PSYA3 - Biological Rhythms powerpoint. 100 slides because there's a lot to know! Condensed it as much as possible. Includes: Biological rhythms - Circadian, Infradian, Ultradian, endogenous pacemakers, exogenous zeitgebers & consequences of disruption of said rhythms Sleep states - lifespan changes, restorative theory, evolutionary evaluations Disorders of sleep - Insomnia & other sleep disorders. There's minimal evaluation for Infradian - so do it yourself :D

1. PSYA4 - Sleep

2. Definitions:
Word Definition
Circadian rhythm Body’s biological, internal clock. Approx.
24 hours. Day/wake cycle.
Ultradian rhythm Recurring function at regular intervals, in
less than 24 hours
Infradian rhythm Regular occurrence in cycles of more than
24 hours
Endogenous pacemakers Internal cues such as SCN
(suprachiasmatic nucleus), pineal gland
and melatonin
Exogenous zeitgebers Light, social cues, temp
Entrainment Resetting the biological clock using
exogenous zeitgebers

3. Ultradian:

4. Stages of sleep: Rechtschaffen and
Kales (1968) (Ultradian):

5. Stages of sleep:
Stage Definition
Stage 1: Drowsiness; small wave freq. (4-7hz), on
EEG, NREM Sleep
Stage 2: Asleep; EEG dominated by theta waves
but hz increases, high energy bursts on
EEG (sleep spindles), NREM Sleep
Stage 3: Delta waves, (1-4hz), less sleep spindles,
NREM Sleep
Stage 4: Deepest stage of NREM, delta waves,
hard to wake, growth hormone released
here, SWS (slow wave sleep)
REM Sleep (paradoxical sleep) Fast desynchronised EEG, body effectively
paralysed, dreaming more likely to occur
Move back to stage 2 (approx 20 mins): Move back into REM, repeat pattern,
approx every 90 minutes, 4/5 a night

6. Comparative: Jouvet (1967)
• Cats and other animals
• Upside-down flowerpots in
tank of water
• Cats went into REM sleep,
muscles became slack,
bodies slumped, fell into
water & woke
• Cats who didn’t go into REM
showed abnormal behaviour
like stress, and eventually
died

7. Ultradian – Dement and Kleitman
(1957):
• Looking at relationship between REM and
dreams
• 9 participants (only 5 studied intensely)
• Lab study – EEG’s used
• Some variables controlled (no
alcohol/caffeine)
• All ppts showed REM every night
• REM predominantly for dreaming, but not
always
Small sample size, subsequent studies haven’t
supported findings, lacks eco validity,
objective methods, variables controlled

8. AO2 for Ultradian Rhythms:
• Further evidence e.g.
Friedman and Fisher (1967),
who found BRAC (basic rest-
activity cycle) followed 90 min
cycle over 6 hr period. 
- May not be generalisable
- Supports Ultradian Rhythms
- Suggests biological mechanism
to sleep Ultradian rhythm…

9. AO2 for Ultradian Rhythms:
• Reductionist  - simplified form
• Only looks at biology, not
psychology/social/individual
differences
• For example, people with
insomnia
• They should look at broader
concepts 
• Other than biological factors,
perhaps the setting (lab studies)
would affect people’s sleep…

10. AO2 for Ultradian Rhythms:
• Ecological Validity  whether the
research is applicable to setting
outside of the experiment
• Lab study, ppts removed from natural
sleep settings
• This may have affected those in
Dement and Kleitman’s (1957)
research
• Lack of eco val. could mean the studies
don’t test what they set out to test.
• Another thing which could reduce
validity may be studies conducted on
animals…

11. AO2 for Ultradian Rhythms:
• Comparative research + ethical
issues 
• Better than human testing
• May not be generalisable to
human studies
• Animals may die
• E.g. Jouvet (1967)
cats/flowerpots died
• Though some studies are
based on science...

12. AO2 for Ultradian Rhythms:
• Objective – based on facts
• Increased replicability, due
to objective tests such as
EEGs (like in Rechtschaffen
and Kales (1968): Sleep
Stages
• More replicable, similar
results = more reliable

13. Infradian:

14. A little bit about the Infradian
rhythms:
• Body rhythms which occur for periods
(ha) over 24 hours.
• An example of which is the menstrual
cycle
• Which is the internal control of
hormones by the endocrine system
• Driven by release of oestrogen from
ovaries (builds up uterine lining)
which is maintained by progesterone
• Pituitary gland near hypothalamus
releases FSH (follicle stimulating) and
LH (luteinizing hormone) to ripen egg
• If egg isn’t implanted, then
menstruation occurs

15. Infradian Rhythms – Russell et al
(1980):
• Menstrual cycles usually controlled
by hormones (Endo. Pacemakers)
• However, Russell used 2 groups of
women, who were kept
separately.
• Sweat from one group of women,
was wiped on the upper lips of the
second group of women. (ew)
• Their menstrual cycles
synchronised.
• Shows that cycles may be linked by
exogenous zeitgebers in the form
of pheromones.

16. McClintock and Stern (1988):
• Investigate affect of women’s pheromones
(exogenous zeitgebers) on other women’s
menstrual cycles
• 29 women aged (20-35 years) with irregular
menstrual cycles tested
• 9 women gave pheromone samples by using
cotton pads they had under their arms for 8
hours+
• Cotton pads were treated with alcohol to
disguise any smells, and then frozen
• The pads were then wiped under the other
20 women’s noses
• 68% of women responded, and their cycles
shortened from 1 to 14 days, or lengthened
1 to 12 days (depending on when the
pheromone samples were collected)

17. Men have Infradian cycles too-
Empson (1977):
• 21 males ppts
• Body temp
&alertness measured
from 49 to 102 days
• Found evidence of
approx. a 20 day
cycle

18. Infradian – SAD (Seasonal affective
disorder):
• Depressed during
winter months
• Due to high
melatonin and
reduced serotonin
• Treatment is via light
box therapy

19. Infradian AO2 – Determinism vs Free
will:
• Ms. English drove a car into her husband’s
house, and blamed it on PMS (Johnson, 1987)
• Supported by Dr. Katherina, who said ‘women
are not responsible for their actions on PMS’
(Deterministic)
SYNOPTIC: do not analyse Born
• One study found people who were told to wake
up earlier had higher levels of the stress
hormone ACTH (which contributes to them
waking up) causing them to wake earlier – Born
et al (1999)
(Free will)

20. Infradian AO2 - Reductionist:
• Only looking at biological aspect i.e. hormones
• But that’s objective, so it’s also good 
• Link to endogenous/exogenous
• Also it’s good for treatment? Like, for S.A.D,
getting to know how the rhythms work mean
we can provide the best treatments possible

21. Infradian AO2 – Further research:
McClintock (1971) Found that
women who work in male
dominated environments
have shorter menstrual
cycles
Shows menstrual cycles further
influenced by exogenous
zeitgebers
This could be seen as an
EVOLUTIONARY ADVANTAGE
as it would provide more
opportunities for pregnancy

22. Infradian AO2 – further further
research:
Reinberg (1967) – showed that
Infradian rhythms were also
affected by LIGHT (exogenous).
Woman lived in a cave for 3
months, and her menstrual
cycle changed to 26 days
(average is 28 days)
Could be from the lack of natural
light that she had

23. Circadian Rhythms:
Circa = circle
Dian = day
One day!

24. A little bit about circadian rhythms:
• Rhythms that occur on a cycle over a period of
24 hours.
• ‘Body’s biological, internal clock. Approx. 24
hours. Sleep/wake cycle.’

25. Introduction to Biological rhythms:
The Case of Michel Siffre (1962):
• Testing internal body clock
• Michel Siffre spent 61 days and nights
underground in a cave
• No exogenous zeitgebers
(lights/clocks/radio)
• Only influence was endogenous
pacemakers (internal body clock)
• Emerged 17th Sept, thought it was 20th
Aug
• Natural rhythm extended to over 24
hours
(Supports endogenous)

26. Biological rhythms:
Aschoff and Wever (1976):
• Researchers placed ppts in
WW2 bunker
• Removed exogenous
cues/social cues
• Most people developed 24-
25 hours
• Some were as long as 29
hours
(Supports endogenous)

27. Biological rhythms:
Folkardet al (1985):
• Seeing the external cue time could be
used to override internal clock
• 12 people lived in a cave for 3 weeks,
isolated from natural light
• Woke up and went to bed when clock
showed particular time
• Researchers sped up clock from 24
hour cycles to 22 hour cycles
• Volunteer’s circadian rhythms matched
the clock initially, but eventually it
returned to 24 hour cycles
(Supports endogenous)

28. Biological Clock, Proteins – Darlington
et al (1998):
• Proteins in the Drosophila fruit fly
• In the morning: CLK-CYC bind
• Once bound, PER-TIM are produced
• Their presence decreases the amount
of CLK-CYC
• Which, in turn, deceases PER-TIM.
• But then it all repeats in a 24hr cycle.
This is known as NEGATIVE FEEDBACK.
• In humans, the main proteins are
CLOCK-Bmal1 and PER-CRY

29. Things that effect circadian rhythm –
Exogenous Zeitgebers:
Light:
One of the most dominant
zeitgebers, it resets the body’s
pacemaker through the SCN
It can reset CRY protein, which is
light-sensitive
This may explain whyCampbell and
Murphy (1998) found that
shining lights on knees caused a
shift in Circadian Rhythm.

30. Exogenous zeitgebers:
Social cues:
Eating at certain times, and the
times we sleep and wake up
Entrained by social convention
rather than biology
Zeitgebers for liver and heart
cells are likely to be
controlled by mealtimes, as
they’re reset by eating
(Davidson, 2006)

31. Exogenous zeitgebers:
Temperature:
Cold-blooded animals are
effected by weather for how
active they are.
Warm-blooded animals (like
humans) suggest changes are
made by their own circadian
clock, and their temps entrain
other circadian(Buhr et al,
2010)

32. Endogenous pacemakers:
• The suprachiasmatic nucleus,
(SCN) is a pair of structures
which lie in the hypothalamus
and are located where the
optic nerves from each eye
cross.
• It obtains info about light even
when our eyes are shut.

33. Endogenous pacemakers:
• The SCN sends signals to the
pineal gland.
• The production of the
hormone melatonin is
increased at night.
• Melatonin induces (causes)
sleep.

34. Endogenous – SCN, Albuset al 2005:
• The SCN is split in two.
One in each hemisphere
• It is further split into
dorsal and ventral
• Ventral is quickly reset by
EXTERNAL CUES like light
• Dorsal is more resistant to
being reset

35. Endogenous pacemakers, – Morgan et
al (1995):
• ‘Role of the SCN’
• Bred mutant hamsters, with
circadian rhythms of 20 hours
instead of 24
• Then transplanted their SCNs into
‘normal’ hamsters
• ‘Normal’ hamsters then displayed
the mutant rhythms
• Shows circadian rhythms may be
controlled by the SCN

36. Endogenous pacemakers –
DeCourseyet al (2000):
• Removed SCNs from 30 chipmunks
• They were returned to natural
habitat & observed
• Alongside 2 other groups: 24 surgical
controls, and 20 controls.
• After 80 days, significantly more of
the SCN-lesioned chipmunks had
been killed by weasels
• Probably because those chipmunks
remained awake, and made noises in
their burrows so weasels could hear.
(Sleep = links to evolutionary)

37. Endogenous pacemakers, artificial
lighting – Stevens (2006):
• If lights do reset the
biological clock, our
artificially lit world
could be damaging
• Stevens (2006)
suggests it disrupts
our rhythm and
melatonin
production

38. AO2 for endogenous pacemakers and
sleep cycles:
• Further supporting evidence 
• Stevens (2006) supports role of
SCN
• Suggests artificial lighting
disrupts circadian rhythms,
disrupting melatonin levels
• Provides further evidence SCN
affected by light
• Although this research is carried
out on humans… Quite a lot of
research is carried out on…

39. AO2 for endogenous pacemakers and
sleep cycles:
• Comparative
studies/generalisability
• DeCourseyet al’s (2000) research on
chipmunks, Morgan et al‘s (1995)
on hamsters
• Biology differs between animals and
humans
• E.g. Reptiles have direct input into
the pineal gland, whereas humans
do not.
• Another issue, is whether or not
animal testing is ethical…

40. AO2 for endogenous pacemakers and
sleep cycles:
• Ethical issues 
• Do the pros outweigh the cons?
• Decoursey removed SCNs which
was detrimental to chipmunks
survival
• They’re unable to say no,
however we could not carry out
these tests on humans
• All of the research thus far has
followed a biological approach…
What about evolutionary?

41. AO2 for endogenous pacemakers and
sleep cycles:
• What about evolution? For
example hibernation? (Though
humans don’t hibernate)
• SCN isn’t only control of
sleep/wake cycle, temp should
also be considered as temp affects
hibernation
• Evolutionary approach not
considered therefore reductionist

42. AO2 for endogenous pacemakers and
sleep cycles:
• Reductionist 
• Doesn’t include individual
differences/social differences/stress,
anxiety, insomnia, blind people (no
optic nerve)… Counter with Campbell
& Murphy (1998) (kneecap light)
• Shows sleep is more complex than
light/temp/biological factors
• To fully understand sleep, biological
factors would have to be considered
including psychological/social factors

43. Disrupting Biological rhythms:

44. Intro…
• Research has shown that
endogenous pacemakers use
exogenous zeitgebers to adjust
the body’s biological rhythms
(Czeisleret al 1982; Siffre, 1962)
• This allows our body to cope
with seasonal changes slowly
over time.
• However there are some faster
changes such as jetlag and shift
work.

45. Jet lag:
Phase Advance (W-E)
Phase Delay (E-W)

46. Jet lag – travelling long distance by plane, so
exo&endo are out of sync (desynchronisation)
Phase delay:
• Endogenous pacemakers
are ahead of local time
• Phase delay is considered
easier to adjust to
• Moves from East to West
• When a train is delayed
‘EWWWWW’ (east to west)
Phase advance:
•Endogenous pacemakers are
behind local time
•Phase advance is more
difficult to adjust to because
our biological clocks ‘lose time’
•Moves from West to East
• When you advance down a
slide ‘WEEEEEEE’ (west to
east)

47. Consequences of jet lag – Rechtet al
(1995):
• Slower mental & physical reactions
• Looking at performance of US
baseballers
• Over a 3 year period
• Teams from E to W won 44% of their
games
• Teams from W to E won 37% of their
games
• Suggests phase delay is easier
• Does not consider individual
differences (the teams may just be bad)
• Longitudinal

48. Consequences of jet lag – Takahashi et
al (2002):
• After 11 hour flight
• Doses of melatonin
reduced symptoms of jet
lag by speeding up
resynchronisation
• Recommended that you
eat meals at the same
time as locals on arrival

49. Shift work:
• Usually found in factories and power
stations
• Work one shift in a 24 hour period
• People who work night shifts have
disrupted biological rhythms –
Desynchronisation of endo&exo
• Some workers move a shift back each
week, causing further
desynchronisation
• ‘moving back’ has the same effect as
phase advance
• It’s been shown a week isn’t long
enough to resync
Phase advance

50. Consequences of shift work:
1. Poor decision making –
anecdotal evidence such
as:
- Chernobyl (1:30am)
- Challenger space disaster
(decision to launch was
made in early hours of
morn)

51. Consequences of shift work:
2. Sleep deprivation
Workers on night shifts have
to sleep during the day,
which is more difficult due
to sunlight, bird sounds etc.
De-synced circadian rhythms

52. Consequences of shift work:
3. Low worker satisfaction and production
(Czeisleret al, 1982)
• Chemical plant, Utah, USA
• Staff on short rotation shifts suffered
more health problems: difficulty sleeping
& stress
• Researchers convinced the plant to put
workers on a ‘Phase-delay’ shift pattern,
where their shifts move forward
• Shift rotation also altered from 7 days to
21 days
• After 9 months, worker satisfaction was
significantly higher

53. Consequences of shift work:
4. Gordon et al (1986):
• Police in Philadelphia from
backwards to forwards
rotation on 18 day cycles
• 30% reduction in sleeping
on job
• 40% reduction in accidents
• Officers had better sleep,
and less stress

54. Lifespan changes in sleep:

55. Lifespan changes in sleep:

56. Lifespan changes in sleep:
• Little babies have the mostest sleep, and the
mostest REM sleep too
• The amount of sleep you get decreases as you
get older
• % amount of REM sleep decreases through life
• This shows sleeping patterns are not resolute
• Doesn’t account for individual differences –
those with insomnia

57. Lifespan changes in sleep – Ohayonet
al (2004):
• Meta analysis of 65 studies
• Age range: 5-102
• Total sleep time decreased. Approx 8
hours at 5 years old, and 6 hours at
70 years old.
• % of 1 and 2 NREM sleep increases
with age
• % of 3 and 4 NREM sleep decreases
with age
• % of REM sleep decreased from 25%
aged 5, to 19% aged 70.

58. Lifespan changes in sleep – Van Cauter
et al (2000):
• Longitudinal study (14 years)
• 149 male ppts (aged 16 to 83)
• Production of growth hormone
decreases, which causes deep
sleep to decrease.
• Deteriorates in 2 stages:
- between 16 and 35
- between 35 and 50 years old
• Little growth hormone means
ability to repair body tissue is
decreased.

59. Evaluation for lifespan changes:
 Uses EEGs to test, which are
reliable as are lab studies and
stuff
 Supporting studies – van
cauter &ohayon
 But using lab studies can be
bad due to unfamiliar settings
which could disrupt sleep
therefore, lacks ecological
validity
 Does this only take night time
sleep into account? What
about elderly folk & babies
who nap during the day?
 Individual differences not
considered, arguably
reductionist

60. Evolutionary explanations:

61. Evolutionary explanations:
• Look at different species to determine key
sleeping features
• Amount of sleep is affected by different
factors:
- Predator/prey
- Safe place to sleep
- Body & brain size
- Metabolic rate

62. Evolutionary – Meddis (1975): (like medicine)
• Proposed that sleep is to keep animals safe
when active behaviour is impossible
• For example at night, when prey animals need
to hide from predators (sheep from foxes)
• For example in DeCourseyet al (2000)’s study
with chipmunks, who were eaten by weasels
when they couldn’t sleep & made noise
• However, it would make more sense for the
animal to be awake & alert?
• It also doesn’t explain why we have 2 types of
sleep

63. Supporting Meddis – Leskuet al
(2006):
- Animals sleeping in dangerous
places sleep less
- Predator (carnivores) animals
sleep more than prey animals
maybe because meat is higher
in energy than say grass.

64. Evaluation – Leskuet al (2006):
• Correlations only show association, not cause
& effect
• Many studies are in artificial environments
(like zoos), are they ecologically valid?
• Takes into account the animal & their
environment, so it’s not reductionist… In fact,
it’s MORE holistic.
• However, it cannot tell us which is the more
important factor determining sleep patterns

65. Evolutionary – Webb (1982):
• Used model of hibernation to propose
that sleep is to conserve energy
• Moreso in smaller animals with higher
metabolic rates
• Supported by positive correlation
between metabolic rate and sleep time
• Doesn’t explain why there’s two types of
sleep
• REM is highly active, and doesn’t
conserve energy (it’s similar to being
awake!)
• But overall, we burn less energy whilst
asleep, which supports Webb’s theory.

66. Supporting Webb – Berger and Philips
(1995):
• Empirical support:
animals sleep more when
food is scarce

67. AO2 evaluation for evolutionary:
• Holistic – Nature and environmental factors
considered
• However, could also be deemed simplistic as it
doesn’t take lifespan changes of sleep into
account
• Why are there 2 types of sleep? (NREM & REM)
• REM is still highly active, is it really conserving
energy?

68. AO2 evaluation for evolutionary:
• Empson (1993), describes sleep
as ‘a complex function of the
brain’ which has a ‘restorative
function’
• Bottlenose dolphin sleeps one
hemisphere of its brain at a time,
so it can remain partly conscious
& still breathe, shows that sleep
is important, as it has had to
develop this intricate sleeping
method. Also links to restorative.
(unihemispheric sleep)

69. • Shows that evolutionary should also consider
than sleep has a restorative function, as sleep
is there to help both the brain and the body
recovery

70. Sleep as a restorative thing…
Oswald (1980) Restoration model
Horne (1988) Core/Optional sleep
model

71. Oswald (1980) Restoration Model:
• High levels of brain activity during REM, reflect recovery of
the brain (EEG)
• Increase in release of hormones, (like growth hormone) in
SWS (Slow wave sleep) which restore body tissues,
suggesting sleep does have a restorative function
• Has not been applied to humans
Supported by:
- Randy Gardner (case study) who only had mild loss of
cognitive functioning
- Jouvet’s study (1967), as cats without sleep died
- Rechtschaffenet al (1983), rats without sleep died after 33
days

72. Horne (1988) – Core/Operational sleep
model:
• Lab studies, showed sleep deprivation only
had mild effects on cognitive functioning
(Randy Gardner)
• Recovery centred on SWS Stage4 & REM
• Suggested SWS and REM is core sleep
needed for brain functioning
• Lighter stages (3&4) known as ‘optional
sleep’
• Body restoration is not purpose of sleep,
which occurs during relaxed wakefulness
• Focussed on human ppts

73. Horne (1988) – supported by…
• Newborn baby spends 50-60% of sleep in REM
compared to normal proportion of 25%, supports
Horne as babies use a lot of cognitive functioning
to be able to take everything in
• Horne (1988) conducted meta-analysis of 50
human sleep deprivation studies, increases
reliability
• Randy Gardner (ha!) (Case study) as he lost his
cognitive functioning

74. Oswald Horne
Sleep is used to restore
both the BRAIN and the
BODY
Core sleep is ONLY used to
restore the brain
The body recovers during
sleep through the release
of hormones
The body recovers during
periods of ‘relaxed
wakefulness’
Could apply to non-
humans
Could only apply to
humans

75. Sleep deprivation studies – supports
Horne:
Peter Tripp (famous DJ):
- 201 hours and 10 minutes awake, mostly in a
booth in Times Square, NY
- Nurses/doctors tried to keep him awake
- Mean body temp declined
- An EEG showed brain waves that he was asleep,
even though he was awake and talking
- Followed 90min cycles of hallucinations & periods
of clarity (like Ultradian rhythms, such as REM) as
though he was dreaming, even though he was
awake
- Suggests that the brain has to go into this sleeping
pattern to recover

76. Sleep deprivation studies – supports
Horne:
Randy Gardner (1965):
Stayed awake for 11 days and nights
Reported malfunctioning cognitive
processes such as blurred vision,
slurred speech, mild paranoia
Despite losing 90 hours of sleep, he
only caught up 11 hours
However, caught up on more REM
and Stage 4 (suggesting these are
the vital stages)
Suffered no long term consequences
(unlike Tripp)

77. Animal sleep deprivation studies –
Supports Oswald:
Rechtschaffenet al (1983)
Placed rats on discs over water
When EEG’s showed they were sleeping,
the discs would rotate, forcing the rat
to walk to stay out of the water
They lost weight, had increased
metabolic rates
After 33 days, all rats were dead
Suggests sleep does have a restorative
function
Animal study/not generalisable/ethical

78. Evaluation of restorative theories of
sleep (supports):
Fatal familial insomnia – genetic defect
leading to messy sleep patterns, until middle
age, where they’re unable to sleep. After 2
years of sleeplessness, they die
- autopsies shown the thalamus degenerates
- suggests we need sleep to recover
- Cases are rare, so it’s difficult to generalise

79. Evaluation of restorative theories of
sleep (supports):
 Reductionist
- Biological
- Looking at nature
- Doesn’t consider individual differences

80. Evaluation of restorative theories of
sleep (refutes):
 No correlation between energy
expenditure and length of sleep –
We’d imagine we’d sleep more after
high levels of activity, and less after
low activity.
Breedlove (aww) et al (2007) found
no relationship between length of
sleep & activity levels prior to sleep.
Giant sloth will sleep up to 20
hours, and it does VERY little (lazy
sod!)

81. Evaluating restorative theory:
• When looking at restorative theory, an
explanation that could help to understand it
would be the evolutionary theory of sleep, as
it looks at both biological influences and
influences of the environment
• So, it’s better to consider different
explanations together to gain full
understanding

82. Sleep disorders:
Narcolepsy, insomnia, sleep walking

83. Sleep disorder - Narcolepsy:
• It’s a disorder where people
fall asleep whilst walking
round.
• If triggered by an emotional
experience, it’s known as
‘cataplexy’
• Lots of research suggests
that it is a genetic disorder
(biological link)

84. Three explanations for narcolepsy –
1. Rapid eye movement (1960s)
REM sleep linked to eye
movements, and body paralysis.
Brain activity similar to if you’re
awake. This explanation suggests
a person experiences elements of
REM sleep whilst they are awake.
Since narcoleptics often collapse
(like paralysis in REM) and can
dream in the brief period they
are asleep

85. Three explanations for narcolepsy –
2. HLA – Human Leukocyte
Antigen (1980’s)
Biological/objective
Caused by mutation in immune
system. Best HLA marker is
HLA-DQB1*0602 which is
present in 90% of
narcolepsy-cataplexy
(Stanford school of medicine)

86. Three explanations for narcolepsy –
3. Hypocretin (yanks call it Orexin)
(1990’s)
Biological/objective
A neurotransmitter that regulates sleep,
appetite and energy conservation. It
helps maintain wakefulness.
Hypocretin-1 is measured in
Cerebrospinal fluid, using a lumbar
puncture. Most people with
narcolepsy-cataplexy have no
hypocretin-1 molecules.

87. Evaluating hypocretin:
• People with narcolepsy
have less Hypocretin-
producing-cells in their
brains (Thannickalet al
2000)
• People with narcolepsy
have low levels of
Hypocretin (Sakurai,
2007)
• Deterministic
• Not 100% concordance
rates between twins,
suggests there’s another
factor that genes
• Reductionist – Only looks
at biology, not social or
psychological factors

88. Narcolepsy – University of Tokyo (study):
• University of Tokyo found a
genetic link
• Genetic variant found in:
79% chance increase of
Narcolepsy in Japanese people
40% chance in other ethnic
groups
Links to CPT1B and CHKB genes

89. Sleep disorder - Insomnia:
• Primary insomnia – No
obvious psychological or
physical cause
• Secondary insomnia – Result
of an existing psychological or
physical problem
• It affects 1/3 of American
population, and a chronic
problem in 1/10 Americans

90. Insomnia:
• Characterised by:
Sleepiness, fatigue, drop in alertness,
difficulty concentrating, depression,
overly emotional state
Dement argues insomnia is a
symptom caused by something else.
If he is correct, we should focus on
what’s causing it, rather than
treating the insomnia.

91. Primary explanations for insomnia:
Idiopathic Insomnia:
- Begins in childhood &v. rare.
- Malfunction in sleep/wake
cycle
- Brain: Raphe nuclei and
Reticular Activating System
(RAS) at fault

92. Idiopathic (cont.)
- During sleep/wake cycle, we’re kept awake by
RAS which creates arousal in brain
- In order to sleep, the RAS must be inhibited
- Those with idiopathic insomnia are predisposed
to greater arousal, and struggle to switch off their
RAS
- Supported by Bonnet and Arand (1995) who
suggest insomniacs have higher levels of cortical
activity both when awake and asleep

93. Primary explanations for insomnia:
Psycho-physiological insomnia:
Insomnia results from learned/behavioural
condition
A) Cycle of anxiety, reduces sleep, self-
reinforcing
B) Regular routines, such as brushing
teeth/getting ready for bed could create
and become associated with stress, as
they link to the thought of insomnia
An example of classical
conditioning/phobia-like

94. Secondary explanations for insomnia:
• Sleeplessness caused by
another disorder such as
depression or a medical
disorder (chronic pain)
• Much more common than
primary
• Monti (2004) found that
treating the CAUSE was
more successful than
treating the insomnia (Like
Dement said!)

95. Secondary explanations for insomnia:
1. Sleep apnoea:
Obstructive sleep apnoea – condition
where air stops flowing into the lungs,
where breathing stops for 10+ seconds,
for 5ish times a night
– Lack of muscle tone in the upper airway
causes airway to fold in & close
This can cause people to wake up again
with a snore/snort
Sleep apnoea trust (2008) found that
people will be forced awake during the
night so are sleepy during the day

96. Causes + symptoms of sleep apnoea:
• Blocked nose (various causes)
• Obesity (fat people = pressure on
throat)
• Drugs (tobacco/alcohol/painkillers)
• Age (more common in old age)
• Adenoids and tonsils (tonsillitis and
all that rank stuff)
Symptoms include – tiredness,
reduced cognitive functioning, poor
concentration, Macey et al (2002)
believes it can damage the brain
due to repeated oxygen starvation

97. Secondary explanations for insomnia:
2. Personality:
Anxious personalities
are more likely to
suffer from insomnia
Anxiety is linked to
higher arousal which
means it would be
more difficult to
sleep

98. Personality & Insomnia – Gregory et al
(2006):
• Gregory et al (2006) studied the effects of family
conflict on insomnia, which linked to high levels of
anxiety
• Longitudinal
• New Zealand kids followed from 1972-2006
• Used questionnaires to find out about household,
recorded life events.
• Extraneous variables were controlled e.g. socio-
economic status, gender, health, depression
• Found a correlation between family conflict
experience by child from (9-15 years) and onset of
insomnia by 18
• Could be a casual correlation between familial
conflict (which leads to anxiety) and insomnia

99. Gregory et al (2006) – evaluation:
• Variables well controlled
• Longitudinal – lots of
information gathered
• Longitudinal – may
suffered attrition rates
• Only followed kids from
NZ (ethnocentric/cultural
bias/cultural relativism?!
Idk)
• Questionnaires are
subjective, may also be
affected by social
desirability bias

100. Sleep disorder – Sleep walking:
• Sleepwalking is when people carry out activities
such as walking, weeing, or moving furniture in
their sleep – as if they were awake.
• It occurs during slow-wave sleep, rather than
REM
• Episodes can last from seconds to over 30mins
• If left undisturbed, sleepwalkers often go back to
sleep, but could fall asleep in unusual places.
• Usually occurs in children aged 5-12, affecting
20% of children, and 3% of adults (Hublinet al
1997)

101. Sleepwalking – Bassetti (2002):
• Looking at genetic evidence
(biology)
• Focussed on the HLA-
DQB1*05 gene
• Volunteer sample (some
sleepwalkers may not even
know they sleepwalk )
• 74 patients (only 16
genetically tested)
• 8 patients had the gene (50%)
• Gene present in 25% of non-
sleep walking population
• May not be representative

102. Bassetti (2002) – evaluation:
• Objective – blood tests to
find genes, replicable +
consistent results = reliable
• Supporting evidence –
Hublinet al (1997) Finnish
twins, found 66%
concordance rates in boys,
and 57% of girls have gene,
suggesting genetic link
• SE – Sleepwalking runs in
fams(Horne, 1992)
• Small sample size, may not
be representative, or
generalisable
• Volunteer sample was silly
because lots of sleepwalkers
don’t even know they do it

103. Sleep walking – Zadraet al (2008):
• Investigating sleep walking &
sleep deprivation
• 40 ppts in lab study over 3 nights
• Night one ‘normal sleep’
measured – 40ppts had total of
32 episodes of sleep walking
• Night two – ppts kept awake for
25 hours
• Night three ‘Recovery sleep’
measured – 40 ppts had total of
92 episodes of sleep walking
• Suggests tiredness can trigger
sleepwalking

104. Zadraet al (2008) – evaluation:
• Findings not found in
those who do not sleep
walk – suggesting a
genetic predisposition
(link to Bassetti, 2002)
• Sleepwalking common in
those with RLS (Restless
leg syndrome), which is a
risk factor of insomnia,
therefore excessive
tiredness (SYNOPTIICCCC)
• Small sample size
• Lowered ecological
validity, as not in their
own beds
- could’ve let them sleep
in the beds for a few
more nights before
observations began

105. Main evaluations for sleepwalking:
• Objective – scientific,
based on fact, replicable +
consistency = reliable
e.g. blood tests in Bassetti
(2002)
• Deterministic – focuses
on biology which is pre-
determined, you’re
unable to change it
• Biological/reductionist –
Looking at HLA DQB1*05
gene in Bassetti (2002)
Zadra (2008) also found
genetic link
• Research conducted in lab
study (esp sleeping) may
reduce ecological validity,
may not be applicable to
real life