Rapid advances in technology, overstimulation and the subsequent
diminishing effort towards emotional growth and awareness are making
some individuals more susceptible to "out of control
behaviors." The concept of self medicating with substances is
well-known, but how about self medicating with behaviors? The use of
repetitive actions, initiated by an impulse that can't be stopped,
causing an individual to escape, numb, soothe, release tension, lessen
anxiety or feel euphoric, may redefine the term addiction to include
experience and not just substance.
The word addiction can be defined in many ways. Traditionally, the
dependence on exogenous drugs of abuse causing neuroadaptation has
served as a primary definition. But some would argue that specific
behaviors in a vulnerable individual can also lead to an addictive
state. Critics, however, report that the inclusion of behavioral
addictions may "medicalize" bad behaviors and blur the line of
demarcation between an excessive bad behavior and a true addiction.
There is a distinct possibility that adding many more disorders to the
Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition
(DSM-IV; APA 2000) may effectively dilute pathological behavior and
pathologize variants of normative behavior, subsequently increasing the
general public's suspicion of the validity of psychiatric
disorders. If everyone meets criteria for a disorder, is there really an
effective diagnostic system?
There is great debate over how to classify nonsubstance addictions
within the diagnostic classification of mental disorders. Many have
suggested that the constellation of symptoms and impairments in
functioning associated with "behavioral disorders" are simply
symptoms of other disorders and do not have enough in common to warrant
their own category let alone individual disorder status such as
"sex addiction," "compulsive shopping" and
"pathological gambling." However, recent findings are shedding
new light on the shared attributes of this class of impulse control
disorders and forging a better understanding of how they develop.
Historically, both the construction and development of DSM criteria
in the field of psychiatry and the boundaries between normative behavior
and disordered or abnormal behavior have been riddled with controversy,
with significant research findings ultimately defining the criteria for
NEUROBIOLOGICAL MECHANISMS OF ADDICTION
When reviewing the neurobiological correlates of addiction, it is
usual to start with the brain reward circuitry. This region is
significant for understanding the origins of how addictive related
behaviors may emerge. Motivation is an ancient and evolutionarily
conserved phenomenon. As a species, the genetic drive for survival
requires incentivizing the acquisition of vital resources such as food,
water, shelter and sex. In an age where resources were scarce and the
availability of these assets was the key to life or death, strongly
imprinting the location and availability of resources and mates ensured
Over time, the brain has developed mechanisms to reinforce these
behaviors; this neural circuit has been defined as the mesolimbic reward
system (Di Chiara 1998). The neuropharmacological mechanisms that
mediate this circuit appear to involve several different
neurotransmitter systems collectively; however the dopaminergic and
endogenous opioid systems appear to be the most influential in
regulating "rewarding behaviors." Addiction has traditionally
been defined as dependence on a drug that can pharmacologically
"hijack" reward circuitry mediated by its effect on the brain
and body (the neuromimetic effect of drug administration). However, it
could be suggested that any stimuli (drug or behavior) that transforms
basic drives required for survival (natural rewards like feeding,
thirst, reproduction) into actions of craving/seeking behaviors or
repetitive out-of-control behaviors may make it plausible that addiction
can occur even in the absence of drug taking. Thus, behavioral
addictions may share many of the same pathways associated with chemical
dependence. A growing theory is that if one can alter neurocircuitry
with illicit drugs and pharmacology, then one can alter it with behavior
as well (Holden 2001).
In addition to similarities in clinical overlap, the common
currency of both drug and behavioral addiction is learning and memory
(Hyman 2005). Cravings are triggered by memories, affective states and
situations associated with both out-of-control behaviors and drug use
(Martin & Petry 2005). Cue-induced behaviors likely evolved along
side the pleasure system to provide a memory of both rewarding as well
as aversive stimuli. These signals would both help drive behaviors that
would benefit us and avoid circumstances that would prove detrimental.
In the case of addictions, cues can be so strong that they reinforce
particular behavioral patterns despite their negative consequences.
Repetitive behavioral patterns help establish and maintain the
cue-induced behaviors associated with addiction through neuroadaptation.
Neuroadaptation and neural plasticity are the hallmarks of the
adaptive brain. In response to a drug or behavior, neuroadaptations
occur in centers of the brain associated with reward, emotion, and
decision-making through plasticity changes and relearning, which elicits
behavioral reinforcement and habit formation during addiction.
Sensitization, a neuroadaptive response, greatly dependent on context
and learning, alters neuronal circuitry involved in the normal processes
of incentive, motivation and reward, and thus is equally applicable to
"out of control drug use" or "non drug" problematic
behaviors (Martin & Petry 2005). These types of neurochemical adaptations also occur in areas of the brain critical to higher order
The reward circuit is closely tied with the executive
function/decision-making centers of the brain, the prefrontal cortex and
orbitofrontal gyrus. Studies suggest that impulse control disorders,
like addiction, lead to dysregulation of the prefrontal cortex circuitry
(Jentsch & Taylor 1999). Impulsivity is often defined as something
that has a sense of urgency or lack of premeditation, an act that
restricts evaluation and decision-making. Indeed all of these features
tend to define the manner in which drug use manifests itself as one
transitions into an "addictive state." An important function
of this brain region is that it acts as the "brake system" for
the brain by sending stop signals to inhibit the execution of distinct
behaviors or actions.
Drugs of abuse have been shown to alter glutamate and dopamine
functioning in the prefrontal cortex which may compromise its ability to
direct inhibitory regulation (Kalivas & O'Brien 2008); the same
may be true for behavioral disorders. It is of note that the prefrontal
cortex receives and sends projections to reward, memory, emotion, and
stress centers of the brain, all regions that play a substantive role in
the addiction process. Thus the impulsive aspects of addiction mediated
by alterations in the prefrontal cortex appear to alter the brain's
behavioral inhibitory system, opening the door for repetitive
A SHARED APPROACH TO ADDICTION
There has been a trend toward thinking about non-drug addictions as
sharing neurobiological mechanisms with substance abuse and dependence (Deadwhyler 2010; Petry 2006; Volkow & Wise 2005). Drugs of abuse
are thought to hijack neural circuits that underlie encoding of natural
rewards and plasticity in this circuitry. It has been suggested that
these changes may be responsible for the behavioral plasticity
associated with increased craving and drug seeking seen in addictive
states (Kalivas & O'Brien 2008). Evidence of hijacking is seen
in several brain regions known to affect executive function, reward
processing and motivation. (Koob & Volkow 2010). It is widely
thought that this plasticity underlies the maladaptive changes in
behavior associated with addiction (Olsen 2011). In humans, some of
these changes include impaired decision-making, anhedonia, craving
tolerance, withdrawal and high rates of relapse (Potenza 2006; Bechara
Similarities between substance and non substance rewards can be
seen in imaging studies as well. Functional neuroimaging studies in
humans have shown that seeing appetizing food (Wang et al. 2004b), the
act of gambling (Breiter et al. 2001), shopping (Knutson et al. 2007)
and playing video games (Hoeft et al. 2008) activate similar brain
regions, including the mesocorticolimbic system and extended amygdala,
as do drugs of abuse (Volkow & Fowler 2000). Looking at a
traditional description of "addicted states," we may find
substance induced and behavioral conditions both meet criteria.
Addictive states are characterized by changed reinforcement
contingencies, significant anhedonia, the incapacity to experience
day-to-day pleasures due to reduced sensitivity to endogenous brain
dopamine, and a striking responsiveness to cues that are both internal
to the individual and within the environment associated with the
behavior or drug use (Volkow & Fowler 2000; Childress et al. 1999).
These behavioral correlates suggest that nonsubstance addictions
share similar neuroadaptations. Further support for this concept comes
from studies showing medication-induced increases in nondrug rewards for
activities including gambling, shopping or sex in patients taking drugs
that activate the dopaminergic system (Evans et al. 2006). Thus it
appears that dopamine dysregulation is a common thread in both chemical
and behavioral addictions.
In looking at the numbers, epidemiological reports estimate
prevalence rates in the United States at 1% to 2% for pathological
gambling (Potenza et al. 2003; Welte et al. 2001), 5% to 6% for
compulsive shopping, (Black 2007; Koran et al. 2006), 3% to 6% for
compulsive sexual behavior (Black 2000), 2.8% for binge eating disorder (Hudson et al. 2007) and .5 to 1% for kleptomania (McElroy et al. 1991).
Currently, the impulse control disorders have a small sectionintheDSM
IV-TR (intermittent explosive disorder, kleptomania, pyromania,
trichotillomania, pathological gambling) with some behaviors simply
classified under impulse control disorder NOS. Although the term
"addiction" is not utilized in the DSM-IV, substance use
disorders are categorized according to the substance causing the
problems and then grouped by abuse, dependence, withdrawal and
intoxication. Within the DSM-IV, behavioral addictions have been grouped
under categories including: "impulse control disorders not
otherwise specified," "eating disorders" and
"substance-related disorders," (Potenza 2006; Holden 2001). As
understanding of these disorders expands, a better grasp of the
etiology, prevalence, and neurobiological underpinnings will likely
emerge around these "behavioral addictions."
Food is an essential component to every organism on the planet.
From single celled bacteria to multicelled organisms such as ourselves,
almost every living thing has some means of consuming and metabolizing
nutrients to get energy for survival. However, the modern era has
ushered in a growing population with an unhealthy relationship to food.
Within this population exists a growing subgroup of compulsive eaters
whose relationship with food in many ways mimics the criteria currently
reserved for addictive disorders. These individuals display both
compulsive consumption and preoccupation with certain foods, leading
some to categorize them as "food addicts."
Compulsive overeating, also referred to as food addiction, is
characterized by an obsessive-compulsive relationship to food. An
individual suffering from compulsive overeating disorder engages in
frequent episodes of uncontrolled eating, during which they may feel
frenzied or out of control, often consuming food past the point of being
comfortably full. Unlike individuals with bulimia, compulsive overeaters
do not attempt to compensate for their binging with purging behaviors
such as fasting, laxative use or vomiting. Compulsive overeaters will
typically eat when they are not hungry. Their obsession is demonstrated
in that they spend excessive amounts of time and thought devoted to
food, and secretly plan or fantasize about eating alone. Binge Eating
Disorder (BED) is the most common eating disorder in the United States,
affecting 3.5% of females and 2% of males, and is prevalent in up to 30%
of those seeking weight loss treatment (Smith et al. 1998). The DSM-IV
(APA 2000) defines Binge Eating Disorder as a type of eating disorder
not otherwise specified, that is characterized by recurrent binge eating
without the regular use of compensatory measures to counter the binge
eating and a minimum of two binge eating episodes a week for at least
The neurobiological mechanisms underlying the behaviors that result
in pathological overeating are multifaceted. "The regulation of
food intake is a complex balance between excitatory and inhibitory
processes. The excitatory processes arise from the body's needs for
nutrients and calories. The inhibitory processes arise from satiety signals after food consumption" (Bassareo & Di Chiara 1999).
From an evolutionary standpoint the drive for food acquisition is
incredibly powerful for humans and animals. The consumption of food is a
vital component of our every day lives. Motivation and cue-induced
behaviors directed toward food sources ensured that early man would
succeed in the race for survival. However, with the advent of the
industrial revolution, resources like food have become more easily
accessible to the masses in a manner never before seen. For some, it may
be that caloric-based resources strongly activate reward and cue based
brain centers in a similar fashion to drugs of abuse.
This compounded with the abundant availability of food to many may
prove a downward spiral into an addiction-like disorder: compulsive
eating. Indeed, neurobiological studies suggest correlates between the
neurocircuitry recruited in substance abuse and compulsive food
consumption. It has been shown that palatable foods have the potential
to increase neuropeptides associated with regulating the brain's
pleasure system (Kelley et al. 2005). Brain imaging studies in humans
implicate the involvement of dopamine-modulated circuits in pathological
eating behavior (Wang et al. 2004a). Further, food cues increase
striatal extracellular dopamine as well as metabolism in the
orbitofrontal cortex, a brain region associated with executive
functions, suggesting activation of both motivational and
decision-making centers of the brain (Wang, Volkow & Thanos 2009).
Just as various drugs promote different degrees of dependence,
foods also differ in their capacity to promote abuse (Volkow & Wise
2005). Highly palatable foods such as those high in fats and sugars have
been shown to strongly activate mesolimbic dopaminergic circuits within
the brain (Sharf, Lee & Ranaldi 2005). Similar to drug-addicted
subjects, striatal dopamine D2 receptor availability is reduced in obese
subjects, which could explain how food could temporarily compensate for
understimulated reward circuits in these individuals. Decreased DA D2
receptors in obese subjects are also associated with decreased
metabolism in prefrontal cortical regions involved in inhibitory
control, which may underlie their inability to control food intake
(Volkow, Wang & Telang 2008); Volkow suggests that, "Dopamine
deficiency in obese individuals may perpetuate pathological eating as a
means to compensate for decreased activation of these circuits." In
conjunction with dopamine, the serotonin system been shown to play a
distinctive role in modulating appetitive behaviors (Blundell 1984).
Evidence suggests that serotonin is a key regulator of the satiety or
"stop eating" signal in the brain (Halford et al. 1998).
Serotonergic agonists and reuptake inhibitors have been shown to
significantly reduce binge-eating frequency and suppress excess food
consumption in human populations (Appolinario & McElroy 2004;
Halford & Blundell 2000). Congruently, the serotonergic system
appears to play a significant role in several drugs of abuse including
cocaine, alcohol, and methamphetamine (Kenna et al. 2009; Filip et al.
2005), indicating that there may be shared pathways between substance
abuse and binge eating disorders. Although the DSM-IV does not classify
food as a substance of abuse, the neurobiological, clinical and
behavioral findings suggest that binge eating fits into the framework of
Treatment options for compulsive eating disorder include
pharmacological and behavioral interventions. Randomized controlled
trials using cognitive behavioral therapy and brief psychoeducation have
led to improved outcomes with binge eating symptoms (Carter et al.
2003). Some success has been seen with antidepressants such as
serotonergic reuptake inhibitors such as fluoxetine, fluvoxamine,
sertraline and citalopram. Other options that have also shown promise
are anticonvulsants like topiramate that modulate voltage-gated ion
channels and glutamatergic receptors (Marazziti et al. 2011; Appolinario
& McElroy 2004), suggesting a role for these transmitter systems in
regulating this behavior. Given the known risks associated with
compulsive overeating, such as obesity and increased morbidity and
mortality, further investigation is warranted to better understand
treatment options and factors that have contributed to this epidemic.
The Substance Use Disorders Workgroup of the American Psychiatric
Association DSM committee has proposed several changes to the current
DSM-IV classification of pathological gambling. The workgroup has
proposed to rename the pathological gambling disorder as disordered
gambling and to reclassify the disorder from the section on impulse
control disorders not elsewhere classified to the substance related
disorders (which is to be renamed as addiction and related disorders)
(Hodgins, Stea & Grant 2011).
The access and availability of gambling opportunity is the highest
it has ever been worldwide. Online gaming environments, casinos,
destination resorts, sports betting, spread betting, bingo, slot
machines, private betting, horse races, card games, and lottery tickets
are collectively receiving increased attention from the general public
throughout the world. The desire and willingness to wager money or other
items of value on randomly established outcomes seems universal.
Although most individuals participate in gambling as an enjoyable social
activity, a small group of people become too seriously involved in terms
of time invested and money wagered and they continue to gamble despite
substantial and negative personal, social, family, and financial
effects. (Hodgins, Stea & Grant 2011)
Epidemiological research, along with studies in treatment-seeking
samples, finds high rates of comorbidity (Petry 2009). In data from the
National Epidemiologic Survey on Alcohol and Related Conditions (NESARC)
study, pathological gamblers had an increased risk of having a diagnosis
of alcohol misuse in their lifetimes by a factor of six and an increased
risk of having a substance use disorder by a factor of four compared to
nongamblers. Also, rates of manic episodes were eight times higher in
pathological gamblers, major depression and dysthymia were three times
higher in pathological gamblers and generalized anxiety disorder, panic
disorder and specific phobias were each more than three times higher
(Petry, Stinson & Grant 2005). Also, most studies of
treatment-seeking samples find that individuals with both substance
abuse and disordered gambling have more severe problems than individuals
with either disorder alone. (Langenbucher et al. 2001)
The research base on pathological gambling is not substantial but
there are comparative studies looking at drug addiction and pathological
gambling (PG). From a clinical perspective, gamblers report subjective
cravings as powerful as drug abusers, they report "highs"
similar to drug highs, they show withdrawal symptoms and autonomic
instability when not gambling, and they may throw away everything in
their life to gamble.
The behaviors that characterize problematic gambling (chasing
losses, preoccupation with gambling, inability to stop) are impulsive in
that they are often premature, poorly thought out, risky, and result in
deleterious long-term outcomes (Chamberlain & Sahakian 2007).
Deficits in aspects of inhibition, working memory, planning, cognitive
flexibility and time management or estimation are more common in
individuals with pathological gambling problems than healthy volunteers
(Hodgins, Stea & Grant 2011). Distorted cognitions in gambling
disorders may include: magnification of gambling skill, superstitious
beliefs, interpretative biases, temporal telescoping, selective memory,
predictive skill, illusions of control over luck, and illusory
associations. (Hodgins, Stea & Grant 2011)
Research studies looking at the relationship between gambling and
substance use disorders reveal similar performance on personality and
neurocognitive assessments of impulsivity, with both groups having high
scores on self-reported measures of impulsiveness and sensation seeking
(Petry 2001). Both show similar clinical courses and similar clinical
characteristics including things like tolerance, withdrawal, craving
states and repeated attempts to cut back or quit. Thus there appears to
be substantive similarities between the systems and circuits associated
with chemical and gambling addictions.
Among those who do seek treatment, Gamblers Anonymous (GA) is the
most commonly utilized approach. GA is a 12-Step support group based on
the principles of Alcoholics Anonymous (Petry 2009). In many
epidemiological studies, an estimated 36% to 46% of pathological
gamblers are in recovery (Hodgins, Wynne & Makarchuk 1999).
Treatment for pathological gambling and problem gambling is varied and
may include: GA, cognitive behavioral therapy, pharmacotherapy,
motivational enhancement therapy, family therapy, brief therapy,
residential treatment and for some, natural recovery.
Neuroimaging studies reveal decreased activation of the
ventro-medial prefrontal cortex (vmPFC) in pathological gambling
subjects during presentation of gambling cues (videos), which resembles
cocaine addicts watching a cocaine video, with relatively less
activation in regions implicated in judgment and motivation (Potenza et
al. 2003). This suggests that the decision-making faculties are
inhibited in these individuals. Neuroimaging studies in pathological
gamblers have indicated diminished ventral striatum, ventromedial
prefrontal cortex and ventrolateral prefrontal cortex activity during
rewarding events, suggestive of a blunted neurophysiological response to
rewards and losses (Reuter et al. 2005). The work of Slutske and
colleagues (2000) strongly suggests that pathological gambling is
genetically related to substance addictions. Low 5-HIAA levels have been
found to correlate with high levels of impulsivity and sensation seeking
and have been found in pathological gambling and substance use disorders
(Potenza, Kosten & Rounsaville 2001). Baseline decreases in
serotonergic tone have been observed in comparison to nongambling
controls (Linnoila et al. 1983) and a euphoric "high" in
gamblers is seen after administration of 5HT2C agonists (Potenza 2008).
Also, PG has been shown to lead to elevations in noradrenaline and
comparatively elevated heart rates (Potenza 2008).
Currently, there are no FDA-approved medications to treat
pathological gamblers. It appears that three types of medications have
some efficacy in treating PG: opiate antagonists, mood stabilizers and
antidepressants. Results from two double-blind, placebo controlled
studies of naltrexone and two multicenter double-blind,
placebo-controlled trials of nalmefene suggest efficacy of opioid
antagonists in reducing the intensity of urges to gamble, gambling
thoughts, and gambling behavior (Hodgins, Stea & Grant 2011). Opiate
antagonists have been shown to decrease the craving for gambling in a
similar fashion to craving in alcoholics, and elevated rates dopamine in
individuals with PG and alterations in the A1 allele of the dopamine D2
receptor gene suggest that the reward associated neurotransmitter
systems are playing a significant role in driving the addiction process
in this disorder (Goodman 2008; Potenza 2008). The use of paroxetine and
other SSRIs, lithium and other mood stabilizers for pathologic gamblers
with bipolar symptoms, and the glutamate modulator N-acetyl cysteine have shown some positive effects. Because improvement in glutamatergic
tone in the nucleus accumbens has been implicated in reducing the
reward-seeking behavior in addictions (Kalivas, Peters & Knackstedt
2006), N-acetyl cysteine has been studied in the treatment of
pathological gambling and has had positive effects on urges and gambling
behavior (Grant, Kim & Odlaug 2007).
Sex addiction (also known as compulsive sexual behavior or
hypersexual disorder) is a controversial topic in both science and
media. There is a lot of press but not much scientific evidence. Sex
addiction could be described as a debilitating problem which may include
impairment in physical health function, cognition, impulse control,
attachment, intimacy and mood or it could simply be a convenient excuse
for an individual's indiscretions.
There will always be controversy when any class of behaviors,
including sexual behaviors, that are considered to be intrinsically
"normal" are medically "pathologized." (Money 1994)
The primary criticism of compulsive sexual behavior or hypersexual
disorder is that it may simply be a symptom of an underlying Axis I
disorder and not a true disorder itself. In one study of compulsive
sexuality, 88% of the sample met diagnostic criteria for an Axis I
disorder at the time of the interview and 100% met criteria for an Axis
I disorder at some time in their lives, with the most common diagnoses
being mood and anxiety disorders (Raymond, Coleman & Miner 2003).
Compulsive sexual behavior has been estimated to have a prevalence of
between 3% and 6% in the United States (Black 2000). Most individuals
with hypersexuality are male but studies that have examined both sexes
report a proportion of 8% to 40% female (Kaplan & Krueger 2010).
Sexuality is dependent on many factors, including individual and
relationship variables, societal values, cultural mores, and ethnic and
religious beliefs. In discussing hypersexuality, these contexts need to
be considered (Kaplan & Krueger 2010). The challenge is in defining
abnormal and pathological sexual practices. For example, a Swedish study
found that simple frequency of sexual activity alone was insufficient to
establish pathology; high frequency of sexual behavior with a stable
partner was associated with better psychological functioning, whereas
solitary or impersonal sexual behavior was associated with psychiatric
disorders and psychosocial dysfunction (Langstrom & Hanson 2006)
In defining aberrant sexual behavior, Carnes and Wilson (2002)
proposed that sexually addictive behaviors include compulsive
masturbation, affairs, use of prostitutes, pornography, cybersex,
prostitution, voyeurism, exhibitionism, sexual harassment and sexual
offending. Coleman, Raymond and McBean (2003) defined compulsive sexual
disorders as compulsive cruising and multiple partners, compulsive
fixation on an unattainable partner, compulsive autoeroticism,
compulsive use of erotica, compulsive use of the Internet, compulsive
multiple love relationships, and compulsive sexuality in a relationship.
Hypersexual Disorder has been proposed as a new psychiatric
disorder for consideration in the Sexual Disorders section for DSM-V.
Hypersexual Disorder is conceptualized as primarily a nonparaphilic
sexual desire disorder with an impulsivity component (Kafka 2010).
Proposed diagnostic criteria for Hypersexual Disorder (American
Psychiatric Association DSM-5 Development 2010) include:
A. Over a period of at least six months, recurrent and intense
sexual fantasies, sexual urges, and sexual behavior in association with
four or more of the following five criteria:
1. Excessive time is consumed by sexual fantasies and urges, and by
planning for and engaging in sexual behavior.
2. Repetitively engaging in these sexual fantasies, urges, and
behavior in response to dysphoric mood states (e.g., anxiety,
depression, boredom, irritability).
3. Repetitively engaging in sexual fantasies, urges, and behavior
in response to stressful life events.
4. Repetitive but unsuccessful efforts to control or significantly
reduce these sexual fantasies, urges, and behavior.
5. Repetitively engaging in sexual behavior while disregarding the
risk for physical or emotional harm to self or others.
B. There is clinically significant personal distress or impairment
in social, occupational or other important areas of functioning
associated with the frequency and intensity of these sexual fantasies,
urges, and behavior.
C. These sexual fantasies, urges, and behavior are not due to
direct physiological effects of exogenous substances (e.g., drugs of
abuse or medications) or to Manic Episodes.
D. The person is at least 18 years of age.
Specify if: Masturbation, Pornography, Sexual Behavior With
Consenting Adults, Cybersex, Telephone Sex, Strip Clubs, Other.
There is a paucity of literature on brain imaging during
conventional or pathological sexual functioning. Research utilizing
neuropsychological testing with self-reported behavior has shown a
positive correlation between hypersexual behavior and global indices of
executive dysfunction including features of impulsivity, cognitive
rigidity, poor judgment, and deficits in emotional regulation (Reid et
al. 2009). Also, diffusion tensor imaging, psychometric testing and the
Go-No-Go procedure revealed higher impulsivity scoring in compulsive
sexual behavior patients than controls, with hypersexual patients having
higher superior frontal region mean diffusivity than controls (Miner et
al. 2009). Patients with hypersexual disorder do report feeling out of
control and anxious, with obsessional thinking, mood instability and
significant impairment in their daily lives.
Reward circuits such as dopaminergic and endogenous opiate systems
have been implicated in the process of sexual behavior in much the same
way as substance abuse (Goodman 2008). An interesting piece of evidence
around the role of the reward system in these disorders comes out of the
Parkinson's field, where treatment with dopamine agonists leads to
increased vulnerability to impulse control disorders such as
pathological gambling, hypersexuality, compulsive shopping and
compulsive eating (Vilas, Pont-Sunyer & Tolosa 2012).
A case study of Internet-based sex addiction involving
preoccupation with Internet pornography, extended and frequent
masturbation and unprotected sex with cyber contacts revealed
interesting diagnostic and treatment-based findings. The patient was
initially prescribed an antidepressant (sertraline) with both individual
and group therapy and 12-Step work with Sex Addicts Anonymous with
little improvement. After the addition of naltrexone (an opiate
antagonist), the patient reported significant improvement in his
cravings. When the naltrexone was discontinued, the patient's
cravings returned and when he was put back on the medication, the urges
diminished (Bostwick & Bucci 2008). Two double-blind,
placebo-controlled studies reveal decreased symptoms using medication
compared to baseline. The first, by Kruesi and colleagues (1992),
compared clomipramine versus desipramine, with a two-week, single-blind
placebo lead in. Both drugs decreased paraphilic symptoms. The second
study by Wainberg (2006) compared citalopram with a placebo for the
treatment of compulsive sexual behaviors in gay and bisexual men. In the
study, results included a significant decrease in sexual desire and
drive as well as frequency of masturbation and pornography use.
Additional treatment includes: cognitive behavioral therapy
psychodynamic psychotherapy (exploring family of origin, trauma and
underlying factors) and 12-Step groups with a focus on sexual behavior,
including Sex and Love Addicts Anonymous, Sex Addicts Anonymous and
Sexaholics Anonymous (Kaplan & Krueger 2010).
COMPULSIVE BUYING DISORDER
Like other behavioral addictions, shopping addiction is a
controversial idea. Many experts recoil at the idea that excessive
spending can constitute an addiction, believing there has to be physical
tolerance and withdrawal to be diagnostically classified as such. One of
the unifying components of all addictions lies in the reinforcing
properties of these behaviors and substances. Although there is
variability in the definition of pathological spending, experts define
compulsive buying disorder (CBD) as a disorder associated with
compulsive thoughts or impulses to purchase unnecessary or large amounts
of items despite its negative consequences. The classification of
compulsive buying disorder remains unclear; however, McElroy and
colleagues (1995) have developed diagnostic criteria for compulsive
shopping in research settings, which include: (1) frequent preoccupation
with shopping or intrusive, irresistible, "senseless" buying
impulses; (2) clearly buying more than is needed or can be afforded; (3)
distress related to buying behavior; and (4) significant interference
with work or social functioning.
Epidemiological reports suggest that there is a 2% to 8% prevalence
of compulsive shopping in the U.S. based on results of a survey in which
the Compulsive Buying Scale (CBS) was administered to 292 individuals in
Illinois (Claes et al. 2011; Black at el. 2001). The data on gender
differences with compulsive buying disorder is mixed; however, some
estimate that the gender ratio is nine to one (female to male) (Claes et
al. 2011; Black at el. 2001). However, Koran and colleagues (2006)
report that compulsive buying disorder is nearly equal in men and women
(5.5% and 6.0%), respectively. This finding implies that the gender
disparity may be smaller than previous reports suggest and that men may
be underrepresented in samples.
Compulsive buying is typically chronic or intermittent, with an age
of onset that ranges from 18 to 30 years and a greater proportion of
these individuals reporting incomes under $50,000 (Black 2007).
Psychiatric comorbidities often include mood disorders (21% to 100%),
eating disorders (8% to 85%), substance abuse disorders (24% to 46%) and
other impulse control disorders. Furthermore, some studies suggest that
nearly 60% of compulsive buyers meet criteria for at least one
personality disorder (Black 2007).
Although widespread consumerism has escalated in recent years,
compulsive shopping is not a new disorder but rather was identified over
a century ago. Kraepelin gave it the name oniomania, which is roughly
translated as "buying mania." As such, it has been a
long-known phenomenon but only recently suggested to fit into the
behavioral addiction spectrum (Brewer & Potenza 2008). Although this
concept has historical recognition, there is no clear consensus on the
difference between normal shopping, occasional splurges and shopping
addiction. Black and colleagues (2001) report that individuals with
compulsive buying disorder are preoccupied with shopping and spending
and typically spend hours each week engaged in these behaviors. They
identified four distinct phases of compulsive buying disorder, including
anticipation, preparation, shopping, and spending. Many compulsive
buyers describe an escalating level of anxiety that can only be relieved
when they engage in the act of spending. Lee and Miltenberger (1997)
reported that negative emotions, such as anger, anxiety, boredom and
self-critical thoughts, were the most common antecedents to shopping
binges, while euphoria or relief of the negative emotions were the most
common consequences. They reported that there are several
characteristics that compulsive buying shares with other addictions. For
instance, shopping addicts become preoccupied with spending, and devote
significant time and money to the activity. Similar to drug abuse,
shopping addiction is highly ritualized and follows an addictive course
where the individual is consumed by thinking and planning the next
shopping trip, and engaging in the act of buying itself or returning
purchases leads to pleasure and relief of negative feelings. The
frequency of pathological shopping episodes can range from once a month
to once a day, depending on available funds. Similar to substance abuse,
after the act of compulsive shopping, the individual may experience
exhaustion or a let down. Once the purchase is complete, it often leads
to feelings of guilt, disappointment and shame.
The etiology and mechanisms of action behind compulsive spending
are poorly understood; however, new research is shedding light on shared
addiction associated circuitry that may mediate this behavior. There is
a distinction to be made between window-shopping and compulsive
spending; the actual addictive process in this disorder is driven by the
process of spending money. The act of compulsive spending subsequently
requires recruitment and possible dysregulation of distinct
decision-making circuits in the brain.
The role of opiate, serotonergic and dopaminergic systems have all
been suggested in compulsive buying disorder (Mueller et al. 2010),
however at present no definitive evidence has strongly linked these
systems with it. Although clinical studies suggest that citalopram, a
selective serotonin reuptake inhibitor (SSRI), may have some beneficial
effects in preventing relapse to compulsive buying disorder patients,
use of other SSRIs like fluvoxamine has proven inconclusive (Koran et
al. 2006). A key indicator seems to stem from the field of
Parkinson's disease, where patients maintained on a dopamine
precursor L-DOPA or dopamine agonists tend to have higher rates of
compulsive shopping, as well as other behavioral addictions (Djamshidian
et al. 2010; Nirenberg & Waters 2006). In fact it has been shown
that L-DOPA increased reward learning and risk taking in human imaging
data (Pessiglione et al. 2006). This suggests that dopamine may play a
distinctive role in driving craving and seeking, reward prediction, and
decision-making aspects of behavioral addictions in a similar manner to
drugs of abuse (Berridge 2007; Volkow & Wise 2005). As shown in
previous sections, these systems play a significant role in regulating
emotional affect as well as reward systems in the brain and thus
represent key components in the addiction process. Compulsive buying
disorder shares behavioral features such as escalation and tolerance, in
the form of needing to spend more money in order to receive fulfillment
from a shopping binge--both hallmarks of addiction. It is clear that the
behavioral traits associated with these maladaptive behaviors share a
substantial homology with substance abuse and it stands to reason that
similar brain systems are recruited and altered during the etiology of
the disorder. However, a more rigorous approach is needed to understand
the neurobiological mechanisms underlying compulsive buying disorder.
The social, psychological and biological factors surrounding
compulsive spending make it an interesting and complex condition.
Additional studies are needed to better understand the etiology,
differential diagnosis and treatment of this disorder. There are no
published reports describing psychotherapy-focused trials for compulsive
buying disorder. However, some preliminary findings suggest that
cognitive behavioral therapy and dialectical behavioral therapy may have
promising effects. Treatment outcome studies using SSRIs such as
citalopram and fluvoxamine also seem to show a therapeutic benefit for
individuals with compulsive buying disorder. However, further research
is needed to identify the mechanisms that drive this behavior in order
to create more efficacious treatment options.
INTERNET ADDICTION DISORDER
There is increasing attention on cyberspace social pathologies,
which some would call technical addictions. As with other behavioral
addictions, Internet abuse has been a controversial idea and one of the
most challenging tasks has been to arrive at a comprehensive definition
of the concept. Experts have not been able to come to a consensus on a
name, however, there are as many as six different terms associated with
Internet addiction, including "Internet Addiction Disorder
(IAD)," "Pathological Internet Use," "Excessive
Internet Use," and "Compulsive Internet Use" (Widyanto,
Griffiths & Brunsden 2011).
Internet addiction is a relatively new concept in psychiatry and
not yet recognized by the DSM-IV. However, some definitions of
compulsive Internet use in the literature have been derived from DSM-IV
criteria for addiction and impulse control disorder. First introduced by
Goldberg (1995) and Substance Abuse
made popular Addiction Medication
research, the term Internet addiction disorder (IAD) has been defined as
"the compulsive overuse of the Internet and the irritable or moody
behavior when deprived of it" (Mitchell 2000). Some prefer a more
holistic definition that suggests that an individual's
psychological state, which includes both mental and emotional states, as
well as scholastic, occupational and social interactions, is impaired by
the overuse of the Internet (Beard 2005). Shapira and colleagues (2003)
state that in order to diagnose the presence of Internet addiction
disorder, individuals must meet the following criteria: (1) the
excessive use of the Internet beyond the time allotted and/or
irresistible urge to be preoccupied with the Internet; (2) an
impairment, distress or poor functioning in social settings caused from
a preoccupation with the Internet; and (3) the excessive use of the
Internet is not associated exclusively with periods of hypomania or
mania and cannot be entirely accounted for by Axis I clinical disorders.
Griffiths (2000) believes that technical addictions are a branch of
behavioral addictions that satisfy six criteria for addiction: salience,
mood modification, tolerance, withdrawal, conflict, and relapse.
true prevalence of Internet addiction in the U.S. is unknown;
however, Young (1998) estimated the figure to be between 5% and 10% of
all online users, which is approximately two and five million Internet
addicts. Other estimates vary greatly, from as low as 3% reported by
Mitchell (2000) and Whang, Lee, and Chang (2003), to as high as 80% in
Young's original study (1998). The demographic on who is more
likely to be affected by Internet addiction is mixed and not a
homogenous group. However, Mafe and Blas (2006) constructed a profile of
Internet-dependent users as young, highly educated individuals having a
close connection with the Internet. Other researchers have identified
Internet addiction-prone individuals as single, males, college students,
gays, middle-aged females and the less educated (Soule, Shell &
Kleen 2003). There is mixed data on gender disparities, although, more
recent research suggests that that there is no correlation between
gender and length of Internet use (Soule, Shell & Kleen 2003).
Common psychiatric comorbidities with Internet addiction include
depression, bipolar disorder, substance abuse disorder, pathological
gambling and sexual compulsions (Morahan-Martin 2005).
After a decade or more of academic research, the etiology and
mechanisms of action behind pathological Internet use are not well
developed. Research in this area is limited, with few studies using
control groups, randomization, or well-validated measures. The
reward-deficiency hypothesis suggests that those who achieve less
satisfaction from natural rewards turn to substances to seek an enhanced
stimulation of reward pathways (Blum et al. 1996). Internet use provides
immediate reward and gratification, similar to substance use.
Individuals with certain personality attributes such as impulsivity, low
self-esteem and introversion have a greater propensity to Internet
addiction. Internet use may be used as a compensatory tool for certain
deficiencies with social skills and interpersonal relationships. There
has been a range of psychological and behavioral theories that have been
proposed to explain Internet addiction. Hammersley (1995) has suggested
a number of psychological reasons why the Internet is highly reinforcing
for some people: (1) it allows correspondence with people who share
mutual interests; (2) it puts people in touch with other people who
would otherwise never meet; (3) the costs of communicating is low; (4)
there is a substantial "puzzle" element to using the Internet,
and many people find puzzling tasks reinforcing; (5) people can download
software toys, some of which are reinforcing; (6) people can keep in
touch with friends with minimal time and financial costs; (7) it gives
people feelings of status and modernity, which may bolster self-esteem;
(8) it allows people to be taken seriously and listened to; and (9) it
allows people to present a "well-managed" persona, which may
deviate in significant ways from one's everyday, face-face persona.
Others have described a cognitive behavioral model (Davis 2001) where
Internet addiction may result when some psychological factor causes an
individual to be vulnerable to dependence on new online content, which
is followed by obsessive thoughts and then the perception that the
Internet is a "friend." This may be reinforced by the
decade-long trend of people spending increasingly more time with
technology than with humans. There has been a shift away from family and
peers to mass media technology as the primary socialization agents.
Treatment strategies for pathological Internet use are
under-researched and there is limited published data on effective
therapeutic modalities. Young (1999) points to the usefulness of
cognitive behavioral therapy for compulsive Internet use. He suggests
that catastrophic thinking might contribute to compulsive Internet use
in proving a psychological escape mechanism to avoid real or perceived
problems. He also hypothesized that those who suffer from negative core
beliefs and cognitive distortions may be more drawn to anonymity of the
Internet in order to overcome perceived adequacies. Cognitive behavioral
therapy and psychoeducation seem to have promising results for the
treatment of Internet addiction (Young 2007).
Unfortunately, there are no published controlled trials to evaluate
pharmacological interventions. Some experts believe that a similar
pattern of cortical arousal exists in pathological gamblers, substance
abusers and Internet abusers, and naltrexone may mitigate problematic
impulse control behaviors in some individuals (Yellowless & Marks
2007). Research has shown adding naltrexone to a mediation regimen that
already includes an SSRI coincided with a decline in symptoms of
Internet addiction (Bostwick & Bucci 2008). More research is needed
to clarify the mechanism by which naltrexone and SSRIs extinguish
There is no doubt that the Internet usage among the general
population will continue to increase over the next few years. Future
studies are needed to examine the quantitative and qualitative effects
of Internet abuse, while also investigating treatment differences among
the various types of Internet addictions.
Video games have been a part of American culture since the late
1950s, and their prominent role in the lives of American youth has led
to increased public scrutiny of the effects and potential harms of video
game usage, including the potential of socially maladaptive behaviors
such as increased short-term aggressiveness and overuse syndromes (CSAPH Report 2006). In June of 2007, the American Medical Association Council
on Science and Public Health considered whether "videogame
addiction" could be a disorder.
In the U.S. alone, the sale of video games and related products
reportedly grossed between $7 and $10 billion in 2004. Although 70% to
90% of U.S. youth play video games, in 2005 a national survey identified
the prototype gamer as a 30-year-old male who averages between 6.8 and
7.6 hours weekly playing video games (ESA 2006, 2005).
Using World Health Organization criteria, a gaming addiction rate
of 12% was found by researchers in the United Kingdom who polled 7,000
gamers (Grusser et al. 2007). Research in the United States has
estimated that anywhere from a small minority to as much as 10% to 15%
of players may be affected (Chak & Leung 2004).
Psychosocial effects of video games are varied. Some studies have
found that exposure to video game violence may promote increased
aggressive behaviors and decreased prosocial behaviors in social
interactions. (Sheese& Graziano 2005; Vastag 2004) Although overuse
can be associated with any type of video game, it is most commonly seen
among those using massively multi-player online role-playing games
(MMORPG), who represent approximately 9% of gamers (ESA 2005). The
MMORPG are very interactive, social and competitive and primarily
focused on fantasy. Researchers have attempted to examine the type of
individual most likely to be susceptible to such games, and current data
suggest these individuals are somewhat marginalized socially, perhaps
experiencing high levels of emotional loneliness and/or difficulty with
real life social interactions. (Allison et al. 2006) Current theory is
that these individuals achieve more control of their social
relationships and more success in social relationships in the virtual
reality realm than in real relationships (CSAPH Report 2006). Symptoms
of time usage and social dysfunction/disruption appear in patterns
similar to that of other addictive disorders (Tejeiro et al. 2002).
Additionally, dependence-like behaviors are more likely in children who
start playing video games at younger ages (Grusser et al. 2007).
Although there are very few research studies looking at imaging or
treatment, evidence for striatal dopamine release during video game
playing was detected in a positron emission tomography study (Koepp et
al. 1998). Areas of research on potential health effects of video games
that are receiving increasing attention include attention
deficit/hyperactivity disorders (ADHD) and neurology (Chan &
OTHER BEHAVIORAL ADDICTIONS
There are many other potential behaviors that may have addictive
properties, but there is little published data on these conditions. The
terms "love addiction or pathological attachment," "work
addiction," "exercise addiction" and others have been
discussed. And of course, the current impulse control disorders listed
in the DSM-IV classification need more data. There is very little
research to support any of these "other" conditions that are
not currently in the DSM being a true disorder, but clinically there are
many individuals who report symptoms that warrant further discussion.
We live in an overstimulated society and rapid advances in
technology and abundant availability to stimuli and resources may play a
role in the increased prevalence of behavioral disorders. The use of
repetitive actions, initiated by an impulse that can't be stopped,
causing an individual to escape, numb, soothe, release tension, lessen
anxiety or feel euphoric, may redefine the term addiction to include
experience and not just substance. The core feature of these behaviors
as well as substance use disorders appears to be impulsivity. Impulse
control disorders primarily involve a hedonic quality--sex, gambling and
stealing are all associated with a rush or a high (Grant, Brewer &
The difficult part of defining impulse control disorders involves
comorbidity and the complex relationship between affect and impulsivity.
How do you know if the symptoms originate from the proposed primary
disorder? Some critics argue that behavioral conditions are simply
secondary manifestations of underlying psychiatric illnesses including
mood disorders, anxiety disorders, ADHD, personality disorders and other
disorders. The repetitive behavior is simply an adaptation or compulsion
to avoid discomfort.
As research in nondrug addiction progresses, knowledge gained from
the fields of drug addiction, motivation and obsessive-compulsive
disorder will contribute to the development of therapeutic strategies
for nondrug addictions (Olsen 2011). There is emerging clinical evidence
that medications used to treat chemical dependency may be successful in
treating nondrug addictions. For example, naltrexone, nalmefine,
N-acetyl-cysteine and modafanil have all been reported to reduce craving
in pathological gamblers (Grant et al. 2006). Opiate antagonists have
also shown promise in the treatment of pathological gambling and
compulsive sexual behavior (Grant & Kim 2001) and topirimate has
shows some success in reducing binge episodes (McElroy et al. 2007).
Similarities between nondrug and drug addictions include craving,
impaired control over the behavior, tolerance, withdrawal and high rates
of relapse (Potenza 2006). It makes sense that natural rewards can cause
neuroadaptation since learned associations between things such as food
or sexual opportunities and the conditions which maximize availability
is beneficial from a survival standpoint and is a natural function of
the brain (Alcock 2005). In some individuals, this plasticity may
contribute to a state of compulsive engagement in behaviors that
resembles drug addiction (Olsen 2011). Similar to chemical addictions,
there appears to be a transition period between moderate and compulsive
use (Grant, Brewer & Potenza 2006). Extensive data suggests that
eating, shopping, gambling, playing video games, and spending time on
the Internet are behaviors that can develop into compulsive behaviors
that are continued despite devastating consequences (Davis & Carter
2009). Clinically, patients may shift from a normative behavioral set
point to a pathological one when influenced by comorbidities or
environmental stimuli. These addiction and related disorders appear to
work on a spectrum.
It is clear there is a substantial amount of overlap between
behavioral addictions and substance abuse. Despite this commonality,
there haven't been many studies evaluating shared neurobiology,
although the research in binge eating and pathological gambling is
slowly growing. At a minimum, we need researchers to better define these
conditions with uniform diagnostic criteria and develop universal, valid
screening measures. Awareness is building and research is beginning to
coalesce around defining the biological systems that drive these types
of disorders. The National Institute on Drug Abuse (NIDA 2002), a
research-funding agency in the United States, has cited the importance
of studying nondrug behaviors/disorders (obesity, pathological gambling,
etc.) in understanding substance dependence. Indeed, in gaining a better
understanding of behavioral addictions it may prove that we gain a
stronger theory of the overall mechanisms that comprise our perception
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Reef Karim, D.O. (a) & Priya Chaudhri, Ph.D. (b)
(a) Assistant Clinical Professor, UCLA Semel Institute for
Neuroscience & Human Behavior, Department of Psychiatry, Los
(b) Adjunct Faculty, University of California, San Diego, San
Please address correspondence to Reef Karim, D.O., The Control
Center, 9777 Wilshire Blvd, Suite 704, Beverly Hills, CA 90210; phone:
(310) 271 8700; email: Reef@doctorreef.com