Sleep and Wellbeing, Now and in the Future
International Journal of
Environmental Research
and Public Health
Editorial
Sleep and Wellbeing, Now and in the Future
Chin Moi Chow 1,2
1 Sleep Research Group, Charles Perkins Centre, University of Sydney, Sydney 2006, Australia;
chin-moi.chow@sydney.edu.au
2 Sydney School of Health Sciences, Faculty of Medicine and Health, University of Sydney,
Sydney 2006, Australia
Received: 17 April 2020; Accepted: 17 April 2020; Published: 22 April 2020
The processes of sleeping, eating and moving, in concert with cognition and learning,
support health and life. Sleeping occurs in the rest phase, whereas the other behaviours occur in the
active phase. It is largely axiomatically understood that “exercise is medicine” [1]. However, research
confirms that the same dictum applies to sleep and nutrition. Indeed, sleep is medicine, as exercise
and nutrition are medicine.
Wellbeing includes three aspects: life satisfaction; feelings of happiness, sadness, anger, stress,
and pain; and a sense of purpose and meaning in life [2]. As such, moment to moment wellbeing,
psychological or physical, is aected by activities evolving around us and can, over time, greatly impact
on our health.
How does sleep directly aect wellbeing? Poor sleep and/or sleep loss (voluntarily curtailed or
circumstantial) has a considerable negative impact on health and wellbeing. Zhao et al. [3] reported
lower happiness in those who had short sleep duration and insomnia. We now know that short
sleep increases the risk of weight gain from increased food intake in response to ghrelin (the hunger
hormone) and decreases in leptin (the satiety hormone) [4]. These physiological data show that short sleep
duration is related to increases in BMI and support the hypothesis that short sleep duration predicts a
higher BMI. We are also aware that sedentary habits, with reduced energy expenditure and excess
food intake, may also be elements that underscore this relationship between short sleep duration and
obesity [5]. Garfield (2019) [6] draws attention to the fact that this relationship could be bidirectional
and that obesity (using BMI cut-opoints) may predict short sleep duration. Longitudinal studies
using objective measures of sleep will help to clarify any causal relationship between sleep duration
and BMI.
Chronic sleep loss increases the risk for the development of diabetes, cardiovascular conditions
and other pathologies [4]. Indeed, short, low-quality and mistimed sleep may threaten metabolic
public health [7]. A chronic lack of sleep directly impacts on a person’s capacity to manage daily tasks,
which, over time, manifests in an overwhelming sense of physical fatigue, malaise, impaired cognition
and diminished wellbeing [8,9].
Sleep can deliver recovery following prolonged waking hours/sleep loss [10,11] or exhaustive
exercise through many of the functions it serves. Sleep has an anabolic function. Growth Hormone
(GH, an anabolic hormone) peaks [12], whereas cortisol (a catabolic hormone with capacity for muscle
catabolism and bone demineralization) concomitantly dips to its nadir [13], within the first two sleep
cycles. Thus, the temporal associations between GH/cortisol and sleep furnish a pathway for tissue
restoration and restorative sleep, contributing to overall wellbeing.
The importance of recovery is illustrated clearly in competing athletes, who have an increased
sleep need to meet the energetic, metabolic and vascular demands of exercise training. Insucient
sleep may be a result of poor sleep due to psychological or social stresses [14], apart from physical
demands. Many athletes have reported diculty in initiating sleep, night-time waking and diculty
in getting up in the morning [15,16]. Thus, the strategic planning of recovery sleep includes napping,
Int. J. Environ. Res. Public Health 2020, 17, 2883; doi:10.3390/ijerph17082883
www.mdpi.com/journal/ijerph
Int. J. Environ. Res. Public Health 2020, 17, 2883
2 of 4
sleep extension for sleep deprived athletes and promoting “best possible” sleep hygiene to facilitate
regular sleep-wake patterns [17], which are cardinal elements for optimising sports performance.
Sleep recovery is not only physically important for athletes but for the general population.
During slow wave sleep, toxic metabolic wastes (e.g., beta-amyloid proteins, a biomarker of Alzheimer
disease) are cleared [18], GH is released [12] and glycogen granules are accumulated in the brain [19,20],
serving as a fuel reserve for the brain at times of neuronal activation.
Sleep can also aect psychological wellbeing. Sleep serves a synthetic function of new nerve
structures (e.g., of synapses) that follows learning and memory consolidation [21]. This memory feature
is particularly critical for our existence, i.e., the ability to recognise, learn, acquire motor procedures,
map physical space, develop language expression and permit creativity. Memories give life purpose
and meaning.
Sleeping diculties are common. Diculties in initiating or maintaining sleep or waking too early
may arise from a variety of factors including sleeping too cold/hot, medication, alcohol and caeine
use, and pain. Eating within 3 h of bedtime is positively associated with nocturnal awakening [22].
Furthermore, dierent psychiatric disorder categories are associated with dierent sleep complaints in
pre-schoolers [23].
Some sleep issues may be mitigated by choosing an appropriate pillow type, e.g., with an
appropriate pillow neck and side height [24], and sleepwear fabric type, e.g., sleeping in wool
promoted improved sleep [25,26]. The food type consumed may also help to promote sleep onset,
e.g., a high glycemic index meal shortened sleep onset compared to a low glycemic index meal [27].
The question remains “why can’t some people sleep”? Pressing issues, especially when acute and
psychological in nature, can often deter sleep. The city doesn’t sleep [28] highlighted social factors such as
socio-economic status, safety/security and future insecurity as weighty social divides of sleep disparity,
suggesting they were sources of stress and anxiety arising from daily living. Hang-ups (not being able
to let go) at bedtime postpone sleep. Stress, worries and anxiety culminate in heightened arousals with
consequential increases in the pulsatility of nocturnal cortisol, when only few, regular cortisol pulses
should exist [29].
Together, stress and anxiety are significant sources of sleeping diculties. Recent developments
in endocannabinoid signalling, which has a key role in the regulation of stress responses and emotional
learning [30], may signpost and prioritise research opportunities in this field. The signalling molecule
2-arachidonoylglycerol (2-AG) appears to protect against stress [31]. In the presence of acute stress
exposure, the failure of 2-AG signalling would result in the strengthening of anxiety-producing
connections between the amygdala and prefrontal corticies [31]. This mouse model research is very
encouraging, since the identification of anxiety-producing signalling pathways may provide an insight
into future treatment possibilities.
Dierent strategies are available for managing sleep loss in shift work. Sleep medicine has come
a long way due to increased public awareness, as highlighted by the study of Savic et al. (2019),
who reported that the nurses in their study had already adopted health-promoting coping strategies
with their night shifts [32], including health practices of physical activity, healthy eating, engaging
with social support and leisure, mindfulness, managing time, and work-related coping strategies.
Nevertheless, the online platforms of mHealth [33] and cognitive behavioural therapy for insomnia
(CBTi) [34] are resourceful, easily accessible materials for shift workers. Forest therapy (originating in
the 1980s in Japan for stress reduction) that improved sleep eciency in cancer patients [35] may be
explored in shift workers in future studies.
Finally, sleep is as individual as the individual. Sleeping behaviour is an individual practice.
An individualised approach to treating sleep diculties is a step towards personalised medicine for
optimising health and both physical and psychological wellbeing.
Funding: This research received no external funding.
Conflicts of Interest: The author declares no conflict of interest.
Int. J. Environ. Res. Public Health 2020, 17, 2883
3 of 4
References
1. Egan, B.; Zierath, J.R. Exercise metabolism and the molecular regulation of skeletal muscle adaptation. Cell
Metab. 2013, 17, 162–184. [CrossRef] [PubMed]
2. Steptoe, A.; Deaton, A.; Stone, A.A. Subjective wellbeing, health, and ageing. Lancet 2015, 385, 640–648.
[CrossRef]
3. Zhao, S.Z.; Wang, M.P.; Viswanath, K.; Lai, A.; Fong, D.Y.T.; Lin, C.-C.; Chan, S.S.-C.; Lam, T.H. Short Sleep
Duration and Insomnia Symptoms were Associated with Lower Happiness Levels in Chinese Adults in
Hong Kong. Int. J. Environ. Res. Public Health 2019, 16, 2079. [CrossRef] [PubMed]
4. Van Cauter, E.; Knutson, K.L. Sleep and the epidemic of obesity in children and adults. Eur. J. Endocrinol.
2008, 159, S59–S66. [CrossRef] [PubMed]
5. Garaulet, M.; Ortega, F.; Ruiz, J.; Rey-Lopez, J.; Beghin, L.; Manios, Y.; Cuenca-Garcia, M.; Plada, M.;
Diethelm, K.; Kafatos, A. Short sleep duration is associated with increased obesity markers in European
adolescents: Eect of physical activity and dietary habits. The HELENA study. Int. J. Obes. 2011, 35,
1308–1317. [CrossRef]
6. Garfield, V. The association between body mass index (BMI) and sleep duration: Where are we after nearly
two decades of epidemiological research? Int. J. Environ. Res. Public Health 2019, 16, 4327. [CrossRef]
7. Cedernaes, J.; Schiöth, H.B.; Benedict, C. Determinants of shortened, disrupted, and mistimed sleep and
associated metabolic health consequences in healthy humans. Diabetes 2015, 64, 1073–1080. [CrossRef]
8. Haack, M.; Mullington, J.M. Sustained sleep restriction reduces emotional and physical well-being. Pain
2005, 119, 56–64. [CrossRef]
9. Goel, N.; Rao, H.; Durmer, J.S.; Dinges, D.F. Neurocognitive consequences of sleep deprivation. In Seminars
in Neurology; Thieme Medical Publishers: New York, NY, USA, 2009; pp. 320–339.
10. Ferrara, M.; De Gennaro, L.; Bertini, M. Selective slow-wave sleep (SWS) deprivation and SWS rebound: Do
we need a fixed SWS amount per night. Sleep Res. Online 1999, 2, 15–19.
11. Beersma, D.; Dijk, D.; Blok, C.; Everhardus, I. REM sleep deprivation during 5 hours leads to an immediate
REM sleep rebound and to suppression of non-REM sleep intensity. Electroencephalogr. Clin. Neurophysiol.
1990, 76, 114–122. [CrossRef]
12. Sassin, J.; Parker, D.; Mace, J.; Gotlin, R.; Johnson, L.; Rossman, L. Human growth hormone release: Relation
to slow-wave sleep and sleep-waking cycles. Science 1969, 165, 513–515. [CrossRef] [PubMed]
13. Kern, W.; Dodt, C.; Born, J.; Fehm, H.L. Changes in cortisol and growth hormone secretion during nocturnal
sleep in the course of aging. J. Gerontol. Ser. A Biol. Sci. Med Sci. 1996, 51, M3–M9. [CrossRef] [PubMed]
14. Jereys, I. A multidimensional approach to enhancing recovery. Strength Cond. J. 2005, 27, 78. [CrossRef]
15. Venter, R.E.; Potgieter, J.R.; Barnard, J.G. The use of recovery modalities by elite South African team athletes.
South Afr. J. Res. Sport Phys. Educ. Recreat. 2010, 32, 133–145. [CrossRef]
16. Erlacher, D.; Ehrlenspiel, F.; Adegbesan, O.A.; Galal El-Din, H. Sleep habits in German athletes before
important competitions or games. J. Sports Sci. 2011, 29, 859–866. [CrossRef]
17. Bird, S.P. Sleep, recovery, and athletic performance: A brief review and recommendations. Strength Cond. J.
2013, 35, 43–47. [CrossRef]
18. Xie, L.; Kang, H.; Xu, Q.; Chen, M.J.; Liao, Y.; Thiyagarajan, M.; O’Donnell, J.; Christensen, D.J.; Nicholson, C.;
Ili, J.J. Sleep drives metabolite clearance from the adult brain. Science 2013, 342, 373–377. [CrossRef]
19. Karadzic, V.; Mrsulja, B. Deprivation of paradoxical sleep and brain glycogen. J. Neurochem. 1969, 16, 29–34.
[CrossRef]
20. Karnovsky, M.; Reich, P.; Anchors, J.; Burrows, B. Changes in brain glycogen during slow-wave sleep in the
rat. J. Neurochem. 1983, 41, 1498–1501. [CrossRef]
21. Colicos, M.A.; Collins, B.E.; Sailor, M.J.; Goda, Y. Remodeling of synaptic actin induced by photoconductive
stimulation. Cell 2001, 107, 605–616. [CrossRef]
22. Chung, N.; Bin, Y.S.; Cistulli, P.A.; Chow, C.M. Does the Proximity of Meals to Bedtime Influence the Sleep of
Young Adults? A Cross-Sectional Survey of University Students. Int. J. Environ. Res. Public Health 2020, 17,
2677. [CrossRef] [PubMed]
23. Chénier-Leduc, G.; Béliveau, M.-J.; Dubois-Comtois, K.; Butler, B.; Berthiaume, C.; Pennestri, M.-H. Sleep
Diculties in Preschoolers with Psychiatric Diagnoses. Int. J. Environ. Res. Public Health 2019, 16, 4485.
[CrossRef] [PubMed]
Int. J. Environ. Res. Public Health 2020, 17, 2883
4 of 4
24. Son, J.; Jung, S.; Song, H.; Kim, J.; Bang, S.; Bahn, S. A Survey of Koreans on Sleep Habits and Sleeping
Symptoms Relating to Pillow Comfort and Support. Int. J. Environ. Res. Public Health 2020, 17, 302. [CrossRef]
25. Shin, M.; Halaki, M.; Swan, P.; Ireland, A.H.; Chow, C.M. The eects of fabric for sleepwear and bedding on
sleep at ambient temperatures of 17 c and 22 c. Nat. Sci. Sleep 2016, 8, 121. [CrossRef] [PubMed]
26. Chow, C.M.; Shin, M.; Mahar, T.J.; Halaki, M.; Ireland, A. The impact of sleepwear fiber type on sleep quality
under warm ambient conditions. Nat. Sci. Sleep 2019, 11, 167. [CrossRef] [PubMed]
27. Afaghi, A.; O’Connor, H.; Chow, C.M. High-glycemic-index carbohydrate meals shorten sleep onset. Am. J.
Clin. Nutr. 2007, 85, 426–430. [CrossRef]
28. Sonnega, J.; Sonnega, A.; Kruger, D. The City Doesn’t Sleep: Community Perceptions of Sleep Deficits and
Disparities. Int. J. Environ. Res. Public Health 2019, 16, 3976. [CrossRef]
29. Vargas, I.; Vgontzas, A.N.; Abelson, J.L.; Faghih, R.T.; Morales, K.H.; Perlis, M.L. Altered ultradian cortisol
rhythmicity as a potential neurobiologic substrate for chronic insomnia. Sleep Med. Rev. 2018, 41, 234–243.
[CrossRef]
30. Ramikie, T.S.; Nyilas, R.; Bluett, R.J.; Gamble-George, J.C.; Hartley, N.D.; Mackie, K.; Watanabe, M.; Katona, I.;
Patel, S. Multiple mechanistically distinct modes of endocannabinoid mobilization at central amygdala
glutamatergic synapses. Neuron 2014, 81, 1111–1125. [CrossRef]
31. Marcus, D.J.; Bedse, G.; Gaulden, A.D.; Ryan, J.D.; Kondev, V.; Winters, N.D.; Rosas-Vidal, L.E.; Altemus, M.;
Mackie, K.; Lee, F.S. Endocannabinoid Signaling Collapse Mediates Stress-Induced Amygdalo-Cortical
Strengthening. Neuron 2020, 105, 1062–1076.e6. [CrossRef]
32. Savic, M.; Ogeil, R.P.; Sechtig, M.J.; Lee-Tobin, P.; Ferguson, N.; Lubman, D.I. How Do Nurses Cope with
Shift Work? A Qualitative Analysis of Open-Ended Responses from a Survey of Nurses. Int. J. Environ. Res.
Public Health 2019, 16, 3821. [CrossRef] [PubMed]
33. Oftedal, S.; Burrows, T.; Fenton, S.; Murawski, B.; Rayward, A.B.; Duncan, M.J. Feasibility and Preliminary
Ecacy of an m-Health Intervention Targeting Physical Activity, Diet, and Sleep Quality in Shift-Workers.
Int. J. Environ. Res. Public Health 2019, 16, 3810. [CrossRef] [PubMed]
34. Peter, L.; Reindl, R.; Zauter, S.; Hillemacher, T.; Richter, K. Eectiveness of an online CBT-I intervention and a
face-to-face treatment for shift work sleep disorder: A comparison of sleep diary data. Int. J. Environ. Res.
Public Health 2019, 16, 3081. [CrossRef] [PubMed]
35. Kim, H.; Lee, Y.W.; Ju, H.J.; Jang, B.J.; Kim, Y.I. An Exploratory Study on the Eects of Forest Therapy on
Sleep Quality in Patients with Gastrointestinal Tract Cancers. Int. J. Environ. Res. Public Health 2019, 16, 2449.
[CrossRef]
© 2020 by the author. Licensee MDPI, Basel, Switzerland. This article is an open access
article distributed under the terms and conditions of the Creative Commons Attribution
(CC BY) license (http://creativecommons.org/licenses/by/4.0/).