Sleep Walking Research Paper

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Sleep Walking Research Paper

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The blue light emitted by your phone, tablet, computer, or TV is especially disruptive. You can minimize the impact by using devices with smaller screens, turning the brightness down, or using light-altering software such as f. Say no to late-night television. Not only does the light from a TV suppress melatonin, but many programs are stimulating rather than relaxing. Try listening to music or audio books instead. Use heavy curtains or shades to block light from windows, or try a sleep mask. Also consider covering up electronics that emit light. Keep the lights down if you get up during the night. If you need some light to move around safely, try installing a dim nightlight in the hall or bathroom or using a small flashlight.

This will make it easier for you to fall back to sleep. People who exercise regularly sleep better at night and feel less sleepy during the day. Regular exercise also improves the symptoms of insomnia and sleep apnea and increases the amount of time you spend in the deep, restorative stages of sleep. Exercise speeds up your metabolism, elevates body temperature, and stimulates hormones such as cortisol. Try to finish moderate to vigorous workouts at least three hours before bedtime. Relaxing, low-impact exercises such as yoga or gentle stretching in the evening can help promote sleep. Your daytime eating habits play a role in how well you sleep, especially in the hours before bedtime. Focus on a heart-healthy diet. Eating a Mediterranean-type diet rich in vegetables, fruit, and healthy fats—and limited amounts of red meat—may help you to fall asleep faster and stay asleep for longer.

Cut back on sugary foods and refined carbs. Eating lots of sugar and refined carbs such as white bread, white rice, and pasta during the day can trigger wakefulness at night and pull you out of the deep, restorative stages of sleep. Limit caffeine and nicotine. You might be surprised to know that caffeine can cause sleep problems up to ten to twelve hours after drinking it! Similarly, smoking is another stimulant that can disrupt your sleep, especially if you smoke close to bedtime. Avoid big meals at night. Try to make dinnertime earlier in the evening, and avoid heavy, rich foods within two hours of bed. Spicy or acidic foods can cause stomach trouble and heartburn.

Avoid alcohol before bed. Avoid drinking too many liquids in the evening. Drinking lots of fluids may result in frequent bathroom trips throughout the night. For some people, a light snack before bed can help promote sleep. For others, eating before bed leads to indigestion and makes sleeping more difficult. If you need a bedtime snack, try:. Do you often find yourself unable to get to sleep or regularly waking up night after night? Residual stress, worry, and anger from your day can make it very difficult to sleep well.

Taking steps to manage your overall stress levels and learning how to curb the worry habit can make it easier to unwind at night. You can also try developing a relaxing bedtime ritual to help you prepare your mind for sleep, such as practicing a relaxation technique, taking a warm bath, or dimming the lights and listening to soft music or an audiobook. Problems clearing your head at night can also stem from your daytime habits. The more overstimulated your brain becomes during the day, the harder it can be to slow down and unwind at night. Then when it comes to getting to sleep at night, your brain is so accustomed to seeking fresh stimulation, it becomes difficult to unwind.

Academic urban legends. Social Studies of Science. Since Why We Sleep was published, Walker published two academic papers that cited it. Many of the claims in both papers originate from Why We Sleep. The first one doi Walker MP. A sleep prescription for medicine. The Lancet. The second one doi Walker MP. A Societal Sleep Prescription. Furthermore, residents made to percent fewer diagnostic errors to begin with. Manuscripts are considered for publication with the understanding that no part of the work has been published previously in print or electronic format. Figure 6. The Lancet paper is on the left. Neuron paper is on the right. Identical text is highlighted in red. Image created with the help of copyleaks. During my undergrad, I took 2 years of statistics, a year of econometrics and worked as a research assistant for an economics prof for about 3 years.

I also took graduate-level psychology, neuroscience, and biology courses. Over the last several years, I spent many hundreds of hours studying biology and neuroscience. Since the publication of this essay, it was read by hundreds of psychologists and neuroscientists who—I believe—also failed to find any serious issues. Regardless of what I believe, you can check the discussions in the links in the beginning of the essay and check whether this is true for yourself.

Some of the scientists wrote to me directly. I myself am a sleep researcher but - I would like to think - of quite a different ilk from the Walker variety. In fact, I was so infuriated by the Walker claims that I bought a copy of the book so that I could review it. Your decision to limit your comments to the first chapter was a great solution to what could have become an intractable morass. First, it is true that some diseases lead to prolonged sleep. However, some diseases also lead to shortened sleep. Post-stroke insomnia in community-dwelling patients with chronic motor stroke: physiological evidence and implications for stroke care. Therefore, if you want to make the argument that the association between longer sleep and higher mortality is not indicative of effect of sleep, you have to accept that the same is true about shorter sleep and higher mortality.

As Cappuccio et al cited in section 1 note, these associations do not have a single accepted reason behind them:. Proposed mechanisms for mortality associated with long sleep include: I long sleep is linked to increased sleep fragmentation that is associated with a number of negative health outcomes; II long sleep is associated with feelings of fatigue and lethargy that may decrease resistance to stress and disease; III changes in cytokine levels associated with long sleep increase mortality risk; IV long sleepers experience a shorter photoperiod that could increase the risk of death in mammalian species; V a lack of physiological challenge with long sleep decrease longevity; VI underlying disease processes mediate the relationship between long sleep and mortality.

Second, at the level of an individual, there do not appear to exist any experimental studies or studies that would reasonably be able to establish causality that would support the claim that sleep restriction cause long-term health problems or an increase in mortality. You could say that it is well-known that short-term acute lack of sleep causes a stress response from the organism. This is true. However, if you make this argument, you should also consider the following argument about the dangers of exercise valid:.

When we exercise, our blood pressure and heart rate would increase. Stress hormones' concentration in the blood rises and the muscles get damaged. Therefore, exercise is bad for your health. In general, be careful to distinguish short-term stress response and long-term stress response. Please see section 18 , section 19 , and section 22 , where I cover problems with chapters 6 and 8. For example, in section 18, I show how Walker literally cuts out the part of a graph that displays the data in contradiction with his argument. My guess is that same is likely true for sleep.

I did look into this. I was not able to find any data on vehicular accidents caused by drowsy driving. However, the data by the National Highway Traffic Safety Administration on accidents that involve drowsy driving a and that involve drugs and alcohol a does not support this assertion. According to this data, 1. However, is there any reason to expect his treatment of sleep and learning to be any more accurate than, for example, his treatment of the relationship between sleep and longevity? Is there any reason to expect that this is one statistic he decides to portray accurately?

Have you considered looking at the scientific literature and seeing if this number checks out? Before doing all of this research, I frequently forced myself to sleep 8 hours, even if I naturally woke up after 7. I no longer do that and I continue to experiment with my sleep. A sleep physician Daniel Erichsen a writes:. Two friends in the sleep field and myself weekly have talked about people that slept well until reading this book. This is the email from a sleep coach Martin Reed a I quoted in Section 7 :. Martin also linked to this episode a of his podcast on insomnia:. Scott slept well his entire life until he listened to a podcast that led him to worry about how much sleep he was getting and the health consequences of insufficient sleep.

That night, Scott had a terrible night of sleep and this triggered a vicious cycle of ever-increasing worry about sleep and increasingly worse sleep that lasted for ten months. SleepyHead a sleep clinic in Exeter, UK writes a :. A reader tweets a :. After a week of forced 8-hour sleep I faced a problem of not falling asleep for more than an hour. Note: this problem was first noticed by Olli Haataja. Figure 7. Likelihood of injury over month period based on hours of sleep per night. Chronic lack of sleep is associated with increased sports injuries in adolescent athletes. Journal of Pediatric Orthopaedics. Walker cites this paper in Chapter 6 and provides an adaptation of this graph:.

Figure 8. The 5 hours of sleep column — which is associated with lower chance of injury than 6 hours of sleep — has simply disappeared. As an aside, that 9 hours of sleep column is based on exactly 1 child being injured out of 6 children who reported sleeping for 9 hours. Many people defend Walker cutting of the data from the graph by saying that he is just trying to make the trend clearer for the popular audience. As I noted in the Introduction of this essay, this argument is indefensible:. Update: Neil Stanley shows another example of Walker cutting off data from the graph to change its conclusion a :.

In Chapter 8, Walker discusses the relationship between sleep and cardiovascular health. In the first paragraph of this discussion, he mentions two studies. He seems to completely misrepresent both of them. Most notably, in the description of both of these studies he inflates their sample sizes. Unhealthy sleep, unhealthy heart. Simple and true. Over a fourteen-year period, those sleeping six hours or less were to percent more likely to suffer one or more cardiac arrests than those sleeping more than six hours.

Although he does not cite the two studies he discusses, he gives enough identifying information that I believe I was able to find both of them. The first one is Sleep duration predicts cardiovascular outcomes: a systematic review and meta-analysis of prospective studies a. Sleep duration predicts cardiovascular outcomes: a systematic review and meta-analysis of prospective studies. European Heart Journal. The second study he appears to describe in that paragraph is The effects of sleep duration on the incidence of cardiovascular events among middle-aged male workers in Japan a.

The effects of sleep duration on the incidence of cardiovascular events among middle-aged male workers in Japan. A reddit comment a :. I was looking into Matthew Walker a bit and it seems odd that where he claims he got his PhD on his own website [ a ] the MRC in London, very prestigious is clearly not where he got his PhD: both his thesis [ a ] and wikipedia page [ a ] show that his PhD was from the University of Newcastle upon Tyne less prestigious. Was he just sloppy in writing up the bio on his own website? Or stretching the truth to tell a better story? Neil Stanley notes on twitter a :.

He may have got funding from the MRC for his studies but his PhD must have been awarded by an academic institution. On forum. Chapter 8 also contains another erroneous description of an existing study. In one of the sessions, the participants were given just five hours of sleep before being put in front of the camera, while in the other session, these same individuals got a full eight hours of sleep. The faces pictured after one night of short sleep were rated as looking more fatigued, less healthy, and significantly less attractive.

Walker completely fails to mention that the individuals who received five hours of sleep were also sleep deprived for 31 hours. This fact is even directly stated in the abstract of the paper:. This completely changes the interpretation of the paper. Being able to tell visually if someone has had 5 hours of sleep is considerably different from being able to tell if they have had five hours of sleep AND have been sleep deprived for 31 hours.

Aric Prather regarding sleep and colds. Walker states that:. Though exceedingly rare, [4] this disorder asserts that a lack of sleep can kill a human being. The first night, he slept well; the second night, less well; and the third, still less, followed by 1—2 sleepless nights. Then the cycle repeated. Finally, statement [3] is also false. Clinical features of fatal familial insomnia: phenotypic variability in relation to a polymorphism at codon of the prion protein gene. Brain Pathology. Detailed analysis of 14 cases from 5 unrelated families showed that patients ran either a short 9.

See discussion of statement [4] in Section 3. He [Walker] has been frustrating to many in the sleep field for years—talks showing bar graphs without any error bars, clear misunderstandings of p-values, etc. Check out this doozy from a review back in It appears he multiplied the numbers from the studies together—but that is by no means a correct methodology! The condition usually emerges between ages ten and twenty years. There is some genetic basis to narcolepsy, but it is not inherited. In Kramis, Bland, and Vanderwolf proposed that in rats there are two distinct types of hippocampal theta rhythm, with different behavioral and pharmacological properties Kramis et al.

Type 1 "atropine resistant" theta, according to them, appears during locomotion and other types of "voluntary" behavior and during REM sleep, has a frequency usually around 8 Hz, and is unaffected by the anticholinergic drug atropine. Type 2 "atropine sensitive" theta appears during immobility and during anesthesia induced by urethane , has a frequency in the 4—7 Hz range, and is eliminated by administration of atropine. Many later investigations have supported the general concept that hippocampal theta can be divided into two types, although there has been dispute about the precise properties of each type.

Type 2 theta is comparatively rare in unanesthetized rats: it may be seen briefly when an animal is preparing to make a movement but hasn't yet executed it, but has only been reported for extended periods in animals that are in a state of frozen immobility because of the nearby presence of a predator such as a cat or ferret Sainsbury et al. Vanderwolf made a strong argument that the presence of theta in the hippocampal EEG can be predicted on the basis of what an animal is doing, rather than why the animal is doing it.

Active movements such as running, jumping, bar-pressing, or exploratory sniffing are reliably associated with theta; inactive states such as eating or grooming are associated with LIA. The faster an animal runs, the higher the theta frequency. In rats, the slowest movements give rise to frequencies around 6. Lesioning the medial septal area, or inactivating it with drugs, eliminates both type 1 and type 2 theta. Under certain conditions, theta-like oscillations can be induced in hippocampal or entorhinal cells in the absence of septal input, but this does not occur in intact, undrugged adult rats.

The critical septal region includes the medial septal nucleus and the vertical limb of the diagonal band of Broca. The lateral septal nucleus, a major recipient of hippocampal output, probably does not play an essential role in generating theta. Some of the projections from the medial septal area are cholinergic; the rest are GABAergic or glutamatergic. A major research problem has been to discover the "pacemaker" for the theta rhythm, that is, the mechanism that determines the oscillation frequency. The answer is not yet entirely clear, but there is some evidence that type 1 and type 2 theta depend on different pacemakers. For type 2 theta, the supramammillary nucleus of the hypothalamus appears to exert control Kirk, For type 1 theta, the picture is still unclear, but the most widely accepted hypothesis proposes that the frequency is determined by a feedback loop involving the medial septal area and hippocampus Wang, Several types of hippocampal and entorhinal neurons are capable of generating theta-frequency membrane potential oscillations when stimulated.

As a rule, EEG signals are generated by synchronized synaptic input to the dendrites of neurons arranged in a layer. Basic EEG theory says that when a layer of neurons generates an EEG signal, the signal always phase-reverses at some level. Thus, theta waves recorded from sites above and below a generating layer have opposite signs. There are other complications as well: the hippocampal layers are strongly curved, and theta-modulated inputs impinge on them from multiple pathways, with varying phase relationships.

The outcome of all these factors is that the phase and amplitude of theta oscillations change in a very complex way as a function of position within the hippocampus. The largest theta waves, however, are generally recorded from the vicinity of the fissure that separates the CA1 molecular layer from the dentate gyrus molecular layer. In rats, these signals frequently exceed 1 millivolt in amplitude. Theta waves recorded from above the hippocampus are smaller, and polarity-reversed with respect to the fissure signals. The dentate gyrus also generates theta waves, which are difficult to separate from the CA1 waves because they are considerably smaller in amplitude, but there is some evidence that dentate gyrus theta is usually about 90 degrees out of phase from CA1 theta.

Direct projections from the septal area to hippocampal interneurons also play a role in generating theta waves, but their influence is much smaller than that of the entorhinal inputs which are, however, themselves controlled by the septum. Theta-frequency activity arising from the hippocampus is manifested during some short-term memory tasks Vertes, Conversely, theta oscillations have been correlated to various voluntary behaviors exploration, spatial navigation, etc. Theta rhythms are very strong in rodent hippocampi and entorhinal cortex during learning and memory retrieval, and are believed to be vital to the induction of long-term potentiation , a potential cellular mechanism of learning and memory.

Phase precession along the theta wave in the hippocampus permits neural signals representing events that are only expected or those from the recent past to be placed next to the actually ongoing ones along a single theta cycle, and to be repeated over several theta cycles. This mechanism is supposed to allow long term potentiation LTP to reinforce the connections between neurons of the hippocampus representing subsequent elements of a memory sequence. In non-human animals, EEG signals are usually recorded using electrodes implanted in the brain; the majority of theta studies have involved electrodes implanted in the hippocampus.

In humans, because invasive studies are not ethically permissible except in some neurological patients, the largest number of EEG studies have been conducted using electrodes glued to the scalp. The signals picked up by scalp electrodes are comparatively small and diffuse and arise almost entirely from the cerebral cortex for the hippocampus is too small and too deeply buried to generate recognizable scalp EEG signals. Human EEG recordings show clear theta rhythmicity in some situations, but because of the technical difficulties, it has been difficult to tell whether these signals have any relationship with the hippocampal theta signals recorded from other species.

In contrast to the situation in rats, where long periods of theta oscillations are easily observed using electrodes implanted at many sites, theta has been difficult to pin down in primates, even when intracortical electrodes have been available. Green and Arduini , in their pioneering study of theta rhythms, reported only brief bursts of irregular theta in monkeys. Other investigators have reported similar results, although Stewart and Fox described a clear 7—9 Hz theta rhythm in the hippocampus of urethane-anesthetized macaques and squirrel monkeys, resembling the type 2 theta observed in urethane-anesthetized rats. Most of the available information on human hippocampal theta comes from a few small studies of epileptic patients with intracranially implanted electrodes used as part of a treatment plan.

In the largest and most systematic of these studies, Cantero et al. The hippocampal oscillations were associated with REM sleep and the transition from sleep to waking, and came in brief bursts, usually less than a second long. Cortical theta oscillations were observed during the transition from sleep and during quiet wakefulness; however, the authors were unable to find any correlation between hippocampal and cortical theta waves, and concluded that the two processes are probably controlled by independent mechanisms. Studies have shown an association of hypnosis with stronger theta-frequency activity as well as with changes to the gamma-frequency activity Jensen et al.

Also, increased theta waves have been seen in humans in ' no thought' meditation. From Wikipedia, the free encyclopedia. Neural oscillatory pattern. Bibcode : PNAS ISSN

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