We've updated our Privacy Policy to make it clearer how we use your personal data. We use cookies to provide you with a better experience. You can read our Cookie Policy here.

Advertisement

Cutting Through the Headlines: Are Morning People at a Higher Risk of Alzheimer’s?

Cutting Through the Headlines: Are Morning People at a Higher Risk of Alzheimer’s? content piece image
Listen with
Speechify
0:00
Register for free to listen to this article
Thank you. Listen to this article using the player above.

Want to listen to this article for FREE?

Complete the form below to unlock access to ALL audio articles.

Read time: 3 minutes

A new study has investigated the links between Alzheimer’s disease (AD), major depressive disorder (MDD) and sleep. This study, armed with a huge cohort of over half a million people, has become the latest in a series of studies to find no causal link between sleep and dementia.

Sleep’s relationship with neurodegenerative brain disease is not straightforward. A recent report by a Lancet Commission
identified 12 risk factors for dementia that, if removed, would reduce worldwide dementia incidence by 40%. Whilst air pollution, obesity and smoking all made the cut, poor sleep was a notable omission. The report examined studies in this area but concluded that “there was not enough comprehensive evidence to definitively link sleep to dementia risk.”

Nevertheless, absence of evidence is not evidence of absence, and studies examining sleep and dementia are still trying to tease out whether these factors are linked. A new study published in
Neurology by researchers at Imperial College London has continued this investigation.

The research, led by Imperial’s Abbas Dehghan, Ph.D, looked into the links between AD, MDD and several aspects of sleep. The study’s real power came from the use of huge cohorts – data was taken from the UK Biobank (N = 446,118), the Psychiatric Genomics Consortium (N = 18,759), and the International Genomics of Alzheimer's Project (N = 63,926). Furthermore, the study used an innovative statistics technique called mendelian randomization that uses genetic variants to tease out cause-effect relationships between observed traits.

The headline finding from this study was that people with genetic backgrounds that put them at higher risk for AD were more likely to be self-defined “morning people”. Further links were found between increased risk of AD and:

  • Shorter sleep duration
  • Lower likelihood of reporting long sleep
  • Smaller number of sleep episodes
  • The least active five hours of the day coming at an earlier time as measured by a wrist-worn accelerometer
  • Lower risk of insomnia

No significant statistical links were found between MDD and sleep or MDD and AD. Taken at face value, these findings suggest that links do exist between sleep and Alzheimer’s risk, but statistical analysis is rarely that simple.

Firstly, these findings are purely associative in nature – no causal links were found. This means that the study cannot conclude that any aspects of sleep lead to AD.

But perhaps even in the absence of causation, an association might be informative for people worried about AD. If being a morning person is linked to a higher risk of the disease, might it be time to finally throw that alarm clock out the window and embrace an 11am wakeup? Not quite. The increase in risk found in the study was just 1%. By comparison, being a smoker
confers a 30-50% increased risk. One study of obesity found a 300% increase in risk for AD versus having a healthy BMI. Does a 1% increase in risk have any real clinical significance, or at least enough significance to encourage us all back into our warm beds until the dawn chorus has ceased?

Speaking to Technology Networks, Dehghan says the increase in risk is “trivial”. He points out that the sleep data in the study comes from a healthy population as part of the UK Biobank, and genetic variants bestow a higher genetic risk of developing AD, rather than a definite diagnosis. This has implications for how the findings should be interpreted. “S
ince it is not in Alzheimer’s patients and merely in those who are genetically at risk of Alzheimer’s, [the observed association] may be due to some common genetic factors,” says Dehghan.

The weak links identified, says Deghhan, are to be “
interpreted with caution.” Far from encouraging people to change their sleep habits to ward off Alzheimer’s, Deghhan instead says that their data is more in agreement with a scenario where sleep disturbances are happening in early stages of the Alzheimer’s disease.” This is a valuable finding – if clinicians can diagnose AD earlier using markers such as changes to sleep patterns, then patients can be enrolled in clinical trials at an earlier stage, and on an individual level, people can have more time to adapt their lifestyle in response to diagnosis. But should late lie-ins be the latest brain health trend? Based on this data, the answer is clearly no. “There is no need to change your sleep pattern to prevent Alzheimer’s disease,” concludes Dehghan.