Eating And Sleep Disorders (Week 8 / Chap 9-10) Flashcards
1
Q
Impact of eating disorders
A
- Up to 20% of people with anorexia die from their disorder (5% within
a decade, e.g., Franko et al., 2013) - This is more than any other disorder, including depression
- The rate of suicide is 50 X higher than in the general population
Arcelus et al., 2011)
2
Q
Bulimia Nervosa in the DSM5
A
- Recurrent episodes of binge eating, meaning:
1. Eating, in a discrete amount of time an amount of food (e.g., within
2 hours), definitely larger than most people would eat in a similar
amount of time
2. Sense of lack of control over eating during the episode - Recurrent inappropriate compensatory behaviours to prevent weight
gain (vomiting, exercise, laxatives, diuretics) - Occurs at least once a week for at least 3 months
- Self‐evaluation is unduly influenced by body shape and weight
- Doesn’t occur exclusively during episodes of anorexia nervosa
3
Q
Bulimia Side effects
A
- Facial distortions from salivary gland enlargement (vomiting)
- Loss of and damage to teeth from vomiting
- Potentially fatal cardiac arrhythmia or kidney failure, from electrolyte
imbalances - Subsequent substance abuse, smoking, (von Ranson, Iacono &
McGue, 2002) and depression (Steiger et al., 2013) - Weight gain (Ludescher et al., 2009) ‐ laxatives and vomiting are not
effective. Most are within 10% of their normal body weight when
they start. - Colon damage or constipation from laxative use
4
Q
Anorexia Nervosa DSM5
A
A. Restriction of energy intake relative to requirements, leading to a
significantly low weight (in context of age, sex, health etc)
B. Intense fear of gaining weight or becoming fat, or persistent behaviour
that interferes with weight gain, even at a significantly low weight
C. Disturbance in the way in which one’s body is experienced, undue
influence of body weight or shape on self‐evaluation, or persistent lack
of recognition of the seriousness of the current body weight
* Specification of whether they had the restricting (no binge/purge – just
restriction and/or excessive exercise) or binge‐eating/purging subtype in
the past 3 months
5
Q
Description / Summary of Anorexia
A
- Intense fear of obesity
- Distorted sense of their body size: Pick your body shape.
- They answer with gross overestimation (McCabe, McFarlane, Polivy &
Olmstead, 2001); they believe they look “fat” - Other observers would estimate the same person’s shape accurately, and
would recognize that they look sickly - They can binge/purge too (eating without control albeit far smaller
amounts of food than those with bulimia and an immediate purge) - They expect continual weight loss. Weight maintenance, even at
dangerously low levels, is anxiety provoking
6
Q
Etiology: Social, gender of Anorexia
A
- Greater sex prevalence in females
- Those whose assigned sex at birth does not match their gender identity, are more likely than cisgender people (assigned sex at birth matches gender identity) are more likely to engage in disordered eating. The odds of past year ED and past month ED symptoms are
significantly higher than the odds of these behaviors in cisgender males (Watson, Veale, & Saewyc, 2017) - Gender nonconforming people assigned a female sex at birth have
increased risk of EDs relative to people who are male‐to‐female or
female‐to‐male (Diemer et al., 2018)
- Gender nonconforming people assigned a female sex at birth have
7
Q
Etiology: Culture, Media portrayal of Anorexia
A
- Overweight men depicted on tv are 2‐5 X more common; magazine
portrayals of women since the 70s have had decreasing weight - Frequent portrayals of women dieting, making disparaging remarks
about their bodies - Previously thin ideals were achieved via corsets not dieting
- An examination of Ebony magazine had less representations of thin
women(Thompson‐Brenner, Boisseau & Paul, 2011); there is a lower
rate of ED in black women (Bodell et al., 2018).
8
Q
Etiology: Family contributions of Anorexia
A
- More likely to have perfectionistic, dieting mom
- Families with preoccupation with others’ sizes
- Having a family member with an ED is stressful and creates family
strife
9
Q
Dieting leading to EDs
A
- People who don’t diet, don’t develop eating disorders
- Teen girls who diet, are 8 x more likely to develop EDs
- Dieting leads to weight gain, which increases preoccupation/concern
- Boring food, after exposure to junk food, leads to anxiety in rats –
when you give them junk food, anxiety decreases – reinforcement - We are all exposed to media images of thin women, why is the rate of
eating disorders less than 1%?
10
Q
Etiology: Biological factors of Anorexia
A
- Heritability of AN of .56 (Bulik et al., 2006) but WHAT is being
inherited? - Also no adoption studies, just twin studies
- Isn’t this the case across all of our disorders?
- A nonspecific biological vulnerability which could be sensitivity to distress?
- Drive for control under uncertainty?
- Responsivity to stress?
- Tendency towards negative mood?
- Low levels of serotonin?
11
Q
Etiology: Psychological factors of Anorexia
A
- Our models have focused on general psychological vulnerability
- What are they?
- Perfectionism
- Anxiety sensitivity
- Need for control
- Low self‐efficacy
- Eating Disorder specific?
- Distortions on body image
- Intolerance of negative mood states
- Fear of becoming fat
12
Q
Integrative Model of Eating Disorders
A
Check text
13
Q
Treatment Rates for Anorexia
A
- Treatment seeking is not as common as you would think, given that AN is the
most fatal - It is more common to seek treatment for the comorbid condition, e.g., MDD]
Check text / slide approximately only 30-40%
14
Q
Treatment options for Anorexia
A
- SSRIs (only for Bulimia, Not For Anorexia)
- CBT‐E (Fairburn, 2008)
- Interpersonal Psychotherapy (IPT)
- family involvement/counseling re: communication around food,
having structured and reinforcing meals, attitudes towards body shape. - Motivational interviewing may be helpful before therapy to enhance
readiness for change (Dunn, Neighbors & Larimer, 2006)
15
Q
Treaments for Anorexia: SSRIs
A
- SSRIs help some with bulimia but not long‐term so they are combined with
CBT, if used at all (Reas & Grillo, 2014); SSRIs not helpful with anorexia
(Kruger & Kennedy, 2000)
16
Q
Treaments for Anorexia: CBT-E
A
- CBT‐E (Fairburn, 2008) is a transdiagnostic treatment with good efficacy
and an approach that addresses the common factors across disorders
eating
17
Q
Treaments for Anorexia: Interpersonal Therapy
A
Interpersonal Psychotherapy (IPT) focuses solely on interpersonal issues
and is as effective as CBT (Fairburn et al., 1993; Agras et al., 2000)
* Even in CBT, there is family involvement/counseling re: communication around food, having structured and reinforcing meals, attitudes towards body shape
18
Q
Treaments for Anorexia: Motivational interviewing
A
Motivational interviewing may be helpful before therapy to enhance
readiness for change (Dunn, Neighbors & Larimer, 2006)
19
Q
- Ingesting insufficient calories (i.e., below body’s needs)
A
Restricted eating
20
Q
- Attempting to follow demanding, rigid, perfectionistic rules to try to
experience sense that one is in control of their eating - Creates a preoccupation/obsession with food
- Ironically attempts to control eating deprive them of a true ability to control
eating - Makes eating anxiety provoking, guilt‐ridden experiences
A
Restrained eating
21
Q
Targeting restricted eating (eating disorders)
A
- Identify dietary rules: What foods do you fear? If you were at a dinner
party, what situations would cause anxiety? - They learn why restricted eating doesn’t work, the adverse consequences and
how ineffective laxatives and vomiting are as strategies - Connect the motivation to the behavior. What would happen if?….
- Make a plan for breaking rules, by creating low stakes situations
(coping plan to prevent binges/purges). Repeat exposures until guilt
and anxiety decrease - CBT‐E prescribes 6 small “meals” at no more than 3 hour intervals to reduce
over eating or restricting and prevention of compensatory behaviours
22
Q
Targeting maladaptive beliefs (eating disorders)
A
- There is nothing inherently good about resisting eating
- There are no bad foods. Quantity and balance takes care of this.
- Goal is not to eat crappy foods—just to have freedom to choose from
a range of foods - Eating should not be restrictive; its something we do to be healthy
- Rules about eating less are like developing rules to breathe less than
others - The right amount of food is the amount needed to maintain a healthy
weight and follow nutritional guidelines
23
Q
Sleep problems
A
▪ Problems associated with sleepiness (e.g., obstructive
sleep apnea)
▪ Problems associated with sleeplessness (e.g., insomnia
disorder)
▪ Other sleep problems (e.g., nightmare disorder)
24
Q
▪ Fall asleep unintentionally outside of the sleep period,
includes dozing, nodding off
▪ Problems causing ________ (not exhaustive)
– Voluntary sleep restriction
– Sleep apnea
– Narcolepsy
– Shift work
– Periodic Limb Movement Disorder
A
Excessive Sleepiness / Hypersomnolence Disorder
25
Hypersomnolence Disorder: DSM-5
A. Self‐reported sleepiness despite a sleep period of at least 7 hours with at
least one of the following:
1. Recurrent periods of sleep or lapses into sleep within the same day
2. Prolonged main sleep period of 9 hours or more that is nonrestorative
3. Difficulty being fully awake when awoken abruptly
B. The hypersomnolence occurs at least three times a week for at least three months
C. Distress or functional impairment
D. Not better accounted for or does not occur exclusively during another
disorder
E. Not attributable to a condition or a substance
F. Co‐existing mental or medical disorder does not adequately explain
26
Epworth Sleepiness Scale
TEXT / SLIDE
27
Quantification of a
behavioral state of
sleepiness
Multiple sleep Latency Test (MSLT)
28
Treatment of Excessive daytime sleepiness / Hypersomnolence Disorder
▪ Address cause if known (e.g., apnea, narcolepsy)
▪ Ensure proper sleep‐wake habits (e.g., Harvey et al., 2015)
▪ Increase daytime alertness (stimulant medications)
▪ Manage sleepiness behaviourally (naps)
▪ Safety assessments
29
Physical Effects of Obstructive Sleep
Apnea
Increased mortality
Headache
Stroke
Depression
Glaucoma
Cardiac Disease
High Blood Pressure
Type II Diabetes
Obesity
Erectile dysfunction
Feet oedema as a
result of heart failure
Car accidents 2-7 x
30
Apnea screening
STOPBANG
Snoring loudly and persistently
Tired, actually sleepy rather than tired
Observed apneas
High Blood Pressure
BMI over 35 kg/m2?
Age: Older than 50 years old?
Neck size larger than 40 cm (15”+)?
Gender: Male?
31
OSA on Polysomnographic Recording (TEXT/SLIDE)
Severity: Number of breathing events per hour of sleep
Breathing event: apnea or hypopnea (hypo‐apnea)
Titration studies review these parameters after the initiation of an
assisted breathing device
32
1. What is the gold standard or best way to treat Obstructive Sleep Apnea
2. Why?
3. Issues with it
1. Positive Airway Pressure (PAP)
2. therapy eliminates events and can reverse the diseases apnea causes
3. BUT, up to 40 % are going to have issues with it
▪ Some will feel claustrophobic using the mask
▪ Some won’t believe it is useful
▪ Some won’t believe the results of the test
▪ Some will find it uncomfortable (e.g., air leakage)
33
1. OSA: Mask + Panic = __
2. Solutions?
1. conditioned arousal
2. Behavioural sleep medicine specialists can treat mask aversion with
exposure therapy (Carney & Edinger, 2010)
34
Narcolepsy: DSM-5
A. Recurrent periods of an irrepressible need to sleep (sleep attacks)
within the same day (at least 3 times per week for at least 3 months)
B. The presence of cataplexy at least a few times a month
C. Hypocretin deficiency in cerebral spinal fluid
D. Sleep onset REM (SOREMs) of less than or equal to 15 minutes or
multiple sleep latency test sleep onset latency < 8 minutes or 2 or
more SOREMsNarcolepsy: DSM-5
35
▪ neurological disorder characterized by an intrusion of REMS into wakefulness.
▪ The classic tetrad of this disorder includes: cataplexy, hallucinations, sleep paralysis and excessive daytime sleepiness (EDS).
▪ Not all have to be present so differing ____ presentations can
ppear quite differently
Narcolepsy
36
a loss of muscle tone in response to increased emotional
arousal
Cataplexy
37
In Narcolepsy, ________ that have the diagnosis have cataplexy
around two thirds
38
Cataplexy
▪ Cataplexy is a loss of muscle tone in response to increased emotional
arousal.
▪ Occurs in around two thirds of those with the diagnosis (Bassetti &
Aldridge, 1996).
▪ The loss of tone may result in total collapse onto the floor or mild buckling
of the legs such that the patient can continue to stand. The head and jaw
often slump forward and the arms often collapse to their sides.
▪ Common emotional triggers include laughing, being frightened, or being
angered.
▪ The person remains aware throughout the attack which can frighten them
and leave them vulnerable to prolonged symptoms.
▪ This can be a life‐threatening condition
39
Mechanisms of cataplexy
**▪ Cataplexy appears to have a genetic basis: a gene turns on an autoimmune
response that attacks hypocretin cells.**
▪ Colony of hypocretin‐knockout Doberman Pinschers raised at Stanford.
▪ Chocolate is a highly palatable food that excites mice, and in mice whose
hypocretins are knocked‐out, the introduction of chocolate is associated
with increased activity in the medial prefrontal cortex (mPFC) and resultant
cataplexy (Oishi et al., 2013) .
– During the cataplexy, there was also increased activity in parts of the limbic system,
namely the hypothalamus and amygdala.
– Blocking mPFC activity in these mice resulted in a reversal of the chocolate‐induced
cataplexy; thus, emotional areas and the mPFC are likely critical for cataplexy
40
Cataplexy treatment
▪ The most common treatment approaches are to:
1) facilitate adrenergic activity with selective reuptake inhibitor
(SSRIs) antidepressant medications such as fluoxetine or
fluvoxamine
2) use gamma hydroxybutyrate (GHB) to consolidate REMS
– Potent, dangerous drug
– Measure out doses and leave by bed
– Highly regulated
– patient can consolidate sleep by taking this medication and it has been shown to help with other narcolepsy symptoms too (U.S. Xyrem Multicentre Study Group,
2004)
41
involving shapes and colours on the wall
but it can also include sounds or music or perception of someone touching
the body.
Hallucinations
42
1. ____ hallucinations occur upon awakening whereas 2. ______
hallucinations occur while falling asleep.
1. Hypnopompic
2. Hypnagogic
43
Two types of hallucinations
1. Hypnopompic
2. Hypnagogic
44
Hallucinations
1. Hypnopompic
2. Hypnagogic
▪ Most often visual hallucinations involving shapes and colours on the wall
but it can also include sounds or music or perception of someone touching
the body.
▪ Like sleep paralysis, hypnopompic or hypnagogic hallucinations can occur
in the normal population (Ohayon, Priest, Caulet, & Guilleminault, 1996).
▪ There are no hallucination‐specific interventions except for
psychoeducation to reassure the patient of the normalcy of this
experience
45
There are 1. ____ hallucination‐specific interventions except for
2. ____ to reassure the patient of the normalcy of this
experience
1. no / zero
2. psychoeducation
46
A. Repeated, extended dysphoric, well‐remembered dreams (usually
threats to survival, security or physical integrity, typically in the
second half of the night)
B. Upon awakening from the bad dream, they are alert
C. Distress or impairment in functioning
D. Not attributable to a substance
E. Co‐existing condition is not enough to explain the nightmares
Nightmare Disorder: DSM-5
47
Nightmares and trauma
Most people who have nightmares following trauma
eventually stop having them. Nightmares gradually change
into less disturbing dreams. This process was not enacted in
PTSD, but IRT can start that process.
▪ Over time, nightmares take on a life of their own. Move
beliefs towards nightmares being caused by habit over
trauma.
▪ Imagery Rescripting and Rehearsal Therapy (IRT) produces
large effects on nightmare frequency/intensity and PTSD
symptoms (Davis et al., 2011; Krakow et al., 2001)
48
Best Treatment for Nightmares and trauma
Imagery Rescripting and Rehearsal Therapy (IRT)
49
People in Canada and the US have significant insomnia symptoms
at any given time
>100 000 000
50
DSM5 Insomnia Disorder (ID)
– Difficulty sleeping (initiating and/or maintaining sleep* OR
nonrestorative sleep)
– Difficulty functioning: contemporary views of insomnia
conceptualize it as a 24‐hour disorder (daytime component) and/or
distress
– At least 3 nights per week
– >3 months duration
– Occurs despite adequate opportunity for sleep
– Not better explained by drug, medical/mental/sleep‐wake disorder
– ID is usually comorbid
51
Wakefulness and Sleepiness: Competing processes
– Process S: Homeostat
– Process C: Circadian/Body Clock
52
The biological systems that promote wakefulness and sleep
are ______
distinct
53
Wakefulness and Sleepiness: Process S
"Homeostat"
- Homeostatic Mechanism Balances Sleep and Wakefulness
- Sleep drive determines the quantity of deep sleep and the quality
- Build sleep drive to sleep deeply
54
1. Wakefulness and Sleepiness: Process C
2. ________ Essentials
1. Circadian/Body Clock
2.
1. TIMING
▪ Clock determines timing of sleep especially REM sleep timing AND timing of alertness
2. MANAGING DRIFT
▪ There is drift in our clock because it is longer than 24 hours
– Regular bedtimes, regular rise times and regular light exposure “set” the clock and manage drift
55
Chronic and acute insomnia are ____
different
- Different etiologies
- Different physiologies
- Different intervention
56
Circadian alerting signals are on a ______
24-Hour Basis
57
How does staying active effect sleep??
Builds sleep drive to sleep deeply (Homeostatic Mechanism)
58
3 Precipitating factor(s) of Insomnia
1. Homeostatic Disruption
2. Circadian Disruption
3. Arousal (Cognitive)
59
1. Precipitating factor(s) of sleep:
Reduced sleep drive = _____
2. _____ Perpetuating Factors
1. Homeostatic Disruption
2. Homeostatic Perpetuating Factors
▪ We need to “build” sleep drive to have
continuous and quality sleep, therefore
behaviours that will have a negative impact
on this build‐up will be:
– Spending increased time in bed relative to how much sleep you can currently
produce
▪ Napping; Sleeping‐in; Going to bed early
– Inactivity (Carney et al., 2006)
Going to bed early: less deep sleep build‐up
Sleep‐in or lay‐in: less deep sleep build‐up
Naps: less deep sleep build‐up
60
1 . Precipitating factor(s) of sleep:
Improper Sleep Scheduling = ____
2. perpetuating factors
1. Circadian Disruption
2. ▪ Optimal sleep is produced during a dynamic,
idiosyncratic timing window, therefore the
following behaviours would have a negative
impact on sleep:
– Variable timing of going to bed and getting out of bed
– Sleeping outside of your optimal window (i.e., keeping late hours if you are a lark or getting up early if you are an owl)
Delayed and Advanced Chronotypes
-Normal Sleep Phase
- Delayed Sleep Phase
- Advanced Sleep Phase
61
1. Precipitating factor(s) of sleep:
Poor sleep habits / Conditioned
arousal = ________
Cognitive Arousal
▪ The arousal system can override the sleep promoting system
– allows us adequate respond to dangerous threats
▪ When overactive, the arousal system interferes with the processes
controlling sleep. Hyperarousal issues:
1. Conditioned arousal
2. Cognitive arousal
3. Physiological arousal
62
We nap for ____, never for ______
sleepiness, sleep
Sleepiness
▪ Can help: even as short as 15
minutes (Dinges, Orne,
Whitehouse & Orne, 1987).
▪ The briefer and earlier in the
day, the less sleep disruptive
Insomnia
▪ They already have low deep
sleep drive
▪ They fear not being able to
cope and need to face that fear
▪ It’s poor stimulus control to
sleep outside the sleep window
63
Increased Physiological (Hyper)arousal
in Insomnia
– Metabolic rate (Kay et al., 2016)
– Sympathetic activation (Gehrman et al., 2016)
– Hypothalamic‐Pituitary‐Adrenal axis (Minkel et al., 2014)
– Cortical arousal
▪ Electroencephalogram and regional brain
metabolism (Riedner et al., 2016)
▪ Multiple Sleep Latency Testing (Bonnet & Arand, 2010)
64
Sleep medications
▪ Sleep medications, approved by Health Canada (Canada) or the Food and Drug Administration (FDA in the United States), are an effective treatment option for insomnia.
▪ Generally, medications have been in the benzodiazepine or non‐benzodiazepine categories.
▪ Benzodiazepines facilitate (agonists) GABA and decrease alertness. An agonist is a drug that potentiates or increases the action of that receptor; in other words it facilitates GABA—an important chemical for the production of sleep (e.g., estazolam, flurazepam, temazepam, triazolam).
▪ The half‐life refers to the time it takes for the drug to lose half of its action (half of the drug is used up). A very long half‐life would be most effective for people with problems staying asleep throughout the night (e.g., dalmane). A long half‐life is also associated with increased sedation throughout the day because the drug remains in the system during the day. A short half‐life is most commonly used for those with sleep onset insomnia only. The
short half‐life would limit the leftover effects of the medication the next day but such drugs would not help the patient if they woke up in the middle of the night
65
Z drugs
▪ Non‐benzodiazepine medications
▪ Less side effects than regular benzodiazepine medications
▪ Do not have a benzodiazepine structure but are GABA agonists that
target very specific alpha receptors.
▪ For example, zolpidem or eszoplicone
▪ Downsides include daytime sedation, psychological dependence,
unwanted involuntary sleep‐walking or sleep‐sex behaviours
66
CBT(I) versus meds for Insomnia
▪ Both are effective
▪ Augmenting approach often preferred but data is mixed for
this practice
▪ Unlike hypnotic treatment, gains achieved during CBT‐I endure months to years after the end of active therapy (e.g., Edinger et al., 1996;1992; 2001; Edinger & Sampson, 2003; Espie, Inglis, Harvey, Tessier, 2000; Morin et al., 1999)
67
CBT‐I and physiology
CBT‐I improves
neurophysiology of
sleep: ↓high frequency
& ↑ slow wave activity
in the EEG (Cervena,
Dauvilliers, Espa, et al., 2004)
68
OTC Melatonin
▪ No compelling evidence of melatonin problems in insomnia
▪ Oral melatonin is somewhat effective in Delayed Phase Circadian Rhythm Disorder because melatonin release occurs much later and thus, sleep onset is delayed. Melatonin not delayed in insomnia
▪ Melatonin taken before bed would have a placebo effect only; taking melatonin when melatonin already present in the brain does nothing—signal was already sent.
▪ Melatonin during day, the brain responds by increasing sleepiness several hours later because no melatonin present in the brain when the pill was taken (Wyatt, Dijk, Cecco, Ronda, & Czeisler, 2006).
▪ Crappy studies reporting positive effects for melatonin are so small that they lack any clinical utility. For example, Brzezinski and colleagues’ (2005) meta‐analysis found an increase of sleep efficiency of only 2% and an increase in
total sleep time across the entire night of only 12 minutes, and a decrease in sleep onset latency of only 4 minutes.
Although there may be some statistical significance for some of these findings, we would not consider these findings to be particularly meaningful. Especially in light of some studies reporting negative findings for melatonin
(i.e., that sleep worsens). For example, in Buscemi and colleagues’ (2007) meta‐analysis, melatonin’s hypnotic effects were negative when given before bed. Thus, melatonin is not used for insomnia in sleep settings despite
the belief by many that it is helpful for insomnia
69
Complementary medicines in insomnia?
▪ In sum, there is a lack of efficacy evidence for any alternative or complementary
medicine approach for insomnia (Meoli et al., 2005).
▪ National Center for Complementary and Alternative Medicine (NCCAM)
70
What is CBT‐I?
An evidence‐based treatment developed from biological and learning
principles:
▪ Stimulus Control (Bootzin, 1972): a set of sleep rules to address
conditioned arousal.
▪ Sleep Restriction (Spielman et al., 1987): a technique to increase
sleep drive by matching the time spent in bed with current sleep
production time.
▪ Sleep Hygiene: a set of rules designed to address sleep‐interfering
habits or substances.
▪ Cognitive Therapy: a set of techniques to modify beliefs about sleep
and fatigue that cause or exacerbate insomnia
71
a set of sleep rules to address
conditioned arousal
Stimulus Control
72
a technique to increase
sleep drive by matching the time spent in bed with current sleep
production time.
Sleep Restriction
73
a set of rules designed to address sleep‐interfering
habits or substances
Sleep Hygiene
74
a set of techniques to modify beliefs about sleep
and fatigue that cause or exacerbate insomnia
Cognitive Therapy
75
Stimulus Control
If wakefulness and the bed have become associated, re‐
associate bed with sleep by:
1. Going to bed only when sleepy
2. Getting out of bed when unable to sleep
3. Getting out of bed at a consistent time each morning
(irrespective of how you slept)
4. Using the bed and bedroom only for sleep (and sex)
5. Refraining from daytime naps
76
Sleep Restriction Therapy (SRT) or
Time‐in‐Bed Restriction
To restore homeostatic sleep drive:
▪ Match time‐in‐bed with current average sleep
production (add 30 minutes for normal sleep onset
latency)
▪ Once sleep normalizes and there is sleepiness (self‐
reported or a mean sleep onset latency 10 min or less or
a sleep efficiency above 90%) we extend time‐in‐bed in
15 or 30 minute increments
77
Sleep extension
Provide MORE time in bed when there is sleepiness:
– Subjective complaints of sleepiness
– Sleep efficiency upwards of 90%
– Sleep onset latencies less than 10 minutes
▪ Renegotiate where to allot the additional 15‐30 minutes.
If sleep suffers, scale back, if sleepiness continues and
sleep is still ok, increase by another 15‐minutes
78
Sleep Hygiene: Focus on Lifestyle Factors not
Implicated in Insomnia
– Caffeine – timing and reduction
– Nicotine reduction/elimination
– Prescribed exercise ‐ timing
– Light bedtime snack (milk, peanut butter)
– Avoid middle of the night eating
– Reduce alcohol, marijuana & other substances
– Optimize environment: light, noise, temperature
▪ American Academy of Sleep Medicine recommends against using sleep
hygiene on its own (Edinger et al., 2021)
▪ Used as a behavioural placebo in clinical trials (e.g. Carney et al., 2017)
79
Summary of Insomia (much needed)
▪ We have two main efficacious treatments for insomnia:
– Hypnotic medications
– Cognitive behaviour therapy for insomnia (CBT‐I)
▪ Hypnotic medications are less effective than CBT‐I long‐term and have a
number of side effects that can make them undesirable.
▪ CBT‐I is comprised of: Stimulus Control, Sleep Restriction, Sleep Hygiene
and Cognitive Therapy
– Stimulus Control helps to disassociate the bed with wakefulness (i.e., conditioned
arousal)
– Sleep Restriction increases the drive for deep sleep
– Sleep Hygiene is sometimes necessary but rarely sufficient to address insomnia
– Cognitive Therapy modifies sleep‐interfering beliefs
80
many people react to disrupted sleep by taking over-the-counter
sleeping pills. Unfortunately, most people are not aware that
______________
rebound insomnia may occur
- hypnotics are almost equally effective as CBT-I, but CBt lasts monthsnor years longer
