Idiopathic intracranial hypertension (IIH) is a disease characterized by increased intracranial pressure (ICP) without identifiable secondary causes. While the increased ICP is a critical diagnostic feature, the underlying pathophysiological mechanisms remain unclear. Previous theories have suggested cerebrospinal fluid (CSF) overproduction, impaired reabsorption, or circulatory obstruction as potential causes. Emerging evidence indicates that IIH may not be solely a central nervous system disorder but also a systemic metabolic disorder. Metabolic and hormonal dysregulation features, including hyperleptinemia, adipocyte leptin hypersecretion, increased insulin resistance, and androgen excess, have been noted in IIH. Furthermore, the targeted blockade of the cortisol- producing enzyme 11 beta-hydroxysteroid dehydrogenase type 1 has demonstrated therapeutic potential in treating IIH. Consequently, the role of metabolic dysfunction and hormonal imbalance in IIH warrants consideration. This review aims to provide a comprehensive update on current theories regarding the mechanisms of metabolic dysfunction in IIH.