anti-Causality


Tuesday, January 18, 2011

Extinction for addiction: Conditioned compensatory response



Note: this describes a purely-behavioral approach, which, by the nature of behaviorism, deliberately ignores underlying factors such as addiction vulnerability (compulsive-impulsive-obsessive continuum?).  In practice, such approaches are unconcerned with specific clients seeking, instead, beneficial statistical outcomes for agency and directorial self-benefit.


Conditioned behavior is a key component of drug addiction, but the conditioned and unconditioned pairing stimuli and responses happen in different, or perhaps opposite, ways than would be expected from basic classical conditioning (J. Dyce, personal communication, n.d.).  In this case the conditioned response is called the conditioned compensatory response, and the conditioned stimulus is called a cue, which serves an important function in this model.  An accepted therapy for drug addiction uses another conditioned behavior process, extinction, in conjunction with this compensatory process.

Cues describe the components of an addict's environment; in lay terms, they serve as a reminder to the addict of his addiction.  As a conditioned stimulus, they stimulate craving for the drug that goes beyond a possible physical addiction, so much so that they cause craving when there is no physical addiction.

When extinction is used as a therapy, a recovering addict is exposed to the cues from his environment but not given the unconditioned stimulus, or drug, to create the unconditioned response, which is drug-induced euphoria.  Eventually, the effect of the cues, or the conditioned stimulus, to create the craving, or conditioned response, diminishes as a result of extinction, and the addict is cured of addiction--at least momentarily.  To maintain the therapeutic benefit of extinction, the addict has to avoid the cues, presumably by not returning to the drug-related cues of his past environment.

There are also internal cues, called pre-drug cues, that complicate the addict's experience and hopeful therapy by increasing tolerance and withdrawal symptoms (Siegel, 2005).  For example, drug-onset describes how a conditioned stimulus will cause a life-long alcoholic to relapse.  The taste of an alcoholic drink, a drug-onset cue, acts as a conditioned stimulus that is associated with the effect of alcohol that triggers the craving that defines addiction.

Siegel, S. (2005). Drug Tolerance, Drug Addiction, and Drug Anticipation. Current Directions in Psychological Science (Wiley-Blackwell), 14(6), 296-300. doi:10.1111/j.0963-7214.2005.00384.x.


Conditioned stimulus (CS cues) causes no response












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Conditioned compensatory responses

1) Pre-condition
Conditioned stimulus (CS cues ) causes no response

Unconditioned stimulus (UCS drug ) causes unconditioned response (UCR euphoria )

Combine CS-cue with UCS-drug to cause UCR-euphoria

2) CS-cue causes CR-craving, does not modify UCR-euphoria to become CR-euphoria

3) CS-cue causes CR-craving (CR) to create behavior to get drug (UCR)

Extinction

Gradual weakening of CR-craving (conditioned response) from CS-cue (conditioned stimulus) when no UCS-drug (unconditioned stimulus) is provided to cause UCR-euphoria (unconditioned response)
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Tolerance is learned:
The stimuli present at the time of drug administration are the conditional stimulus (CS),
while the effect produced by the drug is the unconditional stimulus (UCS).
drug effects involve disruption of the homeostatic level of physiological systems (e.g., alcohol lowers body temperature), and these disruptions elicit compensatory responses that tend to restore functioning to normal levels.
The compensatory, restorative response to a drug effect is the unconditional response (UCR).
usual predrug cues coming to elicit as a conditional response (CR) the compensatory, restorative response

In order to eliminate a CR, it is necessary to present the CS not followed by the UCS, a procedure termed extinction.

Research indicates that the loss of tolerance occurs as a result of extinction of drug-compensatory CRs.

"Conditioned Tolerance." Encyclopedia of Drugs, Alcohol, and Addictive Behavior. 2nd Ed. Ed. Rosalyn Carson-DeWitt. Macmillan-Thomson Gale, 2001.
http://www.enotes.com/drugs-alcohol-encyclopedia/conditioned-tolerance

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Understanding the basis of drug addiction, along with applying therapies to treat it, relies on behavioral science. 
cues associated with drug use (friends, place, smells, behaviors prior to use) cause craving as a CR which is the opposite of the drug pleasure.

Extinction drug approach -- extinction, provide cues but no drugs so that the response to the cues goes away -- without UCS, cravings go away

 conditional response that opposes, rather than being the same as, the unconditional response

drugs
the conditioned compensatory responses produced by taking heroin oppose the desired effects of the drug.

When a drug is taken in a new environment, there will be less conditioned compensatory response and the drug will have an enhanced effect.
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Drug use
cues associated with drug use (friends, place, smells, behaviors prior to use) cause craving which is a conditioned response CR which is craving -- which is not the drug (unlike food)

Hunger and drug are different because they use different bodily functions

Extinction drug approach -- extinction, provide cues but no drugs so that the response to the cues goes away -- without UCS, cravings go away

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interoceptive early-drug onset cues (DOCs) may become associated with the later, larger drug effect (intraadministration associations)

The findings suggest that associative analyses of tolerance should acknowledge the conditional responding elicited by DOCs, and extinction-based addiction treatments should incorporate extinction of DOC-elicited conditional responding.


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The phenomenon, although noted almost 150 years ago, has repeatedly been confirmed in epidemiological and experimental studies.

Siegel, S. (1999). Drug anticipation and drug addiction. The 1998 H. David Archibald Lecture. Addiction, 94(8), 1113-1124. doi:10.1080/09652149932901.



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