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Definition: addiction from Dictionary of Psychological Testing, Assessment and Treatment

Psychological and/or physiological dependency on a drug or other (usually pleasure-giving) substance or event. Common addictions include illegal drugs (drug addiction), alcohol, tobacco, and gambling. If the addiction is purely governed by a psychological drive, then it is known as a

psychological addiction, or psychological dependency. If the patient’s bodily mechanisms require the drug (i.e. if s/he feels physically ill if the drug is withdrawn), then the phenomenon is called physiological addiction or substance dependence (note that there may be a psychological drive as well).


Summary Article: Addiction
From Encyclopedia of the Mind

Addiction is a chronic and relapsing disorder marked by persistent substance use despite a host of negative consequences. The U.S. Drug Enforcement Administration's Controlled Substances Act (CSA) identifies five classes of drugs: narcotics, depressants, stimulants, hallucinogens, and anabolic steroids. Substances within each of these classes, with the possible exception of anabolic steroids, are used to change one's mood or thoughts by way of altering the delicate chemical balance within the central nervous system. It is thought that all substances of abuse are capable of producing euphoria, and the extent to which this euphoria is reliably produced by the substance increases the possibility of the formation of addiction to it.

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), defines two primary forms of substance use disorders (SUDs), namely, substance abuse and substance dependence. Substance abuse is marked by (a) recurrent substance use resulting in the failure to fulfill role obligations (e.g., missing work or school due to the consequences of substance use), (b) recurrent use in physically hazardous situations (e.g., drinking and driving), (c) continued use despite negative interpersonal consequences, or (d) repeated substance-related legal problems. Only one of those symptoms must be present within a 12-month period to warrant the diagnosis of substance abuse. Substance dependence, however, is typically conceptualized as a more severe substance use disorder, which is, in turn, more commonly associated with the term addiction. Substance dependence is marked by the presence of at least three of the following symptoms occurring together within a 12-month period: (a) tolerance (i.e., the need for greater amounts of the substance to achieve the same effect); (b) withdrawal (i.e., a group of symptoms that occurs when the substance is abruptly discontinued or taken in reduced amounts); (c) taking the substance in larger amounts or over longer periods of time than intended; (d) persistent desire or unsuccessful effort to stop or cut down substance use; (e) a great deal of time spent in obtaining, using, and recovering from the effects of a substance; (f) giving up important activities because of substance use; and (g) use despite physical or psychological problems caused or exacerbated by the substance. Revisions to the DSM-IV are under way, and the proposed changes include a single disorder category, namely, substance use disorder specified as moderate or severe. In light of the DSM-IV revisions, there continues to be considerable debate in the field as to the best terminology for substance use disorders and whether they should be collectively referred to as addiction, dependence, or an alternative term. Nevertheless, there is clear recognition that addiction represents a chronic and debilitating disorder with enormous costs to the affected individuals, their families, and society.

In this entry, the epidemiology, etiology, and treatment of addiction will be briefly summarized, with important theories and future directions highlighted.

Epidemiology

Substance use disorders, as currently defined in the DSM-IV, represent highly prevalent mental disorders. Based on results from the National Epidemiologic Survey on Alcohol and Related Conditions in 2007, prevalence, or the total number of individuals diagnosed with alcohol abuse within their lifetime and the past 12 months, is estimated at 17.8% and 4.7%, respectively, while the prevalence of lifetime and 12-month alcohol dependence is 12.5% and 3.8%, respectively. Epidemiological data for drug abuse suggest the prevalence of 12-month and lifetime drug abuse to be 1.4% and 7.7%, with drug dependence being less frequent in 12-month and lifetime estimates at 0.6% and 2.6%, respectively. Results consistently demonstrate that SUDs are highly comorbid with one another and with other forms of psychopathology, particularly mood, anxiety, and personality disorders. Recent research has also shown that despite the debilitating nature of SUDs only a small proportion of individuals with drug abuse and less than half of patients with drug dependence ever seek treatment. A similar pattern of infrequent treatment seeking is seen for alcohol dependence, as only a quarter of individuals diagnosed with this disorder report seeking help. Together, these results suggest that substance use disorders (a) are highly prevalent; (b) are debilitating and often comorbid with other forms of psychopathology; and (c) despite their high frequency and associated impairments, treatment seeking for these disorders remains uncommon.

Etiology

The etiology of SUDs is inherently complex and likely involves the interplay between biological and psychosocial factors. At the biological level, two factors that modulate behavior, reinforcement and neuroadaptation, are implicated in the addictive process. Traditionally, it was assumed that addicts are motivated to take drugs either for the pleasure induced by the drug (positive reinforcement model) or to avoid the unpleasant consequences of withdrawal (negative reinforcement model). Drugs of abuse possess acute positive reinforcing effects because of their interactions with specific neurotransmitter systems within the mesolimbic reward circuitry. This circuitry, which encompasses connections between the ventral tegmental area and the basal forebrain (including the nucleus accumbens, olfactory tubercle, frontal cortex, and amygdala), is known to be involved in modulating behavioral responses to stimuli that activate feelings of motivation (reward) and reinforcement through the neurotransmitter dopamine, among other neurotransmitter systems (e.g., opioid peptides). Dopamine's role in the mesolimbic reward system is widely believed to be crucial for mediating the rewarding effects of drugs, as most drugs of abuse have been found to increase dopamine within the nucleus accumbens.

Recently, however, the positive and negative reinforcement models have been criticized as being neither necessary nor sufficient for the development of SUDs. The lack of strong withdrawal syndromes present in some common drugs of abuse and the dissociation between subjective levels of pleasure and compulsive drug-taking behavior have been proposed as examples of the limitations inherent in these models of addiction etiology. The incentive-sensitization model of drug addiction, which was developed by Terry Robinson and Kent Berridge in response to these limitations, posits that repeated administration of potential drugs of abuse cause long-lasting neural adaptations in the mesolimbic reward circuitry, which renders the brain reward systems sensitized to drugs and drug-associated stimuli. Thus, although the acute reward and initiation of addiction appear to be dependent on dopamine's involvement in the mesolimbic reward system, the sensitized brain regions in this model are thought to mediate a subcomponent of reward termed the incentive salience, or craving, rather than the pleasurable effects of drugs per se. Studies have convincingly demonstrated that, with repeated drug exposure, the dopaminergic response becomes triggered by the presentation of drug cues (e.g., the sight of a needle to an individual addicted to heroin or the smell of tobacco smoke to a smoker) as opposed to the administration of the drug itself, which is consistent with the proposed associative learning processes in addiction. In particular, end-stage addiction has been hypothesized to result primarily from the gradual recruitment of the prefrontal cortex and its glutamatergic projections to the nucleus accumbens. This pathological form of neuroplasticity in excitatory transmission is hypothesized to promote the compulsive nature of drug seeking by decreasing the value of natural rewards, reducing cognitive control over drug-related behavior, and enhancing glutamatergic response to drug-associated stimuli.

Genetic factors are widely accepted as determinants of the risk for substance use disorders. Twin and adoption studies have estimated that approximately 50% of the variance in risk for developing alcoholism is due to genetic factors, while the genetic contribution to drug use disorders ranges between 60% and 80%. Studies have also shown that common genetic and environmental factors that influence the vulnerability to substance use disorders are largely, or entirely, nonspecific to any particular drug class. For example, results from the Harvard Twin Study of Substance Abuse revealed that between 50% and 85% of the vulnerability to drug use is common across different categories of illicit drugs. Common genetic and environment risk factors may also underlie the comorbidity between substance use disorders and other psychiatric illnesses such as mood and anxiety disorders. In short, genetic factors account for a substantial portion of the liability to substance use disorders, although these factors are less specific to drug classes and even to psychiatric disorders than originally thought. Although considerable progress has been made in elucidating the relative contribution of genetic and environmental factors to addiction, the identification of specific risk genes remains elusive.

Treatment

Given the complexity of addiction phenomenology, the available treatment approaches are only modestly effective. The standard of care for addiction consists of initial detoxification for cases in which withdrawal symptoms must be medically managed. Following detoxification, intensive inpatient or outpatient programs are typically recommended. A combination of psychotherapy and pharmacotherapy is likely to give patients the best chance of recovery. In terms of psychotherapy, cognitive behavioral approaches have received the most empirical support for their efficacy. A large multisite treatment study called Project MATCH (1997) has also found support for 12-step facilitation and motivation enhancement for the treatment of alcoholism.

Numerous pharmacological treatments have been proposed for the treatment of substance use disorders, yet few have proven effective at maintaining long-term abstinence. Substitution therapies that replace the addictive substance with another, less detrimental substance have been proven to be efficacious for the treatment of opiate addiction; however, these opioid receptor agonists (e.g., methadone) only manage the disorder and may themselves promote the same neuroadaptive processes as the originally abused drug, thereby maintaining the strength of the addiction rather than treating it. The opioid receptor partial agonist, buprenorphine, has shown greater efficacy for the treatment of opiate dependence and can be administered on an outpatient basis. The Food and Drug Administration (FDA) has approved three medications for the indication of alcoholism, namely, naltrexone, acamprosate, and disulfiram. The opioid antagonist naltrexone and the partial glutamate coagonist acamprosate target the state of craving by blocking the opioid receptors and NMDA glutamate receptors within the reward circuit, respectively. Additionally, a variety of antidepressants have been used in the treatment of addiction, based in part on the assumption that they will alleviate some of the anhedonia, or inability to experience pleasure, reported by patients during protracted withdrawal. Bupropion is one such antidepressant that has been reported to increase abstinence from cigarettes in smokers. More recently, immunotherapies (i.e., vaccines) are being developed for the treatment of cocaine abuse, which stimulate the body's own immune system to attack the substance, thereby reducing the amount of cocaine that reaches the brain. Although promising, these immunotherapies fail to reverse the neuroadaptive processes responsible for addiction, and thus craving for the drug may remain despite treatment.

Summary

Addiction is a chronic and relapsing condition caused by the interplay between genetic and environmental factors. Research on the neurobiological bases of addiction has consistently highlighted the ability of drugs of abuse to potently activate the mesolimbic dopamine system, producing an intense subjective feeling of reward. Although various drugs of abuse have different pharmacological properties and associated intoxication effects, their common activation of this reward circuitry subsequently produces the compulsive drug seeking that characterizes this disorder. Addictive disorders are highly frequent in modern society and associated with devastating psychosocial and health consequences. These disorders often co-occur with other psychiatric illness, such as mood, anxiety, and personality disorders. The currently available treatments for addiction are only moderately effective, and the combination of pharmacotherapy with behavioral therapy is often recommended. Nevertheless, the pharmacological treatment options for various substance use disorders are scarce relative to other psychological disorders, and there is a strong need to develop more effective medications as well as to identify the biological and psychological factors within patients that can guide the selection of effective treatment approaches at the individual level.

See also

  • Behavioral Therapy
  • Reinforcement Learning, Psychological Perspectives
Further Readings
  • Compton, W. M.; Thomas, Y. F.; Stinson, F. S.; Grant, B. F. (2007). Prevalence, correlates, disability, and comorbidity of DSM-IV drug abuse and dependence in the United States: Results from the National Epidemiologic Survey on Alcohol and Related Conditions. Archives of General Psychiatry, 64, 566-576.
  • Hasin, D. S.; Stinson, F. S.; Ogburn, E.; Grant, B. F. (2007). Prevalence, correlates, disability, and comorbidity of DSM-IV alcohol abuse and dependence in the United States: Results from the National Epidemiologic Survey on Alcohol and Related Conditions. Archives of General Psychiatry, 64, 830-842.
  • Kalivas, P. W.; Volkow, N. D. (2005). The neural basis of addiction: A pathology of motivation and choice. American Journal of Psychiatry, 162, 1403-1413.
  • Koob, G. F.; Moal, Le M. (2001). Drug addiction, dysregulation of reward, and allostasis. Neuropsychopharmacology, 24, 97-129.
  • Magill, M.; Ray, L. A. (2009). Cognitive-behavioral treatment with adult alcohol and illicit drug users: A meta-analysis of randomized controlled trials. Journal of Studies on Alcohol and Drugs, 70, 516-527.
  • O'Brien, C. P.; Volkow, N.; Li, T. K. (2006). What's in a word? Addiction versus dependence in DSM-V. American Journal of Psychiatry, 163, 764-765.
  • Robinson, T. E.; Berridge, K. C. (2000). The psychology and neurobiology of addiction: An incentive–sensitization view. Addiction, 95, 91-117.
  • Tsuang, M. T.; Bar, J. L.; Harley, R. M.; Lyons, M. J. (2001). The Harvard Twin Study of Substance Abuse: What we have learned. Harvard Review of Psychiatry, 9, 267-279.
Lara A. Ray
Kelly E. Courtney
© 2013 by SAGE Publications, Inc.

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