Evidence map›Paper›PMID 30263045›Full record

ArticleBMC proceedings2018

Heritability and genetic associations of triglyceride and HDL-C levels using pedigree-based and empirical kinships.

Nicholas B Blackburn, Arthur Porto, Juan M Peralta, John Blangero

Abstract read
In one paragraph

Article in BMC proceedings, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

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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

4 authors.

Nicholas B Blackburn1South Texas Diabetes and Obesity Institute, Department of Human Genetics, University of Texas Rio Grande Valley School of Medicine, One University Blvd., Modular Building #100, Brownsville, TX 78250 USA.
Arthur Porto1South Texas Diabetes and Obesity Institute, Department of Human Genetics, University of Texas Rio Grande Valley School of Medicine, One University Blvd., Modular Building #100, Brownsville, TX 78250 USA.
Juan M Peralta1South Texas Diabetes and Obesity Institute, Department of Human Genetics, University of Texas Rio Grande Valley School of Medicine, One University Blvd., Modular Building #100, Brownsville, TX 78250 USA.
John Blangero1South Texas Diabetes and Obesity Institute, Department of Human Genetics, University of Texas Rio Grande Valley School of Medicine, One University Blvd., Modular Building #100, Brownsville, TX 78250 USA.

Funding

Genetic and Environmental Determinants of TriglyceridesU01HL072524 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI ARNETT, DONNA K · 2002 to 2008
$11.9M
GENETIC ANALYSIS OF COMMON DISEASES: AN EVALUATIONR01GM031575 · NIGMS · UNIVERSITY OF TEXAS RIO GRANDE VALLEY · PI ALMASY, LAURA A. · 1985 to 2016
$7.8M
Genomewide Association Study of Lipid Response to Fenofibrate and Dietary FatR01HL091357 · NHLBI · UNIVERSITY OF KENTUCKY · PI ARNETT, DONNA K · 2008 to 2018
$5.8M
SOLAR-Eclipse Computational Tools for Imaging GeneticsR01EB015611 · NIBIB · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KOCHUNOV, PETER V. · 2012 to 2024
$5.0M
NHLBI NIH HHS R01 HL091357NHLBI NIH HHS U01 HL072524NIGMS NIH HHS R01 GM031575
6 · The paper itself

Abstract

The heritability of a phenotype is an estimation of the percent of variance in that phenotype that is attributable to additive genetic factors. Heritability is optimally estimated in family-based sample populations. Traditionally, this involves use of a pedigree-based kinship coefficient generated from the collected genealogical relationships between family members. An alternative, when dense genotype data are available, is to directly measure the empirical kinship between samples. This study compares the use of pedigree and empirical kinships in the GAW20 data set. Two phenotypes were assessed: triglyceride levels and high-density lipoprotein cholesterol (HDL-C) levels pre- and postintervention with the cholesterol-reducing drug fenofibrate. Using SOLAR (Sequential Oligogenic Linkage Analysis Routines), pedigree-based kinships and empirically calculated kinships (using IBDLD and LDAK) were used to calculate phenotype heritability. In addition, a genome-wide association study was conducted using each kinship model for each phenotype to identify genetic variants significantly associated with phenotypic variation. The variant rs247617 was significantly associated with HDL-C levels both pre- and post-fenofibrate intervention. Overall, the phenotype heritabilities calculated using pedigree based kinships or either of the empirical kinships generated using IBDLD or LDAK were comparable. Phenotype heritabilities estimated from empirical kinships generated using IBDLD were closest to the pedigree-based estimations. Given that there was not an appreciable amount of unknown relatedness between the pedigrees in this data set, a large increase in heritability in using empirical kinship was not expected, and our calculations support this. Importantly, these results demonstrate that when sufficient genotypic data are available, empirical kinship estimation is a practical alternative to using pedigree-based kinships.

Identifiers

PMID30263045
PMCPMC6157025

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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.