• Moore - Supporting evidence for this theory comes from Moore who found that hypocretin producing cells in the hypothalamus were reduced in narcoleptic patients. In dogs they found that a mutation produced this lack of hypocretin but this is not true in humans. Despite this a link has been established between an antigen – HLA and low levels of hypocretin. 90% of narcoleptics have an increased variant of the HLA antigen which causes low levels of hypocretin and therefore narcolepsy.This supports the role of hypocretin in the development of narcolepsy as it shows a potential link between levels of the HLA antigen and hypocretin - 90% of narcoleptics have an increased variant of the HLA antigen - which is believed to genetically predispose narcolepsy.
  • Siegel et al (2000) managed to acquire the preserved brains of 4 narcoleptics and after a close examination they were found to have 93% fewer hypocretin neurons than a non-narcoleptic’s brain. This seems to suggest that the work of Mignot and Dement was relevant to humans too. More recently low levels of hypocretin have been found in the cerebrospinal fluid (CSF) of humans with the disorder. This supports the explanation of narcolepsy as those with fewer hypocretin neurons secreted less hypocretin hormone which resulted in them developing narcolepsy.
  • Broughton (1999) reported that lifestyle adjustments, such as regulated sleep schedules and relaxing before bed, were more successful at treating the symptoms of narcolepsy than drugs.

This suggests that lifestyle plays an important role in managing narcolepsy, which means that it may also play a role in development of the condition. The above theory overlooks the importance of lifestyle, which means that it is insufficient to account for these data.

  • Nishino et al found a link between low levels of hypocretin in the human cerebrospinal fluid and narcoleptic symptoms.This study seems to support the theory because it is the hypocretin which regulates arousal and wakefulness, therefore if there are decreased levels of hypocretin in the cerebrospinal fluid then it is logical to assume an equal decrease in wakefulness.
  • Wang et al (2001) – Patients with chronic primary insomnia and healthy controls (measured by questionnaires). Those who scored higher on the neuroticism, anxiety and impulsivity scales had chronic primary insomnia. This is a result of unusual functioning of the hypothalamus and a neurotransmitter imbalance. This supports the theory of predisposing factors because biological factors are underlying the personality factors of anxiety, impulsivity and neuroticism. The study suggests that patients with insomnia could have a genetic predisposition to have an imbalance of neurotransmitters which contributes to the personality factors, which lead to less sleep (insomnia).
  • Nofzinger et al (2004) found that the transition from being awake to being asleep is usually associated with a decrease in activity in the brain stem, thalamus and prefrontal cortex. Using PET scans, Nolfzinger et al showed that insomniacs experienced a smaller decline in such activity when going to sleep. In fact, they found elevated level of activity in the brains of insomniacs. This suggests that people who suffer from insomnia do so due to high physiological arousal which supports the biological element of the explanation for insomnia.
  • Dement – Studied several cases of sleep-state misconception. One participant suffered severe insomnia whilst being asked to sleep 10 nights in a sleep laboratory. They completed questionnaires which asked how long it took them to fall asleep at night. They reported times ranging from 1-4hours, with a mean time of 90 minutes. They actually never took more than 30 mins to fall asleep. This research showed that poor expectation of sleep worsened insomnia as those who conceived the process of getting to sleep negatively showed more misconceptions of the quality/quantity of sleep. This supports perpetuating factors element of the theory as expecting bad sleep affected insomnia.
  • Bastien et al. (2004) found that 60% of patients with insomnia could identify a trigger for their sleep disturbance, and these tended to be around family, work/school and health.This study supports the idea that precipitating factors have an effect on insomnia because the stress of external factors such family problems (divorce) may have an effect on their health resulting in them not being able to sleep.
  • Ohayon & Roth (2003)interviewed 14,195 participants representative of the general populations of the UK, Italy, Portugal and Germany over the telephone about their psychiatric history and their sleep patterns. They found that people with insomnia were six times more likely to report a mental health problem, such as depression or anxiety, than people without insomniaThis suggests that there are also psychological factors that can be linked to suffering from insomnia.
  • Ohayon researched a sample of 19,136 individuals from 15 states of the U.S. The study showed that people with depression were 3.5 times more likely to sleepwalk than those without, and people with alcohol abuse/dependence or obsessive-compulsive disorder were also significantly more likely to have sleepwalking episodes. This evidence supports the stress part of the explanation as it shows that environmental factors increase the amount of sleepwalking that occurs in individuals for example those who drink a lot of alcohol increased their time spent in SWS sleep which therefore could increase their chances of sleep walking.
  • Hublin et al (1997) Monozygotic (1045) and dizygotic (1899) twins were interviewed about their sleepwalking habits in childhood and adulthood. The study found that there was a link between genetics and sleepwalking.which suggests that one can be predisposed to sleepwalking, supporting the diathesis idea.
  • Oliviero (2008) examined the motor excitability of adult sleepwalkers during wakefulness. Compared to normal controls, the sleepwalkers had signs of immaturity in the relevant neural circuits. This evidence supports the diathesis-stress model, since the participants’ neural circuits were not fully developed, therefore could not reduce motor activity. This led to a state of semi-wakefulness, causing sleep-walking. The study also supports the finding that children sleepwalk more than adults as their brains are still developing.
  • Zadra et al (2008) investigated 40 patients and recorded sleepwalking for one baseline night and during recovery sleep after 25 hours of sleep deprivation. The results show that 32 episodes were recorded from 20 sleepwalkers (50%) at baseline whereas recovery sleep resulted in 92 episodes being recorded from 36 patients (90%). This study also supports the model because the participants were subject to stress caused by sleep deprivation. Most patients who were deprived of sleep showed sleepwalking
  • Lin et al (1999) linked cataplexy in dogs to a gene defect on chromosome 12. This gene is responsible for regulating the neurochemical orexin (also known as hypocretin). The defect means it cannot carry out its normal function.
  • Mellins et al studied 39 people with type 1 narcolepsy and 35 people without the disorder (including four sets of twins in which one twin was affected and the other was not) and found that people with narcolepsy have a subgroup of T cells in their blood that react to particular portions of the hypocretin protein, but narcolepsy-free people do not. T cells are a key part of immune system defences against infection. This supports the theory as it suggests a link between T cells in the bodies of humans and the hypocretin protein, as those with narcolepsy had a subgroup of T cells that were affected, those who didn’t have narcolepsy were not affected.
  • Watson et al (2006). In a twin study, Watson found that 50% of the variance in the risk for insomnia could be attributed to genetic factors.
  • Gregory et al (2006) looked to see whether children growing up in families for whom high levels of conflict had been reported (when the children were between 7 and 15 years) were more likely to have insomnia as young adults (aged18 years). Interestingly, they found the greater the number of assessments at which a family scored in the top 25 per cent for conflict, the more likely the participant was to suffer insomnia at 18 years of age. This study supports that environmental factors can have an effect on whether or not a person suffers from insomnia. People who suffered from more family conflict were more likely to have the disorder.
  • Lecendreux et al (2003) found around 50% concordance in MZ twins compared to 10-15% in DZ twins.These studies support the idea that there is a genetic component to sleep walking but also that stress and other environmental factors increase the likelihood of sleep walking otherwise the concordance rates would be 100%.
  • Broughton (1968) found that the prevalence of sleepwalking in first-degree relatives of those who are affected is at least 10 times higher than in the general population.
  • Mignot et al (1999) found that dogs with narcolepsy had a defective hypocretin receptor 2 gene. This supports the theory of a genetic cause of narcolepsy, as dogs with the gene all suffered narcolepsy and sudden fall into REM sleep. The lack of function in hypocretin receptors could have the same effect of destroying the cells in the hypothalamus which produce the neurotransmitter- the overall effect is that hypocretin does not have an effect.
  • Dement (1999) found evidence to support the hypocretin’s role in narcolepsy. They found that mice who could not make the neurotransmitter in their brains developed symptoms of narcolepsy, including sleep attacks and cataplexy.This study supports the biological theory of narcolepsy because it highlights how certain failures in brain producing specific neurotransmitters can result in symptoms similar to that of narcolepsy such as total loss of muscle control (as in cataplexy) and the attacks of sleep synonymous with narcolepsy.
  • Montplaisir (2007) found abnormal numbers of hypocretinergic and dopaminergic neurons in the brainstems of 16 narcoleptic patients.This suggests that an imbalance of neurotransmitters is associated with narcolepsy. Furthermore it confirms that abnormal levels of hypocretin in the brain may be responsible for the condition. However, it also suggests the involvement of dopamine, so hypocretin alone may not be sufficient to account for the development of narcolepsy in all cases