Evidence map›Paper›PMID 30571417›Full record

ArticleStroke2018

APOE and the Association of Fatty Acids With the Risk of Stroke, Coronary Heart Disease, and Mortality.

Claudia L Satizabal, Cécilia Samieri, Kendra L Davis-Plourde, Barbara Voetsch, Hugo J Aparicio, Matthew P Pase, José Rafael Romero, Catherine Helmer, Ramachandran S Vasan, Carlos S Kase and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Stroke, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 3 pooled it
2.4field-weighted citation impact, top 12% of its field
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

31 citing papers in PubMed, 3 syntheses or guidelines pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Multiple Roles of Palmitic Acid in Cardiovascular Diseases.Journal of inflammation research · 2025
    Review
  12. Article
  13. Article
  14. Assessment of neurovascular uncoupling: APOE status is a key driver of early metabolic and vascular dysfunction.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  15. Assessment of Neurovascular Uncoupling:bioRxiv : the preprint server for biology · 2024
    Article
  16. Article
  17. Understanding the interplay between APO E polymorphism and cognition in the Italian oldest old: results from the "Mugello study".Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Article
  18. Article
  19. Article
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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

13 authors at 8 institutions in 3 countries.

Claudia L SatizabalFrom the Department of Neurology (C.L.S., H.J.A., M.P.P., J.R.R., C.S.K., A.S.B., S.S.), Boston University School of Medicine, MA.
Cécilia SamieriBordeaux Population Health Research Center, UMR U1219-Inserm, University of Bordeaux, France (C.S., C.H., S.D.).
Kendra L Davis-PlourdeFramingham Heart Study, MA (C.L.S., K.L.D.-P., H.J.A., M.P.P., J.R.R., R.S.V., A.S.B., S.S.).
Barbara VoetschDepartment of Neurology, Lahey Hospital & Medical Center, Burlington, MA (B.V.).
Hugo J AparicioFrom the Department of Neurology (C.L.S., H.J.A., M.P.P., J.R.R., C.S.K., A.S.B., S.S.), Boston University School of Medicine, MA.
Matthew P PaseFrom the Department of Neurology (C.L.S., H.J.A., M.P.P., J.R.R., C.S.K., A.S.B., S.S.), Boston University School of Medicine, MA.
José Rafael RomeroFrom the Department of Neurology (C.L.S., H.J.A., M.P.P., J.R.R., C.S.K., A.S.B., S.S.), Boston University School of Medicine, MA.
Catherine HelmerBordeaux Population Health Research Center, UMR U1219-Inserm, University of Bordeaux, France (C.S., C.H., S.D.).
Ramachandran S VasanDepartment of Medicine (R.S.V.), Boston University School of Medicine, MA.
Carlos S KaseFrom the Department of Neurology (C.L.S., H.J.A., M.P.P., J.R.R., C.S.K., A.S.B., S.S.), Boston University School of Medicine, MA.
Stéphanie DebetteBordeaux Population Health Research Center, UMR U1219-Inserm, University of Bordeaux, France (C.S., C.H., S.D.).
Alexa S BeiserFrom the Department of Neurology (C.L.S., H.J.A., M.P.P., J.R.R., C.S.K., A.S.B., S.S.), Boston University School of Medicine, MA.
Sudha SeshadriFrom the Department of Neurology (C.L.S., H.J.A., M.P.P., J.R.R., C.S.K., A.S.B., S.S.), Boston University School of Medicine, MA.
Boston University · USFramingham Heart Study · USBordeaux Population Health · FREmory University · USInserm · FRInstitute for Neurodegenerative Disorders · USLahey Hospital and Medical Center · USUniversité de Bordeaux · FR

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI MEYER, OANH L · 1991 to 2020
$28.3M
PRECURSORS OF STROKE INCIDENCE AND PROGNOSISR01NS017950 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Hugo Javier Aparicio, Jose Rafael Romero · 1985 to 2026
$22.9M
EPIDEMIOLOGY OF DEMENTIA IN THE FRAMINGHAM STUDYR01AG008122 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI AU, RHODA, SESHADRI, SUDHA · 1989 to 2015
$14.4M
Temporal Trends, Novel Imaging and Molecular Characterization of Preclinical and Clinical Alzheimer's Disease in the Framingham CohortsR01AG054076 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI DECARLI, CHARLES, SESHADRI, SUDHA · 2016 to 2020
$12.3M
Collaborative GWAS of Dementia, AD and related MRI and Cognitive EndophenotypesR01AG033193 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SESHADRI, SUDHA · 2009 to 2016
$4.4M
Microglial, Inflammatory and Omics Markers of Cerebral Small Vessel Disease in the CHARGE ConsortiumUH3NS100605 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI FORNAGE, MYRIAM, SESHADRI, SUDHA · 2018 to 2020
$3.0M
CHARGE: Identifying Risk & Protective SNV for AD in ADSP Case-control SampleU01AG049505 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SESHADRI, SUDHA · 2014 to 2017
$3.0M
Microglial, Inflammatory and Omics Markers of Cerebral Small Vessel Disease in the CHARGE ConsortiumUH2NS100605 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FORNAGE, MYRIAM, SESHADRI, SUDHA · 2016 to 2017
$2.0M
ADSP Follow-up in Multi-Ethnic Cohorts via Endophenotypes, Omics & Model SystemsU01AG052409 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI FORNAGE, MYRIAM, SESHADRI, SUDHA · 2016 to 2020
$1.6M
THE FRAMINGHAM HEART STUDY-N01HC25195-268025195-268025195N01HC025195 · HC · TRUSTEES OF BOSTON UNIVERSITY · PI WOLF, PHILIP A · 2002 to 2006
–
NHLBI NIH HHS HHSN268201500001INHLBI NIH HHS N01 HC025195NIA NIH HHS P30 AG010129NIA NIH HHS R01 AG008122NIA NIH HHS R01 AG033193NIA NIH HHS R01 AG054076NIA NIH HHS U01 AG049505NIA NIH HHS U01 AG052409NINDS NIH HHS R01 NS017950NINDS NIH HHS UH2 NS100605NINDS NIH HHS UH3 NS100605
6 · The paper itself

Abstract

Background and Purpose- The role of dietary fat on cardiovascular health and mortality remains under debate. Because the APOE is central to the transport and metabolism of lipids, we examined associations between plasma fatty acids and the risk of stroke, coronary heart disease, and mortality by APOE-ε4 genotype. Methods- We included 943 FHS (Framingham Heart Study) and 1406 3C (Three-City) Bordeaux Study participants. Plasma docosahexaenoic, linoleic, arachidonic, and palmitic fatty acids were measured at baseline by gas chromatography. All-cause stroke, ischemic stroke, coronary heart disease, and all-cause mortality events were identified prospectively using standardized protocols. Each cohort used Cox models to separately relate fatty acid levels to the risk of developing each event during ≤10 years of follow-up adjusting for potential confounders and stratifying by APOE genotype (ε4 carriers versus noncarriers). We then meta-analyzed summary statistics using random-effects models. Results- On average, participants had a mean age of 74 years, 61% were women, and 21% (n=483) were APOE-ε4 carriers. Meta-analysis results showed that, only among APOE-ε4 carriers, every SD unit increase in linoleic acid was associated with a reduced risk of all-cause stroke (hazard ratio [HR], 0.54 [95% CI, 0.38-0.78]), ischemic stroke (HR, 0.48 [95% CI, 0.33-0.71]), and all-cause mortality (HR, 0.70 [95% CI, 0.57-0.85]). In contrast, every SD unit increase in palmitic acid was related to an increased risk of all-cause stroke (HR, 1.58 [95% CI, 1.16-2.17]), ischemic stroke (HR, 1.76 [95% CI, 1.26-2.45]), and coronary heart disease (HR, 1.48 [95% CI, 1.09-2.01]), also in APOE-ε4 carriers only. Results for docosahexaenoic acid and arachidonic acid were heterogeneous between cohorts. Conclusions- These exploratory results suggest that APOE-ε4 carriers may be more susceptible to the beneficial or adverse impact of fatty acids on cardiovascular disease and mortality. In this subgroup, higher linoleic acid was protective for stroke and mortality, whereas palmitic acid was a risk factor for stroke and coronary heart disease. The mechanisms underlying these novel findings warrant further investigation.

Indexed as

AgedApolipoprotein E4Arachidonic AcidCleft LipCoronary DiseaseDietary FatsDocosahexaenoic AcidsFatty AcidsFemaleHumansLinoleic AcidLipid MetabolismMaleMortalityPalmitic AcidProportional Hazards ModelsApolipoprotein E4Arachidonic AcidDietary FatsDocosahexaenoic AcidsFatty AcidsLinoleic AcidPalmitic Acidapolipoproteins Ecardiovascular diseaseshumanslipidsmortality

Identifiers

PMID30571417
PMCPMC6310220
OpenAlexW2899868482

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.