Sleep Restriction Increases the Risk of Developing Cardiovascular Diseases by Augmenting Proinflammatory Responses through IL-17 and CRP
Open accessAbstract
BACKGROUND: Sleep restriction, leading to deprivation of sleep, is common in modern 24-h societies and is associated with the development of health problems including cardiovascular diseases. Our objective was to investigate the immunological effects of prolonged sleep restriction and subsequent recovery sleep, by simulating a working week and following recovery weekend in a laboratory environment. METHODS AND FINDINGS: After 2 baseline nights of 8 hours time in bed (TIB), 13 healthy young men had only 4 hours TIB per night for 5 nights, followed by 2 recovery nights with 8 hours TIB. 6 control subjects had 8 hours TIB per night throughout the experiment. Heart rate, blood pressure, salivary cortisol and serum C-reactive protein (CRP) were measured after the baseline (BL), sleep restriction (SR) and recovery (REC) period. Peripheral blood mononuclear cells (PBMC) were collected at these time points, counted and stimulated with PHA. Cell proliferation was analyzed by thymidine incorporation and cytokine production by ELISA and RT-PCR. CRP was increased after SR (145% of BL; p<0.05), and continued to increase after REC (231% of BL; p<0.05). Heart rate was increased after REC (108% of BL; p<0.05). The amount of circulating NK-cells decreased (65% of BL; p<0.005) and the amount of B-cells increased (121% of BL; p<0.005) after SR, but these cell numbers recovered almost completely during REC. Proliferation of stimulated PBMC increased after SR (233% of BL; p<0.05), accompanied by increased production of IL-1beta (137% of BL; p<0.05), IL-6 (163% of BL; p<0.05) and IL-17 (138% of BL; p<0.05) at mRNA level. After REC, IL-17 was still increased at the protein level (119% of BL; p<0.05). CONCLUSIONS: 5 nights of sleep restriction increased lymphocyte activation and the production of proinflammatory cytokines including IL-1beta IL-6 and IL-17; they remained elevated after 2 nights of recovery sleep, accompanied by increased heart rate and serum CRP, 2 important risk factors for cardiovascular diseases. Therefore, long-term sleep restriction may lead to persistent changes in the immune system and the increased production of IL-17 together with CRP may increase the risk of developing cardiovascular diseases.
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Sleep restriction without circadian disruption resulted in a marked elevation of serum hsCRP levels in men.
“Consistent with previous studies of partial sleep deprivation in healthy young men (37,38), sleep restriction without circadian disruption resulted in a marked elevation of serum hsCRP levels in men.”
From Circadian Misalignment Augments Markers of Insulin Resistance and Inflammation, Independently of Sleep Loss (2014) · cites this paper as [37]
The Results (CRP, Heart rate, blood pressure, and cortisol; page unavailable) report a significant rise in CRP to 145% of baseline after sleep restriction in healthy young men, and the Discussion identifies the measure as serum hs-CRP. The study design kept wake time and meals fixed but moved bedtime from 11 PM to 3 AM; it does not establish that circadian disruption was absent. (LLM, conf=0.83)
Experimental — accuracy not yet measuredWe have earlier shown that cytokine (interleukins IL-1b, IL-6 and IL-17) release as response to in vitro immunological challenge is increased after sleep restriction, as well as serum acute phase protein CRP.
“We have earlier shown that cytokine (interleukins IL-1b, IL-6 and IL-17) release as response to in vitro immunological challenge is increased after sleep restriction, as well as serum acute phase protein CRP7.”
From Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses (2016) · cites this paper as [7]
No changes in the overall cortisol concentration in SR compared to BL was observed.
“No changes in the overall cortisol concentration in SR compared to BL was observed7.”
From Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses (2016) · cites this paper as [7]
Seven nights of restricted sleep raise plasma IL-6 in both sexes, TNF only in men, and inflammatory transcripts for IL-1β, IL-6, and IL-17, with the transcript rise persisting after recovery sleep.
“even shorter periods of sleep restriction (ie, 7 nights) induce increase in plasma concentrations of IL-6 in men and women, increase of TNF in men only (Vgontzas et al, 2004), and increase in inflammatory transcripts of IL-1β, IL-6, and IL-17 (van Leeuwen et al, 2009), which persists even after a night of recovery sleep (van Leeuwen et al, 2009).”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as van Leeuwen et al, 2009
Laboratory studies have shown that physiologic sleep restriction is associated with a proinflammatory state, including elevations in inflammatory cytokines such as IL-1B, IL-6, IL-17, TNF-α, and C-reactive protein.
“Laboratory studies have shown that physiologic sleep restriction is associated with a proinflamma-tory state, including elevations in inflammatory cytokines, such as interleukin 1B (IL-1B),64,65 IL-6,64,66–68 IL-17,64,69 tumor necrosis factor-α,64,68,70–72 and C-reactive protein.64,69,73–76”
From Sleep, Health, and Society (2017) · cites this paper as [69]
Sleep loss is associated with increased levels of proinflammatory cytokines and low-grade inflammation, a condition that may predispose to insulin and leptin resistance.
“Furthermore, sleep loss is associated with increased levels of proinflammatory cytokines and low-grade inflammation (reviewed in chapter 9 “Sleep loss and inflammation”), a condition that may predispose to insulin [69-71] and leptin resistance [72].”
From Role of sleep duration in the regulation of glucose metabolism and appetite (2010) · cites this paper as [70]
TNF-α levels are most often unchanged after partial sleep restriction, but not always.
“TNF-α levels are most often,82,93,112 but not always,107 unchanged after partial sleep restriction.”
From Interacting epidemics? Sleep curtailment, insulin resistance, and obesity (2012) · cites this paper as [112]
Increased plasma IL-6 is reported after partial and total sleep deprivation in most cases, though two studies only reported loss of circadian rhythms.
“Increased plasma levels of IL-6 were reported after partial and total sleep deprivation in most cases,93,106,107,108,112 although two studies only reported a loss of circadian rhythms82,96”
From Interacting epidemics? Sleep curtailment, insulin resistance, and obesity (2012) · cites this paper as [112]
IL-1β is elevated after partial and total sleep deprivation, but one study found no changes after total sleep deprivation.
“IL-1β was elevated after partial,106,112 and total sleep deprivation,96 but one study did not find any changes after total sleep deprivation82”
From Interacting epidemics? Sleep curtailment, insulin resistance, and obesity (2012) · cites this paper as [112]
Effects of sleep curtailment on CRP levels are inconsistent: lower, unchanged, or higher.
“Effects of sleep curtailment on CRP levels are inconsistent: they have been reported lower,96 unchanged,124 or higher.108,112”
From Interacting epidemics? Sleep curtailment, insulin resistance, and obesity (2012) · cites this paper as [112]
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- Authors
- van Leeuwen, W. M. A., Lehto, M., Karisola, P., Lindholm, H., Luukkonen, R., Sallinen, M., Härmä, M., Porkka-Heiskanen, T., & Alenius, H.
- Affiliations
- Finnish Institute of Occupational Health (FI)
- Corresponding author
- Alenius, Harri
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2009-02-25
- Volume
- 4
- Issue
- 2
- Pages
- e4589
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC2643002
- OpenAlex
- W2063611046
- Cited by
- 483
- References
- 32
- Citations by year
- 2026: 24 · 2025: 32 · 2024: 29 · 2023: 32 · 2022: 39 · 2021: 28 · 2020: 28 · 2019: 22 · 2018: 28 · 2017: 21 · 2016: 30 · 2015: 28 · 2014: 37 · 2013: 35 · 2012: 25
- FWCI
- 29.15
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Työväentutkimus Vuosikirja (submittedVersion)
- Funders
- European Commission (MCRTN-CT-2004-512362)
- Työsuojelurahasto (104073, 108203)
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Keywords
- sleep restriction, sleep deprivation, cardiovascular risk, inflammatory cytokines, IL-17, C-reactive protein, IL-1β, interleukin-6, lymphocyte activation, natural killer cells, B cells, peripheral blood mononuclear cells, heart rate, blood pressure, salivary cortisol, recovery sleep, inflammation, young men
- MeSH terms
- Adult, C-Reactive Protein, Cardiovascular Diseases, Heart Rate, Humans, Male, Sleep Deprivation, Time Factors, Interleukin-6, Inflammation Mediators, Interleukin-17, Interleukin-1beta, Young Adult
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