ArticleHuman heredity2026
Generalized Stable Population and Agent-Based Models of Phenotypic Transmission in Human Populations, with an Application to Body Size.
Article in Human heredity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
introductionWe show that generalizations of stable population (GSPM) and agent-based models (ABMs) are useful tools to simulate trajectories of human phenotypes. Although mathematically very different, both classes of models can simultaneously account for multiple determinants of the population distribution of a phenotype across time and space. These include genetic transmission, assortative mating, differential fertility, vertical and horizontal cultural heredity, gene-environments interactions (GxE), and environmental feedback. We propose an application to obesity, a condition that has spread rapidly around the globe, increasing the risk of adult chronic illnesses and mortality.
methodsWe choose body mass index as the target phenotype, and formulate GSPM and ABMs that include genetic inheritance, GxE, assortative mating, and fertility differentials. We exclude, in this version, the role of vertical cultural heredity. The GSPM is built on time-varying stochastic matrices that trace the trajectory of the phenotype by groups. The ABM models the behavior of individual agents integrating a stochastic component modifying each agent's behavior.
resultsThere are four key results. First, differential fertility dominates the phenotype's time trajectory, followed by assortative mating and GxE. Second, contrary to research in other phenotypes, the impact of assortative mating cannot offset the influence of fertility differentials. Third, concerning the formal representation of the transmission process, we show that the use of simple Mendelian models to represent complex phenotypes can produce badly biased inferences. Fourth, despite their mathematical differences, the GSPM and ABM produce virtually identical results.
conclusionsModeling phenotypes with complex genetic transmission and heavily dependent on regimes of fertility differentials, assortative mating and GxE ought not to rely on excessive simplifications, as has traditional been done in past research. Both, the GSPM and ABM are useful, accessible, and effective tools to introduce more realism in the modeling of these phenotypes, and can be used as guides for policy interventions.
Indexed as
Identifiers
What Socratic 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 Socratic graph.