dorsal striatum

From a Drinking Problem to a Thinking Problem?

 

In early recovery I was amazed that some people in recovery said they never thought about alcohol after a few weeks into recovery. Or rather than thoughts related to alcohol rarely drifted across their minds.

I was alarmed by this as thoughts of alcohol rarely left my mind in early recovery.

They came to me rather than me actively going to retrieve thoughts about alcohol myself, consciously or deliberately.

I now realise that this was due to two main reasons.

First of all, fear of drinking is a distress which activates thoughts of alcohol as distress and negative emotions (and negative self perception/schema) seem to automatically retrieve thoughts of alcohol as there has been some habitual fusion of negative emotion with urge to drink in the alcoholic brain.

This is because my alcoholism resulted in compulsive drinking, i.e. my drinking was mainly to do with relieving distress, and that is what compulsion is, automatic behaviours that relieve distress.

Secondly and tied to this point, is that this compulsive drinking in itself is also linked to how chronic my drinking became.

I was completely addicted to alcohol at the end of my drinking so my alcoholism is very chronic.

In terms of neuroscience this means any distress activates a motoric part of my brain, the dorsal striatum,  a part of the brain that deals with stimulus response or automatic response the internal stimulus of distress, which activates an automatic approach or preparation of movement towards getting a drink.

This is expressed in terms of instruction in the brain as automatically occurring intrusive thoughts about drinking alcohol. This is also called an alcohol use schema because as a schema it is procedural way to deal with distress, i.e. have distress automatically deal with it by drinking.

I still find it fascinating that even automatic behaviours have thoughts that accompany them. Although nothing is completely automatic and we have a brief period of time in which to react or not.

By not reacting or acting on this thoughts they appear to lessen in intensity.  The more we do not react the less intense these thoughts become. Finding new ways to cope with distress lessens their grip on us too and eventually they practically disappear.

I have found I have to be very very distressed in recovery for thoughts of alcohol to come revisiting my mind.

This involuntary retrieval of drug related thoughts is thus a hallmark of addicted populations as it happens automatically, implicitly without you having to consciously and explicitly retrieve these thoughts and associated images from your memory banks. They just pop up without your permission.

The intensity of obsessive thoughts about alcohol is said to predict relapse rates (1), with addicts motivated to use drugs to “silence” obsessive thoughts (2).

The idea that abstinence automatically decreases alcohol-related thoughts is challenged by research (3) and supported by clinical observation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than exception (4).

Modell and colleagues (1992) highlighted symptomatic similarities between addiction and obsessive compulsive disorder with subjective craving for drugs or alcohol characterized as having obsessive elements. (eg, the compulsive drive to consume alcohol, recurrent and persistent thoughts about alcohol, and the struggle to control these drives and thoughts) similar to the thought patterns and behaviours of patients with obsessive-compulsive illness (5).

Modell et al. also point to the potential similarities in underlying neural pathways implicated in the two disorders, suggesting that they may share a similar aetiology.

The Obsessive Compulsive Drinking Scale (OCDS) implies that as the severity of this illness progresses, so does the intensity of the obsessive thoughts about alcohol and the compulsive behaviours to use alcohol.

Kranzler et al. (1999) showed relapsers who scored higher in ‘obsessions’ craving measured by the OCDS predicted relapse in the 12 months after treatment completion (6).

This may also be a reflection of addiction severity too! As addicts and alcoholics become more addictive brain imaging shows a shift in “reward processing” from the ventral striatum to the dorsal striatum.

The DS as stated above is in charge of more automatic, compulsive reaction.

This shift from VS to DS  may also be marked by an increased emergence of automatic thoughts, which the authors also suggested as the cognitive thoughts and images of automatized drug action schemata (2).

In fact, this is demonstrated by correlations indicating that dorsal striatum activation is lowest in participants with low OCDS scores. And vice versa, highers OCDS scores with increased DS activation.

 

This means, in simple terms, that more severe addiction may be associated with more intrusive/obsessive thoughts and less severe with less thoughts.  

So if you are in a meeting or in other treatment environments and someone in recovery says they never have any obsessive thoughts or intrusive thoughts consider the possibility that their addiction did not become as severe as your addiction?

Either way these thoughts are not your own but the automatic thoughts of addiction so be careful not to react to them.

They are frightening at first, but gradually becoming irritating and annoying before occurring less and less as recovery and your non reaction progress.

If you learn to habitually not to react emotionally to them they start to lose their grip and become less severely intrusive.

Most days I do not have any intrusive thoughts. This is because my recovery has progressed.

In many ways, recovery usually goes in the opposite direction to addiction.

References

1.. Bottlender, M., & Soyka, M. (2004). Impact of craving on alcohol relapse during, and 12 months following, outpatient treatment. Alcohol and Alcoholism, 39(4), 357-361.

2. 6. Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychological review, 97(2), 147.

3. Caetano, R. (1985). Alcohol dependence and the need to drink: A compulsion? Psychological Medicine,
15(3), 463–469.

4. Hoyer, J., Hacker, J., & Lindenmeyer, J. (2007). Metacognition in alcohol abusers: How are alcohol-related intrusions appraised?. Cognitive Therapy and Research, 31(6), 817-831.

5. Modell, J. G., Glaser, F. B., Mountz, J. M., Schmaltz, S., & Cyr, L. (1992). Obsessive and compulsive characteristics of alcohol abuse and dependence: Quantification by a newly developed questionnaire.
Alcoholism: Clinical and Experimental Research, 16, 266-271.

6. Kranzler, H. R., Mulgrew, C. L., Modesto-Lowe, V. and Burleson, J. A.
(1999) Validity of the obsessive compulsive drinking scale (OCDS): Does craving predict drinking behavior? Alcoholism: Clinical and Experimental Research 23, 108–114.

7. Vollstädt‐Klein, S., Wichert, S., Rabinstein, J., Bühler, M., Klein, O., Ende, G., … & Mann, K. (2010). Initial, habitual and compulsive alcohol use is characterized by a shift of cue processing from ventral to dorsal striatum.Addiction, 105(10), 1741-1749.

 

 

 

Why a “Spiritual Solution” to a Neurobiological Disease?

because it says it all! and for our newcomers…

Inside The Alcoholic Brain

In the first in a series of blogs we discuss the topic of why does the solution to one’s alcoholism and addiction require a spiritual recovery.

This is a much asked question within academic research, although the health benefits of meditation are well known and life styles incorporating religious affiliation are known to increase health and span of life.

I guess people are curious as to how the spirit changes matter or material being when it should perhaps be rephrased to how does application of the ephemral mind affect neuroplasticity of the brain. Or in other words how does behaviour linked to a particular faith/belief system alter the functions and structure of the brain. We have discussed these points in two blogs previously and will do so again in later blogs. Here I just want to highlight in a short summary why spiritual practice helps alcoholics and addicts with with…

View original post 2,028 more words

Explaining the negative consequences of Negative Urgency.

Explaining how negative Negative Urgency can be.

from Inside the Alcoholic Brain by alcoholicsguide

In various blogs we have suggested that one of the main aspects of addictive behaviours is to act as the result of distress-based impulsivity or negative urgency. Here we explore in more details what we mean by that term negative urgency.

Here we borrow from one article (1) which has an excellent review of  negative urgency (1).

The experience of emotion facilitates action. It has long been recognized that emotional processing appears to prepare the body for action (Frijda, 1986; Lang, 1993; Saami, Mumme, & Campos, 1998). In fact, to emote means, literally, to prepare for action (Maxwell & Davidson, 2007). Researchers have theorized that the relationship between emotional experiences and actions involve activation of the motor cortex by limbic structures (Morgenson, Jones, & Yim, 1980).

Some investigations have used neuroimaging techniques to document increased activity in motor areas of the brain during emotional processing (Bremner et al., 1999; Rauch et al., 1996), and nonhuman studies suggest the emotion-action interface may involve connections between the amygdala and the anterior cingulate cortex (ACC: Devinsky, Morrel, & Vogt, 1995).

Hajcak et al. (2007) found that emotionally arousing stimuli increase motor cortex excitability. The authors theorized that there may be individual difference in emotional reactivity that may relate to differences in the amount of activation of the motor cortex areas.

One takes action to meet the need identified by the emotion.Pinker (1997) makes this point by noting that “Most artificial intelligence researchers believe that freely behaving robots . . . will have to be programmed with something like emotions merely for them to know at every moment what to do next” (p. 374).

Intense emotions can undermine rational, advantageous decision making (Bechara, 2004, 2005;Dolan, 2007; Driesbach, 2006; Shiv et al., 2005). It also appears to be true that attempts to regulate negative emotions can impair one’s ability to continue self-control behaviors (Muraven & Baumeister, 2000; Tice & Bratslavsky, 2000; Tice,Bratslavsky, & Baumeister, 2001).

Thus, it is not surprising that individuals engage in other strategies to manage intense emotions that are ill-considered and maladaptive, in that they work against one’s long-term interests. For example, heavy alcohol use may be used to manage emotion. Daily diary studies of alcohol use indicate that individuals drink more on days when they experience anxiety and stress (Swendson et al., 2000).

Indeed, negative affect states have been shown to correlate with a greater frequency of many maladaptive, addictive behaviors, including alcohol and drug abuse (Colder & Chassin, 1997;Cooper, 1994; Cooper et al., 2000; Martin & Sher, 1994;Peveler & Fairburn, 1990). This pattern also is true of bulimic behaviors; individuals tend to participate in more binge eating and purging behaviors on days during which they experienced negative emotions (Agras & Telch, 1998; Smyth et al., 2007). Emotions such as shame, guilt, anger, depression, loneliness, stress, anxiety, boredom, and rejection are often cited as triggers for binge and purge episodes (Jeppson, Richards, Hardman, & Granley, 2003). For bulimic women, engaging in binge eating produces a decline in the earlier negative emotion (Smyth et al., 2007). Because actions like these do appear to reduce negative affect, they are reinforced.

Brain Pathways Related to Emotion-Based Action

Brain system involved in emotion and action -the amygdala, the orbitofrontal cortex (OFC) and its medial sector (the ventromedial prefrontal cortex, or VM PFC:Bechara, 2005), and other areas of the prefrontal cortex (PFC:Barbas, 2007). The amygdala appears to be heavily involved in the experience of negative affect; more broadly, it is thought to play a role in directing attention to emotionally salient stimuli, particularly stressful or disturbing stimuli (Davidson, 2003).

orbitofrontaler_cortex

The OFC appears to be involved in the modulation of emotion-based reactivity (Davidson, 2003).

OFC activity overrides emotional responses, apparently by providing information and a bias toward long-term, goal-directed behavior (Lewis & Todd, 2007).

Davidson and his colleagues (Davidson, 1998, 2000,2003;Davidson & Irwin, 1999; Davidson, Putnam, & Larson, 2000) suggest the experience of intense emotion, and its accompanying potential actions, is inconsistent with one’s long-term goals. The OFC, perhaps particularly the left VM PFC, provides a biasing signal to avoid immediate reward, and thus maintain one’s pursuit of one’s longer-term goals. Davidson (2003) refers to this process as affect-guided planning and anticipation: with healthy left VMPFC functioning, one gains access to the emotion associated with anticipated outcomes consistent with one’s long-term goals. The ability to do so is, Davidson argues, the hallmark of adaptive, emotion-based decision making. At times, long-term affect-guided planning is difficult: the experience of intense emotions unrelated to one’s long-term interests may disrupt processing with regard to those interests (Gray, 1999; Preston, Buchanan, Stansfield, & Bechara, 2007). But healthy functioning of the left VM PFC helps one maintain an affective connection to one’s longer-term goals, and thus plan accordingly.

Damage to the OFC, and perhaps damage specifically to the VM PFC, results in affective lability and rash action particularly in inhibiting the action of amygdaloid reactivity.

Parasagittal_MRI_of_human_head_in_patient_with_benign_familial_macrocephaly_prior_to_brain_injury_(ANIMATED)

 

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The authors of this study put forward various reasons why OFC and VM PFC damage can cause rash action – we consider these before forwarding our own ideas of why OFC/ VM PFC damage may prompt distress based impulsivity.

The OFC, perhaps particularly the left VM PFC, provides a biasing signal to avoid immediate reward, and thus maintain one’s pursuit of one’s longer-term goals. Davidson (2003) refers to this process as affect-guided planning and anticipation: with healthy left VM PFC functioning, one gains access to the emotion associated with anticipated outcomes consistent with one’s long-term goals. Activation of the left VM PFC also appears to inhibit amygdalar activity (Davidson, 1998), thus shortening the time course of the experience of negative affect and attention to stressful stimuli. Because negative affect stimulates autonomic nervous system (ANS) activity, which provides support for action in response to distress, prolonged negative affect leads to prolonged ANS arousal (Davidson, 2000). Perhaps a greater duration of ANS arousal increases the likelihood of affect-triggered action. Activity in the amygdala appears to facilitate this process.

Damage to the OFC, and perhaps damage specifically to the VM PFC, results in affective lability and rash action. Individuals with PFC damage, and with OFC damage in particular, do not; they do not appear to have the normal anticipatory affective response to potential punishment (Bechara, 2004; Bechara, Tranel, Damasio, & Damasio, 1996; Cardinal et al., 2002).

Thus, OFC damage appears to impair affective anticipation of potential risk to one’s actions.

Bechara, Damasio, Damasio, and Anderson (1994) described OFC-damaged individuals as oblivious to the future consequences of their actions, but sensitive to immediate reinforcement and punishment. Thus, their actions tend to be guided by immediate consequences only. These patients had otherwise retained their intellectual capacities, including abstract reasoning skills. They could even describe possible future consequences in realistic language. They appeared simply to lack the anticipatory affect that others have; thus perhaps lacking the affect-guided anticipation described byDavidson (2003).

The authors then  suggest that  associations between the OFC/VM PFC-amygdala system and psychopathy are  consistent with their claim of an association between this system and the urgency traits. In other words, individuals high in psychopathy have reduced VM PFC functioning, and hence lack an affective connection to the consequences of their actions. Other studies have also documented similar OFC functioning deficits among psychopaths (Blair et al., 2006; Mitchell, Colledge, Leonard, & Blair, 2002).

This model is interesting but there is not mention of stress systems in this model although the authors mention distress and negative affect but not the stress chemicals underpinning these affective manifestations.

The authors also do no mention two hugely important points we believe;

a. that this amgydaloid (hyper) activity, caused by PFC dysfunction can also “offline” PFC activity (fig.1)

b. in favour of the compulsive, emotive-motoric behaviour of the dorsal striatum which drives rash action, distress-based impulsivity or compulsivity rendering the individual remote to negative consequence of actions, although he/she may be able to explain clearly these consequences. prior to or after seeming to not consider them. It is chronic stress dysregulation in addiction that “cuts off” access to action-outcome or goal-directed parts of the brain and recruits stimulus response, implicit, “must do” action instead.

fig 1.

nihms197465f5 (1)

This we believe is the mechanism of negative urgency rather than as the authors suggest in this article, but not included, that VMPFC damage renders individuals unknowing of consequence, when rather, consequence, negative or otherwise, has been cut off by this amygdaolid activity rendering action  outcome associations remote to consciousness.  The brain acts implicitly, procedurally or in a stimulus response way to distress we believe in addictive disorders when heightened amgydaloid reactivity  is in charge of behaviour with VMPFC deficit contributing to this amgydaloid dysfunction.

An argument against simply seeing rash behaviour as the result of OFC or VMPFC damage which leads to lack of knowledge of consequence is that it does not really consider the chronic stress that accompanies addictive behaviours and which creates a near constant distress which acts in the way we describe above.

This does not mean that there is a lack of emotionally guided behaviour or action on the part of addicts. It would appear, as discussed in previous blogs, that emotional processing deficits are common in addiction and may not recruit the goal-directed parts of the brain as the authors suggest. They do not guided action or choices effectively. As a result they manifest in perhaps crude, undifferentiated or processed forms as distress signals instead and recruit more limbic, motoric regions of the brain.  Hence they are not use to anticipate future, long term consequence.

We are simply adding that as addiction becomes more chronic, so does stress and emotional distress and this appears to lead to a distress-based “fight or flight” responding to decision making that the authors have mentioned in this article but not elucidated as above. Addicts increasing appear to recruit sub-cortical or limbic areas in decision making and this is prevalent in abstinence as in active using. it is the consequence of chronic and stress dysregulation.

We suggest that this chronic stress prompts negative urgency via an hypofunctioning ACC (2) and by a “emotional arousal habit bias” as seen in post traumatic stress disorder (3) whereby chronic emotional distress increasingly during the addiction cycle comes to implicitly activate dorsal striatal responding “offlining” the PFC in a similar manner to fig. 1.

References

1. Cyders, M. A., & Smith, G. T. (2008). Emotion-based dispositions to rash action: positive and negative urgency. Psychological bulletin, 134(6), 807.

2. Li, C. S. R., & Sinha, R. (2008). Inhibitory control and emotional stress regulation: neuroimaging evidence for frontal–limbic dysfunction in psycho-stimulant addiction. Neuroscience & Biobehavioral Reviews,32(3), 581-597.

3. Goodman, J., Leong, K. C., & Packard, M. G. (2012). Emotional modulation of multiple memory systems: implications for the neurobiology of post-traumatic stress disorder.

 

Why a spiritual solution?

The Alcoholics Guide to Alcoholism

In the first in a series of blogs we discuss the topic of why does the solution to one’s alcoholism and addiction require a spiritual recovery.

This is a much asked question within academic research, although the health benefits of meditation are well known and life styles incorporating religious affiliation are known to increase health and span of life.

I guess people are curious as to how the spirit changes matter or material being when it should perhaps be rephrased to how does application of the ephemral mind affect neuroplasticity of the brain. Or in other words how does behaviour linked to a particular faith/belief system alter the functions and structure of the brain. We have discussed these points in two blogs previously and will do so again in later blogs. Here I just want to highlight in a short summary why spiritual practice helps alcoholics and addicts with with…

View original post 2,028 more words

Understanding Emotional Processing Deficits in Addiction – Guest Blog

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.

Why a spiritual solution?

In the first in a series of blogs we discuss the topic of why does the solution to one’s alcoholism and addiction require a spiritual recovery.

This is a much asked question within academic research, although the health benefits of meditation are well known and life styles incorporating religious affiliation are known to increase health and span of life.

I guess people are curious as to how the spirit changes matter or material being when it should perhaps be rephrased to how does application of the ephemral mind affect neuroplasticity of the brain. Or in other words how does behaviour linked to a particular faith/belief system alter the functions and structure of the brain. We have discussed these points in two blogs previously and will do so again in later blogs. Here I just want to highlight in a short summary why spiritual practice helps alcoholics and addicts with with regulating themselves especially when the areas of their brains which govern self regulation have been taken over by the action of drugs and alcohol, so that they have very limited control over their own selves and their own behaviour.

This seems to be at the heart of addiction and alcoholism, this increasingly limited self control over addictive behaviors. In addressing this need for a spiritual solution we also hope to address choice versus limited control arguments. As we will see, the addicted or alcoholic brain is usurped to such a profound extent by effects of drugs and alcohol and this brain acts so frequently without conscious awareness of the negative consequences of these actions that it is appears undoubtedly the case that addicts and alcoholics have profoundly diminished control over their choices of behaviour.

This is especially pertinent in chronic addicts and alcoholics were the thrill is long gone so why would they continue doing something which has little reward other than because they are compelled to.

In addiction, vital regions of the brain and processes essential to adaptive survival of the species become hijacked or usurped or “taken over” by the combination of the effects of alcohol or drugs or addictive compulsive behaviours (acting as pharmacological stressors)  on pre-existing impairment in certain parts and functions of the brain. The actions of drugs and alcohol lead to a hyperactive stress system which enhances the rewarding aspects of drugs and alcohol in initial use, especially in those with maladaptive stress response such as individuals who have altered stress systems in the brain due to abusive childhood experiences (1-3).

In the second abusing phase, stress interacts with various neurotransmitters especially dopamine to drive this abusive cycle. In this phase of the addiction cycle  stress heightens attention towards cues and creates an  heightened attentional bias towards drugs and alcohol (4,5). Stress chemicals also increase activation of “addiction memory” (6,7). Thus there is multi-network usurping of function in the brain as the addiction cycle progresses (8). Recruited of attention, reward and memory networks are enhanced by the effects of stress chemicals.

Stress also enhances the rewarding effects of alcohol and drugs so makes us want them more (9). Enjoy them more. These are the so-called “good times” some of us look back on, in our euphoric recall.

In the final endpoint phase of addiction, stress incorporates more compulsive parts of the brain, partly by the stimulus response of emotional distress which automatically activates a compulsive response to approach drug and alcohol use while in distress, which is a common reality for chronic addicts and alcoholics.

 

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Thus stress chemicals acting on mainly dopamine  circuits in the brain and other neurotransmitters eventually take over control of the brain in terms of the control of behaviour (8).

In usurping  “survival” or self regulation networks in the brain, control over behaviour “implodes” or collapses inwards, from control over behaviour moving inwards from the action outcome, or goal directed, conscious prefrontal cortex to the unconscious automatic, motoric, subcortical  parts of the brain (10).

This greatly limits one’s conscious self control over one’s own behaviour  if one is addicted or chronically alcoholic. Control of behaviour appears to have becomes a function of hyperactive stress systems in the brain and their manifestation as emotional distress (11,12).

This emotional distress constantly activates a “flight or flight” response in the brain and this means behaviour is carried out without reflection or without explicit knowledge of consequences, usually negative in the case of addiction (13,14).

The alcoholic or addicted brain becomes a reactionary brain not a forward thinking, considering of all possible options type of brain. The addict or alcoholic becomes driven by his brain and to a great extent a passenger in his own reality. Automatic survival networks act or react continually as if the addicted brain is on a constant state of emergency, constantly under threat.

There is a profoundly reduced conscious cognitive control over behaviour. This heighted, excessive and chronic stress and distress cuts off explicit memory of previous negative consequences of our past drinking and drug use and recruits implicit memory systems which are mainly habitual and procedural, they are “do” or “act” without conscious deliberation systems of the brain (14) .

It is as if our alcoholic or addicted brains are doing the thinking for us. Or not as the case may be. Alcoholics are on automatic pilot, fuelled by distress.  This neuroscientific explanation fits almost perfectly with the description of alcoholism in the Big Book of Alcoholics Anonymous, “The  fact is that most alcoholics…have lost choice in drink. Our so-called will power becomes practically nonexistent. We are unable , at certain times,  to bring into our consciousness with sufficient force the memory of the suffering and humiliation of even a week or month ago. We are without defense against the first drink”

The” suffering and humiliation” are now called “negative consequences” in current definitions of addiction…”continued use despite negative consequences”. (15)

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We “cannot bring into our consciousness with sufficient force the memory” because this is an explicit memory cut off by the effects of excessive stress which “offlines” the prefrontal cortex and hippocampal memory in favour of unconscious habitual, implicit or procedural memory (14,16). The memory of drinking not the memory of the “ situations surrounding this drinking”. How is this not a disorder  that has placed us “ beyond human aid” and beyond our own human aid” ? 

The “unable at certain times” are possibly times of great distress or emotional dysregulation and they leave the alcoholic and addict vulnerable to  relapse.

“Once more: The alcoholic, at certain times, has no effective mental defence against the first drink.”

“His defence must come from a Higher Power”

In later blogs we will discuss, in terms of the brain, why we need to recruit parts of the brain, via selfless behaviours, which activate areas outside those implicated in self regulation.

The cited  power greater than ourselves in AA meetings, for example, often follows an experiential trajectory – first it is the first person an alcoholic asks for help whether a family member, loved one or a G.P. – this often leads to an AA meeting or a treatment centre – then they are presented with other alcoholics who suffer from the same disorder – in AA parlance this is the first, and for many alcoholics in recovery, their only experience or attempt to find G.O.D. – this Group. of. Drunks. is like all that preceded it, a power greater than ourselves, regardless on whether we attain a spiritual connection with God after that.

A sizable minority in AA remain agnostic or atheist. This does not mean they have not performed essentially “spiritual” acts such as asking for help, accepting powerless over their life at that present moment. These are all acts of humility of accepting one needs help from beyond oneself. They also attend meetings where no one is in charge apart from God as He may express Himself in our group conscience.

Our first sponsors (mentors) in AA are also a power beyond ourselves as are their sponsors and their sponsors and the people in all their lives who advise and support. From the moment one has wholeheartedly accepted the need for help, one has accepted that help will come from a power greater than themselves.  It is a humbling and I believe spiritual act. A new breath filling one’s life.

All these people are already doing something for us which we could not do ourselves, they are helping us recruit the prefrontal cortex and explicit memories of the disasters alcohol or drug addiction has wrought on our lives – they move, eventually, activity in the brain from the unthinking dorsal striatal to the reasoning prefrontal cortex, helped also by sharing our stories in meetings. They give us a new recovery alcoholic self schema to replace the former drinking alcoholic self schema and stores it in implicit memory.

These people helps us change positive memory association of alcohol with negative associations. They overturn old ideas about the good times with a deep awareness of how bad these so-called good times were. The attentional bias is avoided or is rarely activated as the distress and stress are greatly reduced so as not to activate it.

We find recovery rewarding in the way we formerly (but not latterly) found drinking. In fact we find recovery better than drinking even at it’s best. The worst day in recovery seems much better than the worst day in drinking. We learn how to regulate our emotions so as to avoid prolonged bouts of distress, we ring our sponsors when such moments arise, talk to a loved one.

Again an external prefrontal cortex helps us climb out of the sub-cortical “fear” areas of the dorsal striatum and the anxious amgydala. The solution  is in the prefrontal cortex, in it’s control over emotions, in it’s clear appraisal of our past, in it’s activation of negative, realistic  memories of the past and  in avoiding the people, places and things which remind us of drinking.

The prefrontal cortex becomes more in charge rather than our illness doing the thinking. The prefrontal also gets strengthened by us sharing our experience strength and hope at meetings, it uses a recovery narrative to reconcile the drinking self with the recovering self, making us whole,  it embeds in our mind the truth of the progressive nature of this illness. It helps us see what it was like, what happened and what it is today. It gives us the tools to help others.

In the follow up blog to this we will further explore how this works – this spiritual solution.

 

References

1. Cleck, J. N., & Blendy, J. A. (2008). Making a bad thing worse: adverse effects of stress on drug addiction. The Journal of clinical investigation, 118(2), 454.

2. Koob, G. F., & LeMoal, M. (2001). Drug addiction, dysregulation of reward, and allostasis. Neuropsychopharmacology, 24, 97–129.

3. Sinha, R. (2008). Chronic stress, drug abuse, and vulnerability to addiction. Annals of the New York Academy of Sciences, 1141, 105–130

4. Peciña, S., Schulkin, J., & Berridge, K. C. (2006). Nucleus accumbens corticotropin-releasing factor increases cue-triggered motivation for sucrose reward: paradoxical positive incentive effects in stress?  BMC biology, 4(1), 8.

5. Ventura, R., Latagliata, E. C., Morrone, C., La Mela, I., & Puglisi-Allegra, S. (2008). Prefrontal norepinephrine determines attribution of “high” motivational salience. PLoS One, 3(8), e3044

6. Hyman, S. E. (2007). Addiction: a disease of learning and memory. Focus, 5 (2), 220.

7.  Adinoff , B. (2004) Neurobiologic processes in drug reward and addiction, Harvard Review of Psychiatry

8. Duncan E, Boshoven W, Harenski K, Fiallos A, Tracy H, Jovanovic T, et al  (2007) An fMRI study of the interaction of stress and cocaine cues on cocaine craving in cocaine-dependent men. The American Journal on Addictions, 16: 174–182

9. Berridge, K. C., Ho, C. Y., Richard, J. M., & DiFeliceantonio, A. G. (2010). The tempted brain eats: pleasure and desire circuits in obesity and eating disorders.Brain research, 1350, 43-64.

10. Everitt, B. J., & Robbins, T. W. (2005). Neural systems of reinforcement for drug addiction: From actions to habits to compulsion. Nature Neuroscience, 8, 1481–1489

11. Sinha, R., Lacadie, C., Sludlarski, 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, 171–180.

12. Goodman, J., Leong, K. C., & Packard, M. G. (2012). Emotional modulation of multiple memory systems: implications for the neurobiology of post-traumatic stress disorder.

13. Schwabe, L., Tegenthoff, M., Höffken, O., & Wolf, O. T. (2010). Concurrent glucocorticoid and noradrenergic activity shifts instrumental behavior from goal-directed to habitual control. Journal of Neuroscience, 20, 8190–8196.

14. Schwabe, L., Dickinson, A., & Wolf, O. T. (2011). Stress, habits, and drug addiction: a psychoneuroendocrinological perspective. Experimental and clinical psychopharmacology, 19(1), 53.

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

16. Arnsten, A. F. (2009). Stress signalling pathways that impair prefrontal cortex structure and function. Nature Reviews Neuroscience, 10(6), 410-422.

 

Is the “mental obsession” of the Big Book relative to how severe your addiction is?

Involuntary retrieval of drug related thoughts is a hallmark of addicted populations.

Intensity of obsessive thoughts about alcohol predict relapse rate (1), with addicts motivated to use drugs to “silence” obsessive thoughts (2).  The idea that abstinence automatically decreases alcohol-related thoughts is challenged by research (3) and supported by clinical observation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than exception (4).

Modell and colleagues (1992) highlighted symptomatic similarities between addiction and obsessive compulsive disorder with subjective craving for drugs or alcohol characterized as having obsessive elements. (eg, the compulsive drive to consume alcohol, recurrent and persistent thoughts about alcohol, and the struggle to control these drives and thoughts) similar to the thought patterns and behaviours of patients with obsessive-compulsive illness (5).

Modell et al. also point to the potential similarities in underlying neural pathways implicated in the two disorders, suggesting that they may share a similar aetiology. The Obsessive Compulsive Drinking Scale (OCDS) implies that as the severity of this illness progresses, so does the intensity of the obsessive thoughts about alcohol and the compulsive behaviours to use alcohol.

Kranzler et al. (1999) showed relapsers who scored higher in ‘obsessions’ craving measured by the OCDS predicted relapse in the 12 months after treatment completion (6).

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This may also be a reflection of addiction severity too! As addicts and alcoholics become more addictive brain imaging shows a shift in “reward processing” from the ventral striatum to the dorsal striatum. The DS is in charge of more automatic, compulsive reaction.  This shift from VS to DS  may also be marked by an increased emergence of automatic thoughts, which the authors suggested as the cognitive thoughts and images of automatized drug action schemata (2).

In fact, this is demonstrated by correlations indicating that dorsal striatum activation is lowest in participants with low OCDS scores. This means, in simple terms, that more severe addiction may be associated with more intrusive/obsessive thoughts and less severe with less thoughts.  

 

References 

 

1.. Bottlender, M., & Soyka, M. (2004). Impact of craving on alcohol relapse during, and 12 months following, outpatient treatment. Alcohol and Alcoholism, 39(4), 357-361.

2. 6. Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychological review, 97(2), 147.

3. Caetano, R. (1985). Alcohol dependence and the need to drink: A compulsion? Psychological Medicine,
15(3), 463–469.

4. Hoyer, J., Hacker, J., & Lindenmeyer, J. (2007). Metacognition in alcohol abusers: How are alcohol-related intrusions appraised?. Cognitive Therapy and Research, 31(6), 817-831.

5. Modell, J. G., Glaser, F. B., Mountz, J. M., Schmaltz, S., & Cyr, L. (1992). Obsessive and compulsive characteristics of alcohol abuse and dependence: Quantification by a newly developed questionnaire.
Alcoholism: Clinical and Experimental Research, 16, 266-271.

6. Kranzler, H. R., Mulgrew, C. L., Modesto-Lowe, V. and Burleson, J. A.
(1999) Validity of the obsessive compulsive drinking scale (OCDS): Does craving predict drinking behavior? Alcoholism: Clinical and Experimental Research 23, 108–114.

7. Vollstädt‐Klein, S., Wichert, S., Rabinstein, J., Bühler, M., Klein, O., Ende, G., … & Mann, K. (2010). Initial, habitual and compulsive alcohol use is characterized by a shift of cue processing from ventral to dorsal striatum.Addiction, 105(10), 1741-1749.

 

 

The Distress at the Heart of Addiction and Alcoholism

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?