In the next few weeks we will be asking and attempting to give answers to the following questions

1. What is addictive behaviour?

2. How is it defined?

3. What are the neurobiological models of addiction –

dopaminergic positive reinforcement models,

stress based negative reinforcement models

and thirdly a model of addiction which combines both these models – the model we subscribe to in this blog and which we have contributed towards in a comprehensive theoretical review article, outlining our model.

4. Are there are additional factors which need to be included in a theory of addiction?

What are these factors e.g do cognitive-affective mechanisms interact with altered brain neurobiology in the addiction cycle?

Again we believe that cognitive-affective factors such as stress and emotion dysregulation play in intitiating and sustaining additive behaviour?

Also we have recently submitted a theoretical article which shows how people with addictive behaviours use these behaviours to regulate negative emotions and negative self schemata.

This negative emotion regulation is also linked to altered stress systems in the brain which results in an altered and impaired ability to process emotion, i.e. identify, label and use emotion to guide adaptive decision making.

Instead substance and behavioural addicts seem to engage in distressed based impulsive decision making, recruiting more sub-cortical “flight or fight ” parts of the brain when making decisions rather than prefrontal cortex parts of the brain used in reasoned and evaluative thinking and decision making.

5. Are their underlying similarities in all addictive behaviours? If so, what are these common underlying mechanism?

6. Does environment play a role in the risk of later addictive behaviours?

7. Do genetics play a role in these theories of addiction?

8. Are present definitions and theories of additive behaviour accurate or adequate enough?

9. Our proposal for a re-definition of addictive behaviour?

10.  How do we explain addictive behaviour in those without adversive childhoods?

It occurs to us that when one reads social media accounts of addiction most theoretical, neurobiological models of addiction seem to be dopaminergic. We disagree with this view of addiction.

We can demonstrate  how stress chemicals interact with dopamine throughout the addiction cycle, from pre initial  use of substance or maladaptive behaviour.  We can show how these stress chemicals increasingly impact on the dopaminergic brain circuits governing memory, attention , emotion and reward/motivation.

Thus the process of the brain being  “hijacked” during chronic addictive behaviour is not achieved solely by dopaminergic mechanisms but in relation to the impacting effects of increasingly chronic stress on these dopaminergic systems.

It is increasingly chronic stress reactivity leading to compulsive behaviours to relieve distress that “hijacks” the addicted brain, albeit, via dopaminergic systems in the brain.

In fact dopamine models do not appear to always fully consider the impaired stress reactivity which accompanies the evident abuse, trauma and insecure attachment which accompanies the  childhood of  the vast majority of addicted individuals.

This altered stress reactivity heightens reward sensitivity in the brain and makes substance and behaviour misuse more reinforcing and rewarding because it is not only more stimulating but also it relieves inherent stress, distress and anxiety which are the manifestation of altered stress systems in the brain. So it contributes to a heightened sense of “having our feelings fixed”.

Secondly, there is rarely any real mention of these affective and anxiety type manifestations which appear an integral part of addictive behaviours and which increasingly becomes more severe in the addiction cycle.

Most models suggest that this emotion dysfunction is the consequence of co-morbidity with other affective disorders without much appreciation that emotion dysfunction is central to addictive behaviour.

In fact it seems strange to divorce stress dysregulation from emotion dysregulation or to divorce stress dysregulation from emotion processing deficits such as alexithymia and lack of emotional awareness? They are all interconnected.

If there is trauma, abuse and/or insecure attachment stress in the vast majority of of people suffering addictive behaviour why do dopamine models only consider reduced dopamine in these individuals but not the excessive stress chemicals too which reduce dopamine?

A failure to do so has lasting consequence?

These models then state that addicts relapse due to factors that have come out of dopaminergic models such as “craving” which has never been defined properly, via attentional bias and cue reactivity to things from their past, such as people, places and things that prompt “craving” although this is implicated in only a minority of relapse.

Measures of “craving” are mainly stress based, cortisol, saliva, heart rate, pus self reports of the “craving” experience in terms of anxiety, in relation to cues and negative emotions like fear, sadness, anger, in stress provoked “craving”.

Stress reactivity is intrinsic to the urge or craving experience.

The majority of relapse is due to stress and negative emotion based factors, often in relation to interpersonal factors like relationships with others.  They would report these stress factor as also being “cues” or internal cues.

We, however,  believe this attempts to divorce two aspects which cannot be divorced – the role of altered stress and dopamine systems in the brain.

The majority of people I know who have relapsed have done so  because they could not deal with themselves, with their distress and overwhelming negative emotions.

These distress state activates all the circuits hijacked in the brain and this leads to relapse. They are not dissoluble.

Science needs to come up with a more comprehensive model of addiction which predicts this type of behaviour, this distress based relapse and with more effective treatment which treats this distress at the heart of all addictive behaviour.