ArticleCell & bioscience2025
Genetic influences on the association between DNA methylation and obesity measures: insights from a twin study design.
Article in Cell & bioscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
backgroundBoth obesity and DNA methylation (DNAm) are influenced by genetic factors. Despite more than a thousand of obesity-related DNAm sites (CpGs) being identified, studies that account for genetic influences in these associations are limited.
resultsUsing data from 1,074 twins in the Chinese National Twin Registry and bivariate structural equation models (SEMs), we investigated the phenotypic (Rph), genetic (Ra), and environmental (Re) correlations between genome-wide DNAm and three obesity indices: BMI, waist circumference (WC), and waist-to-hip ratio (WHR). Genome-wide, correlations between DNAm and obesity were small (Rph = 0.04, Ra = 0.08-0.09, Re = 0.02-0.03). For CpGs with high phenotypic correlation (Rph > 0.1), the mean genetic and environmental correlations were 0.23-0.24 and 0.03-0.05, respectively, indicating significant genetic influence on the DNAm-obesity associations. To further investigate the role of genetic influences, we then categorized the CpGs into different groups: high phenotypic correlation (Rph ≥ 0.2); high phenotypic and genetic correlations (Rph > 0.1 and Ra > 0.5); high phenotypic and low genetic correlations (Rph > 0.1 and Ra < 0.5). Association studies were conducted in the full population and in the monozygotic (MZ) twin-paired design, where genetic influences were controlled. For CpGs with Rph ≥ 0.2, 9, 8, and 22 were associated with BMI, WC, and WHR in the full population, but only 6, 1, and 1 CpGs remained significant after controlling for genetic effects in MZ twin-pair analyses. For CpGs with Rph > 0.1 and Ra > 0.5, genetic factors predominantly drove the association, and none of the 155/155/189 CpGs associated with BMI/WC/WHR in the full population were significant in MZ-paired analyses. For CpGs with Rph > 0.1 and Ra < 0.1, genetic effects were minimal or confounding, with 89, 4, and 17 significant in both full population and MZ-paired analyses.
conclusionsOur results highlight the significant genetic influences on the DNAm-obesity relationships, which may explain the low replicability of obesity-related DNAm markers. This indicates that genetic influences should be carefully considered in DNAm-related studies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.