Eating And Sleep Disorders (Week 8 / Chap 9-10)

Question 1

Impact of eating disorders

Answer 1

• 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)

Question 2

Bulimia Nervosa in the DSM5

Answer 2

• 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

Question 3

Bulimia Side effects

Answer 3

• 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

Question 4

Anorexia Nervosa DSM5

Answer 4

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

Question 5

Description / Summary of Anorexia

Answer 5

• 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

Question 6

Etiology: Social, gender of Anorexia

Answer 6

• 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)

Question 7

Etiology: Culture, Media portrayal of Anorexia

Answer 7

• 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).

Question 8

Etiology: Family contributions of Anorexia

Answer 8

• 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

Question 9

Dieting leading to EDs

Answer 9

• 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%?

Question 10

Etiology: Biological factors of Anorexia

Answer 10

• 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?

Question 11

Etiology: Psychological factors of Anorexia

Answer 11

• 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

Question 12

Integrative Model of Eating Disorders

Answer 12

Check text

Question 13

Treatment Rates for Anorexia

Answer 13

• 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%

Question 14

Treatment options for Anorexia

Answer 14

• 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)

Question 15

Treaments for Anorexia: SSRIs

Answer 15

• 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)

Question 16

Treaments for Anorexia: CBT-E

Answer 16

• CBT‐E (Fairburn, 2008) is a transdiagnostic treatment with good efficacy
  and an approach that addresses the common factors across disorders
  eating

Question 17

Treaments for Anorexia: Interpersonal Therapy

Answer 17

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

Question 18

Treaments for Anorexia: Motivational interviewing

Answer 18

Motivational interviewing may be helpful before therapy to enhance
readiness for change (Dunn, Neighbors & Larimer, 2006)

Question 19

• Ingesting insufficient calories (i.e., below body’s needs)

Answer 19

Restricted eating

Question 20

• 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

Answer 20

Restrained eating

Question 21

Targeting restricted eating (eating disorders)

Answer 21

• 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

Question 22

Targeting maladaptive beliefs (eating disorders)

Answer 22

• 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

Question 23

Sleep problems

Answer 23

▪ Problems associated with sleepiness (e.g., obstructive
sleep apnea)
▪ Problems associated with sleeplessness (e.g., insomnia
disorder)
▪ Other sleep problems (e.g., nightmare disorder)

Question 24

▪ 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

Answer 24

Excessive Sleepiness / Hypersomnolence Disorder

Question 25

Hypersomnolence Disorder: DSM-5

Answer 25

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

Question 26

Epworth Sleepiness Scale

Answer 26

TEXT / SLIDE

Question 27

Quantification of a
behavioral state of
sleepiness

Answer 27

Multiple sleep Latency Test (MSLT)

Question 28

Treatment of Excessive daytime sleepiness / Hypersomnolence Disorder

Answer 28

▪ 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

Question 29

Physical Effects of Obstructive Sleep
Apnea

Answer 29

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

Question 30

Apnea screening
STOPBANG

Answer 30

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?

Question 31

OSA on Polysomnographic Recording (TEXT/SLIDE)

Answer 31

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

Question 32

1. What is the gold standard or best way to treat Obstructive Sleep Apnea
2. Why?
3. Issues with it

Answer 32

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)

Question 33

1. OSA: Mask + Panic = __
2. Solutions?

Answer 33

1. conditioned arousal
2. Behavioural sleep medicine specialists can treat mask aversion with
   exposure therapy (Carney & Edinger, 2010)

Question 34

Narcolepsy: DSM-5

Answer 34

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

Question 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

Answer 35

Narcolepsy

Question 36

a loss of muscle tone in response to increased emotional
arousal

Answer 36

Cataplexy

Question 37

In Narcolepsy, ________ that have the diagnosis have cataplexy

Answer 37

around two thirds

Question 38

Cataplexy

Answer 38

▪ 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

Question 39

Mechanisms of cataplexy

Answer 39

▪ 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

Question 40

Cataplexy treatment

Answer 40

▪ 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)

Question 41

involving shapes and colours on the wall
but it can also include sounds or music or perception of someone touching
the body.

Answer 41

Hallucinations

Question 42

1. ____ hallucinations occur upon awakening whereas 2. ______
   hallucinations occur while falling asleep.

Answer 42

1. Hypnopompic
2. Hypnagogic

Question 43

Two types of hallucinations

Answer 43

1. Hypnopompic
2. Hypnagogic

Question 44

Hallucinations

Answer 44

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

Question 45

There are 1. ____ hallucination‐specific interventions except for
2. ____ to reassure the patient of the normalcy of this
experience

Answer 45

1. no / zero
2. psychoeducation

Question 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

Answer 46

Nightmare Disorder: DSM-5

Question 47

Nightmares and trauma

Answer 47

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)

Question 48

Best Treatment for Nightmares and trauma

Answer 48

Imagery Rescripting and Rehearsal Therapy (IRT)

Question 49

People in Canada and the US have significant insomnia symptoms
at any given time

Answer 49

> 100 000 000

Question 50

DSM5 Insomnia Disorder (ID)

Answer 50

– 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

Question 51

Wakefulness and Sleepiness: Competing processes

Answer 51

– Process S: Homeostat
– Process C: Circadian/Body Clock

Question 52

The biological systems that promote wakefulness and sleep
are ______

Answer 52

distinct

Question 53

Wakefulness and Sleepiness: Process S

Answer 53

“Homeostat”

• Homeostatic Mechanism Balances Sleep and Wakefulness
• Sleep drive determines the quantity of deep sleep and the quality
• Build sleep drive to sleep deeply

Question 54

1. Wakefulness and Sleepiness: Process C
2. ________ Essentials

Answer 54

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

Question 55

Chronic and acute insomnia are ____

Answer 55

different

• Different etiologies
• Different physiologies
• Different intervention

Question 56

Circadian alerting signals are on a ______

Answer 56

24-Hour Basis

Question 57

How does staying active effect sleep??

Answer 57

Builds sleep drive to sleep deeply (Homeostatic Mechanism)

Question 58

3 Precipitating factor(s) of Insomnia

Answer 58

1. Homeostatic Disruption
2. Circadian Disruption
3. Arousal (Cognitive)

Question 59

1. Precipitating factor(s) of sleep:
   Reduced sleep drive = _____
2. _____ Perpetuating Factors

Answer 59

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

Question 60

1 . Precipitating factor(s) of sleep:
Improper Sleep Scheduling = ____
2. perpetuating factors

Answer 60

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

Question 61

1. Precipitating factor(s) of sleep:
   Poor sleep habits / Conditioned
   arousal = ________

Answer 61

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

Question 62

We nap for ____, never for ______

Answer 62

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

Question 63

Increased Physiological (Hyper)arousal
in Insomnia

Answer 63

– 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)

Question 64

Sleep medications

Answer 64

▪ 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

Question 65

Z drugs

Answer 65

▪ 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

Question 66

CBT(I) versus meds for Insomnia

Answer 66

▪ 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)

Question 67

CBT‐I and physiology

Answer 67

CBT‐I improves
neurophysiology of
sleep: ↓high frequency
& ↑ slow wave activity
in the EEG (Cervena,
Dauvilliers, Espa, et al., 2004)

Question 68

OTC Melatonin

Answer 68

▪ 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

Question 69

Complementary medicines in insomnia?

Answer 69

▪ 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)

Question 70

What is CBT‐I?

Answer 70

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

Question 71

a set of sleep rules to address
conditioned arousal

Answer 71

Stimulus Control

Question 72

a technique to increase
sleep drive by matching the time spent in bed with current sleep
production time.

Answer 72

Sleep Restriction

Question 73

a set of rules designed to address sleep‐interfering
habits or substances

Answer 73

Sleep Hygiene

Question 74

a set of techniques to modify beliefs about sleep
and fatigue that cause or exacerbate insomnia

Answer 74

Cognitive Therapy

Question 75

Stimulus Control

Answer 75

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

Question 76

Sleep Restriction Therapy (SRT) or
Time‐in‐Bed Restriction

Answer 76

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

Question 77

Sleep extension

Answer 77

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

Question 78

Sleep Hygiene: Focus on Lifestyle Factors not
Implicated in Insomnia

Answer 78

– 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)

Question 79

Summary of Insomia (much needed)

Answer 79

▪ 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

Question 80

many people react to disrupted sleep by taking over-the-counter
sleeping pills. Unfortunately, most people are not aware that
______________

Answer 80

rebound insomnia may occur
- hypnotics are almost equally effective as CBT-I, but CBt lasts monthsnor years longer