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Which paper was it that defined addiction as a release?

Which paper was it that defined addiction as a release?


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I read somewhere that a psychologist in 1949 (or somewhere around that) described sexual addiction as a release. I don't remember the author's name nor the title of the paper.

The gist of that paper was that sexual addiction is not about emotions, no intimacy but it's all about a release of a chemical. And I read in the comments that this idea was followed by universities researchers for a long time.

Any help will be much appreciated.

P.S. : Let me know if this question is off-topic.


Social Media Addiction Research Paper

Social media addiction is a serious issue today. It is the main cause for various Internet associated psychological disorders.

In psychology, any Internet addiction is usually divided on stages. They include the initial stage of a healthy interest in the Internet and pathological dependence on it that affects human performance and begins to harm the person’s social life, undermining his mental health. With social media, the situation is completely analogous.

At the core of the social media addiction, experts say, is primarily low self-confidence and self-doubt. People suffering from a low self-esteem, dissatisfied with their appearance or small attention from their environment are often hooked on the “online needle.” Typically, these are people with humanitarian mindset, prone to fantasies, loving invent things to look better and often having wishful thinking.

We can write your Social Media Addiction research paper from scratch!

Social media addiction has physiological characteristics by which it can be classified as a mental illness, and not just a bad habit. Among its symptoms, there are wet eyes, increased sweating, and chronic insomnia. The fact is that often social media surfing creates increased levels of dopamine – a substance similar to adrenaline – in the brain.

At this activity, an addicted person experiences excitement, which is akin to the gambling fever or sexual arousal. Such a person seeks to experience this state over and over again and starts to use the social networks as a tool for pleasure.

In addition, social media addiction can harm health due to the reduction of communicating with real people. According to experts, the lack of communication may affect the immune system, hormonal balance, state of the arteries and thought processes, which in the long run increases the risk of the emergence and development of diseases such as cancer, cardiovascular disease, and dementia.

According to the experts, his type of addiction is especially dangerous for teenagers, as they form a false impression that love and friendship can be easily won and just as easy destroyed. In addition, according to Dr. Himanshu Tyagi, to people who are accustomed to the rapid flow of Internet life, the reality may seem too boring, and they may try to “revive” it, making impulsive acts, including suicide attempts, because they tend to underestimate the value of effective life.

It is quite simple to detect social media addiction: you need stop using social networks for some time, such as month, and if there is no problem with such an abstention, there is no addiction, if there is irresistible desire, there is possibility of the addiction.

In the fight against the social media addiction in educational and business institutions such services are restricted. The is a bunch of various software which allows to easily restrict access to such services.

Free sample research paper on social media addiction is a good start for non-experienced writer.

Are you looking for a top-notch custom research paper about Social Media Addiction? Is confidentiality as important to you as the high quality of the product?


Which paper was it that defined addiction as a release? - Psychology

Substance-use and addictive disorders are marked by physiological dependence, drug-seeking behavior, tolerance, and/or withdrawal.

Learning Objectives

Summarize the similarities and differences in diagnostic criteria, etiology, and treatment options among substance-use and addictive disorders

Key Takeaways

Key Points

  • Substance use disorder combines the previous DSM-IV-TR categories of “substance abuse” and “substance dependence ” into a single disorder measured on a diagnostic continuum from mild to severe. Each specific substance is addressed as a separate use disorder, such as alcohol or stimulants.
  • Substance use disorder can be diagnosed with physiological dependence, evidence of tolerance or withdrawal, or without physiological dependence.
  • Addiction is the continued repetition of a behavior despite adverse consequences, or a neurological impairment leading to such behaviors. Physiological dependence occurs when the body adjusts to the substance.
  • Tolerance is when body adapts to the substance and requires increasingly more to achieve effects. Withdrawal refers to physical and psychological symptoms experienced when reducing or discontinuing a substance.
  • Gambling disorders include the urge to continuously gamble despite harmful negative consequences or a desire to stop.
  • Theories of the causes of substance-related and addictive disorders include genetic predisposition, the self-medication theory, and factors involved with social/economic development.
  • Most treatment for addictions involves counseling, step-based programs, self-help, peer-support, medication, or a combination of these.

Key Terms

  • dysthymia: A milder form of clinical depression, characterized by low-grade depression which lasts at least 2 years.
  • dual diagnosis: Also called co-occurring disorders the condition of suffering from a mental illness and a simultaneously occurring substance abuse problem.
  • dependence: An irresistible physical or psychological need, especially for a chemical substance.

Defining Substance Use Disorder

Substance use disorder combines the previous DSM-IV-TR categories of “substance abuse” and “substance dependence” into a single disorder, measured on a diagnostic continuum from mild to severe. Each specific substance is addressed as a separate use disorder, such as alcohol or stimulants. Other substances include opioids, sedatives, cocaine, cannabis, amphetamines, inhalants, and nicotine.

Addiction is the continued repetition of a behavior despite adverse consequences, or a neurological impairment leading to such behaviors. Addictions can include, but are not limited to, substance abuse, exercise addiction, food addiction, sexual addiction, computer addiction and gambling. Classic hallmarks of addiction include impaired control over substances or behavior, preoccupation with substance or behavior, continued use despite consequences, and denial. Habits and patterns associated with addiction are typically characterized by immediate gratification (short-term reward), coupled with delayed deleterious effects (long-term costs).

Physiological dependence occurs when the body has to adjust to the substance by incorporating the substance into its ‘normal’ functioning. This state creates the conditions of tolerance and withdrawal. Tolerance is the process by which the body continually adapts to the substance and requires increasingly larger amounts to achieve the original effects. Withdrawal refers to physical and psychological symptoms experienced when reducing or discontinuing a substance that the body has become dependent on. Symptoms of withdrawal generally include but are not limited to anxiety, irritability, intense cravings for the substance, nausea, hallucinations, headaches, cold sweats, and tremors. Chemical and hormonal imbalances may arise. Physiological and psychological stress is to be expected if the substance is not re-introduced.

Substance Use, Addiction, and Effects: Individuals suffering from substance use disorder and addiction may engage in the use of many substances. This can lead to personal problems such as failing health and unemployment, and interpersonal problems such as broken families and alienation.

Epidemiology

Substance-related disorders, a category which includes both substance dependence and substance abuse, can lead to significant personal, interpersonal, and societal problems. These disorders are most prevalent in individuals aged 18–25, with a higher occurrence in men than women, and higher occurrence in urban residents than rural residents. On average, general medical facilities hold 20% of patients with substance-related disorders, which could possibly lead to psychiatric disorders later on. Over 50% of individuals with substance-related disorders will often have a dual diagnosis, where they are simultaneously diagnosed with another psychiatric diagnosis, the most common being major depression, dysthymia, personality disorders, and anxiety disorders.

Most countries have legislation which makes various drugs and drug-like substances illegal. Although the legislation may be justifiable on moral grounds to some, it can make addiction or dependency a much more serious issue for the individual. Reliable supplies of a drug become difficult to secure as illegally produced substances may have contaminants. Withdrawal from the substances or associated contaminants can cause additional health issues, and the individual becomes vulnerable to both criminal abuse and legal punishment.

DSM-5 Diagnostic Criteria

The diagnostic criteria for substance use disorder in DSM-5 is set at two or more criteria from a list of 11. Severity of the substance use disorders is based on the number of criteria endorsed, where 2-3 endorsements indicate a mild disorder, 4-5 indicate a moderate disorder, and 6 or more indicate severe substance use disorder. Substance use disorder can be diagnosed with physiological dependence, evidence of tolerance or withdrawal, or without physiological dependence. In addition, criteria for cannabis and caffeine withdrawal were added.

Defining Gambling Disorder

Problem gambling or gambling addiction is an urge to continuously gamble despite harmful negative consequences or a desire to stop. Severe problem gambling may be diagnosed as clinical pathological gambling if the gambler meets certain criteria and is associated with both social and family costs.

DSM-5 Diagnostic Criteria

The DSM-5 has re-classified the condition as an addictive disorder, with sufferers exhibiting many similarities to those who have substance addictions. In order to be diagnosed, an individual must have at least four of the following symptoms in a 12-month period:

  • Needs to gamble with increasing amounts of money in order to achieve the desired excitement.
  • Is restless or irritable when attempting to cut down or stop gambling.
  • Has made repeated unsuccessful efforts to control, cut back, or stop gambling.
  • Is often preoccupied with gambling (e.g., having persistent thoughts of reliving past gambling experiences, planning the next venture, thinking of ways to get money with which to gamble).
  • Often gambles when feeling distressed (e.g., helpless, guilty, anxious, depressed).
  • After losing money gambling, often returns another day to get even (“chasing” one’s losses).
  • Lies to conceal the extent of involvement with gambling.
  • Has jeopardized or lost a significant relationship, job, or educational or career opportunity because of gambling.
  • Relies on others to provide money to relieve desperate financial situations caused by gambling.

Etiology

Several theories of substance use and addiction exist, some of the main ones being genetic predisposition, the self-medication theory, a psychological predisposition, and factors involved with social/economic development. It has long been established that genetic factors along with social and psychological factors are contributors to substance use and addiction. Epidemiological studies estimate that genetic factors account for 40–60% of the risk factors for alcoholism. Similar rates of heritability for other types of drug addiction have been indicated by other studies. Genetic factors may create a predisposition for substance abuse, which means that an individual may have a tendency toward substance abuse. The self-medication hypothesis suggests that certain individuals abuse drugs in an attempt to self-medicate physical, psychological problems, or social problems. There are strong associations between poverty and addiction.

Understanding how learning and behavior work in the reward circuit of the brain can help in understanding drug-seeking behavior and addiction. Drug addiction is characterized by strong, drug-seeking behaviors in which the person who is addicted persistently craves and seeks out drugs, despite the knowledge of harmful consequences. Addictive drugs produce a reward, which is the euphoric feeling resulting from sustained dopamine concentrations in the synaptic cleft of neurons in the brain. The reward circuit, also referred to as the mesolimbic system, is characterized by the interaction of several areas of the brain.

According to the Illinois Institute for Addiction Recovery, evidence indicates that pathological gambling is an addiction similar to chemical addiction. It has been seen that some pathological gamblers have lower levels of norepinephrine than normal gamblers. According to a study conducted by Alec Roy, formerly at the National Institute on Alcohol Abuse and Alcoholism, norepinephrine is secreted under stress, arousal, or thrill, so pathological gamblers gamble to make up for their under-dosage. Deficiencies in serotonin might also contribute to compulsive behavior, including a gambling addiction. Others argue that social factors are far more important determinants of gambling behavior than brain chemicals and suggest that a social model may be more useful in understanding the issue.

Treatment

Early treatment of acute withdrawal from substances often includes medical detoxification, in which a person goes through the process and experience of withdrawal symptoms while discontinuing a drug. A detoxification program for physical dependence does not necessarily address the precedents of addiction, social factors, psychological addiction, or the often-complex behavioral issues that intermingle with addiction.

Treatments for addiction usually involve planning for specific ways to avoid the addictive stimulus and/or therapeutic interventions intended to help a client learn healthier ways to find satisfaction. Clinical leaders in recent years have attempted to tailor intervention approaches to specific influences that affect addictive behavior, using therapeutic interviews in an effort to discover factors that led a person to embrace unhealthy, addictive sources of pleasure or relief from pain. Several evidenced-based intervention programs have emerged, including behavioral marital therapy, community reinforcement approaches, cue exposure therapy, and contingency management strategies. Most treatment for addictions involves counseling, step-based programs, self-help, peer-support, medication, or a combination of these.

Twelve-step programs (such as Alcoholics Anonymous) are a set of guiding principles, sometimes accepted by members as being ‘spiritual principles’, outlining a course of action for tackling problems of addiction including alcoholism, drug addiction, and compulsion. Alcoholics Anonymous is the largest of all the twelve-step programs (from which all other twelve-steps programs are derived), followed by Narcotics Anonymous


Introduction

Addiction is a term that means compulsive physiological need for and use of a habit-forming substance (like heroin or nicotine), characterized by tolerance and well-defined physiological symptoms upon withdrawal it has also been used more broadly to refer to compulsive use of a substance known by the user to be physically, psychologically, or socially harmful (Maddux and Desmond, 2000). In the following essay, I shall try to explore the meaning of this concept.

A note on the term addiction: I shall use the term addiction, except when I refer to a specific diagnostic system that uses other terms. The term dependence was introduced to reduce the stigma associated with addiction in the 50ties. I generally prefer the term addiction, because the term dependence is sometimes used in a counter-therapeutic fashion: I depend on my heroin/cigarettes etc. Addiction more directly addresses the issue: I am addicted to heroin/cigarettes, which means that I suffer various consequences from using the drug, and I will need to think about whether I will accept these consequences, or do something about my addiction (Maddux and Desmond, 2000).


The nutrition transition theory

The nutrition transition theory first emerged to describe global trends toward a “Western diet” containing refined foods high in fat and sugar, and low in fiber (21). Later the term was used to capture a correlation with increased BMI and changing economic and agricultural factors. Early identified factors include urbanization, economic growth, technical change, and culture (22) while more recent descriptions of the critical underlying factors include technology, urbanization, economic welfare relative to the cost of food, and expansion of global trade (23). The nutrition transition theory is not a new concept. Previous models have included the demographic and epidemiological transitions. Popkin and Gordon-Larsen identify that both historic processes precede the nutrition transition (22). The epidemiological transition describes a shift from high prevalence of disease associated with famine, malnutrition, and poor sanitation, to a pattern of high prevalence of chronic and degenerative disease associated with urban-industrial lifestyles (24). This ecological framework analyzes changes at the societal level, examining how agricultural and food supply chains impact global dietary patterns. The theory suggests that “upstream” interventions (supply-side) will be more effective than addressing the lower hanging fruit (i.e., exercise, calorie restriction).

The nutrition transition theory is also supported by compelling evidence suggesting that a wide range of animals have also been gaining weight in recent years (25, 26). Other terms that support the 𠇎nvironmental theory of obesity” include “globesity” at the most distal levels, and the “neighborhood effect” at more proximal levels (27). Notwithstanding, the “neighborhood effect” has far-reaching social implications, given that the neighborhood where one lives is merely a proxy for socioeconomic status. Recently, other research has suggested that discussions of nutritional inequality emphasizing supply-side factors are less indicative of consumption patterns than demand-side differences (28), lending support to the food addiction (FA) hypothesis.


New definition of addiction: Addiction is a chronic brain disease, not just bad behavior or bad choices

The American Society of Addiction Medicine (ASAM) has released a new definition of addiction highlighting that addiction is a chronic brain disorder and not simply a behavioral problem involving too much alcohol, drugs, gambling or sex. This the first time ASAM has taken an official position that addiction is not solely related to problematic substance use.

When people see compulsive and damaging behaviors in friends or family members -- or public figures such as celebrities or politicians -- they often focus only on the substance use or behaviors as the problem. However, these outward behaviors are actually manifestations of an underlying disease that involves various areas of the brain, according to the new definition by ASAM, the nation's largest professional society of physicians dedicated to treating and preventing addiction.

"At its core, addiction isn't just a social problem or a moral problem or a criminal problem. It's a brain problem whose behaviors manifest in all these other areas," said Dr. Michael Miller, past president of ASAM who oversaw the development of the new definition. "Many behaviors driven by addiction are real problems and sometimes criminal acts. But the disease is about brains, not drugs. It's about underlying neurology, not outward actions."

The new definition resulted from an intensive, four-year process with more than 80 experts actively working on it, including top addiction authorities, addiction medicine clinicians and leading neuroscience researchers from across the country. The full governing board of ASAM and chapter presidents from many states took part, and there was extensive dialogue with the National Institute on Drug Abuse (NIDA).

The new definition also describes addiction as a primary disease, meaning that it's not the result of other causes such as emotional or psychiatric problems. Addiction is also recognized as a chronic disease, like cardiovascular disease or diabetes, so it must be treated, managed and monitored over a life-time.

Two decades of advancements in neurosciences convinced ASAM that addiction needed to be redefined by what's going on in the brain. Research shows that the disease of addiction affects neurotransmission and interactions within reward circuitry of the brain, leading to addictive behaviors that supplant healthy behaviors, while memories of previous experiences with food, sex, alcohol and other drugs trigger craving and renewal of addictive behaviors. Meanwhile, brain circuitry that governs impulse control and judgment is also altered in this disease, resulting in the dysfunctional pursuit of rewards such as alcohol and other drugs. This area of the brain is still developing during teen-age years, which may be why early exposure to alcohol and drugs is related to greater likelihood of addiction later in life.

There is longstanding controversy over whether people with addiction have choice over anti-social and dangerous behaviors, said Dr. Raju Hajela, past president of the Canadian Society of Addiction Medicine and chair of the ASAM committee on the new definition. He stated that "the disease creates distortions in thinking, feelings and perceptions, which drive people to behave in ways that are not understandable to others around them. Simply put, addiction is not a choice. Addictive behaviors are a manifestation of the disease, not a cause."

"Choice still plays an important role in getting help. While the neurobiology of choice may not be fully understood, a person with addiction must make choices for a healthier life in order to enter treatment and recovery. Because there is no pill which alone can cure addiction, choosing recovery over unhealthy behaviors is necessary," Hajela said.

"Many chronic diseases require behavioral choices, such as people with heart disease choosing to eat healthier or begin exercising, in addition to medical or surgical interventions," said Dr. Miller. "So, we have to stop moralizing, blaming, controlling or smirking at the person with the disease of addiction, and start creating opportunities for individuals and families to get help and providing assistance in choosing proper treatment."


Thesis about Drug Addiction

It is extremely important to recognize drug addiction at the right moment, preferably in the beginning, so as not to spoil social relationships and health. It is necessary to understand that the sooner the problem will be attended, the better it is for the treatment progress. There are certain symptoms of drug abuse: when drug is getting people into legal trouble, if because of it people start neglecting their responsibilities, when they use drugs under dangerous conditions, and when they cause problems in relationships.

It is absolutely necessary to prevent drug addiction levels’ raise, and it is necessary for all the people to take part in this prevention program. Only if we…


Neurochemistry of Resilience

&ldquoAllostasis&rdquo refers to the dynamic process through which the body adapts to daily stressors and maintains homeostasis (Sterling and Eyer 1988). Sudden stressful events trigger the release of the &ldquoflight-or-fight&rdquo hormones (i.e., catecholamines) and other stress hormones in the brain, preparing the organism to cope with stress and avert harm. This process is mediated by a stress circuit (see figure 1), which is consistently implicated in stress-related disorders such as mood and anxiety disorders and addictive disorders. Interindividual variability in stress resilience results from differences in the coordinated stress response. This response comprises the function and interactions of numerous hormones, neurotransmitters, and neuropeptides, some of which are discussed below.

Figure 1 Norepinephrine (NE) and dopamine (DA) are the principle chemical messengers employed in central and peripheral sympathetic synapses, and the human NE transporter rapidly clears NE and DA from the synaptic cleft via efficient transport systemattenuating signaling, recycling 90 percent of these synaptic monoamines. NE neurons innervate nearly all parts of the neuroaxis, with the locus coeruleus (LC) being responsible for most of the NE in the brain. NE exerts neuromodulatory effects on the cellular activity of post-synaptic target neurons in many brain circuits, thereby moderating synaptic transmission in target circuits including the thalamus, prefrontalcortex (PFC), ventral striatum (via PFC), and amygdala, which have been implicated in substance use disorders. The widespread and divergent anatomical organization positions the NE system to be involved in widely varying functions including responses to stress, which alters both the electrophysiological activity of NE neurons in the LC and the release of NE in the terminal regions of these cells, as well as crucial cognitive functions, including attention and arousal. NE mediates many of the adaptive and maladaptive consequences of stress exposure, implicating this system in a variety of abnormal behaviors including alcohol dependence.

HPA Axis

The HPA axis is a system regulated by a complex negative-feedback system. CRF, released by the hypothalamus in response to stress, triggers the release of adrenocorticotrophic hormone (ACTH) from the anterior pituitary gland. This process leads to the synthesis and release of cortisol by the adrenal cortex. Cortisol secretion acutely facilitates cognitive, metabolic, immunologic, and behavioral adaptations to stress. It also results, however, in &ldquoallostatic overload&rdquo when stress becomes chronic or overwhelming (McEwen 2003). Resilience is maintained when the stress response is both activated and terminated efficiently. The adaptive responses of the HPA axis are thought to involve an optimal balance of the cortisol-binding receptors GR and mineralocorticoid receptor (de Kloet et al. 2005, 2007).

Studies showing lower plasma levels of ACTH but not cortisol in men with a family history of alcoholism (Dai et al. 2007 Gianoulakis et al. 2005) suggest that HPA axis dysfunction might predate the onset of alcoholism. Long-term alcohol abuse is associated with increased extrahypothalamic CRF signaling and dampened HPA axis responsivity (Richardson et al. 2008). Increases in extrahypothalamic CRF contribute to negative emotional states during abstinence, increasing risk for relapse (Koob and Le Moal 2008). In a recent study, researchers asked alcoholics who had been abstinent for 1 month to imagine a relaxing situation of their choice while listening to a previously recorded audiotape of this situation. A greater cortisol-to-corticotropin ratio (i.e., higher adrenal sensitivity) during this relaxed state was found to predict a shorter time to alcohol relapse, thus suggesting that new treatments aimed a decreasing adrenal sensitivity could reduce relapse rates (Sinha et al. 2011).

Norepinephrine

During the acute stress response, the hormone norepinephrine (NE) is released through direct projections from the brain site where NE is synthesized (i.e., locus coeruleus) and other brain stem nuclei (i.e., structures that act as transit points for brain signals) into the amygdala, hippocampus, nucleus accumbens, prefrontal cortex (PFC), and other brain areas mediating emotional responses. Several studies have linked abnormal regulation of brain NE systems to stress disorders (Krystal and Neumeister 2009 O&rsquoDonnell et al. 2004). As drug dependence develops, levels of the neurotransmitter dopamine decrease and the NE stress system in the brain is activated, contributing to &ldquostress-like states&rdquo and increased vulnerability to stressors during periods of abstinence (Koob and Le Moal 2008). In combination with CRF, NE also might contribute to the consolidation of emotional memories associated with drug use in the amygdala (Koob et al. 2009).

Stress resilience may be enhanced through the regulation of NE system responsiveness, which is mediated through effects on the NE transporter on catecholamine receptors (i.e., &alpha2 adrenoreceptors), as well as interactions between the NE and other neurobiologic systems, such as the dopamine and serotonin systems (Krystal and Neumeister 2009). For example, animal studies have shown that PFC NE nerve cell projections (i.e., axons) have a latent capacity to enhance synthesis and recovery of transmitter, which might underlie the capacity to adapt to stress (Miner et al. 2006). This mechanism deserves further study in humans with positron emission tomography (PET), which uses positron-emitting radiotracers to show where and how compounds act in the brain (Ding et al. 2005). Other targets include the &alpha2a and &alpha2c receptors, which have complementary roles in the regulation of stress responses (Small et al. 2000). Yohimbine, a drug that blocks the &alpha2 receptors (i.e., a receptor antagonist), increases alcohol self-administration and induces reinstatement of alcohol seeking (Le et al. 2005 Marinelli et al. 2007). The recent finding that an &alpha2c receptor polymorphism (Del322-325) reduces feedback inhibition of sympathetic NE release (Neumeister et al. 2005) as well as evidence from studies in mice bred to have an inactivated &alpha2c receptor (i.e., knockout mice) (Sallinen et al. 1999), suggest that interventions targeting this receptor might modulate stress and anxiety responses.

Serotonin

The serotonin (5-HT) system, which consists primarily of neurons from the dorsal raphe nuclei that project widely throughout the brain (including the amygdala, ventral striatum, and PFC), is involved in the regulation of stress and anxiety. Serotonin has an important role in promoting neuroplasticity in the central nervous system, both during development and in adulthood. Serotonin also regulates the neurochemical effects of drugs of abuse, including alcohol, and is involved in modulating impulsivity, known to increase risk for alcohol and drug abuse (Kirby et al. 2011). The 5-HT system is itself modulated by drugs of abuse. For example, alcohol administration elevates 5-HT levels in the nucleus accumbens, ventral tegmental area (VTA), amygdala, and hippocampus, an effect that is more pronounced in alcohol-preferring rats. Reduced activity of the 5-HT system might contribute to depression during withdrawal and increase vulnerability to relapse (Kirby et al. 2011). In studies of macaques, differential function of the 5-HT system in interaction with early life stress was found to affect alcohol consumption: peer-reared female macaques with a specific variant (i.e., the l/s genotype) of the serotonin transporter polymorphism showed higher levels of ethanol preference and increased consumption over time (Barr et al. 2004).

The 5-HT system is extremely complex, including at least 14 receptor subtypes. Of these receptors, the 5-HT1A, 5-HT1B, 5-HT2A, and 5-HT2C receptors are well understood through research on anxiety regulation in both animals and humans (Krystal and Neumeister 2009). The 5-HT1A receptor is thought to counteract the deleterious effects of 5-HT2A receptor activation (i.e., the disruption of brain cell creation), mediated by increased release of the neurotransmitter glutamate and direct glucocorticoid effects (Hoebel et al 2007). Restrained function of another 5-HT receptor, 5HT1B, might be central to resilient stress responses by enhancing synaptic availability of 5-HT in the amygdala and other cortical regions as well as promoting dopamine release in the ventral striatum (Clark and Neumaier 2001 Krystal and Neumeister 2009 Sari 2004) (see figure 2).

Figure 2 Alterations in serotonin 1B receptor (5HT1BR) function might contribute to alcohol dependence by influencing not only serotonin (5HT) input to the ventral striatum via the receptors&rsquo role as 5HT terminal autoreceptors, 1 but also dopaminergic input to the striatum via the role of these receptors as heteroreceptors 2 on GABA terminals within the ventral tegmental area, and glutamatergic activity within the ventral striatum via heteroreceptors on corticofugal projections.

1 Autoreceptor: A site on a neuron that binds the neurotransmitter released by that neuron, which then regulates the neuron&rsquos activity.

2 Heteroreceptor: A site on a neuron that binds a modulatory neuroregulator other than that released by the neuron.

The role of this receptor subtype in addiction disorders recently was studied in humans. The report demonstrated that alcohol dependence in humans, like in rodent models, is associated with increased levels of ventral striatal 5-HT1B receptors (Hu et al. 2010). Additional research is necessary to understand the complex function of the 5-HT system. However, these findings suggest possible novel targets for the treatment of stress-related disorders and, most important, addiction disorders.

Dopamine

Dopaminergic neurons in the ventral tegmental area (VTA) of the midbrain project to the nucleus accumbens and other limbic areas to form the mesolimbic dopamine system, the most studied reward circuit. Dopamine neurons are activated in response to reward or the expectation of reward, and generally are inhibited by aversive stimuli. Dopamine signaling is central to the onset of addiction, as well as to the transition to dependence in interaction with other neurotransmitter systems (Ross and Peselow 2009). Drugs of addiction trigger large but brief increases in extracellular dopamine in the nucleus accumbens. Over time, chronic drug use downregulates dopamine receptors and dopamine release, leading to decreased sensitivity to natural rewards, such as food and sex, and leading also to further drug use (Volkow et al 2010).

Although findings from animal studies suggest that early-life stress can lead to long-lasting changes in gene expression in the mesolimbic dopamine pathway, ultimately increasing vulnerability to addictive disorders, not all individuals with a history of childhood abuse develop addictive or other disorders, thereby stressing the role of protective factors such as genetic variants conferring resilience (Enoch 2010).

Findings from several studies suggest that higher dopamine D2 receptor availability in the striatum might promote resilience to alcohol use disorders. In a study of unaffected members of alcoholic families, higher striatal dopamine D2 receptor availability was associated with higher positive emotionality, discussed above as a protective factor against alcohol use disorders (Volkow et al 2006). Other studies found that higher striatal dopamine D2 receptor availability was associated with resistance to the reinforcing effects of stimulants in healthy volunteers (Volkow et al. 1999, 2002) and in rats (Thanos et al. 2008).

NPY, a 36&ndashamino acid peptide, is widely distributed in the brain. NPY has anxiety-reducing properties in rodents and is thought to enhance resilience to stress in humans (Feder et al. 2009 Morgan et al. 2000). Evidence from animal and human studies suggests that NPY has a key role in regulating alcohol intake, dependence, and withdrawal. Mice genetically modified to overexpress NPY consume less alcohol (Thiele et al. 1998), and administration of NPY into the cerebral ventricles of the brain (i.e., intracerebroventricular infusion) reduces alcohol consumption in alcohol-preferring rats (Thorsell 2007). Infusion of NPY into the central nucleus of the amygdala has been shown to normalize both anxiety behaviors and alcohol intake, suggesting that NPY might work by modulating anxiety responses (Zhang et al. 2010). In rhesus macaques exposed to early life stress, and in human studies, certain NPY gene polymorphisms are associated with differential susceptibility to alcohol or cocaine dependence (Koehnke et al. 2002 Lindell et al. 2010 Mottagui- Tabar et al. 2005 Wetherill et al. 2008).

Endocannabinoids

An emerging body of evidence suggests an important role for the endogenous cannabinoid (eCB) system and specifically the CB1 receptor in alcohol-related behaviors (for review, see Basavarajappa 2007). To date, however, only peripheral measures of eCB function have been collected in living humans with alcohol dependence (AD) (Mangieri et al. 2009), and no human in vivo data on the potentially critical role of the brain CB1 receptor in AD have been collected yet. At a neurobiological level, studies show impairments in decision making in alcohol-dependent patients (Dom et al. 2006), which is associated with altered functions in a cortico-limbic- striatal circuit, including the amygdala, hippocampus, anterior cingulate cortex, insula, and the ventral striatum. Three sets of factors are thought to be responsible for high alcohol relapse rates. First, individual differences in the positive, reinforcing properties of alcohol are known to increase risk of alcoholism and possibly alcohol relapse (Schuckit and Smith 1996). Second, stimuli previously associated with alcohol use and its physiological and subjective effects become paired with alcohol and are thought to serve as &ldquoconditioned cues&rdquo that can increase alcohol craving and subsequent alcohol use (O&rsquoBrien et al. 1998). Finally, stress has been found to increase the risk of alcohol relapse (Brown et al. 1990 Miller et al. 1996 Sinha 2001). All three factors can be linked to the eCB system and its attending CB1 receptor and increasing evidence derived from animal studies suggests a role of the eCB system in alcohol-related behaviors (Vinod and Hungund 2006).

Such research suggests that upregulation of CB1 receptor&ndashmediated G-protein signaling in a brain circuit that mediates AD susceptibility (involving the amygdala, hippocampus, ventromedial prefrontal cortex, insula, and ventral striatum) (Sullivan and Pfefferbaum 2005) might contribute to the increased alcohol consumption in patients with chronic AD. For example, CB1 inactivation (Hungund et al. 2003 Naassila et al. 2004 Poncelet et al. 2003 Thanos et al. 2005) and pharmacological manipulation of CB1 receptor function (Femenia et al. 2010 Maccioni et al. Maccioni et al. 2008 Malinen and Hyytia 2008) result in reduced voluntary alcohol intake. In addition, administration of an agent that binds to the CB1 receptor (i.e., a CB1 receptor agonist) (Colombo et al. 2002 Gallate et al. 1999 Vinod et al. 2008b) enhances alcohol consumption.

In contrast, acute, short-term alcohol intoxication is associated with elevated eCB levels (Basavarajappa et al. 2006 Blednov et al. 2007 Vinod et al. 2008a), reduced activity of the enzyme fatty acid amide hydrolase (FAAH), and reduced CB1 receptor&ndashmediated G-protein signaling (Vinod et al. 2011). This mediates the activation of the mesolimbic dopaminergic system (Cheer et al. 2007 Hungund et al. 2003 ), which has been extensively studied in alcohol dependence. Evidence suggests a functional interaction between these systems, which might be associated with the reinforcing effects of alcohol and therefore may be an important mechanism in the etiology of alcohol dependence. Findings in animal studies recently have stimulated interest in the therapeutic potential of enhancing eCB signaling, with research in humans having just begun (Hill et al. 2009). However, an accumulating body of evidence suggests that the eCB system, and in particular its attending CB1 receptor, provides novel leads for treatment development in alcohol dependence (Bailey and Neumeister 2011).


Contents

  • addiction – a biopsychosocial disorder characterized by persistent use of drugs (including alcohol) despite substantial harm and adverse consequences
  • addictive drug – psychoactive substances that with repeated use are associated with significantly higher rates of substance use disorders, due in large part to the drug's effect on brain reward systems
  • 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 and desirable or as something to approach
  • 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

None of the official diagnostic classification frameworks list "sexual addiction" as a distinct disorder.

DSM Edit

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. [15]

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." [16] The reference to sexual addiction was subsequently removed. [17] The DSM-IV-TR, published in 2000 (DSM-IV-TR), did not include sexual addiction as a mental disorder. [18]

Some authors suggested that sexual addiction should be re-introduced into the DSM system [19] however, sexual addiction was rejected for inclusion in the DSM-5, which was published in 2013. [20] 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. [21] [22]

ICD Edit

The World Health Organization produces the International Classification of Diseases (ICD), which is not limited to mental disorders. The most recent approved 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. [23] The most recent (yet unapproved) version of that document, ICD-11, includes "compulsive sexual behavior disorder" [24] as a diagnosis (code 6C72)—it does not use the addiction model. [25]

CCMD Edit

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. [ citation needed ]

Other Edit

Some mental health providers have proposed various, but similar, criteria for diagnosing sexual addiction, including Patrick Carnes, [26] Aviel Goodman, [27] and the late Jonathan Marsh. [28] 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. [29] No diagnostic proposal for sex addiction has been adopted into any official government diagnostic manual, however. [ citation needed ]

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

In 2011, the American Society of Addiction Medicine (ASAM), the largest medical consensus of physicians dedicated to treating and preventing addiction, [30] redefined addiction as a chronic brain disorder, [31] which for the first time broadened the definition of addiction from substances to include addictive behaviors and reward-seeking, such as gambling and sex. [32]

Borderline personality disorder Edit

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. [33] 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. [34]

Medical reviews and position statements Edit

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." [35]

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. [36]

In 16 November 2017 the Association for the Treatment of Sexual Abusers (ATSA) published a position against sending sex offenders to sex addiction treatment facilities. [37] Those centers argued that "illegal" behaviors were symptoms of sex addiction, which ATSA challenged they had no scientific evidence to support. [ citation needed ]

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. [38] [39] [40] Sexual activity is an intrinsic reward that has been shown to act as a positive reinforcer, [41] strongly activate the reward system, and induce the accumulation of ΔFosB in part of the striatum (specifically, the nucleus accumbens). [38] [39] [40] 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. [39] [42] [43] [44]

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. [38] Current experimental models of addiction to natural rewards and drug reward demonstrate common alterations in gene expression in the mesocorticolimbic projection. [38] [45] 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 [45] it has been implicated in addictions to alcohol, cannabinoids, cocaine, nicotine, opioids, phenylcyclidine, and substituted amphetamines. [38] [45] [46] ΔJunD is the transcription factor which directly opposes ΔFosB. [45] 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). [45]

ΔFosB also plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise. [39] [45] 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. [38] [39] Thus, ΔFosB is also the key transcription factor involved in addictions to natural rewards as well, [38] [40] and sexual addictions in particular, since ΔFosB in the nucleus accumbens is critical for the reinforcing effects of sexual reward. [39] 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. [38] [40]

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
[38]
Behavioral plasticity
Escalation of intake Yes Yes Yes [38]
Psychostimulant
cross-sensitization
Yes Not applicable Yes Yes Attenuated Attenuated [38]
Psychostimulant
self-administration
[38]
Psychostimulant
conditioned place preference
[38]
Reinstatement of drug-seeking behavior [38]
Neurochemical plasticity
CREB phosphorylation
in the nucleus accumbens
[38]
Sensitized dopamine response
in the nucleus accumbens
No Yes No Yes [38]
Altered striatal dopamine signaling ↓DRD2, ↑DRD3 ↑DRD1, ↓DRD2, ↑DRD3 ↑DRD1, ↓DRD2, ↑DRD3 ↑DRD2 ↑DRD2 [38]
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 [38]
Changes in striatal opioid peptides ↑dynorphin
No change: enkephalin
↑dynorphin ↓enkephalin ↑dynorphin ↑dynorphin [38]
Mesocorticolimbic synaptic plasticity
Number of dendrites in the nucleus accumbens [38]
Dendritic spine density in
the nucleus accumbens
[38]

Counseling Edit

As of 2017, none of the official regulatory bodies for Psycho-sexual Counseling 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. [35] As a result, treatment for sex addiction is more often provided by addiction professionals in the counseling field than psychosexual specialists. These counseling professionals typically hold advanced degrees of education including Master's degrees or Doctorates in counseling or a related field like psychology. These counselors can also hold certifications like Licensed Professional Counselors (LPC-S) who are required to hold a Master's degree or higher level of education. Therapists and Psychologists usually also hold a Master's in a related field of study. [47]

Cognitive behavioral therapy is a common form of behavioral treatment for addictions and maladaptive behaviors in general. [48] 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. [29] [49] Their treatments have yet to be subject to peer-review, so it is unclear if they help or harm patients.

Support groups Edit

Online support groups Edit

In-person support groups Edit

In-person support groups are available in most of the developed world. None yet have any scientific evidence to show whether or not they are helpful, so attendees do so at their own risk.

    : For those who want to reduce or eliminate their use of pornography, masturbation, and/or unwanted sexual activity. : Similar to the above. : 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. .

In places where none of the above are available, open meetings of Alcoholics Anonymous or Narcotics Anonymous may be a second-best option. At open AA and NA meetings, non-alcoholics/non-addicts are welcome to observe but not participate.

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.

Medications Edit

Antiviral drugs Edit

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. [ citation needed ]

In the US, most insurance plans cover these drugs. [50]

According to a systematic review from 2014, observed prevalence rates of sexual addiction/hypersexual disorder range from 3% to 6%. [2] Some studies suggest that sex addicts are disproportionately male, at 80%. [51]

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. [52] 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. [ citation needed ]

Controversy Edit

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. [38] 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, [15] these are ill-suited for modelling compulsive behaviors in a clinical setting. [38] 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". [21] 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." [2]

External media
Audio
Robert Weiss & David Ley. Is sex addiction a myth? // KPCC (25 April 2012, 9:29 am)
Video
Nicole Prause, Ph.D. (sexual physiologist). [1] 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. [54] [55] 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). [56] 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. [57] [58] The 1988 paper argued that the condition is instead a way of projecting social stigma onto patients. [57] "Love addiction" falls into the same controversial area as well since it refers to a frequent pattern of intimate relationships which can be a by product of cultural norms and commonly accepted morals. [59]

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." [60] : 8 Klein singled out a number of features that he considered crucial limitations of the sex addiction model [60] : 8 and stated that the diagnostic criteria for sexual addiction are easy to find on the internet. [60] : 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." [60] : 10

Historically, the claim of sex addiction has been the preferred defense of white men who committed felonies. [61]

Popular culture Edit

Sexual addiction has been the main theme in a variety of films including Diary of a Sex Addict, I Am a Sex Addict, Black Snake Moan, Confessions of a Porn Addict, Shame, Thanks for Sharing, Don Jon, and Choke.

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    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.
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  74. 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". Journal of Psychoactive Drugs. 44 (1): 38–55. doi:10.1080/02791072.2012.662112. PMC4040958 . PMID22641964. 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.
  75. ^ abcd
  76. 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. PMC3865508 . PMID23426671. 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
  77. ^
  78. "What is a Sex Addict". Understanding Sexual Addiction . Retrieved 17 October 2020 .
  79. ^
  80. 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. PMC6135092 . PMID27475769. 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
  81. ^
  82. 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. PMID25083822. S2CID19157711.
    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. .

Books that provide overview history and treatment techniques for sexual addiction include:


Drug addiction, dysregulation of reward, and allostasis

This paper reviews recent developments in the neurocircuitry and neurobiology of addiction from a perspective of allostasis. A model is proposed for brain changes that occur during the development of addiction that explain the persistent vulnerability to relapse long after drug-taking has ceased. Addiction is presented as a cycle of spiralling dysregulation of brain reward systems that progressively increases, resulting in the compulsive use and loss of control over drug-taking. The development of addiction recruits different sources of reinforcement, different neuroadaptive mechanisms, and different neurochemical changes to dysregulate the brain reward system. Counteradaptive processes such as opponent-process that are part of normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to form an allostatic state. Allostasis from the addiction perspective is defined as the process of maintaining apparent reward function stability by changes in brain reward mechanisms. The allostatic state represents a chronic deviation of reward set point and is fueled not only by dysregulation of reward circuits per se, but also by the activation of brain and hormonal stress responses. The manifestation of this allostatic state as compulsive drug-taking and loss of control over drug-taking is hypothesized to be expressed through activation of brain circuits involved in compulsive behavior such as the cortico-striatal-thalamic loop. The view that addiction is the pathology that results from an allostatic mechanism using the circuits established for natural rewards provides a realistic approach to identifying the neurobiological factors that produce vulnerability to addiction and relapse.


The nutrition transition theory

The nutrition transition theory first emerged to describe global trends toward a “Western diet” containing refined foods high in fat and sugar, and low in fiber (21). Later the term was used to capture a correlation with increased BMI and changing economic and agricultural factors. Early identified factors include urbanization, economic growth, technical change, and culture (22) while more recent descriptions of the critical underlying factors include technology, urbanization, economic welfare relative to the cost of food, and expansion of global trade (23). The nutrition transition theory is not a new concept. Previous models have included the demographic and epidemiological transitions. Popkin and Gordon-Larsen identify that both historic processes precede the nutrition transition (22). The epidemiological transition describes a shift from high prevalence of disease associated with famine, malnutrition, and poor sanitation, to a pattern of high prevalence of chronic and degenerative disease associated with urban-industrial lifestyles (24). This ecological framework analyzes changes at the societal level, examining how agricultural and food supply chains impact global dietary patterns. The theory suggests that “upstream” interventions (supply-side) will be more effective than addressing the lower hanging fruit (i.e., exercise, calorie restriction).

The nutrition transition theory is also supported by compelling evidence suggesting that a wide range of animals have also been gaining weight in recent years (25, 26). Other terms that support the 𠇎nvironmental theory of obesity” include “globesity” at the most distal levels, and the “neighborhood effect” at more proximal levels (27). Notwithstanding, the “neighborhood effect” has far-reaching social implications, given that the neighborhood where one lives is merely a proxy for socioeconomic status. Recently, other research has suggested that discussions of nutritional inequality emphasizing supply-side factors are less indicative of consumption patterns than demand-side differences (28), lending support to the food addiction (FA) hypothesis.


Introduction

Addiction is a term that means compulsive physiological need for and use of a habit-forming substance (like heroin or nicotine), characterized by tolerance and well-defined physiological symptoms upon withdrawal it has also been used more broadly to refer to compulsive use of a substance known by the user to be physically, psychologically, or socially harmful (Maddux and Desmond, 2000). In the following essay, I shall try to explore the meaning of this concept.

A note on the term addiction: I shall use the term addiction, except when I refer to a specific diagnostic system that uses other terms. The term dependence was introduced to reduce the stigma associated with addiction in the 50ties. I generally prefer the term addiction, because the term dependence is sometimes used in a counter-therapeutic fashion: I depend on my heroin/cigarettes etc. Addiction more directly addresses the issue: I am addicted to heroin/cigarettes, which means that I suffer various consequences from using the drug, and I will need to think about whether I will accept these consequences, or do something about my addiction (Maddux and Desmond, 2000).


Which paper was it that defined addiction as a release? - Psychology

Substance-use and addictive disorders are marked by physiological dependence, drug-seeking behavior, tolerance, and/or withdrawal.

Learning Objectives

Summarize the similarities and differences in diagnostic criteria, etiology, and treatment options among substance-use and addictive disorders

Key Takeaways

Key Points

  • Substance use disorder combines the previous DSM-IV-TR categories of “substance abuse” and “substance dependence ” into a single disorder measured on a diagnostic continuum from mild to severe. Each specific substance is addressed as a separate use disorder, such as alcohol or stimulants.
  • Substance use disorder can be diagnosed with physiological dependence, evidence of tolerance or withdrawal, or without physiological dependence.
  • Addiction is the continued repetition of a behavior despite adverse consequences, or a neurological impairment leading to such behaviors. Physiological dependence occurs when the body adjusts to the substance.
  • Tolerance is when body adapts to the substance and requires increasingly more to achieve effects. Withdrawal refers to physical and psychological symptoms experienced when reducing or discontinuing a substance.
  • Gambling disorders include the urge to continuously gamble despite harmful negative consequences or a desire to stop.
  • Theories of the causes of substance-related and addictive disorders include genetic predisposition, the self-medication theory, and factors involved with social/economic development.
  • Most treatment for addictions involves counseling, step-based programs, self-help, peer-support, medication, or a combination of these.

Key Terms

  • dysthymia: A milder form of clinical depression, characterized by low-grade depression which lasts at least 2 years.
  • dual diagnosis: Also called co-occurring disorders the condition of suffering from a mental illness and a simultaneously occurring substance abuse problem.
  • dependence: An irresistible physical or psychological need, especially for a chemical substance.

Defining Substance Use Disorder

Substance use disorder combines the previous DSM-IV-TR categories of “substance abuse” and “substance dependence” into a single disorder, measured on a diagnostic continuum from mild to severe. Each specific substance is addressed as a separate use disorder, such as alcohol or stimulants. Other substances include opioids, sedatives, cocaine, cannabis, amphetamines, inhalants, and nicotine.

Addiction is the continued repetition of a behavior despite adverse consequences, or a neurological impairment leading to such behaviors. Addictions can include, but are not limited to, substance abuse, exercise addiction, food addiction, sexual addiction, computer addiction and gambling. Classic hallmarks of addiction include impaired control over substances or behavior, preoccupation with substance or behavior, continued use despite consequences, and denial. Habits and patterns associated with addiction are typically characterized by immediate gratification (short-term reward), coupled with delayed deleterious effects (long-term costs).

Physiological dependence occurs when the body has to adjust to the substance by incorporating the substance into its ‘normal’ functioning. This state creates the conditions of tolerance and withdrawal. Tolerance is the process by which the body continually adapts to the substance and requires increasingly larger amounts to achieve the original effects. Withdrawal refers to physical and psychological symptoms experienced when reducing or discontinuing a substance that the body has become dependent on. Symptoms of withdrawal generally include but are not limited to anxiety, irritability, intense cravings for the substance, nausea, hallucinations, headaches, cold sweats, and tremors. Chemical and hormonal imbalances may arise. Physiological and psychological stress is to be expected if the substance is not re-introduced.

Substance Use, Addiction, and Effects: Individuals suffering from substance use disorder and addiction may engage in the use of many substances. This can lead to personal problems such as failing health and unemployment, and interpersonal problems such as broken families and alienation.

Epidemiology

Substance-related disorders, a category which includes both substance dependence and substance abuse, can lead to significant personal, interpersonal, and societal problems. These disorders are most prevalent in individuals aged 18–25, with a higher occurrence in men than women, and higher occurrence in urban residents than rural residents. On average, general medical facilities hold 20% of patients with substance-related disorders, which could possibly lead to psychiatric disorders later on. Over 50% of individuals with substance-related disorders will often have a dual diagnosis, where they are simultaneously diagnosed with another psychiatric diagnosis, the most common being major depression, dysthymia, personality disorders, and anxiety disorders.

Most countries have legislation which makes various drugs and drug-like substances illegal. Although the legislation may be justifiable on moral grounds to some, it can make addiction or dependency a much more serious issue for the individual. Reliable supplies of a drug become difficult to secure as illegally produced substances may have contaminants. Withdrawal from the substances or associated contaminants can cause additional health issues, and the individual becomes vulnerable to both criminal abuse and legal punishment.

DSM-5 Diagnostic Criteria

The diagnostic criteria for substance use disorder in DSM-5 is set at two or more criteria from a list of 11. Severity of the substance use disorders is based on the number of criteria endorsed, where 2-3 endorsements indicate a mild disorder, 4-5 indicate a moderate disorder, and 6 or more indicate severe substance use disorder. Substance use disorder can be diagnosed with physiological dependence, evidence of tolerance or withdrawal, or without physiological dependence. In addition, criteria for cannabis and caffeine withdrawal were added.

Defining Gambling Disorder

Problem gambling or gambling addiction is an urge to continuously gamble despite harmful negative consequences or a desire to stop. Severe problem gambling may be diagnosed as clinical pathological gambling if the gambler meets certain criteria and is associated with both social and family costs.

DSM-5 Diagnostic Criteria

The DSM-5 has re-classified the condition as an addictive disorder, with sufferers exhibiting many similarities to those who have substance addictions. In order to be diagnosed, an individual must have at least four of the following symptoms in a 12-month period:

  • Needs to gamble with increasing amounts of money in order to achieve the desired excitement.
  • Is restless or irritable when attempting to cut down or stop gambling.
  • Has made repeated unsuccessful efforts to control, cut back, or stop gambling.
  • Is often preoccupied with gambling (e.g., having persistent thoughts of reliving past gambling experiences, planning the next venture, thinking of ways to get money with which to gamble).
  • Often gambles when feeling distressed (e.g., helpless, guilty, anxious, depressed).
  • After losing money gambling, often returns another day to get even (“chasing” one’s losses).
  • Lies to conceal the extent of involvement with gambling.
  • Has jeopardized or lost a significant relationship, job, or educational or career opportunity because of gambling.
  • Relies on others to provide money to relieve desperate financial situations caused by gambling.

Etiology

Several theories of substance use and addiction exist, some of the main ones being genetic predisposition, the self-medication theory, a psychological predisposition, and factors involved with social/economic development. It has long been established that genetic factors along with social and psychological factors are contributors to substance use and addiction. Epidemiological studies estimate that genetic factors account for 40–60% of the risk factors for alcoholism. Similar rates of heritability for other types of drug addiction have been indicated by other studies. Genetic factors may create a predisposition for substance abuse, which means that an individual may have a tendency toward substance abuse. The self-medication hypothesis suggests that certain individuals abuse drugs in an attempt to self-medicate physical, psychological problems, or social problems. There are strong associations between poverty and addiction.

Understanding how learning and behavior work in the reward circuit of the brain can help in understanding drug-seeking behavior and addiction. Drug addiction is characterized by strong, drug-seeking behaviors in which the person who is addicted persistently craves and seeks out drugs, despite the knowledge of harmful consequences. Addictive drugs produce a reward, which is the euphoric feeling resulting from sustained dopamine concentrations in the synaptic cleft of neurons in the brain. The reward circuit, also referred to as the mesolimbic system, is characterized by the interaction of several areas of the brain.

According to the Illinois Institute for Addiction Recovery, evidence indicates that pathological gambling is an addiction similar to chemical addiction. It has been seen that some pathological gamblers have lower levels of norepinephrine than normal gamblers. According to a study conducted by Alec Roy, formerly at the National Institute on Alcohol Abuse and Alcoholism, norepinephrine is secreted under stress, arousal, or thrill, so pathological gamblers gamble to make up for their under-dosage. Deficiencies in serotonin might also contribute to compulsive behavior, including a gambling addiction. Others argue that social factors are far more important determinants of gambling behavior than brain chemicals and suggest that a social model may be more useful in understanding the issue.

Treatment

Early treatment of acute withdrawal from substances often includes medical detoxification, in which a person goes through the process and experience of withdrawal symptoms while discontinuing a drug. A detoxification program for physical dependence does not necessarily address the precedents of addiction, social factors, psychological addiction, or the often-complex behavioral issues that intermingle with addiction.

Treatments for addiction usually involve planning for specific ways to avoid the addictive stimulus and/or therapeutic interventions intended to help a client learn healthier ways to find satisfaction. Clinical leaders in recent years have attempted to tailor intervention approaches to specific influences that affect addictive behavior, using therapeutic interviews in an effort to discover factors that led a person to embrace unhealthy, addictive sources of pleasure or relief from pain. Several evidenced-based intervention programs have emerged, including behavioral marital therapy, community reinforcement approaches, cue exposure therapy, and contingency management strategies. Most treatment for addictions involves counseling, step-based programs, self-help, peer-support, medication, or a combination of these.

Twelve-step programs (such as Alcoholics Anonymous) are a set of guiding principles, sometimes accepted by members as being ‘spiritual principles’, outlining a course of action for tackling problems of addiction including alcoholism, drug addiction, and compulsion. Alcoholics Anonymous is the largest of all the twelve-step programs (from which all other twelve-steps programs are derived), followed by Narcotics Anonymous


Thesis about Drug Addiction

It is extremely important to recognize drug addiction at the right moment, preferably in the beginning, so as not to spoil social relationships and health. It is necessary to understand that the sooner the problem will be attended, the better it is for the treatment progress. There are certain symptoms of drug abuse: when drug is getting people into legal trouble, if because of it people start neglecting their responsibilities, when they use drugs under dangerous conditions, and when they cause problems in relationships.

It is absolutely necessary to prevent drug addiction levels’ raise, and it is necessary for all the people to take part in this prevention program. Only if we…


Drug addiction, dysregulation of reward, and allostasis

This paper reviews recent developments in the neurocircuitry and neurobiology of addiction from a perspective of allostasis. A model is proposed for brain changes that occur during the development of addiction that explain the persistent vulnerability to relapse long after drug-taking has ceased. Addiction is presented as a cycle of spiralling dysregulation of brain reward systems that progressively increases, resulting in the compulsive use and loss of control over drug-taking. The development of addiction recruits different sources of reinforcement, different neuroadaptive mechanisms, and different neurochemical changes to dysregulate the brain reward system. Counteradaptive processes such as opponent-process that are part of normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to form an allostatic state. Allostasis from the addiction perspective is defined as the process of maintaining apparent reward function stability by changes in brain reward mechanisms. The allostatic state represents a chronic deviation of reward set point and is fueled not only by dysregulation of reward circuits per se, but also by the activation of brain and hormonal stress responses. The manifestation of this allostatic state as compulsive drug-taking and loss of control over drug-taking is hypothesized to be expressed through activation of brain circuits involved in compulsive behavior such as the cortico-striatal-thalamic loop. The view that addiction is the pathology that results from an allostatic mechanism using the circuits established for natural rewards provides a realistic approach to identifying the neurobiological factors that produce vulnerability to addiction and relapse.


Social Media Addiction Research Paper

Social media addiction is a serious issue today. It is the main cause for various Internet associated psychological disorders.

In psychology, any Internet addiction is usually divided on stages. They include the initial stage of a healthy interest in the Internet and pathological dependence on it that affects human performance and begins to harm the person’s social life, undermining his mental health. With social media, the situation is completely analogous.

At the core of the social media addiction, experts say, is primarily low self-confidence and self-doubt. People suffering from a low self-esteem, dissatisfied with their appearance or small attention from their environment are often hooked on the “online needle.” Typically, these are people with humanitarian mindset, prone to fantasies, loving invent things to look better and often having wishful thinking.

We can write your Social Media Addiction research paper from scratch!

Social media addiction has physiological characteristics by which it can be classified as a mental illness, and not just a bad habit. Among its symptoms, there are wet eyes, increased sweating, and chronic insomnia. The fact is that often social media surfing creates increased levels of dopamine – a substance similar to adrenaline – in the brain.

At this activity, an addicted person experiences excitement, which is akin to the gambling fever or sexual arousal. Such a person seeks to experience this state over and over again and starts to use the social networks as a tool for pleasure.

In addition, social media addiction can harm health due to the reduction of communicating with real people. According to experts, the lack of communication may affect the immune system, hormonal balance, state of the arteries and thought processes, which in the long run increases the risk of the emergence and development of diseases such as cancer, cardiovascular disease, and dementia.

According to the experts, his type of addiction is especially dangerous for teenagers, as they form a false impression that love and friendship can be easily won and just as easy destroyed. In addition, according to Dr. Himanshu Tyagi, to people who are accustomed to the rapid flow of Internet life, the reality may seem too boring, and they may try to “revive” it, making impulsive acts, including suicide attempts, because they tend to underestimate the value of effective life.

It is quite simple to detect social media addiction: you need stop using social networks for some time, such as month, and if there is no problem with such an abstention, there is no addiction, if there is irresistible desire, there is possibility of the addiction.

In the fight against the social media addiction in educational and business institutions such services are restricted. The is a bunch of various software which allows to easily restrict access to such services.

Free sample research paper on social media addiction is a good start for non-experienced writer.

Are you looking for a top-notch custom research paper about Social Media Addiction? Is confidentiality as important to you as the high quality of the product?


Neurochemistry of Resilience

&ldquoAllostasis&rdquo refers to the dynamic process through which the body adapts to daily stressors and maintains homeostasis (Sterling and Eyer 1988). Sudden stressful events trigger the release of the &ldquoflight-or-fight&rdquo hormones (i.e., catecholamines) and other stress hormones in the brain, preparing the organism to cope with stress and avert harm. This process is mediated by a stress circuit (see figure 1), which is consistently implicated in stress-related disorders such as mood and anxiety disorders and addictive disorders. Interindividual variability in stress resilience results from differences in the coordinated stress response. This response comprises the function and interactions of numerous hormones, neurotransmitters, and neuropeptides, some of which are discussed below.

Figure 1 Norepinephrine (NE) and dopamine (DA) are the principle chemical messengers employed in central and peripheral sympathetic synapses, and the human NE transporter rapidly clears NE and DA from the synaptic cleft via efficient transport systemattenuating signaling, recycling 90 percent of these synaptic monoamines. NE neurons innervate nearly all parts of the neuroaxis, with the locus coeruleus (LC) being responsible for most of the NE in the brain. NE exerts neuromodulatory effects on the cellular activity of post-synaptic target neurons in many brain circuits, thereby moderating synaptic transmission in target circuits including the thalamus, prefrontalcortex (PFC), ventral striatum (via PFC), and amygdala, which have been implicated in substance use disorders. The widespread and divergent anatomical organization positions the NE system to be involved in widely varying functions including responses to stress, which alters both the electrophysiological activity of NE neurons in the LC and the release of NE in the terminal regions of these cells, as well as crucial cognitive functions, including attention and arousal. NE mediates many of the adaptive and maladaptive consequences of stress exposure, implicating this system in a variety of abnormal behaviors including alcohol dependence.

HPA Axis

The HPA axis is a system regulated by a complex negative-feedback system. CRF, released by the hypothalamus in response to stress, triggers the release of adrenocorticotrophic hormone (ACTH) from the anterior pituitary gland. This process leads to the synthesis and release of cortisol by the adrenal cortex. Cortisol secretion acutely facilitates cognitive, metabolic, immunologic, and behavioral adaptations to stress. It also results, however, in &ldquoallostatic overload&rdquo when stress becomes chronic or overwhelming (McEwen 2003). Resilience is maintained when the stress response is both activated and terminated efficiently. The adaptive responses of the HPA axis are thought to involve an optimal balance of the cortisol-binding receptors GR and mineralocorticoid receptor (de Kloet et al. 2005, 2007).

Studies showing lower plasma levels of ACTH but not cortisol in men with a family history of alcoholism (Dai et al. 2007 Gianoulakis et al. 2005) suggest that HPA axis dysfunction might predate the onset of alcoholism. Long-term alcohol abuse is associated with increased extrahypothalamic CRF signaling and dampened HPA axis responsivity (Richardson et al. 2008). Increases in extrahypothalamic CRF contribute to negative emotional states during abstinence, increasing risk for relapse (Koob and Le Moal 2008). In a recent study, researchers asked alcoholics who had been abstinent for 1 month to imagine a relaxing situation of their choice while listening to a previously recorded audiotape of this situation. A greater cortisol-to-corticotropin ratio (i.e., higher adrenal sensitivity) during this relaxed state was found to predict a shorter time to alcohol relapse, thus suggesting that new treatments aimed a decreasing adrenal sensitivity could reduce relapse rates (Sinha et al. 2011).

Norepinephrine

During the acute stress response, the hormone norepinephrine (NE) is released through direct projections from the brain site where NE is synthesized (i.e., locus coeruleus) and other brain stem nuclei (i.e., structures that act as transit points for brain signals) into the amygdala, hippocampus, nucleus accumbens, prefrontal cortex (PFC), and other brain areas mediating emotional responses. Several studies have linked abnormal regulation of brain NE systems to stress disorders (Krystal and Neumeister 2009 O&rsquoDonnell et al. 2004). As drug dependence develops, levels of the neurotransmitter dopamine decrease and the NE stress system in the brain is activated, contributing to &ldquostress-like states&rdquo and increased vulnerability to stressors during periods of abstinence (Koob and Le Moal 2008). In combination with CRF, NE also might contribute to the consolidation of emotional memories associated with drug use in the amygdala (Koob et al. 2009).

Stress resilience may be enhanced through the regulation of NE system responsiveness, which is mediated through effects on the NE transporter on catecholamine receptors (i.e., &alpha2 adrenoreceptors), as well as interactions between the NE and other neurobiologic systems, such as the dopamine and serotonin systems (Krystal and Neumeister 2009). For example, animal studies have shown that PFC NE nerve cell projections (i.e., axons) have a latent capacity to enhance synthesis and recovery of transmitter, which might underlie the capacity to adapt to stress (Miner et al. 2006). This mechanism deserves further study in humans with positron emission tomography (PET), which uses positron-emitting radiotracers to show where and how compounds act in the brain (Ding et al. 2005). Other targets include the &alpha2a and &alpha2c receptors, which have complementary roles in the regulation of stress responses (Small et al. 2000). Yohimbine, a drug that blocks the &alpha2 receptors (i.e., a receptor antagonist), increases alcohol self-administration and induces reinstatement of alcohol seeking (Le et al. 2005 Marinelli et al. 2007). The recent finding that an &alpha2c receptor polymorphism (Del322-325) reduces feedback inhibition of sympathetic NE release (Neumeister et al. 2005) as well as evidence from studies in mice bred to have an inactivated &alpha2c receptor (i.e., knockout mice) (Sallinen et al. 1999), suggest that interventions targeting this receptor might modulate stress and anxiety responses.

Serotonin

The serotonin (5-HT) system, which consists primarily of neurons from the dorsal raphe nuclei that project widely throughout the brain (including the amygdala, ventral striatum, and PFC), is involved in the regulation of stress and anxiety. Serotonin has an important role in promoting neuroplasticity in the central nervous system, both during development and in adulthood. Serotonin also regulates the neurochemical effects of drugs of abuse, including alcohol, and is involved in modulating impulsivity, known to increase risk for alcohol and drug abuse (Kirby et al. 2011). The 5-HT system is itself modulated by drugs of abuse. For example, alcohol administration elevates 5-HT levels in the nucleus accumbens, ventral tegmental area (VTA), amygdala, and hippocampus, an effect that is more pronounced in alcohol-preferring rats. Reduced activity of the 5-HT system might contribute to depression during withdrawal and increase vulnerability to relapse (Kirby et al. 2011). In studies of macaques, differential function of the 5-HT system in interaction with early life stress was found to affect alcohol consumption: peer-reared female macaques with a specific variant (i.e., the l/s genotype) of the serotonin transporter polymorphism showed higher levels of ethanol preference and increased consumption over time (Barr et al. 2004).

The 5-HT system is extremely complex, including at least 14 receptor subtypes. Of these receptors, the 5-HT1A, 5-HT1B, 5-HT2A, and 5-HT2C receptors are well understood through research on anxiety regulation in both animals and humans (Krystal and Neumeister 2009). The 5-HT1A receptor is thought to counteract the deleterious effects of 5-HT2A receptor activation (i.e., the disruption of brain cell creation), mediated by increased release of the neurotransmitter glutamate and direct glucocorticoid effects (Hoebel et al 2007). Restrained function of another 5-HT receptor, 5HT1B, might be central to resilient stress responses by enhancing synaptic availability of 5-HT in the amygdala and other cortical regions as well as promoting dopamine release in the ventral striatum (Clark and Neumaier 2001 Krystal and Neumeister 2009 Sari 2004) (see figure 2).

Figure 2 Alterations in serotonin 1B receptor (5HT1BR) function might contribute to alcohol dependence by influencing not only serotonin (5HT) input to the ventral striatum via the receptors&rsquo role as 5HT terminal autoreceptors, 1 but also dopaminergic input to the striatum via the role of these receptors as heteroreceptors 2 on GABA terminals within the ventral tegmental area, and glutamatergic activity within the ventral striatum via heteroreceptors on corticofugal projections.

1 Autoreceptor: A site on a neuron that binds the neurotransmitter released by that neuron, which then regulates the neuron&rsquos activity.

2 Heteroreceptor: A site on a neuron that binds a modulatory neuroregulator other than that released by the neuron.

The role of this receptor subtype in addiction disorders recently was studied in humans. The report demonstrated that alcohol dependence in humans, like in rodent models, is associated with increased levels of ventral striatal 5-HT1B receptors (Hu et al. 2010). Additional research is necessary to understand the complex function of the 5-HT system. However, these findings suggest possible novel targets for the treatment of stress-related disorders and, most important, addiction disorders.

Dopamine

Dopaminergic neurons in the ventral tegmental area (VTA) of the midbrain project to the nucleus accumbens and other limbic areas to form the mesolimbic dopamine system, the most studied reward circuit. Dopamine neurons are activated in response to reward or the expectation of reward, and generally are inhibited by aversive stimuli. Dopamine signaling is central to the onset of addiction, as well as to the transition to dependence in interaction with other neurotransmitter systems (Ross and Peselow 2009). Drugs of addiction trigger large but brief increases in extracellular dopamine in the nucleus accumbens. Over time, chronic drug use downregulates dopamine receptors and dopamine release, leading to decreased sensitivity to natural rewards, such as food and sex, and leading also to further drug use (Volkow et al 2010).

Although findings from animal studies suggest that early-life stress can lead to long-lasting changes in gene expression in the mesolimbic dopamine pathway, ultimately increasing vulnerability to addictive disorders, not all individuals with a history of childhood abuse develop addictive or other disorders, thereby stressing the role of protective factors such as genetic variants conferring resilience (Enoch 2010).

Findings from several studies suggest that higher dopamine D2 receptor availability in the striatum might promote resilience to alcohol use disorders. In a study of unaffected members of alcoholic families, higher striatal dopamine D2 receptor availability was associated with higher positive emotionality, discussed above as a protective factor against alcohol use disorders (Volkow et al 2006). Other studies found that higher striatal dopamine D2 receptor availability was associated with resistance to the reinforcing effects of stimulants in healthy volunteers (Volkow et al. 1999, 2002) and in rats (Thanos et al. 2008).

NPY, a 36&ndashamino acid peptide, is widely distributed in the brain. NPY has anxiety-reducing properties in rodents and is thought to enhance resilience to stress in humans (Feder et al. 2009 Morgan et al. 2000). Evidence from animal and human studies suggests that NPY has a key role in regulating alcohol intake, dependence, and withdrawal. Mice genetically modified to overexpress NPY consume less alcohol (Thiele et al. 1998), and administration of NPY into the cerebral ventricles of the brain (i.e., intracerebroventricular infusion) reduces alcohol consumption in alcohol-preferring rats (Thorsell 2007). Infusion of NPY into the central nucleus of the amygdala has been shown to normalize both anxiety behaviors and alcohol intake, suggesting that NPY might work by modulating anxiety responses (Zhang et al. 2010). In rhesus macaques exposed to early life stress, and in human studies, certain NPY gene polymorphisms are associated with differential susceptibility to alcohol or cocaine dependence (Koehnke et al. 2002 Lindell et al. 2010 Mottagui- Tabar et al. 2005 Wetherill et al. 2008).

Endocannabinoids

An emerging body of evidence suggests an important role for the endogenous cannabinoid (eCB) system and specifically the CB1 receptor in alcohol-related behaviors (for review, see Basavarajappa 2007). To date, however, only peripheral measures of eCB function have been collected in living humans with alcohol dependence (AD) (Mangieri et al. 2009), and no human in vivo data on the potentially critical role of the brain CB1 receptor in AD have been collected yet. At a neurobiological level, studies show impairments in decision making in alcohol-dependent patients (Dom et al. 2006), which is associated with altered functions in a cortico-limbic- striatal circuit, including the amygdala, hippocampus, anterior cingulate cortex, insula, and the ventral striatum. Three sets of factors are thought to be responsible for high alcohol relapse rates. First, individual differences in the positive, reinforcing properties of alcohol are known to increase risk of alcoholism and possibly alcohol relapse (Schuckit and Smith 1996). Second, stimuli previously associated with alcohol use and its physiological and subjective effects become paired with alcohol and are thought to serve as &ldquoconditioned cues&rdquo that can increase alcohol craving and subsequent alcohol use (O&rsquoBrien et al. 1998). Finally, stress has been found to increase the risk of alcohol relapse (Brown et al. 1990 Miller et al. 1996 Sinha 2001). All three factors can be linked to the eCB system and its attending CB1 receptor and increasing evidence derived from animal studies suggests a role of the eCB system in alcohol-related behaviors (Vinod and Hungund 2006).

Such research suggests that upregulation of CB1 receptor&ndashmediated G-protein signaling in a brain circuit that mediates AD susceptibility (involving the amygdala, hippocampus, ventromedial prefrontal cortex, insula, and ventral striatum) (Sullivan and Pfefferbaum 2005) might contribute to the increased alcohol consumption in patients with chronic AD. For example, CB1 inactivation (Hungund et al. 2003 Naassila et al. 2004 Poncelet et al. 2003 Thanos et al. 2005) and pharmacological manipulation of CB1 receptor function (Femenia et al. 2010 Maccioni et al. Maccioni et al. 2008 Malinen and Hyytia 2008) result in reduced voluntary alcohol intake. In addition, administration of an agent that binds to the CB1 receptor (i.e., a CB1 receptor agonist) (Colombo et al. 2002 Gallate et al. 1999 Vinod et al. 2008b) enhances alcohol consumption.

In contrast, acute, short-term alcohol intoxication is associated with elevated eCB levels (Basavarajappa et al. 2006 Blednov et al. 2007 Vinod et al. 2008a), reduced activity of the enzyme fatty acid amide hydrolase (FAAH), and reduced CB1 receptor&ndashmediated G-protein signaling (Vinod et al. 2011). This mediates the activation of the mesolimbic dopaminergic system (Cheer et al. 2007 Hungund et al. 2003 ), which has been extensively studied in alcohol dependence. Evidence suggests a functional interaction between these systems, which might be associated with the reinforcing effects of alcohol and therefore may be an important mechanism in the etiology of alcohol dependence. Findings in animal studies recently have stimulated interest in the therapeutic potential of enhancing eCB signaling, with research in humans having just begun (Hill et al. 2009). However, an accumulating body of evidence suggests that the eCB system, and in particular its attending CB1 receptor, provides novel leads for treatment development in alcohol dependence (Bailey and Neumeister 2011).


Contents

  • addiction – a biopsychosocial disorder characterized by persistent use of drugs (including alcohol) despite substantial harm and adverse consequences
  • addictive drug – psychoactive substances that with repeated use are associated with significantly higher rates of substance use disorders, due in large part to the drug's effect on brain reward systems
  • 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 and desirable or as something to approach
  • 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

None of the official diagnostic classification frameworks list "sexual addiction" as a distinct disorder.

DSM Edit

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. [15]

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." [16] The reference to sexual addiction was subsequently removed. [17] The DSM-IV-TR, published in 2000 (DSM-IV-TR), did not include sexual addiction as a mental disorder. [18]

Some authors suggested that sexual addiction should be re-introduced into the DSM system [19] however, sexual addiction was rejected for inclusion in the DSM-5, which was published in 2013. [20] 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. [21] [22]

ICD Edit

The World Health Organization produces the International Classification of Diseases (ICD), which is not limited to mental disorders. The most recent approved 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. [23] The most recent (yet unapproved) version of that document, ICD-11, includes "compulsive sexual behavior disorder" [24] as a diagnosis (code 6C72)—it does not use the addiction model. [25]

CCMD Edit

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. [ citation needed ]

Other Edit

Some mental health providers have proposed various, but similar, criteria for diagnosing sexual addiction, including Patrick Carnes, [26] Aviel Goodman, [27] and the late Jonathan Marsh. [28] 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. [29] No diagnostic proposal for sex addiction has been adopted into any official government diagnostic manual, however. [ citation needed ]

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

In 2011, the American Society of Addiction Medicine (ASAM), the largest medical consensus of physicians dedicated to treating and preventing addiction, [30] redefined addiction as a chronic brain disorder, [31] which for the first time broadened the definition of addiction from substances to include addictive behaviors and reward-seeking, such as gambling and sex. [32]

Borderline personality disorder Edit

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. [33] 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. [34]

Medical reviews and position statements Edit

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." [35]

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. [36]

In 16 November 2017 the Association for the Treatment of Sexual Abusers (ATSA) published a position against sending sex offenders to sex addiction treatment facilities. [37] Those centers argued that "illegal" behaviors were symptoms of sex addiction, which ATSA challenged they had no scientific evidence to support. [ citation needed ]

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. [38] [39] [40] Sexual activity is an intrinsic reward that has been shown to act as a positive reinforcer, [41] strongly activate the reward system, and induce the accumulation of ΔFosB in part of the striatum (specifically, the nucleus accumbens). [38] [39] [40] 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. [39] [42] [43] [44]

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. [38] Current experimental models of addiction to natural rewards and drug reward demonstrate common alterations in gene expression in the mesocorticolimbic projection. [38] [45] 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 [45] it has been implicated in addictions to alcohol, cannabinoids, cocaine, nicotine, opioids, phenylcyclidine, and substituted amphetamines. [38] [45] [46] ΔJunD is the transcription factor which directly opposes ΔFosB. [45] 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). [45]

ΔFosB also plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise. [39] [45] 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. [38] [39] Thus, ΔFosB is also the key transcription factor involved in addictions to natural rewards as well, [38] [40] and sexual addictions in particular, since ΔFosB in the nucleus accumbens is critical for the reinforcing effects of sexual reward. [39] 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. [38] [40]

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
[38]
Behavioral plasticity
Escalation of intake Yes Yes Yes [38]
Psychostimulant
cross-sensitization
Yes Not applicable Yes Yes Attenuated Attenuated [38]
Psychostimulant
self-administration
[38]
Psychostimulant
conditioned place preference
[38]
Reinstatement of drug-seeking behavior [38]
Neurochemical plasticity
CREB phosphorylation
in the nucleus accumbens
[38]
Sensitized dopamine response
in the nucleus accumbens
No Yes No Yes [38]
Altered striatal dopamine signaling ↓DRD2, ↑DRD3 ↑DRD1, ↓DRD2, ↑DRD3 ↑DRD1, ↓DRD2, ↑DRD3 ↑DRD2 ↑DRD2 [38]
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 [38]
Changes in striatal opioid peptides ↑dynorphin
No change: enkephalin
↑dynorphin ↓enkephalin ↑dynorphin ↑dynorphin [38]
Mesocorticolimbic synaptic plasticity
Number of dendrites in the nucleus accumbens [38]
Dendritic spine density in
the nucleus accumbens
[38]

Counseling Edit

As of 2017, none of the official regulatory bodies for Psycho-sexual Counseling 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. [35] As a result, treatment for sex addiction is more often provided by addiction professionals in the counseling field than psychosexual specialists. These counseling professionals typically hold advanced degrees of education including Master's degrees or Doctorates in counseling or a related field like psychology. These counselors can also hold certifications like Licensed Professional Counselors (LPC-S) who are required to hold a Master's degree or higher level of education. Therapists and Psychologists usually also hold a Master's in a related field of study. [47]

Cognitive behavioral therapy is a common form of behavioral treatment for addictions and maladaptive behaviors in general. [48] 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. [29] [49] Their treatments have yet to be subject to peer-review, so it is unclear if they help or harm patients.

Support groups Edit

Online support groups Edit

In-person support groups Edit

In-person support groups are available in most of the developed world. None yet have any scientific evidence to show whether or not they are helpful, so attendees do so at their own risk.

    : For those who want to reduce or eliminate their use of pornography, masturbation, and/or unwanted sexual activity. : Similar to the above. : 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. .

In places where none of the above are available, open meetings of Alcoholics Anonymous or Narcotics Anonymous may be a second-best option. At open AA and NA meetings, non-alcoholics/non-addicts are welcome to observe but not participate.

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.

Medications Edit

Antiviral drugs Edit

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. [ citation needed ]

In the US, most insurance plans cover these drugs. [50]

According to a systematic review from 2014, observed prevalence rates of sexual addiction/hypersexual disorder range from 3% to 6%. [2] Some studies suggest that sex addicts are disproportionately male, at 80%. [51]

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. [52] 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. [ citation needed ]

Controversy Edit

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. [38] 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, [15] these are ill-suited for modelling compulsive behaviors in a clinical setting. [38] 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". [21] 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." [2]

External media
Audio
Robert Weiss & David Ley. Is sex addiction a myth? // KPCC (25 April 2012, 9:29 am)
Video
Nicole Prause, Ph.D. (sexual physiologist). [1] 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. [54] [55] 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). [56] 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. [57] [58] The 1988 paper argued that the condition is instead a way of projecting social stigma onto patients. [57] "Love addiction" falls into the same controversial area as well since it refers to a frequent pattern of intimate relationships which can be a by product of cultural norms and commonly accepted morals. [59]

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." [60] : 8 Klein singled out a number of features that he considered crucial limitations of the sex addiction model [60] : 8 and stated that the diagnostic criteria for sexual addiction are easy to find on the internet. [60] : 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." [60] : 10

Historically, the claim of sex addiction has been the preferred defense of white men who committed felonies. [61]

Popular culture Edit

Sexual addiction has been the main theme in a variety of films including Diary of a Sex Addict, I Am a Sex Addict, Black Snake Moan, Confessions of a Porn Addict, Shame, Thanks for Sharing, Don Jon, and Choke.

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  72. Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. 61 (7): 1109–1122. doi:10.1016/j.neuropharm.2011.03.010. PMC3139704 . PMID21459101. 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"
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  74. 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". Journal of Psychoactive Drugs. 44 (1): 38–55. doi:10.1080/02791072.2012.662112. PMC4040958 . PMID22641964. 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.
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  76. 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. PMC3865508 . PMID23426671. 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
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  80. 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. PMC6135092 . PMID27475769. 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
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  82. 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. PMID25083822. S2CID19157711.
    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. .

Books that provide overview history and treatment techniques for sexual addiction include:


New definition of addiction: Addiction is a chronic brain disease, not just bad behavior or bad choices

The American Society of Addiction Medicine (ASAM) has released a new definition of addiction highlighting that addiction is a chronic brain disorder and not simply a behavioral problem involving too much alcohol, drugs, gambling or sex. This the first time ASAM has taken an official position that addiction is not solely related to problematic substance use.

When people see compulsive and damaging behaviors in friends or family members -- or public figures such as celebrities or politicians -- they often focus only on the substance use or behaviors as the problem. However, these outward behaviors are actually manifestations of an underlying disease that involves various areas of the brain, according to the new definition by ASAM, the nation's largest professional society of physicians dedicated to treating and preventing addiction.

"At its core, addiction isn't just a social problem or a moral problem or a criminal problem. It's a brain problem whose behaviors manifest in all these other areas," said Dr. Michael Miller, past president of ASAM who oversaw the development of the new definition. "Many behaviors driven by addiction are real problems and sometimes criminal acts. But the disease is about brains, not drugs. It's about underlying neurology, not outward actions."

The new definition resulted from an intensive, four-year process with more than 80 experts actively working on it, including top addiction authorities, addiction medicine clinicians and leading neuroscience researchers from across the country. The full governing board of ASAM and chapter presidents from many states took part, and there was extensive dialogue with the National Institute on Drug Abuse (NIDA).

The new definition also describes addiction as a primary disease, meaning that it's not the result of other causes such as emotional or psychiatric problems. Addiction is also recognized as a chronic disease, like cardiovascular disease or diabetes, so it must be treated, managed and monitored over a life-time.

Two decades of advancements in neurosciences convinced ASAM that addiction needed to be redefined by what's going on in the brain. Research shows that the disease of addiction affects neurotransmission and interactions within reward circuitry of the brain, leading to addictive behaviors that supplant healthy behaviors, while memories of previous experiences with food, sex, alcohol and other drugs trigger craving and renewal of addictive behaviors. Meanwhile, brain circuitry that governs impulse control and judgment is also altered in this disease, resulting in the dysfunctional pursuit of rewards such as alcohol and other drugs. This area of the brain is still developing during teen-age years, which may be why early exposure to alcohol and drugs is related to greater likelihood of addiction later in life.

There is longstanding controversy over whether people with addiction have choice over anti-social and dangerous behaviors, said Dr. Raju Hajela, past president of the Canadian Society of Addiction Medicine and chair of the ASAM committee on the new definition. He stated that "the disease creates distortions in thinking, feelings and perceptions, which drive people to behave in ways that are not understandable to others around them. Simply put, addiction is not a choice. Addictive behaviors are a manifestation of the disease, not a cause."

"Choice still plays an important role in getting help. While the neurobiology of choice may not be fully understood, a person with addiction must make choices for a healthier life in order to enter treatment and recovery. Because there is no pill which alone can cure addiction, choosing recovery over unhealthy behaviors is necessary," Hajela said.

"Many chronic diseases require behavioral choices, such as people with heart disease choosing to eat healthier or begin exercising, in addition to medical or surgical interventions," said Dr. Miller. "So, we have to stop moralizing, blaming, controlling or smirking at the person with the disease of addiction, and start creating opportunities for individuals and families to get help and providing assistance in choosing proper treatment."


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