In our previous neurobiological model, we highlighted how 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 behaviours can be viewed as an extremely maladaptive and dysfunctional “regulation” of negative emotions and emotional distress.
Koob ( ) describes this chronic stress and emotional regulation throughout this work with alexithymic characteristics increasingly the product of the addiction cycle.
So in the addiction cycle, the ability to process and regulate emotions (especially negative emotions) may become increasingly and pathologically impaired.
Two of the main characteristics of alexithymia are: (1) difﬁculty identifying feelings and distinguishing between emotions and corresponding bodily sensations; (2) difﬁculty describing feelings to others.
Research has also demonstrated that alexithymia or emotional processing deficits are also observed in certain children from families with a history of alcoholism who have a higher risk of developing later addictive behaviours such as alcoholism (FH+).
Research has also shown how the ability to process and regulate emotions is also a protective factor in FH- children, those children who have lower risk of developing later alcoholism.
In one study, resilient youth had enhanced monitoring of emotionally arousing stimuli, even compared to typically developing youth. The resilient group had an increased insula activation to negative words. The insula is implicated in evaluating internally generated emotions and the monitoring of ongoing internal emotional state (Phan et al., 2002).
The resilient group did not suppress the emotional experience. They responded to emotional stimuli while demonstrating enhanced monitoring which allowed for the inhibition of inappropriate responding.
In contrast the vulnerable group demonstrated a reactive approach to the world, in which affect was not fully processed. In fact, the authors surmised that vulnerable youth were recruiting an emotional control system that was suppressing emotional response – they did not inhibit inappropriate responding as a result of processing emotions.
In fact a recent study illustrated that reduced connectivity between insula and prefrontal cortex regions may be an important factor in adolescent alcohol use given that reduced inhibitory control has been found to be a factor in alcohol use disorders.
The theoretical model we outline here posits that this inappropriate (or impulsive) responding as the result of impaired emotion processing is central to all addictive behaviours and represents a premorbid vulnerability.
One of the best characterized findings in FH+ is greater impulsivity and difficulties in response inhibition (27,28). FH+ individuals are less able to delay reward gratification compared with their peers (29).
Given the wealth of research into this vulnerability it is surprising that emotional processing and its relationship with executive control has not received much attention in FH+ individuals.
Research examining the relationship between emotional processing and cognition has found affective measures in FH+ alcoholics also relate to deficits in executive functioning, e.g impulsivity (47). This suggests that familial history of AUDs may put individuals at greater risk for problems with emotional processing and associated disruptions in executive functioning (47), which could, in turn, increase risk for later addictive behaviours (49).
Redefining Addictive Behaviour
There are few affect centred theories of addiction (Cheetham), with little centrality afforded to the role of emotional dysfunction in those suffering from 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 part of the most recent American Society for Addiction Medicine (ASAM) definition of addition
In contrast, DSM 5 has treated this emotion dysfunction in substance dependence by relegating any psychiatric symptoms that affect the well-being and social functioning of addicted individuals to the domain of psychiatric comorbidity of e.g. Generalized Anxiety Disorder (GAD) or Major Depression (MDD), although some researchers have demonstrated the transitory nature of these so-called co-morbidities in terms of “substance-induced disorders” (Shuckitt).
In effect, DSM appears to be stating that emotion dysfunction is the consequence of a co-morbid condition.
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. Mark Shuckitt, along with others, show that the prevalence of these conditions within addicted populations to be similar to that of their occurrence in normal populations (approximately 15%).
In 2013, 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”. NIMH suggested a fuller diagnosis should include specific domains of cognition, emotion, or behavior.
Pani et al ( ), in addressing the limitations in the nosology of DSM IV and V, remarked that, unlike other sections in the DSM, such as those on mood disorders, in which diagnosis requires exploration of perception, affect, and cognition, in the case of substance addiction it is implied that an adequate diagnosis can be achieved solely by observing the patient’s current behaviour and altered physiology.
These researchers have also queried why anxiety, mood and impulse-control domains (such as sadness, irritability, diminished interest in activities, affective instability, dysphoria, restlessness, boredom susceptibility, impulsivity, irresponsibility, attention and concentration difficulties); symptoms, almost always associated with addiction and which characterize the everyday life of some patients with addictive disorders, were often located below the threshold for a defined additional disorder?
Indeed these researchers have suggested that “Addiction” reaches beyond the mere result of drug-elicited effects on the brain and cannot be “peremptorily equated only with the use of drugs despite the adverse consequences produced”, and emphasised how addiction is a relapsing chronic condition in which psychiatric manifestations play a crucial role. ()
Thus, as Pani et al have argued, it may not be possible to sever the aetiology of addiction from its psychopathological connotations, particularly in view of “the undeniable presence of symptoms, their manifest contribution to the way addicted patients feel and behave, and to the role they play in maintaining the continued use of substances.”
Important to our theory here is the idea that “latter symptoms frequently precede the addictive process constituting a predisposing psychological background on which substance effects and addictive processes interact, leading to a full-fledged psychiatric disorder.”
In other words, addiction is more than it’s manifest symptoms of chronic addictive behaviour. This disease state, like other disease states, must be driven a pathomechanism.
Although the emotional dysfunction in addiction is varied (Oscar Berman et al) we concentrate here on the role emotion processing and regulation deficits play in prompting distress based impulsivity and impaired decision making. However, the above factors in emotion dysfunction also play a part in difficulties regulating the distress which prompts the rash decision making central to an addicted individual’s behaviour.
Affect-Centred Theories of Addictive Behaviour
Ceetham et al (2010) suggest that models of addiction have not generally provided a comprehensive account of the role of affect and that recent research has focused more upon the neurobiological substrates underlying addiction than on its affective components, although these neural circuitries overlap with those of emotional dysregulation and are thus not incompatible with an affect-centred theory of addiction.
In fact the neurobiological or neuro-endocrinological model we developed (1) in which increasing distress and stress dysregulation appear to increasingly prompt pathological craving and compulsive substance use can be viewed as the an affect-based theory of addiction from a neurobiological perspective.
DSM 4 and 5 , although attempting to maintain an “atheoretical perspective”, however, appears to be influenced by neurobiological theories of addiction. There was even a steering group working on definitions of “Craving”….
These neurobiological accounts have developed experimental paradigms such as cue reactivity, attentional bias, in addition to craving concepts, although these have only ever been demonstrated to account for a minority of relapses. Many addicted individuals in abstinence and recovery also develop strategies to counteract attentional bias and cue reactivity.
Others have challenged these “one dimensional” conditioning accounts of addiction and relapse, with some researchers demonstrating how craving may be the consequence of emotion dysregulation (Thayer, Garland) while others have shown how it is stress and emotion dysregulation that activates more “habit-based” or emotive-motor regions of the brain in chronically addicted individuals in prompting compulsive behaviours.
Thus neurobiological accounts alone cannot successfully predict relapse behaviour, in the majority of relapse scenarios.
It may be that cognitive-affective mechanisms mediate the evidently impaired neurobiological networks demonstrated in addicted individuals to be instrumental in relapse.
This is a particularly pertinent question as it has been suggested that a sizeable majority of relapse is caused by difficulties in regulating negative affect and emotional distress/stress, often within the context of interpersonal relationships – so why do recovering/abstinent addicted individuals have such difficulties with emotional and stress regulation especially if they do not have a co-morbid disorder?”
What is the nature of this emotion dysfunction which appears to contribute to not only vulnerability but as a pathomechanism of addictive behaviour and which also plays a major role in relapse in abstinent and recovering individuals.
What are the “symptoms (which) frequently precede the addictive process constituting a predisposing psychological background on which substance effects and addictive processes interact…”?
The neural circuitry implicated in affective reactivity and regulation is closely related to the circuitry proposed to underlie addictive behaviours ().
Although emotional distress is often said to be related to dysfunctional decision-making processes and impulsivity (negative urgency) and regions involved in affective processing have frequently been found to be impaired in those with various addictive behaviours, there has been little consideration of what these results might mean for impaired affective processing capabilities of those at high risk of developing later addiction. How may they contribute to this pathology?
Like others, in particular we query whether appropriate consideration been given to evident emotion processing and regulation deficits, observed across many different addictive behaviours in two domains which constantly show up in studies of addictive behaviours, namely that of decision making deficits and impulsivity (or negative urgency).
References (to follow)
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