Objective sleep duration and response to combined pharmacotherapy and cognitive behavioral insomnia therapy among patients with co-morbid depression and insomnia: a report from the TRIAD study
- S-Med
- Jun 26
- 2 min read
The current study was conducted to determine whether short sleep duration, as measured objectively, attenuates the treatment responses of patients with insomnia and co-morbid major depressive disorder. We also attempted to determine whether any of the previously tested cutoffs of < 5 hours, < 6 hours, or < 7 hours to define short sleep separated those patients more and less likely to respond to the interventions provided in this study. Whereas previous studies have shown that defining “short sleepers” as those with fewer than 6 or 7 hours of sleep separates patients who do and do not respond to CBT-I, we did not find that to be the case in our co-morbid sample. Only when we used < 5 hours of TST as a cutoff for defining short sleep did we observe statistically significant different treatment responses of the so defined short and longer sleepers. We did hypothesize that the risk for non-remission in patients with ID and MDD would be greatest among those who have < 5 hours of objective sleep duration. Yet it is notable that when short sleep was defined as < 6 or 7 hours of TST, we did not find any differences in insomnia and depression remission rates between those falling above and below these cutoffs. Thus, our findings did not replicate the findings of prior CBT-I treatment studies Consequently, our results suggest that what constitutes treatment confounding short sleep may differ in patients with ID with and without MDD as a co-morbid condition.
In comparing our results with those of prior studies that examined the CBT-I responses of short sleepers, it is important to note that treatment in the current study included antidepressant medication combined with CBT-I. Prior tests of short sleepers not only excluded those with MDD and other psychiatric comorbidities but also tested CBT-I used in isolation. From the data we obtained it is not clear how our combined CBT-I/antidepressant medication treatment served to lower the TST threshold below which CBT-I’ effectiveness markedly diminished. However, it may be useful to consider the putative significance of short sleep in regard to its pathophysiology among patients affected by it. Vgontzas et al have proposed that objectively short sleep duration among individuals with ID connotes a chronic state of physiological hyper-arousal that results in heightened morbidity outcomes and poor response to CBT-I. Vgontzas et al have supported this contention by showing individuals with short sleep and no significant comorbidities have elevated 24-hour cortisol levels that are suggestive of heightened activation of the hypothalamic-pituitary-adrenal axis.
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