Sexual addiction(Redirected from Sexual compulsivity)
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Sexual addiction, also known as sex addiction, is characterized as a state of compulsive participation or engagement in sexual activity, particularly sexual intercourse, despite negative consequences.
|Addiction and dependence glossary|
Proponents of a diagnostic model for sexual addiction consider it to be one of several sex-related disorders within an umbrella concept known as hypersexual disorder. The term sexual dependence is also used to refer to people who report being unable to control their sexual urges, behaviors, or thoughts. Related or synonymous models of pathological sexual behavior include hypersexuality (nymphomania and satyriasis), erotomania, Don Juanism (or Don Juanitaism), and paraphilia-related disorders.
The concept of sexual addiction is contentious. There is considerable debate among psychiatrists, psychologists, sexologists, and other specialists whether compulsive sexual behavior constitutes an addiction, and therefore its classification and possible diagnosis. Animal research has been established that compulsive sexual behavior arises from the same transcriptional and epigenetic mechanisms that mediate drug addiction in laboratory animals; however, as of 2018,[update] sexual addiction is not a clinical diagnosis in either the DSM or ICD medical classifications of diseases and medical disorders. Some argue that applying such concepts to normal behaviors such as sex, can be problematic, and suggest that applying medical models such as addiction to human sexuality can serve to pathologise normal behavior and cause harm.
The ICD-11 created a new condition classification, compulsive sexual behavior, to cover " a persistent pattern of failure to control intense, repetitive sexual impulses or urges resulting in repetitive sexual behaviour".
None of the official diagnostic classification frameworks list "sexual addiction" as a distinct disorder.
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.
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." The reference to sexual addiction was subsequently removed. The DSM-IV-TR, published in 2000 (DSM-IV-TR), did not include sexual addiction as a mental disorder.
Some authors suggested that sexual addiction should be re-introduced into the DSM system; however, sexual addiction was rejected for inclusion in the DSM-5, which was published in 2013. 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.
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 F52.7), subdividing it into satyriasis (for males) and nymphomania (for females). However, the ICD categorizes these diagnoses as compulsive behaviors or impulse control disorders and not addiction. The most recent version of that document, ICD-11, includes "compulsive sexual behavior disorder" as a diagnosis (code 6C72)—it does not use the addiction model.
The Chinese Society of Psychiatry produces the Chinese Classification of Mental Disorders (CCMD), which is currently in its third edition – the CCMD-3 does not include sexual addiction as a diagnosis.
Other diagnostic criteria
Some mental health providers have proposed various, but similar, criteria for diagnosing sexual addiction, including Patrick Carnes, and Aviel Goodman. 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. 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.
In 2011, the American Society of Addiction Medicine (ASAM), the largest medical consensus of physicians dedicated to treating and preventing addiction, redefined addiction as a chronic brain disorder, which for the first time broadened the definition of addiction from substances to include addictive behaviors and reward-seeking, such as gambling and sex.
Borderline personality disorder
The ICD, DSM and CCMD list promiscuity as a prevalent and problematic symptom for Borderline Personality Disorder. Individuals with this diagnosis sometimes engage in sexual behaviors that can appear out of control, distressing the individual or attracting negative reactions from others. There is therefore a risk that a person presenting with sex addiction, may in fact be suffering from Borderline Personality Disorder. This may lead to inappropriate or incomplete treatment.
Medical reviews and position statements
In November 2016, the American Association of Sexuality Educators, Counselors and Therapists (AASECT), the official body for sex and relationship therapy in the United States, issued a position statement on Sex Addiction that states that AASECT, "...does not find sufficient empirical evidence to support the classification of sex addiction or porn addiction as a mental health disorder, and does not find the sexual addiction training and treatment methods and educational pedagogies to be adequately informed by accurate human sexuality knowledge. Therefore, it is the position of AASECT that linking problems related to sexual urges, thoughts or behaviors to a porn/sexual addiction process cannot be advanced by AASECT as a standard of practice for sexuality education delivery, counseling or therapy."
In 2017, three new USA sexual health organizations found no support for the idea that sex or adult films were addictive in their position statement.
In November 16, 2017 the Association for the Treatment of Sexual Abusers (ATSA) published a position against sending sex offenders to sex addiction treatment facilities. Those centers argued that "illegal" behaviors were symptoms of sex addiction, which ATSA challenged they had no scientific evidence to support.
As of 2017, none of the official regulatory bodies for Psychosexual Counselling or Sex and Relationship therapy, have accepted sex addiction as a distinct entity with associated treatment protocols. Indeed, some practitioners regard sex addiction as a potentially harmful diagnosis and draw parallels with gay conversion therapy. As a result, treatment for sex addiction is more often provided by addiction professionals than psychosexual specialists.
Cognitive behavioral therapy is a common form of behavioral treatment for addictions and maladaptive behaviors in general. 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. Their treatments have yet to be subject to peer-review, so it is unclear if they help or harm patients.
Online support groups
In-person support groups
In-person support groups are available in most of the developed world. None yet have any scientific evidence to support that they are helpful, so attend at your own risk. These groups include:
- Sex Addicts Anonymous: For those who want to reduce or eliminate their use of pornography, masturbation, and/or unwanted sexual activity.
- Sex and Love Addicts Anonymous: Similar to the above.
- Sexaholics Anonymous: For those who want to eliminate their use of pornography, masturbation, unwanted sexual activity, and/or sex outside of marriage. Has a stricter definition of sexual sobriety than its competitors.
- SMART Recovery.
Support groups may be useful for uninsured or under-insured individuals. (See also: Alcoholics Anonymous § Health-care costs.) They may also be useful as an adjunct to professional treatment. In addition, they may be useful in places where professional practices are full (i.e. not accepting new patients), scarce, or nonexistent, or where these practices have waiting lists. Finally, they may be useful for patients who are reluctant to spend money on professional treatment.
The term "pre-exposure prophylaxis" (PrEP) generally refers to the use of antiviral drugs to help prevent AIDS. PrEP is an optional treatment for people who are HIV-negative, but have a substantial risk of getting an HIV infection.
In the US, most insurance plans cover these drugs.
According to a systematic review from 2014, prevalence rates of sexual addiction and related sexual disorders ranges from 3% to 6%. Some studies suggest that sex addicts are disproportionately male, at 80%.
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. 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.
Animal research involving rats that exhibit compulsive sexual behavior has identified that this behavior is mediated through the same molecular mechanisms in the brain that mediate drug addiction. 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). 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.
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. Current experimental models of addiction to natural rewards and drug reward demonstrate common alterations in gene expression in the mesocorticolimbic projection. 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; it has been implicated in addictions to alcohol, cannabinoids, cocaine, nicotine, opioids, phenylcyclidine, and substituted amphetamines. ΔJunD is the transcription factor which directly opposes ΔFosB. 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).
ΔFosB also plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise. 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. Thus, ΔFosB is also the key transcription factor involved in addictions to natural rewards as well, and sexual addictions in particular, since ΔFosB in the nucleus accumbens is critical for the reinforcing effects of sexual reward. 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.
|Form of neuroplasticity
or behavioral plasticity
|Type of reinforcer||Sources|
|Opiates||Psychostimulants||High fat or sugar food||Sexual intercourse||Physical exercise
|ΔFosB expression in
nucleus accumbens D1-type MSNs
|Escalation of intake||Yes||Yes||Yes|||
conditioned place preference
|Reinstatement of drug-seeking behavior||↑||↑||↓||↓|||
in the nucleus accumbens
|Sensitized dopamine response
in the nucleus accumbens
|Altered striatal dopamine signaling||↓DRD2, ↑DRD3||↑DRD1, ↓DRD2, ↑DRD3||↑DRD1, ↓DRD2, ↑DRD3||↑DRD2||↑DRD2|||
|Altered striatal opioid signaling||No change or
|↑μ-opioid receptors||↑μ-opioid receptors||No change||No change|||
|Changes in striatal opioid peptides||↑dynorphin
No change: enkephalin
|Mesocorticolimbic synaptic plasticity|
|Number of dendrites in the nucleus accumbens||↓||↑||↑|||
|Dendritic spine density in
the nucleus accumbens
Society and culture
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;drug-induced compulsive sexual behavior has also been noted clinically in some individuals taking dopaminergic drugs. Moreover, some research suggests compulsive engagement in sexual behavior despite negative consequences in animal models.Since current diagnostic models use drug-related concepts as diagnostic criteria for addictions, these are ill-suited for modelling compulsive behaviors in a clinical setting. 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". 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."
|Robert Weiss & David Ley. Is sex addiction a myth? // KPCC (25 April 2012, 9:29 am)|
|Nicole Prause, Ph.D. (sexual physiologist).  CBS (18 July 2013)|
There have been debates regarding the definition and existence of sexual addictions for decades, as the issue was covered in a 1994 journal article. The Mayo Clinic considers sexual addiction 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). 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. The 1988 paper argued that the condition is instead a way of projecting social stigma onto patients.
In a 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.":8 Klein singled out a number of features that he considered crucial limitations of the sex addiction model:8 and stated that the diagnostic criteria for sexual addiction are easy to find on the internet.: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.":10
- 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.
- Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681. PMID 24459410.
Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
- "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February 2015.
- 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.
Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
- 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.
- 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.
- 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.
- 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.
- Carnes, Patrick (1994). Contrary to Love: Helping the Sexual Addict. Hazelden Publishing. p. 28. ISBN 1568380593.
- Schaefer GA, Ahlers CJ (2017). "1.3, Sexual addiction: Terminology, definitions and conceptualisation". In Birchard T, Benfield J. Routledge International Handbook of Sexual Addiction. Routledge. ISBN 1317274253.
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- 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. 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 unfortunate that the Manual avoids use of the term addiction, which provides the best description of the clinical syndrome.
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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.
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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"
- 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 4040958. 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.
- 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 3865508. 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
- 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
- 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. ...
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.
- 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
- 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 3569166. 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.
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- Francoeur, R. T. (1994). Taking sides: Clashing views on controversial issues in human sexuality, p. 25. Dushkin Pub. Group.
- 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.
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- 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.
Books that provide overview history and treatment techniques for sexual addiction include:
- Out of the Shadows: Understanding Sex Addiction by Patrick Carnes. (Hazelden, 1983) ISBN 978-1-56838-621-8
- Sex and Love Addicts Anonymous: The Basic Text for the Augustine Fellowship (Augustine Fellowship, 1986) ISBN 978-0-9615-7011-8
- Sex Lies and Forgiveness: Couples Speaking Out on Healing from Sex Addiction by Jennifer P. Schneider and Burt Schneider. (Recovery Resources Press, 1991) ISBN 978-0-06-255343-0
- Don't Call It Love: Recovery From Sexual Addiction by Bantam, Patrick Carnes. (1992) ISBN 978-0-553-35138-5
- Sex Addiction: Case Studies And Management by Ralph H. Earle and Marcus R. Earle. (Brunner/Mazel, 1995) ISBN 978-0-87630-785-4
- Sexual Addiction: An Integrated Approach by Aviel Goodman. (International Universities Press, 1998) ISBN 978-0-8236-6063-6
- Breaking the Cycle: Free Yourself from Sex Addiction, Porn Obsession, and Shame by George N. Collins, Andrew Adleman. (New Harbinger Publications, 2011) ISBN 978-1-60882-083-2
Books focusing on partners of sex addicts:
- My Secret Life with a Sex Addict – from discovery to recovery by Emma Dawson. (Thornton Publishing, 2004) ISBN 978-1-932344-70-7
- Hope After Betrayal: Healing When Sexual Addiction Invades Your Marriage by Meg Wilson. (Kregel Publications, 2007) ISBN 978-0-8254-3935-3
- Deceived: Facing Sexual Betrayal Lies and Secrets by Claudia Black. (Hazelden, 2009) ISBN 978-1-59285-698-5
- Your Sexually Addicted Spouse: How Partners Can Cope and Heal by Barbara Steffens and Marsha Means. (New Horizon Press, 2009) ISBN 978-0-88282-309-6
- Mending a Shattered Heart: A Guide for Partners of Sex Addicts by Stefanie Carnes. (Gentle Path Press, 2011) ISBN 978-0-9774400-6-1
- Love You, Hate the Porn: Healing a Relationship Damaged by Virtual Infidelity by Mark Chamberlain. (Shadow Mountain; 2.7.2011 edition, 2011. ISBN 1606419366
- A Couple's Guide to Sexual Addiction: A Step-by-Step Plan to Rebuild Trust and Restore Intimacy by Paldrom Collins and George Collins. (Adams Media, 2011) ISBN 978-1-4405-1221-6
- Facing Heartbreak: Steps to Recovery for Partners of Sex Addicts by Stefanie Carnes. (Gentle Path Press, 2012) ISBN 978-0-98327-133-8
Discussions of the concept of sexual addiction: