Hypomania is a mood state characterized by elevated energy, impulsivity, and heightened goal-directed activity, which often manifests in the context of Bipolar Disorder Type II and Cyclothymic Disorder, but also presents independently. Recent research suggests that epigenetic mechanisms may play a significant role in the development of hypomania via their influence on dopamine metabolism control and neural plasticity. This study employs a self-modeling adaptive network model to simulate and computationally analyse the epigenetic mechanisms contributing to hypomania adaptation at five adaptation levels, ranging from neurotransmitter activity and protein expression to DNA methylation and epigenetic alteration. The model has a specific focus on the COMT gene that is considered to have a key role in dopamine regulation. Simulation experiments were conducted, demonstrating how environmental stressors such as sleep deprivation, life changes, and charged atmospheres may trigger long-term epigenetic changes, causing dysregulation of prefrontal cortex, amygdala, and dopamine pathways. The results highlight how stable epigenetic changes can maintain a degree of dopaminergic hyperactivity that generates and perpetuates hypomanic episodes. In this sense the model is in line with qualitative empirical information from the literature. Further research may address the specific role of the COMT gene in hypomania in more depth and getting numerical empirical data enabling quantitative validation as well. By integrating epigenetics, neurobiology, and computational modeling, this research offers a novel framework for the computational analysis of hypomania and a foundation for the exploration of its underlying mechanisms and new therapeutic targets in the future.