Evidence map›Paper›PMID 35606076›Full record

ReviewAtherosclerosis2022

Non-genetic influences on lipoprotein(a) concentrations.

Byambaa Enkhmaa, Lars Berglund

Open access · hybridAbstract readReview
In one paragraph

Review in Atherosclerosis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 4 pooled it
34.2field-weighted citation impact, top 1% 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

78 citing papers in PubMed, 4 syntheses or guidelines pooled it, 166 citations in OpenAlex.

  1. Pooled it
  2. Association between hepatic steatosis and lipoprotein(a) levels in non-alcoholic patients: A systematic review.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2024
    Pooled it
  3. Plasma Lipoprotein(a) Levels in Polycystic Ovary Syndrome: A Systematic Review and Meta-analysis.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2023
    Pooled it
  4. Pooled it
  5. Trial
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  10. Lipoprotein(a): Cardiovascular Risk and Emerging Targeted Therapies.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2026
    Review
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18 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Byambaa EnkhmaaDepartment of Internal Medicine, School of Medicine, University of California Davis, Davis, CA, USA; Center for Precision Medicine and Data Sciences, School of Medicine, University of California Davis, Davis, CA, USA. Electronic address: ebyambaa@ucdavis.edu.
Lars BerglundDepartment of Internal Medicine, School of Medicine, University of California Davis, Davis, CA, USA.
University of California, Davis · US

Funding

Lp(a) and Oxidized Phospholipids - Impact of DietsR01HL157535 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BYAMBAA, ENKHMAA · 2022 to 2025
$2.4M
NHLBI NIH HHS R01 HL157535
6 · The paper itself

Abstract

An elevated level of lipoprotein(a) [Lp(a)] is a genetically regulated, independent, causal risk factor for cardiovascular disease. However, the extensive variability in Lp(a) levels between individuals and population groups cannot be fully explained by genetic factors, emphasizing a potential role for non-genetic factors. In this review, we provide an overview of current evidence on non-genetic factors influencing Lp(a) levels with a particular focus on diet, physical activity, hormones and certain pathological conditions. Findings from randomized controlled clinical trials show that diets lower in saturated fats modestly influence Lp(a) levels and often in the opposing direction to LDL cholesterol. Results from studies on physical activity/exercise have been inconsistent, ranging from no to minimal or moderate change in Lp(a) levels, potentially modulated by age and the type, intensity, and duration of exercise modality. Hormone replacement therapy (HRT) in postmenopausal women lowers Lp(a) levels with oral being more effective than transdermal estradiol; the type of HRT, dose of estrogen and addition of progestogen do not modify the Lp(a)-lowering effect of HRT. Kidney diseases result in marked elevations in Lp(a) levels, albeit dependent on disease stages, dialysis modalities and apolipoprotein(a) phenotypes. In contrast, Lp(a) levels are reduced in liver diseases in parallel with the disease progression, although population studies have yielded conflicting results on the associations between Lp(a) levels and non-alcoholic fatty liver disease. Overall, current evidence supports a role for diet, hormones and related conditions, and liver and kidney diseases in modifying Lp(a) levels.

Indexed as

Cardiovascular DiseasesLipoprotein(a)Cholesterol, LDLEstradiolEstrogen Replacement TherapyEstrogensExerciseFemaleHumansRisk FactorsCholesterol, LDLEstradiolEstrogensLipoprotein(a)DietHormonesKidney diseaseLiver diseaseLp(a) plasma levelPhysical activitySaturated fat

Identifiers

PMID35606076
PMCPMC9549811
OpenAlexW4281257482

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.