Abstract
Sleep restriction therapy (SRT), potentially the most active component of cognitive behavioral therapy for insomnia [1], has emerged as a clinically and cost-effective standalone treatment [2–4]. While efficacious, the mechanisms through which SRT improves insomnia are not fully understood. Maurer et al. [5] proposed the “Triple-R” model to explain the therapeutic effects of SRT, suggesting it principally operates by restricting time in bed, regularizing sleep–wake timing, and reconditioning the bedroom–sleep association. While these three “R’s” represent proximal intervention targets, a cascade effect on underpinning and interacting cognitive-behavioral and physiological processes is suggested to address several different features of insomnia disorder. The model formulates a number of testable hypotheses but empirical support comes from a relatively small number of recent studies (e.g. [6–9]), chiefly because most research on SRT focuses on outcome rather than process and mechanism.