A global analysis shows how modern lifestyles erode microbial diversity, destabilize gut communities, and amplify immune stress signals, revealing hidden biological costs of industrialization.

Study: Industrialization drives convergent microbial and physiological shifts in the human metaorganism. Image Credit: MattL_Images / Shutterstock

*Important notice: bioRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
In a study posted to the bioRxiv preprint* server, an international team of researchers analyzed how lifestyle and levels of industrialization influence the structure of the human gut microbiome.
Their findings indicate links between industrialization and less diverse, more uniform microbiomes. Populations in more industrialized regions also showed signs of reduced community stability and heightened immune activity, including elevated gut stress markers.
How Industrialization Alters Microbiome Diversity
Industrialized lifestyles have repeatedly been associated with major shifts in the gut microbiome, including reduced diversity, altered microbial compositions, and distinct metabolic traits. But these patterns could reflect many confounding factors, such as diet, genetics, geography, immune status, infectious exposures, and inconsistent sampling.
Another open question is whether industrialization-linked microbiome changes destabilize microbial communities or influence host immune and inflammatory responses.
To resolve these issues, researchers require globally diverse populations and standardized, multidimensional microbiome and host datasets. The Global Microbiome Conservancy (GMbC) cohort was created to meet this need.
Global Microbiome Conservancy Cohort Design and Data Collection
The GMbC enrolled 1,015 healthy adults from 12 countries and 35 local populations, representing broad variation in age, BMI, ethnicity, environment, and subsistence strategies. Participants reported no chronic or infectious disease at enrollment. This design captured large gradients in industrialization, urbanization, and subsistence while documenting detailed dietary habits.
Shotgun metagenomic sequencing profiled taxonomic and functional features. Human genotyping defined genetic diversity and admixture. Researchers compiled extensive metadata on lifestyle, diet, environment, and demographics, then reduced it to principal components (PCs) representing industrialization, diet, and host genetics. These PCs informed association tests, multivariate models, and variance partitioning.
Statistical Models Reveal Lifestyle as the Strongest Microbiome Driver
Across the cohort, industrialization emerged as the single strongest determinant of gut microbiome structure. More industrialized populations showed markedly reduced alpha diversity and more homogenized community compositions, patterns observed across continents and within individual countries like Ghana and Cameroon.
Although diet, genetics, geography, age, sex, and BMI contributed meaningfully, industrialization (PC1-Lifestyle) explained the largest share of overall variation. Variance partitioning models showed these factors jointly explained up to 58% of beta diversity and allowed non-redundant effects to be separated.
Species-Level and Functional Shifts Associated With Lifestyle
Many bacterial species displayed consistent lifestyle-linked changes across multiple countries. While canonical “industrialization marker taxa” such as Bacteroides and Prevotella remained significant, others (e.g., Treponema, Akkermansia) lost significance after adjusting for confounders.
Functionally, 1,438 KEGG genes were more strongly associated with lifestyle than diet or genetics. Industrialized microbiomes were enriched in pathways including cobalamin (vitamin B12) biosynthesis and propanoyl-CoA metabolism, suggesting metabolic rewiring during lifestyle transitions.
Network Analyses Show Reduced Ecological Stability in Industrialized Microbiomes
Co-abundance network reconstruction showed that industrialized populations exhibited denser positive associations, fewer negative correlations, and decreased ecological stability, patterns consistent with lower resilience.
Despite the lower prevalence of gut eukaryotic protists in industrialized groups, IgA-sequencing revealed heightened immune activity. Although IgA-targeting patterns were broadly conserved across populations, specific taxa such as Phocaeicola vulgatus and Gemmiger OTUs showed lifestyle-associated differences.
Implications for Disease Models and Global Health Equity
The study highlights that microbiome-based disease prediction models developed in industrialized, primarily European cohorts do not generalize well to other populations. This underscores a significant equity gap and the need for globally representative clinical cohorts.
The elevated gut stress markers in industrialized populations raise the possibility that low-diversity microbiomes may influence physiological disruption or increase vulnerability to disease.
Complementary co-culture experiments from the same GMbC cohort support this hypothesis, showing amplified inflammatory responses to industrialized microbiomes.
Future Directions to Preserve Microbiome Diversity
The authors stress that some variation remains difficult to disentangle due to collinearity between diet and lifestyle. Future efforts will prioritize longitudinal sampling, regional capacity building, and context-specific interventions aimed at conserving global microbiome diversity.
Overall, expanding the GMbC framework will deepen mechanistic understanding, improve disease model accuracy, and ensure that microbiome science reflects diverse human experiences worldwide.

*Important notice: bioRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
Journal reference:
- Preliminary scientific report.
Poyet M., Rühlemann M., Schaan A.P., Ma Y., Moitinho-Silva L., Wacker E.M., Jebens H., Patel L., Nguyen L.T.T., Zimmer A., Plichta D., McDonald D., Stevens C., Agyei A., Afihene M.Y., Asibey S.O., Awuku Y.A., Badiane A.S., Ching L.S., Corzett C., Deme A., Dominguez-Rodrigo M., Duah A., Fezeu A., Froment A., Gibbons S., Girard C., Hooker J., Ibrahim F., Iqaluk D., Juimo V., Kettunen P., Lafosse S., Lango-Yaya E., Lehtimäki J., Lim Y.A.L., Mabulla A., Mahachai V., Mohamed R.S., Moniz K., Mwikarago I.E., Nartey Y.A., Ndiaye D., Noel M., Onyekwere C., Pin T.M., Plymoth A., Roberts L., Ruokolainen L., Rusine J., Segurel L., Shapiro B.J., Sigwazi S., Sistiaga A., Valles K., Vatanen T., Vilaichone R., Rosenstiel P., Baines J., Franke A., Ellinghaus D., Knight R., Daly M., Xavier R.J., Alm E.J., Groussin M. (2025). bioRxiv. DOI: 10.1101/2025.10.20.683358, https://www.biorxiv.org/content/10.1101/2025.10.20.683358v1