Addiction as a Brain Disorder of Emotion Regulation
Neural networks of emotion processing deficits – Alexithymia and addictive Behaviour
Neural Correlates of Alexithymia
Neuroimaging data show higher degrees of alexithymia are associated with altered structure/function in emotion-related brain regions including the insula, ACC, vmPFC, and amygdala ().
Structurally, alexithymia has been directly related to gray matter volume reductions in the insula, ACC, and vmPFC (). Similarly, poorer emotional intelligence and interoceptive awareness, indirect features of alexithymia (), have been linked with gray matter reductions in right anterior insula (aI), dorsal ACC, and vmPFC ().
Some studies have emphasized a right hemisphere deficit in alexithymia [8,9] based on the hypothesis that right hemisphere plays a more important role in emotion processing than the left [10, 11].
More on corpus callosum – dysfunction of the corpus callosum can result in a person experiencing basic emotional feelings but with no conscious cognition concerning these feelings (oooo).
Neural Correlates in Addictive Behaviours
These models of the regions implicated in alexithymia may interact with each other and may also map onto brain regions morphological vulnerability mentioned as being prevalent in addictive behaviours such as with alcoholics.
Magnetic resonance imaging and post-mortem neuropathological studies of alcoholics indicate that the greatest cortical loss occurs in the frontal lobes, with concurrent thinning of the corpus callosum. One might speculate that thinning of the corpus collosum may contribute more generally to emotion processing difficulties (15 ). The inability to identify and describe affective and physiological experiences is itself associated with the elevated negative affect (16) commonly seen in alcoholics, even in recovery (17).
Another study suggested all of the critical areas of alcoholism-related brain damage are important for normal emotional functioning (14).
Cocaine abuse blunts responses in regions important to emotional regulation (15) with reduced grey matter in brain regions critical to executive function, such as the anterior cingulate, lateral prefrontal, orbitofrontal and insular cortices (19-24) (00000).
Men with Gambling Disorder show relatively diminished BOLD signal change in vmPFC. (000000), an area which modulates amgydaloid activity (Cyders) and implicated in Negative Urgency; the disposition to engage in rash action.
Other behavioural addictions also show alteration to the emotion regulation network (Y) and also in response to the increasing cumulative exposure to adverse life events of those who have experienced maltreatment.
All areas are involved in stress, emotion and reward regulation, impulse control and maladaptive decision making.
Vulnerability and Resilience
One study (9), demonstrated relatively increased cerebral blood flow (CBF) in bilateral amygdala and vmPFC and relatively decreased CBF in bilateral insula, right dorsal anterior cingulate cortex (ACC) in high-risk adolescents for an alcohol use disorder (AUD).
As insula and ACC interaction is important to emotional processing ( ), at risk adolescents may have a reduced ability to label and process emotions combined with a tendency to recruit more subcortical regions in emotional responding.
FMRI studies have found reduced BOLD response in adolescent alcohol abusers in brain regions important affective decision-making (13).
In adolescents, the children of individuals with alcohol-use problems demonstrate increased alexithymia that interacts with executive dysfunction in a manner that may raise the risk for future substance use .
A correlation between a component of alexithymia (the DFF factor on the TAS-20) and family history of substance-use problems, also suggests that alexithymia may exist as a vulnerability factor.
A protective factor in FH+ families may be the ability to process and regulate emotions.
In one study, resilient high-risk youth had enhanced monitoring of emotionally arousing stimuli, even compared to typically developing youth ( ).
A Historical Perspective on Addictive Behaviour
Where Psycho-Analytic and Neuroscientifc theories meet
It is illuminating to now consider how aspects of our proposed model have been considered in theories of addiction (mainly with a psycho-analytic focus) as far back as the 1930s.
Affect centred theories of addiction are not a recent development as clinicians have long considered addictive behaviour as the consequence of a failure to cope with distressing, negative, and particularly, undifferentiated emotions. (26)
Rado in 1933, described substance use as a way of coping with these excessively difﬁcult states of emotions (27).
Krystal and Raskin (1970) emphasized the role of undifferentiated emotions of persons suffering from addictive disorders (28). They suggested these emotions are ﬁxed at this level owing to the traumatic nature of the early life of many addicted individuals.
This point is particularly pertinent considering the widespread extent of childhood maltreatment in addicted populations (29-31). Alexithymia may be particularly troublesome for those with developmental trauma as various studies have shown how insecure attachment is associated with alexithymia and addictive behaviours such as alcohol-dependence (40-42).
Individuals are thus posited as using alcohol to escape feelings of rejection and establish a “secure attachment base” (43). Their substance use can thus be recognized as an attempt at “self-treatment.” The self-medication hypothesis of Khantzian (1985) posits the self medicating of overwhelmingly painful emotions (47).
Taylor et al. 1990 also hypothesized that substance abusers take drugs to help manage unpleasant emotional states, which are experienced as unmanageable because of difficulty in understanding and effectively dealing with those emotions () as the result of difficulty in identifying and describing feelings, and difficulty in differentiating feelings from bodily sensations, similar to the interoceptive (a sensitivity to stimuli originating inside of the body confusion proposed by the psycho-analytic theory of Hilde Bruch) which is also associated with attachment style and insecure attachment to primary care givers ( ).
Wurmser (1974), also suggests people with addictive disorders are unable to regulate their undifferentiated feelings, impulses, and pervasive internal stress, and so they turn to psychoactive substances (46).
Particularly relevant to our discussion is Wurmser’s connection between undifferentiated feelings and impulses.
Clinical observations also highlight primarily the presence of undifferentiated, overﬂowing, dominantly negative and painful feelings, and difﬁculties in emotional expression and emotional regulation in addicted individuals, which leads, as identified by MacDougall (1984), to substance use as a compulsive way of canalizing these overﬂowing emotions (45).
Besides clinical observations (11), empirical studies have also shown that people with addictive disorders have difﬁculties with the verbalization and expression of their feelings (48-50).
What is most illuminating is that the unpleasant “undifferentiated emotional” experience of early, mainly psycho-analytic, theories, and associated with alexithymia, is now supported by present day neuroscientific study which demonstrates that it may be these undifferentiated emotion states which prompt individuals to engage in maladaptive addictive behaviors in an effort to regulate emotions.
This historical perspective, married to more recent neuro-scientific research, highlights how it is alexithymic-type characteristics manifest as emotion processing deficits which prompt maladaptive behaviours and that these processing deficits are often genetically inherited, adversely affected by both trauma and development trauma, which results in a developmental delay disorder (brain disorder) regarding the processing of emotion.
Next we begin to explain the neural mechanism through which undifferentiated emotion states prompt individuals to engage in maladaptive addictive behaviors in an effort to regulate emotions.
Particularly as alexithymia has also been shown to mediate the relationship between childhood maltreatment (Gaher, Arens, & Shishido, 2013) and trauma history (Gaher, Hofman, et al., 2013) and urgency, suggesting that deficits in emotional understanding may underlie urgent responding.
How emotion dysregulation prompts impulsive behaviour?
In this section, we posit that individuals with high levels of alexithymia, act rashly in an attempt to immediately reduce psychological and physiological sensations associated with undifferentiated (unpleasant/distressing) emotion states. In other words, negative urgency could be the mechanism that drives dysregulated behaviors in individuals who experience difficulty recognizing and expressing their emotions.
Negative urgency describes the disposition to engage in rash action when experiencing negative affect (5).
A common behavioral measure of impulsivity is the delay discounting task which measures the degree of temporal discounting. Participants are faced with the choice of a small immediate reward, or a larger delayed reward; choosing the smaller immediate reward indicates a higher degree of impulsivity.
Substance users frequently make decisions with a view to immediate gratification (6-10.
Increased discounting of larger delayed rewards has been found in heroin- (13), cocaine- (14), and alcohol (15 -17) – dependent individuals, and other addictive behaviours, such as eating, gambling and hyepersexual disrorders (oooooo)
Various studies have demonstrated delay discounting in high risk individuals (ooooooo)
Also heavy alcohol use during adolescence is also related to poorer neuropsychological functioning, including response inhibition (2), and decision-making (6).
Studies suggest that Negative Urgency may prompt individuals who score high on alexithymia to engage in maladaptive behaviors more than individuals with low scores.
To summarise, it may that low alexithymic individuals rely on reflexive affective (emotional) processes rather than on reflective cognitive processes, to lead their behaviours (Lieberman, 2007; Metcalfe & Mischel, 1999) as the confusing affective experience inherent to alexithymia may be quite upsetting (or unpleasant) and could lead to negative urgency, or a tendency to act rashly to avoid it.
Modelling Distress-based Decision Making
The Iowa gambling task (IGT) was developed to assess decision-making processes based on emotion-guided evaluation.
In one study, using the IGT, nonalexithymics showed activation in the bilateral insula and ACC whereas this was not found in alexithymics who instead showed activation in the caudate, an area of the dorsal striatum implicated in regulation of impulsivity and disinhibition ( ).
Comparison between alexithymics and nonalexithymics also reveals that alexithymics show lower CBF in the vmPFC, an area associated with the use of internal signals accompanying affective evaluation of stimuli, crucial for successful decision-making.
The implication is that alexithmic subjects were not using brain functions related to emotion-based biasing signals.
In another IGT study, children with a family history of alcoholism (FH+) showed greater relative activation in the left dorsal ACC, a region implicated in emotion processing and initiation of motor behavior () and the caudate nucleus ().
This bias in brain decision-making systems towards more motor expressive responding may be an underlying elevated risk for alcoholism.
Measuring Distress Based Compulsivity
These dysregulated physiological responses over many years may result in untoward health effects such as drug and behavioural addiction.
In one study male cocaine-dependent patients also failed to activate the ACC cingulate and other paralimbic regions during stress imagery, suggesting dysregulation of control under emotional distress in these patients (). The greater activation associated with alexithymia in men in the right putamen during stress is broadly consistent with earlier studies implicating the dorsal striatum in emotional motor responses.
References to follow.
Categories: the aetiology of addiction, Theories of Addiction
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