The strongest influencers on the circadian rhythm are melatonin and light. However, there is something called the phase response curve, meaning that the effects of both on the circadian rhythm are dependent on WHEN they are given, so if you expose someone to light or melatonin at one point it may shift their clock forward, but at another time back. The size of the effect is also dependent on timing. That is why I do not recommend people try to manipulate their own rhythm with melatonin for jet lag. However, exposure to bright light in the day, especially the morning, and avoidance of bright light in the evenings helps anchor circadian rhythm. It is important not to forget that lots of other factors also influence the clock. Eating, drinking, exercise temperature. The key thing with reinforcing the circadian rhythm is maintaining a regular pattern. But if you want to shift it, it is a little more complicated.

Before answering this, I would say that good sleepers often do not practise good sleep hygiene. They sleep well regardless. So while sleep hygiene may help the intermittently poor sleeper, it is not going to make a significant difference to people with chronic insomnia. Paradoxical intent may be helpful, but evidence really identifies CBTi as being the best approach. This multimodal therapy combines relaxation techniques, MBT, stimulus control and sleep compression, all with a view to breaking down the negative conditioned response to bed, and rebuild a positive conditioning. Evidence suggests that CBTi is non-inferior to medications, and may well achieve a longer-term positive outcome. Medications have a role in some individuals, particularly if there are co-morbidities, but concerns have been raised regarding the long-term adverse effects, including falls, accidents, habituation, dependency and cognitive dysfunction. There is a signal from the literature that long term hypnotics may be a risk factor for Alzheimer's/MCI, although there remain some unanswered questions in this area - these are detailed in my book. In summary therefore, CBTi would be my first choice, delivered either face to face, via teleconferencing, or even using online platforms.

The issue is more to do with the underlying cause. Psychophysiological insomnia can cause both initiation and maintenance difficulties, but it is more common for people to have difficulties with sleep initiation. The treatment strategies for both are the same. However, if people fall asleep readily during the day (which most people with insomnia cannot do), this raises the possibility of an underlying "biological" sleep disorder mimicking insomnia. For sleep initiation difficulties, these include RLS or delayed sleep phase syndrome. For sleep maintenance issues, conditions like OSA, RLS, or even narcolepsy. And obviously if there is an underlying cause, this needs to be addressed with the most appropriate treatment strategy.

Undoubtedly, treating the trauma symptoms first, as it is the more holistic approach. Once this has been done, the sleep can be focussed on. As you know, PTSD-associated nightmares can remain despite other aspects of PTSD lessening, and in these cases, there are a variety of treatment options with varying levels of evidence - dream imagery rehearsal therapy, CBTi, EMDR, or medications. A popular medication is prazosin, a blood pressure med. A recent RCT showed no effect, but many of us seeing these patients have had some successes with this drug. The AASM recently published a consensus statement on PTSD-associated nightmare disorder, detailing the levels of evidence for these interventions.

There is significantly more evidence for CBTi, in terms of its impact on sleep in anxiety and depression, but also its impact on the underlying mood/anxiety disorder. But the reality is that CBTi is hard to adhere to, so ACTi is a useful adjunct to reduce distress from sleep issues in those who cannot manage the CBTi protocol.

It is important to note that insomnia is associated with anxiety or depression in about 50% of individuals but can exist in the absence of anxiety in the other 50%. The nature of anxiety in the context of insomnia is hugely variable. For many people with insomnia, there is a single and isolated sleep-related anxiety - worry about the night ahead or the day after - and this causes hyperarousal or hypervigilance around bed time, or specifically in bed. However, any more generalised anxiety disorder results in a persistent state of hyperarousal which obviously then impacts on sleep initiation and maintenance. OCD may also lead to bed procrastination and repetitive intrusive thoughts, having much the same effect. It is also important to recognise that insomnia, and indeed sleep deprivation, causes physiological changes such as a hyperadrenergic state, which compounds anxiety, and there are probably neurophysiological changes that also lead to insomnia exacerbating anxiety states. Therefore, in the presence of both insomnia and anxiety, both need to be dealt with simultaneously for best outcome.

The answer is probably both, but there remain so many questions about this. Certainly NREM "deep" sleep is fundamentally important - perhaps one of the most important issues is that in deep sleep, the glymphatic system expands significantly, potentiating the removal of metabolites from the brain. This system has been implicated in the removal of tau and beta-amyloid, both of which have a role in the pathogenesis of Alzheimer's and other neurodegenerative diseases. REM sleep is also important, probably more so for learning, memory and emotional processing. But there are a number of paradoxes when it comes to REM. As we get older, the proportion of REM sleep diminishes, and we have not seen major ill effects from abolition of REM in adults. The likely explanation is that REM is more important and has slightly different roles in infants and children.

Melatonin in tablet form is a synthetic analogue of the melatonin released by our pineal gland, and acts both as a sleep promoter and Zeitgeber - a modulator of our circadian rhythm. Despite early concerns regarding its modulation of autoimmune conditions (not really subsequently borne out), it is held to be very safe. As you probably know, in the US and Canada, it is seen as a health supplement rather than medication, and in some European countries can be bought without a prescription. Have said all that, it would always be best to avoid medication, especially in young people. We know teenagers tend to develop a delayed sleep phase, but there are certain drivers that will make this worse. Exposure to bright light at night, mental stimulation by the use of gadgets, distractions of social life, lack of exposure to sun early in the morning. So it would be preferable to address these issues first rather than reaching for the melatonin. Equally, if it is being given for insomnia, it is worth trying to address the insomnia first, using techniques like CBTi

There are two issues for shift workers. The first is that they are often sleep-deprived, as they are not able to achieve adequate sleep. The second is that their circadian rhythms are disrupted, with resulting negative effects on health. Some of the solutions are structural, related to the nature of working patterns. It is difficult to shift your circadian clock by more that 1 hour per 24 hours, and so rapidly shifting rotas are difficult to cope with. Equally, rotas need to be mindful of giving people adequate sleep opportunity between shifts. On a personal level, the most important thing is to be mindful of light exposure. Adequate bright light after waking, minimising bright light on the journey home (sometimes even resorting to sunglasses on the commute), maintaining a routine that provides opportunity for sleep, and utilising good sleep hygiene to ensure that sleep onset and sleep quality is affected as little as possible. However, it is important to accept if you as an individual are someone who can cope with shift work. If you have a tendency to insomnia or poor sleep anyway, then shift work is simply going to exacerbate that underlying trait.

Sadly, I think there are limited options. Best for both the snorer and the partner is to get the snorer's snoring dealt with! Options such as devices to keep the snorer off their back, dental devices called mandibular advancement devices, or for very carefully selected cases, surgery. Other options are earplugs or a separate bedroom!

The only thing to be done is to ensure you are not sleep-deprived and to address any other sleep issues that you have. The story of sleep and cognitive decline is not fully unravelled, and there remain some unanswered questions, but certainly there is a growing wealth of evidence to suggest that there is some causality there. There are some experimental techniques in development, for example using auditory signals in the form of pink noise timed to brainwaves that have shown some subtle beneficial effects, but this work is at the very early stages

The answer is a clear yes. These are all sedating agents and do not promote sleep in themselves. In fact, many of these drugs increase the proportion of intermediate sleep, not deep sleep. Furthermore, they are often associated with problems like dependency, habituation, risk of falls or road traffic accidents, and there is emerging evidence that they may be associated with risk of cognitive decline. It is not always possible to get people off their hypnotics, but there is clear evidence that CBTi may facilitate drug withdrawal. This should be done in conjunction with a physician though. It is also important that people understand that alcohol actually reduces sleep quality, so while some people find it helpful as a form of sedation, it is one of the worst things you can do to get a decent night's sleep

You are describing sleep-related bruxism. This may have some underlying causes, such as daytime anxiety, SSRIs (which can also cause toothgrinding during the day), and sleep apnoea. Sometimes we see individuals who have brief arousals associated with sleep apnoea that then trigger these teethgrinding events. Options for treatment include anxiety management, treatment of sleep apnoea or a bruxism guard - a dental device. For patients with refractory bruxism, rarely clonazepam or even Botox have been used.

We know that there is huge inter-individual vulnerability to the effects of blue light on circadian rhythm, which is largely genetic. Certainly, there is some evidence that people with delayed sleep phase syndrome may be more vulnerable to the effects of blue light. The answer that I would give is that if you fall asleep easily and wake up refreshed, regardless of your exposure to light then don't worry about it. If you have DSPS, then you need to be aware of the impact of blue light on your rhythm, and restriction of light exposure in the evening through whatever means (including lenses) may provide benefit. However, this in isolation is unlikely to be effective, and needs to be in the context of other changes to behaviour. A note of caution though - studies of night modes on various gadgets has shown that in themselves they do not alter suppression of melatonin in the evening, and need to be used in conjunction with a reduction of screen brightness in order to minimise melatonin suppression. The degree to which that affects sleep quality however remains to be fully determined.

Ha! I hear this question so frequently that I have recently written about this: https://www.ft.com/content/b3f59882-4749-11ea-aee2-9ddbdc86190d In summary, no sleep trackers measure sleep, unless they include EEG electrodes. They measure a variety of physiological parameters that are proxy markers for sleep. Some are more accurate than others, but most are only really accurate about the time you have spent in bed, not sleep stages or sleep efficiency. Furthermore, they are likely to be even less accurate if you have a sleep disorder. But this also relates to another answer that I have given, which is that in insomnia, the objective and subjective experience of sleep is often hugely different, and so a sleep tracker or even a PSG is of very limited value. In my experience, many people with insomnia end up being harmed by sleep trackers - they encourage further obsessionality about sleep and increase sleep-related anxiety further

We know that certain factors that can exeracerbate RLS. These include substances like caffeine, alcohol and nicotine, as well as a range of drugs, such as SSRIs and antihistamines. So avoidance of these substances in the evening can have a huge impact, and if people are taking these medications at night, this should be discussed with their physician. What is frequently under-recognised is that people who have had RLS for many years will develop a secondary psycho-physiological insomnia, and even when the RLS is treated, the insomnia persists. These people frequently obtain benefit from standard sleep hygiene advice (how I hate that term, but everyone knows what it is), and CBT for insomnia. Anecdotally, sufferers often describe benefit from warm baths before bed, gentle exercise like an evening walk, and leg massage.

Iron deficiency is a well-defined risk factor for RLS. Evidence over the last few years points to there being an issue of transport of peripheral iron into the brain in RLS. Therefore, for patients with RLS, we generally recommend iron levels higher than the normal population, both due to improvements in symptoms but also as lower iron levels are associated with a complication of drug treatment termed augmentation. We tend to aim for a ferritin of at least 75 mcg/L, and if it is below that, a course of iron supplementation is recommended. If iron levels remain low despite this, we will consider an intravenous iron infusion. Richard Allen has published extensively on this, and there is a recent consensus statement on use of intravenous iron in RLS.

The first bit of advice is to calm down. These events are far more distressing for the parents than for the child, who tends not to remember anything at all of these events. It is also important to understand that these events are so common as to almost be viewed as a normal developmental variant, are are not representative of any underlying neurological or psychological issue. The best thing to do is to calm your child and guide them gently back to bed. If these are happening very frequently, then one option is to consider pre-emptive awakenings. These events arise from non-REM sleep, and tend to occur at a similar time every night. Waking the child briefly, 20-30 minutes before the expected time can sometimes disrupt sleep enough to avoid such a deep NREM sleep period, reducing the likelihood of night terrors.

Only in specific cases. Pharmacotherapy is generally considered for those individuals who are putting themselves or their bed partners at risk, or in whom the condition is hugely impacting their quality of life. First line treatments should always be to optimise sleep, as fragmented sleep due to any reason, be that biological, such as sleep apnoea, or behavioural/psychological, can precipitate sleepwalking events. Depending on the clinical picture, we will try a variety of stress management/relaxation therapy, CBTi, CBT for anxiety, or treatment of OSA. We have recently published our experience of treatment in over 500 patients with NREM parasomnias, and this is Open Access (Drakatos et al. Sleep Med. 2019 Jan;53:181-188. NREM parasomnias: a treatment approach based upon a retrospective case series of 512 patients.)

This is rather difficult to answer on a thread. It depends on why her sleep is poor and what she is like during the day. Does she have learning difficulties? Does she have pain, contractures, sphincter dysfunction, breathing difficulties? If she is not obviously tired or sleepy during the day, then it is best not to spend prolonged periods of time in bed while awake, as this weakens the positive conditioned response to bed, and strengthens the negative conditioned response. There is a second question around melatonin. This drug has two effects - a sleep promoter and a Zeitgeber, i.e. modulator of circadian rhythm. The effect depends on dose and timing relative to intrinsic circadian rhythm. She may be better off being put to bed at 9pm with a dose of melatonin to consolidate sleep, rather than trying to manipulate her circadian rhythm which by the sounds of it has been unsuccessful so far. I would stress the proviso that there are a number of factors that potentially need to be addressed, and she would benefit from seeing a paediatric sleep physician or neurodisability specialist.

Unfortunately not. To date, no hypocretin analogue has been identified that can deliver to the hypothalamus reliably and safely. No successful strategy to replace or rescue the hypocretin-producing cells has been found. The treatment of narcolepsy relies upon education, optimising sleep patterns and drugs that promote wakefulness during the day, consolidate nighttime sleep, and treat cataplexy (the loss of tone with strong emotion).

For sleep apnoea, the treatment depends on symptoms, severity and nature of the sleep apnoea. For mild sleep apnoea, it can be treated using positional manoeuvres if it is related to being flat on your back, and dental devices called mandibular advancement devices can help. More severe sleep apnoea may need CPAP, a pressurised mask that splints the airway open. Surgery is rarely indicated. For insomnia, the preferred method of treatment is CBTi in the first instance, and addressing any psychological co-morbidities. Medications may have a role, but usually are not first option. I am not sure if your question actually refers to the co-existence of sleep apnoea and insomnia, which does sometimes occur. The treatment in this setting depends on which is more prominent, as people with severe insomnia will not tolerate any treatment of OSA - it will simply make their insomnia worse. So we need to decide on a case by case basis

The answer to this is yes and no. Polysomnography should be viewed as an extension to the clinical evaluation, rather than a definitive test. It is more helpful in some contexts rather than others. We know that PSG is generally not very useful in insomnia - the subjective experience of sleep and the objective demonstration of it often correlate very poorly. For other conditions like sleep apnoea or periodic limb movement disorder, PSG is more helpful. Yet other conditions, like non-REM parasomnias, frequently return normal PSGs. And the truth is that many people have more than one condition influencing their sleep, with environmental, behavioural and psychological factors that no PSG is going to detect.

The association between sleep and appetite also involves other hormones such as leptin and ghrelin, influencing appetite and satiety. Poor sleep upregulates appetite, increases caloric intake, and tends to lead to poor food choices. I am not sure that this actually provides specific avenues of treatment other than to ensure that patients with eating disorders do not have their sleep ignored, using psychological techniques or pharmacotherapy. It is important to ensure that if patients are on medications, these are not disrupting sleep - e.g. SSRIs. On other curious aspect of this area is the phenomenon of sleep-related eating disorder and night eating syndrome, both of which have been linked to eating disorders. A discussion of this area is beyond the scope of a thread, but if you are interested, one entire chapter of my book, The Nocturnal Brain, is dedicated to these conditions.