Sleep Restriction Increases the Risk of Developing Cardiovascular Diseases by Augmenting Proinflammatory Responses through IL-17 and CRP
2009

Sleep Restriction and Cardiovascular Disease Risk

Sample size: 19 publication 10 minutes Evidence: moderate

Author Information

Author(s): van Leeuwen Wessel M. A., Lehto Maili, Karisola Piia, Lindholm Harri, Luukkonen Ritva, Sallinen Mikael, Härmä Mikko, Porkka-Heiskanen Tarja, Alenius Harri

Primary Institution: Finnish Institute of Occupational Health

Hypothesis

Continuous sleep restriction disturbs human immunity which could result in an increased risk of developing cardiovascular diseases.

Conclusion

Prolonged sleep restriction can change immune cell functions and may lead to an increased risk of developing cardiovascular diseases.

Supporting Evidence

  • CRP levels increased significantly after sleep restriction and remained elevated after recovery sleep.
  • Heart rate increased significantly after recovery sleep.
  • The number of NK-cells decreased significantly after sleep restriction.
  • Proliferation of stimulated PBMC increased significantly after sleep restriction.
  • Production of proinflammatory cytokines IL-1β, IL-6, and IL-17 increased significantly after sleep restriction.

Takeaway

Not getting enough sleep can make your body react in ways that might hurt your heart, even if you sleep normally for a couple of nights afterward.

Methodology

The study involved 19 healthy young men who underwent sleep restriction followed by recovery sleep, with various physiological and immunological parameters measured.

Potential Biases

Potential bias due to the controlled laboratory setting and the specific demographic of participants.

Limitations

The study was limited to a small sample size of healthy young men, which may not be generalizable to other populations.

Participant Demographics

Nineteen healthy men, aged 19–29, with a regular sleep-wake schedule.

Statistical Information

P-Value

p<0.005

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0004589

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