Impact of CBTi in COMISA: Could it mean a “masking effect” of the circadian time machinery on psychosocial stress factors?

Cognitive-behavioral approaches, including sleep hygienic measures directed to the correction of inadequate habits and erratic sleep patterns, are effective therapeutic options for patients with insomnia and have been increasingly recognized as a standard of care for this common sleep disorder. Yet some studies have argued that cognitive-behavioral approaches could be more challenging in patients who are depressive, anxious, or stressed, with lower rates of success. In a recently published article on the impact of cognitive-behavioral therapy for insomnia, Sweetman and colleagues¹ suggested that these psychosocial stressors may actually not be an issue in patients with comorbid insomnia and sleep apnea because in their study CBTi succeeded and was not impacted by the above-mentioned conditions.

Circadian misalignment, a mismatch between the social and internal time, can have a major impact on the sleep-wake cycle with consequent complaints of insomnia, excessive daytime sleepiness, and fatigue. Insomnia, in turn, can also lead to circadian clock dysregulation.² Accordingly, it is known that daily variations in sleep patterns are often associated with physical and mental impairment. Even the intraindividual variability of sleep duration, bedtime, and wake-up time has been also suggested to have a link with poorer cognitive function and to worsen the outcomes of affective disorders and stress.³ A number of studies have also showed that sleep-disordered breathing may interact with the synchronization between peripheral oscillators and the central clock within the circadian timing system. This model of disturbed temporal organization impacts, eg, the acquired nondipping pattern of arterial pressure in patients with obstructive sleep apnea or the reversal in the intrinsic circadian rhythm of intraocular pressure, is also frequent among these patients.⁴ An interactive relationship between the circadian timing system and sleep-related breathing control is further highlighted by the severity of obstructive sleep apnea, with a lower and prolonged apnea-hypopnea index in patients with a morning circadian phase, contrasting with a shorter and higher apnea-hypopnea index in patients with a circadian phase corresponding to late afternoon and evening.⁵

All of this interactive role-play between clocks and the pathophysiological aspects of insomnia, sleep-disordered breathing, and psychosocial stressors is potentially exacerbated in patients with comorbid insomnia and sleep apnea, leading to a wider risk spectrum associated with either cardiometabolic health⁶ or cognitive and emotional dysfunction.¹

We therefore hypothesize a more aggressive impact of cognitive-behavioral therapy for insomnia–related strategies in patients with comorbid insomnia and sleep apnea when compared with patients with insomnia. This impact may be associated with directed goals toward circadian misalignment factors of this multicomponent nonpharmacological therapy, even in the presence of comorbid conditions such as depression, anxiety, and stress. Could it actually mean that there is a “masking effect” of the circadian time machinery on such psychosocial stress factors?

DISCLOSURE STATEMENT

Both the authors have seen and approved the submitted manuscript. Both authors report no conflicts of interest.