ArticlePediatric research2026
Genetically mediated causal relationship between gut microbiota composition and childhood obesity.
Article in Pediatric research, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGut microbiota (GM) plays a critical role in maintaining human health and modulating the pathogenesis of various diseases. This study aimed to investigate the causal relationship between gut microbiota and childhood obesity using Mendelian randomization.
methodsIn accordance with preset thresholds, independent genetic loci significantly related to the relative abundance of GM were extracted as instrumental variables using GM genome-wide association study (GWAS) data from the MiBioGen database and childhood obesity GWAS data from the IEU Open GWAS database. Inverse variance weighting was used to examine the causal relationship between GM and childhood obesity.
resultsAn increase in Akkermansia and Butyricimonas abundance can reduce the risk of obesity in children (OR = 0.476, 95% CI: 0.311-0.726, P = 0.001; OR = 0.682, 95% CI: 0.471-0.990, P = 0.044). Ruminiclostridium9 abundance increased the risk of childhood obesity (OR = 2.051, 95% CI: 1.069-3.932, P = 0.031).
conclusionBeneficial GM members Akkermansia and Butyricimonas were positively associated with reduced obesity risk in children. Ruminiclostridium 9 was identified as a potential risk factor for childhood obesity. This study provides genetic evidence supporting a potential causal relationship between GM composition and childhood obesity, offering valuable insights for future research and preventive intervention strategies. IMPACT: Gut microbiota (GM) plays a critical role in maintaining human health and modulating the pathogenesis of various diseases. GM-based interventions have emerged as promising therapeutic approaches for childhood obesity. This study aimed to investigate the causal relationship between gut microbiota and childhood obesity using Mendelian randomization methods, thereby providing genetic evidence to support the potential of GM-targeted strategies in the prevention and management of this condition. The findings reinforce prior observational evidence by demonstrating a causal association between specific gut microbial taxa and childhood obesity. These results provide valuable insights that may guide future research and the development of novel therapeutic interventions.
Identifiers
41882376What OpenQuestion 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 OpenQuestion graph.