Sleep and circadian rhythms in cancer patients and relationship with quality of life

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Systemic consequences of sleep disruption. (A) Sleep disruption-induced inflammation establishes a pro-tumor inflammatory environment in peripheral tissues, including the increase in proinflammatory cytokines like IL-6, IL1-b, and IL-17, mediated by the transcription factor NF-kB. (B) Sleep disruption reduces anti-tumor immunity. Alterations in the number of circulating and intra-tumor lymphocytes and myeloid cells contributes to immunosuppression in cancer. Reduced differentiation of cytotoxic cells further prevents cancer elimination. (C) Sleep disruption engages the HPA axis and autonomic nervous system. Glucocorticoids and catecholamines have widespread effects on the immune system and energy balance important for tumor progression. (D) Sleep disruption alters systemic metabolism. Wake-promoting neurons (e.g., hypocretin/orexin) regulate the activity of others that control food intake and metabolic health (e.g., POMC, AgRP, NPY neurons). (E) Sleep disruption promotes the breakdown of the blood brain barrier (BBB). Disrupted sleep results in vascular endothelial cell dysfunction and inflammation, further contributing to BBB impairment. This allows inflammatory molecules in blood to reach the brain, where they alter the function of sleep/wake regulatory systems (Made with BioRender.com).
Review
19 May 2022
Sleep Disruption and Cancer: Chicken or the Egg?
Adrian Berisha
1 more and 
Jeremy C. Borniger

Sleep is a nearly ubiquitous phenomenon across the phylogenetic tree, highlighting its essential role in ensuring fitness across evolutionary time. Consequently, chronic disruption of the duration, timing, or structure of sleep can cause widespread problems in multiple physiological systems, including those that regulate energy balance, immune function, and cognitive capacity, among others. Many, if not all these systems, become altered throughout the course of cancer initiation, growth, metastatic spread, treatment, and recurrence. Recent work has demonstrated how changes in sleep influence the development of chronic diseases, including cancer, in both humans and animal models. A common finding is that for some cancers (e.g., breast), chronic disruption of sleep/wake states prior to disease onset is associated with an increased risk for cancer development. Additionally, sleep disruption after cancer initiation is often associated with worse outcomes. Recently, evidence suggesting that cancer itself can affect neuronal circuits controlling sleep and wakefulness has accumulated. Patients with cancer often report difficulty falling asleep, difficulty staying asleep, and severe fatigue, during and even years after treatment. In addition to the psychological stress associated with cancer, cancer itself may alter sleep homeostasis through changes to host physiology and via currently undefined mechanisms. Moreover, cancer treatments (e.g., chemotherapy, radiation, hormonal, and surgical) may further worsen sleep problems through complex biological processes yet to be fully understood. This results in a “chicken or the egg” phenomenon, where it is unclear whether sleep disruption promotes cancer or cancer reciprocally disrupts sleep. This review will discuss existing evidence for both hypotheses and present a framework through which the interactions between sleep and cancer can be dissociated and causally investigated.

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Frontiers in Sleep

Reviews in Sleep: 2024
Edited by Stephen Sheldon, Dalva Poyares, Ritchie Edward Brown, Radhika Basheer
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