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While that line of research overwhelmingly supports the prevalence and risks associated with Internet and Internet related addiction, it is outside the scope of this neuroscience focused review.
Thus we believe that it makes sense to limit this review primarily to the studies that meet the most rigorous requirements, studies that address the neurobiochemical and neurophysiological processes known to underlie addiction generally.
We hope that the articles reviewed here will make it clear that the dozens of studies supporting IA and each of its subtypes as being neuroscientifically similar to substance addiction and will demonstrate that all of the possible Internet behaviors must be considered as potentially addictive in the same way, as variations on a theme rather than separate disorders, just as diverse forms of gambling e.
In fact it is the case that most IA studies around the world have considered the various Internet behaviors in this light.
To conduct the research, an extensive literature search and review was performed utilizing a variety of sources: A universal inclusion criterion was publication in a peer-reviewed journal.
Continuous rechecks of the more rapidly emerging subject areas e. As such, an exact number of results reviewed was impossible to calculate as the rechecks often returned results already reviewed.
Some manual screen of ambiguously titled papers was required performed by first author. The reference management tool Zotero was used to build a database of all articles considered.
The scope of this topic was limited to the previous ten years, with primary focus given to articles published in the past five years.
Older publications considered key developments within the scientific advancement of this field were also included for example, Blum et al.
This scope was not time-delimited, as it is an emerging topic whose entire historical context is relevant. Analytical priority, however, was given to literature reviews, and articles published via a newest to oldest methodology.
The following search terms and their derivatives were used in multiple combinations: Multiple combinations of the following search terms and their derivatives were used in conducting the research: As this is another emerging topic, there was no time-scope set for this topic, although priority was given to studies and reviews published in the previous five years.
Special attention to nomenclature was required here, as the disorder is studied under different headings. As such, the following search terms and their derivatives were used in multiple combinations: No time-limitation was placed on this topic, and the following search terms and their derivatives were used in multiple combinations: A less-than-exhaustive final selection approach was taken based on the fact that the APA has already approved IGD as a research-worthy diagnosis, and thus the full volume of articles in this subject area was not needed to support our premise.
Research into the area of addictive sexual behaviors on the Internet began with an inquiry into the various constructs surrounding compulsive sexual behavior.
There was no specific time-delimitation for this search, however, as with behavioral addiction, analytical priority was placed upon literature reviews and articles published via a newest to oldest methodology.
Additional screening was required to differentiate articles about IP included and non-IP not included.
Multiple combinations of the following search terms and their derivatives were used: All drugs of abuse affect the mesolimbic dopamine DA pathway, which originates from the ventral tegmental area VTA and projects into the nucleus accumbens NAcc.
Commonly called the reward center, the NAcc is heavily connected with pleasure, reinforcement learning, reward seeking, and impulsivity.
The mesolimbic dopamine pathway connects with three other key regions to form a collection of integrated circuits commonly called the reward system: The amygdala positive and negative emotions, emotional memory , hippocampus processing and retrieval of long term memories , and the frontal cortex coordinates and determines behavior.
Taken together, the reward system and its connecting regions modulate, among other things, pleasure, reward, memory, attention, and motivation [ 43 ].
Naturally occurring behaviors such as eating and sex, have evolved such that they activate the reward system due to the fact that they reinforce behaviors necessary for survival [ 20 ].
The past decade has yielded multiple theories of addiction, all of which involve the reward system and related brain regions and substrates [ 44 ].
Nora Volkow describes addiction as a neurobiochemically based shift from impulsive action learned through positive reinforcement to compulsive actions learned through negative reinforcement [ 43 ].
This in turn is seen as leading to an addictive cycle that progressively worsens over time. Different classes of drugs activate the reward system through different means, however, the universal result is a flood of dopamine in the NAcc reward center.
This results in acute positive reinforcement of the behavior that initiated the flood. In this impulsive stage, this positive reinforcement results in addictive related learning associations [ 45 ].
Neuroplastic changes begin to occur, however, as the continued release of dopamine in the NAcc leads to an increase in dynorphin levels.
Dynorphin, in turn, decreases the dopaminergic function of the reward system, resulting in a decrease of the reward threshold and an increase in tolerance [ 43 , 45 ].
The resulting negative emotional state leads to activation of brain stress systems and dysregulation of anti-stress systems.
This leads to a decreased sensitivity to rewards and an increase in the reward threshold, which is called tolerance.
This further progresses to negative reinforcement as the individual continues to engage in the addictive behaviors to avoid the negative affect associated with withdrawal.
A key point of this stage is that withdrawal is not about the physiological effects from a specific substance. Rather, this model measures withdrawal via a negative affect resulting from the above process.
Aversive emotions such as anxiety, depression, dysphoria, and irritability are indicators of withdrawal in this model of addiction [ 43 , 45 ].
Researchers opposed to the idea of behaviors being addictive often overlook or misunderstand this critical distinction, confusing withdrawal with detoxification [ 46 , 47 ].
A second component of the reward system comes into play here; the mesocortical dopamine pathway. Specific affected areas within the prefrontal cortex include the dorsolateral prefrontal cortex DLPFC , responsible for key components of cognition and executive function, and the ventromedial prefrontal cortex VMPFC responsible for components of inhibition and emotional response.
Taken together, the mesocortical dopamine pathway affects the cognitive component of reward processing [ 43 , 45 ]. The I-RISA model integrates the increased salience of learned drug-related cues resulting from the aforementioned positive and negative reinforcement of the addictive behavior with newly developed deficiencies in top-down inhibitory control.
This leaves the individual vulnerable to reinstatement of the behavior, and two primary mechanisms have been identified; cue-induced reinstatement and stress-induced reinstatement [ 43 , 45 ].
George Koob proposed an expansion of the second stage of addiction. In the opponent-process model of motivation, a-processes reflect positive hedonic effects and b-processes reflect negative hedonic effects.
The application in addiction is that a-processes occur first and reflect tolerance. In contrast, the b-processes arise after the a-process have concluded and reflect withdrawal.
Solomon and Corbit [ 52 ] used skydivers as an example of the opposite, wherein the novice skydivers experience great fear when they jump b-process and some relief when they land a-process.
As they repeat the behavior, the balance shifts such that experienced skydivers experience some fear when they jump but great relief when they land.
Koob [ 51 ] overlays a detailed biologic model onto the psychological opponent-process theory. The aforementioned elevated levels of dynorphin further elevate CRF, and the engagement of these systems brings about many of the negative affects linked to the withdrawal stage.
Compounding the problem, the brains anti-stress system also becomes dysregulated, as evidenced by decreases in neuropeptide Y a natural anxiolytic in the brain.
The reward system subsequently develops an altered set-point, leaving the individual vulnerable to relapse and dependence. While both the Anti-Reward and I-RISA models include learning components, other theories of addiction focus primarily on the learning aspects of addiction, and the biological underpinnings thereof.
Everitt and Robbins [ 55 , 56 ] propose a model of addiction as a steady transition from voluntary actions to habitual actions to compulsive actions.
Their model includes a combination of classical Pavlovian stimulus-response conditioning and instrumental learning, and they presented evidence illustrating a shift in brain activity from the ventral striatum location of the NAcc to the dorsal striatum brain region established for compulsive behaviors through the course of the development of addiction.
The Incentive Salience theory follows the framework of a hypersensitized mesocorticolimbic DA pathway, however, this theory focuses on the motivational attributions attached to the behavior, rather than pleasure or reward [ 58 ].
Robinson and Berridge [ 61 ] recently updated their model to remove the necessity of the component of liking, illustrating wanting as the only component of Incentive Sensitization theory.
Genetics, as they are relevant here, can be divided into three mechanisms; Genetic heritability, addiction related genetic expression in the individual, and epigenetics intersecting the two.
Volkow and Muenke [ 63 ] report common genetic factors on both sides of dual diagnoses; for example, ADHD and substance abuse. Agrawal and colleauges [ 64 ] performed a literature review and identified addiction related genes as belonging in one of two categories; genes that potentiate metabolic changes in response to specific substances, and genes that influence reward-system behaviors such as DRD2.
These authors also found that early stages of addictive process were more tied to environmental factors, while later stages were more tied to heritability.
These interruptions result in a hypodopaminergic state that yields a predisposition to addictive, compulsive, and impulsive behaviors, as well as several personality disorders.
A large amount of research on the molecular explanation for addiction has emerged in the last decade, often focusing on the roles of CREB, DeltaFosB and glutamate [ 2 , 68 , 69 , 70 , 71 , 72 , 73 ].
The sum of this research indicates that the flooding of dopamine in the reward system triggers an increase in the production of cyclic AMP cAMP , a small molecule that then signals the release of cAMP response element-binding protein CREB.
CREB is a protein that regulates the expression of specific genes. In this case, the result is the release of dynorphin, a protein that slows the release of dopamine and inhibits the VTA, thereby dampening the reward system.
Researchers believe this to be the molecular basis of tolerance, as increased amounts of the drug or behavior are required to overcome the increased amounts of CREB.
This process is also involved with dependence, as the inhibited reward system leaves the individual in a state of anhedonia when abstinent from the source of problematic dopamine release.
When the addict becomes abstinent, CREB levels quickly drop, tolerance fades, and sensitization begins. At this point, DeltaFosB becomes the predominant factor.
DeltaFosB is a transcription factor that operates partially in an opposite manner to CREB, in that it suppresses dynorphin and increases sensitivity in the reward pathway.
Additionally, whereas elevated CREB levels dissipate quickly, the elevated levels of DeltaFosB remain for extended periods—weeks or months.
This enhances response to rewards and reward related cues, leaving the individual sensitive to addiction related cues and vulnerable to compulsive behaviors and relapse.
A third component is the neurotransmitter glutamate. Researchers are finding glutamate to be intimately involved with the learning component of addiction, and the increased amount of dopamine in the mesocorticolimbic pathway leads to an increased sensitivity to glutamate.
Olsen cited fMRI studies showing gambling, shopping, sex orgasm , video games, and the sight of appetizing food to activate the mesocorticolimbic system and extended amygdala in the same manner as do drugs of abuse.
In their review of the genetic heritability of behavioral addiction, Lobo and Kennedy [ 75 ] reported pathological gamblers to be three times more likely to have a parent who is a pathological gambler, and twelve times more likely to have grandparent.
Blum has consistently included addictive behaviors in his constellation of domains impacted by RDS. In an early paper on the reward cascade, Blum et al.
The following list represents specific behavioral problems currently tied to RDS please note here that we use the original terms, although we would not categorize Internet Gaming or Aberrant Sexual Behavior under the term Compulsive Behaviors:.
Exposure to these behaviors, just as occurs with exposure to rewarding drugs, is facilitative of the addiction process rather than causative of addiction.
The state of brain anatomy and physiology is the underlying variable that is more directly causative of addiction.
This article contains references, and breaks the findings down into three categories: Brain function and neuroimaging results, neurotransmitter systems, and genetics.
Gambling, Internet, gaming, shopping, kleptomania, and sex. The left column of the table included a summary of the existing research on the specific behavioral addiction, and the right column contrasted them with corresponding findings for substance abuse.
The authors concluded that there is limited but emerging data connecting different behavioral addictions with existing research on substance abuse.
These authors used Gambling Disorder as the reference model for behavioral addictions, although they next acknowledged binge-eating disorder as showing a common neuropathophysiology with substance addictions.
Included in their findings, these authors report,. As in alcohol dependence, an inverse relationship between ventral striatal activation during reward anticipation and self-reported impulsivity was observed in both the pathological-gambling and alcohol-dependent groups suggesting that this feature of blunted ventral striatal activation across behavioral- and substance-addiction groups relates similarly to impulsivity.
The concept of food as addictive has been particularly studied in recent years, including heavy research into the neurobiological components of binge eating and obesity [ 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 ].
In addition to the aforementioned research into the neurobiology of both substance use disorders SUDs and addictive behaviors, there is a substantial body of research specifically into the neurobiology of Gambling Disorder GD known as Pathological Gambling PG prior to the DSM Indeed, as mentioned in the Fineberg et al.
For example, Potenza [ 91 , 92 ] published two literature reviews specific to the neurobiology of GD. These findings are reinforced in his second study, in which he found multiple brain regions ventral striatum, ventromedial prefrontal cortex, insula, among others , and neurotransmitter systems norepinephrine, serotonin, dopamine, opioid, and glutamate to be altered in disordered gamblers [ 91 ].
The authors illustrated multiple similarities between GD and SUDs in regards to brain function frontal cortices, striatum, and insula and neurotransmitter system research findings dopamine, serotonin, opioids, glutamate, and norepinephrine.
Similarly, el-Guebaly and colleagues published a review investigating the appropriateness of fit of GD as an impulse control disorder or as an additive disorder [ 93 ].
Based on findings of applicable neurotransmitters, neurocircuitry, and genetics as well as response to pharmacotherapies, these authors found that GD and SUDs had more in common than between GD and impulse control disorders.
As a final example, Gyollai et al. This recognition of GD as a non-substance-related disorder i. Since that time, neuroimaging studies and reviews continue to emerge.
For example, Singer et al. In particular they described a number of studies which lend support to the idea that exposure to reward unpredictability can cause aberrant responses in the dopamine systems, which in turn mediates incentive salience to reward-related cues.
The reviewers also touched upon studies suggesting that cortisol plays a role in modulating incentive motivation in the ventral striatum, i.
Finally, a recent review by Romanczuk-Seiferth et al. They examined the recent neuropsychological, neurophysiological, and neuroimaging studies of GD based on the three main clusters of diagnostic criteria: Researchers have been studying IA for nearly two decades.
Among these reviews, at least 10 have reviewed, in part or in whole, the research on the neurobiological findings regarding IA [ 15 , , , , , , , , , ].
Internet addiction comprises a heterogeneous spectrum of Internet activities with a potential illness value, such as gaming, shopping, gambling, or social networking.
Gaming represents a part of the postulated construct of Internet addiction, and gaming addiction appears to be the most widely studied specific form of Internet addiction to date.
Among the peer-reviewed articles, only three articles were actually specifically focused on Internet Gaming [ , , ].
The APA has now focused on Internet gaming. We argue, however, that also other applications can be used addictively Therefore, we summarize results of previous studies on Internet addiction in a broader way, although a great proportion of studies published so far concentrated on Internet gaming.
Similarly, for the purposes of this review, any study that conceptualizes IGD as a subtype of IA is classified as an IA study for the purposes of this review, although many use gaming as the prototypical example.
While this study was not specific to neurobiology, these authors briefly reported on findings in this area, concluding:.
Regardless of nomenclature inconsistencies, it is critical to note that much of the results of both reviews are directly in line with many of the aforementioned neurobiology of addiction findings [ 4 , 43 , 44 , 51 , 55 , 56 , 57 , 61 ].
As part of these findings, the mesocorticolimbic reward system was found to be impacted in the same manner as with substance abuse, as was the cue-induced craving phenomenon.
These researchers investigated the classification, comorbidity, diagnosis, electrophysiology, epidemiology, molecular genetics, neuroimaging, and treatment pharmacological and non-pharmacological of the disorder.
Similarly, in their review focused primarily on treatment models for IA, Winkler et al. One recent review focused on the role of prefrontal control functions in IA and summarized neuropsychological and neuroimaging studies on this topic [ 15 ].
In line with the aforementioned addiction models [ 4 , 43 , 44 , 51 , 55 , 56 , 57 , 61 ], and particularly based on recent results from neuroimaging studies in Internet addicted individuals, the authors concluded that IA seems to be related with structural and, more prominent, functional brain changes in cortical e.
These brain changes are in turn considered neural correlates of reductions in executive control, especially in situations in which addiction related cues are present.
The authors posited that the processes of cue-reactivity and craving might accelerate the problems in executive control functions [ 15 ].
These authors started with 61 articles, which they consolidated to 10 voxel-wise whole-brain analysis studies. In another recent literature review on the neurobiology of IA, Zhu, Zhang and Tian [ ] specifically reviewed molecular mechanisms through neuroimaging studies utilizing functional magnetic resonance imaging fMRI , positron emission tomography PET and single photon emission computed tomography SPECT.
These authors found that IA is associated with dysfunction in the brain dopaminergic systems just like addiction involving substances; and MRI studies have shown structural changes in the brain in IA subjects, with the impaired cognition and behavioral control found in IGD adolescents specifically, being associated with structural brain changes in the pre-frontal cortex and insula that are characteristic of addiction.
A burgeoning number of studies on the genetics of IA are emerging. For example, Montag et al. These researchers found a significant increase in a specific polymorphism on the CHRNA4 gene in the Internet addicted subjects.
Moreover, Lee et al. Additionally, Han et al. In the study of addictive behaviors, both resting state EEG and event related potentials may be employed.
Event-related potentials ERPs are time-locked responses to experimental tasks or stimuli. For example, Yu, Zhao, Li, Wang and Zhou [ ] tested subjects using auditory oddball tasks and found reduced P amplitudes and increased P latencies in IA subjects compared to healthy controls.
Decreased P have been reported in other substance abusers [ ], and suggest poorer memory and attention allocation.
The authors also reported a weakening of gamma oscillation intensity, which has been demonstrated is related to reduced dopamine levels. The IGD group had significantly lower P amplitudes during the finding of rewards, leading the authors to conclude that the blunted P reflected deficits in IGD subjects reward system, a finding in line with substance addictions.
These authors found these P latency increases to return to normal levels after subjects completed a three-month CBT program. A second longitudinal study reported abstinence along with treatment improved short-term memory and normalization of P amplitudes and latencies [ ].
These last two studies suggest that cognitive changes may a consequence of IA. Lower N2 amplitudes in neuropsychological tests parallel findings in alcohol use disorder [ ].
Finally, Yu, Zhao, Wang, Li and Wang [ ] employed a keystroke mismatch task to asses N differences between excessive Internet users and controls.
The N amplitude was lower in excessive Internet users, indicating potential difficulty retrieving conceptual knowledge. Similar findings have been reported for alcohol abusers and heavy cannabis users [ ].
According to these authors, less sensitivity to feedback during risk-taking may contribute to continued use despite negative consequences.
Dong, Zhou and Zhao [ ] tested subjects using a color-word Stroop task, and reported lower medial frontal negativity MFN in IA subjects compared to controls.
Along with more response errors, these authors reported that this finding suggests reduced executive function, a shared feature of addictions.
A single ERP study compared cue-reactivity in excessive computer gamers and casual computer gamers. Finally, two resting state EEG studies have been published.
These studies reported IA subjects had lower absolute power on the delta and beta bands compared to controls. Both studies suggest these differences may be neurobiological markers for IA [ , ].
Taken together, the EEG studies provide additional evidence that those suffering from IA have much in common with those suffering from substance addictions as compared with controls.
IA was formally proposed for inclusion in the DSM-5 two times, once with gaming as a subtype, and once with no subtypes [ 17 , 34 ]. IGD however, was never formally proposed for inclusion in the DSM-5, so it did not go through the formal commenting procedure.
It is understandable that gaming subjects are the most often studied subtype, as much of the leading neuroscientific research into the phenomenon of IA comes from China and South Korea, countries in which IP is outlawed, and therefore research on IPA is generally lacking [ ].
This review follows the original proposals, considering gaming as a subtype of IA. Despite claims of limited research on the topic [ 12 , 16 , 46 , 47 , , , ], a yearly breakdown of primary brain studies excluding reviews on IA and its subtype IGD makes it evident that brain studies in support of IA in this field are mounting rapidly:.
This extensive neuroscientific evidence provides compelling support for the acknowledgment of internet-related addictions as valid disorders. The same subjects were later shown preconscious sexually related visual cues erotic images.
Frascella, Potenza, Brown and Childress [ ] conducted a literature review contrasting three specific behaviors with alcoholism, pathological gambling, obesity, and the mechanics of sexuality.
The authors broadened the scope of the Childress et al. The overlap of classic reward brain areas involved in sexual arousal, love and attachment is complete VTA, NAcc, amygdala, ventral pallidum, orbitofrontal cortex.
Speculation is justified that associates survival-level natural rewards with substance addictions, expanding the brain systems to be addressed in therapy, and increasing our understanding of the necessary tenacity of the behaviors [ ] p.
As stated previously, the RDS model includes problematic sexual behaviors in a list of RDS-related problems [ , , , ]. Perhaps the largest volume of studies indicating a neurobiological basis for compulsive sexual behavior as akin to the addiction model involve the transcription factor DeltaFosB.
It has been well established that drugs of abuse elevate levels of the transcription factor DeltaFosB in the reward system, resulting in enhanced response to rewards and reward related cues, increased sensitivity to addiction related cues, and heightened vulnerability to compulsive behaviors and relapse [ 2 , 73 , , , ].
Note that this line of research must utilize non-human mammals, such as mice, rats, and hamsters, as a required part of the study requires euthanizing the subjects in order to access and measure intracranial DeltaFosB.
For example, researchers have genetically modified mice to overproduce DeltaFosB in the reward system at similar levels to those of drug addicted mice.
When presented with cocaine for the first time, these mice showed increased sensitivity to the drug and respond and behave in manners similar to those of rats who had become addicted through chronic use [ ].
Multiple tests using Syrian hamsters treated to overproduce DeltaFosB have focused on the effects of sexual behavior, and found a similarly enhanced sensitivity to sexual activity [ , ].
These authors found repeated sexual experience significantly increased DeltaFosB levels in the NAcc compared with controls, although the rates of increase were lesser than with drugs of abuse.
Investigating the combination of natural and drug rewards, Pitchers et al. In his highly regarded book on neuroplasticity, The Brain That Changes Itself [ ] Norman Doidge summarized the research on addiction and the reward system, and stated that the continued release of dopamine into the reward system when an individual compulsively and chronically watches Internet pornography stimulates neuroplastic changes that reinforce the experience.
Doidge went on to explain how these neuroplastic changes build brain maps for sexual excitement. The authors provided a short literature review renewing the argument that all manifestations of addiction operate via the same underlying mechanisms.
The authors included many of the previously mentioned studies; the role of DeltaFosB in natural addictions, neuroanatomical changes caused by excessive behaviors, changes in dopamine receptor density, and the influence of excessive behaviors on the reward system.
Hilton published a second and similar literature review [ 24 ], again emphasizing the critical role of DeltaFosB research as informing the study of not only sexuality in general but the more specific scope of internet pornography consumption.
The first fMRI study which explicitly focused on IPA was published in , when the first in a series of Cambridge University studies found the same brain activity as seen in drug addicts and alcoholics [ ].
In this arguably landmark study an experiment was conducted designed to measure the subjective experience of cue-reactivity, as well as the neurobiological markers and correlates, if any, found in subjects with compulsive sexual behavior CSB.
Note that this study included two primary lines of investigation. The subjects were shown the videos both inside and outside of the fMRI scanner.
Each time, subjects were asked to rate their subjective experiences via two specific measures: This line of study yielded two distinct results: These results indicated a dissociation between liking and wanting by CSB-subjects when watching sexually explicit videos.
These results replicated the results of well-established studies on the incentive-salience theory of addiction, wherein addicts report higher levels of wanting but not of liking their salient rewards.
The second primary area of investigation contained within this study regards neuroimaging results of compulsive sexual behaviors CSB , internet pornography in particular.
Prior studies have indicated common brain regions activated during craving states and drug-cue-reactivity for alcohol, cocaine, and nicotine; among others, the amygdala, dACC, and ventral striatum [ ].
While the researchers in the present study found these same regions to become activated within both CSB and non-CSB subjects when shown sexually explicit materials, the researchers found elevated activation in the CSB subjects.
Based on these results, Voon et al. The current and extant findings suggest that a common network exists for sexual-cue reactivity and drug-cue reactivity in groups with CSB and drug addictions, respectively.
Note that this finding is in line with the actual results of a recent study purporting to find otherwise [ ]. Three main results were reported.
First, longer duration and more hours per week of use correlated with lower grey matter volume in the right caudate.
While the caudate serves multiple complex functions, volume changes in the striatum are associated with several addictions, while the direction of change is not consistent.
Second, more years and more hours per week of use correlated with lower left putaminal activity in response to brief, still sexual images.
The authors suggested this lower volume may reflect tolerance brought about by desensitization: Given the stronger response to 9-second explicit video clips in Voon et al.
Alternatively, the non-addicts here examined may be responding differently than addicts would have. Finally, subjects who consumed more pornographic material were found to have less connectivity between the right caudate and left dorsolateral prefrontal cortex DLPFC.
While the DLPFC is concerned with executive functions, it is also associated with cue reactivity to drugs and internet gaming.
Disruptions in this circuit are implicated in drug and behavioral addictions. Specifically, poor functional connectivity between the DLPFC and caudate as found in the current study is implicated in heroin addiction [ ].
Multiple presentations indicating potential upcoming papers on the neurobiology of IPA were delivered at the 2nd International Conference on Behavioral Addictions in Budapest, Hungary.
Note that these are all conference proceedings and have not yet been published in peer reviewed journals. They do provide further proof, however, of the fact that there is a rapidly growing body of research.
These researchers followed a study model [ ], in which researchers found increased sensitivity in response to addictive cues measured by shorter reaction times and blunted response in the ventral striatum when shown non-addictive cues.
In their study, Gola et al. In a similar fMRI study, Brand, Grabenhorst, Snagowski, Laier and Maderwald [ ] found heterosexual males to have increased ventral striatal activity in response to preferred pornographic images.
Further, the increase in activity correlated with the degree of subjective complaints due to their Internet Pornography addiction.
Wehrum-Osinsky, Klucken and Stark [ ] reported on a potentially similar fMRI study they conducted with 20 subjects reporting excessive internet pornography consumption and 20 control subjects.
Although more neuropsychological than neurobiological, multiple studies have been conducted investigating the impacts of internet pornography viewing on cognitive operations.
This line of inquiry is relevant to the present paper in that the neurobiological mechanisms underlying neuropsychological operations have been well established.
For example, Fineberg et al. In their work, these authors provided a table wherein they mapped neurocognitive domains different forms of impulsivity and compulsivity to neuroanatomical and neurochemical findings.
Similarly, in their aforementioned review, Fineberg et al. As such, we believe that reporting the following neuropsychological studies exploring the interference of processing sexual cues and sexual arousal with executive functions has direct applicability to this review of brain science studies focused on the problem of IPA.
Several theories and experimental paradigms have been developed to describe and investigate executive functions [ ].
Generally, executive functioning describes a complex interplay between several cognitive domains in order to facilitate goal-directed behaviors, e.
Regarding the neural correlates of executive functions it was shown that they generally were located in the prefrontal cortex, but vary between the single facets of executive functions [ , , ].
Neuropsychological and neuroimaging studies on substance addictions showed that the prefrontal cortex and executive functions get impaired following substance use [ 46 , ].
This was taken into account to explain repeated drug administration and the preference for short-term reinforcement due to the drug despite severe negative consequences following drug use [ ].
Within the development of addictive sexual behaviors on the Internet it was assumed that anticipating and receiving gratification plays an important role [ ], since sexual arousal is highly reinforcing [ , ].
Experimentally, it was shown that sexual arousal reactions to Internet pornographic cues were related to symptom severity of IPA in heterosexual males and females as well as in homosexual males [ , , , ] and that problematic IP users reacted with increased subjective craving compared to healthy cybersex users when being confronted with Internet pornographic material [ ].
It has been further shown that positive implicit associations as measured by an Implicit Association Task modified with pornographic pictures [ ] and moreover, approach and avoidance tendencies [ ] are linked to symptoms of IPA.
Based upon these observations, the model of specific internet addiction proposed by Brand et al. Reid, Karim, McCrory and Carpenter [ ] found greater self-reported executive dysfunction in a sample of hypersexual patients, another study found no general impairments of executive functions observed using neuropsychological tests [ ].
However, several studies reported an interference of the processing of sexual cues and sexual arousal with executive functions.
Deficits in visual processing caused by bound attention due to erotic stimuli was shown in studies using a choice reaction time task [ ], rapid target perception [ ], and a dot detection task [ , , ].
In line with the above, Laier, Pawlikowski and Brand [ ] used an Iowa Gambling Task modified with pornographic pictures and found that the sexual arousal in a decision making situation can interfere with feedback processing and advantageous decision making.
Similarly, sexual arousal induced by sexual images impaired working memory performance in a pictorial 4-back paradigm [ ] as well as switching and monitoring performance in an executive multitasking paradigm [ ].
The findings of an attentional bias towards sexually explicit cues was replicated and shown to be enhanced in a sample of sexually compulsive individuals [ ].
This is in line with the theoretical suggestion that executive functions should be affected in situations in which individuals are confronted with addiction-related cues eliciting craving reactions [ 15 ].
In the results, no difference in the task performance was observed when comparing video conditions, but differential prefrontal coupling was observed during the two tasks in the erotic video condition.
The authors explain that sexual arousal interfered with cognitive functioning but that task performance was not decreased because of functional adaptations during the task performance, which in turn could be interfered with in craving situations experienced in addiction.
An EEG study on those complaining of problems regulating their viewing of internet pornography has reported the neural reactivity to sexual stimuli [ ].
The study was designed to examine the relationship between ERP amplitudes when viewing emotional and sexual images and questionnaire measures of hypersexuality and sexual desire.
However, the lack of correlations may be better explained by arguable flaws in the methodology. For example, this study used a heterogeneous subject pool males and females, including 7 non-heterosexuals.
Cue-reactivity studies comparing the brain response of addicts to healthy controls require homogenous subjects same sex, similar ages to have valid results.
Additionally, two of the screening questionnaires have not been validated for addicted IP users, and the subjects were not screened for other manifestations of addiction or mood disorders.
Finally, a significant finding of the paper higher P amplitude to sexual images, relative to neutral pictures is given minimal attention in the discussion section.
This is unexpected, as a common finding with substance and internet addicts is an increased P amplitude relative to neutral stimuli when exposed to visual cues associated with their addiction [ ].
In fact, Voon, et al. Similarly, both studies show a correlation between these measures with enhanced desire. Here we suggest that dACC activity correlates with desire, which may reflect an index of craving, but does not correlate with liking suggestive of on an incentive-salience model of addictions.
So while these authors [ ] claimed that their study refuted the application of the addiction model to CSB, Voon et al. Another EEG study involving three of the same authors was recently published [ ].
Unfortunately, this new study suffered from many of the same methodological issues as the prior one [ ]. For example, it used a heterogeneous subject pool, the researchers employed screening questionnaires that have not been validated for pathological internet pornography users, and the subjects were not screened for other manifestations of addiction or mood disorders.
In the new study, Prause et al. As expected, the LPP amplitude relative to neutral pictures increased for both groups, although the amplitude increase was smaller for the IPA subjects.
Specifically, higher pornography use correlated with lower grey matter volume in the dorsal striatum, a region associated sexual arousal and motivation [ ].
One might expect frequent viewers of Internet pornography and controls to have similar LPP amplitudes in response to brief exposure to sexual images if pathological consumption of Internet pornography had no effect.
Instead, the unexpected finding of Prause et al. One might logically parallel this to tolerance. Sexual films produce more physiological and subjective arousal than sexual images [ ] and viewing sexual films results in less interest and sexual responsiveness to sexual images [ ].
Taken together, the Prause et al. In addition, the statement of Prause et al. Moreover, it is critical to note that one of the major challenges in assessing brain responses to cues in Internet pornography addicts is that viewing sexual stimuli is the addictive behavior.
In contrast, cue-reactivity studies on cocaine addicts utilize pictures related to cocaine use white lines on a mirror , rather than having subjects actually ingest cocaine.
Since the viewing of sexual images and videos is the addictive behavior, future brain activation studies on Internet pornography users must take caution in both experimental design and interpretation of results.
For example, in contrast to the one-second exposure to still images used by Prause et al. Unlike the one-second exposure to still images Prause et al.
This review investigated the current body of scientific knowledge regarding neural processes of addiction in relation to both broad areas of psychoactive substances and behaviors such as gambling, sex and internet use, as well as the available research supporting specific behavioral aspects and their subtypes.
Most of the studies used neuroimaging measures, EEGs, or physiological measurements, although some studies used neuropsychological measures.
The net result of this inquiry yielded a very large number of neuroscience based studies that support the application of the addiction model to addictive Internet-related behaviors.
ASAM clearly stated that all manifestations of addiction are about common effects on the brain, not the differences in substances or contents or behaviors.
By this logic, viewing IP excessively and playing internet games excessively are substantively different, despite substantial overlap in activation of the reward system of the brain, and despite the potential for the exhibition of similar psychosocial behaviors and psychosocial consequences.
The essential feature of Internet gaming disorder is persistent and recurrent participation in computer gaming, typically group games, for many hours.
These games involve competition between groups of players Team aspects appear to be a key motivation. Based on this logic, abusing substances in a bar or at a party can constitute substance abuse, but abusing substances while alone does not.
To make an internet-related analogy, this logic dictates that someone playing World of Warcraft excessively is addicted, but someone playing Candy Crush excessively is not.
This review presents strong neuroscientific evidence for viewing internet-related behaviors, including IP use, as potentially addictive, which should be taken into consideration when discussing the classification of IPA.
Todd Love conceived the project, conducted the literature review, and wrote the main part paper. Christian Laier and Matthias Brand contributed theoretically to the manuscript, wrote parts of the manuscript, and revised the manuscript.
Linda Hatch contributed to shaping and outlining the overall ideas presented, and assisted with the editing of the manuscript. Raju Hajela reviewed and edited the medical science, contributed theoretically, and assisted with the editing of the manuscript.
All authors approved the manuscript. National Center for Biotechnology Information , U. Journal List Behav Sci Basel v.
Published online Sep Christian Laier 2 Department of General Psychology: Find articles by Christian Laier. Matthias Brand 2 Department of General Psychology: Andrew Doan, Academic Editor.
Author information Article notes Copyright and License information Disclaimer. Received Jul 2; Accepted Sep 8. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license http: This article has been cited by other articles in PMC.
Abstract Many recognize that several behaviors potentially affecting the reward circuitry in human brains lead to a loss of control and other symptoms of addiction in at least some individuals.
Introduction A revolutionary paradigm shift is occurring in the field of addiction that has great implications for assessment and treatment.
As a result of the growing neuroscientific evidence, the American Society of Addiction Medicine ASAM formally expanded their definition of addiction in to include both behaviors and substances: Method To conduct the research, an extensive literature search and review was performed utilizing a variety of sources: Neurobiology of Addiction The scope of this topic was limited to the previous ten years, with primary focus given to articles published in the past five years.
Neurobiology of Addictive Behaviors This scope was not time-delimited, as it is an emerging topic whose entire historical context is relevant.
Internet Addiction As this is another emerging topic, there was no time-scope set for this topic, although priority was given to studies and reviews published in the previous five years.
Internet Gaming Disorder No time-limitation was placed on this topic, and the following search terms and their derivatives were used in multiple combinations: Internet Pornography Addiction Research into the area of addictive sexual behaviors on the Internet began with an inquiry into the various constructs surrounding compulsive sexual behavior.
Neurobiology of Addiction All drugs of abuse affect the mesolimbic dopamine DA pathway, which originates from the ventral tegmental area VTA and projects into the nucleus accumbens NAcc.
Three-Stage Model of Addiction Nora Volkow describes addiction as a neurobiochemically based shift from impulsive action learned through positive reinforcement to compulsive actions learned through negative reinforcement [ 43 ].
Anti-Reward George Koob proposed an expansion of the second stage of addiction. Neurobiology of Learning, Habit, and Motivation While both the Anti-Reward and I-RISA models include learning components, other theories of addiction focus primarily on the learning aspects of addiction, and the biological underpinnings thereof.
Genetics Genetics, as they are relevant here, can be divided into three mechanisms; Genetic heritability, addiction related genetic expression in the individual, and epigenetics intersecting the two.
Molecular Underpinnings of Addiction A large amount of research on the molecular explanation for addiction has emerged in the last decade, often focusing on the roles of CREB, DeltaFosB and glutamate [ 2 , 68 , 69 , 70 , 71 , 72 , 73 ].
The following list represents specific behavioral problems currently tied to RDS please note here that we use the original terms, although we would not categorize Internet Gaming or Aberrant Sexual Behavior under the term Compulsive Behaviors: Gambling Disorder In addition to the aforementioned research into the neurobiology of both substance use disorders SUDs and addictive behaviors, there is a substantial body of research specifically into the neurobiology of Gambling Disorder GD known as Pathological Gambling PG prior to the DSM Internet Addiction Researchers have been studying IA for nearly two decades.
Internet Gaming Disorder IA was formally proposed for inclusion in the DSM-5 two times, once with gaming as a subtype, and once with no subtypes [ 17 , 34 ].
Despite claims of limited research on the topic [ 12 , 16 , 46 , 47 , , , ], a yearly breakdown of primary brain studies excluding reviews on IA and its subtype IGD makes it evident that brain studies in support of IA in this field are mounting rapidly: Prior to —6 studies,.
Compulsive Sexual Behavior Childress et al. Internet Pornography In his highly regarded book on neuroplasticity, The Brain That Changes Itself [ ] Norman Doidge summarized the research on addiction and the reward system, and stated that the continued release of dopamine into the reward system when an individual compulsively and chronically watches Internet pornography stimulates neuroplastic changes that reinforce the experience.
Conclusions This review investigated the current body of scientific knowledge regarding neural processes of addiction in relation to both broad areas of psychoactive substances and behaviors such as gambling, sex and internet use, as well as the available research supporting specific behavioral aspects and their subtypes.
Author Contributions Todd Love conceived the project, conducted the literature review, and wrote the main part paper. Conflicts of Interest The authors declare no conflict of interest.
References and Notes 1. Is there a common molecular pathway for addiction? The incentive sensitization theory of addiction: Neurobiological mechanisms for opponent motivational processes in addiction.
The neurobiology of substance and behavioral addictions. Introduction to behavioral addictions. Natural rewards, neuroplasticity, and non-drug addictions.
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