Gene-environment interactions due to quantile-specific heritability of triglyceride and VLDL concentrations
Abstract
"Quantile-dependent expressivity" is a dependence of genetic effects on whether the phenotype (e.g., triglycerides) is high or low relative to its distribution in the population. Quantile-specific offspring-parent regression slopes (βOP) were estimated by quantile regression for 6227 offspring-parent pairs. Quantile-specific heritability (h2), estimated by 2βOP/(1 + $$\Gamma$$ spouse), decreased 0.0047 ± 0.0007 (P = 2.9 × 10-14) for each one-percent decrement in fasting triglyceride concentrations, i.e., h2 ± SE were: 0.428 ± 0.059, 0.230 ± 0.030, 0.111 ± 0.015, 0.050 ± 0.016, and 0.033 ± 0.010 at the 90th, 75th, 50th, 25th, and 10th percentiles of the triglyceride distribution, respectively. Consistent with quantile-dependent expressivity, 11 drug studies report smaller genotype differences at lower (post-treatment) than higher (pre-treatment) triglyceride concentrations. This meant genotype-specific triglyceride changes could not move in parallel when triglycerides were decreased pharmacologically, so that subtracting pre-treatment from post-treatment triglyceride levels necessarily created a greater triglyceride decrease for the genotype with a higher pre-treatment value (purported precision-medicine genetic markers). In addition, sixty-five purported gene-environment interactions were found to be potentially attributable to triglyceride's quantile-dependent expressivity, including gene-adiposity (APOA5, APOB, APOE, GCKR, IRS-1, LPL, MTHFR, PCSK9, PNPLA3, PPARγ2), gene-exercise (APOA1, APOA2, LPL), gene-diet (APOA5, APOE, INSIG2, LPL, MYB, NXPH1, PER2, TNFA), gene-alcohol (ALDH2, APOA5, APOC3, CETP, LPL), gene-smoking (APOC3, CYBA, LPL, USF1), gene-pregnancy (LPL), and gene-insulin resistance interactions (APOE, LPL).
- Authors:
-
- Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States). Molecular Biophysics & Integrated Bioimaging Division
- Publication Date:
- Research Org.:
- Lawrence Berkeley National Laboratory (LBNL), Berkeley, CA (United States)
- Sponsoring Org.:
- USDOE Office of Science (SC); National Heart, Lung, and Blood Institute (NHLBI); Boston University; National Institutes of Health (NIH)
- OSTI Identifier:
- 1615321
- Grant/Contract Number:
- AC02-05CH11231; N01-HC-25195; HHSN268201500001I; R21ES020700
- Resource Type:
- Accepted Manuscript
- Journal Name:
- Scientific Reports
- Additional Journal Information:
- Journal Volume: 10; Journal Issue: 1; Journal ID: ISSN 2045-2322
- Publisher:
- Nature Publishing Group
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 59 BASIC BIOLOGICAL SCIENCES
Citation Formats
Williams, Paul T. Gene-environment interactions due to quantile-specific heritability of triglyceride and VLDL concentrations. United States: N. p., 2020.
Web. doi:10.1038/s41598-020-60965-9.
Williams, Paul T. Gene-environment interactions due to quantile-specific heritability of triglyceride and VLDL concentrations. United States. https://doi.org/10.1038/s41598-020-60965-9
Williams, Paul T. Wed .
"Gene-environment interactions due to quantile-specific heritability of triglyceride and VLDL concentrations". United States. https://doi.org/10.1038/s41598-020-60965-9. https://www.osti.gov/servlets/purl/1615321.
@article{osti_1615321,
title = {Gene-environment interactions due to quantile-specific heritability of triglyceride and VLDL concentrations},
author = {Williams, Paul T.},
abstractNote = {"Quantile-dependent expressivity" is a dependence of genetic effects on whether the phenotype (e.g., triglycerides) is high or low relative to its distribution in the population. Quantile-specific offspring-parent regression slopes (βOP) were estimated by quantile regression for 6227 offspring-parent pairs. Quantile-specific heritability (h2), estimated by 2βOP/(1 + $\Gamma$ spouse), decreased 0.0047 ± 0.0007 (P = 2.9 × 10-14) for each one-percent decrement in fasting triglyceride concentrations, i.e., h2 ± SE were: 0.428 ± 0.059, 0.230 ± 0.030, 0.111 ± 0.015, 0.050 ± 0.016, and 0.033 ± 0.010 at the 90th, 75th, 50th, 25th, and 10th percentiles of the triglyceride distribution, respectively. Consistent with quantile-dependent expressivity, 11 drug studies report smaller genotype differences at lower (post-treatment) than higher (pre-treatment) triglyceride concentrations. This meant genotype-specific triglyceride changes could not move in parallel when triglycerides were decreased pharmacologically, so that subtracting pre-treatment from post-treatment triglyceride levels necessarily created a greater triglyceride decrease for the genotype with a higher pre-treatment value (purported precision-medicine genetic markers). In addition, sixty-five purported gene-environment interactions were found to be potentially attributable to triglyceride's quantile-dependent expressivity, including gene-adiposity (APOA5, APOB, APOE, GCKR, IRS-1, LPL, MTHFR, PCSK9, PNPLA3, PPARγ2), gene-exercise (APOA1, APOA2, LPL), gene-diet (APOA5, APOE, INSIG2, LPL, MYB, NXPH1, PER2, TNFA), gene-alcohol (ALDH2, APOA5, APOC3, CETP, LPL), gene-smoking (APOC3, CYBA, LPL, USF1), gene-pregnancy (LPL), and gene-insulin resistance interactions (APOE, LPL).},
doi = {10.1038/s41598-020-60965-9},
journal = {Scientific Reports},
number = 1,
volume = 10,
place = {United States},
year = {Wed Mar 11 00:00:00 EDT 2020},
month = {Wed Mar 11 00:00:00 EDT 2020}
}
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Figures / Tables:
Table 1: Traditional and quantile regression analyses of triglycerides and very low density lipoprotein (VLDL)cholesterol from the Offspring and Third Generation Framingham Cohorts. Triglycerides and log triglycerides: 1174 offspring with one parent and 2507 with two parents, and 6176 full siblings in 2187 sibships; VLDLcholesterol: 2840 full siblings in 1029more »
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