Is the Impulsive Behaviour that Precedes Addiction Hardwired into the Brain?

In various blogs we have forwarded the idea that emotional and stress dysregulation are that the heart of addiction and alcoholism and are also possible present in those at risk to these disorders.

Essentially we suggest that the behavioural endpoint of addictive behaviours, the distress based impulsivity (negative urgency) seen in alcoholics and addicts which shapes decision making may be the consequence of chronic neurotoxic activity (as the consequence of chronic alcohol and drug use)  on brain areas which have a pre-existing impairments or vulnerability such as brain regions involved in emotional regulation, processing, inhibition and stress and reward response.

Here we cite an article (1) which looks at some of these brain regions, specifically those involved in emotional regulation and impulsivity and considers whether these deficits may be “hardwired” into the brain in terms of white and grey matter impairments.

 

Brain areas actively developing during adolescence include the prefrontal cortex, limbic system areas, and white matter myelin ( electrically insulating material that forms a layer, the myelin sheath – the yellow insulation below), usually around only the axon of a neuron. It is essential for the proper functioning of the nervous system.)

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These areas serving cognitive, behavioral, and emotional regulation may be particularly vulnerable to adverse alcohol effects.

Alternatively, deficits or developmental delays in these structures and their functions may underlie liability to accelerated alcohol use trajectories in adolescence.

The prefrontal cortex, limbic brain regions, white matter ( composed of bundles of myelinated nerve cell axons which connect various grey matter areas (the locations of nerve cell bodies) of the brain to each other (see below – grey on outside, white inside) and carry nerve impulses between neurons. Myelin acts as an insulator, increasing the speed of transmission of all nerve signals, and reward circuits undergo active development during adolescence (Chambers et al., 2003; Spear, 2000).

 

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These structures and their functions, involving behavioral, emotional and cognitive regulation, may be particularly vulnerable to the adverse effects of alcohol exposure during adolescence.

Delays or deficits in the development of neural substrates necessary for these psychological regulation abilities to fully develop may be termed neurodevelopmental dysmaturation.

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Psychological Dysregulation

The development of accelerated alcohol involvement in adolescence is not an isolated phenomenon, but is typically presaged by persistent behavioral characteristics including attentional deficits, conduct problems, and irritability (Chassin et al., 1999; Clark et al., 1997a, 2005; Tapert et al., 2002).

Two main psychological factors have been identified: (1) Behavioral Undercontrol, comprised of conduct disorder symptoms and personality characteristics including aggression and diminished constraint, and (2) Negative Emotionality, comprised of depression, anxiety and stress reactivity variables (Martin et al., 2000).

These two factors were significantly correlated. These correlated characteristics have been hypothesized to comprise the early phenotypic manifestations of a core liability for SUDs (Tarter et al., 1999).

The proposed construct manifested by these psychopathologic features has been termed psychological dysregulation (Clark and Winters, 2002). Psychological dysregulation is a deficiency in the ability to regulate attention, emotions and behavior in response to environmental challenges. Psychological regulation is thus the ability to modulate prepotent responses in order to optimize reward opportunities. The skills involved in psychological regulation include executive cognitive functioning (ECF), behavioral inhibition and emotional management.

Deficiencies in psychological regulation may be the result of delays or persistent deficits in the acquisition of behavioral, emotional, and cognitive regulation skills.

Adolescents at risk for developing SUDs exhibit deficits in psychological regulation. Childhood psychological dysregulation, or neurobehaviour disinhibition, correlates with parental substance use disorders (SUDs) and prospectively predicts adolescent alcohol and other substance use as well as related disorders (Clark et al., 2005; Tarter et al., 2003).

The psychological dysregulation dimension integrates several psycho patholological dimensions heretofore considered distinct, including affective disorders and SUDS themselves (Krueger et al., 2002).

Neurobiological Basis of Psychological Dysregulation

The functions subsumed under the construct of psychological dysregulation are thought to be served by the prefrontal cortex (Koechlin and Summerfield, 2007). The capabilities that comprise psychological regulation improve during adolescence (Levin et al., 1991; Welsh et al., 1991). The ongoing development of the prefrontal cortex has been hypothesized to be the primary neurobiological foundation for the advancement of these abilities (Happaney et al., 2004; Spear, 2000). Developmental abnormalities in the frontal cortex have been found in children and adolescents with behavioral problems reflecting psychological dysregulation (Rubia et al., 2000; Spear, 2000).

Diffusion tensor imaging (DTI) studies  indicated that white matter organization increases from early childhood to young adulthood (Klingberg et al., 1999; Nagy et al., 2004; Schmithorst et al., 2002; Zhang et al., 2005).White matter development may underlie advancing executive functioning. The prefrontal cortex is a brain region undergoing relatively late gray matter pruning, and volumes of gray matter appear to decrease over adolescence (Gogtay et al., 2004; Lenroot and Giedd, 2006; Sowell et al., 2001, 2004). Unlike grey matter volume, white matter volume appears to increase during adolescence, particularly in the prefrontal area (Ashtari et al., 2007;Barnea-Goraly et al., 2005; Lenroot and Giedd, 2006).

 

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White Matter Development and Alcohol Exposure

Selective white matter loss has been reported among adults with Alcohol Use Disorders (AUDs) (Carlen et al., 1978, 1986) and with fMRI (Agartz et al., 2003), and postmortem specimens (Krill et al., 1997).  Compared with controls, adolescents with AUDs have been found to have smaller prefrontal white matter volumes (DeBellis et al., 2005). Prefrontal grey and white matter volumes were compared in adolescents with AUDs. Compared with control subjects, subjects with AUDs had significantly smaller prefrontal white matter volumes.Marijuana use has also been found to be associated with smaller white matter volumes in adolescents (Medina et al., 2007b). While these volumetric findings suggest problematic frontal development among adolescents with AUD, the emergence of neuroimaging techniques developed to examine white matter organization may prove to be more specifically relevant to understanding the effects of alcohol on neurodevelopmental maturation.

Changes in gene expression may be involved in alteration of white matter structure in AUDs.  In a postmortem study, myelin-related genes were found to be down-regulated in the AUD group (Lewohl et al., 2000).

While evidence has been presented that alcohol consumption may disrupt white matter organization, the possibility remains that delayed or diminished white matter organization may presage alcohol involvement and constitute a risk factor for AUDs. Immaturity of white matter development and the related deficits in the functional integration of brain areas may in part explain individual differences in psychological regulation during adolescence. For example, disruptive behavior disorders in childhood, particularly conduct disorder, have been found to predict accelerated trajectories of alcohol use, cannabis use, and substance-related problems in adolescence (Clark et al., 1999).

Limbic System Development and Alcohol Exposure

The limbic system is central to the processing of affective stimuli, the successful formation of new memories, and the implementation of related responses. Limbic system structures, including the hippocampus and amygdala, may be susceptible to alcohol-induced dysmaturation.

Smaller hippocampal volumes have been reported in adults with AUDs compared with control adults (Sullivan et al., 1995). As hippocampal development progresses in adolescence (Gogtay et al., 2006), this brain area may be particularly susceptible to the adverse effects of alcohol involvement during this developmental period.

DeBellis et al. (2000) compared the hippocampal volumes of 12 adolescents and young adults with adolescent-onset AUD to those of 24 control subjects. Both left and right hippocampi were significantly smaller in AUD subjects compared to the volumes in controls. Specifically, left hippocampal volumes were smaller in teens with AUD than demographically similar controls, and youth with greater severity of AUD had the smallest left hippocampal volumes (Medina et al., 2007a; Nagel et al., 2005).

The amygdala may also be important for understanding the neurodevelopmental effects of alcohol exposure. The amygdala, along with ventral striatum, has been hypothesized to be involved in reward mechanisms and thereby critical for understanding alcohol use trajectories (Koob, 1999). Amygdala volumes have been found to be relatively smaller in high-risk older adolescents and adults with SUDs compared to that in control subjects (Hill et al., 2001; Makris et al., 2004). Lack of correlation with use levels has led to the suggestion that this may be a predisposing characteristics rather than a substance effect.

Interacting brain areas are involved in reward processing (McClure et al., 2004), motivation (Chambers et al., 2003), and decision-making (Verdejo-Garcia et al., 2006).  The interactions between the prefrontal cortex and subcortical areas, including the amygdala and nucleus accumbens, constitute the neurocircuitry involved in reward responding. In the affective component of reward responding, the amygdala appears to be a network node involved in reactivity to emotional stimuli (Hariri et al., 2006; Schwartz et al., 2003). An understanding of the adolescent development of neural circuits underlying reward processing and decision making is central to considering the role of these systems in the development of alcohol involvement.

Impulsivity, defined as acting without forethought, progressively decreases from childhood into adulthood. This change has been thought to occur as a result of neuromaturation in the prefrontal cortex (Casey et al., 2005).

The generation of behaviors optimizing long-term reward opportunities often involves behavioral inhibition. The activation of prefrontal cortical areas during response inhibition tasks has been found to increase from childhood through adolescence, a change corresponding to the development of abilities to suppress prepotent behaviors (Luna and Sweeney, 2004; Luna et al., 2004). The ability to select an optimally adaptive behavioral response while suppressing a predominant or prepotent response with problematic consequences defines impulse control and is fundamental to psychological regulation skills. Improved abilities in response inhibition and related prefrontal activation during adolescence are thought to involve maturation of functional connectivity subserved by ongoing myelination.

Adolescents with psychopathology predictive of SUDs, similar to adults with alcohol dependence, have difficulty with behavioral inhibition during laboratory tasks (Bjork et al., 2004a; Dougherty et al., 2003; Schweinsburg et al., 2004). Furthermore, adolescents with histories of substantial marijuana use, compared with control adolescents, showed more activation in frontal cortical areas during behavioral inhibition tasks (Tapert et al., 2007). More activitation suggests greater effort was required by the marijuana using group.

 

References

1.  Clark, D. B., Thatcher, D. L., & Tapert, S. F. (2008). Alcohol, psychological dysregulation, and adolescent brain development. Alcoholism: Clinical and Experimental Research, 32(3), 375-385.

 

AA helps to reduce Impulsivity

 

One constant in studies on addiction and in alcoholism, in particular is the  fundamental role played by impulsivity in these disorders. It is seen to be present in early use but appears to be more distress based (i.e. more negative urgency based) as the addiction cycle becomes more chronic. This impulsivity has obvious consequences for propelling these disorders via impulsive behaviours and decision making difficulties.

Thus it then follows that any treatment of these addictive disorders must have treatment of impulsivity at the core as it appears to a fundamental pathomechanism.

 

Here, we review a study that on links  AA attendance and reduced impulsivity using a 16-year prospective study of men and women, who were initially untreated for their drinking problems. Across the study period, there were significant l decreases in impulsivity, and longer AA duration was associated with reductions in impulsivity.

Alcoholics Anonymous (AA) is linked to improved functioning across a number of domains [2,3]. As the evidence for the effectiveness of AA has accumulated, so too have efforts to identify the mechanisms of change associated with participation in this mutual-help group [4].

This study concluded that help-seeking and exposure to the “active ingredients” of various types of help (i.e., AA principles/practices, sponsors), which, in turn, leads to improvements in reduced impulsivity.

Impulsivity is typically higher among individuals in AUD treatment than among those in the general population [5] and, impulse control deficits tend to predate the onset of drinking problems [6-9].

Contemporary research has revealed that traits such as impulsivity can change over time [10]. Mutual-help groups like AA may promote such changes, given that they seek to bolster self-efficacy and coping skills aimed at controlling substance use, encourage members to be more structured in their daily lives, and target deficits in self-regulation [11].

 

impulse control.preview

 

Such “active ingredients” may curb the immediate self-gratification characteristic of disinhibition and provide the conceptual grounds to expect that AA participation can press for a reduction in impulsive inclinations. In turn, given the range of outcomes related to impulsivity (e.g., legal, alcohol-related, and psychosocial problems), decreases in impulsivity may account for part of the association between AA participation and improvements in these outcomes.

AA’s vision of recovery as a broad transformation of character [12], and  explores individual differences in emotional and behavioural functioning as potential mechanisms of change (13,14).

Such groups encourage members to be more structured and goal-directed, which may translate into greater efforts to delay gratification of one’s impulses and  to improve clients’ general coping skills (e.g., reduce avoidance coping).

Given that impulsivity is a risk factor for a host of problematic behaviors and outcomes beyond drinking-e.g., criminality [15], drug abuse [16], reckless driving and sexual practices [17],  lower quality of interpersonal relationships [18], and poor health [19] this reduced impulsivty is beneficial in other aspects too.

Notably, this effect was buffered by a higher quality of social support-a probable active ingredient of AA. Thus, the impact of reducing impulsivity may be widespread across a range of outcomes that are critical for long-term sobriety.

 

Our main caveat on this study is that it does not distinguish between different types of impulsivity and does not mention negative urgency (or distress-based impulsivity) which is more commonly seen is this sample group.

AA’s “active ingredients” may reduce distress, via a new found emotional regulation gained via the steps and use of a sponsor (acting as an external prefrontal cortex to help us inhibit our impulsive and distress based responses)  which in turns reduces our tendency to impulsive decision making and behaviour.

 

It would have been interesting in this study to have also measure how emotional dysregulation changed in the time span of 16 years (using the DERS scale) and to have used a different impulsivity scale i.e. used the UPPS-P scale which would both have helped more specificallylook  at the interaction of how emotional regulation and impulse control changed over the 16 year period.

 

References

 

1.  Blonigen, D. M., Timko, C., & Moos, R. H. (2013). Alcoholics anonymous and reduced impulsivity: a novel mechanism of change. Substance abuse, 34(1), 4-12.

2. Humphreys, K. Circles of recovery: Self-help organizations for addictions. Cambridge Univ Pr; 2004.

3.. Tonigan JS, Toscova R, Miller WR. Meta-analysis of the literature on Alcoholics Anonymous: Sample and study characteristics moderate findings. Journal of Studies on Alcohol. 1995

4. Kelly JF, Magill M, Stout RL. How do people recover from alcohol dependence? A systematic review of the research on mechanisms of behavior change in Alcoholics Anonymous. Addiction Research & Theory. 2009; 17(3):236–259.

5. Conway KP, et al. Personality, drug of choice, and comorbid psychopathology among substance abusers. Drug and alcohol dependence. 2002; 65(3):225–234. [PubMed: 11841894]

6. Caspi A, et al. Behavioral observations at age 3 years predict adult psychiatric disorders: Longitudinal evidence from a birth cohort. Archives of General Psychiatry. 1996; 53(11):1033. [PubMed: 8911226]

7. Cloninger CR, Sigvardsson S, Bohman M. Childhood personality predicts alcohol abuse in young adults. Alcoholism: Clinical and Experimental Research. 1988; 12(4):494–505.

8. Elkins IJ, et al. Personality traits and the development of nicotine, alcohol, and illicit drug disorders: Prospective links from adolescence to young adulthood. Journal of abnormal psychology. 2006; 115(1):26. [PubMed: 16492093]

9. Sher KJ, Bartholow BD, Wood MD. Personality and substance use disorders: A prospective study. Journal of Consulting and Clinical Psychology. 2000; 68(5):818. [PubMed: 11068968]

10. Caspi A, Roberts BW, Shiner RL. Personality development: Stability and change. Annual Review of Psychology. 2005; 56:453–484

11. Moos RH. Active ingredients of substance use focused self help groups. Addiction. 2008; 103(3):387–396. [PubMed: 18269361]

12. White WL. Commentary on Kelly et al. (2010): Alcoholics Anonymous, alcoholism recovery, global health and quality of life. Addiction. 2010; 205:637–638. [PubMed: 20403015]

13. Kelly JF, et al. Mechanisms of behavior change in alcoholics anonymous: does Alcoholics Anonymous lead to better alcohol use outcomes by reducing depression symptoms? Addiction. 105(4):626–636. [PubMed: 20102345]

14. KELLY JF, et al. Negative Affect, Relapse, and Alcoholics Anonymous (AA): Does AA Work by Reducing Anger? Journal of studies on alcohol and drugs.

15. Krueger RF, et al. Personality traits are linked to crime among men and women: Evidence from a birth cohort. Journal of abnormal psychology. 1994; 103(2):328. [PubMed: 8040502]

16. McGue M, Slutske W, Iacono WG. Personality and substance use disorders: II. Alcoholism versus drug use disorders. Journal of Consulting and Clinical Psychology. 1999; 67(3):394. [PubMed: 10369060]

17. Caspi A, et al. Personality differences predict health-risk behaviors in young adulthood: Evidence from a longitudinal study. Journal of Personality and Social Psychology. 1997; 73(5):1052. [PubMed: 9364760]

18. Ozer DJ, Benet-Martinez V. Personality and the prediction of consequential outcomes. Annu. Rev. Psychol. 2006; 57:401–421. [PubMed: 16318601]

19. Bogg T, Roberts BW. Conscientiousness and Health-Related Behaviors: A Meta-Analysis of the Leading Behavioral Contributors to Mortality. Psychological Bulletin. 2004; 130(6):887. [PubMed: 15535742]

 

 

 

 

 

 

 

 

Why erase addiction memories when they can help others?

According to one UK newspaper The Independent, dated the 9th July 2014 “Substance abusers could have their memories of drug addiction wiped in a bid to stop them using illegal narcotics, an award-winning neuroscientist has said.

According to new research by Cambridge University’s Professor Barry Everitt: disrupting the memory pathways of drug users could weaken powerful “compel” cravings, reduce “drug seeking behaviour” and open a new field of addiction therapy.

Professor Everitt  told this week’s Federation of European Neuroscience Societies (FENS) how his research in rodents had found that targeting “memory plasticity” in rats was able to reduce the impact of maladaptive drug memories.

He added that this knowledge could offer a radical new method of treatment of drug addiction in humans, where researchers have already established that the path to addiction operates by shifting behavioural control from one area of the brain to another. This process sees drug use go from a voluntary act to a goal directed one, before finally becoming an compulsive act.

It was this process that Professor Everitt’s research is trying to “prevent” by targeting “maladaptive drug-related memories” to “prevent them from triggering drug-taking and replaces”.

In humans this could potentially be done by blocking brain chemicals.

“It’s the emotional intrusiveness of drug and fear memoirs that can be diminished, rather than an individual’s episodic memory that they did in the past take drugs or had a traumatic experience,” he told The Independent. “Conscious remembering is intact after consolidation blockade, but the emotional arousal [that] leads to drug seeking or distressing feelings of fear that are diminished.”

His research group discovered that when drug memories are reactivated by retrieval in the brain, they enter a pliable and unstable state. By putting rats in this state Professor Everitt was able to prevent memory reconsolidation by blocking brain chemicals or inactivating key genes.

In one study, the team diminished drug seeking behaviours by obstructing a brain chemical receptor linked to learning and memory, thus erasing memories, while in another study it found they could weaken drug use memories by altering a particular gene in the amygdala, a brain area processing emotional memory.

“Of course, inactivating genes in the brain is not feasible in humans,” the professor told FENS. “So we’re directing our research to better identify the underlying brain mechanisms of memory reconsolidation.”

He added: “We specifically examined how we could target these maladaptive drug-related memories, and prevent them from triggering drug-taking and relapse.”

So to recap, this new treatment is based on altering genes in rats!

There is no need to actually wipe an alcoholics’ addiction memories.

In fact it may be very counter productive to recovery from alcoholism. One 80 year old and hyper ecologically valid experiment into the mnemonics of “treating addiction memories”  has shown that by honestly looking at the consequences of one’s actions as the result of one’s alcoholic drinking that the positive associations of previous drinking were reappraised in light of the damage done to oneself, one’s loved ones and family and society at large.

Addiction memories via this profound reappraisal were then more accurately processed in long term explicit memory. Implicit schematic memory was also altered fro a self schema in which one is a drinking alcoholic to one in which one is a recovering alcoholic.

So-called positive associations in long term episodic and explicit memory were,  when labile via recall, then challenged and replaced by more accurate negative associations in long term memory – no memories needed to be erased just reappraised more accurately.

 

mad scientist

 

This type of ongoing experiment is happening on a daily basis at an AA meeting near you.

AA groups have found that memories need not be erased, with possible deleterious knock on effects on fear processing and amgydaloid performance, but rather memories simply need to be faced up to, and via honesty appraisal reprocessed more adaptively in long term memory.

This also means alcoholics in recovery can use their addiction memories in not only clearing away the wreckage of the past, repairing broken relationships with loved ones and society as a whole by  making amends to those involved in this wreckage and also put the memories of the past to excellent therapeutic use by using it to help others with similar memory difficulties.

In fact even academic researchers have found and have demonstrated that abstinent, treatment seeking individuals also have a different cognitive or/and memory bias to active alcoholics. This has been illustrated in findings that the greater “accessibility” for positive vs. negative alcohol- associations in heavy vs. light drinkers was not found to be generalized to alcoholics in treatment vs. social drinkers (2). Rather, there was a trend for treated inpatients, motivated to attain abstinence, to show greater availability and accessibility for negative alcohol-related information.

This is how to use memories of addiction to the best possible use, instead of erasing them, wiping them our and hoping for the best, memories of our addiction can be used to great purpose in helping others. Also “addiction memory” is often activated by those who have not come to terms with their alcoholism and still want to drink. Unless some one has come to terms with their alcoholism little can be done, by erasing memories or otherwise. These are sticking plasters on a gaping wound. They will be replaced with other “addiction memory” as there an underlying condition to alcoholism ( we believe it to be emotional regulation and processing deficits) and it is this that drives this fear-based condition called alcoholism, memories are the result of this malady. Address the underlying conditions and the rest takes care of itself.

It is not brain regions which are the problem either such as activation of the amgydala, it is how this sometimes errant and overactive brain region in alcoholics is tamed via the serenity found in the AA program of recovery.

The compel parts of the brain, Everitt mentions,  are activated by emotional distress, so treat the distress not the symptom of it. He also confuses implicit, automatic memory, with explicit, conscious memory. Either way they are both activated by stress/distress, and are thus both emotional memories.  Again treat the emotional dysregulation, the primary problem not the secondary manifestation of the problem.

As I mentioned above, there has been an ongoing experiment into recovery from alcoholism going on for nearly 80 years now, there is a lab in most areas of town.

It would benefit the world and science, in particular, if neuroscientists would pop in for a coffee and check our our findings.

 

References

2. McCusker CG  Cognitive biases and addiction: an evolution in theory and methodAddiction 2001;96:4756.

 

At Risk Adolescents have Emotional Dysregulation?

Following up from our previous blog on the abnormalities in the ventromedial prefrontal cortex  (vmPFC) in alcoholics,  brain regions which govern emotional regulation, we came across another study which appears to show that adolescents at increased risk for later alcohol use disorders (AUDs) may also be showing an emotion regulation difficulty.

This emotional regulation difficulty may be a biomarker for later alcoholism, which is in keeping with our previous proposals that an emotional processing and regulation difficulty or disorder underpins the aetiolgy of of alcoholism. In order words it is part of the pathomechanism – or the mechanism by which a pathological condition occurs- of later alcoholism.

 

 ventromedial-prefrontal-cortex

 

The area in this study, the vmPFC,   showed relatively increased cerebral blood flow (CBF) in bilateral amygdala and vmPFC and relatively decreased CBF in bilateral insula, right dorsal anterior cingulate cortex (ACC) and occipital lobe cuneus of high-risk adolescents. This suggests that adolescents at relatively high-risk for AUD exhibit altered patterns of resting CBF in distributed corticolimbic regions supporting emotional behaviors.

The authors’ hypothesized that the relatively increased amygdala and ventromedial prefrontal CBF may contribute to increased emotional reactivity and sensitivity to environmental stressors in these individuals while diminished insula/occipital cuneus and dorsal anterior cingulate cortex (ACC) CBF may lead to poor integration of visceral and sensory changes accompanying such emotional stress responses and top-down regulation of amygdala reactivity.

Thus we see our model in a snapshot even in adolescents potentially.  The emotional processing deficits we have discussed previously implicate the insula and ACC, as there appears to be a difficulty in alcoholics in reading emotional or somatic signals/states and integrating these signals into the identifying, labelling and processing of emotions. Equally there appears to be a hyperactivty in the vmPFC and amgydala as with alcoholics which implies emotional dysregulation, a hyper reactive emotional response and a tendency perhaps to a more “fight or flight” response, distress based impulsivity and short termist decision making, wanting it NOW rather than later.

 

References Lin, A. L., Glahn, D. C., Hariri, A. R., & Williamson, D. E. (2008). Basal Perfusion in Adolescents at Risk for Alcohol Use Disorders. In Proc. Intl. Soc. Mag. Reson. Med (Vol. 16, p. 60).

Predicting relapse via extent of emotional dysregulation?

Predicting relapse via extent of emotional dysregulation?

by alcoholicsguide

Even the most experienced counselors have difficultly spotting a recovering alcoholic in danger of relapse. Brain imaging scans might do a better job according to a study last year by researchers at  Yale University.

They suggested that alcoholics with abnormal activity in areas of the brain that control emotions and desires (reward) are eight times more likely to relapse and drink heavily than alcoholics with more normal patterns of activity or healthy individuals (1)

“These areas in the prefrontal cortex are involved in regulating emotion and in controlling responses to reward,” said Rajita Sinha, the Foundations Fund Professor of Psychiatry and professor in the Child Study Center and of Department of Neurobiology. “They are damaged by high levels of alcohol and stress and just do not function well.”

Or both perhaps, i.e. chronic alcohol use impacting on already impaired emotional regulation networks in the brain.

 

Figure6_ADHC_revised_2_7_12

 

This graphic highlights areas of the brain where Yale researchers found significant differences in responses to stress and relaxation-inducing stimuli between alcoholics and healthy controls. Alcoholics who exhibited such patterns of activity during fMRI scans were much more likely to relapse than alcoholics that more closely resembled control subjects.

Areas of the brain governing emotional regulation such as the ventromedial prefrontal cortex which suggests chronic difficulties in emotional dysregulation, which  potentiates the reward network, lying adjacent, and promotes higher relapse – click image for study. 

 

Ironically, the damage shows up on fMRI scans when alcoholics imagine being in their own most relaxing scenarios, like sitting at the beach listening to the waves, or taking a bubble bath. In non-alcoholics, these brain regions regulating emotion show markedly reduced activity during relaxing imagery, as anticipated. However, in alcoholics most likely to relapse, those brain regions remain hyperactive. On the other hand, when recovering alcoholics imagine their own recent stressful events, these control regions of the brain show little change, while in non-alcoholics, they show marked activation in response to stress. Such disrupted responses in areas of the brain governing emotions and reward lead to high cravings in the recovering alcoholic and an increased likelihood of subsequent relapse.

These brain scans in the future might serve as a diagnostic test to help professionals identify those most at risk of relapsing and suggest specific interventions to normalize brain function and prevent high rates of alcohol relapse, Sinha said.

“The findings show the prefrontal region is important for maintaining recovery for alcoholism,” Sinha said.

This is in accord with much of our writing in this blog – alcoholics, in recovery or otherwise, appear to have profound difficulties in regulating stress and emotion, as if the hyperactivity in the ventromedial pefrontal cortex, seen here, is indicative of a brain that never emotionally shuts off, is always on the go (whether this is the consequence of allostasis, the continual readjustment of the brain to stress needs to be further explored) and is primed to relapse effectively via a “fight of flight mechanism, or a distress based impulsivity.

 

References

Dongju Seo; R Todd Constable; Kwang-Ik Hong; Cheryl Lacadie; Keri Tuit; Rajita Sinha
Disrupted ventromedial prefrontal function, alcohol craving, and subsequent relapse risk.
JAMA psychiatry (Chicago, Ill.) 2013;70(7):727-39.

 

Maintaining emotional sobriety (and sanity) via Steps 10-12

When I have did my steps 4-7, noting the situations, the people, the institutions  that have caused persistent resentments in me, then examining what parts of my self have been affected,  I also, thanks to one sponsor was asked me to,  put down exactly what “sins” or defects of character I also experienced during these resentments. This jotting down of the exact sins I was in during these resentments  has proved to be very useful in my recovery ever since.  What I noticed was that I had the same array of sins or negatively (immaturely) expressed emotions in relation to all resentments regardless of the situation or the person I had the resentment, the same web of sins was weaved in every situation.  For me this shows clearly how I do not process and regulate my emotions properly, how it has a canalized form of reaction.

I have found increasingly in recovery that when I want someone or something to be the way I want it and it doesn’t go that way or I want something to stay a certain way or I believe someone is threatening to interfere or take away something that I have (when I am controlling basically), I find I respond by either being dependent or dominating of the person or situation. This is what Bill Wilson also found out in ten years or so of psycho-analysis with Harry Tiebout.

Immature emotional response I call this, followed by emotional reasoning. I rarely react in a balanced manner to these prompts. The situations invariably provoke a fear based response in me which somehow also leads to me suddenly becoming dishonesty in my thinking. It is as if this self centred fear as cut me off from the truthful sunlight of the spirit and I am suddenly in the dark shadow of dishonesty. In fact, according to Father Ralph honesty comes from the Greek to be at one with God funnily enough.

Then I feel shame as the result of my pride being hurt, which can lead to self pity it if I let it. I may also feel guilt. Then I may decide to strike back via being arrogant, impatient or intolerant, in behaviourally expressed sometimes as putting others down to elevate one self. Again immature emotional response. I am obviously also being self centred and selfish while in this process. I can also be envious or jealous of others in the midst of this for taking what I wanted or threatening what I have, like a child in the park or playground with friends. Other ways of fixing my feelings rear their heads and I can be gluttonous as a reaction or become greedy. Eat too much or go on a shopping frenzy. All instead of processing the emotions which are driving this behaviour I react, act out of distress based impulsivity. I can be so distressed that I can tend towards procrastination, which is sloth in five syllables. These sins or negatively expressed emotions truly grip me and these sins seem to  hunt in packs.

I found this fascinating when I first discovered this during my steps. It seemed to map the reactions of my heart when I react via resentments to the world. They describe accurately how I relate to the world especially when the world does not give me what I want or I have stood on it’s toes.

What else is this but an immature emotional reaction based not just on me being the same age as I started drinking  but also on the fact that the regions of the brain which govern emotional regulation in the brain of the alcoholic are immature, are smaller, not connected as well or do not function as well as healthy folk.  This is according to many academic studies and also seen in the brains of children of alcoholics, so our emotional brain regions may never have worked properly and thanks to years of alcohol abuse have gotten a whole lot worse.

When I am not in charge of my emotions they are in charge of me, in other words. They are controlling me and not the other way around. This type of emotional immaturity happens throughout the day sometimes. So there is no point waiting to the end of the day to do a step 10, to see when have I been fearful, dishonest, resentful or selfish. I have to do it continuously throughout the day to maintain my spiritual and emotional equilibrium, because it needs constant attention and maintenance, because I have no naturally maintained balance. I have to manage it. I impose homoestasis to an allostatic system. There is not naturally resting place. I am in charge of my serenity.

So I spot check continuously to ensure my emotional sobriety. Another word for sober is sane. I ike this because  while I am in emotional dysregulation or immaturity, I am far from sane. In fact, I am strangely deluded, distinct from from any reasonableness. I need to do my step ten to be restored to sanity.

The other problem with this emotional lability and dysregulation is that it send streams of distorted thinking into my head. I remember ringing my sponsor in early recovery, a few months in, with the startling relevation, to me,  that my thoughts were all leading me to a place of emotional pain. My emotional dysregulation leading to cognitive distortions which leads to further emotional dyregulation etc.  Spot the negative emotions underpinning these thoughts and they disappear like wispy evaporating clouds. This has similarities here with the practice of mindfulness.

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I do this all in a very simple way – I simply ask God to remove my sins, which are usually fear, dishonesty, pride, shame,guilt, self pity, leading to intolerance, arrogance and impatience and so on, warmed in a dendritic spreading across my heart and polluting of my mind with stinking thoughts.

It is interesting that in the 5th century a religious man called Evagrius Ponticus suggested that one gets rid of troublesome thoughts by pinpointing the negative emotions which were somehow underpin then and weight these thoughts in one’s mind, like anchors weighing down lassoed clouds. I do the same effectively.

I ask God to remove these emotions after I have first identified them and offered them to Him for help in removing. What I am doing, in a sense, is also identifying, labelling and letting go (processing) of the negative emotions that have kept these thunderous grey black clouds of thoughts in my head, and striking my heart with forked pain. I am asking God to help me do what I cannot do for myself it seems; namely emotional regulation.

People outside AA often wonder how this spiritual program can help people recover. As  I blogged about recently recently it does so, I believe partly, because it helps us learn how to practice identifying, labelling  and processing emotions (often by verbalising them to someone or via step 10)  in a way that is not only healthy and adaptive but in a way I was seemingly never able to do prior to coming into AA.  Or had never been taught to do.

I have learnt all these development skills not in my childhood but in my surrogate home of AA.  How many of us have come home in AA?

Processing the Past via the action steps, 4-12!

 

 

Processing the Past via the actions steps, 4-12!

by alcoholicsguide

How The Alcoholics Anonymous’ program of action helps with emotional dysregulation.

When I first came into recovery I was surprised how much more time I spent embroiled in thinking about past incidents and how I had numerous murderous resentments  about people who had supposedly done me wrong, than I did thinking about drinking.

The thought of drinking terrified me rather than enticed me. Fortunately it also made be nauseous and fortunately still does. A full year of vomiting on an empty stomach, throughout each and every interminable day and night, has had some aversion like effect.

I had literally hundreds of thoughts and negative emotions about the past streaming through and around my aching head and piercing my heart. They were like toxic mind darts that flipped my guts and almost made me physically ill. Even thinking back now makes me feel queasy.

It was a constant state of emotional distress, those early days of recovery.

I was shocked as the weeks trudged on painfully that I seemed to have problems other than the drink. I was reassured by many other AAs in meetings when they shared about how difficult life was on life’s terms – how they struggled with resentments and fears and their “emotional disease”. I was was glad it wasn’t just me.

I had finally found a club where I fitted in! After all these years. In fact most people I drank with were also alcoholic! So I have always sought the company of my own. I thought we could only be found in pubs! And here we had rooms of them talking about trying to stay “emotionally sober”. It wasn’t just sobriety it had to be emotional sobriety. I was, through my fading eyesight and mercifully abating alcoholic psychosis, greatly intrigued by this. My life, and their lives, had become unmanageable, they said,  not just because of the drink, but because of some underlying condition.

I was especially interested in why I was so cursed by memories of my past. Why hadn’t they gone away? Why had they come back so prolifically in early recovery. The alcohol must have keep some of them suppressed, at bay. Now they were teeming through, poisoning my mind just as effectively as any alcoholic withdrawal or rattling hangover ever did. It was difficult not to somehow see these rampant, rampaging negative thoughts and emotions as akin to a disease. When they spoke of spiritual disease, it seemed to describe what was happening in my head.

I have “done” the steps three times and each time has offered more insight into this spiritual malady which I call an emotional disease. Why? Well because the sure sign of a spiritual malady, I believe,  is the expression and lack of control over negative emotions. The emotional lability and volatility. The bad temperedness, the indignition at life’s flaws, the perfectionism, the need to control, the righteous anger. We sin via these negative emotions. Have you ever heard of someone sinning via positive emotions? “Yes he wronged me by being so kind and generous, thoughtful and loving, to hell with that man!” So why are we so scared of the e word, emotion.

We sin via, or have defects of character which are, negative expressions of emotion. Intolerance, or impatience, selfishness, fear based dishonesty and so on. All expressions of distress. A fear based illness?  I like the term defect of character because it suggests sometime intrinsic to alcoholics. I call this inherent aspect of this condition called alcoholism, emotional regulation and processing difficulties.

In this blog I will attempt to explain how the 12 steps of AA, principally the action steps 4 through to 12, have not only connected me with a power greater than myself  but they continue to treat, on a daily basis, my unmanageability.  An  unmanageability caused inherently by my difficulties processing and regulating emotions.

 

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I have looked hard for supporting evidence to substantiate what I am about to write and found this link to an interesting piece on the use of EMDR and other therapies in treating the unprocessed emotions caused by emotional dysregulation in those who suffer from trauma. I have used aspects of this to make it applicable to alcoholics. I believe profoundly that steps 4-12 facilitate a profound alteration in our ability to regulate and process emotions.

Steps 4 -7,  in particular help us to embed the numerous unprocessed memories from childhood onwards, that all seem to have been tied together in a terrible mnemonic mesh by aspects of emotional dysregulation such as resentments.  It is in addressing all these that we finally process these associated negative emotions in our memory banks and finally embed all these memories in long term memory.

In short, the Steps allow us to adaptively and healthily process our disturbed pasts. They also allow us to maintain a health and adaptive emotional regulation  on a daily basis and via steps 10-12 in particular allow us to greatly improve our emotional regulation.

I am not rewriting the Big Book of AA here, only to add another angle to understanding it and how it works, so that others in related therapeutic fields can have some insight into how it may work and those who need help feel more inclined to come to AA for help.

http://www.thebody.com/content/art48754.html   – Refer also to the work of Francine Shapiro (1) and her work which shaped development of the EMDR therapy which treats trauma (PTSD) and other disorders. I know it works for PTSD as my wife suffered PTSD after a car accident, and was greatly helped by this type of treatment. It is Shapiro’s insight into the role of unprocessed emotions in causing emotional volatility and a “volcano of unresolved distressing effects” (2) and that  chronic dysfunctional perceptions, responses, attitudes, self-concept, and personality traits are all symptoms of unprocessed memories (3) that shapes my thinking, partly, on how the steps allow us to put the past to bed.

I have to add also that I believe myself to be a sufferer of PTSD also. I have stressed that alcoholism is a psychiatric disorder in it’s own right but would never be silly enough to suggest it does not have co-occurring disorders such as PTSD, as the result of abuse and trauma in earlier life experience. Especially as there as up to 2/3s of dependent people may have had abuse in their early lives and that PTSD sufferers have up to a 50 % co-morbidity with alcoholism and addiction. Perhaps this is why this work by Shapiro strikes a cord with me. I think it is naive to say that abusive early life does not play a role in alcoholism and addition and that this environmental influence on genetic inheritance (alcoholism has a a generic heritability of some 50 – 70% making one of the most inheritable disorders). In other words, some 50 – 70% of alcoholics have alcoholism in their genes.

Throughout our lives, we all experience significant events that impact our perceptions of the world and determine how we interpret and respond to future experiences. These moments represent painful experiences so severe that they overwhelm our ability to cope with the rush of thoughts and feelings they elicit and If left unresolved, these feelings can persist for years in unprocessed emotions.

As a general rule, anything destructive that is left untreated — disease, trauma, stress, psychological disorders, addiction — can become progressively worse over time. Coming to terms with the past is often referred to as “integration,”  of these errant unprocessed emotions and achieving resolution. One way this resolution can be accomplished is by verbally and somatically (by being aware of how they affect one bodily) reprocessing these, like in step 5 when discussing one’s inventory, and the rewards can be transformative.

Mental networks contain visual images of the previous experiences  as well as related thoughts, emotions, and sensations. Previous experiences — including every physical sensation, every emotion, and every perception or interpretation — are encoded and stored in the brain and throughout the body. The processing of information about previous events may be incomplete, perhaps because the person has not developed the emotional or mental faculties to effectively manage or correctly interpret the situation (often the case with children who have faced abuse, trauma, insecure attachment to caregivers) or because processing is hindered by strong negative feelings (such as shame, helplessness, and denial) which I believe may be the consequence of emotional dysregulation.

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The memory of the previous experiences can  therefore be improperly stored without appropriate associative connections and with many elements still unprocessed. This incomplete processing prevents the forging of connections with more adaptive information or new learning which might help the person release the abusive, traumatising, misrepresented, resented, emotionally dysregualted and unprocessed experiences from the past. Finally when we do process these experiences then we can consign them to, embed them, happily in long term memory.

In a previous blog we say how one maladaptive emotional regulations strategies that of self elaboration, where one regulates a negative emotional experience by filtering in through the self and then elaborating on this in a ruminating manner, i.e. only seeing an event in relation to themselves, in self- reference (similar to a resentment)  and that our minds in early recovery are thus filled with these unprocessed memories as the consequence of this type if emotional dysregulation which filtered everything through a self centredness. In many cases we began to see in our step 4 inventory that it was often our emotional dysregultation that caused others to act in certain ways which we interpret, whether for valid reasons or not, in a self centred and distorted way which was base on emotional reasoning. These unprocessed emotions and memories thus lingered on in our minds for decades, festering as resentments and fuelling our drinking and drug use.

Doesn’t Step 4 allow us to record these unprocessed memories, get them down in black and white, with the unprocessed emotions, the resentments and other negative unprocessed emotions, such as anger, fear, selfishness, self-centredness, dishonesty and son on.  Doesn’t it let us use our proper reasoning to see through our purely emotional reasoning?

Don’t we start to process these emotions and thus the attached memories by verbalizing them in a therapeutic sense to our sponsors, mentors, respected religious or spiritual guides, counsellors etc? Don’t we learn to see what has kept us enslaved in feelings of injustice, resentment, of being wronged? Doesn’t it help us see how our emotional dysregulation distorts our perception of reality, and leads to a negative bias in our thinking about life and the people in it? Doesn’t it show us our underlying problem, our underlying psychiatric condition, which the steps helps us then to manage, to help us become manageable. We are not powerless over alcohol when we manage our negative emotions.

The Steps 6 and 7 allow us to have these removed. I believe God remove my many previous unprocessed emotions and memories, helped me consign then to the past and my long term memory. They did not go into ether as i fist thought, but into were processed in long term memory. This is no way lessens the Grace of God or his mercy.  He helps me do what i cannot, He goes deep! Steps 8 and 9 process these emotions even more via making amends for our wrongdoings and getting rid of the potential distress associated with unresolved situations from our past.  The final recognition of the effects our emotional dysregulation has had on our wider community.

Aren’t the steps, primarily to help us manage our emotional dysregulation?

Isn’t this what was unmanageable? Wasn’t it this which gave King Alcohol power over us? Doesn’t the AA program of action help us in a similar way EMDR does with trauma victims?

Step 10 helps us on a daily basis look out for manifestations and examples on how we hurt others with our lack of control over our negative emotional response, our dysfunctional emotional response. It gives us a way to examine and process these emotions and to take action to apologise to those who experienced this emotional volatility. It helps encourage positive, healthy, adaptive emotional expression.

Step 11 helps us self soothe and this helps our emotional regulation, meditation improves  and strengthens the very brain areas which regulate emotion, the dlPFC and ACC, which help control our anxious amygdala, the very the heart of all distress.  And via Step 12 we regulate our emotions in one of the most profound ways possible by helping others. By showing love. There is little dyregulation in love, the most healthy of human  emotional expression. ..and in all our affairs! We do not become intolerance of other is upholding “Principles not personalities”

Love contains the positive assets hopefully also listed in your inventories; selfishness, consideration, patience, tolerance etc  – the aspects of healthy emotional being. Perhaps this is another reason why Step 12 is so profound in helping us manage the unmanageability of our emotional dysregulation.

And fellowship itself, gives us an “earned attachment” especially when many of us had insecure attachments with our parents, grew up in dysfunction, disrupted families, in abuse or trauma. It helps us finally “belong”.  Fellowship  allows us perhaps to express our emotions fully for the first time, allows us to verbalize our concerns and feelings, label them for the first time, regulate and process them. Provides a safe environment in which to emotionally mature. The list goes on and on. AA gives us loving feedback, nurtures us, nourishes us.  Home groups with regular members over many years obviously aid this process of caring and mutual self growth.

It has become more clear while writing this how AA manages this emotional disease we call alcoholism.

The AA program of action helps us change how we feel and think about the world.

References

1. Shapiro, F. EMDR Therapy: Adaptive Information Processing, Clinical Applications and Research Recommendations.

2. Courtois, C. A., & Ford, J. D. (Eds.). (2009). Treating complex traumatic stress disorders: An evidence-based guide. New York, NY: Guilford Press.

3  Alcoholics Anonymous. (2001). Alcoholics Anonymous, 4th Edition. New York: A.A. World Services.

Some references to follow.

When fighting your neural ghosts make sure to surrender!!

When I was in early recovery, in the first weeks and months my brain would continually trick me into thinking I was not an alcoholic and it did this via a combination of  stress and memory.

The process went like this – first I would have an intrusive thought about alcohol and drinking which I did not want and had not consciously put in my own head. Which used to annoy me! So what was it doing there then? I must have put it there right? why else would it be there?

So I must still have wanted to drink?

I would find this thought very threatening, frightening and upsetting. I would try to get rid of it by suppressing it, pushing it out of my consciousness. The problem was this didn’t work.

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In fact, it made the situation a whole lot worse. The intial intrusive thoughts about drinking would then proliferate and there would be other thoughts about drinking; where, at what time, who would be there. I would then have a visual read out of all these scenarios. In the bar, the sunlight streaming through the window, the golden glistening pint of lager in the summer sun matched only by the pearly white smile of the beautiful buxom bar maid slowly pulling my pint, looking at me longingly etc. in a busy atmosphere, full of happy your attractive people laughing and enjoying themselves. people dancing and hugging. Sweet music drifting acorss the bar. You get the picture.

Delusion! This was nothing like the last bar I drank in a can assure you!! It was however the image my brain was evoking partly via memory association partly by motivational embellishment.

I have an alcoholic brain which wants me to drink. It uses, still, memories from the past, to whisper sweet nothings. It never casts images across my feverish mind of violently vomiting, bent over the downstairs toilet, or me staring through half blind eyes at my severely jaundiced face in the bathroom mirror. Or being thrown out of various bars onto the hard concrete pavement outside, on my head. Or the tears and violent rows. And the distress and confusion on loved ones’ faces.

No my alcoholism never accesses these images. Ignores them completely. Instead, as my alcoholic brain wants nothing more or else than to drink, it sends memories like neural ghosts into my head to cast a spell of delusional images and suggestive ideas, mainly promoting the idea of how good it was.

This is why in AA it is said we should wind the tape forward a bit to the disgustingly horrible reality of our final drinking. The constantly wretching and living in isolaton in our alcohol induced psychosis and the shivering terror of delirium tremens.

We have a inner voice of alcoholism that quite simply lies. Distorts our memories. The motivational voice of our alcoholism is a pathological liar. It only wants to drink because it is like a psychotic carer who thinks that drinking is the thing to do when we are in full of stress or in emotional distress. It automatically says hold one I have a solution to this distress, DRINK!

This is what the brain has become hardwired to do when distressed enough.  it is a habitual response of our implicit memory which then recruits our explicit memory which paints the picture of why drinking would be such a good idea.

I have a distress based illness, so I do get distressed from time to time. Sometimes over the most innocuous things sometimes.

Not as badly as in early recovery.  No, things have improved beyond belief since then.

The neural ghosts of my motivation were like intoxicating sirens in early recovery. My impaired reward systems implored me to have liquid release. Both combined to conjure an alternative view of myself from that of my recovering self, which was still in it”s infancy. They seemed to have control of my brain!  I suddenly had a problem beyond my own will power, I couldn’t resolve these things under my own steam.

The thoughts would come and I would suppress them and the thoughts would multiply and then the memories would all chain link  and pretty soon I would have an Amazon warehouse store of memories, all providing evidence against those guys in AA, who were not telling me truth about me being an alcoholic, They were wrong…sure I liked to drink, especially given by traumatic upbringing and all?

All these thoughts and memories floating across my mind like edits in a movie to show me as a drinking person who wasn’t an alcoholic. Not many disorders go to such profound trouble!!

I would fight these images, memories and thoughts to such an extent my brain would quite simply end up paralysed, my brain felt like it had become locked and there was nothing I could do about it. It had frozen into a terrifying inertia. Stalemate. No resolution apart from increased suffering.

Fortunately whatever I had learnt in AA even in the early days would rescue me. I had learnt to habitually grasp at something close to hand, my mobile phone. After a few puzzling moments of indecision I realised I could get help from somewhere. Ring my sponsor!!!!

I had to use someone else’s head to help me with my head, my newly recovering alcoholic head. I needed a recovered head who knew what I was going through and could help me through it! I felt all fragile like a jaundiced chick.

Recovery is tough in the early days, let’s never forget that! Life without a sponsor and right from the start is a key to surviving this alcoholic possession by these deluded memories and these neural ghosts.

This is the most vital period, to keeping those who need help in recovery. Saying someone doesn’t want it enough doesn’t cut it for me anymore. Better to show them what they are missing, namely a solution to their problems. Who ultimately doesn’t want that?

If you have never trusted anyone in your life, like me, this is the time to start if you want to recover. Trust at least one person on God’s earth. One, that’s all. This is the start to a new world in recovery. A world beyond your alcoholic brain’s comprehension.

Anyway, remember that in the feverish brain of a person in early recovery who ends up engaged in this neurobiological possession, thought straightjacket and fighting for his or her life against a mnemonic Hydra when it is the last thing they should be doing, the only way to win is to give in. Surrender!

Ultimately, how we appraise and react to naturally occurring alcohol or drug related thoughts and associated memories  will determine if this process of “craving” is activated. If we use strategies such as acceptance of these thoughts as transitory then the thoughts will not affect this process and if we “Let Go and Let God” then the distress which initially activates this process will not do so. How we react to our thoughts and accompanying distress (as they appear be be coupled) will determine whether the mental obsession mentioned above will be provoked.

Also see Cognitive Craving Part 3  and Part 4

A Cognitive Model of Craving – Pt 3

In an earlier blog we asked the question whether  neurobiological or “conditioning” or reinforcement models of craving predict relapse in abstinent alcoholics and addicts?

For us this is the most essential question. How do we explain relapse in those individuals motivated to remain abstinent, especially when they have followed some form of treatment, including 12 step groups.

We have seen that most relapse seems to be prompted by psychological stressors such as interpersonal relationships and the failure to cope with these.

This is very different to conditioning or reinforcement models that simply posit that people relapse because of the lure of alcohol or drug related stimuli, “cues”, or cues in the presence of stress or negative emotions, which we believe does have some affect.

Equally we have shown that in treatment seeking individuals there seems to be an automatic avoidance of cues so attentional bias does not really apply to this group plus there is a negative memory association bias in this abstinent, treatment seeking group also. So why do these people relapse?

What is the craving process prior to relapse for this group? . This is hugely important as neurobiological accounts do not predict relapse, so what does?

Over the next two blogs we will forward a model of craving or “mental obsessing” which we believe more accurately models the mechanisms which lead these individuals committed to staying sober and in recovery to relapse.

Ultimately we believe it may the maladaptive cognitive-affective reaction to naturally occurring  intrusive thoughts about alcohol or drugs (which are also the function of emotional dysregulation) that creates a proliferation of such thoughts, until they become obsessive, and which escalates stress and emotional distress to such an extent that the individual relapses to silence these tortuous obsessive thoughts.

These thoughts may not always be about alcohol or drugs. They may also contain negative perceptions of self, such as low self esteem and negative self schemas as the consequence of abusive early childhoods. These may result in “I am not good enough” thinking or “to hell with it!” relapse which have little to do with an appetitive urge to drink as in some reinforcement models. They are more akin to escape from self.

So models of addiction tend to focus on neurobiological substrates underlying addiction rather than on how affective (and cognitive) processing mediate addictive behaviours (1) although 80% of problem drinkers after outpatient treatment reported drinking episodes aimed at manipulating thoughts or emotions (2), with the majority of treatment clients attributing their relapse to interpersonal stress or negative emotions (3).

Also the involuntary retrieval of drug related thoughts is a hallmark of addicted populations. Over 70% of smokers stated that urges disrupted their thinking or functioning (4). Intensity of obsessive thoughts about alcohol predict relapse rate (5), with addicts motivated to use drugs to “silence” obsessive thoughts (6).  The idea that abstinence automatically decreases alcohol-related thoughts is challenged by research and supported by clinical observation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than exception (7).

So if emotion regulation difficulties and related intrusive thoughts are so prevalent in recovering abstinent addicts and alcoholics how do we account for this in a satisfactory and comprehensive theory of craving?

One study important to the conceptual framework set out here (6) used heart rate variability (HRV) measures, as a putative index of emotional regulation, to illustrate how craving involves cognitive-emotional processing and how conditioning models may not fully explain  ‘craving’.  This is consistent with the increasing concern in the literature about the applicably of such “one-dimensional” conditioning models explaining the results of cue reactivity studies (6). This study, among various findings, showed a link between HRV and obsessive thoughts,  in simple terms, the greater the emotional dysregulation, the greater the obsessive thoughts about alcohol.

It may even be that these “conditioning” reinforcement models or dopaminergic or stress-based models are describing “urges” rather than craving.  For us “craving” is distinct but interdependent on this “urge” state, it is partly triggered by it, if you like.

As an alternative to such passive “respondent” or “conditioning” models, some researchers have advocated the use of information-processing theory to understand how dependent individuals react in their encounter with “drug-related” cues (external and internal, e.g. stress or negative emotions) (6). Craving may thus be a different phenomenological experience to that of the physiological urges, although one may prompt the other.

According to one ‘info-processing’ view of craving, forwarded by Stephen Tiffany (4), ‘craving’,  occurs only when the automatic approach behaviour commonly seen in addicts in thwarted. This is particularly pertinent to those abstinent, treatment seeking individuals. In addiction, drug use behaviour develops various rituals around the seeking, preparation and consumption of drugs. These habitual procedures become stored in memory, in automatized action schemata  or action plans.

Encoded within these unitized memory systems are prompts such as external events (e.g. sight of a hypodermic syringe,) or internal events such as physical states (e.g. NA). Although activation of these memory structures may not be a sufficient for addicts to respond to ‘urges’, via actual drug seeking, they may stimulate approach behaviours.

Tiffany (1990) proposed “urges”, or what we call craving, are said to be associated with conscious efforts to inhibit the operation of drug use action plans (e.g. prevention of relapse or suppressive reaction to intrusive using-related thoughts). In abstinence, these “urges” involve non-automatic (i.e. conscious, effortful) cognitions that compete with automatic (unconscious effortless) drug use related plans. Thus, relapse may occur under two circumstances: when the action plan operates autonomously and when conscious processes to inhibit the action plan (thought suppression) backfire and are unsuccessful.

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We agree with Tiffany’s (1990) assertion that, like other stereotypic motor acts, some aspects of the drug-use ritual are susceptible to automatization. In fact in relation to automatic using schemas it is only the “nonautomatic” processing where cognitive resources are consciously devoted to disrupting the course of a perceive threat of relapse and prior experience of these self same affective states in the context of use that activate drug- and alcohol related memories (Bradizza, Stasiewcz, & Maisto, 1994.) and cause “craving”.

The “exhaustive and effortful” effects of “urges” (craving)  in abstinent addicts (Tiffany, 1990 p.158) may reflect consciously trying to inhibit these by thought suppression. Whereas, drug using schemas are firmly established and neurally embedded and require few resources to operate, the “abstinence plan” is poorly established and demands vigilance (i.e. attention) and effort to maintain. It is also a relatively new internal voice and not as familiar to the addict. Therefore, it not surprising that many addicts take the path of least resistance and relapse.

Addictive behaviours thus become increasingly automatic or compulsive in the addiction cycle, which supports Tiffany’s ‘cognitive’ model of automatic action plans. ‘Cravings’ are generated, in our model, by non-automatic, cognitive processes which are invoked to thwart (or interfere) with these drug use action plans.

For example, in abstinent addicts, internal stress/emotional distress provokes automatic action plans (and accompanying intrusive thoughts). These individuals then use non-automatic processing i.e. cognitive control/thought suppression) to ‘fight’ these threatening (naturally occurring) automatic thoughts.

The anterior cingualte cortex (ACC) acts a gateway between what is known as explicit (hippocampal) memory (remembered knowledge about things – e.g. where we drank, with whom, how it felt, noises, smells, atmosphere and ourselves in those situations etc) and implicit (dorsal striatal)  memory (the procedural, how to do memory-  the habitualised procedure of Tiffany’s automatic addiction action plans). The dorsal medial striatum (DMS) plays an important part orchestrating the switching between these memories through a “hippocampal-to-striatal pathway” passing through the ACC (41). It may be ACC hypofunctioning, under extreme stress, which aids transition between explicit and implicit memory networks (42).

Addiction severity is suggested as being represented by a shift in reward processing from ventral stiatum (VS) to DS (28) with this marked by an emergence of automatic thoughts, which the authors suggested as the cognitive thoughts and images of automatized drug action schemata (Tiffany 1990). As addiction escalates there appears to be a greater reliance on implicit rather than explicit (hippocampal) memory too. Also emotional distress is known to recruit the DS region also. So in effect the DS becomes involved in memory, reward and affect in later addiction.  So emotional dysregulation will not only provoke intrusive thoughts, but activate automatic approach behaviour, i.e. will prompt a movement towards getting and consuming drugs and alcohol.

Modell et al, 1992, distinguished between  intrusive thoughts – and memories – in a cognitive component to craving and in compulsions, which is more motoric and action component –  the cognitive component may be governed by the dorsal medial which has connections with the ‘associative’ PFC and lateral DS which is more involved in habitual motor activity As we have already discussed, addiction severity corresponds with the extent of obsessive thoughts as measured by the Obsessive Compulsive Drinking Scale (OCDS) which suggest that as the severity of this illness progresses, so does the intensity of the obsessive thoughts about alcohol and the compulsive behaviours to use alcohol. Kranzler et al. (1999) showed relapsers who scored higher in ‘obsessions’ craving measured by the OCDS predicted relapse in the 12 months after treatment completion. It is tempting to ad that emotional dysregulation also worsens as addiction becomes more severe(  ).

‘Cravings’ are thus generated by non-automatic, cognitive processes which are invoked to thwart (or interfere) with these drug use action plans.  The DMS may be very important in the relapse mechanism we are about to explore.

The DMS may have a potential role in cognitive control of behaviour flexibility and mediating behaviours by hippocampal guidance. As such the DMS and DLS may either compete (Misumori, Yeshenko, Gill and Davis, 2004) or cooperate (Devan, MacDonald, White 1999) under different conditions.  For example, DMS may be activated when a reversal of a previously reinforced response, i.e. habitual response, is required (Eichenbaum et al, 1989). Thus in attempting to inhibit stimulus response, i.e. the automatic alcohol approach behaviour of the DLS,    the DMS activates action-outcome pathways

Thus the ‘cognition and imagery of automatized schema’ becomes increasingly obsessive as the consequence of the anterior cingulate cortex (ACC) detecting conflict between memory intrusions and alerting the prefrontal cortex (PFC) to actively suppress unwanted thoughts (169). This only serves to intensify these thoughts as thought suppression ‘rebounds’ unwanted thoughts more intensely and prolifically into consciousness (170).

This, in abstinent addicts, appears to make the situation worse leading to greater stress reactivity and  need to further inhibit habitual response which activates even more action-outcome memory, e.g. the automatic activation of mental representations in associated memory networks of what course of action has normally been followed to affect the outcome of reducing this distress, i.e. which normally has been to drink.

Whereas the DMS normally in adaptive processes competes with the DLS to resolve a situation, for the abstinent addict, it only increases the problem by suggesting solutions which in fact make the situation more acutely adverse.

For the addict attempting to maintain abstinence, declarative memory and controlled processes may often be “corrupted” in service of promoting or rationalizing drug use. This will occur because negative affect is aversive and intrinsically primes escape and avoidance strategies.

Thus the ACC in recruiting explicit memory to counteract the automatic alcohol related thoughts of the DS may unwittingly be increasing memories of drinking and explicit prompts to drink as this is what has normally been the course of action in such situations of negative emotions.

The best and most well-intentioned efforts to remain sober/clean threaten sobriety most; producing a mnemonic ‘Hydra Effect’ whereby attempts to cut off this terrible flowering of intrusive thoughts leads to increased proliferation of these thoughts and accompanying emotional distress.

 

This, we posit, is what occurs in the mind of a recovering/abstinent alcoholic and is more akin to the “mental obsession” of the Big Book that purely neurobiological/physiological urge states.

Equally it should be noted that craving or mental obsession does not suggest that the alcoholic or addict in recovery/abstinence is actually motivated or even wants to relapse to former use. One can engage in this “mental obsession” or cognitive craving simply via a maladaptive emotional dysregulation whereby a defective emotional strategy such as thought suppression of threatening intrusive thoughts can set up a chain of reactions which lead to an unfortunate proliferation of thoughts and memories which promote alcohol and drug use to relieve escalating emotional distress which leads to relapse even if the alcoholic or addict in recovery did not even wish it! What else is this other than a craving beyond one’s mental (cognitive) control!

Relapse can happen to an alcoholic or addict if he does not manage his underlying condition of emotional dysregulation, in other words.

 

 

References (to follow)

1. Cheetham, A., Allen, N. B., Yücel, M., & Lubman, D. I. (2010). The role of affective dysregulation in drug addiction. Clinical psychology review30(6), 621-634.

2. Sanchez-Craig, M., Annis, H. M., Bronet, A. R., & MacDonald, K. R. (1984). Random assignment to abstinence and controlled drinking: evaluation of a cognitive-behavioral program for problem drinkers. Journal of consulting and clinical psychology52(3), 390.

3. Lowman, C., Allen, J., Stout, R. L., & Group, T. R. R. (1996). Replication and extension of Marlatt’s taxonomy of relapse precipitants: overview of procedures and results. Addiction91(12s1), 51-72.

4. Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychological review97(2), 147.

5. Bottlender, M., & Soyka, M. (2004). Impact of craving on alcohol relapse during, and 12 months following, outpatient treatment. Alcohol and Alcoholism39(4), 357-361.

6. Ingjaldsson JT, Laberg JC, Thayer JF. Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry. 2003;54(12):1427–1436.

7.  Hoyer, J., Hacker, J., & Lindenmeyer, J. (2007). Metacognition in alcohol abusers: How are alcohol-related intrusions appraised?

 

. Bradizza, C. M., Stasiewicz, P. R., & Maisto, S. A. (1994). A conditioning reinterpretation of cognitive events in alcohol and drug cue exposure. Journal of Behavior Therapy and Experimental Psychiatry, 25, 15 – 22

Modell, J. G., Glaser, F. B., Cyr, L. & Mountz, J. M. (1992) Obsessive and compulsive characteristics of craving for alcohol in alcohol abuse and dependence. Alcoholism: Clinical and Experimental Research, 16, 272–274.

. Kranzler, H. R., Mulgrew, C. L., Modesto-Lowe, V. and Burleson, J. A. (1999) Validity of the obsessive compulsive drinking scale (OCDS): Does craving predict drinking behavior? Alcoholism: Clinical and Experimental Research 23108–114.

(Misumori, Yeshenko, Gill and Davis, 2004)

(Devan, MacDonald, White 1999)

(Eichenbaum et al, 1989).

How far have we come in understanding this emotional disorder?

A constant thread throughout our blogs so far has been an assertion that alcoholism and addiction are primarily emotional regulation and processing disorders.

So we were thus  very interested to find this article (1) which describes how we are not the first to view alcoholism and addiction this way.

Here we use this article to present a  brief history of research, dating back to the 1930s, that has viewed alcoholism and addiction in a similar way to we do now in 2014.

 

“Life, as we find it, is too hard for us; it brings us too many pains, disappointments and impossible tasks. In order to bear it we cannot dispense with palliative measures. (…), intoxicating substances, which make us insensitive to it” (Freud, 1930, p. 75).

 

Rado (1933) was the first to describe substance use as a way of coping with excessively difficult states of emotions (3).

Others subsequently interpret the phenomena as a maladaptive way of fighting against stress, anxiety, and depression (4-6). Krystal and Raskin(1970) emphasize the undifferentiated and archaic, somatically manifested, emotions of persons suffering from addictive disorders (7).

These emotions are fixed at this level owing to their early traumatic nature.

Later, McDougall (1984) also highlighted the importance of overflowing emotions in the case of people with addictive disorders (8). He identified substanceuse as a compulsive way of canalizing these overflowing emotions. Conclusively, we can see that in all of these mainly psychoanalytically oriented theories, substance use is present as an instrument to regulate emotions.

This approach is elaborated unequivocally in the theories of Leon Wurmser and Edward J. Khantzian. According to Wurmser (1974), people with addictive disorders are unable to regulate their undifferentiated feelings, impulses, and pervasive internal stress, and so they turn to psychoactive substances (9). Their substance use can thus be recognized as an attemptat “self-treatment.” The self-medication hypothesis of Khantzian (1985) also highlights emotion regulation in the background of addictions (10).

He asserts that drug use in fact emerges as the common result of psychopharmacological functioning and overwhelmingly painful emotions. Like Wurmser, Khantzian also points out that the choice of substance is specific to the person’s self-regulation and affect-regulation problems, as well as his/her personality dysfunctions (11).

More recently we have had Cheetham’s affect- centred theories of addiction (12).

Apparently, clinical observations highlight mainly those dimensions in the background of psychoactive substance use—primarily the presence of undifferentiated, overflowing, dominantly negative and painful feelings, and difficulties in emotional expression and emotional regulation—which appear to be basic components of the later Emotional Intelligence (EI)  construct (13). For instance, according to Mayer and Salovey (1997), the main components of EI are: (1) the perception, appraisal, and expression of emotions; (2) the emotional facilitation of thinking; (3) understanding and analyzing emotions, and employing emotional knowledge; and (4) the regulation of emotions.

The most important empirical findings regarding our topic may be those studies, which attempted to explore the relationship between addictions and alexithymia.

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

The four main characteristics of alexithymia are: (1) difficulty identifying feelings and distinguishing between emotions and corresponding bodily sensations; (2) difficulty describing feelings to others; (3) constricted imaginal life and fantasies; and (4) externally oriented cognitive style (17).

The relationship between alexithymia and emotional consciousness or emotional intelligence was confirmed by several studies (18-20). These studies pointed out that a low level of EI correlates with a high level of alexithymia.

These results are hardly surprising, given that the ability to identify and express emotions is an important component of EI.

Besides clinical observations (21), empirical studies have also shown that people with addictive disorders—mainly alcoholic patients or those diagnosed with eating disorders—have difficulties with the verbalization and expression of their feelings, so in their case the problem of alexithymia is more frequent than in the normal population (22-24)

One study looking at a meta analysis of research into emotional aspects of addiction (1) found – 12 of these studies solely measured the ability to identify emotions – Oscar-Berman and colleagues (1990) were the first to draw attention to the fact that alcohol addicts, especially those suffering from Korsakoff‘s syndrome, have difficulties in identifying and decoding emotions mediated by facial expressions (25).

Underlying the inaccuracy of decoding is the overestimation of intensity of emotions, especially negative ones, characteristic of alcohol patients (26-29). They also tend to associate negative emotions more often with each of the presented facial expressions (30). Furthermore, Kornreich and colleagues have pointed out that the ability to identify emotions is tightly and negatively associated with interpersonal problems, and these problems seem to be a mediating factor between emotional identification deficits and alcoholism (31). All of these findings may relate to results stating that people with alcohol addiction tend to interpret facial expressions, like sadness or disgust, falsely as emotions describing interpersonal conflicts, like anger or contempt (32).

This latter result is also supported by an Italian study (33). A further important outcome of these investigations showed that alcohol-addicted patients, in spite of their weaker capacity, rate these emotion-decoding tasks at the same difficulty level as do people from the control groups. It therefore seems as though they are not aware of their difficulties in identifying emotions.

At the same time, however, this distortion in the subjective ratings is not only characteristic of alcohol addiction, but is present in the case of opiate-addicted people as well (34,35). These studies also highlighted that alcoholism is associated with poorer emotion-decoding  abilities than compulsive use of opiates.

causes-of-addiction_mini

 

We have discussed emotional processing deficits in alcoholics and addicts in another blog.

The prevalence rate of alexithymia in alcohol use disorders is between 45 to 67% (36,37). Finn, Martin and Phil (1987) investigated the presence of alexithymia among males at varying levels of genetic risk for alcoholism. They found that the high risk for alcoholism group was more likely to be alexithymic than the moderate and low genetic risk groups (38).

The inability to identify and describe affective and physiological experiences is itself associated with the elevated negative affect (39) commonly seen in alcoholics, even in recovery (40). This latter study also highlighted the link between alexithymia and the emotional dysregulation inherent in addictive disorders.

Thus, the unpleasant “undifferentiated emotional” experience of early theories might prompt individuals to engage in maladaptive behaviors, such as excessive alcohol consumption, in an effort to regulate emotions, or, more specifically, cope with negative emotional states (41).

We now see how neurobiological models can marry statisfactorially wih psycho-analytic theories. This will be especially the case when we blog about alexithymia, addictive and theories of attachment.

We have thus moved from a mainly clinical perspective on the role of emotional difficulties in addiction to providing some neuroscientific evidence that these theories were actually on to something, namely these theories were pointing the way to further conceptualisations of addiction as a disorder of emotional regulation and processing. 

 

References

1. Kun, B., & Demetrovics, Z. (2010). Emotional intelligence and addictions: a systematic review. Substance use & misuse45(7-8), 1131-1160.

2. Freud, S. (1930). Civilization and its discontents. In J. Strachey (Ed.), The standard edition of the complete psychological works of Sigmund freud (Vol. 21, pp. 59–145). London: The Hogarth Press

3. Rado, S. (1933). The psychoanalysis of pharmacothymia (Drug Addiction). Psychoanalytic Quarterly, 2:1–23

4. Chein, I., Gerard, D. L., Lee, R. S., Rosenfeld, E. (1964). The road to H. New York: Basic Books

5. Fenichel, O. (1945). The psychoanalytic theory of neurosis. New York: Norton

6. Hartmann, D. (1969). A study of drug-taking adolescents. Psychoanalytic Study of the Child, 24:384–398.

7. Krystal, H., Raskin, H. A. (1970). Drug dependence. aspects of ego functions. Detroit: Wayne State University Press.

8.  McDougall, J. (1984). The “dis-affected” patient: reflections on affect pathology. Psychoanalytic Quarterly, 53:386–409.

9. Wurmser, L. (1974). Psychoanalytic considerations of the etiology of compulsive drug use. Journal of the American Psychoanalytic Association, 22:820–843.

10. Khantzian, E. J. (1985). The self-medication hypothesis of addictive disorders: focus on heroin and cocaine dependence. American Journal of Psychiatry, 142:1259–1264.

11. Khantzian, E. J. (1991). Self-regulation factors in cocaine dependence – a clinical perspective. NIDA Research Monograph, 110:211–226.

12. Cheetham, A., Allen, N. B., Yücel, M., & Lubman, D. I. (2010). The role of affective dysregulation in drug addiction. Clinical psychology review30(6), 621-634.

13.  Mayer, J. D., Salovey, P. (1997). What is emotional intelligence? In P. Salovey & D. Sluyter (Eds.), Emotional development and emotional intelligence: implications for educators(pp. 3–31). New York: Basic Books.

14. Ruesch, J. (1948). The infantile personality. Psychosomatic Medicine, 10:134–144

15. Nemiah, J. C., Sifneos, P. E. (1970). Affect and fantasy in patients with psychosomatic disorders. In O. W. Hill (Ed.), Modern trends in psychosomatic medicine (Vol. 2, pp. 26–35). London: Butterworths.

16. Sifneos, P. E. (1967). Clinical observations on some patients suffering from a variety of psychosomatic diseases. Acta Medica Psychosomatica, 7:1–10

17.  Nemiah, J. C., Freyberger, H., Sifneos, P. E. (1976). Alexithymia: a view of the psychosomatic process. In O. W. Hill (Ed.), Modern trends in psychosomatic medicine (Vol. 3, pp. 430–439). London: Butterworths

18. Austin, E. J., Saklofske, D. H., Egan, V. (2005). Personality, well-being and health correlates of trait emotional intelligence. Personality and Individual Differences, 38:547–558.

19. Lane, R. D., Sechrest, L., Reidel, R., Weldon, V., Kaszniak, A., Schwartz, G. E. (1996). Impaired verbal and nonverbal emotion recognition in alexithymia.Psychosomatic Medicine, 58:203–210

20. Parker, J. D. A., Taylor, G. J., Bagby, R. M. (2001). The relationship between emotional intelligence and alexithymia. Personality and Individual Differences, 30:107–115.

21. Krystal, H. (1995). Disorders of emotional development in addictive behavior. In S. Dowling (Ed.), The psychology and treatment of addictive behavior(pp. 65–100). Madison, CT: International Universities Press.

22. Handelsman, L., Stein, J. A., Bernstein, D. P., Oppenheim, S. E., Rosenblum, A., Magura, S. (2000). A latent variable analysis of coexisting emotional deficits in substance abusers: alexithymia,
hostility, and PTSD. Addictive Behaviors, 25:423–428

23. Speranza, M., Corcos, M., Loas, G., Stephan, P., Guilbaud, O., Perez-Diaz, F., et al. (2005). Depressive personality dimensions and alexithymia in eating disorders.Psychiatry Research, 135:153–163.

24.Troisi, A., Pasini, A., Saracco, M., Spalletta, G. (1998). Psychiatric symptoms in male cannabis users not using other illicit drugs. Addiction, 93:487–492

25. Oscar-Berman, M., Hancock, M., Mildworf, B., Hutner, N., Weber, D. A. (1990). Emotional perception and memory in alcoholism and aging. Alcoholism: Clinical and Experimental Research, 14:383–393.

26. Foisy, M. L., Kornreich, C., Fobe, A., D’Hondt, L., Pelc, I., Hanak, C., et al. (2007a). Impaired emotional facial expression recognition in alcohol dependence: do these deficits persist with midterm abstinence? Alcoholism: Clinical and Experimental Research, 31:404–410

27. Kornreich, C., Blairy, S., Philippot, P., Hess, U., Noel, X., Streel, E., et al. (2001b). Deficits in recognition of emotional facial expression are still present in alcoholics after mid- to long-term abstinence. Journal of Studies on Alcohol, 62:533–542

28. Philippot, P., Kornreich, C., Blairy, S., Baert, I., Den Dulk, A., Le Bon, O., et al. (1999). Alcoholics’ deficits in the decoding of emotional facial expression. Alcoholism: Clinical and Experimental Research, 23:1031–1038

29. Townshend, J. M., Duka, T. (2003). Mixed emotions: alcoholics’ impairments in the recognition of specific emotional facial expressions.Neuropsychologia, 41:773–782.

30. Foisy, M. L., Kornreich, C., Petiau, C., Parez, A., Hanak, C., Verbanck, P., et al. (2007b). Impaired emotional facial expression recognition in alcoholics: are these deficits specific to emotional cues? Psychiatry Research, 150:33–41.

31. Kornreich, C., Philippot, P., Foisy, M. L., Blairy, S., Raynaud, E., Dan, B., et al. (2002). Impaired emotional facial expression recognition is associated with interpersonal problems in alcoholism. Alcohol and Alcoholism, 37:394–400

33. Frigerio, E., Burt, D. M., Montagne, B., Murray, L. K., Perrett, D. I. (2002). Facial affect perception in alcoholics. Psychiatry Research, 113:161–171

34. Foisy, M. L., Philippot, P., Verbanck, P., Pelc, I., Van Der Straten, G., Kornreich, C. (2005). Emotional facial expression decoding impairment in persons dependent on multiple substances: impact of a history of alcohol dependence. Journal of Studies on Alcohol, 66:673–681

35. Kornreich, C., Foisy, M. L., Philippot, P., Dan, B., Tecco, J., Noel, X., et al. (2003). Impaired emotional facial expression recognition in alcoholics, opiate dependence subjects, methadone maintained subjects and mixed alcohol-opiate antecedents subjects compared with normal controls. Psychiatry Research, 119:251–260.

36. Loas G, Fremaux D, Otmani O, Lecercle C, Delahousse J. Is alexithymia a negative factor for maintaining abstinence? A follow-up study. Comprehensive Psychiatry. 1997;38:296–299.

37. . Ziolkowski M, Gruss T, Rybakowski JK. Does alexithymia in male alcoholics constitute a negative factor for maintaining abstinence. Psychotherapy and psychosomatics. 1995;63:169–173.

38. Finn PR, Martin J, Pihl RO. Alexithymia in males at high genetic risk for alcoholism.Psychotherapy and Psychosomatics.1987;47:18–21

39. 16.  Connelly M, Denney DR. Regulation of emotions during experimental stress in alexithymia. Journal of Psychosomatic Research. 2007;62:649–656

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41. Thorberg FA, Young RM, Sullivan KA, Lyvers M, Hurst CP, Connor JP, Feeney GFX. Alexithymia in alcohol dependent patients is partially mediated by alcohol expectancy. Drug and Alcohol Dependence. 2011;116:238–241