The impact of stress on sleep: Pathogenic sleep reactivity as a vulnerability to insomnia and circadian disorders

Abstract

Sleep reactivity is the trait-like degree to which stress exposure disrupts sleep, resulting in difficulty falling and staying asleep. Individuals with highly reactive sleep systems experience drastic deterioration of sleep when stressed, whereas those with low sleep reactivity proceed largely unperturbed during stress. Research shows that genetics, familial history of insomnia, female gender and environmental stress influence how the sleep system responds to stress. Further work has identified neurobiological underpinnings for sleep reactivity involving disrupted cortical networks and dysregulation in the autonomic nervous system and hypothalamic-pituitary-adrenal axis. Sleep reactivity is most pathologically and clinically pertinent when in excess, such that high sleep reactivity predicts risk for future insomnia disorder, with early evidence suggesting high sleep reactivity corresponds to severe insomnia phenotypes (sleep onset insomnia and short sleep insomnia). High sleep reactivity is also linked to risk of shift-work disorder, depression and anxiety. Importantly, stress-related worry and rumination may exploit sensitive sleep systems, thereby augmenting the pathogenicity of sleep reactivity. With the development of cost-effective assessment of sleep reactivity, we can now identify individuals at risk of future insomnia, shift-work disorder and mental illness, thus identifying a target population for preventive intervention. Given that insomniacs with high sleep reactivity tend to present with severe insomnia phenotypes, patient sleep reactivity may inform triaging to different levels of treatment. Future research on sleep reactivity is needed to clarify its neurobiology, characterize its long-term prospective associations with insomnia and shift-work disorder phenotypes, and establish its prognostic value for mental illness and other non-sleep disorders.

Keywords: Ford insomnia response to stress test; mental health; preventive treatment.

FIGURE 1

Conceptual diagram depicting moderators of the effect of stress on sleep disturbance. Negative event appraisal, greater stressor chronicity, poor coping, greater substance misuse and negative cognitive-emotional factors increase the risk of and severity of sleep disturbance following a stressor

FIGURE 2

Theorized relation of sleep reactivity to other components of stress reactivity

FIGURE 3

The role of sleep reactivity in the relationship between cognitive intrusion (i.e. rumination) and risk of insomnia disorder. In response to the same degree of cognitive intrusion, persons with greater sleep reactivity are more likely to develop insomnia disorder

FIGURE 4

The role of sleep reactivity in the impact of stress on sleep. Although stress disturbs sleep in persons with both low and high sleep reactivity, those with high sleep reactivity experience relatively greater sleep disturbance. Moreover, whereas persons with low sleep reactivity return to normal sleep following a normal stressor, those with high sleep reactivity are less likely to experience such a reprieve, and are thus more likely to develop insomnia disorder

FIGURE 5

Depiction of the cyclical impact of sleep reactivity in sleep disturbance. Sleep reactivity predisposes individuals to sleep disturbance and subsequent neurocognitive factors following stress, including conditioned arousal and cognitive alterations. These in turn presage the development of insomnia disorder, which increases sleep reactivity, heightening the likelihood of future sleep disturbance. PSG, polysomnography