"When Does Sleep Become the Enemy?" Jason Ellis (02.03.2021)

February 08, 2021

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To CiteDCA Citation Guide

00:23OK, hello everyone. I'm Bri
00:24and minor I'm subbing in today
00:27for Lauren Tobias,
00:28who will be working in the ICU.
00:31Thank you to her for her service
00:33and I'd like to welcome you
00:36all to our Yale Sleep Seminar,
00:38afew brief announcements before I
00:40introduce today's speaker first,
00:42please take a moment to
00:44ensure that you are muted.
00:46I think we all know from our
00:49zoom experience that this
00:51is a very important step.
00:53In order to receive CME
00:55credit for attendance,
00:56please see the chat room for instructions.
00:58You can text the unique ID for this
01:01conference anytime until 3:15 PM if
01:03you're not already registered with the LC ME.
01:06You will need to do so first.
01:09If you have questions
01:11during the presentation,
01:12if they are burning questions,
01:13you may put them in the chat.
01:16Otherwise our speaker kindly
01:18requests that you leave questions
01:20till the end of the talk.
01:22A recorded version of this lecture
01:25will be available online within two
01:27weeks at the link provided in the chat,
01:30and finally, Pete.
01:31Please feel free to share the
01:33announcements for this weekly lecture
01:35series to anyone else who may be interested,
01:38or contact Debbie Lovejoy to
01:40be added to our email lists.
01:42So now I will move on to
01:44introduce today's speaker,
01:46doctor Jason Ellis,
01:47who is hailing all the way from the United
01:51Kingdom to join us for our afternoon.
01:53His early evening.
01:55So doctor Ellis.
01:57Has done all of his training
02:00in the United Kingdom,
02:01first starting with a bachelors degree
02:04in psychology and clearly had an
02:06interest in insomnia from the beginning.
02:08He did his dissertation,
02:10which was entitled is chronic
02:12insomnia a resource loss spiral?
02:14He went on to do his Masters work
02:16at the University of Surry where
02:18he studied the role of rumination
02:21and thought control and sleep
02:23disturbance and he got a PhD
02:26also at the University of Surry.
02:28Looking at the cognitive
02:30consolidation model of insomnia,
02:32an examination of the predictors and
02:34consequences of late life insomnia.
02:37And finally,
02:38in 2014 he was recognized by the
02:40European Sleep Research Society as an
02:43expert in behavioral Sleep Medicine.
02:45He now serves as a professor of
02:48sleep science and the director of
02:50the Sleep Research Laboratory at
02:53Northumbria University in Newcastle.
02:55He has editorial appointments
02:57for journals of Behavioral Sleep
02:59Medicine and sleep health.
03:00He serves on committees for
03:02the Sleep Research Society and
03:04the British Sleep Society.
03:06He has many different interests
03:08that have been sort of that I was,
03:11you know,
03:12looking through in his very long CV,
03:15and so I just wanted to to highlight
03:18a couple here that I thought were,
03:21you know, recent and interesting.
03:22He is looking at optimizing sensory
03:25information for sleep in toddlers.
03:27The effects of a multi ingredient
03:30nighttime tea on sleep quality well
03:32being an markers of immune function.
03:35He is looking at development of
03:37of a fatigue management program
03:39for training health care personnel
03:41following shift work.
03:43Behavioral treatment for insomnia
03:44in adults with autism and he has
03:47interesting projects and consulting
03:49looking at determining the most
03:51super riffic reason,
03:52anthems and developing evidence
03:54based sleep hygiene guidelines.
03:56He has over 50 peer reviewed publications,
03:58multiple book chapters. Anna book.
04:01Called the one week Insomnia cure
04:03learned to solve your sleep problems
04:05and he has been invited as a keynote
04:07speaker for multiple professional
04:09societies and universities.
04:11An multiple public engagement
04:12talks and in fact Doctor Tobias,
04:14who couldn't be here today, saw him,
04:17gave a similar talk to this when
04:19he proposes to talk to us today
04:21about found him very engaging and
04:24so he very kindly accepted the
04:26invitation to speak with us today.
04:30So without further ado,
04:31thank you Doctor Ellis and we're
04:33looking forward to your talk.
04:35Read that if you want to sit on
04:38my promotions board at any point,
04:40please feel free.
04:41That's a beautiful introduction.
04:43Thank you to Doctor Miller.
04:44Minor for that introduction. Of course,
04:47Dr Tobias for the invitation and Debbie,
04:49of course for making sure that
04:52I'm correct and appropriate.
04:53OK, So what are we going to talk about today?
04:57We're going to talk really
04:59about acute insomnia.
05:00So when does sleep actually become the enemy,
05:03and what can we do about it?
05:07Before we continue, I'm going to
05:09have to use that just disclosure.
05:12There's no commercial support for
05:13the grand rounds an any conflicts of
05:16interest have already been resolved,
05:18and more than happy to discuss that
05:21if anyone wishes to do so, alright.
05:25Now I always like to start the talk
05:28at the very end and the reason that
05:31I like to start a talk at the very
05:34end is in case people fall asleep.
05:37So let's start with cognitive
05:39behavioral therapy for insomnia, CBT.
05:41I what do we know about CBT?
05:43It's been around for about 30 years now
05:45and we know it demonstrates very good
05:48efficacy and comparative effectiveness
05:50when compared directly to fund therapy.
05:52It's durable, we know that studies where.
05:55CPT is being employed.
05:57We can see at least five to 10
06:00years in terms of treatment gains.
06:03Wilson Heights complex cases.
06:05It's just as effective as it is
06:07with the pure cases and anyone.
06:09Whoever finds that pure case
06:11of insomnia do let me know.
06:13I have been looking for them for 20 years.
06:17And finally.
06:18It confers benefits EBT.
06:21I confers benefits above and
06:23beyond sleep itself.
06:24We see reductions in anxiety,
06:26depression,
06:27paying and so it's a gift that
06:30keeps on giving so that really
06:32leads us to the point of this is
06:36the evidence base that we've got.
06:39So we've got at least 20 meter analysis
06:42now which demonstrate that CBT eye works.
06:45It's effective and it confers
06:47these additional benefits.
06:49So really, we're done.
06:50That's the end of the talk, sorry.
06:54Give everyone CBT I fantastic.
06:57We've beaten the Beast of Insomnia.
07:01There are a couple of issues however,
07:04that we have to be mindful
07:06of in terms of CBT I.
07:08There still very few trained
07:10clinicians and so that is a problem
07:13in terms of widespread dissemination.
07:15It's also prone to quite
07:17high levels of attrition.
07:18We see up to 50% of people who
07:21will enroll into a CBT program,
07:23either clinically or in terms of research,
07:26and then drop out.
07:28A lot of clinicians and a lot of patience,
07:32C CBT is quite labor intensive
07:34and time intensive,
07:35and therefore that prevents
07:37them from engaging fully.
07:40Even when we get people into doing CBT,
07:43I what we see is that we get about a 70
07:47or 80% therapeutic response from CBT.
07:49I but only about 50 to 60% of those
07:53responders go on to achieve a full remission.
07:56So even though we've beaten
07:58the Beast of Insomnia,
07:59there's still a few things
08:02that we need to clear up.
08:04How we managed to try to address
08:07some of these issues with CBT in
08:09terms of very few trained clinicians,
08:12we offer in Group therapy which
08:14certainly reduces our waiting times
08:17and we can now afford to do it online,
08:19so there's lots of online programs,
08:22so that's one way in which we've tried to
08:25address the problem of very few clinicians.
08:28What about that levels of
08:31attrition and nonadherence?
08:32We've been looking more
08:34recently adjuvant therapy,
08:35so can we combine CBT to increase the
08:38overall efficacy and effectiveness
08:40by incorporating a stimulant?
08:42For example,
08:43to keep people awake during the day?
08:46What about with a hypnotic to keep
08:49them asleep when you are affording
08:52them that opportunity to get into bed?
08:55Unfortunately,
08:56in both cases the results really
08:58didn't add much in terms of
09:00increasing efficacy or effectiveness.
09:02More recently,
09:03researchers these crazy researchers
09:04from England include partners.
09:06What about including a partner in CBT?
09:08And that's because we can see when
09:11we've looked at it that partners can
09:14be quite a strong barrier to CBT.
09:17I if we think about some of the things
09:20that we do when we're doing CBT,
09:23I we ask people to do.
09:26Things that really don't make
09:28that much sense to them in terms
09:30of managing their sleep,
09:32and that can create some
09:34difficulties in dyads,
09:35whereby if you actually help manage that,
09:38it does increase efficacy somewhat.
09:41And finally,
09:41the most crazy thing at all
09:43is lucid dreaming training.
09:45If we include lucid dreaming training
09:47on top of CBT I does it impact on both,
09:50and that's a trial that we're
09:52doing at the moment,
09:53which is please feel free to ask me
09:56anything about how I managed to get
09:58myself hooked up into a study on.
10:00Lucid dreaming.
10:03Alright,
10:03So what about this issue of it being
10:06perceived and time and labor intensive?
10:09Well,
10:09the question really is how low can
10:12you go for a therapeutic effect and
10:14we can see that there are quite a
10:18few studies on the brief interventions
10:20for people with chronic insomnia
10:22by Jack Edinger and Anne Germain.
10:24When we look at the average
10:27treatment effect sizes,
10:28however,
10:28there moderate to large and
10:30they're good and we can see that.
10:33We can incorporate brief interventions for
10:35insomnia with a certain degree of efficacy,
10:38so that's another way to address the issue.
10:41The challenge with that, however,
10:43as with the other issues,
10:45is that they're not standardized practice,
10:47and so where some people might
10:49want to do group,
10:51other people may not want
10:53to engage with that.
10:54Other people don't want brief
10:56therapies for chronic insomnia,
10:57so maybe we need to think about
11:00an alternative perspective.
11:01So we're going to go to.
11:04Plan B.
11:05What's the Plan B will to
11:07start looking at what we might
11:10think of in terms of a Plan B.
11:13Let's look at how insomnia is diagnosed.
11:15We've got the DSM 5 wonderful thing.
11:18It starts to talk about no issues
11:20between primary and secondary insomnia.
11:22It's one of its greatest benefits in my mind.
11:26When we start looking down at the
11:28symptom profile, one of the things that
11:30jumped out was the problem has been
11:33evident for at least three months.
11:35In order for it to be diagnosis chronic,
11:37it's gotta be present for three months now.
11:40It's always been a question of mine is
11:42to how do we determine three months?
11:45Because in past iterations of all of
11:47the masallah, geez, we've gone right
11:49the way through from one month,
11:51right way through to six months.
11:53So how did we choose three months?
11:55How do we know?
11:56Insomnia is insomnia.
11:58At three months, the easy answer is we don't.
12:02It seems that that's quite
12:04an arbitrary cutting point.
12:08When the DSM five was being.
12:11Conceptualize one of the other things
12:14that they put out in one of their
12:17position statements was this statement
12:18saying although a minimal duration of
12:21three months is required, insomnia of
12:23shorter duration may still
12:25need clinical attention.
12:26So this starts to give us a
12:29very new opportunity out Plan B,
12:32which is why don't we address asamia
12:35when it's during its acute phase,
12:37when it's not reached its chronic phase.
12:41Now, why would that be important?
12:44What are the benefits of this?
12:46And believe me,
12:47I used to have about 6 slides justifying
12:49why I think acute insomnia is important,
12:53and then a very dear friend and
12:55colleague of mine from Upenn,
12:57Michael Careless, said to me look decent.
13:01An ounce of early intervention with acute
13:04insomnia may be worth a pound of CBT I,
13:07in the context of chronic insomnia.
13:10In essence, what we're saying here
13:12is if we can address it early,
13:15we could probably do a lighter touch,
13:18because there's going to be less
13:20conditioned arousal at this point,
13:22and less self schemata around
13:25having the identity of insomnia.
13:28We can also help in terms of reducing
13:30all of those direct and indirect costs
13:33associated with chronic insomnia.
13:34One of those, of course being.
13:37Depression.
13:39So really,
13:40we've got a good rationale
13:43for intervening early.
13:46In terms of not only helping people,
13:48but also in terms of impacting on costs,
13:52and we could do it lighter and
13:54easier than a full CBT eye protocol.
14:02The problem remains, however,
14:04is to what is acute insomnia.
14:07Believe it or not,
14:08considering the pattern ACOLOGY switch
14:11have covered insomnia since the 70s.
14:13Acute insomnia has always been
14:16defined on the basis of exclusion.
14:18In other words,
14:20in most instances it's assumed that
14:23insomnia that meets all of the criteria.
14:26For insomnia,
14:27except duration is classified as acute.
14:31Now that's a problem,
14:34because we don't really know enough about it,
14:37and it's never really been studied.
14:39In order for us to see whether it might
14:42actually be different and warrant a
14:45different form of treatment strategy,
14:47it might respond better to
14:49a stress based protocol.
14:51So in 2012,
14:52one of the first things that we
14:55did was created our own definition.
14:57Our own working definition of acute insomnia.
15:01Anyone who's familiar with the work of Art,
15:05Spielman, will understand his 3P model
15:08that insomnia is made up of predisposing,
15:11precipitating,
15:12and perpetuating factors.
15:14Now, one of the things that Spielman
15:17said in his model, of course,
15:19is that acute insomnia starts
15:21because of a precipitating event,
15:23a life event that he's talking about,
15:26something like a divorce,
15:27or he's talking about a bereavement,
15:29something that is a major
15:32impact on somebody's life.
15:34One of the first things that we
15:37felt was that actually there are
15:40going to be other circumstances
15:42which will lead somebody over that
15:44threshold of insomnia into having
15:47that diagnosis of acute insomnia.
15:50So the main differentiation that
15:52we've had from the DSM and the ICS D
15:55is really we've taken account of the
15:57fact that not only might there be,
16:00as you can see on the left hand side,
16:04significant life event that takes
16:05somebody over a threshold of insomnia.
16:08But it could also be an accumulation
16:10of daily hassles, for example,
16:12and I think that many of us have
16:14experienced this and we're seeing a
16:16lot of this at the moment due to the
16:19circumstances that we're living in is
16:21that it's not one thing that people
16:23pinpoint that is kicked off their insomnia,
16:26but in accumulation of
16:28things that have built up.
16:30The third group that we talk about in
16:32terms of the precipitants for insomnia.
16:35Somebody who's chronically stressed if
16:37we've got somebody who's caregiving,
16:39for example.
16:40That's going to keep them
16:42quite close to that threshold.
16:44That stress threshold that
16:46goes over into insomnia.
16:47And it might just take one or two things
16:51that push them over the edge into insomnia.
16:54So we've rejected the idea that it
16:57has to be a significant life event.
17:00But they also could be daily
17:03hassles that have accumulated
17:04or indeed a chronic stressor.
17:07Beyond that,
17:08we generally keeping within the
17:10framework of the DSM 5 in that it's
17:13a problem of getting off to sleep,
17:15staying asleep,
17:16waking too early in the morning
17:19despite adequate opportunity.
17:21Three nights a week.
17:22And causing significant daytime
17:25impairment or distress.
17:26But what we're talking about here is period.
17:30Generally between two weeks,
17:32three months.
17:36OK, so we've now got a working
17:39definition for acute insomnia.
17:41That's fantastic. Yay me.
17:44Do we need to do after that?
17:47Well, you know.
17:48As with anything that we're dealing
17:50with in terms of looking for
17:53resource is for healthcare resources,
17:55we need to know what the prevalence is.
17:58We need to know the Epidemiology
18:00of acute insomnia becausw,
18:01is it worth plowing money into this?
18:04If indeed it doesn't exist
18:06and it's not very problematic.
18:08So we conducted the first study
18:10looking at the Epidemiology of
18:12acute insomnia in both the US and.
18:15Can you take?
18:17What we found from that is that the
18:20point prevalence of acute insomnia
18:23is somewhere between 8 and 9%.
18:25So 8 or 9% of the population
18:28are suffering from the acute
18:30insomnia at any given time point.
18:33What about its incidence, however?
18:36When we start to talk about incidents,
18:39we see quite a high incidence rate.
18:41We're looking at an annual incidence
18:44rate of between 31 to 36%,
18:46so almost a third of the population will
18:50develop acute insomnia in a given year.
18:53But for a large majority of those,
18:56they will naturally rumic as opposed to
18:59going on to develop chronic insomnia,
19:02just as a sideline.
19:04You know what we're dealing with
19:06at the moment in terms of covert,
19:09what we're seeing in terms of acute
19:11insomnia is increasing by about 40%,
19:13so we're going to see over this year
19:16and the next year, acute insomnia.
19:19Prevalence rates,
19:20probably in their 20s or even 30s.
19:23Lot of people suffering from acute
19:25insomnia at the moment there's a lot
19:28of uncertainty, anxiety and worry.
19:30Alright,
19:30so now we've got a definition fantastic,
19:33and that made me famous.
19:36Now we've got the prevalence and incidents,
19:38so now we've got some good data behind.
19:42How popular and common it is and
19:45whether we need to address it or not.
19:49So now we really need to know
19:51more about what it looks like.
19:53What does acute insomnia actually look like?
19:56Going back to the apea and
19:58what they suggested in 2012.
20:00Well,
20:01they suggested that this situational or
20:03acute insomnia is often associated with
20:06life events or changes in sleep schedules,
20:09so that's the first part we want to check.
20:12Does this trigger actually need
20:14to occur in order for somebody
20:17to develop acute insomnia?
20:18Starting now to look more into
20:21the analytic Epidemiology of it?
20:25So what if we got in terms
20:28of previous research?
20:30There's only actually one significant paper
20:32on precipitating factors in insomnia,
20:34and this is my cell am Bastian.
20:38University level from 2004.
20:40An what Celine did is she got a group
20:44of patients that were coming through
20:47to clinic for treatment 323 and she
20:50asked them whether they could recall
20:53the precipitant event that kicked off
20:56and triggered their insomnia and what
20:59she found was 78.3% of them said yes
21:03they can recall a specific event.
21:06Now there are two main challenges
21:08with Celine's.
21:09Work here.
21:10The first is that the mean length that
21:13people had insomnia when they went
21:15into the clinic was over 10 years.
21:17So there's gonna be some memory
21:20biases around that.
21:21That we need to be mindful of.
21:23The other issue, of course,
21:25is that she didn't account for
21:27a previous history of insomnia,
21:30and one of the things that we do
21:32know is that a previous episode of
21:35Insomnia is a significant risk factor
21:38for the development of insomnia,
21:40and so we might want to look at
21:43whether there are differences
21:44in precipitating events based on
21:46whether it's your first ever episode,
21:49or indeed whether it is a recurrent episode.
21:52So small scale study.
21:54We've asked people, in essence.
21:58Um,
21:59if there in the first three months
22:01of a recurrent episode,
22:03so they're still in acute insomnia,
22:05but they're going through a
22:07recurrent episode, not their first.
22:09What happens if you ask people?
22:12Can they identify a precipitant an it's
22:15interesting in the sense that 93% of people,
22:18even though there are increased risk for
22:21insomnia because they've had it in the past.
22:24They can still identify a precipitants
22:26or precipitant is needed for.
22:28Even a recurrent episode.
22:32What about if you ask people if
22:34it's their first ever episode?
22:37So you're asking people within the
22:391st three months of their first
22:41ever episode of Acute Insomnia?
22:43Surprise, surprise.
22:45100% everyone interviewed could
22:47identify specific precipitants they may
22:49have been accumulations of daily hassles.
22:52They may have been life events
22:55or chronic stressors with an
22:57additional stress burden on it,
22:59but they could identify something
23:01that triggered off their insomnia.
23:04So it seems like the API is
23:07on the right track.
23:09It is precipitated by an event of some sort.
23:14Alright, so now we know.
23:17But it looks like we now know the
23:20prevalence of it and we now know that it
23:24is in response to a precipitating event.
23:27What about sleep?
23:29It's an interesting thing.
23:31We would probably take it for
23:33granted that its impact is on sleep,
23:36but we really do need to check that
23:39and so very small scale study really.
23:42Just looking at people with acute
23:44insomnia compared to a group of controls,
23:47matched controls and looking at
23:49their sleep diary information when
23:51we look at people sleep Diaries,
23:53what we do see is that there are
23:57significant differences there.
23:58Reporting increased sleep.
23:59Latency's increased wake after
24:01sleep onset and
24:03certainly reduced total sleep time
24:05and a decreased sleep efficiency
24:08compared to our normal sleepers,
24:10so their self reports of sleep are
24:13poor compared to normal sleepers.
24:16When we look at some of their
24:19measures of stress and mood,
24:21they appear to be reporting more life events.
24:24That makes sense with the precipitants.
24:27Depsite stress over the last month,
24:30that is also significantly higher
24:33than our normal sleepers, as are our
24:36symptoms of anxiety and depression,
24:38so it gives us our first indication of
24:41some of the elements that are feeding into
24:45this experience of acute insomnia, wonderful.
24:50What about the actual sleep?
24:52What's happening with
24:54somebody's sleep architecture?
24:55During acute insomnia?
24:56One of the mysteries that we've got,
25:00certainly in the realm of chronic insomnia,
25:03is that we've never really found a
25:05biological signal within sleep architecture,
25:08and so would we find one
25:11within acute insomnia.
25:12Let's find out the answer is,
25:15there does appear to be a tradeoff
25:18when somebody has acute insomnia.
25:20It appears that there seems to
25:23be a switch between N2 and N3.
25:26We reduced the amount of N3,
25:28slow wave sleep and we increase
25:31at about the same rate.
25:33How levels of N2 or stage two sleep?
25:36So there does appear to be a change
25:39in sleep architecture associated
25:41with having acute insomnia.
25:44Now this is all wonderful.
25:46We're mapping out acute insomnia.
25:48It's beautiful,
25:49it's wonderful.
25:51What we really want to know if
25:53we want to start thinking about
25:55intervening and helping is what really
25:57makes somebody go acute to chronic.
26:00That's the key point.
26:01That's what we want to know,
26:04because we know that in the majority of
26:07cases that it should go away on its own.
26:10So.
26:12Let's characterize people.
26:14So we've taken our group of people
26:17with acute insomnia.
26:19We followed them up.
26:22For the next three months and
26:24we've worked out who's gone on to
26:26develop chronic insomnia and who's
26:28naturally emitted from insomnia.
26:30So we've split that group and we're
26:32going to look at those baseline
26:34characteristics around the sleep
26:36diary and sleep architecture.
26:38Are there any signals at that early
26:40stage which start to give us an
26:43indication of who's going to develop
26:45chronic insomnia and who's not
26:47lose naturally going to get better?
26:50So let's look at sleep diary
26:53information first.
26:54No differences,
26:55so it doesn't appear that the severity
26:58or the perceived severity of symptoms
27:00is the thing that fuels somebody
27:03going from acute to chronic insomnia.
27:06No differences in sleep latency,
27:08number of awakenings,
27:09wake after sleep onset,
27:11total sleep time,
27:13or indeed sleep efficiency.
27:16OK,
27:16so it's not about the severity
27:19of the complaint that drives
27:21acute to chronic insomnia.
27:25Let's look at their architecture,
27:27the baseline architecture.
27:28And here we see some curious differences.
27:30What we see is those people who have acute
27:34insomnia but will remit within three months.
27:37In terms of REM latency,
27:39how rapidly there going into REM,
27:41what we are seeing is that they pretty
27:44much the same as normal sleepers
27:47rather than that 9200 minutes.
27:49Other people who go on to
27:51develop chronic insomnia,
27:52their REM latency is actually quite sure
27:55comparatively on average it's 66 minutes.
27:57Similarly,
27:58when we start to look at slow wave sleep,
28:01we see that there is a linear reduction
28:04in slow wave sleep by group status.
28:07With those people who go on
28:10to develop chronic insomnia,
28:11demonstrating the shortest amounts
28:13of slow wave sleep at baseline.
28:16So that starts to give us an indication now.
28:20Is it about stress?
28:22Is it that stress that is fueling
28:24these changes in terms of REM
28:27in terms of slow wave sleep?
28:29Looking at Life Events scale scores,
28:31no real significant difference
28:33between those two groups,
28:34so it doesn't appear to be about
28:37the veracity of the life events.
28:39What about perceived stress,
28:40scale scores so perceived
28:42stress over the last month?
28:44Again, no significant differences there,
28:45So what it appears is it's
28:48not about the stress,
28:49so we're doing this as a
28:51process of elimination.
28:52That's why it's taking me so many years,
28:55and that's why I look so old.
28:58I'm actually only 19.
28:59But in essence,
29:01through our process of elimination,
29:03we've determined that it's not really
29:05about the severity of the complaint,
29:07and it's not about the
29:09severity of the stress itself.
29:12What do we see this pattern in there?
29:14And this is something that sparked a little
29:17sideline is we've seen this pattern before.
29:19We've seen this pattern in the 70s.
29:22I've seriously reduced REM latency
29:24and reduced slow wave sleep.
29:27Is also a marker.
29:30Of potential depression.
29:31So maybe it's the depression that's firming
29:34this up so we looked specifically at
29:38levels of anxiety levels of depression,
29:41and certainly you can see that those
29:44people who go on to develop chronic insomnia.
29:47They have more anxious and
29:50depressive symptomology at baseline,
29:52so that may well be one of our drivers.
29:57Now the thing we got to remember is
29:59that's actually quite a small sample,
30:00so we.
30:00Want to be a bit more mindful
30:02about larger samples before we
30:04can make these judgments?
30:05And I'm going to come on to that
30:08in the next part of the talk.
30:11So we're going to take a break here.
30:13Before I start talking again,
30:15what do we know?
30:16So what do we know about sleeping
30:19with the enemy acute insomnia?
30:22It is associated with a precipitating event.
30:24It's got a pretty high prevalence,
30:278-9 percent annual incidence
30:29is quite high as well.
30:31It's associated with increased stage,
30:34two decrease slow wave sleep at
30:37transition to chronic insomnia is
30:39associated with the fast onset of
30:42REM and decreased slow wave sleep
30:45that does look quite similar to what
30:48we see is the onset of an
30:52affective disorder alright.
30:54Now we've got to a point of thinking right?
30:56Let's talk about intervention.
30:58What are we going to do about intervention?
31:01If we were to create an intervention.
31:05Where would we intervene?
31:06What's the point that we intervene?
31:09And certainly if we think about
31:11it as a precipitating events,
31:13you'd maybe want to look
31:15at a stress framework,
31:16but that doesn't appear to be the case,
31:19so perhaps we should study the
31:22blue area from Spillmans model.
31:24Maybe we should look to see are
31:26these perpetuate ING behaviors and
31:28cognitions and affective issues?
31:30I think present during acute insomnia.
31:35So this is a much larger sample.
31:39And here we got a group of normal sleepers
31:42737 against people with acute insomnia,
31:45and so we've looked at them in
31:48terms of their sleep symptoms and
31:51predisposing factors of personality,
31:53arousal predisposition and of course
31:55stress and insomnia vulnerability.
31:57Then we've looked at
31:59these precipitants again.
32:00Life events, perceived stress,
32:02anxiety and depression and see if that
32:05anxiety and depression comes forward.
32:08We just want to take account of coping.
32:11Of course, it may be that how you
32:13cope with that initial precipitating
32:15event that fuels whether you develop
32:18insomnia in a chronic form or not.
32:21So we're looking at thought
32:23control strategies and maladaptive
32:25and adaptive forms of coping.
32:27Finally,
32:28let's throw in those perpetuating factors
32:30that really should be plainly tiny tiny.
32:33At this point of acute insomnia,
32:36we're going to look at fatigue,
32:38dysfunctional beliefs,
32:39cognitive and behavioral sleep preoccupation.
32:41What we mean by that is when people
32:45adopt cognitive or behavioral actions
32:47which are detrimental to their sleep.
32:50Going to bed early, for example,
32:52lying in drinking more coffee,
32:54worrying about it during the daytime.
32:58The affect if element of sleep preoccupation
33:01is much more focused on rumination.
33:03I can't stop thinking about it.
33:06I can't get over the insomnia itself.
33:09Finally, we also want to
33:11look at pre sleep arousal.
33:13Is it the point that we've actually
33:16created a form of hyperarousal,
33:18be it somatic or cognitive in
33:21terms of fueling this insomnia?
33:23Alright, so looking at differences
33:26between our normal sleepers and now
33:28individuals with acute insomnia, yeah,
33:31there's differences in each domain.
33:33Now they don't tell us much about
33:36what predict who goes chronic,
33:38what they do do is give us
33:40an indication of what does.
33:42Somebody with their cute insomnia look like.
33:45What are those risks and what
33:48are those associated outcomes
33:50with having acute insomnia?
33:52Again, what we really want to do,
33:54however, is figure out.
33:56What is predicting who goes chronic?
34:01Again, got a nice sample here.
34:03Got 129 people with acute insomnia.
34:06We've separated them out into
34:08those people who get better.
34:10Naturally,
34:10Ramit and those people who go on to
34:14develop chronic insomnia in the future,
34:16and we're going to look up all of
34:20those significant variables that we
34:22got from our cross sectional study
34:24to look at what other
34:26predictors. What predicts it
34:29becoming the enemy a long term enemy?
34:33And Interestingly,
34:34which is not quite what we might expect,
34:37is that it's not about predisposing factors.
34:42In terms of precipitants,
34:44even the anxiety does appear
34:46not to be fueling somebody going
34:49acute to chronic more so.
34:52Depression, depressions, measures,
34:53baseline are a good predictor of
34:56who's going to go chronic against
34:59who is going to go from it.
35:02So higher levels of depression
35:05with about our coping.
35:06Nothing comes through from coping.
35:10But what is interesting?
35:11And I think this talks a lot to
35:14spillmans model is when we look at
35:16the factors that are significant
35:18predictors of who will become chronic.
35:21What we can see is it's focused
35:24largely around cognitive factors,
35:26behavioral actions which are used
35:28to address the insomnia during the
35:31acute phase going to bed early,
35:34lying in napping.
35:35Also, those affect, if ruminations,
35:38that we see.
35:40People can't stop thinking about
35:42sleep craving sleep during that
35:45acute phase that also appears to be
35:48driving us into the chronic insomnia.
35:51So what that gives us is the indication
35:54that we don't really want a stressed
35:57based management system in order
35:59to try to manage acute insomnia,
36:01we want a cognitive behavioral framework,
36:04so this is what we've let us
36:06now to our treatment pathway.
36:12Can we circumvent the transition and
36:14we stop people going from acute to
36:17chronic insomnia and we're going to
36:20use something called A1 single shot.
36:23That's a single shot of CBT I.
36:28So let's go back to those brief
36:30interventions because we need to now
36:32frame how much of our intervention,
36:34how much of that weight do we need
36:37to put in there in order to do what
36:39we need to do to circumvent the
36:42transition to chronic insomnia?
36:44So going back to those brief interventions,
36:46what we can see is generally they're
36:48working on about an hour contact time.
36:51Look at the work of Jack Edinger
36:53and Anne Germain works out at about
36:55an hour on average contact time.
36:59And then if we look at the dose
37:02response trial by Jack Edinger,
37:04four sessions helped the greatest
37:06impact in terms of number of clinical
37:08remissions followed by one session,
37:108 sessions, and then two sessions.
37:13Now I don't know about you,
37:15and if you were maybe do CBT.
37:18I offering somebody four sessions of 15
37:21minutes. Will probably have you killed.
37:24So OK, let's then go back and say next.
37:28One down is one session,
37:30so one session of one hour in
37:32order to get some clinical gain
37:35within chronic insomnia,
37:37which should be enough in order to
37:40affect change in acute insomnia.
37:42Just as a sideline,
37:44Jack Edinger also tried a pamphlet.
37:48And because of that I wanted a pamphlet.
37:50No other reason I want to
37:53conflict with Jack had one.
37:55So now I've got to create a pamphlet, yay.
37:58Alright, so here's the pamphlet.
38:01First simple pamphlet and it's taking
38:04quite a few of the elements of CBT,
38:06but doing him in a much lighter touch.
38:09It's framed.
38:10There's something called the 3D's detect.
38:12So that's how to record a sleep
38:15diary and when to seek help.
38:18Detach that gives us our
38:21stimulus control instructions.
38:22If you're awake in bed,
38:24get out of the bed, do something else,
38:28go back to bed when you are tired and
38:32sleepy again, and finally distract.
38:34This is our cognitive techniques.
38:36We've got cognitive control,
38:38constructive worry,
38:39putting the day to bed before you
38:42go to bed and giving people imagery,
38:45distraction techniques.
38:46As per Alison Harvey.
38:48OK, so we've now got our pamphlet
38:50and it is beautiful, isn't it?
38:53It's blue.
38:55First thing we want to do is check out
38:58the feasibility on the pamphlet itself.
39:01Does the pamphlet do anything
39:02because it's got some active
39:04treatment modalities in it?
39:06Is it doing anything?
39:08So we've done a feasibility study
39:10with a sample of individuals with
39:13acute insomnia and what we can see
39:16is even a week after somebody has
39:18been given just the pamphlet alone.
39:20We see significant reductions in terms
39:22of cognitive and somatic arousal.
39:24Fantastic, we're getting there.
39:26What about the hour?
39:27What are you going to do with
39:29somebody in your single session?
39:31In essence, we talk about sleep,
39:33education and sleep hygiene,
39:35but again, very light touch.
39:37Most patients with insomnia I've
39:39already got pretty good sleep hygiene
39:41by the time they come to you.
39:43It's really focused on sleep restriction,
39:45and so we're doing a basic
39:47sleep restriction protocol,
39:48previous weeks total sleep time becomes
39:51time in bed for the following week.
39:53Anchor your time in bed to the
39:56morning and titrate at 15 minutes
39:58after week one and then every.
40:00Subsequent week,
40:02so very standardized CBT based
40:05sleep restriction protocol.
40:07Introduce the pamphlet and then discuss
40:09any barriers to implementation.
40:11So now we've got our intervention.
40:13We've done all of the background work.
40:16Let's take the intervention out for a spin.
40:20So we've got a randomized control trial.
40:23Again, small sample, but adequately powered.
40:2720 randomized to weightless
40:29control and 20 randomized to the
40:32intervention and the delivery of
40:34the intervention was done by me.
40:36And that's important later on.
40:41Single session 60 to 70 minutes and the
40:44pamphlet given one month follow up.
40:47What is the outcome?
40:49In essence, actually pretty good.
40:51We've got a 60% remission rate at one
40:54month compared to our weakness control,
40:56which is only 15%, which is significant.
41:00What's interesting about the first
41:02trial was that by three months
41:04we saw an increase in remission.
41:06In those people that were treated,
41:09it went up to 70, three point, 7%.
41:11That's not unusual to see within
41:14a CBT format, either that it's
41:16the gift that keeps on giving.
41:18We tend to see increases in total sleep
41:21time after the patient has left us,
41:24so this is a good start.
41:26We've got a good start in terms
41:29of randomized control trial.
41:31I don't know about everyone else,
41:33but I am constantly being asked to
41:36do things quicker, cheaper, faster.
41:38So the next step, D.
41:40Oh no, it's not does it impacts on sleep?
41:44I suppose that's quite an important question,
41:46isn't it? Does it impact on sleep?
41:48Absolutely,
41:49we can see some nice effect sizes,
41:51moderately nice effect sizes in
41:53terms of reductions in sleep latency,
41:55wake after sleep onset, and sleep efficiency.
41:58So, as I was saying,
41:59which I gave you all the opportunities,
42:02think about what you're going to say next.
42:05What's faster and quicker and easier?
42:07Can you do it in groups?
42:09Yep, I was asked if I could do it in groups.
42:14So here we've got our group data.
42:18Again, we're looking at our outcome point is,
42:21those people who have gone into
42:23full remission so they completely
42:25do not have insomnia as per the
42:28insomnia severity index.
42:29One month after treatment,
42:30what we can see is there's not much
42:33difference between group and individual.
42:3569% of those people that were
42:38treated in Group format,
42:39they were in remission compared to
42:42the individual group which was 75%.
42:44But we did see a slight difference
42:46in terms of attrition.
42:49People were more likely to drop out
42:51of group than they were individual,
42:54but it wasn't significant.
42:56OK, so we now know that it works.
42:59We can deliver it in groups.
43:01Now what you want to do is take it
43:03into a population that's incredibly
43:06vulnerable. That's the real test, isn't it?
43:08Find out if you've got a group that's
43:11really vulnerable to acute insomnia.
43:13Give it to them and see if they end
43:16up developing chronic insomnia.
43:19And here we've chosen male prisoners.
43:21For some reason. When you go to prison.
43:26You're very likely to develop insomnia,
43:28and so it starts in the prison.
43:31Think about changes,
43:32environment changes in routine.
43:34There's a lot of stress, alot of concern,
43:37sharing those sorts of things lead into
43:40this vulnerability for acute insomnia,
43:42so we've got 30 male category C prisoners,
43:45so these are the ones that we don't let out.
43:50They're not allowed out there, not organic.
43:53They're not free range.
43:55In essence,
43:56done exactly the same as we've
43:58done in the previous trials,
44:00but this is an open label trial.
44:03What are we looking at in terms
44:05of one month post treatment, 70,
44:08three point, 3% remission rate?
44:10So here's an interesting thing.
44:12So in our first study we had a
44:1560% remission rate one month,
44:17and in the second and third,
44:19it's averaging out around 73 to 75%.
44:22Why is this happening?
44:24Remember, I said I took the first one?
44:27Clearly I'm crap because what happened
44:29in the second study and the third study
44:32is that actually trained people to do
44:34the intervention they've delivered it,
44:36and they've got better outcomes than me,
44:38so I should be terribly ashamed
44:41and will not be doing that again.
44:44Alright, so we've looked at it
44:46in a vulnerable population now.
44:48Wonderful, what about impact on mood.
44:51We know that CBT.
44:52I really does have a knock on effect in
44:56terms of anxiety and depression symptoms.
44:59So when we look at pre treatment versus
45:03post treatment in terms of mood,
45:06anxiety, depression,
45:06we're seeing some really good effect sizes.
45:10Here we're seeing reductions of one
45:12month of over 50% in both anxiety
45:16symptoms and in terms of depressants,
45:18symptomology.
45:19So it's doing what we would expect
45:22from a standardized CBT I,
45:24but it's also just doing it in
45:27that early acute insomnia.
45:29Days alright,
45:30so we're coming to the end
45:32of what was an extravaganza.
45:35What can we conclude?
45:37Single shot of CBT I led to a
45:40fourfold increase in remission rate
45:42that is based upon the first study.
45:46We also saw those improvements
45:48in subjectively reported sleep.
45:50Reductions in arousal anxiety
45:54and depressive symptomology.
45:56And people liked it.
45:58People actually liked the fact
46:00that it was a single session and
46:02that they were given something
46:04tangible to go away with,
46:06and that really made it well tolerable.
46:09Certainly in terms of the dropout rates,
46:12we weren't seeing anything near in
46:14any of the trials that relates to what
46:17we might see in a chronic insomnia parameter,
46:20so that's brilliant.
46:21So it's well tolerated as well.
46:24Where is it going now?
46:25Well, we're actually deploying it.
46:27Due to kovit at the moment,
46:30as you can imagine,
46:31there's a lot of issues which are increasing
46:33the vulnerability for acute insomnia.
46:36So we're running a trial.
46:37At the moment we've got 200
46:39people in it at the moment,
46:42which is giving them an online
46:44version of the one shot.
46:46What about primary care?
46:47It's another area of vulnerability
46:50where we'll see a lot of people
46:52who will attend the PCP or the
46:54GP and talk about acute insomnia.
46:56So we're deploying it.
46:58Out in primary care,
46:59but also Interestingly,
47:01we're going to be using it within
47:03other vulnerable populations
47:05during addiction recovery.
47:07One of the things that we know
47:10is that during recovery,
47:11although sleep may not become
47:13a problem during recovery,
47:15it is have been identified by
47:17patients that have undergone addiction
47:19recovery as a vulnerability and a
47:21concern that they feel that if their
47:24sleep goes wonky that they will
47:26end up going back to their drugs or alcohol.
47:29So we're trying to see whether it
47:32circumvents not only the issues
47:34around sleep and that vulnerability,
47:36but maybe it has a knock on effect.
47:39In terms of relapse an we're now
47:41running it out and I think 5 places
47:44these are independent trials.
47:45I'm not running any of these, thankfully.
47:50We're actually running it in oncology
47:53and so this is now being deployed in
47:56the US and Australia and in the UK.
47:58And when somebody gets a diagnosis
48:00of any form of cancer and they're
48:02just about to start treatment
48:04protocols 'cause we know that that's
48:07an increasing vulnerability period.
48:08People have been given the intervention
48:11as a prophylactic, and what we're
48:13looking at in those respects is,
48:15is it impacting on sleep, insomnia,
48:17the development of insomnia itself?
48:20But is it also having an impact on
48:23recovery and treatment pathways?
48:25So some very exciting things
48:27happening in the future.
48:31As with all my talks,
48:33you know I don't do half of this stuff.
48:35You know I have collaborators
48:37from all around the world who
48:39do all of the work for me.
48:41I've got my lab team and
48:43that's a picture of us.
48:44When we were allowed out,
48:46I think we all might look a
48:48little bit different by the time
48:49we're all allowed back in again.
48:51But of course, there's also people
48:53that fund the work that I do,
48:55that I'm always eternally grateful for.
48:57OK, thanks very much.
48:58That's me.
49:01Great, that's really wonderful.
49:03So I'm under is in truck and I'm helping
49:05out Brianne and monitoring the session.
49:07She unfortunately had to run out.
49:11Quickly it at the beginning of the session,
49:14but so thank you for this wonderful talk.
49:16Doctor Ellis is really insightful and
49:18evolution of sleep disorder from its
49:20Genesis all the way to treatment.
49:22It was really nice to see that,
49:24and it's a problem that we encountered
49:26commonly and I'm sure many of the
49:28audience I've encountered it,
49:30especially now that we're having
49:31multiple social and health
49:33stressors during these times.
49:34And so I'd like to invite the
49:36audience to ask some questions.
49:38And while folks are typing
49:39things in and chat,
49:41which I'll be happy.
49:42Train if you wanted to ask
49:43question person just let me know.
49:45I'll I'll be happy to meet you.
49:47I just wanted to start off with.
49:49A question as well,
49:51and so are there some components of
49:53the one shot interventions that use?
49:55Note that might work better than others,
49:58or something you think it's
50:00it's intervention.
50:00It is a cute subtype of insomnia,
50:02something that has to be.
50:04Tailored to each individual
50:05patient by therapist,
50:07it's a
50:08really nice question. Thank you,
50:10that was not set up for everybody else.
50:14One of the things that we did is we.
50:17We interviewed all of the patients in
50:18each of those three studies afterwards
50:20and found you know what worked for you.
50:22What didn't work for you.
50:24What appears anecdotally to be
50:26the strongest element from the one
50:28shot is actually in the pamphlet
50:30rather than the one hour session,
50:33and that is the stimulus
50:35control instructions.
50:36So there is an understanding then
50:39that perhaps if we wanted to
50:41tailor this down even further,
50:43let's just start with stimulus
50:45control and then see what happens.
50:47Stop doing almost a deconstruction study,
50:49which is one of the things that
50:52we're doing at the moment.
50:54It certainly appears people like
50:55the cognitive strategies,
50:57the distraction strategies,
50:58but they are they.
51:00They feel that the benefit is
51:02really coming from stimulus control.
51:05Interesting.
51:07Excellent, well thank you for that.
51:09So let's see there's a question
51:11from you requesting Doctor Ellis.
51:13Do we know how the nature of the
51:15precipitating stressful life events looks
51:17different between acute to remission,
51:19acute to chronic groups?
51:20And of course there is taking
51:22you for a great presentation.
51:24And so I think the question is
51:26whether there's a difference in
51:28stressors in acute versus chronic.
51:30Find Sonia.
51:32It's an interesting point.
51:34It really does speak to model
51:36of insomnia by Colin SP.
51:38You know his psychobiological
51:39inhibition model.
51:40What Collins suggests is
51:41that during the acute phase,
51:43the stress that the sleep
51:45loss should be due to stress,
51:47but then there is a switch point
51:50and I think that's the Holy Grail
51:53of what we're looking for here
51:55is when does it become that the.
51:58This dress causing the sleep loss
52:01becomes the sleep loss as a stressor itself,
52:04and I think that is where we might find
52:08this transition point to chronic insomnia.
52:11When we've looked at the types of stressors.
52:16Between our groups,
52:17those who commit those who don't commit.
52:20Not only is there no differences in
52:22terms of life events or perceived
52:25stress and anxiety depression,
52:27although depression does appear
52:29to be a factor in there.
52:32What is interesting is that
52:34you're seeing financial issues,
52:35so we've asked people more qualitatively,
52:38what are the issues?
52:40Are they financial,
52:41social, environmental,
52:42occupational?
52:42Financial issues appear to be
52:45something that drives chronic
52:47insomnia into it's chronic form,
52:49as opposed to remission.
52:50That's probably because the
52:52longevity of financial issues,
52:54but there weren't really any
52:56other differences in terms of the
52:58types of stressors or the length
53:00of the stressors that really
53:02impacted on whether somebody got
53:04better or somebody got worse.
53:08Interesting, thank you.
53:10Let's see it so there's another
53:12question from folks at the
53:14VA Veteran Affairs Hospital.
53:15So so. Doctor Ellis,
53:16any digital CBT tool that you
53:18personally like and recommend.
53:21Oh
53:24oh, not not
53:25to put you on the spot.
53:29Yeah, I mean, we've got three in the UK.
53:33So sleepy, of course, is the most well
53:35known of the three that are used in
53:37the UK. Yep. I certainly
53:41feel that it digital has got
53:43its place. Because of widespread
53:46dissemination and implementation.
53:48I do worry about
53:50some of the issues around
53:52digital in terms of engagement.
53:54And also when people are doing
53:57online therapy, you know.
54:00When I'm doing therapy face to face,
54:02you have to come see me at the time of which
54:06is specified. If you're doing it remotely,
54:08what's not to stop you from doing it
54:11at 8:00 o'clock nine o'clock at night,
54:13which may well have actually
54:16detrimental impact? And the other
54:18thing before I advocate for anyone.
54:20It is the fact that you know when we look
54:23at the work of Nora Vincent. For example,
54:25when she's looked at stat care models,
54:27there's quite a high level of people
54:29who will not update for digital CBT.
54:31I. So a lot of people don't like it,
54:35don't want it.
54:36There was a really nice idea, but she did.
54:39If I was to advocate for one,
54:42I would advocate for one which
54:44is called sleep Four,
54:45which was developed in the UK.
54:47The reason that I would say that
54:49I fondest fan of that particular
54:51variant is because a I was one
54:53of the beta testers on it,
54:55so I know what it was like.
54:58B, it's free.
55:00Because it was built upon
55:02government money and in the UK,
55:04if you're building it up on NIH money,
55:06or you know government money,
55:08then it has to be made freely available
55:10and we do like a nice freebie.
55:13So
55:14I think those those sort of swing me towards
55:16sleep full as opposed to sleep here,
55:18although I think it's a it's a great product
55:20and please don't tell Colin I said back
55:23I'm going to tell him. I knew it no
55:27no. So I have a
55:29question. What is the
55:31reimbursement like? What
55:32is the reimbursement like is that's
55:34in the US? That's a huge issue.
55:37For CBT I yeah yeah this is been
55:40both a helping a hindrance to
55:43us in the fact that we've got
55:45our National Health Service,
55:47so our socialized medicine
55:48in the sense that there is no
55:51issues around reimbursement.
55:53But the problem is is it's so
55:56sporadic in order to get the CBT
55:59service up and running in the UK,
56:02it's very challenging. Name there's about
56:058 places in the UK where you can
56:08get face to face CBT in the UK.
56:11Which is not great and this is one of
56:14the reasons why online digital CBT I is
56:17becoming a lot more popular in the UK,
56:19and certainly it's going through
56:21at the moment as I'm sitting on
56:24the panel again. Don't
56:25tell Colin I'm sitting on the
56:27panel so that it will become part
56:30of the National Health Service,
56:31so it'll be freely
56:33deliverable from GP surgeries.
56:34OK, so that will improve the situation.
56:37But you know, I always have this
56:39thing about face to face is.
56:41Is a very important factor
56:43because of therapeutic alliance.
56:46Great, well thank you I think just a
56:49couple of more questions in the comments.
56:51So for the folks at the VA who
56:53are asking questions about apps,
56:55there's actually a VA based CBT I coach
56:58that was developed by researchers at the VA,
57:00which you might be familiar with,
57:02and so that's freely available also
57:04to patients and their loved ones
57:06and doctor Schneeberg from our
57:08sleep center is asking whether you
57:10have any tips on delivering CBT.
57:11I via Tele medicine.
57:15You know CBT is selling thing.
57:17I think it's less about therapeutics
57:19'cause they can be delivered
57:21in a variety of contexts.
57:23This is about selling and I think
57:25that you know my my experience of
57:27telling medicine has been limited,
57:29but in that respect,
57:31what we have tended to do is we focused
57:34much more on that interactive process
57:36in terms of the we're trying to get
57:39that therapeutic alliance across.
57:40I think that's the only way to sell
57:43it through therapeutic alliance,
57:45especially when it's removed.
57:48Great, well thank you so much for
57:51a wonderful talk and for great
57:53answers to the questions and this.
57:55I think I know is useful for
57:57everybody in the audience and perhaps
57:58looking forward to having you in our
58:01sessions another time another year,
58:03maybe even in person.
58:04Who knows, we'll go out and say it there,
58:07but just as the call out to the
58:10rest of the group is that we'll
58:12resume our next session next week
58:14and looking forward to a great talk.
58:17Alright, thanks, everybody.
58:18Take care.
58:19So much bye bye.
58:22Bye bye. Goodbye doctor player.
58:28Hi.