Obesity risk is written in more than one language. Part of the story is encoded in DNA, where hundreds of genetic loci have been linked to body weight, fat distribution and energy regulation. Another part is shaped by the conditions in which people grow, work and age. A new systematic review published in the International Journal of Obesity examines how these forces may interact, asking whether socioeconomic position can alter the way genetic susceptibility to obesity appears across the life course.
The review focuses on the concept of gene–environment interaction, often abbreviated as G×E. This framework does not suggest that genes determine an inevitable body-weight outcome. Instead, it proposes that the influence of genetic variants may become stronger or weaker depending on environmental circumstances. A person carrying genetic variants associated with higher adiposity may not express that risk in the same way as someone with the same genetic profile but different access to nutritious food, safe places for physical activity, healthcare, education or financial resources.
Socioeconomic position is a particularly important environmental factor because it affects many of these conditions simultaneously. Researchers commonly measure it through education, household income, occupation and area-level deprivation. These measures are not interchangeable, but each can provide information about the resources and constraints that shape daily life. Lower socioeconomic position may be linked with greater exposure to food insecurity, chronic stress, demanding work schedules, limited recreational space and reduced access to preventive healthcare. Together, these pressures can influence sleep, diet, physical activity, metabolism and long-term weight gain.
The biological question is how such circumstances might modify inherited susceptibility. Genetic risk scores combine the effects of numerous DNA variants, each of which usually has a very small influence on body size. Many of these variants are involved in appetite regulation, satiety, brain reward pathways, adipocyte biology and energy expenditure. Their effects are therefore highly dependent on the surrounding environment. In a setting dominated by inexpensive, energy-dense foods and sedentary routines, genetic differences in hunger or food reward may be expressed more visibly than they would be in an environment that makes healthy choices easier.
The review also considers epigenetic profiles, which provide a possible molecular bridge between social experience and gene activity. Epigenetics refers to chemical and structural changes that influence whether genes are more or less active without altering the underlying DNA sequence. DNA methylation, histone modification and regulatory RNA molecules are among the mechanisms involved. Some epigenetic marks can respond to nutrition, stress, inflammation and other exposures. Researchers are investigating whether these marks help explain how socioeconomic conditions become biologically embedded and contribute to obesity risk.
That process may begin early. Pregnancy, infancy, childhood and adolescence are periods of rapid biological development in which environmental exposures can have lasting consequences. Maternal nutrition, prenatal stress, early feeding, household resources and childhood neighbourhood conditions may influence both later adiposity and the regulation of metabolic pathways. At the same time, genetic predisposition may affect how strongly an individual responds to these exposures. The life-course perspective is therefore essential: an interaction detected in childhood may not look the same in adulthood, and the effects of cumulative disadvantage may emerge only after years of exposure.
According to the review, existing research on these relationships remains fragmented. Studies differ in how they define socioeconomic position, calculate genetic susceptibility and measure obesity. Some examine body-mass index, while others focus on waist circumference, fat distribution or clinical obesity. Age ranges, ancestry groups, study designs and statistical models also vary widely. Epigenetic research introduces further complexity, because molecular signatures can differ across tissues, change over time and reflect both causal exposures and consequences of obesity itself.
These differences make it difficult to combine results or draw simple conclusions. A statistical association between low socioeconomic position, genetic risk and obesity does not automatically demonstrate a biological mechanism. Researchers must account for potential confounding factors, population structure, reverse causation and measurement error. Genetic studies have also historically overrepresented people of European ancestry, limiting the accuracy of genetic risk scores in other populations. The review’s life-course approach highlights the need for larger, more diverse studies that follow participants over time and collect repeated information on social conditions, behaviour, physiology and molecular changes.
The broader implication is that obesity prevention cannot be reduced to personal choice or genetic destiny. If socioeconomic conditions modify the expression of inherited risk, then interventions aimed only at individual behaviour may leave major drivers untouched. Policies that improve access to affordable nutritious food, quality education, stable housing, healthcare and safe environments could reduce obesity risk while also weakening the impact of genetic susceptibility. Understanding epigenetic pathways may eventually help identify sensitive periods for prevention, but it should not be used to label individuals or justify discrimination. The central message emerging from this field is that genetic liability is real, yet its expression remains shaped by society—and changing the environment may change the outcome.
Subject of Research: Socioeconomic position, genetic susceptibility and epigenetic profiles in obesity across the life course
Article Title: Socioeconomic position, genetic susceptibility, and epigenetic profiles in obesity across the life course: a systematic review
Article References: van Uhm, J., Meeusen, R.E.H., Jansen, P.R. et al. “Socioeconomic position, genetic susceptibility, and epigenetic profiles in obesity across the life course: a systematic review.” International Journal of Obesity (2026). https://doi.org/10.1038/s41366-026-02181-5
Image Credits: AI Generated
DOI: 10.1038/s41366-026-02181-5
Keywords: obesity, genetics, gene–environment interaction, socioeconomic position, epigenetics, life course, adiposity, public health, health inequality
Tags: environmental influences on obesity riskgene–environment interaction in obesitygenetic loci linked to body weightimpact of socioeconomic position on genetic susceptibilityinfluence of socioeconomic resources on gene expressionlife course influences on obesity developmentobesity gene-environment interactionsocioeconomic determinants of health and obesitysocioeconomic disparities in obesitysocioeconomic factors affecting epigenetic changessocioeconomic status and epigenetic modifications
