Hypersexuality Addiction and Withdrawal: Phenomenology, Neurogenetics and Epigenetics

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.

Keywords: compulsivity; epigenetics; hypersexuality disorder; neurogenetics; reward deficiency syndrome.

Figure 1. A descriptive map of Hypersexuality Disorder as a subtype of RDS

The figure illustrates interactive neurogenetic and epigenetic effects. Both short-term dopamine blocking and long –term “dopaminergic – homeostasis” -based treatments and dopamine boosting therapies and daily activities are listed. Circles indicate RDS characteristics and boxes indicate RDS behaviors.