We achieved all three objectives. We (1) enabled early identification of insomniacs at risk of depression. We (2) found clues to mechanisms underlying the increased risk by quantification of how insomniacs at risk differ from those that do not develop depression with respect to psychological traits, health history, life events, behavioural habits, environmental exposure, brain structure and brain function (PNAS 2016;113:2538; Lancet Psychiatry 2019;6:151; Brain 2019;142:1783; Sleep 2019;42:zsy268; Curr Biol 2019;29:2351; Transl Psychiatry 2020;10:425; Sleep 2020;zsaa031). We (3) demonstrated effectiveness of risk interventions (Psychother Psychosom 2021).
In more detail:
1. We established the profile of an individual’s psychological traits, health history, life events and brain structures involved in the risk of transitioning from insomnia to depression (Lancet Psychiatry 2019;6:151; Transl Psychiatry 2020;10:425; Sleep 2020;zsaa031). We identified brain functional correlates of maladaptive sleep (PNAS 2016;113:2538; Brain 2019;142:1783; Sleep 2019;42:zsy268; Curr Biol 2019;29:2351).
2. We developed the novel tool of network outcome analysis to demonstrate that the causal chain to the development of depression involves possibly modifiable behavioural and environmental factors that cause or maintain insomnia (Sleep 2020;43:zsz288).
3. We developed the novel tool of network intervention analysis to demonstrate that the causal chain to the development of depression could be acted upon by altering an individual’s modifiable behavioural and environmental factors that cause or maintain insomnia (Psychother Psychosom 2019;88:52). We demonstrated that acting on mentioned profile of an elderly individual’s modifiable behavioural and environmental factors interacting with this make-up to protect from transitioning from insomnia to depression.
4. We obtained the novel insight that insomnia mainly involves limbic circuits rather than sleep-regulating circuits of the brain (Nat Genet 2017;49:1584; Nat Genet 2019;51:394; Neurobiol Learn Mem 2019;160:144; Sleep 2020;zsaa031; Nat Genet 2022;in press). Acting on these limbic circuits could indeed be better targets for the development of novel preventive and therapeutic interventions (Physiol Rev 2021;101:995; PNAS 2016;113:2538; Brain 2019;142:1783; Sleep 2019;42:zsy268; Curr Biol 2019;29:2351).
5. For application in studies on novel interventions targeting specific factors discovered, we delivered diagnostic screening tools for profiling risk, ranging from a questionnaire for application in population-based screening (Lancet Psychiatry 2019;6:151; Sleep 2020;43:zsz288), to comprehensive genotyping (Nat Genet 2017;49:1584; Nat Genet 2019;51:394; Nat Genet 2022;in press) and phenotyping of brain structure (Transl Psychiatry 2020;10:425; Sleep 2020;zsaa031) and brain function (PNAS 2016;113:2538; Brain 2019;142:1783; Sleep 2019;42:zsy268; Curr Biol 2019;29:2351).
6. In a randomized controlled trial, we compared internet-based cognitive behavioural therapy for insomnia (CBT-I), chronotherapy (CT), and their combination to reveal the optimally effective and most cost-effective intervention to date to prevent depression in insomniacs at risk of developing it (Psychother Psychosom 2021).
7. We communicated this finding as best practice recommendation for implementation of the evidence-based most effective presently available intervention to prevent conversion of insomnia to depression (Psychother Psychosom 2021).
