Evidence mapPaperPMID 42547683Full record

ReviewJournal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine2026

Sleep loss as a cardiometabolic risk factor: a narrative review of clinical and public health implications.

Firas K Ghanem, Hrayr Attarian, Zeina Al-Khalil, Colette S Kabrita

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In one paragraph

Review in Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Firas K GhanemGilbert and Rose-Marie Chagoury School of Medicine, Lebanese American University (LAU), Byblos, Lebanon.ORCID http://orcid.org/0009-0001-7323-9261
Hrayr AttarianDepartment of Neurology, Center for Circadian and Sleep Disorders, Feinberg School of Medicine, Northwestern University, 633 N Saint Clair Street, Suite 5000, Chicago, IL, 60611, USA. h-attarian@northwestern.edu.ORCID http://orcid.org/0000-0002-3983-4323
Zeina Al-KhalilFaculty of Medicine, American University of Beirut (AUB), Beirut, Lebanon.ORCID http://orcid.org/0009-0003-0663-7547
Colette S KabritaDepartment of Sciences, Faculty of Natural and Applied Sciences, Notre Dame University-Louaize (NDU), Zouk Mikael, P.O. Box 72, Zouk Mosbeh, Lebanon. ckabrita@ndu.edu.lb.ORCID http://orcid.org/0000-0001-9614-396X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo synthesize current evidence on how sleep deprivation, impaired sleep architecture, and circadian misalignment affect cardiovascular and metabolic regulation across autonomic, hormonal, inflammatory, and behavioral pathways, and to highlight remaining research gaps in cardiometabolic sleep medicine.

methodsA structured literature search was conducted using PubMed, Scopus, and Google Scholar to identify peer‑reviewed primary and review articles published within the past decade, using chronobiological and cardiometabolic search terms. Reference lists of retrieved articles were screened to identify additional relevant studies.

resultsExperimental and epidemiologic data consistently link short or disturbed sleep with increased incidence of hypertension, coronary artery disease, stroke, obesity, type 2 diabetes, and metabolic syndrome. Sleep loss activates the sympathetic nervous system and elevates cortisol, while suppressing growth hormone, thereby promoting vasoconstriction, endothelial dysfunction, and cardiac remodeling. Parallel disruption of leptin, ghrelin, and endocannabinoid signaling increases hunger, caloric intake, and preference for energy‑dense foods, driving weight gain, visceral adiposity, and insulin resistance. Circadian misalignment from shift work and social jet lag further amplifies inflammatory signaling and metabolic risk across the lifespan. Limited interventional data suggest that sleep extension can improve appetite regulation, blood pressure, and some glycemic indices, but mechanistic and long‑term outcomes remain underexplored.

conclusionSleep deprivation and circadian disruption mediate cardiometabolic disease through converging neuroendocrine, autonomic, inflammatory, and behavioral pathways. Future research should employ longitudinal designs and integrated multi- "omics" approaches combined with sleep phenotyping to clarify causal mechanisms and identify novel biomarkers and therapeutic targets in clinical sleep medicine.

Indexed as

Cardiometabolic Risk FactorsCardiovascular DiseasesMetabolic SyndromePublic HealthSleep DeprivationHumansAutonomic dysfunctionCardiometabolic diseaseCircadian misalignmentMetabolic syndromeNeuroendocrine regulationSleep deprivation

Identifiers

PMID42547683
PMCPMC13433680

What Socratic holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.