Abstract
Sleep is not considered a pathological state, but it consumes a third of conscious human life. This share is much more than most optimistic life extension forecasts that biotechnologies or experimental and medical interventions can offer. Are there insurmountable physical or biological limitations to reducing the duration of sleep? How far can it be avoided without fatal consequences? What means can reduce the length of sleep? It is widely accepted that sleep is necessary for long-term survival. Here we review the limited yet intriguing evidence that is not consistent with this notion. We concentrate on clinical cases of complete and partial loss of sleep and on human mutations that result in a short sleep phenotype. These observations are supported by new animal studies and are discussed from the perspective of sleep evolution. Two separate hypotheses suggest distinct approaches for remodeling our sleep machinery. If sleep serves an unidentified vital physiological function, this indispensable function has to be identified before “sleep prosthesis” (technical, biological, or chemical) can be developed. If sleep has no vital function, but rather represents a timing mechanism for adaptive inactivity, sleep could be reduced by forging the sleep generation system itself, with no adverse effects.
Highlights
ALWAYS LOOK ON THE BRIGHT SIDE OF WAKEThis Mini Review was inspired by the striking clinical case of agrypnia reported by Michel Jouvet and his colleagues (Fischer-Perroudon et al, 1974) that was brought back to life in his last book Le sommeil, la conscience et l’éveil (Sleep, Consciousness and Wakefulness) (Jouvet, 2016)
Another autosomal dominant allele from one family with naturally short sleep was identified in the metabotropic beta1 adrenergic receptor (ADRB1) that belongs to the family of 7TM GPCR proteins. Carriers of this mutation have a lifelong tendency to sleep only 4–6 h per night and feel well rested. The introduction of this mutation to mice resulted in a shorter sleep phenotype with approximately 55 min shorter total sleep time compared to wild-type mice, which affected both non-rapid eye movement (REM) and REM sleep (Shi et al, 2019)
If sleep is adaptive and does not serve an unknown vital function, from an evolutionary prospective, sleepless animals would be eliminated from the population not because they die from sleep absence but because extra wake time makes them more vulnerable in the wild
Summary
ALWAYS LOOK ON THE BRIGHT SIDE OF WAKEThis Mini Review was inspired by the striking clinical case ( almost forgotten) of agrypnia (the complete loss of sleep) reported by Michel Jouvet and his colleagues (Fischer-Perroudon et al, 1974) that was brought back to life in his last book Le sommeil, la conscience et l’éveil (Sleep, Consciousness and Wakefulness) (Jouvet, 2016). We concentrate on clinical cases of complete and partial loss of sleep and on human mutations that result in a short sleep phenotype. If sleep has no vital function, but rather represents a timing mechanism for adaptive inactivity, sleep could be reduced by forging the sleep generation system itself, with no adverse effects.
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