Abstract
Abstract Introduction Hypersexuality or Compulsive Sexual Behavior Disorder (CSBD) is characterized by a spectrum of sexual behaviors and fantasies marked by compulsion, obsession, and impulsivity. The pathophysiology of CSBD remains poorly understood despite the arousing of articles exploring the potential biomarkers associated with hypersexuality. Objective We aimed to review the literature regarding the investigation on CSBD pathophysiology from a neuroimaging, neuroendocrine and molecular perspective. Methods We raised papers related on neuroimaging, neuroendocrine and molecular biomarkers investigated in individuals that reached diagnosis of CSBD or similar, written in English language in the last 10 years, through PubMed, Scopus, and Web of Science with biomarkers and compulsive sexual behavior/hypersexuality key terms. Results Neuroimaging studies revealed the activation of the anterior cingulate cortex, ventral striatum, and amygdala, in individuals with CSBD. Neuroendocrine markers revealed abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis, including elevated adrenocorticotropic hormone (ACTH) levels and non-suppression of dexamethasone. Findings concerning the hypothalamic-pituitary-gonadal (HPG) axis, responsible for sexual function regulation, varied among CSBD individuals, including testosterone and luteinizing hormone (LH) levels. Oxytocin levels have been noted to rise in CSBD individuals and subsequently decrease following psychotherapy. Genetic and epigenetic markers associated with CSBD suggest involvement of addiction-related genes and epigenetic modifications near the corticotropin-releasing hormone (CRH) gene. Conclusion Most of the findings point to HPA axis alterations. Molecular analysis is in the beginning, as well as more research on the HPG axis is needed. The exploration of CSBD biomarkers potentially will provide insights into its pathophysiology, diagnosis, and treatment. Financing FAPESP.
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