Addiction: nicotine Flashcards
Explain genetic explanation for smoking initiation
One explanation is that some people inherit a genetic
vulnerability to start smoking and ultimately develop an addiction.
One candidate gene for smoking (and other addictions) is the
A1DRD2 variation. This seems to code for defective and
insufficient dopamine receptors in the brain’s reward circuitry,
meaning some individuals cannot produce pleasure naturally and
may engage in smoking behaviours to raise dopamine to optimal
levels
Action of nictotine
Explain in detail the role of dopamine and behaviour repetition
1- Nicotine stimulates specific acetylcholine (nicotinic acetylcholine receptors - NAcR) receptors which increases alertness, memory function and learning.
2- This action causes a rise in dopamine activity in the ventral tegmental area (VTA): a critical area in the brain’s reward circuitry which is highly populated with NAcR. This gives nicotine a rewarding sensation.
3- The VTA activity caused by nicotine is then projected to the nucleus accumbens, a producer of dopamine that is located deep in the mesolimbic dopamine pathway.
4- The nucleus accumbens is a primary reward centre in the brain and with increased activity: dopamine rises causing users to evaluate ‘smoking’ as very pleasurable, compelling further use.
5- At the same time, the nucleus accumbens is encouraged to release more dopamine as nicotine also stimulates endorphins that reduce GABA activity.
A decrease in GABA correlates with further rises in dopamine (as GABA usually suppresses dopamine).
More and more dopamine forces smokers to engage with further use.
Describe smoking relapse and downregulation
Nicotine triggers the firing of dopamine in the mesolimbic dopamine pathway, and this acts like a reward, or a ‘kick’ to the smoker. The smoker will want this reward again, but tolerance develops.
With long term use, the Nicotine Regulation Model (Shachter, 1977) suggests that the smokers ‘reward system’ becomes temporarily less active/sensitive (downregulation) i.e., specific acetylcholine receptors become unavailable and inactive. This can create anxiety, lethargy and sadness.
To avoid this, smokers continue to smoke more to maintain a certain level of nicotine in their bodies to avoid these unpleasant side effects (negative reinforcement).
Hence, with the downregulation (tolerance) in the mesolimbic pathway, an increased amount of nicotine is needed to achieve the same initial ‘kick’ as the rewarding receptors have been ground down.
Describe upregulation and smoking
As long as the individual is smoking, nicotinic receptors are desensitised and cravings and withdrawal symptoms held off. However, when smokers go without nicotine for a prolonged period of time, nicotine disappears from the body. This allows more nicotine receptors to become functional again (upregulation).
EVALUATING Brain chemistry and dopamine in NICOTINE ADDICTION: evidence
paterson
Paterson et al. (2002) found support for the role of nicotine and dopamine through research with epilepsy drug (Gamma-vinyl GABA).
This drug reduces the surge of dopamine in the nucleus accumbens that occurs after nicotine. This effectively reduces the addictive properties of nicotine, without major side effects.
EVALUATING Brain chemistry and dopamine in NICOTINE ADDICTION: beta bias
Nerin and Jane (2007) argue the onset of smoking addiction is significantly different between the sexes - i.e., women typically start smoking much later than men.
The biological reasoning for this is ignored.
EVALUATING Brain chemistry and dopamine in NICOTINE ADDICTION: neglects to consider nurture
Neglects to consider the role of nurture.
Perhaps the rewarding qualities of nicotine are also gained through the environment - for example the peer acceptance and approval that have been shown to be positively reinforcing.
Research has shown that nicotine activates dopamine - but studies have also shown peer approval activates dopamine as well.
EVALUATING Brain chemistry and dopamine in NICOTINE ADDICTION: scientific
The dopamine account uses both empirical and falsifiable methods to help identify the biochemical action of nicotine.
For instance, dopamine and NAcR can be objectively measured through cerebrospinal fluid (CSF), sophisticated PET scans as well as carefully examining urine for waste products.
EVALUATING Brain chemistry and dopamine in NICOTINE ADDICTION: practical applications
Delivering therapeutic doses of nicotine (without the undesirable parts of tobacco) in the early stages of stopping smoking. This release of nicotine is absorbed much more slowly and steadily than in tobacco.
For instance, there are _____________________ currently available to purchase. The use of inhalers has been shown to keep 28% of the treatment group off cigarettes for 12 months.
- Davison, 2004
What are the 3 parts of learning theory for smoking addiction?
Smoking initiation - Social Learning Theory
Smoking maintenance - Consequential learning and peer acceptance
Smoking maintenance and relapse - Cue reactivity
Outline smoking maintenance (SLT)
Nicotine addiction could be picked up easily through vicarious reinforcement and learning from equal status (peers) and higher status (parent) role models.
E.g., individuals may see mum being particularly stressed out and then smoke a cigarette which appears to remove her stress (and example of vicarious (negative) reinforcement).
If this pattern of behaviour is repeated several times, not only is this legitimising smoking as acceptable, but we are likely to remember this event and be motivated to repeat the behaviour ourselves - chasing this negative reinforcement (stress reduction).
Outline smoking maintenance
Consequential Learning
Skinner: Immediate reinforcers take precedence over the long term consequences.
I.e., short term benefits of smoking (reduced stress) outwight long term costs of smoking (addiction - health risks etc). 25% of inhaled nicotine reaches the brain in less than 10 seconds.
Peer Acceptance
Milton et al. (2008): Young smokers identified peer influence as an important factor in smoking, and the rejection from a peer group as key.
Hence, through social modelling and interaction, peer acceptance acts like reinforcement that helps maintain smoking behaviour.
Outline cue reactivity
Carter and Tiffany (1999)
CC claims smoking addictions are often maintained and relapsed due to triggers or cues in the environment that we have learnt to associate with smoking addiction.
These cues (CS) will elicit a conditioned response even in the absence of the actual smoking behaviour.
MAINTENANCE: As the effects of tobacco start to wear off with repeated exposure users can experience
unpleasant withdrawal symptoms (e.g. nausea, insomnia, cravings). Taking
more nicotine stops these negative experiences occurring. As this further use removes the
negative states and provides more pleasure, this is likely to increase the
frequency of smoking and subsequent addiction. Hence, maintaining pleasurable effects
from tobacco acts as a negative reinforcer.
RELAPSE= Classical conditioning claims smoking (and other addictions) are often maintained and
relapsed due to triggers or CUES in the environment that we have learnt to associate with
smoking addiction. These triggers are referred to as a Conditioned Stimulus (CS). Through CC
these cues (or CS) will elicit C__________________ R____________ even in the absence of
the actual smoking behaviour.
list some of the cues or CS that may reignite smoking and /or create cravings
- PUB
- LIGHTERS
- PEERS
- ALCOHOL
- LOCAL SHOP