Body clock breakdown: A new clue to dementia risk

Inside the body, a 24-hour rhythm, known as the circadian rhythm, quietly coordinates when we sleep, wake, eat and recover. This internal timing system helps keep organs and hormones working in sync.

When it becomes disrupted, the effects may extend well beyond poor sleep, with growing evidence suggesting consequences for long-term brain health.

A large 2025 study of more than 2,000 people with an average age of 79 found that those with a strong circadian rhythm had an almost halved risk of developing dementia. Circadian rhythms regulate daily processes including sleep timing, hormone release, heart rate and body temperature.

Over three years of follow-up, dementia developed in 7% of participants with irregular body clocks, measured using heart rate monitors, compared with 10% of those whose rhythms remained more regular. Disrupted circadian rhythms are often associated with poor sleep.

For decades, poor sleep has been suspected to contribute to both dementia and heart disease, which share several underlying risk factors. In the 2025 study, worse heart health and high blood pressure, both commonly linked to sleep disruption, were accounted for in the analysis. Sleep apnoea, however, was not.

Sleep apnoea is a common condition in which breathing repeatedly stops and starts during sleep, reducing oxygen supply to the brain and raising blood pressure. Its relationship with dementia remains debated, largely because sleep apnoea is more common in people who already have established dementia risk factors such as obesity, diabetes, smoking and alcohol misuse.

This overlap makes it difficult to determine whether sleep apnoea itself increases dementia risk or whether it reflects broader metabolic and cardiovascular vulnerability.

This review suggested that addressing physical inactivity linked to fatigue from disrupted sleep may be a promising approach. Increasing activity could reduce obesity, improve sleep quality and support brain cell health, potentially lowering dementia risk through several pathways at once.

Other explanations may also help clarify the link between disrupted circadian rhythms and dementia. One involves the immune system, which is influenced by circadian rhythms as well as sleep and plays a role in both heart disease and neurodegeneration.

Another is the theory that sleep supports the removal of toxic proteins from the brain, including amyloid plaques that characterise Alzheimer's disease, through a waste clearance system that appears to be more active during sleep.

While this clearance hypothesis is widely discussed, evidence remains mixed. Some animal studies, including those in mice, have shown reduced rather than increased toxin clearance during sleep.

Animal findings must be interpreted cautiously, as sleep patterns in mice differ substantially from those in humans, particularly in later life. The Lancet commission update on dementia prevention concluded that sleeping for longer or shorter durations is unlikely to be a true independent risk factor for dementia.

One reason for this conclusion is that evidence from real-world sleep disruption does not clearly point to sleep duration as the main driver of risk. Although shift work is associated with increased dementia risks, studies do not consistently show higher risk in night shift workers compared with day shift workers.

If sleep disruption alone were responsible, night shifts would be expected to carry a greater risk. This suggests that circadian disruption may matter independently of sleep duration.

However, shift work is also associated with unhealthy lifestyle patterns, including poorer diet, smoking, alcohol use and variable physical activity.

(The writer is Professor of Biological Psychology, Loughborough University, UK)