Obesity is a recognized risk factor for VTE in both children and adults. However, the causal relationship between childhood obesity and the risk of VTE in adulthood remains unclear. This study conducted a bidirectional 2-sample Mendelian randomization (MR) analysis using genome-wide association study data to explore this association. The inverse-variance weighting (IVW) method, along with weighted median and MR-Egger approaches, was employed to assess causality, while linkage disequilibrium score regression (LDSC) evaluated genetic correlations. Sensitivity analyses, including Cochran Q statistics, the MR-Egger intercept test, MR-PRESSO, and leave-one-out analysis, ensured the robustness of the findings. In the forward MR analysis, the IVW analysis identified a significant causal association between childhood body mass index (BMI) and UBK_VTE (OR: 1.005, 95% CI: 1.000-1.008, P = .002), FinnGen_VTE (OR: 1.303, 95% CI: 1.175-1.446, P < .001), FinnGen_pulmonary embolism (PE) (OR: 1.265, 95% CI: 1.079-1.484, P = .004) and FinnGen_deep vein thrombosis (DVT) (OR: 1.345, 95% CI: 1.145-1.58, P < .001). The results remained consistent across different MR methods, with no evidence of pleiotropy or heterogeneity. Reverse MR analysis showed that VTE, including PE and DVT, had no causal effect on childhood obesity. LDSC analysis further confirmed significant genetic correlations between childhood BMI and VTE outcomes (FinnGen_VTE [rg = 0.28, P = 2.21 × 10-7], FinnGen_PE [rg = 0.24, P = 8.62 × 10-5], and FinnGen_DVT [rg = 0.27, P = 1.79 × 10-5]). In conclusion, these findings provide genetic evidence that childhood obesity increases the risk of developing VTE in adulthood, emphasizing the need for early prevention and weight management strategies. Further studies are required to explore underlying biological mechanisms and assess the impact of obesity interventions on VTE risk reduction.