ventromedial prefrontal cortex

Alcoholics Anonymous and Reduced Impulsivity: A Novel Mechanism of Change

Impulsivity or lack of behaviour inhibition, especially when distressed, is one psychological mechanisms which is implicated in all addictive behaviour from substance addiction to behaviour addiction.

It is, in my view, linked to the impaired emotion processing as I have elucidated upon in various blogs on this site.

This impulsivity is present for example in those vulnerable to later alcoholism, i.e. sons and daughters of alcoholic parents or children  from a family that has a relatively high or concentrated density of alcoholics in the family history, right through to old timers, people who have decades of recovery from alcoholism.

It is an ever present and as a result part of a pathomechanism of alcoholism, that is it is fundamental to driving alcoholism to it’s chronic endpoint.

It partly drives addiction via it’s impact on decision making – research shows people of varying addictive behaviours choose now over later, even if it is a smaller short term gain over a greater long term gain. We seem to react to relieve a distress signal in the brain rather than in response to considering and evaluating the long term consequences of a decision or act.

No doubt this improves in recovery as it has with me. Nonetheless, this tendency for rash action with limited consideration of long term consequence is clearly a part of the addictive profile. Not only do we choose now over then, we appear to have an intolerance of uncertainty, which means we have difficulties coping with uncertain outcomes. In other words we struggle with things in the future particularly if they are worrying or concerning things, like a day in court etc. The future can continually intrude into the present. A thought becomes a near certain action, again similar to the though-action fusion of obsessive compulsive disorder. It is as if the thought and possible future action are almost fused, as if they are happening in unison.

Although simple, less worrying events can also make me struggle with leaving the future to the future instead of endless and fruitlessly ruminating about it in the now. In early recovery  especially I found that I had real difficulty dealing with the uncertainty of future events and always thought they would turn out bad. It is akin to catastrophic thinking.

If a thought of a drink entered into my head it was so distressing, almost as if I was being dragged by some invisible magnet to the nearest bar. It was horrendous. Fortunately I created my own thought action fusion to oppose this.

Any time I felt this distressing lure of the bar like some unavoidable siren call of alcohol I would turn that thought into the action of ringing my sponsor. This is why sponsees should ring sponsors about whatever, whenever in order to habitualize these responses to counteract the automatic responses of the addicted brain.

I think it is again based on an inherent emotion dysregulation. Obsessive thoughts are linked to emotion dysregulation.

My emotions can still sometimes control me and not the other way around.

Apparently we need to recruit the frontal part of the brain to regulate these emotions and this is the area most damaged by chronic alcohol consumption.

As a result we find it difficult to recruit this brain area which not only helps regulate emotion but is instrumental in making reflective, evaluative decisions about future, more long term consequence. As a result addicts of all types appear to use a “bottom up” sub-cortical part of the brain centred on the amgydala region to make responses to decisions instead of a “top down” more cortical part of the brain to make evaluative decisions.

We thus react, and rashly act to relieve the distress of undifferentiated emotions, the result of unprocessed emotion rather than using processed emotions to recruit the more cortical parts of the brain.

Who would have though emotions were so instrumental in us making decisions? Two parts of the brain that hold emotions in check so that they can be used to serve goal directed behaviour are the orbitofrontal cortex and the ventromedial prefrontal cortex.

120px-Orbital_gyrus_animation_small2

 

These areas also keep amgydaloid responding in check. Unfortunately these two areas are impaired in alcoholics and other addictive behaviours so their influence on and regulation of the amgydala is also impaired.

This means the sub cortical areas of the amgydala and related regions are over active and prompt not a goal directed response to decision making but a “fight or flight” response to alleviate distress and not facilitate goal directed behaviour.

128px-Amyg

 

Sorry for so much detail. I have read so much about medication recently which does this or that to reduce craving or to control  drinking but what about the underlying conditions of alcoholism and addictive behaviour? These are rarely mentioned or considered at all.

 

We always in recovery have to deal with alcoholism not just it’s symptomatic manifestation of that which is chronic alcohol consumption. This is a relatively simple point and observation that somehow alludes academics, researchers and so-called commentators on this fascinating subject.

Anyway that is some background to this study which demonstrates that long term AA membership can reduce this impulsivity and perhaps adds validity to the above arguments that improved behaviour inhibition and reducing impulsivity is a very possible mechanism of change brought about by AA membership and the 12 step recovery program.

It shows how we can learn about a pathology from the recovery from it!

Indeed when one looks back at one’s step 4 and 5 how many times was this distress based impulsivity the real reason for “stepping on the toes of others” and for their retaliation?

Were we not partly dominated by the world because we could not keep ourselves in check? Didn’t all our decisions get us to AA because they were inherently based on a decision making weakness? Isn’t this why it is always useful to have a sponsor, someone to discuss possible decisions with?

Weren’t we out of control, regardless of alcohol or substance or behaviour addiction? Isn’t this at the heart of our unmanageability?

I think we can all see how we still are effected by a tendency not to think things through and to act rashly.

The trouble it has caused is quite staggeringly really?

Again we cite a study (1) which has Rudolf H. Moos as a co-author. Moos has authored and co-authored a numbered of fine papers on the effectiveness of AA and is a rationale beacon in a sea of sometimes quite controversial and ignorant studies on AA, and alcoholism in general.

“Abstract

Reduced impulsivity is a novel, yet plausible, mechanism of change associated with the salutary effects of Alcoholics Anonymous (AA). Here, we review our work on links between AA attendance and reduced impulsivity using a 16-year prospective study of men and women with alcohol use disorders (AUD) who were initially untreated for their drinking problems. Across the study period, there were significant mean-level decreases in impulsivity, and longer AA duration was associated with reductions in impulsivity…

Among individuals with alcohol use disorders (AUD), Alcoholics Anonymous (AA) is linked to improved functioning across a number of domains [1, 2]. 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 [3]. To our knowledge, however, there have been no efforts to examine links between AA and reductions in impulsivity-a dimension of personality marked by deficits in self-control and self-regulation, and tendencies to take risks and respond to stimuli with minimal forethought.

In this article, we discuss the conceptual rationale for reduced impulsivity as a mechanism of change associated with AA, review our research on links between AA and reduced impulsivity, and discuss potential implications of the findings for future research on AA and, more broadly, interventions for individuals with AUD.

Impulsivity and related traits of disinhibition are core risk factors for AUD [5, 6]. In cross-sectional research, impulsivity is typically higher among individuals in AUD treatment than among those in the general population [7] and, in prospective studies, impulse control deficits tend to predate the onset of drinking problems [8–11]

Although traditionally viewed as static variables, contemporary research has revealed that traits such as impulsivity can change over time [17]. For example, traits related to impulsivity exhibit significant mean- and individual-level decreases over the lifespan [18], as do symptoms of personality disorders that include impulsivity as an essential feature [21, 22]. Moreover, entry into social roles that press for increased responsibility and self-control predict decreases in impulsivity [16, 23, 24]. Hence, individual levels of impulsivity can be modified by systematic changes in one’s life circumstances [25].

Substance use-focused mutual-help groups 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 [26]. 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.

…the idea of reduced impulsivity as a mechanism of change…it is consistent with contemporary definitions of recovery from substance use disorders that emphasize improved citizenship and global health [31], AA’s vision of recovery as a broad transformation of character [32], and efforts to explore individual differences in emotional and behavioral functioning as potential mechanisms of change (e.g., negative affect [33,34]).

Several findings are notable from our research on associations between AA attendance and reduced impulsivity. First, consistent with the idea of impulsivity as a dynamic construct [18, 19], mean-levels of impulsivity decreased significantly in our AUD sample. Second, consistent with the notion that impulsivity can be modified by contextual factors [25], individuals who participated in AA longer tended to show larger decreases in impulsivity across all assessment intervals.

References

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.

Explaining the negative consequences of Negative Urgency.

Explaining how negative Negative Urgency can be.

from Inside the Alcoholic Brain by alcoholicsguide

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

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

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

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

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

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

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

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

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

Brain Pathways Related to Emotion-Based Action

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

orbitofrontaler_cortex

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

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

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

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

Parasagittal_MRI_of_human_head_in_patient_with_benign_familial_macrocephaly_prior_to_brain_injury_(ANIMATED)

 

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

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

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

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

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

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

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

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

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

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

fig 1.

nihms197465f5 (1)

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

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

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

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

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

References

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

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

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

 

Are Alcoholics Emotionally Immature?

Concerted attempts have been made to relate personality factors to alcohol dependence.

In fact, for many years, research attempted to define the so-called alcoholic personality. Attempts to do so have dwindled in recent years.

Potential alcoholics tend to be emotionally immature, expect a great deal of the world, require an inordinate amount of praise and appreciation, react to failure with marked feelings of hurt and inferiority, have a low frustration tolerance, and feel inadequate and unsure of their abilities to fulfil expected male or female roles.1

Although the obvious emotional immaturity often seen in alcoholics seems to cover a number of the more recent findings on bio-psychologcal aspects a alcoholism.

For example, if we partly defined emotional immaturity as containing some of the following, then we appear to be covering a number of much researched and demonstrated aspects of alcoholism. Do these then not come under an umbrella term of emotional immaturity? This list was complied by Psych Central

Dimensions of Emotional maturity

  1. The ability to modulate emotional responses.  Addicts tend to have an all or nothing emotional response.  When they respond they become overly emotional and take a longer time to return to baseline.  They are easily flooded with emotion to the point of impairing functioning.
  1. The ability to tolerate frustration.  Addicts tend to respond to frustrating situations as disasters rather than having any perspective.
  1. The ability to delay gratification.  Emotionally immature people have trouble planning and working toward goals.  The ability to give up immediate gratification is necessary for anyone to go about life in a successful way.
  1. The ability to control impulses.  The mature self has the ability to see that feeling the urge to do something is not the same as doing it.  The recovering addict has a level of control over his or her behavior and can put boundaries around what is inappropriate to say or do.
  1. The ability to be reliable and accountable.  Addicts are often self centered and not good at dealing with the everyday requirements of life like being on time, fulfilling obligations and telling the truth.  As they gain emotional maturity they gain the ability to get out of themselves and think about the impact of their actions on others and on their own lives as well.

 

 photo-for-emotional-maturity

 

According to a list drawn up by alcoholrehab.com

If people are emotionally immature, they may exhibit some of the following symptoms:

* Such individuals will often find it hard to deal with the normal challenges of life. When they are faced with problems they feel unable to cope. They may have developed a psychological state known as learned helplessness.

They struggle to develop meaningful relationships with other people. They may appear too needy or a bit overbearing.
* Those people who are emotionally immature will tend to have a pessimistic outlook on life. They may see the future as a threatening and hostile place.
* This type of person will usually have low self-esteem. This means that they do not value themselves highly so will be willing to accept very little in life as being all they deserve.
* They find it almost impossible to live in the present moment. They are either reliving the past or worrying about the future.
* They can easily lose their temper at the slightest provocation. When they are dealing with uncomfortable emotions they will tend to take things out on other people.

* People who are emotionally immature can have unrealistically high expectations. This means that they are frequently disappointed. Such and individual can have impossibly high expectations for other people yet low expectations for themselves.
* Such individuals can suffer from severe mood swings. This instability of mood can make life a bit uncomfortable.
* If people are emotionally immature, they find it much harder to control their own behavior.

Recognize any of these symptoms?

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We were completely like this before doing the 12 steps.

We, however, do not think that anyone, alcoholics or otherwise choose to behave in this emotional immature way.

We have already looked at the emotional distress accompanies alcoholism and addiction, and will be examining more in the months ahead and it is difficult not to see the above emotional immaturity as all being products of a distress state.

In the course of addiction the alcoholic in particular grows in emotional distress as the stress and emotional dysregulation associated with addiction increases.

This means the brain “collapses” from more cortical, goal-directed (and emotionally regulated) areas of the brain to more sub-cortical areas which are more automatic, unthinking and compulsive.

Emotional distress activates these areas of habit-like compulsive behaviour, acting as a stimulus response, distress the stimulus and compulsive (unthinking)  responding as the response.

This is like a distress based or “fight or flight” reality or a heightened emotional state or “emergency” state. It seems to us that alcoholics live in this region more than cortical regions. They are primed to go off!

They then have a tendency to either run away from situations or to fight “everybody and everything”, to be intolerant of uncertainty, to catastrophize, to be fear-based people to be over reactive, hypervigilant, perfectionist etc These are all distress based states.

Are aspects of the  apparent emotional immaturity mentioned above not also not  a surface manifestation of these deep subcortical processes?

It is this state of heightened uncertainty and fear that whittles away at the alcoholic psyche. This amount of stress/distress promotes implicit, do, memory, over explicit, reflective, evaluative, memory. Distress makes one act without much thought of consequence, it makes one choose short term over greater long term gain, it makes one want to act impulsively or compulsively to alleviate distress. It is this distress that is in charge of action and emotional behaviour. It calls the shots.  A state of emergency has been called in the brain of the alcoholic.

I know it is widely shared at AA meetings that we got stuck in the emotional age of our first drink, in the early teens and never developed our emotional selves or capacity to regulate and process emotions. We are not sure this is completely true as the stress that accompanies alcoholism, as alcohol is literally classified as a pharmacological stressor,  not only causes chronic stress dysregulation but also the emotional dysregulation which accompanies this. It is emotional parts of the brain and the cortical areas that are supposed to keep them in check that are most impaired via chronic alcoholism.

Dr. Stephanie Brown (2) has explored these developmental changes in cognition, which lead to “alcoholic thinking.” She states that these changes refer “not only to rationalization, denial and frame of mind, but also to character traits that frequently accompany drinking. These include grandiosity, omnipotence and low frustration tolerance.” (3) These traits appear to be directly associated with the addictive process rather than with the individual’s personality prior to establishing this abusive cycle.

As alcohol becomes more dominant, the need to deny these changes becomes greater. It appears that there is an interaction between physiological changes and psychological defenses which creates emotional immaturity, self-centeredness and irresponsibility. Alcoholism becomes a thought disorder as well as an addiction to alcohol.

This is the consequence we believe of prefrontal atrophy and subcortical hypertrophy caused by chronic alcohol consumption, a constant injection a pharmacological stressor into the brain, wrecking the ability to maturely deliberate and instead rely on “I want it now!”  type of thinking.

We firmly believe this progression is to a state of constant distress signal in the brain and a cortical hyperarousal.

The alcoholic may not be emotionally distressed all the time but his brain is never satisfied, it constantly needs more, it finds only transient balance, via allostasis, it never finds true balance, i.e. homeostasis. it is always seeking, never reaching satiety, never completely at rest. This is emotionally exhausting.

It may represent, on superficial observation to some, the “emotional immaturity, self-centeredness and irresponsibility” (4) but is it really this simple, seeing these as the primary defenses and interpersonal style typical of normal development in the first three years of life or to characterize the addictive part of self as a “two-year-old child”?

Isn’t it more apt to say instead of  a “two-year-old wounded part of self begins to “drive the bus” and create havoc for all concerned” to say chronic stress manifest  as emotional distress “driving the bus”?

Thus a valid question remains for us and we ask it to our normies or earthling friends (i.e. non-alcoholics), wouldn’t you act in a childish if you were this distressed most of the time, having to rely on impaired emotional regulation and processing parts of the brain?

 

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In fact, to all those normies or earthlings who are reading this blog, how well do you think or consider others when in a state of persistent and daily distress? In this heightened anxiety how good is your action outcome memory, goal-directed planning and awareness of future consequence?

Are you ever moody, emotionally volatile and over reactive in this state of high anxiety? Hyper sensitive? Ever strike out unthinkingly at others although you had not intended to? Leading to guilt and shame, and remorse and self pity which can in the fullest of time lead to depression? This is called a transient emotional dysregulation, distress leading to an emotional cascade. This is the brain of an alcoholic all the time. It can lead to dejection and relapse.

In this sate of nauseating anxiety, how well do you consider the consequence, negative or otherwise, or your fear-based decision making?  Do you choose the short term answer in these anxiety-filled moments just to simply relieve this distress this unpleasant feeling of doom? So do alcoholics!

It is not enough to call the alcoholic emotional immature or stuck in the “terrible twos”, although let’s face it the evidence for it is compelling at times!! Let’s instead understand the reasons for it. Would you like to be in a state of distress most of the time? It’s not a whole lot of fun!

The 12 steps help solve these issues, there is a solution to emotional immaturity – it leads to emotional maturity or emotional sobriety which is blogged about here also.

The next time the alcoholic is your life acts in an immature way don’t ask them why they are acting that way, ask them how they feel. instead. Get them to identify, label and process their feelings  by verbalizing them.

When the anxious amgydala has quelled and  it’s feverish responding quietened,  get them to an AA meeting where many tens of thousands of alcoholics are doing the same, “sharing”, processing their emotions by talking about them and how they really feel.

 

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Not running away from them or intellectualizing about them, not fighting them. Simply saying in words how they feel.

It is a miracle awakening for us in recovery, the emotional regulation normies and earthlings take for granted.

The age of miracles is amongst us and it starts by opening your mouth, asking for help, getting help and getting real about what you are really feeling.

It is through sharing our deepest feelings that we start to mature and grow up.

 

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References

1. Chaudhury, S.K. Das, B. Ukil,  Psychological assessment of alcoholism in males Indian J Psychiatry. 2006 Apr-Jun; 48(2): 114–117. doi: 10.4103/0019-5545.31602

2. Brown S. (1985). Treating the Alcoholic: A Developmental Model of Recovery. New York: John Wiley & Sons, Spring.

3. Brown, S. (1988). Treating Adult Children of Alcoholics: A Developmental Perspective. New York: John Wiley and Sons.

4. http://www.cairforyou.com/alchoholdrugs/alcoholcharacter.htm

 

At Risk Adolescents have Emotional Dysregulation?

Following up from our previous blog on the abnormalities in the ventromedial prefrontal cortex  (vmPFC) in alcoholics,  brain regions which govern emotional regulation, we came across another study which appears to show that adolescents at increased risk for later alcohol use disorders (AUDs) may also be showing an emotion regulation difficulty.

This emotional regulation difficulty may be a biomarker for later alcoholism, which is in keeping with our previous proposals that an emotional processing and regulation difficulty or disorder underpins the aetiolgy of of alcoholism. In order words it is part of the pathomechanism – or the mechanism by which a pathological condition occurs- of later alcoholism.

 

 ventromedial-prefrontal-cortex

 

The area in this study, the vmPFC,   showed relatively increased cerebral blood flow (CBF) in bilateral amygdala and vmPFC and relatively decreased CBF in bilateral insula, right dorsal anterior cingulate cortex (ACC) and occipital lobe cuneus of high-risk adolescents. This suggests that adolescents at relatively high-risk for AUD exhibit altered patterns of resting CBF in distributed corticolimbic regions supporting emotional behaviors.

The authors’ hypothesized that the relatively increased amygdala and ventromedial prefrontal CBF may contribute to increased emotional reactivity and sensitivity to environmental stressors in these individuals while diminished insula/occipital cuneus and dorsal anterior cingulate cortex (ACC) CBF may lead to poor integration of visceral and sensory changes accompanying such emotional stress responses and top-down regulation of amygdala reactivity.

Thus we see our model in a snapshot even in adolescents potentially.  The emotional processing deficits we have discussed previously implicate the insula and ACC, as there appears to be a difficulty in alcoholics in reading emotional or somatic signals/states and integrating these signals into the identifying, labelling and processing of emotions. Equally there appears to be a hyperactivty in the vmPFC and amgydala as with alcoholics which implies emotional dysregulation, a hyper reactive emotional response and a tendency perhaps to a more “fight or flight” response, distress based impulsivity and short termist decision making, wanting it NOW rather than later.

 

References Lin, A. L., Glahn, D. C., Hariri, A. R., & Williamson, D. E. (2008). Basal Perfusion in Adolescents at Risk for Alcohol Use Disorders. In Proc. Intl. Soc. Mag. Reson. Med (Vol. 16, p. 60).

Predicting relapse via extent of emotional dysregulation?

Predicting relapse via extent of emotional dysregulation?

by alcoholicsguide

Even the most experienced counselors have difficultly spotting a recovering alcoholic in danger of relapse. Brain imaging scans might do a better job according to a study last year by researchers at  Yale University.

They suggested that alcoholics with abnormal activity in areas of the brain that control emotions and desires (reward) are eight times more likely to relapse and drink heavily than alcoholics with more normal patterns of activity or healthy individuals (1)

“These areas in the prefrontal cortex are involved in regulating emotion and in controlling responses to reward,” said Rajita Sinha, the Foundations Fund Professor of Psychiatry and professor in the Child Study Center and of Department of Neurobiology. “They are damaged by high levels of alcohol and stress and just do not function well.”

Or both perhaps, i.e. chronic alcohol use impacting on already impaired emotional regulation networks in the brain.

 

Figure6_ADHC_revised_2_7_12

 

This graphic highlights areas of the brain where Yale researchers found significant differences in responses to stress and relaxation-inducing stimuli between alcoholics and healthy controls. Alcoholics who exhibited such patterns of activity during fMRI scans were much more likely to relapse than alcoholics that more closely resembled control subjects.

Areas of the brain governing emotional regulation such as the ventromedial prefrontal cortex which suggests chronic difficulties in emotional dysregulation, which  potentiates the reward network, lying adjacent, and promotes higher relapse – click image for study. 

 

Ironically, the damage shows up on fMRI scans when alcoholics imagine being in their own most relaxing scenarios, like sitting at the beach listening to the waves, or taking a bubble bath. In non-alcoholics, these brain regions regulating emotion show markedly reduced activity during relaxing imagery, as anticipated. However, in alcoholics most likely to relapse, those brain regions remain hyperactive. On the other hand, when recovering alcoholics imagine their own recent stressful events, these control regions of the brain show little change, while in non-alcoholics, they show marked activation in response to stress. Such disrupted responses in areas of the brain governing emotions and reward lead to high cravings in the recovering alcoholic and an increased likelihood of subsequent relapse.

These brain scans in the future might serve as a diagnostic test to help professionals identify those most at risk of relapsing and suggest specific interventions to normalize brain function and prevent high rates of alcohol relapse, Sinha said.

“The findings show the prefrontal region is important for maintaining recovery for alcoholism,” Sinha said.

This is in accord with much of our writing in this blog – alcoholics, in recovery or otherwise, appear to have profound difficulties in regulating stress and emotion, as if the hyperactivity in the ventromedial pefrontal cortex, seen here, is indicative of a brain that never emotionally shuts off, is always on the go (whether this is the consequence of allostasis, the continual readjustment of the brain to stress needs to be further explored) and is primed to relapse effectively via a “fight of flight mechanism, or a distress based impulsivity.

 

References

Dongju Seo; R Todd Constable; Kwang-Ik Hong; Cheryl Lacadie; Keri Tuit; Rajita Sinha
Disrupted ventromedial prefrontal function, alcohol craving, and subsequent relapse risk.
JAMA psychiatry (Chicago, Ill.) 2013;70(7):727-39.

 

The Distress at the Heart of Addiction and Alcoholism

This blog is written for alcoholics and those who love and live with them, by alcoholics in recovery. For those who know what it is like to live with alcoholism but would also like to know why alcoholism affects the alcoholic and those around him in the way it does.

We write this blog to help us and you understand how the alcoholic brain works; why they do the things the do, why they act the way they do. Why is it everything is going great and suddenly the alcoholic in your life “flies off the handle’ and acts in an emotionally immature way, which can often cause hurt to others around them? What is the reason behind this “Jekyll and Hide” emotional responding?

Why do they suddenly cut off their emotions so profoundly it leaves your emotions in limbo, confused and upset?

In this blog we seek to explain, as researchers,  in terms of the processes of the brain, why alcoholics, particularly  those in recovery, do the things the way they do, act the way they do.

We hope to explain this disease state, which alcoholics themselves call a “emotional disease’, a “cancer of the emotions’, a “parasite that feeds on the emotions” or quite simply  “a fear based illness”. It appears that alcoholics in recovery are aware to a large extent of what they suffer from. But why do they do what they do sometimes if they know what is going on? Why do they not seem to be able to help themselves from engaging in certain responses and behaviours?

Why do they endless engage in self defeating resentments,  taking “other peoples’ inventory” or criticizing, why do they project into future scenarios and then get emotionally paralyzed by doing so, why do they run through the list of cognitive distortions on a daily basis, why do they get self absorbed and engage in “me, me, me” behaviour!? Why do they indulge in self pity to the extent they end up in full blown depression?

More importantly, perhaps, how do various therapeutic strategies deal with these behaviours and seek to challenge and address them? And do these therapies, in time through practice and the neuroplasticity (neural reshaping of the brain via behaviour) change how they act, feel and live in this life. In short, how does recovery change the brains of alcoholics for the better?

As we are personally well aware, self knowledge does not bring recovery – only action does. But this action can be based solidly on a better understanding of what goes on in the brain of an alcoholic for example, why should I mediate? What beneficial, adaptive change will that bring, how will that “help me recover”? What is the point of doing the steps, how exactly do they effect change in one’s alcoholic brain? Is there a good healthy neurobiological reason for going to mutual aid group meetings like AA or  SMART?

We also believe that academic research definitions of alcoholism are inadequate – the latest DSM V  equates the emotional difficulties we highlight here as ‘co-morbidities’,  conditions that occur alongside the condition of alcoholism. We disagree, we suggest these ‘co-morbidities’ (co-occurring psychiatric disorders) are a main reason why we become alcoholics, they are what make us vulnerable, along with genes and environment to becoming alcoholic.

Most alcoholics feel they never fitted in, were emotionally hyper “sensitive”,  engaged in risky behaviours, got into trouble without intending to, and other impulsive behaviours which we believe are illustrative of an emotional dysregulation which makes certain individuals vulnerable to becoming alcoholic.

Science tells us there are many such vulnerabilities in children of alcoholics. The alcohol regulated, medicated these errant emotions which caused such distress, even at an early age. It is these emotional processing deficits and emotional dysregualtion (i.e. poor control of emotions, especially when distressed!) which lie at the heart of the this psychopathology or if you like  this psychiatric disorder called alcoholism.

It is a distress-based condition, day in day out, and we formally believe that various therapeutic regimes like the 12 steps, DBT, ACT or CBT, etc all treat this inherent distress state in some way. It is this distress state that activates this “fear-based illness”, that makes one hyper aware of cues, alcohol, it is this distress that provokes memories of drinking, alcohol use schemata, that trains one attention on people places and things from the past. Without this distress our illness barely gets activated! 

For example, does your loved alcoholic, “over do things”on a regular basis, do they engage in short term thinking, or “quick fix ” thinking. Do they resist your attempts at sensible long term , goal directed, “thought through thinking”?

Does your alcoholic work himself to a frazzle, do they easily become exhausted by overdoing it, whatever it is? Do they have a series of new addictions? Are they perfectionist doing too much, or nothing anything at all? Perfectionism is distress based.

Does your alcoholic fear the future, but continually project their thinking into the future? Do they have an intolerance of uncertainty, do they endless ruminate about things, do they react rather than act? Do the most simple decisions provoke a “fight or flight” response? Do they frequently come up with “I know how to do this, I have a great idea!” Only for it to be the opposite of a great idea! Do they give people “rent free room in their heads” because of resentments – replying the same old tape in their minds, over and over and over again? All distress based?

“Fear based” is distress based.

A recent study showed that alcoholics have a part of the brain that helps process emotions but it doesn’t work properly so is overactive all the time; it is exhausting being on red alert, all the time , living on a state of emergency. Hence step 11 in the the 12 steps.

The problem with this hyperactive brain region, called the ventromedial prefrontal cortex, is that it  also cuts out , hypo-activates, when more or excessive stress is applied and another compulsive area of the brain, the basal ganglia, takes over. This part is automatic, habitualized, automatic, compulsive! It results in more more more, and is driven by distress not goal directed consideration. It simple does, does, does, without consideration of future consequence.    Sound familiar??

How did your loved alcoholic get to be this way? What happened to your own alcoholic brain? We believe there is a vulnerability to these aforementioned  emotional difficulties as certain brain areas which regulate emotion not working properly. This means they are smaller, impaired and do not function optimally or are not  connected properly.

Do you know an alcoholic who does not accurately know how he is feeling properly, does not know what emotion he is experiencing? Cannot label to emotion properly which makes processing of it difficult? Can’t rely on a neural feedback to tell himself when  he is tired, angry, hungry  and that he should HALT? This is the insular cortex not working properly.

Does your alcoholic see error everywhere (and worse still give a running commentary on it!?), always whinging about that not being right, or that being wrong. Why can’t they do things properly, be more perfect!! That is partly to do with impairment of the anterior cingulate cortex which monitors error in the environment.

This fear based stuff? That is a hyperactive amgydala, the “anxious amgydala”, and it also acts as a switch between memory systems, from explicit to implicit memory, and recruits the compulsive “go,go, go” area of the dorsal striatum from the always “on the go”, hyperactive, ventromedial cortex.

The amgydala is at the heart of alcoholism and addiction. It not only switches memory but also reward/motivation/ and emotional response so that distress provokes a habitualised “fight or flight response” in the dorsal striatum.

It is said that alcoholics are emotional thinkers, but this region is also an emotional “do” area which means emotional distress acts as a stimulus response. The brain responds to the stimulus of distress in other words. As addiction and alcoholism progress the ways addicts and alcoholics react  become limited in line with addiction severity. The further the alcoholic gets in alcoholism the more he will react out of distress, the more automatic his behaviours become, the more short term his decision making will be, the more he has to fight automatic urges and automatic drink-related thoughts, the more he has to contend with “fight or flight” thinking and feeling.

Add to this a brain that is out of balance, does not have homeostasis, natural neurochemical balance, but has a state called  allostasis, where the brain constantly attempts to finding stability via constant change, and the fact that the alcoholic brain has too much Glutamate,  an excitatory neurotransmitter, the “go neurochemical”, and not enough GABA,  an inhibitory  neurotransmitter, the brains’ natural brakes”, (and which is increased by drinking alcohol) the stop or slow down chemical and  that this also helps slow down an abnormal heart rate variability (HRV) found in alcoholics.

Alcoholics have a different heart rate variability meaning we have a heart rate more suited to being ready for the next (imagined) emergency.  The effects of alcohol are thus more profound on this group, and this HRV is also seen in children of alcoholics so represents a profound vulnerability to later alcoholism.

Add to that depleted levels of of  dopamine, which is very important in the addiction cycle. The problem with dopamine supplies is that our excessive levels of stress reduce our amount of dopamine,  that we are always on the look out for more dopamine. Add to this that stressful states increase our brain in “dopamine seeking” in an attempt at transient allostasis and you have a brain that is always trying to get a buzz out of something, especially when in distress states.

Then there is other deficits to the serotonin system, to the natural opioids  system, to oxytocin, all of which take a beating and are reduced by excessive stress systems. But all are increased via love and looking out for our fellow man, our families, loved ones and other’s in recovery. We can manipulate our brain chemistries, this is what happens in recovery in fact!

Too much stress on the brain spreads like a forest fire throughout the brain, lowering levels of  essential neurotransmitters,  impairing memory and turning one from a goal directed action to a compulsive reaction type of guy. The alcoholic brain is always primed to go off!!

Chronic stress also impairs the prefrontal cortex, the cognitive, conscious “top down” controller of the brain’s emotions and urges, instincts and so on. It doesn’t help that it doesn’t work too well in alcoholics. The brain of an alcoholic is a “spillover” brain, it is a brain that spills over into various types of disinhibition,  impulsivity and compulsivity . It often acts before considering, speaks before thinking. decides this is a great idea with out consulting, reacts without sufficient reason or cause.

It needs help, this alcoholic brain. From another brain, from someone other than himself.

Recovering alcoholics need an external prefrontal cortex to help with the top down cognitive control of the subcortical emotional and motivational states. The problem with emotions are they, in the alcoholic brain, have become entwined with reward. We feel a certain way, negative for example, and fix this negative feeling, with something rewarding, makes us feel better, more positive, less self reflective,  and it seems this has been the case with certain alcoholics since childhood. Dealing with emotions by the granting of treats.

Feeling better by consuming. Fixing feelings via external substances. Sub contracting our emotional regulation.  Finding different feelings in a bottle, or a pill, or a syringe or snorting them up one’s nose. Alcoholics need a spiritual awakening,  a psychic change, a change in consciousness, in self schema;  this sudden change in how we feel about the world (including memories of our past life) because the old feeling about the world will lead to the sane old behaviours. Plus alcohol and drugs were  crude approximates of this change in consciousness, this  spirit awakenings, they dramatically and very instantaneously helped change our feelings, thoughts, perceptions about the world around us. They helped us fit in.

This is the purpose of a spiritual awakening too, a sudden change of consciousness. We believe the best and most sudden way to achieve this is to let go of the thing that causes all the suffering in the first place, the self. It appears we can live without the “self” . It also appears helping others brings a bigger buzz than even helping ourselves.

Helping others reduces our distress. and many many other therapeutic benefits to brain chemistry. This brain also needs some one outside of self, outside the self regulation network in the brain which is so impaired and cannot be relied on because at times it is maladaptive. Can’t be counted on the make the right decision because it favours  short term over the long term, is based on “fight or flight “thinking and rational, hence is distorted by fear.

If we have been thinking in this maladaptive way all our lives it  is no wonder we ended up where we have. We used alcohol to deal with our errant and quite frightening emotions. I positively ran away from my own emotions.

I used to say to my wife, the main reason for my drinking is “to get away from my self”. Now we have to find a solution to living with oneself, these sometimes torturous alien state of emotional sobriety.

I remember being asked by a counsellor to sit with my emotions for half on a hour. I felt I was being possessed by some poltergeist,  the feelings associated with emotional regulation were so alien to me, so frightening. I didn’t know what they were even. I had to have by wife label them for me and help me process them.

I believe steps 4 and  of 12 step programs help one emotional regulation hundreds  and hundreds of unresolved, unprocessed emotions from the past otherwise they will continue to be in there, haunting us like “neural ghosts” from the past, adding emotional distress to our conscious daily experience and encouraging relapse.  This is the case for many newly recovering alcoholics.  Being haunted by a million thoughts produced by  rampant emotional dysregulation.

Resentments swirling around the mind and driving the newcomer back to relapse. What the newcomer finds is that the drink stops working, and the emotional difficulties remain, in fact much worsened by years and years of sticking a neurotoxin down our throats and in into our brains. Havoc is then further reaped on an already not fully functioning  brain.

In AA they often they say that they are stuck at the emotional age of when they started drinking which is usually around the early teens when the cognitive part of the brain that controls emotions is still developing.  But we act much more immaturely than that, we act like the terrible twos or children. Our emotional brains never really grew up. This emotional dysregulation apparent as teens then shaped all our future decisions and eventually our alcoholism. That is what they mean in AA, when they say all your best thinking got you here. So there you have it . Sound familiar? Recognize anyone here?