Addiction

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For other uses, see Addiction (disambiguation).
See also: Substance dependence (drug addiction) and Behavioral addiction

Addiction is the continued repetition of a behavior despite adverse consequences,[1] or a neurological impairment leading to such behaviors.[2]

According to many addiction specialists, potential addictions can include, but are not limited to, drug abuse, exercise addiction, food addiction, computer addiction and gambling. Currently, however, only substance addictions and gambling addiction are recognized by the DSM-5. ΔFosB, a gene transcription factor, is now known to be the critical component and common factor in the development of virtually all forms of behavioral and drug addictions.[3][4][5] Classic hallmarks of addiction include impaired control over substances or behavior, preoccupation with substance or behavior, continued use despite consequences, and denial.[6] Habits and patterns associated with addiction are typically characterized by immediate gratification (short-term reward), coupled with delayed deleterious effects (long-term costs).[7]

Physiological dependence occurs when the body has to adjust to the substance by incorporating the substance into its "normal" functioning.[8] This state creates the conditions of tolerance and withdrawal. Tolerance is the process by which the body continually adapts to the substance and requires increasingly larger amounts to achieve the original effects. Withdrawal refers to physical and psychological symptoms experienced when reducing or discontinuing a substance that the body has become dependent on. Symptoms of withdrawal generally include but are not limited to anxiety, irritability, intense cravings for the substance, nausea, hallucinations, headaches, cold sweats, and tremors.

Substance dependence[edit]

Main article: Substance dependence

Substance dependence can be diagnosed with physiological dependence, evidence of tolerance or withdrawal, or without physiological dependence. DSM-5 substance dependencies include:

Withdrawal[edit]

Main article: Drug withdrawal

Withdrawal is the body's reaction to abstaining from an addictive substance of which it has become dependant and tolerant. Without the substance, physiological functions that were dependent on the substance will react because of the body's tolerance and dependence of the substance. Chemical and hormonal imbalances may arise if the substance is not introduced. Physiological and psychological stress is to be expected if the substance is not re-introduced.

Recovery/Interventions[edit]

In addition to the traditional behavioral self-help groups and programs available for rehabilitation, there is a varied array of preventive and therapeutic approaches to combating addiction. For example, a common treatment option for opiate addiction is methadone maintenance. This process consists of administering the drug, a potent opiate with some potential for abuse, as a drink in a supervised clinical setting. In this way, the brain opiate levels increase slowly without producing the high but remain in the system long enough to deter addicts from injecting heroin.

Another form of drug therapy involves buprenorphine, a drug which seems to be even more promising than methadone.[9] A partial agonist for certain opiate receptors, this treatment blocks the effects of opiates but produces only mild reactions itself. Moreover, this method of detoxification has little value in the drug market.

New research indicates that it may even be possible to develop antibodies which combat a particular drug's effect on the brain, rendering the pleasurable effects null. Recently, vaccines have been developed against cocaine, heroin, methamphetamine, and nicotine. These advances are already being tested in human clinical trials and show serious promise as a preventive and recovery measure for addicts or those prone to addiction.[10][11]

Furthermore, another method of treatment for addiction that is being studied is deep brain stimulation. A serious procedure, DBS targets several brain regions including the nucleus accumbens, subthalamic nucleus, dorsal striatum, and medial prefrontal cortex among others.[12] Other studies have concurred and demonstrated that stimulation of the nucleus accumbens, an area that is apparently one of the most promising regions, allowed a seventy-year-old man to stop smoking without issue and attain a normal weight.[13]

Behavioral addiction[edit]

The term addiction is also sometimes applied to compulsions that are not substance-related, such as compulsive shopping, sex addiction/compulsive sex, overeating, problem gambling, exercise/sport, compulsive or binge travel, and computer addiction. Sometimes the compulsion is not to "do" something but to avoid or "do nothing" e.g. procrastination (compulsive task avoidance).[14][15][16] In these kinds of common usages, the term addiction is used to describe a recurring compulsion by an individual to engage in some specific activity, despite harmful consequences, as deemed by the user themselves to their individual health, mental state, or social life. There may be biological and psychological factors contributing to these addictions.[17]

Biological mechanisms[edit]

Main article: ΔFosB

ΔFosB, a gene transcription factor, has been identified as playing a critical role in the development of addictive states in both behavioral addictions and drug addictions.[3][4][5] Overexpression of ΔFosB in the nucleus accumbens is necessary and sufficient for many of the neural adaptations seen in drug addiction;[3] it has been implicated in addictions to alcohol, cannabinoids, cocaine, nicotine, phenylcyclidine, and substituted amphetamines[3][18][19][20] as well as addictions to natural rewards such as sex, exercise, and food.[4][5] A recent study also demonstrated a cross-sensitization between drug reward (amphetamine) and a natural reward (sex) that was mediated by ΔFosB.[21]

Additional addiction research indicates that biological mechanisms are present. There are many variables, which the studies disagree over, among the primary contributing factors. As discussed in "nature versus nurture" debate the biological "nature" of individual innate qualities can account for many decisions and actions, such as a family history in which genetics, DNA, and other mental disorders remain dormant for generations and then are triggered.[22] Professional treatment providers have differing opinions on this issue.

The risk of a future addictive disorder is greatly increased if an individual gets exposed to repeated stress or engages in drug abuse during adolescence due to it being a critical neuro-developmental stage which is sensitive to such experiences or insults. The reason that stress and substance abuse during adolescence increases the risk of addiction is due to the changes it does to the brain.[23]

Several brain regions are also involved in the biological mechanisms of addiction. Most notably, the release of dopamine into the nucleus accumbens, which is triggered by a wide variety of drugs in a wide variety of ways, plays a role in the reinforcing qualities of stimuli.[24] Since dopamine secretion is also characteristic of natural reinforcing stimuli such as food, water, and sex, it's evident that the addictive nature of drug involves processes that hijack these mechanisms. Research indicates that this process begins in the limbic dopaminergic system and subsequently modifies other parts of the brain that receive input from the affected neurons. Among these areas is the ventral tegmental area.[25]

The mechanisms by which this takes place include the insertion of extra AMPA receptors into the postsynaptic membrane of the DA neurons. Studies with mice indicate that exposure to cocaine for two weeks can cause long-term changes in the ventral tegmental area. Moreover, the pleasurable effects of the drug reinforce the behaviors associated with acquiring and ingesting the drug until they become a habit. Early on, this process takes place largely in the ventral striatum, specifically in the nucleus accumbens but eventually, these changes primarily involve the dorsal striatum. Further studies suggest that the neuronal modifications involved in addiction follow a dorsally cascading sequence of reciprocal connections between the two aforementioned areas.[26]

The changes that happen in the nucleus accumbens and eventually also in the dorsal striatum include alterations in the dopamine receptors on the neurons which send axons to other areas. Dopamine D1 receptors increase which results in excitation and facilitation of behavior, while dopamine D2 receptors lessen, resulting in inhibited and suppressed behavior. Studies have found that certain drug use can also affect acetylcholinergic interneurons which, though few in number, exert their influence on medium spiny neurons in the nucleus accumbens.[27] To summarize, the release of dopamine in the nucleus accumbens results in the early stages of drug addiction, but subsequent alterations in regions such as the dorsal striatum account for the formation of actual drug-taking habitual behaviors. This helps explain why drug addicts are prompted to procure the drug and consume it when environmental cues associated with drug-taking are present but become withdrawn and solemn when participating in drug-free activity.[28]

With regard to initial use and drug addiction, several factors play a role in determining one's predisposition. Moreover, the prefrontal cortex, which has bearing on judgement, risk taking, and impulse control, may be complicit in explaining why adolescents are more prone to drug-taking behavior. In fact, some studies have demonstrated that children, as young as ten to twelve years old, who score lowest on measures of behavioral inhibition displayed the highest risks of developing substance addiction.[29]

Personality theories of addiction[edit]

Role of affect dysregulation in addiction[edit]

Research has consistently shown strong associations between affective disorders and substance use disorders. Specifically, people with mood disorders are at increased risk of substance use disorders.[30] Affect and addiction can be related in a variety of ways as they play a crucial role in influencing motivated behaviours. For instance, affect facilitates action, directs attention, prepares the individual for a physical response, and guides behaviour to meet particular needs.[31] Moreover, affect is implicated in a range of concepts relevant to addiction: negative reinforcement and positive reinforcement, behaviour motivation, regulation of cognition and mood, and reasoning and decision making.[32][33] Emotion-motivated reasoning has been shown to influence addictive behaviours via selecting outcomes that minimize negative affective states while maximizing positive affective states.[34]

Negative affect[edit]

The relationship between negative affect and substance use disorders has been the most widely studied model of addiction. It proposes that individuals who experience the greatest levels of negative affect are at the greatest risk of using substances or behaviours as a coping (psychology) mechanism.[35][36] Here, substances and behaviours are used to improve mood and distract from unpleasant feelings. Once physical dependence has been established, substance abuse is primarily motivated by a desire to avoid negative affective states associated with withdrawal. Individuals high in affective mood disorders (anxiety) most commonly report high levels of negative affect associated with cravings.[37][38][39] However, the relationship between negative affect and addiction is not unidirectional. That is, while positive affect increases the likelihood of initiation of substance use, the negative affective states produced by withdrawal are the most commonly reported factors for continued use.[30]

Key to this concept is the Hedonic Hypothesis, which states that individuals initiate use of the substance or behaviour for their pleasurable effects, but then take it compulsively to avoid withdrawal symptoms, resulting in dependence.[40] Based on this hypothesis, some researchers believe that individuals engaging in risky use of substances or behaviours may be over-responsing to negative stimuli, which leads to addiction.

Negative affect has also been a powerful predictor in terms of vulnerability to addiction in adolescents. High-risk adolescents have been found to be highly reactive to negative stimuli, which increases their motivation to engage in substance use following a negative emotion-arousing situation.[41] Moreover, it has been established that adolescents high in negative affect are at increased risk for moving from recreational use to problematic use despite a family history of addiction.[41]

Furthermore, the trait negative urgency, the propensity to engage in risky behaviour in response to distress, is highly predictive of certain aspects of substance abuse in adolescents.[42] Early individual differences in emotional differences in reactivity and regulation underlie the later emergence of the trait 'negative urgency'.[43]

Positive affect[edit]

Unlike negative affect, positive affect is related to addiction in both high and low forms. For example, individuals high in positive affect are more likely to engage in risky behaviour, such as drug use. Individuals with high positive affect in response to use are more likely to seek out substances for hedonic reasons. Conversely, low positive affect may prompt initial use due to lack of responsiveness to natural rewards.[30]

Extensive personality research has been done that links positive emotional states to individual differences in risky behaviour.[30] The trait positive urgency, defined as the tendency to engage in risky behaviour under conditions of extreme positive affect, is predictive of substance or behavioural problems that lead to addiction.[44] This trait represents an underlying dysregulation in response to extreme affective states and has a direct impact on behaviour. The trait 'positive urgency' has been shown to have a predictive relationship with increases in drinking quantity and alcohol-related problems in college, as well as drug use in college.[42][45] Furthermore, this trait provides important information on how positive affect can increase the likelihood of engaging in substance abuse.

Another important factor to consider is the individual differences in the experience of pleasurable effects brought on by the substance or behaviour. It is reasoned that certain individuals may be more sensitive to the pleasurable effects and thus experience them with greater intensity, resulting in addiction.[30] For example, over-responsiveness to substance affects has been found in cocaine addicts - an increased response to methylphenidate in the brain regions associated with emotional reactivity and mood.[46][47][48] Thus, strong emotional responses that addicted individuals show in response to substances or behaviours might be results of enhanced sensitivity to their effects.

Individuals differ in the way by which they metabolize substances, such as alcohol; these positive reinforcing effects are partly predetermined.[30] Individual reactivity to the effects of substances may affect motivation to use. For example, if a person experiences strong positive (and weak negative) effects from a substance, due to their biochemical profile, their expectations of the positive effects from the substance will be heightened, therefore increasing their desire for continued use, resulting in dependence.[30] According to this model, the experience of the positive mood enhances implicit attention to substance cues and implicit associations between reward and substance use.[49]

Interestingly, many addicts report symptoms of anhedonia (i.e., the inability to experience pleasure).[50] Results of chronic deviation of the brain's reward set point, which follow a prolonged intoxication, diminish responsiveness to natural positive stimuli. This may result in an over-responsiveness to substance-related cues, coupled with an impaired capacity to initiate behaviours in response to natural rewards.[51] Thus, low positive affect inhibits the individual's ability to replace drug-taking with other rewarding activities. It has also been proposed that during substance dependence the somatic states that guide decision-making are weakened in relation to natural rewards, while at the same time they enhance the emotional response to drug-related stimuli.[52]

Compulsive behaviours characterized by addiction are underpinned by two interacting systems: (a) impulsivity, and (b) reflection. Impulsivity is responsible for the rapid signalling of the affective importance of a stimuli. Reflection cognitively evaluates the signal before altering the behavioural response. Dysfunction in impulsivity exaggerates the emotional impact of the drug-related stimuli and attenuates the impact of natural reinforcement.[30] Dysregulation in reflection results in the inability to override impulsivity, thus resulting in addiction.[30] Under-responsiveness to naturally occurring positive stimuli is a crucial element that biases the individual towards the use of substances or behaviours and away from non-drug alternatives.

Effortful control[edit]

Temperamental effortful control is defined as the ability to suppress a dominant response in order to perform a subdominant response.[53] In other words, it is the degree of control the individual has over impulses and emotions, which includes the ability to focus or shift attention. Temperamental effortful control can influence addiction in a number of ways.

Low levels of effortful control can render the individual less able to distract themselves from unpleasant feelings or overcome strong affective impulses, resulting in maladaptive responses to distress - such as continued substance use.[30] Low effortful control may also interact with negative and positive affect, predisposing individuals to substance or behavioural use, and impair their ability to control use.[30]

A general inability to control affective states may impair the conditioning of behaviour associated with rewards and punishment, may increase susceptibility to biasing by substance-related cues, and could tax self-regulatory capacity.[30] Such conditions may render individuals unable to interrupt automatic drug-seeking behaviours. Abnormal levels of positive and negative affect can be increased by low effortful control.[54][55] For example, high positive affect may interact with low effortful control in increasing risk of addiction amongst vulnerable populations.

Gray's reinforcement sensitivity theory[edit]

Gray's Reinforcement sensitivity theory (RST) consists of two motivational systems: the Behaviour Inhibition System (BIS) and the Behaviour Activation System (BAS).[56][57] The BIS is responsible for organizing behaviour in response to adverse stimuli. In other words, stimuli associated with punishment or the omission/termination of reward, are believed to underlie anxiety. The purpose of the BIS is to initiate behaviour inhibition, or interrupt ongoing behaviour, while the BAS is sensitive to stimuli that signal reward and/or relief from punishment (impusivity).[56][57] In accordance with the RST, an association was found between people with extreme scores in BIS/BAS and adjustment problems. BIS and BAS reactivity correspond with individual trait differences in positive affect and negative affect - The BAS is associated with trait impulsivity and positive affect, while the BIS is associated with trait negative affect.[58][59] For instance, it has been postulated that high BIS is related to anxiety, while high BAS is related to conduct disorders or impulsivity.[57][60]

According to this model substance abuse problems may arise under two different personality traits: low BIS and high BAS. Since the BAS promotes the individual to pursue actions that may result in reward, BAS sensitivity is involved in the initiation of addiction. Significant associations have been found between high BAS such as alcohol misuse in school girls, hazardous drinking in men, illicit drug abuse, and tobacco use. BAS sensitivity is a significant predictor of reactivity to substance cues, or cravings.[61][62][63][64][65][66][67][68] Conversely, BIS sensitivity is involved in avoiding negative situations or affect (such as withdrawal). Low BIS has been positively associated with continuing the addiction to relieve feelings of withdrawal, or for continued use to alleviate negative affect.

Model of impulsivity[edit]

The model of impulsivity states that individuals high in impulsivity are at greater risk of addictive behaviours. The model proposes a two dimensional trait characteristic for the initiation and continuation of substance/behavioural abuse:

  • Reward Drive (RD) - reflects individual differences in sensitivities to incentive motivation and engagement of addictive behaviour when reward cues are detected.[69]
  • Rash Impulsiveness (RI) - reflecting individual differences in the ability to modify the addictive behaviour due to negative consequences.[69] Individuals high in RI are oblivious or insensitive to the negative consequences as a result of addictive behaviour when engagement is craved.

Both high RD and RI individuals are found to have difficulty in making decisions that have future consequences. Individuals high in RD experience greater reinforcement when initially engaging in the addictive behaviour, and experience stronger conditioned associations with continued use. Individuals high in RI experience greater difficulty resisting cravings even in the face of negative consequences.[69] Some moderators of RD and RI on the severity of addiction are stress and negative affect (such as feeling depressed).[70] That is, individuals high in RD/RI who also experience high levels of negative affect or stress, present more severe addictive behaviours. For example, if an individual is experiencing emotional distress, the distress experienced may lessen impulse control if they believe that engaging in addictive behaviour will decrease negative affect. According to this model, adolescents who are high in RI are at greater risk for developing addictions. Interestingly, low RI has been shown to moderate some of the risk of addiction due to family history.[71][72][73][74] However, high RI for individual without a family history of addiction has been related to poor decision-making.

Cloninger's tri-dimensional personality theory[edit]

Cloninger's Tri-Dimensional Personality Theory states that personality comprises three genetically independent dimensions:[75]

  • Novelty seeking (NS) - tendency towards exploration and intense exhilaration in response to novel stimuli
  • Harm avoidance (HA) - intense response to adverse stimuli and learned inhibited behaviour to avoid punishment
  • Reward dependence (RD) - resistance to extinction of previously rewarded behaviour.

Each personality dimension lies on a spectrum ranging from low to high. For example, individuals high in NS are impulsive, while individual's low in NS are reflective. Interactions between each of these three personality dimensions lead to different responses to novelty, punishment and rewards.[75]

This model was extended to alcohol use disorders proposing that individuals with alcohol use disorders have extreme temperaments (i.e. are very high or very low in NS, HA, and RD).[76] This model proposes that alcoholics can be classified in two groups based on the combinations of their three personality dimensions:[75]

Type I alcoholics have a late onset of alcohol-related problems, experience guilt and fear associated with consumption, lose control once drinking is initiated, engage in alcohol-related antisocial conduct, and rarely exhibit spontaneous alcohol-seeking behaviour.[77] Type I alcoholics are thought to be low in NS and high in HA and RD, exhibiting behaviors that are motionally dependent, rigid, perfectionistic, anxious, quiet, patient, and introverted.[77]

Type II alcoholics have an earlier onset of alcohol-related problems, less ability to abstain from alcohol, more frequent alcohol-related antisocial behaviour, less loss of control once drinking commenced, and less guilt or fear associated with drinking.[77] These individuals are high in NS, and low in HA and RD, which means they may be typically aggressive, impulsive, active, talkative, and impatient.[77]

Criticism of the addiction model[edit]

In the mid-20th century critics of the addiction model, notably Thomas Szasz, claimed that the concept of addiction was not normatively neutral, but inherently included a normative component that was arguably out of place in scientific discourse. Szasz cited, for example, Goodman and Gilman's The Pharmacological Basis of Therapeutics, which defined "drug abuse" as "the use, usually by self-administration, of any drug in a manner that deviates from the approved medical or social patterns within a given culture."[78] In investigating the history of the word "addiction," Szasz found that until the 20th century, the term meant "simply a strong inclination toward certain kinds of conduct, with little or no pejorative meaning attached to it."[79] The Oxford English Dictionary included examples of addiction "to civil affairs" and "to useful reading."[79] Szasz observed that the term transformed over time into a "stigmatizing label" with "pejorative meaning."[80] Szasz drew an analogy between this stigmatization of minority psychopharmacological habits and the stigmatization of minority sexual habits

Just as socially disapproved pharmacological behavior constitutes "drug abuse," and is officially recognized as an illness by a medical profession that is a licensed agency of the state, so socially disapproved sexual behavior constitutes a "perversion" and is also officially recognized as an illness; and so, more generally, socially disapproved personal behavior of any kind constitutes "mental illnesses."[78]

Szasz's views were criticized for failing to account for the effect of physiological dependence.[81]

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