Sleep Disturbance, the HPA Axis, and Mental Illness

Our reading on sleep discussed a correlation between disordered sleep and mental illness. Problems with sleep are symptomatic of many different psychiatric conditions but could also be caused by or perpetuated by them as well. The chapter on sleep discussed a patient with Bipolar disorder who every 6-8 weeks cycled between depression and mania with great changes in his sleep during these times. He was encouraged to stay in bed in a dark room for fourteen hours per night, and later ten hours per night. After this intervention his mood and sleep stabilized and he maintained these improvements even a year later (Higgins, 2013). To me this shows that sleep regulation plays a much larger part in psychiatry than it is given credit for.

This successful intervention inspired me to look into current research connecting sleep and mental illness. The article Arousal Regulation in Affective Disorders found that disturbed sleep is a core symptom of depression and that many people with this disorder report excessive daytime sleepiness. This sleepiness is usually not the typical understanding of being tired, as in being more likely to fall asleep, instead it is “tiredness/fatigue in the sense of exhaustion with a tonically high inner tension and physiological arousal…Patients are convinced that they could improve their condition by extended bed rest, yet in many cases this only aggravates the underlying problem”  (Hegerl, 2016). This article also discussed that the mood of these patients was inversely correlated with the amount of sleep they had. While the subjects felt the need to sleep, the more they did, the worse their depressive symptoms became.  I found this extremely interesting as our textbook also mentioned that not only is depression worse in the morning, but sleep deprivation can act as a short term antidepressant (Higgins, 2013).

Conversely, other articles I found described the protective power of adequate sleep. Deep sleep inhibits HPA axis, the activation of which causes stress and disrupts the ability to sleep.  Insomniacs (measured here by <70% of time asleep during sleep testing) have higher cortisol levels than their counterparts who get enough sleep. Long term disturbed sleep leads to increased HPA axis activation, which in turn makes it more difficult to sleep, creating a positive feedback loop (Chrousos, 2016). When someone suffers from chronic stress, it may cause the deregulation of their HPA system, and over time can cause disturbed sleep and depression (Schmitt, 2016).

Stress has the potential to have severe impacts on sleep. For example, Post-Traumatic Stress Disorder (PTSD) is associated with sleep disturbances. The neurological changes observed in people with PTSD are very similar to healthy individuals who have experienced sleep deprivation. Sleep deprivation causes increased amygdala reactivity, weaker connections between the amygdala and the medial prefrontal cortex, and stronger connections between the amygdala and the sleep/wake centers. This suggests that decreased sleep leads to increased fear response and arousal. Patients with PTSD are also likely to have decreased hippocampal volume. This is potentially caused by the sleep disturbances themselves (Kelly, 2016).  The hippocampus is important in both stress and sleep as it regulates HPA axis activity (Jacobsen, 1991). When the hippocampus is compromised, the HPA axis can take over, contributing further to stress and  sleep disturbances.

Brain-Derived Neurotrophic Factor (BDNF) plays a part in brain neuroplasticity and is important in pathology of stress-related mood disorders. Increased stress decreases BDNF levels, leading to increased disorders depression. Decreased sleep increased stress susceptibility. In contrast to chronic stress and long term sleep deprivation, partial sleep deprivation is able to cause a rapid increase in BDNF levels, producing an antidepressant effect that is far more immediate than typical antidepressants (BDNF in sleep).

Sleep is highly important to mammalian functioning and is still surrounded with uncertainties. Sleep plays a major role in our mental health, even in people without mental illness. Looking at the research I was alarmed at how many areas create positive feedback loops where stress decreases sleep and that in turn leads to further stress along with other potential complications. This also shows an area that may be undervalued in the treatment process that could be utilized to significantly help patients.

Chrousos, Vgontzas, A. N., & I. Kritikou. (2016).  HPA Axis and Sleep. De Groot LJ.

Higgins, E. S., George, M. S. (2013). The Neuroscience of Clinical Psychiatry:  The Pathophysiology of Behavior and Mental Illness, 2nd edition.  Philadelphia, PA:  Lippincott Williams & Wilkins

Kelly, M.R., Killgore, W.D.S. & Haynes, P.L. (2016). Understanding Recent Insights in Sleep and Posttraumatic Stress Disorder from a Research Domain Criteria (RDoC) Framework.Curr Sleep Medicine Rep

Jacobson, L., & Sapolsky, R. (1991). The Role of the Hippocampus in Feedback Regulation of the Hypothalamic-Pituitary-Adrenocortical Axis*. Endocrine Reviews, 12(2), 118-134.

Hegerl, Sander, & Hensch. (2016) Chapter 12 – Arousal Regulation in Affective Disorders, Systems Neuroscience in Depression, Pages 341-370

Schmitt, K., Holsboer-Trachsler, E., & Eckert, A. (2016). BDNF in sleep, insomnia, and sleep deprivation. Annals of medicine, 48(1-2), 42-51.