The relationship between nonrestorative sleep and persistent post-acute sequelae of COVID-19: a longitudinal study…, 2026, Hazumi+

[SNT Gatchaman]

The relationship between nonrestorative sleep and persistent post-acute sequelae of COVID-19: a longitudinal study of recovery trajectories

Spoiler: Authors

Hazumi, Megumi; Kataoka, Mayumi; Usuda, Kentaro; Miyake, Michi; Nakashita, Ayako; Kitamura, Makiko; Okazaki, Emi; Yoshiike, Takuya; Matsui, Kentaro; Kuriyama, Kenichi; Nishi, Daisuke; Kuroda, Naoaki

Nonrestorative sleep (NRS) may contribute to the persistence of post-acute sequelae of COVID-19 (PASC), but no longitudinal studies have investigated this relationship. This study examined the association between NRS and PASC persistence over one year.

This was a one-year prospective cohort study conducted using an online survey. We conducted a one-year prospective cohort study through an online survey between September 2022 (Time 1, T1) and September 2023 (Time 2, T2). Eligible patients were adults aged 18 years or older who had experienced COVID-19 infection after February 2022 and were more than one month post-infection with at least one PASC symptom. NRS, difficulty initiating sleep (DIS), difficulty maintaining sleep (DMS), and early morning awaking (EMA) were evaluated at T1. PASC persistence was evaluated at T2. Relative risk ratio calculations with multiple imputations were performed to examine associations between sleep disturbances and PASC.

Among 957 participants with PASC at baseline, 559 (58.4%) completed the follow-up assessment. NRS at T1 was associated with PASC persistence at T2 (Relative Risk = 1.33, 95% confidence interval = 1.08 – 1.64). In contrast, DIS, DMS, and EMA showed no significant associations with PASC persistence. Sensitivity analyses using different NRS thresholds yielded consistent trends.

This study suggests that NRS may partly contribute to PASC persistence through a potentially distinct mechanism from DIS, DMS, and EMA.

Web | DOI | PDF | Sleep and Biological Rhythms | Paywall

 

[SNT Gatchaman]

NRS can influence PASC, because sleep disturbances are prevalent in PASC. A meta-analysis indicated that sleep disturbances, including poor sleep quality, conceptually related to NRS, are more strongly associated with PASC than duration or timing of sleep. Additionally, risk factors for NRS, such as obstructive sleep apnea, have been identified as predictors of PASC. NRS is also associated with symptoms commonly observed in PASC, including fatigue, respiratory disease, neuralgic pain, and migraine.

This study is the first to examine the influences of sleep on longitudinal PASC recovery trajectories. While previous studies demonstrated that pre-infection sleep problems, including obstructive sleep apnea, short sleep duration, night-shift work, and other sleep disturbances, predict PASC development, our findings extend this knowledge by showing that NRS during PASC also predicts its persistence.

This longitudinal study suggests that NRS is associated with PASC persistence over one year, different from insomnia symptoms like DIS, DMS, and EMA. This finding indicates that NRS may influence PASC recovery through mechanisms distinct from those involved in DIS, DMS, and EMA. These results highlight the importance of comprehensive sleep assessment in patients with PASC. Future research should explore the biological mechanism underlying this relationship and evaluate whether interventions targeting NRS can improve PASC outcomes.

I don't think it's occurred to them that non-restorative sleep is the result of PASC. No mention or reference of ME/CFS.

I'd love to know what the interventions targeting non-restorative sleep might be. "You're sleeping it wrong" I guess.

 

[Sean]

I don't think it's occurred to them that non-restorative sleep is the result of PASC. No mention or reference of ME/CFS.

I'd love to know what the interventions targeting non-restorative sleep might be. "You're sleeping it wrong" I guess.

It's nuts isn't it. The 'reasoning', as with so many claims in this field, seems to basically boil down to the symptom and/or the resultant behavioural changes are the cause the symptom, that the phenomenon is its own cause.

Nobody is suggesting that non-restorative sleep is helping nor that it does not bring secondary problems of its own.

The question is why is it happening and what, if anything, can be done about it in the absence of an explanation and treatment for its original cause.

Their argument is the same as saying the cause of Fatal Familial Insomnia is lack of sleep and the solution is better sleep hygiene. No, the cause is a long dormant gene switching on, and the solution is figuring out how to either prevent the gene switching on or suppress its action if it does. Sleep hygiene is completely irrelevant.