Dear Feisal,

The following summarizes the moral theory of Le Moal and Koob:

For more details, see attached review article.

Eur Neuropsychopharmacol. 2007 May-Jun;17(6-7):377-93. Epub 2006 Dec 12.

Drug addiction: pathways to the disease and pathophysiological perspectives.

Le Moal M1, Koob GF.

Author information

Abstract

Drug addiction is a medical condition, a chronic relapsing disease. As in other domains of experimental medicine, appropriate experimental investigations are needed in order to better understand the disease. However, to understand the diverse facets of drug effects and of the underlying pathophysiology it is necessary to keep in mind the complexity of the psychopathological processes. The main symptoms that characterize addiction correspond to expressions of dysfunctions within specific circuits and regions. Pathways to addiction are numerous and comorbidity and in the real world poly-drug use are common. Some of these aspects will be examined as well as the role of life events and stress. Theoretical considerations will be proposed [see also: Koob, G.F., & Le Moal, M.. 2005a. Neurobiology of Addiction. Elsevier. 570 pp] to account for the stages of the disease from impulse control disorder to compulsive disorders, for affective dynamics and for the relations between the symptoms and pathophysiology.

Neuropsychopharmacology. 2010 Jan; 35(1): 217–238.

Published online 2009 Aug 26. doi:  10.1038/npp.2009.110

PMCID: PMC2805560

NIHMSID: NIHMS166700

Neurocircuitry of Addiction

George F Koob1,* and Nora D Volkow2

Author information ► Article notes ► Copyright and License information ►

This article has been corrected. See Neuropsychopharmacology. 2010 March 13; 35(4): 1051.

This article has been cited by other articles in PMC.

Go to:

Abstract

Drug addiction is a chronically relapsing disorder that has been characterized by (1) compulsion to seek and take the drug, (2) loss of control in limiting intake, and (3) emergence of a negative emotional state (eg, dysphoria, anxiety, irritability) reflecting a motivational withdrawal syndrome when access to the drug is prevented. Drug addiction has been conceptualized as a disorder that involves elements of both impulsivity and compulsivity that yield a composite addiction cycle composed of three stages: ‘binge/intoxication', ‘withdrawal/negative affect', and ‘preoccupation/anticipation' (craving). Animal and human imaging studies have revealed discrete circuits that mediate the three stages of the addiction cycle with key elements of the ventral tegmental area and ventral striatum as a focal point for the binge/intoxication stage, a key role for the extended amygdala in the withdrawal/negative affect stage, and a key role in the preoccupation/anticipation stage for a widely distributed network involving the orbitofrontal cortex–dorsal striatum, prefrontal cortex, basolateral amygdala, hippocampus, and insula involved in craving and the cingulate gyrus, dorsolateral prefrontal, and inferior frontal cortices in disrupted inhibitory control. The transition to addiction involves neuroplasticity in all of these structures that may begin with changes in the mesolimbic dopamine system and a cascade of neuroadaptations from the ventral striatum to dorsal striatum and orbitofrontal cortex and eventually dysregulation of the prefrontal cortex, cingulate gyrus, and extended amygdala. The delineation of the neurocircuitry of the evolving stages of the addiction syndrome forms a heuristic basis for the search for the molecular, genetic, and neuropharmacological neuroadaptations that are key to vulnerability for developing and maintaining addiction.

Hoping this will be helpful,

Rafik

Dear Feisal,

The following summarizes the moral theory of Le Moal and Koob:

For more details, see attached review article.

Eur Neuropsychopharmacol. 2007 May-Jun;17(6-7):377-93. Epub 2006 Dec 12.

Drug addiction: pathways to the disease and pathophysiological perspectives.

Le Moal M1, Koob GF.

Author information

Abstract

Drug addiction is a medical condition, a chronic relapsing disease. As in other domains of experimental medicine, appropriate experimental investigations are needed in order to better understand the disease. However, to understand the diverse facets of drug effects and of the underlying pathophysiology it is necessary to keep in mind the complexity of the psychopathological processes. The main symptoms that characterize addiction correspond to expressions of dysfunctions within specific circuits and regions. Pathways to addiction are numerous and comorbidity and in the real world poly-drug use are common. Some of these aspects will be examined as well as the role of life events and stress. Theoretical considerations will be proposed [see also: Koob, G.F., & Le Moal, M.. 2005a. Neurobiology of Addiction. Elsevier. 570 pp] to account for the stages of the disease from impulse control disorder to compulsive disorders, for affective dynamics and for the relations between the symptoms and pathophysiology.

Neuropsychopharmacology. 2010 Jan; 35(1): 217–238.

Published online 2009 Aug 26. doi:  10.1038/npp.2009.110

PMCID: PMC2805560

NIHMSID: NIHMS166700

Neurocircuitry of Addiction

George F Koob1,* and Nora D Volkow2

Author information ► Article notes ► Copyright and License information ►

This article has been corrected. See Neuropsychopharmacology. 2010 March 13; 35(4): 1051.

This article has been cited by other articles in PMC.

Go to:

Abstract

Drug addiction is a chronically relapsing disorder that has been characterized by (1) compulsion to seek and take the drug, (2) loss of control in limiting intake, and (3) emergence of a negative emotional state (eg, dysphoria, anxiety, irritability) reflecting a motivational withdrawal syndrome when access to the drug is prevented. Drug addiction has been conceptualized as a disorder that involves elements of both impulsivity and compulsivity that yield a composite addiction cycle composed of three stages: ‘binge/intoxication', ‘withdrawal/negative affect', and ‘preoccupation/anticipation' (craving). Animal and human imaging studies have revealed discrete circuits that mediate the three stages of the addiction cycle with key elements of the ventral tegmental area and ventral striatum as a focal point for the binge/intoxication stage, a key role for the extended amygdala in the withdrawal/negative affect stage, and a key role in the preoccupation/anticipation stage for a widely distributed network involving the orbitofrontal cortex–dorsal striatum, prefrontal cortex, basolateral amygdala, hippocampus, and insula involved in craving and the cingulate gyrus, dorsolateral prefrontal, and inferior frontal cortices in disrupted inhibitory control. The transition to addiction involves neuroplasticity in all of these structures that may begin with changes in the mesolimbic dopamine system and a cascade of neuroadaptations from the ventral striatum to dorsal striatum and orbitofrontal cortex and eventually dysregulation of the prefrontal cortex, cingulate gyrus, and extended amygdala. The delineation of the neurocircuitry of the evolving stages of the addiction syndrome forms a heuristic basis for the search for the molecular, genetic, and neuropharmacological neuroadaptations that are key to vulnerability for developing and maintaining addiction.

Hoping this will be helpful,

Rafik

Perhaps it is all very simple - people would not take drugs if the drugs did not make them "feel better" when they take them (conditioning/learning). If that is so then these people (who take drugs) do so to experience positive emotions and avoid negative emotions. Our brains are wired in such a way as the ensure our survival (and the survival of the species) by maximising positive (feeling good) emotions and minimising negative (feeling bad) emotions. Perhaps at the end of the day it is all about conditioning - and not necessarily a "medical" (illness) condition. Comments?