People think it’s all about misery and desperation and death and all that shite, which is not to be ignored, but what they forget is the pleasure of it. Otherwise we wouldn’t do it. After all, we’re not fucking stupid. At least, we’re not fucking stupid.
Irvine Welsh, Trainspotting
When it comes to addiction a number of questions pop up in our head:
- Why some people become addicted, when most who try a substance do not?
- Why social deprivation, or experiences of social defeat, place people at risk of addiction?
- Why people persist in taking the substance despite obvious harms to themselves and their families?
- Why people who abstain from drugs suffer terrible withdrawal symptoms, and find life more stressful afterwards?
- Why people can relapse to heavy use of substances after a very long period of abstinence, and despite their very best intentions?
Addiction to me is a brain disorder involving specific brain regions and circuits. Thus, I see addiction as the result of a set of brain’s chemical dysregulation and am going to further elaborate this.
The brain regions involved in addiction are the prefrontal cortex (PFC), amygdala, hippocampus, thalamus, i.e. the ventral tegmental area (VTA), and the neurotransmitter involved is dopamine. The mesolimbic system with the VTA is known as the brain region involved in reward-related cognition (classical conditioning and operant reinforcement) as it shapes our motivation or uncontrollable desire for a reward. Consequently addiction and the way we conceive and process reward are indissolubly linked.
Daily natural rewarding activities which are important for our survival release dopamine. Research findings posit that all drugs of abuse cause an increase in dopamine levels, whereas drugs which do not have a street value – which people do not find rewarding- do not.
For example, stimulants like cocaine and amphetamine produce extreme rises in dopamine, because they act directly on the dopaminergic transmission including the synthesis, release, binding and reuptake of dopamine. What this means is that the brain experiences a much stronger signal than it usually would get from an ordinary reward, like food or sex.
The drug’s speed of entry to the brain whether that is intravenously, smoked, or snorted – is important in how stunning our brain considers that experience to be.This is why drugs with no street value are not particularly rewarding, because they enter our system slowly.
Furthermore, variation in dopamine receptors causes an unpleasant feeling (high levels) or a pleasant feeling, a reward (low levels).
How do we know who has high or low dopamine receptors? The associated behavioural phenotype of Reward Impulsivity reveals that. What does this mean? That high Reward Impulsivity is an indicator for low dopamine receptors which suggests more desire for the illicit substance.
So does this mean that my actions and addictions are predetermined? Definitely not. Environmental factors play an important role for the availability of dopamine receptors. Family history plays a role in addictive vulnerability; for example alcoholism vulnerability is linked with alterations in GABA sensitivity. Duration of exposure and amount ingested is also important in the transition to addiction.
Dopamine receptor availability changes following the development of addiction. Those addicted to a substance have lower dopamine receptor availability and this does not normalise before at least several months of abstinence.
Dopamine release occurs in relation to cues rather than the substance itself i.e. a kind of Pavlovian learning. For example Cocaine addicts release dopamine in relation to dopamine-related cues. What fires the rewarding experience is the anticipation of the experience.
Furthermore, research has shown a relationship between dopamine function and the function of the prefrontal cortex (PFC) which promotes cognitive stability and resistance to distraction. PFC is the part of the brain involved in decision-making. The more dopamine receptors we have the better our Orbital Frontal Cortex (OFC), the region of PFC above the orbits, functions . Changes in dopamine release have knock-on effects.
This means there is object alteration in the Addictive Brain leading from frontal control to frontal dis-control, as such addictive behaviour involves a movement from positive reinforcement to negative reinforcement.
On the other hand the Non-Addictive Brain inhibits compulsive behaviour and moves from reward-related behaviour to cue-primed automatic behaviour, the habit.
Consequently, the transition to addiction involves shifts in the reward system so that all rewards are less rewarding but drug cues have added salience.
In addition, research evidence demonstrates that there are also shifts in the stress axis involving changes in Central Nervous System (CNS) expression of Corticotrophin Releasing Hormone (CRH) and Hypothalamic-Pituitary-Adrenal (HPA) axis. CRH and HPA axis co-ordinate the endocrine and sympathetic nervous system response to stress.
Therefore, there is a relationship between stress and substance misuse as illicit drugs stimulate the CRH and HPA axis expression.
These changes do not absolve addicts of personal responsibility but highlight the enduring challenge addicts face and represent therapeutic targets which could improve prognosis.
Literature suggests that opiate dependence is quite distinct from stimulant dependence, however the avoidance of withdrawal symptoms, anxiety, dysphoria and depression is common in addictive behaviours in general. Therefore, the continued use of the addictive drug or behaviour is sustained in order to keep the dysphoria associated with the hyperactivity of the stress system under control.
In conclusion, abnormalities in the Brain’s rewarding and stress systems are increasingly recognised and may lead to a new unifying theory of addiction including behavioural addictions.
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