Do you have Emotional Regulation Difficulties!?

Emotions have always troubled me! I have always found them frightening, always had difficulties labeling and controlling them. I have always seemed to put in an extra effort to keep them in check.

I have recently read a very good chapter from a book (1) which looks at emotional regulation and the role it seems to play in psychopathology. In fact, it is my view that emotional dysregulation lies at the heart of alcoholism, initiates, sustains and perpetuates this chronic disease state.

It was thus illuminating to see that emotional dysregulation is cited as being present in some 75% of disorders listed in The Diagnostic and Statistical Manual of Mental Disorders, DSM-5.

Alcohol Dependence in the DSM has a narrow definition, I believe, of alcoholism as mentioned in previous blogs. It relegates all manifestation of emotional, mood, impulse difficulties to that of “co-morbidities” which means it thinks there is a difficulty with unregulated drinking but the unregulated thinking, emotions and impulsive behaviour it relegates to being the consequence of a co-occurring condition such as anxiety disorder, depression, post traumatic stress disorder and so on. This is not to say that some of these conditions do not co-occur with alcoholism. PTSD and alcoholism co-occur quite frequently.

What I am saying is that a number of conditions/disorders attributed to alcoholism as a co-morbidity may not be co-morbidities at all, for some. They may be aspects of this psychiatric disorder I call alcoholism.

See blogs for more An Emotional Disease? and Current Definitions of Addiction – how accurate are they?

I do not want to rehash arguments mentioned elsewhere on this blog (especially as I want to discuss some emotional regulation difficulties I find are very pertinent to my alcoholism and maybe to yours?) Particularly “self elaboration” which seems to be at the heart of my alcoholism and appears very similar to the alcoholic mentioned in the Big Book of Alcoholics Anonymous.

Emotions are important in readying behavioral, motor,

and physiological responses, in facilitating decision making, in enhancing memory for important events, and for negotiating interpersonal relationships.

But emotions can also hurt as well as help! Emotions are not always helpful!

Psychopathology is largely characterised by excessive negative emotion. In those with emotional dysregulation, emotional regulation strategies helpful in childhood are now unhelpful in adulthood, such as use of an avoidant coping style where they down play threat and suppress feelings. This may have helped in surviving an abusive childhood but is not conducive to intimate adult relationships.

Another difficulty is not allowing a primary emotional response to proceed but instead suppressing it or resisting it e.g it is not okay for me to feel angry at my dying mother. Thereby, creating a maladaptive secondary emotional response e.g. guilt.

Secondary responses for resisted emotions coming from emotions
are experienced as anxiety producing, as reflected in rigid attentional
processes, lack of acceptance, and the activation of negative beliefs about emotions.

In order to ascertain if your emotional regulation is adaptive answer the questions below (and refer perhaps to your early recovery too!)

Do you not immediately react to the external situation or to one’s internal primary emotional response, but pause for a moment and give oneself some breathing room? Thus allowing space for the emotion to begin to arise free of immediate avoidance (e.g., cognitive, behavioral, or emotional avoidance), immediate resistance (e.g., “I shouldn’t want to feel this way”), or impulsive behavioural reaction (e.g reacting angrily or fearfully)?

Are you aware of your primary emotional response and be able to identify what emotion one is having in order to effectively control it?

Can you determine how controllable the situation that
caused the emotion is and how controllable one’s internal reaction to the situation?

For situations or internal thoughts or emotions that are out of one’s control, adaptive regulation is to accept the situation and experience . This is common to most therapeutic regimes.

Finally, how well do you inhibit/control inappropriate or impulsive behaviors when experiencing negative emotions?

All of the above, from a personal perspective, have improved the longer I have been in recovery. Although tiredness, or distress can prompt a quick return to emotional dysregulation.

Emotion regulatory strategies

The two regualtory strategies are two that most apply to me as an alcoholic. Attentional Deployment and Cognitive Change

See if they relate to you too, or to a loved one.

Attentional Deployment

Specific forms of maladaptive attentional deployment include rumination, distraction and worry.

Rumination typically involves repetitive attentional focus on feelings associated with negative events, along with a negative evaluation of their consequences. It has been associated with increased levels of negative emotion. Rumination is constantly implicated in alcoholism.

We discuss this and catastrophizing in later blogs.

Cognitive Change

Before a situation that is attended to gives rise to emotion, the situation needs to be judged as important to one’s goals (i.e., appraisal).This stage of imbuing a situation with meaning can be influenced if one wishes to change the trajectory of the emotional response.

Cognitive change refers to changing how we appraise a situation to alter its emotional significance.

Two categories of reappraisals associated with psychopathology are (1) self-elaboration (e.g. “Others must think poorly of me”) and (2) emotional resistance/non acceptance of one’s current emotional experience (e.g., “I shouldn’t feel bad” ).

I personally find this “self elaboration” very applicable to myself as an alcoholic, this ” the self in reference to a situation can substantially increase the duration and complexity of emotional responses.”

For example, instead of my negative thoughts and feelings being processed and put to bed, they can be reignited throughout the day and can leave me feeling negative for hours afterward rather than just for the period following whatever incident provoked this emotional response initially.

This and other maladaptive emotional regulation strategies like rumination are shared with other disorders such as depression but this doesn’t mean they are the same disorders or that they co-occur. They are disorders which share common emotional dysregulation but ultimately have different behavioural manifestation.

They are not co-morbid but similar in certain ways but not all.

Back to self elaboration – Following my lack of appropriate emotional response above, I may feel negative the rest of the day, I may decide to ruminate, or complain or bitterly gossip with others, I may exhibit all the “defects of character” that came out in my step four inventory, such as pride, arrogance, intolerance, self-centredness, selfishness, anger, resentment, fear, dishonesty and so, all of which I feel are secondary emotional responding or emotional cascades. In fact, I believe step four through to seven helped me process the various episodes of emotional dysregulation I had running around my head and tearing at my heart for the thirty odd years prior to doing the steps.

The more I gossip and backbite, the more I think the person who “wronged me” is incompetent, it’s all his fault, my feelings are down to him! He caused this distress didn’t he? The injustice of it all!! These thoughts will reignite other emotions and thoughts – I should have stuck up for my self – guilt and this situation could be serious – fear. And so the cascade continues.

“I wonder if others think the same way about me, perhaps they don’t like me, perhaps I am not very popular!? – shame, self pity and maybe I am just not very lovable – despair ” and then it can delve into my distant past to my childhood, “well this is how my mother acted sometimes, maybe it is just me ! I’m the problem!”

It is difficult not to see this self-assassination as anything other than emotional dysregulation. My thinking, based on negative emotions, running away with themselves and increasing these negative emotions which then increased by distorted thinking, until “to hell with it, I’m not worth it, let’s get drunk!”

My emotional dysregulation is linked to a heightened reward sensitivity, I really like things that soothe my emotions like drink and drugs and I used them to regulate my emotions. I did not ruminate forever as in depression, I fixed it my external means, I consumed things and they change how I felt.

This makes my condition different to depression although plenty of depressives drink and abuse drugs. For me this heightened reward sensitivity meant I enjoyed them a whole lot more, got a whole lot out of them and decided that they would be part of how I dealt with things, emotions, life.

Our abnormal rejection to drink and drugs is a big part of our condition, our psychopathology, our psychiatric disorder. It has similarities with other conditions based on emotional dysregulation but it is also very different, That is why it demands a different treatment.

The wrong treatment will not Work!

The self elaboration means that I would consider many imagined scenarios all in relation or in reference to my self. The self has to be involved. Unfortunately this elaborates the meaning of my emotional responses and the emotional responses. All of a sudden there is a soap opera running in my head, a committee of wrongdoings, soon becoming a psycho drama. A friend of mine in AA calls it travelling via his intergalactic armchair!

Ruminating on things that did not occur as we think, will not occur as we think and have only caused a temporary insanity.

How is this not a psychiatric disorder!?

The emotions get increasing intense and proliferate. A many headed monster.

All usually because of my initial misperception of something that probably did not occur!

References

Werner, K., & Gross, J. J. (2010). Emotion regulation and psychopathology: A conceptual framework.

Euphoria Re-experienced not Recalled?

I never, never want to drink again, I would rather kill myself.

This does not mean I will not drink again however.

A possible relapse is thus not down to desire for a drink, it is because something in my brain and in my heart goes awry.

I remember being in early recovery and thinking the following line from the Big Book of Alcoholics Anonymous was very strange “Remember that we deal with alcohol—cunning, baffling, powerful! Without help it is too much for us”

What did they mean, alcohol was cunning, baffling, powerful? Surely they meant, alcoholism was cunning, baffling, powerful? Right?

Alcohol itself has not got magical powers? It isn’t a ghost or a spirit that can come and get you lured you back into drinking? Why be wary of a substance?

I suffer from alcoholism not alcohol, don’t I? ISM – I, self, me, the internal spiritual malady treated formerly by alcohol. Right? Alcohol was symptomatic? “Bottles were only a symbol”

Now what is it to be?

In AA, I used to think alcohol got off light, considering the damage it causes to the brain. I always felt alcohol and it’s comprehensive deleterious neuro-toxic effects on my brain have greatly contributed to my difficulties with emotions and thinking and memory and perception etc. The list does go on and on.

One only has to look at a brain image from a fMRI scan to realise that the damage to the brain wrought by alcohol is extensive and some of it irreversible although there is extensive repair in certain regions of the brain in recovery. I have felt for some time that alcohol gradually help change, over years, how I felt and thought and perceived this world.

Alcohol literally moulded my brain. If I emotionally reacted or thought in the same distorted way as I did while drinking or perceived this world in the same jaundiced way I did while drinking ,but while in recovery, then the same behaviours would soon follow.

I would drink.

Like a lot of alcoholics, I had a terrible sense of self, a very negative self perception in other words. I thought I was the lowest of the low, that I had screwed up my life and squandered my talents, that I didn’t even deserve recovery or to recover. I was not even worth that. It was this shame and guilt-fuelled lack of self esteem, this devalued sense of self that helped drive my drinking and which threatened to ruin any chances of recovery.

But what does this have to do with alcohol being cunning, baffling, powerful I hear you ask? Lots, is the answer. This negative self perception, I have had since early childhood, well since I could reflect on my self and the product of emotional and mental abuse and traumatic parenting is ingrained in my brain.

Even now when I reflect on myself I have a tendency to think negatively or poorly about myself and my achievements, I have a negative bias in my thinking about me. It could depress me even, if I indulged in thinking about me for too long.

Again what does this have to do with alcohol? Well these negative perceptions, ingrained in neural structures in my brain have had more than a helping hand by alcohol. Alcohol has helped reinforced this faulty image of my self.

Alcohol had helped colour this jaundiced view of my self and this can has serious repercussions in recovery. This distorted view was partly the result of staring at my refection on the warped glass of a wine bottle or on a glass of beer. It cemented this view or “concretized” it in my self perception neural networks. Every drink helped dig the grave of my self worth.

I have seen many people in recovery relapse after a period of negative self reflection, after not thinking they are good enough to recover. It is immensely sad, tragic but nonetheless true. That is why they need love more than anything when they come into recovery. Not orders or dictats but love, plain and simple, make them feel part of, that they belong, that they have found their place, their surrogate home.

I have seen countless people who were so severely abused that they could not face the self disclosure at the heart of the 12 step program of recovery. I have seem than unconsciously “choose” to drink rather than take the steps. Part of this is something deep inside whispers a barely audible solution. To drink again.

Why is it barely audible? Because it is. It doesn’t actually have a voice. It is the whisper of a neural ghost (1). It is ghost that lives in the machinery of the brain. As alive as you are. It will probably remain to haunt you as an alcoholic in some form and at some time of weakness. Never think otherwise!

It is like a euphoria recalled but also it isn’t!? It may be worse than that; it is actually to a very great extent re-experienced.

Euphoria re-experienced not simply recalled.

Euphoria wasn’t just the pleasure you received but also relief from…negative emotions surrounding the self. Negative self perception, emotional distress and so on. It appears that negative affect (emotions, mood, anxiety) can automatically prompt thoughts of alcohol or drugs (2) and that the neural circuitries of affect, reward, memory and attention are taken over or ‘hijacked’ in the addiction cycle and often prompted into activation by emotional distress so that attention is directed to alcohol to relieve distress, with the resultant ‘craving’ coloured by numerous memory associations ingrained in the brain linked to habitually drinking to relieve negative emotional states.

Also, pertinent to this blog, negative self perception may also prompt relapse. I partly reconcile alcohol being cunning, baffling, powerful and alcoholism by reference to an article I read a while back by Rex Cannon(3).

His observations about a possible role for negative self perception in relapse was based on a study conducted on recovering alcoholics. It found that by measuring their brain frequencies, when thinking about drinking and when thinking about self perception that there was a change in the frequency of their brain waves. In both cases, thinking about drinking and negative self perception, Cannon et al observed that widespread alpha power increases in the cortex, commonly seen by use of certain chemicals, were also present and in the same areas of a common neural circuitry for his study group during their reports of ‘using’ and ‘drinking’ thought patterns as well as in negative self perception.

These reports of ‘using’ and ‘drinking’ thought patterns as well as in negative self perception which appeared to bring the brain into synchrony, if only for a brief period of time, suggesting this to be the euphoria addicted individuals speak so fondly of and one possible reason for difficulty in treating these disorders.

In relation to using thoughts they suggested that “if the brain communicates and orchestrates the affective state of the individual in response to contents and images relating to self and self-in-experience – it is plausible that a large scale feedback loop is formed involving not only perceptual processes but relative automatic functioning.

This process reinforces the addicted person to become habituated to an aroused cortical state (i.e. increased alpha/beta activity) and when there is a shift to ‘normalcy’ (or recovery/sobriety) it is errantly perceived as abnormal thereby increasing the desire or need for a substance to return to the aroused (perceived as normal (or desired)) state”.

This would surely have a profound impact on addicts attempting to contain normal negative emotions when there is an automatic desire state suggesting, unconsciously, an alternative to wrestling with these torturous sober realities.

I have seen a similar process but over a much longer time frame in some alcoholics in recovery who relapse. They seem to disappear into themselves, right in front of you, like they were being lured by some internal, inaudible siren, into a self drowning.

Letting go of the life boat trying to keep them afloat. I have seen it many times, the dimming of the eye’s light, the turning inwards to the alcoholic darkness. A submerging into this illness.

It may be that indulging in one’s negative self perception recreates a neural based virtual reality. One is almost bodily transported back in time. Back to a drinking period. In a neural sense, back in the drink and not fully in sobriety, however fleetingly.

It does leave a neural taste for it, a torturous transient desire.

I remember it, particularly in early recovery, when the ‘recovery’ script was not written yet and I did not have a habitual recovery self schema to automatically activate, to pull me out of this neural reverie, this most bio-chemical vicarious pleasure.

The problem is that it happens to you without you asking it! You can be invoking a negative self schema automatically without wanting to reawaken this ghost.

But that is alcoholsim in a nutshell. It happens to you without your express permission. It takes over the brain step by step, while impairing ones’ ability to observe this progression.

That is why we are are the last to know. It is not just denial, it is brain impairment and limited ability to reflect on what has happened to one’s self.

The self has been ‘hijacked’ so it is nigh impossible to figure this out without the help of others.

It is others that lead you out of the fog, as one has become lost to oneself. If nothing else, in early recovery especially, before the steps are done, it is a dangerous place to visit, the self and it is safer to spend as much time as possible outside of it and working with others!

It is a horrible, frightening experience, the limbo between addicted self and recovery self schemas. It is fraught with danger! I remember bumping into people places and things from the past and experiencing the most excruciating cognitive dissonance of literally being caught in between two worlds and not knowing if I was a drinking or a recovering alcoholic; the sense of self as a drinking alcoholic was much stronger than the recovering self. I would hurry to my sponsor or wife to help pull my sense of self as a recovering alcoholic to the surface, out of the neural swamp of my drinking alcoholism.

But it felt alien as Cannon observes, this sober self. All new, awkward, pained, exposed and frightened. A constant vacillation between two worlds, that of active use and that of recovery. Recovery had not become “concretized” in my neural networks!

This left an oscillating experiential schism, with one caught in two realities almost simultaneously.

I see people relapse because they have no emotional sobriety and they seem to be emotionally drunk before they are actually drunk. Emotionally drunk seems to be like a virtual drunk, brings up the similar feelings or neurochemical reactions as actual drinking.

The best way to stay sober is to act sober and develop this habitual schema so that it can be retrieved instantaneously, automatically, without thinking. We achieve this schema through our actions, so in a sense is also an action schema. Tiffany (4) states that alcoholics and addicts are prompted to relapse by automatized schemata surrounding drug and alcohol use rituals, so we must have automatized schemata surrounding recovery rituals. Such as ringing a sponsor, mentor, friend, doing a step ten, praying, meditating, working with others, letting go and letting God, re-appraising distress, regulating emotions, putting thoughts of others before thoughts of ourselves, living outside self. There are so many automatic schemas in AA and other therapeutic regimes.

Either way, whatever path you choose, make your recovery tools automatic, so that they come to hand without yourself having to think about them.

References

1. Zack, M., Toneatto, T., & MacLeod, C. M. (1999). Implicit activation of alcohol concepts by negative affective cues distinguishes between problem drinkers with high and low psychiatric distress. Journal of Abnormal Psychology, 108(3), 518.

2. Cannon, R., Lubar, J., & Baldwin, D. (2008). Self-perception and experiential schemata in the addicted brain. Applied psychophysiology and biofeedback,33(4), 223-238.

3. 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.

4. Adinoff, B. (2004). Neurobiologic processes in drug reward and addiction.Harvard review of psychiatry, 12(6), 305-320.

So what is emotional dysregulation then?

Emotion dysregulation still involves attempts at regulation, but the process leads to maladjustment rather than adjustment. For example, emotion dysregulation may result in poor interpersonal relationships, difficulty concentrating, feeling overwhelmed by emotions, or inability to inhibit destructive behaviors.

Components of emotional dysregulation include a tendency for emotions to spiral out of control, change rapidly, get expressed in intense and unmodified forms, and/or overwhelm both coping capacity and reasoning. ()

Emotional distress, which is chronically higher in people with emotion dysregulation, appears to potentiate reward systems in the brain ()

This simply means that emotional dysregulation can make more potent or heighten the effects of alcohol and drugs, increasing the chances they will turn to alcohol.

Thus, the combination of emotional dysregulation and high reward sensitivity should be a potent risk factor for the development and/or maintenance of substance abuse and eating disorder.

Self regulatory deficits like these may emerge from an interaction of intrinsic biological factors as well as from chaotic or stressful early life experiences, particularly child abuse and problematic attachments with caregivers ().

We know from our other research into the neurobiology of the brain that children who have abusive childhoods have altered stress systems and this enhances the effects of alcohol and drugs, with initial drug use more rewarding. So difficulties with emotional and stress control are compounded by liking alcohol and drugs so much. It is a greater release if you like, especially from overwhelming emotions.

Personally speaking alcohol appeared to help me regulate my emotions, by this I mean alcohol appeared to take away my fear, gave me positive rather than negative emotions and most importantly in some ways made me more confident and comfortable around people, who had previously frightened me. Thus in a very real sense, alcohol helped to be in charge of my emotions, instead of the other way around. I believe this was embedded in my brain and memory as a survival strategy – alcohol was a place to go to escape.

Emotional Dysregulation may be present in overly restricted emotional expression and avoidance or excessive emotions and excitement seeking ()

Emotional dysregulation is a distinct construct ( ), related to but not reducible to negative effect (moods, anxiety, negative emotions) and may be seen as the result of the developmental capacity to adaptively regulate emotions being disturbed by early disruptive experiences ( ) such as childhood trauma and abuse.

For me, the above means that I have difficulties controlling emotions per se, not just negative, although I do seem to have a negative bias in my thinking as a result of this emotional dysregulation. I have, especially in early recovery real difficulties with feelings of euphoria and elation which sounds strange that these could be problematic but they were because they were always overwhelming and also accompanied by the idea of a drink occurring in my mind because this was an emotional reason for drinking too, “I drank when I felt bad and I drank when I felt good.” It is emotions that activate desire to drink, to escape overwhelming emotions. We are not neurobiological robots, this disease is mediated via our emotions, it acts like “a parasite on our emotions”.

Emotional dysregulatlon heightens the potency of the need to drink. From a neurobiology point of view, elation is a stress response also and this too enhances the motivation to drink. So I suggest it is safer to be not too high or too low with certain emotions.

Maladaptive cognitive emotion regulation strategies such as rumination ( ) and thought suppression () have been linked to a binge-eating (), and other impulsive behaviors () as well as alcoholism and addiction, all of which may all be a result of emotion dysregulation.

Selby (1) addresses the issues of why does emotion dysregulation appear to result in behavioral dysregulation?

The connection may lay in the use of certain cognitive emotion regulation strategies (cognitive emotion dysregulation) that actually increase the intensity of negative emotions and cause an individual to engage in maladaptive behavioral emotion regulation strategies (behavioral dysregulation) in order to down-regulate these intense emotions.

In essence, the way we regulate our emotions may actually cause us to lose control of them. These are often considered “impulsive” behaviors, without premeditation.

While not a behavioral emotion regulation strategy per se, urgency may be part of what causes certain individuals to engage in behavioral dysregulation.

Individuals who exhibit high levels of urgency, feeling the need to act when faced with emotional distress, may be more likely to engage in maladaptive behaviors such as substance abuse as a result of emotion dysregulation.

As we have seen in an another blog on negative urgency, this emotional distress prompts alcoholics to act rashly without premeditation and that we believe these levels of distress increase and become constant as addiction becomes more severe, to the point they act as an internal stimulus for the automatic responding of drinking or relapse to drinking. This relapse is done with little conscious intention.

As we see below, this type of relapse can be accompanied by a “to hell with it!” response after a series of resentments which build up distress levels to the point of “emotionally losing it””and compulsive relapse follows then as a relief from the escalating pressure of this emotional cascade!

The best characterized cognitive emotion regulation strategy is rumination.

Rumination () is the tendency to repetitively think about the causes, situational factors, and consequences of one’s emotional experience. Rumination is an important risk factor for substance abuse ().

Thought suppression is another emotion regulation strategy, as is catastrophizing () the tendency to continuously think about how bad a situation is and the negative effects that the current situation has on the future.

Using catastrophizing as an emotion regulation strategy has been found to increase emotional distress (). All of the cognitive emotion strategies discussed (rumination, thought suppression, and catastrophizing) appear to have a common theme: they all focus attention on emotionally relevant stimuli, usually negative.

Furthermore, evidence has shown that ruminative processes tend to amplify the effect of negative affect. Cognitive emotion dysregulation may then be a result of the intense use of rumination, catastrophizing, and thought suppression when upset.

Yet the tendency to ruminate on negative emotional thoughts increases levels of negative affect, and in turn the increase in negative affect increases levels of rumination followed by a flood of racing negative emotional thoughts, which in turn increase levels of negative affect in a vicious, repetitive cycle – an emotional cascade.

As the Big Book of AA says “resentments kill more alcoholics than anything else”

see blog on Rumination also

References (to be uploaded)

References (to be included)

Bradley, B., DeFife, J. A., Guarnaccia, C., Phifer, J., Fani, N., Ressler, K. J., & Westen, D. (2011). Emotion dysregulation and negative affect: Association with psychiatric symptoms. Journal of Clinical Psychiatry, 72(5), 685-691.

Selby, E. A., Anestis, M. D., & Joiner, T. E. (2008). Understanding the relationship between emotional and behavioral dysregulation: Emotional cascades. Behaviour Research and Therapy, 46(5), 593-611.

Nolen-Hoeksema, S., & Morrow, J. (1991). A prospective study of depression and posttraumatic stress symptoms after a natural disaster: The 1989 Loma Prieta earthquake. Journal of Personality and Social Psychology, 61, 115–121.

Wegner, D. M., Schneider, D. J., Carter, S. R., & White, T. L. (1987). Paradoxical effects of thought suppression. Journal of Personality
and Social Psychology, 53, 5–13.
Wegner, K. E., Smyth, J. M., Crosby, R. D., Wittrock, D., Wonderlich, S. A., & Mitchell, J. E. (2002). An evaluation of the relationship
between mood and binge eating in the natural environment using ecological momentary assessment. International Journal of Eating
Disorders, 32, 352–361.
Whiteside, S. P., & Lynam, D. R. (2001). The ﬁve-factor model and impulsivity: Using a structural model of personality to understand
impulsivity. Personality and Individual Differences, 30, 669–689.

Anestis, M. D., Selby, E. A., Fink, E., & Joiner, T. E. (2007). The multifaceted role of distress tolerance in dysregulated eating behaviors.
International Journal of Eating Disorders, 40, 718–726.
Anestis, M. D., Selby, E. A., & Joiner, T. E. (2007). The role of urgency in maladaptive behaviors. Behaviour Research and Therapy, 45,
3018–3029

How do resentments become the Number one Offender!?

Research suggests (1) suggest individuals with poorly regulated emotions often turn to alcohol to escape from or down-regulate their emotions, creating a risk for diagnosable problems in relation to alcohol difﬁculties as this impairment in emotion regulation is associated with alcohol-related disorders and substance-related disorders (2).

Experiential avoidance of thoughts, emotions, sensations,memories, and urges can lead to a variety of negative outcomes such as problems with substance use, because it paradoxically increases negative thoughts (3)

Thus risk factors include suppression (including both expressive suppression and thought suppression), avoidance (including both experiential avoidance and behavioral avoidance), and rumination.

Emotional distress, which is chronically higher in people with emotion dysregulation, appears to potentiate (heighten) reward systems in the brain (1), and this potentiation may be even greater in individuals high in reward sensitivity, increasing the chances they will turn to alcohol. Intake of alcohol will be reinforced both by the satisfaction of high appetitive drives and by the reduction of negative emotions these individuals otherwise cannot regulate. Thus, the combination of emotional dysregulation and high reward sensitivity should be a potent risk factor for the development and/or maintenance of substance abuse and eating disorder.

Emotion dysregulation may occur if emotions are experienced as intense and overwhelming, when individuals have not learned how or when to apply effective strategies, when strategies are not applied flexibly, when the strategies fail, or when strategies are overused, emotion regulation patterns may interfere with the ability to successfully achieve goals. Emotion dysregulation still involves attempts at regulation, but the process leads to maladjustment rather than adjustment. For example, emotion dysregulation may result in poor interpersonal relationships, difficulty concentrating, feeling overwhelmed by emotions, or inability to inhibit destructive behaviors.

Emotional Dysregualtion may be present in overly restricted emotional expression and avoidance or excessive emotionality and excitement seeking. This research (4) highlighted that the idea that emotional dysregualtion is a distinct construct, related to but not reducible to negative effect (anxiety, mood, negative emotions) and may be seen as the result of the developmental capacity to adaptively regulate emotions being disturbed by early disruptive experiences. In other words, abuse in early childhood can help determine how we cope with our emotions.

Maladaptive cognitive emotion regulation strategies such as rumination (5 ) and thought suppression (6) have been linked to a number of negative psychological outcomes. Binge-eating (7), and other impulsive behaviors (8) may all be a result of emotion dysregulation.

Selby (9 ) addresses the issues of why does emotion dysregulation appear to result in behavioral dysregulation? The connection may lay in the use of certain cognitive emotion regulation strategies (cognitive emotion dysregulation) that actually increase the intensity of negative emotions and cause an individual to engage in maladaptive behavioral emotion regulation strategies (behavioral dysregulation) in order to down-regulate these intense emotions.

In essence, the way we regulate our emotions may actually cause us to lose control of them. These are often considered “impulsive” behaviors, without premeditation. While not a behavioral emotion regulation strategy per se, urgency may be part of what causes certain individuals to engage in behavioral dysregulation. Individuals who exhibit high levels of urgency, feeling the need to act when faced with emotional distress, may be more likely to engage in maladaptive behaviors such as substance abuse as a result of emotion dysregulation.

The best characterized cognitive emotion regulation strategy is rumination. Rumination (5) is the tendency to repetitively think about the causes, situational factors, and consequences of one’s emotional experience. Rumination is an important risk factor for substance abuse (10)

Thought suppression is another emotion regulation strategy as is catastrophizing (11) the tendency to continuously think about how bad a situation is and the negative effects that the current situation has on the future. Using catastrophizing as an emotion regulation strategy has been found to increase emotional distress (12)

All of the cognitive emotion strategies discussed (rumination, thought suppression, and catastrophizing) appear to have a common theme: they all focus attention on emotionally relevant stimuli, usually negative.

Furthermore, evidence has shown that ruminative processes tend to amplify the effect of negative affect.

As a recovering alcoholic, this rumination and catastrophizing is very similar to what we call resentments the constant resending of negative emotions and accompany thoughts, each cycle making the emotions and thoughts more distressing.

Mixed with the self elaboration we discussed in another blog, then more has a heady cocktail of distressing resentments.

As the Big Book of Alcoholics Anonymous says “resentments kill more alcoholics than anything else”

It is thus difficult to see alcoholism as anything other than a disorder of emotional regulation.

References

1. Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). Emotion-regulation strategies across psychopathology: A meta-analytic review. Clinical psychology review, 30(2), 217-237.

2. Berking, M., Margraf, M., Ebert, D., Wupperman, P., Hofmann, S. G., & Junghanns, K. (2011). Deficits in emotion-regulation skills predict alcohol use during and after cognitive–behavioral therapy for alcohol dependence. Journal of consulting and clinical psychology, 79(3), 307.

3. Hayes, S. C., Strosahl, K. D., & Wilson, K. G. (1999). Acceptance and commitment therapy: An experiential approach to behavior change. New York: Guilford Press.

4. Bradley, B., DeFife, J. A., Guarnaccia, C., Phifer, J., Fani, N., Ressler, K. J., & Westen, D. (2011). Emotion dysregulation and negative affect: Association with psychiatric symptoms. Journal of Clinical Psychiatry, 72(5), 685-691.

5. Nolen-Hoeksema, S. (1991). Responses to depression and their effects on the duration of depressive episodes. Journal of Abnormal
Psychology, 100(4), 555–561.

6. Wegner, D. M., Schneider, D. J., Carter, S. R., & White, T. L. (1987). Paradoxical effects of thought suppression. Journal of Personality
and Social Psychology, 53, 5–13.

7. Anestis, M. D., Selby, E. A., Fink, E., & Joiner, T. E. (2007). The multifaceted role of distress tolerance in dysregulated eating behaviors.
International Journal of Eating Disorders, 40, 718–726.

8. Whiteside, S. P., & Lynam, D. R. (2001). The ﬁve-factor model and impulsivity: Using a structural model of personality to understand
impulsivity. Personality and Individual Differences, 30, 669–689.

9. Selby, E. A., Anestis, M. D., & Joiner, T. E. (2008). Understanding the relationship between emotional and behavioral dysregulation: Emotional cascades. Behaviour Research and Therapy, 46(5), 593-611.

10. Nolen-Hoeksema, S., Stice, E., Wade, E., & Bohon, C. (2007). Reciprocal relations between rumination and bulimic, substance abuse, and depressive symptoms in female adolescents. Journal of abnormal psychology, 116(1), 198.

11. Garfnefski, N., Kraaij, V., & Spinhoven, P. (2001). Negative life events, cognitive emotion regulation, and emotional problems.
Personality and Individual Differences, 30, 1311–1327.

12. Sullivan, M. J. L., Bishop, S. R., & Pivik, J. (1995). The pain catastrophizing scale: Development and validation. Psychological
Assessment, 7, 524–532.

Is there an emotional processing problem in alcoholics?

As there is very few studies looking at emotional processing deficits in alcoholics and addicts we have had to search around the subject to make so progress on this subject.

I know personally that when I first came into recovery a number of years ago I did not have a clue about my emotions, they were the things that drove your to the pub as far as I was concerned.

I drank to get away from my emotions, to regulate them through alcohol.

I used to tell my wife that the chief reason I drank was “to get away from myself” which brought out a very quizzical expression on her face.

What does that mean?

I have also found it difficult controlling my emotions, I have always found them frightening, alien, threatening, difficult to label and control. I have always been moody, “sensitive”, easily upset.

My mother would tell me she could watch by moody emotions wash across my face one after the other. One blending into the other without any ‘brakes’ on them to differentiate them from each other. A stream of emotions.

When I first came into treatment I was told to just sit with my emotions, so I did, with my wife for moral support. I sat there and felt ‘possessed’ by these alien feelings as they surged around my body. They were horrible. I could feel them but did not know what to do with them. It was like they were out to get me. My wife asked me to label them and tell her what emotions I was experiencing and I could not. She was amazed at this. I learnt to verbalize these feeling and via that process I started to label and process my emotions.

I wasn’t used to processing my emotions. This is why an important part the solution to our problem, especially in early recovery, is to ‘share’ with others how we are feeling as it is not obvious to us what the emotions are we are experiencing.

It is not just emotions – I had and still have difficulties reading my body states, or reading feedback from my body in terms of how tired I am, how hungry I am or what emotions are affecting me. This is probably why AA suggests HALT when hungry, angry, lonely and tired.

The insular cortex is implicated in reading these internal body states, “introception” is the term used (1). Poor introception is suggestive of an impaired insula, which is actually impaired in alcoholics.

Given the relative paucity of research into emotional processing of emotions (as opposed to recognition of emotions etc) we have considered how a known disorder of emotional processing Alexithymia relates to 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).

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.

See blog on Rumination also

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.

So how is your decision making?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Distressed Based Impulsivity?

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

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

These findings highlight a specific role for emotion.

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

The impact of emotional processing on cognitive performance.

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

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

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

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

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

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

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

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

The impact of emotion on impulsive action and decision making

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Looking Inside the Brain

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

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

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

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

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

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

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

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

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

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

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

The future is now in other words.

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

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

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An Emotional Disease?

Is Addiction an Emotional Disease!?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

How Research Helped Saved My Life!

One Christmas, I nearly relapsed.

I did not wish to relapse, in fact I would rather put a gun to my head and blow my brains out!

Nonetheless, I was indeed about to relapse. It seemed urgently inevitable. The emotional distress I had suffered all over Christmas, prompted by sad unresolved feelings about my deceased parents’s had built up, aided by a few bitter arguments with my frustrated wife, into into a sheer, blind terror.

My emotions overwhelmed me and had started to rush like a startled herd of fear through the remaining mental barricades, exploding into a crashing cascade of stress chemicals rushing around my whole body, making my limbs weak, achy and feeble.

Somehow I had the sense to shakily climb the stairs to the top of the house to tell my wife that I was in trouble. Real nauseatingly frightening trouble. I needed help. “Let’s stop arguing, I am in danger!”

My wife’s facial expression quickly flickered from hurt to heightened concern. She could tell by my quivering voice and ashen complexion that I was in trouble.

I shakily walked over to sit near her. Out of the corner of my eye I could see a bottle of white spirits, which glowed invitingly with some spiritual lustre.

My attention seemed ‘locked into’ this bottle of spirits. Somewhere there was voice in my head saying “You could drink that, soon get rid of this terror” My wife had been trying to talk to me, get through to me. I looked at her. I recognised her face but couldn’t remember her name or the fact she was my wife. It was as if some habitual behaviour, some automatic pilot had activated my legs and brought me here for help.

My wife and I couldn’t remember her name!!? What the ….? I was consumed with a rampant rampaging terror that flipped by guts. Hallucinatory terror. I was going to drink the white spirits. I have never drunk white spirits during my active alcoholism but had heard of plenty of alcoholics who had, and their wife’s perfume and many other such unthinkable liquids. It had, via these accounts, become a viable option. Something I could drink if need be!

It seemed like this was one of those moments.

“What do you normally do?” was all I heard. What? “What do you mean, what do I normally do….?” I hesitantly replied in a hushed almost child-like voice. “When you are like this, what do you normally do?” her voicing becoming more urgent . I could see the white spirits glisten and almost feel it evaporate, on my tongue, harshly as it deeply burnt my chest with a warm reassuring heat, move glowingly outwards from there in little dendritic branches of smoothing warmth and the whispering promised of blessed relief and good cheer. When alcoholism whispers sweet nothings it is sweeter than your lover.

“You better drink it” sounded in my head. I couldn’t remember what I normally do, or who was this asking this I head was jumbled and terrified. “You’d better do it”, the internal voice insisted. All I could feel was huge surges of stress chemicals surging through my veins like little scuttling manic spiders, speeding through my veins, up and down the insides of my legs, my limbs, scurrying frantically.

For some inexplicable reason, I thought, or a thought occurred to me “once I would have thought this a massive craving!” but now I felt I knew better. This wasn’t an appetitive craving, I didn’t fancy a wee drinky winky, wouldn’t that be nice. I knew this was a stress based urge and nothing to do with desire.

Nonetheless, I would kill for a drink, but paradoxically I didn’t even want one!? It wasn’t for pleasure but to escape this escalating aversion.

I knew somewhere, and know more now, that the stress chemicals swirling around my nervous system were activating my reward (or survival) brain systems. I knew it because I had read about it. Many, many times. Enough times. Stress and emotional distress activated the inner beast.

Massive amounts of stress and distress cuts off the action outcome memory, the explicit memory, the remembering of knowledge of what I would normally do in this type of situation, the “what do you normally doing this situation?” my wife had implored me to recall. It was completely cut off, I couldn’t get to it, access it. It might as well have belonged to someone else.

In there, in that explicit memory, was my wife’s name and other life saving stuff like what I normally did when faced with inevitable relapse, apart from staring at a bottle of spirits and salivating! Stuff like the tips of recovery that I had learnt so proficiently that they were ingrained in my explicit memory, for occasions such as this one!?

Some of this recovery memory had become habitualized in my implicit memory too, thank God. It was this memory that had prompted me to climb the stairs to my wife’s help on my uncertain legs. To automatically ask for help. This was implicit recovery. The very memory I could now not access now was explicit, because the excessive stress had cut if off. The what to do now I have asked for help memory. I knew this from my research as well.

The “flight or fight “mechanism, a cascade of noradrenaline, the actions of chronic stress on switching explicit to implicit memory from the action outcome to the stimulus response, to the compulsive automatised, you see it and then you do it, memory. The stimulus response memory.

The distress was the stimulus and drinking to alleviate it would be the response. Your life can depend on this memory, like when fleeing an approaching tiger, so it does not ease it’s grip on your mind too readily or easily. This is the memory with no insight of future negative consequence. It acts now and too hell with the later consequences. The “let’s deal with this now!” memory, not later.

The “what I usually did as a chronic drinking alcoholic during extreme moments of distress”, a compulsive action hardwired into my brain. I drank alcohol previously at such prompting. It had become a unpremeditated, compulsive reaction to distress. It was how I survived back then.

But then was now.

Not only did it shut off my escape route via my explicit memory and knowledge of how to get out of this life threatening crisis but it locked me into “your life is in danger, act without thinking, just do the thing your have normally done over the past 25 odd years” routine. It showed me images of doing it before, drinking, in case I had forgotten, fleeting glimpses of the people I did it with and where, when, and whispered to me that this this person was actually the real me. Not this quivering sober fraud, in this torturous alien sober reality. That I was kidding myself.

The response was positively motoric. Get up and go over there and…drink! Lots! Drink, although you would rather kill yourself than drink.

Where was the choice there in this? Where had it gone, disappeared with my explicit memory no doubt? As my wife further implored me to do something, the voice in my heading was now screeching orders at me “Drink now!” “Drink now or you..will, die!!!” Drink for God’s sake, drink!!”

So it wasn’t to be a case of I will relapse because “hey one will not hurt” sort of reasoning, rationalising and justification. I was being implored to drink because my life was at risk if I did not!! I could die. I could die if I didn’t!

How badly is an alcoholics reward/survival system hijacked…usurped when this brain is imploring him to do the very thing that will kill him? And in order to help, save him from this nightmare, help him survive like some psychotic caregiver would suggest. How far down the road from full cognitive control over one’s behaviour had I gone. Answer: about as far as I could go! How much stress surges through the alcoholics brain to close down the mnemonic survival kit. When you can’t access your “recovery” survival kit, the old alcoholic one kicks in! The alcoholic self schema overrides the recovering alcoholic schema.

I slumped to my knees and implored through tear blurred eyes for help from somewhere. I gave in profoundly, I was beat. I surrendered. The stress retreated like waves scuttling away from a beach. All action stations became deactivated and the red swirling light in my head and the honking siren turned off. I was emotionally traumatised but still sober.

I had given up on the idea that I, my self, could solve this terrifying dilemma. The answer was outside of my self, my survival network, it was in letting go. Letting go of the distress and all the brain regions it was activating; memory, attention. emotion, reward/survival. It is regions that make up the self that are taken over in the course of alcoholism. The self can no longer be fully trusted in matters such as these. It needs to escape to brain regions outside of self or to the helping arms and reassurance of someone who knows how to help, and external prefrontal cortex of reason. One armed combat with the self will end up in crushing defeat. At certain times we are beyond our own mental control.

It was the most terrifying eureka moment imaginable. I have confirmed in experiential terms what I had spent the previous two years researching. Research had partly saved my life and I hope it also does yours or at the very least help you understand this disease more fully. It had proved my ‘theory’ as far as I was concerned, highlighted the mechanisms of my torture, the psycho-neural pullies and the strings.

It is this and other related theories that we hope to share while posting to this blog. Emotional distress appears to lie at the very heart of my alcoholism, my “emotional disease”, as I have heard many alcoholics in recovery call it or this parasite that feeds on( my poorly regulated and processed) emotions, as described to me by a treatment centre counselor. The same emotional difficulties that had made alcohol such a stupendous release and comfort, such a seemingly wonderful way to regulate my emotions, to approach and be with people who used to scare and confuse me, to belong among them, however fleetingly; now the thrill had long gone, my emotional difficulties were what remained, the daily managing of this emotional dysregulation is at the heart of my recovery. If we do not manage them then they manage us.

So there we have it: how research saved my life. Researchers need to consult and observe, listen and learn from those they study. As one researcher said about educational theories, the best way to disprove or ruin your beloved theory was to set it in a classroom environment. I suggest that researchers into alcoholisim and addiction ruin or disprove their own cherished theories by applying them to those they meet at a treatment centre. Who knows they may even improve on their theories, and in doing so treatment of the alcoholics and addicts they research.

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?

	Brittany Palmer on An Addicted Brain but a Recove…
	Richard L Walz-Smith on Acceptance is the Key
	Chapter 10 – R… on “The Bottled Scream” A Disease…
	Chapter 1 “Rock Bott… on Do we have to Hit Rock Bottom…
	Chapter 4 – Wh… on Acceptance is Always the …
	Chapter 5 – My… on Simplifying the Complex?
	Chapter 4 – Wh… on The psychic change as continua…
	Chapter 3 – Th… on 12 Steps
	Chapter 1 “Rock Bott… on Do we have to Hit Rock Bottom…
	“The Bottled Scream”… on Chapter 5 – My Sobering…
	“The Bottled Scream”… on Chapter 3 – The First…
	“The Bottled Scream”… on Chapter 1 “Rock Bottom”
	The First Step Is Th… on “The Bottled Scream” A Disease…
	Don’t They Kno… on “The Bottled Scream” A Disease…
	A Chemical Colonisat… on “The Bottled Scream” A Disease…

The Alcoholics Guide to Alcoholism

Blogging The Language of the Heart

Month: May 2014