Insomnia harms the heart: from restless nights to cardiovascular diseases

Updated and contextualized version of an article originally published on July 21, 2020
The article retains its original focus by presenting it through a scholarly and accessible perspective, supported by verifiable references.

Authors

• Dr. M. Bitonti – Biologist
• Roberto Panzironi –Independent researcher 

Note editoriali

• First publication: July 21, 2020
• Last update: April 20, 2026
• Version: 2026 narrative revision  

IN BRIEF

• Sleep disturbances and fragmented sleep are associated with an increase in inflammatory markers and signs of atherosclerosis in epidemiological observations.
• A large-scale study found that sleep fragmentation is linked to an increase in neutrophils, which partly mediate the association with coronary calcification.
• Evidence mostly comes from observational studies and sleep deprivation experiments; the causal relationship remains partial and mediated by multiple factors.
• Interventions that improve nocturnal breathing (e.g., CPAP for apnea) appear to reduce inflammatory markers, but the direct impact on cardiac events requires further evidence.
• For those suffering from insomnia or fragmented sleep, it is advisable to consult professionals, consider appropriate diagnostic evaluations, and discuss possible treatments with a doctor.

Abstract: what does science say?

Poor quality sleep and fragmented sleep have been associated with an increase in inflammatory markers and a higher prevalence of signs of cardiovascular disease in the population. Observational evidence and some deprivation experiments indicate that repeated alterations in rest can modify the immune system, increasing cell populations such as neutrophils and monocytes and pro-inflammatory molecules (e.g., IL-6, CRP). Studies on large cohorts show associations between sleep duration and regularity and cardiovascular risk; medium and high-quality studies suggest that the treatment of specific sleep disorders, such as obstructive apnea, can reduce inflammatory markers. However, the transition from association to causality is complex: the dose and frequency of deprivation, the presence of comorbidities, obesity, and therapeutic support intervene. The evidence supports the biological plausibility of an inflammatory pathway linking disturbed sleep to atherosclerosis, but additional diagnostic procedures and clinical studies are needed to define effective and safe therapeutic settings.

The link between fragmented sleep, white blood cells, and hardened arteries

In recent years, interest has grown in the mechanisms linking sleep disturbances to cardiovascular disease. An analysis of a large cohort combining polysomnography and actigraphy data showed that sleep fragmentation—i.e., frequent awakenings or micro-awakenings during the night—is associated with higher circulating levels of neutrophils and, to a lesser extent, monocytes, as well as increased coronary artery calcification. The proposed mechanism is mediated: fragmented sleep → increase in certain types of inflammatory white blood cells → increased coronary calcific deposition, an indicator of subclinical atherosclerosis. This model remains a hypothesis supported by statistical mediation analyses: the observed relationship persists even after adjusting for known factors such as age, body mass index, hypertension, and smoking [1].

Sleep, inflammation, and biological markers

The association between sleep disorders and inflammation is documented at multiple levels: cohort studies and meta-analyses show that chronic patterns of insomnia or abnormal sleep duration (very short or very long) tend to correlate with higher levels of C-reactive protein (CRP), interleukin-6 (IL-6), and other pro-inflammatory cytokines. Controlled sleep deprivation experiments demonstrate that repeated nights of insufficient sleep lead to transcriptional and cellular activation of inflammatory pathways, with increased production of cytokines and monocyte responses. These systemic changes provide biological plausibility for the possible influence of sleep on atherosclerotic pathogenesis, while leaving open the question of the strength and directionality of the effect in the general population [2].

What kind of studies support these conclusions?

Evidence comes from various sources: large international observational studies that associate sleep duration and quality with cardiovascular disease events or signs; cohort studies with objective sleep measures (polysomnography and actigraphy) linked to blood tests and coronary imaging; controlled sleep deprivation or fragmentation experiments; and meta-analyses that synthesize the overall effect on inflammatory markers. An important methodological limitation is that most associations are observational, thus susceptible to confounding and shared variables (e.g., obesity, sedentary lifestyle, obstructive sleep apnea). For this reason, interpretations must be cautious and focused on plausibility and association, not on definitive conclusions of causality [1][2][3].

What does a key study show?

A study on a diverse cohort combined one night of polysomnography and one week of actigraphy with blood analyses and a measurement of coronary calcification. Researchers found that sleep fragmentation measured with actigraphy was associated with higher neutrophil counts and higher coronary calcification scores. Mediation analyses suggested that the increase in neutrophils partly explained the link between fragmentation and calcification, indicating a possible inflammatory pathway [1].

What it means in practice

For the average person and for general practitioners, the results described do not immediately imply new prescriptions or universal therapies. However, they reinforce some practical and prudent ideas: evaluating sleep quality as part of cardiovascular prevention; investigating possible specific disorders (e.g., obstructive sleep apnea) that can be treated with proven therapies and which, in aggregated studies, have shown reductions in some inflammatory markers after adequate treatment [5]. Improving sleep hygiene (regular hours, favorable environment, limiting evening stimuli) is a reasonable and low-risk measure. In the presence of chronic insomnia, frequent awakenings, or symptoms of nocturnal apnea (snoring, excessive daytime sleepiness), it is advisable to consult specialists for a diagnostic evaluation; therapeutic choices, including behavioral therapies with evidence of effectiveness, must be discussed on a case-by-case basis.

Role of specific interventions

In the case of obstructive sleep apnea, CPAP use is the reference treatment in appropriate patients, and meta-analyses show reductions in CRP and other inflammatory markers, especially with continuous treatment and good adherence [5]. For chronic insomnia, cognitive-behavioral therapies have evidence of efficacy; the use of supplements or medications should be carefully evaluated on an individual basis. The use of melatonin shows modest and selective effects on sleep parameters, and recent synthetic literature suggests considering targets, dosages, and populations to evaluate its clinical utility [7][8].

KEY POINTS TO REMEMBER

• Fragmented sleep and poor sleep quality are associated with increases in inflammatory markers and signs of subclinical atherosclerosis in observational studies [1][2].
• Neutrophils may represent a plausible biological mediator linking disturbed sleep and coronary calcification, but causal evidence is incomplete [1][4].
• Specific interventions for sleep disorders (e.g., CPAP for OSA) can reduce some indices of inflammation; the effect on cardiovascular events requires further confirmation [5].
• Sleep hygiene measures and medical evaluation of nocturnal disturbances remain prudent and low-risk approaches.
• Available evidence comes from studies with different designs: observational, experimental, and meta-analytic; interpreting the results requires caution.

Limitations of Evidence

It is important to distinguish between association and causation. Much of the relationship between sleep and cardiovascular disease is based on observational data, which is subject to confounding factors (e.g., lifestyle, comorbidities, obesity). Experimental sleep deprivation studies show inflammatory changes, but often over short time horizons and in controlled contexts that do not always reflect chronic real-world exposure. Furthermore, methodological variability (subjective vs. objective sleep measures, follow-up duration, studied populations) complicates synthesis. For these reasons, claims such as "fragmented sleep causes atherosclerosis" cannot be made without further confirmation from targeted clinical trials and longer, well-controlled intervention studies [2][3].

Editorial Conclusion

Restless nights and fragmented sleep are not merely a subjective annoyance: scientific literature indicates that repeated sleep disturbances are associated with biological markers of inflammation and subclinical signs of cardiovascular disease. The suggested biological pathway—an increase in pro-inflammatory white blood cells that promotes atherosclerotic processes—is plausible and supported by observational studies and mediation analyses. However, proof of causality is incomplete and mediated by numerous factors. For clinical practice and public health, it is reasonable to value sleep diagnostics when indicated, promote good sleep habits, and offer appropriate treatments for identified disorders. Large-scale intervention studies with prolonged follow-ups are still needed to definitively establish the impact of improved sleep on cardiovascular events.

SCIENTIFIC RESEARCH

1. Vallat R, Shah VD, Redline S, Attia P, Walker MP. Broken sleep predicts hardened blood vessels. PLoS Biol. 2020 Jun 4;18(6):e3000726. https://doi.org/10.1371/journal.pbio.3000726
2. Irwin MR, Olmstead R, Carroll JE. Sleep disturbance, sleep duration, and inflammation: a systematic review and meta-analysis of cohort studies and experimental sleep deprivation. Biol Psychiatry. 2016 Jul 1;80(1):40-52. https://doi.org/10.1016/j.biopsych.2015.05.014
3. Wang C, et al. Association of estimated sleep duration and naps with mortality and cardiovascular events: a study of 116,632 people from 21 countries. Eur Heart J. 2019;40(20):1620–1629. https://doi.org/10.1093/eurheartj/ehy695
4. Graham KA, et al. Neutrophils in cardiovascular disease: warmongers, peacemakers, or both? Cardiovasc Res. 2022;118(12):2596–2609. https://doi.org/10.1093/cvr/cvab302
5. Xie X, Pan L, Ren D, Du C, Guo Y. Effects of continuous positive airway pressure therapy on systemic inflammation in obstructive sleep apnea: a meta-analysis. Sleep Med. 2013 Nov;14(11):1139-1150. https://doi.org/10.1016/j.sleep.2013.07.006
6. Ridker PM, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med. 2017;377(12):1119-1131. https://doi.org/10.1056/NEJMoa1707914
7. Choi K, Lee YJ, Park S, Je NK, Suh HS. Efficacy of melatonin for chronic insomnia: Systematic reviews and meta-analyses. Sleep Med Rev. 2022; (review). https://doi.org/10.1016/j.smrv.2022.101692
8. Ferracioli-Oda E, Qawasmi A, Bloch MH. Meta-Analysis: Melatonin for the Treatment of Primary Sleep Disorders. PLoS One. 2013;8(5):e63773. https://doi.org/10.1371/journal.pone.0063773