Addiction
Characteristics of addiction:
In 2005, Griffiths suggested six criteria which diagnose addiction. These were:
Salience – when the particular activity becomes the most important activity in their life and
dominates their thoughts and feelings. Even if they aren’t engaged in the activity they’re
thinking about the next time they will be
Mood modification – Subjective consequence that people report of engaging in the activity.
The persons’ activity of choice is able to have mood modifying effects e.g. using nicotine in
the morning gives energy from the “nicotine rush” but it could also be used in the evening to
destress
Tolerance – This is the process where increasing amounts of the activity are required to
experience previous effects e.g. heroin addicts need increasing amounts of their “fix” to
achieve the same sensations as previously
Withdrawal symptoms – unpleasant mental and physical effects that occur when the activity
is discontinued e.g. nausea and irritability
Conflict – Addiction can cause interpersonal conflict with the people around the addict as
well as intrapsychic conflict (conflict withing themselves due to poor life decisions
Relapse – the tendency to revert to the activity after a period of abstinence e.g. smokers
after a few cigarettes
Walters created characteristics known as the four P’s. These were:
Preoccupation – when the addict is engrossed by their addictive activity
Persistence – continuing with activity despite difficulty and conflict
Progression – engaging more and more as tolerance increases
Perceive – addict feels as though they’ve lost control
Biological explanation one – addictive genes:
The DRD2 gene is a dopamine gene
Individuals with the A1 variation of DRD2 gene have fewer dopamine receptors
Consequently, less pleasure is experienced in the nucleus accumbens when participating in
activities like sex or eating so the person has to overcompensate for the lack of satisfaction
by engaging in more stimulative activities
Comings et al found that around 49% of smokers or ex-smokers and 51% of gambling addicts
had the A1 variant compared with 26% of the general population
Drinking alcohol puts people at risk of adverse health effects like alcoholism and cancer but
some people are at higher risk
Research shows alcohol related problems are influenced by individual variation in alcohol
metabolism controlled by genetic factors like variation in enzymes that break down alcohol.
This means some are at risk whilst others are protected by their genetic make-up.
The genes responsible for the process are ADH and ALDH
Normally, alcohol is metabolised into acetaldehyde by enzyme alcohol dehydrogenase (ADH).
Then the enzyme acetaldehyde dehydrogenase (ALDH) breaks it down into acetic acid and
water
The type of ADH and ALDH genes someone carries is shown to influence their risk for
developing alcoholism.
, A fast ADH enzyme or a slow ALDH enzyme can cause toxic acetaldehyde to build up in the
body making drinking unpleasant because you feel nauseous, flushing and rapid heard rate
therefore people who carry these genes tend to drink less so are at lower risk of alcoholism
This reaction is found in larger quantities amongst east Asians explaining lower alcoholism
rates in these cultures.
Conversely, people with a slow ADH enzyme break down alcohol at a slower rate so they’re
more likely to drink and become addicted
Addictive genes evaluation:
Strength – This explanation helps us to understand why some people become addicts and
not others. This reduces blame placed on addicts because they cannot control a biological
reason. This can prove important when the individual is trying to overcome their addiction
and reduces a sense of guilt.
Weakness – However, this deterministic view could cause the individual to view their
addiction as an unstoppable consequence of their genetics so they’re less likely to take
responsibility for their own recovery which could hinder their ability to change and
overcome the addiction.
Strength – There is supporting evidence for this explanation. Kendler and Prescot
interviewed around 2000 twins. Concordance rate for cocaine initiation in monozygotic twins
was 54% compared to 42% in dizygotic twins. But, the concordance rate for addiction of
cocaine was 35% in MZ twins and 0% in DZ twins. Although environmental and social factors
affected initiation, genes affected addiction. This suggests genetic factors have a large role to
play in addiction.
Weakness – On the other hand, Ojelade et al found when the Rsu1 gene was functioning
incorrectly in fruit flies, they had a lower sensitivity to alcohol. Brain imaging tested for this
in humans and there was a correspondence found between this gene and alcohol addiction.
This shows there isn’t simply one gene linked to addiction. DRD2 is also linked to other
disorders like autism and Tourette’s but these people don’t tend to suffer from addiction.
Therefore, the link between the DRD2 gene and addiction is more complex and unclear than
simply saying the A1 variant causes addiction.
Weakness – Furthermore, another weakness is that biological explanations focus on
addiction as a disease which requires treatment the same way as a physical illness does.
Neuroscientist Marc Lewis suggests that this is unhelpful to addicts because labelling it as a
disease can lower self esteem and we should consider changes in the brain as a form of
learning not disease. This will help addicts overcome the addiction.
Conclusion – In conclusion, this explanation enables us to understand why some individuals
are at risk of addiction however, labelling it as a disease and explaining the behaviour in
biological terms leads to a sense of helplessness from the addict and they make not take
responsibility for their own recovery if they believe it’s fault of their genetic make up. There
is supporting evidence for this explanation such as the findings of Kendler and Prescot
proving that genetics do play and important role in addiction but, it is not solely the DRD2
gene which is important – there are many genes and it is more complex that saying one gene
causes addiction.
Characteristics of addiction:
In 2005, Griffiths suggested six criteria which diagnose addiction. These were:
Salience – when the particular activity becomes the most important activity in their life and
dominates their thoughts and feelings. Even if they aren’t engaged in the activity they’re
thinking about the next time they will be
Mood modification – Subjective consequence that people report of engaging in the activity.
The persons’ activity of choice is able to have mood modifying effects e.g. using nicotine in
the morning gives energy from the “nicotine rush” but it could also be used in the evening to
destress
Tolerance – This is the process where increasing amounts of the activity are required to
experience previous effects e.g. heroin addicts need increasing amounts of their “fix” to
achieve the same sensations as previously
Withdrawal symptoms – unpleasant mental and physical effects that occur when the activity
is discontinued e.g. nausea and irritability
Conflict – Addiction can cause interpersonal conflict with the people around the addict as
well as intrapsychic conflict (conflict withing themselves due to poor life decisions
Relapse – the tendency to revert to the activity after a period of abstinence e.g. smokers
after a few cigarettes
Walters created characteristics known as the four P’s. These were:
Preoccupation – when the addict is engrossed by their addictive activity
Persistence – continuing with activity despite difficulty and conflict
Progression – engaging more and more as tolerance increases
Perceive – addict feels as though they’ve lost control
Biological explanation one – addictive genes:
The DRD2 gene is a dopamine gene
Individuals with the A1 variation of DRD2 gene have fewer dopamine receptors
Consequently, less pleasure is experienced in the nucleus accumbens when participating in
activities like sex or eating so the person has to overcompensate for the lack of satisfaction
by engaging in more stimulative activities
Comings et al found that around 49% of smokers or ex-smokers and 51% of gambling addicts
had the A1 variant compared with 26% of the general population
Drinking alcohol puts people at risk of adverse health effects like alcoholism and cancer but
some people are at higher risk
Research shows alcohol related problems are influenced by individual variation in alcohol
metabolism controlled by genetic factors like variation in enzymes that break down alcohol.
This means some are at risk whilst others are protected by their genetic make-up.
The genes responsible for the process are ADH and ALDH
Normally, alcohol is metabolised into acetaldehyde by enzyme alcohol dehydrogenase (ADH).
Then the enzyme acetaldehyde dehydrogenase (ALDH) breaks it down into acetic acid and
water
The type of ADH and ALDH genes someone carries is shown to influence their risk for
developing alcoholism.
, A fast ADH enzyme or a slow ALDH enzyme can cause toxic acetaldehyde to build up in the
body making drinking unpleasant because you feel nauseous, flushing and rapid heard rate
therefore people who carry these genes tend to drink less so are at lower risk of alcoholism
This reaction is found in larger quantities amongst east Asians explaining lower alcoholism
rates in these cultures.
Conversely, people with a slow ADH enzyme break down alcohol at a slower rate so they’re
more likely to drink and become addicted
Addictive genes evaluation:
Strength – This explanation helps us to understand why some people become addicts and
not others. This reduces blame placed on addicts because they cannot control a biological
reason. This can prove important when the individual is trying to overcome their addiction
and reduces a sense of guilt.
Weakness – However, this deterministic view could cause the individual to view their
addiction as an unstoppable consequence of their genetics so they’re less likely to take
responsibility for their own recovery which could hinder their ability to change and
overcome the addiction.
Strength – There is supporting evidence for this explanation. Kendler and Prescot
interviewed around 2000 twins. Concordance rate for cocaine initiation in monozygotic twins
was 54% compared to 42% in dizygotic twins. But, the concordance rate for addiction of
cocaine was 35% in MZ twins and 0% in DZ twins. Although environmental and social factors
affected initiation, genes affected addiction. This suggests genetic factors have a large role to
play in addiction.
Weakness – On the other hand, Ojelade et al found when the Rsu1 gene was functioning
incorrectly in fruit flies, they had a lower sensitivity to alcohol. Brain imaging tested for this
in humans and there was a correspondence found between this gene and alcohol addiction.
This shows there isn’t simply one gene linked to addiction. DRD2 is also linked to other
disorders like autism and Tourette’s but these people don’t tend to suffer from addiction.
Therefore, the link between the DRD2 gene and addiction is more complex and unclear than
simply saying the A1 variant causes addiction.
Weakness – Furthermore, another weakness is that biological explanations focus on
addiction as a disease which requires treatment the same way as a physical illness does.
Neuroscientist Marc Lewis suggests that this is unhelpful to addicts because labelling it as a
disease can lower self esteem and we should consider changes in the brain as a form of
learning not disease. This will help addicts overcome the addiction.
Conclusion – In conclusion, this explanation enables us to understand why some individuals
are at risk of addiction however, labelling it as a disease and explaining the behaviour in
biological terms leads to a sense of helplessness from the addict and they make not take
responsibility for their own recovery if they believe it’s fault of their genetic make up. There
is supporting evidence for this explanation such as the findings of Kendler and Prescot
proving that genetics do play and important role in addiction but, it is not solely the DRD2
gene which is important – there are many genes and it is more complex that saying one gene
causes addiction.
