Biological model of addiction

(writing in purple is A02 A03 marks)

psychology unit 4 aqa a A2 

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  • Created by: lauren
  • Created on: 15-06-12 10:21

Genetics

Initiation

Family studies - alcohol dependance been linked to genetic inheritance, with heritability estimes of around 50-60% for men and women - McGue - Illicit drug abuse has also been shown to have high heritability estimates of 45-79% - Agrawal and Lynksey

Twin studies - Kendler - anaylsed data from Virginia Twin Registry in the USA and found that a common genetic factor linked to a general predisposition towards behavioural disorders which may lead to alcohol dependence or illicit drug abuse or to antisocial behavioural disorders - ethnocentrism? we cannot assume that these results will be the same in all countries - element of culture bias?

Genetic explanations can account for individual differences - some people are more vulnerable to develop an addiction because of their genetic prediposition but external cues are needed to trigger that innate predisposition - diathesis-stress model - may also explain why some people are more resistant to treatment than others and why they are more likely to relapse

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Genetics

What is inherited? Research found a link betwen the gene for the D2 dopamine receptor DRD2 and alcoholism - Noble - A1 variant of this gene is more commonly found in alcoholics - Blum - and found among children born to alcoholics supporting the idea of a genetic predisposition 

A1 variant more common among smokers - about 50% compared to 26% of non-smokers - Comings

Noble - DRD2 gene is the 'reward gene' - individuals with the A1 variant gene appear to have fewer dopamine receptors in the brains pleasure centers - drugs increase dopamine levels by stimulating what few dopamine receptors there are - addiction is maintained because it is only the drug that make these individuals feel good

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Genetics

Research support by Caine - research on mice - Mice like humans develop a craving for the drug cocaine but those that are bred to lack another dopamine receptor, the D1 dopamine receptor, dont self-administer themselves with cocaine when given the chance to do so unlike other mice who will keep returning for more- reinforces the claim that dopamine plays a key role in addiction - use of animal research - human animals and non-human animals have a differeny physiology and a different level of cognitive ability - humans have the chance to choose whether or not they take a drug whereas mice lack this ability and so are more likely to do it because of genetic factors - different physiology so it is not clear if humans will react the same - difficult to generalise results - also need to make sure that they follow the BPS guidelines for conducting research such as researchers only use as few as possible mice as they can - and when they 'engineer' the mice they have to be put under an anesthetic and given painkillers so that they feel as little pain as possible

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Genetics

Research support for dopamine in non-drug addictions - Botswick and Bucci reported successful treatment of sex addiction using naltrexone, a drug that blocks the release of dopamine - blocking the reward extinguished the addictive power of that behaviour

Findings of DRD2 gene are inconsistent - meta-analysis (using a meta-anaylsis can introduce the file-drawer effect where researchers only use studies that benefit the hypothesis they are using, also all the studies they use may not have the same methodology which would make findings and conclusions unreliable as the methodology for all studies is inaccurateby Noble - 48% severe alcoholics - 32% less severe alcoholics - 16% of controls are carriers of this A1 variant  - supporting the idea that in some way this A1 variant influenced the development of addiction BUT Several subsequent studies such as Edenberg have failed to find any relationship between alcoholism and the DRD2 gene, or have only found a very weak relationship


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Genetics

DRD2 gene may not be the reward gene - Comings - A1 variant occurred in some people with several disorders, including autism and Tourettes syndrome as often as it appeared with alcoholics - this finding creates issues for the idea of the DRD2 gene being a reward gene since people with autism and tourettes are not thought to be especially pleasure-seeking

Biological explanations are reductionist - they reduce a complex phenomenom such as addiction down to a relatively simple level of explanation such as an imbalance of brain chemicals which influence specific genes - although there are potential advantages to this approach as it suggests effective drug treatments, it ignores all other potential influences such as irrational though processes and so on

Deterministic - suggests if you are born with this inherited gene or predisposition you are going to develop it later in life - however there are findings such as that by Comings that show that people can go through life carrying this A1 variant of the DRD2 gene but not develop an addiction, suggesting that other factor are involves such as environment and cognitive influences (16% of healthy controls carried the gene but didnt develop an addiction)

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The disease model

Initiation - addictive drugs stimulate the brains reward system - crack cocaine activates dopamine receptors in the mesolimbic pathway - lasting memories are created that link the drug to a pleasureable reward - incentive sensitisation theory - Robinson and Berridge - repeated exposure to drugs of abuse increases the sensitivity to their desireability

Mainetenance - Chronic exposure to drugs eventually results in a reduction in the acitivty of these positive reward circuits - downregulation - and the drug levels that are needed to trigger the brain reward system increase - Koob and Kreek

Relapse - brain continues to recieve difficult-to-resist signals of imminent reward , even if the addict knows that a reward is not really coming - this is because the pre-frontal cortex has become less effective at making decisions and judging the consequences of actions

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The disease model

Research support - Volkow - gave ritalin (lifts dopamine levels) to adult volunteers - using volunteers could create a sample bias as these adults are more likely to posses certain characteristic such as having a high motivation and extra time on their hands - could be people who do not have jobs - would create a volunteer bias - using brain scanning (scientific method) found that those who enjoyed the sensation had fewer d2 receptors than those who hated it - could explain why some people, after experimenting with drugs, might go on and develop and addiction and others, despite having the same intial experience might not

Link between dopamine and poverty - experiment with monkeys - Grant - showed that animals that lost social status also lost D2 receptors - has implications for human beings whose lives are characterised by poverty and stress whereas dopamine systems of those who have more stimulating lives are less likely to need an aritifical boost from alcohol or drugs - use of monkeys again - although they are a close ancestor - we still do not have the same physiology - may not replicate the action of D2 receptors in humans - issues when generalising

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The disease model

Animal research - Hackham and Redelmeier argue that even high quality animal studies of drug addiction rearely replicate human research - but there have been some successes such as Czoty who used monkeys to establish the feasibility of treating cocaine addiction by substituting a less addictive 'replacement' drug that mimics the action of cocaine but has less potential for abuse

Implications for treatement - neurochemical explanations create the possibility that addiction may be treated by various pharmacological methods - more progessive approach than those that treat addicts as delinquents who must be punished

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