Sexual addiction

Addiction and dependence glossary[1][2][3][4]
• addiction – a medical condition characterized by compulsive engagement in rewarding stimuli despite adverse consequences
• addictive behavior – a behavior that is both rewarding and reinforcing
• addictive drug – a drug that is both rewarding and reinforcing
• dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
• drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
• drug withdrawal – symptoms that occur upon cessation of repeated drug use
• physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue and delirium tremens)
• psychological dependence – dependence that involves emotional–motivational withdrawal symptoms (e.g., dysphoria and anhedonia)
• reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
• rewarding stimuli – stimuli that the brain interprets as intrinsically positive or as something to be approached
• sensitization – an amplified response to a stimulus resulting from repeated exposure to it
• substance use disorder - a condition in which the use of substances leads to clinically and functionally significant impairment or distress
• tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose

Sexual addiction, also known as sex addiction, is a state characterized by compulsive participation or engagement in sexual activity, particularly sexual intercourse, despite negative consequences.[5] Proponents of a diagnostic model for sexual addiction, as defined here, consider it to be one of several sex-related disorders within an umbrella concept known as hypersexual disorder.[6] In clinical diagnostics, the term sexual dependence may also refer to a conceptual model that is used to assess people who report being unable to control their sexual urges, behaviors, or thoughts. Related models of pathological sexual behavior include hypersexuality, erotomania, nymphomania, satyriasis, Don Juanism (or Don Juanitaism), and paraphilia-related disorders.[7][8][9]

Clinicians, such as psychiatrists, sociologists, sexologists, and other specialists, have differing opinions on the classification and clinical diagnosis of sexual addiction. As a result, "sexual addiction" does not exist as a clinical entity in either the DSM or ICD medical classifications of diseases and medical disorders.

Neuroscientists, pharmacologists, molecular biologists, and other researchers in related fields have identified a transcriptional and epigenetic model of drug and behavioral (including sexual) addiction pathophysiology. Diagnostic models, which use the pharmacological model of addiction (this model associates addiction with drug-related concepts, particularly physical dependence, drug withdrawal, and drug tolerance),[10] do not currently include diagnostic criteria to identify sexual addictions in a clinical setting. In the alternative reward-reinforcement model of addiction, which uses neuropsychological concepts to characterize addictions, sexual addictions are identifiable and well-characterized.[11][12] In this model, addictive drugs are characterized as those which are both reinforcing and rewarding (i.e., activates neural pathways associated with reward perception).[10] Addictive behaviors (those which can induce a compulsive state) are similarly identified and characterized by their rewarding and reinforcing properties.

Mechanisms

Current research on sexual addiction within the context of the reward-reinforcement model indicates that it is well-characterized as an addiction[11][12] and that it develops through the same biomolecular mechanisms that induce drug addictions.[11][13] Specifically, sexual activity is an intrinsic reward that has been shown to act as a positive reinforcer, strongly activate the reward system, and induce the accumulation of ΔFosB in part of the striatum (specifically, the nucleus accumbens).[11][12][13] Chronic and excessive activation of certain pathways within the reward system and the accumulation of ΔFosB in a specific group of neurons within the nucleus accumbens has been directly implicated in the development of the compulsive behavior that characterizes addiction.[12][14][15][16]

In humans, a dopamine dysregulation syndrome, characterized by drug-induced compulsive engagement in sexual activity or gambling, has also been observed in some individuals taking dopaminergic medications.[11] Current experimental models of addiction to natural rewards and drug reward demonstrate common alterations in gene expression in the mesocorticolimbic projection.[11][17] ΔFosB is the most significant gene transcription factor involved in addiction, since its viral or genetic overexpression in the nucleus accumbens is necessary and sufficient for most of the neural adaptations and plasticity that occur;[17] it has been implicated in addictions to alcohol, cannabinoids, cocaine, nicotine, opioids, phenylcyclidine, and substituted amphetamines.[11][17][18] ΔJunD is the transcription factor which directly opposes ΔFosB.[17] Increases in nucleus accumbens ΔJunD expression can reduce or, with a large increase, even block most of the neural alterations seen in chronic drug abuse (i.e., the alterations mediated by ΔFosB).[17]

ΔFosB also plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise.[12][17] Natural rewards, like drugs of abuse, induce ΔFosB in the nucleus accumbens, and chronic acquisition of these rewards can result in a similar pathological addictive state.[11][12] Thus, ΔFosB is also the key transcription factor involved in addictions to natural rewards as well,[11][13] and sex addictions in particular, since ΔFosB in the nucleus accumbens is critical for the reinforcing effects of sexual reward.[12] Research on the interaction between natural and drug rewards suggests that psychostimulants and sexual reward possess cross-sensitization effects and act on common biomolecular mechanisms of addiction-related neuroplasticity which are mediated through ΔFosB.[11][13]

Summary of addiction-related plasticity
Form of neuroplasticity
or behavioral plasticity		 Type of reinforcer Sources
Opiates Psychostimulants High fat or sugar food Sexual intercourse Physical exercise
(aerobic)		 Environmental
enrichment
ΔFosB expression in
nucleus accumbens D1-type MSNs		 ↑ ↑ ↑ ↑ ↑ ↑ [11]
Behavioral plasticity
Escalation of intake Yes Yes Yes [11]
Psychostimulant
cross-sensitization		 Yes Not applicable Yes Yes Attenuated Attenuated [11]
Psychostimulant
self-administration		 ↑ ↑ ↓ ↓ ↓ [11]
Psychostimulant
conditioned place preference		 ↑ ↑ ↓ ↑ ↓ ↑ [11]
Reinstatement of drug-seeking behavior ↑ ↑ ↓ ↓ [11]
Neurochemical plasticity
CREB phosphorylation
in the nucleus accumbens		 ↓ ↓ ↓ ↓ ↓ [11]
Sensitized dopamine response
in the nucleus accumbens		 No Yes No Yes [11]
Altered striatal dopamine signaling ↓DRD2, ↑DRD3 ↑DRD1, ↓DRD2, ↑DRD3 ↑DRD1, ↓DRD2, ↑DRD3 ↑DRD2 ↑DRD2 [11]
Altered striatal opioid signaling No change or
↑μ-opioid receptors 		↑μ-opioid receptors
↑κ-opioid receptors 		↑μ-opioid receptors ↑μ-opioid receptors No change No change [11]
Changes in striatal opioid peptides ↑dynorphin
No change: enkephalin 		↑dynorphin ↓enkephalin ↑dynorphin ↑dynorphin [11]
Mesocorticolimbic synaptic plasticity
Number of dendrites in the nucleus accumbens ↓ ↑ ↑ [11]
Dendritic spine density in
the nucleus accumbens		 ↓ ↑ ↑ [11]

Diagnosis

DSM

The American Psychiatric Association (APA) publishes and periodically updates the Diagnostic and Statistical Manual of Mental Disorders (DSM), a widely recognized compendium of mental health diagnostics.[10]

The version published in 1987 (DSM-III-R), referred to "distress about a pattern of repeated sexual conquests or other forms of nonparaphilic sexual addiction, involving a succession of people who exist only as things to be used."[19] The reference to sexual addiction was subsequently removed.[20] The DSM-IV-TR, published in 2000 (DSM-IV-TR), did not include sexual addiction as a mental disorder.[21] The DSM-IV-TR included a miscellaneous diagnosis called sexual disorders not otherwise specified, stating: "distress about a pattern of repeated sexual relationships involving a succession of lovers who are experienced by the individual only as things to be used." (Other examples include: compulsive fixation on an unattainable partner, compulsive masturbation, compulsive love relationships, and compulsive sexuality in a relationship.)[21]

Some authors suggested that sexual addiction should be re-introduced into the DSM system;[22] however, sexual addiction was rejected for inclusion in the DSM-5, which was published in 2013.[23] Darrel Regier, vice-chair of the DSM-5 task force, said that "[A]lthough 'hypersexuality' is a proposed new addition...[the phenomenon] was not at the point where we were ready to call it an addiction." The proposed diagnosis does not make the cut as an official diagnosis due to a lack of research into diagnostic criteria for compulsive sexual behavior, according to the APA.[24][25]

Borderline personality disorder

The APA uses the Diagnostic and Statistical Manual of Mental Disorders to define and classify mental illnesses and in the DSM-IV version of the document, it lists borderline personality disorder (BPD) as an Axis II – Cluster B personality disorder with the code 301.83. The DSM-5 dropped the multiaxial system, but BPD still retains the same numerical code of 301.83.[24] The World Health Organization (WHO) produces the International Classification of Diseases (ICD) and lists BPD under the name "Emotionally unstable personality disorder". The latest version of the document (ICD-10) lists the disorder in Chapter X which is reserved for "Disorders of adult personality and behaviour" and has the code F60.3.[26] The Chinese Society of Psychiatry uses the Chinese Classification of Mental Disorders (CCMD), which is in its third edition (CCMD-3) and has a diagnosis of "Nonorganic sexual dysfunction" (numerical code 52.9), of which sexual promiscuity may be a symptom. Personality disorders, Habit and impulse disorders, Psychosexual disorders in the CCMD-3 fall in Chapter 6 and under code 6.60 are listed the personality disorders. The CCMD-3 lists "impulsive personality disorder" (numerical code 60.4),[27] which is equivalent to what the DSM refers to as "borderline personality disorder" and what the ICD-10 refers to as "emotionally unstable personality disorder". All three classification manuals and documents list sexual promiscuity as a prevalent and problematic symptom for patients with this particular pathology. Hypersexuality along with high-risk sexual behaviour, seductive behaviour, and promiscuity are an often due to the marked impulsivity common to this group of patients. Individuals with borderline personality disorder (emotionally unstable personality disorder or impulsive personality disorder) not only are prone to promiscuity, but in many cases, co-morbid paraphilias and fetishistic behaviour are commonly associated with their sexual behaviours. Common paraphilic compulsions among individuals with this diagnosis include urolagnia ("golden showers"), sadomasochism, voyeurism, autassassinophilia, partialism, and in some cases paraphilic drives may be more extreme and dangerous – such as erotophonophilia, necrophilia, biastophilia, pedophilia, and anthropophagy. Both males and females with this personality disorder often have a strong desire and compulsion to get involved in illicit sex, affairs, and relationships with married or otherwise pre-attached individuals. Consequently, individuals with borderline personality disorder often experience love and sexuality in perverse and violent qualities which they cannot integrate with the tender, intimate side of relationships.[28][29]

ICD

The World Health Organization produces the International Classification of Diseases (ICD), which is not limited to mental disorders. The most recent version of that document, ICD-10, includes "excessive sexual drive" as a diagnosis (code F52.8), subdividing it into satyriasis (for males) and nymphomania (for females).[30]

CCMD

The Chinese Society of Psychiatry produces the Chinese Classification of Mental Disorders (CCMD), which is currently in its third edition – the CCMD-3 and Chapter 5 of the document lists "Physiological disorders related to psychological factors" and under code 52 are disorders that are "Nonorganic sexual dysfuction," and within that category are listed a number of disorders, one of which is "other or unspecified sexual dysfunction" (numerical code 52.9).[31] This is roughly equivalent to the ICD-10 diagnosis of "other sexual dysfunction not due to a substance or known physiological condition" (specifier excessive sexual drive) (F52.8) and "unspecified sexual dysfunction not due to a substance or known physiological condition" (F52.9).[32]

Diagnostic criteria

Several mental health providers have proposed various, but similar, criteria for diagnosing sexual addiction, including Patrick Carnes,[33] and Aviel Goodman.[34] Dr. Carnes authored the first clinical book about sex addiction in 1983 based on his own empirical research. His diagnostic model is still largely utilized by the thousands of certified sex addiction therapists (CSATs) trained by the organization he founded.[35] No diagnostic proposal for sex addiction has been adopted into any official government diagnostic manual, however.

During the update of the Diagnostic and Statistical Manual to version 5 (DSM-5), the APA rejected two independent proposals for inclusion.

The International Classification of Diseases (ICD-10) of the WHO, however, does include an entry for "excessive sexual drive."[36] and another entry – applying to children and adolescants – "excessive masturbation"[37]

In 2011, the American Society of Addiction Medicine (ASAM), the largest medical consensus of physicians dedicated to treating and preventing addiction,[38] redefined addiction as a chronic brain disorder[39] which for the first time broadened the definition of addiction from substances to include addictive behaviors and reward-seeking, such as gambling and sex.[40]

Treatment

Behavioral therapy

Cognitive behavioral therapy is a common form of behavioral treatment for addictions and maladaptive behaviors in general.[41] Dialectical behavior therapy has been shown to improve treatment outcomes as well. Certified Sex Addiction Therapists (CSAT) – a group of sexual addiction therapists certified by the International Institute for Trauma and Addiction Professionals – offer specialized behavioral therapy designed specifically for sexual addiction.[35][42]

Twelve-step programs

Involvement in twelve-step programs for sex addiction can also serve as an adjunct therapy to supplement clinical treatment. Self-help groups exist in most of the developed world. Such programs include Sexaholics Anonymous, Sex Addicts Anonymous, Sex and Love Addicts Anonymous, Celebrate Recovery, and others.

Medications

Epidemiology

According to a systematic review from 2014, prevalence rates of sexual addiction and related sexual disorders ranges from 3% to 6%.[6]

History

Sex addiction as a term first emerged in the mid-1970s when various members of Alcoholics Anonymous sought to apply the principles of 12-steps toward sexual recovery from serial infidelity and other unmanageable compulsive sex behaviors that were similar to the powerlessness and un-manageability they experienced with alcoholism.[43] Multiple 12-step style self-help groups now exist for people who identify as sex addicts, including Sex Addicts Anonymous, Sexaholics Anonymous, Sex and Love Addicts Anonymous, and Sexual Compulsives Anonymous.

Society and culture

Controversy

External media
Images
The History and Rise of Sex and Love Addiction (INFOGRAPHIC)
Audio
Robert Weiss & David Ley. Is sex addiction a myth? // KPCC (25 April 2012, 9:29 am)
Video
Nicole Prause, Ph.D. (sexual physiologist). CBS (18 July 2013)

The controversy surrounding sexual addiction is centered around its identification, through a diagnostic model, in a clinical setting. As noted in current medical literature reviews, compulsive sexual behavior has been observed in humans;[11][12] drug-induced compulsive sexual behavior has also been noted clinically in some individuals taking dopaminergic drugs.[11] Moreover, current medical research involving neuropsychological models has identified sexual addictions (i.e., the compulsive engagement in sexual behavior despite negative consequences) as a true form of addiction (i.e., it possesses all the necessary characteristics to classify it as one) in animal models.[11][12] Since current diagnostic models use drug-related concepts as diagnostic criteria for addictions,[10] these are ill-suited for modelling compulsive behaviors in a clinical setting.[11] Consequently, diagnostic classification systems, such as the DSM, do not include sexual addiction as a diagnosis because there is currently "insufficient peer-reviewed evidence to establish the diagnostic criteria and course descriptions needed to identify these behaviors as mental disorders".[24] A 2014 systematic review on sexual addiction indicated that the "lack of empirical evidence on sexual addiction is the result of the disease's complete absence from versions of the Diagnostic and Statistical Manual of Mental Disorders."[6]

There have been debates regarding the definition and existence of sexual addictions for decades, as the issue was covered in a 1994 journal article.[44][45] According to a 2014 systematic review, sexual addiction (including excessive masturbation and pornography addiction) is a diagnosable behavioral addiction with estimable prevalence rates.[6] The Mayo Clinic considers sexual addiction to be a form of obsessive compulsive disorder and refer to it as sexual compulsivity (note that by definition, an addiction is a compulsion toward rewarding stimuli).[46] A paper dating back to 1988 and a journal comment letter published in 2006 asserted that sex addiction is itself a myth, a by-product of cultural and other influences.[47][48] The 1988 paper argued that the condition is instead a way of projecting social stigma onto patients.[47]

In a non-academic opinion report from 2003, Marty Klein, stated that "the concept of sex addiction provides an excellent example of a model that is both sex-negative and politically disastrous."[49]:8 Klein singled out a number of features that he considered crucial limitations of the sex addiction model[49]:8 and stated that the diagnostic criteria for sexual addiction are easy to find on the internet.[49]:9 Drawing on the Sexual Addiction Screening Test, he stated that "the sexual addiction diagnostic criteria make problems of nonproblematic experiences, and as a result pathologize a majority of people."[49]:10

Popular culture

Sexual addiction has been the main theme in films such as 2001 film Diary of a Sex Addict, 2005 film I Am a Sex Addict, 2006 film Black Snake Moan, 2008 film Confessions of a Porn Addict, 2011 film Shame, 2012 film Thanks for Sharing, and others.

See also

References

  1. ↑ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN 9780071481274.
  2. ↑ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681Freely accessible. PMID 24459410.
  3. ↑ "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February 2015.
  4. ↑ Volkow ND, Koob GF, McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". N. Engl. J. Med. 374 (4): 363–371. doi:10.1056/NEJMra1511480. PMID 26816013.
  5. ↑ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–365, 375. ISBN 9780071481274. The defining feature of addiction is compulsive, out-of-control drug use, despite negative consequences. ...
    compulsive eating, shopping, gambling, and sex–so-called "natural addictions"– ... Indeed, addiction to both drugs and behavioral rewards may arise from similar dysregulation of the mesolimbic dopamine system.
  6. 1 2 3 4 Karila L, Wéry A, Weinstein A, Cottencin O, Petit A, Reynaud M, Billieux J (2014). "Sexual addiction or hypersexual disorder: different terms for the same problem? A review of the literature". Curr. Pharm. Des. 20 (25): 4012–20. doi:10.2174/13816128113199990619. PMID 24001295. Sexual addiction, which is also known as hypersexual disorder, has largely been ignored by psychiatrists, even though the condition causes serious psychosocial problems for many people. A lack of empirical evidence on sexual addiction is the result of the disease's complete absence from versions of the Diagnostic and Statistical Manual of Mental Disorders. ... Existing prevalence rates of sexual addiction-related disorders range from 3% to 6%. Sexual addiction/hypersexual disorder is used as an umbrella construct to encompass various types of problematic behaviors, including excessive masturbation, cybersex, pornography use, sexual behavior with consenting adults, telephone sex, strip club visitation, and other behaviors. The adverse consequences of sexual addiction are similar to the consequences of other addictive disorders. Addictive, somatic and psychiatric disorders coexist with sexual addiction. In recent years, research on sexual addiction has proliferated, and screening instruments have increasingly been developed to diagnose or quantify sexual addiction disorders. In our systematic review of the existing measures, 22 questionnaires were identified. As with other behavioral addictions, the appropriate treatment of sexual addiction should combine pharmacological and psychological approaches.
  7. ↑ Coleman, Eli (June–July 2003). "Compulsive Sexual Behavior: What to Call It, How to Treat It?" (PDF). SIECUS Report. The Debate: Sexual Addiction and Compulsion. ProQuest Academic Research Library. 31 (5): 12–16. Retrieved 15 October 2012.
  8. ↑ Coleman, E. (2011). "Chapter 28. Impulsive/compulsive sexual behavior: Assessment and treatment". In Grant, Jon E.; Potenza, Marc N. The Oxford Handbook of Impulse Control Disorders. New York: Oxford University Press. p. 375. ISBN 9780195389715.
  9. ↑ Carnes, Patrick (1994). Contrary to Love: Helping the Sexual Addict. Hazelden Publishing. p. 28. ISBN 1568380593.
  10. 1 2 3 4 Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–368. ISBN 9780071481274. The defining feature of addiction is compulsive, out-of-control drug use, despite negative consequences. ...Addictive drugs are both rewarding and reinforcing. A reward is a stimulus that the brain interprets as intrinsically positive or as something to be approached. A reinforcing stimulus is one that increases the probability that behaviors paired with it will be repeated. Not all reinforcers are rewarding; for example, a negative or punishing stimulus might reinforce avoidance behaviors. ... Familiar pharmacologic terms such as tolerance, dependence, and sensitization are useful in describing some of the time-dependent processes that underlie addiction. ...
    Dependence is defined as an adaptive state that develops in response to repeated drug administration, and is unmasked during withdrawal, which occurs when drug taking stops. Dependence from long-term drug use may have both a somatic component, manifested by physical symptoms, and an emotional–motivation component, manifested by dysphoria. While physical dependence and withdrawal occur with some drugs of abuse (opiates, ethanol), these phenomena are not useful in the diagnosis of addiction because they do not occur with other drugs of abuse (cocaine, amphetamine) and can occur with many drugs that are not abused (propranolol, clonidine). The official diagnosis of drug addiction by the Diagnostic and Statistic Manual of Mental Disorders (2000), which makes distinctions between drug use, abuse, and substance dependence, is flawed. First, diagnosis of drug use versus abuse can be arbitrary and reflect cultural norms, not medical phenomena. Second, the term substance dependence implies that dependence is the primary pharmacologic phenomenon underlying addiction, which is likely not true, as tolerance, sensitization, and learning and memory also play central roles. It is ironic and unfornate that the Manual avoids use of the term addiction, which provides the best description of the clinical syndrome.
  11. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. 61 (7): 1109–1122. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704Freely accessible. PMID 21459101. Cross-sensitization is also bidirectional, as a history of amphetamine administration facilitates sexual behavior and enhances the associated increase in NAc DA ... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. The transcription factor delta FosB is increased in the NAc, PFC, dorsal striatum, and VTA following repeated sexual behavior (Wallace et al., 2008; Pitchers et al., 2010b). This natural increase in delta FosB or viral overexpression of delta FosB within the NAc modulates sexual performance, and NAc blockade of delta FosB attenuates this behavior (Hedges et al, 2009; Pitchers et al., 2010b). Further, viral overexpression of delta FosB enhances the conditioned place preference for an environment paired with sexual experience (Hedges et al., 2009). ... In some people, there is a transition from "normal" to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a). ... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex (Evans et al, 2006; Aiken, 2007; Lader, 2008)."Table 1"
  12. 1 2 3 4 5 6 7 8 9 Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M (2012). "Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms". J. Psychoactive Drugs. 44 (1): 38–55. doi:10.1080/02791072.2012.662112. PMC 4040958Freely accessible. PMID 22641964. It has been found that deltaFosB gene in the NAc is critical for reinforcing effects of sexual reward. Pitchers and colleagues (2010) reported that sexual experience was shown to cause DeltaFosB accumulation in several limbic brain regions including the NAc, medial pre-frontal cortex, VTA, caudate, and putamen, but not the medial preoptic nucleus. Next, the induction of c-Fos, a downstream (repressed) target of DeltaFosB, was measured in sexually experienced and naive animals. The number of mating-induced c-Fos-IR cells was significantly decreased in sexually experienced animals compared to sexually naive controls. Finally, DeltaFosB levels and its activity in the NAc were manipulated using viral-mediated gene transfer to study its potential role in mediating sexual experience and experience-induced facilitation of sexual performance. Animals with DeltaFosB overexpression displayed enhanced facilitation of sexual performance with sexual experience relative to controls. In contrast, the expression of DeltaJunD, a dominant-negative binding partner of DeltaFosB, attenuated sexual experience-induced facilitation of sexual performance, and stunted long-term maintenance of facilitation compared to DeltaFosB overexpressing group. Together, these findings support a critical role for DeltaFosB expression in the NAc in the reinforcing effects of sexual behavior and sexual experience-induced facilitation of sexual performance. ... both drug addiction and sexual addiction represent pathological forms of neuroplasticity along with the emergence of aberrant behaviors involving a cascade of neurochemical changes mainly in the brain's rewarding circuitry.
  13. 1 2 3 4 Pitchers KK, Vialou V, Nestler EJ, Laviolette SR, Lehman MN, Coolen LM (February 2013). "Natural and drug rewards act on common neural plasticity mechanisms with ΔFosB as a key mediator". J. Neurosci. 33 (8): 3434–3442. doi:10.1523/JNEUROSCI.4881-12.2013. PMC 3865508Freely accessible. PMID 23426671. Drugs of abuse induce neuroplasticity in the natural reward pathway, specifically the nucleus accumbens (NAc), thereby causing development and expression of addictive behavior. ... Together, these findings demonstrate that drugs of abuse and natural reward behaviors act on common molecular and cellular mechanisms of plasticity that control vulnerability to drug addiction, and that this increased vulnerability is mediated by ΔFosB and its downstream transcriptional targets. ... Sexual behavior is highly rewarding (Tenk et al., 2009), and sexual experience causes sensitized drug-related behaviors, including cross-sensitization to amphetamine (Amph)-induced locomotor activity (Bradley and Meisel, 2001; Pitchers et al., 2010a) and enhanced Amph reward (Pitchers et al., 2010a). Moreover, sexual experience induces neural plasticity in the NAc similar to that induced by psychostimulant exposure, including increased dendritic spine density (Meisel and Mullins, 2006; Pitchers et al., 2010a), altered glutamate receptor trafficking, and decreased synaptic strength in prefrontal cortex-responding NAc shell neurons (Pitchers et al., 2012). Finally, periods of abstinence from sexual experience were found to be critical for enhanced Amph reward, NAc spinogenesis (Pitchers et al., 2010a), and glutamate receptor trafficking (Pitchers et al., 2012). These findings suggest that natural and drug reward experiences share common mechanisms of neural plasticity
  14. ↑ Koob GF, Volkow ND (August 2016). "Neurobiology of addiction: a neurocircuitry analysis". Lancet Psychiatry. 3 (8): 760–773. doi:10.1016/S2215-0366(16)00104-8. PMID 27475769. Drug addiction represents a dramatic dysregulation of motivational circuits that is caused by a combination of exaggerated incentive salience and habit formation, reward deficits and stress surfeits, and compromised executive function in three stages. The rewarding effects of drugs of abuse, development of incentive salience, and development of drug-seeking habits in the binge/intoxication stage involve changes in dopamine and opioid peptides in the basal ganglia. The increases in negative emotional states and dysphoric and stress-like responses in the withdrawal/negative affect stage involve decreases in the function of the dopamine component of the reward system and recruitment of brain stress neurotransmitters, such as corticotropin-releasing factor and dynorphin, in the neurocircuitry of the extended amygdala. The craving and deficits in executive function in the so-called preoccupation/anticipation stage involve the dysregulation of key afferent projections from the prefrontal cortex and insula, including glutamate, to the basal ganglia and extended amygdala. Molecular genetic studies have identified transduction and transcription factors that act in neurocircuitry associated with the development and maintenance of addiction that might mediate initial vulnerability, maintenance, and relapse associated with addiction. ... Substance-induced changes in transcription factors can also produce competing effects on reward function.141 For example, repeated substance use activates accumulating levels of ΔFosB, and animals with elevated ΔFosB exhibit exaggerated sensitivity to the rewarding effects of drugs of abuse, leading to the hypothesis that ΔFosB might be a sustained molecular trigger or switch that helps initiate and maintain a state of addiction.141,142
  15. ↑ Ruffle JK (November 2014). "Molecular neurobiology of addiction: what's all the (Δ)FosB about?". Am. J. Drug Alcohol Abuse. 40 (6): 428–437. doi:10.3109/00952990.2014.933840. PMID 25083822.
    The strong correlation between chronic drug exposure and ΔFosB provides novel opportunities for targeted therapies in addiction (118), and suggests methods to analyze their efficacy (119). Over the past two decades, research has progressed from identifying ΔFosB induction to investigating its subsequent action (38). It is likely that ΔFosB research will now progress into a new era – the use of ΔFosB as a biomarker. ...

    Conclusions
    ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a ‘‘molecular switch’’ (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction.
  16. ↑ Biliński P, Wojtyła A, Kapka-Skrzypczak L, Chwedorowicz R, Cyranka M, Studziński T (2012). "Epigenetic regulation in drug addiction". Ann. Agric. Environ. Med. 19 (3): 491–496. PMID 23020045. For these reasons, ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence. These newly constructed networks function very efficiently via new pathways as soon as drugs of abuse are further taken ... In this way, the induction of CDK5 gene expression occurs together with suppression of the G9A gene coding for dimethyltransferase acting on the histone H3. A feedback mechanism can be observed in the regulation of these 2 crucial factors that determine the adaptive epigenetic response to cocaine. This depends on ΔFosB inhibiting G9a gene expression, i.e. H3K9me2 synthesis which in turn inhibits transcription factors for ΔFosB. For this reason, the observed hyper-expression of G9a, which ensures high levels of the dimethylated form of histone H3, eliminates the neuronal structural and plasticity effects caused by cocaine by means of this feedback which blocks ΔFosB transcription
  17. 1 2 3 4 5 6 Nestler EJ (December 2012). "Transcriptional mechanisms of drug addiction". Clin. Psychopharmacol. Neurosci. 10 (3): 136–143. doi:10.9758/cpn.2012.10.3.136. PMC 3569166Freely accessible. PMID 23430970. ΔFosB has been linked directly to several addiction-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states.
  18. ↑ Kanehisa Laboratories (2 August 2013). "Alcoholism – Homo sapiens (human)". KEGG Pathway. Retrieved 10 April 2014.
  19. ↑ American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders (3rd ed., rev.). Washington, DC: Author.
  20. ↑ Kafka, M. P. (2010). "Hypersexual Disorder: A proposed diagnosis for DSM-V" (PDF). Archives of Sexual Behavior. 39 (2): 377–400. doi:10.1007/s10508-009-9574-7. PMID 19937105.
  21. 1 2 American Psychiatric Association. (2000). Diagnostic and Statistical Manual of Mental Disorders (fourth edition, text revision). Washington, DC: Author.
  22. ↑ Irons, R.; Irons, J. P. (1996). "Differential diagnosis of addictive sexual disorders using the DSM-IV". Sexual Addiction & Compulsivity. 3: 7–21. doi:10.1080/10720169608400096.
  23. ↑ Psychiatry's bible: Autism, binge-eating updates proposed for 'DSM' USA Today.
  24. 1 2 3 American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. pp. 481, 797–798. ISBN 978-0-89042-555-8. Thus, groups of repetitive behaviors, which some term behavioral addictions, with such subcategories as "sex addiction," "exercise addiction," or "shopping addiction," are not included because at this time there is insufficient peer-reviewed evidence to establish the diagnostic criteria and course descriptions needed to identify these behaviors as mental disorders.
  25. ↑ Rachael Rettner (6 December 2012). "'Sex Addiction' Still Not Official Disorder". LiveScience. Retrieved 2 January 2013.
  26. ↑ "International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10) Version for 2010". International Statistical Classification of Diseases and Related Health Problems. World Health Organization. Retrieved 3 July 2014.
  27. ↑ "CCMD-3". Chinese Society of Psychiatry. Chinese Classification of Mental Disorders (third edition). Retrieved 3 July 2014.
  28. ↑ Mitchell, Stephen (1995). Freud and Beyond: A History of Modern Psychoanalytic Thought. New York: Basic Books. ISBN 978-0-465-01405-7.
  29. ↑ Hull J. W.; Clarkin J. F.; Yeomans F. (1993). "Borderline personality disorder and impulsive sexual behavior". Psychiatric Services. 44 (10): 1000–1001. doi:10.1176/ps.44.10.1000.
  30. ↑ International Classification of Diseases Expert Coding Manual for Physicians, 2016 update.
  31. ↑ "Chinese Society of Psychiatry". Chinese Classification of Mental Disorders (CCMD). Ministry of Health. Retrieved 3 July 2014.
  32. ↑ "ICD-10-CM – 2016 update". Retrieved 2 March 2016.
  33. ↑ Patrick Carnes; David Delmonico; Elizabeth Griffin (2001). In the Shadows of the Net. p. 31. ISBN 1-59285-149-5.
  34. ↑ Goodman, Aviel (1998). Sexual Addiction: An Integrated Approach. Madison, Connecticut: International Universities Press. pp. 233–234. ISBN 978-0-8236-6063-6
  35. 1 2 IITAP Official Website
  36. ↑ "2012 ICD-10 Diagnosis Code F52.7 : Excessive sexual drive". Retrieved 22 February 2013.
  37. ↑ "2012 ICD-10-CM Diagnosis Code F98.8 : Other specified behavioral and emotional disorders with onset usually occurring in childhood and adolescence". Icd10data.com. Retrieved 22 June 2012.
  38. ↑ "2011 New definition of addiction: Addiction is a chronic brain disease, not just bad behavior or bad choices". Retrieved 15 August 2011.
  39. ↑ "2011 Addiction Now Defined As Brain Disorder, Not Behavior Issue". Retrieved 15 August 2011.
  40. ↑ "2011 ASAM: The Definition of Addiction". Retrieved 12 April 2011.
  41. ↑ Hollon SD, Beck AT (2013). "Chapter 11 Cognitive and Cognitive-Behavioral Therapies". In MJ Lambert. Bergin and Garfield's Handbook of Psychotherapy and Behavior Change (6th ed.). Hoboken, NJ: John Wiley & Sons. pp. 393–394. ISBN 9781118418680.
  42. ↑ Stefanie Carnes. Mending a Shattered Heart: A Guide for Partners of Sex Addicts. Gentle Path Press; Second Edition. (4 October 2011) page 139 ISBN 978-0-9826505-9-2
  43. ↑ Augustine Fellowship (June 1986). Sex and Love Addicts Anonymous. Augustine Fellowship. ISBN 0-9615701-1-3. OCLC 13004050.
  44. ↑ Francoeur, R. T. (1994). Taking sides: Clashing views on controversial issues in human sexuality, p. 25. Dushkin Pub. Group.
  45. ↑ Kingston, D. A.; Firestone, P. (2008). "Problematic hypersexuality: A review of conceptualization and diagnosis". Sexual Addiction and Compulsivity. 15 (4): 284–310. doi:10.1080/10720160802289249.
  46. ↑ Mayo Clinic Website
  47. 1 2 Levine, M. P.; Troiden, R. R. (1988). "The myth of sexual compulsivity". Journal of Sex Research. 25 (3): 347–363. doi:10.1080/00224498809551467.
  48. ↑ Giles, J. (2006). "No such thing as excessive levels of sexual behavior". Archives of Sexual Behavior. 35 (6): 641–642. doi:10.1007/s10508-006-9098-3. PMID 17109229.
  49. 1 2 3 4 Klein, Marty (June–July 2003). "Sex Addiction: A Dangerous Clinical Concept" (PDF). SIECUS Report. ProQuest Academic Research Library. 31 (5): 8–11. Retrieved 15 October 2012.

Further reading

There are several books which offer overview history and treatment techniques for sexual addiction, including the following
There are also books focusing on partners of sex addicts
The interested reader can find discussions of the concept of sexual addiction in

External links

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