ArticleObesity (Silver Spring, Md.)2018
A Mathematical Model for Predicting Obesity Transmission with Both Genetic and Nongenetic Heredity.
Article in Obesity (Silver Spring, Md.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- Generalized Stable Population and Agent-Based Models of Phenotypic Transmission in Human Populations, with an Application to Body Size.Human heredity · 2026Article
- Article
- Dynamic Empirically Based Model for Understanding Future Trends in US Obesity Prevalence in the Context of Social Influences.Obesity (Silver Spring, Md.) · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
objectiveObesity is transmissible across generations through both genetic and nongenetic routes, but distinguishing between these factors is challenging. This study aimed to quantitatively examine the contribution of these genetic and nongenetic effects to assess their influence on obesity prevalence.
methodsA mathematical model was proposed that incorporated both the genetic and nongenetic effects of obesity. Model parameters were estimated by using observational data. Model simulations were used to assess the sensitivity of model parameters. To strengthen the study's approach, parameter estimation and simulation using data from the United Kingdom were also performed.
resultsIndividuals homozygous for a "hypothetical obesogenic gene" were suggested to be more susceptible to both socially contagious risk and spontaneous weight gain risk. The model predicted that obesity prevalence would reach 41.03% (39.28, 44.31) and 26.77% (25.62, 28.06) at 2030 in the United States and United Kingdom, respectively. The socially contagious risk factor had a greater overall impact on the distribution of the population with obesity than did spontaneous weight gain risk or mother-to-child obesity transmission risk.
conclusionsAlthough the proposed "first approximation" model captured the complex interactions between the genetic and nongenetic effects on obesity, this framework remains incomplete. Future work should incorporate other key features driving the obesity epidemic.
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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 Socratic graph.