Background and Aims Pancreatic cancer is a malignant tumor with a very poor prognosis, and obesity, as a widespread health issue, is thought to be associated with various cancers. This study uses Mendelian randomization (MR) to analyze the causal relationship between obesity and pancreatic cancer to provide scientific evidence for preventing and intervening in pancreatic cancer.Methods Single nucleotide polymorphism (SNP) data for eight obesity-related anthropometric measures were downloaded from the IEU database as instrumental variables. Genome-wide association study (GWAS) data for pancreatic cancer were also obtained from the Finnish R10 database. The study employed inverse variance weighting (IVW), Mendelian randomization-Egger (MR-Egger), and Cochran's Q test to assess data heterogeneity. Potential causal relationships were further evaluated using IVW, MR-Egger, weighted median, weighted mode, Bayesian weighted Mendelian randomization, and constrained maximum likelihood Meta-analysis. MR-PRESSO and leave-one-out analyses were also used to identify and exclude outlier SNPs, ensuring result accuracy.Results Using 6 MR analysis methods to assess potential causal relationships, the study found that pancreatic cancer has a possible causal relationship with body mass index (BMI), basal metabolic rate, hip circumference, trunk fat mass, trunk fat-free mass, trunk predicted mass, and whole body fat-free mass (all P<0.05). No evidence of horizontal pleiotropy or heterogeneity was found. The consistent direction of β values across the 6 different MR analysis methods further confirmed that BMI, hip circumference, and trunk fat mass were positively correlated with an increased risk of pancreatic cancer, providing robustness to the results.Conclusion There is a causal relationship between obesity and pancreatic cancer, suggesting that improving obesity status may reduce the risk of pancreatic cancer.