Executive dysfunctions

Impulsivity is an Independent Predictor of 15-Year Mortality Risk among Individuals Seeking Help for Alcohol-Related Problems

Posted on by alcoholicsguide

In yesterday’s blog we looked at how AA membership and the 12 step program of recovery helped reduce impulsivity in recovering alcoholics.

We mentioned also that impulsivity was present as a pathomechanism of alcoholism from vulnerability in “at risk” children from families, were there was a history of alcoholism, right the way through to recovering alcoholics in long term recovery (i.e. many years of recovery).

We cited and used excerpts from a study written by the same authors as the study we cite now (1).

This study shows and highlights how, if untreated, by recovery programs such as AA’s 12 steps, that “trait” impulsivity can lead to increased mortality in alcoholics.

This study interestingly shows there is a difference from “state-like” impulsivity in early recovery when recovering people are still distressed and “trait-like” which is after Year 1 of recovery when some of the severity of withdrawal from alcohol has long since abated and some recovery tools have been learnt.

The fact that this impulsivity continues to contribute to relapse and mortality may suggest it is a trait state in alcoholics and possibly a vulnerability to later alcoholism also.

In effect, it illustrates the role impulsivity plays as a pathomechanism in alcoholism, i.e. it is a psychological mechanism that drives addiction and alcoholism forward to it’s chronic endpoint.

Again research shows us how we can learn about a pathology from the recovery from it!

 

impulse control.preview

“Abstract

Background

Although past research has found impulsivity to be a significant predictor of mortality, no studies have tested this association in samples of individuals with alcohol-related problems or examined moderation of this effect via socio-contextual processes. The current study addressed these issues in a mixed-gender sample of individuals seeking help for alcohol-related problems.

Results

…higher impulsivity at baseline was associated with an increased risk of mortality from Years 1 to 16; higher impulsivity at Year 1 was associated with an increased risk of mortality from Years 1 to 16, and remained significant when accounting for the severity of alcohol use, as well as physical health problems, emotional discharge coping, and interpersonal stress and support at Year 1. In addition, the association between Year 1 impulsivity and 15-year mortality risk was moderated by interpersonal support at Year 1, such that individuals high on impulsivity had a lower mortality risk when peer/friend support was high than when it was low.

Conclusions

The findings highlight impulsivity as a robust and independent predictor of mortality.

Introduction

…personality traits related to impulsivity (e.g., low conscientiousness) have been identified as significant predictors of poor health-related outcomes including mortality (Bogg and Roberts, 2004; Roberts et al., 2007). Although there is a well-established association between disinhibitory traits and alcohol use disorders (AUDs) (Labouvie and McGee, 1986; McGue et al., 1999;Sher et al., 2000), to our knowledge, no studies have tested these traits as predictors of mortality among individuals with alcohol-related problems or examined moderation of this effect via socio-contextual processes.

Predictors of Mortality Risk among Individuals with Alcohol Use Disorders

Relative to the general population, individuals with AUDs are more likely to die prematurely (Finney et al., 1999; Johnson et al., 2005; Valliant, 1996). Accordingly, several longitudinal studies have aimed to identify the most salient risk factors for mortality in this population (for a review, see Liskow et al., 2000)

…more reliance on avoidance coping, less social support, and more stress from interpersonal relationships increase the risk of mortality among individuals with AUDs (Finney and Moos, 1992; Holahan et al., 2010; Mertens et al., 1996; Moos et al., 1990).

Impulsivity and Risk for Mortality: Relevance for Individuals with Alcohol Use Disorders

Despite the litany of variables that have been examined as predictors of mortality among individuals with AUDs, tests of the significance of individual differences in personality are noticeably absent from this literature. In the clinical and health psychology literatures, however, personality traits have long been identified as possible risk factors for mortality (Friedman and Rosenman, 1959), with low conscientiousness emerging as one of the most consistent, trait-based predictors of poor health and reduced longevity (Kern and Friedman, 2008; Roberts et al., 2007). Conscientiousness is a broad domain of personality reflecting individual differences in the propensity to control one’s impulses, be planful, and adhere to socially-prescribed norms (John et al., 2008).

(previously) no studies in this literature have tested impulsivity as an independent predictor of mortality in a sample of individuals with alcohol-related problems. This is a surprising omission, given that impulsivity is a well-established risk factor for alcohol misuse (Elkins et al., 2006; McGue et al., 1999; Sher et al., 2000) and therefore may be an especially potent predictor of mortality among individuals with AUDs. Furthermore, the role of impulsivity as an independent predictor of mortality risk among individuals with AUDs is relevant from the standpoint of the stage of the alcohol recovery process.

Thus, we sought to examine the impulsivity-mortality link at baseline and one year after participants had initiated help-seeking for their alcohol use problems. At baseline, participants were in a state of distress due to their problematic alcohol use, whereas at Year 1 most participants had obtained help for their alcohol-related problems and reduced their drinking (Finney and Moos, 1995).

Given prior research on acute clinical states and self-report assessments of personality (e.g., Brown et al., 1991; Peselow et al., 1994;Reich et al., 1987), we hypothesized that individuals’ self-reports of impulsivity at Year 1 would be less a reflection of their alcohol problems – and therefore more likely to be independently linked to mortality risk – than their reports at baseline, which may be more closely associated with concurrent alcohol use and problems (i.e., state effects).

Discussion

…impulsivity at baseline was a significant predictor of mortality risk from Years 1 to 16; however, this effect was accounted for by the severity of alcohol use at baseline. In contrast, impulsivity at Year 1 was associated with an increased risk of mortality over the subsequent 15 years…

In addition, a significant interaction was observed between impulsivity and peer/friend support at Year 1, which suggested that, among individuals high on impulsivity, the mortality risk may be reduced for those high on support from peers/friends. Collectively, these findings highlight impulsivity as an independent risk factor for mortality in AUD samples…

…It is also conceivable that, given participants were in a state of crisis at baseline, their reports of their impulsive tendencies at that time partly captured “state” effects (e.g., psychiatric distress from concurrent substance use; withdrawal symptoms) and therefore were less an indication of their typical or “characterological” pattern of impulsivity, independent of alcohol use. However, at Year 1, most participants had reduced their drinking and were not in a state of crisis; thus, their reports at that time may have been a better reflection of their “trait-like” pattern of impulsivity, which in turn may be a more robust independent predictor of long-term outcomes such as mortality. Accordingly, future studies that seek to test impulsivity as an independent predictor of mortality among individuals with AUDs should consider the stage of the alcohol recovery process.

Moderation of the Impulsivity-Mortality Link via the Social Context

The results of the moderator analyses suggest that the effects of impulsivity on mortality may become manifest through interactions between traits and socio-contextual process (Friedman, 2000). That is, the dire effects of impulsivity on risk for mortality may not reach fruition for individuals who are able to maintain a strong peer support network. Conceivably, by virtue of their strong bond with a high-risk individual, such peers may have sufficient leverage to discourage expression of the individual’s impulsive tendencies and encourage consideration of the long-term consequences of his/her actions.

Such a perspective is consistent with evidence from the AUD treatment-outcome literature that social support networks are a key mechanism by which Alcoholics Anonymous (AA) and other psychosocial treatments can improve long-term drinking-related outcomes (Humphreys and Noke, 1997; Kaskutas et al., 2002).

Furthermore, from the standpoint of treatment, the present findings suggest that interventions for AUDs may benefit from an ecological perspective that considers the contexts in which dispositional tendencies, such as impulsivity, become expressed in individuals’ everyday lives. Notably, based on prior work with this sample, longer duration in AA and alcohol treatment was associated with a decline in impulsivity (Blonigen et al., 2009). In combination with the present findings, it appears that formal and informal help for AUDs may include “active ingredients” that can help curtail expression of impulsive tendencies (e.g., social integration, peer bonding; Moos, 2007,2008) and buffer the otherwise deleterious impact of such tendencies on health and longevity.

References

1. Blonigen, D. M., Timko, C., Moos, B. S., & Moos, R. H. (2011). Impulsivity is an Independent Predictor of 15-Year Mortality Risk among Individuals Seeking Help for Alcohol-Related Problems. Alcoholism, Clinical and Experimental Research, 35(11), 2082–2092. doi:10.1111/j.1530-0277.2011.01560.x

AA helps to reduce Impulsivity

Posted on by alcoholicsguide

 

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]

 

 

 

 

 

 

 

 

Understanding Emotional Processing Deficits in Addiction – Guest Blog

Posted on by alcoholicsguide

Understanding Emotional Processing Deficits in Addiction

by alcoholicsguide

We recently blogged on how alcoholics, and children of alcoholics, have difficulty with recognizing and differentiating external signs of emotions such as facial emotional expressions, now we will consider increasing evidence that alcoholics have difficulties with identifying and differentiating internal emotional states also.

Both these areas of research point to real difficulties in alcoholics in relation to the processing of emotion.

As we shall explain below, this deficit in emotional processing has real consequence for decision making capabilities and this has an important role to play in the initiation and maintenance of substance abuse and eventual addiction.

Alexythymia and Addiction

Effective emotion regulation skills include the ability to be aware of emotions, identify and label emotions, correctly interpret emotion-related bodily sensations, and accept and tolerate negative emotions (2,3).

Alexithymia is characterized by difficulties identifying, differentiating and expressing feelings. The prevalence rate of alexithymia in alcohol use disorders is between 45 to 67% (4,5)

Finn, Martin and Pihl (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 (6).

Higher scores on alexithymia were associated poorer emotion regulation skills, fewer percent days abstinent, greater alcohol dependence severity (7). Some studies have emphasized a right hemisphere deficit in alexithymia [8,9] based on the hypothesis that right hemisphere plays a more important role in emotion processing than the left [10, 11].

Dysfunction of the anterior cingulate cortex has been frequently argued, e.g., [12], and others have focused on neural substrates, such as the amygdala, insula, and orbitofrontal cortex (see the review in [13]). All different components of the the emotional regulation  network.

These models may interact with each other and also map onto the brain region morphological vulnerability mentioned as being prevalent in alcoholics.

Magnetic resonance imaging and post-mortem neuropathological studies of alcoholics indicate that the greatest cortical loss occurs in the frontal lobes, with concurrent thinning of the corpus callosum. Additional damage has been documented for the amygdala and hippocampus, as well as in the white matter of the cerebellum. All of the critical areas of alcoholism-related brain damage are important for normal emotional functioning (14) .

One might speculate that thinning of the corpus collosum may render alcoholics less able to inhibit negative affect in right hemisphere circuits.

Alcoholics are thus vulnerable to thinning of the corpus collosum and perhaps even to emotional processing difficulties (15 ). The inability to identify and describe affective and physiological experiences is itself associated with the elevated negative affect (16) commonly seen in alcoholics, even in recovery (17.

Thus, this unpleasant experience 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 (18 )

One neuroimaging study (19) looked at and compared  various models of alexithymia showing people with alexithymia showed reduced activation in the dorsal ACC and right anterior insula (AI), and suggested individuals who exhibit impaired recognition of their own emotional states may be due to a dysfunction of the ACC-AI network, given these regions’ important role in self-awareness. These studies suggest alexithymics may not be able to use feelings to guide their behaviour appropriately.

The Iowa gambling task (IGT) was developed to assess decision-making processes based on emotion-guided evaluation. When alexithymics perform the IGT, they fail to learn an advantageous decision-making strategy and show reduced activity in the medial prefrontal cortex, a key area for successful performance of the IGT, and increased activity in the caudate, a region associated with impulsive choice (20).

ep neg

The neural machinery in alexithymia is therefore activated more on the physiologic, motor-expressive level, similar to the study on children of alcoholics and thus may represent a vulnerability.

The function of the caudate is to regulate or control impulsivity and disinhibition. Individuals with alexithymia may work on the IGT impulsively rather than by using emotion-based signals. This IGT study suggests that individuals with alexithymia may be unable to use feelings to guide their behavior appropriately.

Alexithymic individuals thus may be unable to use emotion for flexible cognitive regulation. Thus, there may be dysfunction in the interaction of the aspects of the emotional response system in alexithymia with greater activation in the caudate (basal ganglia) and less activation in the mPFC in alexithymics during the IGT.

Thus alexithymics show weak responses in structures necessary for the representation of emotion used in conscious cognition and stronger responses at levels focused on action. This ties in with the blog on an emotional disease? and also  so how is your decision making? which suggested that alcoholics do not use emotion to guide decision making and rely on more motor, or automatic/compulsive parts of the brain to make decisions.

Consequently, alexithymics experience inflexible cognitive regulation, owing to impairment of the emotion guiding system. These dysregulated physiological responses over many years may result in untoward health effects such as drug addiction.

To illustrate this, one study demonstrated that patients with cocaine dependence had higher alexithymia scores compared with healthy control subjects (21).

In a study of 46 inpatients with alcohol abuse or dependence, the total TAS (Toronto Alexithymia Scale) score was significantly higher among those who relapsed after discharge than among those who did not, even when depressive symptoms were taken into account(4)

Cocaine-dependent patients also failed to activate the anterior cingulate and other paralimbic regions during stress imagery, suggesting dysregulation of control under emotional distress in these patients (22).

Instead, cocaine-dependent patients demonstrated greater craving-related activation in the dorsal striatum, a region that has been implicated in reward processing and obsessive–compulsive behaviours. The greater activation associated with alexithymia in men in the right putamen during stress is broadly consistent with earlier studies implicating the striatum in emotional motor responses.

This also corresponds to  the study of  children of alcoholics show significantly more activation in the left dorsal anterior cingulate cortex and left caudate nucleus a region associated with impulsive choice, illustrating perhaps in children of alcoholics a bias in brain decision-making systems as an underlying  elevated risk for alcoholism.

We have also suggested previously a ‘compulsive’ emotional  habit bias in endpoint addiction which reflects a stiumulus response or automatic behaviour in the face of emotional distress, which then influences an automatic decision making profile. This may be the effect of chronic drug use impacting on an inherited emotional expressive-motor decision making vulnerability seen in children of alcoholics.

In simple terms, these vulnerable individuals may recruit more automatic rather than goal-directed areas of the brain when making decisions. This would result in impulsive/compulsive decisions which do not fully consider consequences, negative or otherwise, of their decisions and resultant actions. This decision making profile would then have obvious consequences in terms of a propensity to addiction.

 

References (to be finished)

1. Naqvi, N. H., & Bechara, A. (2009). The hidden island of addiction: the insula.Trends in neurosciences, 32(1), 56-67.

2. Berking M, Margraf M, Ebert D, Wupperman P, Hogmann SG, Junghanns K. Deficits in emotion-regulation skills predict alcohol use during and after cognitive-behavioral therapy for alcohol dependence. Journal of Consulting and Clinical Psychology. 2011;79:307–318

3. Gratz KL, Roemer L. Multidimensional assessment of emotion regulation and dysregulation: Development, factor structure, and initial validation of the Difficulties in Emotion Regulation Scale. Journal of Psychopathology and Behavioral Assessment.2004;26:41–54

4. 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.

5. 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.

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

7.  Moriguchi, Y., & Komaki, G. (2013). Neuroimaging studies of alexithymia: physical, affective, and social perspectives. BioPsychoSocial medicine, 7(1), 8.

8. Miller L. Is alexithymia a disconnection syndrome? A neuropsychological perspective. Int J Psychiatry Med. 1986;7:199–209. doi: 10.2190/DAE0-EWPX-R7D6-LFNY.

9. Sifneos PE. Alexithymia and its relationship to hemispheric specialization, affect, and creativity.Psychiatr Clin North Am. 1988;7:287–292.

10. Buchanan DC, Waterhouse GJ, West SC Jr. A proposed neurophysiological basis of alexithymia. Psychother Psychosom. 1980;7:248–255. doi: 10.1159/000287465.

11. Shipko S. Further reflections on psychosomatic theory. Alexithymia and interhemispheric specialization. Psychotherapy and psychosomatics.

12. Lane RD, Reiman EM, Axelrod B, Yun LS, Holmes A, Schwartz GE. Neural correlates of levels of emotional awareness Evidence of an interaction between emotion and attention in the anterior cingulate cortex. J cognitive neuroscience. 1998;7:525–535. doi: 10.1162/089892998562924.

13. Wingbermühle E, Theunissen H, Verhoeven WMA, Kessels RPC, Egger JIM. The neurocognition of alexithymia: evidence from neuropsychological and neuroimaging studies.Acta Neuropsychiatrica. 2012;7:67–80. doi: 10.1111/j.1601-5215.2011.00613.x.

14. Oscar-Berman, M., & Bowirrat, A. (2005). Genetic influences in emotional dysfunction and alcoholism-related brain damage.

15. Sperling W, Frank H, Martus P, et al. The concept of abnormal hemispheric organization in addiction research. Alcohol Alcohol.2000;35:394–9.

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

17. Stasiewicz, P. R., Bradizza, C. M., Gudleski, G. D., Coffey, S. F., Schlauch, R. C., Bailey, S. T., … & Gulliver, S. B. (2012). The relationship of alexithymia to emotional dysregulation within an alcohol dependent treatment sample.Addictive Behaviors, 37(4), 469-476.

18.  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

19. Moriguchi, Y., & Komaki, G. (2013). Neuroimaging studies of alexithymia: physical, affective, and social perspectives. BioPsychoSocial medicine, 7(1), 8.

20.  Kano M, Fukudo S. The alexithymic brain: the neural pathways linking alexithymia to physical disorders. BioPsychoSocial medicine. 2013;7:1. doi: 10.1186/1751-0759-7-1.

21.  Li, C. S. R., & Sinha, R. (2006). Alexithymia and stress-induced brain activation in cocaine-dependent men and women. Journal of psychiatry & neuroscience,31(2).

22.  Sinha, R., Lacadie, C., Skudlarski, P., Fulbright, R. K., Rounsaville, B. J., Kosten, T. R., & Wexler, B. E. (2005). Neural activity associated with stress-induced cocaine craving: a functional magnetic resonance imaging study.Psychopharmacology, 183(2), 171-180.

Do alcoholics drive through life with Faulty Brakes!

Posted on by alcoholicsguide

There has been a lot of debate in the last thirty – forty years about genetic inheritance – with at least half of children of alcoholic families at risk for later alcoholism. What is less known is what exactly is inherited in our genes? What marks us out for later alcoholism? Prior to drinking are there aspects of our behaviour, personality or emotional responding that marks us out compared to so-called normal healthy types.

Recently research has looked at brain systems which overlap in decision making such as cognitive control over impulsive behaviour and also emotional processing. Children from alcoholics seem to have difficulties with both these overlapping circuits in the brain – they are not only impulsive but also do not seem to process emotions in the same way their “health” peers do. Research has also begun  to show that emotional processing is indeed important to making decisions, as is the ability to inhibit impulsive responses.

It seems  young alcoholics in the making, are not using our emotions  to make decisions and  are also prone to being impulsive. This difficulty with making decisions must shape all other future decisions ?

Youth for families with a history of alcoholism (FH+) are more likely to engage in early adolescent alcohol use (1), they may be more prone to experience the neurotoxic effects of alcohol use during adolescence.

_54075099_teenage_girl_drinking_

Heavy alcohol use during adolescence is related to poorer neuropsychological functioning, including response inhibition (2), working memory (3-5), and decision-making (6).

Neuroimaging studies have shown that alcohol abusing teens have atypical grey matter volume in the PFC (7,8), and subcortical structures, such as the hippocampus (9,10) OFC and the amgydala.

Further, they have reduced integrity of white matter pathways, in both long-range connections between frontal and parietal brain regions as well as in pathways connecting subcortical and higher-order brain areas (11,12).

FMRI studies have found reduced BOLD response in adolescent alcohol abusers
in brain regions important affective decision-making (13).

The raging debate in research has been to whether these deficits are a consequence of heavy alcohol use or if genetic and environmental factors, such as family history of alcoholism, may contribute.

Risk Factor for Alcohol Use Disorders (AUDs): Family History of Alcoholism

The observation that alcoholism runs in families has long been documented
(14-16). Over the past few decades, adoption (17,18) and twin (19)
studies have suggested that there is an increased likelihood of individuals with a family history of alcoholism to develop the disorder themselves (20, 21).

These studies indicate that familial alcoholism is one of the most robust predictors of the development of an AUD during one’s lifetime. Furthermore, this risk factor appears to be stable over time, since it also predicts the chronicity of alcohol dependence at multiple time points (22).
This indicates that higher familial density is often associated with greater
risk (23), with genetic vulnerability accounting for about 30-50% of
individual risk (24-26).

 

One of the best characterized findings in individuals with familial alcoholism are greater impulsivity and difficulties in response inhibition which are commonly seen in this population (27,28), and FH+ individuals are less able to delay reward gratification compared with their peers (29).

Emotional processing and its relationship with executive control has received much less
attention in FH+ individuals.

Alcohol Use Disorders and Emotional Processing

Emotion Recognition and Affective Processing – Research suggests that alcohol use disorder (AUDs)  are associated with deficits in emotion recognition
(30-33), which may be related to atypical brain structure and functioning observed in the
limbic system among alcoholics (34-37).

Alcoholics not only tend to overestimate the intensity of emotions seen in faces  but they also make more negative emotional attributions and often confuse one emotion for another, such as mislabeling disgust as anger or contempt (32). Additionally, these deficits seem to be specific to alcoholism, since alcoholics, both recently abstinent and long-term abstinent, perform poorer on emotion recognition tasks than individuals with other drug abuse history (38). Alcoholics have also been shown to have slower reaction time when recognizing emotions (39).
Furthermore, poorer accuracy on emotion recognition tasks in alcoholics does not improve across the duration of the task, even though better performance is seen over time with other drug abusers (38).

Polysubstance abusing adults, the majority of whom were alcohol abusers, showed emotion recognition deficits on angry, disgusted, fearful, and sad faces (40). Based on the evidence of emotion recognition deficits in alcoholics, it is necessary to determine whether similar difficulties are present in FH+ youth that could be disruptive to emotional functioning and may contribute to the ultimately higher prevalence of alcohol abuse in this population.

Ultimately we may be observing here external emotional processing difficulties in the same manner we observed “internal” emotional processing difficulties in those with alexithymia, the reduced ability to “read” internal emotions of which a majority of alcoholics appear to suffer.

In summary, alcoholics and children of alcoholic families appear to have both external, i.e. recognition of other people’s emotions as well as their own and these may relate to immature development of brain regions which govern emotional, processing, recognition and regulation, which appears to contribute greatly to the initiation and progression of alcohol abuse.

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In addition to emotional processing deficits, alcoholics have various structural
and functional abnormalities in affective processing brain regions. Studies of the limbic system have found reduced volume in subcortical structures, including the amygdala, thalamus, ventral striatum, and hippocampus among adult alcoholics (41,42). Alcoholics with smaller amygdalar volumes, are more likely to continue drinking after six months of abstinence (37).

Marinkovic et al. (2009) alcoholics exhibited both amygdalar and hippocampal hypoactivity during face encoding, and when recognizing deeply encoded faces, alcoholics had significantly reduced amygdalar activity to positive and negative emotional expressions compared with controls (35). These results help explain findings in behavioral studies of alcoholics that have found considerable evidence for emotion recognition deficits in this population.

Furthermore, during emotion identification, alcoholics showed comparable
performance to controls, but had reduced brain response in the affective division of the
anterior cingulate cortex (ACC) to disgust and sadness, with this lack of affective response to aversive stimuli believed to underlie disinhibitory traits in AUDs (36).

There is also evidence to suggest that non-alcohol abusing FHP individuals
share similar deficits in affective systems to alcohol abusers, including reduced
amygdalar volume, less amygdalar activity in response to emotional stimuli, and high
rates of internalizing symptoms such as anxiety and depression (37; 45-47).

Furthermore, research examining the relationship between emotional
processing and cognition has found that poor inhibition in individuals with co-morbid
substance and alcohol abuse is associated with atypical arousal in response to affective images (48), and affective measures in FH+ alcoholics also relate to deficits in executive functioning, e.g impulsivity (47).

This suggests that familial history of AUDs may put individuals at greater risk for problems with emotional processing and associated disruptions in executive functioning (47), which could, in turn, increase risk for alcohol abuse (49).

As we suggested previously, in relation to decision making profiles, in those at risk, those with alexithymia and also with cocaine addicts, decision making often involves more emotion expressive-motor areas of the brain like the caudate nucleus which is more of a “feel it-do it” type of reaction to decision making or a emotionally impaired or distress-based impulsivity. If there is a difficulty  processing emotions, these emotions can not be used as a signal to guide adaptive, optimal decisions. Decisions appear more compulsive and short term.

It may be this tendency to act now, rather than later,  that defines the vulnerability in FH+ children. It is like driving through life with faulty brakes on decision making, which sets up a chain of maladaptive choices such as alcohol abuse which then damages these affective based decision making regions of the brain even more, with increasing  deleterious consequences as the addiction cycle progresses until the endpoint of addiction of very limited choice of behaviour as emotional distress acts eventually as a stimulus response to alcohol use.  Emotional processing usurped by compulsive responding.

 

References

Main reference – Cservenka, A., Fair, D. A., & Nagel, B. J. (2014). Emotional Processing and Brain Activity in Youth at High Risk for Alcoholism. Alcoholism: Clinical and Experimental Research.

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2. Ferrett, H.L., Cuzen, N.L., Thomas, K.G., Carey, P.D., Stein, D.J., Finn, P.R., Tapert, S.F., Fein, G., 2011. Characterization of South African adolescents with alcohol use disorders but without psychiatric or polysubstance comorbidity. Alcohol Clin Exp Res 35, 1705-1715.

3. Brown, S.A., Tapert, S.F., 2004. Adolescence and the trajectory of alcohol use: basic to clinical studies. Ann N Y Acad Sci 1021, 234-244.

4.   Brown, S.A., Tapert, S.F., Granholm, E., Delis, D.C., 2000. Neurocognitive functioning of adolescents: effects of protracted alcohol use. Alcohol Clin Exp Res 24, 164-171.

5.   Squeglia, L.M., Schweinsburg, A.D., Pulido, C., Tapert, S.F., 2011. Adolescent binge drinking linked to abnormal spatial working memory brain activation: differential gender effects. Alcohol Clin Exp Res 35, 1831-1841.

6. Johnson, C.A., Xiao, L., Palmer, P., Sun, P., Wang, Q., Wei, Y., Jia, Y., Grenard, J.L.,  Stacy, A.W., Bechara, A., 2008. Affective decision-making deficits, linked to a dysfunctional ventromedial prefrontal cortex, revealed in 10th grade Chinese adolescent binge drinkers. Neuropsychologia 46, 714-726.

7. De Bellis, M.D., Narasimhan, A., Thatcher, D.L., Keshavan, M.S., Soloff, P., Clark, D.B.,  2005. Prefrontal cortex, thalamus, and cerebellar volumes in adolescents and young adults with adolescent-onset alcohol use disorders and comorbid mental disorders. Alcohol Clin Exp Res 29, 1590-1600.

8.  Medina, K.L., McQueeny, T., Nagel, B.J., Hanson, K.L., Schweinsburg, A.D., Tapert, S.F., 2008. Prefrontal cortex volumes in adolescents with alcohol use disorders: unique gender effects. Alcohol Clin Exp Res 32, 386-394.

9.  De Bellis, M.D., Clark, D.B., Beers, S.R., Soloff, P.H., Boring, A.M., Hall, J., Kersh, A., Keshavan, M.S., 2000. Hippocampal volume in adolescent-onset alcohol use disorders. Am J Psychiatry 157, 737-744.

10.  Nagel, B.J., Schweinsburg, A.D., Phan, V., Tapert, S.F., 2005. Reduced hippocampal volume among adolescents with alcohol use disorders without psychiatric comorbidity. Psychiatry Res 139, 181-190.

11.  Bava, S., Jacobus, J., Thayer, R.E., Tapert, S.F., 2013. Longitudinal changes in white matter integrity among adolescent substance users. Alcohol Clin Exp Res 37 Suppl 1, E181-189.

12.   McQueeny, T., Schweinsburg, B.C., Schweinsburg, A.D., Jacobus, J., Bava, S., Frank, L.R., Tapert, S.F., 2009. Altered white matter integrity in adolescent binge drinkers. Alcohol Clin Exp Res 33, 1278-1285.

13. Xiao, L., Bechara, A., Gong, Q., Huang, X., Li, X., Xue, G., Wong, S., Lu, Z.L., Palmer, P., Wei, Y., Jia, Y., Johnson, C.A., 2012. Abnormal Affective Decision Making Revealed in Adolescent Binge Drinkers Using a Functional Magnetic Resonance Imaging Study. Psychol Addict Behav.

14. Cotton, N.S., 1979. The familial incidence of alcoholism: a review. J Stud Alcohol 40, 89-116.

15. Goodwin, D.W., 1979. Alcoholism and heredity. A review and hypothesis. Arch Gen Psychiatry 36, 57-61.

16.  Schuckit, M.A., 1985. Genetics and the risk for alcoholism. Jama 254, 2614-2617

17. Bohman, M., 1978. Some genetic aspects of alcoholism and criminality. A population of adoptees. Arch Gen Psychiatry 35, 269-276.

18. Cloninger, C.R., Bohman, M., Sigvardsson, S., 1981. Inheritance of alcohol abuse. Cross-fostering analysis of adopted men. Arch Gen Psychiatry 38, 861-868.

19. Merikangas, K.R., Stolar, M., Stevens, D.E., Goulet, J., Preisig, M.A., Fenton, B., Zhang, H., O’Malley, S.S., Rounsaville, B.J., 1998. Familial transmission of substance use disorders. Arch Gen Psychiatry 55, 973-979

20. Finn, P.R., Kleinman, I., Pihl, R.O., 1990. The lifetime prevalence of psychopathology in men with multigenerational family histories of alcoholism. J Nerv Ment Dis 178, 500-504.

21. Goodwin, D.W., 1985. Alcoholism and genetics. The sins of the fathers. Arch Gen Psychiatry 42, 171-174.

22. Hasin, D., Paykin, A., Endicott, J., 2001. Course of DSM-IV alcohol dependence in a community sample: effects of parental history and binge drinking. Alcohol Clin Exp Res 25, 411-414.

23. Hill, S.Y., Yuan, H., 1999. Familial density of alcoholism and onset of adolescent drinking. J Stud Alcohol 60, 7-17.

24.   Heath, A.C., Bucholz, K.K., Madden, P.A., Dinwiddie, S.H., Slutske, W.S., Bierut, L.J., Statham, D.J., Dunne, M.P., Whitfield, J.B., Martin, N.G., 1997. Genetic and environmental contributions to alcohol dependence risk in a national twin sample: consistency of findings in women and men. Psychol Med 27, 1381-1396.

25. Kaprio, J., Koskenvuo, M., Langinvainio, H., Romanov, K., Sarna, S., Rose, R.J., 1987. Genetic influences on use and abuse of alcohol: a study of 5638 adult Finnish twin brothers. Alcohol Clin Exp Res 11, 349-356.

26.  Knopik, V.S., Heath, A.C., Madden, P.A., Bucholz, K.K., Slutske, W.S., Nelson, E.C., Statham, D., Whitfield, J.B., Martin, N.G., 2004. Genetic effects on alcohol dependence risk: re-evaluating the importance of psychiatric and other heritable risk factors. Psychol Med 34, 1519-1530.

27. Acheson, A., Richard, D.M., Mathias, C.W., Dougherty, D.M., 2011a. Adults with a family history of alcohol related problems are more impulsive on measures of response initiation and response inhibition. Drug Alcohol Depend 117, 198-203.

28.  Saunders, B., Farag, N., Vincent, A.S., Collins, F.L., Jr., Sorocco, K.H., Lovallo, W.R., 2008. Impulsive errors on a Go-NoGo reaction time task: disinhibitory traits in relation to a family history of alcoholism. Alcohol Clin Exp Res 32, 888-894.

29.  Acheson, A., Vincent, A.S., Sorocco, K.H., Lovallo, W.R., 2011b. Greater discounting of delayed rewards in young adults with family histories of alcohol and drug use disorders: studies from the Oklahoma family health patterns project. Alcohol Clin Exp Res 35, 1607-1613.

30. Foisy, M.L., Kornreich, C., Petiau, C., Parez, A., Hanak, C., Verbanck, P., Pelc, I., Philippot, P., 2007b. Impaired emotional facial expression recognition in alcoholics: are these deficits specific to emotional cues? Psychiatry Res 150, 33-41.

31.  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. J Stud Alcohol 66, 673-681.

32.  Philippot, P., Kornreich, C., Blairy, S., Baert, I., Den Dulk, A., Le Bon, O., Streel, E., Hess, U., Pelc, I., Verbanck, P., 1999. Alcoholics’ deficits in the decoding of emotional facial expression. Alcohol Clin Exp Res 23, 1031-1038.

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

34.  Gilman, J.M., Hommer, D.W., 2008. Modulation of brain response to emotional images by alcohol cues in alcohol-dependent patients. Addict Biol 13, 423-434.

35. Marinkovic, K., Oscar-Berman, M., Urban, T., O’Reilly, C.E., Howard, J.A., Sawyer, K., Harris, G.J., 2009. Alcoholism and dampened temporal limbic activation to emotional faces. Alcohol Clin Exp Res 33, 1880-1892.

36.  Salloum, J.B., Ramchandani, V.A., Bodurka, J., Rawlings, R., Momenan, R., George, D., Hommer, D.W., 2007. Blunted rostral anterior cingulate response during a simplified decoding task of negative emotional facial expressions in alcoholic patients. Alcohol Clin Exp Res 31, 1490-1504.

37.  Wrase, J., Makris, N., Braus, D.F., Mann, K., Smolka, M.N., Kennedy, D.N., Caviness, V.S., Hodge, S.M., Tang, L., Albaugh, M., Ziegler, D.A., Davis, O.C., Kissling, C., Schumann, G., Breiter, H.C., Heinz, A., 2008. Amygdala volume associated with alcohol abuse relapse and craving. Am J Psychiatry 165, 1179-1184.

38.  Kornreich, C., Foisy, M.L., Philippot, P., Dan, B., Tecco, J., Noel, X., Hess, U., Pelc, I., Verbanck, P., 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 Res 119, 251-260.

39.  Maurage, P., Campanella, S., Philippot, P., Martin, S., de Timary, P., 2008. Face processing in chronic alcoholism: a specific deficit for emotional features. Alcohol Clin Exp Res 32, 600-606.

40.  Fernandez-Serrano, M.J., Perez-Garcia, M., Schmidt Rio-Valle, J., Verdejo-Garcia, A., 2010. Neuropsychological consequences of alcohol and drug abuse on different components of executive functions. J Psychopharmacol 24, 1317-1332.

41.  Durazzo, T.C., Tosun, D., Buckley, S., Gazdzinski, S., Mon, A., Fryer, S.L., Meyerhoff, D.J., 2011. Cortical thickness, surface area, and volume of the brain reward system in alcohol dependence: relationships to relapse and extended abstinence. Alcohol Clin Exp Res 35, 1187-1200.

42.   Makris, N., Oscar-Berman, M., Jaffin, S.K., Hodge, S.M., Kennedy, D.N., Caviness, V.S., Marinkovic, K., Breiter, H.C., Gasic, G.P., Harris, G.J., 2008. Decreased volume of the brain reward system in alcoholism. Biol Psychiatry 64, 192-202.

43.   Benegal, V., Antony, G., Venkatasubramanian, G., Jayakumar, P.N., 2007. Gray matter volume abnormalities and externalizing symptoms in subjects at high risk for alcohol dependence. Addict Biol 12, 122-132.

44.  Glahn, D.C., Lovallo, W.R., Fox, P.T., 2007. Reduced amygdala activation in young adults at high risk of alcoholism: studies from the Oklahoma family health patterns project. Biol Psychiatry 61, 1306-1309.

45.   Hill, S.Y., De Bellis, M.D., Keshavan, M.S., Lowers, L., Shen, S., Hall, J., Pitts, T., 2001. Right amygdala volume in adolescent and young adult offspring from families at high risk for developing alcoholism. Biol Psychiatry 49, 894-905.

46.  Oscar-Berman, M., Bowirrat, A., 2005. Genetic influences in emotional dysfunction and alcoholism-related brain damage. Neuropsychiatr Dis Treat 1, 211-229.

47.  Sinha, R., Parsons, O.A., Glenn, S.W., 1989. Drinking variables, affective measures and neuropsychological performance: familial alcoholism and gender correlates. Alcohol 6, 77-85

48.  Verdejo-Garcia, A., Bechara, A., Recknor, E.C., Perez-Garcia, M., 2006. Executive dysfunction in substance dependent individuals during drug use and abstinence: an examination of the behavioral, cognitive and emotional correlates of addiction. J Int Neuropsychol Soc 12, 405-415.

49.  Fox, H.C., Hong, K.A., Sinha, R., 2008. Difficulties in emotion regulation and impulse control in recently abstinent alcoholics compared with social drinkers. Addict Behav 33, 388-394

 

Emotional Dysregulation, recovery and relapse

Posted on by alcoholicsguide

Throughout our blogs thus far, we have attempted to highlight how emotional dysregulation appears to prevalent to all aspects of alcoholism and addiction from pre-morbid vulnerability to endpoint compulsive addictive behaviours.

Here we highlight a few articles which have considered how prevalent is emotional dysregulation in alcoholism and addiction in early abstinence/recovery. 

Early abstinence from chronic alcohol dependence is associated with increased emotional sensitivity to stress-related craving as well as changes in brain systems associated with stress and emotional processing.

Early abstinence from alcohol is associated with changes in neural stress and reward systems that can include atrophy in subcortical and frontomesal regions (1).

Moreover, recent imaging studies have shown that these brain regions are also associated with the experience and regulation of emotion (2).

While alcohol-related changes in emotion, stress and reward-related brain regions have been well documented difficulties in emotion regulation (ER) have not been studied much.

bar_of_destruction_1874__medium

One study (3) examined ER in early abstinent alcohol-dependent individuals compared with social drinkers using the Difficulties in Emotion Regulation Scale (DERS).

The DERS is an inclusive scale and defines ER in terms of four major factors: the understanding of emotion, the acceptance of emotion, the ability to control impulsive behavior and the ability to access ER strategies benefiting the individual and the specific goals of the situation. The scale has been validated in cocaine dependent patients (4) and on alcohol dependent individuals.

ER difficulties in treatment-engaged alcohol dependent (AD) patients during a period of early abstinence that is marked by an overall distress state. AD patients reported an overall problem with emotion regulation compared with SDs in the first few days of abstinence; in particular with emotional awareness and impulse control. Following protracted abstinence, AD patients significantly improved awareness and clarity of their emotional experience, and only significant problems with impulse control persisted.

This is consistent with neuro-imaging studies showing chronic alcohol abuse to be associated with stress and cue-related neuroadaptations in the medial prefrontal and anterior cingulate regions of the brain (6), which are strongly implicated in the self-regulation of emotion and behavioral self-control (7). As impulsivity in distress states may reflect a change in priority from self-control to affect regulation (8 ).

As we have seen in other blogs and articles (5) these areas are those which improve in short term abstinence/recovery.

Cocaine-dependent individuals also report emotion regulation difficulties, particularly during early abstinence (4). Additionally, protracted distress-related impulse control problems suggest potential relapse vulnerability Difficulties concerning emotional clarity and awareness compared with controls were observed which suggests that cocaine dependent individuals were less able to acknowledge and/or have a clear understanding of their emotions.

Clarity and awareness of emotions could represent early processing components of emotional competence (9) and may be integral to the maintenance of drug use.

The cocaine addicts appeared to have greater difficulty in developing effective emotional coping strategies  (i.e. they would be more likely to believe that little could be  done to change an emotionally stressful situations.) They were also found to report significantly higher scores on the Impulse subscale of the DERS compared with controls, indicating difficulties with regard to inhibiting inappropriate or impulse behaviors under stressful situations which can prompt relapse.

References

1. Bartsch, A. J., Homola, G., Biller, A., Smith, S. M., Weijers, H. G., Wiesbeck, G. A., et al. (2007). Manifestations of early brain recovery associated with abstinence from alcoholism. Brain, 130(Pt 1), 36−47

2. Fox, H. C., Hong, K. A., & Sinha, R. (2008). Difficulties in emotion regulation and impulse control in recently abstinent alcoholics compared with social drinkers. Addictive Behaviors, 33(2), 388-394.

3. Ochsner, K.N., Gross, J.J., 2005. The cognitive control of emotion. Trends Cogn. Sci. 9, 242–249

4. Fox, H. C., Hong, K. A., & Sinha, R. (2008). Difficulties in emotion regulation and impulse control in recently abstinent alcoholics compared with social drinkers. Addictive Behaviors, 33(2), 388-394.

5. Sinha, R., & Li, C. S. (2007). Imaging stress- and cue-induced drug and alcohol craving: Association with relapse and clinical implications. Drug and Alcohol Review, 26(1), 25−31.

6. Connolly, C. G., Foxe, J. J., Nierenberg, J., Shpaner, M., & Garavan, H. (2012). The neurobiology of cognitive control in successful cocaine abstinence. Drug and alcohol dependence, 121(1), 45-53.

7. Baumeister, R.F., Heatherton, T.F., Tice, D.M., 1994. Loosing Control: How and Why People Fail at Self-regulation. Academic Press, San Diego, CA

8.  Tice, D.M., Bratslavsky, E., Baumeister, R.F., 2001. Emotional distress regulation takes precedence over impulse control: if you feel bad, do it! J. Pers Soc. Psychol. 80, 53–67.

9. Salovey, P., Stroud, L.R., Woolery, A., Epel, E.S., 2002. Perceived emotional intelligence, stress reactivity, and symptom reports: further explorations using the trait Meta-mood scale. Psychol. Health 17, 611–627

 

Intolerance of Uncertainty

Posted on by alcoholicsguide

Like many recovering alcoholics I know I have a real problem with “Not projecting into the future” but staying in the moment or even the day. Why is this? When I “project” or even consider a near future event I can feel distressed by it. I want to do something about it now! Not later.

The future seems to be urgently now.

I have long researched why this is? I seem to become overwhelmed at times by future tense and it is not even due to future events being that distressing in themselves. I just have this constant need to act now rather than later. I have an urgency or a negative urgency or in other words a  distress based impulsivity which prompts a desire to act now, make a decision now rather than later. I call this a compulsion to act  because a distress state compels me to make a decision to act now.

As I have mentioned in previous blogs, alcoholics appear to have a bias in decision making towards choose the short term solution over a long term one, even though the long term solution will yield greater gains. There are various  theories on why this is so. Sometimes it appears like a “fight or flight” response!

My theory is that I am very poor at tolerating uncertainty and what is the future but uncertain. I have  an “unconscious” negative bias about the future, linked at times to a tendency to then catastrophize.

This intolerance of uncertainty is seen in other disorders, such as anxiety, obsessive-compulsive and post traumatic stress disorders as well as in eating disorders but it is rarely researched in alcoholism.

I believe when confronted with a decision about the future I often make a decision to relieve a distress which manifests as an unpleasant feeling state which compels me, via a stimulus response to act now. Distress is the stimulus, acting now is the response.

I am not saying that I have to be in a negative frame of mind for this to occur. It is simply a decision making bias I have when left to my own devices.   It is the reason I speak to others when making important decisions in life because the need to relief distress can show in the mind as a good idea when it is often on reflection not such a great idea.

This is due to distress being a stress-fuelled experience and excessive stress reduces the awareness of future consequence of a decision. It seems like a good idea at the time because it relieves distress. To the brain this is a good idea.  It is a automatic response of the dorsal striatum, an implicit memory (procedural) system, that requires one to retrospectively rationalise and justify the automatic responding of this area of the brain, it justifies a previous action in other words, thus a decision is represented in the mind as a good idea, what was most urgently required!

These rationalisations and justifications through time can become automatic schemas and are automatically activated following a compulsive response. Some of us are probably familiar with these schemas being a big part of our alcohol and drug use. As we needed to use, we had automatic addiction schemas following shortly after our decisions to head to the pub or to score some drugs or even to propel some decisions, as the consequence of distress states. It is these habitual response, based on distress states which bias decisions making to acting now, even in recovery.

I came across an article (1) which looked at this intolerance of uncertainty in relation to decision making and came up with similar conclusions to the above. “high IU (intolerance of uncertainty) predicted shorter wait times and more frequent selection of the immediate, less valuable (and riskier) reward. We take this tendency as evidence that IU was associated with an aversion to waiting in a state of uncertainty. One might argue that choices for the more immediate, less valuable reward might reflect an aversion to waiting per se…, the delay associated with the more valuable reward in the
current study appears to have magnified the unpleasant affective responses to uncertainty… delay is provoking unpleasant affective responses, choices for the smaller, immediate reward can be seen as avoidance of distress.” Decisions are thus like an “escape route” and more based on emotional avoidance.  “That is, the affective consequences of uncertainty may play a more central role in determining behavior than uncertainty itself…decision  making tendencies among those high in IU may be maintained through negative reinforcement…to  reduce or eliminate affectively unpleasant circumstances that accompany waiting in uncertainty.”

These “unpleasant affective responses” are distress based and lead to a negative urgency to act now.

References

1. Luhmann, C. C., Ishida, K., & Hajcak, G. (2011). Intolerance of uncertainty and decisions about delayed, probabilistic rewards. Behavior therapy, 42(3), 378-386.

 

 

 

 

So how is your decision making?

Posted on by alcoholicsguide

 

In this blog we will look at something  which we believe is apparent in alcoholics,  the decision making difficulties very present  in active alcoholism and to a lesser extent in recovery.

By this we mean there is a tendency to use the short term fix over more long term considerations, a more “want it now” than delayed gratification. This may be down to internal body (somatic signals) which can give rise to an unpleasant feeling at times prior making a decision, as if we sometimes make decisions based on a distress feeling rather than forward thinking, that we choose a decision to alleviate this feeling. It has been suggested by some authors that emotions do not guide the decision making of alcoholics and addicts properly and this is the reason why they are maladpative.

Equally it may be that certain somatic states such as the so-called ‘primary inducers’ of feeling, mainly centring on  the “anxious” amgydala which helps in our responding to body states associated with chronic drug and alcohol abuse, such as alleviated, chronic stress (and it’s manifestation as emotional distress) have the potential to dominate decisions, to treat decisions in a habitual, automatic manner and not in via  a thoughtful consideration of the possible outcome of our decisions.  

Once science thought we make sensible reasonable decision based on pure reason but it has become clear in recent decades that we use emotional signals ,”gut feelings” to make decisions too.

It appears that if we don’t access these emotional signals we are destined to make the move decisions over and over again, regardless of their outcome and consequence.

The extreme example of emotions guiding decisions, would be running from a rampaging lion, this decision is make emotionally, via the quick and dirty route, the “low road” according to Le Doux. The amygdala, which directs signal traffic in the brain when danger lurks, receives quick and dirty information directly from the thalamus in a route that neuroscientist Joseph LeDoux dubs the low road.

This shortcut allows the brain to start responding to a threat within a few thousandths of a second. The amygdala also receives information via a high road from the cortex. Although the high road encodes much more detailed and specific information, the extra step takes at least twice as long— and could mean the difference between life and death. 

Emotional dysregulation and altered reward sensitivity may underpin impulsive behavior and poor decision-making.

Both of these tendencies can be seen in the “real-world” behavior of addicted individuals, but can also be studied using laboratory-based paradigms.

Addiction is associated with a loss of control over drug use which continues in spite of individuals’ awareness of serious negative consequences.

Increased reward  alone, as seen in alcoholics and resulting in attentional bias and automatic responding to cues (internal and external)  do not seem a sufficient explanation for this persistent maladaptive behavior of addiction.

Instead there must be additional deficits in decision-making and/or inhibiting these maladaptive behaviours and which critically involve  emotional factors exerting a detrimental effect on cognitive function.

The term “impulsivity” is often used to describe behavior characterized by excessive approach with an additional failure of effective inhibition (1) and has consistently been found to be associated with substance dependence (2,3).

Impulsivity is a complex multifaceted construct which has resulted in numerous additional definitions such as, “the tendency to react rapidly or in unplanned ways to internal or external stimuli without proper regard for negative consequences or inherent risks” (4), or “the tendency to engage in inappropriate or maladaptive behaviors” (2).

This we suggest could be the consequence of either the push or pull of dsyregulated emotions.

By this we mean we either do not use emotions properly to feel the right  decision as we cannot process them properly to use them as “guides” in decision making or these dsyregulated emotions become distressing and prompt more compulsive decision making, effectively to relieve the distress of these negative emotional states.

Either way it appears that not only do alcoholics, but also children of alcoholics, use a more motor-expressive style of decision making, i.e. they recruit more compulsive regions of the brain rather than prefrontal cortex areas normally used used to make planned, evaluative decisions.

It appears that emotional dsyregulation is at the heart of maladaptive decison making in alcoholics and addicts.

Distressed Based Impulsivity?

Emotional impulsivity more closely reflects the interaction between emotional and cognitive processes. Negative urgency,   the disposition to engage in rash action when experiencing extreme negative affect (mood, emotion or anxiety), or in simple terms, distress-based impulsivity, was found to be the best predictor of alcohol, drug, social, legal, medical, and employment problems (5).

Substance users frequently make decisions with a view to immediate gratification (6-10), and may be less sensitive to negative future outcome (‘myopia for the future’) (11,12). It has been hypothesized that substance users are less able to use negative feedback to guide and adjust ongoing behavior (12).

These findings highlight a specific role for emotion.

Emotional impulsivity traits appear distinct from other impulsivity traits and particularly pertinent for dependence, reliably differentiating substance users from controls, and also predicting poorer outcomes in dependent individuals.

The impact of emotional processing on cognitive performance.

A common behavioral measure of impulsivity is the delay discounting task which measures the degree of temporal discounting. Participants are faced with the choice of a small immediate reward, or a larger delayed reward; choosing the smaller immediate reward indicates a higher degree of impulsivity.

Increased discounting of larger delayed rewards has been found in heroin- (13), cocaine- (14), and alcohol (15 -17) -dependent individuals.

Enhanced discounting is also seen during opiate withdrawal, possibly reflecting the emergence of negative affect states during withdrawal (18).

Withdrawal is a period of heightened noradrenaline ( a “stress” chemical”) and this excessive stress has a bearing on decision making, and in relapse.

High levels of negative affect, anxiety/stress sensitivity a in substance dependent individuals may therefore contribute to observed deficits on decision-making tasks. Stress mechanisms are considered to be important mechanisms underlying relapse (19), suggesting these emotional traits impair real life decision-making.

Studies directly assessing the role of emotional states on decision-making in opiate addiction have shown that trait and state anxiety are negatively correlated with performance on the the Iowa Gambling Task – IGT (20). Furthermore, stress induction using the Trier Social Stress Test, was shown to produce a significant deterioration in IGT performance in long term abstinence and newly abstinent heroin users, but not in comparison subjects.

Treatment with the B adrenocepter antagonist propranolol blocked the deleterious effect of stress on IGT performance, supporting the role of the noradrenergic system in the generation of negative emotional states in substance dependence (21).

These findings indicate that conditioned emotional responses, i.e. stress based emotional response, impair decision-making.

The impact of emotion on impulsive action and decision making

Planning systems (also referred to as deliberative, cognitive, reflective or executive systems) are “goal-directed” systems that allow an agent to consider the possible consequences or outcomes of its actions to guide behavior. Habit systems mediate behaviors that are triggered in response to certain stimuli or situations but without consideration of the consequences.

“Habit” systems do not mean we are calling addiction is a habit, it simply means behaviour is automatic, ingrained, individuals respond immediately, without future consequence  to certain stimulus, such as stress or emotional distress. It is a conditioned response!

Brain areas underlying these conditioned or Pavlovian responses include the amygdala, which identifies the emotional significance or value of external stimuli, and the ventral  striatum, which mediates motivational influences on instrumental responding (22), and their connections to motor circuits (23).

Thus, it has been argued that emotions constitute a decision-making system in their own right, exerting a dominant effect on choice in situations of opportunity or threat (24).

It should be noted here, that in the addiction cycle, as it progresses towards endpoint addiction and compulsive use of substances, there is a stress based reduction  in prefrontal cognitive control over behaviour, and a responding more based on automatic emotive-motoric regions of the brain such s the dorsal striatal (DS) (and basal ganglia). Reward processing moves to the DS also from the ventral striatum (VS).

Thus stress modulates instrumental action in favour of the DS-based habit system at the expense of the PFC-based goal-directed system, also seen in hypertrophy of the DS and hypotrophy of the PFC.

This shift from cognitive to automatic is also the result of  excessive engagement of habitual processes, by partly by affecting the contribution of multiple memory systems on behaviour. We suggest that emotional stress via amgydaloid activity knocks out the hippocampal (explicit) memory in favour of the DS which is also a memory system, that of implicit memory, the procedural memory.

In lien with addiction severity, the brain appears to implode inwards towards compulsive behaviours of sub-cortical areas such as the DS modulated by the amgydala from more conscious cognitive control areas of the cortex. In fact, it is possible to say that this conscious cognitive control diminishes.

Recent evidence suggests this role of stress in shifting goal-directed control to habitual control of behavior (25). This effect appears to be mediated by the action of both cortisol and noradrenaline (26).

More importantly, perhaps for our argument is that , this shift from hippcampal to DS memory is also a function of a “emotional arousal habit bias”, as seen in post traumatic stress disorder,  via amgydaloid hyperactivity, or distress based hyperactivity,  which results in emotional distress acting as a stimulus to the automatic responding of the DS. Affect related behaviour, in essence, becomes more compulsively controlled also.

In simple terms, negative urgency, may bias an automatic responding towards amgydaloid activation of the dorsal striatum and away from cortical areas such as the ventromedial cortex  – vmPFC (27 ) which is involved in emotionally guided decision making and this may have consequence for decision making as decision making involves  responding to stimulus such as emotionally provoking stimuli.

One study (28) showed this vmpfc to be hyperactive in recently abstinent alcoholics, perhaps as the result of altered stress systems which create a state called allostasis, and when further stressed responding moved to the more compulsive regions of the brain listed above. This suggest to us, that there are inherent difficulties with emotional dysregulation, particularly in early abstinence/recovery and that these resources when taxed further by seemingly stressful decision making may be dealt with via a need to make a decision to relieve this “distress” feeling rather than achieve a long term outcome. Relieving this distress is thus the outcome most urgent.

Thus for some alcoholics there is an overtaxing of the areas implicated in emotional regulation and thus emotionally guided decision making and under extreme stress we suggest this switches to more a more compulsive decision making profile.

The habit system chooses actions based upon stored associations of their values from past experience; through training, an organism learns the best action to take in a certain situation. Upon recognition of the situation again this “best action” will automatically be initiated, without consideration of consequences of such an action. This process is very fast but inflexible, unable to adapt quickly to changes in the value of outcomes (29,30).

Thus although emotion can guide decision-making when it is integral to the task at hand, emotional responses that are excessive can be detrimental (31).

Dorsal prefrontal regions are also involved in the regulation of affective states (32). Excessive emotion is likely to require increased regulation by these areas (33,34).

Dorsal prefrontal regions are additionally important in decision-making and inhibitory control, thus high levels of emotion that require regulation may limit resources available for these functions, which may contribute to deficits in decision-making.

As we mentioned this PFC control becomes impaired in the addiction cycle with automatic responding becomes more prevalent. This is especially the result of the emotional manifestation of chronic stress which is distress. We suggest this distress can act as a switch between conscious and automatic (unconscious) responding and this has consequences for decision making.

Given the crucial role of emotions in the processes of decision-making as described above, it follows that dysregulation of emotional processing may contribute to the observed decision-making deficits observed in substance dependent individuals. Decisions are driven by distress or negative affect and appear to favour now over then/later.

Looking Inside the Brain

A consistent finding of neuroimaging studies of decision-making in substance dependence is hypoactivation of the prefrontal cortex (35-37), 

Chronic drug use is consistently associated with VPFC, DLPFC and antior cingulate or ACC  gray matter loss in cocaine and alcohol dependence (38-42) and reduced prefrontal neuronal viability in opiate dependence (43,44). VPFC and DLPFC loss have been shown to predict both impaired performance on the IGT (45) and preference for immediate gratification in delay discounting tasks (37)

These areas and others involved in emotional regulation such as the hippocampus, orbitofrontal cortex  and insula show morphological abnormalities and the  emotional regulation neural network as a whole appears to have functionality and connectivity impairments.

These all suggest emotions are not being utilized properly to guide decisions. This may even appear as unregulated and distressing with the brain experiencing this distress rather than processed emotions.

A similar decision making profile is seen in alexithymia, where there is a difficulty labelling and processing emotions and thus using them to guide decision making which appears to result in recruitment of more compulsive or motor expressive areas of the brain outlined here. There are also similar morphological, neurobiological and connectivity impairments as seen in addiction. Cocaine addicts also  have a similar decision making profile as do children of alcoholics, before they start to use substances.

Whether these separate groups all have distress prompting this decision making profile  or whether it is unpleasant feeling state based on not fully processing emotion is open to debate.

As the prefrontal regions of the planning system are impaired in substance dependence, this compromises both the ability to generate affective states relating to long term goals and the ability to exert executive inhibitory control over drug-seeking thoughts and actions .

Dorsal prefrontal regions are involved in the regulation of affective states . Therefore excessive anxiety  would require increased regulation by these areas. Studies have shown dorsal prefrontal regions to be important in regulating reducing amygdala activity . Considering these prefrontal regions are important for  decision-making and anxiety regulation would limit the resources available for effective decision-making within the planning system and would not be able to inhibit more amgydaloid, or compulsive responding.

Bechara  concluded that  an impaired ability to use affective signals to guide behavior underlie impaired decision-making in these individuals. We forward the idea that distress signals guide this decision making and behaviour via a compulsive desire to automatically act to relieve a distress state. Whether via an unprocessed emotional state or as the consequence of the addiction cycle and excessive chronic distress recruiting compulsive parts of the brain.

Either way emotional processing and regulation deficits lie at the heart of these decision making difficulties! 

Now is chosen instead of later, short term gains rather than long term higher gains, because of the negative urgency to act now, to relieve a distress, which automatically, not consciously, devalues future outcome.

The future is now in other words.

There is a distress based urgency to act this moment, not later.  It is this desire to compulsively act which may give rise to obsessive compulsive behaviours, based on the desire to relieve distress not on the relative merits of a future consequence.

It can appear as a “little emergency” not a choice, the “flight or fight” response that delay discounting could possible be measuring and that excessive noradrenaline and glucocorticoids (stress chemicals) prompt – it has to be done, needs to be done now!

 

References (to  be included)

 

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An Emotional Disease?

Posted on by alcoholicsguide

Is Addiction an Emotional Disease!?

“Addiction”, is widely viewed as a chronic, relapsing, neurobiological disorder, characterized by compulsive use of alcohol or substances, despite serious negative consequences. It involves both physiological and psychological dependence and leads to the emergence of a negative emotional state.  The Diagnostic and Statistical Manual of Mental Disorders, DSM-5, combines DSM-IV categories of substance abuse and dependence into a single disorder, on a continuum from mild to severe.  The previous definition of addiction by the American Society of Addiction Medicine (ASAM) includes the terms, craving, persistent risk, and emphasizes risk of relapse after periods of abstinence triggered by exposure to substance-related cues and emotional stressors . This conceptualisation points to the role of substance-related cues, e.g., environmental stimuli that are strongly associated with the effects of the administration of substances and acquire incentive salience through Pavlovian conditioning, as well as stress (an internal cue), as major determinants of relapse.

For example in terms of the reasons for relapse implicated in much research, alcoholics relapse due to ‘cue-reactivity’ i.e. they see ‘people, places, or things’ associated with their drinking past and they are drawn to it and simply relapse.

 In some years of recovery, we have rarely heard of a committed abstinent alcoholic addict in recovery who relapsed simply because he/she was lured siren like to some cue associated stimuli. That is not to say cue reactivity is not a valid construct, it is obviously. Recovering alcoholics  exhibit an automatic, that is involuntary,  attentional bias towards drug and alcohol-related “cues”. This is a torturous aspect of early recovery thus most therapeutic regimes advise those in early abstinence and recovery to avoid “people, places and things” that act as  cue-associated stimuli. In fact, some in early recovery do challenge this only to learn painfully as the result by thinking they can spend time, like before, in drinking establishments,  only to find that it is “like sitting in a hairdressors  all day and not expecting to eventually get a haircut!”

A more recent  ASAM definition includes “Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social and spiritual manifestations. Addiction is characterized by inability to consistently abstain, impairment in behavioral control, craving, diminished recognition of significant problems with one’s behaviors and interpersonal relationships, and a dysfunctional emotional response.”

We appreciate the role now afforded to “dysfunctional emotional response” in this new definition as we believe it is dysfunctional emotional response which is at the heart of alcoholism and addiction.

Our own experience of recovery, coupled with our neuroscientific research over several years, has  made us curious as why the ways addicts and alcoholics talk about their condition or the explanations they forward all generally point to what they would call an “emotional disease” or “a parasite the feeds on their emotions”, an “emotional cancer” or a “fear based disease” yet these are rarely countenanced in any theory of addiction, whether neurobiological, psychological, psycho-analytical (although there have been very interesting ideas based on attachment within this methodology).

How could addicts and alcoholics be so wrong about themselves and what ails them? Especially when they see it also in hundreds of others with the same condition? We doubt that they are wrong, in fact, we have in recent years taken the opposite approach and started to explore, in terms of research, if addiction and alcoholism, especially, have their roots in emotional dysregulation and emotional processing deficits

In even more recent times, we have been encouraged that these difficulties also shape decision making difficulties, distress based impulsivity (leading to compulsivity) lack of inhibition across various psychological domains, as well as more revealingly the cognitive and executive dysfunctions and ‘flight or flight’ reactions which seem common to this group, over reacting in other words.

There appears to be a short term decision making profile which we suggest is distress based, which implicates more emotive-motoric “automatic,compulsive”regions of the brain rather than goal-directed. A more “let’s do it NOW!”way of making decisions.  This is also seen in children of alcoholics.

Could this be an important vulnerabilty to alcoholism? In order to get this debate going we will now consider whether there are possibilities for re-defining the DSM criterion in relation to the manifest difficulties observed in these clinical groups in relation to emotional dysregulation. The “official” nosology (e.g. DSM IV) is largely limited to physical manifestations of addiction although addicted individuals display additional psychiatric symptoms that affect their well-being and social functioning but which have been relegated to the domain of psychiatric “comorbidity.” 

Although the relationship of these psychiatric symptoms with addiction is very close, substance abuse may modify pre-existing psychic structures and lead to addiction as a specific mental disorder, inclusive of symptoms pertaining to mood/anxiety, or impulse control dimensions, decision making difficulties or, as we suggest, the various characteristics of emotional dysregulation. All of which suggests the current DSM based nosology of addiction-related mental comorbidity does not consider the overlap of the biological substrates and neurophysiology of addictive processes and psychiatric symptoms associated with addiction, so fails to include specific mood, anxiety, and impulse control dimensions and decision making difficulties in the psychopathology of addictive processes.

Addiction reaches beyond the mere result of drug-elicited effects on the brain and cannot be peremptorily equated only with the use of drugs despite the adverse consequences produced. Addiction is a relapsing chronic condition in which these psychiatric manifestations play a crucial role. Thus it may be that the aetiology of addiction cannot be severed from its psychopathological underpinning, it’s roots.  In may have been initiated by these mechanisms and also the addiction cycle may be continually perpetuated by them. Particularly in view of the undeniable presence of symptoms, of their manifest contribution to the way addicted patients feel and behave, and to the role they play in maintaining the continued use of substances.

In other words, the latter symptoms frequently precede the addictive process constituting a predisposing psychological background on which substance effects and addictive processes interact, leading to a full-fledged psychiatric disorder. Within the frame of the current DSM, numerous relevant psychiatric issues in substance abuse disorders may have been overlooked.   Even in the absence of psychiatric diagnosis, specific psychological vulnerabilities may constitute a background for the development of  disorders. The neural circuitry implicated in affective reactivity and regulation is closely related to the circuitry proposed to underlie addictive behaviours.  Affect is related to dysfunctional decision-making processes and risky behaviours,  In fact, we suggest these affective processing difficulties cause inherent decision making difficulties and constitute a premorbid vulnerability.

Substance dependence is associated with significant emotional dysregulation that influences cognition via numerous mechanisms. This dysregulation comes in the form of heightened reward sensitivity to drug-related stimuli, reduced sensitivity to natural reward stimuli, and heightened sensitivity of the brain’s stress systems that respond to threats. Such disturbances have the effect of biasing attentional processing toward drugs with powerful rewarding and/or anxiolytic effects. 

Emotional dysregulation can also result in impulsive actions and influence decision-making. It appears clear in addiction and alcoholism (substance dependence)  and that emotional processing significantly impairs cognition in substance dependence. Emotionally influenced cognitive impairments have serious negative effects with both the resultant attentional bias and decision-making deficits being predictive of drug relapse. 

The influence of emotion is clearly detrimental in substance dependence, and many of the detrimental effects observed are due to the ability of drugs of abuse to mimic the effects of stimuli or events that have survival significance. Drugs of abuse effectively trick the brain’s emotional systems into thinking that they have survival significance!

They trick the alcoholic into thinking he needs to drink to survive! 

It is important to note that the neural mechanisms implicated in neurobiological accounts of the transition to endpoint addiction from initial use are also experienced emotionally in human beings, in addicted individuals. That human beings, addicted individuals have to live with these profound alterations and impairments of various regions and neural networks in the brain. And that it is in treating these human manifestation of this neurobiological disease, i.e. one’s “dysfunctional emotional responses” in every day life that is required for long term recovery. We have to manage the emotional difficulties which perpetuate this disease, this “parasite on our emotions”, otherwise these dysfunctional overwhelming emotions manage us.   

It is through this emotional dysregulation that the addiction cycle is experienced and via emotional means perpetuated! It is through living “emotionally light” and spiritually aware lives which help manage our emotions that perpetuate our long term recovery.

Emotional distress is at the heart of addiction and alcoholism, and relief from it on a continually, daily basis is at the heart of recovery.    

References

American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. pp. 5–25.

Pani, Pier Paolo, et al. “Delineating the psychic structure of substance abuse and addictions: Should anxiety, mood and impulse-control dysregulation be included?.” Journal of affective disorders 122.3 (2010): 185-197.

Murphy, A., Taylor, E., & Elliott, R. (2012). The detrimental effects of emotional process dysregulation on decision-making in substance dependence. Frontiers in integrative neuroscience, 6.

Cheetham, A., Allen, N. B., Yücel, M., & Lubman, D. I. (2010). The role of affective dysregulation. in drug addiction. Clinical Psychology Review, 30(6), 621-634.

The Distress at the Heart of Addiction and Alcoholism

Posted on by alcoholicsguide

This blog is written for alcoholics and those who love and live with them, by alcoholics in recovery. For those who know what it is like to live with alcoholism but would also like to know why alcoholism affects the alcoholic and those around him in the way it does.

We write this blog to help us and you understand how the alcoholic brain works; why they do the things the do, why they act the way they do. Why is it everything is going great and suddenly the alcoholic in your life “flies off the handle’ and acts in an emotionally immature way, which can often cause hurt to others around them? What is the reason behind this “Jekyll and Hide” emotional responding?

Why do they suddenly cut off their emotions so profoundly it leaves your emotions in limbo, confused and upset?

In this blog we seek to explain, as researchers,  in terms of the processes of the brain, why alcoholics, particularly  those in recovery, do the things the way they do, act the way they do.

We hope to explain this disease state, which alcoholics themselves call a “emotional disease’, a “cancer of the emotions’, a “parasite that feeds on the emotions” or quite simply  “a fear based illness”. It appears that alcoholics in recovery are aware to a large extent of what they suffer from. But why do they do what they do sometimes if they know what is going on? Why do they not seem to be able to help themselves from engaging in certain responses and behaviours?

Why do they endless engage in self defeating resentments,  taking “other peoples’ inventory” or criticizing, why do they project into future scenarios and then get emotionally paralyzed by doing so, why do they run through the list of cognitive distortions on a daily basis, why do they get self absorbed and engage in “me, me, me” behaviour!? Why do they indulge in self pity to the extent they end up in full blown depression?

More importantly, perhaps, how do various therapeutic strategies deal with these behaviours and seek to challenge and address them? And do these therapies, in time through practice and the neuroplasticity (neural reshaping of the brain via behaviour) change how they act, feel and live in this life. In short, how does recovery change the brains of alcoholics for the better?

As we are personally well aware, self knowledge does not bring recovery – only action does. But this action can be based solidly on a better understanding of what goes on in the brain of an alcoholic for example, why should I mediate? What beneficial, adaptive change will that bring, how will that “help me recover”? What is the point of doing the steps, how exactly do they effect change in one’s alcoholic brain? Is there a good healthy neurobiological reason for going to mutual aid group meetings like AA or  SMART?

We also believe that academic research definitions of alcoholism are inadequate – the latest DSM V  equates the emotional difficulties we highlight here as ‘co-morbidities’,  conditions that occur alongside the condition of alcoholism. We disagree, we suggest these ‘co-morbidities’ (co-occurring psychiatric disorders) are a main reason why we become alcoholics, they are what make us vulnerable, along with genes and environment to becoming alcoholic.

Most alcoholics feel they never fitted in, were emotionally hyper “sensitive”,  engaged in risky behaviours, got into trouble without intending to, and other impulsive behaviours which we believe are illustrative of an emotional dysregulation which makes certain individuals vulnerable to becoming alcoholic.

Science tells us there are many such vulnerabilities in children of alcoholics. The alcohol regulated, medicated these errant emotions which caused such distress, even at an early age. It is these emotional processing deficits and emotional dysregualtion (i.e. poor control of emotions, especially when distressed!) which lie at the heart of the this psychopathology or if you like  this psychiatric disorder called alcoholism.

It is a distress-based condition, day in day out, and we formally believe that various therapeutic regimes like the 12 steps, DBT, ACT or CBT, etc all treat this inherent distress state in some way. It is this distress state that activates this “fear-based illness”, that makes one hyper aware of cues, alcohol, it is this distress that provokes memories of drinking, alcohol use schemata, that trains one attention on people places and things from the past. Without this distress our illness barely gets activated! 

For example, does your loved alcoholic, “over do things”on a regular basis, do they engage in short term thinking, or “quick fix ” thinking. Do they resist your attempts at sensible long term , goal directed, “thought through thinking”?

Does your alcoholic work himself to a frazzle, do they easily become exhausted by overdoing it, whatever it is? Do they have a series of new addictions? Are they perfectionist doing too much, or nothing anything at all? Perfectionism is distress based.

Does your alcoholic fear the future, but continually project their thinking into the future? Do they have an intolerance of uncertainty, do they endless ruminate about things, do they react rather than act? Do the most simple decisions provoke a “fight or flight” response? Do they frequently come up with “I know how to do this, I have a great idea!” Only for it to be the opposite of a great idea! Do they give people “rent free room in their heads” because of resentments – replying the same old tape in their minds, over and over and over again? All distress based?

“Fear based” is distress based.

A recent study showed that alcoholics have a part of the brain that helps process emotions but it doesn’t work properly so is overactive all the time; it is exhausting being on red alert, all the time , living on a state of emergency. Hence step 11 in the the 12 steps.

The problem with this hyperactive brain region, called the ventromedial prefrontal cortex, is that it  also cuts out , hypo-activates, when more or excessive stress is applied and another compulsive area of the brain, the basal ganglia, takes over. This part is automatic, habitualized, automatic, compulsive! It results in more more more, and is driven by distress not goal directed consideration. It simple does, does, does, without consideration of future consequence.    Sound familiar??

How did your loved alcoholic get to be this way? What happened to your own alcoholic brain? We believe there is a vulnerability to these aforementioned  emotional difficulties as certain brain areas which regulate emotion not working properly. This means they are smaller, impaired and do not function optimally or are not  connected properly.

Do you know an alcoholic who does not accurately know how he is feeling properly, does not know what emotion he is experiencing? Cannot label to emotion properly which makes processing of it difficult? Can’t rely on a neural feedback to tell himself when  he is tired, angry, hungry  and that he should HALT? This is the insular cortex not working properly.

Does your alcoholic see error everywhere (and worse still give a running commentary on it!?), always whinging about that not being right, or that being wrong. Why can’t they do things properly, be more perfect!! That is partly to do with impairment of the anterior cingulate cortex which monitors error in the environment.

This fear based stuff? That is a hyperactive amgydala, the “anxious amgydala”, and it also acts as a switch between memory systems, from explicit to implicit memory, and recruits the compulsive “go,go, go” area of the dorsal striatum from the always “on the go”, hyperactive, ventromedial cortex.

The amgydala is at the heart of alcoholism and addiction. It not only switches memory but also reward/motivation/ and emotional response so that distress provokes a habitualised “fight or flight response” in the dorsal striatum.

It is said that alcoholics are emotional thinkers, but this region is also an emotional “do” area which means emotional distress acts as a stimulus response. The brain responds to the stimulus of distress in other words. As addiction and alcoholism progress the ways addicts and alcoholics react  become limited in line with addiction severity. The further the alcoholic gets in alcoholism the more he will react out of distress, the more automatic his behaviours become, the more short term his decision making will be, the more he has to fight automatic urges and automatic drink-related thoughts, the more he has to contend with “fight or flight” thinking and feeling.

Add to this a brain that is out of balance, does not have homeostasis, natural neurochemical balance, but has a state called  allostasis, where the brain constantly attempts to finding stability via constant change, and the fact that the alcoholic brain has too much Glutamate,  an excitatory neurotransmitter, the “go neurochemical”, and not enough GABA,  an inhibitory  neurotransmitter, the brains’ natural brakes”, (and which is increased by drinking alcohol) the stop or slow down chemical and  that this also helps slow down an abnormal heart rate variability (HRV) found in alcoholics.

Alcoholics have a different heart rate variability meaning we have a heart rate more suited to being ready for the next (imagined) emergency.  The effects of alcohol are thus more profound on this group, and this HRV is also seen in children of alcoholics so represents a profound vulnerability to later alcoholism.

Add to that depleted levels of of  dopamine, which is very important in the addiction cycle. The problem with dopamine supplies is that our excessive levels of stress reduce our amount of dopamine,  that we are always on the look out for more dopamine. Add to this that stressful states increase our brain in “dopamine seeking” in an attempt at transient allostasis and you have a brain that is always trying to get a buzz out of something, especially when in distress states.

Then there is other deficits to the serotonin system, to the natural opioids  system, to oxytocin, all of which take a beating and are reduced by excessive stress systems. But all are increased via love and looking out for our fellow man, our families, loved ones and other’s in recovery. We can manipulate our brain chemistries, this is what happens in recovery in fact!

Too much stress on the brain spreads like a forest fire throughout the brain, lowering levels of  essential neurotransmitters,  impairing memory and turning one from a goal directed action to a compulsive reaction type of guy. The alcoholic brain is always primed to go off!!

Chronic stress also impairs the prefrontal cortex, the cognitive, conscious “top down” controller of the brain’s emotions and urges, instincts and so on. It doesn’t help that it doesn’t work too well in alcoholics. The brain of an alcoholic is a “spillover” brain, it is a brain that spills over into various types of disinhibition,  impulsivity and compulsivity . It often acts before considering, speaks before thinking. decides this is a great idea with out consulting, reacts without sufficient reason or cause.

It needs help, this alcoholic brain. From another brain, from someone other than himself.

Recovering alcoholics need an external prefrontal cortex to help with the top down cognitive control of the subcortical emotional and motivational states. The problem with emotions are they, in the alcoholic brain, have become entwined with reward. We feel a certain way, negative for example, and fix this negative feeling, with something rewarding, makes us feel better, more positive, less self reflective,  and it seems this has been the case with certain alcoholics since childhood. Dealing with emotions by the granting of treats.

Feeling better by consuming. Fixing feelings via external substances. Sub contracting our emotional regulation.  Finding different feelings in a bottle, or a pill, or a syringe or snorting them up one’s nose. Alcoholics need a spiritual awakening,  a psychic change, a change in consciousness, in self schema;  this sudden change in how we feel about the world (including memories of our past life) because the old feeling about the world will lead to the sane old behaviours. Plus alcohol and drugs were  crude approximates of this change in consciousness, this  spirit awakenings, they dramatically and very instantaneously helped change our feelings, thoughts, perceptions about the world around us. They helped us fit in.

This is the purpose of a spiritual awakening too, a sudden change of consciousness. We believe the best and most sudden way to achieve this is to let go of the thing that causes all the suffering in the first place, the self. It appears we can live without the “self” . It also appears helping others brings a bigger buzz than even helping ourselves.

Helping others reduces our distress. and many many other therapeutic benefits to brain chemistry. This brain also needs some one outside of self, outside the self regulation network in the brain which is so impaired and cannot be relied on because at times it is maladaptive. Can’t be counted on the make the right decision because it favours  short term over the long term, is based on “fight or flight “thinking and rational, hence is distorted by fear.

If we have been thinking in this maladaptive way all our lives it  is no wonder we ended up where we have. We used alcohol to deal with our errant and quite frightening emotions. I positively ran away from my own emotions.

I used to say to my wife, the main reason for my drinking is “to get away from my self”. Now we have to find a solution to living with oneself, these sometimes torturous alien state of emotional sobriety.

I remember being asked by a counsellor to sit with my emotions for half on a hour. I felt I was being possessed by some poltergeist,  the feelings associated with emotional regulation were so alien to me, so frightening. I didn’t know what they were even. I had to have by wife label them for me and help me process them.

I believe steps 4 and  of 12 step programs help one emotional regulation hundreds  and hundreds of unresolved, unprocessed emotions from the past otherwise they will continue to be in there, haunting us like “neural ghosts” from the past, adding emotional distress to our conscious daily experience and encouraging relapse.  This is the case for many newly recovering alcoholics.  Being haunted by a million thoughts produced by  rampant emotional dysregulation.

Resentments swirling around the mind and driving the newcomer back to relapse. What the newcomer finds is that the drink stops working, and the emotional difficulties remain, in fact much worsened by years and years of sticking a neurotoxin down our throats and in into our brains. Havoc is then further reaped on an already not fully functioning  brain.

In AA they often they say that they are stuck at the emotional age of when they started drinking which is usually around the early teens when the cognitive part of the brain that controls emotions is still developing.  But we act much more immaturely than that, we act like the terrible twos or children. Our emotional brains never really grew up. This emotional dysregulation apparent as teens then shaped all our future decisions and eventually our alcoholism. That is what they mean in AA, when they say all your best thinking got you here. So there you have it . Sound familiar? Recognize anyone here?