Theories of Addiction

Addiction As a Brain Disorder of Emotion Regulation – Part 4

Addiction As a Brain Disorder of Emotion Regulation

Fourth and Final Part


Alexithymia as Stress Dysregulation 


In this section, we further focus on the specific neural mechanism implicated in alexithymic emotion processing and how it prompts a more maladaptive motor-expressive responding to emotion experience in decision making rather than adaptive cognitive processing of emotion.

This may be the specific endocrinological mechanism, underlying emotion processing deficits and in distress-based decision making.

In other words, the inability to modulate emotions (and process) leading to a discharge of tension arising from unpleasant emotional states through impulsive acts or compulsive behaviors may also be explained in terms of stress dysregulation,  in prolonged elevations of the autonomic nervous system (ANS) and neuroendocrine systems (Taylor 1997).

A study which examined the association of alexithymia, with it’s subfactors according to Toronto Alexithymia Scale (TAS), on cortisol response, found that alexithymia was associated with significantly increased cortisol at baseline but not during stress exposure.

This increased cortisol was linked to ‘‘the difficulty in describing feelings’’ factor (DDF) of TAS.  Subjects in this study scoring low on this factor increased their cortisol from low value at onset to high value at peak whereas high scorers already evidenced maximal cortisol in anticipation of stress.

The authors concluded that the DDF subfactor may be related to the finding that affect labelling decreases amygdala activation in response to affective stimuli (Lieber man et al., 2007) as impaired labelling of DDF might increase amygdala activation, to modulate the anticipation of the stressor rather than the response to the stressor itself and resultant cognitive processing of emotions.

Instead of dampening amgydaloid activity (and subsequent neuro-endocrine release) in order to identify and label emotion in order to cognitively process, alexythmics may do the opposite.

They appear to increase amgydaloid and neuro-endocrine activity, which recruits more automatic, implicit and motoric regions in responding to affective stimuli. Emotion is thus not labelled as a resource to be cognitive processed but almost treated in a compulsive threat or “fight or flight” stimulus; an undifferentiated emotion distress relieved via motoric responding.

Other studies have had similar findings, showing the ability to differentiate emotion was related to autonomic reactivity XXX  that alexithymic patients exhibited higher levels of executive dysfunction, psychological distress, norepinephrine-to-cortisol (NE/CORT ratio explain) which was also associated with greater difficulty describing feelings  XXXX, which highlights a probable neural mechanism for “distress-based” impulsivity.

Other studies have shown similar results; that increased HPA activity was again related to only one alexithymia subfactor, the difficulty in differentiating feelings and distinguishing them from bodily sensations and emotion arousal. XXXXX

These findings are consistent with the idea that alexithymic deficits are specific to processing emotional arousal, and suggest difficulties with parasympathetic control and emotion regulation XXXXXX


Implications for Treatment


Alexithymia and Treatment Outcome

Alexithymia is also frequently seen in participants who are undergoing drug abuse treatment [36], and research has suggested that alexithymia itself may be a difficult characteristic to change.

Alexithymia in healthy populations appears stable, as evidenced in a large sample after an 11-year follow-up period [40•]

In addition, if alexithymia were brought upon by drug dependence, then cessation of use may reduce alexithymia symptoms.

However, alexithymia did not change over an 8-week course of treatment using computerized cognitive-behavioral therapy (CBT) [44•].

Similarly, other treatment comparison studies in populations with cocaine use disorder [45] and polysubstance-use disorders [46] also revealed no change in alexithymia scores over time, regardless of the type of treatment delivered. Alexithymia also remained stable over a 6-week course of treatment in individuals with polysubstance-use disorders [47•]

In 60 men with alcohol-use disorders in outpatient treatment, those with higher alexithymia reported more episodes of relapse after 1 year than those with low levels of alexithymia [53]

Speranza and colleagues (2007) found that alexithymia predicted eating disorder treatment outcome in a three year prospective study meaning high levels of alexithymia can interfere with treatment response even more than the actual severity of the presenting problem (61).

Although alexithymia seems a difficult stable characteristic to address in treatment, improvements in emotion processing and in regulation are reported as being important to longer term abstinence and recovery.

Alcohol-dependent patients reported significant differences in emotional awareness and impulse control during week 1 of treatment. Significant improvements in awareness and clarity of emotion were observed following 5 weeks of protracted abstinence (2)

Abstinent cocaine abusers have shown reduced metabolism in left anterior cingulate cortex (ACC), greater activation in right ACC and right dorsolateral prefrontal cortex (DLPFC).

Interestingly the abstinent groups of cocaine addicts showed more elevated activity in the DLPFC, a finding that has also been observed in abstinent marijuana users (8) and the elevation of frontal activity also appears to undergo a shift from the left to right hemisphere over the course of abstinence.  The right is used more in processing (labelling/identifying) of emotion.

Although alexithymic type emotion processing deficits may persist they can improve via abstinence and recovery.


Summary and Conclusion


The areas of the emotion processing and regulation network implicated in alexithymia are also those implicated in premorbid vulnerability and across a range of addictive behaviours.

These area must then be crucial areas to address in recovery from these conditions.


As this was an academic paper, we have not mentioned much of 12 step recovery which helps in a multitude of ways in addressing this deficit in emotion processing and regulation. Not only do the 12 steps  alleviate the accumulated emotional distress of the past, a number of recovery practices are essential in improving emotion awareness, processing and regulation. These including “sharing” emotions at meetings or privately with sponsors and other recovery buddies and reappraising, via daily “stop checks”, emotional well being.

In early recovery describing distressing emotions to other helps with the identifying, labelling and processing or emotion so that subsequent regulation is more optimal.  This process of allowing others to help with processing emotions in turn helps develop areas of the brain implicated in emotion processing. This has positive effects on long term recovery.

These above reasons may be some of the reasons “How It Works” to quote 12 step literature?


References to follow


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