Jump to content

Addiction

From Wikipedia, the free encyclopedia

This is an old revision of this page, as edited by 66.60.156.2 (talk) at 21:24, 8 May 2014 (→‎Recovery/Interventions). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

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]

Addictions can include, but are not limited to, drug abuse, exercise addiction, food addiction, computer addiction and gambling. Classic hallmarks of addiction include impaired control over substances or behavior, preoccupation with substance or behavior, continued use despite consequences, and denial.[3] Habits and patterns associated with addiction are typically characterized by immediate gratification (short-term reward), coupled with delayed deleterious effects (long-term costs).[4]

Physiological dependence occurs when the body has to adjust to the substance by incorporating the substance into its "normal" functioning.[5] 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

Main article: Substance dependence

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

Withdrawal

Main article: Drug withdrawal

Italic text

==Recovery/Interventions==ocedure, DBS targets several brain regions including the nucleus accumbens, subthalamic nucleus,

Behavioral addiction

Main articles: Behavioral addiction and Addictive behavior

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 and computer addiction. Sometimes the compulsion is not to "do" something but to avoid or "do nothing" e.g. procrastination (compulsive task avoidance).[6][7][8] 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.[9]

Biological mechanisms

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.[10] 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.[11]

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.[12] 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.[13]

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.[14]

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.[15] 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.[16]

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.[17]

Personality theories of addiction

Role of affect dysregulation in addiction

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.[18] 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.[19] 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.[20][21] Emotion-motivated reasoning has been shown to influence addictive behaviours via selecting outcomes that minimize negative affective states while maximizing positive affective states.[22]

Negative affect

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.[23][24] 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.[25][26][27] 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.[18]

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.[28] 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.[29] 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.[29]

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.[30] Early individual differences in emotional differences in reactivity and regulation underlie the later emergence of the trait 'negative urgency'.[31]

Positive affect

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.[18]

Extensive personality research has been done that links positive emotional states to individual differences in risky behaviour.[18] 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.[32] 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.[30][33] 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.[18] 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.[34][35][36] 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.[18] 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.[18] According to this model, the experience of the positive mood enhances implicit attention to substance cues and implicit associations between reward and substance use.[37]

Interestingly, many addicts report symptoms of anhedonia (i.e., the inability to experience pleasure).[38] 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.[39] 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.[40]

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.[18] Dysregulation in reflection results in the inability to override impulsivity, thus resulting in addiction.[18] 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

Temperamental effortful control is defined as the ability to suppress a dominant response in order to perform a subdominant response.[41] 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.[18] 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.[18]

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.[18] 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.[42][43] For example, high positive affect may interact with low effortful control in increasing risk of addiction amongst vulnerable populations.

Gray's reinforcement sensitivity theory

Gray's Reinforcement sensitivity theory (RST) consists of two motivational systems: the Behaviour Inhibition System (BIS) and the Behaviour Activation System (BAS).[44][45] 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).[44][45] 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.[46][47] For instance, it has been postulated that high BIS is related to anxiety, while high BAS is related to conduct disorders or impulsivity.[45][48]

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.[49][50][51][52][53][54][55][56] 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

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.[57]
  • Rash Impulsiveness (RI) - reflecting individual differences in the ability to modify the addictive behaviour due to negative consequences.[57] 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.[57] Some moderators of RD and RI on the severity of addiction are stress and negative affect (such as feeling depressed).[58] 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.[59][60][61][62] However, high RI for individual without a family history of addiction has been related to poor decision-making.

Cloninger's tri-dimensional personality theory

Cloninger's Tri-Dimensional Personality Theory states that personality comprises three genetically independent dimensions:[63]

  • 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.[63]

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).[64] This model proposes that alcoholics can be classified in two groups based on the combinations of their three personality dimensions:[63]

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.[65] 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.[65]

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.[65] These individuals are high in NS, and low in HA and RD, which means they may be typically aggressive, impulsive, active, talkative, and impatient.[65]

Criticism of the addiction model

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."[66] 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."[67] The Oxford English Dictionary included examples of addiction "to civil affairs" and "to useful reading."[67] Szasz observed that the term transformed over time into a "stigmatizing label" with "pejorative meaning."[68] 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."[66]

Szasz's views were criticized for failing to account for the effect of physiological dependence.[69]

References

  1. ^ Angres DH, Bettinardi-Angres K (October 2008). "The disease of addiction: origins, treatment, and recovery". Dis Mon. 54 (10): 696–721. doi:10.1016/j.disamonth.2008.07.002. PMID 18790142.
  2. ^ American Society for Addiction Medicine (2012). "Definition of Addiction". {{cite journal}}: Cite journal requires |journal= (help)
  3. ^ Morse RM, Flavin DK (August 1992). "The definition of alcoholism. The Joint Committee of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism". JAMA. 268 (8): 1012–4. doi:10.1001/jama.1992.03490080086030. PMID 1501306.
  4. ^ Marlatt GA, Baer JS, Donovan DM, Kivlahan DR (1988). "Addictive behaviors: etiology and treatment". Annu Rev Psychol. 39: 223–52. doi:10.1146/annurev.ps.39.020188.001255. PMID 3278676.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ Torres G, Horowitz JM (1999). "Drugs of abuse and brain gene expression". Psychosom Med. 61 (5): 630–50. PMID 10511013.
  6. ^ Procrastinators Anonymous website http://procrastinators-anonymous.org/node/8
  7. ^ Pychyl, T. (February 20, 2012). Due Tomorrow. Do Tomorrow. Psychology Today, Retrieved Feb 20 2012 from http://www.psychologytoday.com/blog/dont-delay/201202/due-tomorrow-do-tomorrow
  8. ^ Fiore, Neil A (2006). The Now Habit: A Strategic Program for Overcoming Procrastination and Enjoying Guilt- Free Play. New York: Penguin Group. p. 5. ISBN 978-1-58542-552-5.
  9. ^ Pargman D, Burgess S (1977). "Hooked on Exercise: A Psycho-Biological Explanation". 1977 Annual Meeting of North American Society for the Psychology of Sport and Physical Activity. OCLC 425154924.
  10. ^ Tsuang, M. T.; M. J. Lyons; J. M. Meyer; T. Doyle (1998). "Co-occurrence of abuse of different drugs in men: The role of drug-specific and shared vulnerabilities". Archives of General Psychiatry (55): 967–972. {{cite journal}}: |access-date= requires |url= (help)
  11. ^ Crews, FT.; Vetreno, RP. (2011). "Addiction, adolescence, and innate immune gene induction". Front Psychiatry. 2: 19. doi:10.3389/fpsyt.2011.00019. PMID 21629837.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  12. ^ Salamone, J.D. (1992). "Complex motor and sensorimotor function of striatal and accumbens dopamine: Involvement in instrumental behavior processes". Psychopharmacology (107): 160–174. {{cite journal}}: |access-date= requires |url= (help)
  13. ^ Kauer, J.A.; R.C. Malenka (2007). "Synaptic plasticity and addiction". Nature Reviews Neuroscience (8): 844–858. {{cite journal}}: |access-date= requires |url= (help)
  14. ^ Belin, D.; B.J. Everitt (2008). "Cocaine Seeking habits depend upon dopamine-dependent serial connectivity linking the ventral with the dorsal striatum". Neuron (57): 432–441. {{cite journal}}: |access-date= requires |url= (help)
  15. ^ Witten, I; S.-C. Lin; M Brodsky (2010). "Cholinergic interneurons control local circuit activity and cocaine conditioning". Science (330): 1677–1681. {{cite journal}}: |access-date= requires |url= (help)
  16. ^ Volkow, N. D.; G.-J Wang; J. S. Fowler (2011). "Addiction: Beyond dopamine reward circuitry". Proceedings of the National Academy of Science (108): 15037–15042. {{cite journal}}: |access-date= requires |url= (help)
  17. ^ Tarter, R. E.; L. Kirisci; A. Mezzich; J. R. Cornelius (2003). "Neurobehavioral disinhibition in childhood predicts early age at onset of substance use disorder". American Journal of Psychiatry (160): 1078–1085. {{cite journal}}: |access-date= requires |url= (help)
  18. ^ a b c d e f g h i j k l Cheetham A, Allen NB, Yücel M, Lubman DI (August 2010). "The role of affective dysregulation in drug addiction". Clin Psychol Rev. 30 (6): 621–34. doi:10.1016/j.cpr.2010.04.005. PMID 20546986.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  19. ^ Gross JJ (September 1998). "The emerging field of emotion regulation: An integrative review". Review of General Psychology. 2 (3): 271–299. doi:10.1037/1089-2680.2.3.271.
  20. ^ Bechara A, Damasio H (2002). "Decision-making and addiction (part I): impaired activation of somatic states in substance dependent individuals when pondering decisions with negative future consequences". Neuropsychologia. 40 (10): 1675–89. doi:10.1016/S0028-3932(02)00015-5. PMID 11992656.
  21. ^ Quirk SW (May 2009). "Emotion concepts in models of substance abuse". Drug and Alcohol Review. 20 (1): 95–104. doi:10.1080/09595230125185.
  22. ^ Westen D, Blagov PS, Harenski K, Kilts C, Hamann S (November 2006). "Neural bases of motivated reasoning: an FMRI study of emotional constraints on partisan political judgment in the 2004 U.S. Presidential election". J Cogn Neurosci. 18 (11): 1947–58. doi:10.1162/jocn.2006.18.11.1947. PMID 17069484.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ^ McCollam JB, Burish TG, Maisto SA, Sobell MB (April 1980). "Alcohol's effects on physiological arousal and self-reported affect and sensations". J Abnorm Psychol. 89 (2): 224–33. doi:10.1037/0021-843X.89.2.224. PMID 7365134.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ Measelle JR, Stice E, Springer DW (September 2006). "A prospective test of the negative affect model of substance abuse: moderating effects of social support". Psychol Addict Behav. 20 (3): 225–33. doi:10.1037/0893-164X.20.3.225. PMC 1560098. PMID 16938060.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ Childress AR, Ehrman R, McLellan AT, MacRae J, Natale M, O'Brien CP (1994). "Can induced moods trigger drug-related responses in opiate abuse patients?". J Subst Abuse Treat. 11 (1): 17–23. doi:10.1016/0740-5472(94)90060-4. PMID 8201629.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  26. ^ Cooney NL, Litt MD, Morse PA, Bauer LO, Gaupp L (May 1997). "Alcohol cue reactivity, negative-mood reactivity, and relapse in treated alcoholic men". J Abnorm Psychol. 106 (2): 243–50. doi:10.1037/0021-843X.106.2.243. PMID 9131844.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  27. ^ Fox HC, Bergquist KL, Hong KI, Sinha R (March 2007). "Stress-induced and alcohol cue-induced craving in recently abstinent alcohol-dependent individuals". Alcohol. Clin. Exp. Res. 31 (3): 395–403. doi:10.1111/j.1530-0277.2006.00320.x. PMID 17295723.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  28. ^ Robinson TE, Berridge KC (2003). "Addiction". Annu Rev Psychol. 54: 25–53. doi:10.1146/annurev.psych.54.101601.145237. PMID 12185211.
  29. ^ a b Randall DM, Cox WM (February 2001). "Experimental mood inductions in persons at high and low risk for alcohol problems". Am J Drug Alcohol Abuse. 27 (1): 183–7. doi:10.1081/ADA-100103126. PMID 11373034.
  30. ^ a b Cyders MA, Smith GT, Spillane NS, Fischer S, Annus AM, Peterson C (March 2007). "Integration of impulsivity and positive mood to predict risky behavior: development and validation of a measure of positive urgency". Psychol Assess. 19 (1): 107–18. doi:10.1037/1040-3590.19.1.107. PMID 17371126.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  31. ^ Whiteside SP, Lynam DR (March 2001). "The Five Factor Model and impulsivity: using a structural model of personality to understand impulsivity". Personality and Individual Differences. 30 (4): 669–689. doi:10.1016/S0191-8869(00)00064-7.
  32. ^ Cyders MA, Smith GT (November 2008). "Emotion-based dispositions to rash action: positive and negative urgency". Psychol Bull. 134 (6): 807–28. doi:10.1037/a0013341. PMC 2705930. PMID 18954158.
  33. ^ Zapolski TC, Cyders MA, Smith GT (June 2009). "Positive urgency predicts illegal drug use and risky sexual behavior". Psychol Addict Behav. 23 (2): 348–54. doi:10.1037/a0014684. PMC 2709762. PMID 19586152.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  34. ^ Volkow ND, Wang GJ, Fowler JS, Logan J, Gatley SJ, Gifford A, Hitzemann R, Ding YS, Pappas N (September 1999). "Prediction of reinforcing responses to psychostimulants in humans by brain dopamine D2 receptor levels". Am J Psychiatry. 156 (9): 1440–3. PMID 10484959.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  35. ^ Volkow ND (November 2004). "The reality of comorbidity: depression and drug abuse". Biol. Psychiatry. 56 (10): 714–7. doi:10.1016/j.biopsych.2004.07.007. PMID 15556111.
  36. ^ Volkow ND, Wang GJ, Ma Y, Fowler JS, Wong C, Ding YS, Hitzemann R, Swanson JM, Kalivas P (April 2005). "Activation of orbital and medial prefrontal cortex by methylphenidate in cocaine-addicted subjects but not in controls: relevance to addiction". J. Neurosci. 25 (15): 3932–9. doi:10.1523/JNEUROSCI.0433-05.2005. PMID 15829645.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  37. ^ Cox WM, Klinger E (May 1988). "A motivational model of alcohol use". J Abnorm Psychol. 97 (2): 168–80. doi:10.1037/0021-843X.97.2.168. PMID 3290306.
  38. ^ Janiri L, Martinotti G, Dario T, Reina D, Paparello F, Pozzi G, Addolorato G, Di Giannantonio M, De Risio S (2005). "Anhedonia and substance-related symptoms in detoxified substance-dependent subjects: a correlation study". Neuropsychobiology. 52 (1): 37–44. doi:10.1159/000086176. PMID 15942262.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  39. ^ Koob GF, Le Moal M (October 1997). "Drug abuse: hedonic homeostatic dysregulation". Science. 278 (5335): 52–8. doi:10.1126/science.278.5335.52. PMID 9311926.
  40. ^ Bechara A (2003). "Risky business: emotion, decision-making, and addiction". J Gambl Stud. 19 (1): 23–51. doi:10.1023/A:1021223113233. PMID 12635539.
  41. ^ Rothbart MK, Ellis LK, Rueda MR, Posner MI (December 2003). "Developing mechanisms of temperamental effortful control". J Pers. 71 (6): 1113–43. doi:10.1111/1467-6494.7106009. PMID 14633060.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  42. ^ Colder CR, Chassin L (June 1997). "Affectivity and impulsivity: Temperament risk for adolescent alcohol involvement". Psychology of Addictive Behaviors. 11 (2): 83–97. doi:10.1037/0893-164X.11.2.83.
  43. ^ Hussong AM, Chassin L (November 1994). "The stress-negative affect model of adolescent alcohol use: disaggregating negative affect". J. Stud. Alcohol. 55 (6): 707–18. PMID 7861800.
  44. ^ a b Gray JA (August 1970). "The psychophysiological basis of introversion-extraversion". Behav Res Ther. 8 (3): 249–66. doi:10.1016/0005-7967(70)90069-0. PMID 5470377.
  45. ^ a b c McNaughton N, Gray ,JA (2000). The neuropsychology of anxiety: an enquiry into the function of the septo-hippocampal system. Oxford [Oxfordshire]: Oxford University Press. ISBN 0-19-852270-3.{{cite book}}: CS1 maint: multiple names: authors list (link)
  46. ^ Campbell-Sills L, Liverant GI, Brown TA (September 2004). "Psychometric evaluation of the behavioral inhibition/behavioral activation scales in a large sample of outpatients with anxiety and mood disorders". Psychol Assess. 16 (3): 244–54. doi:10.1037/1040-3590.16.3.244. PMID 15456380.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  47. ^ Jorm AR, Christensen H, Henderson AS, Jacomb PA, Korten AE, Rodgers B (January 1998). "Using the BIS/BAS scales to measure behavioural inhibition and behavioural activation: Factor structure, validity and norms in a large community sample". Personality and Individual Differences. 26 (1): 49–58. doi:10.1016/S0191-8869(98)00143-3.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  48. ^ Quay HC (February 1997). "Inhibition and attention deficit hyperactivity disorder". J Abnorm Child Psychol. 25 (1): 7–13. doi:10.1023/A:1025799122529. PMID 9093895.
  49. ^ Franken IHA, Muris P (2006). "BIS/BAS personality characteristics and college students' substance use". Personality and Individual Differences. 40 (7): 1497–1503. doi:10.1016/j.paid.2005.12.005.
  50. ^ Genovese JE, Wallace D (December 2007). "Reward sensitivity and substance abuse in middle school and high school students". J Genet Psychol. 168 (4): 465–9. doi:10.3200/GNTP.168.4.465-469. PMID 18232522.
  51. ^ Kimbrel NA, Nelson-Gray RO, Mitchell JT (April 2007). "Reinforcement sensitivity and maternal style as predictors of psychopathology". Personality and Individual Differences. 42 (6): 1139–1149. doi:10.1016/j.paid.2006.06.028.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  52. ^ Knyazev GG (September 2004). "Behavioural activation as predictor of substance use: mediating and moderating role of attitudes and social relationships". Drug Alcohol Depend. 75 (3): 309–21. doi:10.1016/j.drugalcdep.2004.03.007. PMID 15283952.
  53. ^ Loxton NJ, Dawe S (November 2006). "Reward and punishment sensitivity in dysfunctional eating and hazardous drinking women: associations with family risk". Appetite. 47 (3): 361–71. doi:10.1016/j.appet.2006.05.014. PMID 16846665.
  54. ^ Loxton NJ, Dawe S (April 2007). "How do dysfunctional eating and hazardous drinking women perform on behavioural measures of reward and punishment sensitivity?". Personality and Individual Differences. 42 (6): 1163–1172. doi:10.1016/j.paid.2006.09.031.
  55. ^ O’Connor RM, Stewart SH, Watt MC (March 2009). "Distinguishing BAS risk for university students' drinking, smoking, and gambling behaviors". Personality and Individual Differences. 46 (4): 514–519. doi:10.1016/j.paid.2008.12.002.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  56. ^ Pardo Y, Aguilar R, Molinuevo B, Torrubia R (October 2007). "Alcohol use as a behavioural sign of disinhibition: evidence from J.A. Gray's model of personality". Addict Behav. 32 (10): 2398–403. doi:10.1016/j.addbeh.2007.02.010. PMID 17407802.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  57. ^ a b c Dawe S, Loxton NJ (May 2004). "The role of impulsivity in the development of substance use and eating disorders". Neurosci Biobehav Rev. 28 (3): 343–51. doi:10.1016/j.neubiorev.2004.03.007. PMID 15225976.
  58. ^ Koob GF, Le Moal M (February 2001). "Drug addiction, dysregulation of reward, and allostasis". Neuropsychopharmacology. 24 (2): 97–129. doi:10.1016/S0893-133X(00)00195-0. PMID 11120394.
  59. ^ Brook JS, Kessler RC, Cohen P (1999). "The onset of marijuana use from preadolescence and early adolescence to young adulthood". Dev. Psychopathol. 11 (4): 901–14. doi:10.1017/S0954579499002370. PMID 10624731.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  60. ^ Lynskey MT, Fergusson DM, Horwood LJ (October 1998). "The origins of the correlations between tobacco, alcohol, and cannabis use during adolescence". J Child Psychol Psychiatry. 39 (7): 995–1005. doi:10.1111/1469-7610.00402. PMID 9804032.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  61. ^ King KM, Chassin L (September 2004). "Mediating and moderated effects of adolescent behavioral undercontrol and parenting in the prediction of drug use disorders in emerging adulthood". Psychol Addict Behav. 18 (3): 239–49. doi:10.1037/0893-164X.18.3.239. PMID 15482079.
  62. ^ Tarter RE, Kirisci L, Habeych M, Reynolds M, Vanyukov M (February 2004). "Neurobehavior disinhibition in childhood predisposes boys to substance use disorder by young adulthood: direct and mediated etiologic pathways". Drug Alcohol Depend. 73 (2): 121–32. doi:10.1016/j.drugalcdep.2003.07.004. PMID 14725951.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  63. ^ a b c Cloninger CR (June 1987). "A systematic method for clinical description and classification of personality variants. A proposal". Arch. Gen. Psychiatry. 44 (6): 573–88. doi:10.1001/archpsyc.1987.01800180093014. PMID 3579504.
  64. ^ Howard MO, Kivlahan D, Walker RD (January 1997). "Cloninger's tridimensional theory of personality and psychopathology: applications to substance use disorders". J. Stud. Alcohol. 58 (1): 48–66. PMID 8979213.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  65. ^ a b c d Cloninger CR (April 1987). "Neurogenetic adaptive mechanisms in alcoholism". Science. 236 (4800): 410–6. Bibcode:1987Sci...236..410C. doi:10.1126/science.2882604. PMID 2882604.
  66. ^ a b Thomas Szasz, Ceremonial Chemistry (1974), p. 9
  67. ^ a b Thomas Szasz, Ceremonial Chemistry (1974), p. 6
  68. ^ Thomas Szasz, Ceremonial Chemistry (1974), p. 7
  69. ^ See, for example, David M. Warburton, Addiction Controversies (1992).

Further reading

Look up addiction or -holism in Wiktionary, the free dictionary.
Retrieved from "https://en.wikipedia.org/w/index.php?title=Addiction&oldid=607689317"