In my PhD I was attempting, to show, that there is an inherent decision making deficit in a variety of addictions and that this is due to an emotional processing deficit which means the prefrontal cortical, rational areas of the brain are not recruited in relatively simple task in which there is some uncertainty about outcome and instead undifferentiated emotions act like a distress signal to prompt more subcortical, limbic or emotionally reactive responding.
This results in a tendency to be impulsive/compulsive and to choose short term smaller gain over delayed, but longer term greater gain. In other words addicts of various types seem to react in order to relieve this distress, this unpleasant undifferentiated feeling state rather than after the reflective deliberation of the pros and cons, the cost benefit analysis of a set of possible decisions. This may be linked also to an intolerance of uncertainty often seen in obsessive compulsive disorder.
Even the most neuro-biological models of addiction such as that forwarded by an esteemed researcher, like George Koob, would point to an increasingly severe stress and emotional dysregulation during the addiction cycle and an increasing alexithymia (the inability to recognise, identity, label, and verbalise emotions) as addiction becomes more chronic.
Other models such as that forwarded by another esteemed researcher at Yale, Rajita Sinha point to impaired abilty to control behaviour in the face of stress and negative emotions which results in the recruiting of brain regions involved in more compulsive habitual responding. These models suggest that there is an emotional dysregulation at the heart of addiction and certainly it’s endpoint at least.
However, it may be that this self dysregulation may be a fundamental part of the aetiology of addiction which simply worsens over time due to the toxic effects of alcohol and drugs or via the neuro-plasticity caused by maladaptive addictive behaviours.
There is in fact much evidence that those vulnerable to later alcoholism substance and behavioural addictions all have inherited an emotional processing and regulation deficit.
First I want to challenge present definitions of addiction as forwarded by organisations like the American Psychiatric Association which seem to have a limited perspective on not only diagnosing addictive disorders but also with regards to the diagnostics of other psychiatric disorders.
I borrow from an article I wrote earlier in the year for Recovery SI.
Roughly about a year and a half ago, “the mental health world was just gearing up for the appearance of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition1, DSM-5. Just weeks before, the National Institute of Mental Health (NIMH), the world’s largest funding agency for research into mental health, noted the need for an alternative to the DSM, citing “weakness” and “lack of validity.”
Others observed that “DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure” and asked whether “Patients with mental disorders deserve better.”
At the end of 2014, the question remains very pertinent.
NIMH went on to suggest what might be inserted into a fuller diagnosis of mental health conditions: Consider mental disorders as biological disorders involving brain circuits; disorders that implicate specific domains of cognition, emotion, or behavior.
Other authorities (2) note that the DSM’s classification of addiction is largely limited to physical manifestations that can be objectively observed, in the interest of maintaining an “atheoretical” perspective. DSM-5 relegates other psychiatric symptoms that affect the well-being and social functioning of addicted individuals to the domain of psychiatric comorbidity – we will discuss so-called comorbidity or “substance-induced disorders” in other blogs.
As an example, the relationship between addiction and symptoms associated with depression or anxiety disorders is apparently very close (the association is frequently supposedly observed and noted by clinicians and researchers.) However, this doesn’t rule out the possibility that addiction itself may modify pre-existing psychic structures via chronic drug or alcohol use.
The neural mechanisms that are manifested through various behaviors could be worsened or made more chronic through substance abuse. As a specific mental disorder, addiction might include symptoms pertaining to mood, such as depression or anxiety. Addiction itself may have impulse control dimensions that promote cognitive, executive and emotional dysfunction.
I would add that based on observed, underlying emotional processing and regulation deficits, decision making difficulties are inherent in addiction (3). All these symptoms can be included under the umbrella term “emotional dysregulation.”
I believe emotional dysregulation initiates, maintains and perpetuates the disease to its emotionally distressing endpoint—compulsive addictive behavior. It is via emotional dysregulation that the impaired neurobiology of addiction can be made clearly visible.
It’s also illuminating to see that elements of emotional dysregulation are cited as being present in some 75% of disorders listed in DSM-5 (4). Emotional dysregulation may be manifested differently in different disorders, therefore requiring different treatments.
Addiction should be treated as addiction. The emotional distress that drives the sufferer to the endpoint of addiction is illustrated in maladaptive emotional strategies that are similar to, but not the same as, apparent “co-morbidities.” The differences are evidenced through behaviour such as relapse to drug or alcohol abuse.
In short, while it may have similarities to other disorders, the emotional dysregulation that characterizes addiction is not the same.
Pier Paolo Pani and colleagues suggest that the state of addiction reaches beyond the result of drug-elicited effects on the brain. It can’t be equated only with the use of drugs despite adverse consequences.
Addiction is a relapsing chronic condition in which psychiatric manifestations play a crucial role. Thus, its etiology cannot be severed from its psychopathological manifestations, particularly in view of the undeniable presence of symptoms and their obvious contribution to the way addicted patients feel and behave, and to the continued use of substances.
Indeed, the psychopathology frequently precedes the addictive process. This constitutes a predisposing background on which substance effects and addictive processes interact, leading to a full-fledged psychiatric disorder.
This predisposing background may be that of emotional processing and regulation difficulties which initiate and accelerate initial use, as emotional dysregulation appears to heighten reward, i.e. makes alcohol and drugs more stimulating and through increased use these substances (and behaviours) become a way to regulate emotions, particularly negative emotions to the endpoint of addiction whereby emotional distress appears to be the stimulus to the automatic responding of compulsive drug use. Hence this increasing emotonal dysregulation proves to be the main factor for relapse as emotional distress leads to an automatic craving state which compels those in recovery to relapse. Hence it is evident in vulnerability, initial use, abuse, endpoint addiction and an ever present danger to relapse.
(to be continued)
- American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. pp. 5–25.
- Pani, Pier Paolo, et al. “Delineating the psychic structure of substance abuse and addictions: Should anxiety, mood and impulse-control dysregulation be included?.” Journal of affective disorders 122.3 (2010): 185-197.
- Murphy, A., Taylor, E., & Elliott, R. (2012). The detrimental effects of emotional process dysregulation on decision-making in substance dependence. Frontiers in integrative neuroscience, 6.
- Werner, K., & Gross, J. J. (2010). Emotion regulation and psychopathology: A conceptual framework.