A review recently published in PLOS Mental Health describes the mechanisms and bidirectional interactions between sleep and psychiatric disorders. As discussed here, rather than sleep disturbances (including insomnia and hypersomnia) being strictly a consequence of mental illness, they are now recognized to be “active contributors to the onset, course, and relapse of a psychiatric disorder,” in part because of biological pathways shared by both sleep dysregulation and psychopathology.
There are many examples of this bidirectional relationship. For one, chronic insomnia carries a 2-to 3-fold increase in risk for depression, along with a more frequently relapsing course. Indeed, a meta-analysis of 13 studies published in Sleep Medicine Reviews found that insomnia was associated with a 183% higher risk for depression, 223% higher risk for anxiety, and 28% higher risk for psychosis. In the other direction, rumination (common with low mood) and worry/intrusive nighttime thoughts can interfere with sleep quality and duration. Rumination specifically may mediate the effects of emotional dysregulation on sleep disruption and interrupt REM sleep, during which emotional processing and memory consolidation occur. Higher REM density has been considered a biomarker for depression in some, but not all, studies, while difficulties with sleep initiation and continuity are extremely common among people with depression.
People with depression (including remitted depression) have also been shown to have a higher cortisol awakening response than those without, as well as corticotropin-releasing hormone and glucocorticoid excess, suggesting involvement of the HPA axis. Circadian disruption is also common among people with anxiety, mood, and psychotic disorders, as are changes in neurotransmitter function, including serotonin, dopamine, and gamma-aminobutyric acid (GABA) activity. The review in PLOS Mental Health also describes the brain structures most commonly affected by sleep and mental health disorders, including the prefrontal cortex, amygdala, and hippocampus. For example, one small study that utilized functional magnetic resonance imaging found that inducing a sleep debt over a 5-day period increased activity in the left amygdala in response to a facial expression of fear, while decreasing connectivity between the amygdala and the ventral anterior cingulate cortex (vACC), linked to mood deterioration.
Among the other shared mechanisms are an upregulation in inflammatory signals, including C-reactive protein (CRP) and interleukin-6 (IL-6), as well as metabolic dysregulation, marked by reduced insulin sensitivity and impaired glucose tolerance, along with changes in appetite and related hormones (e.g., leptin and ghrelin).
Given this bidirectional nature and shared pathophysiology, it’s important to recognize that effective interventions may have broad benefits. For example, CBT-I (cognitive therapy for insomnia) has been shown to both enhance sleep and reduce symptoms of depression, with the major limitation being lack of availability or awareness (including by practitioners). Similarly, adjunctive bright light therapy has been found to improve both sleep and depressive symptoms among people with bipolar depression, and melatonin is also a promising candidate. Other interventions worth considering are mindfulness-based stress reduction, exercise, and anti-inflammatory therapies.