Editing Insomnia (section)

== Mechanism ==

Two main models exist regarding the mechanism of insomnia: cognitive and physiological. The cognitive model suggests that rumination and hyperarousal contribute to preventing a person from falling asleep and might lead to an episode of insomnia.

The physiological model is based upon three major findings in people with insomnia; firstly, increased urinary [[cortisol]] and [[catecholamines]] have been found suggesting increased activity of the HPA axis and arousal; second, increased global cerebral glucose utilization during wakefulness and NREM sleep in people with insomnia; and lastly, increased full body metabolism and heart rate in those with insomnia. All these findings taken together suggest a deregulation of the arousal system, cognitive system, and [[HPA axis]], all contributing to insomnia.<ref name="Th2007"/><ref>{{cite journal | vauthors = Bonnet MH | title = Evidence for the pathophysiology of insomnia | journal = Sleep | volume = 32 | issue = 4 | pages = 441–42 | date = April 2009 | pmid = 19413138 | pmc = 2663857 | doi = 10.1093/sleep/32.4.441 }}</ref> However, it is unknown if the hyperarousal is a result of, or cause of insomnia. Altered levels of the inhibitory [[neurotransmitter]] [[GABA]] have been found, but the results have been inconsistent, and the implications of altered levels of such a ubiquitous neurotransmitter are unknown. Studies on whether insomnia is driven by circadian control over sleep or a wake-dependent process have shown inconsistent results, but some literature suggests a deregulation of the circadian rhythm based on core temperature.<ref>{{cite journal | vauthors = Levenson JC, Kay DB, Buysse DJ | title = The pathophysiology of insomnia | journal = Chest | volume = 147 | issue = 4 | pages = 1179–92 | date = April 2015 | pmid = 25846534 | pmc = 4388122 | doi = 10.1378/chest.14-1617 }}</ref> Increased beta activity and decreased delta wave activity has been observed on [[electroencephalogram]]s; however, the implication of this is unknown.<ref>{{cite journal | vauthors = Mai E, Buysse DJ | title = Insomnia: Prevalence, Impact, Pathogenesis, Differential Diagnosis, and Evaluation | journal = Sleep Medicine Clinics | volume = 3 | issue = 2 | pages = 167–74 | date = 1 January 2008 | pmid = 19122760 | pmc = 2504337 | doi = 10.1016/j.jsmc.2008.02.001 }}</ref>

Around half of post-menopausal women experience sleep disturbances, and generally, sleep disturbance is about twice as common in women as men; this appears to be due in part, but not completely, to changes in hormone levels, especially in post-menopause.<ref name=Santoro2015rev/><ref>{{cite journal | vauthors = Shaver JL, Woods NF | s2cid = 23937236 | title = Sleep and menopause: a narrative review | journal = Menopause | volume = 22 | issue = 8 | pages = 899–915 | date = August 2015 | pmid = 26154276 | doi = 10.1097/GME.0000000000000499 }}</ref>

Changes in [[sex hormone]]s in both men and women as they age may account in part for an increased prevalence of [[sleep disorder]]s in older people.<ref>{{cite journal | vauthors = Lord C, Sekerovic Z, Carrier J | title = Sleep regulation and sex hormones exposure in men and women across adulthood | journal = Pathologie-Biologie | volume = 62 | issue = 5 | pages = 302–10 | date = October 2014 | pmid = 25218407 | doi = 10.1016/j.patbio.2014.07.005 }}</ref>