Abstract

Hypersexuality is now part of the DSM-V and has been defined as abnormally increased sexual activity. Epidemiological and clinical studies have shown that this non-paraphilic condition consists of “excessive” sexual behaviors and disorders accompanied by personal distress and social and medical morbidity. Hypersexual disorder is conceptualized as primarily a non-paraphilic sexual desire disorder with impulsivity. Pathophysiological perspectives include dysregulation of sexual arousal and desire, sexual impulsivity, sexual addiction, and sexual compulsivity. The nucleus accumbens, situated within the ventral striatum, mediates the reinforcing effects of drugs of abuse, such as cocaine, alcohol, nicotine, and food as well as music. Indeed, it is believed that this structure mandates behaviors elicited by incentive stimuli. These behaviors include natural rewards like feeding, drinking, sexual behavior, and exploratory locomotion. An essential rule of positive reinforcement is that motor responses will increase in magnitude and vigor if followed by a rewarding event. Here, we are hypothesizing that there is a common mechanism of action (MOA) for the powerful effects drugs, music, food, and sex have on human motivation. The human drive for the three necessary motivational behaviors “hunger, thirst, and sex” may all have common molecular genetic antecedents that, if impaired, lead to aberrant behaviors. We hypothesize that based on a plethora of scientific support hypersexual activity is indeed like drugs, food, and music that activate brain mesolimbic reward circuitry. Moreover, dopaminergic gene and possibly other candidate neurotransmitter-related gene polymorphisms affect both hedonic and anhedonic behavioral outcomes. There is little known about both the genetics and epigenetics of hypersexuality in the current literature. However, we anticipate that future studies based on assessments with clinical instruments combined with genotyping of sex addicts will provide evidence for specific clustering of sexual typologies with polymorphic associations. The authors are also encouraging both clinical and academic scientists to embark on research using neuroimaging tools to examine natural dopaminergic agonistic agents targeting specific gene polymorphisms to “normalize” hyper- or hyposexual response.

Highlights

  • BackgroundCertainly, hypersexual behavior has been documented within clinical and research settings over the past decade [1]

  • Sexual addiction is defined as any compulsive sexual behavior that interferes with normal living and causes severe stress on the family, friends, loved ones, and one's work environment

  • We are proposing hypersexuality disorder as a subtype of reward deficiency syndrome (RDS) sharing characteristics with substance and non-substance addictive behaviors with its clinical expression being partly affected by both genetics and epigenetics. Untested at this time, we propose shortterm FDA-approved medication-assisted treatments (MAT) favoring blocking dopamine function followed by gentle activation of dopaminergic pathways leading to long-term dopamine homeostasis

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Summary

Introduction

Hypersexual behavior has been documented within clinical and research settings over the past decade [1]. The basic tenant of these investigators suggested that hypersexuality constituted persistent socially deviant sexual behavior(s) in both males and females with excessive sexual appetite being maladaptive. In 1969, Allen suggested satyriasis for males and nymphomania in females supported by Ellis and Sagarin [6,7]. Since DSM-5 does not currently include "hypersexuality," we hereby encourage continued research into this very important area and applaud the major accomplishments of Kafka, Reid, Bancroft and even the World Health Organization among others [8,9,10,11]

Literature methodology
Conclusions
Disclosures
Rush B
Stroller RJ: Perversion
22. Basson R
Findings
27. Hanson RK
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