Sultan Qaboos University Med J, February 2015, Vol. 15, Iss. 1, pp. e4–6, Epub. 21 Jan 15
Submitted 27 Oct 14
Revision Req. 10 Nov 14; Revision Recd. 15 Nov 14
Accepted 18 Nov 14

In this issue of SQUMJ, Al-Maddah et al. reported a significant association between sleep deprivation among medical trainees 
and depressive indices using the Beck Depression 
Inventory-2.1 Using a cross-sectional study design, 
the authors found that depressive symptoms were 
more profound with acute rather than chronic sleep 
deprivation. They attributed the emerging depressive 
symptoms among medical residents to the acute lack 
of sleep because of long working hours, but not to the 
number of on-call nights per week.1 However, there 
was no follow-up to ascertain the cause-and-effect 
relationship between chronic sleep deprivation and 
depressive indices. 

Sleep occupies about a third of our lives and 
is vital to fulfil physiological needs, particularly in 
terms of cognitive function and mood. Disrupted 
sleep is very distressing for most individuals and may 
have a negative impact on their quality of life. Sleep 
deprivation has been shown to alter performance 
among medical professionals and shift workers, 
with several studies addressing its association with 
depressive symptoms.2–4 Residents and medical interns 
often suffer from reduced sleep which may lead to 
neurobehavioural impairment. Rosen et al. reported 
that medical interns with chronic sleep deprivation 
displayed high levels of depression and burnout over a 
period of one working year.5 In another study, Papp et 
al. found that chronic sleep loss had a negative impact 
on residents’ personal lives and their ability to perform 
their work.6 This supports the idea that chronic rather 
than acute sleep deprivation may result in depression, 
contrary to the findings of Al-Maddah et al.1 

Night shift work is a well-known cause of daytime 
sleepiness and mood disorders among workers. These 
results might also be attributable to chronic sleep 
loss and changes in circadian rhythm.7 However, 

one night of fragmented sleep was shown to cause 
normal subjects to feel sleepier during the day, impair 
subjective assessments of their mood and decrease 
mental flexibility and sustained attention.8 Therefore, 
clinical depression might result from the accumulative 
effect of chronic sleep fragmentation, deprivation 
and disturbance.8

There is a strong bi-directional relationship 
between sleep deprivation/disturbance and depre-
ssion. Although disturbed sleep is associated with 
psychiatric disorders and is traditionally considered to 
be a symptom of depression,9 research suggests that 
the relationship between sleep changes and mood 
disorders may work in the other direction as well.10 In 
addition to being a symptom, disrupted or a lack of 
sleep may also be a causal factor that contributes to the 
development of mood disorders.10,11 Chronic insomnia 
was found to increase the odds ratio of developing 
depression in several longitudinal studies.9,12 Alterations 
in sleep patterns are associated with depression, a fact 
which has been reported in the literature for over 
three decades.11,12 Additionally, certain sleep breathing 
disorders have a strong association with depression. 
Obstructive sleep apnoea syndrome is significantly 
associated with an impairment in cognitive function 
due to sleep disturbance and subsequent daytime 
sleepiness.13 Peppard et al. found a dose-response 
association between sleep-related breathing disorders 
and depression.14 This finding might be attributed 
to frequent awakening due to the sleep apnoea, in 
addition to repeated hypoxic stress to the brain as a 
result of desaturation.14

Contrarily, acute sleep deprivation has been 
long reported to be beneficial in treating depression. 
An early study revealed that a single night of sleep 
deprivation had an antidepressive effect.15 Therapeutic 
sleep deprivation was performed either as total sleep 

Department of Clinical Physiology, Sultan Qaboos University Hospital, Muscat, Oman
E-mail: malabri@squ.edu.om

احلرمان من النوم واالكتئاب
ارتباط ثنائي االجتاه

حممد عبد اهلل العربي

editorial

Sleep Deprivation and Depression
A bi-directional association

Mohammed A. Al-Abri



Mohammed A. Al-Abri

Editorial |e5

deprivation or with selective non-rapid eye movement 
(REM) sleep deprivation.16,17 The efficacy of either 
method has not yet been well investigated, although 
the impression received suggests that total sleep 
deprivation is superior to the selective technique.15 

Nonetheless, therapeutic sleep deprivation is not free 
of side-effects. Depressed individuals may experience 
increases in impulsiveness and drive.17 In addition, 
they would also suffer from excessive daytime 
sleepiness, which might be difficult to distinguish, 
especially in non-responders, with a worsening of the 
depressive symptoms.17

Two processes mainly regulate sleep. Firstly, the 
circadian process regulates the daily rhythms of the 
body and brain.18 The circadian pacemaker is found in 
a group of cells in the suprachiasmatic nucleus of the 
hypothalamus.18,19 These cells provide an oscillatory 
pattern of activity that drives rhythms such as sleep-
wake activity and endocrine secretions. They are 
markedly affected by light and darkness and, to some 
extent, by temperature.19 Bright light in the evening 
will delay the ‘clock’ and bright light in the morning 
is necessary to synchronise individuals to a 24-hour 
rhythm. All animals have a form of this process 
and the specific period and timing appear to be 
dependent on particular genes, which are similar in 
fruit flies and mammals.20

There is strong evidence to support the role 
of the sleep-wake cycle and circadian rhythm in 
the pathogenesis of major psychiatric disorders, 
particularly depression.18 Melatonin, a peptide 
synthesised by the pineal gland, has been shown to 
play a role in the modulation of the circadian rhythm.21 

Disrupted melatonin secretion and abnormal circadian 
rhythms have been reported among depressed 
subjects and the elderly; this could be the cause of 
sleep-phase shifts and consequent daytime sleepiness 
among these groups.22,23 As part of the circadian clock, 
the drive to sleep in normal sleepers slowly begins 
to increase a few hours after sunset and gradually 
reaches a peak in the early morning. The timing of 
REM sleep is linked to the circadian rhythm, closely 
mirroring the core temperature of the body. Thus, the 
maximum propensity for REM sleep is usually in the 
second half of the night with the onset of slow-wave 
sleep at the beginning of the night.24,25 The occurrence 
of REM sleep during daytime naps indicates a patho- 
logical daytime sleepiness, as can be observed in cases 
of narcolepsy.24

Secondly, the homeostatic process is the other 
important regulatory factor for sleep. It increases via 
sleep deprivation and peaks 16 hours after morning 
awakening and then decreases again during sleep. 
When there is a lack of sleep or the duration of 

sleep is shorter than usual, there is an increase in 
the homeostatic process. Consequently, this works 
to ensure that the sleep deprivation is made up for 
during the next sleep period, by accelerating the time 
before sleep and by possibly increasing sleep depth 
and duration.25

In animal models, chronic sleep restriction 
for more than a week was shown to lead to 
alterations in the neurotransmitter receptor systems 
(serotonin-1A receptor and corticotropin-releasing 
hormone receptor systems) and neuroendocrine 
stress systems (hypothalamic-pituitary-adrenal axis).26 
These changes are similar to those reported for major 
depression. The link between sleep and depression 
occurs through the serotoninergic system, which is 
active during wakefulness and inactive during sleep. 
Serotonin release is very much inhibited during slow-
wave and REM sleep.22 Endogenous depression is 
associated with the functional impairment of several 
neurotransmitter systems, particularly monaminergic 
neurotransmission. Likewise, evidence of decreased 
serotoninergic activity was observed in the brains of 
depressed patients.27

In conclusion, chronic sleep deprivation rather 
than acute sleep loss may lead to depression that is 
potentially attributable to the neurochemical changes 
that occur in the brain. On the other hand, depression 
may lead to disturbed sleep which could manifest as a 
symptom of a mood disorder. Short sleep duration has 
been shown to be increasing in prevalence worldwide 
with a concurrent increase in depressive symptoms, 
mainly among the younger population.28 Further 
epidemiological studies are required to ascertain the 
prevalence of such an association among the local 
population in Oman.

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