxidative stress in the gut also prevented the early death of these flies. Consequently, a causal link was now established between oxidative stress in the gut with sleep deprivation and early death.
It had already previously been shown that sleep loss is linked to gastrointestinal damage, however the extent of this was not realised until now to be a major factor causing death. Furthermore, this finding is interesting because although sleep is generated in our brains, this organ is not the most affected when sleep is taken away. Instead, the significant damage is found in the gut. Even when given mild sleep deprivation, a build-up of oxygen species (albeit at a slower rate) is still observed. This finding could be important for improving treatment for sufferers of insomnia and chronic sleep disorders.
The paper ultimately shows a cause of death from sleep deprivation, but it is not known how this deficiency in sleep leads to a build-up of ROS. Perhaps the next step in this investigation is to try and understand this. Whilst this research could be potentially very promising for insomniacs. It is important to understand that knowing the cause of death from a lack of sleep will not tell us if this is the main purpose of sleep in the body. Sleep deprivation does indeed damage the gut but whether the primary function of sleep is to support the gut is yet to be observed.
The full paper can be found here: https://pubmed.ncbi.nlm.nih.gov/32502393/