Evidence map›Paper›PMID 26073395›Full record

Trial reportJournal of clinical lipidology

Dose-response effects of marine omega-3 fatty acids on apolipoproteins, apolipoprotein-defined lipoprotein subclasses, and Lp-PLA2 in individuals with moderate hypertriglyceridemia.

Ann C Skulas-Ray, Petar Alaupovic, Penny M Kris-Etherton, Sheila G West

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Journal of clinical lipidology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Review
  6. Dietary and Pharmacological Fatty Acids and Cardiovascular Health.The Journal of clinical endocrinology and metabolism · 2020
    Review
  7. Article
  8. Review
  9. Article
  10. Article
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 at 2 institutions in 1 country.

Ann C Skulas-RayDepartment of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA. Electronic address: aus164@psu.edu.
Petar AlaupovicLipid and Lipoprotein Laboratory, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
Penny M Kris-EthertonDepartment of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA.
Sheila G WestDepartment of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA; Department of Biobehavioral Health, The Pennsylvania State University, University Park, PA, USA.
Pennsylvania State University · USOklahoma Medical Research Foundation · US

Funding

Penn State Clinical and Translational Science InstituteUL1TR000127 · NCATS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI SINOWAY, LAWRENCE I · 2012 to 2015
$17.1M
PENN STATE CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTEUL1RR033184 · NCRR · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI SINOWAY, LAWRENCE I · 2011 to 2011
$4.5M
NCATS NIH HHS UL1 TR000127NCRR NIH HHS UL1 RR033184
6 · The paper itself

Abstract

backgroundApolipoprotein (apo) distribution and lipoprotein (Lp)-associated markers of inflammation, such as lipoprotein-associated phospholipase A2 (Lp-PLA2), influence the atherogenicity of circulating lipids and lipoproteins. Little evidence exists regarding the dose-response effects of the marine omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on apos, apo-defined Lps, and Lp-PLA2.

objectiveThe purpose of this study was to compare the effects of 0, 0.85, and 3.4 g/d of EPA + DHA on Lp-PLA2 mass and activity in individuals with moderate hypertriglyceridemia. We also measured effects on concentrations of apoAI, apoAII, apoB, apoC, apoD, and apoE-defined Lp subclasses.

methodsThe study was a randomized, doubleblind, crossover design with 8-week treatment periods and 6-week washout periods. During the 3 treatment periods, subjects (n = 25) received 0 g/d EPA + DHA, 0.85 g/d EPA + DHA (low dose), and 3.4 g/d EPA + DHA (high dose) in random order.

resultsapoB and apoC-III were significantly decreased by the high dose relative to placebo and low dose (P < .01), as was very low-density lipoprotein cholesterol (P < .005). The low dose had no effect on Lp outcomes compared with placebo. The high- and low-dose effects differed significantly for heparin-precipitated apoC-III, LpB, LpA-I, and apoB/apoA-I ratio (P < .05). There was a trend for a decreased Lp-PLA2 mass with the high dose (P = .1).

conclusionThe effects of 3.4 g/d EPA + DHA on apoB and apoC-III may reduce atherosclerotic plaque progression in individuals with elevated triglycerides.

Indexed as

1-Alkyl-2-acetylglycerophosphocholine EsteraseApolipoprotein A-IApolipoprotein C-IIIApolipoproteins BCross-Over StudiesDocosahexaenoic AcidsDose-Response Relationship, DrugDouble-Blind MethodEicosapentaenoic AcidFemaleHumansMaleMiddle Aged1-Alkyl-2-acetylglycerophosphocholine EsteraseApolipoprotein A-IApolipoprotein C-IIIApolipoproteins BDocosahexaenoic AcidsEicosapentaenoic AcidPLA2G7 protein, humanApolipoproteinsDocosahexaenoic acidEicosapentaenoic acidFish oilLipoproteinsLp-PLA(2)Omega-3Triglycerides

Identifiers

PMID26073395
PMCPMC4677829
OpenAlexW2066520896

What OpenQuestion holds

Textmetadata
LicenceTDM
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.