Sleep is an evolutionary paradox. In pre-historic times, periods of sleep would have been windows of opportunity for predators and periods of susceptibility to dangerous natural calamities. The chances of losing life for early humans during sleep must have been very very high. Yet sleep has persisted throughout evolution in practically all animals — why?

Recent research on mammalian sleep has shed some light on its role in maintaining a state of health.

Sleep deprivation hampers the regeneration of neurons in the hippocampus — a part of the brain which regulates memory as well as emotional responses to external stimuli. Neuronal precursor cells in the dentate gyrus of the hippocampus divide to produce new neurons. This process is hampered by extra periods of wakefulness. Disturbance of REM sleep and fragmentation of sleep are factors that can inhibit the proliferation of neurons. The current opinion is that extended periods of wakefulness, rather than absence of sleep dependent biochemical processes, can result in impaired neuron growth.

The sleep-wake cycle is regulated by diurnal variations in the secretion of melatonin. Disruption of sleep patterns and misalignment of melatonin secretion with duration of daytime are seen in patients who display mild cognitive impairment (MCI) — a stage that precedes the development of Alzheimer’s disease (AD). Onset of secretion of melatonin is early in patients with MCI than that seen in healthy individuals.

In a study of community-dwelling adults, disruption of sleep patterns and reduction in the duration of night-time sleep was positively correlated to the burden of the beta- amyloid peptide in the brain. Deposits of beta-amyloid were imaged in these patients and sleep patterns were reported by elderly members of the community.

Recent studies indicate that sleep is a period of “housekeeping” for the brain. Clearance of toxic metabolites such as the beta-amyloid peptide is enhanced during periods of sleep. The intercellular gaps between neurons increase during periods of sleep. Increased flux of cerebrospinal fluids through these channels (recently christened the ‘glymphatic system’) facilitates clearance of metabolites and toxins, such as the beta-amyloid peptide, from neurons during sleep. This is a significant discovery that provides an explanation for the association between poor sleep and development of AD.

Disruption of sleep patterns is also a risk factor for development of FrontoTemporal Dementia (FTD). Elderly patients (age 60 and above) with a confirmed diagnosis of FTD showed disruption of sleep macrostructure at an earlier age than patients diagnosed with AD. Although the profile of primary sleep disorders in both groups was similar, video-recordings of sleep and self-reported sleep patterns by patients show that loss of good sleep is evident to a greater degree in FTD patients than in AD patients.

Acute sleep deprivation, such as that experienced by on-call doctors, can affect the autonomous regulation of cardiovascular system. It can also result in increased levels of inflammatory cytokines such as interferon-gamma. Loss of sleep is also associated with a greater risk of developing insulin resistance as well as obesity.

A small pilot study has indicated that acute sleep deprivation (24 h) can cause an increase in stress response hormones like cortisol, epinephrine and norepinephrine. Loss on concentration and poor working memory was also evident in these subjects.

Disruption of circadian rhythms, owing to working night shifts, can cause disruptions in endocrine secretion in women and lead to problems with menstruation and conception.

People who habitually sleep for 6 hours or less show poor performance in attention based tasks and novel sensory inputs. These individuals show inefficient switching from memory-based tasks to attention-based tasks that demand quick processing of novel sensory inputs. What this study indicates is that new learning abilities may be compromised in people who sleep less on a regular basis. The recovery from habitual sleep deprivation may take several weeks and efficient performance in attention-based tasks can be achieved only after long-term normalization of duration of sleep.

Taking this research together, we have learned that sleep represents a period of daily recovery and reboot from environmental and metabolic stress. Getting eight hours of restful sleep in a regular pattern seems to be crucial for regulating mammalian metabolism in toto.

References

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Tobaldini E, Cogliati C, Fiorelli EM, Nunziata V, Wu MA, Prado M, Bevilacqua M, Trabattoni D, Porta A, & Montano N (2013). One night on-call: sleep deprivation affects cardiac autonomic control and inflammation in physicians. European journal of internal medicine, 24 (7), 664-70 PMID: 23601527

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