emotional processing

The Roots of All Our Troubles!?

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Most of my distress and emotional pain in recovery comes from wanting stuff, and not getting my way or not accepting things as they are.

As Bill Wilson noted, we seem to get distressed when we don’t get what we want or feel people or trying to take away what we have.

This was his observation after a decade of psycho analysis with the psycho analyst Harry Tiebout.

A decade of therapy also showed Bill Wilson he has two default settings in his relationship to other human beings – he either tried to dominate them or he became dependent on them for his sense of self and emotional well being. In other words, he became dependent on others, on external means for approval and elevating his self esteem.

This is similar to relying on external means, i.e. alcohol, drugs, addictive behaviours to regulate our emotions and bolster our low self esteem.

We are in a sense co-dependent on other people for our sense of esteem.  We rely on others in terms of how we feel about ourselves.

As a result we are guarded against those that we perceive will reject us or be negative to us, harm us in some way and we seek to dominate these folk or we are dependent on those who are kind to us, help us and care for us. We swing at times between these extremes.

Some of us are “people pleasers”, some of us are dismissive towards others. I can be a dismissive person more than a people pleaser. It is all manipulating our interaction with others to our selfish ends.

Some of these tendencies are the result of our childhoods and how closely attached we were to our parents.

Some of us have this knawing feeling of not being good enough, have a hole in the soul which we are/were kinda always unconsciously trying to protect, shield from the world.

It is a strange feeling of not wanting to be found out of being less than, not good enough. “If people realise what the real me is like, they will reject me!” type thinking although a lot of this is unconscious and does not pop in to our minds as thoughts but is an unconscious self schema that shapes our behaviours.

In simple terms we manipulate via people pleasing or we push people away via being dismissive and putting others down, we guard against any threat of perceived rejection or threats to the self via defense mechanisms such as projecting what we do not like about ourselves on to others.

We often do not like traits in others because they somehow mirror traits in ourselves although we are not always conscious of this.

We have difficulties in our relationships with others, these relationships are often unhealthy and ill.

Some of this is touched on in the Big Book of Alcoholics Anonymous, but much of it comes from later observations by Bill Wilson after the publication of the Big Book and my and others’ observations since.

I have seen in myself how fear and shame seem to drive most of my maladaptive behaviour.

My illness of addictive behaviours.

I have an illness of chronic malcontent, things are rarely good enough and I am rarely good enough, according to my “out of kilter”  thinking which  I usually try to ignore, turn over to God or on occasion challenge via reasoning and sharing with other people.

My thoughts are often not my friends, they are often not in the service of my ongoing well being, quite the opposite in fact.

This is how a mental health disorder manifests itself as distorted fear based thinking which appear, if acted upon, to make one’s situation a whole lot worse.

We can not rely on our thoughts and feelings or, in other words, our Self Will. Our self will has become impaired and is no longer in the service of our successful survival.

I have found over the last decade in recovery that when I turn my Will over to the care of the God of my understanding that I am restored to sanity and my thoughts are sound, they are on a higher plane as the Big Book tells me.

I can become the fullest expression of me in the God, not the ill, deluded version while running under my own self will. That has been my experience.

It is only with God’s help that I get restored to sanity or reasonableness.

When I have a fear of not getting stuff and this is linked to insecurity, as mentioned in the Big Book, it is usually in relation to my pocket book, financial insecurity, personal relationships, self esteem etc.

I will now look at this fear based reaction to my security which is mainly to do with stuff out  there (external) such as work, people and how they affect my sense of self before looking at how my internal sense of self, based on the fear based emotion of shame seems to play a pivotal role in my relationship with others and the world around me.

I am assailed externally by fear of what other’s think about me and internally about what I think of me – when these two line up it can have a powerful and damaging effect on my psyche.

Desiring stuff seems at the root of my fear based stuff – the exquisite torture of desire which soon loses it’s so-called relish and just becomes torturous.

Alcoholics do not seem want stuff like normal folk, but have a pathological wanting, an all consuming need to get stuff regardless of it’s worth or value.

We seem to compulsively seek to relieve an inherent distress of not having what we set out to get. Our decision making seems fueled at times by this need to relieve distress rather than the intrinsic value of what we are seeking.

We seem to become manic in our pursuit of things and end up overdoing whatever we are doing via this stress-based manic activity.

This seems compounded by not always being able to read our emotions or somatic states.

One of my own difficulties is realising I am hungry or tired and I can often end up exhausted by over-doing stuff especially manual work around my house. My stop button broke a long time a ago and probably did not work very well to begin with.

So we have  stress-based compulsive need to do something and very limited brakes in the brain stopping us and very little emotional feedback going on, a limited consideration of  “aren’t we overdoing this a bit?”

Desire obviously runs contrary to the idea of being in God’s will, in fact it is being in Self Will that seems to create distress in many people with addictive behaviours.

I would add to this that I also get distress via fears of rejection from others, I suffer from fear based shame to a chronic extent.

Shame, also the consequence of being in Self Will, was not really mentioned in the Big Book of Alcoholics Anonymous, mainly because it was not really known about as a psychological or psycho-therapeutic concept then.

Much of the Big Book was influenced by  psycho-analysis which did not consider shame, but rather guilt, in psychological disturbance.

In fact, it has only started considering the role of shame in the last few decades.

So I would add fear of not getting what we want or having something taken away is also complemented by shame-based fears of being rejected.

For example there is an undercurrent in fear of things being taken away, of it being because we are not good enough, deserving enough, have failed in some way, which are shame based reactions.

In fact the Big Book gives me a good idea of the “sins” or “defects of character” I have when I have a resentment but does not explain why I have resentments in the first place.

It explains this as selfishness, self centredness… the root of all our troubles.

It does not, for me, clearly explain why we resort to these selfish, immature, emotional reactions or why we persist with resentments?

It does not explain the emotional immaturity at the heart of alcoholism,  this spiritual malady of inappropriate emotional response to the world around us?

Bill Wilson was struck himself, when he started working with other alcoholics, how much they were plagued constantly by various resentments. How they were haunted by memories of situations in the past, how they swirl around and pollute their minds in the present. How they could not let go of events in their past?

For me he was seeing the root of this spiritual malady, this emotional disease.

For me we engage futilely and distressingly in resentment because we have an inability to process and control our emotions, they overwhelm us and we often react by people pleasing (shame) or react via various defense mechanisms (also shame based).

Defense mechanisms are central to psycho-analytic thought – such as projection etc, the idea that we  expel “out of ourselves what we do not like about ourselves onto others.

Sometimes others expel the same negative emotions on to us. I have found this a fairly common trait among male alcoholics in recovery settings and meetings.

I was discussing this with a newcomer last week, how people who seek to “put us down”  do so out of shame and induce in us all the negative emotions they are experiencing themselves!

The newcomer gave me an example of a resentment he was experiencing after this guy at a meeting said “get off your pink cloud” a phrase that refers to the sometimes  mildly ecstatic feelings of early recovery.

This made the newcomer ashamed that he could have been so stupid for being on this pink cloud, as if this was a selfish indulgence!?

I explained to him that his pride had been hurt, he was in shame and his “apparent” depression every since was simply prolonged self pity.

If we leave self pity to fester long enough it becomes depression, that is my experience anyway.

I said the other guy was probably “hurt” to see a newcomer having such a good period of recovery (God does want us to be happy, joyous and free after all) – I said his false pride was hurt too, that he was not having the recovery experience at present of the newcomer (possibly because he wasn’t putting the effort in) and was in shame (not good enough) and self pity. This mesh of negative emotions can link up fairly instantaneously I find.  It is the web my spiritual malady seeks to ensnare me in.

The guy was probably in guilt too as he could been working on his recovery more.

As a result this guy put the newcomer down to alleviate his own sense of self, his low self esteem.

He “had to” react with arrogance, dismissiveness, impatience and intolerance, because his shame, which is a fear based emotion, made him fearful of his own recovery and fear makes one strangely dishonest (at times deluded), This is my experience.

All because a newcomer had the temerity to be enjoying his recovery?

Not completely, this is half the answer.

The other part is that this guy, if an alcoholic like me, has real difficulties accessing in his heart and mind how he actually “feels” at any particular time. Or rather what emotions he is experiencing at any particular time.

This guy could have been experiencing guilt or shame for example.

Instead of saying to himself I am feeling guilt that my recovery is flabby  compared to this newcomer or that I am being an arrogant “know it all”, putting this newcomer in his place because  he had been in recovery longer – although being in recovery and being sober are different things I have found.

Either way, if he could perhaps of had the ability to say this is how exactly I am feeling he could have acted on this emotional information rather than reacted to it.

What do I mean by this?

Well, if I was feeling guilty about this newcomer it would cause a disturbance in me because I have difficulties processing my emotions.

It would have turned up therefore as a resentment of someone having something I do not have and as them taking away the illusion that my recovery was going OK?

I would have found this threatening to my sense of self so I would have reacted via defense mechanisms. I would have strangely blamed this person for making me feel the way I did! Even if this person had no such intention of hurting my feelings I would blame him nonetheless via my defensive reactions.

It is as if my emotional well being is dependent on other people and their behaviours, this is my spiritual malady, my emotional disease.

As I would have had a resentment, it would have had a wolf pack of negative emotions attached.

In this instance I might have have acted differently.

If I had been in God I would have been more sane for a start and had more loving tolerance for a newcomer.

I would have been acting not reacting. I would have had empathy for where the newcomer  “was at in his recovery” as I had been there once too.

This love and tolerance for the newcomer evolves the displaying of virtues (the opposite of defects are virtues).

What virtues? Well as the newcomer was relatively new I would attempted to be patient, empathetic, kind, gentle, tolerant, considerate  etc. These prevent the defects occurring I find.

If we practice virtues instead of defects then the brain changes for the better and we recover quicker. Our positive loving, healthy behaviours change us and our brains via neuroplasticity for the better.

Attempting to live according to God’s Will (which is a state of Love) also helps me not react but to act with Grace.

In Grace we can still experience negative emotions but God allows us to see them for what they are and not react. His Grace takes the distress out of thee negative emotions. This is my experience.

This allows me to do a quick inventory of my negative emotions and a prayer to God to have them removed. My experience is that they are always removed and that we are immediately restored to sanity.

I do not necessarily have to react to my feelings of negativity about myself, someone else does not need to experience the consequence of my resentments.

I can manage my spiritual malady or emotional dysfunction, I have the tools to do so.

I also impressed upon the newcomer that what the other guy was experiencing and was reacting is also how he, the newcomer, reacts and how I react too.

It is what our spiritual malady looks like I believe, it is the map of my impaired emotional responding.

I also impressed upon him that mostly I can manage this emotional dysfunction but often I fail to and get into a resentful anger.

This is why I have to forgive the other guy as I have been forgiven but also to forgive myself (or ask God to forgive me my shortcomings) for my reactions.

We are not perfect, far from it. We are far from being Saints but have a solution Saints would approve and achieve a kind of transient sanctity in this 12 step solution of letting go and letting God.

We have to show love and tolerance for each other as we suffer the same illness/malady. Dismissing others like us for having what we have and acting as we do is like a form of self loathing. We have to forgive ourselves and each other for being ill. Self compassion allows us to be compassionate  towards others.

Also we need to be aware what we project on to other alcoholics is the same thing as they project on to use and sometimes we project if back.

So we have two main ailments, distressed based wanting which results in the same negative emotions as being in a shame- based fear of rejection.

I can get out of the distress of wanting/needing stuff by asking God to remove those negative emotions which block me off from Him.

For example, if I really want something and feel someone is preventing me getting that thing or that they are taking this thing away from me I have a hunting pack of negative emotions running through by heart and pulsating through my veins, propelling me to want that thing even more! As if my very life depended on it?

These feelings are translated as “how dare you take that thing/stop me getting that thing” – False Pride – followed by fear of being rejected – Shame (this is because I am not good enough)  and possible Guilt (for something I must have done wrong as usual) – then leading to “poor me” and feelings of Self pity, all because I am in Self, so I am being Self Centred and not considering someone else’s view so I am Selfish.

I retaliate via by “I”ll show you/I’ll get you” emotions of Dismissiveness, Intolerance, Arrogance and Impatience – my “I’ll put you down to make me feel better!”

All because I am fearful that you are taking away something from me or rejecting  me –  Fear and Fear is always accompanied by dishonesty.

I will act out on these somethings, if I do now use my spiritual tools and let Go and Let God, usually by eating too much, Gluttony, having a shopping spree, Greed, engaging  sexual fantasy/activity Lust of “freezing” through fear in the subltle sin of Sloth (procrastination).

A perceived slight or a rejection can have an incredible emotional effect on me

This is all emotion dysfunction and immaturity. I have resentments because they are a true sign of emotion dysfunction.

The mature way to to access, identfiy and label how one is feeling and use this information to reasonably express how one is feeling. This way we do not retaliate, fight, flee or freeze. Instead our emotions do what they are supposed to do. They are suppose the tell the fronts of our brains to find words for our feelings. Not to tell the bottom of our brains to fight back or run or freeze.

Let me use an example.

I had an argument with a guy once who suddenly proclaimed he was upset by what I had said. I was amazed as this guy was reading his emotions, identifying verbalising/expressing them to me in a way I have never been able to do.

My alcoholism is rooted in an impaired ability to read, identify, label and express my emotions (otherwise called emotion processing) – as a result my emotions have always troubled me and been so troubling in their undifferentiated state that I have always either avoided them or ran away from them.

I have sought refuge from my negative emotions in alcohol, drugs and other addictive behaviours. It is this that propelled my addictions, this inability to deal with my negative emotions. I dealt with them externally via addictive behaviours, not internally via emotion processing.

My emotions became wedded in time to being undifferentiated arousal states that prompted me to seek an external way to deal with these troubling emotional/arousal states.

Today when I engage in the above emotion dysfunction, engage in the above web of defense mechanisms it is because I have not been able to locate in me what feeling is disturbing me ?

On occasion it is, as the guy above said, because I am upset. I have not learnt the ability to say that I am upset etc. The words for these feeling states somehow can continue to elude me unless I am in God’s Grace.

God does for us what we can not do for ourselves!

Finding out what is really going on with us emotionally is at the heart of recovery. That is why we have to constantly share how we are feeling with others so that we can find out what we are feeling.

Unless, we let Go and Let God and ask God to remove these negative emotions/sins/defects of character we end up in a futile increasingly distressed spiral of negative emotions.

We end up cultivating much greater misery.

As soon as you can, let Go and Let God.

 

Phew! So it’s going much better than I thought!?

I have often written about all the difficulties I have had with reading my emotions. Especially in early recovery when I could not even identify and label the most intense negative emotions.

That experience has set me on a near decade-long search to better understand emotions and the way a lack of awareness of emotions plays in addiction and in recovery.

Today I would say the effective and rational/reasonable control of emotions is one area that has become noticeably better.

I tolerate negative emotions better, their intensity is much reduced compare to early recovery, the duration of these emotions is much much shorter than before. I seem to also make better decisions in my life based on not being overwhelmed by my emotions, particularly negative emotions.

It is said by much research that addicts, alcoholics and those with behavourial addictions have something skin to alexithymia, an impaired ability to read emotions and act on them in making decisions.

Humans seem to use emotions to make decisions which is something I never realized before.

When I ask my wife how have I changed she always says I have become more considerate and more mature in my emotional reactions.

This to me shows recovery as a process of handling emotions better, in a more emotional mature as opposed to immature way.

I also have looked at lots of research that says this emotional immaturity is there for many pre-using drugs or alcohol or engaging in unhealthy behaviours. So it may be a part of the aetiology of addictive behaviours.

When I first came into recovery I remember my wife would drive me to AA meetings. This was before my sponsor said I would be either walking or getting the bus from now on!

I was mortified?

ME!? Doesn’t he know who I am?

I have chauffeur, thank you very much?.

I had become so emotional dependent on my wife. It was like another addiction/dependency.

Recovery has been a long, at times painful, process of growing up, however reluctantly at times!

I was not only powerless over alcohol but fairly hopeless too when it came to living life on lives terms.

The more chronic my addictions became the more I regressed emotionally.

The more I recovered the more I matured emotionally,  is my point.

Even today I often have to “talk my emotions out” to see what I feel really, before I can label and identify what I am feeling really.

Before I can act maturely on what I am feeling instead of emotionally reacting which is what I always used to do.

As a fellow recovering person said in this article (1)  . . “. sit down with people and bounce some ideas off each other and get it off your chest and stuff. That’s very helpful and that kind of helps me, like saying it out loud to identify where I’m actually at.”

This is why ringing sponsors and talking to fellow recovering people is essential  especially in early recovery.

We do not how we feel clearly what we are really feeling otherwise, delude ourselves everything is fine, continue to make poor decisions to the point of becoming emotionally  drunk and then often relapsing to physically drunk.

We do all of this sometimes not because we want to drink but because we think we can do it alone when we cannot.

Sometimes in early recovery we haven’t go a clue what is going on, our arrogant pride however resists this idea and keeps missing the point of what is really going on.

Our errant emotion processing does not result in clear thinking, it results in negative, strangely deluded thinking.

By deluded I mean divorced from the reality of things as they really are. It takes some weeks and months to realize we cannot fully rely on our own thinking and this can be a blow to the pride.

The concluding part of this study (1) was very revealing to me and explained part of the “feeling” that often accompanies early recovery, the feeling of not recovering fast enough of not recovering NOW!

Addicts and alcoholics want everything NOW even recovery, they want the recovery of ten years in ten weeks!

” …some  participants interpreted negative feelings as global markers of overall emotional ill health and poor progress in recovery, for example, “I think I should be feeling better now” and “I thought I was progressing but in a lot of ways I haven’t and that’s not good.”

Here, participants realize they are experiencing negative feelings and understand it as suggestive of a larger negative phenomenon, for example, that they are not “better now” and not “progressing” as previously thought. This type of negative globalization is a type of cognitive distortion.”

A cognitive distortion is a deluded thought like those mentioned above. Our errant negative emotions produce distorting thinking.

Our negative feelings rarely tell us the truth. They give some jaundiced view of reality.

This is why we need to have constant contact with others in recovery to offload these negative feelings.

Just as with sharing with a sponsor or a friend to find out what we feel, we need to share with others to undistort our negative thinking. Negative emotions often give rise to negative thinking.

“As one participant said “And I know [recovery] is not a magic fix either because I didn’t expect, if you get sober to be all of a sudden everything is perfect. That’s not the way it works. . . . So it’s going to take you a little longer to feel better.””

I would add to this that it is  progress not perfection.

I would also add that we can feel better quicker than we think on a basis, one day at a time.

Ring someone, talk to someone and try to verbalise how you feel.

This straightens out your thinking and you will feel better right away.

We drank to go “phew!” a release from our thinking and negative heads, now we “share” with others what is really going on with us, to get to understanding what emotions ail us and this leads to the same feeling of release, to the same feeling of “phew!”

We never have to drink again to go “phew”, talk to someone instead.

We will discover things are never as negative as our thinking has lead us to believe, and are usually a whole better in fact!

We recover together.

 

References

1. Krentzman, A. R., Higgins, M. M., Staller, K. M., & Klatt, E. S. (2015). Alexithymia, Emotional Dysregulation, and Recovery From Alcoholism Therapeutic Response to Assessment of Mood. Qualitative health research,25(6), 794-805.

Forgiving Others is the Number One Healer!?

“Resentment is the “number one” offender. It destroys more alcoholics than anything else… In dealing with resentments, we set them on paper. We listed people, institutions or principles with whom we were angry… The first thing apparent was that this world and its people were often quite wrong. To conclude that others were wrong was as far as most of us ever got. The usual outcome was that people continued to wrong us and we stayed sore. Sometimes it was remorse and then we were sore at ourselves. But the more we fought and tried to have our own way, the worse matters got…It is plain that a life which includes deep resentment leads only to futility and unhappiness…If we were to live, we had to be free of anger. The grouch and the brainstorm were not for us. They may be the dubious luxury of normal men, but for alcoholics these things are poison…We saw that these resentments must be mastered, but how?… (1)”

Later, p.77, it suggests  “a helpful and forgiving spirit.”

In the 12 Steps and 12  Traditions, p.78, in reference to step 8 it suggests “why shouldn’t we start out by forgiving them, one and all?

These truncated passages from the Big Book (1)  and the 12 and 12 (3) illustrates how resentments cause relapse and that they need to by treated with the antidote of forgiveness.

We suggest also that the myriad of resentments which swirl around our minds in early recovery are also negative emotions unprocessed and thus unregulated from the past. They continually haunt us because we have not put them “to bed” in long term memory.

We have not dealt with them, by clearly identifying, labelling, sharing via verbalising them with others and then by letting go of them via forgiveness. “Letting go” is another emotional regulatory strategy that healthy people use.

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Instead of constantly holding on to memories and incidents from the past, endlessly ruminating on them we maturely face up to them and consign them to the past.

We were thus interested in a study which was not using 12 step recovery but which came to the same conclusion but via another route (2).

“Anger and related emotions have been identified as triggers in substance use. Forgiveness therapy (FT) targets anger, anxiety, and depression as foci of treatment. Fourteen patients with substance dependence from a local residential treatment facility were randomly assigned to and completed either 12 approximately twice-weekly sessions of individual FT or 12 approximately twice-weekly sessions of an alternative individual treatment based. Participants who completed FT had significantly more improvement in total and trait anger, depression, total and trait anxiety, self-esteem, forgiveness, and vulnerability to drug use than did the alternative treatment group. Most benefits of FT remained significant at 4-month follow-up.

The levels of anger and violence observed among alcohol and other substance abusers are far higher than the levels found in the general population.

Alcohol and other substance abusers administered the State-Trait Anger Expression Inventory typically have been shown to have higher state and trait anger, to be more likely to express anger to others, and to have less control of their anger.

Reducing levels of anger and its related emotions is now seen as an important feature of recovery programs. For example, according to the Project Match 12-step facilitation therapy manual, “Anger and resentment are pivotal emotions for most recovering alcoholics. Anger that evokes anxiety drives the alcoholic to drink in order to anesthetize it. Resentment, which comes from unexpressed (denied) anger, represents a constant threat to sobriety for the same reason” (Nowinski, Baker, & Carroll, 1999, p. 83).

Marlatt (1985) emphasized the importance of anger and frustration as triggers for relapse in both the intrapersonal and interpersonal domains. He noted that 29% of relapses are related to intrapersonal frustration and anger and that 16% are related to interpersonal conflict and associated anger and frustration.

Litt, Cooney, and Morse (2000) reported that those alcoholics who had urges to use after treatment had higher degrees of alcohol dependence, anxiety, and trait anger than those without such urges.

Forgiveness is an important way to resolve anger and restore hope (Enright & Fitzgibbons, 2000). In helping clients move toward forgiveness, it is essential to differentiate forgiving from condoning, pardoning, reconciling, or forgetting.

Forgiveness is a personal decision to give up resentment and to respond with beneficence toward the person responsible for a severe injustice that caused deep, lasting hurt. FT helps the wronged person examine the injustice, consider forgiveness as an option, make a decision to forgive or not, and learn the skills to forgive.

Findings – Our clients came to the program with trait anxiety and trait anger scores substantially above the published norms for adults; after treatment, however, FT participants exhibited scores comparable to the average.  In other words, the treatment did not lead simply to a change in anxiety and anger (particularly the reportedly more stable trait anxiety) but to a change toward normal profiles. In contrast, patients in the alternative treatment condition had anxiety scores well above average, especially in terms of trait anxiety, which showed little change at post test and only minimal improvement at follow-up.

FT did not focus on drug vulnerabilities, whereas the alternative treatment did. Urges to use substances are not necessary for relapse, they are important indicators.

FT  treatment is centered more on clients’ thoughts, feelings, and behaviors about someone other than themselves: an offender who hurt them deeply and unfairly. In FT, a potential reason for substance use is examined, that of avoiding painful memories of betrayal, violence, or abuse. When patients are allowed to heal, their motivation to abuse substances may be substantially reduced…(it) is worth considering as a way to address core issues of emotional pain.

resentment

 

This can lead to a reduction in negative emotions and increases in self-esteem and forgiveness… it moves to the heart of the matter for some clients. Deep hurts borne out of unfair treatment seem to play a part in substance use and abuse. Even when clients have many people to forgive…we find that they seem to know which person is most crucial to forgive first before moving to other offenders. Substance use, from this perspective, is a symptom of underlying resentments and related emotional disruptions.

If we fail to realize this, we may end up treating only symptoms rather than underlying causes. ”

 

This process seems practically the same as the inventory of Step 4 and the forgiveness implicit to steps 8 and 9. This study also highlights that we through forgiveness we actually tackle the underlying condition of emotional dysregulation. It is this emotion dysregulation (or spiritual disease) which appears to drive addiction so needs to be fundamentally addressed. By addressing these issues via the steps especially step 4 we begin to see how it works!

It was interesting that forgiveness led to higher self esteem, as if being tied to the past was akin to being tied to a former negative self schema, that people from our pained past did actually have the power to control us! Especially how we feel about ourselves. We change how we feel about ourselves and our past by simply forgiving, it is such a powerful tool in recovery.

Importantly by viewing studies like this (2)  we get beyond negative views of 12 step recovery to show that the recovery program’s effectiveness is clearly highlighted by the success of other psychological treatments getting the same positive results by using exactly the same strategies.

12 step groups provide a battery of the most profoundly effective psychological therapies for addiction ever contained within one treatment philosophy.

Don’t we all need to re-appraise how we see 12 step recovery?

Can’t we all benefit from stepping to one side and looking via a different angle to see why 12 step recovery is effective?

 

Reference

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

2. Lin, W. F., Mack, D., Enright, R. D., Krahn, D., & Baskin, T. W. (2004). Effects of forgiveness therapy on anger, mood, and vulnerability to substance use among inpatient substance-dependent clients. Journal of consulting and clinical psychology, 72(6), 1114.

3.   Twelve steps and twelve traditions. (1989). New York, NY: Alcoholics Anonymous World Services

How the Brain Recovers in Abstinence and Recovery

If addiction is characterized by loss of control over the use of substances and behaviour and a severely diminished self control or volitional control over behaviour is recovery the regaining over control over behaviours?

 

This study (1)  looked at the recovery of grey matter (and brain function in cocaine addicts (CD).  This study used a brain imaging technique called voxel based morphometry (VBM) to assess how local grey matter (GM) volume varies with years of drug use and length of abstinence in a cross-sectional study of cocaine users (presently or formerly inpatients or outpatients at treatment centres) with various durations of abstinence (1–102 weeks) and years of use (0.3–24 years).

“Extensive evidence indicates that current and recently abstinent cocaine abusers compared to drug-naïve controls have decreased grey matter in regions such as the anterior cingulate, lateral prefrontal and insular cortex. Relatively little is known, however, about the persistence of these deficits in long-term abstinence despite the implications this has for recovery and relapse.

Lower grey matter volume associated with years of use was observed for several regions including anterior cingulate, inferior frontal gyrus and insular cortex. Conversely, higher grey matter volumes associated with abstinence duration were seen in regions that included the anterior and posterior cingulate, insular, right ventral and left dorsal prefrontal cortex. Grey matter volumes in cocaine dependent individuals crossed those of drug-naïve controls after 35 weeks of abstinence, with greater than normal volumes in users with longer abstinence.

The asymmetry between the regions showing alterations with extended years of use and prolonged abstinence suggest that recovery involves distinct neurobiological processes rather than being a reversal of disease-related changes. Specifically, the results suggest that regions critical to behavioral control may be important to prolonged, successful, abstinence.

Findings suggest a cumulative effect of cocaine use wherein the longer the period of substance use the lower the grey matter volume [22]. That these effects were observed in abstinent users is consistent with prior reports of GM deficits in alcoholism that last from 6–9 months to more than a year or, in some reports, up to at least 6 years following abstinence [42]–[44].

Similarly, decreased GM as a function of years of use of heroin [6], [45], [46] and cocaine [15] have previously been reported. in regions important to emotional regulation…given that emotional reactivity has been implicated as a factor modulating vulnerability to drug abuse [49], this may have been a preexisting factor that served to increase the likelihood of the development and prolongation of drug abuse.

If addiction can be characterized as a loss of self-directed volitional control [22], abstinence and its maintenance may be characterized by a reassertion of these aspects of executive function [24]

Current cocaine users demonstrate reduced GM in brain regions critical to executive function, such as the anterior cingulate, lateral prefrontal, orbitofrontal and insular cortices [6]–[11]. In contrast, the group of abstinent CD users reported here show elevations in GM as a function of abstinence duration that exceeds control levels after 36 weeks, on average, of abstinence. One possible explanation for this is that abstinence may require reassertion of cognitive control and behavior monitoring that is diminished during current cocaine dependence [11], [50], [51].

 

We, and others, have previously hypothesized that drug abusers may develop increased cerebellar activity to compensate for reduced prefrontal activity in tasks demanding elevated levels of cognitive control [52], [53] and that this may play a role in maintaining abstinence [24]. Reassertion of behavioral control may produce a practice-related expansion [54] in GM regions such as the anterior insula, anterior cingulate, cerebellum, and dorsolateral prefrontal cortex and is consistent with our previous reports of elevated activity levels, compared to controls, in long-term abstinent substance users [24], [55].

 

It should be noted that we also observed regions displaying increased GM with abstinence in bilateral cingulate gyri that did not overlap with those showing decreased GM with years of use. This suggests that the brain is capable of compensating in response to changes in demands, such as the maintenance of abstinence [54], [76].”

It would have been interesting to correlate the findings of this type of research with more information on the treatment undertaken, e.g. was it a 12 step facilitation treatment, to assess the nature of this behaviour-based neuro-plasticity. We need more research into translating the elements of “how it works” into the areas of the brain to observe where it works. In other words how do new attitudes and behaviours shape the brain literally. How does the brain recover volume, connectivity, functionality via behavioural change?

The brain areas which regain volume are implicated also in emotion regulation. It is interesting that the authors point to a possibility that the decreased brain volume in certain areas regulating emotion may also be a pre-existing condition, or in other words, a vulnerability to later addiction risk.

It may be that in recovery some of us learn to master or at least attempt to manage and control emotions in a way we could not previously.

For us this is an essential part of the pathomechanism of addictive  behaviours,  this emotion processing and regulation deficit; a deficit we learn to overcome in recovery. An unmanageability that we learn to manage in recovery.

In our next blog we will look at how these emotional factors drive the addiction cycle to it’s chronic endpoint.

We will look at how emotional dysregulation around forgiveness has contributed to a need to continually distance ourselves chemically from the incidents that needed our forgiveness. It will also look at how forgiveness itself is a emotional regulation strategy in itself, just like “letting go” is. We learn so many emotion regulation strategies in recovery and these appear essential to long term recovery.

References

1. Connolly, C. G., Bell, R. P., Foxe, J. J., & Garavan, H. (2013). Dissociated Grey Matter Changes with Prolonged Addiction and Extended Abstinence in Cocaine Users. PLoS ONE, 8(3), e59645. doi:10.1371/journal.pone.0059645

 

 

What recovers in Recovery? – Cognitive Control over emotions?

 In recent blogs we have called for an increase in research into the neurobiology of recovery to add to the extensive research already published on the neurobiology of the addiction cycle.
There has been extensive research into the neurobiology of addiction, most of this has focused on reward and motivation networks of the brain.  In effect this suggests there is a pathological wanting in addicts, an excessive motivation towards drug taking over all other rewarding activities.
This view does not fully consider that this pathological wanting is in itself a product of dysregulated stress systems in the brain, many the product of neglect, abuse and maltreatment in childhood. These stress factors are also reflective of the role of emotional distress in the addiction cycle . This distress is we feel a product of the emotion processing and regulation deficits commonly seen in all addictive behaviours such as alcohol and substance addiction, eating and gambling disorders and sex addiction etc (and often reflective of childhood maltreatment).
In fact , this emotion processing and  regulation deficit is also apparent in certain children of alcoholics and may be a vulnerability to later alcoholism as these children demonstrate a deficit in impulsivity (common to alcoholics and addicts) and a decision making profile based on choosing now over later (short term gains based) and which recruits more subcortical and motor expressive (compulsive) parts of the brain rather than cortical and reflective/evaluative parts of the brain.
This means they make decisions to alleviate the distress of decisions (as undifferentiated emotions appear to be distressing) not via evaluative processes). This has obvious consequence for decision making over a life span.
This emotion dysregulation is also seen in active addicts and alcoholics and at the endpoint of addiction there is a fairly complete reliance of this compulsive decision making profile, which begs the question, does the decision making deficits seen in at risk children simply get worse in the addiction cycle via the neuro toxic effects of substance abuse?
This emotion (and stress) dysregulation also potentiates reward (makes things more rewarding) so alcohol is seen as more stimulating than for non risk children. This vulnerability may lead to the need  to regulate, especially negative, emotions ( and low self esteem ) via the stimulating and highly rewarding effects of alcohol make perpetuate the addiction cycle to it’s chronic endpoint where chronic emotional distress acts as a compulsive stimulus to the responding of chronic alcohol and drug use.
This emotion dysregulation also seems to play a huge part in relapse – so it begs the question does this emotion regulation improve in time via recovery, particularly long term recovery?
In the next two blogs we look at how the emotion regulation areas of the brain become reinforced, strengthened by the process of recovery or in other words we appear to develop the brain capacity for controlling and regulating our emotions more adaptively and this reduces the stress/distress which often prompts relapse.
Personally, I can wholeheartedly say, that the one main aspect I have developed in my recovery has been the awareness and skills in regulating/controlling emotions. Via recovery I have learnt to identify, label, describe by verbalising and sharing with others how I feel. This processes and regulates the emotions that used to cause me so much distress.
I have also developed a more acute awareness of the the emotional expression and needs of yours. These were previously aspects of my life which were completely lacking and frustrating/confusing as a result.
By emotionally engaging in with the world, by becoming more emotionally literate, I can converse with the world in a way that was previously beyond my capabilities.
The research we look at in the next two blogs asks the question – is cognitive control over emotions, lacking in active addiction, one of the main brain functions that improve in recovery?
A core aspect of alcohol dependence is poor regulation of behavior and emotion.
Alcohol dependent individuals show an inability to manage the appropriate experience and expression of emotion (e.g., extremes in emotional responsiveness to social situations, negative affect, mood swings) (1,2). Dysfunctional emotion regulation has been considered a primary trigger for relapse (1,3) and has been associated with prefrontal dysfunction.
While current alcohol dependence is associated with exaggerated bottom-up (sub-cortical) and compromised top-down (prefrontal cortex) neural network functioning, there is evidence suggesting that abstinent individuals may have overcome these dysfunctional patterns of network functioning (4) .
Neuro-imaging studies showing chronic alcohol abuse to be associated with stress neuroadaptations in the medial prefrontal and anterior cingulate regions of the brain (5 ), which are strongly implicated in the self-regulation of emotion and behavioral self-control (6).
One study (2) looking at how emotional dysregulation related to relapse, showed compared with social drinkers, alcohol-dependent patients reported significant differences in emotional awareness and impulse control during week 1 of treatment. Significant improvements in awareness and clarity of emotion were observed following 5 weeks of protracted abstinence.
Another study (7) which did not look specifically at emotional regulation but rather on the recovering of prefrontal areas of the brain known to be involved also in the inhibition of  impulsive behaviour and emotional regulation showed that differences between the short- and long-abstinence groups in the patterns of functional recruitment suggest different cognitive control demands at different stages in abstinence.

In one study, the long-term abstinent group (n=9) had not consumed cocaine for on average 69 weeks, the short-term abstinent (SA) group (n=9) had an average 0f 2.4 weeks.

Relative to controls, abstinent cocaine abusers have been shown to have reduced metabolism in left anterior cingulate cortex (ACC) and right dorsolateral prefrontal cortex (DLPFC), and greater activation in right ACC.
In this study  the abstinent groups of cocaine addicts showed more elevated activity in the DLPFC ; a finding that has also been observed in abstinent marijuana users (8).
The elevation of frontal activity also appears to undergo a shift from the left to right hemisphere over the course of abstinence.  The right is used more in processing (labelling/identifying) of emotion.
Furthermore, the left inferior frontal gyrus (IFG) has recently been shown to be important for response inhibition (9) and in a task similar to that described here, older adults have been shown to rely more on left PFC (10). Activity observed in these regions is therefore likely to be response inhibition related.
The reliance of the SA group on this region suggests that early in abstinence users may adopt an alternative cognitive strategy in that they may recruit the LIFG in a manner akin to children and older adults to achieve behavioral results similar to the other groups.
In longer,  prolonged abstinence a pattern topographically typical of normal, healthy controls may emerge.
In short-term abstinence there was an increased inhibition-related dorsolateral and inferior frontal activity indicative of the need for increased inhibitory control over behaviour,  while long-term abstinence showed increased error-related ACC activity indicative of heightened behavioral monitoring.
The results suggest that the improvements in prefrontal systems that underlie cognitive control functions may be an important characteristic of successful long-term abstinence.
Another study (11) noted the loss of grey matter in alcoholism that last from 6–9 months to more than a year or, in some reports, up to at least 6 years following abstinence (12 -14).
It has been suggested cocaine abuse blunts responses in regions important to emotional regulation (15)
Given that emotional reactivity has been implicated as a factor in vulnerability to drug abuse (16)  this may be a preexisting factor that  increased the likelihood of the development and prolonging of drug abuse
If addiction can be characterized as a loss of self-directed volitional control (17),  then abstinence (recovery) and its maintenance may be characterized by a reassertion of these aspects of executive function (18)  as cocaine use has been shown to reduce grey matter in brain regions critical to executive function, such as the anterior cingulate, lateral prefrontal, orbitofrontal and insular cortices (19-24) .
The group of abstinent cocaine addicts (11) reported here show elevations in  (increased) grey matter in abstinence exceeded those of the healthy control in this study after 36 weeks, on average, of abstinence .
One possible explanation for this is that abstinence may require reassertion of cognitive control and behavior monitoring that is diminished during current cocaine dependence.
Reassertion of behavioral control may produce a expansion (25)  in grey matter  in regions such as the anterior insula, anterior cingulate, cerebellum, and dorsolateral prefrontal cortex .
All brain regions implicated in the processing and regulating of emotion. 
References
1. Berking M, Margraf M, Ebert D, Wupperman P, Hofmann SG, Junghanns K. Deficits in emotion-regulation skills predict alcohol use during and after cognitive-behavioral therapy for alcohol dependence. J Consult Clin Psychol. 2011;79:307–318.
2.  Fox HC, Hong KA, Sinha R. Difficulties in emotion regulation and impulse control in recently abstinent alcoholics compared with social drinkers. Alcohol Clin Exp Res. 2008;33:388–394.
3..Cooper ML, Frone MR, Russell M, Mudar P. Drinking to regulate positive and negative emotions: A motivational model of alcohol use. J Pers Soc Psychol. 1995;69:990
4. Camchong, J., Stenger, A., & Fein, G. (2013). Resting‐State Synchrony in Long‐Term Abstinent Alcoholics. Alcoholism: Clinical and Experimental Research, 37(1), 75-85.
5. Sinha, R., & Li, C. S. (2007). Imaging stress- and cue-induced drug and alcohol craving: Association with relapse and clinical
implications. Drug and Alcohol Review, 26(1), 25−31.
6. Beauregard, M., Lévesque, J., & Bourgouin, P. (2001). Neural correlates of conscious self-regulation of emotion. Journal of
Neuroscience, 21(18), RC165
7. Connolly, C. G., Foxe, J. J., Nierenberg, J., Shpaner, M., & Garavan, H. (2012). The neurobiology of cognitive control in successful cocaine abstinence. Drug and alcohol dependence, 121(1), 45-53.
8.  Tapert SF, Schweinsburg AD, Drummond SP, Paulus MP, Brown SA, Yang TT, Frank LR. Functional MRI of inhibitory processing in abstinent adolescent marijuana users.Psychopharmacology (Berl.) 2007;194:173–183.[PMC free article]
9. Swick D, Ashley V, Turken AU. Left inferior frontal gyrus is critical for response inhibition. BMC Neurosci. 2008;9:102.[PMC free article]
10. Garavan H, Hester R, Murphy K, Fassbender C, Kelly C. Individual differences in the functional neuroanatomy of inhibitory control. Brain Res. 2006;1105:130–142
11. Connolly, C. G., Bell, R. P., Foxe, J. J., & Garavan, H. (2013). Dissociated grey matter changes with prolonged addiction and extended abstinence in cocaine users. PloS one, 8(3), e59645.
12. Chanraud S, Pitel A-L, Rohlfing T, Pfefferbaum A, Sullivan EV (2010) Dual Tasking and Working Memory in Alcoholism: Relation to Frontocerebellar Circuitry. Neuropsychopharmacol 35: 1868–1878 doi:10.1038/npp.2010.56.
13.  Wobrock T, Falkai P, Schneider-Axmann T, Frommann N, Woelwer W, et al. (2009) Effects of abstinence on brain morphology in alcoholism. Eur Arch Psy Clin N 259: 143–150 doi:10.1007/s00406-008-0846-3.
14.  Makris N, Oscar-Berman M, Jaffin SK, Hodge SM, Kennedy DN, et al. (2008) Decreased volume of the brain reward system in alcoholism. Biol Psychiatry 64: 192–202 doi:10.1016/j.biopsych.2008.01.018.
15, Bolla K, Ernst M, Kiehl K, Mouratidis M, Eldreth D, et al. (2004) Prefrontal cortical dysfunction in abstinent cocaine abusers. J Neuropsychiatry Clin Neurosci 16: 456–464 doi:10.1176/appi.neuropsych.16.4.456.
16.  Piazza PV, Maccari S, Deminière JM, Le Moal M, Mormède P, et al. (1991) Corticosterone levels determine individual vulnerability to amphetamine self-administration. Proc Natl Acad Sci USA 88: 2088–2092. doi: 10.1073/pnas.88.6.2088
17.  Goldstein RZ, Volkow ND (2002) Drug addiction and its underlying neurobiological basis: neuroimaging evidence for the involvement of the frontal cortex. Am J Psychiatry 159: 1642–1652. doi: 10.1176/appi.ajp.159.10.1642
18. Connolly CG, Foxe JJ, Nierenberg J, Shpaner M, Garavan H (2012) The neurobiology of cognitive control in successful cocaine abstinence. Drug Alcohol Depend 121: 45–53 doi:10.1016/j.drugalcdep.2011.08.007.
19.  Liu X, Matochik JA, Cadet JL, London ED (1998) Smaller volume of prefrontal lobe in polysubstance abusers: a magnetic resonance imaging study. Neuropsychopharmacol 18: 243–252 doi:10.1016/S0893-133X(97)00143-7.
20.  Bartzokis G, Beckson M, Lu P, Nuechterlein K, Edwards N, et al. (2001) Age-related changes in frontal and temporal lobe volumes in men – A magnetic resonance imaging study. Arch Gen Psychiatry 58: 461–465. doi: 10.1001/archpsyc.58.5.461
21. Franklin TR, Acton PD, Maldjian JA, Gray JD, Croft JR, et al. (2002) Decreased gray matter concentration in the insular, orbitofrontal, cingulate, and temporal cortices of cocaine patients. Biol Psychiatry 51: 134–142. doi: 10.1016/s0006-3223(01)01269-0
22.  Matochik JA, London ED, Eldreth DA, Cadet J-L, Bolla KI (2003) Frontal cortical tissue composition in abstinent cocaine abusers: a magnetic resonance imaging study. NeuroImage 19: 1095–1102. doi: 10.1016/s1053-8119(03)00244-1
23.  Lim KO, Wozniak JR, Mueller BA, Franc DT, Specker SM, et al. (2008) Brain macrostructural and microstructural abnormalities in cocaine dependence. Drug Alcohol Depend 92: 164–172 doi:10.1016/j.drugalcdep.2007.07.019.
24.  Ersche KD, Barnes A, Jones PS, Morein-Zamir S, Robbins TW, et al. (2011) Abnormal structure of frontostriatal brain systems is associated with aspects of impulsivity and compulsivity in cocaine dependence. Brain 134: 2013–2024 doi:10.1093/brain/awr138.
25.  Ilg R, Wohlschlaeger AM, Gaser C, Liebau Y, Dauner R, et al. (2008) Gray matter increase induced by practice correlates with task-specific activation: A combined functional and morphometric magnetic resonance Imaging study. J Neurosci 28: 4210–4215 doi:10.1523/JNEUROSCI.5722-07.2008.

Inability to make fine-grained distinctions regarding negative emotions prompts impulsivity.

When I first came into recovery I was assigned a task which has gone on to shape much of my thinking about my alcoholism and addiction. I was prompted by my wife to sit with my emotions, that is, to sit in one place beside my wife and not suddenly get up and go elsewhere to avoid whatever emotional state consumed me, terrified me.

I have to say it was the bizarre experience. In my drinking any negative emotions would prime my thoughts towards alcohol and any increased intensity of such thoughts would practically have me skipping to the nearest drinking establishment.

Ever since I was a child, emotions were something to be avoided, tamed or feared. They were destructive, counterproductive things which somehow weakened you.

Now I was being asked to do something I had never accomplished in over thirty years. To sit with, not run from, whatever emotions starting to arise in my mind. As the first undifferentiated blobs of emotions arose I was struck my how I could not recognise them or say with any conviction what emotions they were exactly. In this undifferentiated state they felt like waves of feeling, like possessions, like being haunting by mute poltergeists!

The urge to flee these unpleasant feeling states was overwhelming. I asked my wife for help “what was happening to me!?” “What are these feeling things?”

My wife calmly said they are simply feelings, you are experiencing emotions in their entirety. It was horrible. How the hell had I not done this before, sat with my emotions instead to constantly escaping them somehow?

In fact, I am willing to say that I knew next to nothing about emotions when I arrive in recovery. These is why they have come to fascinate me and inspired my research into affective and clinical/psychiatric neuroscience.

How is it that a grown man got to this stage, to the stage where all his undifferentiated emotions propelled him into movement away from them?

The answer to this question may have been demonstrated in this study (1).

 

rumination2

“Affective functioning plays a prominent role in several etiological models of substance use (e.g., Kassel et al., 2010; McCarthy, Curtin, Piper, & Baker, 2010; Simons, Wills, & Neal, in press). These models suggest that individuals with poor affect regulation show a diminished capacity to handle intense emotion states and often rely upon maladaptive coping strategies, such as substance or alcohol use, to manage their emotions (Lavallo, 2007; Spence & Courbasson, 2012).

One factor related to emotion regulation is emotion differentiation. Emotion differentiation is the ability to make fine grained distinctions between similarly valenced emotion states (Feldman Barrett, 2004). Individuals differ greatly in their ability to differentiate their affective experiences. Some tend to describe their emotional experiences in more global terms, such as feeling “good” or feeling “bad” and find it difficult to make more subtle distinctions, while others make these nuanced differentiations easily. These differences have been shown to impact the ability to regulate emotions and consequential behaviors (Feldman Barrett, Gross, Conner Christensen, & Benvenuto, 2001; Tugade, Fredrickson, & Feldman Barrett, 2004). In support of this, emotional differentiation has been shown to moderate associations between negative emotion and alcohol consumption (Kashdan, Ferssizidis, Collins, & Muraven, 2010).

This research suggests that the inability to differentiate emotion may foster maladaptive behavior when emotionally aroused.

Hence, it is possible that the inability to differentiate emotions may
be related to urgency, defined as rash action in response to intense emotion. Along these lines, research on alexithymia, a construct related to deficits in identifying and describing emotions, shows that these deficits are positively associated with urgency, with urgency often fully mediating the relationship between alexithymia and problematic outcomes, including alcohol consequences (Gaher, Hofman, Simons, & Hunsaker, 2013; Shishido, Gaher, & Simons, 2013).

Moreover, alexithymia has been shown to mediate the relationship between childhood maltreatment (Gaher, Arens, & Shishido, 2013) as well as trauma history
(Gaher, Hofman, et al., 2013) and urgency, suggesting that deficits in
emotional understanding may underlie urgent responding.

The findings of this study (1) showed that negative emotion differentiation was associated with both negative urgency and alcohol which suggests that the inability to make fine-grained distinctions regarding the experience of negative emotions contributes to behavioral disinhibition when in a state of high emotional arousal.

References

1. Emery, N. N., Simons, J. S., Clarke, J. C., & Gaher, R. M. (2014). Emotion Differentiation and Alcohol-Related Problems: The Mediating Role of Urgency.Addictive Behaviors.

 

“I don’t know how I feel, therefore I act!”

One of my pet hates in experimental study is researchers suggesting that one can generalise findings from a non-clinical group of participants in a particular study to a clinical  group, not in the study. For example, most studies in Psychology and in Neuroscience are conducted on very well informed, healthy undergraduate Psychology students with the suggestion that the findings will also be seen in a clinical groups such as alcoholics or addicts. That the findings have ecological validity, they will also be observed in the reality of addicts in real everyday life.

Obviously this is very controversial. How can you one really say that brain processes in a perfectly healthy undergraduate psychology student are similar to those suffering from a mental disorder such as addiction?

It is clear that the behavioural responses of someone with an addictive disorder will be different to those with a perfectly healthy adaptive brain and adaptive behavioural choices. The point of addiction, is that individuals with an addictive disorder often make maladaptive choices and make poor decisions as many brain processes and mechanisms have become chronically impaired. They tend to choose now over then, be very emotional reactive, use “fight or flight” responding to situations rather than reflective, evaluative, goal-directed, action-outcome type of thinking…the list goes on and on, believe me!

In other words, they tend to act in a very different way to healthy undergraduate studies!

I do not have a problem with using undergraduate studies but please do not attempt to generalise findings to a clinical group, or in other words, a group suffering a psychiatric disorder. It is like saying that a study observed in healthy 19-20 year olds could also be said to exist or occur in middle aged schizophrenics? Most rational people would view this as quite peculiar, to say the least. So why do this very same thing with those suffering another mental disorder, called addiction?

 

lab-rat

So why do it at all, use students as participants? Well the study I refer to in this blog shows why using a student sample may have utility. If nothing else this sampling of students provides a control group – that is a group that can act as a “healthy” group compared to a later study  which has used a clinical group as participants. This way we can compare results to observe differences in both sample groups and this can highlight fundamental differences (and sometimes similarities) in healthy and clinical groups and may help highlight specific difficulties which may need to be considered in treating these clinical groups.

Also, and importantly for our overall discussion, through many of our blogs thus far,  regarding the role of emotional processing deficits in impulsivity and decision making deficits in addiction, this type of study can look at “proof of concept” which can then be studied in clinical groups such as those with addictive disorders.

But one must also have the proviso that generalising to this clinical group is not without it’s pitfalls. Just because a certain behavioral manifestation is seen in one healthy group, which has also been seen in a more severe from in a clinical  group , it does not follow that this severity is simple down to using a substance more chronically.

Severity may also be a function of genetic expression within a specific type of environment, e.g. a genetic vulnerability in an “at risk” son of an alcoholic reared in a emotionally abusive background may be a main reason for certain behavioural manifestation rather than simply chronic substance use. Altered stress systems may represent in a similar manner to the chronic toxic effects of chronic drug use but not actually be driven by the same mechanisms or underlying processes.

Regardless on these many sensible caveats, it is still possible to look at certain psychological  traits and relate them to certain behaviours before testing whether these are also observed in a clinical  group such as those with addictive disorders.

The study we refer to here (1) used a large sample of 429 undergraduate students and examined the nature of the relationship between alexithymia and impulsivity.  “Alexithymia is a multifaceted personality construct that is characterized by difficulty identifying and describing feelings  (Taylor, 2000). Alexithymia is associated with a range of disorders, many of which are associated with poor impulse control (Parker, Wood, Bond, & Shaughnessy, 2005; Thorberg, Young, Sullivan, & Lyvers, 2009).
The development of emotional awareness and skills to express feelings are strongly linked to cognitive development because humans use language to identify and express their feelings. According to Taylor, Bagby, and Parker (1997), all individuals have emotions (i.e., neurophysiological arousal), but how we feel the emotions differ
based on our subjective cognitive understanding and experiences.
Without adequate words to describe various neurophysiological stimuli, we cannot feel (identify and describe) them accurately and precisely, and thus we have difficulties regulating our behaviors that follow the emotions (Lane & Schwartz, 1987; Taylor et al., 1997).
The emotional awareness theory presented by Lane and Schwartz (1987) has provided some explanations for the development of alexithymia (Taylor, 2000; Taylor et al., 1997). According to this theory, individuals with alexithymia are considered to be on the first two levels of emotional awareness (i.e., sensorimotor reflexive and sensorimotor enactive) as their abilities to cognitively identify
various feelings precisely by recognizing specific physiological signs of emotions are not yet fully developed (Taylor et al., 1997).
Perhaps, lack of cognitive representations for neurophysiological stimuli may make individuals with alexithymia distressed…and thus they may use alcohol to alleviate their discomfort (Kauhanen et al., 1992; Thorberg et al., 2009; Uzun, 2003)… impulsive individuals tend to rely on reflexive affective (emotional) processes rather than on reflective cognitive processes, to lead their behaviors (Lieberman, 2007; Metcalfe & Mischel, 1999)… impulsivity and alexithymia research emphasize the necessity of using reflective and sophisticated cognitive processes in order to
better regulate emotions and behaviors (Carlson, 2007; Cyders & Smith, 2008)… it is plausible that alexithymia and impulsivity are related under a higher order structure, namely neuroticism, and thus they robustly predict behaviors associated with emotion dysregulation.

This study demonstrated that individuals with alexithymia are more likely to act impulsively when experiencing heightened negative affect…and thus engage in more drinking or experience more negative consequences after drinking.

2013-05-en-Rat-Park-09

 

These results support the use of treatment models that emphasize awareness of feelings and psychological mindfulness as these treatment approaches help clients learn to identify and acknowledge their feelings first, in order to learn how to better regulate them. The results indicate that deficits in the cognitive representation of emotional experience may contribute to impulsive action when emotionally aroused. The current findings may help explain why alexithymia has been identified
as a risk factor for many psychological problems that involve emotional and behavioral regulation deficits, including substance use related disorders (Kauhanen et al., 1992; Troisi et al., 1997).”

Essentially this study on undergraduates has observed similar findings as seen in addicted individuals but this does mean the findings generalise. It means that there is theoretical utility in further exploring this link between emotional processing deficit, alexithymia, the psychological trait of impulsivity and the behavioural manifestation of chronic addiction. Finally it may also be possible by scrutinizing results to identify key differences between these two samples which may aid treatment, intervention and even prevention. We have often mentioned that prevention may in the future involve the identification of emotional processing and regulation deficits in “at risk” children and helping them process emotions more adaptively and effectively.

Addiction seems even more tragic if one considers addiction as the consequence of processes that could possible be rectified or improved in early childhood. Emotional dysregulation heightens the effects of drugs and alcohol also and sets up a viscous cycle of use that often leads to chronic addiction.

It may be the source or rather the heart of the problem.  Prevention would then need to act at the heart of this disorder.

 

References

Shishido, H., Gaher, R. M., & Simons, J. S. (2013). I don’t know how I feel, therefore I act: alexithymia, urgency, and alcohol problems. Addictive behaviors, 38(4), 2014-2017.

Explaining the negative consequences of Negative Urgency.

Explaining how negative Negative Urgency can be.

from Inside the Alcoholic Brain by alcoholicsguide

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

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

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

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

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

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

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

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

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

Brain Pathways Related to Emotion-Based Action

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

orbitofrontaler_cortex

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

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

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

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

Parasagittal_MRI_of_human_head_in_patient_with_benign_familial_macrocephaly_prior_to_brain_injury_(ANIMATED)

 

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

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

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

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

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

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

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

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

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

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

fig 1.

nihms197465f5 (1)

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

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

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

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

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

References

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

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

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

 

Processing Emotions by verbalising them!?

The Therapeutic Benefits of “Sharing”

In early recovery I did not have a clue what emotions I was experiencing. I was not able to identify, label or process them. As a result of his failure to process emotions I seemed to be constantly distressed and and, as we seen in previous blogs, this distress leads to a distress-based impulsivity and a negative urgency to either engage in “fight or flight” behaviour, i.e. running away from fearful situations or ignoring the Big Book of AA’s recommendation not to fight anybody or anything.

The only way I could handle these troublesome and frightening emotions was by talking about them to my sponsor or my wife or other people in recovery.

In recent years it has become evident to that what I have been doing all these years have been using a technique of verbalising my emotions to actually process them. I now believe this is a fundamental part of my recovery and that I sometimes need to verbalise my emotions in order to process them. How does this work?

I recently came across an article (1) which might shed some light on this process.

Putting feelings into words (affect labeling) has long been thought to help manage negative emotional experiences. Affect labeling or naming emotions diminishes the response of the amygdala and other limbic regions to negative emotional images.  A  brain imaging study by UCLA psychologists reveals why verbalizing our feelings makes our sadness, anger and pain less intense.

When people see a photograph of an angry or fearful face,they have increased activity in a region of the brain called the amygdala, which serves as an alarm to activate a cascade of biological systems (including stress chemicals) to protect the body in times of danger. Scientists see a robust amygdala response even when they show such emotional photographs subliminally, so fast a person can’t even see them.

But does seeing an angry face and simply calling it an angry face change our brain response? The answer is yes, according to Matthew D.Lieberman, UCLA associate professor of psychology.

“When you attach the word ‘angry,’ you see a decreased response in the amygdala,” said Lieberman, lead author of the study. The study showed that while the amygdala was less active when an individual labeled the feeling, another region of the brain was more active: the right ventrolateral prefrontal cortex.

This region is located behind the forehead and eyes and has been associated with thinking in words about emotional experiences. It has also been implicated in inhibiting behavior and processing emotions.

“What we’re suggesting is when you start thinking in words about your emotions —labeling emotions — that might be part of what the right ventrolateral region is responsible for,” Lieberman said.

If a newcomer to recovery one is sad or angry or resentful , getting them person to talk or write may many have benefits.

In Lieberman’s study  participant’s viewed images of individuals making different emotional expressions. Below the picture of the face they either saw two words, such as “angry” and “fearful” and chose which emotion described the face, or they saw two names,such as “Harry” and “Sally,” and chose the gender-appropriate name that matched the face.

“When you attach the word ‘angry,’ you see a decreased response in the amygdala,” Lieberman said. “When you attach the name ‘Harry,’you don’t see the reduction in the amygdala response.

“When you put feelings into words, you’re activating this prefrontal region and seeing a reduced response in the amygdala,” he said. “In the same way you hit the brake when you’re driving when you see a yellow light,when you put feelings into words, you seem to be hitting the brakes on your emotional responses.”

As a result, an individual may feel less angry or less sad.

“This is ancient wisdom,” Lieberman said.

Putting our feelings into words helps us heal better and if we can get newcomers to talk about them, that  will make them feel better. They will experience part of the “solution” right way and be encouraged to come back for more.

So putting feelings into words helps with not only regulating and modulating the intensity of emotions, but helps with processing them, reduces distress and distress based impulsivity and shows there is a solution to unruly negative  emotions.

In my experience this process has been a fundamental part of how it works!

 

 References

Lieberman, M. D., Eisenberger, N. I., Crockett, M. J., Tom, S. M., Pfeifer, J. H., & Way, B. M. (2007). Putting feelings into words affect labeling disrupts amygdala activity in response to affective stimuli. Psychological Science, 18(5), 421-428.

 

lieberman_affect_labelling_scan_small

What makes some children of alcoholics vulnerable, and some resilient?

I come from a family of four siblings, two of whom are alcoholic and two who are not. I have often wondered why this is the case? Why is it the case that certain children of alcoholic parents will grow up to become alcoholics and why some will not? What is it that makes certain children vulnerable to alcoholism and other children, from the very same family, protected. What do these children have that protects them from later alcoholism?

This is especially important to know in terms of prevention strategies to help children at risk.

Obviously environment has an impact on vulnerability but does an inherited protectiveness help prevent this sometimes dysfunctional and abusive childhood environment of alcoholic parenting from having the same impact as those children who have inherited a genetic vulnerability?

Throughout our blogs has been a thread suggesting alcoholics, and children of alcoholics, may have difficulties in processing and regulating emotions. Is this the vulnerability, is there a difference in affective/emotional circuitry in the brain?

We cite a very interesting article here  Affective circuitry and risk for alcoholism in late adolescence: Differences in frontostriatal responses between vulnerable and resilient children of alcoholic parents

in setting out an argument that children of alcoholics who are at greater risk of later alcoholism may have inherited impairments in brain neural circuitry which is responsible for affective/emotional processing.

Children of alcoholics (COAs) are at elevated risk for alcohol use disorders (AUD), yet not all COAs will develop AUD. One aim of this study was to identify neural activation mechanisms that may mark protection or vulnerability to AUD in COAs.

 

Thoughtful little girl

 

Some differences between alcohol abusers and control samples may precede alcoholism onset and thus constitute markers of precursive risk. After all, behavioral and affective markers early in life can predict later alcoholism (Caspi et al., 1996; Mayzer et al., 2001). Thus, it is reasonable to hypothesize that pre-alcoholic differences in the functioning of relevant neural systems will be related to risk for alcoholism.

In hoping to identify neural activation mechanisms that may mark protection or vulnerability to AUD in children of alcoholic fathers, the guiding conceptual framework was that the functioning of affective and behavioral regulation networks in the brain may serve as such mechanisms.

Consistent with that framework, the resilient and vulnerable groups were distinguished from one another by remarkably consistent inverse or opposite patterns of activation in the brain in response to the processing of emotional stimuli and which were most apparent with regard to negative affective stimuli and the vulnerable group.

These results suggest separate pathways of risk and resilience in the COA’s. First, the COA group that was not prone to early problem drinking (the resilient group) had more activation of the orbital frontal gyrus (OFG) than controls in response particularly to negative affect stimuli, but also to some extent in response to positive affect stimuli. The OFG is involved in the monitoring and evaluation of the affective value of stimuli, allowing for appropriate behavioral responses (Kringelbach and Rolls, 2004; Rolls, 2004).

The resilient group also had increased left insula activation to negative words. The insula is involved in evaluating internally generated emotions and the monitoring of ongoing internal emotional state (Phan et al., 2002).

The present findings, then, are consistent with the hypothesis that resilient youth have enhanced monitoring of emotionally arousing stimuli, even compared to typically developing youth. Yet, in an important nuance, they did not suppress the emotional experience.

They were prepared to modify behavioral response while maintaining affective response to these stimuli. This pattern of response in resilient youth may represent increased flexibility in emotional and social behavior.  These youth may be exhibiting precisely an ability to delay external response to arousing stimuli, while internally processing those stimuli. In short, this may be a “reflective” pattern of approach to the world.

It is not difficult to speculate how this pattern might protect these at risk youth from substance misuse: they are able to respond to the emotional stimuli, but demonstrate enhanced monitoring that may allow for the inhibition of inappropriate responding, buying time for flexible response options based on well-processed information.

Interestingly, the vulnerable group displayed no differences from the control group in emotional monitoring and behavioral regulation systems (OFG and insula), suggesting that weakness in that system is not a risk factor. Rather, they demonstrated over-activation of DMPFC and an atypical under-activation of key emotion processing regions (particularly extended amygdala and ventral striatum). This pattern was more notable in regard to negative affect, it was also observed to a lesser extent with positive affect.

All of this may be consistent with a reactive approach to the world, in which affect is not fully processed.

Supporting this interpretation, neuroimaging studies have consistently shown the involvement of the DMPFC with conscious self-monitoring of emotional responses (Beauregard et al., 2001; Kuchinke et al., 2006; Levesque et al., 2003; Levesque et al., 2004; Phan et al., 2005). For example, during the voluntary suppression of negative affect in healthy adults, activation in the dorsal medial and lateral prefrontal cortex increased and that in the nucleus accumbens and extended amygdala decreased (Phan et al., 2005). It has been suggested that emotional information is conveyed from limbic regions to the prefrontal cortex allowing conscious, voluntary emotional self-regulation (Levesque et al., 2003; Levesque et al., 2004).

Therefore, one interpretation of the present findings is that the vulnerable youth were recruiting an emotional control system that was suppressing emotional response.

 

References

Heitzeg, M. M., Nigg, J. T., Yau, W. Y. W., Zubieta, J. K., & Zucker, R. A. (2008). Affective circuitry and risk for alcoholism in late adolescence: differences in frontostriatal responses between vulnerable and resilient children of alcoholic parents. Alcoholism: Clinical and Experimental Research, 32(3), 414-426.