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Insomnia Phenotypes, Cardiovascular Risk and Their Link to Brain Health
Julio Fernandez-Mendoza. Circulation research, 2025-08-14
Topic: Brain imaging, connectivity and assessment
Plain-language summary
About 30% to 40% of the general population experiences insomnia symptoms of difficulty initiating or maintaining sleep, and another 10% to 15% of the general population experiences chronic insomnia disorder. The prevalence of insomnia is disproportionately higher in people with cardiometabolic risk factors, cardiovascular diseases, cerebrovascular diseases, and neurocognitive disorders, including vascular cognitive impairment. In fact, recent meta-analytic evidence from epidemiological studies has demonstrated that insomnia, especially when accompanied by objective short sleep duration, is a risk factor for incident hypertension, type 2 diabetes, heart failure, stroke, cognitive impairment, Alzheimer disease, and all-cause mortality. Insomnia should, thus, be part of the prevention and management of these adverse health outcomes. However, randomized clinical trials have not demonstrated whether treatment with cognitive-behavioral therapy for insomnia, the first-line guideline-recommended treatment, or hypnotics/sedatives improves heart- or brain-related outcomes. Studies have also failed to consider insomnia a heterogeneous disorder consisting of distinct phenotypes that result from the relative contribution of biological versus cognitive-behavioral perpetuating factors. Objective short sleep duration has emerged as a marker of physiological hyperarousal in insomnia (ie, dysregulation of the hypothalamic-pituitary axis, increased sympathetic nervous system activation, and increased inflammation), as a predictor of insomnia-related adverse heart and brain health outcomes and, potentially, poor response to cognitive-behavioral therapy for insomnia. This review summarizes the meta-analytic evidence on the association of insomnia with cardiometabolic risk factors, cardiovascular diseases, cerebrovascular diseases, and neurocognitive disorders, including current knowledge on the heterogeneity of the disorder. This review also summarizes the potential pathophysiologic mechanisms that lead to heart and brain morbidity, which vary across insomnia phenotypes based on objective sleep duration. This review suggests that basic and clinical sciences need to unveil the molecular, cellular, and behavioral mechanisms at play across insomnia phenotypes, as the public health and clinical implications of their association with adverse heart and brain health are demanding immediate attention.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Fernandez-Mendoza, J. (2025). Insomnia Phenotypes, Cardiovascular Risk and Their Link to Brain Health. Circulation research. https://doi.org/10.1161/circresaha.125.325686
Vancouver
Fernandez-Mendoza J. Insomnia Phenotypes, Cardiovascular Risk and Their Link to Brain Health. Circulation research. 2025. doi:10.1161/circresaha.125.325686. PMID: 40811499.
BibTeX
@article{fernandezmendoza2025-40811499,
author = {Fernandez-Mendoza, Julio},
title = {{Insomnia Phenotypes, Cardiovascular Risk and Their Link to Brain Health}},
journal = {Circulation research},
year = {2025},
doi = {10.1161/circresaha.125.325686},
pmid = {40811499},
url = {https://doi.org/10.1161/circresaha.125.325686}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- In fact, recent meta-analytic evidence from epidemiological studies has demonstrated that insomnia, especially when accompanied by objective short sleep duration, is a risk factor for incident hypertension, type 2 diabetes, heart failure, stroke, cognitive impairment, Alzheimer disease, and all-cause mortality.
- However, randomized clinical trials have not demonstrated whether treatment with cognitive-behavioral therapy for insomnia, the first-line guideline-recommended treatment, or hypnotics/sedatives improves heart- or brain-related outcomes.
- Studies have also failed to consider insomnia a heterogeneous disorder consisting of distinct phenotypes that result from the relative contribution of biological versus cognitive-behavioral perpetuating factors.
- This review suggests that basic and clinical sciences need to unveil the molecular, cellular, and behavioral mechanisms at play across insomnia phenotypes, as the public health and clinical implications of their association with adverse heart and brain health are demanding immediate attention.
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Study details
- Evidence strengthHigh
How this study scored 50/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multicenter collaboration and free to read, so those were left out: it earned 28 of the 56 points we could judge it on, which is 50 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Circulation research) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 5 / 5 | Rated “high” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 4 / 5 | 2025 — within 3 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40811499) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 28 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 28 of the 56 points we could judge it on is 50 out of 100. |
| Total | 50 / 100 | — |
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