Evidence map›Paper›PMID 26126546›Full record

ArticleJournal of the American Heart Association2015

Sex-Specific Parental Effects on Offspring Lipid Levels.

Irene M Predazzi, Rafal S Sobota, Serena Sanna, William S Bush, Jacquelaine Bartlett, Jessica S Lilley, MacRae F Linton, David Schlessinger, Francesco Cucca, Sergio Fazio and 1 more

Open access · goldAbstract readComparative StudyMulticenter Study
In one paragraph

Article in Journal of the American Heart Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 22% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

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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

11 authors at 6 institutions in 2 countries.

Irene M PredazziAtherosclerosis Research Unit, Departments of Medicine and Pharmacology, Vanderbilt University Medical Center, Nashville, TN (I.M.P., J.S.L., M.R.F.L., S.F.) Knight Cardiovascular Institute, Center for Preventive Cardiology, Oregon Health and Science University, Portland, OR (I.M.P., S.F.).
Rafal S SobotaCenter for Human Genetics Research, Vanderbilt University Medical Center, Nashville, TN (R.S.S., W.S.B.) Department of Genetics, Geisel School of Medicine, Dartmouth College, Hanover, NH (R.S.S., J.B., S.M.W.).
Serena SannaIstituto di Ricerca Genetica e Biomedica (IRGB), CNR, Monserrato, Italy (S.S., F.C.).
William S BushCenter for Human Genetics Research, Vanderbilt University Medical Center, Nashville, TN (R.S.S., W.S.B.) Department of Epidemiology and Biostatistics, Case Western Reserve University, Cleveland, OH (W.S.B.).
Jacquelaine BartlettDepartment of Genetics, Geisel School of Medicine, Dartmouth College, Hanover, NH (R.S.S., J.B., S.M.W.).
Jessica S LilleyAtherosclerosis Research Unit, Departments of Medicine and Pharmacology, Vanderbilt University Medical Center, Nashville, TN (I.M.P., J.S.L., M.R.F.L., S.F.) Division of Endocrinology, Department of Pediatrics, University of Mississippi School of Medicine, Jackson, MS (J.S.L.).
MacRae F LintonAtherosclerosis Research Unit, Departments of Medicine and Pharmacology, Vanderbilt University Medical Center, Nashville, TN (I.M.P., J.S.L., M.R.F.L., S.F.).
David SchlessingerLaboratory of Genetics, NIA, Baltimore, MD (D.S.).
Francesco CuccaIstituto di Ricerca Genetica e Biomedica (IRGB), CNR, Monserrato, Italy (S.S., F.C.).
Sergio FazioAtherosclerosis Research Unit, Departments of Medicine and Pharmacology, Vanderbilt University Medical Center, Nashville, TN (I.M.P., J.S.L., M.R.F.L., S.F.) Knight Cardiovascular Institute, Center for Preventive Cardiology, Oregon Health and Science University, Portland, OR (I.M.P., S.F.).
Scott M WilliamsDepartment of Genetics, Geisel School of Medicine, Dartmouth College, Hanover, NH (R.S.S., J.B., S.M.W.).
Dartmouth College · USInstitute of Genetic and Biomedical Research · ITVanderbilt University Medical Center · USCase Western Reserve University · USOregon Health & Science University · USUniversity of Mississippi · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Non-coding RNA & Bioinformatics CoreP01HL116263 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI DAVIES, SEAN STEPHEN · 2014 to 2025
$24.7M
Quantitative Biology Research InstituteP20GM103534 · NIGMS · DARTMOUTH COLLEGE · PI AMOS, CHRISTOPHER I. · 2012 to 2016
$8.6M
Aging-related Traits and Disease Risk Factors in a Sardinian Population CohortZIAAG000675 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2021
$5.7M
NHLBI NIH HHS 2R01HL057986‐15A1NHLBI NIH HHS 2T32HL007751‐16A2NHLBI NIH HHS 5R01HL106845‐03NHLBI NIH HHS HL116263NHLBI NIH HHS P01 HL116263NIA NIH HHS N01‐AG‐1‐2109NIGMS NIH HHS P20GM103534NIGMS NIH HHS T32 GM007347
6 · The paper itself

Abstract

backgroundPlasma lipid levels are highly heritable traits, but known genetic loci can only explain a small portion of their heritability. METHODS AND

resultsIn this study, we analyzed the role of parental levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TGs) in explaining the values of the corresponding traits in adult offspring. We also evaluated the contribution of nongenetic factors that influence lipid traits (age, body mass index, smoking, medications, and menopause) alone and in combination with variability at the genetic loci known to associate with TC, LDL-C, HDL-C, and TG levels. We performed comparisons among different sex-specific regression models in 416 families from the Framingham Heart Study and 304 from the SardiNIA cohort. Models including parental lipid levels explain significantly more of the trait variation than models without these measures, explaining up to ≈39% of the total trait variation. Of this variation, the parent-of-origin effect explains as much as ≈15% and it does so in a sex-specific way. This observation is not owing to shared environment, given that spouse-pair correlations were negligible (<1.5% explained variation in all cases) and is distinct from previous genetic and acquired factors that are known to influence serum lipid levels.

conclusionsThese findings support the concept that unknown genetic and epigenetic contributors are responsible for most of the heritable component of the plasma lipid phenotype, and that, at present, the clinical utility of knowing age-matched parental lipid levels in assessing risk of dyslipidemia supersedes individual locus effects. Our results support the clinical utility of knowing parental lipid levels in assessing future risk of dyslipidemia.

Indexed as

Adult ChildrenFathersMothersAdultBiomarkersCholesterolCholesterol, HDLCholesterol, LDLDyslipidemiasFemaleGene-Environment InteractionGenetic Predisposition to DiseaseHeredityHumansItalyLipid MetabolismBiomarkersCholesterolCholesterol, HDLCholesterol, LDLLipidsTriglyceridescholesterolgeneticslipidsrisk factorssex

Identifiers

PMID26126546
PMCPMC4608079
OpenAlexW2129996150

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Registered trials

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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.