Abstract
Given the role of sleep in the development and treatment of major depressive disorder (MDD), it is becoming increasingly clear that elucidation of the biological mechanisms underlying sleep disturbances in MDD is crucial to improve treatment outcomes. Sleep disturbances are varied and can present as insomnia and/or hypersomnia. Though research has examined the biological underpinnings of insomnia in MDD, little is known about the role of biomarkers in hypersomnia associated with MDD. This paper examines biomarkers associated with changes in hypersomnia and insomnia and as predictors of improvements in sleep quality following exercise augmentation in persons with MDD. Subjects with non-remitted MDD were randomized to augmentation with one of two doses of aerobic exercise: 16 kilocalories per kilogram of body weight per week (KKW) or 4 KKW for 12 weeks. The four sleep-related items on the clinician-rated Inventory of Depressive Symptomatology (sleep onset insomnia, mid-nocturnal insomnia, early morning insomnia and hypersomnia) assessed self-reported sleep quality. Inflammatory cytokines (tumor necrosis factor-alpha, interleukin (IL)-1β, IL-6) and brain-derived neurotrophic factor (BDNF) were assessed in blood samples collected before and following the 12-week intervention. Reduction in hypersomnia was correlated with reductions in BDNF (ρ=0.26, P=0.029) and IL-1β (ρ=0.37, P=0.002). Changes in these biomarkers were not associated with changes in insomnia; however, lower baseline levels of IL-1β were predictive of greater improvements in insomnia (F=3.87, P=0.050). In conclusion, improvement in hypersomnia is related to reductions in inflammatory markers and BDNF in persons with non-remitted MDD. Distinct biological mechanisms may explain reductions in insomnia.
Highlights
Sleep has a significant role in the development treatment of major depressive disorder (MDD)
Increases in brain-derived neurotrophic factor (BDNF) have been associated with increased non-rapid eye movement sleep and slow wave activity during sleep.[9]
The purpose of this paper is to identify biological correlates and predictors of improvements in self-reported hypersomnia and insomnia through a secondary analysis of the Treatment with Exercise Augmentation for Depression (TREAD) trial
Summary
Sleep has a significant role in the development treatment of major depressive disorder (MDD). Distinguishing between atypical and melancholic depression has important clinical relevance as differential treatment responses have been observed in patients with atypical features.[13,14,15] previous research of these biological correlates of sleep disturbances is limited in that it does not distinguish between insomnia and hypersomnia. Exercise has proven efficacious as a monotherapy as well as augmentation treatment for MDD.[16,17,18,19,20] BDNF and inflammatory cytokines have been implicated in the antidepressant effects of exercise.[21,22,23] exercise has been shown to reduce insomnia independent of improvement in depressive symptoms.[24] The purpose of this paper is to identify biological correlates and predictors of improvements in self-reported hypersomnia and insomnia through a secondary analysis of the Treatment with Exercise Augmentation for Depression (TREAD) trial. We hypothesize the following: (1) increases in BDNF but decreases in proinflammatory cytokines will be associated with improvements in self-reported insomnia and hypersomnia and (2) baseline levels of these biomarkers will predict improvements in self-reported insomnia and hypersomnia
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