Skip to main content
Dryad

Early life proteomic and microbiome features signal obesity risk across 26 years of follow-up

Data files

May 27, 2026 version files 3.62 MB

Click names to download individual files

Abstract

Early-life drivers of obesity are incompletely understood. Childhood obesity is rising globally, and yet few studies have examined the microbiome and proteome in early childhood, in relation to this outcome, and most are cross-sectional by design. Early-life factors in the ABIS birth cohort (n = 16,683) were associated with obesity up to age 26 (mean follow-up 25.3 years, range 23.7-26.5 years): psychosocial stressors, smoking, infections, and diet in the first year of life. Biological markers including the metabolome (n = 290) and proteome (n = 358) at birth and gut microbial at age one (n = 1,743) were assessed. Significant differences were found in infants with future obesity, including elevated ANGPTL4, FST, and HGF (independently of maternal weight) and reduced isocaproic acid, tryptophan, and oleic acid, with prenatal mediation. Akkermansia, asaccharolytic bacteria (Phascolarctobacterium and Senegalimassiliensia), and equol-producers (Adlercreutzia and Slackia) were depleted at age one. Machine learning models selecting the 40 most predictive features showed long-term prediction from birth proteomics and bacterial taxa at age one (AUC = 0.83 ± 0.05, n = 1,877) and additional metrics e.g., parental and child BMI in the first eight years (AUC = 0.89 ± 0.02, n = 1,877), suggesting durable biological encoding. The processed data (biological and metadata) used in the published study include 16S rRNA relative abundances (bac_ variables) and normalized Olink protein NPX values (NPX_ variables), as well as responses from the ABIS questionnaires. No identifiable information is included. The outcome variable is coded as 0/1 in meta_ObesitasDiag_2024. Collectively, our findings suggest clinically relevant biomarkers pointing to early-life regulation of bile acid metabolism, lipid storage vs. oxidation, and immune–metabolic signaling and paths to prospectively prevent childhood and adult-onset obesity, even across a 26-year predictive gap.