Evidence map›Paper›PMID 19776641›Full record

ReviewJournal of nutrigenetics and nutrigenomics2009

Polyunsaturated fatty acids and cardiovascular disease: implications for nutrigenetics.

Hooman Allayee, Nitzan Roth, Howard N Hodis

Open access · goldAbstract readReview
In one paragraph

Review in Journal of nutrigenetics and nutrigenomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
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  7. Review
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  15. Nutrigenetics and nutrigenomics of atherosclerosis.Current atherosclerosis reports · 2013
    Review
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  18. 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

3 authors at 2 institutions in 2 countries.

Hooman AllayeeDepartment of Preventive Medicine, Keck School of Medicine, University of Southern California, 2250 Alcazar Street, Los Angeles, CA 90033, USA. hallayee@usc.edu
Nitzan Roth
Howard N Hodis
General Department of Preventive Medicine · VNUniversity of Southern California · US

Funding

Biologic Response of Menopausal Women to 17B-EstradiolR01AG024154 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HODIS, HOWARD NEIL · 2004 to 2012
$13.8M
RESEARCH TRAINING IN GERONTOLOGYT32AG000037 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JENNIFER A AILSHIRE, EILEEN M CRIMMINS · 1985 to 2026
$13.2M
Phytoestrogens/Progression of Atherosclerosis SUPPLEMENTU01AT001653 · NCCIH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HODIS, HOWARD NEIL · 2003 to 2008
$9.2M
Role of the 5-Lipoxygenase Pathway in AtherosclerosisR01HL079353 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ALLAYEE, HOOMAN · 2005 to 2009
$2.8M
EXTRAMURAL RESEARCH FACILITIES CONSTRUCTIONC06RR010600 · NCRR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KEDES, LAURENCE H · 1994 to 1994
–
RESEARCH FACILITIES IMPROVEMENT PROGRAM AND REMODELINGC06RR014514 · NCRR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KEDES, LAURENCE H · 1999 to 1999
–
EXTRAMURAL RESEARCH FACILITIES CONTRUCTION PROJECTC06CA062528 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KEDES, LAURENCE H · 1993 to 1994
–
NCCIH NIH HHS AT 001653NCCIH NIH HHS U01 AT001653NCI NIH HHS C06 CA062528NCI NIH HHS CA 62528-01NCRR NIH HHS C06 RR014514NCRR NIH HHS RR 10600-01NCRR NIH HHS RR 14514-01NHLBI NIH HHS HL 079353NHLBI NIH HHS R01 HL079353NIA NIH HHS AG 024154NIA NIH HHS R01 AG024154NIA NIH HHS T32 AG000037NIA NIH HHS T32 AG 00037
6 · The paper itself

Abstract

Cardiovascular disease (CVD) arises as a result of genetic predisposition in the context of a disease-promoting environment. While several risk factors have been identified for CVD, such as elevated serum lipid levels and hypertension, most of the genes identified thus far do not appear to involve such 'conventional' risk factors. Moreover, the interactions between genes and environment, such as a diet high in certain fats, adds another level of complexity to CVD and renders identification of the underlying genetic factors even more difficult. Polyunsaturated fatty acids (PUFAs), such as the omega-6 and omega-3 fatty acids, which have multiple roles in membrane structure, lipid metabolism, blood clotting, blood pressure, and, in particular, inflammation, have been linked to the reduction in CVD. Linoleic (omega-6) and alpha-linolenic acid (omega-3) are essential fatty acids that can be converted into long-chain PUFAs, such as arachidonic acid (AA) and eicosapentaenoic acid (EPA)/docosahexaenoic acid (DHA), respectively. These long-chain PUFAs are metabolized by enzymatically catalyzed systems via cyclooxygenases and lipoxygenases. The 5-lipoxygenase (5-LO)/leukotriene (LT) biosynthesis pathway has been biochemically and genetically associated with CVD traits in mice and humans, particularly in the context of dietary AA and EPA/DHA. In this review, we summarize the biochemical metabolism of omega-3 and omega-6 PUFAs, evaluate the evidence for genetic and nutrigenetic contributions of 5-LO pathway genes to CVD, and discuss the potential of future studies that could identify other gene-dietary interactions between PUFAs and CVD traits.

Indexed as

AtherosclerosisCardiovascular DiseasesFatty Acids, UnsaturatedHumansInflammationRisk FactorsFatty Acids, Unsaturated

Identifiers

PMID19776641
PMCPMC2820567
OpenAlexW2131780182

What OpenQuestion holds

Textmetadata
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.