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January 29 - April 23, 2025
The culprit is an anomaly of a gene called PrNP, which stands for prion protein.
One region that this malfeasant protein attacks, and attacks comprehensively, is the thalamus—that sensory gate within the brain that must close shut for wakefulness to end and sleep to begin.
Due to this puncturing attack by the prion proteins, the sensory gate of the thalamus was effectively stuck in a permanent “open” position. Patients may not be able to switch off their conscious perception of the outside world and, as a result, cannot drift off into the sleep that they so desperately needed.
Current treatment prospects are few. There has been some interest in an antibiotic called doxycycline, which seems to slow the rate of the rogue protein accumulation in other prion disorders, such as Creutzfeldt-Jakob disease, or so-called mad cow disease.
The genetic certainty raises a eugenically fraught question: If your family’s genes mean that you could one day be struck down by the fatal inability to sleep, would you want to be told your fate? Furthermore, if you know that fate and have not yet had children, would that change your decision to do so, knowing you are a gene carrier and that you have the potential to prevent a next-step transmission of the disease?
Research studies in animals have, however, provided definitive evidence of the deadly nature of total sleep deprivation, free of any comorbid disease.
Unlike starvation, where the cause of death is easily identified, the researchers could not determine why the rats had died following sleep’s absence, despite how quickly death had arrived.
Some hints emerged from assessments made during the experiment, as well as the later postmortems.
First, despite eating far more than their sleep-rested counterparts, the sleep-deprived rats rapidly began losing body mass during the study. Second, they could no longer regulate their core body temperature. The more sleep-deprived the rats were, t...
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The third, and perhaps most telling, consequence of sleep loss was skin deep.
The fatal final straw turned out to be septicemia—a toxic and systemic (whole organism) bacterial infection that coursed through the rats’ bloodstream and ravaged the entire body until death.
Far from a vicious infection that came from the outside, however, it was simple bacteria from the rats’ very own gut that inflicted the mortal blow—one that an otherwise healthy immune system would have easily quelled when fortified by sleep.
If you impose a total absence of sleep on an organism, rat or human, it indeed becomes an emergency, and you will find the biological equivalent of this shattered glass strewn throughout the brain and the body, to fatal effect. This we finally understand.
Well-respected media outlets touted the findings as proof that human beings do not, after all, need a full eight hours of sleep, some suggesting we can survive just fine on six hours or less.
The sleep opportunity that these tribespeople provide themselves is therefore almost identical to what the National Sleep Foundation and the Centers for Disease Control and Prevention recommend for all adult humans: 7 to 9 hours of time in bed.
The problem is that some people confuse time slept with sleep opportunity time.
They, unlike us, give themselves more sleep opportunity than we do.
The next erroneous conclusion drawn from the findings was that humans must, therefore, naturally need a mere 6.75 hours of sleep, and no more. Therein lies the rub.
Need is not defined by that which is obtained (as the disorder of insomnia teaches us), but rather whether or not that amount of sleep is sufficient to accomplish all that sleep does.
Weak immune systems are a known consequence of insufficient sleep, as we have discussed in great detail.
I should also note that one of the most common immune system failures that kills individuals in hunter-gatherer clans are intestinal infections—something that shares an intriguing overlap with the deadly intestinal tract infections that killed the sleep-deprived rats in the above studies.