Jonathan Cedernaes

Mechanisms For how Disrupted Sleep and Disrupted Circadian Rhythms Increase Disease Risk in Humans

In my research group, we focus on uncovering novel mechanisms and biomarkers for how impaired sleep and disruption of 24-hour circadian rhythms increase the risk of cardiometabolic diseases and brain disorders in humans.

Chronic sleep disruption and circadian disruption are very common today: approximately 30-40% of the adult population reports getting ≤6 hours of sleep per night on a regular basis—significantly shorter than the recommended duration of 7-9 hours. Additionally, an even larger proportion (up to 50%) report poor sleep quality. Furthermore, up to 20% of the adult working population engages in some form of shift work, a work pattern that both disrupts sleep and our biological rhythms, which follow an approximately 24-hour cycle (i.e., circadian rhythms). Notably, chronic sleep loss and shift work—whether prior or ongoing—have been associated with an increased risk of common public health conditions, including type 2 diabetes, obesity, Alzheimer’s disease, and various forms of cardiovascular disease. However, the underlying mechanisms remain relatively unknown, particularly at the molecular and metabolic tissue levels.

Using advanced clinical interventions, in vitro and in vivo models, our group focuses on delineating novel molecular mechanisms underlying disrupted sleep and circadian misalignment. For instance, we have found that circadian disruptions in skeletal muscle and adipose tissue—two tissues crucial for normal blood sugar regulation—appear to play a significant role in how shift work negatively impacts metabolism in humans. Our findings also suggest that epigenetic changes may be involved—changes that regulate gene expression over longer time periods.

In our research, we also aim to determine how other lifestyle factors, such as diet and physical activity, interact with the effects of sleep loss and circadian disruption. Through intervention studies and complementary in vivo models, we employ both broad and targeted approaches to identify novel molecular mechanisms by which disturbed sleep and disrupted circadian rhythms impact metabolic health. At the same time, we hope to identify biomarkers to identify individuals at increased risk of adverse cardiometabolic effects from chronic sleep deprivation and prolonged shift work.

Impaired sleep and shift work have also been robustly associated with an increased risk of neurodegenerative diseases, including dementia and Alzheimer’s disease. Part of our ongoing work focuses on identifying novel molecular mechanisms that may causally mediate this relationship, and how such mechanisms are impacted by interactions in lifestyle factors. This involves studying blood markers and their communication with metabolic tissues.

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