Sakurai (2007) highlighted how there are about 10,000-20,000 hypocretin-producing cells in a normal hypothalamus, but people with narcolepsy have a significantly lower amount, resulting in low levels of the neurotransmitter hypocretin which may cause narcolepsy.
Supporting evidence for the hypocretin theory comes from narcoleptic dogs that had a genetic mutation which disrupted to processing of hypocretin.
Nishino et al (2000) applied the findings from narcoleptic dogs and confirmed them in humans, for instance it was confirmed that human narcoleptics had lower level of hypocretin than normal in their cerebrospinal fluid.
On the other hand, this research highlights a correlation between hypocretin and narcolepsy but does not establish a cause and effect between the two variables, for instance low hypocretin could be a consequence of narcolepsy.
If narcolepsy was truly a case of a faulty gene, this would suggest a genetic liability passed on to offspring. However, refuting evidence by Mignot suggests that it is not genetically inherited because in a twin study of MZ twins who share all their genes genes, there was a low concordance rate of 2.3% when 100% would be expected.
It is more likely that the lower levels of hypocretin are due to brain injury, infection, diet, stress or the result of an autoimmune attack, thus making the studies into hypocretin low in internal validity.
On the other hand, researchers have found that narcolepsy might be linked to a malfunction of the neural mechanisms controlling REM sleep; this can thereby explain some of the symptoms of narcolepsy such as cataplexy, which is a loss of