How Might Escaping Technology Help Improve Our Sleep Problems?

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“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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Sleep’s Positive Impact on Traumatic Memories

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Sleep is inescapable. Some will see it as a necessary evil and others will claw at it with limited success. It may leave us (largely) immobile but it is anything but a passive state. Sleep paves the way for new neural connections to be made, clears the brain of harmful waste products, is protective against mental and physical illness, and is preferable to leaving the bed on a cold Monday morning. There is still plenty of debate as to the true function of sleep, but one key area which it appears to be important for is memory.

Broadly speaking, it is argued that sleep enhances the consolidation of recently learned information compared to wakefulness. For example, a nap as short as 5-10 minutes has been shown to enhance memory and improve problem solving compared to wakefulness following learning. Moreover, rapid eye movement sleep has been linked to enhanced memory for emotional information, and to reducing the emotional strength of such memories. This suggests that different aspects of sleep are important for different types of memories and highlights some potential ways we can modify the impact of negative ones. What if we could interfere with the brain’s ability to form negative memories? More specifically, what if we could interfere with traumatic and intrusive memories which form the basis of illnesses such as post-traumatic stress disorder (PTSD)? Recent research seems to suggest this may be possible.

PTSD is a psychiatric disorder characterised by flashbacks and nightmares, avoidance of the situation in which the trauma occurred, and emotional numbing. It is the result of a traumatic event which can be wide in scope (e.g. warfare, sexual abuse, hospital admission) and individuals with PTSD will often find themselves transported back to the event. These ‘memories’ are intrusive in nature and, understandably, highly distressing. It has been suggested that interfering with the consolidation of intrusive memories at the time they are formed (or shortly afterwards) may help those who are likely to go on to experience PTSD. Evidence to support this would unlock a powerful early intervention tool for those likely to experience trauma (e.g. refugees or soldiers). One way this can be achieved, as you have likely guessed, is through manipulating sleep.

In 2015, a study conducted at the University of Oxford explored whether sleep deprivation might be protective against intrusive traumatic memories. Participants were brought into the laboratory and randomised to either a sleep deprivation or sleep group. They were then shown a film containing traumatic scenes which lasted just over 15 minutes. Following the film, participants were either kept awake or allowed to sleep. On the following day, participants completed a questionnaire measure of PTSD symptomology and were then asked to complete a diary to track the intrusiveness, content, distress, and presence of mental imagery associated with the traumatic film for 6 days.

The Oxford group, led by Dr. Kate Porcheret, found that a night of sleep deprivation, compared to sleep as normal, reduced the intrusiveness of experimental-trauma memories. The sleep deprivation group reported fewer intrusive memories, lower PTSD symptoms scores, and (non-significantly) reduced distress of the intrusive memories. However, this effect was only found for the first two days and sleep deprivation was found to confer no protection against intrusive memories after 6 days. This suggests that sleep deprivation immediately after the traumatic experience can reduce its intrusiveness but only in the short term. Sorted. Sleep deprivation, paradoxically, confers some protective against traumatic memories. Right? Well, to quote Ben Goldacre, “I think you’ll find it’s a bit more complicated than that”.

A study published last December in the aptly named journal SLEEP has injected additional complexity to this issue. Dr. Birgit Kleim and colleagues assessed the impact of a single night of sleep deprivation on distress and intrusiveness of traumatic memories for seven, rather than six, days. They asked 65 female participants to watch two 12 minute films of a neutral (nature documentary) or traumatic (horror film) nature in a randomised order. Participants were either allowed to sleep at home or kept awake. They were then asked to keep an intrusion diary which required participants to note when they experienced intrusive memories related to the film and rate their vividness, intrusiveness, content, and distress each day. The participants were then followed-up a week later.

So, what did they find? For the first two days following the films, there was no significant difference between the sleep or wake groups on distress or intrusiveness of the traumatic film. However, by days 6 and 7 there was a significant reduction in distress and intrusiveness for the sleep compared to wake group. By contrast, there were no difference in intrusiveness or distress of the neutral film for the sleep and wake groups. The effects found were specific for the traumatic, emotional, memory.

This second study showed that sleep deprivation does not provide a protective effect against intrusive emotional memories. Instead, they argued that sleep immediately following the trauma experience has long-term benefits on reducing the distress and intrusions associated with the traumatic memory. Nonetheless, this study does not directly contradict the one conducted by Porcheret and colleagues at Oxford. Although non-significant, distress was higher for the sleep compared to sleep deprivation group which suggests that sleep deprivation may serve an immediate protective role against traumatic memories. However, this effect seems to reverse in the relative long-term.

Why should this be so? Well, we know that memories – particularly emotional ones – are strengthened by a period of sleep. This would suggest that sleep following a traumatic experience would strengthen the memory for that experience and thus enhance the intrusiveness of a traumatic memory. This could explain why sleep deprivation produced a reduction in intrusiveness and distress for the Oxford study as the lack of sleep interfered with the ability to lay down the negative memory. However, the explanation for these studies is less clear. The authors argue that sleep deprivation is protective against intrusive memories in the short term but not the long-term. Kleim and colleagues claim that sleep following the traumatic experience may initially make it more distressing but also encourage appropriate integration of the memory alongside existing memories. This, they argue, reduces the chance that the traumatic memory will be intrusive and uncontrollable – a cardinal symptom of PTSD.

We already know that rapid eye movement sleep (REM) is associated with a reduction in the intensity of emotional images (van der Helm et al., 2011). Kleim’s study found that increased REM was associated with more, not less, intrusions. Instead, they argue that other stages of sleep are responsible for the reduction in distress and intrusions seen perhaps through a different mechanism. However, this does not state that the memory should be remembered more poorly (i.e. deliberate recall of the film would be unaffected). Rather it seems that deliberate memory recall and intrusive memories may be guided by different mechanisms and differentially affected by sleep. Neither the Porcheret or Kleim study asked participants to take a memory test of their explicit recall of the films. However, the diary studies suggest that all participants were accurate in recalling the films throughout the study period and deliberate recall does not appear to be associated with intrusive memory frequency.

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A similar distinction between intrusive and deliberate recall of memories was found by another study attempting to reduce the negative impact of traumatic memories. Indeed, these are the not the first studies which have attempted to interfere with the consolidation of traumatic memories. A more colourful way of achieving this has been shown through getting people to play Tetris. For the uninitiated, Tetris is a simple game whereby you match coloured bricks of different shapes into lines of 4. They fall from the top of the screen and you have to rotate the shapes to make them line-up and disappear. In 2009, Dr Emily Holmes and colleagues at the University of Oxford showed that if they got participants to play Tetris for 10 minutes, half an hour after a traumatic film, they saw a reduction in subsequent intrusions or “flashbacks”. This effect was found for over a week follow-up during which an intrusion diary was kept. Interestingly, deliberate recall of the film was not impaired when tested at one-week follow-up. This also suggests it is possible to reduce the intrusive nature of a traumatic memory without reducing the memory for the event.

Of course, it is difficult to get someone in a warzone to take out their Tetris ration or take a nap following a fire-fight, but it highlights that it is possible to reduce the negative impact of traumatic memories. These pieces of research suggest that manipulating sleep is a viable way to reduce the ‘flashback’ quality of traumatic memories. Although promoting sleep for those having recently experienced a traumatic episode might raise its own difficulties, it heralds a step towards early intervention for PTSD. If nothing else, they remind us that sleep is important for the consolidation of memory alongside existing memory networks and how little we know about the effect of sleep on memory.

One thing we do know for sure: sleep is anything but a passive and simple state.

Inquisitive Tortoise

References:

Holmes, E. A., James, E. L., Coode-Bate, T., & Deeprose, C. (2009). Can playing the computer game “Tetris” reduce the build-up of flashbacks for trauma? A proposal from cognitive science. PloS one, 4(1), e4153.

Kleim, B., Wysokowsky, J., Schmid, N., Seifritz, E., & Rasch, B. (2016). Effects of Sleep After Experimental Trauma on Intrusive Emotional Memories. Sleep.

Porcheret, K., Holmes, E. A., Goodwin, G. M., Foster, R. G., & Wulff, K. (2015). Psychological effect of an analogue traumatic event reduced by sleep deprivation. SLEEP, 38(7).

van der Helm, E., Yao, J., Dutt, S., Rao, V., Saletin, J. M., & Walker, M. P. (2011). REM sleep depotentiates amygdala activity to previous emotional experiences. Current Biology, 21(23), 2029-2032.

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Bad Memory (Header)

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What Have Fairy Tales Got to Do With Sleep Medicine?

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“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.

Treatment

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

References:

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.

Image Credits:

Sleeping Beauty (Header)

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Why Do We Dream?

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Key Dream Research Equipment

“What does my dream mean?!”

“Sorry…?”

“I’ve heard you study sleep. I mean I think I’ve worked it out myself but I wanted an expert opinion.”

“Erm…”

It doesn’t take long to drift into questions about dream analysis when I tell people that I study sleep. I don’t entirely blame them. It’s a subject which has fascinated society for millennia and it doesn’t look like that is going to stop any time soon. I’m sure most of us have had a dream which we are convinced has some greater significance: a dream about facing our fears or that person who you hadn’t thought about for years.

In the distant past, dreams were associated with divine will and prophetic qualities. Ancient Egyptian and Greek scholars produced dream manuals which were used to interpret nightly visions. Flash forward to the 19th and early 20th century and there was a shift towards understanding dreams in terms of their psychological causes and consequences. It was not until 1953 with the discovery of rapid eye movement (REM) sleep that the objective study of dreaming was possible.

Since then, we have come to appreciate that not all dreams are not created equal. Depending on which stage of sleep the dream is recalled from will depend on the type of dream. Firstly, dreaming does not only occur during rapid eye movement (REM) sleep but can occur at any stage during the sleep cycle. Dreams at sleep onset and during short naps appear to be relatively faithful, if not stripped back, representations of daily activities. By contrast, dreams reported during REM sleep and after longer periods of sleep appear more bizarre and less clearly linked to daytime activities.

So why do we dream? What attempts have there been to try to understand these nightly visions of the surreal?

Wish Fulfilment

Freud stated in ‘The Interpretation of Dreams’ that all dreams were wish fulfilment of our uninhibited desire. The dream provided an outlet for these desires and prevented them seeping into wakefulness. The dream (manifest) content could thus be interpreted and inform the analyst about the unconscious desires of an individual. The latent, or unremembered and unconscious, dream content could be reached through employing dream analysis and psychoanalytic techniques. Although you can still buy manuals which claim to teach you how to analyse dreams in line with early psychoanalytical thought, the validity of these are questionable at best. The steps required to reach the ‘latent content’ can be idiomatic and despite claims that an airplane can represent unconscious desires sometimes “…a cigar is just a cigar”.

Dreaming to Remember

It has been shown that dreaming is linked to the activities which we complete during the day. This should come with little surprise to most. We can often pinpoint our dreams back to activities we have completed during the day – even if they appear in bizarre contexts.

Robert Stickgold at the Department of Psychiatry, University of Harvard, showed this with a simple experiment. Participants were required to play Tetris at fixed periods and to sleep in a monitored laboratory setting. During this time, participants were asked about their thoughts and dreams in the first hour of attempted sleep.  He found that by asking participants to play Tetris for extended period of time that a significant number of sleep-onset dreams and images were found to be linked to Tetris (i.e. images of the blocks falling into place and lines of blocks disappearing when complete).

tetris

A study from the same group led by Erin Wamsley at the University of Harvard built on this by exploring whether the presence of task-relevant dreams was associated with performance. They asked participants to complete a virtual navigation task whereby they had to reach a goal (e.g. a tree). Participants were then re-tested just over 4 hours after the initial completion of this task.

Half of the group were then provided with an opportunity to nap and the other half remained awake. Unsurprisingly, from what we already know, the nap group were found to show a greater improvement on the task at re-test. Interestingly, and importantly for dreaming, the participants who dreamed about the maze during the nap also reported the greatest re-test improvement. Okay, perhaps this might simply have been due to the fact that these participants were simply thinking of the task more? However, this doesn’t appear to be the case. The wake participants were also asked about their task-relevant thoughts but the researchers found no benefit to re-test performance here.

Collectively, these studies suggest that dreaming may be a result of the brain consolidating and organising new memories alongside existing ones. However, they don’t tell us that dreaming is responsible for our improvement but that dreaming may be a marker of it.

Activation Synthesis Theory (and Dreaming to Forget)

Other theories suggest that dreaming has little relevance to memory or other functions. The Activation Synthesis theory proposed by Allan Hobson and Robert McCarley in 1977 claims that dreaming is the product of seemingly random or automatic brain activity produced during REM sleep.

These ‘random’ activations have their origin in the brain stem and are transmitted to the forebrain during REM sleep. The cortex then compares this activation against previous memories to make sense of the neural activity produced by the brain stem. It is claimed that a similar mechanism may explain non-sleep hallucinations and dreaming. This theory forms the basis for another hypothesis for why we dream: not to remember but to forget. This should seem counter-intuitive based on what we know about sleep and memory – and all that advice you’re given by teachers or colleagues before an important exam or meeting.

However, Francis Crick (yes, that Francis Crick) and Graeme Mitchison argued in 1983 that sleep has an important role in identifying faulty connections within the brain – an inevitable problem facing a neural network of sufficient complexity. These ‘faults’ arise during development and as a part of the multitudinous memories and connections we develop throughout any ordinary day. During REM sleep, these ‘faults’ are dampened down and their connections weakened. This ensures the brain works efficiently.

So, where does dreaming fit in?

Quite simply the ‘faults’ in the brain are experienced as dreams. Our dreams are the connections which our brains’ are trying to suppress during REM sleep. The overall purpose of such a mechanism is to ensure the efficient functioning of a brain with finite processing power.

However, if our dreams are the memories we are trying to erase, in one form or another, why do we have recurrent dreams? Crick claims that this is tricky for the theory but may be as a result of the threatening nature of recurrent dreams. The anxiety and fear associated with such dreams is likely to wake up the dreamer and to subsequently be remembered. This may interfere with the reverse learning process.

Primitive instinct rehearsal theory of dreaming

Another appealing theory is that dreaming is not a product of vital or random brain activity but rather that it serves an evolutionary advantage. More specifically, it has been claimed that dreams may help us deal with threatening situations in our daily lives by giving us an opportunity to practise overcoming them. In turn this increases our survival odds and also increases the chance we will successfully reproduce – passing on that ability to dream to our offspring.

Anecdotally this might explain why anxiety and fearful dreams are commonly reported by many different people, and why they share a common theme. However, like Freud, this theory assumes that dream content must have a distinct purpose. It’s hard to falsify such a theory and provide evidence which would conclusively disprove its existence as many dreams could conceivably be interpreted in a practise or threat-related manner.

Dreaming and Creativity

Finally, it’s an old claim that creativity and dreaming are linked together. Authors such as Mary Shelley and Steven King relate their tales of horror back to dreams they’ve remembered. Salvador Dali enjoyed the phantasmagorical images produced through his dreams and used them as inspiration for his surrealist art.

What does the science say about creativity and dreaming?

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Surveys of students’ ability to remember and recall dreams correlates with openness to new experiences, fantasy proneness, and may even be associated with a lesser ability to filter out environmental input. Cumulatively, this suggests that traits associated with creativity and ‘thinking outside the box’ are associated with an ability to recall dreams. However, this does not mean that we dream in order to improve creativity but that creativity is likely a product of bizarre, frightening and fantastical dreams. We benefit from dreaming but only insomuch as an incidental source of inspiration.

Overall, even though the content of your dreams may not necessarily provide a convenient road to your hidden thoughts and desires, they can provide us some fascinating insights into the sleeping brain. Despite frustrated responses from others, that remains my response when they ask about last night’s dream about planes, trains and giant chickens.

Don’t ask.

Inquisitive Tortoise

References:

Crick, F., & Mitchison, G. (1983). The function of dream sleep. Nature, 304(5922), 111-114.

Stickgold, R., Malia, A., Maguire, D., Roddenberry, D., & O’Connor, M. (2000). Replaying the game: hypnagogic images in normals and amnesics. Science, 290(5490), 350-353.

Wamsley, E. J., & Stickgold, R. (2010). Dreaming and offline memory processing. Current Biology, 20(23), R1010-R1013.

Wamsley, E. J., Perry, K., Djonlagic, I., Reaven, L. B., & Stickgold, R. (2010). Cognitive replay of visuomotor learning at sleep onset: temporal dynamics and relationship to task performance. Sleep, 33(1), 59-68.

Image Credits:

Dream Catcher (Header)

Tetris (Body Text)

Nightmare (Body Text)

 

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

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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

References:

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).

Extra Reading:

http://www.huffingtonpost.com/margaux-mcgrath/social-jet-lag-and-sleep_b_7842074.html

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Should We Be Napping More?

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Please tweet me and other sleep scientists at the University of Manchester your sleep questions using the hashtag above! #msf16

 

“Why don’t you just take a nap if you’re so tired? It’ll probably help and give me a break from your whining…”

“I can’t nap! I feel all groggy after a nap. Besides, I find the complaining is helping me through the fatigue”

“…”

Napping is something which divides opinions. It’s no yeast-based snack featured heavily in the news recently, but there are certainly strong proponents of the will-nap and won’t-nap camps. However, what does the research say about napping? Can it help us get through the day and feel better able to deal with the challenges which face us?

Firstly, sleep in general is something taken for granted. We’re all guilty of it. On average we need about eight hours sleep, with some individual variation, but yet on average the general population is shy of this by one and a half hours. Although we should really be focusing on ensuring we get the right amount of sleep, at the right time, for our own body, it may be that napping may alleviate some of the symptoms of poor sleep such as fatigue and mood changes.

Regardless of your own personal views on this topic, it seems that naps are effective in easing fatigue, increasing our concentration, improving mood and even reaction times. Interestingly enough, even a relatively short nap of 10 minutes has been shown to improve alertness and decrease feelings of fatigue. Moreover, the positive effects were more immediate than for short (e.g. 10 minutes) compared to longer naps (e.g. 30 minutes). On a more practical level, there is evidence to suggest that a 15-minute nap could help reduce the number of road accidents.

It is key to remember that napping is a broad term. The short periods of sleep, typically during the day, which we call naps can vary in their duration and in the type of sleep which an individual might get. This could start to explain why some people love to nap and others despise it, but more on that later.

Great, so we should all be trying to sneak a nap in during office hours? Well you might want to think about the time at which you take a brief trip into sleep. During the average day, we tend to have a post-lunch dip in concentration and energy which lasts from around 1pm-4pm. Research has found that naps, whether brief or long, are most effective when taken during this post-lunch dip.

At this point, it looks like napping, albeit at the right time, can have some benefits. Yet, why might some people not actually end up benefiting? There are two possible explanations for this.

One is that disgruntled nappers may sleep for too long and focus on the grogginess upon awakening. The longer an individual naps for, the more likely they are to feel sluggish upon awakening – also referred to as sleep inertia. The positive effects of longer naps are felt for longer, but it takes longer for them to be realised.

Another explanation may depend on how serious nappers are about well… napping! Those who have more experience with napping were found to benefit more from a brief nap than those who don’t nap. This suggests that napping might have a greater effect for those who do it more frequently. Then again, it may simply be that habitual nappers are habitual because of the fact they benefit from those short slumbers. Rather than experience, it may just be individual differences. This is a question we don’t have the answer to quite yet before you try to discipline yourself into daily naps!

So what’s the verdict overall? Napping can be beneficial and if you can work through the sleep inertia longer naps will have a longer effect on your functioning. That been said, even naps as short as 10 minutes can have a positive impact. There are individual differences in our response to napping but that shouldn’t hinder us from feeling rested. Napping may be useful to ease fatigue but the ideal way to manage daytime sleepiness is to make sure you are getting better quality sleep during the night. Naps should not be a substitute for poor sleep if it can be helped!

One more thing…

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Time for ‘shameless plug time’. I am volunteering with the Manchester Science Festival as part of their sleep installation known as the Chronarium. It aims to immerse participants in specially selected lights and sounds which are used to promote relaxation and sleep. Would-be nappers are suspended in sturdy hammocks and are gently rocked into a peaceful state while the hustle and bustle of the busy shopping centre outside the fabric walls feels like a distant world.

The Chronarium is currently open as part of the Manchester Science Festival and can be found in the Manchester Arndale Centre. It is open until the 30th October. For those Mancunion readers amongst you, it’s free entry and well worth trying out!

Inquisitive Tortoise

References:

Tietzel, A. J., & Lack, L. C. (2002). The recuperative value of brief and ultra‐brief naps on alertness and cognitive performance. Journal of sleep research, 11(3), 213-218.

Brooks, A., & Lack, L. (2006). A brief afternoon nap following nocturnal sleep restriction: which nap duration is most recuperative?. SLEEP-NEW YORK THEN WESTCHESTER-, 29(6), 831.

Reyner, L. A., & Horne, J. A. (1997). Suppression of sleepiness in drivers: combination of caffeine with a short nap. Psychophysiology, 34(6), 721-725.

For more info on the Chronarium:

The Chronarium Sleep Lab

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Can a Lack of Sleep Kill You?

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“Have you forgotten so easily?” the subject asked. “We are you. We are the madness that lurks within you all, begging to be free at every moment in your deepest animal mind. We are what you hide from in your beds every night. We are what you sedate into silence and paralysis when you go to the nocturnal haven where we cannot tread.”

Surviving participant from ‘The Russian Sleep Experiment’ in the late 1940s. This volunteer went 15 days without sleep.

Before you start looking over your shoulder for the demonic presence presented above, don’t be alarmed. The quote above is from a piece of horror fiction from a website called Creepy Pasta and is completely fake. I hope.

I wanted to start with this as Halloween is fast approaching and I thought that a more fiendish sleep myth was worth looking at. Can a lack of sleep be directly responsible for your death?

A complete lack of sleep is something new parents and those of us with upcoming deadlines may know all too well. It’s draining, depressing, and leaves us eyeing up any available floor space as prime real-estate for your exhausted brain and body.

We have already looked at the effects of getting too little or too much sleep in my earlier post, but not the more extreme side of this. Research conducted with animals at the end of the 19th and the start of the 20th century suggests that not only is sleep important, but that it is vital for sustaining life. In experiments which looked at puppies, cats and rats, it was found that after anything from a few days to around a month of no to very little sleep would lead to death in these animals. This should be taken with a pinch of salt as animals tend to have to be forced to stay awake, and this is typically through stressful contraptions.

How about humans though? What is the longest any one has gone without sleep and gone on to tell the tale?

Well there are two main sources which we can look at. Firstly, there are the people who have willingly deprived themselves of sleep and secondly we can look at people who no longer sleep. Starting with those strange souls who willingly deprive themselves of shut-eye we can look towards a reality TV-show, our trusty sleep-deprived student population, and a couple of radio DJs to start to answer this question.

People are seemingly keen to show off their endurance when it comes to neglecting or overindulging in the necessities of life. Some will do it to win a fabulous prize and others because… Well I’m sure they know why they do it. Anyway, one such contest is relevant here.

The reality TV show ‘Shattered’ provided contestants a chance to win £100,000. All they had to do was be the last one standing in a competition to stay awake the longest. The show was screened on channel 4 in 2004 and its questionable premise didn’t put off a group of eager participants keen to deprive themselves of sleep for fame and glory. The winner stayed awake ultimately for 178 hours. The show capped the length of time participants could remain awake for, and a number of increasingly soporific tasks eventually weeded out one overall victor. If you are interested in this ‘experiment’ you can watch it here.

However, 178 hours was meagre compared to the next contenders. It seems that at the end of the 1950s and early 1960s there was a surge in radio DJs attempting to promote themselves and further their careers in bizarre ways. Collectively they felt that staying awake and parading their increasingly fatigued selves in a department store window was the way to do this.

Our first member of the media to tackle a lack of sleep was a young radio announcer referred to as W.A. He managed to stay awake for a total of 220 hours or just over 9 days. Previously, another radio DJ by the name of Peter Tripp had managed to last 201 hours without sleep. Finally, our last radio DJ, Tom Rounds, shortly after moving to Honolulu in 1959, managed to stay awake for 260 hours and appeared to suffer no long-term effects of his sleep deprivation.

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Is sleep necessary for sustaining life?

However, their collective records did not last long. The radio DJs were swiftly beaten in 1964 by the efforts of a student called Randy Gardener. Randy was a 17 years old student who felt that he could provide something more interesting than a papier-mâché volcano to present at his school’s science fair. He went without sleep for 264.4 hours, which equates to about 11 days and 24 minutes, and supposedly suffered no long-term problems. The often cited report claims that Randy suffered no ill effects of his experiment, yet others claim he experienced hallucinations, paranoia, fluctuations in mood, and problems in short term memory and concentration. The latter would fit with what we know about acute sleep disturbances (Petrovsky et al. 2014; Kahn-Greene et al., 2007).

Interesting, there have been reports of others having seemingly beaten Randy’s record and by a sizeable margin. These have not been validated in part due to scientists and those responsible for recording ‘world records’ not wanting to encourage these record attempts. For example, the Guinness Book of World Records no longer prints updates to the sleep deprivation record since Randy Gardener.

Okay, so far it looks like we can go a long time without sleep and survive. This seems to suggest that although we need sleep (try not sleeping tonight if you’re not convinced), an acute loss is not going to be directly responsible for your demise (but likely indirectly).

Let’s move to the second source of human sleep loss evidence now: those who no longer possess the ability to sleep.

We’ve already looked at people who for one reason or another have decided to willingly deprive themselves of sleep. Yet, for some the ability to sleep is lost. Although insomnia fits this bill, in this case we are referring to the rare genetic brain disease known as Fatal Familial Insomnia (FFI). As the name suggests, this disease is associated with a prolonged and severe insomnia which ultimately leads to death. There are some experimental treatments to delay the fatal consequences but these may only provide a couple of extra years at best.

Fatal familial insomnia is a prion disease. Prions are misfolded proteins that cause damage to the brain as they clump together. In the case of FFI, these prions clump at a specific part of the brain known as the thalamus. The thalamus plays a prominent role in regulating sleep and in coordinating the brain as it drifts deeper and deeper in somnolence. As a result, as the damage to the thalamus accumulates this unsurprisingly leads to worsening insomnia.

These individuals seemingly sleep very little or not at all and will survive from a few months to about several years following the presentation of symptoms. The course of this illness would suggest that it is possible to die from sleep deprivation, at least at extreme durations. However, we can’t say that it is the complete lack of sleep alone which kills those with FFI as damage to the thalamus affects other functions rather than just sleep. Moreover, as this disease is so rare that it would be wrong to make a firm conclusion based on this alone. More likely, it seems that the lack of sleep contributes significantly, but not completely, to the decline of those with this illness.

So, what’s the verdict on sleep deprivation being capable of deadly consequences?

The research in animals suggests it can be but the human studies tell another story. Although common myths and horror stories might like to toy with our inbuilt fears about the unknown, it looks like a lack of sleep will not directly lead to your death. Instead, the host of effects already covered may be the true driver between mortality and sleep loss.

Inquisitive Tortoise

References:

Luby, E. D., Frohman, C. E., Grisell, J. L., Lenzo, J. E., & Gottlieb, J. S. (1960). Sleep deprivation: effects on behavior, thinking, motor performance, and biological energy transfer systems. Psychosomatic Medicine, 22(3), 182-192.

Petrovsky, N., Ettinger, U., Hill, A., Frenzel, L., Meyhöfer, I., Wagner, M., … & Kumari, V. (2014). Sleep deprivation disrupts prepulse inhibition and induces psychosis-like symptoms in healthy humans. The Journal of Neuroscience, 34(27), 9134-9140.

** http://creepypasta.wikia.com/wiki/The_Russian_Sleep_Experiment

**In case you find yourself wanting to read the rest of the fictitious foray into the effects of sleep deprivation.

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Why Do We Sleep? Keeping Those Pesky Excitable Neurons in Line

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“The subject of sleeplessness is once more under public discussion. The hurry and excitement of modern life is quite correctly held to be responsible for much of the insomnia of which we hear: and most of the articles and letters are full of good advice to live more quietly and of platitudes concerning the harmfulness of rush and worry. The pity of it is that so many people are unable to follow this good advice and are obliged to lead a life of anxiety and high tension. Hence the search for some sovereign panacea…” (British Medical Journal, SEPT. 29, 1894, Sleeplessness)

I am sure until you glanced at the date you could easily be forgiven for thinking this quotation was written only last week. The disturbance of “modern life” is far from a novel phenomenon that plagues the 21st century, and smartphones and technology cannot be solely to blame for the problems we see. As the quotation continues (you can read the full article here, page 719), it is clear that attempts to treat insomnia were not all that different from remedies people might turn to now.

Disturbed sleep is something we’ve all experienced at one point or another. That sleepless night before an important meeting, interview, or exam stress leaves us feeling groggy, less responsive, and annoyingly less prepared for the problem we have to face. It’s clear that even a night of poor sleep can cause a plethora of problems which make restoration theories of sleep enticing and convincing. However, it is still not certain how sleep might rectify the impaired functioning associated with a night of tossing and turning in bed.

One theory argues that sleep acts to quieten down brain activity which becomes increasingly noisy during the day. This ‘noise’ makes it harder to function in terms of laying down new memories, remaining vigilant, and maintaining a positive mood. There are plenty of studies which highlight problems in each of these areas following poor, or a complete absence of, sleep for even a single night.

Now, the brain is a noisy organ and is constantly busy keeping you alive and functioning. Even when you’re not ‘thinking’ anything, it is still possible to detect a network of activity associated with this resting state. However, when ‘noisy’ is used here, it is in reference to noise which may be more indiscriminate and impede normal brain functioning.

Synaptic Homeostasis Hypothesis

This theory is known as the synaptic homeostasis hypothesis and was put forward in 2003 by the psychiatrist, Dr. Giulio Tononi of the University of Wisconsin-Madison. This theory centres on the important role of slow wave sleep (SWS) during a night’s sleep. SWS is the predominant neural signal found during the third stage of NREM sleep, and is characterised by slow-synchronised oscillations across the cortex. It is associated with the deepest stage of sleep and with many restorative properties of sleep.

A paper by Christoph Nissen and colleagues, published just this week in Nature Communications, has shed more light on how sleep may help us function on a day to day basis, and has provided further support for the synaptic homeostasis hypothesis. Currently, most of the evidence for this theory comes from animal studies and indirect evidence from a handful of human studies. That is what made the recent study by Nissen particularly exciting.

Christoph Nissen and colleagues at the University of Freiburg explored how sleep, compared to sleep deprivation, was associated with changes in memory encoding, cortical excitability and neural mechanisms behind brain plasticity and learning. They examined a group of 20 healthy university students who all took part in the normal sleep and sleep deprivation portions of the experiment.

The team examined cortical excitability following a normal night’s sleep and sleep deprivation using transcranial magnetic stimulation (TMS) to induce a twitch in a participant’s hand. The TMS device allows scientists to deliver a pulse which can be used to inhibit or excite the neurons underneath its coil. A pulse to the appropriate location on the right side of the brain will produce a corresponding twitch to the muscle in the participant’s left hand. The strength of the pulse needed to produce a response, or twitch, can be used as a marker of how excitable that particular patch of neurons is. As a result, this technique provides a non-invasive and relatively simple way to test one of the synaptic homeostasis hypothesis’ predictions.

In addition, the group examined brain activity using electroencephalography (EEG) to further explore alterations produced by extended wakefulness.They also tested performance by examining participant’s memory through the use of a simple word pair test, and through their capacity for LTP-like plasticity using a paired stimulation method.  LTP, or long-term potentiation to give it its full name, has been argued to be the mechanism within the nervous system through which learning occurs. It is argued to play a large role in memory formation and so provides the researchers with another way to assess performance following extended wakefulness or sleep.

In their student sample, Nissen and colleagues found evidence of increased cortical excitability, poorer memory performance, and reduced LTP-like plasticity following a night of sleep deprivation compared to wakefulness. All of these support the synaptic homeostasis hypothesis and support the role of sleep in ‘resetting’ the neural activity to a baseline. It is argued that this is what allows us to continue on at our best after a night’s sleep and allows us to start efficiently storing memories of cute animal videos while at work.

Yet, the evidence for this is still in its infancy and it would be unwise to jump to conclusions about this research. Rather, it is another hat to throw into the ring of sleep science.

This work is still just a start, but it is an interesting and exciting foray into further understanding how sleep serves its important role in our lives. Furthermore, it also provides some interesting avenues for therapies which might try to capitalise on the ability of sleep to return neural activity to a set-point. There is already some evidence to support short-term sleep deprivation to help depression. A further understanding of sleep’s impact on the brain, or lack thereof, may help us manipulate this to our advantage.

Inquisitive Tortoise

References:

Kuhn, M. et al. Sleep recalibrates homeostatic and associative synaptic plasticity in the human cortex. Nat. Commun. 7:12455

Tononi, G., & Cirelli, C. (2003). Sleep and synaptic homeostasis: a hypothesis. Brain research bulletin, 62(2), 143-150.

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Why Do We Sleep? The Brain’s Waste Disposal System

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How does sleep help this fellow’s tubular brain remain healthy?

“Okay, smart guy so why do we sleep then? Bet you can’t answer that one…”

“Well… How long have you got? There’s a fair bit of content to co- Hey! Don’t run away! It won’t take me that long, honest!”

Sleep is complex and despite the intuitive explanation for why we drift off on a daily basis, we are still in our infancy when it comes to understanding how and why this occurs. We know that for the most part a good night’s sleep is refreshing and important for paying attention at work, school, or carrying out most tasks.However, how sleep keeps us functioning is less black and white.

There is no one reason why we need to sleep. For example, it maintains us mentally and physically in a number of ways, including:

  • Memory consolidation
  • Growth
  • Mental health
  • Brain maintenance

We could spend a lot of time covering all of these in considerable detail, but for now we’ll look at brain maintenance. Brain maintenance may seem like a broad category but it fits into our recent developments in understanding how the brain deals with waste materials.

The Brain’s Waste Disposal System

All cells in the body produce waste products of some description. This may be as a result of metabolic functioning, protein synthesis, and cell death, and these are filtered out via the lymphatic system.

The brain, unsurprisingly, is no different. However, until recently it was not clear how the brain solved this waste management problem. That was until the recent discovery of the glymphatic system.

Glymphatic System: The Brain’s Clearance System?

So what is the glymphatic system, and why should we care? Well firstly, its discovery has been hailed as important step in understanding major neuropathologies such as Alzheimer’s disease. Although, there’s a while to go before we should get too excited about this.

As mentioned above, the cells within your body work and produce potentially toxic waste products. The body has an effective way of getting rid of these through multitudinous lymphatic vessels. Yet, until recently it wasn’t known how the central nervous system, that is the spinal cord and the brain, manage to remove their waste products.

In a similar way to the lymphatic system, it has been proposed than the glymphatic system works by removing waste products from the central nervous system (e.g. spinal cord and brain). This is achieved, in part, by the exchange of solutes or waste products between cerebrospinal fluid (CSF) and interstitial fluid (ISF).

The system is comprised of a series of channels which appears to “piggyback” off blood vessels within the brain. It is argued that the movement of arteries, as a result of blood-flow, helps to move the cerebrospinal fluid through the brain (CSF). This enables the movements of waste between interstitial fluid (ISF) which bathes cells and CSF which runs alongside blood vessels in the brain. However, the glymphatic system also includes the presence of specific glial cells, known as astrocytes, alongside these channels. The function of the astrocytes is to facilitate the movement of particles between CSF and ISF. Without their presence, the movement of waste would be too sluggish to respond appropriately to the changing demands of the hungry organ we call the brain. It is the presence of glial cells, and the similarities to the lymphatic system, which give this glymphatic system its name.

Waste Disposal While You Sleep

How does all of this relate to sleep? Well, a recent collection of studies has provided some evidence that sleep may facilitate the movement of toxins from the brain via the increased activity of the glymphatic system.

One particular toxin produced as a waste product of brain cell activity is called amyloid beta. This toxin is linked to severe progressive diseases such as Alzheimer’s, and there is considerable research trying to work out how to mitigate its destructive effects. Last year, a group of scientists lead by Professor Maiken Nedergaard at the University of Rochester Medical Centre found that the brain’s drainage of amyloid beta was increased during sleep and anaesthesia-induced unconsciousness compared to during wakefulness in mice. More specifically, it seems that the capacity of the brain to flush out such harmful toxins is enhanced due to the area between cells, interstitial space, expanding by as much as 60 per cent. This seemingly enables a greater opportunity for such toxins to be removed via the glymphatic system.

In addition, the same group also found earlier this year that this process of washing harmful toxins out of the brain during sleep is enhanced based on the position of the mice studied. It was found that the removal of amyloid beta was enhanced when the mice slept on their side rather than their back. Interestingly, in both cases, it seems that anaesthetised mice showed the same effects as sleeping mice for the removal of amyloid beta and benefit of sleep posture.

This suggests that sleep may help with the maintenance of our brains by enhancing the waste disposal system we have in place. It may also provide some evidence as to why dementia and serious psychiatric illnesses are associated with sleep disturbances prior to the emergence of symptoms. However, this is all speculative and uncertain at this point. For a start, these studies have only been conducted on mice, and due to the nature of the experiment it is not likely that they would be conducted on humans any time soon. That’s not to say that the same mechanism might not be occurring within humans, but it is rash to jump the gun and assume it is.

Regardless, it will be exciting to see how research in this area advances and what it can teach us about the importance of sleep.

Inquisitive Tortoise

References:

Lee, H., Xie, L., Yu, M., Kang, H., Feng, T., Deane, R., … & Benveniste, H. (2015). The effect of body posture on brain glymphatic transport. The Journal of Neuroscience, 35(31), 11034-11044.

Xie, L., Kang, H., Xu, Q., Chen, M. J., Liao, Y., Thiyagarajan, M., … & Takano, T. (2013). Sleep drives metabolite clearance from the adult brain.science, 342(6156), 373-377.

Further Reading:

https://www.urmc.rochester.edu/labs/Nedergaard-Lab/projects/glymphatic_system (From the horse’s mouth; a better description of what I’ve tried to convey in this post!)

Image Credits:

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Filed under Psychology, Sleep Science

Sleep Roundup 12/07/16

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So, being the geek that I am I come across lots of interesting sleep talks online and resources which help me with my day to day research. Here’s a roundup of the current sleep talks / podcasts online over this past week or so which grabbed my attention.

This may become a regular thing if I find enough interesting sleep research / talks (organisation permitting, no doubt).

For now enjoy two the latest episode of the Infinite Monkey Cage which is focused on sleep in general and How Much Sleep Do We Need from the BBC. Also, if you don’t already listen to the infinite monkey cage, do so now!

Inquisitive Tortoise

 

 

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Filed under General Interest, Media, Sleep Science