A recent study published in the Nature and Science of Sleep examined the relationship between sleep behaviors and primary open-angle glaucoma (POAG).
Give me some background first.
With POAG being the most common form of glaucoma, extensive research has been conducted investigating various causes and risk factors.
Sleep-related behavioral phenotypes and POAG have displayed bidirectional relationships, and thus, evidence for a causal relationship has been growing.
Go on..
However, some studies have also reported no associations between the two, and potential confounding variables have further room for exploration.
As a result, researchers set out to gain a better understanding between sleep-related phenotypes and POAG.
Now, talk about the study.
Data for this analysis was taken from publicly available genome-wide association studies (GWAS) at the summary level. This study then utilized a two-sample Mendelian randomization (MR) method.
More on this GWAS data.
The GWAS data included eight sleep-related phenotypes from a “large genetic consortia” included in PubMed in IEU databases. These eight sleep traits included:
- Self-reported chronotype (morning/evening person)
- Ease of getting up in the morning
- Sleep duration
- Napping during the day
- Insomnia
- Daytime dozing/narcolepsy
- Snoring
- Obstructive sleep apnea (OSA)
Potential for confounding variables was taken into account through the conventional linear multivariable MR (MVMR) approach to isolate the effects of sleep traits on POAG.
Findings?
The results of the study demonstrated that the genetic disposition for ease in getting up in the morning and sleep duration both could cause POAG susceptibility.
In terms of sleep duration, the MR estimate in this study found a 1.66-fold higher risk of POAG for those with worse sleep compared to normal levels.
These findings were consistent after testing for confounding variables; no reverse causality was found.
Expert opinion?
Within the discussion, the authors suggested that this association might be due to underlying mechanisms between sleep-related behaviors and POAG, such as systemic inflammation-related processes.
They also mention vascular factors, such as recurrent hypoxia, and how OSA might predispose patients to optic nerve dysregulation.
Go on…
They follow up by mentioning that furthermore, chronic insomnia may result in elevated IOP through dysregulation of cortisol hormone. Ultimately, they maintain that the complex interactions within sleep behaviors and POAG need to be further studied.
Anything else?
The authors’ discussion referenced various studies on sleep and POAG, between which they noted contradictions.
They suggested that this could be attributed to both the control of potential confounders and reverse caution.
Limitations?
This study consisted of data from European individuals and thus might not be generalizable to broader populations. Additionally, much of the data was self-reported, opening the door to potential biases.
The authors also spoke to other potential confounders such as stress and depression on sleep duration; they also mentioned the need for future observational studies.
Take home.
The authors spoke to the study’s demonstration of the connection between suboptimal sleep patterns and increased risk of POAG, specifically in sleep duration and ease of getting up in the morning.
They concluded: “To better understand and manage both phenotypes in our clinical implications, potential ophthalmologic screening and intervention among individuals with chronic sleep problems should be made to help prevent POAG."