Obesity is a multifactorial condition influenced by genetic predisposition, environmental factors, and epigenetic changes. Although studies have identified key genes such as LEP, POMC, and MC4R associated with monogenic obesity, most cases are polygenic and shaped by dynamic gene–environment interactions. Epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNA activity, mediate the relationship between environmental factors and genetic expression. Adverse childhood experiences (ACEs) have emerged as significant contributors to obesity through their impact on stress-regulatory pathways, particularly involving the hypothalamus–pituitary–adrenal (HPA) axis. Epigenetic modifications in stress-regulating genes such as NR3C1 and FKBP5 influence cortisol regulation and metabolic responses, while neurotrophic factors like brain-derived neurotrophic factor (BDNF) modulate neural plasticity and metabolic balance. This review synthesizes current evidence linking epigenetic changes associated with ACEs to obesity and highlights mechanisms like FKBP5 hypermethylation, NR3C1 dysregulation, and BDNF modulation. Understanding these pathways may facilitate targeted interventions for mitigating the long-term health impacts of early-life adversity and obesity.