1. What do these statements define?
7) ‘User takes substance to avoid social or emotional discomfort, Substance becomes the centre of user's life, determining daily activity’
Physical Dependance
Psychological Dependance
Addiction
Drug Compensatory Response
7) ‘User takes substance to avoid social or emotional discomfort, Substance becomes the centre of user's life, determining daily activity’
Physical Dependance
Psychological Dependance
Addiction
Drug Compensatory Response
6) ‘Repeated, compulsive use, Preoccupation with substance, need to maintain its supply, Used to get an effect’
Physical Dependance
Psychological Dependance
Addiction
Abuse
8) ‘Previous levels of substance no longer have a desired affect’
Tolerance
Adaption
Addiction
8) ‘Previous levels of substance no longer have a desired affect’
Tolerance
Adaption
Addiction
~ To play the quiz, start the ‘slide show’
9) ‘Higher levels of substance needed to produce desired affect, substance use increases’
Tolerance
Adaption
Addiction
Abuse
9) ‘Higher levels of substance needed to produce desired affect, substance use increases’
Tolerance
Adaption
Addiction
Abuse
6) ‘Repeated, compulsive use, Preoccupation with substance, need to maintain its supply, Used to get an effect’
Physical Dependance
Psychological Dependance
Addiction
Abuse
5) ‘Painful physical and psychological effects that occur when substance use stops’
Physical Dependance
Psychological Dependance
Tolerance
Withdrawal
2) ‘Use of a substance infrequently without harm’
Use
Misuse
Abuse
Addiction
‘Use of a substance resulting in a problem’
Use
Misuse
Abuse
Addiction
‘Use of a substance resulting in a problem’
Use
Misuse
Abuse
Addiction
2) ‘Use of a substance infrequently without harm’
Use
Misuse
Abuse
Addiction
3) ‘Use of a substance resulting in harm’
Use
Misuse
Abuse
Addiction
4) ‘Substance needed to maintain a normal state, user experiences withdrawal symptoms eg. stomach cramps if substance isn't used’
Physical Dependance
Psychological Dependance
Addiction
Tolerance
4) ‘Substance needed to maintain a normal state, user experiences withdrawal symptoms eg. stomach cramps if substance isn't used’
Physical Dependance
Psychological Dependance
Addiction
Tolerance
3) ‘Use of a substance resulting in harm’
Use
Misuse
Abuse
Addiction
5) ‘Painful physical and psychological effects that occur when substance use stops’
Physical Dependance
Psychological Dependance
Tolerance
Withdrawal

2. Key Terms of ‘Addiction Cycle’
Initiation - the process where individuals start to become addicted
Maintenance - the process whereby people continue to behave addictively even in the face of adverse consequences
[Cessation Process – intervention with current behavioural patterns; prevention of relapse]
Relapse - the process whereby individuals who have managed to give up their addictive habits start to show signs and symptoms of the behaviour again
At what stages do our quiz keywords come in?

3. Biological Explanations Of Addictive Behaviour
The Mesolimbic Pathway
(‘Pleasure Centre’)

4. The Genetics of Addiction (AO1)
Specific genes, specific drugs
Noble et al (1991): Link between D2 dopamine receptor gene (DRD2) to severe alcoholism. A1 variant of gene present in 2/3deceased alcoholics Vs 1/5 non-alcoholics.
Individuals with A1 variant appeared to have significantly fewer dopamine receptors in pleasure centres of the brain.
People with A1 more likely to become addicted to drugs that increase dopamine (alcohol, cocaine, heroin, nicotine) which compensates the deficiency by stimulating the few receptors they have = drugs only way they ‘feel good’.

5. The Genetics of Addiction (AO1)
Initiation: insights from family studies
 McGue (1999): genes contribute to alcohol dependence, with hereditability estimates between 50% and 60% for both men and women.
Argrawal & Lynskey (2006): significant genetic influence- heritability estimates 45% to 79%.
Kendler (2003): genetic influence on alcohol and drug dependence manifests itself in a general disposition towards behavioural disorders.

6. The Genetics of Addiction (AO1)
Initiation: insights from twin studies
McGue (1992): higher concordance rate of alcohol abuse in MZ twins (77%) compared to DZ twins (54%) suggesting a genetic link to addictive behaviours.
Kendler (2003): twins concordance rates for using, abusing, & being dependent on drugs higher for DZ than MZ twins. MZ DZ
Use
54%
42%
Abuse
47% 8%
Dependence
35% 0%

7. The Genetics of Addiction (AO2)
Explaining individual differences - 
Genetic explanations can explain why some people become addicted, yet others who have the same environmental experiences and life pressures do not.
Some people are more vulnerable to develop an addiction because of their genetic predisposition.
This idea of genetic vulnerability may also explain why some people are more resistant to treatment for their addiction and more likely to relapse.

8. The Genetics of Addiction (AO2)
Inconsistent research findings- 
Noble meta-analysis: 48% of more severe alcoholics, 32% of less severe alcoholics, and 16% of controls are carriers of the A1 variant of DRD2 gene, thus supporting the claim that this gene was an important influence in development of drug and alcohol addiction.
However, several subsequent studies have failed to find any relationship between alcoholism and the DRD2 gene, or have only found a very weak relationship.

9. The Genetics of Addiction (AO2)
DRD2 and other disorders- 
Comings et al (1996): A1 variant occurred with several disorders, including autism and tourettes syndrome.
The A1 variant of the DRD2 gene was present in 45% of the tourettes patients compared with 25% of controls.
This find creates a problem for the idea that DRD2 being a reward gene as people with tourettes and autism are not thought to be especially pleasure seeking.

10. The Disease Model- role of dopamine (AO1)
Initiation- 
Addictive drugs stimulate a reward circuit in the brain.
Rewarding experiences, such as drug taking, trigger the release of the neurotransmitter dopamine, effectively telling the brain to do it again.
E.g. crack cocaine causes a large and rapid activation of dopamine receptors in the mesolimbic pathway.
Robinson & Berridge - incentive sensitisation theory- suggest that reported exposure to abusive drugs leads to increased sensitivity of the brain to their desirability.

11. The Disease Model- role of dopamine (AO1)
Maintenance- 
Chronic exposure to alcohol or drugs eventually leads to down-regulation (i.e. desensitisation to DA  tolerance)
The negative state then becomes the driving force to the drug taking. e.g. user no longer takes drugs to obtain pleasure (positive reinforcement) but takes them to avoid an un-pleasurable state (negative reinforcement).
Drugs must be taken to avoid withdrawal.

12. The Disease Model- role of dopamine (AO1)
Relapse –
 Desire for the drug becomes more important than most other desires.
Addicts have learned to expect a rewarding experience from the drug, and for the individual trying to abstain from it, they are surrounded by cues.
e.g. reminders of the drug that cause the release of dopamine and therefore predict a reward.

13. Recap & Restart What is the ‘Disease Model’ of Addiction?
What role does Dopamine (in the ‘pleasure centre’ of the brain) play in the Disease Model?
What role do Genetics play in the Disease Model? (in relation to Dopamine activity)

14. Role of Dopamine (AO2) Supporting research evidence-
Volkow (2001): gave Ritalin, which lifts dopamine levels, to a group of adult volunteers. Some of them loved the drug while the others hated the way it made them feel.
Those who loved the rush had fewer D2 receptors than those who hated it.
They concluded that some people are particularly vulnerable to the added rush of dopamine, but others have a circuitry that can’t take the additional stimulation.
Would explain why some people after experimenting the first initial experience will become addicted and some would not.

15. Role of Dopamine (AO2) Limitations of neuro-chemical explanations-
Neurotransmitters have complex effects and these are not fully understood
Neuro-chemical explanations ignore other causal factors including the social context of alcohol or drug taking behaviours.
Thus only offer treatment by various pharmacological methods.

16. Role of Dopamine (AO2)
DA sensitivity & addiction inevitability linked? - 
Grant (1998): monkeys’ DA system influenced by social interactions!  Lost social status also lost D2 receptors.
Implies that humans who have live in poverty & stress are more vulnerable to addiction.
Volkow (2003): people in stimulating environments & healthy social interactions protected from addiction. Even if don't have a naturally responsive DA system, if they have more chances to get excited by natural stimuli, they are less likely to need artificial boost.

17. Synoptics (AO3) The value of animal research-
Researchers have discovered animal preferences for the same drugs that humans use in socially problematic ways.
Banks et al: used monkeys to establish treating cocaine addiction by substituting a less addictive replacement drug that minimises action of cocaine.
Duplicates what was found in smaller human studies, suggesting monkeys have a useful role to play in testing effectiveness of potential treatments.

18. Synoptics (AO3) Reductionism-
Biological explanations of addiction reduce a complex phenomenon such as addiction down to a relatively simple level of explanation. i.e. imbalance of brain chemicals.
While there are potential advantages to this approach such as studying the family history of addiction or offer possibilities of treatment, but it also has its limitations.
Reducing addiction to just the action of genes or chemicals ignores all other potential influences(e.g. irrational thought processes, social context).

19. Intervention - Biological treatments
Addicts given a drug to help overcome their addiction.
Can be Aversive, Agonist or Antagonist.
Mainly given to those with a chemical addiction, but can be given to those with behavioural addictions (gambling, sex, shopping)

20. Intervention - Biological treatments
Aversive Agent treatment
Agonist Maintenance
Antagonist Narcotic
Antabuse is an emetic which when combined with alcohol, produces nausea & possibly vomiting.
Synthetic opiates (methadone) are given to prevent withdrawal- & decrease cravings.
Blocks effects of opiates (naltrexone). Partial agonists (bupropion) can also be used. Repeated lack of desire breaks the drug habit.

21. THIS CONCLUDES our Overview of the Biological Approach as a whole.
Intermission
THIS CONCLUDES our Overview of the Biological Approach as a whole.
Next, we consider how it ‘plays out’ in ‘smoking’ and ‘gambling’ addiction

22. Smoking: Initiation
Nicotine is the active and addictive ingredient; effects Central Nervous System.
Berke and Hyman (2000): nicotine activates mesolimbic dopamine system, which may explain its addictiveness.
Griffiths (1996): use usually begins in early adolescents; early age smokers are more likely to develop a more severe addiction than later starters.
Lerman(1999) : gene SLC6A3-9 (simple little children, 6 and 3  9) reduces risk of starting smoking and time/difficulty it takes to quit. Linked to dopamine regulation.

23. Smoking: Maintenance
SLC6A3-9 regulates dopamine transmission to a steady level, which curbs the nicotine effect of DA boost, and reduces the need for such a boost  less incentive to smoke
Studies on rats and snails found nicotine amplifies the reward system. This makes other behaviours more enjoyable and rewarding.
If this is the case for humans, people could keep smoking to make tasks seem less boring, or neutral tasks more fun. [caution in generalising to humans]
Shacter (1977) – withdrawal symptoms are unpleasant. People keep smoking, maintaining nicotine to avoid withdrawal symptoms.

24. Smoking: Relapse
When people quit smoking they are faced with withdrawal symptoms. They may restart their smoking as a way of eliminating these symptoms
Lerman (1999) – smokers that were deprived of nicotine had an increase in activity of other parts of the brain. After one night with no nicotine there was increased blood flow in parts of the brain linked with attention, memory and reward*. These parts are active during times of craving.
Some people are more prone to this and therefore more likely to relapse.
* Why those three functions do you think??

25. Smoking Intervention - Bio treatments
NRT desensitises nicotine receptors in brain so if a person does smoke, it is less satisfying.
Stead et al (2008): meta-analysis NRT products; using NRT 1.5 to 2 times more likely to abstain from smoking at follow-up than placebo or control condition.
Varenicline: causes the release of dopamine. Found to block the effect of nicotine. Reduces risk of relapse after 12 weeks, but limited long term research.
New (in trial) vaccine that blocks effect of nicotine.

26. Gambling: Bio Approach
Evidence of serotonin deficiencies/fluctuation in pathological gamblers (George and Murali, 2005).
However serotonin may not be the only neuro- transmitter involved in addiction, as DA activity increases as result of gambling  DA deficiency plays a role in predisposition?
Positive Reward Theory: After placing a bet, a period of anticipation follows. The excitement leads to an adrenaline rush. This pleasurable adrenaline rush can be addictive. Initiation linked to reward adrenaline rush.

27. Gambling: Initiation
Shah (2005): Twin study found evidence of genetic transmission of gambling in men  gambling predisposition could be inherited
Comings et al (1996): More gambler have A1 variant of gene DRD2 than control group [50.9% versus 25.9%]. Highest percentage were pathological gamblers [63.8%].
Black et al (1997): First degree relatives of pathological gamblers were more likely to also develop pathological gambling in comparison to distant relatives

28. Gambling: Maintenance
FMRI scans: brain blood flow is different in gamblers
Potenza (2003) – examined craving states in pathological gamblers with FMRI scans of neural activity. When viewing gambling videos (cues), PG demonstrate decreased activity in brain regions implicated in impulse regulation (not found when watching happy/sad situations).
Addiction may relate to an inability to control behaviour and make decisions. This could be why they maintain the addiction.
Caveaini et al (2002): A number of studies shown link between frontal lobe dysfunction and problem gambling

29. Gambling: Relapse
Although withdrawal symptoms are not as severe as smoking, people still keep gambling to avoid it.
Rosenthal et al (1992): over 60% of pathological gamblers reported physical withdraw, and these could be compared with withdrawal of drugs
Ciarrochi et al (1987): gamblers often have coinciding problems, e.g. alcohol & shopping. When quitting gambling, they switch to these behaviours. When these behaviours become too much of a problem, they switch back to gambling to keep the positive-reward feeling.

30. Gambling Intervention - Bio treatments
SSRIs (selective serotonin reuptake inhibitor) regulate serotonin levels, which could reduce the urge to partake in addictive behaviours.
Hollander et al (2000) found that gamblers treated with SSRIs to increase serotonin levels showed significant improvement compared to a control group (Blanco et al could not replicate findings).
Neltrexone inhibits the release of dopamine that results from gambling - Kim & Grant (2001): decrease in gambling thoughts and behaviour after 6 weeks.