The exact cause of<unk>  is unknown, and it may be caused by several distinct factors. The mechanism involves the loss of orexin-releasing neurons within the lateral hypothalamus (about 70,000 neurons). Some researches indicated that people with type 1<unk> <unk>  with cataplexy) have a lower level of orexin (hypocretin), which is a chemical contributing to the regulation of wakefulness and REM Sleep. It also acts as a neurotransmitter to enable nerve cells to communicate. In up to 10% of cases there is a family history of the disorder. Family history is more common in<unk>  with cataplexy. There is a strong link with certain genetic variants, which may make T-cells susceptible to react to the orexin-releasing neurons (autoimmunity) after being stimulated by infection with H1N1 influenza. In addition to genetic factors, low levels of orexin peptides have been correlated with a past history of infection, diet, contact with toxins such as pesticides, and brain injuries due to head trauma, brain tumors or strokes. Genetics The primary genetic factor that has been strongly implicated in the development of<unk>  involves an area of chromosome 6 known as the human leukocyte antigen (HLA) complex. Specific variations in HLA genes are strongly correlated with the presence of<unk> ; however, these variations are not required for the condition to occur and sometimes occur in individuals without<unk> . These genetic variations in the HLA complex are thought to increase the risk of an auto-immune response to orexin-releasing neurons in the lateral hypothalamus. The allele HLA-DQB1*06:02 of the human gene HLA-DQB1 was reported in more than 90% of people with<unk> , and alleles of other HLA genes such as HLA-DQA1*01:02 have been linked. A 2009 study found a strong association with polymorphisms in the TRAC gene locus (dbSNP IDs rs1154155, rs12587781, and rs1263646). A 2013 review article reported additional but weaker links to the loci of the genes TNFSF4 (rs7553711), Cathepsin H (rs34593439), and P2RY11-DNMT1 (rs2305795). Another gene locus that has been associated with<unk>  is EIF3G (rs3826784). H1N1 Influenza Type 1<unk>  is caused by hypocretin/orexin neuronal loss. T-cells have been demonstrated to be cross-reactive to both a particular piece of the hemagglutinin flu protein of the pandemic 2009 H1N1 and the amidated terminal ends of the secreted hypocretin peptides. Genes associated with<unk>  mark the particular HLA heterodimer (DQ0602) involved in presentation of these antigens and modulate expression of the specific T cell receptor segments (TRAJ24 and TRBV4-2) involved in T cell receptor recognition of these antigens, suggesting causality. A link between GlaxoSmithKline's H1N1 flu vaccine Pandemrix and<unk>  has been found in both children and adults. In 2010, Finland's National Institute of Health and Welfare recommended that Pandemrix vaccinations be suspended pending further investigation into<unk> . In 2018, it was demonstrated that T-cells stimulated by Pandemrix were cross-reactive by molecular mimicry with part of the hypocretin peptide, the loss of which is associated with type I<unk> .
Narcolepsy
Heart failure
Erotolepsy
Major depressive disorder
Nicotine withdrawal
Anemia
Dancing mania
Sleep apnea