Chronic interferon-alpha administration disrupts sleep continuity and depth in patients with hepatitis C: association with fatigue, motor slowing, and increased evening cortisol
Open accessAbstract
Background Consequences of chronic exposure to cytokines of the innate immune system on sleep in humans and the association of cytokine-induced sleep alterations with behavior, motor performance, and cortisol secretion are unknown. Methods Thirty-one patients with hepatitis C without pre-existing sleep disorders underwent nighttime polysomnography, daytime multiple sleep latency testing, behavioral assessments, neuropsychological testing, and serial blood sampling at baseline and after ∼12 weeks of either treatment with the innate immune cytokine interferon (IFN)-alpha (n = 19) or no treatment (n = 12). Fatigue and sleepiness were assessed using the Multidimensional Fatigue Inventory and Epworth Sleepiness Scale. Results Interferon-alpha administration led to significant increases in wake after sleep onset and significant decreases in stage 3/4 sleep and sleep efficiency. Rapid eye movement latency and stage 2 sleep were significantly increased during IFN-alpha treatment. Decreases in stage 3/4 sleep and increases in rapid eye movement latency were associated with increases in fatigue, whereas decreases in sleep efficiency were associated with reduced motor speed. Increased wake after sleep onset was associated with increased evening plasma cortisol. Despite IFN-alpha-induced increases in fatigue, daytime sleepiness did not increase. In fact, IFN-alpha-treated patients exhibited decreased propensity to fall asleep during daytime nap opportunities. Conclusions Chronic exposure to an innate immune cytokine reduced sleep continuity and depth and induced a sleep pattern consistent with insomnia and hyperarousal. These data suggest that innate immune cytokines may provide a mechanistic link between disorders associated with chronic inflammation, including medical and/or psychiatric illnesses and insomnia, which, in turn, is associated with fatigue, motor slowing, and altered cortisol.
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IFN-α treatment led to decreases in stage 3/4 sleep over 12 weeks.
“In particular, IFN-α treatment led to increased awakenings after sleep onset, decreases in stage 3/4 sleep and sleep efficiency, increases in REM latency, and decreases in stage 2 sleep over 12 weeks (Raison et al., 2010).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Raison et al., 2010
IFN-α treatment led to increased awakenings after sleep onset over 12 weeks.
“In particular, IFN-α treatment led to increased awakenings after sleep onset, decreases in stage 3/4 sleep and sleep efficiency, increases in REM latency, and decreases in stage 2 sleep over 12 weeks (Raison et al., 2010).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Raison et al., 2010
IFN-α treatment led to decreases in sleep efficiency over 12 weeks.
“In particular, IFN-α treatment led to increased awakenings after sleep onset, decreases in stage 3/4 sleep and sleep efficiency, increases in REM latency, and decreases in stage 2 sleep over 12 weeks (Raison et al., 2010).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Raison et al., 2010
An IFN-α study in patients with hepatitis C showed that inflammation alters objective measures of sleep.
“An IFN-α study in patients with hepatitis C showed that inflammation alters objective measures of sleep, and began to identify the specific components of sleep disrupted by inflammation using polysomnography (Raison et al., 2010).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Raison et al., 2010
IFN-α treatment led to increases in REM latency over 12 weeks.
“In particular, IFN-α treatment led to increased awakenings after sleep onset, decreases in stage 3/4 sleep and sleep efficiency, increases in REM latency, and decreases in stage 2 sleep over 12 weeks (Raison et al., 2010).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Raison et al., 2010
IFN-α treatment led to decreases in stage 2 sleep over 12 weeks.
“In particular, IFN-α treatment led to increased awakenings after sleep onset, decreases in stage 3/4 sleep and sleep efficiency, increases in REM latency, and decreases in stage 2 sleep over 12 weeks (Raison et al., 2010).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Raison et al., 2010
Exogenously-induced inflammation using both endotoxin and IFN-α also led to a suppression of REM sleep.
“However, exogenously-induced inflammation using both endotoxin and IFN-α also led to a suppression of REM sleep (Mullington et al., 2000; Raison et al., 2010), which is the opposite of changes observed in depressed patients (Palagini et al., 2013; Riemann et al., 2001; Tsuno et al., 2005).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Raison et al., 2010
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Why Sleep Is Important for Health: A Psychoneuroimmunology Perspective
Irwin, M. R. (2015) · Annual Review of Psychology · doi:10.1146/annurev-psych-010213-115205 · Cited by 1,325 · see citing works
Reciprocal regulation of the neural and innate immune systems
Irwin, M. R., & Cole, S. W. (2011) · Nature Reviews Immunology · doi:10.1038/nri3042 · Cited by 910 · see citing works
Inflammation: Depression Fans the Flames and Feasts on the Heat
Kiecolt-Glaser, J. K., Derry, H. M., & Fagundes, C. P. (2015) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2015.15020152 · Cited by 844 · see citing works
Is depression an inflammatory disorder?
Raison, C. L., & Miller, A. H. (2011) · Current Psychiatry Reports · doi:10.1007/s11920-011-0232-0 · Cited by 524 · see citing works
Self-citationAnnual research review: re-thinking the classification of autism spectrum disorders
Lord, C., & Jones, R. M. (2012) · Journal of Child Psychology and Psychiatry · doi:10.1111/j.1469-7610.2012.02547.x · Cited by 290 · see citing works
The evolutionary significance of depression in Pathogen Host Defense (PATHOS-D)
Raison, C. L., & Miller, A. H. (2013) · Molecular Psychiatry · doi:10.1038/mp.2012.2 · Cited by 253 · see citing works
Self-citationIrwin, M. R., Olmstead, R., Breen, E. C., Witarama, T., Carrillo, C., Sadeghi, N., Arevalo, J. M. G., Ma, J., Nicassio, P., Bootzin, R., et al. (2015) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.01.010 · Cited by 227 · see citing works
Dooley, L. N., Kuhlman, K. R., Robles, T. F., Eisenberger, N. I., Craske, M. G., & Bower, J. E. (2018) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2018.09.006 · Cited by 176 · see citing works
Sleep disturbance, inflammation and depression risk in cancer survivors
Irwin, M. R., Olmstead, R. E., Ganz, P. A., & Haque, R. (2013) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2012.05.002 · Cited by 173 · see citing works
Therapeutic Implications of Brain–Immune Interactions: Treatment in Translation
Miller, A. H., Haroon, E., & Felger, J. C. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2016.167 · Cited by 152 · see citing works
Self-citationThe role of dopamine in inflammation-associated depression: mechanisms and therapeutic implications
Felger, J. C. (2016) · Current Topics in Behavioral Neurosciences · doi:10.1007/7854_2016_13 · Cited by 115 · see citing works
Redman, K. N., Karstaedt, A. S., & Scheuermaier, K. (2018) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2018.02.002 · Cited by 62 · see citing works
Hayley, S., Scharf, J., & Anisman, H. (2013) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2012.07.023 · Cited by 48 · see citing works
Felger, J. C., Alagbe, O., Pace, T. W. W., Woolwine, B. J., Hu, F., Raison, C. L., & Miller, A. H. (2011) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2011.02.015 · Cited by 41 · see citing works
Self-citationSchmidt, E.-M., Linz, B., Diekelmann, S., Besedovsky, L., Lange, T., & Born, J. (2015) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2014.11.012 · Cited by 41 · see citing works
- Authors
- Raison, C. L., Rye, D. B., Woolwine, B. J., Vogt, G. J., Bautista, B. M., Spivey, J. R., & Miller, A. H.
- Affiliations
- Emory University (US)
- Corresponding author
- Miller, Andrew H.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2010-11
- Volume
- 68
- Issue
- 10
- Pages
- 942-949
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC2937202
- OpenAlex
- W2053607004
- Cited by
- 116
- References
- 85
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 3 · 2023: 6 · 2022: 9 · 2021: 8 · 2020: 8 · 2019: 8 · 2018: 6 · 2017: 6 · 2016: 12 · 2015: 9 · 2014: 12 · 2013: 5 · 2012: 11
- FWCI
- 10.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (K23 MH064619, R01 MH070553, K05 MH069124, R01 HL073921, T32 MH020018)
- Clinical and Translational Science Award Program (UL1 RR025008)
- General Clinical Research Center Program (M01 RR0039)
- National Center for Research Resources
- Centocor
- GlaxoSmithKline
- Schering-Plough
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Keywords
- interferon-alpha, hepatitis C, sleep continuity, sleep depth, fatigue, motor slowing, cortisol, cytokines, insomnia, hyperarousal, sleep efficiency, REM latency, daytime sleepiness, chronic inflammation
- MeSH terms
- Interferon alpha-2, Antiviral Agents, Fatigue, Female, Hepatitis C, Humans, Hydrocortisone, Male, Middle Aged, Polyethylene Glycols, Reaction Time, Recombinant Proteins, Sleep Wake Disorders, Tumor Necrosis Factor-alpha, Case-Control Studies, Interferon-alpha, Receptors, Tumor Necrosis Factor, Type II
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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