Explanations of sleep disorders

Narcolespy is linked to the neurotransmitter hypocretin.

• Hypocretin(or orexin) regulates arousal, wakefulness and appetite. 
• The loss of hypocretin can reuslt in narcolepsy, where the individual falls rapidly into REM sleep.
• The brain only contains around 10-20,000 neurons in the hypothalamus that produce hyprocretin.
• In the HLA complex on chromosome 6, a gene  variationcan predipose people to narcolepsy.
• The variation incraeses risk of an immune response to the cells that produce hypocretin.
• People with narcolepsy often have vastly reduced numbers of hypocretin-neurons in their brain.
• The auto-immune response can also be cuased by a flu vaccination.

T.E. Scammel

• observed one case where a young man suffered a hypthalamic stroke, destroying hypocretin producing cells.
• He then suffered narcolepsy.

This supports the theory because the loss of these cells, and therefofre a lack of hypocretin, would result in a lack of control over wakefullness. This lead to narcolepsy.

Nishino

• Found a link betwene low levels of hypocretin in the cerebrospinal fluid and narcolpetic symptoms.

This also supports the theory,as  a lack of the wakefullness-controlling chemical, hypocretin, would logically result in a lack of control over sleep.

CAUSALITY?

MIGNOT

• 16 pairs of monozygotic twins
• 5 pairs were concordant for narcolepsy

This supports the genetic theory because the concordance rate is much higher than the general population.

However, since there isn't a 100% concordance rate, the condition isn't compleely genetic, and tehre must be environmental factors. These are described by the explanation, so this research cannot fully justify the theory.

Broughton

• reported that lifestyle adjustments , such as regulated sleep schedules and relaxing before bed, were more succesfful than drugs.
• This suggests that environmental factors have a larger influence over narcolepsy than biological factors.

The explanation does not account for these environmental factors, and so it could be called an incomplete explanation of the disorder.

Good:

• High ecological validity- case study and twins are real life cases, so are not artifical.
• High internal control- the genes and hypocretin cells were the studied variable, and all resulted in narcolepsy.
• BASICALLY THERE IS A LINK!

Bad:

• Low populational validity- case studies and twins are not a fair represneattion of all sufferers of narcolepsy.
• Other potential causes: hypothalamic stroke could have affected release of other neurotransmitters, causing narcolepsy.
• CAUSALITY- nishino find a link between hypocretin levels and narcoleptic does not ensure than hypocretin CAUSES narcolepsy. Instead, a lack of sleep may result in lower levels of hypocretin.

Reductionist

The theory suggetss the dirsorder is caused entirely by teh biological factor of a lack of hypocretin functioning within the brain. It does not explain or even suggest the environmental factors that culd come about to cause thisn laclk of hypocretin, and is therefore likely to be an oversimplification. However, the approach also allows potential medical cures or treatment.

Practical Applications

• Actually minimal medical applications so far.
• Hypocretins are large molecules and difficult to get into the brain.
• Gene therapy techniques may be developed, but are expensive and unreliable.

Very scientfic

• The research, depsite low population validity, is comeplling and highly controlled, making this explanation compelling and scientific.

ANIMAL STUDIES

• A lot of research into hypocretin has been carried out on animals.e.g. autosomal recssive gene in dogs showed a increase in narcolepsy.
• There are ethical and methodological problems.

The diathesis-stress model

• There are pre-disposing factors (diathesis) and environemntal causes to teh diroder (the stress.)
• Sleepwalking occurs in SWS.
• The genetic predisposition is likely to be incomplete arousal, which may be determined by the adenosine deaminase gene, found on chromosome 20.
• This may be linked to the release of gammapaminobutyric acid (GABA), an chemical messenger which usually suppresses motor acitivity.
• EEGs of the brain during sleep walking shows typical SWS delta waves, but higher frequency beta waves- characteristic of an awake state.
• Maturation of key neural circuits and the release of GABA in the brain is key to stopping sleepwalking, which is why most people grow out of it. If they don't mature fully, adults can continue to sleepwalk.
• Factors that increase amount of SWS can increase sleepwalking e.g. sleep deprivation, drinking alcohol, being a child.

Bakwin

9/19 MZ pairs were concordant for sleepwalking, wherease only 1/14 DZ pairs were concordant.

Hublin

Concordance rate for MZ twins was 0.55 v concordance rate for DZ twins was 0.35.

Self reported study

1045 monozygotic twins

1899 dizygotic twins

found the concordance rate was was 5 times higher in MZ.

The concordance rates are much higher than for the general population, and so suggetss there is definitely a genetic link for insomnia. It is not 100% concordance rates, and so the stress part of the model is still justified by this research.

Zadra

• 40 patients who sleep walked, and 15 of which had injured themselves
• They were prevented from falking asleep.
• After 25 hours they were allowed to sleep.
• With sleep deprivation, 90% of the patentions showed signs of sleep walking, compared to 50% with a normal nights sleep.
• Sleep deprivation does not lead to SW in normal individuals.

This supports the theory, because the genetic predisposition was exacerbated by environmental conditrions, such a sleep deprivation. Therefore, the daithesis-stress model represents a clear interaction betwene nature and nurture, when it comes to sleep walking.

Ohayon

• 19136 indivudals across 15 US states
• People with depression are 3.5x more likely to sleepwalk.
• People with alcohol abuse or OCD are also more liekly to sleepwalk.

This research supports the stress part of the model, because its hwos that environmental factirs such as alcohol can affect sleepwalking, perhaps by lengthening the amount of time in SWS.

The depression statistic shows that other conditions could cause or exacerbate sleepwalking, also providing a basis for the stress aspect of the explanation.

Oliverio

• examine adult sleep walkers motor- excitability during wakefulness.
• Compared to the control they sleep walkers had high levels of immaturity in their neural circuits.

This supports the diathesis model, as a lack of development in the circuits means a lack of control over motor excitability. These leads to state of semi-awakeness.

This also supports the explnanation of why children sleepwalk more than adults.

Population validity- many twins involved, but maybe twins are more predispositioned to sleep walking than general population. Zadra used just 40 people. BUT 19,136 people in Ohayon and Roth, which is good-- BUT JUST AMERICANS.

Artifical conditions- Zadras study was executed in a sleep lab, which could have increased or decreased teh amount of sleepwalking. This lowers teh cological and predictive validity, as sleep deprivation may be more or less affective in a real life situtaion.

Self reported study- one twin study was self reported. This means it is more suceptible to incorrect answers e.g. someone may have remembered tehmsleves sleep walking but never actually did. 

HOWEVER- high control over all studys (MZ compared to DZ twins so social factors are controlled for. Zadra used EEG's and strict observations. This increases the reliability of the reserach and increases the internal validity as well.

Nature v nurture

The theory involves both aspects of the nature nurture debate. The biological basis of the diathesis-stress model is sueful, as it's reductionsit nature makes it easier to test empirically and experimentally. This could lead to idenytofocation of  cause-andeffect mechanism, which may later allow a treatment or cure for sleep walking.

However, the acknowledgment of environemental factors also allows a more positive outlook, as a determinists diagnosis of 'genetic predispostion' may cause people to lose hope of getting better.

MANY PRACTICAL APPLICATIONS

• Due to the integrated nature of the theory, there are many practical applications. Those who are predisposed to sleep walking can be advised to avoid alcohol, sleep deprivation and other exacerbatory factors.
• However, the genetic side does mean that certain people will be more likely to sleep walk, and this is genetically determined. Therefore there is less applications.
• CRIMINAL ACTS: Some people have commiteed criminal and violent acts and claimed to be sleep walking. The theory may allow us to measure their amount of SWS (if it is more than normal) their neaural dveelopment (if it is immature) and even if they the allele variation. This would allow us to identify real sleep walkers. This is very useful for the theory, if if can ever be fully proven. At the moment, evidence does not have strong enough predictive validity.

Speilman and Glovinsky

• There are predisposing, precipitating and perpetuating facyors that explain primary insomnia.
• Predisposing-- genetic vulnerability to the physiological state of hyperarousal. Some research has linked the Cul3- a neural pathway proetin- to imnsomnia.
• Precipitating factors incolude stress and environmental change wthat make it more difficlt to get to sleep e.g. hnaging time zones. Women and older people suffer more from insomnia, so these are precipitating fcators too. Events that disrupt the circaian rythym, such as oherr illnesses and travelling.
• Perpetuating factors- these maintain insomnia. Examples include being tense or being scared of not being able to fall asleep. These are key to chronic primary insomnia.

Stavropoulos et al

• 21000 fruit flies 
• Normal fruit fly slep an average of 927 minutes a day.
• Fruit flies with the insomniac gene slept about 1/3 of this.

This supports the research because the genetic change, associated with the Cul3 pathway, resulted in different sleep ebhaviour in the fruit flies. This could suggets that sleep behvaipour can be directly linked to genetics in humans too.

Drake et al

• 988 MZ twins and 1086 DZ twins
• Measured sleep reactivity, which is the difficulty in sleeping after one of nine situtaions e.g. stressful experiences, watching a scary film
• Heritability of sleep reactivuty was 36%
• The heritability for insomnia was 49%

This shows a substantial genetic component for insomnia and its symptoms.

BASTIEN

• 345 patients
• completed survey and semi-structured interview
• Found that most common precipiatating factors were related to family, health or work-school events.
• 65% of these had negative effects on insomnia.

This resaerch shows how different events and worries can cause insomnia to worsen.

Ohayon and Roth

• interviewed 14,195 particoants in general population of several european countries
• Over the ohone
• Found that people with insomnia were 6x more likely to suffer from a mental health problem, than those without insomnia.

This suggests that other mental health issues and psychologcial factors are linked to suffering insomnia, which could help explain spart of the 'stress' factor of the explanation.

HOWEVER- not causality-- maybe the insomnia caused the other condition.

Animal research-

• the fruit fly study shows that a certain gene can control sleep behaviour in flies, but this cannot be generalised completely to humans.
• Some peope consider animal research cruel and an iniefficent way of studying human conditions.

VALIDITY

• ecological- bastiens study was non-invasive, and the twin studies were carried out in their own homes. This increases ecological validity.
• Population validity is good for numbers (Ohayon = 14,000+), but there is a definite ethnocentric bias- all studies are focused on western insomniacs, whereas symptoms and causes may vary by culture. This reduces generalisability.

RELIABLITY

• Very repeatablle studies and high control
• Self-report surveys are vulnerable to demand characteristics and social desirability bias.

Nature v nurture

The theory looks at both aspects of the nature nurture debate. The predispsoing factors suggest that insomnia may have a biological side, but the ackowledgment of precpitating and perpetuating factors also suggest that insomnia is affected by environmental factors.

The biological side can be easily tested using empirical methods e.g. the identification of a specific gene. This could also allow effective treatments to prevent or reduce insomnia.

The nurture side also has practical applications because we can inform people about what may cause insomnia, or make it worse.

Practical Applications

• Also has an integrated aporoach to the condition, resulting in many practical applications.
• Reducing precipating factors e.g. travelling, alcohol or scary.stressful events
• Reducing perpetuating factors e.g. CBT to prevent anxiety over sleeplessness

Vague genetic explanation

• The genetic side of the theory has not been fully eplained or demonstrated.
• This makes the theory weaker, as it cannot be ully justfied.
• HOWEVER- mor eresaerch is being done, and its still early days in gene technology.