Cognitive behavioral therapy for insomnia treatment attrition in patients with weekly nightmares.

STUDY OBJECTIVES: This study's objective was to evaluate the effect of nightmares (NMs) on attrition and symptom change following cognitive behavioral therapy for insomnia (CBT-I) treatment using data from a successful CBT-I randomized controlled trial delivered to participants with recent interpersonal violence exposure. METHODS: The study randomized 110 participants (107 women; mean age: 35.5 years) to CBT-I or to an attention-control group. Participants were assessed at 3 time periods: baseline, post-CBT-I (or attention control), and at time 3 (T3) post-cognitive processing therapy received by all participants. NM reports were extracted from the Fear of Sleep Inventory. Participants with weekly NMs were compared with those with fewer than weekly NMs on outcomes including attrition, insomnia, posttraumatic stress disorder, and depression. Change in NM frequency was examined. RESULTS: Participants with weekly NMs (55%) were significantly more likely to be lost to follow-up post-CBT-I (37%) compared with participants with infrequent NMs (15.6%) and were less likely to complete T3 (43%) than patients with less frequent NMs (62.5%). NMs were unrelated to differential treatment response in insomnia, depression, or posttraumatic stress disorder. Treatment with CBT-I was not associated with reduced NM frequency; however, change in sleep-onset latency from post-CBT-I to T3 predicted fewer NMs at T3. CONCLUSIONS: Weekly NMs were associated with attrition but not a reduced change in insomnia symptoms following CBT-I. NM symptoms did not change as a function of CBT-I, but change in sleep-onset latency predicted lower NM frequency. CBT-I trials should screen for NMs and consider augmenting CBT-I to specifically address NMs. CITATION: Hamilton NA, Russell JA, Youngren WA, et al. Cognitive behavioral therapy for insomnia treatment attrition in patients with weekly nightmares. J Clin Sleep Med. 2023;19(11):1913-1921.

Sleep Fragmentation and Estradiol Suppression Decrease Fat Oxidation in Premenopausal Women.

CONTEXT: Body fat gain associated with menopause has been attributed to estradiol (E2) withdrawal. Hypoestrogenism is unlikely to be the only contributing factor, however. OBJECTIVE: Given the links between sleep and metabolic health, we examined the effects of an experimental menopausal model of sleep fragmentation on energy metabolism. METHODS: Twenty premenopausal women (age 21-45 years) underwent a 5-night inpatient study during the mid-to-late follicular phase (estrogenized; n = 20) and the same protocol was repeated in a subset of the participants (n = 9) following leuprolide-induced E2 suppression (hypo-estrogenized). During each 5-night study, there were 2 nights of unfragmented sleep followed by 3 nights of fragmented sleep. Indirect calorimetry was used to assess fasted resting energy expenditure (REE) and substrate oxidation. RESULTS: Sleep fragmentation in the estrogenized state increased the respiratory exchange ratio (RER) and carbohydrate oxidation while decreasing fat oxidation (all P < 0.01). Similarly, in the hypo-estrogenized state without sleep fragmentation, RER and carbohydrate oxidation increased and fat oxidation decreased (all P < 0.01); addition of sleep fragmentation to the hypo-estrogenized state did not produce further effects beyond that observed for either intervention alone (P < 0.05). There were no effects of either sleep fragmentation or E2 state on REE. CONCLUSION: Sleep fragmentation and hypoestrogenism each independently alter fasting substrate oxidation in a manner that may contribute to body fat gain. These findings are important for understanding mechanisms underlying propensity to body fat gain in women across the menopause transition.