Ethan Green
Research Mentor(s): Philip Cheng
Mentor Department: Henry Ford Health System
Authors: Ethan Green, Philip Cheng
Session: Session 2 (10:00am – 10:50am)
Presentation Type: Poster 26
Abstract
Even with current light therapy techniques, gaps in the causal mechanisms of shift work disorder (SWD) continue to perpetuate a prevalent medical disorder that poses a risk to public health and safety. Often night shift workers will undergo light therapy to have their circadian rhythms shifted. This mitigates drowsiness during their shift by changing when the body begins producing melatonin. However, individuals will sometimes experience persistent SWD leading to further research. Subsequently, researchers found that stress may play a role in this phenomenon. This relationship was named sleep reactivity and was separated into two groups corresponding to how easily disturbed an individual’s sleep is: high reactivity, easy to disturb, and low reactivity, hard to disturb. This study aims to further study this relationship by examining if sleep reactivity is a causal mechanism and predictor of insomnia and sleepiness in SWD independent of circadian misalignment. To do so, 150 participants will be recruited with 120 participants having their circadian misalignment experimentally reduced, and the rest undergoing a control light condition so that we can control for light’s effect on a participant’s sleep quality. From there, approximately 74 of the group of 120 participants will continue to the next part of the study and subsequently be re-randomized to ensure that symptoms can be attributed to sleep reactivity. Participants will then again be split into two therapy groups. One will receive cognitive behavioral therapy (CBT) and the other sleep education emails. Previous research has shown that sleep reactivity can be probed with CBT, and we predict that participants with high sleep reactivity who underwent CBT will experience reduced symptoms. While the other participants will remain largely symptomatic. Thereby supporting our initial hypothesis, and by doing so, allowing for a better treatment of SWD by uncovering another causal mechanism of the disorder.
