On this episode, Dominik Polasek tells us about his summer as a visiting research assistant at Harvard University’s Sleep Lab. We also discuss how to get involved in research in the department and find your own international internship.
If you’d like to learn more about sleep research at Harvard you can check out their website here.
To learn more about our sleep research at Northumbria, check out this page.
If you’re a NU Psychology student and want to find out more about getting involved in research, look out for Dr. Michael Craig’s monthly updates on Volunteer Research Assistantships or email him at michael2.craig@northumbriapsy
To follow Dominik’s continued research you can follow him on LinkedIn or Instagram @dominikpolasek
If you’re a student from the Czech Republic looking for funding to come to Northumbria University, check out The Kellner Foundation at their website here.
A good night’s sleep is important for many reasons. It helps our body repair itself and function as it should, and is linked to better mental health and lower risk of many health conditions – including heart disease and diabetes. It’s also been shown that not getting enough sleep is linked to cognitive decline and conditions such as Alzheimer’s disease.
But more isn’t always better, as one recent study found. Researchers from the Washington University School of Medicine have published a paper that indicates that just like getting too little sleep, sleeping too much may also be linked with cognitive decline.
The research team wanted to know how much sleep was linked to cognitive impairment over time. To do this, they looked at 100 older adults in their mid-to-late-70s on average, and tracked them for between four and five years. At the time of their study, 88 people did not show any signs of dementia, while 12 showed signs of cognitive impairment (one with mild dementia and 11 with the pre-dementia stage of mild cognitive impairment).
Throughout the study, participants were asked to complete a range of commonplace cognitive and neuropsychological tests to look for signs of cognitive decline or dementia. Their scores from these tests were then combined into a single score, called the Preclinical Alzheimer Cognitive Composite (PACC) score. The higher the score, the better their cognition was over time.
Sleep was measured using a single-electrode encephalography (EEG) device, which participants wore on their forehead while sleeping, for a total of between four to six nights. This was done once, three years after people first completed their annual cognitive tests. This EEG allowed the researchers to accurately measure brain activity, which would tell them whether or not someone was asleep (and for how long), and how restful that sleep was.
Although sleep was only measured at one period during the study, this still gave the research team a good indication of participants’ normal sleep habits. While using an EEG to measure brain activity may be somewhat disruptive to sleep on the first night, as people get used to the equipment, sleep tends to return to normal the following night. This means that when sleep is tracked from the second night onwards it’s a good representation of a person’s normal sleep habits.
The researchers also took into account other factors that can affect cognitive decline – including age, genetics and whether a person had signs of the proteins beta-amyloid or tau, which are both linked to dementia.
Overall, the researchers found that sleeping less than 4.5 hours and more than 6.5 hours a night – alongside poor quality sleep – was associated with cognitive decline over time. Interestingly, the impact of sleep duration on cognitive function was similar to the effect of age, which is the greatest risk factor for developing cognitive decline.
A good night’s sleep
We know from previous research that lack of sleep is linked to cognitive decline. For example, one study showed that people who reported sleep disturbances, such as insomnia or excessive daytime sleepiness, have a greater risk of developing dementia compared to people who don’t. Other research has shown that people who have short sleeping times have higher levels of beta-amyloid in their brain – which is commonly found in the brains of people who have Alzheimer’s disease.
Researchers don’t know for certain why lack of sleep is linked to cognitive decline. One theory is that sleep helps our brain flush out harmful proteins that build up during the day. Some of these proteins – like beta-amyloid and tau – are thought to cause dementia. So interfering with sleep might interfere with our brain’s ability to get rid of these. Experimental evidence even supports this – showing that even just one night of sleep deprivation temporarily increases beta-amyloid levels in the brain of healthy people.
But it’s less clear why long sleep is linked with cognitive decline. Previous studies have also found a link between over-sleep and cognitive performance, but most relied upon participants self-reporting how long they sleep nightly – which means the data is less accurate than using an EEG to measure brain activity. This new study therefore adds weight to such findings.
What’s surprising about this study’s findings is that the optimal sleep duration is much shorter than that which previous studies have suggested are problematic. The study showed that sleeping longer than 6.5 hours was associated with cognitive decline over time – this is low when we consider that older adults are recommended to get between seven and eight hours of sleep every night.
It could be the case that it isn’t necessarily the length of the sleep that matters, but the quality of that sleep when it comes to risk of developing dementia. For instance, this study also showed that having less “slow-wave” sleep – restorative sleep – particularly affected cognitive impairment.
What we also cannot tell from this study is if long sleep durations can independently predict cognitive decline. Essentially, we can’t rule out that participants who slept longer than 6.5 hours every night might not have already had pre-existing cognitive problems of brain changes suggestive of dementia that weren’t picked up on the tests. And although the researchers were careful to adjust for dementia-related factors, longer sleepers may also have had other pre-existing conditions that might have contributed to their cognitive decline which weren’t taken into account. For example, this could include poor health, socioeconomic status or physical activity levels. All of these factors together may explain why longer sleep was linked to cognitive decline.
There are many factors which can impact on both our sleep quality, and whether we experience cognitive decline. While some factors aren’t preventable (such as genetic predisposition), there are many things we can do alongside getting a good night’s sleep to help reduce our likelihood of developing dementia – such as exercising and eating a healthy diet. But while the researchers of this study seem to suggest there’s an optimal sleep duration – between 4.5 and 6.5 hours every night – the occasional weekend lie-in is unlikely to do your brain any harm.
It should be one of the most relaxing times of the day. You climb into bed, get comfortable and cosy, start to feel your brain slowing down … and then suddenly you experience a shocking falling sensation. It’s like you misjudged the number of stairs you were walking down, leaving your leg in mid air for just a bit longer than you expected. Not pleasant.
This bedtime tumbling sensation is the phenomenon known as the “hypnic jerk” and may sometimes be accompanied by a visual hallucination. You may have heard it called a “sleep start”, the “hypnagogic jerk” or the “myoclonic jerk”, but for the sake of sanity we’ll just stick with the former.
So what is it?
The hypnic jerk occurs when the muscles, usually in the legs (although they can be observed throughout the body), involuntarily contract quickly, almost like a twitch or spasm. Although the reasons behind this are not that well understood, the evolutionary perspective suggests that it serves at least two important but interrelated functions, the former of which is still relevant today.
First, this sudden awakening allows us to check our environment one last time, an opportunity to ensure that it really is safe to go to sleep by creating a startle-like response. You might have accidentally dropped off somewhere dangerous, after all.
Another suggested evolutionary function is that it allowed us – or at least our early ancestors – to check the stability of our body position before we went to sleep, especially if we started to fall asleep in a tree. The jerk would allow us to test our “footing” before unconsciousness set in. https://www.youtube.com/embed/Mg_66TRsb6Y?wmode=transparent&start=0
The other main theory suggests that the hypnic jerk is merely a symptom of our active physiological system finally giving in, albeit sometimes reluctantly, to our sleep drive, moving from active and volitional motor control to a state of relaxation and eventual bodily paralysis. In essence, the hypnic jerk may be a sign of the eventual switch over between the brain’s recticular activating system (which uses arousal neurotransmitters to aid wakefulness) and the ventrolateral preoptic nucleus (which utilises inhibitory neurotransmitters to reduce wakefulness and promote sleep).
When jerks go bad
Either way, although in most cases a normal and natural phenomenon, the hypnic jerk can be a rather disconcerting or frightening experience. In extreme cases – whether in terms of frequency or the velocity and violence of the jerk – it can keep people awake, preventing them from entering the normal sleep onset process, resulting, in the longer-term, in a form of sleep-onset insomnia.
As the hypnic jerk is related to motor activity, anything that is going to keep your motor system active at night is likely to increase the chances of you having one – and possibly even a more intense one, too.
As such, caffeine (or other stimulants) and/or vigorous exercise in the evening and high stress and anxiety levels at night are associated with an increased chance of a spontaneous hypnic jerk and should, where possible, be avoided. Other associations include being overtired or fatigued, sleep deprived or having an erratic sleep schedule. Here, keeping a good regular sleep/wake pattern can help. https://www.youtube.com/embed/39a_XWaJ7As?wmode=transparent&start=0
Finally, from a nutritional perspective, it has been suggested, albeit anecdotally, that deficiencies in magnesium, calcium and/or iron can also increase the chances of experiencing a spontaneous hypnic jerk. That said, it has also been suggested that hypnic jerks can be evoked through sensory stimulation, during the sleep onset period, so ensuring that your sleep environment is cool, dark and quiet may be helpful in reducing the frequency and intensity of them.
There is actually very little research on the topic, presumably because it is largely seen as a normal phenomenon, making it difficult to suggest a definitive “treatment”. However, we do know that as we get older the number of hypnic jerks we will experience should decrease naturally. The main issue to consider here is whether the hypnic jerk is causing you or your bed partner a problem? If it is, then it is time to see a sleep specialist. The difficulty is there are a number of sleep disorders, such as sleep apnoea, that have symptoms which mimic the experience.
And if all else fails, perhaps just blame the ancestors.
Over the last 12 years at Northumbria Sleep Research we have been studying the pathophysiology of insomnia. In other words, how can two people have the same experiences in life and yet one develops insomnia and the other does not?
As there was no working definition of acute insomnia (the period prior to it being classed as a sleep disorder), prior to us starting this work, the first thing we had to do was create a clinical definition of acute insomnia. We did this in terms of having existing vulnerabilities, how it can start, how long someone should have it to be classified, what symptoms they should experience and how frequently they should experience those symptoms every week.
Using this definition, we then demonstrated how many people in the general population are affected by it at any given time (prevalence = 7.9%) and how many people will be affected by it over the course of a year (annual incidence = 31-36%) in the UK and USA. We then went on to examine what makes people with acute insomnia different from normal sleepers and people with chronic insomnia along several dimensions (genetic, physiological, neuropsychological, psychological, social, behavioural and environmental).
These findings include, changes in the timing of the human body clock, differences in brain-wave activity during sleep, how preoccupied we are with our sleep during the day, our levels of depression and how much time we spend in bed awake worrying.
Why is preventing chronic insomnia important in the context of COVID?
We have seen a sharp increase in people reporting acute insomnia over the crisis. This increase has been attributed not only to fears and concerns about the virus itself but worry and anxiety about family and friends. There have also been increases in financial and work-related pressures and lifestyle and routine changes due to the lockdown which can also negatively impact on sleep.
If left untreated, acute insomnia can develop into a chronic insomnia which increases the risk, significantly, for several physical and psychological illnesses (for example Northumbria Sleep Research were the first to demonstrate that untreated acute insomnia significantly increases the risk for a first episode of depression).
Within the context of COVID specifically, there is lots of evidence that good sleep can; i) minimise the chances of contracting a virus, if exposed, ii) increase the recovery rate after contracting a virus and iii) increase the speed at which immunity occurs following vaccination. Together, this underscores the reasons why identifying and preventing chronic insomnia is so important at the moment.
How are staff in the Northumbria Centre for Sleep Research helping?
One of the most important things about doing research, at least in our view, is that it must have implications for practice, policy and/or changes in individual’s behaviour (real-world impact). Based upon the findings from our research and the intervention, we have already contributed to guidelines for managing sleep during COVID for the British Psychological Society, British Sleep Society, Public Health England, NHS England, the European Sleep Research Society and the Society for Behavioral Sleep Medicine in the USA. Additionally, to date, we have trained over two hundred clinicians in the UK, USA, Japan and Holland on how to use our intervention to help students, front-line healthcare workers, carers and vulnerable populations manage their sleep during the crisis.
Sleep disturbance in young adults who are at risk of suicide are a warning sign of worsening suicidal thoughts, according to new research from Stanford University. These findings held true regardless of the study participants’ current levels of depression.
Suicide is the second leading cause of death in young people in the US and the leading cause in the UK. Having a better understanding of the signs of suicidal thought is important as it could help prevent suicide. Previous research has shown a link between suicidal thoughts and poor sleep, but the Stanford researchers went beyond this research by closely examining which aspects of disrupted sleep predicted suicidal thought.
The researchers examined sleep objectively, using sleep tracking devices, and subjectively, using sleep diaries and records of suicidal thoughts. A group of 50 undergraduate students was selected for the study on the basis that they had recent suicidal thoughts or a history of suicide attempts. The students’ sleep was monitored for seven days continuously. They were also asked to complete a questionnaire – at the beginning, middle (day seven) and end of the study (day 21) – that asked them about the severity of suicidal thoughts, depression, insomnia, nightmares and alcohol use. The researchers found that changes in when the students went to sleep and when they woke up predicted suicidal thought, as did increased symptoms of insomnia and nightmares.
It has long been known that poor sleep, in general, and insomnia, in particular, are associated with a wide variety of mental health conditions. As research in the area advanced it became clear that this relationship was not just an association but rather that insomnia posed a significant risk for the development of many mental health problems, most notably depression.
A strong association
Over the past ten to 15 years, researchers have widened the scope of sleep and mental health research to investigate the relationship between poor sleep – including insomnia – and an increased risk of suicide. Within this framework various research groups around the world began to examine whether poor sleep was related to increased suicidal thoughts but also whether a person who sleeps poorly is more likely to attempt, or complete, a suicide or not.
It soon became clear that a strong association between poor sleep and suicide existed and that the severity and duration of insomnia symptoms and nightmares were associated with increased suicidal thoughts. Especially interesting is that in almost all these studies the relationship between poor sleep and suicide existed independently of a diagnosis of depression or the number of depressive symptoms experienced, as in the current study. But, as most of this previous research was based on self-reported symptoms (of both sleep problems and suicidal thoughts), it was unclear whether the relationship between poor sleep and suicide was based on how the person actually slept or how they felt they had slept – two surprisingly different concepts. The fact that the Stanford researchers objectively measured sleep is a particular strength of their study.
But the reasons for the relationship between poor sleep and suicide have yet to be determined. However, there are three avenues of research which, although still in their infancy, may shed light on why poor sleep is so strongly related to suicide. One, there are significant overlaps between brain circuits that are involved in both emotion regulation and sleep. As such, if sleep is disrupted the likelihood is that mood will also be disrupted, and vice versa. Two, there may be changes in the structure of sleep itself, as a result of poor sleep and insomnia, which makes us more vulnerable to a variety of mood disturbances, including suicidal thought. And, three, the daytime fatigue, caused by poor sleep, affects our ability to think and act rationally.
As yet, we simply don’t know what underscores the relationship between poor sleep and insomnia but, with these avenues in mind, a preventative strategy for suicide is definitely getting closer. And the likelihood is that it will involve the management of sleep.
The Samaritans can be contacted in the UK on 116 123. Papyrus is contactable on 0800 068 41 41 or by texting 07786 209 697 or emailing firstname.lastname@example.org. In the US, the National Suicide Prevention Hotline is 1-800-273-8255. In Australia, the crisis support service Lifeline is on 13 11 14. Hotlines in other countries can be found here.