emotional processing

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).

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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.

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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.

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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

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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.

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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.

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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

 

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

Posted on by alcoholicsguide

 

 

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

by alcoholicsguide

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

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

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

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

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

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

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

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

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

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

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

 

12 steps pic

 

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

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

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

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

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

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

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

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

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

images (3)

 

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

Some references to follow.

How far have we come in understanding this emotional disorder?

Posted on by alcoholicsguide

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

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

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

 

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

causes-of-addiction_mini

 

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

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

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

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

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

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

 

References

1. Kun, B., & Demetrovics, Z. (2010). Emotional intelligence and addictions: a systematic review. Substance use & misuse, 45(7-8), 1131-1160.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40. 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.

 

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

 

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

 

How meditation helps with “emotional sobriety”!

Posted on by alcoholicsguide

In this blog we have considered two main and fundamental areas:-

1. that alcoholism appears to be an emotional regulation and processing disorder which implicates impaired functioning of brain regions and neural networks involved in regulation and processing emotion such as the insular cortex, anterior cingulate cortex and dorsolateral prefrontal cortex.

2. that in early and later recovery there appears to be increased functioning in these areas especially the dorsolateral prefrontal cortex (dlPFC) and anterior cingulate cortex (ACC) which is important not only in regulating emotions but also in abstinence success.

Our third point is that mediation, of various types, appears to strengthen the very areas implicated in emotional regulation and processing, which ultimately helps with “emotional sobriety” and long term recovery.

Various studies have shown that mindfulness mediation training in expert meditators, as well as novices,  influenced areas of the brain involved in attention, awareness and emotion (1,2).

 

Meditation-in-Brain-660

 

A key feature of mindfulness meditators may be the ability to recognise and accurately label emotions (3). Brain FMRI studies have shown more mindful people having increased ability to control emotional reactions in various areas associated with emotional regulation such as the amgydala, dlPFC, and ACC (4).

In a study (5) on the the effects of long term meditation on physical structure of the above brain regions, practitioners of mindful meditation who meditated 30-40 minutes a day, had increased thickness due to neuroplasticity of meditation in brain regions associated with attention and interoception (sensitivity to somatic or internal bodily stimuli) than the matched controls used in this study. Again the regions observed to have greater thickness via increased neural activity (neuroplasticity) were the PFC, right insula (interoception and this increased appreciation of bodily sensations and emotions) as well as the ACC in attention (and possible self awareness as ACC is also linked to consciousness) .

A structural MRI study (6) showed that experienced mindfulness meditators also had increased grey matter the right interior insula and PFC as well as, in unpublished data, in the hippocampus, which is implicated in memory but also in stress regulation. Thus mindfulness meditation and the fMRI and MRI studies show it is possible to train the mind to change brain morphology and functionality through the neuroplastic behaviour of meditating.

Brain regions consistently strengthen or which grow additonal “neural muscles” are those associated with emotional regulation and processing such as the dlPFC, ACC, insula and amgydala.   Thus if we want, as recovering individuals,  to shore up our early recovery, by strengthening the brain regions implicated in recovery success we meditate on a regular basis, daily, so that we can also improve those underlying difficulties in emotional regulation and processing.

By relieving emotional distress we greatly lessen the grip our condition has on us on a daily basis, We recover these functions.  We will discuss the role of meditation on reducing emotional distress in later blogs.

 

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References

1. Cahn, B. R., & Polich, J. (2006). Meditation states and traits: EEG, ERP, and neuroimaging studies. Psychological bulletin, 132(2), 180.

2,  Lutz, A., Slagter, H. A., Dunne, J. D., & Davidson, R. J. (2008). Attention regulation and monitoring in meditation. Trends in cognitive sciences, 12(4), 163-169.

3.  Analayo. (2003). Satipatthana: The Direct Path to Awakening. Birmingham, UK: Windhorse Publications.

4.  Creswell, J. D., Way, B. M., Eisenberger, N. I., & Lieberman, M. D. (2007). Neural correlates of dispositional mindfulness during affect labeling.Psychosomatic Medicine, 69(6), 560-565.

5.  Lazar, S. W., Kerr, C. E., Wasserman, R. H., Gray, J. R., Greve, D. N., Treadway, M. T., … & Fischl, B. (2005). Meditation experience is associated with increased cortical thickness. Neuroreport, 16(17), 1893.

6. Hölzel, B. K., Ott, U., Hempel, H., Hackl, A., Wolf, K., Stark, R., & Vaitl, D. (2007). Differential engagement of anterior cingulate and adjacent medial frontal cortex in adept meditators and non-meditators. Neuroscience letters, 421(1), 16-21.

 

see also  Hijacking the Brain