Have you considered sleep with that? How global warming may stop us getting a good night’s sleep

Insomnia and Heat

When we think about increasing global temperatures we tend to think melting ice caps, flooding, and conspiracy theorists who believe scientists (or the Chinese) make this stuff up to exert some unknown power and influence. However, the temperature at night has a direct influence on the quality of our sleep too. So, I’m back to talking about sleep again (the sigh of relief from my adoring crowd is audible – thank you). A recent paper, published in Science, has shown that global warming will not just have an effect on political alliances but also on our sleep. Trump, take note.

The premise of the recent paper, by Dr Nick Obradovich and colleagues, is a simple but profound one. As the summer months trundle on by (and yes, we get some occasional sunshine here in the UK too) you are probably acutely aware of the nightly sojourn to bed and futile attempts at sleep in the oppressive heat. Unless you have the advantage of a trusty fan or even a hint of a breeze outside you know you are going to toss, turn, and throw the covers around until you eventually nod off for a few fragmented hours. Temperature has an evident ability on our ability to get to sleep. This is shown clearly when we consider the changes in body temperature throughout a typical night. As we drift off our body temperature reduces and remains lowered during the sleep period until we wake up. At this point, it starts to rise again helping to improve alertness during the day. This pattern, or circadian rhythm, is no accident – it helps to send us off to sleep. This rise and fall is important and if we increase our temperature too much (e.g. lying in a particularly stuffy room) then we delay the time at which we drop off and are more likely to wake up during the night.

It is this quirk that a research group explored in relation to global warming. In light of what we know, will the increase in global temperature negatively influence our sleep? We can assess this by looking at unseasonably hot days during a month and correlate this with the reported number of nights of poor sleep in the population. This is exactly what Obradovich and colleagues did. They assessed the temperature changes from the average in a number of cities across the US and identified the sleep habits of hundreds of thousands of respondents to a large survey assessing health and disease. They controlled for potential confounders and found that as the temperature increased from the average, for any given month, that there was an increase in reports of nights with disturbed sleep. In fact, as the temperature rises then so does the number of disturbed nights of sleep. When the group compared low and high earners and young and old populations they found that those who were poorer and older tended to suffer more from the effects of temperatures spikes. Finally, as would be expected, they found that these effects were only significant when they looked at the summer months.

This highlighted largely what we already know: that temperature negatively impacts on sleep quality by interfering with the normal process of drifting to sleep. However, the interesting point comes from the next finding of their study. They identified the predicted increases in global temperature until the end of the century from NASA. They then plugged in these values from the first part of the study to identify the effect of increasing temperatures of the number of nights sleep loss until the end of the century. Somewhat worryingly, they found that over the next century the number of nights poor sleep increases in line with the increases in temperature in part due to global warming and climate change. This has implication for physical and mental health which has consistently been tied to the quality and duration of our sleep.

It is important to note that there are plenty of caveats to this study. For example, its indirect and correlational measure of sleep and temperature should raise some concerns about the validity of the findings. Furthermore, it’s important to note that sleep was assessed with a single self-report question, “During the past 30 days, for about how many days have you felt you did not get enough rest or sleep?”. As the authors suggest, further experimental data is needed to back up their claims.  However, the findings from this study do fall in line with what we already know about the effect of temperature on sleep. It is not a stretch to claim that global warming, ignoring other external factors, will have a negative impact on our sleep. There are of course ways to mitigate the negative effects of increasing global temperature but this study also accounted for that. The poorest and oldest stand to suffer most as they cannot afford to keep air conditioning running all night. Therefore, although this is one admittedly large-scale study there is still additional research which needs to further understand the true impact our warming climate will have on our sleep and subsequent health. For the time being, it raises an important reminder that the effects of global warming are far reaching and ignoring the clear evidence for its existent is nothing short of irresponsible and short-sighted. Again, take note Mr. President.

Image Credit:

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References:

Obradovich, N., Migliorini, R., Mednick, S. C., & Fowler, J. H. (2017). Nighttime temperature and human sleep loss in a changing climate. Science Advances, 3(5), e1601555.

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Filed under Media, Politics, Psychology, Sleep Science, Work and Society

The Human Microbiome: A Teeming Ecosystem Within Your Own Body

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Meet the neighbours: here’s Paul, Sandra, Jack, Lily, and so on and so on

“Why have you stopped speaking about sleep?”

“I can have other interests!”

“I don’t know man, you’ve changed. Why should I care about anything you have to say now?”

“…”

What is a microbiome? That’s a very good question. For a start, it’s not some artificial eco-project which is attempting to save the world or even, I’m sorry to disappoint you, some form of miniaturised food either. The microbiome refers to the different ecosystems of microbes which we have all over our body. These microbes use us as their home and in turn can benefit us, live mutually alongside us, or cause us problems. They form a complex and important addition to the multitude of cells which make up our own bodies and recent estimates suggest there are as many microbial cells as there are cells which make us up. One particularly well studied microbiome requires us to get to the bowels of every one of us. Quite literally. This ecosystem is the one we find in the human gut. This microbiome has also attracted a lot of interest because of its impact on the brain known as the gut-brain axis (more of this in the next article). In general, microbiome research is still in its infancy and everyone wants a piece of it. This is likely because it seems to play an important role in a number of different mental and physical functions and there is even talk of this ecosystem containing our ‘second genome’. So, what does this all really mean and why should we care?

The ecosystem of microbes (e.g. bacteria, fungi and viruses) which live alongside us help to break down food, protect us from invaders and produce nutrients necessary for our health. One good example of the benefits of the gut microbiome is evident in looking at babies and breast milk. There is a particular group of complex sugars known as human milk oligosaccharides (HMOs) which make up a considerable amount of breast milk. However, despite their prevalence in mother’s milk babies do not have the ability to break them down. This should make them rather useless to the baby and a waste of resources for the already energy-stretched mother. Indeed, this finding initially stumped scientists as breast milk has evolved to be the perfect nutrition for an infant – why should it contain something a baby cannot digest? However, it seems that a specific HMO, B. infantis, in the infant’s gut is the intended target of this sugar instead. B. infantis can break down the complex sugar and in turn flourish in its presence. Why is this a good thing? Well it is hypothesised that the healthy colony of B. infantis force out more harmful bacteria from making their home in the infant and act as decoys for potential pathogens keen on harming the bleary eyed newborn. Moreover, this rather nifty bacterium promotes gut health and has anti-inflammatory properties. The mother’s breast milk helps ensure this positive bacterium survives and in turn the bacterium ensures the baby is more likely to survive.

How about in adulthood though? What are some of the functions of our microbiomes scattered around our body? Well the ‘second genome’ seems to play an important role in our behaviour and health. For example, in a series of experiments which looked at the effects of transferring human bacteria from obese and lean twins to germ-free mice. The researchers found that when the mice were given the bacteria from the lean twin they stayed the same weight; however, when the bacteria were from an obese twin they gained weight. This is despite the mice all being given the same amount of food to eat. Furthermore, it seems that lean mice which live together with obese mice have the capacity to transfer their ‘healthy’ microbiome. Yet, the obese mice could not transfer their bacteria to the lean mice. This, it is argued, was because the obese mice have a lower diversity of bacteria within their gut microbiome and this leaves space for new species (found in the lean mice) to colonise and flourish. The bacteria of the lean mice tend to win in these situations. However, the positive effect of the transfer of bacteria on the obese mice is not universal. It requires that the obese mice have the right diet in the first place. If the obese mice were fed a westernised diet high in junk food and saturated fats then the positive impact of the bacteria from lean mice was non-existent. The positive effect was seen only if the obese mice were eating a healthier diet from the start. It could be speculated that this is because the high-fat diet does not promote the survival of the bacteria found in the lean mice’s gut. This opens up the exciting possibility that our gut bacteria are having an important role in our weight and health. It is possible that a particular diet might be able to promote the colonisation of new species of bacteria within our microbiome and, in turn, help promote weight-loss.

The human microbiome has also been linked to illnesses characterised by disruption of the normal functioning of the immune system. It has been argued that autoimmune conditions such as crohn’s disease and ulcerative colitis may be linked to a failure of the gut microbiome to develop appropriately during childhood. It’s claimed that this is because of the increased use of antibiotics and high-fat, low-fibre, diets which characterise the western world. The presence of these environmental factors reduces the diversity of the gut microbiome and interferes with the normal process of teaching the immune system how to function. In addition, certain species of bacteria appear to have anti-inflammatory effects which researchers are trying to capitalise on as treatment possibilities for inflammatory bowel diseases (IBD).

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Understanding the gut microbiome holds promise for the treatment of IBD.

So, it looks like the gut microbiome can have profound effects on our health. With this in mind, can we change our gut bacteria? Well, there are a lot of potential problems with this. Our gut microbiome seems to be influenced by the microbes which our mother and father impart upon us at birth (particularly from our mother). However, during infancy we go through a fluctuating development of our microbiota and the constituent microbes change considerably as we progress to adulthood. This is why some researchers believe that it is during early childhood that any attempts to modify the microbiome will be most effective. It is during this period of flux for our plucky neighbours that attempts to modify the microbiome are likely to be most effective and long-lasting. If there is a link between our gut microbiome and autoimmune disorders it is likely that this stage of our development is critical to reduce the risk of IBD. However, during adulthood there is more stability of our microbiome. The gut microbiome appears resilient to change following diet in the short-term but it is possible that long-term dietary changes might create a more favourable environment for new microbial species. For example, when the initial gut bacteria colonise an area they change the environment so it is more beneficial to their survival compared to other species. Therefore, although there is an obvious benefit to improving our diet, whether this boosts our microbiome is not quite known yet.

The human microbiome is not confined to our guts but our mouths, throats, noses, genitals and skin, to name but a few, are also examples of microbiota within the human body. For example, we contain our own signature of gut bacteria on our hands although there is considerable variation between individuals and even between our own two hands. It is not known exactly what is responsible for this variation but a mixture of genetic and environmental (e.g. hand-washing, climate, sex, etc.) factors seem to be important. It is also possible to shift the microbial constitution of someone else’s hand through direct contact – a handshake. How long the changes remain, however, is not clear and it is likely that the ecosystem carved out by your own skin microbiome favours the microbes usually residing on and in your skin. This is perhaps something to keep in mind when meeting your hero and desperately trying to shake their hand. It may be that greatness can rub off on others through a firm handshake. Also, in a similar manner to the gut microbiome, the composition of microbes on the skin has also been linked to health and disease. A good example of this is psoriasis which involves the development of plaques on the skin of those affected. In a similar manner to the gut microbiome, it is likely that a wider diversity of the skin microbiome has anti-inflammatory properties which are protective against auto-immune disorders such as psoriasis.

So, does this mean that all of us need to alter our eating habits to ensure that our gut bacteria are working at their best? Probably not for the time being. This is the nature of any research in its infancy and beware of any book or news article which claims that changing your microbiome through diet will improve your health. Despite all the excitement surrounding the microbiome at the moment we need to be aware of the limitations of research which seems to be ‘in vogue’. There is plenty of high-quality research which is being carried out in this area but much of this research is conducted in mice and the human research is largely correlational. It’s currently difficult to infer cause and effect – does poor health causes changes in our microbiome or vice-versa or, more likely, is it a mixture of the two? We need to be aware of how little we really know about the microbiome at this current moment. For example, we don’t know what a healthy microbiome looks like. Is there one individual ‘optimal’ combination of microbes to strive for or is it that a greater diversity, in general, is best? There seems to be some evidence of ‘types’ of stable microbiomes in adults but this work is still in development. There is also some evidence which links a healthier, fibre-rich, diet to a greater diversity of microbes within the gut microbiome but it is unclear what impact this has on health and behaviour. Currently, the Human Microbiome Project is trying to understand what the normal limits of the microbial ecosystems look like and how they might be implicated in health and disease. Although they started in 2008 and have received considerable funding there is still a long way to go before we see these findings directly influencing health. There is plenty of excitement about the microbiome but it is still early days for this field. For now, the human microbiome holds a plethora of secrets yet to be unlocked about the teeming, fluctuating, and enigmatic organisms we share our body with.

Image Credits:

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References / Recommended Reading:

http://www.nature.com/news/bacteria-from-lean-cage-mates-help-mice-stay-slim-1.13693#/ref-link-1

https://www.nature.com/articles/srep32484

http://www.nytimes.com/2013/05/19/magazine/say-hello-to-the-100-trillion-bacteria-that-make-up-your-microbiome.html

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535073/

https://www.nature.com/cti/journal/v5/n4/full/cti201612a.html

http://www.nature.com/news/scientists-bust-myth-that-our-bodies-have-more-bacteria-than-human-cells-1.19136

http://hmpdacc.org/ (Human Microbiome Project Website)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3577372/

https://www.ncbi.nlm.nih.gov/pubmed/20668239/

http://www.newyorker.com/tech/elements/breast-feeding-the-microbiome (An extract from the amazing Ed Yong’s book, ‘I contain multitudes’)

http://www.radiolab.org/story/funky-hand-jive/ (A hilarious and brilliant podcast on this topic)

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Filed under General Interest, IBD, Microbiome, Psychology

How can escaping into virtual reality improve healthcare?

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You slowly creep towards the door while being acutely aware that the slightest sound will get you caught. As you reach for the handle and steadily open the large wooden door you hear a slight creak. Suddenly, the expansive and exposed wall to your right explodes in a flurry of shrapnel, wallpaper and dust. A figure starts to emerge from the wound in the wall and stares directly at you with a terrifying smile. You’ve been found out…

Virtual reality isn’t always quite so terrifying but the above example reminds us that the virtual world has the capacity to make us believe what is thrust directly in front of us. The fear is real and the experience is one which mimics the experience of navigating a trap ridden residence. Besides terrifying us and fuelling visions of humanity being locked in a virtual world to escape the real one, what is the future of virtual reality? Well, one emerging area appears to be concerned with improving mental health.

Use of virtual reality to treat mental health difficulties

Psychosis, a cardinal symptom of schizophrenia, is the presence of delusions and hallucinations which can cause considerable distress. Delusions can take many forms and the nature of these seem to be tied to the diagnosis present (e.g. bipolar disorder, depression or schizophrenia). One delusion common to those diagnosed with schizophrenia is paranoia which can, understandably, cause significant distress and impairment in an individual’s life. However, what if we could challenge the paranoid thoughts of those experiencing psychosis and illustrate their unfounded nature? A real-world setting is likely to be too anxiety-provoking for obvious reasons but what if we could recreate paranoia-inducing environments in the relative safety of virtual reality?

This is exactly what a group at the University of Oxford led by Professor Daniel Freeman has explored in their study for the British Journal of Psychiatry last year. They exposed individuals with persecutory delusions (e.g. paranoid thoughts) to one of two mock real-life setting through virtual reality and asked them to do one of two things. One group was simply exposed to the virtual environment and asked to simply experience the situation. The effect of this on their their paranoia was assessed. The second group, by contrast, was asked to drop their guard, stop using their safety behaviours, and actively put their paranoid thoughts to the test (e.g. Do people in this environment see me as an easy target and do they actually do things to belittle me?). This second condition was known as the cognitive therapy group as they were encouraged to actively re-evaluate their delusions in the safe confines of the virtual environment.

There were 30 participants tested and they were randomised to either an exposure or cognitive therapy condition. They were tested in a real-life setting initially, then gradually introduced to the virtual reality environment, and then finally tested in the real life setting once again. At each point participants were tested before and after their immersion to either real-life or virtual reality on a scale assessing the conviction and distress of paranoid thoughts. As a test of ‘credibility’ the participants were also asked whether they believed the virtual reality setting would help them overcome their paranoid thoughts. Participants were tested in one of two different virtual reality settings. The first setting was a typical one for any Londoner: a tube journey. The second was a lift which the participant walked into and could inspect the other passengers.

So, what did they find? They found that there was a significant and large reduction in conviction and distress of delusions following the cognitive therapy group’s immersion into the virtual environments. Interestingly, these findings also carried over to the real-world setting. On average, they found a reduction in scores of around 20% for the cognitive therapy vs the exposure virtual reality condition. This suggested that getting individuals with paranoid delusions to test out their threat beliefs in a safe environment had the impact of reducing their paranoia. This should be considered in light of the difficulty to achieve this in a real life setting due to considerable anxiety and stress. This suggests that virtual reality is a simple and effective way to combat threat beliefs in paranoia.

However, this was only completed over a single day and the long-term impacts of using virtual reality is this way are currently unknown. Is there a dose-dependent effect of VR on threat beliefs? How long do the therapeutic gains last for? Are there individuals for whom this works better or worse? Are there any unintended side effects of using VR for multiple sessions in a patient population? And many other questions which remain to be answered. Psychosis is not the only field where virtual reality has started to prove its worth in treatment and research but anxiety, depression and eating disorders are also highlighted in the recent review by Professor Freeman earlier this year.

It should be noted that virtual reality is by no means only being realised within mental health but it is starting to be used extensively within physical healthcare too. VR provides an optimal way to train new surgeons, doctors, and nurses in medical procedures. This is what current research is exploring and virtual reality is only one avenue. Augmented reality is becoming more common and apps such as VR in the OR allow us to witness surgical procedures in an interactive manner from the comfort of your own home.

Basic Science and Mechanisms Research

So, there appears to be promise for using virtual reality as a way to deliver therapy but what about research more basic, mechanistic, research (e.g. what causes paranoid thinking in the first place)? Surely if we can create a convincing setting then we could start to study how threat beliefs are generated, in the case of psychosis, or understand what might reduce of exacerbate mental health difficulties in general. In an earlier study conducted in 2003, Prof. Freeman showed that paranoid thoughts could be seen in a virtual reality setting with healthy individuals. In their early foray into the use of VR they found that a small number of participants in their sample attributed hostility towards the avatars present in the environment. The researchers argued that this showed that VR could be used to study paranoia and provide a more realistic environment to test predictors of paranoia in a social setting.

Finally, because we can treat these virtual realities as realistic and convincing, they provide a great landscape in which to explore situations which might prove difficult for those at risk for certain mental illnesses. This allows researchers to test out hypotheses without unnecessarily exposing participants to a threatening situation, and with the ease of removing the headset instantly if the situation becomes distressing. For example, it would be possible to further probe the effect of sleep on mood and how this might contribute to mental health difficulties through the use of virtual reality. Now, as with any science, the worth of the study is not dependent on how flashy the toys are which are used but the strength of the research question and design. Although VR may strike some as flashy, it is useful in that it provides a way to recreate reality but in the controlled and safe confines of the lab. VR may currently be synonymous with jump scares and large price tags it is also being used to improve the health of the public. The widespread use of VR across healthcare settings is still a while off. For now, we shall just have to be content with scaring ourselves senseless with Resident Evil and other horror games.

References

Freeman, D., Bradley, J., Antley, A., Bourke, E., DeWeever, N., Evans, N., … & Slater, M. (2016). Virtual reality in the treatment of persecutory delusions: randomised controlled experimental study testing how to reduce delusional conviction. The British Journal of Psychiatry, 209 (1), 62-67.

Freeman, D., Reeve, S., Robinson, A., Ehlers, A., Clark, D., Spanlang, B., & Slater, M. (2017). Virtual reality in the assessment, understanding, and treatment of mental health disorders. Psychological Medicine, 1-8.

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Virtual Reality (Header)

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Filed under Psychology, Schizophrenia, Work and Society

Can we modify specific stages of sleep to improve our memory?

Sleeping Kitten

Our memory is far from perfect. You have probably gone into another room and completely forgot what you went in there for. You stare into space and hope it will come back to you. Was it to pick up keys, tidy something or speak to someone? Nope, it just doesn’t come and you walk back slightly dazed and annoyed at your ailing memory. This is just a small example of the times our memory fail us during our day-to-day lives. However, what if we could improve our memory while we sleep?

Sleep is important. I’d like to think that I’ve impressed on you all by now. It protects us from certain metabolic disorders, keeps us alert to our surroundings and maintains our mental health and overall mood. There is some evidence to suggest it helps the brain’s natural waste disposal systems but that’s still in its very early days (despite some bold claims in the mainstream media). All of these areas have garnered substantial interest from scientists but memory is the one we’ll be focusing on. Typically, studies show that our ability to lay down new memories improves after a simple nap or a good night’s sleep. This, of course, isn’t always practical but it provides us some insight into what is happening in the brain when we drift off. It also should remind anyone revising for exams that sacrificing sleep is a false economy – unless of course you need to cram. Sleep can only help you so far there.

The link between sleep and memory raises an interesting question: what is it about this period of seeming inactivity that may help improve our memory? Sleep is far from a unitary construct and if we could identify the specific stage or stages which are crucial for memory then perhaps we could capitalise on this. We go through different stages of sleep, broadly, broken down into Non-REM and REM, and these are made up of different brain cell oscillations (see picture below) within the brain. Through probing the different stages, we can start to understand which are more important for memory. So, what are some of the candidates for sleep’s role in memory? The main contenders are sleep spindles and slow wave sleep (although REM has also been claimed to play a role in memory too).

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Stages of sleep recorded from EEG

Sleep spindles are characteristic of sleep stage 2 and are brief bursts of activity seen when using a brain imaging device known as electroencephalography (EEG). Imagine one of the funny caps with electrodes protruding out as you probably have a good idea of the typically EEG setup. Sleep spindles have been claimed to be important for memory consolidation and form a key part of one of the main hypotheses for how sleep might boost our memory. More specifically, it is argued that sleep spindles may facilitate the movement of memories from temporary consolidation in a part of the brain known as the hippocampus to the rest of the brain. Interestingly, sleep spindle activity correlates with performance on memory recall following sleep, and spindles show an increase following learning. The activity location of the spindles seems to be associated with the location of brain activity engaged during intensive learning of a specific function. As a result, some have suggested that sleep spindle activity may be used as a marker for learning potential (Fogel & Smith, 2011). However, the reality is likely more complex than this. Nonetheless, it does point towards spindles as a potential marker of memory consolidation during sleep.

In addition, slow wave activity (SWA) has also been shown to be important for memory. These are the slow (1Hz) oscillations characteristic of deep sleep. It has been this stage of sleep which has primarily been targeted to improve memory in previous studies. More recently, slow wave activity and sleep spindles have been successfully modified through the use of electrical stimulation of the scalp, drugs, playing sounds throughout the night (specifically timed and not so loud as to wake the participants), and even by presenting odours present at the time words were initially memorised.  These manipulations have been shown to improve memory and it seems it does this by increasing the amount of slow wave activity and sleep spindles. This work, although still in its infancy, suggests that it possible to stimulate specific features of sleep and, in turn, improve a vital cognitive function. It is at this point that a recent study in the aptly titled journal ‘Sleep’ comes in.

A group at the University of Helsinki in March this year (https://www.ncbi.nlm.nih.gov/pubmed/28364428) built on these previous findings by trying to identify a way to automate this process of stimulating slow wave activity. The success of this aim would increase the ease of introducing this technique into a home-setting and allow for the modification of sleep coveniently. The group decided to try to find a way to target sound stimuli to slow waves automatically in the hope of improving specific types of memory without affecting the sleep quality or mood of the participant. This is crucial as it is little use improving memory and modifying sleep if it causes other problems at the same time.

How did the researchers attempt to automate this process? They recorded electrical activity from the brain during sleep and were able to identify slow wave activity automatically by looking out for a specific frequency band (i.e. how often a waveform occurs over a set period of time). Whenever slow wave activity, indicative of deep sleep, was identified in the sleeping participant, a computer program sent a message to another device which played a brief sound. This meant that the sound was played just after a period of slow wave activity. Following this, there was a break of least 2 seconds between each sound being played. The loudness of the noise was changed automatically in response to cues from the participant. For example, if it seemed that the participant was waking up then the sound was lowered.

With the system in place, a total of 15 participants were invited into the lab for three days, each day separated by a week, to test out the automated approach to increase slow wave activity. The first day involved a familiarisation night so that the participants could get used to sleeping in the lab and with the equipment setup. During day two, one half of the participants heard the automated sounds and the other half did not. This was then switched for the third and final day. This allowed the researchers to compare performance on memory tasks when the sounds were not played and when they were not.

So, what did they find? Firstly, and importantly, they showed that their automated enhancement of slow wave activity was successful and viable. It managed to increase slow wave activity and sleep spindles. Moreover, the automated sounds were also found to increase memory overnight. They showed that word-pairs could be enhanced by playing a relatively quiet sound during slow wave activity. The interesting outcome of this study is that the possibility of having an automated system which people could use at home to boost memory. For populations who have poor memory this could hold promise as a therapeutic tool. It is a while off anything like this being available but it tells us something about how sleep contributes to memory and the potential ways we can exploit this in the future.

Although it is still unclear how exactly sleep is linked to memory, it is research like this which is starting to uncover that our brains are anything but quiet during sleep. Although there is likely to be no device which will improve your memory overnight on the market any time soon, scientists are working on the concepts necessary for this to become a reality. For now, perhaps you could try writing down what you’re about to do before walking into a new room?

ResearchBlogging.org Leminen MM, Virkkala J, Saure E, Paajanen T, Zee PC, Santostasi G, Hublin C, Müller K, Porkka-Heiskanen T, Huotilainen M, & Paunio T (2017). Enhanced Memory Consolidation Via Automatic Sound Stimulation During Non-REM Sleep. Sleep, 40 (3) PMID: 28364428

Additional References

Fogel, S. M., & Smith, C. T. (2011). The function of the sleep spindle: a physiological index of intelligence and a mechanism for sleep-dependent memory consolidation. Neuroscience & Biobehavioral Reviews, 35(5), 1154-1165.

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Sleeping Cat (Header)

Sleep Stages (Body Text)

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Filed under General Interest, Memory, Psychology, Sleep Science

Trauma, Tetris and Memory: A Cheap Way to Reduce the Impact of Intrusive Memories

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What if I was to tell you that playing video games can be good for you? That despite derision and their use in political point scoring, games such as Tetris and Candy Crush could one day be used to help people deal with traumatic events in their lives? You might be initially sceptical but there is growing evidence to support this. Although not a new idea, Tetris has been shown to be useful in reducing the uncontrollable intrusions associated with a traumatic experience.

So, how can we use a video game such as Tetris to interfere with traumatic memories? Well, in much the same way that you would interfere with any memory. As you create a new memory and have converted all the constituent parts into a form which the brain can understand, it goes through a period of consolidation. That is where the memory is stored within your brain so you are able to recall it at a later point. Now if we interfere with the memory during this period of consolidation it is less likely that we will recall said memory. For example, if we can provide some competition for the neural real estate the original memory is vying for then we can weaken the strength of that original memory. It seems to be important that the type of memory is relatively specific and needs to match the original memory’s modality (e.g. a visual-spatial task needs another visual-spatial task to compete with it effectively). This is essentially where Tetris comes in. The authors argued that if both the trauma memory and Tetris rely on the same visual-spatial resources then you can reduce the intrusiveness of the initial trauma memory.

This is exactly what Emily Holmes at the University of Oxford and her collaborators found in studies conducted over the past eight years. If you ask a participant to play Tetris 30 minutes after a lab-controlled trauma induction you can reduce the impact of the traumatic memory compared to a control condition. These early studies showed that, at least in the lab, you could interfere with traumatic memories in a therapeutic way by reducing their intrusive nature. Although they were not carried out in a naturalistic setting they provided evidence that the proposed mechanism existed and could be manipulated. It is also key to keep in mind that this study showed that playing Tetris reduced specifically the intrusiveness of the traumatic memories and not the deliberate recall memory for the event. As the uncontrollable nature of the traumatic memory is a source of considerable distress in PTSD it is important that any intervention can have a targeted effect. What about evidence for the use of Tetris to deal with naturally occurring trauma outside of the lab? This is where their latest study, published in Molecular Psychiatry, last week comes into play (it’s open access so you can read the full article yourself here).

In a small-scale naturalistic study in Oxford, Emily Holmes, and colleagues at the Karolinska Institute in Sweden, examined individuals in A&E who had recently (within 6 hours) experienced a motor accident as a driver, passenger or pedestrian.  They randomised 71 eligible participants to either an intervention or control condition to test the real-life application of their previous findings. In the intervention condition, participants were asked to recall the traumatic event initially and to then spend at least 10 minutes (maximum 20 minutes) playing Tetris. By contrast, the control condition asked participants to write down all the activities they carried out during their time in A&E (e.g. completing a crossword, speaking to a friend, etc.). Participants were assessed at one week and one month following either the control or intervention task. During the initial week participants were required to complete a daily diary of the number of intrusive memories they experienced which were related to the trauma (e.g. motor accident). The participants were instructed not to report “memories recalled deliberately or general verbal thoughts”. The number of intrusions provided a primary way to assess the success of the use of the intervention (memory cue and Tetris).

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So, what did the researchers find? Primarily, they showed that the use of Tetris and memory recall was an effective intervention. The number of intrusions was significantly reduced in the intervention group after one week (9 intrusions on average) compared to the control condition (23 intrusions on average). Furthermore, they also found that the intervention group also reported significantly less distress after one week. However, this reduction in distress did not remain when participants were followed up after one month. To supplement this data, the authors also asked the participants about their subjective experience of using the intervention. Their reports were positive and it was apparent that they appreciated the distraction from the accident which playing Tetris offered. One participant highlighted this clearly with, “it certainly took my mind off of it at a time when I probably would have sat brooding and feeling very sorry for myself…”. Another participant, who had not played Tetris before, was keen to keep playing it following the allotted 20 minutes. The intervention thus proved to be both feasible and acceptable.

Together, these findings support the usefulness and viability of using Tetris to combat intrusive traumatic memories in a real-life setting. The reduction in the number of intrusions following a natural traumatic event (e.g. motor accident) supports the intervention and suggests it could be a low-cost, easy to administer, therapy. As the authors highlight in the paper, waiting times in A&E can be as long as 4 hours and this would be an ideal time to target individuals who have experienced a traumatic accident. As a well-tolerated, and simple, intervention it seems ideal. However, this study is simply the beginning of translating Tetris, or similar aproaches, into the realms of clinical practice. Although this trial did not show an effect on distress at a one month follow-up, a larger trial may be better suited to pick out subtle effects for longer periods of time. Furthermore, additional doses of the intervention may also prove effective as a ‘booster’ to the initial dose. As any good piece of research, this trial raises more questions and exciting avenues for further study.

Alongside the compelling results, why should we be so excited about this research? It provides clear evidence that marrying cognitive neuroscience and clinical practice are vital for progress in both fields. It is still early days for this collaborative approach but hopefully this soon blossoms into a powerful and fruitful relationship. Basic science studies can be blamed for being too distant from the disorders and clinical fields they are trying to unpick and affect. However, with a greater understanding of the mechanisms at work behind mental distress we can develop novel therapies, like the use of Tetris, to target them and help real people. Personally, that is one of the amazing things about research and one of the reasons why I fell in love with science in the first place. More work is needed to validate these findings but, at least for the time being, they provide you with a great retort to anyone who claims video games are good for nothing. To quote Emily Holmes’ original Tetris paper in 2009, “…clearly not all computer games are bad for you.”

ResearchBlogging.org

Iyadurai, L., Blackwell, S., Meiser-Stedman, R., Watson, P., Bonsall, M., Geddes, J., Nobre, A., & Holmes, E. (2017). Preventing intrusive memories after trauma via a brief intervention involving Tetris computer game play in the emergency department: a proof-of-concept randomized controlled trial Molecular Psychiatry DOI: 10.1038/mp.2017.23

Additional 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.
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Tetris Building (Body)

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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.

tetris

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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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.

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.

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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?

dreaming2

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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Filed under PhD, Psychology, Sleep Science, Uncategorized, Work and Society