Poor sleep at age 40 is linked to accelerated brain aging

Poor sleep at age 40 was associated with accelerated brain aging patterns at age 55, longitudinal data showed.

A dose-response relationship emerged between the number of poor sleep characteristics in early midlife and brain age 15 years later, Clémence Cavaillès, PhD, of the University of California, San Francisco, and coauthors reported in neurology.

Individuals with two or three poor sleep characteristics had a brain age 1.6 years older than those without more than one of the six sleep characteristics assessed (β = 1.61, 95% CI 0.28 -2.93). Those with more than three poor sleep characteristics had a brain age 2.6 years older (β = 2.64, 95% CI 0.59–4.69).

Poor sleep characteristics include short sleep duration, poor sleep quality, difficulty initiating sleep, difficulty maintaining sleep, early morning awakening, and daytime sleepiness.

Sleep disorders have been linked to poor cognitive performance and an increased risk of dementia, including Alzheimer’s disease, Cavaillès noted.

“However, most studies include older adults, which raises concerns given the long neurodegenerative process in conditions such as Alzheimer’s disease, where lesions (beta-amyloid plaques and tau tangles) accumulate years before symptoms appear,” he said. MedPage today.

“Advanced brain aging is associated with cognitive decline and atrophy patterns related to Alzheimer’s,” Cavaillès continued. “Therefore, poor sleep may be an important target for early interventions aimed at preventing neurocognitive decline, even before amyloid and tau accumulation begins.”

Good quality sleep is very important, observed Nicolas Cherbuin, PhD, of the Australian National University in Canberra, who was not involved in the study.

“That’s because one of the functions of sleep is to help remove toxic substances, malformed proteins and damaged cellular debris from the brain,” which becomes increasingly important with age, he said. MedPage today.

Other research has linked poor sleep quality in middle age to brain shrinkage or cognitive problems, Cherbuin noted.

“Midlife is when the accumulation of damage becomes more easily detectable and is also a period of life where risk factors for brain and cognitive aging combine, such as poor mental health, stress, obesity, diabetes, hypertension, hypercholesterolemia and physical inactivity are growing concerns,” he said. “Consequently, good sleep quality in mid-life and beyond becomes even more important for brain health, thinking skills and mental well-being.”

Cavaillès and colleagues used CARDIA, a long-term study of cardiovascular disease risk in young adults, to analyze baseline sleep data in 589 participants.

Sleep characteristics were self-reported. Brain MRIs were obtained 15 years later and used to determine the age of the brain based on atrophy using a machine learning approach.

The mean initial age was 40.4 (±3.4) years. Approximately half (53%) of the participants were female and 39% were black.

About 70% of participants reported no more than one characteristic of poor sleep; 22.4% reported two or three, and 8.3% reported more than three. Compared with participants who had one or none of the poor sleep characteristics, those with two or more were more likely to be black, have hypertension or depressive symptoms, and have less education.

After a mean follow-up of 15 years, the mean brain age was 54.3 years and the mean chronological age was 55.3 years.

A subsample of 566 participants reported sleep information 5 years after baseline. These data showed that persistent poor sleep quality, difficulty initiating and maintaining sleep, early morning awakening, and daytime sleepiness were associated with greater brain age at 15 years of follow-up.

The findings of this study “are critical because they demonstrate that the link between sleep disturbances and brain health extends beyond adulthood, suggesting that poor sleep in early midlife can already contribute to accelerated brain aging,” said Cavaillès.

The study had limitations, the researchers acknowledged. Sleep characteristics were self-reported and may have been misclassified. Brain age may have been influenced by unmeasured neuropathology. As this was an observational study, a causal relationship cannot be assumed.