Abstract Introduction Insomnia with short sleep duration (ISSD) represents a distinct phenotype linked to elevated cardiometabolic risk, unlike insomnia with normal sleep duration (INSD). Cognitive-behavioral therapy for insomnia (CBT-I) is the first-line, guideline-recommended treatment for the disorder, yielding reductions in symptom severity. Recent studies suggest that the ISSD and INSD phenotypes may respond differently to CBT-I, highlighting a need for further inquiry in real-world clinical samples. Methods Participants included a pool of 71 adults (47.99±15.8 years old, 66.2% female, 19.2% minority) who received CBT-I at the Behavioral Sleep Medicine (BSM) program of Penn State Health Sleep Research 45.1%) and INSD (PSG total sleep time6h; 54.9%). Participants completed the Insomnia Severity Index (ISI) at their consultation visit and each subsequent treatment visit. Linear mixed-effects models examined changes in ISI across insomnia phenotypes and CBT-I sessions, adjusting for sex, age, race/ethnicity, timing, psychiatric and medical comorbidities. Results A significant main effect of CBT-I on ISI scores indicated significant improvement across 8 CBT-I sessions (F(7,236)=17.66, p.001). A significant interaction between insomnia phenotype (ISSD vs. INSD) and CBT-I sessions showed that ISSD patients had higher ISI scores than INSD patients across sessions (F(7,236)=3.29, p=.002). INSD patients exhibited a continuous decline in ISI scores, while ISSD patients showed blunted symptom improvement. By session 6 of CBT-I, INSD patients showed ISI scores in the full remission range (6.8±1.5), whereas ISSD patients continued to show ISI scores in the subthreshold range (10.9±1.4). Conclusion In a BSM clinical sample, CBT-I reduced insomnia severity in both ISSD and INSD phenotypes, yet INSD patients exhibited greater and more sustained improvement with treatment. In contrast, ISSD patients showed early improvement followed by a plateau and persistently elevated end-of-treatment ISI scores, suggesting a blunted overall treatment response. These pilot findings provide further evidence that distinct insomnia phenotypes exhibit differential treatment responses requiring phenotype-specific therapeutic approaches. Support (if any)
Lenker et al. (Fri,) studied this question.
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