Circadian depression: A mood disorder phenotype. (July 2021)

• Record Type: Journal Article
• Authors: Carpenter, Joanne S.; Crouse, Jacob J.; Scott, Elizabeth M.; Naismith, Sharon L.; Wilson, Chloe; Scott, Jan; Merikangas, Kathleen R.; Hickie, Ian B.
• Is Part Of: Neuroscience and biobehavioral reviews. Volume 126(2021)
• Page Start: 79
• Page End: 101
• Publication Date: 2021-07
• Subjects: Circadian rhythms -- Sleep-wake cycles -- Mood disorders -- Depression -- Bipolar disorder; Psychophysiology -- Periodicals; Human behavior -- Periodicals; Animal behavior -- Periodicals; Neurology -- Periodicals; Behavior -- Periodicals; Ethology -- Periodicals; Neurology -- Periodicals; Psychophysiologie -- Périodiques; Comportement humain -- Périodiques; Animaux -- Mœurs et comportement -- Périodiques; Neurologie -- Périodiques; Animal behavior; Human behavior; Neurology; Psychophysiology; Periodicals; Electronic journals; 573.8
• DOI: 10.1016/j.neubiorev.2021.02.045
• Languages: English
• ISSNs: 0149-7634

Abstract

Highlights: Clinicopathological evidence is outlined for a clinical phenotype: 'circadian depression.' Phenotype is associated with circadian, cardiometabolic, and inflammatory markers. Identification and validation of this phenotype may guide circadian-specific interventions. Abstract: Major mood syndromes are among the most common and disabling mental disorders. However, a lack of clear delineation of their underlying pathophysiological mechanisms is a major barrier to prevention and optimised treatments. Dysfunction of the 24-h circadian system is a candidate mechanism that has genetic, behavioural, and neurobiological links to mood syndromes. Here, we outline evidence for a new clinical phenotype, which we have called 'circadian depression'. We propose that key clinical characteristics of circadian depression include disrupted 24-h sleep-wake cycles, reduced motor activity, low subjective energy, and weight gain. The illness course includes early age-of-onset, phenomena suggestive of bipolarity (defined by bidirectional associations between objective motor and subjective energy/mood states), poor response to conventional antidepressant medications, and concurrent cardiometabolic and inflammatory disturbances. Identifying this phenotype could be clinically valuable, as circadian-targeted strategies show promise for reducing depressive symptoms and stabilising illness course. Further investigation of underlying circadian disturbances in mood syndromes is needed to evaluate the clinical utility of this phenotype and guide the optimal use of circadian-targeted interventions.