Below is an article I was writing with two Professors from a University here in the UK.

The article remains in an incomplete state but contains lots of valuable research into how addiction can be seen as a disorder of emotion processing and regulation (stress dysregulation).

Addiction in terms of pathomechanism is akin to a parasite on this emotion and stress dysregulation and like with other disease states involves some parasitic influence on gene expression, in this case under the vulnerabilities of emotion and stress dysregulation.

In other words not being able to fully process and regulate emotion leads a stress dysregulation which can threaten recovery and lead to relapse.

As we never fully seem able to fully and automatically regulate stress and emotion in a optimal and health way, this parasitic influence is always active in the disease state of addiction, in the networks of self regulation such as memory, affect and motivation (reward) activated by stress dyregulation, emotionally expressed as distress.

Thus distress is the parasite force in addiction, even in recovery and needs to be managed on a daily basis via strategies to reduce distress, such as mediation, prayer and working with others.

In fact, one of the most powerful antidotes to this parasite is by sharing with others how you are feeling, to identify and differentiate emotion and relieve distress states. This will also help with subsequent decision making, usually based on our emotions.

This highlights the importance of a sponsor, mentor or recovery friends in helping us regulate our emotional states.

I have ceased doing purely academic research as  I have found it is of limited utility in helping alcoholics and addicted individuals in their recovery.

I still research the neuroscience of addiction but will be explaining  my research in more simple terms via podcasts and via vlogging, with the help of my wife, so stay tuned for more details on that.

The article blow is quite long, some 5,000 words so I have split into various parts – here is part 1.

References to follow.

Addiction As A Brain Disorder of Emotion Regulation

Abstract

The American Society for Addiction Medicine has defined addiction as a brain disorder which manifests in various neuro-psychological domains such as stress and reward dysregulation, emotion dysfunction, impaired judgement, maladaptive decision making, distress based impulsivity and executive dysfunction. However this definition may not fully consider that these apparently separate domains may be caused by the same brain impairments. Namely, these particular impairments seem to stem from the pathogenesis of inherent emotion processing and regulation deficits, often genetically inherited, frequently made more severe by adverse childhood experiences and developmental trauma. They can also made more severe by chronic consumption of substances or the long term consequence of maladaptive behaviours. These emotion processing and regulation deficits appear common and integral to the aetiology of all addictive behaviours.  As such we hypothesize that the brain disorder, which results in addictive behaviour, manifests via a lag in self-development and affect regulation and, in a major subgroup of addicted individuals, represents a development delay disorder.  In simple terms, a possible pathomechanism common to all addictive behaviour, both behavioural (e.g., gambling) and substance addictions, centres on a diminished ability to put words to emotions, or articulate feelings, which means feelings are not acted on in goal directed manner but instead are treated as undifferentiated emotion (distress) which prompt repetitive compulsive behaviours to relieve this distress.  This distress-based, impulsive decision-making impairs judgement via delay discounting and diminished awareness of future consequence. The implications for treatment are profound with emotion processing and stress coping skills efficacious in both treatment and prevention.

Key Words

alexithymia, affect, negative urgency, developmental delay 

Introduction

There has been a steady increase in the number of research papers (1,2) looking at the primary role of emotion dysfunction in addiction with affective functioning playing a prominent role in several etiological models of substance abuse (3).

These studies suggest that individuals with poor affect regulation show a diminished capacity to handle intense emotion states and often rely upon maladaptive coping strategies, such as addictive behaviours, to manage their emotions (4,5)

We have previously argued (6) that the addiction cycle may be viewed as a transition towards increasingly chronic stress and emotional dysregulation, with persistent states of emotional distress, at the endpoint of addiction, ultimately acting as a stimulus response to the activation of compulsive addictive behaviours.

In essence, chronic substance consumption or addictive behaviour can be viewed as a progressively dysfunctional “regulation” of resultant, often negative emotions, and emotional distress.

Koob and le Moal (7) describe more pronounced, impaired emotion processing (or alexithymic) characteristics as increasingly the result of the addiction cycle and the consequence of increasing stress dysregulation in the addiction cycle as the result of escalating substance abuse.

Equally, however, this chronic abuse may be acting on already impaired stress and emotion regulatory networks. In a major subgroup of addicted individuals, these networks may be impaired pre-morbidly.

There has been limited consideration of how impairments in affective processing may mediate addictive behaviours (8), particularly via their contribution to decision making deficits or how these affective processing deficits often constitute a premorbid vulnerability (9).

Emotion dysfunction in the aetiology of addictive behaviours

Regardless of the relative paucity in research into the centrality of emotion dysfunction in the aetiology of addictive behaviours, it has been included as a direct and indirect manifestation of the brain disorder of addiction as part of the American Society for Addiction Medicine (ASAM) definition of addiction (10).

The most recent ASAM definition has considered various aspects of addiction such as stress and reward dysregulation, emotional dysfunction, impaired judgement, maladaptive decision making, negative urgency (or distress based impulsivity) and executive dysfunction. However, there is no consideration of the possibility that these seemingly separate manifestations of addicted behaviour may be caused by the same brain impairments, namely those of emotion processing and regulation deficits.

We expand on this possibility, arguing that these emotion processing and regulation deficits are often genetically inherited, frequently made more severe by adverse childhood experiences/upbringing factors, with further dysfunction caused by the chronic consumption of substances or the long term consequence of maladaptive behaviours.

These emotion processing and regulation deficits also appear common and integral to the aetiology of all addictive behaviours, both substance and behavioural addictions, including gambling, eating and hypersexual disorders (9,11-15).

In this review, we will demonstrate that addictive behaviour is the consequence of a brain disorder and the central disorder is impaired ability to process and subsequently regulate emotion.

It is this emotion dysfunction that prompts the distress-based impulsivity and judgement/decision making deficits often seen in addicted individuals. Emotion dysfunction also appears to contribute to the emotional and stress dysregulation which potentiates reward networks, heightens craving (), cognitive distortions that combine with distress based impulsivity to drive addictive behaviour (6,16,17).

Finally, we posit that these emotion processing deficits also implicate endocrine dysfunction, which effects the processing of emotion and impacts on optimal decision making capabilities.

The implication in terms of treatment is potentially profound as it suggests that specific therapeutic areas should focus on addressing areas such as emotional literacy and having a greater awareness of emotion processing deficits (18) to reduce relapse and promote recovery. It also has profound implications for prevention strategies in those vulnerable to later develop addictive behaviour.

Defining Addictive Behaviour

In this section we consider two prominent definitions of addictive behaviour.

American Society for Addiction Medicine (ASAM)

ASAM’s definition of addiction as a brain disorder includes, ”Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry…fundamental in the manifestations of altered impulse control, altered judgment, and the dysfunctional pursuit of rewards…”

Impaired neural mechanisms result also in “cognitive and affective distortions, which impair perceptions and compromise the ability to deal with feelings…problems in interpersonal relationships…”

These may partly be the result of “…Exposure to trauma or stressors that overwhelm an individual’s coping abilities…”

There may also be “The presence of co-occurring psychiatric disorders in persons who engage in substance use or other addictive behaviors…”

These aspects of ASAM’s definition, we hypothesize, can all be explained by emotion processing deficits.

Diagnostic and Statistical Manual of Mental Disorders (DSM)

Any emotion dysfunction in addiction, according to DSM IV and V, appears to have treated by relegating psychiatric symptoms that affect the well-being and social functioning of addicted individuals to the domain of psychiatric co-morbidity of e.g. Generalized Anxiety Disorder (GAD) or Major Depression (MDD), although certain researchers have demonstrated the transitory nature of these so-called co-morbidities in terms of “substance-induced disorders” (19, 20).

In effect, DSM classification may be stating that emotion dysfunction is the consequence of a co-morbid condition rather than intrinsic to the condition of addiction itself.

This definition, however, would perhaps fail to account for continued emotion dysfunction after so-called symptoms of apparent co-morbidities such as GAD or MDD appear to dissipate within weeks and, months of abstinence and recovery (21).

Shuckitt (21) has shown the prevalence of co-occurring conditions, such as GAD and MDD, within addicted populations to be similar to that of their occurrence in normal populations (approximately 15%).

Equally, DSM definitions also appears to fail to explain the emotion  dysfunction-based impulsivity and emotion regulation difficulties demonstrated to be present in abstinence (22,23) other than to state it is the consequence of co-morbidity, despite this apparent “co-morbidity” often dissipating in recovery/abstinence?

Our model forwards research evidence, that for a major subgroup of addicted individuals, impulsivity is present premorbidly (24) and contributes to the onset of abusing maladaptive behaviours. Hence it is part of aetiology of this condition.

That is not to say that other co-occurring conditions do not have a pivotal role in initiating and sustaining addictive behaviour.

For example, in this model, we  consider the fundamental effects of trauma (PTSD) and the consequences of insecure attachment (developmental trauma) on addictive behaviour as each appears to alter the emotion regulation network of the brain and, via reciprocal mechanisms, can contribute to the severity of the emotion processing and regulation deficits that appear to propel addictive behaviour.

Equally there may be emotion processing deficits in the presence and the absence of co-occurring conditions.

We argue that there is often a genetic vulnerability in emotion regulation which is impacted on, in sequelae, which can include adverse childhood experiences /developmental trauma and increase risk of addictive behaviours, where changes to the brain caused by chronic substance use or compulsive behaviours can furthermore negatively affect emotion regulation.

TBC