Theories of Addiction

Addiction As a Brain Disorder of Emotion Regulation – Part 2

Part 2

Redefining Addictive Behaviour

Critiquing DSM

Pani et al (25), in addressing the limitations in the nosology of most recent DSM diagnostic classifications, 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 affective instability and impulsivity); almost always associated with addiction, were often located below the threshold for a defined additional disorder.

They suggest 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 emphasized 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 mental health connotations, particularly in view of “the undeniable presence of psychopathological 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.”

Pani et al grouped these symptoms under various psychological domains which we suggest are all aspects of emotion dysregulation.

This dysfunctional emotion regulation has often been considered a primary trigger for relapse (1,3).

We argue that emotion processing deficits result in a diminished ability to put words to emotions, or articulate feelings, with the consequence that feelings cannot be acted on with goal directed behaviour, but are instead treated as undifferentiated emotion distress, prompting repetitive compulsive behaviours.


Emotion and Behaviour

 In this section we very briefly discuss how emotion prompts behaviour via processing capabilities.

Emotion processing appears to prepare the body for action (62, 63), in fact, to emote means, literally, to prepare for action (64).

Researchers differentiate between emotions and feelings. Emotions are considered nonconscious and embodied whereas feelings are our conscious awareness of emotions (65).

Thus an individual takes action to respond to feelings to meet the need identified by the emotion (66).

Emotion Processing and Regulation

According to Taylor, Bagby, and Parker (1997), all individuals have emotions (i.e., neurophysiological arousal), but how we feel the emotions differs based on our subjective cognitive understanding of them (67), how accurately we cognitively represent them or “put words to them”.

Without adequate words to describe various neurophysiological stimuli, we cannot feel (identify and describe) our emotions accurately and precisely, and will thus have difficulties regulating the behaviors that follow our emotions (67, 68). In other words, emotion regulation is a product of initial emotion processing.

Thus effective emotion regulation skills include the ability to be aware of emotions, identify and label them, correctly interpret emotion-related bodily sensations, and accept and tolerate negative emotions (69,70).


Emotion Regulation Networks

 Affect regulation is a complex process, involving reciprocal interactions between three different domains, the neurophysiological, motor-expression, and cognitive-experiential domains respectively (73).

Neural Correlates of Emotion Processing and Regulation

Lane (74) conceptualized a cognitive-development model for understanding the organization of emotional experience with five levels of emotional organization and awareness in the model: awareness of physical sensations,  sensorimotor reflexive (level 1), sensorimotor action tendencies (level 2), single emotions (level 3), blends of emotions (level 4), and (the capacity to appreciate complexity in the experiences of self and others, level 5).

The levels are hierarchically related in that functioning at each level adds to and modifies function of the previous levels.

Levels 1 and 2 involve implicit processes, these are automatic (do not require conscious processing), modular and cognitively impenetrable.

Emotion is implicit in the sense that the specific quality of experience (an emotional feeling) needed to call it an emotion is lacking and requires processing at higher levels.

Implicit aspects of emotion can be conceptualized as the automatic motor expressions of emotion that include the autonomic, neuroendocrine components of emotional responses. (75) Neural substrates of level 1 may include the thalamus, hypothalamus (diencephalon) and brainstem.

At level 2, crude distinctions between globally positive and globally negative states take place, which would be regulated by the thalamus, amygdala, and ventral striatum. Furthermore, the subsequent behavioural displays of emotional expression would take place in the basal ganglia would play a role in the automatic behavioral displays of emotional expression.

Levels 3, 4, and 5 on the other hand consist of explicit, conscious emotional feelings with increasingly higher levels of complexity, which are influenced by higher cognitive processes.

They are hypothesized to be mediated by the structures involved with levels 1 and 2 as well as paralimbic structures, including the anterior cingulate cortex (ACC) and insula, and the medial PFC ( ), including the ventromedial prefrontal cortex (vmPFC)

The rostral ACC/mPFC, in particular, appear to be necessary for the representation of emotion used in conscious cognition (73).


Emotion Processing Deficits


Emotion processing deficits have been operationalised in terms of alexithymia.

The concept of alexithymia (14) was created by Ruesch (1948) but the definition of Nemiah and Sifneos is more widely known (15,16).

Two main characteristics of alexithymia are: difficulty identifying feelings and distinguishing between feelings and the bodily sensations of emotional arousal as well as difficulty describing feelings to other people (33-36). We also consider another characteristic, that of externally orientated thinking.

The development of emotional awareness and skills to express feelings are strongly linked to the infants’ cognitive development because humans use language to identify and express their feelings.

According to Lane and Schwartz (1987), individuals with alexithymia are considered to be on the first two levels of emotional awareness (i.e., sensorimotor reflexive and sensorimotor enactive)  as their abilities to cognitively identify  various feelings precisely by recognizing specific physiological signs of emotions are not yet  fully developed (68, Taylor et al., 1997).

Alexithymia is typically measured with the Toronto alexithymia scale (TAS-20) [8•] and provides total scores (ranging from 20 to 100) and has three factors that reflect the original description of alexithymia by Sifneos, including difficulty describing feelings (DDF), difficulty identifying feelings (DIF), and externalization of emotion, or externally oriented thinking (EOT).

Genetics of Alexithymia

The results from a large, population-based sample of 8,785 twins suggest that genetic factors have a noticeable and similar impact (a genetic heritability around 30–33%) on all facets of alexithymia. (o)

Another study, with sample of 729 twins, suggested genetic factors accounted for 42% of individual differences in alexithymia.

Non-genetic factors unique to each twin accounted for most of the variation in alexithymia and its facets  (22) with unshared environmental factors accounting for 56% of variation in TAS-20 score, while in a small study (21) the estimate of the contribution of unshared environmental factors was between 44 -61% (22).

Both studies reported that unshared environmental influences accounted for most of the variation in difficulties identifying feelings, DIF, difficulty describing feelings DDF, and externally orientated thinking EOT (21,22)


Environmental Influences on Alexithymia

Environmental factors are a major determinant of individual differences in alexithymia. family factors, such as pathological family interactions (17), dysfunctional family environment in childhood (4), poor family expressiveness (5,37), perceived dysfunctional parenting (6,7), living in a broken family (38), and childhood emotional, sexual, and physical abuse (8-10) have been demonstrated (oo)

Alexithymia may be particularly troublesome for those who have experienced past trauma (44).

In the development of alexithymia, psycho-analytic attachment theories stress the importance of significant others in childhood (37, 38) with evidence suggesting that alexithymia is related to dysfunctional parenting (39).

A high incidence of insecure attachment (developmental trauma) has furthermore also been documented with evidence that this can affect emotion processing and regulation (32).

Mothers of insecurely attached children often speak about external events rather than their child’s emotional states that lead to difficulty in recognizing and expressing emotions.

This may also influence externally orientated thinking styles.



Although alexithymia is seen in association with co-occurring conditions such as depressive [56, 57] and anxiety [58] disorders,  it may represent a separable construct from co-occurring disorders  [60], as  not all individuals with co-occurring alexithymia and substance dependence demonstrate affective disorders [44•].

Alexithymia may also be associated with affect and cognitive regulation regardless of the presence of other mental illnesses, with the tendency of alexithymia individuals to instead identify emotion as physiological distress [61] and this distress may be independent of any co-occurring affective disorder.

One study of eating disorders demonstrated evidence of a global emotion-processing deficit independent of affective disorders, such as anxiety and depression (the so-called co-morbidities of DSM V) (13).


Alexithymia and Addictive Behaviour

 The prevalence of alexithymia in alcohol use disorders has been suggested to be as high as 78 % [ooo]

Other studies report prevalence to be between 45% and 67% (T) while research has shown 50% in other SUDs [52-54) are reported, compared to between 8,10 or 15% in the general population (55).

Research also suggests a high prevalence of alexithymia in behavioural addictions, with 56% in bulimia and 63% in anorexia nervosa (56), pathological gamblers 44% (57), 41% in posttraumatic stress disorder (58), with 25.1% and 20.2% reported in two studies looking at alexithymia and sexual disorders (59, 60), pointing to a common emotion processing deficit pathomechanism in both substance and behavioural addictions.

Finn, Martin and Phil (1987) investigated the presence of alexithymia among males at varying levels of genetic risk for alcoholism, finding that the high risk for alcoholism group was more likely to be alexithymic than the moderate and low genetic risk groups (38).

Based on genetic and familial influence, a higher percentage of alexithymia may be expected in parents and other family members of alexithymic patients.

Research has shown that high alexithymic substance use disorder patients were also more likely to have fathers or both fathers and mothers with alcohol problems compared to low alexithymic SUD-patients.

Interestingly paternal family history of alcoholism (FHA) may also relate to the degree of alexithymia, independent of disturbed family functioning.

A study on eating disorders showed that neither level of emotional awareness scores nor alexithymia scores were correlated with the duration of illness which suggests that emotional internal life impoverishment is not due to the severity of the disorder.

The emotion processing deficit may predate the occurrence of the disease, potentially favouring the development of eating disorders. This hypothesis is in line with the point of view of some authors who consider alexithymia to be a predisposing factor in addictive behaviours (Taylor, 1997a, 1997b).


References to follow

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