emotional distress

There is a map of Emotional Responding Tattooed on my Heart.

Posted on by alcoholicsguide

When I was doing my step four inventory as part of my 12 step programme of recovery  I did it pretty much as suggested in the Big Book.

My sponsor at the time asked me to do an additional part that is not explicitly mentioned in the Big Book.

He said to list all the negative emotions (or defects of character) that I had been in the grip of and exhibiting in relation to my various misdemeanors and the resentments I had held against various people and institutions over the preceding decades.

This turned out to be a brilliant idea for two reasons.

First it showed me that  I held a multitude of resentments because I had a problem of emotion regulation.

I did not realise that the engine driving this emotion dysregulation was chronic shame.

I realised when doing my step 4 that that I had not previously been able to leave various supposed slights and abuses from my past in the past because I did not have the emotional maturity to look at these episodes reasonably and objectively.

In other words, I had not processed these episodes emotionally and embedded these events in my long term memory like healthy more emotionally mature people do.

Hence when I came into recovery I had hundreds and hundreds of resentments swirling around my mind, poisoning my thoughts and sending constant emotional daggers into my heart.

My past constantly assailed me emotionally, randomly attacking my mind.

My step 4 and then 5 showed me that I did  not have the natural ability to deal with my negative emotions.

Secondly, listing all the negative emotions I had when I held a resentment against someone was very revealing in that when I held a resentment, any resentment, and against a wide variety of people, the negative emotions listed where generally the same! In fact they were all interlinking in a pattern of emotional reacting, one activating the other. It was like a emotion web that ensnared one in increasingly frustrating states of emotional distress and inappropriate responding.

This was quite a revelation!? That I respond in exactly the same way to my sense of self being threatened?

That there was a map of emotional responding tattooed on my heart.

I was drawing up a web of my emotional dysregulation, a route map of all the wrong ways to go, to emotional cul de sacs.

It was a list of the negative emotions which appear always when I felt anger and resentment against someone for hurting me and my feelings.

Just as revealing where the negative emotions listed which clearly showed how  I react, and can still react to people who I believe have caused my hurt or rejection.

In fact it seems now that I treat all insult, intentional or otherwise, in a very similar way.

I have spent years trying to work our why?

I got as far as deciding it was an inherent problem with processing negative emotions, which it is.

However, there seems to be a problem specifically with a patterned mesh of negative emotions which are activated when someone upsets me.

In fact I think this pattern of interlinked negative emotions occurs simply because of inability to identify, label and share the simple fact that I have been upset  by what someone has said or acted towards me.

“Shame is a fear-based internal state being, accompanied by beliefs of being unworthy and basically unlovable. Shame is a primary emotion that conjures up brief, intense painful feelings and a fundamental sense of inadequacy. Shame experiences bring forth beliefs of “I am a failure” and “I am bad” which are a threat to the integrity of the self. This perceived deficit of being bad is so humiliating and disgraceful that there is a need to protect and hide the flawed self from others. Fears of being vulnerable, found out, exposed and further humiliated are paramount. Feelings of shame shut people down so that they can distance from the internal painful state of hopelessness.”

“… unacknowledged thoughts and feelings become repressed and surface later through substitute emotions and dysfunctional behavior. Other emotions are substituted to hide the shame and maintain self esteem. Anger, exaggerated pride, anxiety and helplessness are substituted to keep from feeling the total blackness of being bad. The buried shame is expressed through defense mechanisms that shield negative unconscious material from surfacing.

Anger responses are modeled and learned in some families. The anger response is more comfortable than feeling the shame for some individuals. Families where coercive and humiliating methods of discipline are used develop children who are shame prone. Behavior become driven by defenses that function to keep from feeling bad. Reality becomes distorted to further protect the self from poor self esteem. The transfer of blame to someone else is an indicator of internal shame.

Children who live with constant hostility and criticism learn to defend against the bad feelings inside and externalize blame on others. External assignment of blame is a defense against shame. People who are super critical have a heavy shame core inside.”

I was working with someone last year and we had a disagreement and this guy said to me “I am upset” and “You have hurt my feelings” I was taken aback. I thought I never say things like that. This guy was an Olympic champion at expressing how he feels compared to me. I never say I am upset because it also seems to be an undifferentiated emotion that I have trouble accessing, mentalising and expressing.

I have not been taught as a child or since to simply say I am upset.

Instead of acting on my upset by saying to someone,  you have hurt my feelings  I do the opposite,   I react and attack them in my head, my thoughts, my words and sometimes in my actions. Sometimes I “get them back” somehow. I make them pay in some way.

Honesty is the heart of recovery and I am being honest. The years of recovery reveal many different things, some of them not so palatable.

I grew up in a family that did not express emotions like the ones I had mentioned. We reacted via anger and put downs hence I have grown up to be dismissive.

My dismissiveness and my arrogance are parts of defence mechanism against rejection, they guard my inherent sense of shame. I am full of shame, more so than fear, although these two overlap. Shame is in fact fear evoking.

I hide my shame away under an anger of emotional hostility, stay away or else! I will get you back somehow. Sometimes I am in shame and offend via my attitudes.

I also have other ways of reacting in an emotionally unhealthy way that my step 4 showed.

If someone hurts me, according to my step 4, my angry resentment of what they have said or done makes me ashamed. This can quickly prick my sense of self pity (uselessness and hopelessness) which is something I have always rage against (rage is an essential part of shame plus I rally against this feeling of powerlessness) and I retaliated via excessive pride (I am better than you, I will put you down and see how you like it!) I put you down in my mind or through the words uttered from my mouth by arrogance, dismissiveness, impatience and intolerance.

I do so because I am being dishonest and fearful.

I do some because I am self centred and selfish.

These are all parts of my emotionally entangled web that is spun when I react to some sense of rejection.

Sometimes the shame persists for some time and I try to relieve it by behavioral addictions, too much shopping, too much eating, too much objectification of the opposite sex.

Not enough action, or effort to change my feelings in a healthy manner.

My step 4  showed me this is the unhealthy fruit of my greed, gluttony, my lust, my sloth.

My spiritual malady.

Add in perfectionism because that is the quick way to do nothing, a fear of failure  that paralyses.

These are my main negative emotional  reactions to the world that often scare me and make me feel ashamed.

I have felt powerless via your comments so try to to steal some power back by making my self seem more powerful over you.

I respond to feelings of humiliation by humiliating you, I react to my chronic shame by attempting to created shame in you.

Some days I react more adversely than others.

For example, this family have just moved into my neighbourhood, they seem wild and out of control.

I am not only fearful (leading to dishonesty in my thinking, catastrophizing, intolerance of uncertainty about how they will behave etc) I have reacted to their arrival via shame based defence mechanisms and reactions. I am shamed and disgusted that my neighourhood has come to this. I am dismissive of them, intolerant, impatient and arrogant towards them. All shame based reactions.

Last night the police were called to their home and one of them was handcuffed and put in the back of the police van.

My head went “I told you so!”

It was a very shameful scene for the whole family.

When things had died  down and calm restored I spent the evening not in my fear or shame but in empathy and compassion.

How embarrassing for them how shameful.

I relate to them as they are out of control, my family was at varying times completely out of control too, traumatic and this is what has created a chronic shame in me, even still now after 10 years of recovery!

My shame responded and related to their shame.

Nobody wants to be out of control, to be teetering on the verge of the next disaster, the next moving of home, the next calling of the police,  the next swirling carousel of unmanageabiilty.

No one.

I related and all my negative emotions retreated to source like a evening tide on a beach.

I relate to my fellow human beings when I am not in fear or shame.

When I am in fear and shame the same pattern of negative reactions entrap my heart in its’ poisonous grip and I react in a way I would not choose to, if more reasonable.

This is what the heart of my alcholism looks like. Not a pretty sight some days.

The most beautiful thing about me most days is the fruits of my recovery.

Now at least I can see how I react and can take steps to deal with it.

I have a spiritual tool kit that deals with this emotional disease.

Whether  I stay in fear or shame is now my choice. A choice I once did not seem to have.

This is what recovery has given to me.

I do not have to cultivate my own misery through blind reaction.

Via an Amazing Grace I can now see what ails me.

Via AA I now have the tools, never taught to me in my family or in my troubled home environment.

I have gone home in AA. I learnt an attachment to those in AA and others.

I share my feelings of shame with those who know what that feels like.

Together we share our pain and we recover.

Reference

1. http://www.angriesout.com/teach8.htm

 

The Power of Identification!!

Posted on by alcoholicsguide

The main reason I am alive today, sober and have recovered from a seemingly hopeless condition of alcoholism is simple!

Or rather the first step can be simple.

The first step on my recovery journey was to identify with the life stories of other recovering alcoholics.

Not necessarily with where they grew up, or the damage alcoholism had inflicted on their lives. Although many alcoholics talk themselves, or their illness talks them, out of the possibility of recovery by saying I am not as bad as that guy, or that woman.

You may not be as bad “YET!” – the “yets” are often talked about in AA – you may not have done the damage others have, yet? Keep drinking and you are bound to. You, like them, will have no choice.

Alcoholism increasingly takes away choice.

It takes over your self will.

Your self will, your self regulation, is a combination of your emotional, attentional, memory and reward/survival/motivation networks.

Alcoholism takes over these networks, progressively, over time.

Neuroscience has shown this, over the last twenty odd years.

A superb longitudinal study, “The Natural History of Alcoholism” by George Vaillant  clearly showed this progression in six hundred alcoholics over a 60 year period!

In my own research and in articles, with two highly respected Professors at a UK University, I have shown how the alcoholic brain progressively “collapses inwards” to subcortical responding.

In other words, we end up with a near constant “fight or flight” reaction to the world,  with alcoholism causing distress based compulsion at the endpoint of this addiction.

All the above neural circuits become governed by a region of the brain which deals with automatic,  compulsive behaviour. All the self regulation parts of the brain progress to an automatic compulsive behaviour called alcoholism and we are then often without mental defence against the next drink!

I identified with this one simple fact – the progression of this neurobiological, emotional, and spiritual disease state called alcoholism. I saw it in my own life, this progression over years of drinking.

The “invisible line” that is crossed, according to AA members, can be viewed on a brain image, I believe.

Can you see it in your life?

Like these recovering alcoholics I had not taken my first drink hoping to end up an alcoholic

It was something that had happened to me,  happened despite my very strong will not because my will is weak. I am as wilful a person as you would hope to me. How come I became an alcoholic then?

I did also relate to other things these people shared.

I identified with the damage caused by alcoholism  in their lives and the lives of their family.  How this illness affects everyone in the immediate and even extended family.

I had never considered the effect on others, apart from me?

I listened and identified with how they talked about a “hole in the soul”, how they never felt part of, felt different from others, detached. I related to this. That was me too.

Alcohol made me feel more me! I became attached to it and grew to love it like someone would love another person, more so perhaps? Alcohol came first, loved ones second.

Alcoholism takes away all the good things in life and then your life too.

All of this was the case with me too.

I identified with all this.

I identified too with their solution.

I identified with and wanted what these now happy people in recovery had.

I decided to take the same steps as they had towards this happiness.

There is a solution.

We do recover!

The terror of “Locked In” Attention!

Posted on by alcoholicsguide

I remember when I was in the first days, weeks and months of early recovery I used to give myself such a hard time when my attention was drawn to some alcohol-related cue, like someone drinking ,or finding it difficult not dealing with some  reminder of people places and things from my alcohol abusing past; finding that I found it nigh on impossible dragging my attention away from these and related memories associated with my drinking past.

It was as if I was entranced by it, in some of tunnel vision. It used to scare the life out of me.

I rarely found these thoughts appetitive but if I dwelt on these thoughts or trained my attention on cues I would find that the adverse, fearful things would turn to more desire based physiological reactions like salivating and so on.

I took these to mean that I actually wanted to drink and not stay sober. My sponsor at the time said two things which helped – a. I have an alcoholic brain that wants to drink period, 2. cues from my past may always have this effect on me. Accept it, don’t fight it.

That was what I had been doing in fact. Fighting it, these cues reminders and their automatically occurring intrusive thoughts about the past. It is in fighting these thoughts that they proliferate and then become “craving”.

Years later after much research I found that all alcoholics seem to have an attentional bias towards alcohol-related cues which leads to a cue reactivity.

Originally I thought this meant that I simply wanted to drink but found out that in  any manifestation of urge to drink (which is slightly different from a craving which requires an affective response on the part of the alcoholic in order to become a craving similar to mental obsession of the Big Book ) there is a stress reponse like the hear beat quickening, differences in galvanic skin conductance, increased saliva production etc .

Thus this cue reactivty seems to involve not only appetitive or desire states, i.e. it activates the reward system in the brain to motivate one to drink but also contains a stress based reactivity.

Any so-called “craving” state also manifests as either an anxiety state in simple cue reactivity e.g. the sight of alcohol or in negative emotions such as fear, anger and sadness in terms of a stress based craving.

Together, i.e. a cue based reactivity in the face stress/distress leads to a greater urge to drink than by either alone. By reacting to these one is increasing the stress/distress.

To the alcoholic brain having a drink or the desire to drink is the brain suggesting to us as alcoholics that this is the best way to attain transient homeostasis from an allostatic state of distress because this is how we used to balance the effects of emotional distress when we were drinking. We experience distress and automatically had thoughts about drinking. Thus alcoholism is a distress-based condition. We think it is us wanting the drink but it is the distress prompting the wanting of the drink!!

The distress does the drinking for us, itgets us out of our seats and down the street to the bar, it gets us on the bar stool….We may think it is our actions as we use rationalisng and justifying schemata afterwards to justify behaviour that had, in fact, been automatic or compulsive, compulsive meaning to relieve a distress state.

As a schema, which is implicit, i.e. it is automatically prompted and activated by distress also. We are not even in charge of this. We feel and think that we are in control over behaviour bit this is not the case as self control has become so impaired and limited it is distress doing the action and the subsequent rationalising.

The compusive part of the brain, the dorsal striatum, is the only part of the brain that requires us to make a post hoc rationalisation of why we did an action that was essentially automatic and compulsive.

We have become passengers in our own lives. Distress is now doing the driving.

So the brain thinks it is simply telling us the best way to survive this distress or in other words to regulate this distress. Thus it is an incredibly impaired way to regulate stress and emotional distress.

I want to further explain how some of this is linked to low heart rate variability. If we have low HRV we find it difficult inhibiting automatic responses and in changing behaviour. We become behaviourally rigid, and locked into attending to things like cues when we don’t really want to.

This is often the result of distress reducing the ability of the heart rate variability to inform and change our responses.

I cite and use excerpts form one of my favourite articles again by co-authored by Julian Thayer (1).

 

“The recovering alcoholic must face the difficulty of having his or her ambition to remain abstinent challenged in various situations in which memories about the pleasurable effects of alcohol are activated and the striving for abstinence no longer seems meaningful (Anton 1999; Marlatt and Gordon 1985). The odds for successful coping with such temptations are related to numerous factors, such as one’s subjective affective state and the ability to shift one’s focus from the automatic impulse to drink toward a cognitive reconstruction of the situation (Palfai et al 1997b; Tiffany 1990). Despite the importance of  attentional flexibility in effectively modulating such “highrisk” situations, research on the topic is scarce.

Thayer and Lane (2000) suggested that the interplay between positive (excitatory) and negative (inhibitory) feedback circuits in the nervous system (NS) allows for flexible and adaptive behavior across a wide range of situations. The uniqueness of this model lies with its emphasis on the importance of inhibitory processes in effective modulation of affective experience. In short, these researchers propose that the defects in neurovisceral regulation of affective experience seen in various psychiatric conditions (e.g., anxiety disorders) may be better explained by faulty inhibitory function in the NS than by unitary arousal models.

Tonic heart rate variability (HRV) may be a physiologic indicator of such inhibitory processes (Friedman and Thayer 1998a; Porges 1995). Heart rate variability refers to the complex beat-to-beat variation in heart rate produced by the interplay of sympathetic and parasympathetic (vagal) neural activity at the sinus node of the heart.

Importantly, heart rate (HR) is under tonic inhibitory control via the vagus nerve (Levy 1990). These neural connections to the heart are linked to brain structures involved in goal-directed behavior and adaptability (Thayer and Lane 2000). Compelling evidence now exists to show that high levels of HRV are related to cognitive flexibility (Johnsen et al 2003), modulation of affect and emotion (see Bazhenova 1995, cited in Porges 1995), and increased impulse control (Allen et al 2000; Porges et al 1996).

The hypothesis that reduced HRV is related to defective affective and emotional regulation has been supported in recent research in which reduced HRV was present in clinical disorders such as generalized anxiety disorder (Thayer et al 1996), panic disorder (Friedman and Thayer 1998b), posttraumatic stress disorder (Cohen et al 1997) several scientific arguments suggest that impaired inhibitory function may play a role in chronic alcohol abuse.

First, alcoholics have repeatedly been shown to have problems shifting attention and directing their attention away from task-irrelevant information (Johnsen et al 1994; Setter et al 1994; Stormark et al 2000). Second, frontal areas of the brain are most affected by the acute and chronic effects of alcohol, and these structures are of crucial importance in inhibitory functioning and self-control (Lyvers 2000). Third, acute effects of alcohol ingestion result in reductions in HRV, implying that chronic alcohol ingestion may result in a long-lasting impairment of the vagal modulation of HR (Reed et al 1999; Weise et al 1986)

Fourth, severely dependent alcoholics show a sustained phasic HR acceleration when processing alcohol information, indicating defective vagal modulation of cardiac function (Stormark et al 1998). Tonic HRV has similarly been found to be a useful measure of physiologic activity in challenging situations (Thayer and Lane 2000). Appropriate modulation of HRV (increases, decreases, or no change) depends on the type of challenge and the characteristics of individuals as they interact with specific contextual manipulation (Friedman and Thayer 1998a; Hughes and Stoney 2000; Porges et al 1996; Thayer et al 1996).

For example, during attention demanding tasks, healthy individuals show appropriate reductions in HRV (Porges 1995). In general, high tonic levels of HRV allow for the flexible deployment of organism resources to meet environmental challenges. With respect to attention, it is suggested that high levels of HRV reflect flexible attentional focus, whereas low HRV is related to “locked in attention” (Porges et al 1996). Moreover, increased tonic vagal activity is related to adaptive development and lack of behavioral and emotional problems (Hughes and Stoney 2000; Porges et al 1996).

Furthermore, it has been demonstrated that increases in vagal activity during challenging tasks discriminates between individuals who have experienced traumatic events and managed to recover from them and those who still suffer from chronic symptoms of posttraumatic stress (Sahr et al 2001). Such increases in vagal activity during challenging tasks are particularly interesting because studies on alcohol abusers have found increases in HRV after exposure to alcohol-related cues (Jansma et al 2000; Rajan et al 1998).

One could speculate that such enhanced vagal activity could be a sign of compensatory coping aimed at taming automatic drinking related processes (Larimer et al 1999). Such an interpretation is in agreement with cognitive theories predicting that alcoholics and other drug users do not simply respond passively to exposure to drug-related cues, but, on the contrary, in such situations conscious processes are invoked, inhibiting execution of drug-related cognition (Tiffany 1990, 1995). If this explanation is correct, alcoholics who have more effective coping resources should show stronger increases in vagal activity during such challenging exposure than alcoholics who express greater difficulty in resisting drinking-related impulses.

Also  general differences in HRV between alcoholics and nonalcoholics are interesting indicators of defective inhibitory functioning, a measure of rigid thought-control strategies and lack of cognitive control should be an important indicator of defective inhibitory function and “positive feedback loops” reflected as low HRV (Wegner and Zanakos 1994).

Linking these measures to the physiologic index of HRV makes a stronger case for attributing reduced vagal tone (HRV) to a defective regulatory mechanism resulting in unpleasant affective states and maladaptive coping with psychologic stressors

The main results of our study may be summed as follows. First, as expected, alcoholic participants had lower HRV compared with the nonalcoholic control group. Second, the imaginary alcohol exposure increased HRV in the alcoholic participants. Third, across the groups, an inverse association was found between HRV and negative mood and a positive association between positive mood and HRV. Fourth, HRV was negatively correlated with compulsive drinking during the imaginary alcohol exposure in the alcoholic participants. Fifth, within the alcoholic group, HRV was negatively associated with chronic thought suppression (WBSI).

Generally, these findings are in agreement with the neurovisceral integration model and the polyvagal theory that suggests HRV is a marker of the level of cognitive, behavioral, and emotional regulatory abilities (Thayer and Lane 2000).

The fact that the alcoholic group had generally lower tonic HRV compared with the nonalcoholic control group indicates that such reduced HRV may also be a factor in alcohol abuse; however, such group differences in HRV provide only indirect support for the theory that low HRV in alcoholics may be related to impaired inhibitory mechanisms

Because HRV is related to activity in frontal brain areas involved in cognition and impulse control (Thayer and Lane 2000), we speculated that tonic HRV would be an index of nonautomatic inhibitory processes aimed at suppressing and controlling automatic drug-related cognitions. To test this hypothesis more directly, the association between HRV and problems with controlling drinking-related impulses were studied.

Consistent with this hypothesis, the compulsive subscale of the OCDS was found to be inversely associated with HRV in the alcohol-exposure condition, thus suggesting that HRV may be an indirect indicator of the level of impulse control associated with drinking. These findings are therefore consistent with Stormark et al (1998), who found that sustained HR acceleration (lack of vagal inhibition) when processing alcohol-related information was related to compulsive drinking and “locked-in attention.”

Post hoc analysis further suggested that alcoholics who expressed a relatively high ability to resist impulses to drink (OCDS) had the clearest increase in HRV under the alcohol exposure this study suggests that alcoholics may actively inhibit or compensate for their involuntary attraction to alcohol-related information by activation of higher nonautomatic cognitive processes (Tiffany 1995). Such conscious avoidance has previously been demonstrated in studies on attentional processes in alcoholics (Stormark et al 1997) and by the fact that frontal brain structures involved in inhibition and control of affective information are often highly activated in the processing of alcohol related cues (Anton 1999). Furthermore, this interpretation is in agreement with other studies suggesting that high HRV during challenging tasks is associated with recovery from acute stress disorders (Sahr et al 2001).

Several studies have indicated that low HRV is associated with impaired cognitive control and perseverative thinking (Thayer and Lane 2002). Consistent with these reports a negative association was found between HRV and chronic thought suppression. The WBSI assesses efforts to eliminate thoughts from awareness while experiencing frequent intrusions of such “forbidden” thoughts and thus represents an interesting and well-validated measure of ineffective thought control (Wegner and Zanakos 1994). Thought suppression has been found to be an especially counterproductive strategy for coping with urges and craving (Palfai et al 1997a, 1997b) and may even play a causal role in maintaining various clinical disorders (Wenzlaff and Wegner 2000).

To our knowledge, this is the first time a link between physiologic indicators of a lack of cognitive flexibility (low HRV) and chronic thought suppression has been demonstrated.

Thayer and Friedman (2002) have reviewed evidence indicating that there is an association between vagally mediated HRV and the inhibitory role of the prefrontal cortex. Consistent with Thayer and Lane (2000), this study suggests that impaired inhibitory processes are significantly related to ineffective thought control.

The fact that this association between HRV and WBSI was only found in the alcoholics may be related to the fact that only this clinical group shows signs of such faulty thought control.

Wegner and Zanakos (1994) suggested that thought suppression is particularly ineffective when the strategic resources involved in intentional suppression are inhibited or blocked (Wegner 1994). Consistent with this hypothesis, our findings show that those reporting high scores on WBSI show signs of impaired inhibitory functioning as indexed by low vagally mediated HRV.”

This excellent article fro me is also alluding to the fact that those with increased HRV was related to successfully related to regulating negative emotion,  stress/distress and affect, not just the thoughts that these affective states gave rise to .

Thus any strategies that help with improving  the ability to increase HRV will likely have positive results in coping with cue associated materials.

We look at one of these therapeutic strategies next…that of mindfulness meditation.

 

References

1. Ingjaldsson, J. T., Laberg, J. C., & Thayer, J. F. (2003). Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry, 54(12), 1427-1436.

 

 

 

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

Posted on by alcoholicsguide

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

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

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

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

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

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

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

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

 

impulse control.preview

“Abstract

Background

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

Results

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

Conclusions

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

Introduction

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

Predictors of Mortality Risk among Individuals with Alcohol Use Disorders

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

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

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

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

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

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

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

Discussion

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

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

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

Moderation of the Impulsivity-Mortality Link via the Social Context

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

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

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

References

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

What recovers in Recovery? – Cognitive Control over emotions?

Posted on by alcoholicsguide

 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.

Gambling Disorder and Emotional Dysfunction

Posted on by alcoholicsguide

Following on from our recent blog on emotional dysfunction in sexual addiction we continue our series which explores the inherent role of  emotional dysfunction in all addictive disorders.

We will explore eating disorders later.

Here we use excerpts from a very interesting article (1)  on

Deficits in emotion regulation associated with pathological gambling.

 

“Pathological gambling is recognized as an impulse-control disorder characterized by a loss of control over gambling, deception about the extent of one’s involvement with gambling, and significant family or job disruption (American Psychiatric Association, 1994). Failures in self-control, therefore, represent a defining feature of pathological gambling. Self-control involves over-riding impulses by substituting another response in its place (Tice & Bratslavsky, 2000), and failures in self-control are primarily associated with the desire for short-term gains despite associated long-term negative consequences (Baumeister, 1997, Baumeister, Heatherton, & Tice, 1993).

Failures in control over gambling are likely to be influenced by individual coping styles. Problem-focused coping includes active and effortful problem solving, while emotion-focused coping includes escape and avoidance behaviours (Lazarus & Folkman, 1984). Scannell, Quirk, Smith, Maddern, and Dickerson (2000) suggested that loss of control over gambling is associated with emotion-focused coping such as avoidance or escape. This suggestionhas been supported by evidence that gamblers demonstrate deficits in coping repertoires (McCormick, 1994) and some rely on gambling to provide an escape from personal or familial problems (Corless & Dickerson, 1989; Lesieur & Rosenthal, 1991). Finally, in a sample of adolescent gamblers, those identified as at-risk for developing pathological gambling behaviours were those who exhibited more emotion-focused coping styles
(Gupta & Derevensky, 2001).

Gambling behaviours, therefore, seem to be associated with a deficit in self-control
processes that may be exacerbated by reliance on coping styles characterized by
avoidance and escape. At a more basic level, difficulties managing emotions effectively may contribute to the use of maladaptive coping strategies and result in failures in self regulation and impulse control. Optimal self-regulation relies on being able to focus on long-term goals in the presence of emotional distress that tends to shift attention to the immediate present (Tice & Bratslavsky, 2000). In addition, struggling with one’s feelings may deplete coping resources and leads to decreased self-control (Baumeister, Muraven, & Tice, 2000), leading to increased risk of disinhibited or impulsive behaviour.

Finally, individuals who are feeling acute emotional distress will likely wish to escape via activities that promise immediate pleasure (Tice, Bratslavsky, & Baumeister, 2001) and pathological gamblers often report using gambling to escape from negative mood states (Blaszczynski & McConaghy, 1989; Getty, Watson, & Frisch, 2000).

Emotion regulation refers to strategies to influence, experience, and modulate
emotions (Gross, 1999). Although there are several factors that influence whether a
certain emotion-regulation strategy is adaptive in a particular situation, certain strategies appear to be costly and maladaptive. For example, suppression or avoidance of emotions is associated with increased negative effect and anxiety, physiological activity, and physical pain (Campbell-Sills, Barlow, Brown, & Hoffman, 2006; Gross & Levenson, 1997; Levitt, Brown, Orsillo, & Barlow, 2004; Masedo & Esteve, 2007). Experimental investigations also support the notion that the effort of suppressing emotions drains mental resources (Richards & Gross, 2000), which could lead to decreased self-control.

Ricketts and Macaskill (2003) investigated several techniques that gamblers use to
modify their emotions, one of which was the technique of ‘shutting off’ or using gambling in order to stop an unpleasant emotional state. Participants receiving treatment for gambling were interviewed or watched during treatment sessions and administered questionnaires. Patients who used the technique of ‘shutting off’ were often the ones who also reported poorly tolerating emotional discomfort (Ricketts & Macaskill, 2003).

According to Baumeister, Zell, and Tice (2007), emotional distress leads to an increase in self-awareness, which consequently leads to a desire to decrease ones self-awareness, but at the cost of self-regulation. If one is unable to self-regulate, this could lead to an addiction or a relapse of an addictive behaviour (Sayette, 2004).

Impulse control represents one of the major behavioural aspects of emotion regulation (Gratz & Roemer, 2004) and has been identified as an important component of addictive processes (Evenden, 1999). More specifically, research has demonstrated that failures of emotion regulation are associated with addictive behaviours (Coffey & Hartman, 2008; Fox, Axelrod, Paliwal, Sleeper, & Sinha, 2007; Goudriaan, Oosterlaan, De Beurs, & Van Den Brink, 2008; Lakey, Campbell, Brown, & Goodie, 2007).

Several recent studies have employed the Difficulties in Emotion-Regulation Scale (DERS), a recently developed and validated measure of emotion regulation, in assessing behavioural addictions (Bonn-Miller, Vujanovic, & Zvolensky, 2008; Fox et al., 2007; Fox, Hong, & Sinha, 2008). The DERS assesses both general deficits in emotion regulation and deficits in specific domains of regulation. It is based on a model of emotion dysregulation that includes: (1) deficits in awareness and understanding of emotional experience (i.e., clarity), (2) minimal access to strategies to manage one’s emotions, (3) non-acceptance of emotions (i.e., reactivity to one’s emotional state), and (4) impaired ability to act in desired ways regardless of emotional state (i.e., impulsivity and an inability to engage in goal-directed behaviour).

The goal of the present study was therefore to examine emotion regulation difficulties among individuals being treated in a specialist gambling clinic and
to compare the use of strategies to a mixed clinical comparison group and a sample
of healthy community controls. Specifically, we investigated the association between
emotion-regulation deficits and gambling pathology using two measures of emotion
regulation, the DERS and the Emotional Regulation Questionnaire (ERQ; Gross & John, 2003). The ERQ examines the habitual use of two specific emotion-regulation strategies, namely expressive suppression and cognitive reappraisal. The use of suppression reduces the outward expression of emotions in the short term, but is less effective in reducing emotions in the long term and is, therefore, considered a maladaptive emotion-regulation strategy (Gross, 1998; John & Gross, 2004). Cognitive reappraisal involves changing the meaning associated with a particular situation so that the emotional impact is altered (Gross, 1999; Siemer, Mauss, & Gross, 2007). Reappraisal is considered an adaptive strategy to regulate one’s internal states and is associated with higher self-reported positive emotions and fewer depressive symptoms (Gross & John, 2003; Mauss, Cook, Cheng, & Gross, 2007).

gambling-slots-cover (1)

 

 

Discussion

As expected, we found a significant relationship between self-reported problem,
gambling behaviour, and negative effect as measured by the DASS, as well as deficits
in emotion regulation as measured by the DERS.

With respect to group differences, the gambling group reported a greater lack
of awareness of their emotions compared to both comparison groups.

With respect to the overall findings of emotional dysregulation, Blaszczynski and
Nower (2002) proposed a pathway model of the determinants of gambling and identified three separate trajectories into problem gambling. Of relevance to the current study, the authors identified an emotionally vulnerable group of problem gamblers who used gambling as a way to regulate affective states by providing either emotional escape or arousal.

According to the pathway model, once a habitual pattern of gambling behaviours has been established, the combination of emotional vulnerabilities, conditioned responses, distorted cognitions, and decision-making deficits maintain the cycle of pathological gambling. Blaszczynski and Nower (2002) suggest that such emotional vulnerabilities make treatment more difficult in this particular group of gamblers and emphasize the need to address these underlying vulnerabilities in addition to directly targeting gambling behaviours in therapy. It may, therefore, be of therapeutic benefit to specifically assess for and target emotion-regulation strategies in this population of gamblers.

Given the gamblers in the current study demonstrated limited access to effective strategies for managing difficult emotions, it may be important for clinicians to address coping strategies (including emotion-focussed strategies) as a part of any comprehensive treatment package. Gamblers need to be able to recognize and modify unhelpful thinking patterns (both in relation to problem gambling situations and, more generally, to other life stressors).

It is also important that the clinician is aware of any deficits in emotion-regulation strategies to ensure that the client is prepared to guard against relapse, given that the ability to tolerate distress is associated with increased length of abstinence from gambling (Daughters et al., 2005).

. More specifically, given the finding that gamblers were less aware of their feelings, mindfulness strategies may be useful to increase awareness of one’s
emotions. This could potentially be helpful in reducing automatic and habitual responses, particularly in high-risk situations. Decreasing emotional avoidance through mindfulness may also assist pathological gamblers in better understanding the impact of various mood states on their behaviour. Individuals who experience heightened awareness of emotions, and who learn to observe and act in a more aware manner, are less likely to engage in maladaptive behaviours such as gambling (Lakey et al., 2007).”

 

References

1. Williams, A. D., Grisham, J. R., Erskine, A., & Cassedy, E. (2012). Deficits in emotion regulation associated with pathological gambling. British Journal of Clinical Psychology, 51(2), 223-238.

AA helps to reduce Impulsivity

Posted on by alcoholicsguide

 

One constant in studies on addiction and in alcoholism, in particular is the  fundamental role played by impulsivity in these disorders. It is seen to be present in early use but appears to be more distress based (i.e. more negative urgency based) as the addiction cycle becomes more chronic. This impulsivity has obvious consequences for propelling these disorders via impulsive behaviours and decision making difficulties.

Thus it then follows that any treatment of these addictive disorders must have treatment of impulsivity at the core as it appears to a fundamental pathomechanism.

 

Here, we review a study that on links  AA attendance and reduced impulsivity using a 16-year prospective study of men and women, who were initially untreated for their drinking problems. Across the study period, there were significant l decreases in impulsivity, and longer AA duration was associated with reductions in impulsivity.

Alcoholics Anonymous (AA) is linked to improved functioning across a number of domains [2,3]. As the evidence for the effectiveness of AA has accumulated, so too have efforts to identify the mechanisms of change associated with participation in this mutual-help group [4].

This study concluded that help-seeking and exposure to the “active ingredients” of various types of help (i.e., AA principles/practices, sponsors), which, in turn, leads to improvements in reduced impulsivity.

Impulsivity is typically higher among individuals in AUD treatment than among those in the general population [5] and, impulse control deficits tend to predate the onset of drinking problems [6-9].

Contemporary research has revealed that traits such as impulsivity can change over time [10]. Mutual-help groups like AA may promote such changes, given that they seek to bolster self-efficacy and coping skills aimed at controlling substance use, encourage members to be more structured in their daily lives, and target deficits in self-regulation [11].

 

impulse control.preview

 

Such “active ingredients” may curb the immediate self-gratification characteristic of disinhibition and provide the conceptual grounds to expect that AA participation can press for a reduction in impulsive inclinations. In turn, given the range of outcomes related to impulsivity (e.g., legal, alcohol-related, and psychosocial problems), decreases in impulsivity may account for part of the association between AA participation and improvements in these outcomes.

AA’s vision of recovery as a broad transformation of character [12], and  explores individual differences in emotional and behavioural functioning as potential mechanisms of change (13,14).

Such groups encourage members to be more structured and goal-directed, which may translate into greater efforts to delay gratification of one’s impulses and  to improve clients’ general coping skills (e.g., reduce avoidance coping).

Given that impulsivity is a risk factor for a host of problematic behaviors and outcomes beyond drinking-e.g., criminality [15], drug abuse [16], reckless driving and sexual practices [17],  lower quality of interpersonal relationships [18], and poor health [19] this reduced impulsivty is beneficial in other aspects too.

Notably, this effect was buffered by a higher quality of social support-a probable active ingredient of AA. Thus, the impact of reducing impulsivity may be widespread across a range of outcomes that are critical for long-term sobriety.

 

Our main caveat on this study is that it does not distinguish between different types of impulsivity and does not mention negative urgency (or distress-based impulsivity) which is more commonly seen is this sample group.

AA’s “active ingredients” may reduce distress, via a new found emotional regulation gained via the steps and use of a sponsor (acting as an external prefrontal cortex to help us inhibit our impulsive and distress based responses)  which in turns reduces our tendency to impulsive decision making and behaviour.

 

It would have been interesting in this study to have also measure how emotional dysregulation changed in the time span of 16 years (using the DERS scale) and to have used a different impulsivity scale i.e. used the UPPS-P scale which would both have helped more specificallylook  at the interaction of how emotional regulation and impulse control changed over the 16 year period.

 

References

 

1.  Blonigen, D. M., Timko, C., & Moos, R. H. (2013). Alcoholics anonymous and reduced impulsivity: a novel mechanism of change. Substance abuse, 34(1), 4-12.

2. Humphreys, K. Circles of recovery: Self-help organizations for addictions. Cambridge Univ Pr; 2004.

3.. Tonigan JS, Toscova R, Miller WR. Meta-analysis of the literature on Alcoholics Anonymous: Sample and study characteristics moderate findings. Journal of Studies on Alcohol. 1995

4. Kelly JF, Magill M, Stout RL. How do people recover from alcohol dependence? A systematic review of the research on mechanisms of behavior change in Alcoholics Anonymous. Addiction Research & Theory. 2009; 17(3):236–259.

5. Conway KP, et al. Personality, drug of choice, and comorbid psychopathology among substance abusers. Drug and alcohol dependence. 2002; 65(3):225–234. [PubMed: 11841894]

6. Caspi A, et al. Behavioral observations at age 3 years predict adult psychiatric disorders: Longitudinal evidence from a birth cohort. Archives of General Psychiatry. 1996; 53(11):1033. [PubMed: 8911226]

7. Cloninger CR, Sigvardsson S, Bohman M. Childhood personality predicts alcohol abuse in young adults. Alcoholism: Clinical and Experimental Research. 1988; 12(4):494–505.

8. Elkins IJ, et al. Personality traits and the development of nicotine, alcohol, and illicit drug disorders: Prospective links from adolescence to young adulthood. Journal of abnormal psychology. 2006; 115(1):26. [PubMed: 16492093]

9. Sher KJ, Bartholow BD, Wood MD. Personality and substance use disorders: A prospective study. Journal of Consulting and Clinical Psychology. 2000; 68(5):818. [PubMed: 11068968]

10. Caspi A, Roberts BW, Shiner RL. Personality development: Stability and change. Annual Review of Psychology. 2005; 56:453–484

11. Moos RH. Active ingredients of substance use focused self help groups. Addiction. 2008; 103(3):387–396. [PubMed: 18269361]

12. White WL. Commentary on Kelly et al. (2010): Alcoholics Anonymous, alcoholism recovery, global health and quality of life. Addiction. 2010; 205:637–638. [PubMed: 20403015]

13. Kelly JF, et al. Mechanisms of behavior change in alcoholics anonymous: does Alcoholics Anonymous lead to better alcohol use outcomes by reducing depression symptoms? Addiction. 105(4):626–636. [PubMed: 20102345]

14. KELLY JF, et al. Negative Affect, Relapse, and Alcoholics Anonymous (AA): Does AA Work by Reducing Anger? Journal of studies on alcohol and drugs.

15. Krueger RF, et al. Personality traits are linked to crime among men and women: Evidence from a birth cohort. Journal of abnormal psychology. 1994; 103(2):328. [PubMed: 8040502]

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Why erase addiction memories when they can help others?

Posted on by alcoholicsguide

According to one UK newspaper The Independent, dated the 9th July 2014 “Substance abusers could have their memories of drug addiction wiped in a bid to stop them using illegal narcotics, an award-winning neuroscientist has said.

According to new research by Cambridge University’s Professor Barry Everitt: disrupting the memory pathways of drug users could weaken powerful “compel” cravings, reduce “drug seeking behaviour” and open a new field of addiction therapy.

Professor Everitt  told this week’s Federation of European Neuroscience Societies (FENS) how his research in rodents had found that targeting “memory plasticity” in rats was able to reduce the impact of maladaptive drug memories.

He added that this knowledge could offer a radical new method of treatment of drug addiction in humans, where researchers have already established that the path to addiction operates by shifting behavioural control from one area of the brain to another. This process sees drug use go from a voluntary act to a goal directed one, before finally becoming an compulsive act.

It was this process that Professor Everitt’s research is trying to “prevent” by targeting “maladaptive drug-related memories” to “prevent them from triggering drug-taking and replaces”.

In humans this could potentially be done by blocking brain chemicals.

“It’s the emotional intrusiveness of drug and fear memoirs that can be diminished, rather than an individual’s episodic memory that they did in the past take drugs or had a traumatic experience,” he told The Independent. “Conscious remembering is intact after consolidation blockade, but the emotional arousal [that] leads to drug seeking or distressing feelings of fear that are diminished.”

His research group discovered that when drug memories are reactivated by retrieval in the brain, they enter a pliable and unstable state. By putting rats in this state Professor Everitt was able to prevent memory reconsolidation by blocking brain chemicals or inactivating key genes.

In one study, the team diminished drug seeking behaviours by obstructing a brain chemical receptor linked to learning and memory, thus erasing memories, while in another study it found they could weaken drug use memories by altering a particular gene in the amygdala, a brain area processing emotional memory.

“Of course, inactivating genes in the brain is not feasible in humans,” the professor told FENS. “So we’re directing our research to better identify the underlying brain mechanisms of memory reconsolidation.”

He added: “We specifically examined how we could target these maladaptive drug-related memories, and prevent them from triggering drug-taking and relapse.”

So to recap, this new treatment is based on altering genes in rats!

There is no need to actually wipe an alcoholics’ addiction memories.

In fact it may be very counter productive to recovery from alcoholism. One 80 year old and hyper ecologically valid experiment into the mnemonics of “treating addiction memories”  has shown that by honestly looking at the consequences of one’s actions as the result of one’s alcoholic drinking that the positive associations of previous drinking were reappraised in light of the damage done to oneself, one’s loved ones and family and society at large.

Addiction memories via this profound reappraisal were then more accurately processed in long term explicit memory. Implicit schematic memory was also altered fro a self schema in which one is a drinking alcoholic to one in which one is a recovering alcoholic.

So-called positive associations in long term episodic and explicit memory were,  when labile via recall, then challenged and replaced by more accurate negative associations in long term memory – no memories needed to be erased just reappraised more accurately.

 

mad scientist

 

This type of ongoing experiment is happening on a daily basis at an AA meeting near you.

AA groups have found that memories need not be erased, with possible deleterious knock on effects on fear processing and amgydaloid performance, but rather memories simply need to be faced up to, and via honesty appraisal reprocessed more adaptively in long term memory.

This also means alcoholics in recovery can use their addiction memories in not only clearing away the wreckage of the past, repairing broken relationships with loved ones and society as a whole by  making amends to those involved in this wreckage and also put the memories of the past to excellent therapeutic use by using it to help others with similar memory difficulties.

In fact even academic researchers have found and have demonstrated that abstinent, treatment seeking individuals also have a different cognitive or/and memory bias to active alcoholics. This has been illustrated in findings that the greater “accessibility” for positive vs. negative alcohol- associations in heavy vs. light drinkers was not found to be generalized to alcoholics in treatment vs. social drinkers (2). Rather, there was a trend for treated inpatients, motivated to attain abstinence, to show greater availability and accessibility for negative alcohol-related information.

This is how to use memories of addiction to the best possible use, instead of erasing them, wiping them our and hoping for the best, memories of our addiction can be used to great purpose in helping others. Also “addiction memory” is often activated by those who have not come to terms with their alcoholism and still want to drink. Unless some one has come to terms with their alcoholism little can be done, by erasing memories or otherwise. These are sticking plasters on a gaping wound. They will be replaced with other “addiction memory” as there an underlying condition to alcoholism ( we believe it to be emotional regulation and processing deficits) and it is this that drives this fear-based condition called alcoholism, memories are the result of this malady. Address the underlying conditions and the rest takes care of itself.

It is not brain regions which are the problem either such as activation of the amgydala, it is how this sometimes errant and overactive brain region in alcoholics is tamed via the serenity found in the AA program of recovery.

The compel parts of the brain, Everitt mentions,  are activated by emotional distress, so treat the distress not the symptom of it. He also confuses implicit, automatic memory, with explicit, conscious memory. Either way they are both activated by stress/distress, and are thus both emotional memories.  Again treat the emotional dysregulation, the primary problem not the secondary manifestation of the problem.

As I mentioned above, there has been an ongoing experiment into recovery from alcoholism going on for nearly 80 years now, there is a lab in most areas of town.

It would benefit the world and science, in particular, if neuroscientists would pop in for a coffee and check our our findings.

 

References

2. McCusker CG  Cognitive biases and addiction: an evolution in theory and method. Addiction 2001;96:47–56.

 

Why a spiritual solution?

Posted on by alcoholicsguide

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

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

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

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

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

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

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

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

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

 

10350601_792571304116059_8113905016770358871_n

 

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

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

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

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

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

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

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

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

images (15)

 

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

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

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

“His defence must come from a Higher Power”

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

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

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

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

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

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

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

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

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

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

 

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

Posted on by alcoholicsguide

 

 

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

by alcoholicsguide

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

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

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

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

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

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

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

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

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

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

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

 

12 steps pic

 

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

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

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

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

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

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

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

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

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

images (3)

 

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

Some references to follow.