Category Archives: Work and Society

How Might Escaping Technology Help Improve Our Sleep Problems?


“Won’t someone please think of the children?!”

Besides infancy, we don’t initially think of sleep as a big problem in childhood. Yet, a slew of recent articles have highlighted that insomnia and other sleep problems are not simply an issue of adulthood. A BBC Panorama documentary released last week commented on the surge in problems with sleep in children. Although there were a number of culprits identified for this increase in the problems with children’s sleep, one key point was technology and later exposure to artificial light.

We are all glued to our smartphones, laptops, and Fitbits. Modern artificial lighting allows us to work and entertain ourselves further into the night than natural light permits but the normality surrounding their use before bed is negatively influencing sleep. As people are educated more about the effects of technology on sleep, these issues should hopefully reduce but whether education can effect this change is uncertain. The question remains: How can we improve sleep without dragging people away from technology? One love-it or hate-it option may be camping.

Last month, a research group led by Kenneth Wright carried out two studies which examined how artificial light interferes with our natural sleep rhythms and our body’s concept of day and night. Study one assessed the sleep of participants firstly during artificial lighting and then natural lighting during the winter. The second study attempted to understand the impact of weekend camping on sleep. The researchers studied sleep by asking them to wear a watch to track movements and by tracking changes in a hormone called melatonin. Melatonin is released prior to sleep, reaches a midpoint during the first half of sleep and dips as you wake up. During the day, it is only detectable at trace levels because in the presence of light melatonin’s production is inhibited. This, in part, explains why we feel tired and want to go to bed at night rather than during the day. As a result, melatonin serves as a useful and precise marker of the internal biological night (i.e. when the body feels we should be sleeping).

The first study had participants spend a week, during winter, camping with no artificial light (e.g. torches or phones) and then a week in their normal, modern, environment which served as a baseline. Participants’ melatonin levels were measured during sleep after about 6 days of the modern environment and after 6 days of the natural light, camping, condition.

This initial study found that the internal biological night (e.g. melatonin onset, midpoint, and offset) is affected by seasonal fluctuations. Specifically, internal biological night is longer during winter and shorter during the summer. In the camping condition, melatonin onset and sleep onset were around 2 hours earlier compared to the modern, artificially lit, condition. However, melatonin offset and sleep offset were similar between camping and baseline. When comparing the winter data to previously collected summer data, the melatonin onset was earlier and melatonin offset was significantly later in the winter condition. More specifically, they showed a four-hour difference in internal biological night between winter and summer. However, there were no change in internal biological night between summer and winter offset when comparing the artificial light conditions. The modern, artificially lit, environment had extinguished the seasonal fluctuations in melatonin and sleep patterns.

The second study then went on to assess whether weekend exposure to natural light (i.e. camping) could help reduce the effects of social jet lag – the mismatch between the time you wake up during the weekday and weekend. We tend to delay our sleep during the weekend and this contributes to why it is so hard to wake up on a Monday morning. In this study, fourteen participants were first tested in their normal, artificially lit, environment and their melatonin levels during the night (onset, midpoint and offset) were assessed. Participants were then separated to a camping condition (n=9; natural light) or normal condition (n=5; artificial light).

What did they find? For the camping condition, the time at which participants went to sleep and woke up were similar between weekday and weekend. However, for the artificial light condition the onset of sleep was found to be delayed by almost 2 hours and participants woke up around an hour and a half later during the weekend compared to the weekday. People were staying up later and waking up later during the weekend presumably when they didn’t have work. Overall sleep duration and efficiency were similar across and within both groups. So, participants were not sleeping for longer under artificial light but were delaying their sleep schedule.

What about the data for internal biological night? In the camping condition, melatonin onset and midpoint were about an hour earlier during the weekend compared to weekday despite there being no changes in sleep timing. Interestingly, changes in melatonin were not only seen in the camping condition but also the modern setting. Melatonin onset, midpoint and offset were delayed by about an hour compared to the weekday for the modern, artificial light, condition. This is problematic if you have to get up earlier on the Monday morning for work and is linked to what we know as social jet lag. If you feel sleepier later and want to wake up later then you may find yourself being groggy and sleep deprived during the week.

Yet, when participants went camping over the weekend, they did not see a shift in their sleep onset or offset, and their biological night became advanced (started earlier) slightly. This suggests that weekend exposure to natural light (e.g. camping) may help diminish the negative effects of living in the current, high-paced, environment we currently have. The small sample size and short sampling period makes it hard to draw definite conclusions from this study but it does highlight that artificial lighting is having a definable impact on our sleep and the biochemistry underpinning it. It also provides some preliminary evidence of the biological impact of social jet lag.

You may, quite rightly, think that the results of this study are rather obvious: we stay up later during the weekend and our biology is going to follow suit unless we hike out to the middle of nowhere for the weekend. However, it highlighted the biological impact of our modern, well-lit, environment on our body’s internal clock. We know that using our devices before bed are generally bad for sleep but very few of us actually do anything about this. We may try to adopt better bedtime habits but this may be thwarted by technology (e.g. using a kindle to read just before bed)

Also, it is key to remember that light is not the only regulator of our sleep rhythms and in societies not exposed to artificial light the key determinant of the sleep cycle is temperature. This should make us think about not a single factor (i.e. light) but a multitude of issues may cause issues with our sleep. Interestingly, such individuals in cultures not exposed to artificial light also reported problems with insomnia but at a reduced rate than reported in modern society.

Nonetheless, light from devices, rich in low-wavelength blue-light, resets our biological clocks and inhibits the release of melatonin. As a result, we feel sleepier later even though we still have to get up at the same time and go to school, college or work. The recurrent sleep deprivation can in turn lower our mood, concentration and put us at increased risk of illness and metabolic disorders. Now, it is unlikely that the rise of childhood sleep problems can be fixed by wrenching tablets from children and throwing them out into the wilderness every Friday until Sunday. Nonetheless, we can think about what these devices are doing to our sleep – at the very least when we’re sleeping poorly to begin with.

Inquisitive Tortoise


ResearchBlogging.orgStothard ER, McHill AW, Depner CM, Birks BR, Moehlman TM, Ritchie HK, Guzzetti JR, Chinoy ED, LeBourgeois MK, Axelsson J, & Wright KP Jr (2017). Circadian Entrainment to the Natural Light-Dark Cycle across Seasons and the Weekend. Current biology : CB, 27 (4), 508-513 PMID: 28162893


Additional References:

Chang, A. M., Aeschbach, D., Duffy, J. F., & Czeisler, C. A. (2015). Evening use of light-emitting eReaders negatively affects sleep, circadian timing, and next-morning alertness. Proceedings of the National Academy of Sciences, 112(4), 1232-1237.

Yetish, G., Kaplan, H., Gurven, M., Wood, B., Pontzer, H., Manger, P. R., … & Siegel, J. M. (2015). Natural sleep and its seasonal variations in three pre-industrial societies. Current Biology, 25(21), 2862-2868.


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What Have Fairy Tales Got to Do With Sleep Medicine?

Sleeping Beauty.jpg

“Fairy tales? That’s the best you could think of to drag people in?”

“What’s wrong with it? It’s accurate…”

“I dunno man, you used to be all about the science. Now this feels all click-bait territory *shudders*”


By fairy tales, I am of course referring to sleeping beauty. Not a champion of feminist thought, this story tells the tale of a young woman who awaits the kiss of a prince to awaken her from an eternal slumber. Although there is no disorder which makes you sleep indefinitely there is a close contender with something called Kleine-Levin syndrome (KLS) – also known as ‘sleeping beauty’ syndrome.

What is Kleine-Levin syndrome?

Kleine-Levin syndrome is an episodic and extremely rare sleep disorder whereby the individual goes through periods of excessive sleepiness (hypersomnia). We all go through periods of feeling exhausted and may find ourselves sleeping for that bit longer. Maybe in extreme cases we’ve found that we’ve spent the whole day in bed fast asleep (thanks new year’s). However, imagine spending up to 20 hours a day asleep for weeks, or even months with no indication when you’ll ‘wake up’ and go back to normal. You miss school, friends, hobbies, and significant portions of your life as your teenage years drifts steadily away. Your dreams seem more real than reality and you lose interest in everything around you. This is a taste of what those with KLS experience and have to deal with.

Other than spending most of the day asleep, sufferers also experience memory, speech, and comprehension problems. In addition, hallucinations, derealisation (feeling as if in a dream), hypersexuality and megaphagia (increased eating behaviour) and paranoia also co-occur with the sleep and cognitive symptoms. It usually tends to emerge around adolescence and usually runs its course over about 8 years (with individual variability). Unsurprisingly, KLS causes significant disruption to academic performance, social lives, and sometimes memory of affected individuals.

What is its prevalence?

It is such a rare disorder that it has been difficult to get an accurate representation of its prevalence. We do know is that it is more prevalent in males but it seems to persist for longer in females for yet unknown reason. Some studies claim the prevalence is as low as 1 in a million but there is little research to support this number. Due to its rarity, most of our available knowledge on this study has been gained through case studies.

What causes this disorder?

This is uncertain although there is research attempting to shed light on this enigmatic illness. A systematic review carried out just over a decade ago found that in over 40% of reported cases, the first episode of KL-syndrome was preceded by an infection or fever. However, in 39% of cases there was no obvious precipitating trigger and the same lack of trigger is found in 84% of subsequent episodes of KL-syndrome. Although onset tends to occur during the latter months of the year, there is no strong argument for why this might be the case. Moreover, the disease may appear to disappear with little understanding why the symptoms disappear.

The link between infections and KLS has led some to argue that it may have an immune-system cause. However, there is little evidence for a link between dysfunctional immune functioning and KLS. Researchers have found some support for a link between certain types of hypersomnia and autoimmunity disorders but it is still unclear whether this extends to KLS.

A study by Dr. Jing Wang and colleagues at the Binzhou Medical University Hospital examined a large group of individuals with KLS (N=44) to identify potential markers of KLS. They found that a large subset of these individuals (N=34) were found to have reductions in a chemical called orexin in their cerebrospinal fluid (CSF) during a relapse compared to a period of remission. Orexin is a neurochemical which is important for wakefulness and is reduced in another disorder characterised by hypersomnia – narcolepsy. However, levels of orexin were not as low as those seen in narcolepsy. Interestingly, this cohort also showed a similar pattern of viral infection preceding the initial episode of hypersomnia / KLS.


Again, it should come with little surprise that there are limited treatment options for those with KLS. One route is to reduce the fatigue through stimulants. However, this approach is not effective for other symptoms of the disorder. A different approach is to treat KLS using a mood stabiliser, lithium, which has shown some promise in reducing the length and frequency of episodes, and in reducing the behavioural symptoms. However, evidence for the efficacy of this treatment is limited and it forms one of many possible pharmacological treatments which require wider study.

Difficulties in Diagnosis

This is an extremely rare disorder and not many will have had experience with this diagnosis. However, it is treated with scepticism from some physicians and the general public. Some see it as laziness or not unusual for adolescents and students to sleep for most of the day. It is also not unusual for an individual with KLS to be given a diagnosis of depression in light of similar symptoms to an unknowing physician. A diagnosis of KLS can be laborious to reach as it will be given after identifying whether the individual’s symptoms are not better explained by a whole host of other diagnoses or causes. We have known about this disorder for more than a century and yet we have no convincing theory for why it occurs or how to treat it.

Although there is a lot we don’t know about KLS there is still active research determined to better understand and treat this disorder. If you’re interested in learning more about what it’s like to live with this illness this documentary is a good start.

Inquisitive Tortoise


Arnulf, I., Zeitzer, J. M., File, J., Farber, N., & Mignot, E. (2005). Kleine–Levin syndrome: a systematic review of 186 cases in the literature. Brain,128(12), 2763-2776.

Barateau, L., Lopez, R., Arnulf, I., Lecendreux, M., Franco, P., Drouot, X., … & Dauvilliers, Y. (2017). Comorbidity between central disorders of hypersomnolence and immune-based disorders. Neurology, 88(1), 93-100.

Kornum, B. R., Rico, T., Lin, L., Huang, Y. S., Arnulf, I., Jennum, P., & Mignot, E. (2015). Serum cytokine levels in Kleine–Levin syndrome. Sleep medicine, 16(8), 961-965.

Leu-Semenescu, S., Le Corvec, T., Groos, E., Lavault, S., Golmard, J. L., & Arnulf, I. (2015). Lithium therapy in Kleine-Levin syndrome An open-label, controlled study in 130 patients. Neurology, 85(19), 1655-1662.

Poppe, M., Friebel, D., Reuner, U., Todt, H., Koch, R., & Heubner, G. (2003). The Kleine-Levin Syndrome. Neuropediatrics, 34(03), 113-119.

Wang, J. Y., Han, F., Dong, S. X., Li, J., An, P., Zhang, X. Z., … & Yan, H. (2016). Cerebrospinal Fluid Orexin A Levels and Autonomic Function in Kleine-Levin Syndrome. Sleep, 39(4), 855.

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Sleeping Beauty (Header)

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Juggling sleep with work: what are the long-term effects?


It’s 6am again. The unrelenting tone from your bedside table reminds you it’s time to roll out of your duvet cocoon and get ready to face the working world. You swat your shrieking phone as it gets louder and more persistent. A quick swipe of the screen and you notice the day. It’s Friday.

A relieved smile spreads across your face.

Well, at least tomorrow means a lie-in.

The typical working week for most will involve dragging ourselves out of our warm, cosy beds and forcing our legs to make the long cold trek to the bathroom. Yet, we know that come the weekend we will be able to catch up, even briefly, on the sleep denied to us during the week. Although we will moan to friends and colleagues, our society seems perfectly content with depriving ourselves of sleep during the working week only to catch it up during the weekend. We would likely prefer a few minutes (or hours) more in the morning, but many of us don’t consider this practice as detrimental to our health. The shift from short to long sleep is considered a part of life.

This is far from sensible as the effects of sleep deprivation are well known, even if you don’t spend your days buried in journals with helpful names such as ‘Sleep’.

There is a name (there always is) for the shifting of sleep patterns throughout the working week – social jet lag. This refers to the changes in our sleep timing and duration depending on when we’re working (e.g. sleeping less on workdays and more on free days), and how this can confuse our internal clocks which try to keep our sleep patterns regular and predictable. These are the same internal clocks which influence whether you are an owl or a lark – an evening or morning person. This misalignment affects people differently, and it is not hard to see why night owls, who want to sleep later and wake up later, may suffer more.

Social jet lag is a problem for society. It is associated with depression, an increased risk for heart disease, more frequent smoking, and increased stimulant use in general. Understandably, the effects seen from sleep deprivation, including difficulties in concentration, memory, social functioning and mood, are also associated with social jet lag.

Despite the mental and physical health issues reported, the available data had been largely correlational. This makes it hard to draw definite conclusions on whether society’s current schedule of sleep is bad for us in the long-term.

However, a recent study published earlier this year has attempted to address this.  A team of researchers at the University of Harvard sought to understand whether repetitive patterns of sleep restriction and catch-up sleep have a negative impact on our health and wellbeing, or whether we may simply get used to it.

More specifically, they wanted to try to work out whether there is a difference in our own subjective view of this sleep pattern and how our body, behind the scenes, might respond in terms of stress and immune functioning. Do we adapt to the sleep loss in both domains? Previous evidence suggested we might not but this hadn’t been convincingly tested over a long period until now.

To assess these questions, they recruited 14 participants who were studied in a controlled hospital setting over three weeks. During each week, the participants spent 5 days sleeping for 4 hours and 2 days sleeping for 8 hours. After a few months, the same participants were invited back to conduct the same experiment sleeping for 8 hours each day over the 25-day experiment. The results of each were compared to try to understand the impact of the working week’s sleep patterns.

The group asked participants about how sleepy they felt, their perceived effort to do anything, and how stressed they felt each day at 4 hour intervals throughout the study. Alongside this, objective measures of stress and immune functioning were also assessed via blood samples collected on 7 of the 25 study days. Specifically, they looked at the levels of a chemical messenger of the immune system known to promote inflammation, interleukin-6, and the levels (total and stability) of cortisol, a hormone released in response to stress (amongst other factors).

The participants’ diet and exercise were controlled to reduce the impact of these variables, and they could have visitors to reduce the impact of isolation, and deviation from normal routines, where possible.

So, what did they find?

Over the three weeks, when participants were restricted to only 4 hours’ sleep they (unsurprisingly) felt sleepier and reported a greater effort to do anything compared to when than when they could sleep for 8 hours (e.g. during the weekend in the restricted condition and every day for the control condition). Interestingly, the ‘effort to do anything’ ratings became increasingly similar for the restricted and control condition over the three weeks, and participants reported no extra stress when asked to halve their sleep to 4 hours for the restriction condition. Overall, this suggests that participants, although sleepy, were subjectively fine with the simulated typical work sleep pattern. There was even evidence that participants started to adapt as their reported effort to carry out tasks diminished by the third week of only 4 hours sleep.

By contrast, the objective results showed a less optimistic picture. The researchers found an increased dysregulation of cortisol as the weeks of sleep restriction went on, and an increase in morning cortisol compared to the control condition. However, both returned to normal following recovery sleep at the weekends. In terms of immune system functioning, unstimulated IL-6 levels were significantly higher for the first week of sleep restriction and then remained elevated but non-significantly so compared to the control condition. For the stimulated IL-6 levels, these were significantly elevated during the week for the second and third week of the restriction condition compared to the control.

These results highlight that although participants seemed to be no more stressed subjectively in depriving themselves of sleep during the week, it seems that this pattern of sleep was not something the body simply ‘gets used to’. Instead it seems that the body still shows an increase in the inflammatory marker IL-6, increased cortisol upon awakening, increased dysregulation of cortisol, and inhibition of IL-6 in the presence of cortisol-like molecule. This hints at a heightened stress and immune response which, importantly, does not appear to adapt to the effects of chronic sleep loss during the week. Although recovery sleep during the weekend mitigated this effect somewhat, there was some evidence to suggest that two days was not enough to return immune functioning (stimulated IL-6) back to normal.

You may be thinking that increases in IL-6 and increased inhibition of IL-6 seem counter-intuitive, but the authors had a potential explanation. They highlighted that this may be the product of a particularly active immune response following chronic sleep to deal with its physiological effects (i.e. the increased sensitivity to cortisol’s effect is lessened due to a need to remove toxins built up in the brain).

In addition, you may also want to argue that 4 hours sleep during the week is hardly typical of most people’s work schedule, and that this experiment is far from representative of real life. However, this is a weak argument as the effects of sleep deprivation have already shown to be cumulative. It is more likely that losing an hour or two during the workday has negative effects but over longer periods than are suggested by this study.

So, it seems that even though we may consider depriving ourselves of sleep during the week manageable, and even get used to it, the same cannot be said for our body. This study suggests that we don’t get used to sleep loss during the working week. Moreover, recovery sleep during the weekends may not be enough to compensate for a week of fighting our internal clocks.

Although this study only examined a small number of people and a small number of specific measures, it still highlights the persistent effects of restricted sleep on our immune and stress systems. It also provides some hints as to how we may be able to successfully convince ourselves that this pattern of sleep is not detrimental to our health. If we feel subjectively okay, if not slightly lethargic, about this lifestyle then there would be no immediate drive to change it – at an individual or society level.

Granted, necessity and an inability to pay the bills may also be powering this too…

Inquisitive Tortoise


Rutters, F., Lemmens, S. G., Adam, T. C., Bremmer, M. A., Elders, P. J., Nijpels, G., & Dekker, J. M. (2014). Is social jetlag associated with an adverse endocrine, behavioral, and cardiovascular risk profile?. Journal of biological rhythms, 0748730414550199.

Simpson, N. S., Diolombi, M., Scott-Sutherland, J., Yang, H., Bhatt, V., Gautam, S., … & Haack, M. (2016). Repeating patterns of sleep restriction and recovery: Do we get used to it?. Brain, Behavior, and Immunity.

Van Dongen, H. P., Maislin, G., Mullington, J. M., & Dinges, D. F. (2003). The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation. SLEEP-NEW YORK THEN WESTCHESTER-, 26(2), 117-129.

van Leeuwen, W. M., Lehto, M., Karisola, P., Lindholm, H., Luukkonen, R., Sallinen, M., … & Alenius, H. (2009). Sleep restriction increases the risk of developing cardiovascular diseases by augmenting proinflammatory responses through IL-17 and CRP. PloS one, 4(2).

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