Radically different
Time spent in daylight could lower the risk of dementia and offer extra benefits for people at particularly high risk, new research suggests. The findings, published in General Psychiatry, could provide a low-cost way to support brain health.
Having less than 0.7 hours of bright daytime light per day was a stronger predictor of dementia than six traditional risk factors. Moderately bright natural light exposure—equivalent to an overcast day outdoors—was linked with a 16% reduction in the risk of dementia.
“Daytime light exposure may serve as a novel indicator of dementia risk,” said researcher Hongliang Feng, PhD, from Guangzhou Medical University in China. Natural cycles of darkness at night followed by bright light during the day are fundamental to entrain circadian rhythms. These regulate physiology, behavior, and cognition, with circadian disruptions common among people with dementia.
Noting that modern lifestyles limit daytime exposure to natural light, the researchers investigated exposure to day- and nighttime light using actigraphy devices that track body movements with built-in light sensors.
The study included 87,577 UK Biobank participants who wore accelerometers on their wrists to measure physical activity and natural light exposure for seven days. Over a median follow-up of 8.1 years, 741 of these people (0.85%) developed dementia.
Higher daytime light, both in terms of average exposure and the duration in bright light, was significantly associated with a lower dementia risk. Daytime light exposure above 1000 lux—a moderately bright light level equal to an overcast day outdoors—was associated with a hazard ratio of 0.84 for dementia. Longer exposure to brighter light of at least 0.70 hours with at least 5000 lux was linked with a further risk reduction, and a hazard ratio of 0.83.
In exploratory analyses, circadian rest-activity rhythms (CRAC) and brain structures mediated up to a third of this association, supporting the idea that improvements in circadian rhythms may have contributed to these results. Dementia protection from light exposure was stronger in people with high levels of nighttime light exposure, those with a “night owl” evening chronotype, or who carried the APOE ε4 allele, with a risk reduction of up to 41%.
Having more than 0.7 hours per day of bright daytime light of at least 5000 lux outperformed the established dementia risk predictors, including alcohol consumption, obesity, air pollution, hearing loss, use of vitamin D supplements, and traumatic brain injury.
However, nighttime light showed no significant association with dementia risk.
The findings point to the importance of higher daytime light exposure in reducing the chances of dementia and offer a simple, cost-free way to reduce this risk.
“Practical implementation pathways could include optimizing indoor lighting at home, community‐based outdoor activity promotion programs, and workplace lighting modifications designed to increase daytime light exposure, such as ensuring adequate illumination and access to natural light,” the researchers suggested.
They added: “Our findings underscore a more pronounced protective association of daytime light exposure in individuals with higher average nighttime light exposure, an evening chronotype, or APOE ε4 carrier status.
“In other words, these findings suggest a targeted approach to mitigate dementia risk by increasing daytime light levels for these populations.”
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Research led by Edith Cowan University in Australia suggests the impact of genetic mutations that impact Alzheimer’s disease risk are influenced by a person’s sleep habits.
As reported in the journal Alzheimer’s & Dementia, the researchers confirmed links with aquaporin-4 gene (AQP4) variants and changes in brain volume, atrophy and cognition linked to Alzheimer’s disease.
The investigators also showed how long people sleep, how long it takes them to fall asleep, how often their sleep is disturbed, and how good or poor their sleep is overall contributed to the effect of these mutations.
“Our study shows that individuals carrying certain AQP4 variants showed faster grey matter loss when they reported shorter sleep,” said study co-author Ayeisha Milligan Armstrong, PhD, a researcher at Edith Cowan University, in a press statement.
“It’s not just which genes you carry—it’s how those genes interact with the world around you. The same variant can look protective or detrimental depending on how someone is sleeping. That’s important, because sleep is one of the few modifiable factors people can actually act on.”
Researchers now think the brain gets rid of amyloid‑beta using a kind of plumbing system that washes waste away along the outside of blood vessels. In this system, fluid moves through the spaces around blood vessels, helped by tiny water channels called aquaporin‑4, encoded by AQP4, which sit on the parts of astrocyte cells that wrap tightly around those vessels.
“Given that AQP4 has been identified as an important mediator of brain amyloid beta clearance, variation within the AQP4 gene has been investigated in relation to neurodegenerative diseases and their associated phenotypes,” write the authors.
“A bi-directional relationship has been observed between suboptimal sleep and increasing brain amyloid beta accumulation…Importantly, a previous study utilizing data from the Australian Imaging, Biomarker and Lifestyle cohort reported that the relationship between sleep and cross-sectional brain amyloid beta burden was moderated by genetic variants in AQP4.”
To investigate this link further, the researchers studied 351 cognitively normal people already showing ongoing build‑up of brain amyloid‑beta on positron emission tomography (PET) imaging. They genotyped the group for 13 mutations in the AQP4 gene and also assessed sleep duration and quality, brain volume, amyloid burden and cognition scores.
Several AQP4 variants interacted with sleep measures to predict gray‑matter atrophy, brain ventricular volume, white‑matter volume, and cognitive decline. For example, people carrying certain variants who also had shorter sleep duration were more likely to have faster grey‑matter loss, and other variants magnified the impact of poorer global sleep quality on ventricular enlargement in the brain.
One variant showed a direct association with better global cognitive performance and two other variants seemed to be linked to less cognitive decline as sleep disturbances increased.
“We’ve known for a while that poor sleep and Alzheimer’s risk are linked,” said first author Tenielle Porter, PhD, also a researcher at Edith Cowan University.
“What this shows is that rather than assuming everyone at risk follows the same pathway, a more targeted and personalized approach to Alzheimer’s prevention may be needed. But we’re not at the point of recommending genetic testing; our findings need replication in larger and more diverse cohorts.”
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