A cross-sectional study presents evidence that sleeping supine could be a modifiable risk factor for diseases such as Alzheimer’s, Parkinson’s, and mild cognitive impairment.

Interview by Alyx Arnett

Imagine if a secret to safeguarding brain health lay in the simple act of changing your sleeping position. This possibility is at the core of research that delves into the connection between the way we sleep and the risk of neurodegenerative diseases.

The study builds on the investigators’ previous work, which suggested sleep position could influence the development of Alzheimer’s, Parkinson’s spectrum disorders, and mild cognitive impairment. 

For this study, researchers analyzed sleep data from people with cognitive impairment compared to subjects without a known cognitive disorder to compare the frequency of the supine sleep position.

The new results provide further evidence for a “relatively strong” association between supine sleep and neurodegeneration in Alzheimer’s, Parkinson’s spectrum disorders, and mild cognitive impairment patients.

Study authors Daniel J. Levendowski, MBA, and Erik K. St. Louis, MD, discuss the study with Sleep Review via email. 

[Editor’s Note: Read the study, “Head position during sleep: potential implications for patients with neurodegenerative disorders,” in Sleep Advances.]

How did earlier studies influence your approach? 

Levendowski: Our original study, published in 2019, found supine sleep time was the most predictive variable in distinguishing controls with normal cognition from a relatively small cohort of patients with a neurodegenerative disorder, which included over one-half diagnosed with mild cognitive impairment. If our hypothesis was correct, ie, supine sleep was associated with neurodegeneration, then the patterns should be consistent across neurodegenerative disorder sub-groups.    

What were your main findings? 

Levendowski: The proportion of patients who slept supine over two hours per night was significantly greater in the Alzheimer’s dementia (n=29), Parkinson’s spectrum disorder (n=35), and mild cognitive impairment (n=41) cohorts when compared to those with normal cognition (n=170). These findings remained consistent as we expanded the number of patients in each neurodegenerative disorder cohort. 

What was the most surprising finding? 

Levendowski: The night-to-night variability in supine sleep time was so low that we observed substantial agreement in both supine sleep time and abnormal supine sleep time. 

How do you interpret the higher incidence of supine sleep in patients with Parkinson’s disease, Alzheimer’s disease, and mild cognitive impairment compared to the control group? 

Levendowski: Lee et al’s original observation, ie, sleeping rats experienced less efficient glymphatic clearance in the supine position, may apply to humans. 

What is the potential mechanism of action?  

St. Louis: Simka et al suggested that the partial collapse of the internal jugular that occurs in the lateral positions but not the supine position decreases flow resistance in the extracranial veins, thereby optimizing cerebral venous outflow and glymphatic clearance of potentially neurotoxic metabolites and proteins from the brain during sleep.   

What are the clinical implications?  

St. Louis: The potential association of the supine sleep position with clinical, imaging, and cerebrospinal fluid neurodegenerative markers in cohorts of neurodegenerative disorder patients should be further explored in additional confirmatory large-scale cross-sectional studies and, ideally, ultimately in future prospective longitudinal cohort studies of older community adults.  

A recent additional provocative report by Ligouri et al has also found that supine sleep in Parkinson’s disease patients was associated with both disease duration and motor impairment. An implication of these formative works is that potential future interventions might be developed for limiting the frequency and duration of supine positional sleep as a preventative therapy for prodromal neurodegenerative disorders such as isolated REM sleep behavior disorder or subjective mild cognitive impairment with biomarker evidence for neurodegenerative disorders. 

What are the next steps in this line of research?  

St. Louis: Future studies could include neurodegenerative disorders, OSA, and control groups undergoing an intervention involving sleep positional avoidance feedback training to restrict sleep duration in the supine position, with outcome measures of neurodegenerative disorder biofluids and imaging biomarkers for disease conversion, severity, and progression. 

Are there any preliminary considerations you might suggest for individuals with neurodegenerative disorders or those at risk? 

St. Louis: Since it is a relatively easy intervention to adopt and without known risks, limiting sleep duration in the supine position would seem to be sensible advice for now.

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