A Mathematical Model for Predicting Obesity Transmission With Both Genetic and Nongenetic Heredity

OBJECTIVE: Obesity is transmissible across generations through both genetic and nongenetic routes, but distinguishing between these factors is challenging. We aimed to quantitatively study the contribution of these genetic and nongenetic effects to assess their influence on obesity prevalence. METHODS: We proposed a mathematical model that incorporated both 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 our approach, we also performed the parameter estimation and simulation using data from the UK. RESULTS: Individuals homozygous for a ‘hypothetical obesogenic gene’ are suggested to be more susceptible to both social contagious risk and spontaneous weight gain risk. The model predicted that obesity prevalence reaches 41.03% (39.28, 44.31) and 26.77% (25.62, 28.06) at 2030 in the US and UK, respectively. The social 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. CONCLUSIONS: Although 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.