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      Neurochemical and Hormonal Contributors to Compulsive Sexual Behavior Disorder

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          Abstract  

          Purpose of Review

          Compulsive sexual behavior disorder has been recently included in the 11th revision of the International Classification of Diseases (ICD-11), and the possible contribution of neurochemical and hormonal factors have been reported. However, relatively little is known concerning the neurobiology underlying this disorder. The aim of this article is to review and discuss published findings in the area.

          Recent Findings

          Evidence suggests that the neuroendocrine systems are involved in the pathophysiology of compulsive sexual behavior. The hypothalamus-pituitary adrenal axis, the hypothalamus-pituitary–gonadal axis, and the oxytocinergic system have been implicated.

          Summary

          Further studies are needed to elucidate the exact involvement of neuroendocrine and hormonal systems in compulsive sexual behavior disorder. Prospective longitudinal studies are particularly needed, especially those considering co-occurring psychiatric disorders and obtaining hormonal assessments in experimental circumstances with appropriate control groups.

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          Most cited references83

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          Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse.

          Patrick McGowan, Aya Sasaki, Ana C D'Alessio … (2009)
          Maternal care influences hypothalamic-pituitary-adrenal (HPA) function in the rat through epigenetic programming of glucocorticoid receptor expression. In humans, childhood abuse alters HPA stress responses and increases the risk of suicide. We examined epigenetic differences in a neuron-specific glucocorticoid receptor (NR3C1) promoter between postmortem hippocampus obtained from suicide victims with a history of childhood abuse and those from either suicide victims with no childhood abuse or controls. We found decreased levels of glucocorticoid receptor mRNA, as well as mRNA transcripts bearing the glucocorticoid receptor 1F splice variant and increased cytosine methylation of an NR3C1 promoter. Patch-methylated NR3C1 promoter constructs that mimicked the methylation state in samples from abused suicide victims showed decreased NGFI-A transcription factor binding and NGFI-A-inducible gene transcription. These findings translate previous results from rat to humans and suggest a common effect of parental care on the epigenetic regulation of hippocampal glucocorticoid receptor expression.
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            Hypersexual disorder: a proposed diagnosis for DSM-V.

            Martin P. Kafka (2010)
            Hypersexual Disorder is proposed as a new psychiatric disorder for consideration in the Sexual Disorders section for DSM-V. Historical precedents describing hypersexual behaviors as well as the antecedent representations and proposals for inclusion of such a condition in the previous DSM manuals are reviewed. Epidemiological as well as clinical evidence is presented suggesting that non-paraphilic "excesses" of sexual behavior (i.e., hypersexual behaviors and disorders) can be accompanied by both clinically significant personal distress and social and medical morbidity. The research literature describing comorbid Axis I and Axis II psychiatric disorders and a purported relationship between Axis I disorders and Hypersexual Disorder is discussed. Based on an extensive review of the literature, Hypersexual Disorder is conceptualized as primarily a nonparaphilic sexual desire disorder with an impulsivity component. Specific polythetic diagnostic criteria, as well as behavioral specifiers, are proposed, intended to integrate empirically based contributions from various putative pathophysiological perspectives, including dysregulation of sexual arousal and desire, sexual impulsivity, sexual addiction, and sexual compulsivity.
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              The role of childhood trauma in the neurobiology of mood and anxiety disorders: preclinical and clinical studies.

              Christine Heim, Charles Nemeroff (2001)
              Epidemiologic studies indicate that children exposed to early adverse experiences are at increased risk for the development of depression, anxiety disorders, or both. Persistent sensitization of central nervous system (CNS) circuits as a consequence of early life stress, which are integrally involved in the regulation of stress and emotion, may represent the underlying biological substrate of an increased vulnerability to subsequent stress as well as to the development of depression and anxiety. A number of preclinical studies suggest that early life stress induces long-lived hyper(re)activity of corticotropin-releasing factor (CRF) systems as well as alterations in other neurotransmitter systems, resulting in increased stress responsiveness. Many of the findings from these preclinical studies are comparable to findings in adult patients with mood and anxiety disorders. Emerging evidence from clinical studies suggests that exposure to early life stress is associated with neurobiological changes in children and adults, which may underlie the increased risk of psychopathology. Current research is focused on strategies to prevent or reverse the detrimental effects of early life stress on the CNS. The identification of the neurobiological substrates of early adverse experience is of paramount importance for the development of novel treatments for children, adolescents, and adults.
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                Author and article information

                Contributors
                Andreas Chatzittofis: (View ORCID Profile)
                Journal
                Title: Current Addiction Reports
                Abbreviated Title: Curr Addict Rep
                Publisher: Springer Science and Business Media LLC
                ISSN (Electronic): 2196-2952
                Publication date Created: March 2022
                Publication date (Electronic): January 06 2022
                Publication date (Print): March 2022
                Volume: 9
                Issue: 1
                Pages: 23-31
                Article
                DOI: 10.1007/s40429-021-00403-6
                SO-VID: 8b021e66-b20e-4ac3-a2d0-c68b2c7c5a64
                Copyright © © 2022
                License:

                https://creativecommons.org/licenses/by/4.0

                https://creativecommons.org/licenses/by/4.0

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