Poor Sleep in Midlife Is Linked to Faster Brain Atrophy

For adults in midlife, difficulty getting to sleep and waking up too early may accelerate brain atrophy that is associated with dementia.

The brain naturally begins to atrophy beginning in one’s 30s and 40s. But this can become much more pronounced with dementia and disorders like traumatic brain injury, stroke and, in some cases, multiple sclerosis.

Even if the cause of dementia is unrelated to sleep, it’s possible that poor sleep may advance or exacerbate cognitive symptoms.”

To estimate the effects of sleep quality on the brain, the researchers surveyed approximately 600 adults on how well they slept. The participants were asked the same questions five years later and underwent brain scans 10 years after this.

The researchers used machine learning, leveraging data from the scans, to estimate the brain age of each participant based on the actual degree of brain shrinkage. They found that even after adjusting for age, sex, education, health and lifestyle factors, the brains of those participants who slept poorly were more atrophied than those who slept well.

Compared to the 70% of the sample who reported having little trouble sleeping, those with moderate difficulty (22%) had brains that were 1.6 years older, while those with the most difficulty (8%) had brains that were 2.6 years older.

The study publishes in Neurology on Oct. 23.

“While we can’t say that poor sleep causes dementia, earlier research has established an association,” said first author Clémence Cavaillès, PhD, of the UCSF Department of Psychiatry and Behavioral Sciences. “Even if the cause of dementia is unrelated to sleep, it’s possible that poor sleep may advance or exacerbate cognitive symptoms.”

The participants, who were 40 years old on average when they enrolled, were part of the Coronary Artery Risk Development in Young Adults (CARDIA) study, which investigates the factors that influence cardiovascular disease, as well as how they may relate to dementia. They were asked about short sleep duration, poor quality of sleep, difficulty getting to sleep, difficulty staying asleep, early morning awakening and daytime sleepiness.

Lack of sleep not a factor … or is it?

Surprisingly, lack of sleep was not one of the characteristics relating to brain aging. “Sleep problems frequently emerge in midlife,” said Cavaillès. “They’re likely due to work stress, family caregiving and menopause,” she said. “Although the study found inadequate sleep duration was not an issue in brain atrophy in this study, we cannot say there is no association,” she said, noting that a previous CARDIA study showed that shorter sleep was associated with worse white matter integrity, indicating lower cognitive functioning.

Future research should investigate the life-course effect of sleep on brain health in young populations.”

Poor sleep that persisted over five years, especially when it related to difficulty getting to sleep and early morning awakening, was found to be highly relevant to brain aging.

“The study shows that poor sleep could be a target for early interventions to prevent possible cognitive decline,” said senior author Kristine Yaffe, MD, of the UCSF departments of Psychiatry and Behavioral Sciences, Neurology, and Epidemiology and Biostatistics.

“Public health initiatives could include emphasizing sleep quality over quantity in midlife – and recognizing the long-term impact of poor sleep quality on the brain,” added Yaffe, who is a member of the first team of experts to determine that 30% of dementia risk is preventable. “Future research should investigate the life-course effect of sleep on brain health in young populations.”

Co-Authors: Cristina Dintica, PhD, and Yue Leng, PhD, of UCSF; Mercedes R. Carnethon, PhD, of Northwestern University; and Mohamad Habes, PhD, of the Glenn Biggs Institute for Neurodegenerative Disorders and the University of Texas Health Science Center.

Funding: The CARDIA study is conducted and supported by the National Heart, Lung, and Blood Institute in collaboration with the University of Alabama at Birmingham (75N92023D00002 & 75N92023D00005), Northwestern University (75N92023D00004), University of Minnesota (75N92023D00006) and Kaiser Foundation Research Institute (75N92023D00003). Also supported in part by (NIA) R35AG071916 and (NIA) R01AG063887. The authors report no relevant disclosures.