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Setiawan et al (2013)

Setiawan et al (2013) carried out a study to investigate the role the dopamine and the mesolimbic reward pathway in alcohol use disorders. This study could be used for the following learning objectives:

Research methods used in the biological approach.

Techniques for studying the brain and behaviour.

Localization of function

The role of neurotransmitters in behaviour

Ethics in the study of the brain and behaviour

 

Background information

The biological origins of alcohol use disorders (AUDs) are still an area of active investigation. Two traits that have been shown to reliably predict AUD are personality traits and one's response to alcohol ingestion. For individuals with lower rates of sensitivity to alcohol - that is, they do not feel the intoxicating effects to the same level as others who consume the same amount of alcohol - there is a higher risk of AUD. It has also been found that there may be a genetic link to this low level of sensitivity as it runs in families and is stable over time. It is argued that individuals with these low levels of response to alcohol (LLR) drink more in order to achieve the desired effect of alcohol consumption.

The link to personality may also be biological. It has been hypothesized that vulnerability for AUD increases in individuals who have greater reward-seeking behaviour. The origin of such behavior is believed to be linked to the mesolimbic reward pathway which includes the ventral tegmental area [VTA], nucleus accumbens, amygdala, hippocampus, and prefrontal cortex.  Dopamine plays an important role in this reward pathway.

The researchers argued that alcohol is an agonist for dopamine, connecting to dopamine receptor sites and causing the neurons to fire. It is hypothesized that people with a potential for alcoholism have a greater response to the agonist than those at low-risk.  Research shows that those with a low level of dopamine neuron activity as a result of alcohol consumption often get tired after drinking a small amount of alcohol.  This is because the higher level of dopamine activity counteracts the sedative effects of alcohol.  By studying the way in which alcohol acts as an agonist on dopamine neurons, it is also possible that researchers could find ways to treat the disorder.

The following study by Setiawan et al (2013) tested this "vulnerability hypothesis" by investigating whether one's level of sensitivity to alcohol and personality traits are related to dopamine responses in the brains of young, healthy social drinkers.

Procedure and results

The researchers studied 26 healthy young social drinkers from the city of Montreal and the university community at McGill. The sample ranged from 18 - 30 years old.  The sample consisted of 8 women and 18 men.  In order to participate, they had to be free of any diagnosis of mental illness or drug dependence other than nicotine or caffeine. None of the participants was identified as having AUD, but 11 of the participants reported having a family member with AUD.

Participants were asked to first fill in a series of questionnaires - including a lifetime drug and alcohol use questionnaire ad the Tridimensional Personality Questionnaire.  The researcher categorized the drinkers as either high or low risk for alcoholism based on personality traits and having a lower intoxication response to alcohol - that is, they did not feel as drunk despite having drunk the same amount as other drinkers.

Each participant underwent two PET scans on separate days.  The conditions were counterbalanced. Before the scan, a urine drug test and a breathalyzer test were used to confirm that the participants were drug-free. They were also asked to abstain from nicotine and caffeine on the day of each scan.

Participants were told that they may or may not receive alcohol on either day. 30 minutes prior to the scan, they were asked to drink a mixture of orange juice and lemon-lime soda - or the same volume of the same drink, but including alcohol. Blood samples were taken before the drink, and then at 30, 60, and 90 minutes thereafter to measure blood alcohol levels.

It was found that when drinking alcohol, those who were considered "high risk" for alcoholism showed significantly greater activity in the mesolimbic reward pathway - that is, greater dopamine levels in response to alcohol consumption. It should be noted that there was no significant difference in the two groups' lifetime exposure to alcohol, suggesting that the result is not simply because of one's past history with alcohol consumption.  Members of the low-risk group, on the other hand, showed a decreased dopamine response.

Evaluation

The study has good internal validity.  There is an attempt to control for other drugs as well as the use of a placebo to control for demand characteristics.  The study is also a repeated measures design to control for participant variability and it is counter-balanced to control for order effects.

Several questionnaires were used to increase the credibility of the "high-risk" vs "low-risk" group. So, although the information is self-reported, data triangulation allows the researchers to establish whether the reports are consistent.

The use of a PET scan is not without risk as it uses a radioactive tracer.  Some people may be allergic to the tracer. This is why it was important that informed consent be given so that the individuals in the study understood the risks.

The sample size is small - only 26 participants. When trying to make generalizations about how the brain works, it is important that sample sizes are relatively large.  However, the cost of using a PET scan as well as the ethical and logistical concerns (access) means that often such studies are small.  This is why meta-analyses are often used to determine the reliability of the data.

The study takes a reductionist approach to understanding alcoholism.  This has both a positive and negative aspect.  Potentially, this type of reseach could lead to a treatment based on the regulation of dopamine levels or allow physicians to have discussions with their patients about the risks of alcoholism based on their dopamine profile.  However, reductionist arguments can also be seen as an oversimplification.  The study does not address social and cognitive factors that may be linked to AUDs. 

Finally, the study is experimental and done under controlled conditions, but drinking alcohol and then lying in a PET scanner is a rather artificial experience which may have an effect on the findings. Although it is unlikely that the PET scan led to the difference in the two groups, the study's ecological validity is low.  We cannot know how other situational factors may play a role on the brain's activity when engaged in social drinking.

Better understanding the brain

For a better understanding of the role of dopamine in drug addiction, the following video is a good introduction.